INTERNAL MEDICINE EOR EXAM REVIEWCRITICAL CAREAcute adrenal insufficiency

MC cause of primary adrenal insufficiency is Addison dzAdrenal crisis occurs in the following situations:

1) stress2) sudden withdrawal of adrenocortical hormone in pt with chronic insufficiency or chronic use of

corticosteroids = MC cause of secondary insufficiency3) following bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed

the other adrenal4) following sudden destruction of the pituitary gland (necrosis)5) when thyroid hormone is given to pt with hypoadrenalism6) following injury to both adrenals by trauma, hemorrhage, anticoag therapy, thrombosis, infection

following admin of etomidate – used for IV anesthesia induction or intubations/s: h/a, lassitude, n/v, abd pain, diarrhea, confusion, coma, fever >40.6, low BPsometimes: cyanosis, dehydration, skin hyperpigmentation, sparse axillary hairhypoglycemia with lessening required need for insulin in Type I DM ptsLab: eosinophil count high, Low Na and high K, Hypoglycemia, >’d CaDx made by: cosyntropin stimulation test (normal cortisol level is >20 mcg/dL) and plasma ACTH (>200 pg/mL)Tr: 2 phases

1) acute phase: draw blood to determine cortisol level and treat with hydrocortisone 100-300 mg IV and saline immediately without waiting for the results. Following, give hydrocortisone phosphate or hydrocortisone sodium succinate 100 mg IV immediately and continue IV infusions 50-100 mg q 6 hrs for 1st day. Give the same amt every 8 hrs on the 2nd day, then adjust dose based on clinical picture.

2) Convalescent phase: hydrocortisone PO 10-20 mg q6hrs, and reduce to maintenance level as needed (typically given q12hrs 10-20 mg am and 5-10mg pm + fludrocortisone acetate .05-.2mg PO daily.

After rapid treatment and crisis has passed, assess for possible cause and permanent treatment optionsThyroid storm Extreme thyrotoxicosis triggered by:

1) stressful illness2) thyroid sx3) RAI administration

s/s: marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, very high fevermortality hightr: thiourea drug (eg methimazole 15-25 mg PO qhrs) or propylthiouracil 150-250mg PO q6hrs)+ Ipodate sodium 500 mg/day PO 1 hr after thiourea+ iodine (Lugol solution 10 drops 3x’s/day PO or sodium iodine ig IV slowly) given 1 hr later+ propranolol 0.5-2mgIV q4hrs or 20-120 mg PO q6rs+ hydrocortisone is usually given in doses of 50 mg orally q6hr (reduce rapidly as pt improves)

Diabetic Ketoacidosis/acute hypoglycemia

Can be initial manifestation of type I DM, or d/t >’d insulin requirement in type 1DM during infection, trauma, MI, or sx; may occur in Type 2DM with severe stress (sepsis, trauma)Mortality greater in elderly than <40Poor compliance = MC causes/s: precedes with polyuria, polydipsia, fatigue, n/v, mild hypothermia, hypotension and tachycardia, cholecystitis or pancreatitis -> mental stupor -> comaPE: stuporous pt w/ rapid deep breathing and a “fruity” breath odor of acetone = strong suggestion of dxLabs: moderately severe:Glucose 350-900 mg/dLSerum ketones at a dilution of 1:8 or greaterHyperkalemia 5-8 mEq/L – occurs despite total body K depletion b/c shift of K from intra to extracellular spaces d/t systemic acidosis

Slight hyponatremia 130 mEq/L – d/t vomiting and polyuriaHyperphosphatemia 6-7 mg/dLElevated blood urea nitrogen and serum creatinineAcidosis severe ranging from 6.9-7.2Serum bicarb 5-15 mEq/LPCO2 is low related to hyperventilationFluid depletionHyperosmolar coma – occurs when osmolality exceeds 320-330Mild = pH 7.25-7.3 – alert – treat in ERMod = pH 7.0-7.24 – either alert or a little drowsy – admission to ICUSevere = <7.0 – stuporose – admission to ICUTreatment:

1) gastric intubation to prevent vomiting/aspiration2) indwelling cath3) Swan-Ganz cath to motior hypovolemia in pts with preexisting cardiac or renal insuff.4) Blood glucose and electrolytes recorded every hour, pH q2hrs5) No opioids and sedatives6) Fluid replacement – 0.9%saline = fluid of choice 1L/hr for 1st 1-2 hrs; after 2L, infuse 300-400 mL/h –

not to exceed 5L in 8 hrs; if glucose falls, change to 5%glucose-containing solution7) Insulin replacement – after fluid replacement has started, give regular insulin IV bolus 0.1 unit/kg,

followed with 0.1 IV unit/kg/h continuously infused – corrects acidosis; if glucose doesn’t fall in 1st hour, then another bolus 0.1 should be given

8) Potassium – once acidosis is fixed, then K flows back into cells and hypokalemia can result – substitute with KCl 10-30 mEq/h in 2nd or 3rd hour after of therapy; if K is <3.5, delay insulin until level is >3.5. EKG monitoring necessary

9) Sodium Bicarb – severe cases when pH <7.0 – 1 or 2 ampules to 1L of .45% saline rapidly – given only until pH reaches 7.1 = fatal arrhythmia

10) Phosphate - only in severe hypophosphatemia < 1 mg/dLHyperchloremic acidosis – usually resolves by itself after 12-24 hrs after initiation of treatment

Acute glaucoma

Only occurs with closure of preexisting narrow anterior chamber anglePredisposing factors: age, farsightedness, inheritance (Asians and inuits)Primary - Usually precipitated by pupillary dilation – dark rooms, times of stress, sympathomimetic agentsSecondary causes: ant uveitis, dislocation of lens, or topiramate.s/s: extreme pain, blurred vision, halos around lights, nausea, abd pain possible, eye is red, cornea cloudy, pupil moderately dilated and nonreactive to lightIOP >50 mm HgTr: primary:Reduction of IOP – single 500 mg IV acetazolamide followed by 250 mg PO 4x’s/dayOsmotic diuretics – glycerin PO and urea or mannitol IV 1-2 g/kg – may be necessary if there is no response to acetazolamideLaser therapy to peripheral iris or ant chamber paracentesisAfter IOP has <’d, topical 4% pilocarpine, 1 drop q15min FOR 1 HR AND THEN 4X’S/day - to reverse underlying angle closureDefinitive tr = laser peripheral iridectomy or surgical peripheral iridectomy.Prophylactic laser peripheral iridotomy to unaffected eye should be done, unless it has already been doneSecondary: systemic acetazolamide

Pulmonary embolism

Can be d/t air, amniotic fluid, fat, foreign bodies, parasitic eggs, septic emboli (infectious endocarditis), tumor cells.MC = thrombus, which can arise anywhere in venous system. MC = DVT in lower leg that propagate proximally to the popliteal and ileofemoral veings50-60% of DVT will develop into a PErisk factors of PE: venous stasis, injury to the vessel wall, and hypercoagulability (Virchow’s triad)

leads to right ventricular failure, hypoxemia through right to left shunting, <’d cardiac output, and surfactant depletionreflex bronchoconstriction promotes wheezing and >’d work of breathings/s: difficult to dxdyspnea and pain on inspiration, tachypnea, chest pain with breathing, 30% hemoptysis, coughinglabs: ECG NORMAL, arterial blood gases – hypoxia with normal chest radiograph in absence of preexisting lung dz is highly suspicious for PE; D-Dimer elevation; Toponin I, Troponin T and plasma beta-natriuretic peptide (BNP) elevationimaging: CXR – to r/o other lung dzCT – helical CT pulmonary angiography for initial dx study for suspected PEV/Q scan – not as specificVenous ultrasound – to assess proximal DVTPulmonary angiography = reference standard for dxTr:Anticoag – not definitive, but more preventative – Heparin + 6 mo of WarfarinThrombolytic tr – Streptokinase, urokinase, and recombinant tissue plasminogen activator (rt-PA, alteplase) – contraindicated in those with uncontrolled HTN and surgery/trauma in last 6 wksPossible IVC filter for recurrent and high risk ptsSurgical extraction for high risk pts who can’t tolerate thrombolytic therapyWell’s criteria for Risk of DVT:CLINICAL FEATURE POINTS

Active cancer (treatment within 6 months, or palliation) 1

Paralysis, paresis, or immobilization of lower extremity 1

Bedridden for more than 3 days because of surgery (within 4 weeks) 1

Localized tenderness along distribution of deep veins 1

Entire leg swollen 1

Unilateral calf swelling of greater than 3 cm (below tibial tuberosity) 1

Unilateral pitting edema 1

Collateral superficial veins 1

Alternative diagnosis as likely as or more likely than DVT −2

Total points:

Risk score interpretation (probability of DVT): 3 points: high risk (75%); 1 to 2 points: moderate risk (17%);<1 point: low risk (3%).

Wells criteria for PE:

CLINICAL FEATUREPOINTS

Clinical symptoms of DVT 3

Other diagnosis less likely than PE 3

Heart rate greater than 100 beats per minute [corrected] 1.5

Immobilization or surgery within past 4 weeks 1.5

Previous DVT or PE 1.5

Hemoptysis 1

Malignancy 1

Risk score interpretation (probability of DVT): >6 points: high risk (78.4%); 2 to 6 points: moderate risk (27.8%); <2 points: low risk (3.4%)

Acute Respiratory Distress/failure

Acute hypoxemic respiratory failure following a systemic or pulmonary insult w/o evidence of heart failure. d/t pro-inflammatory cytokines relased from stimulated inflammatory cells causing lung injury; causes < surfactant production, leading to pulmonary edema, alveolar collapse, and hypoxemiaRisk factors: sepsis, aspiration of gastric contents, shock, infection, lung contusion, nonthoracic trauma, toxic inhalation, near-drowning, and multiple blood transfusionss/s: profound dyspnea (12-48 hrs after event), labored breathing, tachypnea, intercostal retractions, and crackles.labs: CXR shows bilateral widespread pulmonary infiltrates. Patchy and diffuse -> confluent, sparing

costophrenic angles.Can cause multiple organ failure, particularly kidneys, liver, gut, CNS, and CV systems.Tr: ID and treat underlying precipitating and secondary conditions. Hypoxemia tr with intubation and positive pressure ventilation. Lowest level of PEEP and supplemental O2 required to maintain PaO2 above 55mgHg or SaO2 >60%, not to exceed 60% FiO2.Hemodynamic monitoring and fluid management for pts with acute lung injuryPx: mortality of 30-40%; of those that survive, chronic cough, dyspnea, and sputum production

Pneumothorax Accumulation of air in pleural space, classified as spontaneous (primary or secondary) or traumatic:Traumatic: penetrating or blunt traumaIatrogenic: following procedures – thoracocentesis, pleural biopsy, subclavian or internal jugular vein catheter placement, percutaneous lung biopsy, bronchoscopy with transbronchial biopsy, and + poressure mechanical vents/s: acute onset of unilateral chest pain and dyspnea, minimal physical exam findings in mild cases; unilateral chest expansion, <’d tactile fremitus, hyperresonance, diminished breath sounds, mediastinal shift, cyanosis and hypotension in tension pneumopresence of pleural air on CXR

Angina pectoris Stable Angina Unstable AnginaSigns & symptoms-Gradual onset chest pain due to myocardial ischemia that occurs predictably and reproducibly on exertion-May also have SOB-Relieved by rest or NG-Usually lasts 2-5 minutes-Diffuse discomfortManagement-Goal is to relieve symptoms and prevent future cardiac events-Nitrates and β-blockers are initial DOCs-CCB for refractory symptoms-Exercise-Daily aspirin-CV risk reduction: BP control, smoking cessation, statins, weight reduction, glycemic control-Periodic reevaluation with EKGs-Revascularization therapy an option for select candidates

Signs & symptoms-Chest pain refractory to NG treatment or chest pain at rest or nocturnally-May be associated with SOB, nausea, diaphoresisManagement-Treat like other ACS: admission, MOANS, serial troponins, EKGs-Stabilize-Antiplatelet therapy and possible reperfusion for select patients- β-blockers-Statins-ACEI with DM, HF, LV EF < 40%, or HTN-CV risk reduction

MI Signs & symptoms-Sudden onset chest pain, nausea, vomiting, diaphoresis, SOB-Jaw, neck, scapular, throat, or arm pain-DOE-Chest pain > 30 min not responsive to NG-Hypovolemia-HTN or hypotension-Tachy or bradycardia-S3 or S4-Signs of CHF-Systolic murmurs-Friction rub if day 2 or later

Workup-Obtain 12 lead within 10 min of arrival and repeat every 10 minutes if initial EKG is not diagnostic (1st EKG is negative 40% of the time)-Look for early peaked T waves, ST elevation, Q waves, J point elevation-NSTEMI does not have EKG changes because the infarction is in an electrically silent area-Emergent cardiac consult for patients with cardiogenic shock, left heart failure, or sustained ventricular tachyarrhythmia-Electrolytes, coagulation studies, H/H-Serial troponins: specific cardiac damage marker, including damage from defibrillation, arrhythmias, cardiac procedures, CHF, vasospasms, etc;

Additional STEMI Treatment-Antiplatelet and anticoagulant therapy for allpatients (in addition to aspirin)-Emergent stent if < 3 hours from symptom onset-Alternative is lytic therapy if not contraindicated,symptoms < 12 hours, and PCI unavailablewithin 90-120 minutes-CABG rarely performed during acute MIAdditional NSTEMI Treatment-Antiplatelet therapy for all patients (in addition toaspirin)-Anticoagulant therapy for all patients-Invasive intervention based on presence of highrisk factors (recurrent angina at rest, elevatedtroponin, ST depression, high risk stress test result,EF < 40%, hemodynamic instability, sustained VT,recent PCI, prior CABG)Treatment of Cocaine-Related ACS

-Remember that women, the elderly, and diabetics may have atypical presentations

elevation begins within 1 hour and remains ↑ for 5-14 days-CK: found in skeletal muscle throughout the body; shows up in 1-6 hours and lasts up to 1.5 days-CK-MB: cardiac specific CK; shows up in 2 hours and declines after 24-72 hoursEmergent Management (any ACS)-Morphine, oxygen (only if sats < 90% or resp distress), aspirin, NG-Treat HF if present with NG, furosemide-Give β-blocker if HF is not present in order to reduce myocardial oxygen demand-Begin 80 mg atorvastatin for pts not already on

-Benzos every 15 minutes PRN-DON’T give β-blockersPrognosis-33% are fatal-Complications: CHF, RV infarction, ventricular rupture, arrhythmias, mural embolus, stroke,pericarditis, postinfarction angina-For USA and NSTEMIs, can estimate 14-day riskof death, recurrent MI, or need for urgentrevascularization using TIMI score (Skyscape)

Cardiac arrest Abrupt cessation of cardiac mechanical function, which may be reversible by a prompt intervention but will lead to death (sudden cardiac death) in its absence; complete cessation of heartbeatMechanism: Ventricular fibrillation, ventricular tachycardia, asystole, bradycardia, pulseless electrical activity, mechanical factorsStructural causes: Coronary heart dz, coronary abnormalities, chronic atherosclerotic lesions, thrombosis, MI (acute or healed), Myocardial hypertrophy; hypertrophic cardiomyopathy (obstructive, nonobstructive), dilated cardiomyopathy, inflammatory and infiltrative disorders (myocarditis, noninfectious inflammatory dz, infiltrative dz), valvular heart dz,electrophysiologic abnormalities, WPW syndrome, conducting dzFunction contributing factors: coronary blood flow alterations, transient ischemia, reperfusion after ischemia, low cardiac output states, HF (chronic, acute, shock), systemic metabolic abnormalities (electrolyte imbalance, hypoxemia, acidosis, neurologic distrubances), toxic responses (cocaine, digitalis, drug interactions)s/s: Usually, the first sign of sudden cardiac arrest (SCA) is loss of consciousness (fainting). At the same time, no heartbeat (or pulse) can be felt.Some people may have a racing heartbeat or feel dizzy or light-headed just before they faint. Within an hour before SCA, some people have chest pain, shortness of breath, nausea (feeling sick to the stomach), or vomiting.Dx: EKG, Echo, cardiac MRI, cardiac cath, electrophysiology, CMP (electrolyte abnormalities), BNP, troponin, CPK-MBTr: CABG, PCI, ICD, angioplasty

Cardiac arrhythmias and blocks

Bradyarrhythmias-Either a delay in impulse formation or conductionEtiologies-Hypoxia-↑ ICP-Hypothermia-Hypothyroid-Hyperkalemia-Sarcoidosis or amyloidosis-Degenerative disease of conduction system-Ischemia-Lyme-Rheumatic heart disease-Drugs: CCBs, β-blockers, digoxin

Signs & symptoms-Syncope or presyncope-Dyspnea from CHF-Angina pectoris-HypotensionDifferential-Regular rate sinus brady, complete heart block,2:1 AV block, sinus arrest with escape rhythm, “regularized” slowa-fib-Irregular rate sick sinus syndrome,2° AV block (Wenckebach or Mobitz type II), slow a-fib

Tachyarrhythmias

-Either a result of abnormal impulse formation or abnormal propagation (reentry)-Risk factors for SVT: hyperthyroid, HTN, mitral valve disease, COPD, post cardiac surgery-Risk factors for VT: prior MI, ischemia, long QT syndrome, antiarrhythmics, TCAs, hypoMg, hypo or hyperK

Signs & symptoms-Syncope or presyncope-Palpitations-Diaphoresis-Chest painDifferential-Narrow complex afib, multifocal atrial tachycardia,aflutter, atrial tachycardia, sinus tachycardia, WPW,junctional tachycardia, AVNRT-Wide complex torsades, polymorphic VT,AF with aberrant conduction, VT, SVT

AV Blocks Signs and symptoms ManagementFirst degree

-Asymptomatic -Treat reversible causes such as ischemia, increased-EKG showing lengthened PR interval vagal tone, or meds; pacemaker usually not-Determine site of block using EKG recommendedfindings, atropine, exercise, or vagal maneuvers

Second degree Wenckebach Mobitz I

-Typically asymptomatic -Treat reversible causes; pacemaker if there is-EKG shows progressive PR symptomatic bradycardiaprolongation for several beats priorto nonconducted P wave-Beats classically occur in ratios of 3:2, 4:3, or 5:4-Can be a result of inferior MI

Mobitz type II

-May be asymptomatic or have signs of -Treat reversible causes; most pts will required pacehypoperfusion or HF-PR interval remains unchanged prior to anonconducted P wave

Third degree

-May have dizziness, presyncope, syncope, v-tach, v-fib, worsening HF, or angina-P waves don’t correlate to QRS-Escape rhythm takes over for QRS (junctional or ventricular)

1st degree EKG:

2nd degree Mobitz type 1:

Mobitz type II:

3rd degree: Cardiac failure Most often a result of ischemic

heart disease (systolic HF) myocardial remodeling-Other causes: bad valves, HTN (diastolic HF), myocarditis, pericarditis, alcoholism (R HF), substance abuse, COPD or other lung disease (R HF)-Usually associated with low cardiac output but can be highAcute/flash pulmonary edema with acute MI, severe illness, PE, HTN, end stage valvular diseaseBeware acute HF with massive MI, tachyarrhythmias, or endocarditis with valve rupture: severe SOB, cool skin, diaphoresis, AMS, pallor, cyanosisDecompensated HF with new or worsening sx, new murmur, pt is “cold and wet”, CHF “decision rule” predicts 30 day mortality, avoid β-blockers

Signs & symptoms-R CHF ascites, + hepatojugular reflex, weight gain, JVD, hepatomegaly, edema, abdominal distension, mostly clear lungs with dullness at the bases, ↑ JVP with hepatojugular reflux, tricuspid regurg, peripheral edema-L CHF (mostly heart and lung sx) dyspnea, cough, S3 or S4, crackles, wheezes, dullness at bases, frothy or pink sputum, pulse alternans (alternating strong-weak pulse), palpitations, fatigue, diaphoresis, displaced PMI, mitral regurg, pulmonary edema, orthopnea, PNDBut research shows there are no hard and fast physical exam differentiations for R vs L CHF; all of these s/s can overlap!Workup-Referral for echo-EKG for LVH-Stress test-CXR for pulmonary edema (Kerley B lines)-Labs: BNP, CBC, CMP, fasting glucose, lipids-Cardiovascular MRI can help distinguish ischemic heart disease from cardiomyopathy

Other Management-Salt restriction, daily weights-Avoid NSAIDs, CCBs-ATP III recommends giving aspirin to reduce prothrombotic state-Exercise training program for stable NYHA class II to III-Devices: AICD, intra-aortic pump, LVAD

Drugs with proven mortality benefit-Note that there is only evidence for systolic HF for these drugs; use with diastolic CHF is not yet substantiated-ACEI or ARB

-Hydralazine + isosorbide dinitrate: most beneficial for black man as an add on therapy to those already on β-blocker and ACEI that are still symptomatic-β-blockers-Aldosterone antagonistsPrognosis-Diet and prescription noncompliance are a major cause of hospital readmission for CHF

Main causes of death are arrhythmia and progressive pump failure

Hypertensive crisis

Hypertensive urgency = stable or no end organ damage, no raised ICP-May have SOB, headache, BPs usually > 220/110-Tx is to lower BP in clinic slowly over several hours (≤160/100) with labetalol, clonidine, captopril-Close follow-upHypertensive emergency = rapidly progressing end organ damage-Papilledema if malignant

-Chest pain, AMS, weakness, MI, acute CHF, renal failure, ICH, eclampsia, aortic dissection-Don’t lower BP by more than 25% original valueMonitoring HTN:-Annual urine microalbumin-Annual BMP-Annual lipids

-Baseline EKG, look for LVHPharm for HTN single agents only lower by 10-20 mm Hg, may need a 2nd agents

Thiazides: HCTZ, chlorthalidone -DOC for HTN but can’t use once CrCl < 30-Ca sparing = good for osteoporosis pts-Need to check BMP before and after starting-Chlorthalidone has the most evidence but my preceptor thinks itcauses a lot of hypokalemia

Loops: furosemideK-sparing: spironolactone, eplerenone

Not very potent

ACEi’s: benazepril, enalapril, lisinopril

-Cough-Can cause renal failure = need to monitor BMP 1 week and 1 monthafter starting and periodically after that, STOP if serum Cr ↑ by 30%-Ok to use in patients with no renal function left-Pregnancy D

ARBs: irbesartan, losartan, olmesartan, valsartan

-Same AEs as ACEIs and also pregnancy D

CCB’s: dihydropyridine (nifedipine, amlodipine)and non-dihydropyridine (verapamil and diltiazem)

-Useful in the elderly-FDA warning about amlodipine, verapamil, and diltiazemuse with simvastatin-Contraindicated in heart failure

Other direct vasodilators: hydralazine, minoxidilα-blockers -Clonidine: only for refractory HTN due to risk of falls

-Methyldopa: DOC for HTN in pregnancyβ-Blockers -Questionable role in the treatment of essential HTN unless patient

also has CHF or MI-Need strict β-1 blockers for asthma/COPD patients so that bronchial relaxation is not blocked (atenolol or metoprolol)-Propranolol and labetalol block at multiple sites-Can mask signs of hypoglycemia-Contraindications: heart block

Acute Gastrointestinal bleed

Upper GI bleed causes: coffee ground or red hematemesis -> bleeding proximal to the ligament of Treitz. Frank blood -> mod to severe bleeding that may be ongoing; coffee ground -> limited bleeding

Lower GI bleed: melena (black tarry) proximal to the ligament of Treitz; Hematochezia (red or maroon blood in stool) -> lower GI bleed or massive upper GI bleed that’s associated with orthostatic hypotension

Potential sources of GI bleed: varices or portal hypertensive gastropathy w/ liver dz or alcohol abuseAorto-enteric fistulaAngiodysplasiaPUD w/ H pyoloriMedication hx – aspirin or NSAID use, antiplatelet agents, iron, bismuthEsophageal ulcerMallory-weiss tearVariceal hemorrhageMalignancyPE: mild to mod hypovolemia (resting tachy), stool color, abd pain, rebound tenderness and involuntary guarding can indicate perforationLab: CBC (hemoglobin loss with normocytic/chromic RBC’s), CMP, ALT/AST, Alk Phos, PTT/PT, INR, EKG,

cardiac enzymes with MI risk pts with chest pain/dyspnea; elevated BUN/CR ratio (higher ratio = upper GI)Dx studies: upper endoscopy, angiography for upper GI, colonscopy for Lower GI bleedTriage: all pts w/ hemodynamic instability -> admit to ICU for resuscitation and close monitoringOxygen, fluid resuscitation (500mL normal saline or lactate Ringer over 30 minutes), type and crossed, and transfused for pts <7 g/dL hemoglobin (with the exception of variceal bleeding, only transfuse to <10 g/dL)

Meds: PPI, prokinetics (erythromycin or metoclopramide) for upper GI bleed to clear visualization for endoscope, Somatostatin for variceal bleeding (Octreaotide 20-50 mcg bolus + 25-50 mcg/hr; ABX for pts with cirrhosis

SEIZURESHistory & Physical Focal seizures:

w/o impairment of consciousness aka “simple partial” seizures- focal motor symptoms (convulsive jerking)- somatosensory symptoms (eg, paresthesias or tingling) that spread (or “march”) to

different parts of the limb or body- special sensory symptoms (eg, light flashes or buzzing) indicate involvement of visual,

auditory, olfactory, or gustatory regions of the brain- there may be autonomic symptoms or signs (eg, abnormal epigastric sensations, sweating,

flushing, pupillary dilation).- The sole manifestations of some seizures are phenomena such as dysphasia, dysmnesic

symptoms (eg, déjà vu), affective disturbances, illusions, or structured hallucinations, but such symptoms are usually accompanied by impairment of consciousness.

With impairment of consciousness – aka “complex partial” seizures- Impaired consciousness or responsiveness may be preceded, accompanied, or followed by

the various symptoms mentioned above, AND automatisms may occur.Absence seizures

- impairment of consciousness, sometimes w/ mild clonic, tonic, or atonic components (ie, reduction or loss of postural tone), autonomic components (eg, enuresis), or accompanying automatisms

- Onset and termination of attacks are abrupt- If attacks occur during conversation, the patient may miss a few words or may break off in

midsentence for a few seconds.- The impairment of external awareness is so brief that the patient is unaware of it- Absence (“petit mal”) seizures almost always begin in childhood and frequently cease by

the age of 20 years or are then replaced by other forms of generalized seizure.Atypical absence seizures

- More marked changes in tone or attacks may have more gradual onset and termination than in typical absence seizures

- Commonly occur in patients w/ multiple seizure types, may be accompanied by developmental delay or mental retardation

Myoclonic seizures- Myoclonic seizures consist of single or multiple myoclonic jerks.

Tonic-clonic (“grand mal”) seizures- Tonic phase - sudden loss of consciousness, the patient becomes rigid and falls to the

ground, and respiration is arrested; usually lasts for < 1 min- followed by a clonic phase - jerking of the body musculature that may last for 2 or 3

minutes- followed by a stage of flaccid coma- During the seizure, the tongue or lips may be bitten, urinary or fecal incontinence may

occur, and the patient may be injured. Immediately after the seizure, the patient may recover consciousness, drift into sleep, have a further convulsion without recovery of consciousness between the attacks (status epilepticus), or after recovering consciousness have a further convulsion (serial seizures).

- In other cases, patients will behave in an abnormal fashion in the immediate postictal

period, without subsequent awareness or memory of events (postepileptic automatism).- Headache, disorientation, confusion, drowsiness, nausea, soreness of the muscles, or some

combination of these symptoms commonly occurs postictally.Tonic, clonic, or atonic seizures

- Loss of consciousness may occur with either the tonic or clonic accompaniments described above, especially in children. Atonic seizures (epileptic drop attacks) have also been described.

Symptoms & Signs- Nonspecific changes such as HA, mood alterations, lethargy, myoclonic jerking alert some

patients to an impending seizure hours before it occurs- External precipitants

o Lack of sleepo Missed mealso Emotional stresso Menstruationo Alcohol ingestiono Use of certain drugso Fever and nonspecific infections

- In a few patients, seizures are provoked by specific stimuli – flashing lights, flickering TV set (photosensitive epilepsy), music, or reading

Physical exam- Exam b/w seizures shows no abnormality in patients with idiopathic epilepsy- In immediate postictal period, extensor plantar responses may be seen- Presence of lateralized or focal signs suggest that seizures may have a focal origin- In symptomatic epilepsy, findings on exam will reflect underlying cause

Diagnostic studies - MRI is indicated for patients with focal neurologic symptoms or signs, focal seizures, or electroencephalographic findings of a focal disturbance

- some clinicians routinely order MRI for all patients with new-onset seizure disorders- studies should be performed in patients with clinical evidence of a progressive disorder

and in those with new onset of seizures after the age of 20 years because of the possibility of an underlying neoplasm.

- Initial investigations should include CBC, serum glucose, electrolytes, creatinine, calcium, magnesium, and liver function tests to exclude various causes of seizures and to provide a baseline for subsequent monitoring of long-term effects of treatment

- A lumbar puncture may be necessary when any sign of infection is present or in the evaluation of new-onset seizures in the acute setting.

- Electroencephalography may support the clinical diagnosis of epilepsy (by demonstrating paroxysmal abnormalities containing spikes or sharp waves), provide a guide to prognosis, and help classify the seizure disorder.

Diagnosis DDx of focal seizures- TIA- Panic attacks

DDx of generalized seizures- Syncope- Cardiac disease- Brainstem ischemia- Psychogenic nonepileptic seizure (PNES)

Clinical therapeutics

Monotherapy- Monotherapy is preferable to the use of several drugs because fewer toxic effects, less

likelihood of drug interactions, and better compliance.- The drug of choice should be slowly increased until seizures are controlled or until clinic

of toxicity develop.- If seizures are not adequately controlled at the maximum to dosage, a second AED is slowly

introduced. After the second drug attains therapeutic levels, the first drug is gradually

withdrawn.- Monotherapy adequately control onset epilepsy in about two-thirds of the patients.

Polytherapy- Polytherapy with a combination of two AEDs (usually one traditional and one newer

AED) may necessary only if monotherapy with two or more first-line AEDs been unsuccessful.

- When using two AEDs, select those with different mechanism of action.- Avoid using more than two AEDs simultaneously.

After two appropriate AEDs fail to control seizures, monotherapy with a third AED or polytherapy is successful in only 4% of the patients.

STATUS EPILEPTICUSHistory & Physical - A brief history and physical examination should be directed toward discovery of the cause

of the seizures and to any injury that may have resulted- Any of the causes of seizures may result in status epilepticus

Clinical Therapeutics

Initial Supportive Care 1. Maintain airway with cervical spine precautions. 2. Deliver oxygen by nasal cannula.

3. Monitor ECG and blood pressure. 4. Maintain normal temperature.

Pharmacologic Therapy 1. Establish IV, administer thiamine 100 mg IV 2. Administer 1 amp of D50 IV in an adult unless obviously hyperglycemic. 3. Administer IV lorazepam or diazepam initially (midazolam 0.2 mg/kg)

o Lorazepam is considered the initial agent of choice d/t it’s longer duration of action (12-24 h); more effective than phenytoin or phenobarbital

4. If seizures persist, give fosphenytoin or phenytoin.o Phenytoin should not be mixed with any glucose-containing IV fluid and

should not be given IM due to erratic absorption. The drug is contraindicated in the presence of second- or third-degree atrioventricular block

5. If seizures persist, give phenobarbital, paraldehyde. 6. If still no response, obtain emergency neurosurgery and anesthesiology consultations.

Scientific concepts Definition: The traditional definition of status epilepticus (SE) is a prolonged seizure, or cluster of seizures, without a return to baseline, lasting longer than 30 minutes. A revised operational definition, proposed to lower morbidity and mortality, is any seizure lasting more than five minutes.

SHOCKHistory & Physical History

- Check for unsuspected trauma, unsuspected/known pregnancy, new meds, allergies, overdose, or depression

- Look for potential drug interactions such as sildenafil & nitroglycerin- Obtain travel hx (SARS)- Tampon-use hx (toxic shock syndrome)- CP & dyspnea ACS or PE- Fever or hypothermia sepsis

Essentials of diagnosis- Hypotension, tachycardia, oliguria, altered mental status, metabolic acidosis d/t elevated

lactic acid- Peripheral hypoperfusion and impaired oxygen delivery

Hypovolemic shock (20-30% volume loss)- Oliguria, AMS, cool extremities, jugular venous pressure is low, narrow pulse pressure

Cardiogenic shock- L-sided heart failure: pulmonary edema- R-sided heart failure: peripheral edema, JVD

Distributive shock- Hyperdynamic heart sounds- Warm extremities initially- Wide pulse pressure indicative of large stroke volume

Diagnostic studies Labs

- CBC, coagulation studies, electrolytes, BUN, creatinine, arterial blood gas, and serum lactate- In septic shock, obtain pan cultures.- Obtain urinalysis in all patients and perform urine pregnancy testing in all women of child-

bearing age.- Type and crossmatch the patients for packed RBCs.- In cardiogenic shock, obtain cardiac enzymes.

Imaging- A chest radiograph and ECG are valuable initial examinations with further testing dictated

by clinical suspicion- Bedside U/S can have a key role with evaluation of pericardial fluid and hemoperitoneum

but complex imaging studies should wait until the patient is resuscitated.Diagnosis

Clinical therapeutics

- ABCs- Establish multiple short-length, large-bore peripheral IV access- Cardiac monitor- Identify if reversible condition

o Traumatic blood loss – CXR, USo Nontraumatic blood loss – check for abd mass (AAA), GI bleedo Dysrhythmiao Tension pneumothoraxo Cardiac tamponadeo Massive pulmonary embolismo Overt anaphylaxiso Spinal cord injuryo Problem w/ SVR

Hypovolemic shock- Crystalloid infusion of NS or lactated ringer’s solution of 20 cc/kg as general resuscitation

measuresHemorrhagic shock

- Type-specific or type O neg. PRBCs or whole blood (provides extra volume & clotting factors) should be given if not responding to crystalloid infusion of 40 cc/kg

Cardiogenic shock- Supportive measures oxygen, aspirin, heparin, fluid challenges (250cc) if no overt

pulmonary edema- Vasopressors – dopamine, norepinephrine, dobutamine- For STEMI – revascularization by PCI or emergent CABG

Anaphylactic shock- Early intubation- -agonist aerosol - albuterol nebulizerβ- epinephrine- H1 & H2 histamine receptor blockade- Steroids

Septic shock- Aggressive volume resuscitation

- Early antibiotic use- Supportive care

Neurogenic shock- Evaluation of other potential causes of shock- Fluid challenge of 20 cc/kg x 2- If volume replacement is unsuccessful, vasopressors w/ activityα

Obstructive shock- Tension pneumothorax – immediate needle decompression followed by chest tube

thoracostomy- Pericardial tamponade – pericardiocentesis- Massive PE – BP should be augmented w/ appropriate vasopressor (norepinephrine);

thrombolytics if no contraindicationsScientific concepts

COMAHistory & Physical - Pupillary enlargement w/ loss of light reaction & loss of vertical & adduction movements of

the eyes = lesion in upper brainstem- Preservation of pupillary light reactivity & of eye movements = widespread structural

lesions or metabolic suppression of cerebral hemispheres- Fever – systemic infection, bacterial meningitis, encephalitis, heat stroke, neuroleptic

malignant syndrome, malignant hyperthermia d/t anesthetics or anticholinergic drug intoxication

- Hypothermia – characteristic of coma from alcohol or barbiturate intoxication, internal hemorrhage, MI, sepsis, profound hypothyroidism, or Addisonian crisis

Diagnostic studies - Chemical-toxicologic analysis of blood and urine- Cranial CT or MRI- EEG- CSF examination

Diagnosis 1. Diseases that cause no focal or lateralizing neurologic signs, usually with normal brainstem functions; CT scan and cellular content of the CSF are normal

a. Intoxications: alcohol, sedative drugs, opiates, etc.b. Metabolic disturbances: anoxia, hyponatremia, hypernatremia, hypercalcemia, diabetic acidosis, nonketotic hyperosmolar hyperglycemia, hypoglycemia, uremia, hepatic coma, hypercarbia, addisonian crisis, hypo- and hyperthyroid states, profound nutritional deficiencyc. Severe systemic infections: pneumonia, septicemia, typhoid fever, malaria, Waterhouse-Friderichsen syndromed. Shock from any causee. Postseizure states, status epilepticus, subclinical epilepsyf. Hypertensive encephalopathy, eclampsiag. Severe hyperthermia, hypothermiah. Concussioni. Acute hydrocephalus

2. Diseases that cause meningeal irritation with or without fever, and with an excess of WBCs or RBCs in the CSF, usually without focal or lateralizing cerebral or brainstem signs; CT or MRI shows

no mass lesiona. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, traumab. Acute bacterial meningitisc. Viral encephalitisd. Miscellaneous: fat embolism, cholesterol embolism, carcinomatous and lymphomatous meningitis, etc.

3. Diseases that cause focal brainstem or lateralizing cerebral signs, with or without changes in the CSF; CT and MRI are abnormal

a. Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large middle cerebral artery territory) with secondary brainstem compressionb. Brainstem infarction due to basilar artery thrombosis or embolismc. Brain abscess, subdural empyemad. Epidural and subdural hemorrhage, brain contusione. Brain tumor with surrounding edemaf. Cerebellar and pontine hemorrhage and infarctiong. Widespread traumatic brain injuryh. Metabolic coma (see above) with preexisting focal damagei. Miscellaneous: Cortical vein thrombosis, herpes simplex encephalitis, multiple cerebral emboli due to bacterial endocarditis, acute hemorrhagic leukoencephalitis, acute disseminated (postinfectious) encephalomyelitis, thrombotic thrombocytopenic purpura, cerebral vasculitis, gliomatosis cerebri, pituitary apoplexy, intravascular lymphoma, etc.

Clinical therapeutics

- ABCs- IV access- Hypotension, hypoglycemia, hypercalcemia, hypoxia, hypercapnia, and hyperthermia

should be corrected rapidly.- naloxone and dextrose are administered if narcotic overdose or hypoglycemia are

possibilities- thiamine is given along with glucose to avoid provoking Wernicke's disease in

malnourished patients- In cases of suspected basilar thrombosis with brainstem ischemia, IV heparin or a

thrombolytic agent is often utilized, after cerebral hemorrhage has been excluded by a neuroimaging study.

- Physostigmine may awaken patients with anticholinergic-type drug overdose but should be used only with careful monitoring

Scientific concepts Definition – deep sleeplike state from which the patient cannot be arousedPrincipal causes of coma

- (1) lesions that damage the RAS (reticular activating system) in the upper midbrain or its projections

- (2) destruction of large portions of both cerebral hemispheres- (3) suppression of reticulocerebral function by drugs, toxins, or metabolic derangements

such as hypoglycemia, anoxia, uremia, and hepatic failure.CARDIAC TAMPONADE

History & Physical - tachycardia, decreased cardiac output, and hypotension, although hypertension occasionally is present.

- Dyspnea & coughCharacteristic features of tamponade

– Tachycardia– Tachypnea– Narrow pulse pressure– Preserved systolic pressure

Diagnostic studies - primary diagnostic imaging modality for cardiac tamponade is transthoracic Doppler echocardiography

- Electrocardiographic features of tamponade include low voltage and electrical alternan

- A paradoxical pulse is the most helpful clinical test for cardiac tamponade

Clinical therapeutics

- The presence of cardiac tamponade should be considered a medical emergency, warranting admission to an intensive care unit with prompt consultation of a cardiovascular diseases specialist to perform an urgent pericardiocentesis. If the patient becomes pulseless, pericardiocentesis should be performed immediately, even by inexperienced practitioners.

- Removal of the pericardial fluid with pericardiocentesis is the definitive treatment for cardiac tamponade.

Scientific concepts - The rate of fluid accumulation is very important; if slow, the pericardium stretches over time and large volumes (up to several liters) may collect before causing hemodynamic difficulty

- if the fluid accumulates quickly, the noncompliant pericardium does not stretch and tamponade can be caused by as little as 150 to 200 mL. As pericardial pressure increases, transmural ventricular pressures decrease despite increased intracavitary pressures.

PERICARDIAL EFFUSIONHistory & Physical • Pain in acute inflammatory pericarditis; neoplastic and uremic effusions are often painless

• Dyspnea and cough• Other symptoms reflect primary disease• Pericardial friction rub may be present (even with large effusions)• Pulsus paradoxus (> 10 mm Hg decline in systolic pressure during inspiration) is common• Elevation of central venous pressure, edema, or ascites in chronic processes• Hypotension, paradoxical pulse and an elevated jugular venous pressure all important signs

Diagnostic studies • ECG– Often reveals nonspecific T wave changes and reduced QRS voltage– Electrical alternans is pathognomonic

• Chest radiograph: normal or enlarged cardiac silhouette with a globular configuration• Echocardiography is primary mode of diagnosis• Diagnostic pericardiocentesis or biopsy is often indicated for microbiologic and cytologic studies• Yield of diagnostic pericardial tap is low

Clinical therapeutics • Small effusions can be followed clinically and by echocardiogram• Urgent pericardiocentesis is required for tamponade• Partial pericardiectomy may be required for recurrent effusion in neoplastic disease and uremia, either by video-assisted thoracic surgery (VATS) or thoracotomy• Additional therapy (eg, dialysis) for the primary disease

Scientific concepts - Can develop from any form of pericarditis- Slow development of large effusions may produce no hemodynamic effects- Rapid appearance of smaller effusions can cause cardiac tamponade (elevated

intrapericardial pressure that restricts venous return and ventricular filling), leading to shock and death

CardiologyINTERNAL MED EOR EXAM STUDY GUIDE: CHF

Scientific Concepts SYMPTOM COMPLEX, NOT DX Condition from any functional or structural cardiac disorder that

impairs the ability of the heart to fill or pump a sufficient amount of blood through the body. (or a combo of both)

Systolic - depressed ejection fraction (this is more common dysfunction, dilation)

Diastolic - preserved ejection fraction. Not enough blood volume. Passive stiffness

Causes:o CAD (with or without MI)o Ischemic Cardiomyopathy (CMO)- Most Common ( –

ischemic event that caused an exacerbation acutelyo Non-Ischemic CMO (rare- sarcoid/amyloid)o Systemic Hypertension

Stages of Heart Failure

CHF Prognosis Risk increases with diastolic dysfunction and worsening prognosis (because the pulmonary system is getting worse- affecting everything behind it)

Improving with use of ACEI and Beta blockersCHF History and Physical Symps

o Dyspnea (at rest and exertional)o Orthopneao Paroxysmal Nocturnal Dyspnea (PND)o Chronic cough (non-productive) –vascular congestiono Nocturiao Fatigueo With RV Failure: RUQ Pain, Nausea, Loss of appetite,

Peripheral edema, Ascites PE

o Vitals: can be normal, may have Tachycardia, Hypotension , Decreased pulse pressure, Diaphoresis, Cool extremities

o WEIGHT! Follow very closelyo JVDo Thyromegalyo Carotid pulse- Aortic Stenosis (AS)o Lungs: Crackles, Wheezes, Rhonchi, Pleural effusionso LV lift or sustained pulsationo Diminished first sound: annulus around the valves change,

not getting closing snapo S3 gallopo Murmurso RV failure: hepatomegaly

CHF Lab Eval and Workup CBC – Anemia BMP- Renal insufficiency (BUN and Cr increased, but still making

urine)/Renal Failure Electrolytes (K, Mg), Decreased Na, Hypokalemia in Afib

Thyroid BNP (BRAIN NATRIURETIC PEPTIDE)

o Major source is the cardiac ventricleso direct proportion to ventricular volume expansion and

pressure overload.CHF Workup: EKG Hypertrophy

Arrhythmia : ie A-fib MI Non-specific *Compare priors

CHF Workup: CXR Cardiomegaly – silhouette should not be more than one half the size of the chest

Pulmonary venous hypertension Perivascular edema (haziness of vessel outlines) Interstitial edema Pleural effusions (transudate)

CHF Treatment Underlyingo Valvular diseaseo MI : Stent, Angioplasty, CABGo HTNo Arrhythmiaso Alcoholo Drugs: CA++ channel blockerso Pericardial disease

Diuretics

o Most effective for symptomso Careful for excessive useo Electrolyte abnormalities (K+ )o Thiazide diuretics

HCTZ 25mg Daily Metolazone 2.5-5 mg Daily Chlorthalidone 50 mg Daily Works on distal loop, prevention of absorbtion of

Na+ Worsening HF (adding more diuretics – want to assess by

symptomology)o Furosemide (Lasix) 20-40 mg Daily, titrateo Bumetinide (Bumex) 0.5-2 mg Dailyo Torsemideo BID preferredo Watch electrolytes

K+ sparing drugs (aldosterone antagonists)o Spironolactone (Aldactone) 25-50 mg Dailyo Triamtereneo Amilorideo Eplerenone (Inspra)o Along with ACE and diuretics, reduction in mortality and

improve symps ACEI

o Prevents hospitalizationso Increased exercise toleranceo Decreases symptomso Enalapril, Ramipril, Benazepril, Avoid if Renal artery

stenosiso ACEI First line tx in pts with EF < 40%o Used in combo with diuretics: Potential side effects are

hypotension and hyponatremia.o Cough, angioedema, hypotension

ARB’so Not to be used with ACEIo Chronic Failure: Candesartan or valsartan can benefit as

alone or in addition to diuretico Losartan (Cozaar®)

Beta Blockers (Carvedilol, Metoprolol)o Decreased HR allows more time for the heart to fill.o Clinical effects: improve long term symps; reduce

hospitalizations, sudden death; improve survival; reduce remodling/progression

Caution: Could worsen LV function Detrimental to use a pure beta blocker for HF

Digoxin/Digitaliso Only oral positive inotropeo Used in conjunction with patients with atrial fibrillationo Enhances sympathetic tone which delays AV conductiono Can be given with other medso Amiodarone (CORDARONE)

o Quinidineo Propafenone (RYTHMOL)o Verapamil

Vasodilators/Nitrateso Reduction of AV afterloado Need an agent or a combination of agents to improve

both factorso NTG, Sodium Nitroprusside, Isosorbide 20-80 mg TID,

NTG pasteo Hydralazine

Potent arterial vasodilator Markedly increased CO Stand alone does not perform well to improve

symptoms or exercise tolerance Combination of nitrate and hydralazine has

greater hemodynamic effects (BiDil: Hydralazine + Isosorbide)

Frequently limited by side effects GI, HA,Hypotension

Dobutamine/Milrinone: positive inotropes, role is limited to pts with hypoperfusion and deteriorating kidney function, or pts awaiting transplant. Continuous therapy increases mortality.

CHF Tx: CCB’s May accelerate progression of HF Exception is Amlodipine (NORVASC) General rule is to avoid use unless treating HTN associated angina

Anticoagulation LV failure and reduced EF can give risk of intra-cardiac thrombus formation and systemic embolus

Antiarrhythmic Therapy Moderate to severe failure can have increased incidence of arrhythmia

Tx: Implantable Defibrillators Reduction of sudden death from heart failure related arrhythmia (EF <30%, risk of sudden cardiac death increases significantly)

INDICATED IN CLASS III HF for primary prevention of sudden deathNon-Pharm Tx Diet, exercise management

o Reduction in weight, sodium intakeo Exercise training to reverse deconditioning

Biventricular Pacing For use in widened QRS complex situations Can improve EF and exercise tolerance Reduction in death and hospitalizations

Cardiac Transplantation Last ends of care

INTERNAL MED EOR STUDY GUIDE: HYPERTENSIONJNC7 Classification

Diagnosis Serial blood pressure measurements on at least 3 separate occasions Major exceptions to single elevated BP measurement

o Unequivocal evidence of life-threatening end-organ damage

(hypertensive emergency)o BP is >220/125 mm Hg, but life-threatening end-organ damage is

absent (hypertensive urgency)Patient Evaluation 1. Assess CV risk factors and comorbidities

2. Reveal identifiable causes of HTN3. Assess presence of target organ damage and CVD

Risk Factors and Comorbidities

Identifiable Causes HTN

Target Organ Damage and CVD

Scientific Concepts: Primary Essential HTN

**95% of hypertensive patients, onset between ages 25 and 50Genetic and Environmental Factors

Sympathetic NS hyperactivity: Younger persons with tachycardia and elevated CO

RAAS: High Renin Activity, Caucasian and younger Elevated intracellular sodium and calcium levels

Exacerbating factors Obesity, Sleep apnea, Increased salt, ETOH, Cigarettes, Polycythemia, NSAID’s,

Low potassium intakeHistory and Physical Symptoms

o Asymptomatic : “Silent killer”o Nonspecific: HA, Blurred vision, Dizziness, Facial flushingo Severe Symps: N/V, Irregular HR, Tinnitus, Dyspnea

PEo BMIo Verify contralat armo Funduscopic exam

o Palpate peripheral pulseso Bruits (carotid, renal, femoral)o Thyroid gland enlargement or masseso Cardiac (LVH)o Kidney enlargemento Abdominal masses and AAA pulsationo BLE edema and pulseso Neurological assessment (cerebrovascular dz)

Diagnostic Studies Labs UA FBG or HgA1c, K+, creatinine, GFR, Ca++ Fasting lipid panel Hematocrit

Target organ damage Labs, radiologic studies, EKG- but echo better

Complications of Longstanding Hypertension

CV: LVH, CAD, CHF, Afib Cerebrovascular Disease: Stroke, hemorrhage, encephalopathy Renal: Nephrosclerosis, accelerates DM Nephropathy Aortic Dissection: HTN contributing factor

Hypertensive Emergencies

Require substantial reduction of BP within 1 hour to avoid risk of serious morbidity or death

Includes:o Hypertensive encephalopathy (HA, irritability, confusion, AMS)o Hypertensive nephropathy (hematuria, proteinuria, progressive

kidney dysfunction)o Intracranial hemorrhage, aortic dissection, preeclampsia-eclampsia,

pulmonary edema, unstable angina, MI Malignant Hypertension

o Elevated BP results in target organ damage (CNS, CV, renal system)o Characterized by encephalopathy or nephropathy with accompanying

papilledema (must be present)o Progressive kidney disease results if treatment not providedo Same treatment as other hypertensive emergencies, table 11-12

CMDT. Depends on organ affected, includes: Nicardipine, Ntg + Labetalol or Esmelol, Fenoldopam, Clevidipine, Labetalol

Health Maintenance& Treatment Goals

Primary focus is reaching SBP goal, most reach DBP goal once SBP goal is reached

Treating to <140/90 is associated with decrease in CVD complications Goal is <130/80 for patients with HTN and DM or renal dz Lifestyle: sodium recommended 1500 mg, no more than 2300 mg/day or 1 TSP F/U monthly intervals for adjustment of medications until BP goal is reached

and assess for adverse reactions More frequent visits for stage 2 HTN or if complicating comorbid conditions Labs: Serum potassium and creatinine 1-2 times/year and other labs as

indicated BP to goal and stable: 3 to 6 months intervals

Clinical Therapeutics Multidrug treatmento 2 drugs at lower doses avoid adverse effects that may occur with

higher doses of single agent

Thiazide Diuretics Chlorthaizide, Chlorthalidone, HCTZ, Polythiazide, Indapamide, Metolazone Initial therapy for most patients with HTN Enhance the antihypertensive effects of multi-drug regimens (ACEI, BB) Adverse: Decrease K, Mg, Ca, Na; Increase uric acid, glucose, lipid Hypotension, HA, weakness, muscle cramps, photosensitivity, rash, ED

ACE Inhibitors Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril, Quinapril, Ramipril, Trandolapril

More effective in Caucasians and younger patients Less effective in African Americans and older patients Benefits

o Slow progression of loss of kidney function (diabetic nephropathy and CKD)

o Reduce LVH and indicated for CHF Adverse Effects

o Increase K, uric acid; elevated BUN/Cro Hypotension,** cough **angioedema (severe rxn)o If cough, switch to ARB

Angiotensin II Receptor Blockers

Candesartan, Eprosartan, Irbesartan, Losartan, Olmesartan, Telmisartan, Valsartan

Benefitso Less side effects than ACEI (cough and angioedema)o Effectiveness and enhanced interaction with diuretics is similar to

ACEIso Prevention of stroke,o Possibly diminish progression of Alzheimer’s

ADE’s similar to ACEICalcium Channel Blockers

Benefits: Effective in treating arrhythmias Adverse reactions: HA, peripheral edema, bradycardia, heartburn, constipation

Beta Blockers Atenolol, Betaxolol, Bisoprolol, Metoprolol, Nadolol, Propranolol, Timolol Cardioselective – primarily beta-1 receptors (heart) Nonselective – beta-1 and beta-2 (lungs, blood vessels, tissues Benefits

o Cardioprotectiveo Useful in patients with angina, prior MI, stable CHFo Treatment for migraines and anxiety

Adverse reactionso Worsen chronic lung disorderso Possibly worsen heart failure and peripheral vascular diseaseo Abrupt withdrawal may trigger angina or MI in patients with heart

diseaseo Dizziness, fatigue, insomnia, depression, erectile dysfunction,

Raynaud’s, increase TGTreatment: Compelling Indications

INTERNAL MED EOR EXAM STUDY GUIDE: HEART MURMURSAortic Stenosis Harsh systolic ejection murmur heard best at right upper sternal border

(RUSB)o Mid to late peako Reduced intensity of second heart soundo Radiates to carotidso Pulses-parvus et tardus (slow and late)o Narrow pulse pressureo Begins after S1, ends before A2

Aortic Insufficiency (aka regurgitation)

High pitched diastolic decrescendo murmuro Louder along left sternal border in third to fourth intercostal

space Widened pulse pressure Water hammer/Corrigan pulse Optimum auscultation: diaphragm, pt leaning forward, breath held in

expiration Austin Flint: Aortic Regurg may be associated with low pitched mid-

diastolic murmur at apexMitral Stenosis Opening snap following A2

Low pitched diastolic rumble heard best at apex, Lt Lat position, using

bell Left sided after expiration

Mitral Regurgitation Holosystolic murmur heard best at left sternal border and radiates to axilla

Loudest over PMI Begins with S1 and ends at or after A2

Mitral Valve Prolapse Mid systolic click with late systolic murmur Ausculatory findings accentuated in the standing position or valsalva

Pulmonic Insufficiency diastolic decrescendo murmurPulmonary Stenosis systolic murmur with S2 splitTricuspid Regurgitation pansystolic murmur, right heart failure

Best heard at third to fifth ICS along left sternal border Can be hard to hear, blowing, coarse or musical Begins with S1 and fills systole Louder during inspiration

Tricuspid Stenosis Rumble often follows audible opening snap Heard at third to fifth ICS along lefts sternal border out to apex. Murmur increases with inspiration

Murmurs in Stable Angina Occasionally a gallop rhythm and apical systolic murmur due to transient mitral regurg from papillary muscle dysfunction

**Here is a youtube video with a mnemonic to remember the diastolic vs systolic murmurs **http://www.youtube.com/watch?v=sL0vHiXLZ-4INTERNAL MED EOR EXAM STUDY GUIDE: VALVULAR HEART DISEASE

Definitions Stenosis- abnormal narrowing Regurgitation- backward flowing of blood

Aortic Stenosis (AS) Congenital: Unicuspid or bicuspid valves, younger population Rheumatic

Untreated Strep pharyngitis- usually between 5-15y Fusion of the leaflets, also effects mitral valve

Degenerative calcific (most cases > 70y) Lipid accumulation, inflammation and calcification

AS pathophysiology Bulky calcification > obstruction of the outflow tract leads to hypertrophy of the left ventricle >

eventually leads to less compliance > diastolic dysfunction (elevated LVEDP) AS symptoms

3 cardinal symptoms: Angina, Syncope, Dyspnea AS treatment

Surgical aortic valve replacement (gold standard) Mechanical vs bioprosthetic Transcatheter aortic valve replacement (TAVR) Palliative percutaneous aortic balloon valvuloplasty Medical therapy

Aortic Insufficiency Regurgitation of aortic valve into left ventricle Multiple etiologies- endocarditis, iatrogenic, bicuspid vs acute in setting of aortic dissection Prognosis determined by symptoms and LV size/function

AI clinical manifestations Diagnosed with auscultation/echocardiogram

AI treatment options Medical therapy to help slow progression of symptoms ACEi, Diuretics Surgical valve replacement if evidence of LV systolic dysfunction with or without symptoms

Mitral Stenosis Thickening and immobility of mitral valve leaflets (fusion or shortening of chordae tendonae)>

increased pressure in left atrium > increased pressure in pulmonary vasculature > elevated pressures in right heart

Etiology: Rheumatic fever (majority), Congenital MS clinical manifestations

Dyspnea Pulmonary hypertension- can progress to right heart failure Hemoptysis Embolic events (mostly with Afib) Atrial fibrillation PE: Evidence of right heart failure- JVD, lower extremity edema, hepatomegaly

MS management Medical management: Diuretics, Beta blockers, +/- Anticoagulants (if Afib), Statins Mitral balloon valvuloplasty (PMBV) Surgical valve replacement

Mitral Regurgitation (MR) Etiologies: Mitral valve prolapse, Rheumatic , Flail leaflet, Endocarditis

MR manifestations Exercise intolerance, Dyspnea on exertion, Easy fatigability

MR treatment Medical therapy- ACEi/ARB, beta blockers, diuretics SURGERY if severe MR with LV impairment and/or pulmonary hypertension or new onset atrial

fibrillation (with or without symptoms) Mitral Valve Repair (ring annuloplasty) may be superior to replacement

Mitral Valve Prolapse female predominance Causes: myxomatous degenerative changes, connective tissue disorders, ruptured chord or papillary

muscles, enlarged annulus or trauma Non-specific symptoms- chest pain, dizziness, dyspnea, lightheadedness, exercise intolerance, anxiety

disorders

Pulmonic Insufficiency Causes: Dilation of pulmonic ring, Abnormality of leaflets, Congenital

Pulmonary stenosis Congenital is MC

Tricuspid Regurgitation Causes: Abnormality of valve leaflets , Endocarditis, Dilation of right ventricle

Treatment: diuretics, surgery