Produced in response to hyperglycaemia Released by beta

Which of the following statements is true of glucagon?

Produced in response to hyperglycaemia

Released by beta cells

Inhibits gluconeogenesis

Produced in response to an increase of amino acids

Composed of 2 alpha polypeptide chains linked by hydrogen bonds

Glucagon is a protein comprised of a single polypeptide chain. Produced by alpha cells of pancreatic islets of Langerhans in response to hypoglycaemia and amino acids. It increases plasma glucose and ketones. Please rate this question:

Discuss and give feedback

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Glucagon

Glucagon, the hormonal antagonist to insulin, is released from the alpha cells of the Islets of Langerhans in the pancreas. It will result in an increased plasma glucose level.

Stimulation Inhibition

Decreased plasma glucose Somatostatin

Increased catecholamines Insulin

Increased plasma amino acids

Increased free fatty acids and keto acids

http://emrcs.com/question/question.php?q=0#left-panel

Sympathetic nervous system Increased urea

Acetylcholine

Cholecystokinin

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A 28 year old man undergoes a completion right hemicolectomy for treatment of a 5cm appendiceal

carcinoid. As part of his follow up he is due to undergo 24 hour urine collection for 5-HIAA. Which of

the following causes an elevated 5-HIAA in a 24-hour urine collection?

Naproxen

Oranges

Flucloxacillin

Amiodarone

Beef

It is important to be aware of what can falsely elevate 5-HIAA to avoid diagnosing carcinoid

syndrome incorrectly. These include:

Food: spinach, cheese, wine, caffeine, tomatoes

Drugs: Naproxen, Monoamine oxidase inhibitors

Recent surgery

Please rate this question:


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Carcinoid syndrome

Carcinoid tumours secrete serotonin Originate in neuroendocrine cells mainly in the intestine (midgut-distal ileum/appendix)

Can occur in the rectum, bronchi Hormonal symptoms mainly occur when disease spreads outside the bowel


Clinical features

Onset: insidious over many years Flushing face Palpitations Pulmonary valve stenosis and tricuspid regurgitation causing dyspnoea

Asthma Severe diarrhoea (secretory, persists despite fasting)

Investigation

5-HIAA in a 24-hour urine collection Somatostatin receptor scintigraphy CT scan

Blood testing for chromogranin A

Treatment

Octreotide Surgical removal

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A 52 year old man develops septic shock following a Hartmans procedure for perforated diverticular disease. He is started on an adrenaline infusion. Which of the following is least likely to occur?

Peripheral vasoconstriction

Coronary artery vasospasm

Gluconeogenesis

Lipolysis

Tachycardia

It's cardiac effects are mediated via β 1 receptors. The coronary arteries which have β 2 receptors are unaffected. Please rate this question:


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Adrenaline

Fight or Flight response

- Catecholamine (phenylalanine and tyrosine) - Neurotransmitter and hormone - Released by the adrenal glands - Effects on α 1 and 2, β 1 and 2 receptors - Effect on β 2 receptors in skeletal muscle vessels-causing vasodilation - Increase cardiac output and total peripheral resistance - Vasoconstriction in the skin and kidneys causing a narrow pulse pressure Actions

α adrenergic receptors:

Inhibits insulin secretion by the pancreas

Stimulates glycogenolysis in the liver and muscle Stimulates glycolysis in muscle


β adrenergic receptors:

Stimulates glucagon secretion in the pancreas Stimulates ACTH

Stimulates lipolysis by adipose tissue

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Intra cranial pressure is governed by the principles of the Monroe-Kellie doctrine. To which of the following does this concept not apply?

A 2 month old child

A 2 year old child

A 5 year old child

A 10 year old child

An adult

The Monroe-Kelly Doctrine assumes that the cranial cavity is a rigid box. In children with non fused fontanells this is not the case. Please rate this question:


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Applied neurophysiology

Pressure within the cranium is governed by the Monroe-Kelly doctrine. This considers the skull as a closed box. Increases in mass can be accommodated by loss of CSF. Once a critical point is reached (usually 100- 120ml of CSF lost) there can be no further compensation and ICP rises sharply. The next step is that pressure will begin to equate with MAP and neuronal death will occur. Herniation will also accompany this process.

The CNS can autoregulate its own blood supply. Vaso constriction and dilatation of the cerebral blood vessels is the primary method by which this occurs. Extremes of blood pressure can exceed this capacity resulting in risk of stroke. Other metabolic factors such as hypercapnia will also cause vasodilation, which is of importance in ventilating head injured patients.

The brain can only metabolise glucose, when glucose levels fall, consciousness will be impaired.

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Which of the following is not caused by cortisol in the stress response?

Anti-inflammatory effects

Hypoglycaemia

Skeletal muscle protein breakdown

Stimulation of lipolysis

Mineralocorticoid effects

An 'anti insulin' effect occurs leading to hyperglycaemia. Please rate this question:


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Stress response: Endocrine and metabolic changes

Surgery precipitates hormonal and metabolic changes causing the stress response. Stress response is associated with: substrate mobilization, muscle protein loss, sodium and

water retention, suppression of anabolic hormone secretion, activation of the sympathetic nervous system, immunological and haematological changes.

The hypothalamic-pituitary axis and the sympathetic nervous systems are activated and there is a failure of the normal feedback mechanisms of control of hormone secretion.

A summary of the hormonal changes associated with the stress response:

Increased Decreased No Change

Growth hormone Insulin Thyroid stimulating hormone

Cortisol Testosterone Luteinizing hormone



Renin Oestrogen Follicle stimulating hormone

Adrenocorticotrophic hormone (ACTH)

Aldosterone

Prolactin

Antidiuretic hormone

Glucagon

Sympathetic nervous system

Stimulates catecholamine release

Causes tachycardia and hypertension

Pituitary gland

ACTH and growth hormone (GH) is stimulated by hypothalamic releasing factors, corticotrophin releasing factor (CRF) and somatotrophin (or growth hormone releasing factor)

Perioperative increased prolactin secretion occurs by release of inhibitory control Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH) and follicle

stimulating hormone (FSH) does not change significantly

ACTH stimulates cortisol production within a few minutes of the start of surgery. More ACTH is produced than needed to produce a maximum adrenocortical response.

Cortisol

Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).

The usual negative feedback mechanism fails and concentrations of ACTH and cortisol remain persistently increased.

The magnitude and duration of the increase correlate with the severity of stress and the response is not abolished by the administration of corticosteroids.

The metabolic effects of cortisol are enhanced:

Skeletal muscle protein breakdown to provide gluconeogenic precursors and amino acids for protein synthesis in the liver Stimulation of lipolysis 'Anti-insulin effect' Mineralocorticoid effects Anti-inflammatory effects Growth hormone

Increased secretion after surgery has a minor role Most important for preventing muscle protein breakdown and promote tissue repair by insulin

growth factors

Alpha Endorphin

Increased


An important vasopressor and enhances haemostasis Renin is released causing the conversion of angiotensinogen to angiotensin I Angiotensin II formed by ACE on angiotensin 1, which causes the secretion of aldosterone

from the adrenal cortex. This increases sodium reabsorption at the distal convoluted tubule

Insulin

Release inhibited by stress

Occurs via the inhibition of the beta cells in the pancreas by the α2-adrenergic inhibitory effects of catecholamines

Insulin resistance by target cells occurs later The perioperative period is characterized by a state of functional insulin deficiency

Thyroxine (T4) and tri-iodothyronine (T3)

Circulating concentrations are inversely correlated with sympathetic activity and after surgery there is a reduction in thyroid hormone production, which normalises over a few days.

Metabolic effect of endocrine response Carbohydrate metabolism

Hyperglycaemia is a main feature of the metabolic response to surgery

Due to increase in glucose production and a reduction in glucose utilization Catecholamines and cortisol promote glycogenolysis and gluconeogenesis Initial failure of insulin secretion followed by insulin resistance affects the normal responses The proportion of the hyperglycaemic response reflects the severity of surgery Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism

Initially there is inhibition of protein anabolism, followed later, if the stress response is severe, by enhanced catabolism

The amount of protein degradation is influenced by the type of surgery and also by the nutritional status of the patient

Mainly skeletal muscle protein is affected The amino acids released form acute phase proteins (fibrinogen, C reactive protein,

complement proteins, a2-macroglobulin, amyloid A and ceruloplasmin) and are used for gluconeogenesis

Nutritional support has little effect on preventing catabolism

Lipid metabolism Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency, promotes lipolysis and ketone body production. Salt and water metabolism

ADH causes water retention, concentrated urine, and potassium loss and may continue for 3 to 5 days after surgery

Renin causes sodium and water retention

Cytokines

Glycoproteins Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor

Synthesized by activated macrophages, fibroblasts, endothelial and glial cells in response to tissue injury from surgery or trauma

IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery and increase by the degree of tissue damage Other effects of cytokines include fever, granulocytosis, haemostasis, tissue damage limitation and promotion of healing.

Modifying the response

Opioids suppress hypothalamic and pituitary hormone secretion

At high doses the hormonal response to pelvic and abdominal surgery is abolished. However, such doses prolong recovery and increase the need for postoperative ventilatory support

Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and epinephrine changes, although cytokine responses are unaltered

Cytokine release is reduced in less invasive surgery Nutrition prevents the adverse effects of the stress response. Enteral feeding improves

recovery

Growth hormone and anabolic steroids may improve outcome Normothermia decreases the metabolic response

References Deborah Burton, Grainne Nicholson, and George Hall Endocrine and metabolic response to surgery . Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp/mkh040

Next question

Which of the following features does not put a patient at risk of refeeding syndrome?

BMI < 16 kg/m2

Alcohol abuse

Thyrotoxicosis

Chemotherapy

Diuretics

Diuretics increase the risk of re-feeding syndrome through a process of increasing the risk of depletion of key electrolytes. Please rate this question:


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Nutrition - Refeeding syndrome

Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. The metabolic consequences include:

Hypophosphataemia Hypokalaemia

Hypomagnesaemia Abnormal fluid balance

These abnormalities can lead to organ failure. Re-feeding problems If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels High risk for re-feeding problems If one or more of the following:

BMI < 16 kg/m2 Unintentional weight loss >15% over 3-6 months Little nutritional intake > 10 days


Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)

If two or more of the following:

BMI < 18.5 kg/m2

Unintentional weight loss > 10% over 3-6 months Little nutritional intake > 5 days History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and

antacids

Prescription

Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days

Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and supplements

Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)

Next question

Which of the following statements relating to the regulation of renal blood flow is untrue?

In a healthy 70Kg male, the glomerular filtration rate will be the same at a systolic blood

pressure of 120mmHg as a systolic blood pressure of 95 mmHg

Over 90% of the blood supply to the kidney is distributed to the cortex

The kidney receives approximately 25% of the total cardiac output at rest

A decrease in renal perfusion pressure will cause the juxtaglomerular cells to secrete renin

Systolic blood pressures of less than 65mmHg will cause the mesangial cells to secrete

aldosterone

The kidney autoregulates its blood supply over a range of systolic blood pressures. Drop in arterial pressure is sensed by the juxtaglomerular cells and renin is released leading to the activation of the renin-angiontensin system. Mesangial cells are contractile cells that are located in the tubule and have no direct endocrine function. Please rate this question:


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Renal Physiology

Overview

Each nephron is supplied with blood from an afferent arteriole that opens onto the glomerular capillary bed.

Blood then flows to an efferent arteriole, supplying the peritubular capillaries and medullary vasa recta.

The kidney receives up to 25% of resting cardiac output.

Control of blood flow

The kidney is able to autoregulate its blood flow between systolic pressures of 80- 180mmHg so there is little variation in renal blood flow.

This is achieved by myogenic control of arteriolar tone, both sympathetic input and hormonal signals (e.g. renin) are responsible.


Glomerular structure and function

Blood inside the glomerulus has considerable hydrostatic pressure. The basement membrane has pores that will allow free diffusion of smaller solutes, larger

negatively charged molecules such as albumin are unable to cross. The glomerular filtration rate (GFR) is equal to the concentration of a solute in the urine,

times the volume of urine produced per minute, divided by the plasma concentration (assuming that the solute is freely diffused e.g. inulin).

In clinical practice creatinine is used because it is subjected to very little proximal tubular secretion.

Although subject to variability, the typical GFR is 125ml per minute. Glomerular filtration rate = Total volume of plasma per unit time leaving the capillaries and

entering the bowman's capsule

Renal clearance = volume plasma from which a substance is removed per minute by the kidneys

Substances used to measure GFR have the following features: 1. Inert 2. Free filtration from the plasma at the glomerulus (not protein bound) 3. Not absorbed or secreted at the tubules 4. Plasma concentration constant during urine collection Examples: inulin, creatinine GFR = urine concentration (mmol/l) x urine volume (ml/min) -------------------------------------------------------------------------- plasma concentration (mmol/l)

The clearance of a substance is dependent not only on its diffusivity across the basement membrane but also subsequent tubular secretion and / or reabsorption.

So glucose which is freely filtered across the basement membrane is usually reabsorbed from tubules giving a clearance of zero.

Tubular function

Reabsorption and secretion of substances occurs in the tubules.

In the proximal tubule substrates such as glucose, amino acids and phosphate are co-transported with sodium across the semi permeable membrane.

Up to two thirds of filtered water is reabsorbed in the proximal tubules.

This will lead to increase in urea concentration in the distal tubule allowing for its increased diffusion.

Substances to be secreted into the tubules are taken up from the peritubular blood by tubular cells.

Solutes such as paraaminohippuric acid are cleared with a single passage through the kidneys and this is why it is used to measure renal plasma flow. Ions such as calcium and phosphate will have a tubular reabsorption that is influenced by plasma PTH levels.

Potassium may be both secreted and re-absorbed and is co-exchanged with sodium.

Loop of Henle

Approximately 60 litres of water containing 9000mmol sodium enters the descending limb of the loop of Henle in 24 hours.

Loops from the juxtamedullary nephrons run deep into the medulla. The osmolarity of fluid changes and is greatest at the tip of the papilla. The thin ascending limb is impermeable to water, but highly permeable to sodium and

chloride ions.

This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with adjacent interstitial fluid.

In the thick ascending limb the reabsorption of sodium and chloride ions occurs by both facilitated and passive diffusion pathways.

The loops of Henle are co-located with vasa recta, these will have similar solute compositions to the surrounding extracellular fluid so preventing the diffusion and subsequent removal of this hypertonic fluid.

The energy dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this osmotic gradient.

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A 39 year old lady undergoes a laparoscopic cholecystectomy as a daycase. The operation is more difficult than anticipated and the surgeon places a drain to the liver bed. In recovery 1.5 litres of blood is seen to enter the drain. Which of the following substances is the first to be released in this situation?

Angiotensinogen

Renin

Angiotensin I

Angiotensin II

Aldosterone

The decrease in blood pressure will be sensed by the juxtaglomerular cells in the kidney. This will cause renin secretion. Please rate this question:


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Shock

Shock occurs when there is insufficient tissue perfusion. The pathophysiology of shock is an important surgical topic and may be divided into the

following aetiological groups:

Septic Haemorrhagic Neurogenic Cardiogenic Anaphylactic

Septic shock Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure. Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response

Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3, altered mental state


or hyperglycaemia (in absence of diabetes). Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis. Those with organ failure have severe sepsis and those with refractory hypotension -septic shock. During the septic process there is marked activation of the immune system with extensive cytokine

release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those ofexcessive inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for attention:

Prompt administration of antibiotics to cover all likely pathogens coupled with a rigorous search for the source of infection.

Haemodynamic stabilisation. Many patients are hypovolaemic and require aggressive fluid administration. Aim for CVP 8-12 cm H2O, MAP >65mmHg.

Modulation of the septic response. This includes manoeuvres to counteract the changes and includes measures such as tight glycaemic control. The routine use of steroids is not advised.

In surgical patients, the main groups with septic shock include those with anastomotic leaks, abscesses and extensive superficial infections such as necrotising fasciitis. When performing surgery the aim should be to undertake the minimum necessary to restore physiology. These patients do not fare well with prolonged surgery. Definitive surgery can be more safely undertaken when physiology is restored and clotting in particular has been normalised. Haemorrhagic shock The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will equate to 5 litres. This changes in children (8-9% body weight) and is slightly lower in the elderly. The table below outlines the 4 major classes of haemorrhagic shock and their associated physiological sequelae:

Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml

Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased


Respiratory rate 14-20 20-30 30-40 >35

Urine output >30ml 20-30ml 5-15ml <5ml

Symptoms Normal Anxious Confused Lethargic

Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative myocardial ischaemia. The cardiac index gives a numerical value for tissue oxygen delivery and is given by the equation: Cardiac index= Cardiac output/ body surface area. Where Hb is

haemoglobin concentration in blood and SaO2 the saturation and PaO2 the partial pressure of oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not for part A, although you should understand the principle. In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the following may also be the cause or occur concomitantly:

Tension pneumothorax

Spinal cord injury Myocardial contusion Cardiac tamponade

When assessing trauma patients it is worth remembering that in order to generate a palpable femoral pulse an arterial pressure of >65mmHg is required. Once bleeding is controlled and circulating volume normalised the levels of transfusion should be to maintain a Hb of 7-8 in those with no risk factors for tissue hypoxia and Hb 10 for those who have such risk factors. Neurogenic shock This occurs most often following a spinal cord transection, usually at a high level. There is resultant interruption of the autonomic nervous system. The result is either decreased sympathetic

tone or increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance mediated by marked vasodilation. This results in decreased preload and thus decreased cardiac output (Starlings law). There is decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types of shock peripheral vasoconstrictors are used to return vascular tone to normal. Cardiogenic shock In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct

myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal

fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but they are less useful in delineating the extent of myocardial trauma than following MI. When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the heart is the most likely site of injury with chamber and or valve rupture. These patients require surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may require intra aortic balloon pump as a bridge to surgery. Anaphylactic shock Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction. Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated. Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible. The recommended doses for adrenaline, hydrocortisone and chlorpheniramine are as follows:

Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 in 1,000) 25 mg 250 mcg/kg

6 months - 6 years 150 mcg (0.15ml 1 in 1,000) 50 mg 2.5 mg

6-12 years 300 mcg (0.3ml 1 in 1,000) 100 mg 5 mg

Adult and child 12 years 500 mcg (0.5ml 1 in 1,000) 200 mg 10 mg

Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the anterolateral aspect of the middle third of the thigh. Common identified causes of anaphylaxis

food (e.g. Nuts) - the most common cause in children drugs venom (e.g. Wasp sting)

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Which of the following drugs causes hyperkalaemia?

Heparin

Ciprofloxacin

Salbutamol

Levothyroxine

Codeine phosphate

Both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by inhibition of aldosterone secretion. Salbutamol is a recognised treatment for hyperkalaemia. Please rate this question:


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Hyperkalaemia

Plasma potassium levels are regulated by a number of factors including aldosterone, acid-base balance and insulin levels.

Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule.

ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia

Acute renal failure

Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**

Metabolic acidosis Addison's

Tissue necrosis/rhabdomylosis: burns, trauma Massive blood transfusion


Foods that are high in potassium

Salt substitutes (i.e. Contain potassium rather than sodium) Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

*beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment **both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by inhibition of aldosterone secretion

Next question

A 25-year-old man who has been morbidly obese for the past five years is reviewed in the surgical bariatric clinic. In this patient, release of which of the following hormones would increase appetite?

Leptin

Thyroxine

Adiponectin

Ghrelin

Serotonin

Obesity hormones

leptin decreases appetite

ghrelin increases appetite

Whilst thyroxine can increase appetite it does not fit with the clinical picture being described. Please rate this question:


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Obesity: physiology

Leptin Leptin is thought to play a key role in the regulation of body weight. It is produced by adipose tissue and acts on satiety centres in the hypothalamus and decreases appetite. More adipose tissue (e.g. in obesity) results in high leptin levels. Leptin stimulates the release of melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY) Ghrelin Where as leptin induces satiety, ghrelin stimulates hunger. It is produced mainly by the fundus of the stomach and the pancreas. Ghrelin levels increase before meals and decrease after meals

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Which of the following is not linked to excess glucocorticoids?

Osteonecrosis

Osteoporosis

Hypokalaemia

Hyponatraemia

Growth retardation in children

There are many adverse effects associated with excess glucocorticoids. Thinning of the skin, osteonecrosis and osteoporosis are all common. Steroids are associated with retention of sodium and water. Potassium loss may occur and hypokalaemic alkalosis has been reported. Please rate this question:


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Cortisol

Glucocorticoid

Released by zona fasiculata of the adrenal gland 90% protein bound; 10% active Circadian rhythm: High in the mornings Negative feedback via ACTH

Actions

Glycogenolysis

Gluconeogenesis Protein catabolism Lipolysis Stress response

Anti-inflammatory Decrease protein in bones Increase gastric acid Increases neutrophils/platelets/red blood cells Inhibits fibroblastic activity


A 54-year-old woman is admitted to the Surgical Admissions Unit with abdominal pain. Blood tests taken on admission show the following:

Magnesium 0.40 mmol/l (normal value 0.7-1.0 mmol/l)

Which one of the following factors is most likely to be responsible for this result?

Excessive resuscitation with intravenous saline

Digoxin therapy

Diarrhoea

Hypothermia

Rhabdomyolysis



Next question

Hypomagnasaemia

Cause of low magnesium

Diuretics Total parenteral nutrition Diarrhoea

Alcohol Hypokalaemia, hypocalcaemia

Features

Paraesthesia

Tetany Seizures Arrhythmias


Decreased PTH secretion → hypocalcaemia ECG features similar to those of hypokalaemia Exacerbates digoxin toxicity

Next question

A 43 year old man has a nasogastric tube inserted. The nurse takes a small aspirate of the fluid from the stomach and tests the pH of the aspirate. What is the normal intragastric pH?

0.5

2

4

5

6

Theme from January 2012 Exam The intragastric pH is usually 2. Administration of proton pump inhibitors can result in almost complete abolition of acidity Please rate this question:


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Gastric secretions

A working knowledge of gastric secretions is important for surgery because peptic ulcers are common, surgeons frequently prescribe anti secretory drugs and because there are still patients around who will have undergone acid lowering procedures (Vagotomy) in the past. Gastric acid

Is produced by the parietal cells in the stomach pH of gastric acid is around 2 with acidity being maintained by the H+/K+ ATP ase pump. As

part of the process bicarbonate ions will be secreted into the surrounding vessels. Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus.

This sets up a negative potential across the membrane and as a result sodium and potassium ions diffuse across into the canaliculus.

Carbonic anhydrase forms carbonic acid which dissociates and the hydrogen ions formed by dissociation leave the cell via the H+/K+ antiporter pump. At the same time sodium ions are actively absorbed. This leaves hydrogen and chloride ions in the canaliculus these mix and are secreted into the lumen of the oxyntic gland.


This is illustrated diagrammatically below:

Image sourced from Wikipedia

Phases of gastric acid secretion There are 3 phases of gastric secretion: 1. Cephalic phase (smell / taste of food)

30% acid produced

Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells

2. Gastric phase (distension of stomach )

60% acid produced

Stomach distension/low H+/peptides causes Gastrin release

http://en.wikipedia.org/wiki/Gastric%20acid

http://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb028b.jpg


3. Intestinal phase (food in duodenum)

10% acid produced High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion

via enterogastrones (CCK, secretin) and neural reflexes.

Regulation of gastric acid production Factors increasing production include:

Vagal nerve stimulation

Gastrin release Histamine release (indirectly following gastrin release) from enterchromaffin like cells

Factors decreasing production include:

Somatostatin (inhibits histamine release) Cholecystokinin Secretin

The diagram below illustrates some of the factors involved in regulating gastric acid secretion and the relevant associated pharmacology


Below is a brief summary of the major hormones involved in food digestion:




Source Stimulus Actions

Gastrin G cells in

antrum of the stomach

Distension of

stomach, extrinsic

nerves

Inhibited by: low

antral pH,

somatostatin

Increase HCL, pepsinogen and IF secretion,

increases gastric motility, trophic effect on gastric mucosa

CCK I cells in

upper small

intestine

Partially digested

proteins and

triglycerides

Increases secretion of enzyme-rich fluid

from pancreas, contraction of gallbladder

and relaxation of sphincter of Oddi,

decreases gastric emptying, trophic effect on

pancreatic acinar cells, induces satiety

Secretin S cells in

upper small

intestine

Acidic chyme, fatty acids

Increases secretion of bicarbonate-rich fluid

from pancreas and hepatic duct cells,

decreases gastric acid secretion, trophic effect on pancreatic acinar cells

VIP Small

intestine,

pancreas

Neural Stimulates secretion by pancreas and

intestines, inhibits acid and pepsinogen

secretion

Somatostatin D cells in the

pancreas and

stomach

Fat, bile salts and

glucose in the

intestinal lumen

Decreases acid and pepsin secretion,

decreases gastrin secretion, decreases

pancreatic enzyme secretion, decreases

insulin and glucagon secretion

inhibits trophic effects of gastrin, stimulates gastric mucous production

Next question

Which of the following is the equivalent of cardiac preload?

End diastolic volume

Stroke volume

Systemic vascular resistance

Mean arterial pressure

Peak systolic arterial pressure

Preload is the same as end diastolic volume. When it is increased slightly there is an associated increase in cardiac output (Frank Starling principle). When it is markedly increased e.g. over 250ml then cardiac output falls. Please rate this question:


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Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high pressure systems.

The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on the left.

At rest diastole comprises 2/3 of the cardiac cycle. The product of the frequency of heart rate and stroke volume combine to give the cardiac

output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are on the syllabus). However, they are a very popular topic for surgical physiology in the MRCS B exam. Electrical properties

Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is capable of contraction.

In the normal situation the cardiac impulse is generated in the sino atrial node in the right atrium and conveyed to the ventricles via the atrioventricular node.


The sino atrial node is also capable of spontaneous discharge and in the absence of background vagal tone will typically discharge around 100x per minute. Hence the higher resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting membrane potential is lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at which point an action potential is generated.

Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA node will depolarise first. The cells have a refractory period during which they cannot be re-stimulated and this period allows for adequate ventricular filling. In pathological tachycardic states this time period is overridden and inadequate ventricular filling may then occur, cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation. Cardiac cycle


Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic pressure is high.

Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic

volume 130-160ml.

http://en.wikipedia.org/wiki/Cardiac%20cycle

http://d2zgo9qer4wjf4.cloudfront.net/images_eMRCS/swb034b.png


Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave associated with closure of the aortic valve increases aortic pressure. The pressure dip before this rise can be seen on arterial waveforms and is called the incisura. During systole the atrial pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if the neck veins are exposed to air. This patient positioning is important in head and neck surgery to avoid this occurrence if veins are inadvertently cut, or during CVP line insertion. Mechanical properties

Preload = end diastolic volume

Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.

It states that for hollow organs with a circular cross section, the total circumferential wall tension depends upon the circumference of the wall, multiplied by the thickness of the wall and on the wall tension.

The total luminal pressure depends upon the cross sectional area of the lumen and the transmural pressure. Transmural pressure is the internal pressure minus external pressure and at equilibrium the total pressure must counterbalance each other.

In terms of cardiac physiology the law explains that the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have impaired systolic function.

Starlings law

Increase in end diastolic volume will produce larger stroke volume. This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke

volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output.

Baroreceptor reflexes

Baroreceptors located in aortic arch and carotid sinus.

Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.

They are stimulated by arterial stretch.

Even at normal blood pressures they are tonically active. Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node. *Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke volume. *Decreased sympathetic discharge to venous system causing increased compliance. *Decreased peripheral arterial vascular resistance Atrial stretch receptors

Located in atria at junction between pulmonary veins and vena cava.

Stimulated by atrial stretch and are thus low pressure sensors. Increased blood volume will cause increased parasympathetic activity. Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors:

theBainbridge reflex.

Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by juxtaglomerular apparatus-Increase in angiotensin II.

Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

Next question

A 48 year old man undergoes a right hemicolectomy for a large caecal polyp. In the immediate post operative period which of the physiological processes described below is least likely to occur?

Glycogenolysis

Increased production of acute phase proteins

Increased cortisol production

Bronchoconstriction

Release of nitric oxide by vessels



Next question

Response to surgery


Noradrenaline from sympathetic nerves and adrenaline from adrenal medulla

Blood diverted from skin and visceral organs; bronchodilatation, reduced intestinal motility, increased glucagon and glycogenolysis, insulin reduced

Heart rate and myocardial contractility are increased

Acute phase response

TNF-α, IL-1, IL-2, IL-6, interferon and prostaglandins are released Excess cytokines may cause SIRS Cytokines increase the release of acute phase proteins

Endocrine response

Hypothalamus, pituitary, adrenal axis


Increases ACTH and cortisol production:

increases protein breakdown increases blood glucose levels

Aldosterone increases sodium re-absorption

Vasopressin increases water re-absorption and causes vasoconstriction

Vascular endothelium

Nitric oxide produces vasodilatation

Platelet activating factor enhances the cytokine response Prostaglandins produce vasodilatation and induce platelet aggregation

Next question

A 73 year old female is referred to the surgical clinic with an iron deficiency anaemia. As part

of the diagnostic work up the doctor requests a serum ferritin level. Which of the conditions

listed is most likely to lead to a falsely elevated result?

Locally perforated sigmoid colonic adenocarcinoma

Colonic angiodysplasia

Dieulafoy lesion of the stomach

Transitional cell carcinoma of the bladder

Endometrial adenocarcinoma

A locally perforated colonic tumour will typically cause an intense inflammatory response and

if peritonitis is not present clinically then at the very least a localised abscess. This

inflammatory process is the most likely (from the list) to falsely raise the serum ferritin level.

Angiodysplasia and dieulafoy lesions are mucosal arteriovenous malformations and unlikely

to result in considerable inflammatory activity.



Next question

Ferritin

Ferritin is an intracellular protein that binds iron and stores it to be released in a controlled

fashion at sites where iron is required. Because iron and ferritin are bound the total body

ferritin levels may be decreased in cases of iron deficiency anaemia. Measurement of serum

ferritin levels can be useful in determining whether an apparently low haemoglobin and

microcytosis is truly caused by an iron deficiency state.

Ferritin is an acute phase protein and may be synthesised in increased quantities in

situations where inflammatory activity is ongoing. Falsely elevated results may therefore be

encountered clinically and need to be taken in context of the clinical picture and full blood

count results.


Which of the following is least likely to cause a prolonged prothrombin time?

Cholestatic jaundice

Disseminated intravascular coagulation

Prolonged antibiotic treatment

Liver disease

Acquired factor 12 deficiency

Vitamin K deficiency results from cholestatic jaundice and prolonged antibiotic therapy.

Acquired factor 12 deficiency causes prolonged APTT.



Next question

Abnormal coagulation

Cause Factors affected

Heparin Prevents activation factors 2,9,10,11

Warfarin Affects synthesis of factors 2,7,9,10

DIC Factors 1,2,5,8,11



Liver disease Factors 1,2,5,7,9,10,11

Interpretation blood clotting test results

Disorder APTT PT Bleeding time

Haemophilia Increased Normal Normal

von Willebrand's disease Increased Normal Increased

Vitamin K deficiency Increased Increased Normal

Next question

Which statement about peristalsis is true?

Longitudinal smooth muscle propels the food bolus through the oesophagus

Secondary peristalsis occurs when there is no food bolus in the oesophagus

Food transfer from the oesophagus to the stomach is 4 seconds

Circular smooth muscle is not involved in peristalsis

Peristalsis only occurs in the oesophagus



Next question

Peristalsis

Circular smooth muscle contracts behind the food bolus and longitudinal smooth muscle propels the food through the oesophagus

Primary peristalsis spontaneously moves the food from the oesophagus into the stomach (9 seconds)

Secondary peristalsis occurs when food, which doesn't enter the stomach, stimulates stretch receptors to cause peristalsis

In the small intestine each peristalsis waves slows to a few seconds and causes mixture of chyme

In the colon three main types of peristaltic activity are recognised (see below)

Colonic peristalsis

Segmentation contractions Localised contractions in which the bolus is subjected to local forces to maximise mucosal absorption

Antiperistaltic contractions

towards ileum

Localised reverse peristaltic waves to slow entry into colon and

maximise absorption


Mass movements Waves migratory peristaltic waves along the entire colon to

empty the organ prior to the next ingestion of food bolus

Next question

A 24 year old man is injured in a road traffic accident. He becomes oliguric and his renal function

deteriorates. Which of the options below would favor acute tubular necrosis over pre renal uraemia?

No response to intravenous fluids

Urinary sodium < 20mmol/L

Bland coloured urinary sediment

Increased urine specific gravity

None of the above

In acute tubular necrosis there is no response to intravenous fluids because the damage occurs from

within the renal system rather than as a result of volume depletion.



Next question

Acute renal failure: Pre renal failure vs. acute tubular necrosis

Prerenal uraemia - kidneys retain sodium to preserve volume

Pre-renal uraemia Acute tubular necrosis

Urine sodium < 20 mmol/L > 30 mmol/L


Pre-renal uraemia Acute tubular necrosis

Fractional sodium excretion* < 1% > 1%

Fractional urea excretion** < 35% >35%

Urine:plasma osmolality > 1.5 < 1.1

Urine:plasma urea > 10:1 < 8:1

Specific gravity > 1020 < 1010

Urine 'bland' sediment brown granular casts

Response to fluid challenge Yes No

*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x

100

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

Next question

Which of the following is not an effect of cholecystokinin?

It causes gallbladder contraction

It increases the rate of gastric emptying

It relaxes the sphincter of oddi

It stimulates pancreatic acinar cells

It has a trophic effect on pancreatic acinar cells

It decreases the rate of gastric emptying. Please rate this question:


Next question

Gastric secretions



part of the process bicarbonate ions will be secreted into the surrounding vessels.

Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus. This sets up a negative potential across the membrane and as a result sodium and potassium ions diffuse across into the canaliculus.






30% acid produced



60% acid produced








Regulation of gastric acid production

Factors increasing production include:




Somatostatin (inhibits histamine release)

Cholecystokinin Secretin








Gastrin G cells in


Distension of

stomach, extrinsic

nerves

Inhibited by: low

antral pH,

somatostatin



CCK I cells in

upper small

intestine

Partially digested

proteins and

triglycerides






Secretin S cells in

upper small

intestine





VIP Small

intestine, pancreas


intestines, inhibits acid and pepsinogen secretion


pancreas and

stomach

Fat, bile salts and

glucose in the

intestinal lumen






Next question

Which part of the jugular venous waveform is associated with the closure of the tricuspid valve?

a wave

c wave

x descent

y descent

v wave

JVP: C wave - closure of the tricuspid valve

The c wave of the jugular venous waveform is associated with the closure of the tricuspid valve. Please rate this question:


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Jugular venous pressure

As well as providing information on right atrial pressure, the jugular vein waveform may provide clues to underlying valvular disease. A non-pulsatile JVP is seen in superior vena caval obstruction. Kussmaul's sign describes a paradoxical rise in JVP during inspiration seen in constrictive pericarditis 'a' wave = atrial contraction

large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension absent if in atrial fibrillation

Cannon 'a' waves

caused by atrial contractions against a closed tricuspid valve are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single

chamber ventricular pacing


'c' wave

closure of tricuspid valve not normally visible

'v' wave

due to passive filling of blood into the atrium against a closed tricuspid valve giant v waves in tricuspid regurgitation

'x' descent = fall in atrial pressure during ventricular systole 'y' descent = opening of tricuspid valve


Next question

http://emrcs.com/question/question.php?q=0



Which one of the following serum proteins is most likely to increase in a patient with severe sepsis?

Transferrin

Transthyretin

Ferritin

Albumin

Cortisol binding protein

Ferritin can be markedly increased during acute illness. The other parameters tend to decrease during an acute phase response. Please rate this question:


Next question

Acute phase proteins

Acute phase proteins

CRP procalcitonin ferritin fibrinogen

alpha-1 antitrypsin caeruloplasmin serum amyloid A haptoglobin complement

During the acute phase response the liver decreases the production of other proteins (sometimes referred to as negative acute phase proteins). Examples include:

albumin

transthyretin (formerly known as prealbumin) transferrin


retinol binding protein cortisol binding protein

Levels of CRP are commonly measured in acutely unwell patients. CRP is a protein synthesised in the liver and binds to phosphocholine in bacterial cells and on those cells undergoing apoptosis. In binding to these cells it is then able to activate the complement system. CRP levels are known to rise in patients following surgery. However, levels of greater than 150 at 48 hours post operatively are suggestive of evolving complications.

Next question

Theme: Critical care

A. Hypovolaemia

B. Normal

C. Cardiogenic shock

D. Septic shock

For each of the scenarios outlined in the tables below, please select the most likely diagnosis from

the list. Each option may be used once, more than once or not at all.

72. A 45 year old man is admitted to the intensive care unit following a laparotomy. He has a central

line, pulmonary artery catheter and arterial lines inserted. The following results are obtained:

Pulmonary artery occlusion

pressure Cardiac output

Systemic vascular

resistance

Low Low High

Hypovolaemia

Theme from April 2012 Exam

Cardiac output is lowered in hypovolaemia due to decreased preload.

73. A 75 year old man is admitted to the intensive care unit following a laparotomy. He has a central




Systemic vascular

resistance

High Low High

You answered Hypovolaemia

The correct answer is Cardiogenic shock

In cardiogenic shock pulmonary pressures are often high. This is the basis for the use of

venodilators in the treatment of pulmonary oedema.

74. A 22 year old lady is admitted to the intensive care unit following a laparotomy. She has a central




Systemic vascular

resistance

Low High Low

You answered Hypovolaemia

The correct answer is Septic shock

Decreased SVR is a major feature of sepsis. A hyperdynamic circulation is often present. This is the

reason for the use of vasoconstrictors.



Next question

Pulmonary artery occlusion pressure monitoring

The pulmonary artery occlusion pressure is an indirect measure of left atrial pressure, and thus filling

pressure of the left heart. The low resistance within the pulmonary venous system allows this useful


measurement to be made. The most accurate trace is made by inflating the balloon at the catheter

tip and "floating" it so that it occludes the vessel. If it is not possible to occlude the vessel in this way

then the measurement gained will be the pulmonary artery end diastolic pressure.

Interpretation of PAOP

PAOP mmHg Scenario

Normal 8-12

Low <5 Hypovolaemia

Low with pulmonary oedema <5 ARDS

High >18 Overload

When combined with measurements of systemic vascular resistance and cardiac output it is possible

to accurately classify patients.

Systemic vascular resistance

Derived from aortic pressure, right atrial pressure and cardiac output.

SVR=80(mean aortic pressure-mean right atrial pressure)/cardiac output

Next question

A 23 year old man has a routine ECG performed. Which part of the tracing obtained represents atrial repolarisation?

P wave

T wave

Q-T Interval

P-R interval

None of the above

The process of atrial repolarisation is generally not visible on the ECG strip. It occurs during the QRS complex. Please rate this question:


Next question

The normal ECG



P wave

Represents the wave of depolarization that spreads from the SA node throughout the atria

Lasts 0.08 to 0.1 seconds (80-100 ms) The isoelectric period after the P wave represents the time in which the impulse is traveling

within the AV node

P-R interval

Time from the onset of the P wave to the beginning of the QRS complex Ranges from 0.12 to 0.20 seconds in duration Represents the time between the onset of atrial depolarization and the onset of ventricular

depolarization

QRS complex

Represents ventricular depolarization Duration of the QRS complex is normally 0.06 to 0.1 seconds

http://en.wikipedia.org/wiki/ECG



ST segment

Isoelectric period following the QRS Represents period which the entire ventricle is depolarized and roughly corresponds to the

plateau phase of the ventricular action potential

T wave

Represents ventricular repolarization and is longer in duration than depolarization

A small positive U wave may follow the T wave which represents the last remnants of ventricular repolarization.

Q-T interval

Represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential.

Interval ranges from 0.2 to 0.4 seconds depending upon heart rate. At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-T

interval. Therefore the Q-T interval is expressed as a "corrected Q-T (QTc)" by taking the Q-T interval and dividing it by the square root of the R-R interval (interval between ventricular depolarizations). This allows an assessment of the Q-T interval that is independent of heart rate.

Normal corrected Q-Tc interval is less than 0.44 seconds.

Next question

A 72-year-old woman is admitted to the acute surgical unit with profuse vomiting. Admission bloods show the following:

Na+ 131 mmol/l

K+ 2.2 mmol/l

Urea 3.1 mmol/l

Creatinine 56 µmol/l

Glucose 4.3 mmol/l

Which one of the following ECG features is most likely to be seen?

Short PR interval

Short QT interval

Flattened P waves

J waves

U waves

Hypokalaemia - U waves on ECG

J waves are seen in hypothermia whilst delta waves are associated with Wolff Parkinson White syndrome. Please rate this question:


Next question

ECG features in hypokalemia

U waves Small or absent T waves (occasionally inversion)

Prolonged PR interval ST depression Long QT interval


One registered user suggests the following rhyme!

In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!

Next question

The oxygen-haemoglobin dissociation curve is shifted to the left in:

With decreased 2,3-DPG in transfused red cells

Respiratory acidosis

High altitude

Pyrexia

Haemolytic anaemia

S shaped curve

The curve is shifted to the left when there is a decreased oxygen requirement by the tissue. This includes: 1. Hypothermia 2. Alkalosis 3. Reduced levels of DPG:

DPG is found in erythrocytes and is reduced in non exercising muscles, i.e. when there is reduced glycolysis.

4. Polycythaemia Please rate this question:


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Oxygen Transport

Oxygen transport Almost all oxygen is transported within erythrocytes. It has limited solubility and only 1% is carried as solution. Therefore the amount of oxygen transported will depend upon haemoglobin concentration and its degree of saturation. Haemoglobin

Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring surrounding an iron atom in its ferrous state. The iron can form two additional bonds; one with oxygen and the other with a polypeptide chain. There are two alpha and two beta subunits to this polypeptide chain in an adult and together these form globin. Globin cannot bind oxygen but is able to bind to carbon dioxide


and hydrogen ions, the beta chains are able to bind to 2,3 diphosphoglycerate. The oxygenation of haemoglobin is a reversible reaction. The molecular shape of haemoglobin is such that binding of one oxygen molecule facilitates the binding of subsequent molecules. Oxygen dissociation curve

The oxygen dissociation curve describes the relationship between the percentage of saturated haemoglobin and partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration.

Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the curve to the right

Haldane effect

Shifts to left = for given oxygen tension there is increased saturation of Hb with oxygen i.e. Decreased oxygen delivery to tissues

Bohr effect

Shifts to right = for given oxygen tension there is reduced saturation of Hb with oxygen i.e. Enhanced oxygen delivery to tissues



Shifts to Left = Lower oxygen delivery

HbF, methaemoglobin, carboxyhaemoglobin

low [H+] (alkali)

low pCO2

low 2,3-DPG

low temperature

Shifts to Right = Raised oxygen

delivery

raised [H+] (acidic)

raised pCO2

raised 2,3-DPG*

raised temperature

*2,3-diphosphoglycerate

Next question

http://en.wikipedia.org/wiki/Oxygen%E2%80%93haemoglobin%20dissociation%20curve


A homeless 42 year old male had an emergency inguinal hernia repair 24 hours previously. He has a BMI of 15. He has been put on a feeding regime of 35 kcal/kg/day with no additional medications. The nursing staff contact you as he has become confused and unsteady. On examination the patient is disorientated to place, has diplopia and nystagmus. What is the most likely diagnosis?

Cerebellar stroke

Acute dystonic reaction

Cerebrovascular accident

Parkinsonism

Wernickes encephalopathy

Triad of Wernicke encephalopathy:

Acute confusion Ataxia

Opthalmoplegia

This patient has received a carbohydrate rich diet without any thiamine or vitamin B co strong replacement. This has led to Wernickes encephalopathy, which classically presents with confusion, ataxia and opthalmoplegia. Characteristically it is associated with chronic alcoholism, however it is also known to occur post bariatric surgery. Please rate this question:


Next question



Hypophosphataemia

Hypokalaemia Hypomagnesaemia Abnormal fluid balance


These abnormalities can lead to organ failure. Re-feeding problems If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels High risk for re-feeding problems If one or more of the following:

BMI < 16 kg/m2

Unintentional weight loss >15% over 3-6 months Little nutritional intake > 10 days Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)


BMI < 18.5 kg/m2 Unintentional weight loss > 10% over 3-6 months Little nutritional intake > 5 days

History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

Prescription

Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co

strong 1 tds and supplements


Next question

A 22 year old lady receives intravenous morphine for acute abdominal pain. Which of the following best accounts for its analgesic properties?

Binding to δ opioid receptors in the brainstem

Binding to δ opioid receptors at peripheral nerve sites

Binding to β opioid receptors within the CNS

Binding to α opioid receptors within the CNS

Binding to µ opioid receptors within the CNS

4 Types of opioid receptor:

δ (located in CNS)- Accounts for analgesic and antidepressant effects

k (mainly CNS)- analgesic and dissociative effects µ (central and peripheral) - causes analgesia, miosis, decreased gut motility Nociceptin receptor (CNS)- Affect of appetite and tolerance to µ agonists.

Theme from April 2012 Exam Please rate this question:


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Morphine

Strong opiate analgesic. It is a pro- type narcotic drug and its effects mediated via the 4 types of opioid receptor. Its clinical effects stem from binding to these receptor sites within the CNS and gastrointestinal tract. Unwanted side effects include nausea, constipation, respiratory depression and, if used long term, addiction . It may be administered orally or intravenously. It can be reversed with naloxone.

Next question


Which one of the following reduces the secretion of renin?

Erect posture

Adrenaline

Hyponatraemia

Hypotension

Beta-blockers



Next question

Renin

Renin is secreted by juxtaglomerular cells and hydrolyses angiotensinogen to produce angiotensin I Factors stimulating renin secretion

Hypotension causing reduced renal perfusion Hyponatraemia Sympathetic nerve stimulation Catecholamines

Erect posture

Factors reducing renin secretion

Drugs: beta-blockers, NSAIDs

Next question


Which of the following stimulates prolactin release?

Leutinising hormone

Dopamine

Thyrotropin releasing hormone

Oestrogen

Follicle stimulating hormone

TRH stimulates prolactin release. Dopamine suppresses the release of prolactin.



Next question

Prolactin

Prolactin is a peptide hormone released from the anterior pituitary. It is under tonic dopamine

inhibition, thyrotropin releasing hormone has a stimulatory effect on release. Prolactin release

stimulates milk production but also reduces gonadal activity. It decreases GnRH pulsatility at the

hypothalamic level and to a lesser extent, blocks the action of LH on the ovary or testis.

Next question


Theme: Vitamin deficiency

A. Vitamin A

B. Vitamin B1

C. Vitamin B12

D. Vitamin B3

E. Vitamin C

F. Vitamin K

G. Vitamin D

Please select the vitamin deficiency most closely associated with the situation described. Each

option may be used once, more than once or not at all.

82. A 3 year old child presents with Rickets

You answered Vitamin A

The correct answer is Vitamin D

Vitamin D is needed to help mineralise bone. When this is deficient, mineralisation is inadequate

and deformities mayt result.

83. A 44 year old lady presents with jaundice. Following a minor ward based surgical procedure she

develops troublesome and persistent bleeding.

You answered Vitamin A

The correct answer is Vitamin K

Patients who are jaundiced usually have impaired absorption of vitamin K. This can result in loss

of the vitamin K dependent clotting factors and troublesome bleeding.

84. A 69 year old man who has been living in sheltered accommodation for many months, with

inadequate nutrition notices that his night vision is becoming impaired.

Vitamin A

Loss of vitamin A will result in impair rhodopsin synthesis and poor night vision.



Next question

Vitamin deficiency

Vitamin Effect of deficiency

A Night blindness

Epithelial atrophy

Infections

B1 Beriberi

B2 Dematitis and photosensitivity

B3 Pellagra

B12 Pernicious anaemia


C Poor wound healing

Impaired collagen synthesis

D Rickets (Children)

Osteomalacia (Adults)

K Clotting disorders

Next question

A 55 year old man undergoes a laparotomy and repair of incisional hernia. Which of the following hormones is least likely to be released in increased quantities following the procedure?

Insulin

ACTH

Glucocorticoids

Aldosterone

Growth hormone

Insulin and thyroxine are often have reduced levels of secretion in the post operative period. This, coupled with increased glucocorticoid release may cause difficulty in management of diabetes in individuals with insulin resistance. Please rate this question:


Next question













Aldosterone

Prolactin


Glucagon


Stimulates catecholamine release

Causes tachycardia and hypertension

Pituitary gland



stimulating hormone (FSH) does not change significantly ACTH stimulates cortisol production within a few minutes of the start of surgery. More ACTH

is produced than needed to produce a maximum adrenocortical response.

Cortisol

Significant increases within 4-6 hours of surgery (>1000 nmol litre-1). The usual negative feedback mechanism fails and concentrations of ACTH and cortisol

remain persistently increased. The magnitude and duration of the increase correlate with the severity of stress and the

response is not abolished by the administration of corticosteroids. The metabolic effects of cortisol are enhanced:


Increased secretion after surgery has a minor role

Most important for preventing muscle protein breakdown and promote tissue repair by insulin growth factors

Alpha Endorphin

Increased


An important vasopressor and enhances haemostasis

Renin is released causing the conversion of angiotensinogen to angiotensin I Angiotensin II formed by ACE on angiotensin 1, which causes the secretion of aldosterone


Insulin

Release inhibited by stress Occurs via the inhibition of the beta cells in the pancreas by the α2-adrenergic inhibitory

effects of catecholamines

Insulin resistance by target cells occurs later The perioperative period is characterized by a state of functional insulin deficiency



Metabolic effect of endocrine response

Carbohydrate metabolism

Hyperglycaemia is a main feature of the metabolic response to surgery Due to increase in glucose production and a reduction in glucose utilization Catecholamines and cortisol promote glycogenolysis and gluconeogenesis Initial failure of insulin secretion followed by insulin resistance affects the normal responses

The proportion of the hyperglycaemic response reflects the severity of surgery Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism



Mainly skeletal muscle protein is affected

The amino acids released form acute phase proteins (fibrinogen, C reactive protein, complement proteins, a2-macroglobulin, amyloid A and ceruloplasmin) and are used for gluconeogenesis





Cytokines

Glycoproteins

Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor Synthesized by activated macrophages, fibroblasts, endothelial and glial cells in response to

tissue injury from surgery or trauma



Opioids suppress hypothalamic and pituitary hormone secretion At high doses the hormonal response to pelvic and abdominal surgery is abolished.

However, such doses prolong recovery and increase the need for postoperative ventilatory support



recovery Growth hormone and anabolic steroids may improve outcome

Normothermia decreases the metabolic response

References

Deborah Burton, Grainne Nicholson, and George Hall Endocrine and metabolic response to surgery . Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp/mkh040

Next question

Which of the following is not a major function of the spleen in adults?

Iron reutilisation

Storage of platelets

Storage of monocytes

Haematopoeisis in haematological disorders

Storage red blood cells

The reservoir function of the spleen is less marked in humans than other animals (e.g. pigs) and in normal individuals it can sequester between 5 and 10% of the red cell mass. The other stated processes are major splenic functions and this accounts for the answer provided. Please rate this question:


Next question

Spleen

The spleen is located in the left upper quadrant of the abdomen and its size can vary depending upon the amount of blood it contains. The typical adult spleen is 12.5cm long and 7.5cm wide. The usual weight of the adult spleen is 150g. The exact position of the spleen can vary with respiratory activity, posture and the state of surrounding viscera. It usually lies obliquely with its long axis aligned to the 9th, 10th and 11th ribs. It is separated from these ribs by both diaphragm and pleural cavity. The normal spleen is not palpable. The shape of the spleen is influenced by the state of the colon and stomach. Gastric distension will cause the spleen to resemble the shape of an orange segment. Colonic distension will cause it to become more tetrahedral. The spleen is almost entirely covered by peritoneum, which adheres firmly to its capsule. Recesses of the greater sac separate it from the stomach and kidney. It develops from the upper dorsal mesogastrium, remaining connected to the posterior abdominal wall and stomach by two folds of peritoneum; the lienorenal ligament and gastrosplenic ligament. The lienorenal ligament is derived from peritoneum where the wall of the general peritoneum meets the omental bursa between the left kidney and spleen; the splenic vessels lie in its layers. The gastrosplenic ligament also has two layers, formed by the meeting of the walls of the greater sac and omental bursa between spleen and stomach, the short gastric and left gastroepiploic branches of the splenic artery pass in its layers.


Laterally, the spleen is in contact with the phrenicocolic ligament. Relations

Superiorly Diaphragm

Anteriorly Gastric impression

Posteriorly Kidney

Inferiorly Colon

Hilum Tail of pancreas and splenic vessels (splenic artery divides here, branches pass to the

white pulp transporting plasma)

Contents

White

pulp

Immune function. Contains central trabecular artery. The germinal centres are supplied

by arterioles called penicilliary radicles.

Red pulp Filters abnormal red blood cells.

Function

Filtration of abnormal blood cells and foreign bodies such as bacteria. Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for

phagocytosis.

Haematopoiesis: up to 5th month gestation or in haematological disorders. Pooling: storage of 40% platelets. Iron reutilisation Storage monocytes

Disorders of the spleen Massive splenomegaly

Myelofibrosis Chronic myeloid leukaemia Visceral leishmaniasis (kala-azar)

Malaria Gaucher's syndrome

Other causes (as above plus)

Portal hypertension e.g. secondary to cirrhosis

Lymphoproliferative disease e.g. CLL, Hodgkin's Haemolytic anaemia

Infection: hepatitis, glandular fever Infective endocarditis Sickle-cell*, thalassaemia Rheumatoid arthritis (Felty's syndrome)

*the majority of adult patients with sickle-cell will have an atrophied spleen due to repeated infarction

Next question

Which one of the following is associated with increased lung compliance?

Kyphosis

Pulmonary oedema

Emphysema

Pulmonary fibrosis

Pneumonectomy



Next question

Respiratory physiology: lung compliance

Lung compliance is defined as change in lung volume per unit change in airway pressure Causes of increased compliance

age emphysema - this is due to loss alveolar walls and associated elastic tissue

Causes of decreased compliance

pulmonary oedema pulmonary fibrosis pneumonectomy kyphosis

Next question


Which of the following areas is predominantly concerned with thermoregulation?

Hypothalamus

Anterior pituitary

Cerebellum

Brain stem

Temporal lobe

Theme from 2012 Exam The hypothalamus is primarily concerned with thermoregulation. It may relay to the cerebral cortex to induce behavioural adaptation to facilitate the thermoregulatory process. Please rate this question:


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Thermoregulation

The hypothalamus is the main centre for thermoregulation. Peripheral and central thermoreceptors relay to this region.

Central thermoreceptors play the main role in maintenance of core temperature. Hypothalamus may initiate involuntary motor responses to raise body temperature

(e.g.shivering). It will also stimulate the sympathetic nervous system to produce peripheral vasoconstriction and release of adrenaline from the adrenal medulla.

Heat loss is governed by behavioural responses and by autonomic responses including peripheral vasodilation.

Heat loss can be maintained within the thermoneutral zone (25 to 30 degrees) although the absolute value depends upon atmospheric humidity.

Sepsis results in the release of cytokines that reset the thermoregulatory centre resulting in fever.

Next question


Theme: Acid - base disorders

A. pH 7.64 pO2 10.0 kPa pCO2 2.8 kPa HCO3 20

B. pH 7.25 pO2 8.9 pCO2 3.2 HCO3 10

C. pH 7.20 pO2 6.2 pCO2 8.2 HCO3 27

D. pH 7.60 pO2 8.2 pCO2 5.8 HCO3 40

E. pH 7.45 pO2 7.2 pCO2 2.5 HCO3 24 Please match the diagnosis with the arterial blood gas result. Each option may be used once, more than once or not at all.

89. Pulmonary embolus

You answered pH 7.64 pO2 10.0 kPa pCO2 2.8 kPa HCO3 20

The correct answer is pH 7.45 pO2 7.2 pCO2 2.5 HCO3 24

A combination of hypoxia and respiratory alkalosis should suggest a pulmonary embolus.

The respiratory alkalosis is due to hyperventilation associated with the pulmonary

embolism.

90. High output ureterosigmoidostomy



There is acidosis. To compensate the patient will attempt to raise the pH level in the blood

by hyperventilating, hence the low CO2 level .

91. Widespread mesenteric infarction



This is usually associated with acidosis, hyperventillation and reduction in bicarbonate.



Next question


Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A, both in the SBA and EMQ sections. The acid-base normogram below shows how the various disorders may be categorised


Metabolic acidosis

This is the most common surgical acid - base disorder.

Reduction in plasma bicarbonate levels. Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis) 2. Loss of base (e.g. from bowel in diarrhoea) - Classified according to the anion gap, this can be calculated by: (Na+ + K+) - (Cl- + HCO3

-). - If a question supplies the chloride level then this is often a clue that the anion gap should be calculated. The normal range = 10-18 mmol/L Normal anion gap ( = hyperchloraemic metabolic acidosis)

Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula

http://en.wikipedia.org/wiki/Acid-base%20homeostasis



Renal tubular acidosis Drugs: e.g. acetazolamide Ammonium chloride injection Addison's disease

Raised anion gap

Lactate: shock, hypoxia Ketones: diabetic ketoacidosis, alcohol

Urate: renal failure Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:

Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)

Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis

Usually caused by a rise in plasma bicarbonate levels.

Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.

Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or gastrointestinal tract

Causes

Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)

Diuretics Liquorice, carbenoxolone Hypokalaemia Primary hyperaldosteronism

Cushing's syndrome Bartter's syndrome Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis

Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised

aldosterone levels

In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality


Rise in carbon dioxide levels usually as a result of alveolar hypoventilation Renal compensation may occur leading to Compensated respiratory acidosis

Causes

COPD

Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema

Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis

Hyperventilation resulting in excess loss of carbon dioxide This will result in increasing pH

Causes

Psychogenic: anxiety leading to hyperventilation Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude Early salicylate poisoning*

CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis Pregnancy

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

Next question

A 45 year old male is diagnosed with carcinoma of the head of the pancreas. He reports that his stool sticks to the commode and will not flush away. Loss of which of the following enzymes is most likely to be responsible for this problem?

Lipase

Amylase

Trypsin

Elastase

None of the above

Theme from April 2014 Exam Loss of lipase is one of the key features in the development of steatorrhoea which typically consists of pale and offensive stools that are difficult to flush away. Please rate this question:


Next question

Pancreatic cancer

Adenocarcinoma Risk factors: Smoking, diabetes, adenoma, familial adenomatous polyposis Mainly occur in the head of the pancreas (70%) Spread locally and metastasizes to the liver

Carcinoma of the pancreas should be differentiated from other periampullary tumours with better prognosis

Clinical features

Weight loss

Painless jaundice Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a late feature) Pancreatitis Trousseau's sign: migratory superficial thrombophlebitis


Investigations

USS: May miss small lesions CT Scanning (pancreatic protocol). If unresectable on CT then no further staging needed

PET/CT for those with operable disease on CT alone ERCP/ MRI for bile duct assessment Staging laparoscopy to exclude peritoneal disease

Management

Head of pancreas: Whipple's resection (SE dumping and ulcers). Newer techniques include pylorus preservation and SMA/ SMV resection

Carcinoma body and tail: poor prognosis, distal pancreatectomy, if operable Usually adjuvent chemotherapy for resectable disease ERCP and stent for jaundice and palliation

Surgical bypass may be needed for duodenal obstruction

Next question

Which of the following drugs does not interfere with the laboratory analysis of serum cortisol levels?

Dexamethasone

Prednisolone

Hydrocortisone IV

Hydrocortisone PO

Hydrocortisone IM

Prednisolone and it's metabolites can chemically mimic cortisol in radio-immunoassay techniques of laboratory analysis.

Dexamethasone can be given as glucorticoid replacement during testing for addisons or adrenal insufficiency as it does not interfere with cortisol levels. For example, if you have a patient with polymyalgia rheumatica and they are on long term prednisolone, you can replace the prednisolone with dexamethasone to undertake a short synacthen test. Please rate this question:


Next question

Cortisol

Glucocorticoid Released by zona fasiculata of the adrenal gland 90% protein bound; 10% active Circadian rhythm: High in the mornings

Negative feedback via ACTH

Actions

Glycogenolysis

Gluconeogenesis Protein catabolism Lipolysis Stress response Anti-inflammatory


Decrease protein in bones Increase gastric acid Increases neutrophils/platelets/red blood cells Inhibits fibroblastic activity

Next question

An elderly lady who presented with weight loss and malabsorption was found to have amyloid of the

small bowel. On presentation she was found to have osteomalacia and was hypocalcaemic. Over

the past seven days she has received total parenteral nutrition with adequate calcium replacement.

Despite this she remained hypocalcaemic. Deficiency of which of the following electrolytes is most

likely to account for this process?

Magnesium

Potassium

Sodium

Phosphate

None of the above

Theme from September 2015 Exam

Patients with malabsorption may develop magnesium deficiency, although her TPN feeds may have

contained magnesium it may not have been sufficient to correct her losses. Sodium, phosphate and

potassium would not have this effect on serum calcium.



Next question

Combined deficiency of magnesium and calcium

Magnesium is required for both PTH secretion and its action on target tissues. Hypomagnesaemia

may both cause hypocalcaemia and render patients unresponsive to treatment with calcium and

vitamin D supplementation.

Magnesium is the fourth most abundant cation in the body. The body contains 1000mmol, with half

contained in bone and the remainder in muscle, soft tissues and extracellular fluid. There is no one


specific hormonal control of magnesium and various hormones including PTH and aldosterone affect

the renal handling of magnesium.

Magnesium and calcium interact at a cellular level also and as a result decreased magnesium will

tend to affect the permeability of cellular membranes to calcium, resulting in hyperexcitability.

Next question

A 19 year old man is attacked outside a club and beaten with a baseball bat. He sustains a blow to the right side of his head. He is brought to the emergency department and a policy of observation is adopted. His glasgow coma score deteriorates and he becomes comatose. Which of the following haemodynamic parameters is most likely to be present?

Hypertension and bradycardia

Hypotension and tachycardia

Hypotension and bradycardia

Hypertension and tachycardia

Normotension and bradycardia

Theme from April 2013 Exam Hypertension and bradycardia are seen prior to coning. The brain autoregulates its blood supply by controlling systemic blood pressure. Please rate this question:


Next question

Head injury

Patients who suffer head injuries should be managed according to ATLS principles and extra cranial injuries should be managed alongside cranial trauma. Inadequate cardiac output will compromise CNS perfusion irrespective of the nature of the cranial injury. Types of traumatic brain injury

Extradural

haematoma

Bleeding into the space between the dura mater and the skull. Often results from

acceleration-deceleration trauma or a blow to the side of the head. The majority

of extradural haematomas occur in the temporal region where skull fractures

cause a rupture of the middle meningeal artery.

Features

Raised intracranial pressure

Some patients may exhibit a lucid interval


Subdural

haematoma

Bleeding into the outermost meningeal layer. Most commonly occur around the

frontal and parietal lobes. May be either acute or chronic.

Risk factors include old age and alcoholism.

Slower onset of symptoms than a extradural haematoma.

Subarachnoid

haemorrhage

Usually occurs spontaneously in the context of a ruptured cerebral aneurysm, but

may be seen in association with other injuries when a patient has sustained a

traumatic brain injury.

Pathophysiology

Primary brain injury may be focal (contusion/ haematoma) or diffuse (diffuse axonal injury)

Diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons

Intra-cranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact

Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia

The Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event

Management

Where there is life threatening rising ICP such as in extra dural haematoma and whilst theatre is prepared or transfer arranged use of IV mannitol/ frusemide may be required.

Diffuse cerebral oedema may require decompressive craniotomy

Exploratory Burr Holes have little management in modern practice except where scanning may be unavailable and to thus facilitate creation of formal craniotomy flap

Depressed skull fractures that are open require formal surgical reduction and debridement, closed injuries may be managed non operatively if there is minimal displacement.

ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.

ICP monitoring is mandatory in those who have GCS 3-8 and abnormal CT scan. Hyponatraemia is most likely to be due to syndrome of inappropriate ADH secretion. Minimum of cerebral perfusion pressure of 70mmHg in adults. Minimum cerebral perfusion pressure of between 40 and 70 mmHg in children.

Interpretation of pupillary findings in head injuries

Pupil size Light response Interpretation

Pupil size Light response Interpretation

Unilaterally dilated Sluggish or fixed 3rd nerve compression secondary to tentorial

herniation

Bilaterally dilated Sluggish or fixed Poor CNS perfusion

Bilateral 3rd nerve palsy

Unilaterally dilated or

equal

Cross reactive (Marcus -

Gunn)

Optic nerve injury

Bilaterally constricted May be difficult to

assess

Opiates

Pontine lesions

Metabolic encephalopathy

Unilaterally

constricted

Preserved Sympathetic pathway disruption

Next question

Which of the following drugs does not cause pseudohaematuria?

Rifampicin

Quinine

Noradrenaline

Levodopa

Phenytoin

Rifampicin, phenytoin, levodopa, methyldopa, and quinine all cause pseudohaematuria. Please rate this question:


Next question

Haematuria

Causes of haematuria

Trauma Injury to renal tract

Renal trauma commonly due to blunt injury (others penetrating

injuries)

Ureter trauma rare: iatrogenic

Bladder trauma: due to RTA or pelvic fractures

Infection Remember TB

Malignancy Renal cell carcinoma (remember paraneoplastic syndromes):

painful or painless

Urothelial malignancies: 90% are transitional cell carcinoma, can

occur anywhere along the urinary tract. Painless haematuria.

Squamous cell carcinoma and adenocarcinoma: rare bladder

tumours

Prostate cancer


Penile cancers: SCC

Renal disease Glomerulonephritis

Stones Microscopic haematuria common

Structural

abnormalities

Benign prostatic hyperplasia (BPH) causes haematuria due to

hypervascularity of the prostate gland

Cystic renal lesions e.g. polycystic kidney disease

Vascular malformations

Renal vein thrombosis due to renal cell carcinoma

Coagulopathy Causes bleeding of underlying lesions

Drugs Cause tubular necrosis or interstitial nephritis: aminoglycosides,

chemotherapy

Interstitial nephritis: penicillin, sulphonamides, and NSAIDs

Anticoagulants

Benign Exercise

Gynaecological Endometriosis: flank pain, dysuria, and haematuria that is cyclical

Iatrogenic Catheterisation

Radiotherapy; cystitis, severe haemorrhage, bladder necrosis

Pseudohaematuria For example following consumption of beetroot

References Http://bestpractice.bmj.com/best-practice/monograph/316/overview/aetiology.html

Next question

A 74-year-old woman with thyroid cancer is admitted due to shortness of breath. What is the best

investigation to assess for possible compression of the upper airways?

Arterial blood gases

Forced vital capacity

Transfer factor

Peak expiratory flow rate

Flow volume loop

Flow volume loop is the investigation of choice for upper airway compression.



Next question

Flow volume loop

A normal flow volume loop is often described as a 'triangle on top of a semi circle'

Flow volume loops are the most suitable way of assessing compression of the upper airway

Next question


Which of the following statements relating to cerebrospinal fluid is untrue?

The choroid plexus is only present in the lateral ventricles

Total CSF volume is 100-150ml

CSF pressure is usually 10-15mmHg

The cerebral aqueduct connects the third and fourth ventricles

The foramen of Luschka are paired and lie laterally in the fourth ventricle

The choroid plexus lies in all ventricles. Please rate this question:


Next question

Cerebrospinal fluid

The CSF fills the space between the arachnoid mater and pia mater (covering surface of the brain). The total volume of CSF in the brain is approximately 150ml. Approximately 500 ml is produced by the ependymal cells in the choroid plexus (70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations which project into the venous sinuses. Circulation

1. Lateral ventricles (via foramen of Munro) 2. 3rd ventricle 3. Cerebral aqueduct (aqueduct of Sylvius) 4. 4th ventricle (via foramina of Magendie and Luschka) 5. Subarachnoid space 6. Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus Composition

Glucose: 50-80mg/dl

Protein: 15-40 mg/dl Red blood cells: Nil White blood cells: 0-3 cells/ mm3

Next question


Which substance can be used to achieve the most accurate measurement of the glomerular filtration rate?

Glucose

Protein

Inulin

Creatinine

Para-amino hippuric acid

Theme from April 2016 exam Creatinine declines with age due to decline in renal function and muscle mass. Glucose, protein (amino acids) and PAH are reabsorbed by the kidney. Please rate this question:


Next question

Renal Physiology

Overview



















Tubular function








Loop of Henle



chloride ions.





Next question

A 45 year old man sustains a closed head injury. He is initially alert, however, his level of consciousness deteriorates on arrival at hospital. An intra cranial pressure monitor is inserted. What is the normal intracranial pressure?

35 - 45mm Hg

45 - 55mm Hg

<15mm Hg

25 - 35mm Hg

25 - 30 mm Hg

The normal intracranial pressure is between 7 and 15 mm Hg. The brain can accommodate increases up to 24 mm Hg, thereafter clinical features will become evident. Please rate this question:


Next question

Applied neurophysiology

Pressure within the cranium is governed by the Monroe-Kelly doctrine. This considers the skull as a closed box. Increases in mass can be accommodated by loss of CSF. Once a critical point is reached (usually 100- 120ml of CSF lost) there can be no further compensation and ICP rises sharply. The next step is that pressure will begin to equate with MAP and neuronal death will occur. Herniation will also accompany this process.

The CNS can autoregulate its own blood supply. Vaso constriction and dilatation of the cerebral blood vessels is the primary method by which this occurs. Extremes of blood pressure can exceed this capacity resulting in risk of stroke. Other metabolic factors such as hypercapnia will also cause vasodilation, which is of importance in ventilating head injured patients.

The brain can only metabolise glucose, when glucose levels fall, consciousness will be impaired.

Next question


A 55-year-old man with a history of type 2 diabetes mellitus, bipolar disorder and chronic obstructive pulmonary disease has bloods taken during a pre operative assessment of an inguinal hernia repair:

Na+ 125 mmol/l

K+ 3.8 mmol/l

Bicarbonate 24 mmol/l

Urea 3.7 mmol/l

Creatinine 92 µmol/l

Due to his smoking history a chest x-ray is ordered which is reported as normal. The Consultant asks you what is the most likely cause for the hyponatraemia?

Metformin

Lithium

Carbamazepine

Sodium valproate

Pioglitazone

SIADH - drug causes: carbamazepine, sulfonylureas, SSRIs, tricyclics

Lithium can cause diabetes insipidus but this is generally associated with a high sodium. Lithium only tends to cause raised antidiuretic hormone levels following a severe overdosage. Please rate this question:


Next question

syndrome of inappropriate antidiuretic hormone (SIADH): causes

Malignancy

especially small cell lung cancer


also: pancreas, prostate

Neurological

stroke

subarachnoid haemorrhage subdural haemorrhage meningitis/encephalitis/abscess

Infections

tuberculosis pneumonia

Drugs

sulfonylureas SSRIs, tricyclics carbamazepine vincristine

cyclophosphamide

Other causes

positive end-expiratory pressure (PEEP) porphyrias

Next question

A 24 year old man is involved in a road traffic accident. His right leg is trapped for 6 hours whilst he is moved. On examination his foot is insensate and a dorsalis pedis pulse is only weakly felt. Which of the biochemical abnormalities listed below is most likely to be present?

Alkalosis

Hypercalcaemia

Hypocalcaemia

Hyperkalaemia

Hyponatraemia

In this scenario the patient will have a compartment syndrome, delayed diagnosis and muscle death. The effect of muscle death will result in the release of potassium. It is also highly likely that there will be a degree of renal impairment, the result of which is that the serum potassium is likely to be high. Please rate this question:


Next question

Hyperkalaemia

Plasma potassium levels are regulated by a number of factors including aldosterone, acid-base balance and insulin levels.

Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule.

ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole

Causes of hyperkalaemia

Acute renal failure Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers,

spironolactone, ciclosporin, heparin** Metabolic acidosis Addison's Tissue necrosis/rhabdomylosis: burns, trauma


Massive blood transfusion

Foods that are high in potassium

Salt substitutes (i.e. Contain potassium rather than sodium)

Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

*beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment **both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by inhibition of aldosterone secretion

Next question

A 39 year old lady has recurrent attacks of biliary colic. What is the approximate volume of bile to

enter the duodenum per 24 hours?

500 mL

50 mL

100 mL

2000 mL

150 mL

Between 500 mL and 1.5 L of bile enters the small bowel daily. Most bile salts are recycled by the

enterohepatic circulation. When the gallbladder contracts the lumenal pressure is approximately

25cm water, which is why biliary colic may be so painful.



Next question

Bile

Bile is produced at a rate of between 500ml and 1500mL per day. Bile is composed of bile salts,

bicarbonate, cholesterol, steroids and water. There are three main factors regulating bile flow;

hepatic secretion, gall bladder contraction and sphincter of oddi resistance. Bile salts are absorbed

in the terminal ileum (and recycled to the liver). Over 90% of all bile salts are recycled in this way,

such that the total pool of bile salts is recycled up to six times a day.

Primary bile salts

Cholate and chenodeoxycholate.

Secondary bile salts


Formed by bacterial action on primary bile salts. These are deoxycholate and lithocholate. Of these

deoxycholate is reabsorbed, whilst lithocholate is insoluble and excreted.

Pathophysiology of gallstones

Bile salts have a detergent action. They aggregate to form micelles and these have a lipid centre in

which fats may be transported. Excessive quantities of cholesterol cannot be transported in this way

and will tend to precipitate, resulting in the formation of cholesterol rich gallstones.

Next question

At which of the following sites is the most water absorbed?

Right colon

Left colon

Stomach

Jejunum

Duodenum

Water absorption in the gastrointestinal tract predominantly occurs in the small bowel (jejunum and

ileum). The colon is an important site of water absorption, however, its overall contribution is

relatively small. The importance of the colonic component to water absorption may increase

following extensive small bowel resections.



Next question

Water absorption

During a 24 hours period the average person will ingest up to 2000ml of liquid orally. In addition a

further 8000ml of fluid will enter the small bowel as gastrointestinal secretions. Intestinal water

absorption is a passive process and is related to solute load. In the jejunum the active absorption of

glucose and amino acids will create a concentration gradient that water will flow across. In the ileum

most water is absorbed by a process of facilitated diffusion (with sodium).

Approximately 150ml of water enters the colon daily, most is absorbed, the colon can adapt to, and

increase this amount following resection.

Next question


Which of the following is not a characteristic of the proximal convoluted tubule in the kidney?

Up to 95% of filtered amino acids will be reabsorbed at this site

It is a risk of damage in a patient with compartment syndrome due to a tibial fracture

It is responsible for absorbing more than 50% of filtered water

Its secretory function is most effective at low systolic blood pressures (typically less than

100mmHg)

Glucose is reabsorbed by a process of facilitated diffusion

The proximal convoluted tubule may undergo necrosis in situations such as compartment syndrome. It is responsible for reabsorbing up to two thirds of filtered water. Low systolic blood pressures (below the renal autoregulatory range) are a risk factor for acute tubular necrosis. Within the autoregulatory range the absolute value of systolic BP has little effect. Please rate this question:


Next question

Renal Physiology

Overview



















Tubular function








Loop of Henle



chloride ions.





Next question

An arterial blood gas sample is taken and the following results obtained;

PaO2 8kPa

PaCO2 4kPa

pH 7.4

With which of the following are these values most consistent?

Compensated metabolic alkalosis

Pulmonary atelectasis

Alveolar hypoventilation

Residing at 4500M for 48 hours

LAD occlusion

The patient has low oxygen tension and low carbon dioxide. The pH is normal so there is

compensation for a long standing condition in which oxygenation is reduced. There is neither

alkalosis, nor hypoventilation as the carbon dioxide is low. At very high altitude, the low oxygen

tension can exceed the anaerobic threshold and carbon dioxide levels increase.



Next question

Arterial blood gas interpretation


In advanced life support training, a 5 step approach to arterial blood gas interpretation is advocated.

1. How is the patient?

2. Is the patient hypoxaemic?

The Pa02 on air should be 10.0-13.0 kPa

3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)

4. What has happened to the PaCO2?

If there is acidaemia, an elevated PaCO2 will account for this

5. What is the bicarbonate level or base excess?

A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2 mmol)

A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2 mmol)

Next question

Which of the following does not cause a normal anion gap acidosis?

Pancreatic fistula

Acetazolamide

Uraemia

Ureteric diversion

Renal tubular acidosis

Normal Gap Acidosis: HARDUP H - Hyperalimentation/hyperventilation A - Acetazolamide R - Renal tubular acidosis D - Diarrhoea U - Ureteral diversion P - Pancreatic fistula/parenteral saline

Uraemia will typically cause a high anion gap acidosis. It is one of the unmeasured anions. Please rate this question:


Next question

Disorders of acid - base balance

Disorders of acid- base balance are often covered in the MRCS part A, both in the SBA and EMQ sections. The acid-base normogram below shows how the various disorders may be categorised



Metabolic acidosis

This is the most common surgical acid - base disorder.

Reduction in plasma bicarbonate levels. Two mechanisms:

1. Gain of strong acid (e.g. diabetic ketoacidosis) 2. Loss of base (e.g. from bowel in diarrhoea) - Classified according to the anion gap, this can be calculated by: (Na+ + K+) - (Cl- + HCO3

-). - If a question supplies the chloride level then this is often a clue that the anion gap should be calculated. The normal range = 10-18 mmol/L Normal anion gap ( = hyperchloraemic metabolic acidosis)

Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula

Renal tubular acidosis Drugs: e.g. acetazolamide Ammonium chloride injection Addison's disease

Raised anion gap

http://en.wikipedia.org/wiki/Acid-base%20homeostasis



Lactate: shock, hypoxia Ketones: diabetic ketoacidosis, alcohol Urate: renal failure Acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:

Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns) Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

Metabolic alkalosis

Usually caused by a rise in plasma bicarbonate levels.

Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.

Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or gastrointestinal tract

Causes

Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)

Diuretics Liquorice, carbenoxolone Hypokalaemia Primary hyperaldosteronism Cushing's syndrome Bartter's syndrome

Congenital adrenal hyperplasia

Mechanism of metabolic alkalosis

Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor

Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised

aldosterone levels In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to

maintain neutrality


Rise in carbon dioxide levels usually as a result of alveolar hypoventilation Renal compensation may occur leading to Compensated respiratory acidosis

Causes

COPD Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary

oedema

Sedative drugs: benzodiazepines, opiate overdose

Respiratory alkalosis

Hyperventilation resulting in excess loss of carbon dioxide

This will result in increasing pH

Causes

Psychogenic: anxiety leading to hyperventilation

Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude Early salicylate poisoning* CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis Pregnancy

*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis

Next question

Which one of the following would cause a rise in the carbon monoxide transfer factor (TLCO)?

Emphysema

Pulmonary embolism

Pulmonary haemorrhage

Pneumonia

Pulmonary fibrosis

Transfer factor

raised: asthma, haemorrhage, left-to-right shunts, polycythaemia low: everything else

Where alveolar haemorrhage occurs the TLCO tends to increase due to the enhanced uptake of carbon monoxide by intra-alveolar haemoglobin. Please rate this question:


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Transfer factor

The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)

Causes of a raised TLCO

asthma

pulmonary haemorrhage (Wegener's, Goodpasture's)

left-to-right cardiac shunts

polycythaemia

hyperkinetic states

Causes of a lower TLCO

pulmonary fibrosis

pneumonia

pulmonary emboli

pulmonary oedema

emphysema


male gender, exercise anaemia

low cardiac output

KCO also tends to increase with age. Some conditions may cause an increased KCO with a normal or reduced TLCO

pneumonectomy/lobectomy scoliosis/kyphosis neuromuscular weakness

ankylosis of costovertebral joints e.g. ankylosing spondylitis

Next question

Which of the following is least likely to be associated with hypercalcaemia?

Thiazides

Antacids

Coeliac disease

Sarcoidosis

Zolinger-Ellison syndrome

Mnemonic for the causes of hypercalcaemia: CHIMPANZEES C alcium supplementation H yperparathyroidism I atrogentic (Drugs: Thiazides) M ilk Alkali syndrome P aget disease of the bone A cromegaly and Addison's Disease N eoplasia Z olinger-Ellison Syndrome (MEN Type I) E xcessive Vitamin D E xcessive Vitamin A S arcoidosis

Patients with coeliac disease tend to develop hypocalcaemia due to malabsorption of calcium by the bowel. Please rate this question:


Next question

Hypercalcaemia

Main causes

Malignancy (most common cause in hospital in-patients) Primary hyperparathyroidism (commonest cause in non hospitalised patients)


Less common

Sarcoidosis (extrarenal synthesis of calcitriol ) Thiazides, lithium

Immobilisation Pagets disease Vitamin A/D toxicity Thyrotoxicosis MEN Milk alkali syndrome

Clinical features

Stones, bones, abdominal groans, and psychic moans High serum calcium levels result in decreased neuronal excitability. Therefore sluggish reflexes, muscle weakness and constipation may occur.

Next question

Release of somatostatin from the pancreas will result in which of the following?

Decrease in pancreatic exocrine secretions

Contraction of the gallbladder

Increase in the rate of gastric emptying

Increased synthesis of growth hormone

Increased insulin release

Octreotide reduces exocrine pancreatic secretions so is used to treat high output pancreatic fistulae

(though parenteral feeding is most effective). Other uses include variceal bleeding and treatment of

acromegaly.

Inhibits growth hormone and insulin release (when released from pancreas).

Somatostatin is also released by the hypothalamus causing a negative feedback response on

growth hormone.



Next question

Somatostatin

Somatostatin is produced in the D cells of the pancreatic islets. It is also produced in the gut

(enterochromaffin cells) and is found in brain tissue. Those substances that stimulate insulin release

will also induce somatostatin secretion. It is an inhibitor of growth hormone, it also delays gastric

emptying and reduces gastrin secretion.

It reduces pancreatic exocrine secretions and may be used therapeutically to treat pancreatic

fistulae.


Somatostatinomas are rare pancreatic endocrine tumours and will result in the clinical

manifestations of diabetes mellitus, gallstones and steatorrhoea.

Next question

A 34 year old lady develops septic shock and features of the systemic inflammatory response syndrome as a complication of cholangitis. Which of the following is not a typical feature of this condition?

Body temperature less than 36oC or greater than 38oC

Respiratory rate >20

Lactate <4 mmol/L

High levels of tumour necrosis factor α

WCC >12,000 mm3

Septic shock will typically result in end organ hypoperfusion and as a result lactate levels will often be high. In the surviving sepsis campaign it is suggested that elevated lactate levels are an independent indicator for vasopressor support in patient with sepsis. The WCC may be paradoxically low in severe sepsis, although it is most often elevated. Please rate this question:


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Shock

Shock occurs when there is insufficient tissue perfusion. The pathophysiology of shock is an important surgical topic and may be divided into the

following aetiological groups: Septic Haemorrhagic Neurogenic Cardiogenic

Anaphylactic

Septic shock

Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure. Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response

Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90


beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes). Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis. Those with organ failure have severe sepsis and those with refractory hypotension -septic shock. During the septic process there is marked activation of the immune system with extensive cytokine

release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those ofexcessive inflammation, coagulation and fibrinolytic suppression. The surviving sepsis campaign (2012) highlights the following key areas for attention:




In surgical patients, the main groups with septic shock include those with anastomotic leaks, abscesses and extensive superficial infections such as necrotising fasciitis. When performing surgery the aim should be to undertake the minimum necessary to restore physiology. These patients do not fare well with prolonged surgery. Definitive surgery can be more safely undertaken when physiology is restored and clotting in particular has been normalised. Haemorrhagic shock The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will equate to 5 litres. This changes in children (8-9% body weight) and is slightly lower in the elderly. The table below outlines the 4 major classes of haemorrhagic shock and their associated physiological sequelae:



Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140






Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative myocardial ischaemia. The cardiac index gives a numerical value for tissue oxygen delivery and is given by the equation: Cardiac index= Cardiac output/ body surface area. Where Hb is haemoglobin concentration in blood and SaO2 the saturation and PaO2 the partial pressure of oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not for part A, although you should understand the principle. In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the following may also be the cause or occur concomitantly:

Tension pneumothorax

Spinal cord injury Myocardial contusion Cardiac tamponade


tone or increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance mediated by marked vasodilation. This results in decreased preload and thus decreased cardiac output (Starlings law). There is decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types of shock peripheral vasoconstrictors are used to return vascular tone to normal.

Cardiogenic shock In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct

myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but they are less useful in delineating the extent of myocardial trauma than following MI. When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the heart is the most likely site of injury with chamber and or valve rupture. These patients require surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may require intra aortic balloon pump as a bridge to surgery. Anaphylactic shock Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction. Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated. Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible. The recommended doses for adrenaline, hydrocortisone and chlorpheniramine are as follows:







food (e.g. Nuts) - the most common cause in children drugs venom (e.g. Wasp sting)

Next question

Which of the following stimulates gastric acid secretion?

Cholecystokinin

Gastric inhibitory peptide

Secretin

Histamine

Somatostatin

Gastrin: From G cells: stimulates gastric acid production

Pepsin: Digestion of protein, secretion occurs simultaneously with gastrin

Secretin: From mucosal cells in the duodenum and jejunum: inhibits gastric acid, stimulates bile and

pancreatic juice production

Gastric inhibitory peptide: (produced in response to fatty acids) inhibits gastrin release and acid

secretion from parietal cells

Cholecystokinin: From mucosal cells in the duodenum and jejunum (produced in response to fatty

acids) inhibits acid secretion from parietal cells, causes gallbladder contraction and relaxation of

sphincter of Oddi

Somatostatin: From D cells



Next question

Hormonal control of gastric acid secretion



Gastrin G cells in

antrum of the

stomach

Distension of

stomach, extrinsic

nerves

Inhibited by: low

antral pH,

somatostatin


increases gastric motility, trophic effect on gastric

mucosa

CCK I cells in upper

small intestine

Partially digested

proteins and

triglycerides

Increases secretion of enzyme-rich fluid from

pancreas, contraction of gallbladder and

relaxation of sphincter of Oddi, decreases gastric

emptying, trophic effect on pancreatic acinar

cells, induces satiety

Secretin S cells in

upper small

intestine

Acidic chyme, fatty

acids

Increases secretion of bicarbonate-rich fluid from

pancreas and hepatic duct cells, decreases gastric

acid secretion, trophic effect on pancreatic acinar

cells

VIP Small

intestine,

pancreas

Neural Stimulates secretion by pancreas and intestines,

inhibits acid and pepsinogen secretion


pancreas and

stomach

Fat, bile salts and

glucose in the

intestinal lumen

Decreases acid and pepsin secretion, decreases

gastrin secretion, decreases pancreatic enzyme

secretion, decreases insulin and glucagon

secretion

inhibits trophic effects of gastrin, stimulates

gastric mucous production

Next question

Which of the following statements relating to gastric acid secretions are untrue?

In parietal cells carbonic anhydrase generates hydrogen ions which are then actively

secreted

The cephalic phase is abolished following truncal vagotomy

The intestinal phase accounts for 60% of gastric acid produced

Histamine acts in a paracrine manner on H2 receptors

H2 receptor antagonists will not completely abolish gastric acid production

The intestinal phase of gastric acid secretion accounts for only 10% of gastric acid produced. Please rate this question:


Next question

Gastric secretions










30% acid produced Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells


60% acid produced Stomach distension/low H+/peptides causes Gastrin release







Regulation of gastric acid production Factors increasing production include:




Somatostatin (inhibits histamine release) Cholecystokinin Secretin








Gastrin G cells in


Distension of

stomach, extrinsic

nerves

Inhibited by: low

antral pH,

somatostatin



CCK I cells in

upper small

intestine

Partially digested

proteins and

triglycerides






Secretin S cells in

upper small

intestine





VIP Small

intestine,

pancreas


intestines, inhibits acid and pepsinogen

secretion


pancreas and

stomach

Fat, bile salts and

glucose in the

intestinal lumen






Next question

A 22 year old man is undergoing a daycase excision of a sebaceous cyst. He is needle phobic and as the surgeon approaches with the needle the patient begins to hyperventilate. He soon develops circumoral parasthesia and muscular twitching. Which of the following is the most likely explanation for this event?

Temporal lobe epilepsy

Reduction in ionised calcium levels

Increase in ionised calcium levels

Fall in serum PTH levels

Rise in serum PTH levels

50% of plasma calcium is ionised. Hyperventilation will induce a state of alkalosis which will lower ionised plasma calcium levels. Please rate this question:


Next question

Calcium homeostasis

Calcium ions are linked to a wide range of physiological processes. The largest store of bodily calcium is contained within the skeleton. Calcium levels are primarily controlled by parathyroid hormone, vitamin D and calcitonin. Hormonal regulation of calcium

Hormone Actions

Parathyroid hormone (PTH) Increase calcium levels and decrease phosphate

levels

Increases bone resorption

Immediate action on osteoblasts to increase ca2+ in

extracellular fluid

Osteoblasts produce a protein signaling molecule

that activate osteoclasts which cause bone

resorption


Hormone Actions

Increases renal tubular reabsorption of calcium

Increases synthesis of 1,25(OH)2D (active form

of vitamin D) in the kidney which increases

bowel absorption of Ca2+

Decreases renal phosphate reabsorption

1,25-dihydroxycholecalciferol (the

active form of vitamin D)

Increases plasma calcium and plasma phosphate

Increases renal tubular reabsorption and gut

absorption of calcium

Increases osteoclastic activity

Increases renal phosphate reabsorption

Calcitonin Secreted by C cells of thyroid

Inhibits intestinal calcium absorption

Inhibits osteoclast activity

Inhibits renal tubular absorption of calcium

Both growth hormone and thyroxine also play a small role in calcium metabolism.

Next question

Which of the following inhibits gastric acid secretion?

Histamine

Nausea

Calcium

Parasympathetic vagal stimulation

Gastrin

Nausea inhibits gastric secretion via higher cerebral activity and sympathetic innervation. Please rate this question:


Next question

Gastric secretions










30% acid produced



60% acid produced






















Gastrin G cells in


Distension of

stomach, extrinsic

nerves

Inhibited by: low

antral pH,

somatostatin



CCK I cells in

upper small

intestine

Partially digested

proteins and

triglycerides






Secretin S cells in

upper small

intestine





VIP Small

intestine, pancreas




pancreas and

stomach

Fat, bile salts and

glucose in the

intestinal lumen






Next question

A 73 year old lady is diagnosed with hyperaldosteronism. From which of the following structures is

aldosterone released?

Zona fasciculata of the adrenal gland

Juxtaglomerular apparatus of the kidney

Zona reticularis of the adrenal gland

Adrenal medulla

Zona glomerulosa of the adrenal cortex

Aldosterone serves to conserve sodium and water. It is produced in the zona glomerulosa of the

adrenal cortex.



Next question

Aldosterone

Aldosterone is secreted by the zona glomerulosa of the adrenal cortex. It is a mineralocorticoid

hormone. Secretion is regulated by the renin- angiotensin system, and by plasma levels of sodium

and potassium. Aldosterone conserves sodium by stimulating the reabsorption of sodium in the

distal nephron in exchange for potassium. Lack of aldosterone release will result in hyperkalaemia

and hyponatraemia.

Next question


Which of the following hormonal agents will increase secretions of water and electrolytes in

pancreatic juice?

Secretin

Aldosterone

Somatostatin

Cholecystokinin

Adrenaline

Secretin causes secretion of water and electrolytes

Cholecystokinin causes enzyme secretion

While secretin will typically increase electrolyte and water volume of secretions, the enzyme content

in increased by cholecystokinin. Somatostatin will decrease the volume of secretions. Aldosterone

will tend to conserve electrolytes.



Next question

Pancreas exocrine physiology

Composition of pancreatic secretions

Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.

Secretion Source Substances secreted

Enzymic Acinar cells Trypsinogen


Procarboxylase

Amylase

Elastase

Aqueous Ductal and

Centroacinar cells

Sodium

Bicarbonate

Water

Potassium

Chloride

NB: Sodium and potassium reflect their plasma levels; chloride

and bicarbonate vary with flow rate

Regulation

The cephalic and gastric phases (neuronal and physical) are less important in regulating the

pancreatic secretions. The effect of digested material in the small bowel stimulates CCK release and

ACh which stimulate acinar and ductal cells. Of these CCK is the most potent stimulus. In the case

of the ductal cells these are potently stimulated by secretin which is released by the S cells of the

duodenum. This results in an increase in bicarbonate.

Enzyme activation

Trypsinogen is converted via enterokinase to active trypsin in the duodenum. Trypsin then activates

the other inactive enzymes

Next question

A 43 year old lady is admitted with cholestasis secondary to a stone impacted at the level of the

ampulla of vater. Which of the following tests is most likely to be predictive of bleeding diathesis at

the time of ERCP in this particular case?

Bleeding time

Prothrombin time

APTT

Platelet count

Factor I levels

PT: Vitamin K dependent factors 2, 7, 9, 10

APTT: Factors 8, 9, 11, 12

Jaundice will impair the production of vitamin K dependent clotting factors. This is most accurately

tested by measuring the prothrombin time. APTT can be affected by vitamin K deficiency (due to

factor 9 deficiency), however this occurs to a lesser extent and is normally associated with severe

liver disease. The bleeding time is a measure of platelet function.



Next question

Abnormal coagulation




Heparin Prevents activation factors 2,9,10,11

Warfarin Affects synthesis of factors 2,7,9,10

DIC Factors 1,2,5,8,11

Liver disease Factors 1,2,5,7,9,10,11

Interpretation blood clotting test results

Disorder APTT PT Bleeding time

Haemophilia Increased Normal Normal

von Willebrand's disease Increased Normal Increased

Vitamin K deficiency Increased Increased Normal

Next question

Which of the following mechanisms best accounts for the release of adrenaline?

Release from the adrenal medulla in response to increased angiotensin 1 levels

Release from the zona fasiculata from the adrenal gland in response to increased

sympathetic discharge

Release from the adrenal medulla in response to increased noradrenaline levels

Release from the adrenal medulla in response to sympathetic stimulation from the

splanchnic nerves

None of the above

The adrenal gland releases adrenaline in response to increased sympathetic discharge from preganglionic sympathetic fibres of the splanchnic nerves. These cause the chromafin cells of the medulla to release adrenaline (which is preformed) by exocytosis. Please rate this question:


Next question

Adrenaline

Fight or Flight response

- Catecholamine (phenylalanine and tyrosine) - Neurotransmitter and hormone - Released by the adrenal glands - Effects on α 1 and 2, β 1 and 2 receptors - Effect on β 2 receptors in skeletal muscle vessels-causing vasodilation - Increase cardiac output and total peripheral resistance - Vasoconstriction in the skin and kidneys causing a narrow pulse pressure Actions

α adrenergic receptors:

Inhibits insulin secretion by the pancreas

Stimulates glycogenolysis in the liver and muscle Stimulates glycolysis in muscle


β adrenergic receptors:

Stimulates glucagon secretion in the pancreas Stimulates ACTH

Stimulates lipolysis by adipose tissue

Next question

The acute phase response to injury does not include:

Pyrexia

Decreased albumin

Hepatic sequestration of cations

Increased transferrin

Increased serum amyloid A

The acute phase response includes:

Acute phase proteins Reduction of transport proteins (albumin, transferrin) Hepatic sequestration cations Pyrexia

Neutrophil leucocytosis Increased muscle proteolysis Changes in vascular permeability



Next question












Aldosterone

Prolactin


Glucagon


Stimulates catecholamine release Causes tachycardia and hypertension

Pituitary gland



stimulating hormone (FSH) does not change significantly

ACTH stimulates cortisol production within a few minutes of the start of surgery. More ACTH is produced than needed to produce a maximum adrenocortical response.

Cortisol

Significant increases within 4-6 hours of surgery (>1000 nmol litre-1). The usual negative feedback mechanism fails and concentrations of ACTH and cortisol

remain persistently increased.

The magnitude and duration of the increase correlate with the severity of stress and the response is not abolished by the administration of corticosteroids.

The metabolic effects of cortisol are enhanced:


Increased secretion after surgery has a minor role

Most important for preventing muscle protein breakdown and promote tissue repair by insulin growth factors

Alpha Endorphin

Increased


An important vasopressor and enhances haemostasis

Renin is released causing the conversion of angiotensinogen to angiotensin I Angiotensin II formed by ACE on angiotensin 1, which causes the secretion of aldosterone


Insulin

Release inhibited by stress

Occurs via the inhibition of the beta cells in the pancreas by the α2-adrenergic inhibitory effects of catecholamines

Insulin resistance by target cells occurs later

The perioperative period is characterized by a state of functional insulin deficiency



Metabolic effect of endocrine response

Carbohydrate metabolism

Hyperglycaemia is a main feature of the metabolic response to surgery Due to increase in glucose production and a reduction in glucose utilization Catecholamines and cortisol promote glycogenolysis and gluconeogenesis

Initial failure of insulin secretion followed by insulin resistance affects the normal responses The proportion of the hyperglycaemic response reflects the severity of surgery Hyperglycaemia impairs wound healing and increase infection rates

Protein metabolism



Mainly skeletal muscle protein is affected The amino acids released form acute phase proteins (fibrinogen, C reactive protein,

complement proteins, a2-macroglobulin, amyloid A and ceruloplasmin) and are used for gluconeogenesis





Cytokines

Glycoproteins Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor

Synthesized by activated macrophages, fibroblasts, endothelial and glial cells in response to tissue injury from surgery or trauma



Opioids suppress hypothalamic and pituitary hormone secretion

At high doses the hormonal response to pelvic and abdominal surgery is abolished. However, such doses prolong recovery and increase the need for postoperative ventilatory support



recovery

Growth hormone and anabolic steroids may improve outcome Normothermia decreases the metabolic response

References Deborah Burton, Grainne Nicholson, and George Hall Endocrine and metabolic response to surgery . Contin Educ Anaesth Crit Care Pain (2004) 4(5): 144-147 doi:10.1093/bjaceaccp/mkh040

Next question

Which of the following statements relating to blood transfusions in surgical patients is false?

Packed red cells typically have a haematocrit of between 55 and 75%

Clotting factor activity in whole blood decreases in samples stored for longer than 7 days

After 3 weeks of storage blood has a pH of 6.9

Gamma irradiated blood products are not required routinely

Patients should be transfused to achieve a target haemoglobin of 10 g/dl and a haematocrit

of 30%

Patients can generally be managed without transfusion as long as the Hb is 7 or greater. The exact level depends upon patient factors such as co-morbidities. Old blood functions less effectively and should not be used during massive transfusions. Please rate this question:


Next question

Blood products

Whole blood fractions

Fraction Key points

Packed red cells Used for transfusion in chronic anaemia and cases where infusion of large

volumes of fluid may result in cardiovascular compromise. Product obtained by centrifugation of whole blood.

Platelet rich

plasma

Usually administered to patients who are thrombocytopaenic and are bleeding

or require surgery. It is obtained by low speed centrifugation.

Platelet Prepared by high speed centrifugation and administered to patients with


concentrate thrombocytopaenia.

Fresh frozen

plasma

Prepared from single units of blood.

Contains clotting factors, albumin and immunoglobulin.

Unit is usually 200 to 250ml.

Usually used in correcting clotting deficiencies in patients with hepatic

synthetic failure who are due to undergo surgery.

Usual dose is 12-15ml/Kg-1.

It should not be used as first line therapy for hypovolaemia.

Cryoprecipitate Formed from supernatant of FFP.

Rich source of Factor VIII and fibrinogen.

Allows large concentration of factor VIII to be administered in small

volume.

SAG-Mannitol

Blood

Removal of all plasma from a blood unit and substitution with:

Sodium chloride

Adenine

Anhydrous glucose

Mannitol

Up to 4 units of SAG M Blood may be administered. Thereafter whole blood

is preferred. After 8 units, clotting factors and platelets should be considered.

Cell saver devices These collect patients own blood lost during surgery and then re-infuse it. There are two main types:

Those which wash the blood cells prior to re-infusion. These are more expensive to purchase and more complicated to operate. However, they reduce the risk of re-infusing contaminated blood back into the patient.

Those which do not wash the blood prior to re-infusion.

Their main advantage is that they avoid the use of infusion of blood from donors into patients and this may reduce risk of blood borne infection. It may be acceptable to Jehovah's witnesses. It is contraindicated in malignant disease for risk of facilitating disease dissemination. Blood products used in warfarin reversal

In some surgical patients the use of warfarin can pose specific problems and may require the use of specialised blood products Immediate or urgent surgery in patients taking warfarin(1) (2):

1. Stop warfarin 2. Vitamin K (reversal within 4-24 hours) -IV takes 4-6h to work (at least 5mg) -Oral can take 24 hours to be clinically effective 3. Fresh frozen plasma Used less commonly now as 1st line warfarin reversal -30ml/kg-1 -Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid overload) -Need blood group -Only use if human prothrombin complex is not available 4. Human Prothrombin Complex (reversal within 1 hour) -Bereplex 50 u/kg -Rapid action but factor 6 short half life, therefore give with vitamin K References

1. Dentali, F., C. Marchesi, et al. (2011). "Safety of prothrombin complex concentrates for rapid anticoagulation reversal of vitamin K antagonists. A meta-analysis." Thromb Haemost 106(3): 429-438. 2. http://www.transfusionguidelines.org/docs/pdfs/bbt-03warfarin-reversal-flowchart-2006.pdf

Next question

Which of the following statements relating the fluid physiology of a physiologically normal 70 Kg

adult male is false?

He will have more water per unit of body weight than a female of similar weight

Plasma will comprise 25% of his body weight

Interstitial fluid will account for up to 24% of body weight

Approximately 65% of total body water is intracellular

60% of his body weight is composed of water

The 60-40-20 rule:

60% total body weight is water

40% of total body weight is intracellular fluids

20% of body weight is extracellular fluids

Plasma typically accounts for 4-6% of body weight in healthy individuals.

Males typically have more water per unit weight than females, as females have a higher fat content.



Next question

Fluid compartment physiology

Body fluid compartments comprise intracellular and extracellular compartments. The latter includes

interstitial fluid, plasma and transcellular fluid.

Typical figures are based on the 70 Kg male.

Body fluid volumes


Compartment Volume in litres Percentage of total volume

Intracellular 28 L 60-65%

Extracellular 14 L 35-40%

Plasma 3 L 5%

Interstitial 10 L 24%

Transcellular 1 L 3%

Figures are approximate

Next question

A 17 year old lady with long standing anorexia nervosa is due to undergo excision of a lipoma. Which of the following nutritional deficiencies is most likely to be implicated in poor collagen formation as the wound heals?

Deficiency of copper

Deficiency of iron

Deficiency of ascorbic acid

Deficiency of phosphate

None of the above

Theme from January 2011 Vitamin C is involved in the cross linkage of collagen and impaired wound healing is well described in cases of vitamin C deficiency. Please rate this question:


Next question

Collagen

Collagen is one of the most important structural proteins within the extracellular matrix, collagen together with components such as elastin and glycosaminoglycans determine the properties of all tissues.

Composed of 3 polypeptide strands that are woven into a helix, usually a combination of glycine with either proline or hydroxyproline plus another amino acid

Numerous hydrogen bonds exist within molecule to provide additional strength Many sub types but commonest sub type is I (90% of bodily collagen), tissues with increased

levels of flexibility have increased levels of type III collagen Vitamin c is important in establishing cross links Synthesised by fibroblasts

Collagen Diseases Disorders of collagen range from relatively common, acquired defects (typically aging), through to rarer congenital disorders. The latter are exemplified by conditions such as osteogenesis imperfecta


and Ehlers Danlos syndromes. Osteogenesis imperfecta: -8 Subtypes -Defect of type I collagen -In type I the collagen is normal quality but insufficient quantity -Type II- poor quantity and quality -Type III- Collagen poorly formed, normal quantity -Type IV- Sufficient quantity but poor quality Patients have bones which fracture easily, loose joint and multiple other defects depending upon which sub type they suffer from. Ehlers Danlos: -Multiple sub types -Abnormality of types 1 and 3 collagen -Patients have features of hypermobility. -Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to many other diseases related to connective tissue defects.

Next question

A 45 year old man is undergoing a small bowel resection. The anaesthetist decides to administer an

intravenous fluid which is electrolyte rich. Which of the following most closely matches this

requirement?

Dextrose / Saline

Pentastarch

Gelofusine

Hartmans

5% Dextrose with added potassium 20mmol/ L

Theme from April 2012 Exam

Hartmans solution is the most electrolyte rich. However, both pentastarch and gelofusine have more

macromolecules.



Next question

Intra operative fluid management

Composition of commonly used intravenous fluids mmol-1

Na K Cl Bicarbonate Lactate

Plasma 137-147 4-5.5 95-105 22-25 -


0.9% Saline 153 - 153 - -

Dextrose / saline 30.6 - 30.6 - -

Hartmans 130 4 110 - 28

Recommendations for intra operative fluid management

The latest set of NICE guidelines produced in 2013 relating to intravenous fluids did not specifically

address the requirements of intra operative fluid administration. The reason for this is that

administration of fluids in this specific situation does not lend itself to rigid algorithms.

With the introduction of enhanced recovery programmes 10 years ago there was an increasing

emphasis of the concept of fluid restriction. Historically, patients received very large volumes of

saline rich solutions peri-operatively. Clearing the sodium load of a single litre of saline may take up

to 36 hours or more. This can have deleterious effects on the tissues including the development of

oedema. This results in poor perfusion, increased risk of ileus and wound breakdown. A tailored

approach to fluid administration is now practiced and far greater usage is made of cardiac output

monitors in providing goal directed fluid therapy.

References

British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical Patients

GIFTASUP (2009) Revised May 2011.

Frost P. Intravenous fluid therapy in adult inpatients. BMJ 2015 (350): 31-34.

Next question

A 16 year old girl develops pyelonephritis and is admitted in a state of septic shock. Which of the following is not typically seen in this condition?

Increased cardiac output

Increased systemic vascular resistance

Oliguria may occur

Systemic cytokine release

Tachycardia

Cardiogenic Shock: e.g. MI, valve abnormality increased SVR (vasoconstriction in response to low BP) increased HR (sympathetic response) decreased cardiac output decreased blood pressure Hypovolaemic shock: blood volume depletion e.g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during major operations increased SVR increased HR decreased cardiac output decreased blood pressure Septic shock: occurs when the peripheral vascular dilatation causes a fall in SVR similar response may occur in anaphylactic shock, neurogenic shock reduced SVR increased HR normal/increased cardiac output decreased blood pressure

Theme from January 2012 Exam The SVR is reduced in sepsis and for this reason a vasopressor such as noradrenaline may be used if hypotension and oliguria remain a concern despite administration of adequate amounts of intravenous fluids. Please rate this question:


Next question

Shock

Shock occurs when there is insufficient tissue perfusion.

The pathophysiology of shock is an important surgical topic and may be divided into the following aetiological groups:

Septic Haemorrhagic Neurogenic

Cardiogenic Anaphylactic

Septic shock Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess of 40%. In those who are admitted to intensive care mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure. Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response

Syndrome (SIRS). This is characterised by body temperature outside 36 oC - 38 o C, HR >90

beats/min, respiratory rate >20/min, WBC count >12,000/mm3 or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes). Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis. Those with organ failure have severe sepsis and those with refractory hypotension -septic shock. During the septic process there is marked activation of the immune system with extensive cytokine

release. This may be coupled with or triggered by systemic circulation of bacterial toxins. These all cause endothelial cell damage and neutrophil adhesion. The overall hallmarks are thus those ofexcessive inflammation, coagulation and fibrinolytic suppression.

The surviving sepsis campaign (2012) highlights the following key areas for attention:




In surgical patients, the main groups with septic shock include those with anastomotic leaks, abscesses and extensive superficial infections such as necrotising fasciitis. When performing surgery the aim should be to undertake the minimum necessary to restore physiology. These patients do not fare well with prolonged surgery. Definitive surgery can be more safely undertaken


when physiology is restored and clotting in particular has been normalised. Haemorrhagic shock The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will equate to 5 litres. This changes in children (8-9% body weight) and is slightly lower in the elderly. The table below outlines the 4 major classes of haemorrhagic shock and their associated physiological sequelae:



Blood loss % <15% 15-30% 30-40% >40%

Pulse rate <100 >100 >120 >140





Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative myocardial ischaemia. The cardiac index gives a numerical value for tissue oxygen delivery and is given by the equation: Cardiac index= Cardiac output/ body surface area. Where Hb is haemoglobin concentration in blood and SaO2 the saturation and PaO2 the partial pressure of oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not for part A, although you should understand the principle. In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the following may also be the cause or occur concomitantly:

Tension pneumothorax Spinal cord injury

Myocardial contusion Cardiac tamponade


tone or increased parasympathetic tone, the effect of which is a decrease in peripheral vascular resistance mediated by marked vasodilation. This results in decreased preload and thus decreased cardiac output (Starlings law). There is decreased peripheral tissue perfusion and shock is thus produced. In contrast with many other types of shock peripheral vasoconstrictors are used to return vascular tone to normal. Cardiogenic shock In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct myocardial trauma or contusion is more likely. Evidence of ECG changes and overlying sternal fractures or contusions should raise the suspicion of injury. Treatment is largely supportive and transthoracic echocardiography should be used to determine evidence of pericardial fluid or direct myocardial injury. The measurement of troponin levels in trauma patients may be undertaken but they are less useful in delineating the extent of myocardial trauma than following MI. When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the heart is the most likely site of injury with chamber and or valve rupture. These patients require surgery to repair these defects and will require cardiopulmonary bypass to achieve this. Some may require intra aortic balloon pump as a bridge to surgery. Anaphylactic shock

Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction. Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication. The Resuscitation Council guidelines on anaphylaxis have recently been updated. Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible. The recommended doses for adrenaline, hydrocortisone and chlorpheniramine are as follows:







food (e.g. Nuts) - the most common cause in children

drugs venom (e.g. Wasp sting)

Next question

Which of the following statements are not typically true in hypokalaemia?

It may occur as a result of mechanical bowel preparation

Chronic vomiting may increase renal potassium losses

It may be associated with aciduria

It may cause hyponatraemia

It often accompanies acidosis

Potassium depletion occurs either through the gastrointestinal tract or the kidney. Chronic vomiting in itself is less prone to induce potassium loss than diarrhoea as gastric secretions contain less potassium than those in the lower GI tract. If vomiting produces a metabolic alkalosis then renal potassium wasting may occur as potassium is excreted in preference to hydrogen ions. The converse may occur in potassium depletion resulting in acid urine. Hypokalemia is very commonly associated with metabolic alkalosis. This is due to 2 factors: 1) the common causes of metabolic alkalosis (vomiting, diuretics) directly induce H+ and K loss (via aldosterone) and thus also cause hypokalemia and 2) hypokalemia is a very important cause of metabolic alkalosis by three mechanisms. The initial effect is by causing a transcellular shift in which K leaves and H+ enters the cells, thereby raising the extracellular pH. The second effect is by causing a transcellular shift in the cells of the proximal tubules resulting in an intracellular acidosis, which promotes ammonium production and excretion. Thirdly, in the presence of hypokalemia, hydrogen secretion in the proximal and distal tubules increases. This leads to further reabsorption of HCO3-. The net effect is an increase in the net acid excretion. Please rate this question:


Next question

Hypokalaemia

Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends to be associated with acidosis because as potassium levels rise fewer hydrogen ions can enter the cells Hypokalaemia with alkalosis

Vomiting Diuretics


Cushing's syndrome Conn's syndrome (primary hyperaldosteronism)

Hypokalaemia with acidosis

Diarrhoea Renal tubular acidosis Acetazolamide Partially treated diabetic ketoacidosis

Next question

A man is admitted after a period of prolonged self, induced starvation. Naso gastric feeding is planned. Which of the following is least likely to occur?

Hypokalaemia

Increased risk of cardiac arrhythmias

His haemoglobin will have decreased affinity for oxygen

Hypophosphataemia

Hypoalbuminaemia

The process of starvation may lower DPG levels, in practice this is unlikely to occur early as it is generated during glycolysis. Altered metabolism in starvation may be more acidotic and this would also tend to impair oxygen carriage. Please rate this question:


Next question



Hypophosphataemia Hypokalaemia Hypomagnesaemia Abnormal fluid balance

These abnormalities can lead to organ failure. Re-feeding problems If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels High risk for re-feeding problems

If one or more of the following:

BMI < 16 kg/m2


Unintentional weight loss >15% over 3-6 months Little nutritional intake > 10 days Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)


BMI < 18.5 kg/m2 Unintentional weight loss > 10% over 3-6 months Little nutritional intake > 5 days

History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids

Prescription

Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co

strong 1 tds and supplements


Next question

v

Where does spironolactone act in the kidney?

Glomerulus

Proximal convoluted tubule

Descending limb of the loop of Henle

Ascending limb of the loop of Henle

Distal convoluted tubule



Next question

Potassium sparing diuretics

Potassium-sparing diuretics may be divided into the epithelial sodium channel blockers (amiloride and triamterene) and aldosterone antagonists (spironolactone and eplerenone). {Amiloride} is a weak diuretic which blocks the epithelial sodium channel in the distal convoluted tubule. Usually given with thiazides or loop diuretics as an alternative to potassium supplementation. {Spironolactone} is an aldosterone antagonist which acts act in the distal convoluted tubule. Indications

ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used

heart failure nephrotic syndrome Conn's syndrome

Next question


Which receptor does noradrenaline mainly bind to?

α 1 receptors

α 2 receptors

β 1 receptors

β 2 receptors

G receptors

Theme from September 2015 Exam

Noradrenaline is the precursor of adrenaline. It is a powerful α 1 stimulant (although it will increase

myocardial contractility). Infusions will produce vasoconstriction and an increase in total peripheral

resistance. It is the inotrope of choice in septic shock.



Next question

Inotropes and cardiovascular receptors

Inotropes are a class of drugs which work primarily by increasing cardiac output. They should be

distinguished from vasoconstrictor drugs which are used specifically when the primary problem is

peripheral vasodilatation.

Catecholamine type agents are commonly used and work by increasing cAMP levels by adenylate

cyclase stimulation. This in turn intracellular calcium ion mobilisation and thus the force of

contraction. Adrenaline works as a beta adrenergic receptor agonist at lower doses and an alpha

receptor agonist at higher doses. Dopamine causes dopamine receptor mediated renal and

mesenteric vascular dilatation and beta 1 receptor agonism at higher doses. This results in

increased cardiac output. Since both heart rate and blood pressure are raised, there is less overall


myocardial ischaemia. Dobutamine is a predominantly beta 1 receptor agonist with weak beta 2 and

alpha receptor agonist properties. Noradrenaline is a catecholamine type agent and predominantly

acts as an alpha receptor agonist and serves as a peripheral vasoconstrictor.

Phosphodiesterase inhibitors such as milrinone act specifically on the cardiac phosphodiesterase

and increase cardiac output.

Inotrope Cardiovascular receptor action

Adrenaline α-1, α-2, β-1, β-2

Noradrenaline α-1,( α-2), (β-1), (β-2)

Dobutamine β-1, (β 2)

Dopamine (α-1), (α-2), (β-1), D-1,D-2

Minor receptor effects in brackets

Effects of receptor binding

α-1, α-2 vasoconstriction

β-1 increased cardiac contractility and HR

β-2 vasodilatation

D-1 renal and spleen vasodilatation

D-2 inhibits release of noradrenaline

Next question

Adult lung volumes. Which statement is false?

In restrictive lung disease the FEV1/FVC ratio is increased

Residual volume is increased in emphysema

Functional residual capacity is measured by helium dilution test

The tidal volume is approximately 340mls in females

The vital capacity is increased in Guillain Barre syndrome

FEV1/FVC is normal or >80% in restrictive lung disease such as pulmonary fibrosis. The ratio is reduced in obstructive airways disease. The functional residual capacity, residual volume and the total lung capacity cannot be measured with spirometry. They can only be measured by helium dilution. The vital capacity is reduced in: 1. Pulmonary fibrosis/infiltration/oedema/effusions 2. Weak respiratory muscles e.g. MG, GBS, myopathies 3. Skeletal abnormalities e.g. chest wall abnormalities Please rate this question:


Next question

Lung volumes

The diagram demonstrates lung volumes and capacities



Definitions

Tidal volume (TV) Is the volume of air inspired and expired during each

ventilatory cycle at rest.

It is normally 500mls in males and 340mls in females.

Inspiratory reserve

volume (IRV)

Is the maximum volume of air that can be forcibly inhaled

following a normal inspiration. 3000mls.

Expiratory reserve

volume (ERV)

Is the maximum volume of air that can be forcibly exhaled

following a normal expiration. 1000mls.

Residual volume (RV) Is that volume of air remaining in the lungs after a maximal

expiration.

RV = FRC - ERV. 1500mls.

Functional residual

capacity (FRC)

Is the volume of air remaining in the lungs at the end of a

normal expiration.

FRC = RV + ERV. 2500mls.

Vital capacity (VC) Is the maximal volume of air that can be forcibly exhaled after

a maximal inspiration.

VC = TV + IRV + ERV. 4500mls in males, 3500mls in

females.

http://en.wikipedia.org/wiki/Lung%20volumes



Total lung capacity

(TLC)

Is the volume of air in the lungs at the end of a maximal

inspiration.

TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.

Forced vital capacity

(FVC)

The volume of air that can be maximally forcefully exhaled.

Next question

A 47 year old lady is diagnosed as suffering from a phaeochromocytoma. From which of the

following amino acids are catecholamines primarily derived?

Aspartime

Glutamine

Arginine

Tyrosine

Alanine

Catecholamine hormones are derived from tyrosine, it is modified by a DOPA decarboxylase

enzyme to become dopamine and thereafter via two further enzymic modifications to noradrenaline

and finally adrenaline.



Next question

Adrenal physiology

Adrenal medulla

The chromaffin cells of the adrenal medulla secrete the catecholamines noradrenaline and

adrenaline. The medulla is innervated by the splanchnic nerves; the preganglionic sympathetic fibres

secrete acetylcholine causing the chromaffin cells to secrete their contents by exocytosis.

Phaeochromocytomas are derived from these cells and will secrete both adrenaline and nor

adrenaline.

Adrenal cortex

Three histologically distinct zones are recognised:


Zone Location Hormone Secreted

Zona glomerulosa Outer zone Aldosterone

Zona fasiculata Middle zone Glucocorticoids

Zona reticularis Inner zone Androgens

The glucocorticoids and aldosterone are mostly bound to plasma proteins in the circulation.

Glucocorticoids are inactivated and excreted by the liver.

Next question

Theme: Events in wound healing

A. Platelets

B. Neutrophil polymorphs

C. Endothelial cells

D. Lymphocytes

E. Myofibroblasts

F. Granulomas Please select the dominant cell type present in a wound at the specified timeframe. Each option may be used once, more than once or not at all.

132. 10 weeks following injury

You answered Platelets

The correct answer is Myofibroblasts

These differentiated cell types facilitate wound contraction.

133. 25 seconds following injury

You answered Neutrophil polymorphs

The correct answer is Platelets

Platelet degranulation and haemostasis are some of the earliest events in wound healing.

134. 7 days following injury

You answered Neutrophil polymorphs

The correct answer is Endothelial cells

Angiogenesis which is characterised by endothelial cell proliferation and microvessel

formation is a key step in successful wound healing. It is maximal between 1 and 2 weeks

following injury and wounds may have a reddish appearance during this time.



Next question


Phases of wound healing

Phase Key features Cells Timeframe

Haemostasis Vasospasm in adjacent vessels

Platelet plug formation and

generation of fibrin rich clot

Erythrocytes and

platelets

Seconds/

Minutes

Inflammation Neutrophils migrate into wound

(function impaired in diabetes).

Growth factors released, including

basic fibroblast growth factor and

vascular endothelial growth factor.

Fibroblasts replicate within the

adjacent matrix and migrate into

wound.

Macrophages and fibroblasts

couple matrix regeneration and clot

substitution.

Neutrophils,

fibroblasts and

macrophages

Days

Regeneration Platelet derived growth factor and

transformation growth factors

stimulate fibroblasts and epithelial

cells.

Fibroblasts produce a collagen

network.

Angiogenesis occurs and wound

resembles granulation tissue.

Fibroblasts,

endothelial cells,

macrophages

Weeks

Remodelling Longest phase of the healing

process and may last up to one year

(or longer).

During this phase fibroblasts

become differentiated

(myofibroblasts) and these

facilitate wound contraction.

Collagen fibres are remodelled.

Microvessels regress leaving a pale

scar.

Myofibroblasts 6 weeks to 1

year

Next question

Where are the arterial baroreceptors located?

Carotid sinus and aortic arch

Carotid sinus only

Superior vena cava

External carotid artery

None of the above

Theme from September 2015 Exam They lie in the carotid sinus and aortic arch. Please rate this question:


Next question

Cardiac physiology

The heart has four chambers ejecting blood into both low pressure and high pressure systems.

The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on the left.

At rest diastole comprises 2/3 of the cardiac cycle. The product of the frequency of heart rate and stroke volume combine to give the cardiac

output which is typically 5-6L per minute.

Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are on the syllabus). However, they are a very popular topic for surgical physiology in the MRCS B exam. Electrical properties

Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is capable of contraction.

In the normal situation the cardiac impulse is generated in the sino atrial node in the right atrium and conveyed to the ventricles via the atrioventricular node.


The sino atrial node is also capable of spontaneous discharge and in the absence of background vagal tone will typically discharge around 100x per minute. Hence the higher resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting membrane potential is lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at which point an action potential is generated.

Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA node will depolarise first. The cells have a refractory period during which they cannot be re-stimulated and this period allows for adequate ventricular filling. In pathological tachycardic states this time period is overridden and inadequate ventricular filling may then occur, cardiac output falls and syncope may ensue.

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation. Cardiac cycle


Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic pressure is high.

Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic

volume 130-160ml.

http://en.wikipedia.org/wiki/Cardiac%20cycle



Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).

Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml (i.e. Volume ejected).

Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave associated with closure of the aortic valve increases aortic pressure. The pressure dip before this rise can be seen on arterial waveforms and is called the incisura. During systole the atrial pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure falls (y -descent )

The negative atrial pressures are of clinical importance as they can allow air embolization to occur if the neck veins are exposed to air. This patient positioning is important in head and neck surgery to avoid this occurrence if veins are inadvertently cut, or during CVP line insertion. Mechanical properties

Preload = end diastolic volume

Afterload = aortic pressure

It is important to understand the principles of Laplace's law in surgery.

It states that for hollow organs with a circular cross section, the total circumferential wall tension depends upon the circumference of the wall, multiplied by the thickness of the wall and on the wall tension.

The total luminal pressure depends upon the cross sectional area of the lumen and the transmural pressure. Transmural pressure is the internal pressure minus external pressure and at equilibrium the total pressure must counterbalance each other.

In terms of cardiac physiology the law explains that the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have impaired systolic function.

Starlings law

Increase in end diastolic volume will produce larger stroke volume. This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke

volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output.

Baroreceptor reflexes

Baroreceptors located in aortic arch and carotid sinus.

Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.

They are stimulated by arterial stretch.

Even at normal blood pressures they are tonically active. Increase in baroreceptor discharge causes:

*Increased parasympathetic discharge to the SA node. *Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke volume. *Decreased sympathetic discharge to venous system causing increased compliance. *Decreased peripheral arterial vascular resistance Atrial stretch receptors

Located in atria at junction between pulmonary veins and vena cava.

Stimulated by atrial stretch and are thus low pressure sensors. Increased blood volume will cause increased parasympathetic activity. Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors:

theBainbridge reflex.

Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by juxtaglomerular apparatus-Increase in angiotensin II.

Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

Next question

Which one of the following cells secretes the majority of tumour necrosis factor in humans?

Neutrophils

Macrophages

Natural killer cells

Killer-T cells

Helper-T cells



Next question

Tumour necrosis factor

Tumour necrosis factor (TNF) is a pro-inflammatory cytokine with multiple roles in the immune system TNF is secreted mainly by macrophages and has a number of effects on the immune system, acting mainly in a paracrine fashion:

activates macrophages and neutrophils

acts as costimulator for T cell activation key mediator of bodies response to Gram negative septicaemia similar properties to IL-1 anti-tumour effect (e.g. phospholipase activation)

TNF-alpha binds to both the p55 and p75 receptor. These receptors can induce apoptosis. It also cause activation of NFkB Endothelial effects include increase expression of selectins and increased production of platelet activating factor, IL-1 and prostaglandins TNF promotes the proliferation of fibroblasts and their production of protease and collagenase. It is thought fragments of receptors act as binding points in serum


Systemic effects include pyrexia, increased acute phase proteins and disordered metabolism leading to cachexia TNF is important in the pathogenesis of rheumatoid arthritis - TNF blockers (e.g. infliximab, etanercept) are now licensed for treatment of severe rheumatoid

Next question

Which of the following is responsible for the rapid depolarisation phase of the myocardial action

potential?

Rapid sodium influx

Rapid sodium efflux

Slow efflux of calcium

Efflux of potassium

Rapid calcium influx



Next question

Electrical activity of the heart

Myocardial action potential

Phase Description Mechanism

0 Rapid depolarisation Rapid sodium influx

These channels automatically deactivate after a few ms

1 Early repolarisation Efflux of potassium


Phase Description Mechanism

2 Plateau Slow influx of calcium

3 Final repolarisation Efflux of potassium

4 Restoration of ionic

concentrations

Resting potential is restored by Na+/K+ ATPase

There is slow entry of Na+ into the cell decreasing the potential

difference until the threshold potential is reached, triggering a new

action potential

NB cardiac muscle remains contracted 10-15 times longer than skeletal muscle

Conduction velocity

Atrial conduction Spreads along ordinary atrial myocardial fibres at 1 m/sec

AV node

conduction

0.05 m/sec

Ventricular

conduction

Purkinje fibres are of large diameter and achieve velocities of 2-4 m/sec (this allows a

rapid and coordinated contraction of the ventricles

Next question

Which of the following is not a feature of normal cerebrospinal fluid?

It has a pressure of between 10 and 15 mmHg.

It usually contains a small amount of glucose.

It may normally contain up to 5 red blood cells per mm3.

It may normally contain up to 3 white blood cells per mm3.

None of the above

It should not contain red blood cells. Please rate this question:


Next question

Cerebrospinal fluid

The CSF fills the space between the arachnoid mater and pia mater (covering surface of the brain). The total volume of CSF in the brain is approximately 150ml. Approximately 500 ml is produced by the ependymal cells in the choroid plexus (70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations which project into the venous sinuses. Circulation

1. Lateral ventricles (via foramen of Munro) 2. 3rd ventricle 3. Cerebral aqueduct (aqueduct of Sylvius) 4. 4th ventricle (via foramina of Magendie and Luschka) 5. Subarachnoid space 6. Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus Composition

Glucose: 50-80mg/dl

Protein: 15-40 mg/dl Red blood cells: Nil White blood cells: 0-3 cells/ mm3

Next question


Which of the following is not an effect of somatostatin?

It stimulates pancreatic acinar cells to release lipase

It decreases gastric acid secretion

It deceases gastrin release

It decreases pepsin secretion

It decreases glucagon release

It inhibits pancreatic enzyme secretion. Please rate this question:


Gastric secretions


Is produced by the parietal cells in the stomach

pH of gastric acid is around 2 with acidity being maintained by the H+/K+ ATP ase pump. As part of the process bicarbonate ions will be secreted into the surrounding vessels.







30% acid produced



60% acid produced






















Gastrin G cells in


Distension of

stomach, extrinsic

nerves

Inhibited by: low

antral pH,

somatostatin



CCK I cells in

upper small

intestine

Partially digested

proteins and

triglycerides






Secretin S cells in

upper small

intestine





VIP Small

intestine, pancreas




pancreas and

stomach

Fat, bile salts and

glucose in the

intestinal lumen






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