Final OSCE Flashcards

Question

Primary Prevention of ASCVD in Age 20-39

Answer 1

* **Estimate lifetime risk** to encourage lifestyle to reduce ASCVD risk * Consider statin if family hx, premature ASCVD and **LDL-C ≥ 160mg/**dL

Answer 2

10-year ASCVD risk percent begins risk discussion: * _\<5%: “low risk”_ * emphasize lifestyle to reduce risk factors * _5-\<7.5%: “borderline risk”_: * If risk enhancers present then risk discussion regarding moderate-intensity statin therapy * _≥7.5-\<20%_: “Intermediate Risk” * Risk discussion: * if risk estimate + risk enhancers favor statin, initiate **moderate-intensity** statin to reduce LDL-C by 30-49% * if unsure, can use CAC score * _≥ 20%: “high risk”_: * initiate statin to reduce LDL-C ≥ 50%

Answer 3

LDL-C ≥ **190** mg/dL

Answer 4

Diabetes Mellitus age 40-75yo Risk assessment to consider high-intensity statin

Answer 5

Coronary Artery Calcium Score * if risk decision is uncertain in age 40-75yo with intermediate risk (≥7-\<20%) * **_CAC = zero_** * (lower risk; consider no statin unless diabetes, family hx of premature CHD, or cigarette smoking are present) * **_CAC = 1-99_** * favors statin (esp. after age 55) * **_CAC = 100+ and/or ≥75th percentile:_** * initiate statin therapy * Calculate MESA score with CAC, will give you a percentage by which to evaluate whether to initiate statin

Answer 6

* **Statins** (**Rosuvastatin, atorvastatin, etc****)** → inhibit HMG Co-A reductase * impair production of cholesterol in the liver → upregulation of LDL receptors * **Bile Acid Sequestrants (****Cholestyramine, colesevelam, colestipol****) & Cholesterol absorption inhibitors (****Ezetimibe****)** * impair enterohepatic recirculation and gut absorption → less hepatic cholesterol → upregulation of LDL receptors

Answer 7

* **Fibrates** **(fenofibrate, gemfibrozil****)**: inhibit triglyceride synthesis = Drug of Choice;**gemfibrozil should NOT be given with statins** * **Niacin**

Answer 8

* **Niacin** * **Fibrates** **(feno**_fibr_**ate, gem**_fibr_**ozil****)**: inhibit triglyceride synthesis = Drug of Choice;**gemfibrozil should NOT be given with statins**

Answer 9

_secondary hypercholesterolemia_ = **WITH** known clinical CV disease * **high-intensity statin** * can add **ezetimibe** if inadequate response (\<50% LDL reduction); goal is LDL \<70 mg/dL

Answer 10

_secondary hypercholesterolemia_ = **WITH** known clinical CV disease * **high-intensity statin** * can add **ezetimibe** * can also add **PCSK9 monoclonal antibody (****Alirocumab, Evolocumab****)** : blocks PCSK9 binding to LDL receptor → direct upregulation of LDL receptors → lowers LDL 30-60%; injections Q2-3 weeks * goal is LDL \<55 mg/dL

Answer 11

* Low HDL \<40 mg/dL * High LDL \> 190 mg/dL * high LDL in diabetic \>70 mg/dL * high total cholesterol \>250 mg/dL * high fasting triglyceride \>150 mg/dL

Answer 12

* _Definition_: fasting blood triglyceride level of **\>150 mg/dL** * _Etiology_: * diabetes mellitus, EtOH, obesity, steroids, estrogen * _S/sxs_: * **pancreatitis**, eruptive xanthomas, lipemia retinalis (creamy white discoloration of the retinal vessels), corneal arcus (grey arc of deposit on outer iris) * _Dx_: * **fasting lipid panel** * Severity: * 150-499: mild * 500-886: moderate * \>886: severe * _Tx_: * **Best meds to lower elevated triglycerides → Fibrates (****fenofibrate, gemfibrozil****)**, niacin * **Best meds to lower elevated LDL → Statins**, bile acid sequestration * **Best meds to increase HDL → Niacin (****Nicotinic Acid****)**, fibrates * Type II DM → statins, fibrates * **Fibrates** **(fenofibrate, gemfibrozil****)**: inhibit triglyceride synthesis = Drug of Choice;**gemfibrozil should NOT be given with statins** * **Nicotinic Acid (Niacin)**: increases HDL levels, causes flushing * **fish oil supplements** * **Lifestyle modification:** avoid alcohol & refined sugars, lower caloric intake, exercise

Answer 13

* _Definition_: * resting **systolic ≥ 130** or **diastolic ≥ 80** on at least **2 readings** on at least **2 separate visits** with **no identifiable cause** * \*\*need to measure BP in **Both Arms**\*\* * _PE:_ * fundoscopic exam: hypertensive retinopathy → AV nicking * _Diagnosis_: * see above definition * **BP\>15 mmHg higher in one arm** than the other is **associated with a higher mortality** **→** eval of upper vasculature is required!! * Other tests you can order: -**urinalysis and spot urine albumin: creatinine ratio** * **blood tests** (creatinine, K, Na, fasting plasma glucose, lipid profile, and TSH * **ECG**

Answer 14

* _ACC/AHA_: * **goals**: \<130/80 * AntiHTN therapy initiated in the following populations: 1. **all pts with stage 2 HTN** (baseline ≥140/90) 2. **pts with stage 1 HTN** (130-139/80-89 mmHg) who have **1+ of the following**: * ASCVD * Type II DM * CKD * 10-year calculated ASCVD risk ≥ 10% * **Lifestyle Modifications**: * DASH diet, increase fruits and veggies * **Sodium** reduction **\<2.3grams/day** (1 tsp) * **reduce alcohol** intake: * **→ Men: 1-2 drinks daily max** * **→ Women: 1 drink daily max** * _Exercise goals_: * → **\>150 minutes** of moderate intensity/week * → **\>75 minutes** of vigorous intensity/week * **ONE drug given initially**: * for **non-black pts, including DM** give either: * → **ACE-I** or **ARB** * **→** long acting **CCB** (often a dihydropyridine like amlodipine) * → or a **thiazide-like diuretic** (chlorthalidone, or indapamide) * **for stage 2 HTN or a black adults:** * recommendation is * → **2 BP-lowering meds** from **different classes** * If **Target BP is not achieved in 1 month**, dose of drug can be increased or a second drug added → BP should be checked monthly until the target is met

Answer 15

* _Definition_: **\>180 systolic and/or \>120 diastolic** **_WITH_** signs of **damage to target organs** (except papilledema = hypertensive retinopathy) → encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI * _Diagnosis_: * **BP measurement** * ECG * urinalysis * ophthalmic exam * serum BUN * serum creatinine * _Tx_: * **sodium nitroprusside** = drug of choice * pt should be admitted to ICU * If pt has: Aortic dissection, severe pre-eclampsia or eclampsia or pheochromocytoma crisis * → **reduce SBP to _\<140mmHg_ during first hour and then to \<120 mmHg in aortic dissection** * If pt does NOT have any of the above: * **Reduce BP by** (10-20%) **max 25% over first hour, then to 160/100-110 mm/Hg over next 2-6 hours, then to normal over next 24-48 hours**

Answer 16

* _Definition_: **SBP \>180 and/or DBP \>120** without target-end organ damage * _Dx_: * BP measurement * ECG * urinalysis * ophthalmic exam * serum BUN, serum creatinine * _Tx_: * **immediate BP reduction is NOT required** * **Clonidine** = drug of choice

Answer 17

* _Definition_: **SBP ≥130 and/or DBP ≥80 WITH identifiable cause** * _Causes_: * **Primary aldosteronism** = MOST COMMON * renal vascular disease * pheochromocytoma * adrenal tumor that secretes catecholamines (ie norepi and epi) * Cushing's Syndrome * activation of the renin-angiotensin system * Congenital Adrenal Hyperplasia * Hyperthyroidism * Myxedema * associated with hypothyroidism * Coarctation of the Aorta * Excessive alcohol intake * Use of Oral Contraceptives

Answer 18

* _Red Flags_: * HTN at an early age \<25 without a family hx * HTN first develops \>50 yo * previously controlled now refractor * **Pt is refractory on antihypertensive medications** or has severe BP * _Dx_: * when HTN is newly diagnosed consider ordering: * **urinalysis** * s**pot urine albumin: creatinine ratio** → albuminuria ratio = \>30mg/day * indicative of CKD * **Blood tests** * creatinine, K, Na, fasting glucose = _BMP_ * lipid panel * TSH * **EKG** * _Tx_: * tx the underlying condition and aim for **BP \<130/80**

Answer 19

* _Mixed Venous O2_: * amount of oxygen that is in the venous blood upon return to the heart * Normal: * Superior Vena Cava = 65% (brain uses most oxygen) * Inferior Vena Cava = 75% * Abnormal: **\<65%** * **\<50% = danger zone** * _A-VO2 difference_: * arterial O2 (~98%) - venous O2 saturation * **normal \<30%** * **higher the difference = the WORSE the situation** * As mixed venous O2 drops, AVO2 difference will increase (inverse relationship)

Answer 20

DO2 = CO x CaCO2 delivery of oxygen is affected by cardiac output and arterial oxygen content

Answer 21

* _Definition_: * **reduction in intravascular volume/preload** → decreased CO → insufficient perfusion * _Etiologies_: * **hemorrhagic**: trauma, GI bleed, ruptured aneurysm, post-operative, open central line * **non-blood fluid loss**: vomiting, diarrhea, 3rd spacing, burns, dehydration, DKA, over-diuresis * _Pathophys_: * loss of blood/fluid volume → increased HR & vasoconstriction, increased epi, vasopressin, & angiotensin * _S/sxs_: * **tachycardia/tachypnea** * **narrowed pulse pressure (d/t vasoconstriction)** * **oliguria (d/t decreased CO)** * hypotension * pale, cool dry skin and extremities * cap refill \>3 sec * decreased skin turgor * dry mucous membranes * AMS

Answer 22

* _Preload_: decreased (volume depletion) * _Cardiac Output_: decreased * _Afterload_: increased (vasoconstriction) * _BP_: low * _Organ perfusion_: decreased * _AVO2 Difference_: high (b/c heart is delivering less blood so tissues are using more O2 from the available blood)

Answer 23

* _Adults_: 7% IBW (75ml/kg) * → 70kg adult = 5.5 Liters or approx 15 units * _Children_: 9% IBW (90 ml/kg) IBW = ideal body weight

Answer 24

* **_Compensated_**: **0-24.9% blood loss** (500-1250cc) * normal SBP/pulse pressure/ pulse, alert * **_Uncompensated_**: **25-40%** (1250-2000cc) * decreased SBP/ pulse pressure, tachycardic, anxious * **_Irreversible_**: **\>40%** **blood loss** * decreased SBP/ pulse pressure, very tachycardic, lethargic

Answer 25

* ABCs * **Volume resuscitation: Crystalloids (LR or NS)** * usually 3-4 liters: * initially **1-2 NS boluses** to restore tissue perfusion and continued at rapid rate until clinical signs of hypovolemia improve * control the source of hemorrhage +/- packed RBCs if severe * **maintain body temp** (prevent hypothermia)

Answer 26

* _Definition_: **excessive vasodilation in small vessels** & altered distribution of blood flow with shunting from vital organs to non-vital tissues * _Pathophys_: * dilation of all blood vessels so the “tank” becomes too big * _Etiologies_: * **Septic**: overwhelming infx → systemic inflammatory response → systemic vasodilation * **Anaphylactic**: severe rxn to allergen → systemic histamine release → widespread vasodilation * **Neurogenic**: acute spinal injury that results in loss of sympathetic tone that normally keeps vessels constricted → vessel walls veno/vasodilate * **Endocrine**: adrenal insufficiency

Answer 27

* _Sepsis_: “Warm shock" “warm shock” * **warm, flushed extremities** (d/t systemic vasodilation of capillaries) * **wide pulse pressure** * bounding pulses * hypotension * _Anaphylactic Shock_: * pruritus, urticaria * angioedema * hoarseness * _Neurogenic_: * warm skin * bradycardia or normal HR * wide pulse pressure

Answer 28

Type of Distributive Shock * _Preload_: decreased * _Afterload_: decreased * _Cardiac Output_: decreased * _BP_: low * _Organ perfusion_: decreased * **Mixed venous O2: HIGH** (oxygen is not reaching tissues and is not getting used due to loss of vascular tone) * **AVO2 difference**: **LOW** (oxygen is not reaching tissues and is not getting used due to loss of vascular tone) * so mixed venous o2 is high and arterial o2 is also high

Answer 29

Type of Distributive Shock * _Preload_: decreased * _Afterload_: decreased * _Cardiac Output_: **increased** * _BP_: low * _Organ Perfusion_: normal (b/c of good cardiac output so normal organ perfusion) * _AVO2 difference_: normal

Answer 30

* **_Septic Shock_**: * broad spectrum IV abx * IV fluid resuscitation, then a vasopressor (vasoconstrictor: **epinephrine, norepi/phenylephrine)** * **_Anaphylactic Shock_**: * -Epi * -Airway management * -antihistamines * **_Neurogenic Shock_**: * IV fluid resuscitation * vasopressors +/- corticosteroids * **_Endocrine Shock_**: * hydrocortisone

Answer 31

* _Definition_: **mechanical block to heart's outflow or inflow** * _Etiology_: * very large PE * pericardial tamponade * tension pneumo * aortic dissection * _Tx_: **Tx the underlying cause** * PE: heparin, thrombolytics (TPA, TKI) * Tamponade: pericardiocentesis * Tension Pneumo: needle decompression * oxygen, isotonic fluids, inotropic support (**dobutamine, epi, milrinone)**

Answer 32

* _Definition_: **primary myocardial dysfunction** (pump failure) → low cardiac output → inadequate tissue perfusion * _Etiology_: * **Pump Failure**: * ischemia (CAD), acute MI, myocarditis, valve dysfunction (mitral regurg secondary to papillary rupture), cardiomyopathy, post-operative, myocardial contusion, acute ventricular septal or L ventricular rupture * Arrhythmia, toxic/metabolic * _S/sxs_: * **Acute hypotension** (you can only compensate with increasing afterload [vasoconstriction) **BP \<90/60** * tachycardia, tachypnea * weak pulses * mottled skin * diaphoretic * AMS * anxiety/restlessness * **Elevated JVP** * oliguria

Answer 33

* _Preload_: **increased** (due to decreased stroke volume) * _Afterload_: increased * _Cardiac Output_: decreased * _BP_: low * _Organ Perfusion_: decreased * _AVO2 difference_: **high** (b/c heart is delivering less blood, so tissues are using more O2 from the blood available)

Answer 34

**Tx the underlying cause** * if acute MI: revascularize * **i****notropic Support****(****dobutamine, epinephrine, milrinone****)** * can use a vasodilator if BP is okay (**dobutamine, milrinone**) * if hypotensive then use vasopressor (**Epi, norepi/phenylephrine**) * intra-aortic balloon counterpulsation * oxygen * isotonic fluids: AVOID large amounts of fluid * if you use fluids, will eventually need to diurese (**Lasix [furosemide])**

Answer 35

**autosomal dominant** * _Pathophys_: * subaortic **outflow obstruction** d/t **asymmetrical septal hypertrophy** & systolic **anterior motion of the mitral valve** * \*\*Hypercontractile\*\* * can have myocardial ischemia d/t increased muscle mass and increased demand for O2 * _Risk Factors_: * young age, fam hx of sudden death, gene mutations prone to SCD, sustained VT or SVT, recurrent syncope, brady arrhythmias * **#1 cause of sudden death in competitive athletes \<35 yo**

Answer 36

* _S/sxs_: * **dyspnea, syncope** * angina * palpitations * dizziness * fatigue * **sudden cardiac death** * _PE_: * _Hypertrophic Obstructive Cardiomyopathy Murmur:_ **Crescendo-decrescendo systolic murmur** (best heard at R sternal border) * **increased with decreased venous return** (valsalva or standing) * → d/t less volume in L ventricle meaning that the obstruction from the septum is more severe, (vs when it has more volume it pushes the septum to its “normal” place making the murmur less severe) * loud S4 (di-a-stol-ic) * mitral regurg * _Dx_: * Echo: * **asymmetrical ventricular wall thickness** * systolic anterior motion of the mitral valve * small LV chamber * EKG: * **Left ventricular hypertrophy** * Septal Q-waves * R. atrial enlargement

Answer 37

* _Tx_: * **Beta-blockers** = 1st line, or CCB * Diuretics if CHF symptoms * surgery (if gradient \>50 mmHg at rest or class III-IV heart murmur) * alcohol septal ablation * dual chamber pacing * cardiac transplant * Pt should avoid dehydration, extreme activity, **& competitive sports** (low-risk older pts can speak with a cardiologist) * _Complications_: * can progress to dilated cardiomyopathy * a.fib, stroke * clinical deterioration is slow

Answer 38

* _Definition_: * rigid ventricular wall with impaired ventricular filling & **reduced diastolic fnx** in a non-dilated ventricle. No change in contractility * Least common form of cardiomyopathy * _Etiology_: * **amyloidosis = most common** * Sarcoidosis * Scleroderma * Hemochromatosis * _S/sxs_: * R & L HF: * R: peripheral edema, **JVD**, hepatomegaly, ascites, GI sxs * L: dyspnea, fatigue * Other: Kussmaul sign, S4

Answer 39

* _Dx_: * Echo: * non-dilated ventricles with normal thickness * marked dilation of both atria * **abnormal mitral flow** (LA to LV) * **\*\*Endomyocardial biopsy = definitive diagnosis\*\*** * amyloid on biopsy may be d/t primary amyloidosis or secondary to **multiple myeloma** & **hypergammaglobulinemia** * _Tx_: * Tx the underlying disorder * use drugs with caution: diuretics, vasodilators, CCB * **DO NOT USE DIGITALIS (DIGOXIN)** & other inotropic agents * Tx of **hemochromatosis**: phlebotomy & chelation therapy → cardiac fnx may normalize

Answer 40

For Acute Coronary syndrome to tell you if the patient is low, medium, or high risk * H: History * E: EKG * A: Age * R: Risk factors (DM, dyslipidemia, HTN, smoking, CKD, prior CAD or PAD) * T: Troponin

Answer 41

* _Definition_: infection of a **normal valve** with a virulent organism (usually **S. Aureus**). * **Rapidly destructive** (fatal \< 6 weeks if untreated)

Answer 42

* _Definition_: indolent infection (causing little or no pain) of **abnormal valves** with less virulent organisms (**S. Viridians** = normal oral flora) * **slower onset**, longer duration (may continue for weeks-months before fatal)

Answer 43

* _General Definition_: * **infx of the _endocardium_** (usually the valve) secondary to colonization. **Mitral valve** = most common valve involved (M\> A\> T \>P) * _Risk Factors_: * **\>60 yo**, males, **IV drug abusers, poor dentition** * pre-existing structural cardiac abnormality, prosthetic heart valve, prior episode, intravascular device (**indwelling catheter**), congenital heart disease, hemodialysis, HIV, co-morbidities * _S/sxs_: * **Fever** * Chills/sweats * Anorexia & weight loss * Malaise, fatigue * Arthralgias & myalgias

Answer 44

1. **_Native Valve Endocarditis_:** \*\***majority of cases\*\***, infx of mitral & aortic valves with streptococci, enterococci (GI/GU), staphylococci, or normal mouth organisms 2. _._**_Prosthetic valve endocarditis_:** 10-20% of cases, **S. epidermidis** = most common 3. **_.IV Drug Associated endocarditis_**: infx of right-sided valves (**tricuspid**, pulmonic) with **S. aureus (acute bacterial endocarditis)** (or fungi, gram -)

Answer 45

* _Community associated:_ * if diagnosed **within 48 hours** of hospital admission * _Healthcare Associated_: * if recent contact with healthcare setting with **onset of symptoms \> 48 hours** after hospitalization (25-30% of cases)

Answer 46

* _PE_: * **murmur** → **new or worse** **regurg murmur** * splenomegaly * arterial **emboli** * **petechiae** (appear in crops then disappear in 2-3 days) * neurological features, clubbing, arrhythmia, scleral hemorrhage * **Osler’s nodes** (small, painful, purple-red SQ nodules on digits and palms) * **Roth’s spots** (oval retinal hemorrhages with pale center) * **Janeway Lesions** (small, non-tender hemorrhagic macules or nodules on palms & soles) * **Splinter hemorrhages** (linear reddish brown lesions under the nail bed) * _Tests to Order_: * Labs: * **BLOOD CXs** : 3 sets \> 1 hour apart * ESR or CROP: elevated * Rheumatoid factor: positive * Leukocytosis * Anemia * Proteinuria, microscopic hematuria * _Transesophageal Echocardiogram_: * more sensitive than TTE but obtain TTE first → looking for endocardial vegetations

Answer 47

**DUKE CRITERIA** * _Duke Criteria-_**_Major_:** 1. **Sustained bacteremia**: 2 positive blood cultures by organism known to cause endocarditis 2. **Echocardiogram** showing vegetation, dehiscence, or abscess 3. **New** valvular **regurgitation** * _Duke Criteria_ **_Minor_**: 1. Predisposition (heart condition or IVDA) 2. Fever \>38C (100.4F) 3. Vascular: emboli to organs/brain hemorrhages 4. Immunologic: glomerulonephritis, Osler’s nodes, Roth spots, RF 5. Positive blood culture not meeting major criteria (1 positive) 6. Echocardiogram not meeting major criteria * \***Definitive Endocarditis**: 2 major criteria; 1 major + 3 minor criteria; 5 minor criteria or histological findings * \***Possible Endocarditis**: 1 major + 1-2 minor, 3 minor * \***Rejected Endocarditis**: resolution within \<4 days of abx, alternate dx made, no evidence of IE at surgery or autopsy, definite or possible criteria not met

Answer 48

\*\*Recommended prior to procedures which may introduce bacteria into the bloodstream of patients who are at high risk of developing bacterial endocarditis\*\* * _Indicated Cardiac Conditions_: * Prosthetic Cardiac Valve, heart repairs with prosthetic material, prior endocarditis, Cyanotic congenital heart disease, cardiac transplant * _Procedures_: * dental: * (manipulation of gums, roots of teeth, oral mucosa perforation) * respiratory: * respiratory mucosa manipulation, rigid bronchoscopy * Skin/MSK tissue procedures * including abscess I&D * GI/GU → NO longer recommended * _Regimen_: * **2g amoxicillin PO 1H before procedure** (if allergic: 500mg Azithro, 2g cephalexin, 600mg clinda)

Answer 49

* Refractory CHF * **persistent/ uncontrolled infx (sepsis**) * recurrent emboli * endocarditis-associated valve dysfunction causing HF * **invasive infection (causing development of abscess, fistula, heart block**) * fungal infx * **pedunculated vegetation \>1-2cm in size**

Answer 50

* **Duration: 4-6 weeks of high dose therapy** (indwelling catheter often used) * _Native:_ * anti-staph penicillin (nafcillin, oxacillin) **+** ceftriaxone or gentamicin * _Prosthetic_: * vancomycin + gentamicin + rifampin * _Fungal_: * Amphotericin B

Answer 51

* _Definition_: * inflammation or infection of the pericardium (outer layer of the heart) * Pericardium has 3 layers: fibrous pericardium, parietal pericardium (lines fibrous pericardium), and visceral pericardium (lines the epicardium) * _Etiology_: * infectious: viral, bacterial (**TB**), fungal * noninfectious: **secondary to MI (DRESSLER SYNDROME), neoplastic**, uremic, traumatic * Hypersensitivity/autoimmune: rheumatic fever, SLE, RA, scleroderma, drug-induced (phenytoin, INH, procainamide, hydralazine) * _Classification:_ * **Acute pericarditis: \<6 weeks** * subacute pericarditis: 6wks -6months * Chronic pericarditis: \> 6 months * _Types_: * serous: surface of heart look rough * fibrinous: “junk” stuck between layers * adhesive * hemorrhagic * purulent * constrictive

Answer 52

* _S/sxs_: * **chest pain: sudden onset of pleuritic, persistent, postural CP** (\*\*Worse when supine, relieved by sitting up & leaning forward) * aggravated with cough, breathing * may radiate to back, shoulder, or neck * _PE_: * **Pericardial friction rub**: * heard during both systole & diastole, high-pitched scratching/grating, loudest during inspiration, 2-3 components, may come and go

Answer 53

* _EKG_: * **diffuse ST segment elevation (concave)** in most limb leads & precordial v2-v6 * **ST depression in aVR +/- V1** * sinus tach common d/t pain or infx * _Stage 1_: widespread ST elevation with reciprocal changes in aVR * _Stage 2_: Normalization of ST changes, T wave flattening * _Stage 3:_ flattened T-waves or inverted * _Stage 4_: EKG returns to normal * _Echo_: * useful for showing pericardial effusion +/- tamponade → can be performed at bedside * _Diagnosis_ (**2 criteria must be met for diagnosis)**: * typical CP * pericardial friction rub * typical EKG changes * new/worse pericardial effusion * elevated CRP * \*\*no biomarkers for pericarditis → BUT 30% of pats have troponin elevation d/t **myopericarditis**

Answer 54

tx the underlying disorder * _Tx_: * Anti-inflammatory: **NSAIDs x 2 weeks**: aspirin 600-900mg QID, or indomethacin * **Colchicine x 3 months** * possibly steroids * **AVOID anticoags** (system is irritated so it is likely to bleed) **& activity** * _Admission Factors_: * fever \> 38C * subacute course * large pericardial effusion (\>20mm) * immunosuppressed pts * use of anticoags * acute trauma * **failure to improve** **after 7 days of NSAIDs + Colchicine** * elevated cardiac troponin (suggest myopericarditis)

Answer 55

* _Definition_: **inflammation of the myocardium** caused by infectious & noninfectious conditions. Focal or diffuse involvement * _Pathophys_: myocellular damage leads to myocardial necrosis & dysfunction → **heart failure** * _Etiology_: * 1st world = **parvovirus B19, herpes virus 6**, coxsackie B (enterovirus)– used to be the most cause, adenovirus, hepatitis C, COVID-19, lymphocytic, giant cell * 3rd world: HIV, chagas disease, rheumatic fever * _Epidemiology_: * most common in **20-50yo with \*\*\*_hx of recent viral infx\*\*\*_** * _Classifications_: * acute \< 3 months * chronic \> 3 months

Answer 56

* _S/sxs_: * \*many cases go undetected due to subclinical signs * **chest pain, myalgia, fever, fatigue** * CHF: dyspnea, fatigue * **arrhythmia**, sudden death * megacolon * _PE_: * **S3 or S4** * mitral/tricuspid regurg * edema (hepatic & peripheral) * low cardiac output (shock) * tachycardia * _Profiles_: 1. **Acute Coronary Syndrome-Like**: 1. severe, recurrent acute CP 1-4 weeks after viral illness, ST elevation or depression, T-wave inversion, global or regional LV +/- RV dysfunction, +/- troponin elevated 2. **New onset or worsening HF:** 1. new onset or progressive HF over 2weeks - 3months with symptoms, impaired LV +/- RV systolic function 3. **Life-threatening Condition:** 1. life threatening arrhythmias or aborted sudden death, cardiogenic shock

Answer 57

* _Dx_: * Labs: CBC, BMP, acute phase reactants (CRP, sed rate), **troponin (may be elevated**), BNP (**increased**) * _CXR_: * **congestion (not usually cardiomegaly yet)** * _EKG_: nonspecific ST changes, PACs/PVCs * _Echo_: * LV dilation, wall motion abnormalities, decreased systolic dysfunction * _MRI_: * inflammatory hyperemia, edema, wall motion abnormalities, global function, size/geometry * **_Endomyocardial Biopsy_**: **definitive diagnosis** * infiltration of lymphocytes with necrosis of myocardial tissue * Nasal swab: PCR for viruses * _DDx_: * ischemic heart disease, valvular heart disease, other causes of cardiomyopathy, congenital heart disease, pulmonary disease, takotsubo, pericarditis

Answer 58

* _When to suspect_: * onset of otherwise unexplained cardiac abnormality such as CHF, shock, arrhythmia, in a **20-50 yo with a hx of viral illness** * LV dysfunction without apparent etiology * pericarditis with accompanying troponin elevation * Acute Mi presentation without hx of CAD & negative angiogram * ECG changes * _Management_: * **supportive care**: oxygen, inotropes, diuretics, antiarrhythmics, afterload reduction (ACEI), anticoag, mechanism support * _Steroids:_ anti-inflammatory but suppresses the immune system * IVIG * Antivirals (if documented) * plasmapheresis: takes out immunoglobulins that are attacking the heart * immunosuppression

Answer 59

* _Definition_: **Accumulation of fluid in the pericardial space** (normal pericardial space has about 5-50cc) * _Etiology_: * **Acute pericarditis** (viral, bacterial, TB, idiopathic) serous or purulent * autoimmune disease * Post Mi or cardiac surgery → serous or hemorrhagic * blunt or sharp chest trauma → hemorrhagic * **Mediastinal radiation (d/t Hodgkin's or breast cancer)** * **Renal failure with uremia** * Myxedema (hyperthyroidism) * aortic dissection extending into the pericarium * Drugs

Answer 60

* _S/sxs_: chest pain, dyspnea, fatigue * _PE_: * **decreased (muffled) heart sounds** d/t fluid → as fluid increases friction rub may disappear & heart sounds may become faint * _Dx_: * EKG: **electrical alternans** (alternating amplitudes of the QRS complexes) * **low QRS voltage** (something b/w the heart & EKG leads → fluid) * Echo: **Diagnostic test of choice** * increased fluid in the pericardial space * CXR: “water bottle appearance” * Labs: gram stain & bacterial/fungal culture, cytology, AFB stain, PCR

Answer 61

* _When to suspect_: * in all cases of acute pericarditis * unexplained **new radiographic cardiomegaly without pulmonary congestion** * presence of isolated left pleural effusion * fever of hemodynamic deterioration in a pt with another disease process involving the pericadium * _Tx_: * if _minimal (_**_\<20mm_**_)_ or no evidence of hemodynamic compromise: **no immediate intervention** needed but may treat conservatively with therapy aimed at underlying cause & hemodynamic monitoring * if **_progressively_** _enlarging_ or symptoms suggest cardiac tamponade then **pericardiocentesis** is indicated * if _related to pericarditis_ treat with **NSAIDS (2weeks) & Colchicine (x3mo)** * if _chronic_ consider surgery: **pericardial window**

Answer 62

* _Definition_: * **pericardial effusion causing significant pressure on the heart, impeding cardiac filling, leading to decreased cardiac output and shock.** The **Rate of accumulation of fluid is more critical than volume.** (slow accumulation of large volume is OKAY if pericardium is compliant) * _Etiology_: * **Malignancy**, idiopathic pericarditis, & uremia (renal failure) are the most common causes * _S/sxs_: * Dyspnea * Fatigue * peripheral Edema * **BECK's Triad**: * distant (muffled) heart sounds * increased JVP * systemic hypotension * _PE_: * EKG: * **Electrical Alternans** (alternating amplitudes of the QRS complexes) * **low QRS voltage** * Echo: * pericardial effusion & diastolic collapse of teh cardiac champers * CXR: * “water bottle” appearance

Answer 63

* immediate: oxygen, IV fluids, type & culture * **Don’t give pain meds**, **sedate, or intubate** (causes vasodilation which will lower BP even further) * **Pericardiocentesis**

Answer 64

“water bottle” appearance associated with pericardial effusion/ cardiac tamponade

Answer 65

Associated with Cardiac Tamponade 1. elevated JVP 2. muffled heart sounds 3. systemic hypotension

Answer 66

**MOAN & BASH** **Morphine**, **oxygen** if O2 \<90%, **Aspirin** 162 mg, **Nitro** q 5 min (don't give to pts with systolic \<90, or to inferior MI with R ventricular involvement → dependent on preload and nitro decreases preload) **Beta blockers** (Decrease remodeling, decrease oxygen demand of heart, decreases HR, improve L ventricular hemodynamic funx, reduce incidence of ventricular arrhythmias; *Contraindication in Heart block, high risk for cardiogenic shock*) **, ACE-I/ARB** (more for long term use → improve L ventricular EF, mortality rate)**, Statin, Heparin** (antithrombotic therapy → impede progression of thrombus in coronary artery) **TPA** if pt cannot have reperfusion from cath lab in \<90minutes from door to lab

Answer 67

Post-MI pericarditis tx = aspirin or colchicine

Answer 68

1. **JVD** 2. **Clear Lungs** 3. **Positive Kussmaul Sign** 1. paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)

Answer 69

elderly, women, diabetics

Answer 70

Myoglobin ## Footnote **My O My you are fast**

Answer 71

**CRESCENDO- DECRESCENDO** **murmur R 2nd intercostal space** * increased murmur when leaning forward (ERBs) and increased venous return (squatting, supine, leg raise) * **pulsus parvus et tardus** (weak, delayed carotid pulse) * _Etiology_: * degenerative: calcifications \> 70 yo * congenital & bicuspid valve \<70 yo * _S/sxs_: **ASH** * angina * syncope * heart failure * _Dx_: * ECHO = best test * ECG = L ventricular Hypertrophy * _Tx_: aortic valve replacement = ONLY effective treatment

Answer 72

**Diastolic** _high-pitched_ **blowing DECRESCENDO** **murmur along LSB +/- apex** * murmur LOUDER when sitting up and leaning forward * _Etiology_: * acute → MI, aortic dissection, endocarditis * chronic → aortic dilation, rheumatic fever, HTN * _Physical Exam_: * _Water hammer pulse_: swift upstroked and rapid fall of radial pulse accentuated with wrist elevation * _De-Musset's Sign_: head-bobbing with heart beat * _Hill's Sign_: popliteal artery systolic pressure \> brachial artery by 60 mmHg (**most sensitive)** * _Quincke's Pulses_: visible pulsations in the fingernail bed * _Muller's Sign_: visible systolic pulsations of the uvula * _Dx_: * Echocardiogram → regurgitant jet * L ventricular dilation as compensation * _Tx_: * **decrease the afterload** improves the forward flow (e.g. ACE-I, ARBs, nifedipine, hydralazine) * surgery = definitive tx *

Answer 73

* **Diastolic murmur heard best at the apex** * **LOUD S1** (forceful closure of mitral valve) **with OPENING SNAP** (forceful opening of mitral valve →**early diastolic sound** followed by a **mid-diastolic rumbling murmur**. * → initial rumble during passive filling of ventricle, followed by active rapid filling during atrial “kick” * _Etiology_: **rheumatic heart disease = most common cause!** * _S/sxs_: increased L atrial pressure/volume overload → **pulm congestion** → pulm HTN → CHF * _Dx_: * ECG = **L atrial enlargement, A fib, pulmonary HTN** (RVH, R axis deviation) * ECHO = most useful non-invasive tool * Cardiac Cath = most accurate but rarely done * _Tx_: * percutaneous balloon valvuloplasty

Answer 74

**Systolic murmur** **Blowing Holosystolic murmur** **heard best at the APEX** → murmur radiates to the axilla, can be heard well in the LLD position * _Etiology_: **Mitral Valve prolapse = most common cause in the US** * rheumatic fever = most common in developing countries * MI/ischemia → papillary muscle dysfunction * dilated cardiomyopathy → ruptured chordae tendineae * _S/sxs_: * **dyspnea = most common**, blood backs up into L atrium then lungs * _Dx_: * **ECHO = most useful non-invasive test** * _Tx_: sx control by **reducing afterload** (ACE-I, ARBs) * surgery = repair \> replacement

Answer 75

**_Mid-late systolic ejection click_** best heard at the apex * → **any maneuver that makes the LV smaller (decreases preload) results in an earlier click** & longer murmur duration (e.g. valsalva, standing) due to increased prolapse * **MVP = MOST common cause of mitral regurgitation** * _Population_: * **Most common in young women** * _Dx_: * **ECHO** → posterior bulging leaflets * _Tx_: * MVP is associated with good prognosis → **reassurance** * beta-blockers for pts with autonomic dysfunction * mitral valve repair only for severe regurg and CHF

Answer 76

**harsh mid-systolic** **crescendo-decrescendo murmur** * murmur increases with inspiration (bigger preload) * _Pathophys_: * **Right ventricle** encounters more resistance → hypertrophy → less preload→ blood backs up * _epidemiology_: * almost always congenital and in the young * _Tx_: balloon valvuloplasty

Answer 77

**Diastolic decrescendo murmur** **best heart at the L upper sternal border** * murmur **increases with inspiration** and venous return * _Pathophys_: * retrograde blood flow from the pulmonary artery into the **Right Ventricle** causing R-sided volume overload * _Etiology_: * almost always congenital

Answer 78

**mid-diastolic rumbling murmur** at the lower left sternal border * blood backs up into the **R atrium** causing R atrial enlargement which may lead to R-sided heart failure * _Tx_: * decrease R atrial volume overload with diuretics and Na restriction * surgery

Answer 79

**Holocystolic murmur** at 4th ICS left midsternal border * **may radiate to liver** * _Pathophys_: * blood flows back into the **R atrium** * _Etiology:_ * functional overload (pulm HTN, RV dilation) * **dirty needles** (staph etc often up on tricuspid valve) * _PE_: * **_Carvallo’s Sign_**: * holosystolic murmur that becomes **louder during inspiration** * _Tx_: * tx the underlying condition * valve replacement

Answer 80

Sys-tol-ic Murmur can be normal in young and athletic hearts associated with a dilated ventricle (more compliant ventricle)

Answer 81

di-a-stol-ic atrial kick against a stiff wall, associated with **hypertrophy or scar** NEVER normal

Answer 82

Left lateral decubitus position with the bell

Answer 83

sitting up and leaning forward

Answer 84

increases intensity of all murmurs EXCEPT hypertrophic cardiomyopathy, mitral valve prolapse “the **MVP H**ates **C**onforming to the rules”

Answer 85

MS. PRARTS DIED MS = mitral stenosis PR = pulmonary regurg AR = aortic regurg TS = tricuspid stenosis DIED = **diastolic,** everything else is a systolic murmur

Answer 86

lying supine squatting lifting legs

Answer 87

standing valsalva maneuver

Answer 88

Right Side: **RINSPIRATION** → increases the sound of murmurs on the R side

Answer 89

Left side → increases sound of all murmurs on the L side

Answer 90

_How to_: handgrip, phenylephrine * increased resistance decreases forward flow & increases backward flow → increases aortic regurg, mitral regurg (regurgitant murmurs) * decreases AS, MVP, hypertrophic cardiomyopathy

Answer 91

How to: Amyl Nitrate * direct arteriolar vasodilator increases forward flow through the aortic valve * increases AS, MVP, hypertrophic cardiomyopathy * decreases AR, MR (regurgitant murmurs)

Answer 92

a murmur will be **high-pitched** if there is a **large pressure gradient** across the pathologic lesion and _low pitched_ if the _pressure gradient is low_ (Ex. aortic stenosis is high pitched d/t t the large pressure gradient b/w aorta and ventricle

Answer 93

weak, delayed carotid pulse often seen in Aortic Stenosis

Answer 94

* _Definition_: persistent communication between the descending thoracic aorta and the main pulmonary artery after birth → **L to R Shunt** * _Pathophys_: * continued **Prostaglandin E1 production** & low arterial oxygen content promotes patency. → Enlarged R atrium, R Ventricle, & L Ventricle * _Risks_: * **Prematurity**, female, fetal hypoxia

Answer 95

* _S/sxs_: * Most are asymptomatic: * but some have → poor feeding, weight loss, frequent URIs * if they experience Eisenmenger Syndrome → left-to-right shunt switches to a right-to-left shunt → **Cyanosis** * _PE_: * **Continuous Machinery Murmur** loudest at the Left upper sternal border (*PDA → personal digital assistant = machine*) * **wide pulse pressure** (bounding pulses)

Answer 96

* _Dx_: **ECHO = best initial test** * _Tx_:**I****ndomethacin, ibuprofen** (inhibits prostaglandin) * surgical: left thoracotomy * clip the premature babies * ligate the neonates & infants * divide and oversew the toddlers & infants * Catheter based: * coil device → for older infants & children

Answer 97

* Pulmonary HTN & Cyanotic heart disease occuring when a left-to-right shunt shunt switches to a right-to-left shunt → **Cyanosis**

Answer 98

Most common **cyanotic** congenital heart disease (right-to-left shunt) * _4 components_' 1. **RV outflow obstruction** (sometimes call pulm stenosis) 2. **R ventricular hypertrophy** 3. **Overriding Aorta** (shifted to the R; sits right over the VSD) 4. **Ventricular Septal Defect**

Answer 99

* _S/sxs_: * **infants:** **Cyanosis** * **Older Children**: TET spells: paroxysms of cyanosis relieved with squatting or pulling legs up * (increased peripheral vascular resistance causes the shunt to switch to left-to-right shunt ) * _PE_: * **Harsh systolic murmur at left mid-to-upper sternal border** changes similar to HOCM (louder with decrease in ventricular volume- blue, softer with increase in ventricular volume -pink) → **children will squat or pull legs to chest to increase peripheral vascular resistance** * R. ventricular heave * digital clubbing * cyanosis * \*Often dynamic (TOF spells) & progressive

Answer 100

* _Dx_: **Echo = test of choice** * CXR: **Boot shaped heart** (prominent R ventricle) * EKG: RVH, R. Atrial Enlargement * _Tx_: * DO NOT LET THEM GET DEHYDRATED → TOF spells (need to treat gastroenteritis aggressively) * **surgical repair by 3-6 months** or sooner if blue

Answer 101

Boot Shaped Heart Associated with **Tetralogy of Fallot** demonstrates prominent **R ventricle** due to **RV outflow obstruction**

Answer 102

* _Definition_: * abnormal opening in the ventricular septum, associated with a left-to-right shunt. **Most common type of congenital heart defect!!** * Most common defect in **Trisomy 21 (Down Syndrome)** * _Types_: * **Membranous =** **most common type**, hole in the LV outflow tract near tricuspid valve (higher up on the septum) * Muscular: multiple holes in “swiss cheese” pattern → these may resolve on their own

Answer 103

* _S/sxs_: * **Small VSDs**: may be asymptomatic * **Large VSDs**: symptoms manifest within 6 months of age: * **Failure to thrive** (have to pump more blood, breath harder → higher caloric demand, and decreased ability to feed) * **Poor growth** * **Tachypnea** * **GERD** * (liver enlarges due to heart failure and pushes on stomach) * **Frequent URIs** * (due to wet lungs) * _PE_: * high pitched **holosystolic murmur** best heard at the LLSB * **smaller VSDs are louder with more palpable thrills** * normal pulses

Answer 104

* _Dx_: * **Echo =** determines size & location of VSD * CXR: cardiomegaly &/or congestion * _Tx_: * Diuretics, ACEI +/- Digoxin * some may close or get smaller on their own * **Indications for Surgery**: * unmanageable heart failure * failure of medication management * shunt greater than 1.5-2x with or without sxs (babies hearts can accommodate 1.5-2x the volume often before symptoms) * \***\*Want to try to get them to 3-6 months of age before surgery, but not necessary if FTT or other issues\*\***

Answer 105

* _Definition_: * congenital **narrowing of the aortic lumen** at the **juxtaductal area** (insertion of ductus arteriosus distal to left subclavian artery) * Often associated with **Turner syndrome** and bicuspid aortic valve * _Pathophys_: * narrowing of the aorta most commonly → HTN in the arteries proximal to the lesion with hypotension in the lower extremities * overtime, the body develops collaterals around the coarctation

Answer 106

* _S/sxs_: * **Neonates**: Failure to thrive * poor feeding * tachypnea, irritability * CHF * \*\*Severe Coarctation: LV failure & Shock after birth when the _ductus closes_\* * **Older children/Teens**: * headache * nosebleeds * absent or diminished femoral pulses * **Unexplained HTN\*\*\*** * _PE_: * **upper extremity systolic HTN with lower extremity hypotension** * **Diminished or delayed lower extremity pulses** (vs. VSD that has normal pulses * Systolic murmur at LUSB with radiation to the **scapula** (back) * _Dx_: * _CT-angiography_ = **Gold standard** * CXR: cardiomegaly * **posterior rib notching** (due to increased intercostal artery collateral flow) after several years * **3 sign** (narrowed aorta looks like the notch of the number 3) * ECG: LVH * Echo: useful but difficult to visualize coarctation

Answer 107

* _Dx_: * CXR: cardiomegaly * **posterior rib notching** (due to increased intercostal artery collateral flow) after several years * **3 sign** (narrowed aorta looks like the notch of the number 3) * ECG: LVH * Echo: useful but difficult to visualize coarctation * _Tx_: * **surgical**: left thoracotomy with extended end-to-end anastomosis; stents reserved for recurrent coarctations * **Prostaglandin E1 (****Alprostadil**) can be used to open the ductus arteriosus and relax the narrowed aortic segment * Early referral saves lives!

Answer 108

**3 Sign** associated with **Coarctation of the Aorta** narrowed aorta looks like the notch of the number 3

Answer 109

Coarctation-Rib Notching Associated with **Coarctation of the Aorta** due to increased intercostal artery collateral flow after several years

Answer 110

Hyperoxia test

Answer 111

* truncus did not separate into aorta and pulmonary artery * **Large VSD** → R-L shunt * repair: VSD closure, RV-PA conduit, usually operate in first 2 weeks of life * associated with DiGeorge Syndrome 22q11

Answer 112

Benign Murmur * SYSTOLIC, grade 1-2/6 * best heard at APEX of heart & LL sternal border * best heard with BELL of stethoscope * represents the normal sound of blood gushing out _into the aorta during contraction_ * healthy 3-7 year old children

Answer 113

* anything DIASTOLIC * anything \>II/VI * → get an echo

Answer 114

* _Rotation_: * tetralogy of fallot * transposition of the great arteries (TGA) * _Septation_: * ventricular septal defects * atrial septal defects * truncus arteriosus * _Migration_: * total anomalous pulmonary venous drainage (TAPVR)

Answer 115

* flat, nonpalpable * \<1cm in diameter

Answer 116

* flat, non-palpable * \>1cm

Answer 117

* elevated, round * \<1cm in diameter

Answer 118

* elevated, circumscribed * \>1cm in diameter

Answer 119

* elevated, circumscribed * large volume than papule often \> 2cm * involves the **dermis** * greatest mass may be beneath the skin surface

Answer 120

* elevated, circumscribed * \<1cm in diameter * primarily filled with clear fluid, **may become pustular**

Answer 121

* elevated, circumscribed * larger vesicle, \>1cm * filled with clear fluid

Answer 122

* aka hive * firm, edematous plaque * tend to be transient

Answer 123

* elevated, circumscribed * usually \<1cm * filled with purulent fluid

Answer 124

* lichenoid

Answer 125

* hyperkeratosis *

Answer 126

* exogenous injury to all or part of the epidermis * secondary feature of pruritus * due to **scratching**

Answer 127

* **epidermal atrophy:** thinning of the epidermis, leading to wrinkling and a shiny appearance * **dermal atrophy**: loss of dermal collagen and/or elastin leading to a depression

Answer 128

* thickening of the epidermis and accentuation of the natural skin lines i. e. acanthosis nigricans

Answer 129

* 1-6: * 1: white * 2: white * 3: Beige * 4: Brown * 5: Dark Brown * 6: Black

Answer 130

* generalized unexplained pruritus

Answer 131

* means "flower breaking out" * used to describe a skin breakout that is due to internal disorder such as an infection or drug * i.e. viral exanthem

Answer 132

* "measles-like" * maculopapular that becomes confluent

Answer 133

* visible hemorrhage into the skin or mucus membranes * these are **non-blanchable**

Answer 134

* less than or equal to 3mm and macular * small purpura

Answer 135

* usually \>1cm * trauma in the history is typical * a **hematoma** is when it is **palpable**

Answer 136

* blue or discolored network * think of Mallory's legs during cold soccer workouts * pale with the blue and discolored network of lacy coloration

Answer 137

* well circumscribed papules, plaques with hyperkeratosis (scaling) * often associated with: * psoriasis * pityriasis rosea * lichen planus * tinea corporis * seborrheic dermatitis

Answer 138

* itch/scratch cycle * multiple discreet, firm papulonodules with central scale/crust due to chronic **scratching and picking** * **butterfly sign** = everwhere except where the pt cannot reach

Answer 139

* plaques that are either skin colored, pink, or hyperpigmented with exaggerated skin lines and a **leathery** appearance due to habitual scratching/rubbing

Answer 140

* prickling, burning, stinging, and **itching** that may develop within 30 min of water exposure regardless of temperature or salinity * →indicative of **polycythemia vera** * increased blood cell levels * due to overproduction by bone marrow

Answer 141

* neurological pruritus * tends to be unilateral on the upper to mid back * **hyperpigmented patch** may be present * tx: **capsaicin**, **ice packs, gabapentin**

Answer 142

* neuropathic pruritus * tends to affect **the arms and the neck bilaterally** * tx: **capsaicin**, **ice packs,** and **gabapentin** * tends to affect women with light skin tones more than men * 35-45 yos

Answer 143

* abnormal sensation that can be spontaneous or evoked * may include pain, pruritys, tingling, burning, or 'pins and needles' \*\*\*\*Cocnerning if symptoms are sudden, severe, or worsen significantly→ need to image the appropriate area of the spine\*\*\*

Answer 144

1. apply cold, wet cloth or ice pack to skin that is itching 2. take an oatmeal bath 3. moisturize the skin 4. apply topical anesthetics that contain **pramoxine** 5. apply cooling agents, such as **menthol** or **calamine**

Answer 145

* aka post-infectious cough * no specific etiological agent * cough lasting from 3-8 weeks following a viral URI or bronchitis * usually normal CXR

Answer 146

* cough lasting \> 8 weeks in adults * cough lasting \>4 weeks in children * can be sign of underlying condition: * GERD * ACE inhibitor use (lisinopril) * asthma * upper airway cough sundrome * sarcoidosis, TB, cancer * CXR to r/o other causes * if cause can't be identified: * consider chest CT scan * pft * refer to pulmonologist

Answer 147

“Blue Bloaters” * chronic cough **with phlegm** for 3months of the year for 2+ years → without acute cause * PE: crackles and wheezes, percussion = normal * Dx: FEV₁/FVC = \<0.7 * **increased HGB and HCT** → chronic hypoxemia * CXR: peribronchial and **perivascular markings** * TX: SABAs for mild, LAMA for moderate-severe or LABA +/- ICS * SAMA (ipratroprium) = main inhaler for COPD

Answer 148

chronic bronchitis + emphysema proteases \> anti-proteases Causes: smoking, pollution, chronic damage to lungs, family hx, occupational exposure to dust, vapors, fumes and other chemicals, childhood factors (frequent respiratory infx, low birth weight) alpha 1 antitrypsin deficiency Post-bronchodilater FEV₁/FVC must be \<0.7 for a diagnosis by GOLD criteria tend to be \>40 years old for acute exacerbation aim for SpO₂ of 88-92%

Answer 149

part of COPD “Pink Puffers” * enlarged air spaces as a result of damage to alveolar septae → decreased lung function → **chronic hyperventilation** * S/sxs: **quiet lungs, thin, barrel chest**, minimum sputum, underweight, pursed lips to increase resistance of exhale * PE: diminished breath sounds, **prolonged expiration**, and **diminished heart sounds**, _hyperresonance_ on percussion * Dx: * CXR: loss of lung markings, hyperinflation, flattened diaphragm, small thin appearing heart * **subpleural blebs** = pathognomonic * Tx: SAMA (ipratropium bromide) or albuterol inhaler * oxygen * PO steroid burst during exacerbation * abx if increased sputum production, increased purulence, or increased dyspnea

Answer 150

Most commonly caused by **RSV** in fall and winter * common in infants and children * S/sxs: **wheezing**, tachypnea, respiratory distress, fever * often have _prodromal viral sxs_ (fever, uri) for 1-2 days **followed by respiratory distress** * PE: expiratory wheezes, may have normal serous nasal discharge * Diagnosis: CXR = normal * test for influenza, **RSV** (antigen test or nasal washing monocloncal antibody test) * Tx: Supportive tx → humidifed air, antipyretics, **beta-agonists**, nebulized **racemic epi** * **_oxygen = mainstay of tx_** * Palivizumab prophylaxis (Synagis) for immunocompromised, premature infants etc

Answer 151

**cough \> 5 days**, can last 1-3 weeks most often _viral (95%)_, but bacterial = Moraxella, S. pneumo, chlamydia pneumoniae * S/sxs: cough \>5 days, low fever, malaise, dyspnea, **URI sxs** * may have **hemoptysis** (most common cause of hemoptysis, followed by carcinoma) * PE: less severe than PNA (normal vitals) **no crackles or egophany** * may have **rhonchi or wheezing** * → _rhonchi that clears with cough_ * Dx: clinical, can obtain CXR if uncertain * Tx: supportive → fluids, rest, **corticosteroids** if underlying RAD * **Dextromethrophan (Tessalon Pearls)** * **Guaifenesin (robitussin)** * SABAs for wheezing * antipyrettics * **Ribavirin** if severe lung or heart disease * if O₂\<96% on RA→ hospitalize

Answer 152

Medical Emergency → usually caused by Hflu Males\> females, DM =risk factor in adults; most common in age 3mo-6yr * S/sxs: fever, odynophagia (pain with swallowing), _Tripoding_ , dyspnea * 3Ds: **drooling, dysphagia** (difficulty swallowing), Respiratory **distress** * PE: **_inspiratory stridor**_, muffled hot-potato voice, hoarseness, _**Thumb print sign_** * Diagnosis: **laryngoscopy** * tx: secure airway then cx for Hflu * intubate if necessary, supportive care * **ceftriaxone** (or 2nd or 3rd gen cephs)

Answer 153

* aka Croup * \*\*barking cough most commonly caused by **parainfluenzae virus**\*\* * abrupt onset of symptoms * \*\***Steeple Sign\*\*** * home treatment: symptomatic care maybe with some **dexamethasone** * **Nebulized epi with IV/oral/IM dexamethasone** * \*\*the WESLEY CROUP SCORE\*\* \>12 → send to the hospital * mild = 2 * Moderate 3-7 * severe \>/= 8 * impending respiratory failure \>/=12

Answer 154

sxs \< 2x/month * Controller: * TAke ICS whenever SABA is taken * Reliever: * SABA

Answer 155

short acting beta agonist

Answer 156

sxs 2x/month + but less than 4-5days/week * Controller: * low dose maintenance ICS * Reliever: * PRN SABA

Answer 157

inhaled corticosteroid

Answer 158

sxs most days, or waking with asthma once/week + * Controller: * low dose maintenance ICS-LABA * Reliever: * PRN SABA

Answer 159

long acting beta 2 agonist

Answer 160

leukotriene receptor antagonist i.e. singulair (montelukast)

Answer 161

sxs most days, or waking with asthma once/week+, or low lung function * Controller: * medium/high dose maintenance ICS-LABA * Reliever: * PRN SABA

Answer 162

* Controller: * add on LAMA * refer for phenotypic assessment * +/- anti-IgE, anit-IL5/5R, anti-IL4R * consider high dose ICS-LABA * Reliever: * PRN SABA

Answer 163

6-11 years old

Answer 164

sxs \<2x/month * Controller: * low dose ICS whenever SABA is taken; or daily low dose ICS * Reliever: * PRN SABA

Answer 165

sxs 2x/month+ but less than daily * Controller: * daily low dose ICS * other: * daily LTRA, or low dose ICS taken whenever SABA taken * Reliever: * PRN SABA

Answer 166

sxs most days, or waking with asthma 1x/week+ * Controller: * low dose maintenance ICS-LABA or medium dose ICS * Other: * low dose ICS + LTRA * Reliever: * PRN SABA

Answer 167

sxs most days or waking with asthma 1x/week + AND low lung function * Controller: * medium dose ICS-LABA and **refer for expert advice** * other: * high dose ICS-LABA, or add on tiotropium or add on LTRA * Reliever: * PRN SABA

Answer 168

* Controller: * Refer for phenotypic assessment + add-on therapy. e.g. anti-IgE * other: * add-on anti-IL5, or add on low dose OCS but consider side-effects * Reliever: * PRN SABA

Answer 169

Short acting beta-2 agonists * albuterol * levalbuterol * metaproterenol * Terbutaline

Answer 170

SABA: MDI and neb * _dosing_: 2puffs Q4-6hours (90mcg/puff) * stimulates beta-2 receptors = bronchial muscle relaxation * _SEs_: **_HypoK_** especially during continuous neb * beta-2 stimulation causes cellular uptake of K+ = decreased srum K+ * also **tachycardia** (because not very selective and will stimulate beta-1 receptors)

Answer 171

SABA: MDI and neb * steroisomer of albuterol, but higher affinity for beta-2 so less sysstemic sympathetic effects = b/c less binding to beta-1 * _SEs_: **_HypoK_**

Answer 172

long acting beta-2 agonists * salmeterol DPI (Serevent Diskus) * Formoterol DPI (Foradil) * Arformoterol (Brovana) * not for kids * Indacaterol (Arcapta) * not for kids * Olodaterol (striverdi Respimat) * (**Some Fish Are Inherently Odorous)**

Answer 173

LABA **do not use as monotherapy** * partial agonist

Answer 174

LABA * helpful for nighttime sxs * full agonist * onset = to that of albutero but DO NOT USE FOR ACUTE BRONCHOSPASM * _SEs:_ **paradoxical bronchospasm**

Answer 175

MOA: inhibit inflammatory cells (mast cell, eosinophils, neutrophils) and cytokines (histamine, leukotriens) **\*\*Flat dose response curve = double the dose adds limited additional effect \*\*** **BID Dosing is better (need more in smokers)** * Beclomethasone HFA (QVAR) * Budesonide DPI (Pulmicort) * Ciclesonide (Alvesco) * Fluticasone HFA (Flovent) * Fluticasone DPI (Flovent Diskus) * Flunisolide (Aerobid) * Mometasone DPI (Asmanex) * _SEs_: * oral candidiasis * cough * Dysphonia * Adrenal Suppression (at high dose)

Answer 176

monoclono- **anti-IgE antibody** * stops release of inflammatory mediatorys * used for moderate to severe asthma * **significantly reduces ICS use** * SQ injection * _SEs:_ * injection site rxn, bruising, redness, pain, stinging, itching etc * anaphylaxis (rare) * monitor 2 hours after injection for 3 months then 30 min thereafter

Answer 177

* Fluticasone/Salmeterol (Advair) DPI * Fluticasone/Vilanterol (Breo Ellipta) * +3A4 inhibitors (both advair and breo) = increased LABAs = **QT prolongation** * Budesonide/Formoterol HFA (Symbicort) * Mometasone/Formoterol (Dulera) * _SEs_: Thrush * dysphonia * pharyngitis * HA * nausea * tremor

Answer 178

for COPD * Gold 1: FEV₁ \>80% * mild * Gold 2: FEV₁ 50-79% * moderate * Gold 3: FEV₁ 30-49% * severe * Gold 4: FEV₁ \<30% * very severe

Answer 179

* First Line: * SABA prn or SAMA prn (bronchodilators) * Second Line: * LAMA or LABA or SABA + SAMA

Answer 180

* First line: * LAMA or LABA (long acting bronchodilators) * Second Line: * LAMA + LABA

Answer 181

* First line: * ICS + LABA or **LAMA** * Second Line: * LAMA + LABA * LAMA + PDE4i * LABA + PDE4i

Answer 182

* First Line: * ICS + LABA and/or LAMA * Second Line: * ICS + LABA and LAMA * ICS + LABA and PDE4i * LAMA + LABA * LAMA + PDE4i

Answer 183

inhibit breakdown of cAMP = reduction of inflammation **Roflumilast (Dalirespt)** * for prevention of COPD * _SEs_: * diarrhea, decreased appetite, weight loss, abdominal pain * headache, insomnia * anxiety and depression * DDI: CYP 1A2 and 3A4 * inducers: butalbital, phenytoin, rifampin, carbamazepine (avoid use) * inhibitors: amiodarone, clarithromycin, cimetidine, ketoconazole (use with caution)

Answer 184

* Mild: * strep pneumo, H.flu, Moraxella * Severe: * E.coli, Klebsiella, enterobacter, pseudomonas

Answer 185

1. 4 or more courses of abx over the past year 2. recent hospitalization (2+ days in past 90) 3. isolation of pseudomonas during a previous hospital visit 4. severe underlying COPD 1. FEV₁\<50

Answer 186

long acting muscarinic antagonists * Tiotroprium * alcidinium * glycopyrrolate * Umeclidinium

Answer 187

* Albuterol/Ipratroprium (Combivent Respimat) * Duoneb * _SEs_: paradoxical bronchospasm * palpitations/tremor/tachy * **CONTRAINDICATION: soy or peanut allergy** * NOT for Children

Answer 188

only for asthma (LTRA) * montelukast (Singulair) * Zileuton (Zyflo) * SEs: **hepatotoxicity** * DDIs: * **inducers**: rifampin, carbamazepine, St. John's wort * **inhibitors**: fluconazole, amiodarone, fluvoxamine, metronidazole, voriconazole

Answer 189

Mild, no abx needed cardinal sxs: increased dyspnea, sputum volume, or purulence

Answer 190

macrolide 2nd and 3rd gen ceph doxy Septra (TMP/Sulfamethoxazole)

Answer 191

respiratory FQs (moxi/levo/gemi) Amoxicillin/Clavulanate (Augmentin)

Answer 192

FQ (levo PO or IV) Cephalosporins (Cefepime IV or Ceftazidime IV) Zosyn IV (piperacillin + tazobactam)

Answer 193

FQ (levo or Moxi) Cephalosporins (ceftriaxone or cefotaxime)

Answer 194

FEV₁\<50% age \>65 \>/= 3 exacerbations/year cardiac disease

Answer 195

ssRNA Hemagglutinin spikes→ allow virus to bind to host(targeted by IZs) , neuraminidase→ allow virus to bud (targeted by meds) * S/sxs: **sudden onset** high fever, chills, malaise, sore throat, headache, and coryza, **myalgias** (especially legs and lumbosacral), non-productive cough * **_classic triad: FEVER, DRY COUGH, MYALGIAS_** * PE: ill appearance, mild pharyngeal edema, cervical adenopathy +/-, serous nasal drainage * Dx: **rapid antigen test**, serology = more accurate, WBC does not correlate well with severity → often normal or low (if \>15K → suggests secondary bacterial) * Tx: mild disease & healthy? → supportive tx (acetaminophen, fluids, and rest) * hospitalized or at-risk? → neuraminidase inhibitors (Oseltamivir or Zanamivir (Dr. Oz txs the flu)) → need to be initiated within 48 hours of onset * empiric antiviral tx: children \<2, pregnant, 65+, women up to 2 weeks post-partum, chronic or immunosuppressed

Answer 196

aka Whooping Cough → causative agent **bordetella pertussis** → gram -, coccobacillus common in children \<2 yrs, respiratory droplet transmission * S/sxs: consider in adults with cough \> 2weeks * _catarrhal stage_: cold like sxs, poor feeding and sleeping * _paroxysmal stage_: high-pitched **inspiratory whoop** *between coughing fits* → post-tussive emesis is highly indicative of this infx * _convalescent stage_: residual cough (up to 100 days) * Dx: nasopharyngeal swab for cx and PCR * Tx: supportive care +/- steroids/SBAS * **Macrolides** (clarithromycin, azithromycin) * DTaP, TDap Izs * Complications: **PNA**, encephalopathy, otitis media, sinusitis, seizures

Answer 197

Causative Agents: **S. Pneumo (rusty color sputum**, common in after splenectomy), **S. aureus (salmon colored sputum**, lobar, after influenza), Hflu, **Klebsiella (alcohol abuse; currant jelly sputu**m, aspiration); atypicals → **mycoplasma (young ppl living in dorms**, (+) cold agglutination), **chlamydia (college kids**, sore throat), **legionella (air conditioning**, low Na⁺, GI sxs and high fever) * S/sxs: tachycardia, tachypnea, **fever**, pleuritic chest pain, dyspnea +/- rigors (associated with strep pneumo) * PE: CXR: **infiltrate/consolidation** * Typical: percussion → dull, increased tactile fremitus, egophony and crackles * atypical: pulmonary exam is often normal (may have crackles) * Dx: CXR, **blood cxs x 2** , sputum gram stain * Tx: outpt → **doxycycline, macrolides (500mg 1st day, then 250mg for days 2-5)** * CURB-65: Confusion, uremia (BUN \>19), RR \>30, BP \<90/\<60, age 65+ * inpatient tx: * **ceftriaxone + azithromycin, respiratory fluoroquinolones** (Moxi, levo)

Answer 198

\*\*\*most common cause of lower respiratory tract infx in children world wide\*\*\* leading cause of pna and bronchiolitis * S/sxs: rhinorrhea, **wheezing/coughing**, persists for months, low grade fever, nasal flaring/ retractions, often prodomal sxs for 1-2 days before **respiratory distress** * PE: visible retractions * Dx: nasal washing, **RSV antigen test** * CXR can show diffuse infiltrates * Tx: oxygen \<95-96% → hospitalize, same with tachypnea, difficulty feeding * supportive tx * should resolve in 5-7 days * albuterol via neb, humidified O₂

Answer 199

1-2% of lung cancers → carcinoid syndrome tumors that arise from **neuroendocrine cells** → lead to excess secretion of _serotonin_, bradykinin, and histamine * \*\*\*often start at appendix, mesastasize to liver then travel via blood stream to the **lungs**\*\*\* * S/sxs: flushing, diarrhea, wheezing, and low blood pressure * vasodilation and flushing = increased histamine and bradykinin * PE: heart valve dysfunction → tricuspid regurge due to _increased serotonin_ that causes **collagen fiber thickening, fibrosis** * Dx: **CT-scan**, **_octreoscan_** (radiolabeled somatostatin analog binds to receptors on tumor cells) * urinalysis: shows increased **5-hydroxyindoleacetic acid (5-HIAA)** = main metabolite of serotonin * **pellagra** (vitamin B3 deficiency/ niacin) * Tx: **surgical excision** * octreotide: somatostatin analog binds to somatostatin receptors and **decreases the serotonin being secreted** by the tumor * niacin supplement

Answer 200

non-small cell lung cancer **characterized by _keratin_ production** * S/sxs: cough, weight loss, night sweats, hemoptysis (superficial squamous cells burst in lungs), chestpain/back pain, SOB * **located in bronchial tubes (where it starts**) * paraneoplastic syndrome → **hypercalcemia** of malignancy = think stones, bones, and psychiatric overtones * → mediated by **PTHrP** (parathyroid hormone related peptide) * Tx: stage I and II: surgery * Stage IIIa: surgery +chemo * Advanced disease (IIIB and IV): * treat the driver mutation * if PDL1 is expressed by tumor → **pembrolizumab** (PDL1 inhibitor) * if PDL1 expression \<50% → **tradition chemo + PDL1 inhibitor** * _Pancoast Tumor_: should pain, horner's syndrome, brachial plexus compression * _Horner's Syndrome_: unilateral miosis, ptosis, and anhydrosis

Answer 201

non-small cell cancer most common type of lung cancer, and _most common type of lung cancer to occur in never smokers_ * **begins in periphery of lungs** * also associated with smoking and asbestos exposure * paraneoplastic syndrome: _thrombophlebitis_ * tx:

Answer 202

non-small cell cancer most common type of lung cancer, and _most common type of lung cancer to occur in never smokers_ * **begins in periphery of lungs** * PATHOLOGY: * neoplastic gland formation * also associated with smoking and asbestos exposure * paraneoplastic syndrome: _thrombophlebitis_ * tx:Tx: stage I and II: surgery * Stage IIIa: surgery +chemo * Advanced disease (IIIB and IV): * treat the driver mutation * if PDL1 is expressed by tumor → **pembrolizumab** (PDL1 inhibitor) * if PDL1 expression \<50% → **tradition chemo + PDL1 inhibitor**

Answer 203

non-small cell carcinoma very fast doubling time but causes sxs late * rare: only 5% * usually begins on the outer edges of the lungs * _paraneoplastic syndrome_: **gynecomastia** * Tx: stage I and II: surgery * Stage IIIa: surgery +chemo * Advanced disease (IIIB and IV): * treat the driver mutation * if PDL1 is expressed by tumor → **pembrolizumab** (PDL1 inhibitor) * if PDL1 expression \<50% → **tradition chemo + PDL1 inhibitor**

Answer 204

“All of the Ss" * grow very quickly → 54-132 day doubling rate * (if faster growth than this = decreased risk of malignancy) * **aggressive and metastic** * All the Ss: * Smoking, Sentrally located, Super Aggressive, SVC syndrome, Sitting to Standing (Lambert-Eaton Myasthenic Syndrome), Sodium/SIADH→ leads to low sodium through SIADH * **TX: surgical excision is NOT an option** * _limited stage disease_ → chemo and radiation * _extensive stage disease_ → chemo + immunotherapy * _Superior Vena Cava Syndrome_: cancer pushes on superior vena cava and traps blood in upper body * _Lambert-Eaton Myasthenic Syndrome_: similar to myasthenia gravis → *proximal muscle weakness* * _Syndrome of Inappropriate Secretion of ADH_ (SIADH): * euvolemic hyponatremia → retaining too much water * _Cushing Syndrome_: too much cortisol * central obesity, purple striae, hyperglycemia * * _Carcinoid syndrome_: flushing, diarrhea, telangiectasia

Answer 205

pts 50-80 yo; with \>20 year pack hx of smoking, with either current smoking or having quit \<15 years ago

Answer 206

nodule \<3cm (coin lesion), mass \>3cm * smooth, well defined edges → most likely benign * **ill-defined, lobular, spiculated edges** → most likely cancer * when found as incidental finding: * _Fleischner society pulmonary nodule recommendation_ * when found as part of cancer screening: * **Lung-RADS**

Answer 207

excess fluid in the pleural space * S/sxs: dyspnea, discomfort or sharp pain that worsens with inspiration * PE: _dullness to percussion_ * **decreased** tactile fremitus, **decreased** breath sounds * may have a pleural friction rub * CXR: **blunting of costophrenic angles** + _meniscus sign_ * lateral decubitus film (pt lying on their side) = best to detect smaller effusions * differentiates b/w loculations and empyema from new effusions and scarring * Tx: * **_thoracocentesis_ is both diagnostic and therapeutic** * if _empyema_ (pleural fluid pH \<7.2, glucose \<40mg/dL, or positive gram stain of pleural fluid) → can inject **streptokinase** to break up loculations * chronic effisions or recurrent and causing sxs: * **pleurodesis** (pleural space is artificially obliterated) or by intermittent drainage with an indwelling catheter

Answer 208

**the compartmentalization of a fluid-filled cavity into smaller spaces** (locules) by fibrous septa

Answer 209

collapse lung caused by an accumulation of air in the pleural space * **Primary**: occurs in absence of underlying disease (tall, thin males age 10-30) * **secondary**: in presence of underlying disease (COPD, asthma, CF, interstitial lung disease) * **Tension Pneumothorax**: penetrating injury → air into pleural space increased and unable to escape * S/sxs: **acute onset** ipsilateral chest pain and **dyspnea** * non-exertional, sudden * PE: decreased tactile fremitus, deviated trachea, hyperresonance, diminished breath sounds * _tension pneumo_: **mediastinal shift** to the contralateral side and impaired ventilation, **increased JVP, systemic hypotension** * Dx: * CXR: pleural air * ABG: shows hypoxemia * Tx: depends on size * \<15% (small)= will resolve **spontaneously** * **can also do high flow 100% oxygen** * \>15% (large) and symptomatic = **chest tube placement** * need to do **serial CXR every 24 hours** until resolved * _tension pneumo_: * MEDICAL EMERGENCY!!! large bore needle to allow air of the chest + chest tube for decompression * Pt Education: * avoid pressure changes 2+ weeks

Answer 210

Right Ventricular enlargement → eventually leads to R heart failure secondary to a lung disorder that causes pulmonary HTN * Etiology: * COPD (most common), pulmonary embolism, vasculitis, asthma, ARDS * S/sxs: * worsening dyspnea, purulent sputum production, inspiratory crackles, ventricular gallop * PE: lower extremity edema, JVD distention, hepatomegaly, parasternal lift * tricuspid/pulmonic insufficiency **loud S2** * EKG: **S1Q3T3** * \*\*\*\*occurs after pulmonary HTN\*\*\*\*\* * Dx: tx the underlying condition b4 the cardiac structure change becomes irreversible * **diuretics are not helpful and MAY BE HARMFUL!**

Answer 211

obstruction of pulmonary blood flow due to a blood clot (usually thrombosed from a DVT) * Risk Factors: **Virchow's Triad:** 1. Damage (trauma, infx, inflammation) 2. Stasis: immobilization, surgery, prolonged sitting \> 4 hours 3. hypercoagulability: protein C or S deficiency, factor V leiden mutation, Oral contraceptive pills, malignancy, pregnancy, smoking * S/sxs: Classic Triad: * **dyspnea, pleuritic chest pain,** hemoptysis (classic but rare), cough * PE: Tachypnea (most common sign), tachycardia, low-grade fever, lung exam = normal * if large PE = syncope, hypotension, pulseless electrical activity * Dx: **helical (spiral) CT angiography** * _pulmonary angiography_ = GOLD STANDARD (may order if high suspicion and negative CT or VQ scan) * D-Dimer or ABG = respiratory alkalosis secondary to hyperventilation * _Westermark sign_: avascular markings distal to PE * _Hampton hump_: wedge-shaped infiltrate due to infarction * **atelectasis** = most common abnormal finding * Tx: **Heparin** and **oral direct thrombin inhibitors** (_dabigatran_)

Answer 212

blood pressure in lungs is usually **very low** (15/5) pulmonary HTN → \>25mmHg usually caused by underlying disorder: constrictive pericarditis, mitral stenosis, L ventricular failure * Risk Factors: middle-aged or young women (mean age = 50), **BPMR2 gene defect** → usually inhibits pulmonary vessel smooth muscle growth and vasoconstriction * S/sxs: * dyspnea on exertion, fatigue, chest pain, edema * PE: **loud pulmonic component of S2 due to prominent P2,** may have a fixed or paradoxically split P2 * signs of R heart failure: * JVD, ascites, hepatojugular reflux * lower limb edema * pulmonary regurg, R ventricular heave, systolic ejection click * Dx: **R heart catheterization** = _GOLD STANDARD_ * CXR: enlarged pulmonary arteries, lung fields may not be clear, depends on underlying cause * **Echocardiogram**: increased pressure in pulmonary arteries, Right ventricles→ dilated pulmonary artery, dilation/hypertrophy of R atrium/ventricle * **ECG**: right heart strain pattern: T-wave inversion in R precordial leads (V1-4), and inferior leads (II, III, aVF) **cor pulmonale** * Tx: * identify and tx underlying cause * heart-lung transplant = definitive

Answer 213

scarring of the lungs due to unknown cause \*\*\*most common in men \>40, smokers\*\*\* * S/sxs: Worsening dyspnea, non-productive (dry) cough * PE: fine, dry, bibasilar inspiratory crackles * clubbing of fingers * Dx: * CXR: **basal predominant reticular opacities _(honeycombing)_** * Chest CT: Preferred imaging\*\*\*\* **reticular honeycombing, focal ground-glass opacifications**, bronchiectasis * PFTs: **demonstrate a restrictive pattern** (opposite of asthma) * → decreased lung volume with a normal or increased FEV₁/FVC * Tx: lung transplant → only cure

Answer 214

lung disease caused by asbestos Occupation: insulation, demolition, construction, shipworker * S/sxs: dyspnea **on exertion**, cough * PE: bibasilar crackles * **restrictive lung pattern**: normal or increased FEV₁/FVC, normal or decreased FVC, decreased lung volume (shifted to the R on loop) * Dx: * CXR: * reticular **linear pattern** with **basilar predominance, opacities**, and **honey combing** * “**shaggy heart sign**” ground glass obscures the heart * Biopsy: may show **linear asbestos bodies** * Tx: no therapy → bronchodilators, O₂, corticosteroids, +/- lung transplant * \*\*\*can progress to bronchogenic carcinoma or mesothelioma\*\*\*

Answer 215

aka black lung disease occurs when coal dust is inhaled and leads to scarring in the lungs * S/sxs: dyspnea, cough, fine crackles * **caplan syndrome**: coal worker pneumoconiosis + RA (serologically positive) * PE: bibasilar crackles * **restrictive lung pattern**: normal or increased FEV₁/FVC, normal or decreased FVC, decreased lung volumes * Dx: * CXR: **small nodules** especially in the **upper lung fields** with hyperinflation of the lower lobes in an obstructive pattern (looks like emphysema) * _Lung Biopsy_: show dark “black” lungs (not needed for diagnosis) * Tx: supportive care

Answer 216

inhalation of silicone dioxide Risk factors: quarry work with **granite, slate, quartz**, pottery, sandblasting, glass, etc * s/sxs: * acute: dyspnea, cough, weight loss, fatigue * chronic: often asymptomatic, dyspnea on exertion, non-productive cough, crackles * Dx: many small (\<10mm) round nodular opacities (**miliary papttern**) mostly in the upper lobes * **_eggshell calcification_** of hilar and mediastinal nodes * bilateral nodular densities that progress * Tx: removal from exposure= MAINSTAY * nonspecific management: corticosteroids, O₂, rehab

Answer 217

granulomatous pulmonary disease caused by exposure to beryllium used for aerospace material→ high risk: ceramics, tool and dye manufacturing, jewelry making, fluorescent light bulbs * S/sxs: dyspnea, cough, joint pain, fever weight loss * Dx: * CXR: hilar lymphadenopathy, and increased interstitial lung markings (looks like sarcoidosis) → diffuse infiltrates * tx: chronic corticosteroid use * oxygen * methotrexate if corticosteroids do not work * **associated with risk of lung, stomach, and colon cancer**

Answer 218

unknown cause, chronic multisystem inflammatory **granulomatous disease** (exaggerated T-cell response to antigens or self-antigens that leads to central immune system activation, granuloma formation, and peripheral immune depression) Risk factors: female, African American, N. Europeans, age 20-40 * S/Sxs: dry cough, dyspnea, chest pain, and crackles * affects lymph nodes as well * may have abnormal masses or nodules (granulomas) * PE: * **erythema nodosum (**classic), **lupus pernio**, maculopapular rash, anterior uveitis, restrictive cardiomyopathy, arrhythmias, heart block * Dx: serum blood tests show: **hypercalcemia** and **ACE levels x4 normal** * ESR = elevated * CXR: Bilateral hilar lymphadenopathy * _Diagnosis_: biopsy of peripheral lesion or fiber-optic bronchoscopy for central pulmonary lesion * PFTS: **restrictive pattern** * Tx: * Symptomatic pts: CORTICOSTEROIDS (1mg/kg **prednisone)** **methotrexate** and other immunosuppressive meds * **ACE inhibitors** for periodic HTN * → leading cause of death = pulmonary fibrosis

Answer 219

intermittent obstructive airflow → results in periods of apnea at night Risk factors: OBESITY!!! structural abnormalities of the upper airway, family hx, alcohol/sedatives/opiates, hypothyroidism * S/sxs: * SNORING and **daytime sleepiness**! caused by disrupted nocturnal sleep * personality changes: poor mood and mental dysfunction * **morning headaches**, polycythemia * can lead to systemic and pulmonary HTN and **Afib** * Diagnosis: * **Polysomnography = GOLD STANDARD** * can also do home sleep apnea testing but rarely covered by insurance * _Obesity-Hypoventilation Syndrome_: -obesity (\>30BMI), -awake alveolar hypoventilation PaCO₂\>45mmHg, -alternative causes of hypercapnia and hypoventilation ruled out * Tx: * WEIGHT LOSS, exercise, avoiding alcohol/sedatives, and not sleeping supine * **oral appliances** → mild to moderate * → **BiPAP** or **CPAP** * **Uvulopalatopharyngoplasty (UPPP) →** remove extra tissue from oropharynx * **tracheostomy**

Answer 220

type of **respiratory failure** that is **fluid collection in the lungs** and prevents exhange of O₂ * usually occurs in **critically ill** or someone with **significant injuries** * S/sxs; **rapid onset** of _sever dyspnea_ occurring 12-24 hours after a precipitating event * PE: tachycardia, **pink, frothy sputum**, diffuse crackles * Dx: sxs develop within 1 week, bilateral diffuse infiltrates on CXR (not explained by congestive heart failure) * CXR: shows **air bronchograms & bilateral fluffy infiltrate** * tx: * identify and tx underlying cause * tracheal intubation

Answer 221

ssRNA hemagluttinin and neuraminidase tx: neuraminidase inhibitors vaccines: target hemagluttinin Type A = most common Type B= humans only Type C = nonsymptomatic, little medical concern SHIFT vs DRIFT

Answer 222

* Histoplasma * S**ystemic fungi and mold → yeast at 37C** * inhalation from bats/ birds: CAVES and TREE REMOVAL * acute pneumonia sometimes developes * infect Macrophages * bone marrow disruption * apical pulmonary lesions resembling cavitary TB * tx: **itraconazole**

Answer 223

* **yeast** that can end up in the brain but is inhaled! * \*\***Defining opportunistic infection in aids patients**\*\* * skin lesions that look similar to acne, molloscum contagiosum, or basal cell carcinoma * CNS: low grade fever, ocular or facial palseys, headache * Lungs: pneumonia, AIDS (severe dyspnea) tx: **Fluconazole for non CNS, CNS: amphotericin B**

Answer 224

* yeast: pneumocystis jirovecii * \*\*only issue for immunocompromised people\*\* * aerosolized: fever, dyspnea and DRY cough tx: **Bactrim (sulfamethoxazole/trimethoprim )** high risk for HIV pts with CD4 counts \<200/mcL

Answer 225

* gram + diplococci, ENCAPSULATED * causes pneumonia: * rusty mucus * productive cough * fever * malaise * sudden onset chills and rigors (violent shaking) * causes: bacteremia and meningitis * tx: **Ceftriaxone**

Answer 226

most common cause in adults: **Influenza;** most common cause in children **RSV, Parainfluenza virus** * S/sxs: **persistent** sxs of sore throat, HA, myalgias, malaise for **more than 3-5 days** then **_new respiratory sxs_** _-→_ dyspnea, cyanosis * Dx: CXR: **bilateral lung involvement with interstitial infiltrate** * Rapid antigen test for influenza * _RSV_ nasal swab * _cold agglutinin titer_ to r/o Mycoplasma (should be negative with this) * Tx: flu → oseltamivir, zanamivir * RSV → **Ribavirin**

Answer 227

most common cause in adults: **Influenza;** most common cause in children **RSV, Parainfluenza virus** * S/sxs: **persistent** sxs of sore throat, HA, myalgias, malaise for **more than 3-5 days** then **_new respiratory sxs_** _-→_ dyspnea, cyanosis * Dx: CXR: **bilateral lung involvement with interstitial infiltrate** * Rapid antigen test for influenza * _RSV_ nasal swab * _cold agglutinin titer_ to r/o Mycoplasma (should be negative with this) * Tx: flu → oseltamivir, zanamivir * RSV → **Ribavirin**

Answer 228

**reversible** chronic, inflammatory airway disease → recurrent attacks of breathlessness and wheezing that affects the trachea to the terminal bronchioles * caused by **mast cell mediators** * diminished FEV₁ that is improved with inhaler * s/sxs: dyspnea, wheezing, cough, chest tightness (NOT PAIN) * worse at night * increased mucus production * PE: wheezing, prolonged expiratory phase * Diagnosis: * **GOLD STANDARD**: FEV₁/FVC \< 75-80% in adults, below 85% in children * \>12% increase in FEV₁ after bronchodilator * exhaled nitric oxide = can be used to measure eosinophilic airway inflammation * if pt \<5 yo = RAD, not asthma * GINA guidelines

Answer 229

**_Autosomal Recessive Disorder_** mutation in the CFTR gene → abnormal production of mucus by most exocrine glands → pulm infx most common cause of death (staph and HIB acute, chronic = pseudomonas) * lungs normal at birth then begin to develop pulmonary disease often during infancy or childhood * _infancy_: **meconium ileus**, failure to thrive (FTT), diarrhea from malabsorption (can lead to rectal prolapse) * _pulmonary:_: CF = **most common cause of bronchiectasis in the US** (dilation and destruction of the bronchi due to chronic infx and inflammation * PE: rhonchi and crackles * CXR may show hyperinflation, mucus pluggung and focal atelectasis * Dx: elevated sweat chloride test on **two different days** * use pilocarpine → NaCL \>60mEq/L * Tx: **CFTR genotyping** to see if they are approved for CFTR modulator therapy * hypertonic saline and chest physiotherapy → clears the secretions from the airways * tx infections * replacement of pancreatic enzymes: **supplement fat-soluble enzymes (A, D, E, K)**

Answer 230

usually lodges in the larynx or trachea can lead to chronic, recurrent infx if left for a while→ PNA, ARDS, asphyxia * Risk factors: \>85 yo, \<2 yo, poor dentition, alcohol use, sedative use, institutionalization * S/sxs: Inspiratory stridor * Dx: CXR first * tx: rigid bronchoscopy = preferred for children * soft or rigid bronchoscopy for adults * surgical removal * Cxs if PNA is suspected

Answer 231

aka Hyaline membrane disease * affects **preterm infants** when they have not produced enough **surfactant** → poor lung compliance and atelectasis * \*\*\*most common cause of respiratory distress in pre-term infants\*\*\* * Risk factors: caucasion, male, multiple births, maternal diabetes * S/sxs: * respiratory distress at birth (tachypnea \>60 /min, tachycardia, chest wall retractions, grunting, nasal flaring, cyanosis) * Dx: CXR: diffuse bilateral atelectasis that cause a **ground glass appearance** and air bronchograms * Tx: * antenatal steroids within 24-48 hours of birth → **betamethasone IM x 2** * **artificial surfactant** via ET tube * mechanical ventilation with positive pressure

Answer 232

chronic widening or enlargement of the bronchi and their branches → increased risk of infection

Answer 233

furosemide, bumetanide, torsemide * inhibits water, Na, K, Cl transport * inhibits Ca and Mg absorption across the thick ascending limb in the loop of henle * causes dilute urine * increased prostaglandin synthesis -→ improves renal blood flow * Indication: * HTN, edema (pulmonary, peripheral edema due to CHF, nephrotic syndrome, and cirrhosis), hypercalcemia, hypermagnesemia-→does not cause hyponatremia -→ loose more water than salt * SEs: * **decreased electrolytes (**hypoK, hypoCa, HypoMg, HypoCl) * **hyperglycemia, hyperuricemia** (can precipitate gout) * NSAIDs may decrease efficacy * ContraIndicated in pt with sulfa allergy

Answer 234

* hydrochlorothiazide, chlorthalidone, chlorothiazide * MOA: block NaCl reabsorption at the **early distal convoluted tubule (diluting segment)** * leads to diuresis and inability to produce a dilute urine * electrolyte imbalances caused by thiazide diuretics: * **hyponatremia** * **hypokalemia** * **hypercalcemia**

Answer 235

aka Vitamin D * increased absorption of calcium and phosphorous in gut

Answer 236

hypercalcemia, hypophosphatemia

Answer 237

hypocalcemia, hypophosphatemia

Answer 238

* Causes: renal losses-→ HyperPTH * GI: severe malnutrition, malabsorption, alcoholism, phosphate binders * S/sxs: Muscle weakness, bone pain, rickets, osteomalacia * tx: mild or moderate: milk, sodium, or K-phosphate tablets * SEVERE = \<1mg/dL → IV phosphorus replacement

Answer 239

* causes: CKD, AKI, hypoPTH, tissue breakdown: rhabdomyolysis, hemolysis, tumor lysis (these are problems that cause hypocalcemia as a result of hyper K) * tx: management in CKD: low phosphorus diet, phosphate binders, dialysis

Answer 240

* causes: in CKD, Mg containing antacids, enemas, epsom salts, magnesium citrate, milk of magnesia * iatrogenic: pre-eclampsia * Sxs: **Mg = vasodilator** * levels \> 4-6 mg/dL: hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus * levels \> 8-12: flaccid paralysis, respiratory arrest, cardiac arrest * Tx: Mild: d/c mg supplements * severe: IV calcium (to protect heart), saline diuresis (to flush excess Mg), furosemide * Dialysis

Answer 241

chemo drug “punches holes” in renal tubules → hypoK and hypoMg

Answer 242

* Causes: polyuria from osmotic diuresis, DKA, AKI, **PPIs**, **diuretic use** * extracellular volume expansion: reduced Na and H20 reabsorption in PCT, so less passive Mg reabsorption * Hypercalcemia = reduced Mg reabsorption * Drugs: Cisplatin, aminoglycosides, amphotericin B * S/sxs: * _cardiac_: repolarization abnormalities, ventricular arrhythmias * _Neuromuscular_: tremor, twitching, tetany, seizures, migraine * \*\*\*can cause unexplained **hypocalcemia** (due to impaired PTH secretion) **and hypokalemia** (due to released inhibition of ROMK channel so increased distal K secretion\*\*\* * Tx: * _Severe_: Mg levels \<1mg/dL * 1-2 grams of Magnesium sulfate * **can cause diarrhea** * _minimal or no sxs_: * oral repletion (diarrhea side effect) * preferred: sustained release Magnesium chloride * **Amiloride = prevents Mg wasting**

Answer 243

prevents Mg wasting reduces renal Mg excretion by increasing its reabsorption in the distal nephron Mg repletion in CKD or AKI = half dosage with close monitoring

Answer 244

* due to **volume loss**, **heart failure**, or **loss of peripheral vascular resistance** → all lead to loss of perfusion in kidneys * NSAIDs also can cause this (vasoconstriction of the afferent arteriole) * ACEI and ARB block effect of angiotensin (vasodilation of the efferent arteriole) * Diuretics * \*\*\***Kidneys are working fine, the organs that perfuse the kidneys arent working properly\*\*\***

Answer 245

* _S/sx_: weak oliguria (decreased urine output), dizziness, sunken eyes, tachycardia, orthostatic BP changes * _Dx_: **BUN:Cr \> 20:1**, urine osmolality \> 500, FeNa \<1%, FeUrea \<35%, **Urine Na \<20 mEq/L** * _Tx:_ tx with fluids, cardiac support, and/or tx shock

Answer 246

* Risk: * GFR: increased SCr x 1.5 or GFR decrease greater than 25% * UO (urine output): \<0.5 ml/kg/h x 6 hours * Injury: * GFR: increased SCr x 2 or GFR decrease greater than 50% * UO: \< 0.5mL/kg/h x 12 hours * Failure: * GFR: increased SCr X 3, GFR decrease by 75% * OR SCR \>4mg/dL * UO: \< 0.3mL/kg/h x 24 hours or anuria x 12 hours * **LOSS:** persistent AKI = complete loss of kidney function \> 4 weeks * **ESKD**: greater than 3 months

Answer 247

* _Stage 1_: Absolute SCr: ≥ 0.3mg/dL * % SCr: 150-200% (1.5-2x) * UO: \<0.5mL/kg/hr x 6 hours * → no need for renal replacement therapy * _Stage 2_: % SCr: 200-300% (2-3x) * UO: \<0.5mL/kg/hour x 12+ hours * → no need for renal replacement therapy * _Stage 3_: Absolute SCr: ≥ 4mg/dL with an acute increase of at least 0.5mg/dL * %SCr: 300% + (≥ 3x) * UO: \<0.3mL/kg/hr x 24 hours or anuria x 12 hours * → need for renal replacement therapy indicates stage 3 regardless of serum creatinine or UO

Answer 248

* _Etiology_: obstruction (**most common = prostate**), bilateral outlet obstruction or bilateral ureteral obstruction * _S/sxs_: oliguria or anuria +/- **suprapubic pain** * _Dx_: foley catheter placement to find source of obstruction * if large urine output after foley = bladder, urethra, BPH * if low urine output after foley = ureter obstruction or pathology * **Renal U/S** but **CT is most specific!!** * _tx_: removal of obstruction → if done rapidly = quick reversal of AKI

Answer 249

* \*\*\*Type of Intrinsic AKI\*\*\* * _Etiology_ = kidney ischemia or toxins * **prolonged pre-renal AKI = most common cause** * _Major Causes_: * **drugs and toxins:** ampho B, cisplatin, sulfa drug, aminoglycosides, radiocontrast media, NSAIDs, ACEI, cocaine use * **ischemic related ATN** : dehydration, shock, sepsis, hypotension * **endogenous toxins**: heme from hemolysis, myoglobin from rhabdomyolysis (iron is myoglobin is toxic to renal epithelial cells), tumor lysis syndrome, muscle breakdown in a marathon runner

Answer 250

* _S/sxs_: Oliguria, increased SCr etc * _Dx_: urinalysis = **muddy brown casts** (renal tubule epithelial cells), myoglobinuria, hemoglobinuria * **FeNa \>2%**, FeUrea \>35%, Urine Osmolality \<350 * _Tx:_ **remove toxin** or **re-perfuse kidney** via IV fluids * can use loop diuretics if pt is euvolemic and not urinating * \*\*\*most pts return to baseline within 7-21 days \*\*\*

Answer 251

* _Etiology:_ **immune-related response** * due to: * **drugs**: PCN, sulfa (bactrim), NSAIDs, phenytoin, Diuretics, etc * **immunologic & infx disease**: strep (get an ASO antibody), SLE, CMV, Sjogren's, sarcoidosis

Answer 252

* \*\*\*type of intrinsic AKI\*\*\* * _S/sxs_: oliguria, increased SCr * _Dx_: **urinalysis = WBC cats, WBCs, and eosinophils** * acute azotemia (accumulation of nitrogenous waste, BUN) * **diagnosed with RENAL BIOPSY** → interstitial inflammatory cell infiltrates * _Tx_: d/c offending drug, **corticosteroids, dialysis PRN** * → usually self-limiting if caught early * most people recover kidney function within 1 year

Answer 253

* glomerular damage results in **higher loss of proteins in the urine** * _Most common_ **_primary_** _causes_: * **membranous nephropathy**: most common in non-DM adults associated with *malignancy* * **MINIMAL CHANGE DISEASE**: most common cause in children, idiopathic nephrotic syndrome sxs improve after tx * **focal segmental glomerulosclerosis**: obese pts, heroin, and HIV (+) black males * _Most common Secondary Cause:_ * **lupus** * **DM**

Answer 254

* _S/sxs_: peripheral or **periorbital edema**, ascites, weight gain, fatigue, and HTN, **_frothy urine_** * _Dx_: serologic testing and renal biopsy * **proteinuria \>3.5g/day = diagnostic** ( 24h urine collection) * _urinalysis_: **free lipid or oval fat bodies** or **fatty casts** → lipiduria * **Hypoalbuminemia** \< 3.5g/dL * **hyperlipidemia** LDL \> 130mg/dL, Triglycerides \> 150mg.dL * _Tx_: * tx the causative disorder, **corticosteroids**

Answer 255

* inflammation of the glomeruli due to blockage from immune complexes → **immune response causes this** * _Post-Infectious Group A strep_ → diagnosed with **ASO titers** and low serum complement * _IgA Nephropathy_ **_(berger disease_**_)_: *Most common cause of acute glomerulonephritis* * young males **after URI or GI infx** (within 24-48 hours) → IgA immune complexes are first line defense in respiratory/GI secretions so infx → overproduction which damages the kidneys * more common in asian population * _Membranoproliferative Glomerulonephritis_: caused by SLE, viral hepatitis (Hep C) * secondary to **immune-complex deposition** or **complement mediated mechanism**

Answer 256

* _S/sxs_: edema + HTN + hematuria + **RBC casts**, jaundice, HTN * _Dx_: urinalysis = **hematuria \>3 RBCs/HPF + RBC casts + proteinuria (1-3.5g/day)** * ASO titer for post-strep * **serum complement = decreased** (not always * **RENAL BIOPSY = GOLD STANDARD** * _Tx:_ steroids and immunosuppressive drugs to control inflammation due to immune response * dietary management = salt and fluid restrictions * **Dialysis if symptomatic azotemia** * **ACEI/ARBs (enalapril** or **losartan**) are renoprotective → BP goal \<130/80 * use meds to control hyperkalemia

Answer 257

Chronic Kidney Disease * Stage 1: **Normal** GFR ≥ 90mL/min/1.73m2 * either persistent albuminuria or known structural or hereditary renal disease * Stage 2: **Mild** GFR 60-89 mL/min/1.73m2 * Stage 3: **Moderate** GFR 30-59 mL/min/1.73m2 * Stage 4: **Severe** GFR 15-29 mL/min/1.73m2 * Stage 5: **Kidney Failure** GFR \< 15mL/min/1.73

Answer 258

dx: **GFR \< 60mL/min/1.73m2** for **3 months** or any of the following: * _albuminuria_: urine albumin: creatinine ratio **\>30mg/day** * _proteinuria_: urine protein: creatinine ratio **\> 0.2** * _hematuria_ * _structural renal abnormalities_ ( solitary kidney, hx of abnormal renal histology hx of renal transplant)

Answer 259

* Diabetes = **MOST COMMON CAUSE (30%)** * HTN (25%) * chronic glomerulonephritis (15%) * interstitial nephritis, polycystic kidney disease, obstructive uropathy

Answer 260

* **Pruritus = common**, but difficult to tx * _Cardio_: HTN → caused by salt and water retention → decreased GFR = stimulation of RAAS → increased BP → CHF due to volume overload, HTN, anemia → pericarditis * _GI_: (usually due to uremia) nausea, vomiting, loss of appetite * _Neuro_: lethargy, confusion, tetany → (due to **hypocalcemia**), uremic seizures, peripheral neuropathy * _Heme_: normocytic, normochromic anemia (secondary to **deficiency of erythropoietin**) * bleeding secondary to platelet dysfunction→ platelets **do not degranulate in _uremic environment_** * _Endo/Metabolic_: * Ca²⁺/Phosphorus disturbances→ decreased renal secretion of phosphate leads to **hyperphosphatemia** → decreased production of 1,25-dihydroxy vitamin D → **hypocalcemia** → **hyperparathyroidism** * hyperkalemia → decreased secretion and **acidosis** * _Fluid & Electrolyte problems_: * **volume overload**: watch for pulm edema * **hyperkalemia**: due to decreased urinary secretion * **hypermagnesemia**: secondary to reduced urine secretion * **hyperphosphatemia**: decreased clearance of phosphate * **metabolic acidosis**: due to loss of renal mass (& therefore decreased ammonia production) & kidneys' inability to secrete H⁺

Answer 261

* Dx: **GOLD STANDARD = GFR** * _urinalysis_: **waxy casts, or granular casts** → show dilation and hypertrophy of remaining nephrons * _Proteinuria_ * elevated _BUN & creatinine_ * **hyperphosphatemia & hypocalcemia** * low **_erythropoietin levels_** (due to loss of renal function) * Tests to order: CBC, chem panel (CMP), iron studies, lipid profile, urinalysis

Answer 262

* Tx: **ACEI and ARBs** → slow progression of renal dysfunction * manage the comorbidities!! : control HTN, glycemic control (A1C 6.5-7.5%), cholestrol control, tobacco cessation * **Maintain HGB at 11-12 g/dl** → Do not want to bring pt up to normal hgb levels → pro-thrombotic b/c it thickens the blood & increases mortality * **Dietary management**: protein restriction, calcium and vitamin D supplements, limit water, sodium, and potassium and phosphorus * **Need for hemodialysis or kidney transplant** * **PCV-23** * Fluid overload management: dietary salt \<2 gm/day * **GFR \> 30** → thiazide diuretics (hydrochlorothiazide, chlorthalidone) * **GFR \<30** → loop diuretics (furosemide, torsemide, bumetanide) * can use phosphorus binders to reduce hyperPTH → **calcium carbonate, calcium acetate, sevelamer, lanthanum, iron** * tx the acidosis: may reduce risk of CKD progression → NaHCO3- → goal bicarb level \>22

Answer 263

caused by secondary hyperPTH often as a result of CKD * increased phosphate due to decrease in secretion in kidneys → decreases production of 1,25-dihydroxy vitamin D (Calcitriol) → hypocalcemia → hyperparathyroidism * body then break down bones to increase serum calcium

Answer 264

* Urinary Tract obstruction that leads to the collecting system in one or both kidneys to **dilate** * _Etiology_: kidney stones (uretral), tumors, bladder outlet obstruction (BPH or prostate cancer) and sloughed off renal papillae * _S/sxs_: * usually asymptomatic * can have change **in urine output (_Difficulty urinating/hesitancy)_, HTN, hematuria**, and CVA tenderness, pain in the side, abdomen, or groin * _Dx_: * UA→often benign but may show hematuria or elevated pH * may have a **palpable abdominal or flank mass** caused by an enlarged kidney * Labs: may have increased serum creatinine * U/S: **initial imaging that you should do → will show dilation of the collecting system in one or both kidneys** * CT Scan: indicated for those with flank pain and suspected nephrolithiasis or in pts whom visualization of the ureters is needed * _Tx_: * **Removal of obstruction** → rapidly reversible if removed quickly, can lead to UTIs and possible ESRD

Answer 265

**Autosomal Dominant** → mutations of *PKD1* or *PKD2* → causes 10% of ESRD * _formation & enlargement of kidney cysts_ (cysts also common in the liver (most common), then spleen and pancreas * _Pathophys_: * vasopressin (ADH) stimulates cytogenesis and eventually leads to ESRD over time * _S/sxs_: **renal → abdominal pain & flank pain**, nephrolithiasis, UTI and hematuria * ~10% of pts **have brain aneurysms** (so be concerned about headache complains) * **abdominal fullness** * mitral valve prolapse and L ventricular hypertrophy * _Dx_: **U/S → shows fluid filled cysts**, CT scan will show large renal size and thin walled cysts * **need to U/s rest of direct family members** * _Tx_: no cure, only supportive to ease sxs * control HTN \<130/80 with use of **ACE-I & ARBs** * infx should be treated quickly/vigorously with abx * dialysis or transplant should be considered when renal insufficiency becomes life threatening

Answer 266

aka renovascular HTN * **HTN caused by renal artery stenosis** in one or both kidneys * \*\*\*MOST COMMON cause of _secondary HTN_\*\*\* * _Pathophys_: decreased renal blood flow leads to activation of RAAS * _Etiologies_: **atherosclerosis** = most common in elderly, **fibromuscular dysplasia** = most common cause in women \<50 * _S/sxs_: * suspect in pts with **headache & HTN \<20 years** * or **\>50 years, severe HTN** or **HTN** resistant to 3+ drugs * or **abdominal bruits** * or it pt develops **AKI after the initiation of ACE-I therapy** * _Dx_: * non-invasive option: **CT angiography**, MR angiography, Duplex doppler (duplex doppler = less sensitive, specific) * **Renal Catheter Arteriography = GOLD STANDARD and definitive** → revascularization can be performed during the same procedure if stenosis is found (not used in pts with renal failure) * _Tx_: * **Revascularization = definitive management** * **angioplasty with stent** → performed if creatinine \>4.0, increased creatinine with ACE-I tx, or \>80% renal stenosis * Bypass if angioplasty is not successful * Medical Management: * **ACE-I or ARBs** (BUT these are contraindicated in pts with bilateral stenosis or solitary kidney b/c can cause AKI due to ischemia

Answer 267

End Stage Renal Disease * Stage 5 CKD → GFR \<15, complete loss of kidney function for more than 3 months * **Most Common Cause = DM** * _Dx_: * **GFR \<15mL/min/1.73m2 for ≥3months** * low EPO levels * metabolic acidosis * **increased potassium, phosphate, and PTH** * **low calcium, sodium, bicarb** * “_Waxy” cats_ **with low urine flow** * _Tx_: * **Dialysis & kidney transplant** * Manage co-morbidities: * bring HGB up to 11-12 (no higher or else possibility of clots) * **dietary management**: protein restrictiion, Calcium and Vitamin D supplements, limit water, sodium, potassium, and phosphorus * **ACE-I & ARBs** = slow progression of renal dysfunction * **Loop diuretics**: preferred addition to the management of edema associated with HTN due to ESRD * **Pneumococcal vaccine**

Answer 268

End stage renal disease * _S/sxs_: * **pruritus** * **HTN,** may have A/B nicking, copper wire changes on retina * **S4 heart sound** * Kidneys affected by ESRD cannot regulate levels of electrolytes → **sodium excess** = retention of water * **potassium excess** = abnormal heart rhythm, can lead to cardiac arrest * **magnesium deficit** = can affect heartbeat and cause changes in mental state * _Hormones_: cannot absorb calcium and bones become weak and may break (**renal osteodystrophy)** * **erythropoietin production decrease** = normochromic, normocytic anemia * _Enzymes_: kidneys affected by ESRD respond to lower GFR by making too much renin → keeps blood pressure levels high → difficult to tx

Answer 269

* shortened QT * ST depression * Peaked T wave

Answer 270

* decreased T-wave amplitude * ST depression * increased U-wave amplitude

Answer 271

* _Urine potassium \< 20mmol/L_ * metabolic acidosis: diarrhea, laxative * _Urine potassium \> 20 mmol/L_ * *metabolic acidosis*: * proximal RTA, or distal RTA * *Metabolic Alkalosis + Normal or Low BP* 1. Low urine chloride (**\<20)** 1. vomiting 2. High Urine Chloride **(\>20)** 1. Lasix 2. thiazide 3. Mg depletion 4. Bartter's 5. Gitelman's * *Metabolic Alkalosis + High BP* * increased renin + increased aldosterone: * renal artery stenosis or renal tumors * decreased renin + increased aldosterone * primary aldosteronism * decreased renin + decreased aldosterone * Cushings * liddles * apparent mineralocorticoid excess (licorice, drugs) * MR mutation

Answer 272

**identify and tx underlying causes** * NaHCO₃^- indicated when: * **renal dysfunction**→ not enough HCO3- is regenerated * **Severe acidemia:** pG \<7.10 * goal: increase HCO3- by 10mEq/L; and ph\> 7.2 * **½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours** * \*\*\*\*1mEq/kg/dose and monitor\*\*\*

Answer 273

used to treat metabolic acidosis * can be used with loop diuretics to avoid too much fluid (fluid overload) * indicated when: * **renal dysfunction** → not enough HCO3- regenerated * **severe acidemia**: pH\<7.10 * **½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours** * **one amp is 50mL (or 50mEq)** * **can give up to 3 amps + 1L D5W**

Answer 274

used to tx metabolic acidosis * helpful when the acidosis is coupled with hypoK+ * **be cautious with renal impairment → needs to be avoided if pt has hyperK+ (can cause increased HyperK+)**

Answer 275

* pts rarely have symptoms due to alkalemia * sxs often related to volume depletion * muscle cramps * dizziness depending on position * HypoK+ → muscle weakness, polyuria, polydipsia * **Tx**: **tx the underlying cause** * i.e. meds, **citrate** containing products (K-citrate used to tx metabolic acidosis), or acetate in parenteral nutrition → causes HCO3- levels to rise * alkalosis caused by vomiting, NG suction, or diarrhea +/- urinary Cl- (\<25mEq/L) → **saline infusion** * **acetazolamide** (carbonic anhydrase inhibitor) → reduces HCO3- concentration * \*\*\*\*\*\***Hemodialysis** or **HCl infusion** for life-threatening metabolic alkalosis\*\*\*\*\*\*

Answer 276

represents ventilation failure or impaired control of ventilation * hypoxemia + hypercapnia * severe, acute respiratory acidosis = * HA, blurred vision, restlessness and anxiety, tremors, somnolence, and/or delirium * Tx = identify cause and tx that: * opiate/opioids → **naloxone** * acute bronchospasm/asthma → bronchodilators * assisted ventilation and mod-severe acidosis → BiPAP * NOTE: NaHCO3 may actually worsen acidemia due to increased CO2 generation so do NOT use this * Goals: * careful monitoring of pH * maintain oxygenation * improve alveolar ventilation

Answer 277

represents hyperventilation * sxs: irritability of central and peripheral nervous system * light headedness, altered consciousness, cramps, syncope * s**evere cases: HypoPhos** shifts from ECF to ICF * tx: identify cause and tx accordingly * f**or mild-moderate** severity in spontaneously breathing pts → no specific tx * **severe alkalosis**: * rebreathing * rebreathing mask, or paper bag * mechanical ventilation * high level sedation or paralysis is a good option

Answer 278

Na+, Cl-, HCO3-

Answer 279

K+, Mg2+, PO₄^2-, SO₄^2-

Answer 280

* at least 1-2 L of NS as rapidly as possible (bolus) * restores tissue perfusion * fluid replacement is continued at rapid rate until clinical signs of hypovolemia improve

Answer 281

* *Hypernatremia = \>145 Na+* * **Hypovolemic Hypernatremia** * **loss of water \>\>\>\>\> sodium** * *Isovolemic Hypernatremia* * *water loss only* * **Hypervolemic Hypernatremia** * **body has excess sodium and water** * **sodium \>\>\>\>\>\>water**

Answer 282

NSAIDs reduce renal prostaglandins and prostaglandins inhibit the action of ADH so NSAID use can increase action of ADH and cause increased water reabsorption

Answer 283

synthetic analogue of ADH Act on V2-receptors at the collecting duct → reabsorption of water used to tx central diabetes insipidus → the underlying pathophys behind isovolemic hypernatremia

Answer 284

When to tx? \<3.5 mEq/L and/or pt is symptomatic * treatment: * oral: **K-chloride, KPO₄, K-acetate, K-citrate, k-gluconate** * IV: if \>10 mEq/L should be monitored via telemetry * other: diuretic induced (**spironolactone- K+ sparing diuretic**) * correct hypomagnesemia * \*\*\*\*low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently\*\*\*\*\* * correct acid-base imbalance

Answer 285

* _Symptomatic (urgent/emergent_) * **IV calcium** to stabilize the heart membrane * **insulin +/- glucose/dextrose** to temporarily push K+ back into the cell * **albuterol** to also temporarily push K+ back into the cell * **Sodium bicarb** to be considered to tx acidosis * **Eliminate Source**: IV, total parenteral nutrition (TPN), tube feeds, oral supplements, K sparing diuretics * _Symptomatic_: * **sodium polystyrene sulfonate (Kayexelate)** → binds potassium, slower onset, but duration of 4-6 hours (constipation though…) * **Loop diuretics** (lasix) * _Asymptomatic_; * eliminate source * kayexelate (sodium polystyrene sulfonate) → binds potassium * loop diuretics

Answer 286

* **potassium \<3.5 mEq/L** * _Etiology:_ * increased urinary/Gi losses * diuretic therapy, vomiting, diarrhea; renal tubule acidosis * increased intracellular shifts * metabolic acidosis, beta-2 agonists, hypothermia, insulin, aldosterone * hypomagnesemia * decreased intake→ rare * _S/sxs_: * neuromuscular: severe muscle weakness, rhabdomyolysis * nephrogenic DI: **polyuria** (affects renal concentrating ability), cramps, n/v, ileus (obstruction of ileum * cardiac: palpitations, arrhythmias * ***no change in mental status*** * _Dx_: * BMP: potassium \<3.5mEq/L, *magnesium, glucose, and bicarb should be ordered in work up* * Spot Urine K \> 20 mmol/L (renal cause) * Spot Urine K \< 20mmol/L (non-renal cause) * **ECG findings**: _T-wave flattenedfollowed by a prominent_ **_u-wave_** * _Tx_: potassium replacement→ KCl oral if possible, IV KCl if rapid/severe tx needed * potassium sparing diuretic (**spironolactone, amiloride)** * check for hypomagnesemia (need to correct for this 1st or concurrently) * \*\*\*Use non-dextrose IV solutions b/c dextrose will cause spike in insulin release which will cause more K to shift into the cells \*\*\*

Answer 287

**serum potassium \> 5-5.5mEq/L** * Etiology: * **decreased renal excretion: acute/chronic renal failure** * decreased *aldosterone* → hypoaldosteronism, adrenal insufficiency * _Meds_: K+ supplements, K+ sparing diuretics (thiazides, spironolactone, amiloride), **ACEI/ARBs**, digoxin, beta-blockers, NSAIDs, cyclosporin * Cell lysis → rhabdomyolysis, hypovolemia, thrombocytosis, tumor lysis syndrome * K redistribution → metabolic acidosis * _S/sxs_: * **neuromuscular**: weakness (progressive ascending), fatigue, paresthesias (tingling), flaccid paralysis * cardiac: palpitations and cardiac arrhythmias * GI: abdominal distention, diarrhea * _Dx_: * ECG: **peaked T-waves, prolonged QRS, St depression** * BMP: potassium \> 5.0 mEq/L, *glucose and bicarb part of the workup +/- CBC (hemolysis)* * _Tx_: repeat blood draw to ensure that increased K isnt from hemolysis (since venipuncture may cause this) * **IV Calcium Gluconate** → stabilize the cardiac membrane → only for severe symptoms, K \>6.5, + significant ECG findings * → **insulin with glucose/dextrose** → insulin shifts K+ intracellularly * **Kayexalate (sodium polystyrene sulfonate)** → enhances GI excretion of K+, lowers total K+ * **SABA**: albuterol (4-8x dosing for asthma) * **loop diuretics;** dialysis if severe

Answer 288

* **serum sodium \>145 mEq/L** * caused by increased free water loss, hypotonic fluid loss, or hypertonic sodium gain * _Etiology_: **diabetes insipidus**, diarrhea, sweating, burns, fever, insensible loss * → infants, elderly, debilitated pts or impaired thirst mechanism → water intake decreased * _S/sxs_: PRIMARILY CAUSED BY SHRINKAGE OF BRAIN CELLS → dehydration * **thirst = most common initial sx** * confusion, lethargy, disorientation, fatigue, N/V, muscle weakness, *seizures, coma, brain damage resp. arrest* * _PE_: **dry mouth, mucus membranes, decreased skin turgor**, tachycardia, hypotension * _Dx_: **serum studies** → serum Na, urine osmolarity, serum osmolarity, assess volume status * _Tx_: **hypotonic fluids**: pure water oral, D5W, 0.45%NS, * isotonic fluids if hypovolemic to replenish volume then *hypotonic fluids* * if Central **diabetes insipidus → desmopressin (synthetic analog to ADH)** * renal diabetes insipidus → **NSAIDs** (constrict afferent renal arteriole and reduce GFR) * **rapid correction (\>0.5mEq/L.hr)** → can results in **_Cerebral edema_**

Answer 289

**serum sodium \<135 mEq/L** * due to _increased free water_ * clincially significant → hypotonic hyponatremia * _etiology_: * hypertonic hyponatremia → due to *hyperglycemia or mannitol infusion* * Isotonic Hyponatremia → lab error due to hyperproteinemia or hypertrigliceridemia * _Hypotonic Hyponatremia_ → * **hypovolemic** → renal volume loss (diuretics, ACEI); extraneal volume loss → GI loss (diarrhea & vomiting), burns, fever * **Isovolemic:** SIADH, hypothyroidism, adrenal insufficiency water intoxication, MDMA, tea and toast syndrome * **hypervolemic**: edematous states → CHF, nephrotic syndrome, cirrhosis * _S/sxs_: **primary caused by cerebral edema** → confusion, lethargy, disorientation, fatigue, N/V, cramps, *Seizures, coma, respiratory arrest* * _PE_: * **hypervolemia** → edema, JVD, HTN; decreased HCT, serum protein, BUN:creatinine * **hypovolemia→** poor skin turgor, dry mucus membranes, flat neck veins, hypotension; increased hct, serum protein, BUN:creatinine ratio \>20:1 * _Dx_: * 3 steps: 1. measure serum sodium 2. serum osmolality (**275-295 mOsm/kg**) 3. assess volume status (if hypotonic/decreased osmolality)

Answer 290

* **causes rapidly progressive Glomerulonephritis (nephritic syndrome)** * _anti-glomerular basement membrane_ * _presentation_: * lungs/kidneys hemorrhage * teenagers & \>50 years * rapidly progressive→ _fatal_ * _Pathology:_ * antibodies against the glomerular basement membranne * often associated with crescent formation * _Tx_: * **cyclophosphamide + corticosteroids + plasmapheresis** * due to high fatality → START RX while waiting for dx

Answer 291

* _Presentation_: * E.coli O157:H7 (foodborne), Salmonella, etc. → undercooked meat consumption * *bloody diarrhea that has resolved* * **fever; low platelets; AKI** * Dx: * often via serum assays * _Treatment_: symptomatic manage,ent * HUS may require dialysis, 10% death rate

Answer 292

* type of nephritic syndrome → **cause of _rapidly progressive glomerulonephritis_** * _Presentation_: **hematuria + signs of necrotizing small vessel vasculitis** (diffuse skin lesion, lung hemorrhage, sinusitis, etc.) * _Tx:_ aggressive tx with steroids, cyclophosphamide or rituximab * **plasmapheresis** → severe disease

Answer 293

* _S/sxs_: usually hx of lupus * SLE more common in female AA population * **proteinuria, hematuria**, + **elevated creatinine** * _Tx_: dependent on biopsy classifications

Answer 294

Rhabdomyolysis

Answer 295

albumin * can have a false negative if proteinuria composed of light chains * → will be detected in protein precipitation test aka **sulfosalicyclic Acid (SSA)**

Answer 296

albumin * can have a false negative if proteinuria composed of light chains * → will be detected in protein precipitation test aka **sulfosalicyclic Acid (SSA) → Myeloma**

Answer 297

\< 0.2 or 200 aka SPOT urine protein/SPOT urine creatinine

Answer 298

\<200mg/day

Answer 299

30-300mg/g

Answer 300

when the “nephritis” is causing an AKI that is rapidly progressive over days to weeks * _Nephritis_: * RBC casts * proteinuria \<3.5g

Answer 301

Non-oliguria: \>400mL/day Oliguria: 100-400 mL/day Anuria: \<50mL/day

Answer 302

A: severe metabolic Acidosis E: Electrolyte Problems (Hyperkalemia) I: Intoxication (Antifreeze) O: Overload of fluids U:Uremic symptoms (pericarditis, altered mental status)

Answer 303

3-4+ proteins, RBCs and RBC casts, granular & epithelial casts, oval fat bodies

Answer 304

**GFR \<30 ml/min/1.73m2 \*CKD stage 4-5)**

Answer 305

* Advantages: * less sxs f * continuous theraoy * fewer dietary restrictions * needleless * home therapy * flexibility with schedule * easy night-time therapy * easier travel * Disadvantages: * daily (as opposed to 3 times a week) * training required * weight gain, sugar-load * need for clean space in room for PD and supplies * peritonitis risk (though balanced by bacteremia risk of HD)

Answer 306

15 years more

Answer 307

generally okay to keep going as long as: * K controlled * creatinine increases \<20-30% within 6-8 weeks at start * no abrupt AKI * no other SEs (ACEi → cough, angioedema, etc. so can use an ARB instead)

Answer 308

* Urine Na: **\>40mEq/L** * urine osmolality: \<350 * BUN/Creatinine Ratio: 10:1 * FeNa: \>2% * FeUrea: \>35%

Answer 309

to calculate expected pCO₂ * Expected pCO₂ = (1.5 x bicarb) + 8 +/- 2 * if pCO_{2 = higher than expected → additional respiratory acidosis} * if PCO_{2 = lower than expected → additional respiratory alkalosis}

Answer 310

urine albumin: creatinine ratio **\>30 mg/g (per day)**

Answer 311

urine protein: creatinine ratio **\>0.2g/g** or **\>200mg/g**

Answer 312

along afferent arteriole that detect blood pressure if BP = low → secrete renin and activate RAAS system

Answer 313

Decr ADH in Central Diabetes Insipidus (neuro issue) Urine osmo \<300, corrects w/ ADH administration Decr sensitivity to ADH in Nephrogenic Diabetes Insipidus (renal issue) Urine osmo \<300, does NOT correct w/ ADH **Hypernatremia will only occur if water intake is inadequate**

Answer 314

Insensible losses GI losses Fluid shift into cells Urine osmo \>800 Urine Na \<10 **Hypernatremia will only occur if water intake is inadequate**

Answer 315

Causes K excretion in principal cells of CD and K reabsorption in intercalated cells of CD

Answer 316

urine [K+] \> 20 mmol/L = renal cause urine [K+] \< 20 mmol/L = nonrenal cause

Answer 317

GFR: \< 60 mL/min = CKD \< 30 mL/min = referral to nephrology \< 20 mL/min = eligible for transplant listing \< 10 mL/min = dialysis

Answer 318

Stage 1: Incr SCr by **0.3 mg/dL x 48 hrs** or **+50% x 7d**, UOP \<0.5 mL/kg x \>6h Stage 2: UOP \<0.5 mL/kg x \>12h Stage 3: UOP \<0.3 mL/kg x \>24h or anuria \>12h

Answer 319

1st line therapy for HTN in early CKD as they "tell kidneys to take a break & not filter so hard" Will cause slight incr in SCr. Expected and ok as long as \<30% and proteinuria is improving. Watch K as ACEi/ARB can increase **Do not use ACEi & ARB together d/t incr risk of AKI, hyperkalemia, hypotension**

Final OSCE Flashcards

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