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IM > CVS > Flashcards

CVS Flashcards

1
Q

AORTIC STENOSIS

A

MURMUR: systolic crescendo-decrescendo w/ ejection click

L&R: upper sternal border -> radiates to carotids

OTHER FINDINGS:
paradoxical S2 split
S4
narrow pulse pressure

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2
Q

AORTIC INSUFFIECIENCY

A

MURMUR: early decrescendo diastolic

L&R: left lower sternal border

OTHER FINDINGS:
de Musset sign
Quincke’s sign

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3
Q

MITRAL INSUFFICIENCY

A

MURMUR: holosystolic murmur

L&R: apex; radiates to back or clavicular area

OTHER FINDINGS:
diminished S1
wide S2
S3 gallop

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4
Q

MITRAL STENOSIS

A

MURMUR: S2 w/ opening snap then low pitched diastolic rumble

L&R: left lateral decubitus position with bell

OTHER FINDINGS:
high left atrium pressure

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5
Q

MITRAL VALVE PROLAPSE

A

MURMUR: midsystolic click -> systolic murmur

L&R: apex

OTHER FINDINGS:
standing: inc murmur
Squattinf: dec murmur

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6
Q

PULMONARY INSUFFICIENCY

A

MURMUR: crescendo-decrescendo

L&R: Left upper sternal border

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7
Q

PULMONARY STENOSIS

A

MURMUR: diastolic crescendo-decrescendo

L&R: Right upper sternal border

OTHER FINDINGS:
ejection click

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8
Q

TRICUSPID INSUFFICIENCY

A

MURMUR: blowing holosystolic murmur

L&R: Left lower sternal border

OTHER FINDINGS:
Carvallo’s sign
S3 & S4

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9
Q

TRICUSPID STENOSIS

A

MURMUR: diastolic rumble

L&R: Left lower sternal border

OTHER FINDINGS:
ejection click

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10
Q

SYSTOLIC MURMURS

A

Aortic stenosis
Pulmonary stenosis
Tricuspid regurgitation
Mitral regurgitation

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11
Q

DIASTOLIC MURMURS

A

Aortic regurgitation
Pulmonary regurgitation
Tricuspid stenosis
Mitral stenosis

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12
Q

FINDINGS THAT SUGGEST A LARGE INFARCT IN NSTEMI

A

Diaphoresis
Sinus tachycardia
3rd or 4th heart sounds
Bibasilar rales
Hypotension

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13
Q

RUPTURED PLAQUE HAS _____

A

Thin fibrous cap
Collagen poor fibrous cap
Large lipid core
Many macrophages
Fibrin rich thrombus

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14
Q

MAJOR DETERMINANTS OF MYOCARDIAL O2 DEMAND

A

Heart rate
Myocardial contractility
Myocardial wall tension

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15
Q

DETERMINANTS OF ADEQUATE SUPPLY OF O2

A

Level of O2 carrying capacity of blood determined by inspired O2, pulmonary function, and Hgb concentration, & level of coronary flow

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16
Q

Histology findings in simulant induced cardiomyopathy (due to cocaine or amphetamine use)

A

Microinfarcts and thrombus secondary to endothelial dysfunction

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17
Q

Histology findings in acute viral myocarditis

A

Massive myocardial lymphocytic infiltration with clear myocyte damage

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18
Q

Histology findings in alcoholic cardiomyopathy

A

Cardiomyocyte atrophy with interstitial and perivascular fibrosis and hyperplasia of small mitochondria

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19
Q

Histology findings in amyloidosis

A

Birefringence pattern of congo red staining between myocardial fubers under polarized light

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20
Q

Pericarditis that happens after myocardial infarction

A

Dressler’s syndrome

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21
Q

Diagnosed when a typical viral syndrome occurs without cardiac symptoms but with elevated biomarkers

A

Possible subclinical myocarditis

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22
Q

Diagnosed when there is histologic or immunohistologival evidence of inflammation on endomyocardial biopsy

A

Definite myocarditis

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23
Q

Risk factors for peripartum cardiomyopathy

A

Increased maternal age
Incresed parity
Twin pregnancy
Malnutrition
Use of tocolytic therapy for premature labor
Preeclampsia or toxemia of pregnancy

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24
Q

Alternating strong and weak pulse resulting from variations in left ventricular stroke volume with every cardiac cycle because of incomplete LV recovery

A

Pulsus alternans

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25
Q

Exaggerated fall in a patient’s BP during inspiration by >10mmHg; seen in cardiac tamponade and constrictive pericarditis

A

Pulsus paradoxus

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26
Q

Weak pulse seen in patients with aortic stenosis

A

Pulsus parvus et taedus

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27
Q

Increased pulse with double systolic peak seen in AR

A

Pulsus bisferiens

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28
Q

Concentric hypertrophy

A

Increased mass is out of proportion to chamber volume

Pressure overload
Increased LV mass
Increase relative wall thickness

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29
Q

Eccentric hypertrophy

A

Increase in cavity size or volume

Volume overload
Increased LV mass
Normal relative wall thickness

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30
Q

Presents with severe sharp or tearing pain in retrosternal area

A

Acute aortic dissection

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31
Q

Presents with a few seconds of sharp chest pain reproduced by preaaure on the chest

A

Costochondritis

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32
Q

Presents with chest discomfort radiating to trapezius

A

Acute pericarditis

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33
Q

Presents with substernal or epigastric pain sometimes related to food intake

A

GI disorders (GERD/esophageal spasm)

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34
Q

Contraindications to exercise stress testing

A

Rest angina within 48 hours
Unstable rhythm
Severe aortic stenosis
Acute myocarditis
Uncontrolled HF
severe pulmonary hypertension
Active infective endicarditis

35
Q

Indications for revascularization

A

Unstable phase of disease
Intractable symptoms
High risk coronary anatomy
DM
Impaired LV function

36
Q

RELATIVE CI TO FIBRINOLYTICS IN PX WITH STEMI

A
  1. Current use of anticoagulants (INR >/=2)
  2. Recent (<2 weeks) invasive or surgical procedure
  3. Prolonged (>10 min) CPR
  4. Known bleeding diathesis
  5. Pregnancy
  6. Hemorrhagic ophthalmic condition (e.g. hemorrhagic diabetic retinopathy)
  7. Active PUD
  8. Hx of severe HPN that is currently controlled
37
Q

ABSOLUTE CI TO FIBRINOLYTICS AMONG PX WITH STEMI

A
  1. History of cerebrovascular hemorrhage at any time
  2. Non-hemorrhagic stroke or other cerebrovascular event within the past year
  3. Marked hypertension (reliably determined systolic AP >180 mmHg and/or a diastolic pressure >110mmHg) at any time during acute presentation
  4. Suspicion of aortic dissection and active internal bleeding (excluding menses)
38
Q

Raynaud’s Phenomenon

A

Characterized by:
- Episodic digital ischemia
- Sequential development of digital blanching, cyanosis, and rubor of the fingers after cold exposure and subsequent rewarming
- sensation of cold or numbness or paresthesia of the digits often accompanies the phases of pallor and cyanosis
- occurs in patients whose vocations require the use of vibrating hand tools

39
Q

Pernio

A

Vasculitic disorder associated to exposure to cold
Raised erythematous lesions develop most commonly on the toes or fingers in cold weather

40
Q

Erythromelalgia

A

Characterized by burning pain and erythema of extremities

Feet are more involved more frequently that the hands

Males affected more frequently females

41
Q

Acrocyanosis

A

Arterial vasoconstriction and secindary dilatation of the capillaries and venules with resultung persistent cyanosis of the hands, less frequently the feet

42
Q

Originates from GIT; associated with colonic polyps and tumors

A

Streptococcus gallolyticus (S.bovis biotype 1)

43
Q

Located in the oral cavity, skin, and URT

A

Viridand streptococci
Staphylococci
HACEK (Haemophilus, Aggregatibacter, Cardiobacterium hominis, Eikenella corrodens, & Kingella kingae)

44
Q

Isolated from cultures of human rectum, vagina, cervix, urethra, skin, and pharynx

A

Streptococcus agalactiae (GBS)

45
Q

Most common bacterial species causing IE

A

Staphylococcus aureus

46
Q

Most common bacterial species causing IE

A

Staphylococcus aureus

47
Q

Diagnosed when typical viral syndrome occurs without cardiac symptoms, but with elevated biomarkers of cardiac injury, ECG suggestive of acute injury, and/or reduced left ventricular EF or regional wall motion abnormality

A

Possible subclinical acute myocarditis

48
Q

Diagnosed when criteria for myocarditis are met and accompanied by cardiac symptoms such as SOB, chest pain, etc.

A

Probable acute myocarditis

49
Q

Diagnosed when histologic or immunohistologic evidence of inflammation on endomyocardial biopsy is present

A

Definite myocarditis

50
Q

Most commonly diagnosed non-infective inflammatory process affecting the myocardium

A

Granulomatous myocarditis
Sarcoidosis
Giant Cell Myocarditis

51
Q

Mechanism of paroxysmal a.fib

A

Automaticity

52
Q

Mechanism of Torsades de pointes

A

Early afterdepolarization

53
Q

Mechanism of ventricular tachycardia from digoxin toxicity

A

Delayed afterdepolarizations

54
Q

Mechanism of atrial flutter

A

Reentry

55
Q

Blocks multiple cardiac ionic currentd and has sympatholytic activity; most effevtive anti-arrhythmic for supressing VAs

A

Amiodarone

56
Q

Reversal agent of Dabigatran

A

Idarucizumab

57
Q

Reversal agent of rivaroxaban, apixaban, edoxaban, & apixaban

A

Andexanet alfa

58
Q

Reversal agent of warfarin

A

FFP, Prothrombin complex concentrate, Vit K

59
Q

Direct vasodilator that has antioxidant and nitric kxide enhancing actions

A

Hydralazine

60
Q

Non-selective aldosterone antagonist; binds progesterone and androgen receptors; SE include gynecomastia, impotence, and menstrual abnormalities

A

Spironolactone

61
Q

Newer agent that doesn’t have the same SE as spironolactone; selective aldosterone antagonist

A

Eplerenone

62
Q

Indications for using CCB for IHD

A
  1. Inadequate responsiveness to the combination of BB and nitrates
  2. AE/SE to BB (eg. depression, sexual disturbances, and fatigue)
  3. Angina and hx of asthma or COPD
  4. Sick sinus syndrome or significant atrioventricular conduction distubrances
  5. Prinzmetal angina
  6. Symptimatic PAD
63
Q

Severe asymptomatic HPN (SBP >180 OR DBP >120)

A

Hypertensive urgency

64
Q

BP Parameters similar to HPN urgency + acute target organ damage

A

Hypertensive emergency

65
Q

Patients with BP persistently >140/90 despite taking 3 or more anti-hypertensive including a diuretic

A

Resistant HPN

66
Q

Associated with abrupt increase in BP in a patient with underlying HPN or related to sudden onset HPN in a previously normotensive individual

Recognized by progressive retinopathy (arteriolar spasm, hemorrhages, exudates, and papilledema), deteriorating renal function with proteinuria, microangiopathic hemolytic anemia, and encephalopathy

A

Malignant hypertension

67
Q

Autosomal dominant disorder characterized by elevated plasma levels of LDL-C with relatively normal TG levels; mutation on LDLR gene

A

Familial hypercholesterolemia

68
Q

Adipose tissue in certain fat depots is impaired; loss of subcutaneous fat in the extremities and buttocks; accompanied by increased visceral fat; patients described to have muscular appearance

A

Familial Partial Lipodystrophy

69
Q

Recessive disorder; mixed hyperlipidrmia (elevated TG and LDL) due to accumulation of remnant lipoprotein particles (chylomicron and VLDL or IDL)

A

Familial dysbetalioproteinemia

70
Q

Fasting TGs >150 mg/dl and evidence of elevated cholesterol containing lipoproteins such as LDL-C >130 mg/dl or non-HDL-C >160 mg/dl)

A

Mixed hyperlipidemia

71
Q

Most common familial lipid disorder; mixed lipidemia (plasma TG levels bet 150 and 500 mg/dl and total cholesterol bet 200 and 400 mg/dl; usually with HDL-C levels <40 mg/dl in men and <50mg/dl in women) and a family history of mixed dyslipidemia and/or premature CHD

A

Familial combined hyperlipidemia

72
Q

Lipids primarily influenced by obesity, insulin resistance, and T2DM

A

Triglycerides

73
Q

Lipids primarily influenced by diet that is high in saturated and trans fat

A

LDL

74
Q

ABCA1 deficiency or Tangier disease

A

Extremely low circulating plasma levels of HDL-C <5mg/dl and apoA-I <5 mg/dl

Cholesterol accumulates in the reticuloendothelial system resulting in hepatosplenomegaly and pathognomic enlarged grayish yellow or orange tonsils

75
Q

Cholesterol absorption inhibitor that binds directly to and inhibits NCP1L1 and blocks intestinal absoprtion of cholesterol

A

Ezetimibe

76
Q

dec inhibtion of cholesterol synthesis -> inc hepatic LDL receptors

A

HMG COA reductase inhibitors

  • lovastatin, rosuvastatin, simvastatin, atorvastatin
77
Q

dec inhibtion of cholesterol synthesis -> inc hepatic LDL receptors

A

HMG COA reductase inhibitors

  • lovastatin, rosuvastatin, simvastatin, atorvastatin
78
Q

Inc bile acid secretion -> inc LDL receptors

A

Bile acid sequestrants
- cholestyramine, colestipol, colesevelam

79
Q

Dec PCSK9 activity due to Ab inhibition -> inc LDL receptors

OR

Dec PCSK9 synthesis due to siRNA silencing -> inc LDL receptors

A

PCSK9 inhibitors
- evolocumab
- alirocumab
- incilisiran

80
Q

Dec inhibition of cholesterol synthesis -> inc LDL receptors

A

ATP citrate lyase inhibitor
- bempedoic acid

81
Q

MTP inhibition -> dec VLDL assembly and secretion

A

MTP inhibitor
- lomitapide

82
Q

Dec ApoB synthesis due to ASO silencing -> dec ApoB/VLDL secretion

A

ApoB inhibitor
- mipomersan

83
Q

Dec ANGPTL3 activity due to Ab inhibition -> inc LPL activity, inc LDL catabolism

A

ANGPTL3 inhibitor
- Evinacumab

IM (2 decks)

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