Cardio 2 disease approach

[Most likely diagnosis] Soft yellow plaques on the medial eyelids and a deposit on the Achilles tendon. What lipid problem should you suspect?

Dyslipidemia (xanthelasma on the eyelids, xanthoma on the tendon) | Why: Both are lipid deposits. Xanthelasma is specific to the medial eyelids; xanthomas sit in skin or on tendons. | Source: Lecture slides

[Best initial test] Dyslipidemia: Adult with suspected dyslipidemia. Test, and when does routine screening start?

Lipid panel (total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, non-HDL-C); screening starts at age 19 | Why: The lipid panel gives every number the targets are based on, e.g. LDL-C desirable <100 mg/dL. Age 19 was circled on your slide; repeat at least every 5 years if risk is low. | Source: Lecture slides

[Initial treatment of choice] Dyslipidemia: Elevated low-density lipoprotein (LDL). Drug class to start, and what to add if LDL is still high?

Statin (e.g. atorvastatin, rosuvastatin), then add ezetimibe | Why: Statins block cholesterol made in the liver; ezetimibe blocks cholesterol absorbed from the gut, so they add together. Your note: if high LDL, statin then ezetimibe. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (alirocumab, evolocumab) are the single most effective LDL lowering drugs. | Source: Lecture (your handwritten note)

[Initial treatment of choice] Dyslipidemia: Elevated triglycerides. Drug choices?

Fibrates (gemfibrozil, fenofibrate) or omega 3 fatty acids (EPA, DHA, icosapent ethyl) | Why: These are the two classes whose indication is lowering triglycerides. Fibrates carry gallstone risk and cause myopathy when combined with statins. | Source: Lecture slides

[Initial treatment of choice] Dyslipidemia: Low high-density lipoprotein (HDL). Most effective drug?

Niacin (nicotinic acid, vitamin B3) | Why: Raising HDL is niacin's standout job. Its classic side effect is prostaglandin flushing. | Source: Lecture slides

[Initial treatment of choice] Dyslipidemia: Pregnant patient with itching from cholestasis of pregnancy. Lipid drug of choice?

Bile acid sequestrant (cholestyramine) | Why: It binds bile acids in the gut and is safe in pregnancy. Statins, fibrates and niacin are contraindicated in pregnancy. | Source: Lecture slides

[Most likely diagnosis] Average BP of 150/96 on two separate visits, no identifiable cause. Diagnosis and stage?

Primary (essential) hypertension, stage 2 | Why: Stage 2 is ≥140 or ≥90, so systolic 150 alone qualifies. Primary means no other cause is found after workup; it is the most common type. | Source: Practice question set

[Best initial test] Primary Hypertension: Office BP readings are elevated. How do you confirm the diagnosis?

Home BP monitoring (HBPM) or ambulatory BP monitoring (ABPM), with average readings on at least 2 separate occasions | Why: Readings outside the office confirm the BP is truly high, and averaging across visits avoids labeling one bad reading as hypertension. | Source: Lecture slides

[Initial treatment of choice] Primary Hypertension: Newly diagnosed hypertension. First step in management and BP goal?

Lifestyle management (weight loss, exercise, limit alcohol, DASH diet, smoking cessation); goal <130/80 | Why: Lifestyle management was circled on your slide. DASH diet = more fruits, vegetables and whole grains, less sodium and saturated fat. | Source: Lecture slides

[Initial treatment of choice] Primary Hypertension: Uncomplicated hypertension needing medication (non Black patient). Drug class choices?

Thiazide diuretic, angiotensin converting enzyme inhibitor (ACEI), angiotensin II receptor blocker (ARB) or calcium channel blocker (CCB), alone or combined (e.g. hydrochlorothiazide, lisinopril, losartan, amlodipine) | Why: These four classes are the first line options; combine classes if BP is not controlled. | Source: Lecture slides

[Initial treatment of choice] Primary Hypertension: Black/African American patient starting antihypertensives. Drug classes?

Thiazide diuretic or calcium channel blocker (CCB) | Why: This is the narrower list from the slide and the practice set. Angiotensin converting enzyme inhibitor (ACEI)/angiotensin II receptor blocker (ARB) are the tempting wrong answer. | Source: Lecture slides + review session

[Initial treatment of choice] Primary Hypertension: New hypertension in a patient with diabetes and chronic kidney disease. Drug of choice?

ACEI (e.g. lisinopril) | Why: ACEI indications include diabetes, proteinuria and nephropathy. Your note: it slows diabetes' effect on the kidneys. | Source: Practice question set

[Initial treatment of choice] Primary Hypertension: Hypertension plus benign prostatic hyperplasia. Drug class?

Alpha 1 blocker (prazosin, terazosin, doxazosin) | Why: One drug treats both. Warn about 1st dose syncope. | Source: Lecture slides

[Most likely diagnosis] Hypertension resistant to 3 drugs, abdominal bruit, hypokalemia, and acute kidney injury (AKI) right after starting an angiotensin converting enzyme inhibitor (ACEI). Diagnosis?

Renal artery stenosis (renovascular hypertension), the most common cause of secondary hypertension | Why: Low renal blood flow activates the renin angiotensin aldosterone system (RAAS); aldosterone holds sodium and dumps potassium. The stenotic kidney depends on angiotensin, so an ACEI drops its filtration. | Source: Lecture slides

[Most likely diagnosis] Woman under 50 with renal artery stenosis vs a man over 65 with renal artery stenosis. Most likely cause of each?

Woman <50: fibromuscular dysplasia. Elderly >65: atherosclerosis | Why: Fibromuscular dysplasia is abnormal artery wall growth in younger women; atherosclerosis is the common cause in older patients. | Source: Lecture slides

[Best initial test] Renovascular Hypertension (Renal Artery Stenosis): Suspected renal artery stenosis. Best initial (noninvasive) imaging?

CT angiography or MR angiography | Why: Highlighted "non invasive" on your slide. Your note: both need IV contrast. | Source: Lecture slides

[Gold standard / definitive test] Renovascular Hypertension (Renal Artery Stenosis): Renal artery stenosis. Gold standard test, and the classic finding in fibromuscular dysplasia?

Renal catheter arteriography (invasive); "string of beads" appearance | Why: It is the gold standard but invasive, so noninvasive angiography usually comes first. String of beads = alternating narrowing and widening of the renal artery. | Source: Lecture slides

[Initial treatment of choice] Renovascular Hypertension (Renal Artery Stenosis): Renal artery stenosis. First line medical therapy?

Angiotensin converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) | Why: They block the overactive renin angiotensin aldosterone system (RAAS). Use caution with bilateral stenosis or a solitary kidney and monitor creatinine and electrolytes. | Source: Lecture slides

[Definitive treatment] Renovascular Hypertension (Renal Artery Stenosis): Renal artery stenosis. Definitive chronic treatment?

Revascularization (angioplasty or bypass) | Why: Restoring renal blood flow removes the trigger for renin angiotensin aldosterone system (RAAS) activation. | Source: Lecture slides

[Most likely diagnosis] BP 190/125 with headache, no end organ damage. Diagnosis?

Hypertensive urgency (BP >180 and/or >120 WITHOUT end organ damage) | Why: Same numbers as emergency; the only difference is whether organs are being damaged. | Source: Lecture slides

[Initial treatment of choice] Hypertensive Urgency: Hypertensive urgency. How fast do you lower BP, and with what?

Lower mean arterial pressure (MAP) by no more than 25% over the first 48 hours (goal <160/<100), e.g. clonidine, captopril, furosemide, labetalol, nicardipine | Why: Your note: lowering too fast risks ischemic stroke from underperfusing the brain. Clonidine is a centrally active alpha agonist. | Source: Lecture slides

[Most likely diagnosis] BP 220/130 with confusion and retinal hemorrhages. Diagnosis?

Hypertensive emergency (BP >180 and/or >120 WITH end organ damage) | Why: End organ damage can be in the eyes, kidney, brain or heart (your note). Highlighted on the slide. | Source: Lecture slides

[Initial treatment of choice] Hypertensive Emergency: Hypertensive emergency. BP lowering goal?

IV medication; lower mean arterial pressure (MAP) 10-20% in the 1st hour, then another 5-15% over the next 23 hours | Why: Gradual lowering protects perfusion. Your note: the exact numbers matter less than knowing BP is sometimes allowed to stay high (stroke). | Source: Lecture slides

[Initial treatment of choice] Hypertensive Emergency: Hypertensive emergency with aortic dissection vs ischemic stroke not getting reperfusion. How do the BP goals differ?

Dissection: lower fast, systolic blood pressure (SBP) 100-120 within 20 minutes. Ischemic stroke: permissive hypertension up to 220/120 | Why: Dissection needs low pressure to stop the tear; a stroke needs pressure to perfuse the at-risk brain. If giving IV thrombolysis, lower to <185/110. | Source: Lecture slides

[Initial treatment of choice] Hypertensive Emergency: Hypertensive emergency with stroke (ischemic or hemorrhagic). IV drugs?

Nicardipine or labetalol | Why: Highlighted on every neuro line of the slide. | Source: Lecture slides

[Most likely diagnosis] Ischemic chest pain at rest, ECG with ST depressions, troponins normal on serial checks. Diagnosis?

Unstable angina | Why: Ischemia without cell death: partial occlusion on ECG, but no troponin rise. Your note: the muscle isn't dying, but ischemia is still occurring. | Source: Lecture slides + review session

[Best initial test] Unstable Angina: Suspected acute coronary syndrome (ACS). Best initial tests and timing?

12-lead ECG within 10 minutes of arrival + high-sensitivity troponin | Why: Review session: the test of choice is a prompt ECG plus high-sensitivity troponin. A normal first ECG or one negative early troponin does not rule out ACS. | Source: Review session

[Next best step] Unstable Angina: Suspected acute coronary syndrome (ACS), no ST elevation, first troponin normal. Next best step?

Serial ECGs and troponins (repeat troponin every 2-3 hours) | Why: MI needs a rise/fall in troponin, so you follow the trend. Normal troponins confirm unstable angina; rising troponins mean non ST elevation myocardial infarction (NSTEMI). | Source: Review session

[Initial treatment of choice] Unstable Angina: Unstable angina or non ST elevation myocardial infarction (NSTEMI). Initial treatment? (review session mnemonic)

MONA HepB: Morphine (if pain persists), Oxygen (if oxygen saturation (SpO2) <90%), Nitroglycerin, Antiplatelets (aspirin + clopidogrel or ticagrelor), Heparin, Beta blocker | Why: Aspirin is the most important drug; every acute coronary syndrome (ACS) patient gets it. Dual antiplatelets + heparin stop further clot; beta blockers protect the heart. Fibrinolytics are NOT given in unstable angina or NSTEMI. | Source: Review session

[Most likely diagnosis] Chest pain, ST depressions and T wave inversions, troponin rising on repeat. Diagnosis?

NSTEMI (non ST elevation myocardial infarction) | Why: Partial occlusion (no ST elevation) but heart cells are dying, so troponin rises. That rise is what separates it from unstable angina. | Source: Lecture slides + review session

[Initial treatment of choice] NSTEMI: Non ST elevation myocardial infarction (NSTEMI). Initial management?

Same as unstable angina: aspirin + 2nd antiplatelet (clopidogrel or ticagrelor), heparin, beta blocker, nitroglycerin, oxygen if oxygen saturation (SpO2) <90%, high-intensity statin | Why: Your note: the initial medications are the same for ST elevation myocardial infarction (STEMI) and NSTEMI. Fibrinolytics are only for STEMI. | Source: Lecture (your handwritten note)

[Most likely diagnosis] ST elevation ≥1 mm in 2 contiguous leads with reciprocal ST depressions. Diagnosis? What else counts as ST elevation myocardial infarction (STEMI)?

STEMI (total occlusion); a NEW left bundle branch block is STEMI until proven otherwise | Why: Contiguous leads look at the same part of the heart. Reciprocal changes support the diagnosis (PAILS). | Source: Lecture slides

[Next best step] STEMI: ECG shows ST elevation myocardial infarction (STEMI), troponin not back yet. Next best step?

Activate emergent reperfusion; do NOT wait for troponin | Why: The ECG drives the decision in STEMI; waiting on labs costs heart muscle. | Source: Lecture slides + review session

[Definitive treatment] STEMI: ST elevation myocardial infarction (STEMI). Preferred reperfusion and time goal?

Primary percutaneous coronary intervention (PCI): ≤90 min from first contact at a PCI-capable hospital, ≤120 min if transfer is needed | Why: PCI (percutaneous coronary intervention) opens the artery with a balloon and usually a stent, through the radial artery (preferred) or femoral. | Source: Lecture slides + review session

[Definitive treatment] STEMI: ST elevation myocardial infarction (STEMI), symptoms <12 hours, percutaneous coronary intervention (PCI) not possible within 120 minutes. Treatment?

Fibrinolytics (alteplase, tenecteplase, reteplase) with door-to-needle ≤30 min, then transfer to a PCI-capable hospital | Why: Fibrinolytics dissolve the clot. Only for STEMI, never non ST elevation myocardial infarction (NSTEMI) or unstable angina. Prior intracranial hemorrhage is a contraindication (practice set). | Source: Lecture slides + review session

[Definitive treatment] STEMI: When is coronary artery bypass grafting (CABG) chosen over percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS)?

Failed PCI, complex multivessel disease (especially diabetes), significant left main disease, mechanical complications of MI, cardiogenic shock when PCI isn't feasible | Why: CABG (coronary artery bypass grafting) bypasses blockages that are too complex for stents. | Source: Lecture slides

[Initial treatment of choice] STEMI: STEMI (not inferior). Initial medications?

MONA HepB: Morphine if pain persists, Oxygen if oxygen saturation (SpO2) <90%, Nitroglycerin, Antiplatelets (aspirin + clopidogrel or ticagrelor), Heparin, Beta blocker (cardioselective: atenolol, metoprolol, esmolol) | Why: Aspirin is the most important drug. Unfractionated heparin is the preferred anticoagulant. | Source: Lecture slides + review session

[Initial treatment of choice] STEMI: After ST elevation myocardial infarction (STEMI): which two drugs start early, and when?

High-intensity statin within 24 hours (atorvastatin or rosuvastatin); angiotensin converting enzyme inhibitor (ACEI) after the patient is stabilized (lisinopril, ramipril, enalapril) | Why: Statins stabilize plaque; ACE inhibitors prevent ventricular remodeling. Also get an echo to assess ejection fraction (review session). | Source: Lecture slides + review session

[Initial treatment of choice] STEMI: MI after cocaine use. Treatment, and which drug class must you avoid?

Benzodiazepines (lorazepam); do NOT give beta blockers | Why: Beta blockade leaves alpha-1 receptors unopposed, causing vasoconstriction and worse ischemia. | Source: Lecture slides

[Most likely diagnosis] ST elevation in II, III, aVF with hypotension, jugular venous distension (JVD), clear lungs and bradycardia. Diagnosis and artery?

Inferior MI with right ventricular involvement; right coronary artery (RCA) | Why: The RCA supplies the inferior wall, the right ventricle (RV) and usually the atrioventricular (AV) node (hence bradycardia/AV block). Clear lungs because the left heart is fine. | Source: Lecture slides + review session

[Next best step] Inferior and Right Ventricular MI: Inferior MI on the ECG. Next best step?

Get a right sided ECG; ST elevation in V4R is the most specific finding for right ventricle (RV) infarction | Why: Highlighted. Your note: you don't know it is a right heart attack unless you do a right sided ECG. | Source: Lecture slides

[Initial treatment of choice] Inferior and Right Ventricular MI: Right ventricular MI. Initial management?

IV fluids to maintain preload + antiplatelets, heparin, oxygen if oxygen saturation (SpO2) <90%; inotropes (dopamine, dobutamine) if needed | Why: The right ventricle (RV) is preload dependent. Your note: the only MI where you give IV fluids. Review question: hypotensive inferior ST elevation myocardial infarction (STEMI) = oxygen, dual antiplatelets, heparin and fluids. | Source: Lecture slides + review session

[Initial treatment of choice] Inferior and Right Ventricular MI: Right ventricular MI. Which drugs do you avoid?

Nitroglycerin, morphine, beta blockers (and calcium channel blocker (CCB)), diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs) except aspirin | Why: Nitro, morphine and diuretics drop preload, which this right ventricle (RV) can't afford. | Source: Lecture slides + review session

[Most likely diagnosis] ST depressions in V1-V4 (review: isolated in V1-V2, tall R waves). Diagnosis?

Posterior wall MI (circumflex or right coronary artery (RCA)) | Why: The 12-lead doesn't see the posterior wall directly, so its elevation shows up flipped in the anterior leads. Your note: the only ST elevation myocardial infarction (STEMI) where you look for depressions. | Source: Lecture slides + review session

[Next best step] Posterior MI: Suspected posterior MI. Next best step?

Obtain posterior leads V7-V9 | Why: Review session: posterior or right ventricle (RV) infarction can be missed without extra leads. | Source: Review session

[Most likely diagnosis] Chest pain at rest after cocaine, cold weather or pseudoephedrine, with transient ST elevation. Diagnosis?

Prinzmetal (vasospastic) angina | Why: Coronary spasm, not plaque rupture. Triggers: cocaine/amphetamines, cold, pseudoephedrine, oxymetazoline, smoking, catheter manipulation. | Source: Lecture slides + review session

[Next best step] Prinzmetal (Vasospastic) Angina: Transient ST elevation in a suspected Prinzmetal patient. Next best step?

Treat as a ST elevation myocardial infarction (STEMI) and go to the cath lab until proven otherwise | Why: You can't tell spasm from occlusion on the ECG; your note: treat like a STEMI at first. | Source: Lecture slides + review session

[Gold standard / definitive test] Prinzmetal (Vasospastic) Angina: What confirms Prinzmetal angina?

Coronary angiography showing vasospasm with NO stenosis or obstruction | Why: Highlighted on your slide. No fixed blockage means no stent. | Source: Lecture slides

[Initial treatment of choice] Prinzmetal (Vasospastic) Angina: Prinzmetal angina. Treatment of choice, and which class to avoid?

Calcium channel blockers (diltiazem, amlodipine) + sublingual (SL) nitroglycerin as needed; avoid beta blockers (review session) | Why: Calcium channel blockers (CCBs) and nitrates relax the spasming artery. Review session: beta blockers can worsen vasospasm. Chronic: avoid triggers, stop smoking. | Source: Lecture slides + review session

[Most likely diagnosis] Faints after stress or pain, with warning symptoms beforehand. Diagnosis?

Reflex (vasovagal) syncope | Why: It has a prodrome and comes from increased vagal tone. Highlighted. | Source: Lecture slides

[Most likely diagnosis] Faints during exertion with NO warning symptoms. Concern?

Cardiogenic syncope (arrhythmia or mechanical cause like aortic stenosis or hypertrophic cardiomyopathy) | Why: No prodrome and exertional onset are the red flags that separate it from vasovagal. | Source: Lecture slides

[Best initial test] Syncope and Orthostatic Hypotension: Suspected orthostatic hypotension. Best initial test and what defines it?

Orthostatic vital signs (supine, seated, standing immediately and after ≥5 minutes); drop of ≥20 mmHg systolic and/or ≥10 diastolic | Why: Common in older men, with hypovolemia, blood loss and vasodilators. Clinical tip: watch the HR too. | Source: Lecture slides

[Most likely diagnosis] On standing, HR rises by 35 bpm without a BP drop. Diagnosis?

POTS (postural orthostatic tachycardia syndrome): HR increase >30 bpm or to >120 bpm | Why: The problem is the heart rate response, not the BP, which is why the tip says pay attention to HR. | Source: Lecture slides

[Most likely diagnosis] Trauma or GI bleed with tachycardia, hypotension, cool pale extremities, cap refill >2 seconds, low urine output. Shock type?

Hypovolemic shock | Why: Blood or fluid loss empties the intravascular space; the body clamps down, so the skin is cool and pale. | Source: Lecture slides

[Initial treatment of choice] Hypovolemic Shock: Hypovolemic shock. Initial treatment, and which drug class do you avoid?

Airway, breathing, circulation (ABCs), 2 large bore intravenous lines (IVs), IV fluids (normal saline (NS) or lactated ringers (LR)), blood transfusion if needed; AVOID vasopressors | Why: Your note: if they're missing blood, what is the heart going to circulate? Fluids before blood. | Source: Lecture slides + review session

[Definitive treatment] Hypovolemic Shock: Hypovolemic shock. Definitive treatment?

Treat the underlying cause (e.g. surgery for the bleeding source) | Why: Fluids buy time; stopping the loss fixes it. | Source: Lecture slides

[Most likely diagnosis] Hypotension, cold extremities and pulmonary edema right after a large anterior MI. Shock type and most common cause?

Cardiogenic shock; most commonly acute MI | Why: Pump failure: low output despite enough volume. Also myocarditis, cardiomyopathy, valve problems, arrhythmias. | Source: Lecture slides

[Initial treatment of choice] Cardiogenic Shock: Cardiogenic shock. First-line drug, and what you add if output stays low?

Norepinephrine (Levophed); add dobutamine | Why: Your note: vasopressors, very important. Avoid routine IV fluid boluses unless hypovolemia or right ventricle (RV) infarction is suspected. | Source: Lecture slides

[Definitive treatment] Cardiogenic Shock: Cardiogenic shock from MI. Definitive treatment?

Immediate reperfusion (PCI); mechanical support if needed (Impella, venoarterial extracorporeal membrane oxygenation (VA-ECMO), intra-aortic balloon pump) | Why: Opening the artery restores the pump. Coronary artery bypass grafting (CABG) if PCI isn't feasible. | Source: Lecture slides

[Most likely diagnosis] Shock from a massive pulmonary embolism (PE), tension pneumothorax or pericardial tamponade. Shock type?

Obstructive shock (an extracardiac cause of pump failure) | Why: Something outside the heart blocks filling or outflow. Highlighted: extracardiac. | Source: Lecture slides

[Initial treatment of choice] Obstructive Shock (Tension Pneumothorax): Tension pneumothorax. Immediate treatment, then definitive?

Needle decompression at the 2nd intercostal space (ICS) midclavicular line, then chest tube at the 5th ICS midaxillary line | Why: Release the trapped air first, then drain it. Treating the obstruction treats the shock. | Source: Lecture slides

[Most likely diagnosis] Infection with hypotension; warm flushed skin early, then cool mottled skin with cap refill >2 seconds. Diagnosis?

Septic shock (most common type of distributive shock) | Why: Vasodilation and maldistribution of flow. Early = warm; late = cool and mottled. Highlighted. | Source: Lecture slides

[Best initial test] Septic Shock: Suspected sepsis. Key labs?

Lactate (organ perfusion, repeat after fluids), procalcitonin (bacterial), WBC (>12,000 or <4,000) | Why: Elevated lactate signals poor perfusion and poor prognosis. | Source: Lecture slides

[Next best step] Septic Shock: Septic shock. What must you do before antibiotics if possible?

Draw blood cultures | Why: Antibiotics first can sterilize the cultures. Then give empiric broad spectrum antibiotics within the 1st hour. | Source: Lecture slides

[Initial treatment of choice] Septic Shock: Septic shock. Initial treatment sequence?

Weight-based IV fluid bolus within the first 3 hours, broad spectrum antibiotics within 1 hour (e.g. vancomycin + piperacillin-tazobactam), norepinephrine if BP doesn't respond | Why: Your note: WEIGHT BASED, MUST KNOW. The slide amount (30 mL/kg) is context only. | Source: Lecture slides

[Initial treatment of choice] Anaphylactic Shock: Anaphylaxis. Treatment of choice and route?

Epinephrine intramuscular (IM) in the mid outer thigh, repeat every 5-15 minutes as needed; no absolute contraindications | Why: IM was circled. Adjuncts (diphenhydramine, famotidine, methylprednisolone, albuterol) never replace epinephrine. Monitor 4-6 hours. | Source: Lecture slides

[Most likely diagnosis] Spinal cord injury with hypotension, bradycardia and warm extremities. Shock type?

Neurogenic shock | Why: Loss of sympathetic tone leaves vagal tone unopposed. Your note: the only shock without tachycardia. | Source: Lecture slides

[Initial treatment of choice] Neurogenic Shock: Neurogenic shock with severe bradycardia. Treatment?

Atropine or external pacing | Why: Treats the unopposed vagal slowing directly. | Source: Lecture slides

[Initial treatment of choice] Endocrine Shock (Myxedema Coma, Adrenal Crisis): Shock from myxedema coma. Treatment?

IV levothyroxine, IV fluids, vasopressors as needed, passive rewarming | Why: Your note: hypothermic and cold, so rewarm. | Source: Lecture slides

[Initial treatment of choice] Endocrine Shock (Myxedema Coma, Adrenal Crisis): Shock from Addisonian (adrenal) crisis. Treatment?

IV hydrocortisone + IV fluids | Why: Replacing the missing hormone reverses the vasodilation and volume loss. | Source: Lecture slides

[Most likely diagnosis] Unilateral leg swelling, pain, warmth, erythema, calf pain with dorsiflexion after a long flight. Diagnosis?

DVT (deep venous thrombosis); calf pain on dorsiflexion = positive Homan sign | Why: Virchow's triad: intimal damage, venous stasis (flight >4 hrs), hypercoagulability. | Source: Lecture slides

[Best initial test] Deep Venous Thrombosis: Suspected deep venous thrombosis (DVT). Best initial test?

Venous duplex ultrasound (compression with Doppler) | Why: Noninvasive and practical as the first test. | Source: Lecture slides

[Gold standard / definitive test] Deep Venous Thrombosis: Deep venous thrombosis (DVT). Gold standard test?

Contrast venography | Why: Definitive but invasive, so ultrasound comes first. | Source: Lecture slides

[Initial treatment of choice] Deep Venous Thrombosis: Deep venous thrombosis (DVT). Initial treatment options, and which one is NOT acceptable?

Anticoagulation ≥3 months: low molecular weight heparin (LMWH) + warfarin, LMWH + dabigatran or edoxaban, or rivaroxaban or apixaban alone. Warfarin alone is NOT acceptable | Why: Warfarin only appears paired with LMWH; rivaroxaban and apixaban are the only monotherapy options (practice set). | Source: Lecture slides + review session

[Definitive treatment] Deep Venous Thrombosis: Deep venous thrombosis (DVT) when anticoagulation fails or is contraindicated. Treatment?

Inferior vena cava (IVC) filter | Why: The filter catches clots on their way to the lungs. | Source: Lecture slides

[Most likely diagnosis] Brownish hyperpigmentation and weeping erosions near the ankle, ulcer over the medial malleolus, normal pulses, leg pain worse standing and better elevated. Diagnosis?

Chronic venous insufficiency with stasis dermatitis | Why: Leaky valves let blood pool. Normal pulses and warmth rule out arterial disease; the medial malleolus is the venous ulcer spot. | Source: Lecture slides + review session

[Initial treatment of choice] Chronic Venous Insufficiency: Chronic venous insufficiency. Initial treatment?

Compression stockings, leg elevation, skin care, exercise | Why: These push pooled blood back up. | Source: Lecture slides

[Definitive treatment] Chronic Venous Insufficiency: Chronic venous insufficiency not responding to conservative care. Next?

Refer for surgery | Why: Nonoperative care comes first. | Source: Lecture slides

[Most likely diagnosis] Dilated, tortuous superficial leg veins in a woman who stands all day. Diagnosis?

Varicose veins (failed saphenous valves causing superficial vein dilation) | Why: Risk factors: prolonged standing, estrogen (oral contraceptive pills (OCPs), pregnancy), chronic venous insufficiency, obesity. | Source: Lecture slides

[Definitive treatment] Varicose Veins: Varicose veins not controlled with conservative care. Surgical options?

Endovenous thermal ablation, ligation and stripping, compression sclerotherapy | Why: Your note: these raise deep venous thrombosis (DVT) risk, so get an ultrasound. | Source: Lecture slides

[Most likely diagnosis] Woman over 50 with new headache, jaw pain when chewing and vision changes. Diagnosis?

Giant cell arteritis (often overlaps with polymyalgia rheumatica) | Why: Headache is the most common symptom; jaw claudication and amaurosis fugax come from narrowed carotid branches. | Source: Lecture slides

[Best initial test] Giant Cell Arteritis: Suspected giant cell arteritis. Best initial labs?

Erythrocyte sedimentation rate (ESR) and CRP (elevated); normocytic normochromic anemia | Why: Inflammatory markers support the diagnosis. Your note: on the blueprint. | Source: Lecture slides

[Gold standard / definitive test] Giant Cell Arteritis: Giant cell arteritis. Gold standard test and finding?

Temporal artery biopsy: multinucleated giant cells, granulomatous inflammation | Why: Highlighted and starred. | Source: Lecture slides

[Next best step] Giant Cell Arteritis: Suspected giant cell arteritis, biopsy scheduled for next week. Next best step?

Start high dose glucocorticoids NOW; don't delay for the biopsy | Why: Vision loss can be permanent. Highlighted. | Source: Lecture slides

[Initial treatment of choice] Giant Cell Arteritis: Giant cell arteritis. Treatment and adjuncts?

High dose systemic glucocorticoids; add aspirin; tocilizumab (interleukin-6 (IL-6) inhibitor) if glucocorticoids aren't tolerated | Why: Aspirin lowers vision loss, transient ischemic attack (TIA) and stroke risk. | Source: Lecture slides

[Most likely diagnosis] A flutter, not anticoagulated, now sudden painful, pale, cold, pulseless foot with paresthesias. Diagnosis?

Acute arterial occlusion (embolic): the 6 P's | Why: Pain, pallor, pulselessness, paresthesias, poikilothermia, paralysis. Your note: arteries, not veins. | Source: Lecture slides + practice question set

[Best initial test] Acute Arterial Occlusion: Acute arterial occlusion. Bedside test, then imaging of choice?

Bedside Doppler, then duplex ultrasound (CT angiography or catheter angiography also used; NOT MRI) | Why: Catheter angiography can also treat. MRI is not on the list (practice set). | Source: Lecture slides + practice question set

[Initial treatment of choice] Acute Arterial Occlusion: Acute arterial occlusion. Immediate drug?

IV heparin | Why: Anticoagulation stops the clot from extending while you plan revascularization. | Source: Lecture slides

[Definitive treatment] Acute Arterial Occlusion: Acute arterial occlusion. Definitive treatment?

Surgical revascularization (thrombectomy, bypass, patch angioplasty, intraoperative thrombolysis); amputation is the last line | Why: Restoring flow saves the limb. | Source: Lecture slides

[Most likely diagnosis] Calf cramping with walking that goes away with rest; shiny hairless skin, weak pulses, ulcers on the lateral malleolus and toe tips. Diagnosis?

Peripheral arterial disease (PAD) with claudication | Why: Muscles outgrow their narrowed supply during walking. Rest pain at night, relieved by dangling the foot, means severe disease. | Source: Lecture slides

[Best initial test] Peripheral Arterial Disease: Suspected peripheral arterial disease (PAD). Best initial test and cutoff?

Ankle brachial index (ABI): <0.9 = PAD, <0.5 = severe | Why: ABI compares ankle to arm BP. Duplex ultrasound helps further evaluate. | Source: Lecture slides

[Gold standard / definitive test] Peripheral Arterial Disease: Peripheral arterial disease (PAD). Gold standard test?

Arteriography | Why: Defines the anatomy before any intervention. | Source: Lecture slides

[Initial treatment of choice] Peripheral Arterial Disease: Peripheral arterial disease (PAD). First line management, and the most effective drug for claudication symptoms?

Supportive care (smoking cessation, exercise, control diabetes and lipids); cilostazol for symptoms; aspirin or clopidogrel + statin to lower MI and stroke risk | Why: Your note: cilostazol is the HIGH YIELD drug. | Source: Lecture slides + practice question set

[Definitive treatment] Peripheral Arterial Disease: Peripheral arterial disease (PAD) with rest pain or refractory symptoms. Next?

Refer for angioplasty | Why: Revascularization when medical care fails. | Source: Lecture slides

[Most likely diagnosis] Abrupt tearing chest pain to the back, BP 168/90 right arm vs 132/76 left, neuro deficit or new diastolic murmur. Diagnosis?

Aortic dissection | Why: Review session: chest/back pain + neuro deficit or pulse/BP difference is very concerning; don't anchor on acute coronary syndrome (ACS). Most important risk factor: hypertension; also Marfan syndrome. | Source: Lecture slides + review session

[Best initial test] Aortic Dissection: Suspected aortic dissection, hemodynamically STABLE. Best test?

CT angiography (CTA) chest | Why: The usual first-line study in a stable patient. A normal chest x-ray does NOT exclude dissection. | Source: Lecture slides + review session

[Best initial test] Aortic Dissection: Suspected aortic dissection, hemodynamically UNSTABLE. Best test?

TEE (transesophageal echocardiogram) at the bedside | Why: Unstable patients can't travel to CT. Stability changes the test. | Source: Lecture slides + review session

[Initial treatment of choice] Aortic Dissection: Aortic dissection. First drug, goals, and what comes second?

IV beta blocker first (esmolol or labetalol), goal systolic blood pressure (SBP) 100-120 and HR <60; then a vasodilator (nitroprusside, nicardipine) if BP stays high | Why: Beta blockers cut HR and aortic wall stress. Vasodilators alone come only after beta blockade. | Source: Lecture slides + review session

[Definitive treatment] Aortic Dissection: Type A vs Type B dissection. Definitive treatment?

Type A (ascending, Stanford A/DeBakey I and II): emergent surgery. Uncomplicated Type B (descending): medical, beta blockers. Complicated Type B (rupture, malperfusion, refractory pain/hypertension (HTN)): surgery | Why: Review session: Type A, Ascending, Always requires surgery. Your note: proximal matters more for surgery. | Source: Lecture slides + review session

[Most likely diagnosis] 68 year old male smoker with flank pain, BP 88/60, HR 112, pulsatile abdominal mass. Diagnosis?

Ruptured AAA (abdominal aortic aneurysm) | Why: Rupture triad: hemodynamically unstable + abdominal mass/distension + back, flank or abdominal pain. Most important risk factor: smoking; most common location: infrarenal (review). | Source: Lecture slides + review session