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R5 - Internal Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

txs for refractory or decompensated HF

A
  • IV (+) inotropic agent and/or vasodilator: dobutamine, milrinone, nitroprusside, NTG, and nesiritide (improves hemodynamics and sxs; milrinone has inotropic and vasodilator activity)
  • Swan Ganz catheters: used to monitor CVP, pulm artery and capillary wedge pressure, CO, systemic and pulm vascular resistance
  • Extracorporeal ultrafiltration: removes intravasc. fluid - compensatory movment of fluid from interstitial compartment, relives pulm and periph edema and improves HF class, restores responsiveness to loop diuretic
  • Mechanical circ support: intra-aortic balloon pump (best for short term use), cardiopulm assistive device (full cardiopulm support but limited use outside cath lab), left vent assist device (temporary support until transplant, can be long-term for those not candidates for transplant), Cardiac transplantation = DEFINITIVE
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2
Q

Myocarditis

A
  • Viruses: COXSACKIE A VIRUS, parvovirus 19, HHV-6
  • Bacteria: group A strep, lyme dz, mycoplasma
    • lupus, meds (sulfonamides), idiopathic
  • Classic: YOUNG M
  • sxs: asxatic OR viral prodrome - fatigue, fever, malaise, myalgias, HF sxs (dysp at rest, exercise intol, syncope)
  • signs: tachypnea, tachycardia, hepatomegaly, S3 +/- S4, HoTN, dec pulses, AMS
  • complications: pericarditis, CHF, toxic megacolon, arrhythmias, death
  • diagnostics: elevated cardiac enzymes (CK-MB, troponin), ESR high, endomyocardial bx (definitive, GOLD STANDARD): infiltrations of lymphocytes with myocardial tissue necrosis
    • imaging: CXR cardiomeg, EKG sinus tach, Echo ventricular dysfn
  • tx: supportive (diuretics i.e. ACEi, inotropic drugs i.e. dopamine, dobutamine, milrinone), treat underlying cause and any complications
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3
Q

Acute pericarditis

A
  • most commonly IDIOPATHIC or dt viral infxn (coxsackie virus), lupus
  • MC in men <50yo, post-viral illness, 1-2wk after MI (dressler syndrome), renal failure (uremia)
  • sxs: pleuritic (substernal radiating chest pain - sharp, worse with deep insp.), positional (relieved by sitting upright and leaning forward, worse with lying supine, coughing, swallowing
  • signs: pericardial friction rub: specific, not always present - heard during exp, pt sitting up, leaning forward, intermittent, scratching high pitched sound
  • dx: leukocytosis, diffuse ST elevation and PR depression in precordial leads, echo is normal (r/o tamponade)
  • tx: NSAIDs or aspirin, colchicine, steroids if refractory, abx if infectious
  • prognosis: most recover in 1-3wks
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4
Q

Pericardial effusion

A
  • secondary to pericarditis, uremia, or cardiac trauma: restrictive pressure on the heart
  • sxs: painful or painless, cough and dyspnea, atypical chest discomfort, dizziness (low BP), palps
  • signs: periph edema, distant heart sounds
  • complications: as effusion increases, CO and BP dec, falling to critical levels (tamponade)
  • dx: CXR or echo determine extent of effusion or calcification (inc pericardial fluid, cardiomeg), EKG shows nonspec T wave changes, low QRS voltage (alternans)
  • tx: pericardiocentesis to relieve fluid accumulation; if recurrent, surgery with a pericardial window
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5
Q

cardiac tamponade

A
  • fluid compromises cardiac filling and impairs cardiac output
  • signs: beck’s triad - biphasic scratching sound (muffled heart sounds), HoTN, JVD, tachycardia, tachypnea, Kussmaul’s sign, pulsus paradoxus
  • dx: echo shows increased pericardial fluid, diastolic collapse of cardiac chambers, narrow pulse pressure
  • tx: pericardiocentesis
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6
Q

pulsus paradoxus, Kussmaul’s sign, pericardial knowck, electrical alternans

A
  • pulsus paradoxus: >10mm drop in systolic plood pressure with inspiration; pulses disappear with insp as well
  • Kussmaul’s sign: increased JVP with insp
  • Pericardial knock: high pitched third heart sound from sudden cessation of ventricular filling in early diastole dt thick inelastic pericardium
  • Electrical alternans: alteration of QRS complex height on EKG dt mvmt of the heart within pericardial sac
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7
Q

stress EKG

A
  • confirms angina, evaluates response of tx, identifies pts with CAD with high risk of ACS
    • if ST depression or if pt has CP, HoTN, or significant arrhythmias
      • if +, send pt for cardiac catheterization
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8
Q

stress echo

A
  • performed before and after exercise
  • more sensitive than stress EKG for ischemia
  • if +, cardiac cath
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9
Q

cardiac catheterization

A
  • most accurate method for specific cardiac diagnosis
  • provides info on hemodynamics, intracardiac pressure, CO, O2 sat
  • Indications:
    • after + stress test
    • pt w/ angina when noninvasive tests are nondiagnostic, angina occuring despite meds, angina soon after MI, dx dilemma
    • severely sxatic pt needing urgent dx
    • evaluation of valve dz
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10
Q

Coronary CT angiography

A
  • definitive test for CAD (GOLD STANDARD)
  • most accurate method
  • determines whether revasc is needed
  • can perform PCI at same time with balloon or stent
  • stenosis >70% is significant
  • if severe (left main or 3-vessel), refer for CABG
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11
Q

PCI vs CABG

A
  • administer aspirin indefinitely and P2Y12 antag for 1-3mos after implantation of bare metal stent to reduce coronary thrombus formation
  • administer aspirin indef + P2Y12 antag for at least 1 yr after implantation of drug-eluting stent
  • defer noncardiac surg for at least 12mos
  • use of drug-eluting stents that locally deliver antiproliferative drugs can reduce restenosis to less than 10%
  • CABG: anastomosis of one or both internal mammary arteris or a radial artery to the coronary artery distal to obstructive lesion is preferred procedure; section of vein (usually saphenous) is used to form connection between aorta and coronary artery distal to obstructive lesion
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12
Q

PCI indications, benefits, CI, and prognosis

A
  • indications: symptom-limiting angina pectoris, despite medical tx, accompanied by evidence of ischemia during stress test
    • tx stenoses in native coronary arteries as well as in bypass grafts in pts who have recurrent angina after CABG
  • benefits: more effective than medical tx for relief of angina, improves outocmes in pts w/ unstable angina or early in MI w/ and w/out cardio shock, less invasive than CABG
  • CI: left main coronary artery stenosis
  • Prognosis: adequate dilation with relief of angina in >95% cases
    • recurrent stenosis occurs in 20% cases w/in 6mos
    • restenosis MC in pts w/ DM, small arteries, incomplete dilation of stenosis, long stents, occluded vessels, obstructed vein grafts, dilation of LAD, and stenoses containing thrombi
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13
Q

CABG indications, benefits, CI, prognosis

A
  • indications: L main coronary a. stenosis
    • ideal candidate = male, <80yo, no other complicated dz, angina not controlled by medical tx or cant tolerate medical tx
  • benefits: safe, mortality rates <1%, superior to PCI in preventing death, MI, and repeat revasc. in pts with DM and multivessel dz
  • CI: none
  • prognosis: angina abolished or greatly reduced in 90% pts
    • w/in 3y, angina recurs in 25% pts but is rarely severe
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14
Q

stable angina etiology, RF, sxs

A
  • etiology: fixed atherosclerosis narrowing arteries
    • O2 supply < )2 demand
  • major RF: DM (worst), HLDL (high LDL), HTN (most common), smoking, age (m>45, w>55), FHx premature CAD or MI in 1st degree relative, low HDL
    • minor RF: obesity, sedentary, stress, ETOH
  • sxs: CP or substernal pressure (lasts <10-15m, heaviness, pressure, squeezing, tightness, rarely sharp), gradual onset pain, increases with exertion or emotion, relieved with rest or NTG
    • Levine sign: clenched fist over sternum and clenched teeth when describing CP
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15
Q

stable angina dx and tx

A
  • dx: EKG - normal, Q-waves (prior MI)
    • cardiac stress test
  • tx: sublingual NTG - IV NTG
    • coronary angiography: if severely sxatic despite medical tx
  • prognosis: depends on LVEF: <50% = increased mortality
    • vessels involved: left main = poor prognosis, 2-3 vessels total = worst prognosis
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16
Q

congestive heart failure

A
  • decompensated: evidence on PE or chest radiograph of pulm edema, audible 3rd heart sound or increased JVP
  • Left ventricular failure: sxs of low cardiac output and congestion (SOB) dt systolic or diastolic dysfn
  • R ventricular failure: sxs of fluid overload almost always dt LVF
  • MCC systolif HF (reduced EF): ISCHEMIC CARDIOMYOPATHY (CAD with resultant MI an dloss of fning myocardium)
  • systolic dysfn: difficulty with ventricular contraction
  • diastolic dysfn: difficulty with ventricular relaxation; results from HTN and associated with aging; related to myocardial m. stiffness and LVH
  • HF with preserved EF
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17
Q

congestive heart failure etiology, RF, and sxs

A
  • MCC: CAD, HTN, DM
    • LV remodeling: dilation, thinning, mitral valve incompetence, RV remodeling
    • 75% have preexisting HTN
    • MCC of transudative (extravascular fluid) pleural effusions
    • mostly >65yo
  • sxs:
    • exertional dyspnea (SOB), then dyspnea with rest, chronic nonproductive cough, worse in recumbent position
    • fatigue, orthopnea, night cough, relieved by sitting up or sleeping with additional pillows, paroxysmal nocturnal dyspnea, nocturia
  • signs:
    • cheyne-stokes breathing, edema (ankles, pretibial (cardinal)), RALES, additional heart sounds:
      • S4 = diastolic HF (preserved EF)
      • S3 = systolic HF (reduced EF) with volume overload - tachycardia, tachypnea
    • jugular venous pressure >8cm
    • cold extremities, cyanosis, hepatomegaly (ascites, jaundice, peripheral edema)
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18
Q

congestive heart failure dx and tx

A
  • dx:
    • labs: CBC, CMP, UA +/- gluc, lipids, TSH
    • Serum BNP: increases with age and renal impairment, elevated in HF, differentiates SOB in HF from noncardiac issues
    • 12-lead EKG
    • CXR: kerley B lines
    • Echo: differentiates HF _/- preserved LV diastolic fn
    • Reduced pulse pressure and SVR
  • tx:
    • acute management: LMNOP
      • Lasix
      • Morphine (reduces preload)
      • Nitrates (reduces preload)
      • O2
      • Position
    • ACEi
    • CCB in diastolic HF
  • poor prognostic factors: CKD, DM, low LVEF, severe sxs, old
  • 5y mortality = 50%
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19
Q

when to refer HF vs admit

A
  • Refer: new sxs no explained by obvious cause, continued sxs and reduced LVEF (<35%)
  • Admit: unexplained new or worsening sxs or + biomarkers indicating acute MI, hypoxia, fluid overload, pulm edema not resolved as outpt
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20
Q

hypertension sxs, dx, and tx

A
  • sxs: >140/90 during at least 2 separate visits
    • mostly asx w/ nonsepcific HA
  • signs: BMI and waist circumference, BP in both arms, compare radial and femoral pulses
    • examine for abdominal aortic masses, PMI, murmurs, bruits, fundoscopic exam for eye changes
  • dx: EKG: LVH with strain
    • CXR
    • Labs: CBC, CMP, tox, preg, TSH
      • Hgb/Hct (decreased)
      • BUN, Cr, glucose (increased)
      • urinary gluc, prot, sediment: renal dz or DM
      • UA: hematuria or proteinuria
      • lipid profile
  • tx: Goal = <140/90 for gen pop, DM, and renal dz
    • older than 60 = <150/90
    • lifestyle modification = first line
      • DASH diet, weight loss, smoking cessation, limit ETOH and Na
    • Meds: ACEi (DM or renal dz), thiazide (AA), CCB, aldo antagonists (for refractory HTN, post MI, HF), alpha blockers (BPH), hydralazine (refractory HTN)
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21
Q

Primary (essential) HTN

A
  • 90-95% of cases
  • Multifactorial: genetic predisp (old age, AA), environmental (high Na, obese), sympathetic NS, abnl cardio or renal development, imbalance in RAAS, deficit in sodium secretion, abnl Na-K exchange
  • Exacerbating facotrs: excessive ETOH, tobacco, sedentary, polycythemia, NSAIDs, low K intake
  • tx: Goal = <140/90 for gen pop, DM, and renal dz
    • older than 60 = <150/90
    • lifestyle modification = first line
    • DASH diet, weight loss, smoking cessation, limit ETOH and Na
    • Meds: ACEi (DM or renal dz), thiazide (AA), CCB, aldo antagonists (for refractory HTN, post MI, HF), alpha blockers (BPH), hydralazine (refractory HTN)
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22
Q

secondary HTN

A
  • parenchymal dz, renal artery stenosis, coarctation of aorta, pheochromocytoma, Cushings syndrome (excess cortisol), hyperthyroidism, primary hyperaldosteronism, chronic steroid use, estrogen use, NSAID use, sleep apnea
  • tx: treat underlying dz
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23
Q

hypertensive urgency

A
  • BP needs to be reduced within hours
  • Persistently elevated higher than 220 systolic or 125 diastolic or accompanied complications without end-organ damage
  • tx: oral agents: clonidine, captopril, nifedipine, labetolol
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24
Q

Hypertensive emergency (malignant hypertension)

A
  • elevated BP with papilledema or retinal hemorrhage and either encephalopathy or nephropathy, confusion, left ventricular failure, intravascular coagulation
  • Difference: HTN emergency always has retinal papilledema and flame-shaped hemorrhages and exudates
  • must be reduced within 1 h to prevent progression to end organ damage or death
  • diagnostic criteria: persistently elevated higher than 220 systolic, diastolic >130
  • Complications: encephalopathy, nephropathy, ICH, aortic dissection, pulmonary edema, unstable angina, MI, stroke
    • ​on fundoscopic: retinal hemorrhages, exudates, papilledema
  • Hallmark complication: fibrinoid necrosis of the arterioles in the kidney
  • Tx: DONT REDUCE TOO RAPIDLY - can cause ischemia
    • sodium nitroprusside (short acting, titratable, potential for thiocyanate and cyanide tox with prolonged use or renal/hep fail)
    • labetalol (alpha and beta blocker) - preferred in dissection and ESRD
    • Neuro emergencies:
      • encephalopathy, stroke, ICH, SAH: labetalol, nicardipine, esmolol. AVOID nitroprusside and hydralazine
        • reduce MAP 25% over 8h
        • for MI us NTG or BB
      • aortic dissection: use nitroprusside and BB
      • Hydralazine during preg
      • lower BP within first 24-48h by 25%
        • 90% will die after 1-2y
25
Q

endocarditis etiology, RF, and sxs

A
  • MC native valve infection (strep viridans, staph aureus, enterococci)
  • IVDU: staph aureus, tricuspid
  • Prosthetic valve: staph aureus, gram neg or fungi
  • most pts have underlying regurgitant defect providing a nidus
  • sxs: fever, nonspecific sxs (dyspnea, cough, CP, arthralgias, back or flank pain, GI complaints)
  • signs: stable murmur (90%), palatal, conjunctival, or subungal petechiae, splinter hemorrhages, pallor, splenomegaly
  • diagnostic signs:
    • osler nodes (painful, violaceous, raised lesions on fingers, toes, feet)
    • janeway lesions (painless red lesions on palms/soles of feet)
    • roth spots (exudative lesions in retina)
26
Q

endocarditis dx and tx

A
  • dx: 3 sets of blood cultures at least 1h apart, before starting abx
    • echo: required to make dx and identify involved valves (vegetation)
  • tx: empiric abx cover staph, strep, enterococci
    • native valve: vanco alone or + cefazolin
    • Ill pts w/ HF: gentamicin plus cefepime and vanco
    • aortic valve replacement if refractory or abscess (funcal infxn)
  • prophylaxis: abx recommended before invasive dental work or surgical procedures: prosthetic valves, previous IE, some congenital heart dzs (transposition, tetrology), acquired valve disorders, HCM, cardiac transplant pts with valvulopathy
    • ALL OF THE ABOVE GET AMOX 1 hr before procedure (clarith or azith if PCN allergy)
27
Q

Modified duke criteria

A
  • For detecting endocarditis
  • must have one of the following criteria:
    • 2 major
    • 1 major and 3 minor
    • 5 minor
  • Major:
      1. two pos blood cultures of typical causative microorganism
      1. echo showing new valve regurg
  • Minor:
      1. predisposing factor
      1. fever >100.4
      1. vascular phenomena (embolic dz or pulm infarct)
      1. immunologic phenomena (glomeruloneph, osler nodes, roth spots)
        • blood cuture not meeting major criteria
28
Q

hyperlipidemia etiology, RF and sxs

A
  • elevated LDLs increase risk of CAD; higher HDLs = protective; elevated TGs are risk factor for atherosclerosis; severe elevations can cause pancreatitis
    • Recommended screening for pts with no evidence of CVD and NO RISK FACTORS - 35yo
    • NCEP recommends screening at age 20 regardless of risk factors
  • genetic: primary HLD, familial hypercholesterolemia; secondary to DM, ETOH, hypothyroid, obesity, sedentary lifestyle, renal or liver dz, drugs
  • RF: DM (CAD risk equivalent), smoking, HTN, HDL <40, age (>45 men, >55 women), HIV (CAD risk equivalent
  • sxs: eruptive or tendinous xanthomas
    • 2/3 ppl with xanthelasmas affecting eyelidshave normal lipid profiles
    • severe: premature arcus senilis; lipemia retnalis (cream-colored retinal vessels) seen with TG levels >2000mg/dL
29
Q

hyperlipidemia dx and tx

A
  • dx: without RF, order total cholesterol
  • tx: lifestyle changes = first line: reduce total fat intake, saturated fat, dietary cholesterol <200, 30 min aerobic exercise daily, increase antioxidants from fruits and veggies, soluble fiber may reduce LDL
    • CAD prophylaxis (81mg aspirin) unless CI
    • smoking cessation
    • statin tx
  • health maintenance: pts with any evidence of CVD or CAD risk equivalent (DM, HIV should be screened with fasting complete lipid profile)
30
Q

Statins

A
  • HMG-CoA reductase inhibitors
  • reduce cholesterol production in liver and increase ability of liver to remove LDL from blood
  • BEST AT DECREASING LDL, moderate decrease in TGs and increase in HDL
  • Adverse effects: myalgias, mild GI upset; severe = myositis, liver tox, rhabdo
  • monitoring: LFTs and creatinine-phosphokinase if myalgias develop, monitor lipids every 6wk until goals met
31
Q

Niacin

A
  • Reduces long-term risk of CAD by reducing production of VLDL, lowering LDL and increasing HDL; may also reduce TG
  • moderate decrease in LDL, TG; best at elevating HDL
  • adverse effects: prostaglandin-induced NIACIN FLUSHING (may be reduced by taking ASA 30 min prior or a daily NSAID)
  • Monitoring: baseline LFTs, LFTs q6-12wks first year, then q6mo; lipid panel, blood sugar (DM) or platelets and PT (if on anticoagulants), uric acid (gout)
32
Q

Bile-acid sequestrants

A
  • cholestyramine, colesevelam, colestipol
  • bind bile acids in the intestine; resins reduce the incidence of coronary events in middle aged men; no effect on mortality
  • second best at decreasing LDL, mild decrease in TGs, mild elevation HDL
  • Adverse effects: constipation, gas
  • monitoring: fasting lipid profile prior to treatment, then 3 mo after initiation, then 6-12mo thereafter
33
Q

Fibric acid derivatives

A
  • gemfibrozil, clofibrate
  • peroxisome proliferator-activated receptor alpha (PPAR alpha) agonists - most important meds for lowering of TG levels and raising HDL
  • best at lowering TGs, second best at increasing HDL
  • adverse effects: may induce gallstones, hepatitis, myositis
  • monitoring: periodic LFT, CBC, cholesterol in the first year
34
Q

hyperlipidemia goals

A
  • HDL: >40 men, >50 women
  • LDL: <100
  • TG: <150
  • Total cholesterol: <200
35
Q

Coronary artery disease

A
  • risk factor mod: SMOKING CESSATION - cuts risk by 50%
  • Medical tx: ASA + BB
    • Sublingual NTG (for angina)
    • ASA (decreases morbidity and mortality)
    • BB (atenolol and metoprolol are first-line)
    • ACEi (for pts with heart failure)
    • Morphine (venodilation, decreases preload and O2 demand)
    • Nitrates (long acting - need 8 to 10 hr nitrate free interval to prevent tolerance; dilates coronary arteries, reduces preload and myocardial O2 demand; adverse effects = HA, ortho HoTN, tolerance, syncope)
    • CCB - coronary vasodilation, afterload reduction, reduces contractility; secondary tx when BB or NTG not fully effective or maxed out
    • Statins (stabilizes plaques and lower cholesterol)
  • revascularization - does NOT REDUCE RISK OF MI, but improves sxs
    • PCI, CABG, antiplatelet tx
  • Thrombolytic tx (alteplase): first line tx
    • pts who present late and PCI contraindicated, administer ASAP upt to 24hrs after onset of CP, best if given in first 6hrs
36
Q

Peripheral vascular dz or peripheral arterial dz

A
  • in absence of limb-threatening ischemia, sxs of PAD tend to remain stable with med tx
  • if revascularization is needed, percutaneous revasc first, reserve surgery for when arterial anatomy is unfavorable
  • clinical features used to determine if thrombolytic therapy or surg revasc is most appropriate:
    • presumed etiology (embolus vs thrombus)
    • location
    • duration of sxs
    • availability of autologous vein for bypass grafting
    • suitability of pt for surg
  • proximal embolus at bifurcation of common fem artery is ideal lesion for embolectomy
    • embolus to distal vessel Ii.e. tibial a.) may be tx with thrombolytic agent
    • major use of percutaneous transluminal angioplasty (PTA) is in the tx of underlying lesion after clot has been lysed with thrombolytic tx
  • Leriche syndrome: triad of 1) claudication, 2) absent or diminished femoral pulses, and 3) erectile dysfunction
37
Q

intermittent claudication

A
  • occurs distal to level of stenosis or occlusion (calf pain with walking 10-35% of ppl with PAD)
  • sxs: reproducible pain aggravated by sustained exercies, relieved with rest, aching, dull pain, leg pain occurs after certainwalking distances, resolving within 10min, cramping, numbess, weakness, giving way
    • Physical: hair loss on bilateral lower extremities, thinning of skin, diminished pulses
  • dx: treadmill testing using ABIs at rest and after exercise - <0.9 = diagnostic
  • tx: stop smoking (first line), graduated exercise, foot care, control HLD, HTN, weight, DM, avoid extremes of temp, ASA + ticlopidine or clopidogrel (sx relief), cilostazol (PDE inhibitors)
    • surgery: angioplasty, bypass grafting
38
Q

Asx PAD

A
  • screen in pts with abnormal/absent pedal pulses, age >70, age 50-69y with hx of smoking or DM
  • sxs: none
  • dx: ABI - if <0.9 is dx; if 0.91-1.3 normal and no further testing; if >1.3 doppler ankle waveforms and toe pressures
  • tx: preventative = ASA, lipid lowering, blood pressure control
39
Q

PAD or PVD etiology, RF, and sxs

A
  • occlusive atherosclerotic dz of lower extremities
    • superficial femoral artery is MC, popliteal, aortoiliac
  • RF: smoking HLD, DM, HTN
    • Men >40y, AA
  • MCC: atherosclerosis
    • Considered to be a coronary artery disease risk equivalent
    • Common in pts with ESRD
    • 20-50% are asx and 40-50% present with atypical leg pain
  • Sxs: pain in one or more lower extremity muscle groups (cramping thigh, calf, or buttock pain’ intermittent claudication; worse with elevation (reclining))
    • Rest pain felt over distal metatarsals, prominent at night (wakes pt up from sleep), hangs foot over side of bed or stands to relieve pain
  • signs: diminished/absent pulses, muscular atrophy, hair loss distal to obstruction, thick toenails, decreased skin temp, localized skin necrosis (toes), nonhealing, infarction, or gangrene, pallor of elevation and rubor of dependency
40
Q

PAD or PVD dx and tx

A
  • dx: hypercholesterolemia >240, hypertTG >250
    • ABI testing - if <0.9 = dx
    • doppler - reduced or interrupted flow
    • Arteriography (gold standard)
  • tx: prevention of atherosclerosis (control HLD, HTN, weight, DM
    • manage primary HLD: statins, diet exercise (walk to point of claudication, rest, then continue walking), foot care
    • reduce BP, STOP SMOKING (most important)
    • Medical intervention: ASA and ticlopidine or clopidogrel (sx relief), cilostazol (PDE inhib)
    • Surgery: angioplasty (preferred), adjunctive stenting, bypass grafting
41
Q

aortoiliac dz

A
  • inflow dz
  • sxs: buttock or thich claudication = more disabling
  • tx: percutaneous transluminal angioplasty (PTA) - iliac artery and stenting
    • aortoiliac bypass
    • aortofemoral bypass
42
Q

femoropopliteal dz

A
  • disease below inguinal ligament = outflow dz
  • tx: balloon angio/stenting of femoral or superficial femoral artery
    • surgical bypass (femoral to above-knee popliteal bypass, femoral to below-knee bypass
43
Q

coronary artery vasospasm (Prinzmetal variant) etiology, RF, sxs

A
  • etiology: smooth muscle constriction (spasm) of the coronary artery w/out obstruction - leads to MI, ventricular arrhythmias, sudden death
  • known triggers: hyperventilation, cocaine, tobacco use, provocative agents (acetylcholine, ergonovine, histamine, serotonin)
  • Nitric oxide deficiency: increased activity of potent vasoconstrictors and stimulators of smooth muscle proliferation
  • 50yo, females
  • sxs: nonexertional chest pain similar to unstable angina
    • normal exercise tolerance
    • pain is cyclical (most occur in morning hours, no correlaiton to cardiac workload)
44
Q

Prinzmetal angina dx and tx

A
  • dx: EKG (ST segment or Twave abnormalities)
    • Cardiac enzyme: normal troponin, CK-MB
    • Check Mg level, CBC, CMP, lipid panel
  • tx: stress testing with myocardial perfusion imaging or coronary angiography
    • pharmacotherapy (SL, topical, or IV nitrates (initial), antiplatelet, thrombolytics, statins, BB
    • once dx made, CCB and long-acting nitrates used for long term prophylaxis (amlodipine)
45
Q

pharm tx of ACS/chest pain (angina)

A
  • Clopidogrel: reduces incidence of MI in pts with USA compared with ASA alone
  • LMWH: continue for at least 2d; PTT not followed
  • UFH: PTT 2-2.5x normal if using UFH
  • start pt with USA or NSTEMI with high LDL on statin
46
Q

Unstable angina

A
  • O2 demand unchanged, supply decreased, secondary to low resting coronary flow
  • sxs: chronic angina increasing in frequency, duration, or intensity of pain OR
    • new onset angina that is severe and worsening OR
    • angina at rest
  • dx: EKG shows ST segment or Twave abnl
    • cardiac enzymes show normal troponin and CK-MB
  • tx: admit to unit with continuous cardiac monitoring, establish IV access, O2, pain control with NTG and morphine
    • ASA, clopidogrel, BB (first line), LMWH, replace electrolytes, if response to med tx - stress test to determine if catheterization/revascularization necessary
    • reduce RF: stop smoking, weight loss, tx DM/HTN/HLD
    • heparin
  • NOT BENEFICIAL: thrombolytics and CCB
47
Q

NSTEMI and STEMI etiology, RF, sxs

A
  • NSTEMI: caused by severely narrowed artery that is not 100% blocked
  • STEMI: caused by 100% blockage of a coronary artery, necrosis of myocardium (thrombotic occlusion), asx in 1/3 of pts
  • sxs: CP (intense, substernal, crushing), radiation to neck, jaw, arms, back, left side, similar to angina pectoris but more severe and lasts longer, pain doesnt respond to NTG, epigastric, SOB, sweating, nausea, vomiting, weakness fatigue, syncope
48
Q

NSTEMI and STEMI dx and tx

A
  • dx:
    • NSTEMI: EKG shows pathologic Q waves, elevated trop and CK-MB
    • STEMI: EKG shows peaked T-waves, ST elevation, Q waves, T wave inversion
    • in both, monitor BP/HR, cardiac enzymes
  • tx: admit to ccu, establish IV access, O2, NTG/morphine
    • MONA: morphine, O2, nitrates, ASA
    • BB, ACE, heparin, statin
  • prognosis: 30% mortality rate
49
Q

dressler syndrome

A
  • post-MI syndrome occurs 1-2 wk post-MI
  • sxs: fever, malaise
  • complications: pericarditis, pleuritis
  • dx: CBC shows leukocytosis
  • tx: ASA (first line), ibuprofen
50
Q

hypertriglyceridemia

A
  • often caused or exacerbated by uncontrolled DM, obesity, sedentary habitus
  • RF: CAD, usually asymptomatic until TG >1000-2000 mg/dl
  • sxs: GI: midepigastric pain, but can occur in chest or back areas; nausea or vomiting
  • signs: TTP over midepigastric, RUQ/LUQ, hepatomegaly, dyspnea, xanthomas, corneal arcus, xanthelasmas, memory loss, dmentia, depression
  • dx: decreased pedal pulses or ABI index in presence of PAD, lipid panel, chylomicron determination, FBG, TSH, UA, LFTs
  • tx: lifestly mod (diet exercise, weight loss, smoking cessation, limit ETOH)
    • pharm: fibric acid derivatives, niacin, omega 3 FAs, statins
    • plasmapheresis in setting of severe hyperTG
51
Q

cardioversion vs defib

A
  • Cardioversion indicated for A-fib, A-flutter, VT WITH PULSE, SVT
  • Defibrillation indicated for VT WITHOUT PULSE, V-fib
  • Automatic implanted defib: VT not controlled by med tx, V-fib
  • Pharm cardioversion (ibutilide, procainamide, flecainide, sotalol, amiodarone): if pharm cardioversion fails
52
Q

chronic venous insufficiency (venous stasis) etiology, sxs

A
  • mostly dt valvular dysfn - leads to loss of compartmentalization of veins, leads to distention and increased pressure - transmitted to microvasc - basement membrane thickening, inc capillary elongation, skin changes
  • varicose veins, postphelbitic syndrome
  • age 30-40, F > M, 2% of gen pop
  • aggravating factors: preg, inc blood volume, inc cardiac output or venocaval pressure, progesterone
  • RF: family hx, DVT, female, estrogen, age, obesity, prolonged standing
  • sxs: heaviness or aching of leg (lower extrem edema) - worse with prolonged standing and relieved by walking, relief with elevation, edema worse at end of day and with standing, shoes feel tight in evening, night cramps, itching 2/2 irritation
  • signs: hyperpig, distal edema, erythema, dry tight skin, ulceration
  • complications: 50% have varicose veins, fibrosis, atrophy
53
Q

chronic venous insufficiency (venous stasis) dx and tx

A
  • duplex US to assess valve closure (nl = 0.5-1s), <0.5s = diagnostic, CEAP classification
  • tx: conservative = for at least 3 mos, graduated compression hose (1st line), compression for open ulcer
    • vein ablation tx = indications are vein hemorrhage superficial thrombophlebitis, CIs are preg, DVT, mod to severe PAD, and joint dz
    • injection sclero (initial) - for telangiectasias (CEAP cat 1), reticular veins, small varicose veins
    • vein ligation/excision for CEAP cat 2 (>3mm)
    • thermal ablation, venous reconstruction
54
Q

varicose veins

A
  • “blow out” of incompetent veins, 10-30% of gen pop, MC in F
  • sxs: enlarged, tortuous superficial leg veins (seen best with standing), painful and itchy
  • dx: tourniquet test: applied to leg that has been elevated; release after pt stands and veins fill instantly
  • tx: injection sclero with prolonged compression, vasc surg for ligation and removal saphenous veins, endoscopic subfascial dissection of perforating veins
55
Q

Dilated Cardiomyopathy

A
  • MC type (95%) associated with reduced strength of vent contraction, resulting in dilation of L vent, most Idiopathic (50%), age 20-60, CAD with prior MI is common cause, genetic abnormalities, excessive ETOH, postpartum, doxorubicin, endocrinopathy, myocarditis
  • Sxs: dyspnea, fatigue, sx of L and R HF
  • Signs: S3 gallop, pulm crackles (rales), inc JVP
  • Complications: arrhythmias, sudden death, embolic events (10%)
  • Dx: EKG shows nonspec ST and T wave changes, conduction abnlities, vent ectopy, CXR cardiomeg, pulm congestion, echo
  • Tx: CHF supportive tx (ACEi, diuretics, BB, Na restriction), digoxin, vasodilators, ICD if EF <30-35%, cardiac transplant, poor prognosis (most die within 5y
  • Health maint: abstinence from ETOH
56
Q

Hypertrophic Cardiomyopathy

A
  • Asian descent, elderly
  • Most: autosomal dominant trait
  • Stiff, hypertrophied ventricle with elevated diastolic filling pressures (diastolic dysfn)
  • Secondary HCM: dt longstanding HTN or aortic stenosis (not true HCM)
  • Sxs: dyspnea, angina, syncope and arrhythmias common (palps, dizziness), sudden cardiac death
  • Signs: sustained PMI or triple apical impulse, loud S4 gallop, variable systolic murmur, bisferious pulse (carotid pulse with two upstrokes), jucular venous pulse without prominent “a” wave, harsh systolic, crescendo-decrescendo murmur heard at LUSB (better with squatting, lying down or straight leg raise, sustained handgrip), worse with exercise, Valsalva, standing (decrease preload and afterload)
  • Dx: CXR unremarkable, EKG nonspecific ST and T wave changes, septal Q waves, LVH, echo asymmetrical septal hypertrophy, systolic anterior motion of mitral valve, small left ventricle, diastolic dysfunction
  • Tx: BB (1st line or CCB; disopyramide for neg inotropic effects, inc vent diastolic filling time, caution use of digoxin, nitrates, and diuretics), surgery (momectomy – resection of hypertrophied septum, for sever, refractory pts), alcohol septal ablation (ethanol destroys extra myocardial tissue ), dual chamber pacing, implantable defibrillator, mitral valve replacement)
  • Health maintenance: avoid extreme exertion or strenuous exercise, avoid dehydration
57
Q

Restrictive cardiomyopathy

A
  • Infiltraion of myocardium – impaired diastolic vent filling dt dec vent compliance
  • MCC: collagen defect dz (amyloidosis, radiation, post-op changes, DM, endomyocardial fibrosis)
  • Sxs: dyspnea, dec exercise tolerance, advanced = right sided congestive HF sxs (periph edema, hepatic congestion)
  • Signs: pulm HTN, HSM, RUQ tenderness, hepatojugular reflex, JVD, Kussmaul’s sign, S3
  • Dx: CXR mild to mod enlarged cardiac silhouette (enlarged atria), EKG low volt changes, echo ventricles not dilated with normal wall thickness, marked dilation of both atria, diastolic dysfn with normal systolic fn, high pulm cap wedge pressure, endomyocardial bx = GOLD STANDARD
  • Tx: diuretics and vasodilators, tx underlying probs (hemochromatosis – phlebotomy and deferoxamine, sarcoidosis – glucocort, amyloidosis – no tx, systolic dysfn - digoxin
58
Q

acute rheumatic fever

A
  • supporting RF: previous (+) throat cx or RAT (66%), elevated or rising strep ab titer
  • complications: mitral stenosis
  • major criteria: polyarthritis, carditis, chorea, erythema marginatum (red patches with central clearing), subcutaneous nodules)
  • minor criteria: fever (>39), arthralgia, elevated CRP or ESR, prolonged PR interval (mitral regurg)
  • dx: throat cx or RAT, ASO titer establishes recent strep infxn
    • dx criteria: 2 major or 1 major and 2 minor + supporting evidence
    • exceptions: chorea or indolent carditis with normal anti strep ab levels
  • tx: PO ASA QID for 2-4 wk, 1.2 million U benzathine PCN IM, prednisone,
  • prophylaxis: benzathine PCN G

R5 - Internal Medicine (10 decks)

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