All of medicine in 12 hours… Dr. Alan McLeod (F2)

All of medicine in 12 hours…

Dr. Alan McLeod (F2)

The Plan

Day One

• A systematic approach• Chest Pain• Acute sob• Chronic sob• Haemoptysis• TATT• Painful Limb• Breast Pain• Emergency management

Day Two

• Maximising your marks• Swallowing• Change in bowel habits• Hepatomegaly• Abdo pain • Pregnancy / Birth • Recurrent Infections• Headache• Stroke• Pharmacology basics

2 Minutes

10 Causes of Chest Pain

Puzzled?

You Need A SYSTEM…

Puzzled?

What do I do?

I GET VINO…

I Infectious / inflammatory

G Genetic / Idiopathic

E Endocrine

T Trauma

V Vascular

I Iatrogenic / ingested

N Neoplastic

O Organs

2 Minutes

10 Causes of Chest Pain

Chest Pain? Where’s that wine…

I Infectious / inflammatory Pneumonia, pleurisy, Costochonditis

G Genetic / ideopathic

E Endocrine

T Trauma Fractured rib, pulled muscle, pneumothorax

V VascularMyocardial infarction, angina, aortic dissection, PE

I Iatrogenic / ingested Surgical scar

N Neoplastic Bony mets

O Organs / other

Oesophagus (spasm, reflux), heart (pericarditis)Lung, Aorta, bones, muscle, cartilege, anxiety

Ischaemic Heart Disease

• Approx 1/3rd of all male deaths

• Approx ¼ of all female deaths

• Atheroma of coronary vessels

Right: Right Ventricle, most of Right Atrium, Part of Left Atrium

Left: Left Ventricle, part of Right atrium, most of Left atrium

Left circumflex: Left margin of heart and its entire posterior wall, Left atrium, posterior IV septum

LAD: Anterior 2/3 of IV septum, anterior portion of LV, whole apex

SA Node: Right 51-65%, Left 35-45%, Bilateral <10%

AV Node: Right 80-90%, Left 10-20%

ALL HIGHLY VARIABLE!!!

Coronary Arteries: Fill During DIASTOLE

Arterial Disease

Arteriosclerosis• Thickening and

hardening of wall– Reduced lumen

– Reduced flow

– Reduced elasticity– Reduced contrractility

• Diabetes• Hypertension

Atherosclerosis• Commonest cause of

arteriosclerosis• Specific disease• Tunica intima• Mostly large and

medium vessels• Small in prolonged

systemic hypertension

Atherosclerosis

• Changes in intima thrombus formation

• Reduced lumenal size– Poor

perfusion/hypoxia– Tissue death

• Loss of elasticity– Aneurysm formation

Smaller vessel atherosclerosis

• Ischaemic heart disease

• Most strokes• Peripheral heart

disease

Plaque Formation

Plaque Anatomy

Plaque Anatomy (early)• Free Lipid• Foam cells• Increased myointimal

cells• Collagen• Disruption of internal

elastic lamina

Plaque Anatomy (later)• Collagen cap• Extracellular lipid mass• Foam cells• Myointimal cells• Disrupted internal elastic

lamina• Pressure atrophy of

muscle collagenous replacement

Atheroma – Risk factors

Non-preventable• Increasing age• Male sex• Family history

Preventable• Hyperlipidaemia

– LDL and Cholesterol

• Hypertension– Diastolic most

important

• Diabetes• Smoking

Fibrous Pericardium

Parietal Layer of Serous PericardiumParietal Layer of

Serous Pericardium

MyocardiumMyocardium

Pericardial Space

EndocardiumEndocardium

FoldFold

Visceral Layer of Serous PericardiumVisceral Layer of

Serous Pericardium

Layers of the Heart

Compare Skeletal and Cardiac Muscle

Muscle Comparison

Skeletal Cardiac Smooth

Voluntary Involuntary Involuntary

Striated Striated Non-striated

Multinucleated Mononucleated Mononucleated

Unbranched Branched Unbranched

No gap junctions Gap junctions No gap junctions

Myocyte Action Potential

Phase Ion Voltage

0 Na+ IN +ve (rapid)

1 K+ OUT -ve

2Ca++ INK+ OUT

Steady

3 K+ OUT -ve

4 K+ OUT -ve (slow)

NAK-CAKKK

In Detail

Pacemaker Action Potential

Ca++ In K+ Out

Comparison of action potentials

Pacemaker cell Myocyte

Slow diastolic repolarisation in phase 4

Constant phase 4 (resting) potential

Pot. Approx -65 to -40mV Resting Pot. approx -90 mV

Phase 0 less steep Phase 0 more steep

Phase 0 via slow channels Phase 0 via fast Na channels

Plateau not sustained Plateau sustained

Repolarisation more gradual Repolarisation less gradual

Excitation-contraction coupling

• Electrical signal• Stimulates contraction

Generally• Signal causes

depolarisation• CA++ entry results• Causing contraction

• In The Heart• Calcium induced

calcium release• Act Pot from SA Node

L Type Calcium Channel

Ca++Ca++

Excitation

Ca++Ca++

Ryanodine Receptor

Ca++Ca++

Ryanodine Receptor

Ca++Tropomysin

Ca++ Ca++

Tropomysin

Contraction

Describe Sliding Filament Theory

Sliding Filament Theory

http://uk.youtube.com/watch?v=gJ309LfHQ3M&feature=related

• Calcium enters• Binding sites on actin

uncovered by movement of Tropomyosin / troponin complex

• Myosin binds to site powerstroke

• ATP binds to myosin release from binding

• ATP ADP + Pi – cocks myosin for another Powerstroke

• Continues as long as ATP and Ca present

Sliding Filament Theory

Normal Lead 2

A Segment is Shorter than an interval

The Normal ECG

PR interval: first deflection of P first deflection of QRS– 120-200 ms (3-5 small sq)

QRS interval: first deflection of QRS end of last deflection– <100 ms (<3 small sq)

QT interval (QTc is QT corrected for heart rate). Start of QRS end of T wave– 360-440 ms (<11 small sq)

Additional Abnormalities

• Pathological Q wave– Duration > 1 small sq

• ST Depression– 1mm or more over

isoelectric line

• ST Elevation– 0.5mm or more below

isoelectric line

• T wave abnormality– Normally upright in I, II

& V1 – V3– Normally inverted in

aVr– Variable in others

STEMI and NSTEMI

STEMI• ST Elevation MI

• ST elevation on ECG• Positive enzyme tests

NSTEMI• Non ST Elevation MI

• No ST elevation• Positive enzyme tests

STEMI and NSTEMIA: Normal ECG

B: ST Elevation

C: ST Depression

ST elevation in response to Isoelectric line (I)

P TQRS

ST Segment

Evolution of ECG Changes in STEMI

• Minutes to hours– Peaked T waves

• Hours– ST elevation

• Hours to days– T wave inversion– Loss of R wave

• Days– Pathological Q wave

Cardiac Enzymes

Fibrinolysis

• tPa

• Streptokinase

ACS? GO CARDIO ABCDG GTN

O Oxygen

C Clot prevention - enoxaparin

A Aspirin ± clopidogrel

R Raised position

D Diamorphine + antiemetic

I Investigate: ECG, enzymes, Troponin, CXR

O Observe: Repeat ECG + Basic obs,

AACE inhibitor within 24 hours

B Beta blocker

C Cholesterol - statin

D Diabetic control – tight control for at least 24 hours

2 Minutes

5 Causes of acute Dyspnoea

Acute Dyspnoea? Need alcohol!

I Infectious / inflammatoryAsthma, Pneumonia, COPD exacerbation (e.g. upper resp tract infection)

E Endocrine

T Trauma Pneumothorax

V Vascular Myocardial infarction, PE

I Iatrogenic / ingested Foreign body (mostly children)

N Neoplastic

O Organs / other Lungs

Lung Anatomy

3 Lobes2 Lobes

Diaphragmatic

MediastinalCupular

Costal

The Alveolus

Muscles of Breathing

Diaphragm• Phrenic nerve C3,4 & 5

Intercostal muscles• External• Internal

Compare the bronchial and pulmonary arteries

Vessels in the Lung

• Pulmonary Artery– Deoxygenated blood– From Right Ventricle– Oxygenated in lungs– Affected in PE

• Bronchial Artery– Oxygenated blood– From systemic supply– Supplies tissues of lung

• Pulmonary vein– Oxygenated blood– From lungs– To Left atrium

Velocity and Flow

Velocity• Displacement of single

particle per unit time • Inversely proportional to

cross sectional area– Faster in thinner tubes

• Aorta is thinner than total mass of capillaries– V slow capillary flow– Time for gaseous exch

Flow• Volume of fluid passing

point A at time B• Proportional to pressure

difference• Inversely proportional to

tube length• Proportional to r4

• Inversely proportional to viscosity

Resistance (R)

In Parallel:1/RTOT = 1/R1 + 1/R2 + 1/R3

In Series: RTOT = R1 + R2 + R3

Resistance may be varied in arteries and arterioles by control of lumen cross sectional area via smooth muscle

contraction / relaxation

Laminar and Turbulant Flow

Laminar:• Concentric thin

adjacent layers of fluid

• ‘Rings within rings’• Speed max at centre• Elements stay in one

lamina

Laminar and Turbulant Flow

Turbulant:• Fluid elements not

contained in one lamina

• Radial and circumferential mixing

• Vortex generation• Pressure needed to

maintain flow is increased

Venous Thromboembolism

Virchow’s Triad• Or FECing blood…

– Flow disturbances• Stasis• Slow• turbulant

– Endothelial damage• E.g. atheroma• Stasis / turbulance

– Coagulability changes• Genetic• Oral contraceptive pill

Genetic Disorders• Factor V Leiden

– Factor V not inactivated

• Anticoagulant lack– Protein C deficiency

– Protein S deficiency

– Antithrombin III defic.

• You may not need to know these…

Consequences of VTE

PORT• Propagation

– Grows along vessel

• Organisation– Granulation tissue

• Recanalisation– New passages through

granulation tissue

• Thromboembolism– E.g PE

Embolism

A Variety of materials

• Thrombus

• Tumour mass

• Fat/ bone marrow

• Amniotic fluid

• Air

A variety of consequences

• Unstable angina

• Stroke / TIA

• Pulmonary embolism

• Other infarct

• Lower limb muscle

‘Occlusion of a vessel by a mass of material transported through the bloodstream’

DVT and PE

From Vein to Artery…• DVT in leg• Loss of embolus

– Travels in systemic circ

• Lodges in pulmonary artery– 85% Minor PE

– 10% Major

– 5% Massive

– Rarely recurrent

Major• Dyspnoea• Haemoptysis• Pleuritic chest pain

Minor• Possibly assymptomatic• Dyspnoea• Pleuritic chest pain

Predisposing Factors

To PE• Previous PE• DVT

To DVT• Immobility• Post-operative• Pregnancy / post

partum• OCP• Nephrotic syndrome• Trauma esp severe

burns• Cardiac failure

Asthma

Airway

COS of Three Pathologies

Constriction Oedema Secretions

ABGs - pH

Henderson-Hasselbalch (H-H) equation

pH = 6.1 + log [HCO3-] / pCO2 x 0.23

What are the main factors measured on an ABG?

What are the Reference Ranges?

Reference Ranges

pH: 7.35 – 7.45

pCO2: 4.7 – 6.0 kPa (about 35-45 mmHg)

pO2: >10.6 kPa (>80 mmHg)

[HCO3-]: 22-25 mmol/L*

Base excess:

+/- 2 mmol/L*

* standardised, as if pCO2 were 5.3

2 Minutes

5 Causes of Chronic Dyspnoea

Chronic Dyspnoea? Gimme Wine!

I Infectious / inflammatory COPD

E Endocrine

T Trauma

V Vascular Anaemia

N Neoplastic Lung Cancer

O Organs / otherLungs: fibrosis, pleural effusionHeart: failure, pericardial effusion

Heart Failure

'failure of heart to pump blood forwards at a sufficient rate to meet metabolic demand'

(forward failure)

'ability to pump sufficient blood to meet metabolic demand only if cardiac filling pressures are abnormally high’

(backward demand)

Heart Failure

• Left sided (varied causes – see right)

• Right sided – caused by LEFT heart failure or cor pulmonale

• Congestive failure – failure of both left and right sides

Pathological causes• Myocardial disease

– Myocardial infarction

• Volume overload– Regurgitation– Arteriovenous shunts

• Pressure overload– Hypertension (including

pulmonary in RHF)– Stenosis

Define Preload and Afterload

Useful Terms

Preload• Stretch on myocardial

fibre before contraction

Afterload• Ventricular wall tension

during contraction– The resistance that

must be overcome

Ejection fraction• Fraction of end

diastolic volume ejected from ventricle during systole– 55-70% normal

Remember• CO = SV x HR

List Clinical Features of Right Heart failure

Heart Failure - Features

L e f t s i d e d

•Tachypnoea•Haemoptysis•Tachycardia•Sweating

R i g h t s i d e d

•Swollen legs•RUQ discomfort•Nausea•Anorexia

•Pitting periph. oedema•Elevated JVP•Hepatomegaly

Central Venous Pressure

• Pressure measured in central veins.• Indicates mean right atrial pressure • Frequently used as an estimate of right ventr. preload.• CVP rises with poor right ventr. Function or obstructed

pulmonary circulation.

Measuring CVP• Central Line• Catheter placed thorugh subclavian vein• Invasive• Alternative is CVP

Measuring CVP

Jugular venous pressure• Use right internal jugular

vein • Patient at a 45° angle,

head to the left • Light source that shines

obliquely from the left • Locate the anatomical

landmarks • Locate the JVP• Measure the level of the

Anatomical landmarks• Medial end of clavicle• To ear lobe• Under medial aspect of

sternocleidomastoid

• Level is measured from the sternal angle of Louis to top of column

JVP vs Carotid pulse• The JVP pulse is • Not palpable • Obliterated by pressure • Characterised by a

double waveform • Varies with respiration -

decreases with inspiration • Enhanced by the

hepatojugular reflux

The Hepatojugular Reflux• Firm pressure is applied

to the right upper quadrant using the palm of the hand

• A transient increase in the JVP will be seen in normal patients

• There may be a delayed recovery back to baseline which is more marked in right ventricular failure

Jugular venous waveform

a wave: rise in right atrial pressure during atrial contraction

x descent: atrial relaxation + RV contraction (pulls atrium downward)

c wave: bowing of tricuspid valve into RA during systole

v wave: right atrial filling, tricuspid valve closed

y descent: emptying of right atrium after tricuspid valve opens

Starling Curve

• RAP=Right Atrial Pressure

• CO=Cardiac Output

• Remember: too much stretch reduces ability to contract… (blue dashed line)

Normal physiological range, high sensitivity to RAP changes

Heart has reached limit of response, insensitive to further changes in RAP

RAP (mmHg)

Flow / Volume Loops

List the common diastolic and systolic murmurs

A Piratical Crew…Dire Stolic Ms ARrrrrr

A Piratical Crew…

DIASTOLIC murmurs are:

MS: Mitral stenosis

AR: Atrial regurg.

MS ARrrrrr…

Systolic? Meet MR ASs

Sympathetic stimulation

Location Receptor Type Action if stimulated

Heart Beta Increased HR and contractility

Blood vessels in skeletal muscle

Beta Vasodilatation

Blood vessels elsewhere

Alpha Vasoconstriction

Bronchioles Beta Relaxes smooth musc.

Pupil of eye Beta Dilates (darkness)Salivary glands Beta Little, thicker secrSweat glands Alpha Promotes sweatLiver Alpha, Beta Glycogenolysis

GluconeogenesisGut Secretion None -Gut motility Alpha, Beta Inhibits peristalsis

http://uk.youtube.com/watch?v=tOcGbnBCdMM

http://uk.youtube.com/watch?v=bU4955rLv_8&feature=related

GPCR Summary

• Receptor complex + G protein

• G Protein has 3 subunits (alpha, beta & gamma)

• Receptor binds ligand

• Conformational change

• Loss of GDP from G protein alpha subunit

• Binding of GTP

• Separation of alpha subunit from beta-gamma dimer

• Alpha and beta-gamma freed to interact with effectors.

• Cascade effect.

• Cycle starts again

GPCRs in the heart

Beta receptors

• GPCRs

• Gs activates adenylate cyclase– Increased cAMP

– ATP cAMP

• cAMP activates PKA

• PKA phosphorylates alpha-1 subunit on voltage-gated Ca++ channels

• Increased Ca++ influx

• Increased inotropy

• Increased rate

Ca++ In

Beta-adrenergic antagonists

‘Beta blockers’• Combat the harmful

activation of the sympathetic nervous system

• Decrease HR• Decrease contractility

Examples• Propranalol• Sotalol

Side effects• Bronchoconstriction• Bradycardia

GPCRs in the lung

Beta receptors• GPCRs• Gs actvates

adenylate cyclase– Increased cAMP– ATP cAMP

• cAMP causes relaxation of the smooth muscle

• Decreases sensitivity of the IP3 receptor, decreasing release of calcium from intracellular stores in response to IP31

• Some proponents argue for a cAMP independent PKA mechanism as well2

Parasympathetic stimulation

Location Action if stimulated

Heart Decreased HR

Blood vessels in skeletal muscle -

Blood vessels elsewhere -

Bronchioles -

Pupil of eye Constricts (light)

Salivary glands Abundant watery secr

Sweat glands -

Liver Glycogen formation

Gut Secretion Stimulates

Gut motility Stim peristalsis

Parasympathetic vs Sympathetic

Synapse Near Target Organ

Synapse Near CNS Origin

Target Organ

Long Postsynaptic N

Long Presynaptic N

ParasympatheticCN 3, 7, 9, 10S2,3,4

SympatheticT1 – L2

ACE Inhibitors

• In HF the renin-angiotensin-aldosterone pathway is activated inappropriately– Poor renal perfusion– Sympathetic activation

(beta receptors)– Diuretics

Effects• Reduce vasc.

resitance– Reduce afterload– Improve perfusion

• Inhibit aldosterone & reduce Na+ reabsorp– Cause naturiuresis

• Proven to prolong life

Heart Failure – ACE Inhibitors

• Reduce ATII formation

• So reducing Na+ reabsorption

• So reducing water retention

• So reducing central venous pressure

• So reducing load upon heart

TB (or not TB…)

Re-emerging organism• HIV• Drug resistance

• Mycobacterium– Mycolic acid wax coat– Resistant to drying– Acid fast– Slow growing

Spread:• Coughed into air• Remain for hours as

micronuclei• Bypass cilliary cells• Enter alveoli• Enter resident

macrophages

Two disease forms

Primary• 91% no disease• 3% progressive

systemic leading to death

• Remainder pulmonary or extrapulmonary TB

Secondary• Reactivation• Damage is from host

immune response

Tuberculosis

Features• Shortness of breath • Fever and sweating,

especially at night • Haemoptysis • Loss of appetite • Weight loss • Fatigue and tiredness • Lymphadenopathy

Demographics• Black African (211 per

100,000)• Pakistani (145 per

100,000) • Indian (104 per

100,000)

Diagnosis and Management

Diagnosis

• PPD / Mantoux • Sputum culture

– Acid Fast Stain (ZN)

• Chest X-ray• Bronchoscopy ±

biopsy

Management

BCG Vaccine

• Rifampicin 6 months

• Isoniazid 6 months

• Pyrazinamide 2 months

• Ethambutol 2 months

What is meant by ‘concordance’

Social Science: Taking the pills…

• Compliance– Extent to which

patient’s behaviour matches recommendations from the prescriber

• Adherence– Extent to which the

patient’s behaviour matches agreed recommendations from the prescriber.

• Concordance– Extent to which the

patient’s behaviour matches agreed recommendations from the prescriber after exploring and discussing the patients beliefs, views and opinions.

Social Science: Taking the pills…

Poor concordance• The homeless• Minority groups• Learning difficulties• Dementia • Psychological illness• Those with a history

of non-concordance

Increasing concordance• Directly observed

therapy• Key workers• Home visits• Health education• Reminder letters• Foreign lang

materials

2 Minutes

5 Causes of Haemoptysis

Haemoptysis? Where’s that wine…

I Infectious / inflammatory Pulmonary tuberculosis

G Genetic / idiopathic

E Endocrine

T Trauma Chest trauma

V Vascular Pulmonary embolism

N Neoplastic Bronchial carcinoma

O Organs / otherNose: epistaxis; oesophagus: maller weiss tearLung: bronchiectasis; Heart: mitral stenosis

Lung cancer

• Male: Female 7:1• Decreasing

• Male peak in 60s• Female peak in 70s• Rare under 25 years

Presenting complaints• 90% symptomatic

– 40% Haemoptysis– 75% Anorexia– 75% Dyspnoea– 75% Cough– 75% Pain

• Remember Weight Loss

• 10% Incidental imaging

Lung Cancer - Diagnosis

• Imaging– Plain film– CT– MRI

• Cytology– Sputum– Bronchoscopic

washings

Biopsy• Peripheral lesions

– Percutaneous biopsy

• Proximal lesions– Bronchoscopic biopsy

• Pleural Effusions– Fine needle aspiration

Lung Cancer

• Small Cell (20-30%)

• Non-small Cell– Large Cell (10-15%)

– Adenocarcinoma (~20%)• Commonest non-smoking

– Squamous cell carcinoma (40-60%)

• Commonest smoking related

Treatment

• Small cell– Early metastasis

– Chemotherapy and radiotherapy first line

• Non-small cell– Surgery first line

• Lobectomy

• Pneumonectomy

– Radio / chemo as req

Haemostasis

Stops your blood falling on the floor…

• Vasoconstriction

• Platelet aggregation

• Clotting cascade

Platelets

• Made from Megakaryocytes

• Last ~10 days

• Do nothing until activated

• Collagen

• Thromboxane A2 (TXA2)

• Thrombin (from clotting)

• ADP

Platelet Aggregation

Activated Platelets• Release TXA2• Change form• Form plug by adhering to

– Other platelets– Collagen under epithelium– Via Von Willibrand’s Factor

• Promote Coagulation

• Prostacyclin and CD39 prevent activation

Clotting

Damage to tissue outside vessel

Tissue Thromboplastin

Tissue Thromboplastin Clotting cascadeClotting cascade

Damage to the blood vessel

Factor X (inactive)Factor X (inactive)

Factor Xa (active)

Factor II - Prothrombin (inactive)

Factor IIa - Thrombin (active)

FibrinogenFibrinogen FibrinogenFibrinogen ClotClot

Extrinsic Intrinsic

Common

Clotting

Factor Xa (active)

Factor 9Factor 9Factor 8Factor 8

Extrinsic Intrinsic

Common

Clotting

Factor Xa (active)

Extrinsic Intrinsic

Common

Haemophilia A

Haemophilia B

Clotting

Factor Xa (active)

Extrinsic Intrinsic

Common

INR / PT aPTT (PTT)

Haemophilia

X-Linked Recessive

What is the role of vitamin K in blood clotting?

Vitamin KReductase

Vitamin K and Warfarin

• Factors 2,7,9 & 10 must be gamma carboxylated

• Vitamin K is a vital cofactor

• Warfarin inhibits enzyme– Prevents Vitamin K

recycling

Vitamin KReductase

Oxidised Vitamin K

ReducedVitamin K

Factors 2,7,9 & 10

Gamma carboxylated

Vitamin K

Warfarin

Vitamin K Dependent Factors

Intrinsic Pathway Extrinsic Pathway

Common Pathway

aPTT (PTT)

INR / PT

ATIII and Unfractionated Heparin

IIaIIaIIa

Heparin

Factor IIa(Thrombin)

XaFactor

* Note the change in ATII conformation

ATIII and LMW Heparin

IIaIIaIIaLMW

Heparin

XaFactor

* Note the change in ATII conformation

No substrate binding

No substrate binding needed

ATIII and Heparin - Summary

• Antithrombin III deactivates clotting factors IIa (thrombin) & Xa

• It does NOT need heparin to do this

• BUT heparin makes it go FASTER

• LMWH only works on Xa

• Longer molecules in unfractionated heparin work on IIa (thrombin) as well

The Clot

• Platelet activation• Fibrinogen fibrin• Fibrin assembles into

long fibrils• Platelets + Fibils =

Clot• RBCs join later

2 Minutes

10 Causes of a Painful Limb

Painful Limb? Time for some Wine!

I Infectious / inflammatory Cellulitis, septic arthritis

G Genetic / ideopathic Osteogenesis imperfecta related fracture

E Endocrine Osteoporosis related fracture

T TraumaFracture, dislocation, pulled muscle, ligamentous injury

V Vascular Claudication

I Iatrogenic / ingested Corticosteroid osteoporis fracture

N Neoplastic Bony mets, Primary bone cancer (rare)

O Organs / otherJoints: osteoarthritis, rheumatoid arthritis Nerves: sciatica

Fracture

• Pain• Swelling• Deformity• Loss of function

• High impact• Repetitive impact

(stress)• Pathologic

Fractured Neck of Femur

Blood supply to head

- In order of importance• Capsular supply

– From Med + Lat circumflex

– From Deep femoral

• Nutrient artery– From deep femoral

• Ligamentum teres– From Medial epiphyseal

Fractured Neck of Femur

Colles & Smiths Fractures

Colles• Distal radius• Dorsal angulation• FOOSH• Elderly• Osteoporosis

Smiths - as above but• Volar angulation

Scaphoid fracture

• FOOSH• Tenderness in

anatomical snuffbox– Structures of

snuffbox

• Three X-ray views• Blood supply enters

distally– Potential avascular

necrosis

Humeral fracture

• Most Commonly at Surgical neck– Axillary nerve damage

• Also mid shaft• If involves radial groove

– Radial nerve damage

• Distal radius uncommon

Humeral fracture

Distal radius uncommon

• Supracondylar– Median nerve

• Medial epicondyle– Ulnar Nerve

What is this fracture?

Monteggia and Galleazzi

Medics Monteggia (a)

Under Ulnar shaft

Pressure Proximal Radio-ulnar Joint

Get Galleazzi (b)

Really Radial Shaft

Drunk Distal RUJ

Fracture-dislocations

Fracture Management

The “Three R’s”• Reduce• Retain

– Cast– Internal fixation– External fixation

• Rehabilitate

Pulled elbow

• Mostly Children 1-4 yrs

• Dislocation of radial head from annular ligament

• 50% have no Hx

• Not using limb

• Extension + pronation No deformity

In adults Monteggia fracture dislocation is likely differential

Bone Healing

Mins – 3 days

• Haematoma and Necrotic tissue

2 days – 2 weeks

• Phagocytosis

• Provisional callus

3 weeks on

• Firm callus

• Mineralisation

Weeks - months

• Remodeling

Factors influencing Healing

Local• Tissue damage• Tissue loss• Infection• Foreign body

Systemic• Patient age• Nutritional status• Smoking / alcohol• Steroids• Systemic illnesses such as

diabetes, renal, lung, cardiac.

Video Link

Synovial Joint

CollagenSynthesis

http://depts.washington.edu/bonebio/ASBMRed/collagen/collagen.swf

Compare and contrast rheumatoid arthritis with

osteoarthritis

Osteo and Rheumatoid

Osteoarthritis• Disease of cartilage• No immune

component– M=F– Rheumatoid factor -ve

• Assymetric• Large > small joints• DIP Joints

Rheumatoid arthritis• Disease of synovium• Autoimmune

– M<F (approx 1 : 3-4)– Rheumatoid factor

• Symmetrical• Small > large joints• MCP + PIP Joints

Septic Arthritis

‘joint inflammation caused by the presence of live intra-articular micro-organisms’

•Acute•Painful•Swollen•Effectively immobile

Risk of rapid joint loss

Management• Aspirate pus

– Send for analysis

• Surgical washout• IV antibiotics

• Differential: Gout

Septic Arthritis

Routes of infection

1.Haematogenous

2.Direct Trauma

3.Iatrogenic

4.Osteomyelitis

5.Inflamed extraarticular structures

2 Minutes

5 Causes of Breast pain

Breast Pain? Back to the Drinking…

I Infectious / inflammatory Costochonditis

E Endocrine

T Trauma

V Vascular Cardiac Pain

N Neoplastic Benigng or malignant breast cancer

O Organs / otherOesophagus: spasm; Heart :cardiac painLung: pleurisy

Non-cancer conditions

Abnormalities of development

• Cyclical mastalgia• Non-cyclical mastalgia• Epithelial Hyperplasia• Sclerosis• Cysts• Fibroadenoma• Duct ectasia

Benign tumours• Ductal papilloma• Lipoma• Oil cysts• Sebaceous cysts• Lymph nodes

• TB

Cancers

Non-invasive• Lobular carcinoma in

situ• Ductal carcinoma in

Invasive• 80% carcinomas are

ductal– 5% lobular – poorer

outcome

Management• Social / psych support• Surgery

– Local / mastectomy– reconstruction

• Radiotherapy– Breast / axilla

• Chemotherapy

Modifying Oestrogen

• Oestrogen• Progesterone

• Normal breast tissue• AND 60% of tumours

• Pre-menopause prod.– Ovaries

• Post Menopause– Peripheral fats

• Therapy aims to reduce oestrogen production

• Ovarian ablation– GNRH agonists– Surigal or radiation

• Aromatase Inhibitors– Post menopausal

Risk factors• Menarche <11• Menopause >54• Western diet• OCP and HRT• Radiation

• Family history (only 5% of Br. Ca are familial)

Inherited breast cancers• BRCA1

– 51% by age 50– 85% by age 70– Also ovarian cancer

• BRCA2– Male breast cancer– Prostatic cancer– Ovarian cancer

• Present early with advanced disease

Risk Assessment

Think Benign• Young patient• No family history• Smooth lump• Movable lump• Cyclical symptoms

Think Malignant• Patient >55• Family history br. Ca.• Fixed mass

Testing for breast cancer

Triple Assessment• Physical examination• Imaging

– Ultrasonography (<35)– Mammography

• Sampling– USS guided core

biopsy– Or FNA + cytology– Ideally after imaging

The screening programme

• Women• Aged 50+• Every 3 years• 2 view mammography

• Will save ~1,250 lives annually by 2010

• 1 / 500 screened

Describe some of the features that make a disease suitable

for screening

A good screening Programme

• An important public health problem

• In which early detection is possible and advantageous

• With a reliable, acceptable test

• And available, effective treatment

• There should be agreement on who is suitable to investigate and treat.

Neoplasia

• 'Irreversible changes in genetic material of cells, due to exposure to certain noxious stimuli, leading to abnormal cellular growth patterns.’

• Tumours develop from a single cell – they are monoclonal

• Normal tissue is polyclonal

• Learn– Breast– Bowel– Lung

Neoplasia

• Oncogenes– Abnormal expression– Genes controlling cell

growth– Dominant

• Tumor suppressor genes– Loss of activity– Protect against

neoplasia– Recessive

Neoplasia

• Tumor suppressor genes– Loss of activity– Protect against

neoplasia– Recessive

• p53, Chromosome 17 – initiates DNA repair– prevents division of

cells with irreparable DNA damage

• Rb, Chromosome 13.– Abnormal copies of

this gene are implicated in retinoblastoma.

Growth Characteristics

Benign Malignant

Expands onlyGrows locally

Expands and invades local tissuesMay metastasise

Generally slower Generally faster

Cytoplasmic Characteristics

Benign Malignant

Normal or slight increase in nucleus:cytoplasm ratio

High nucleus:cytoplasm ratio

Resembles cell of origin (well differentiated)

Failure of differentiation

Retains specialisations Loses specialisationsDiploid Range of ploidy

Histological CharacteristicsBenign Malignant

Few Mitoses Many mitoses – some of which are abnormal

Cell uniform throughout tumour

Cells vary in shape and size (cellular pleomorphism) and/orNuclei vary in shape and size (nuclear pleomorphism)

Organised tissue Disorganised tissue

Invasion and Metastasis

• Invasion is the spread into adjacent tissues – may occur along natural tissue planes such as along nerves

• Metastasis is the spread of cells to distant parts of the body – there are several mechanisms for this

To Metastasise

• Changes occur in only some cells of the tumour

• By random mutation

• Binds to basement membr

• Becomes motile• Becomes able to attach

to extracellular matrix• Becomes able to degrade

extracellular matrix

• Must be able to survive and grow at site of implantation

Routes of

Metastasis

• Vascular

• Lymphatic

• Coelomic

Local and systemic effects

Local• Pressure• Invasion• Ulceration• Obstruction

Systemic• Weight loss

(cachexia)• Loss of appetite

(anorexia)• Fever• Anaemia• General Malaise• Paraneoplastic

Who gets Cancers?

Inherited tendencies• Xeroderma

pigmentosum• Down’s syndrome• Ataxia telangectasia

Diseases predisposing to cancer

• FPC: Colon• HNPPC: Colon

Genes• Breast / ovarian

– BRCA1– BRCA2

• Colon– MLH1

• DNA mismatch repair• Dominant

– MSH2

What is a carcinogen? Suggest one together with its

mode of action.

Carcinogens

Cigarette smoke

Chemicals• PAH• Aromatic amines• Nitrosamines

UV Radiation

Ionising radiation• Radiotherapy• Radon gas (lung)• Industry/military

Carcinogens

Viruses• EBV (Epstein-Barr)• HPV (Papilloma virus)• HBV (Hepatitis B

virus)

Stages in carcinogenesis

• Initiation• Promotion• Progression

All of medicine in 12 hours… Dr. Alan McLeod (F2)

Documents

McLeod CH04

DIOCESAN CYCLE OF PRAYER - ShaftesburyCofE.org.uk · Clergy: Sarah Pix, Patches Chabala, Barry Lomax, Ray Forbes, Everton McLeod. LLMs: David Scouse, Alan Field, Ralph Dodds, Barbara

McLeod CH01

Referensi Mcleod Raymond

Mcleod final project

McLeod CH08

MIS McLeod CH01

Mcleod Russel

McLeod Motors LTD

The rest of medicine in six hours Dr. Alan McLeod (F2)

McLeod CH02

McLeod Business Library1 McLeod Business Library Room 2034, Alan B. Miller Hall College of William and Mary Mason School of Business

IBSc: Question 3 By Alan McLeod Tested by Natalie Hayes

Lewis Mcleod

Winter 2006CISC121 - Prof. McLeod1 Welcome to CISC121 Prof. (Alan) McLeod – mcleod@cs.queensu.ca Web site at: All

Mcleod Mar09 TandF

Alan McCulloch: cartoonist of distinction · painter and art critic, author and fine cartoonist of distinction, Alan McCulloch. Alan McLeod McCulloch was born in 1907 in the Melbourne

A, McLEOD,

Mary McLeod Bethune!!!!

Mary McLeod Bethune