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Final OSCE Flashcards

1
Q

Dilated Cardiomyopathy:

Pathophys, Etiology & Epidemiology

A
  • Def: systolic dysfunction (S3 gallop) leading to a dilated, weak heart with EF <40%
  • Pathophys:
    • increased heart size & weight, ventricular dilation, thinned ventricular walls (usually due to increased volume)
  • Etiology:
    • Idiopathic = most common cause
    • alcohol (#2)
    • myocarditis (#3)
    • cocaine
    • doxorubicin
    • infection (viruses eg coxsackie, HSV 6, adenovirus)
  • Epidem:
    • age 20-60
    • most COMMON type of cardiomyopathy
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2
Q

Dilated Cardiomyopathy: S/sxs

A
  • Sxs:
    • pulm congestion (Left HF): dyspnea, orthopnea, rales
    • systemic congestion (Right HF): peripheral edema, JVD, nausea, abdominal pain, nocturia, enlarged liver
    • Low CO: fatigue, weakness
  • Other:
    • HTN or hypotension
    • tachycardia, tachypnea
    • S3 gallop
    • mitral/tricuspid regurg: papillary muscles stretches with dilation -→ valvular dysnfunction
    • PMI shifted laterally
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3
Q

Dilated Cardiomyopathy: Dx

A
  • Diagnostic Criteria:
    • inclusion: EF <40%
      • LVEDD >177% of predicted
  • Labs to order:
    • BNP
    • Na, Mg, K
    • BUN, Cr (CMP)
    • Hemoglobin (CBC with diff)
  • CXR:
    • cardiomegaly
    • pulmonary edema
    • pleural effusion
  • EKG:
    • wide QRS
    • LBBB
  • Echocardiogram:
    • L ventricular dilation
    • thin ventricle walls
    • decreased ejection fraction (<50%, but often <30%)
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4
Q

Dilated Cardiomyopathy: Dx

A
  • Diagnostic Criteria:
    • inclusion: EF <40%
      • LVEDD >117% of predicted
  • Labs to order:
    • BNP
    • Na, Mg, K
    • BUN, Cr (CMP)
    • Hemoglobin (CBC with diff)
  • CXR:
    • cardiomegaly
    • pulmonary edema
    • pleural effusion
  • EKG:
    • wide QRS
    • LBBB
  • Echocardiogram:
    • L ventricular dilation
    • thin ventricle walls
    • decreased ejection fraction (<50%, but often <30%)
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5
Q

Dilated Cardiomyopathy: Tx

A
  • tx just like systolic heart failure
    • beta-blockers (metoprolol, carvedilol) + [ACE-I (lisinopril, captopril, enalapril) =mainstay of tx] + Loop diuretic (furosemide)
    • Anticoag if EF <30%
  • if you need increased contractility = digoxin (digitalis)
  • Pt education:
    • limit activity
    • salt restriction <2g/day
    • fluid restriction <2L/day
  • extreme cases = heart transplant or L ventricular assist device
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6
Q

Canadian Cardiovascular Society Classification System: Angina

A
  • Stage I: angina with strenuous activity
  • Stage II: slight limitation of ordinary activity; angina walking 2 blocks, up stairs rapidly
  • Stage III: marked limitation of ordinary activity; angina walking 1-2 blocks
  • Stage IV: Angina at rest
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7
Q

Major Risk Factors of Coronary Artery Disease (CAD)

A
  • Diabetes Mellitus (Worst risk factor, considered a CAD equivalent)
  • Smoking (Most important modifiable risk factor)
  • Hyperlipidemia, HTN
  • Men >45yo, Women >55yo
  • Fam Hx of CAD: (first degree relative – father or brother before age 55, mother or sister before age 65)
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8
Q

Etiology of Acute Coronary Syndrome

A
  • Etiology:
    • atherosclerosis = most common cause -→ acute coronary artery thrombosis with platelet adhesion with fibrin formation
    • coronary artery vasospasm: prinzmetal variant angina, cocaine induced
  • Silent MI:
    • 25% are atypical, more common in women, elderly, diabetics, obese patients; sxs include: dyspnea, epigastric pain, syncope, or sudden death
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9
Q

NSTEMI: def, s/sxs, dx, & tx

A
  • Definition: myocardial necrosis (evidenced by elevated troponins & cK-MB) without acute ST segment elevation; coronary artery not completely blocked, subendocardial infarct
  • S/sxs:
    • Chest pain, SOB
  • Dx:
    • EKG: ST-depression, T-wave inversion
    • Troponins: positive, usually need 2+ draws on this, troponins take up to 3 hours to become elevated
  • Tx:
    • First line: oxygen of o2 <95%
      • sublingual nitroglycerin (1-2 sprays Q5 min, max of 3)
      • Aspirin (inhibits platelet activation)
    • either IV unfractionated heparin (inhibits factor IIa (thrombin, and factor Xa) OR SQ enoxaparin (low molecular weight heparin, only inhibits factor Xa)
    • clopidogrel 300mg
    • if going for PCI → high dose statin prior to angiography
    • Then eventually: BAAAS (b-blocker, ace-i or ARB, stain)
    • ***Do NOT use Thrombolytics***
    • “go to cath lab if not responding to treatment and still having chest pain, significant ST changes etc. Not all NSTEMI go to Cath emergently, many do not need to. Can cath semi-electively” -Dr Pearl
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10
Q

STEMI: def, s/sxs, dx & Tx

A
  • Definition: myocardial necrosis (evidenced by elevated troponin & CK-MB) with acute ST-segment elevation or Q-waves; coronary artery completely blocked; full thickness infarct
  • S/sxs:
    • Chest pain
    • SOB
    • pain radiating to jaw and/or arm
  • PE:
    • Inferior Wall MI:
      • bradycardia or heart block (R. coronary artery supplies the AV node)
      • epigastric pain
      • may have S4
    • Triad of R ventricle MI:
      1. JVD
      2. Clear lungs
      3. positive Kussmaul sign : paradoxical JVP that occurs during inspiration -→ heart cannot accommodate extra blood that returns via the venous system when the intrathoracic pressure becomes negative during inspiration
  • Dx:
    • EKG: new ST-elevation in two contiguous leads of >1mm
      • reciprocal changes in opposite leads
      • **progression: hyperacute T-waves → ST elevations → Q waves
    • Troponin:
      • positive → returns to baseline in 7-10 days
      • **may be falsely positive in pts with renal failure, advanced heart failure, acute PE, or CVA**
  • Tx: a) prevent further clot formation by inhibiting platelet function- Aspirin and Clopidogrel
    • b) Prevent thrombus formation by blocking Fibrin with Heparin
    • c) Decrease Myocardial Oxygen demand (while working to improve supply)- Beta Blockers
    • d) Vasodilate coronaries (spasm may occur as well with ischemia) and decreases preload as well by vasodilation- NTG
    • e) Oxygen- only if sats below about 95%
    • f) Morphine-used less frequent now- need a good BP, avoid in right ventricular infarction
    • g) ACE inhibitor may be added later for remodeling and for afterload reduction, can use sooner if hypertensive
  • Definitive care:
    • If < 3-5 hours and having STEMI go emergently to Cath lab for PTCA ( Balloon and Stent). Goal is 90 minutes door to reperfusion.
    • IF > 3 hours before one can get to a cath lab then use Thrombolytic Therapy TPA or TKI etc. for STEMI
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11
Q

Post MI Complications

A
  • Pericarditis: 1-3 weeks post MI (Dressler Syndrome)
  • VSD (ventricular septal defect: 1-5 days post MI: shock, new murmur, pulmonary edema
  • Acute Mitral Regurg: shock, apical murmur, pulmonary edema
  • new or recurrent MI: chest pain, new ECG changes possible, new bump in troponins
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12
Q

Stable Angina

A

Coronary Artery Disease

  • predictable and occuring with exertion → typically same distance each time
  • relieved with rest or NTG
  • Workup:
    • EKG: Normal, q-waves (if prior MI)
    • Cardiac Stress Test: pt should be able to walk 6 min on treadmill or else unreliable, goal is 85% of max predicted HR
      • bruce protocol (increase by 2% grade & 0.8mph q 3 minutes)
      • monitor: BP, EKG, Echo, sxs (CP, SOB)
    • coronary angiography:
      • provides a definitive dx → defines location and extent of CAD but only used if:
        • pt is severely symptomatic despite medical therapy and being considered for PCI
        • pt with sxs difficult to dx
        • angina sxs in pts who have survived cardiac death event and ots with ischemia on non-invasive testing
  • Tx:
    • NBC (mnemonic to remember)
      • beta blockers: decrease HR, contractility, blood pressure → decreased demand (metoprolol, carvedilol)
      • nitroglycerin: sublingual or IV: decrease preload/afterload, vasodilate coronary arteries
      • Calcium channel blockers: decrease afterload/blood pressure (velocity) , may dilate coronary arteries (non-dihydropyridine CCBs → diltiazem, verapamil)
      • Statins: improve endothelial function
      • aspirin: prevent thrombus formation (anti-platelet activation)
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13
Q

Unstable Angina

A
  • Definition: occurs at rest (Canadian Angina Classification Level 4), or not relieved by rest or NTG. Some include exertional angina that is occurring more frequently, with lesser exertion, more intense, lasting longer (Crescendo Angina
  • Dx:
    • EKG = ST segment depression >1 mm
    • Troponins: Negative (no cell death)
    • angiography = gold standard for diagnosing CAD but only used when revascularization is being considered
  • Tx:
    • antiplatelet drugs (aspirin and/or clopidogrel (plavix) ticagrelor)
    • beta-blockers (metoprolol, carvedilol)
    • nitroglycerin & Ca channel blockers for symptom control
    • Revascularization if sxs persist despite medical therapy
    • ACE-I + statins
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14
Q

Stress Test (Exercise Testing)

A
  • Pt must be able to walk 6 min on a treadmill: goal is 85% of max predicted HR
  • initial test in pts who are stable and able to exercise
    • Bruce Protocol: increase grade by 2% and speed by 0.8mph q 3 minutes
    • Monitor: BP, EKG, symptoms (CP, SOB)
    • Duke Treadmill Score: (duration of exercise in min) - (ST segment depression in mm)x (5) - (angina score)x(4)
  • if patient cannot exercise:
    • can use adenosine for myocardial perfusion imaging
    • can use dobutamine for a stress echo
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15
Q

Angina- Prinzmetal Variant

A
  • Definition:
    • Coronary artery vasospasm causing transient ST-segment elevations, not associated with clot. Usually happens at night or early morning
    • risks: COCAINE ABUSE, female >50yo, hx of vasospastic disorders
    • triggers: cold weather, exercise, alpha-agonists, hyperventilation
  • S/sxs:
    • chest pain at rest (usually midnight to early morning, non-exertional & not relieved with rest)
    • Preserved exercise capacity
  • Dx:
    • EKG: transient ST-elevation that resolves with symptom resolution
      • inverted U-waves
  • Tx:
    • calcium channel blockers: first line monotherapy -→ given at NIGHT (Non-dihydropyridine: diltiazem, verapamil Qday)
      • → can add long acting nitrate (Isosorbide mononitrate ER 30-60mg QAM: SEs: Methemoglobinemia, severe hypotension)
    • Nitroglycerin IR for sx relief (1-2 sprays sublingual Q5 min PRN, max of 3 doses)
    • AVOID BETA-Blockers! → may cause unopposed vasospasm
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16
Q

Acute vs. Chronic Heart Failure

A
  • S/sxs:
    • Chronic Heart Failure (compensated):
      • congestion
      • laterally displaced apical impulse
    • Acute Heart Failure:
      • breathlessness
      • rapid weight gain
      • fluid build-up in the lungs and around the body
      • inadequate time for compensation: largely systolic (HTN crisis, acute MI, papillary muscle rupture); often fatal
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17
Q

Systolic Heart Failure

A
  • Definition: heart failure with decreased ejection fraction
    • impaired contractility
    • thin ventricular walls (DILATED)
    • S3 gallop (sys-tol-ic)
  • Etiology:
    • ischemic heart disease, rapid HTN, dilated cardiomyopathy (LEADING CAUSE), myocarditis, congenital, post-surgical, PE, sepsis
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18
Q

Diastolic Heart Failure

A
  • Definition: Heart failure with preserved ejection fraction
    • impaired filling/relaxation
    • thick ventricular walls (**Hypertrophied**)
    • S4 gallop (Di-a-stol-ic)
  • Etiology:
    • HTN, aortic stenosis, restrictive & hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, normal aging, CAD scarring
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19
Q

Management goals of Heart Failure

A
  1. Afterload: make it easier for the heart to empty
  2. preload: appropriate stretch, get the heart back on the proper part of the Sterling curve
  3. contractility: help the heart function better (pump, squeeze, relaxation, rate & rhythm)

**Uncompensated heart failure: diuretics, afterload reduction, inotropes, mechanical support, transplantation

**Compensated heart failure: diuretics, afterload reduction, beta-blockers

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20
Q

Tx of Heart Failure

A
  • **initial management usually consists of an ACEI & (maybe a beta blocker) + diuretic (for sxs)**
  • Long Term Tx (Afterload reduction:
    • ACE Inhibitors (Captopril, Enalapril, Lisinopril): reduce afterload by vasodilation & BP reduction, useful in pts with EF <35%,mainstay of tx, (adverse effects: hyperkalemia, cough, angioedema, & elevated creatinine)
    • Angiotensin II Receptor Blockers (Losartan, Valsartan): blocks effects of angiotensin II, indicated in pts who cannot tolerate ACEI (cough)
    • Angiotensin Receptor Neprilysin Inhibitor (Sacubitril/Valsartan): inhibits breakdown of BNP so BNP no longer becomes a reliable marker in pts taking this
    • Beta-Blockers (Carvedilol, Metoprolol, Bisprolol): usually added after ACEI or AR
  • Long Term Tx (Preload Reduction)
    • Loop Diuretics (furosemide, bumetanide, torsemide): inhibit water transport across the Loop of Henle, effective for sx tx.
    • potassium sparing diuretics (spironolactone, eplerenone): aldosterone antagonist, decreased mortality
    • Thiazides (hydrochlorothiazide, Metolazone): inhibits DCT reabsorption of Na+
  • Long Term Tx (Positive Inotropes):
    • Digoxin: positive inotrope; 2nd line for pts in CHF with sinus rhythm, 1st line for pts with afib + CHF
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21
Q

Left-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE

A
  • Pathophys: leads to increased pulmonary venous pressure from fluid backing up into the lungs. Increased hydrostatic pressure drives protein-poor fluid into alveoli through an intact barrier
    • → resolution depends on Na+ reabsorption and lymphatic drainage
  • Etiology:
    • Coronary artery disease, HTN = most common
  • S/sxs:
    • dyspnea: exertional, paroxysmal nocturnal dyspnea, orthopnea
    • fatigue
    • cough with frothy sputum
    • activity intolerance
  • PE:
    • pulmonary edema & congestion → crackles, rhonchi, wheezing, tachypnea
    • cheyne-stokes breathing: deep, fast breathing with gradual decrease in episodes of apnea
    • cyanosis
    • S3 or S4 gallop
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22
Q

Right-Sided Heart Failure: Pathophys, Etiology, S/sxs, PE

A
  • Pathophys:
    • leads to increased systemic venous pressure from fluid backing up into the IVC, SVC, and hepatic circulation
  • Etiology:
    • left sided heart failure = most common
    • pulmonary disease (COPD, pulmonary HTN), mitral stenosis
  • S/sxs/Pe:
    • inferior vena cava:
      • peripheral edema
    • Superior Vena Cava:
      • jugular vein distention
    • hepatic: anorexia, weight loss, n/v, hepatojugular reflex
    • hepatosplenomegaly
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23
Q

Hypercholesterolemia: primary vs secondary, etiology, risk factors

A
  • primary: WITHOUT known CV disease (carotid, heart, arteries)
  • Secondary: with known clinical CV disease
  • Etiology:
    • hypothyroidism, pregnancy, kidney failure
  • Risk Factors:
    • sex, age, HTN, DM, smoking, family hx of coronary heart disease
      • 1st degree male relative with CHD before age 55
      • 1st degree female relative with CHD before age 65
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24
Q

Primary Prevention of ASCVD in age 0-19 years

A
  • lifestyle to prevent or reduce ASCVD risk
  • Diagnosis of familial hypercholesterolemia?
    • statin
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25
Q

Primary Prevention of ASCVD in Age 20-39

A
  • Estimate lifetime risk to encourage lifestyle to reduce ASCVD risk
  • Consider statin if family hx, premature ASCVD and LDL-C ≥ 160mg/dL
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26
Q

Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to <190 mg/dL without diabetes mellitus

A

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%
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27
Q

At what LDL-C level do you initiate high intensity statin with no risk assessment?

A

LDL-C ≥ 190 mg/dL

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28
Q

What population do you initiate a moderate-intensity statin regardless of risk factors?

A

Diabetes Mellitus age 40-75yo

Risk assessment to consider high-intensity statin

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29
Q

CAC

A

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
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30
Q

Best meds to lower elevated LDL

A
  • 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
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31
Q

Best Meds to Lower Triglycerides

A
  • Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
  • Niacin
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32
Q

Best Meds to Increase HDL

A
  • Niacin
  • Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
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33
Q

Treatment of Secondary Hypercholesterolemia without high-risk (clinically stable)

A

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
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34
Q

Treatment of Secondary Hypercholesterolemia with High Risk (unstable)

A

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
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35
Q

Abnormal Lipid Values

A
  • 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
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36
Q

Hypertriglyceridemia

A
  • 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
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37
Q

Essential HTN: definition, PE, and diagnosis

A
  • 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
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38
Q

Essential HTN: Tx

A
  • 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
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39
Q

ACC/AHA Classification of BP

A
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40
Q

Hypertensive Emergency: definition, Dx, & Tx

A
  • 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
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41
Q

Hypertensive Urgency: Definition, Dx, & Tx

A
  • 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
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42
Q

Secondary HTN Definition and Causes

A
  • 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
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43
Q

Secondary HTN Red Flags, Dx, & Tx

A
  • 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
      • spot 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
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44
Q

Mixed Venous O2 vs A-VO2 difference

A
  • 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)
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45
Q

Delivery of oxygen is affected by

A

DO2 = CO x CaCO2

delivery of oxygen is affected by cardiac output and arterial oxygen content

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46
Q

Hypovolemic Shock: Definition, Etiologies, Pathophys, S/sxs

A
  • 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
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47
Q

Features of Hypovolemic Shock

A
  • 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)
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48
Q

Normal Blood Volume

A
  • Adults: 7% IBW (75ml/kg)
    • → 70kg adult = 5.5 Liters or approx 15 units
  • Children: 9% IBW (90 ml/kg)

IBW = ideal body weight

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49
Q

Phases of Hypovolemic Shock

A
  • 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
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50
Q

Tx of Hypovolemic Shock

A
  • 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)
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51
Q

Distributive Shock: Definition, Pathophys, & Etiologies

A
  • 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
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52
Q

Distributive Shock: S/sxs of Sepsis, Anaphylaxis, and Neurogenic Shock

A
  • 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
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53
Q

Features of Septic Shock

A

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
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54
Q

Features of Neurogenic Shock

A

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
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55
Q

Tx of Distributive Shocks

A
  • 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
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56
Q

Obstructive Shock: Definition, Etiology & Tx

A
  • 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)
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57
Q

Cardiogenic Shock: Definition, Etiology, & S/sxs

A
  • 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
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58
Q

Features of Cardiogenic Shock

A
  • 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)
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59
Q

Tx of Cardiogenic Shock

A

Tx the underlying cause

  • if acute MI: revascularize
  • inotropic 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])
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60
Q

Hypertrophic obstructive Cardiomyopathy: Pathophys & Risk Factors

A

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
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61
Q

Hypertrophic Cardiomyopathy: S/sxs & PE

A
  • 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
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62
Q

Tx of Hypertrophic Cardiomyopathy

A
  • 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
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63
Q

Restrictive Cardiomyopathy: Definition, Etiology, & S/sxs

A
  • 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
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64
Q

Restrictive Cardiomyopathy: Dx & Tx

A
  • 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
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65
Q

HEART Score

A

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
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66
Q

Acute Bacterial Endocarditis Definition and organism

A
  • Definition: infection of a normal valve with a virulent organism (usually S. Aureus).
  • Rapidly destructive (fatal < 6 weeks if untreated)
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67
Q

Subacute Bacterial Endocarditis: Definition & Organism

A
  • 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)
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68
Q

Bacterial Endocarditis: General Definition, Risk factors, & Sxs

A
  • 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
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69
Q

Types of Endocarditis

A
  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 -)
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70
Q

Community Associated vs Healthcare Associated Endocarditis

A
  • 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)
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71
Q

Bacterial Endocarditis: PE and tests to order

A
  • 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
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72
Q

Diagnosis of Bacterial Endocarditis

A

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
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73
Q

Prophylaxis of Bacterial Endocarditis: Indicated cardiac conditions, Procedures, & Regimen

A

**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)
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74
Q

Indications for Surgery in Bacterial Endocarditis

A
  • 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
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75
Q

Tx of Bacterial Endocarditis

A
  • 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
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76
Q

Acute Pericarditis: Definition, Etiology, Classification, & Types

A
  • 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
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77
Q

Acute Pericarditis: S/sxs & PE

A
  • 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
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78
Q

Acute Pericarditis: Diagnosis

A
  • 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
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79
Q

Acute Pericarditis: Tx & Admit factors

A

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)
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80
Q

Myocarditis: Definition, Pathophys, Etiology, Epidemiology, Classifications

A
  • 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
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81
Q

Myocarditis: S/sxs, PE, and Profiles

A
  • 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
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82
Q

Myocarditis: Dx & DDx

A
  • 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
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83
Q

Myocarditis: When to suspect & Tx

A
  • 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
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84
Q

Pericardial Effusion: Definition & Etiology

A
  • 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
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85
Q

Pericardial Effusion: S/sxs, PE, & Dx

A
  • 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
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86
Q

Pericardial Effusion: When to suspect & Tx

A
  • 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
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87
Q

Cardiac Tamponade: Definition, Etiology, S/sxs, & PE

A
  • 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
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88
Q

Cardiac Tamponade: Tx

A
  • immediate: oxygen, IV fluids, type & culture
  • Don’t give pain meds, sedate, or intubate (causes vasodilation which will lower BP even further)
  • Pericardiocentesis
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89
Q
A

“water bottle” appearance

associated with pericardial effusion/ cardiac tamponade

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90
Q

Beck’s Triad

A

Associated with Cardiac Tamponade

  1. elevated JVP
  2. muffled heart sounds
  3. systemic hypotension
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91
Q

Mnemonic to Remember Medical Tx of STEMI

A

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

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92
Q

Dressler’s Syndrome

A

Post-MI pericarditis

tx = aspirin or colchicine

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93
Q

Triad of R Ventricular Infarction

A
  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)
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94
Q

3 populations with atypical sxs for acute MI

A

elderly, women, diabetics

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95
Q

Which cardio biomarker peaks the fastest?

A

Myoglobin

My O My you are fast

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96
Q

Aortic Stenosis

A

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
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97
Q

Aortic Regurgitation

A

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
      *
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98
Q

Mitral Stenosis

A
  • 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
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99
Q

Mitral Regurgitation

A

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
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100
Q

Mitral Valve Prolapse

A

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
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101
Q

Pulmonary Stenosis

A

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
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102
Q

Pulmonary Regurgitation

A

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
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103
Q

Tricuspid Stenosis

A

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
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104
Q

Tricuspid Regurgitation

A

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
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105
Q

S3

A

Sys-tol-ic Murmur

can be normal in young and athletic hearts

associated with a dilated ventricle (more compliant ventricle)

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106
Q

S4

A

di-a-stol-ic

atrial kick against a stiff wall, associated with hypertrophy or scar

NEVER normal

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107
Q

What can accentuate mitral murmurs

A

Left lateral decubitus position with the bell

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108
Q

What can accentuate aortic murmurs

A

sitting up and leaning forward

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109
Q

What does increasing venous return do?

A

increases intensity of all murmurs EXCEPT hypertrophic cardiomyopathy, mitral valve prolapse

“the MVP Hates Conforming to the rules”

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110
Q

Pneumonic to remember which murmurs are diastolic

A

MS. PRARTS DIED

MS = mitral stenosis

PR = pulmonary regurg

AR = aortic regurg

TS = tricuspid stenosis

DIED = diastolic, everything else is a systolic murmur

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111
Q

Maneuvers to increase venous return

A

lying supine

squatting

lifting legs

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112
Q

Maneuvers to decrease venous return

A

standing

valsalva maneuver

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113
Q

Inspiration increases venous return to which side of the heart

A

Right Side: RINSPIRATION

→ increases the sound of murmurs on the R side

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114
Q

Expiration increases venous return to which side of the heart

A

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

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115
Q

Increased Total Peripheral Resistance & Murmurs

A

How to: handgrip, phenylephrine

  • increased resistance decreases forward flow & increases backward flow → increases aortic regurg, mitral regurg (regurgitant murmurs)
  • decreases AS, MVP, hypertrophic cardiomyopathy
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116
Q

Decreased Total Peripheral Resistance & Murmurs

A

How to: Amyl Nitrate

  • direct arteriolar vasodilator increases forward flow through the aortic valve
    • increases AS, MVP, hypertrophic cardiomyopathy
    • decreases AR, MR (regurgitant murmurs)
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117
Q

What does the pitch tell you about the murmur?

A

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

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118
Q

Pulsus parvus et tardus

A

weak, delayed carotid pulse

often seen in Aortic Stenosis

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119
Q

Patent Ductus Arteriosus: Definition, Pathophys, & Risks

A
  • 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
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120
Q

Patent Ductus Arteriosus: S/sxs, PE

A
  • 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)
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121
Q

Patent Ductus Arteriosus: Dx & Tx

A
  • Dx: ECHO = best initial test
  • Tx:Indomethacin, 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
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122
Q

Eisenmenger Syndrome

A
  • Pulmonary HTN & Cyanotic heart disease occuring when a left-to-right shunt shunt switches to a right-to-left shunt → Cyanosis
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123
Q

Tetralogy of Fallot: 4 components

A

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
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124
Q

Tetralogy of Fallot: S/sxs & PE

A
  • 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
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125
Q

Tetralogy of Fallot: Dx, Tx, and Mnemonic

A
  • 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
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126
Q
A

Boot Shaped Heart

Associated with Tetralogy of Fallot

demonstrates prominent R ventricle due to RV outflow obstruction

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127
Q

Ventricular Septal Defect: Definition & Types

A
  • 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
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128
Q

Ventricular Septal Defect: S/sxs & PE

A
  • 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
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129
Q

Ventricular Septal Defect: Dx, Tx, & Mnemonic

A
  • 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**
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130
Q

Coarctation of the Aorta: Definition & Pathophys

A
  • 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
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131
Q

Coarctation of the Aorta: S/sxs & PE

A
  • 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
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132
Q

Coarctation of the Aorta: Dx & Tx

A
  • 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!
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133
Q
A

3 Sign

associated with Coarctation of the Aorta

narrowed aorta looks like the notch of the number 3

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134
Q
A

Coarctation-Rib Notching

Associated with Coarctation of the Aorta

due to increased intercostal artery collateral flow after several years

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135
Q

How do you distinguish hypoxia from pulmonary disorders from cardiac disease?

A

Hyperoxia test

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136
Q

Truncus Arteriosus

A
  • 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
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137
Q

Still’s Murmur

A

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
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138
Q

Murmurs that are never normal

A
  • anything DIASTOLIC
  • anything >II/VI
  • → get an echo
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139
Q

3 problems with developmental heart processes that leads to congenital heart disease

A
  • 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)
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140
Q

Total Anomalous Pulmonary Venous Drainage (TAPVR)

A
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141
Q

Macule

A
  • flat, nonpalpable
  • <1cm in diameter
142
Q

Patch

A
  • flat, non-palpable
  • >1cm
143
Q

Papule

A
  • elevated, round
  • <1cm in diameter
144
Q

Plaque

A
  • elevated, circumscribed
  • >1cm in diameter
145
Q

Nodule

A
  • elevated, circumscribed
  • large volume than papule often > 2cm
  • involves the dermis
  • greatest mass may be beneath the skin surface
146
Q

Vesicle

A
  • elevated, circumscribed
  • <1cm in diameter
  • primarily filled with clear fluid, may become pustular
147
Q

Bulla

A
  • elevated, circumscribed
  • larger vesicle, >1cm
  • filled with clear fluid
148
Q

Wheal

A
  • aka hive
  • firm, edematous plaque
  • tend to be transient
149
Q

pustule

A
  • elevated, circumscribed
  • usually <1cm
  • filled with purulent fluid
150
Q

Flat topped

A
  • lichenoid
151
Q
A
152
Q
A
153
Q

Scale

A
  • hyperkeratosis
    *
154
Q

Excoriation

A
  • exogenous injury to all or part of the epidermis
  • secondary feature of pruritus
    • due to scratching
155
Q

Atrophy

A
  • 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
156
Q

Lichenification

A
  • thickening of the epidermis and accentuation of the natural skin lines
    i. e. acanthosis nigricans
157
Q

Fitzpatrick Scale of Skin Phototypes

A
  • 1-6:
  • 1: white
  • 2: white
  • 3: Beige
  • 4: Brown
  • 5: Dark Brown
  • 6: Black
158
Q

What type of pruritus requires a full workup

A
  • generalized unexplained pruritus
159
Q

Exanthem

A
  • 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
160
Q

Morbiliform

A
  • “measles-like”
  • maculopapular that becomes confluent
161
Q

Purpura

A
  • visible hemorrhage into the skin or mucus membranes
  • these are non-blanchable
162
Q

Petechiae

A
  • less than or equal to 3mm and macular
  • small purpura
163
Q

Ecchymosis

A
  • usually >1cm
  • trauma in the history is typical
  • a hematoma is when it is palpable
164
Q

Levido Reticularis

A
  • blue or discolored network
  • think of Mallory’s legs during cold soccer workouts
    • pale with the blue and discolored network of lacy coloration
165
Q

Papulosquamous eruption

A
  • well circumscribed papules, plaques with hyperkeratosis (scaling)
  • often associated with:
    • psoriasis
    • pityriasis rosea
    • lichen planus
    • tinea corporis
    • seborrheic dermatitis
166
Q

Prurigo Nodularis

A
  • 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
167
Q

Lichen Simplex Chronicus

A
  • plaques that are either skin colored, pink, or hyperpigmented with exaggerated skin lines and a leathery appearance due to habitual scratching/rubbing
168
Q

Aquagenic pruritus

A
  • 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
169
Q

Notalgia parasthetica

A
  • neurological pruritus
  • tends to be unilateral on the upper to mid back
  • hyperpigmented patch may be present
  • tx: capsaicin, ice packs, gabapentin
170
Q

bracioradial pruritus

A
  • 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
171
Q

Dysesthesia

A
  • 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***

172
Q

General Pruritus Treatment

A
  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
173
Q

Post-Viral Cough

A
  • aka post-infectious cough
  • no specific etiological agent
  • cough lasting from 3-8 weeks following a viral URI or bronchitis
  • usually normal CXR
174
Q

Chronic Cough

A
  • 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
175
Q

Chronic Bronchitis

A

“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
176
Q

COPD definition

A

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%

177
Q

Emphysema

A

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
178
Q

Acute Bronchiolitis

A

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
179
Q

Acute Bronchitis

A

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
180
Q

Acute Epiglottitis

A

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)
181
Q

Acute Laryngotracheitis

A
  • 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
182
Q

Step 1 therapy for Asthma in Adults

A

sxs < 2x/month

  • Controller:
    • TAke ICS whenever SABA is taken
  • Reliever:
    • SABA
183
Q

SABA

A

short acting beta agonist

184
Q

Step 2 therapy for Asthma in Adults

A

sxs 2x/month + but less than 4-5days/week

  • Controller:
    • low dose maintenance ICS
  • Reliever:
    • PRN SABA
185
Q

ICS

A

inhaled corticosteroid

186
Q

Step 3 Therapy for Asthma in Adults

A

sxs most days, or waking with asthma once/week +

  • Controller:
    • low dose maintenance ICS-LABA
  • Reliever:
    • PRN SABA
187
Q

LABA

A

long acting beta 2 agonist

188
Q

LTRA

A

leukotriene receptor antagonist

i.e. singulair (montelukast)

189
Q

Step 4 Therapy for Asthma in Adults

A

sxs most days, or waking with asthma once/week+, or low lung function

  • Controller:
    • medium/high dose maintenance ICS-LABA
  • Reliever:
    • PRN SABA
190
Q

Step 5 Therapy for Asthma in Adults

A
  • Controller:
    • add on LAMA
    • refer for phenotypic assessment
    • +/- anti-IgE, anit-IL5/5R, anti-IL4R
    • consider high dose ICS-LABA
  • Reliever:
    • PRN SABA
191
Q

Age for pediatric asthma tx

A

6-11 years old

192
Q

Step 1 therapy for Asthma in Peds

A

sxs <2x/month

  • Controller:
    • low dose ICS whenever SABA is taken; or daily low dose ICS
  • Reliever:
    • PRN SABA
193
Q

Step 2 Therapy for Asthma in Peds

A

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
194
Q

Step 3 Therapy for Asthma in Peds

A

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
195
Q

Step 4 Therapy for Asthma in Peds

A

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
196
Q

Step 5 Therapy of Asthma for Peds

A
  • 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
197
Q

SABAs

A

Short acting beta-2 agonists

  • albuterol
  • levalbuterol
  • metaproterenol
  • Terbutaline
198
Q

Albuterol (Proventil-HFA; Proair-HFA)

A

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)
199
Q

Levalbuterol (Xopenex-HFA)

A

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
200
Q

LABAs

A

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)
201
Q

Salmeterol DPI (Serevent Diskus)

A

LABA

do not use as monotherapy

  • partial agonist
202
Q

Formoterol DPI (Foradil)

A

LABA

  • helpful for nighttime sxs
  • full agonist
  • onset = to that of albutero but DO NOT USE FOR ACUTE BRONCHOSPASM
  • SEs: paradoxical bronchospasm
203
Q

Inhaled Corticosteroids (ICS)

A

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)
204
Q

Omalizumab (Xolair)

A

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
205
Q

Combined ICS/LABA

A
  • 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
206
Q

GOLD 1-4

A

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
207
Q

ABCD categorization of COPD

A
208
Q

Stage A COPD Tx

A
  • First Line:
    • SABA prn or SAMA prn (bronchodilators)
  • Second Line:
    • LAMA or LABA or SABA + SAMA
209
Q

Stage B COPD Tx

A
  • First line:
    • LAMA or LABA (long acting bronchodilators)
  • Second Line:
    • LAMA + LABA
210
Q

Stage C COPD Tx

A
  • First line:
    • ICS + LABA or LAMA
  • Second Line:
    • LAMA + LABA
      • LAMA + PDE4i
      • LABA + PDE4i
211
Q

Stage D COPD Tx

A
  • First Line:
    • ICS + LABA and/or LAMA
  • Second Line:
    • ICS + LABA and LAMA
    • ICS + LABA and PDE4i
    • LAMA + LABA
    • LAMA + PDE4i
212
Q

Phosphodiesterase (PDE)-4 inhibitors

A

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)
213
Q

Most common bacterial organisms associated with mild exacerbation of COPD and More Severe COPD

A
  • Mild:
    • strep pneumo, H.flu, Moraxella
  • Severe:
    • E.coli, Klebsiella, enterobacter, pseudomonas
214
Q

Pseudomonas risk factors

A
  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
215
Q

LAMAs

A

long acting muscarinic antagonists

  • Tiotroprium
  • alcidinium
  • glycopyrrolate
  • Umeclidinium
216
Q

SABA + Anticholinergic

A
  • Albuterol/Ipratroprium (Combivent Respimat)
  • Duoneb
  • SEs: paradoxical bronchospasm
    • palpitations/tremor/tachy
    • CONTRAINDICATION: soy or peanut allergy
    • NOT for Children
217
Q

Leukotriene Inhibitors

A

only for asthma (LTRA)

  • montelukast (Singulair)
  • Zileuton (Zyflo)
    • SEs: hepatotoxicity
    • DDIs:
      • inducers: rifampin, carbamazepine, St. John’s wort
      • inhibitors: fluconazole, amiodarone, fluvoxamine, metronidazole, voriconazole
218
Q

Abx for COPD exacerbation outpt (⅓ cardinal sxs)

A

Mild, no abx needed

cardinal sxs: increased dyspnea, sputum volume, or purulence

219
Q

Abx for COPD exacerbation outpt (⅔) no risk factors

A

macrolide

2nd and 3rd gen ceph

doxy

Septra (TMP/Sulfamethoxazole)

220
Q

Abx for COPD exacerbation outpt (⅔ cardinal signs) with risk factors

A

respiratory FQs (moxi/levo/gemi)

Amoxicillin/Clavulanate (Augmentin)

221
Q

Abx for COPD exacerbations in hospital (⅔ of cardinal) with risk factors for pseudomonas

A

FQ (levo PO or IV)

Cephalosporins (Cefepime IV or Ceftazidime IV)

Zosyn IV (piperacillin + tazobactam)

222
Q

Abx for COPD exacerbations in hospital (⅔ cardinal) with no pseudomonas risk

A

FQ (levo or Moxi)

Cephalosporins (ceftriaxone or cefotaxime)

223
Q

Complicated COPD

A

FEV1<50%

age >65

>/= 3 exacerbations/year

cardiac disease

224
Q

Influenza

A

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
225
Q

Pertussis

A

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
226
Q

Bacterial Pneumonia

A

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 sputum, 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)
227
Q

RSV

A

***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
228
Q

Carcinoid Tumors

A

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
229
Q

Squamous Cell Carcinoma

A

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
230
Q

Adenocarcinoma

A

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:
231
Q

Adenocarcinoma

A

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
232
Q

Large Cell Carcinoma

A

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
233
Q

Small Cell Lung Cancer

A

“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
234
Q

When to Screen for Lung Cancer

A

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

235
Q

Pulmonary Nodules

A

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
236
Q

Pleural Effusion

A

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
237
Q

loculations

A

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

238
Q

Pneumothorax

A

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
239
Q

Cor Pulmonale

A

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!
240
Q

Pulmonary Embolism

A

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)
241
Q

Pulmonary HTN

A

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
242
Q

Idiopathic Pulmonary Fibrosis

A

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
243
Q

Asbestosis

A

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***
244
Q

Coal Worker’s Pneumoconiosis

A

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
245
Q

Silicosis

A

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
246
Q

Berylliosis

A

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
247
Q

Sarcoidosis

A

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
248
Q

Obstructive Sleep Apnea

A

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
249
Q

Acute Respiratory Distress Syndrome (ARDS)

A

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
250
Q

Influenza

A

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

251
Q

Histoplasmosis

A
  • Histoplasma
  • Systemic 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
252
Q

Cryptococcosis

A
  • 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

253
Q

Pneumocystis

A
  • 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

254
Q

Strep pneumoniae

A
  • gram + diplococci, ENCAPSULATED
  • causes pneumonia:
    • rusty mucus
    • productive cough
    • fever
    • malaise
    • sudden onset chills and rigors (violent shaking)
  • causes: bacteremia and meningitis
  • tx: Ceftriaxone
255
Q

Viral PNA

A

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
256
Q

Viral PNA

A

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
257
Q

Asthma

A

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
258
Q

Cystic Fibrosis

A

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)
259
Q

Foreign Body Aspiration

A

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
260
Q

Newborn Respiratory Distress Syndrome

A

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
261
Q

Bronchiectasis

A

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

262
Q

Loop Diuretics

A

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
263
Q

Thiazide Diuretics

A
  • 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
264
Q

Net effect of increased calcitriol

A

aka Vitamin D

  • increased absorption of calcium and phosphorous in gut
265
Q

Net Effect of Increased PTH

A

hypercalcemia, hypophosphatemia

266
Q

Net Effect of increased Calcitonin

A

hypocalcemia, hypophosphatemia

267
Q

Hypophosphatemia causes, s/sxs, txs

A
  • 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
268
Q

Hyperphosphatemia causes and tx

A
  • 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
269
Q

Hypermagnesemia causes, sxs, and tx

A
  • 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
270
Q

Cisplatin

A

chemo drug

“punches holes” in renal tubules → hypoK and hypoMg

271
Q

Hypomagnesemia causes, s/sxs, treatments

A
  • 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
272
Q

Amiloride

A

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

273
Q

Causes of Pre-Renal Acute Renal Failure

A
  • 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***
274
Q

PreRenal Acute Renal Failure S/sxs, Dx, and Tx

A
  • 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
275
Q

RIFLE criteria and AKI

A
  • 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
276
Q

AKIN Classification/Staging Classification & AKI

A
  • 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
277
Q

PostRenal AKI Etiology, S/sxs, dx, tx

A
  • 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
278
Q

Acute Tubular Necrosis Etiology

A
  • ***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
279
Q

Acute Tubular Necrosis S/sxs, Dx, Tx

A
  • 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 ***
280
Q

Etiology of Interstitial Nephritis

A
  • 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
281
Q

Interstitial Nephritis S/sxs, Dx, & Tx

A
  • ***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
282
Q

Etiology of Nephrotic Syndrome

A
  • 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
283
Q

Nephrotic Syndrome S/sxs, Dx, & Tx

A
  • 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
284
Q

Etiology of Glomerulonephritis

A
  • 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
285
Q

Glomerulonephritis S/sxs, Dx, & Tx

A
  • 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
286
Q

Staging of CKD

A

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
287
Q

Definition of CKD

A

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)
288
Q

Etiology of CKD

A
  • Diabetes = MOST COMMON CAUSE (30%)
  • HTN (25%)
  • chronic glomerulonephritis (15%)
  • interstitial nephritis, polycystic kidney disease, obstructive uropathy
289
Q

S/sxs of CKD

A
  • 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+
290
Q

Dx of CKD

A
  • 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
291
Q

Tx of CKD

A
  • 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
292
Q

Renal Osteodystrophy

A

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
293
Q

Hydronephrosis

A
  • 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
294
Q

Polycystic Kidney Disease

A

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
295
Q

Renal Vascular Disease

A

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
296
Q

ESRD, Etiology, Dx, and Tx (NOT S/Sxs)

A

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
297
Q

S/sxs of ESRD

A

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
298
Q

Hyperkalemia and EKGs

A
  • shortened QT
  • ST depression
  • Peaked T wave
299
Q

Hypokalemia and EKGs

A
  • decreased T-wave amplitude
  • ST depression
  • increased U-wave amplitude
300
Q

Hypokalemia Causes

A
  • 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
301
Q

Treatment of Metabolic Acidosis

A

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***
302
Q

NaHCO3 IV

A

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
303
Q

K-citrate

A

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+)
304
Q

Tx of Metabolic Alkalosis

A
  • 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******
305
Q

Tx of Respiratory Acidosis

A

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
306
Q

Tx of Respiratory Alkalosis

A

represents hyperventilation

  • sxs: irritability of central and peripheral nervous system
    • light headedness, altered consciousness, cramps, syncope
    • severe cases: HypoPhos shifts from ECF to ICF
  • tx: identify cause and tx accordingly
    • for 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
307
Q

Major Extracellular Ions

A

Na+, Cl-, HCO3-

308
Q

Major Intracellular Ions

A

K+, Mg2+, PO42-, SO42-

309
Q

General Tx strategy for severe volume depletion or hypovolemic shock

A
  • 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
310
Q

Types of Hypernatremia

A
  • Hypernatremia = >145 Na+
  • Hypovolemic Hypernatremia
    • loss of water >>>>> sodium
  • Isovolemic Hypernatremia
    • water loss only
  • Hypervolemic Hypernatremia
    • body has excess sodium and water
      • sodium >>>>>>water
311
Q

NSAIDs and Sodium

A

NSAIDs reduce renal prostaglandins

and prostaglandins inhibit the action of ADH

so NSAID use can increase action of ADH and cause increased water reabsorption

312
Q

Desmopressin (DDVAP)

A

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

313
Q

Hypokalemia Tx

A

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
314
Q

Hyperkalemia Tx

A
  • 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
315
Q

Hypokalemia Etiology, S/sxs, Dx, & Tx

A
  • 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 ***
316
Q

Hyperkalemia Etiology, S/sxs, Dx, & Tx

A

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
317
Q

Hypernatremia Etiology, S/sxs, Pe, Dx, & Tx

A
  • 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
318
Q

Hyponatremia Etiology, S/sxs, PE, & Dx

A

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)
319
Q

Goodpasture’s Syndrome

A
  • 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
320
Q

Hemolytic Uremic Syndrome

A
  • 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
321
Q

Pauci-Immune Vasculitis S/sxs & Tx

A
  • 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
322
Q

Lupus Nephritis S/sxs & Tx

A
  • S/sxs: usually hx of lupus
    • SLE more common in female AA population
    • proteinuria, hematuria, + elevated creatinine
  • Tx: dependent on biopsy classifications
323
Q

Dipstick positive for hemoglobin and myoglobin but no RBCs?

A

Rhabdomyolysis

324
Q

What type of protein is tested for on the urine dipstick?

A

albumin

  • can have a false negative if proteinuria composed of light chains
    • → will be detected in protein precipitation test aka sulfosalicyclic Acid (SSA)
325
Q

What type of protein is tested for on the urine dipstick?

A

albumin

  • can have a false negative if proteinuria composed of light chains
    • → will be detected in protein precipitation test aka sulfosalicyclic Acid (SSA) → Myeloma
326
Q

Normal Urine protein/creatinine ratio

A

< 0.2 or 200

aka SPOT urine protein/SPOT urine creatinine

327
Q

Normal Urine 24 hour protein

A

<200mg/day

328
Q

Microalbuminuria

A

30-300mg/g

329
Q

Macroalbuminuria

A

>300mg/g

330
Q

Rapidly Progressive Glomerulonephritis (RPGN)

A

when the “nephritis” is causing an AKI that is rapidly progressive over days to weeks

  • Nephritis:
    • RBC casts
    • proteinuria <3.5g
331
Q

Non-Oliguria vs Oliguria vs Anuria

A

Non-oliguria: >400mL/day

Oliguria: 100-400 mL/day

Anuria: <50mL/day

332
Q

Indications for Acute Dialysis

A

A: severe metabolic Acidosis

E: Electrolyte Problems (Hyperkalemia)

I: Intoxication (Antifreeze)

O: Overload of fluids

U:Uremic symptoms (pericarditis, altered mental status)

333
Q

Urinalysis Findings of Rapidly Progressive Glomerulonephritis

A

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

334
Q

What is the avg life expectancy after typical patient starts dialysis?

A

4-5 years

335
Q

At what GFR should we refer to nephrology?

A

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

336
Q

Peritoneal Dialysis compared to HemoDialysis

A
  • 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)
337
Q

How many added years would you expect your patient to live with a transplant compared to staying to dialysis?

A

15 years more

338
Q

ACEIs or ARBs in CKD

A

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)
339
Q

Urine Electrolytes for Intrinsic AKI

A
  • Urine Na: >40mEq/L
  • urine osmolality: <350
  • BUN/Creatinine Ratio: 10:1
  • FeNa: >2%
  • FeUrea: >35%
340
Q

Winter’s Formula

A

to calculate expected pCO2

  • Expected pCO2 = (1.5 x bicarb) + 8 +/- 2
  • if pCO2 = higher than expected → additional respiratory acidosis
  • if PCO2 = lower than expected → additional respiratory alkalosis
341
Q

Albuminuria

A

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

342
Q

Proteinuria

A

urine protein: creatinine ratio >0.2g/g

or >200mg/g

343
Q

JG cells

A

along afferent arteriole that detect blood pressure

if BP = low → secrete renin and activate RAAS system

344
Q

Hypernatremia d/t renal cause

A

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

345
Q

Hypernatremia d/t extrarenal cause

A

Insensible losses
GI losses
Fluid shift into cells

Urine osmo >800
Urine Na <10

Hypernatremia will only occur if water intake is inadequate

346
Q

Aldosterone

A

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

347
Q

Spot Urine (K)

A

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

348
Q

Evaluating GFR

A

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

349
Q

AKIN AKI Criteria

A

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

350
Q

ACEI/ARBs in CKD

A

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

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