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Cardiovascular FA > dif to remember > Flashcards

dif to remember Flashcards

1
Q

Myocardial infraction complication - Interventricular septal rupture, papillary muscle rupture, ventricular pseudoaneurysm, ventricular free wall rupture - time

A

Interventricular septal rupture –> 3-5 d
papillary muscle rupture –> 3-4 d
ventricular pseudoaneurysm –> 3-14 d
ventricular free wall rupture –> 5-14 d

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2
Q

antiarrhytmics Class IC - clinical use

A
  1. SVT (including atrial fibrillation)

2. Only last resort in refractory VT

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3
Q

GPIIb/IIIa inhibitors - clinical use / pt

A

acute coronary sundromes (only unstable angina and non-stemi) in those who are to undergo angioplasty and stenting
they lead to reduction in mortality on those with ST depression, esp with high enzymes who then develop muocardial infraction requiring PCI with stenting

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4
Q

AR - valve replacement

A
  • EF less than 55 or LVESD greater than 55

- Repairing the valve means tightening the ends of the valve with sutures

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5
Q

MR - valve replacement

A

When LVESD is above 40 mm or EF drops below 60%

–> surgical valve repair or replacement

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6
Q

MI criteria

A
  1. at least 1 mm segment elevation in at least 2 contiguous limb leads
  2. 2mmm elevation in 2 continguous precordial limbs
  3. New LBBB
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7
Q

Diastolic dysfunction - treatment

A
  • the management here is not as clear as in the systolic
  • b-blockers have clear benefits
  • digoxin and spironolactone has no benefit and should not used
  • diuretics to control symptoms
  • unclear benefit for ACEi and ARBs and hydralazine
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8
Q

AR - physical findings (not the murmur)

A
  1. wide pulse pressure
  2. water-hammer (wide,dounding) pulse
  3. Quincke pulse (puslations in the nail)
  4. Hill sign (BP in legs as much as 50 above arm)
  5. head bobbing (de Musset sign)
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9
Q

HF with preserved EF - spironolactone

A
  • not decreased mortality
  • reduced hospitalisation rate
  • indication in peripheral edema and lung congestion fnsaid
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10
Q

drug that is contraindicated in patients with dilated cardiomyopathy and why

A

NSAID

worsen afterload by inhibiting prostagladin synthesis and by counteracting the benefits of ACEi

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11
Q

large vessel vasculitis types (and epidemiology)

A
  1. Temporal (giant cels) arteritis (older female)

2. Takayasu arteritis (usually asian females under 40)

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12
Q

Medium-vessel arteritis types

A
  1. Polyarteritis nodosa
  2. Kawasaki disease
  3. Buerger disease (thrommboangiitis obliterans)
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13
Q

small vessel vasculitis types

A
  1. Granulomatosis with polyangiitis (Wegener)
  2. Microscopic polyangiitis
  3. Eosinophilic granulomatosis with polyangiitis (Chung strauss)
  4. Henoch-Schonlein purpura
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14
Q

Takayasu arteritis - sign and symptoms

A
  1. weak upper extremity pulses (pulseless disease)
  2. fever 3. night sweats 4. arthritis 5. myalgias
  3. skin nobules 7. ocular disturbances
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15
Q

Polyarteritis nodosa - symptoms

A
  1. fever 2. weight loss 3. malaise 4. headache
  2. GI (abdominal pain, MELENA) 6. hypertension
  3. neurologc dysfunction 8. cutaneous eruption
  4. renal damage
    typically involves renal and visceral vessels
    NOT PULMONARY ARTERIES
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16
Q

Polyarteritis nodosa - histological appearance

A

transmural inflammation of the arterial wall with fibrinoid necrosis

17
Q

Polyarteritis nodosa - association with (and proportion)

A

hepatitis B seropositivity in 30% of patients

18
Q

Beurger disease (thromboangitis obliterans) - symptoms

A
  1. intermittent claudication may lead to gangere
  2. autoamputation of digits
  3. superficial nodular phlebitis
  4. Raynaud phenomenon
19
Q

Kawasaki disease - Mucocutaneous lymph syndrome

A

mnemonic: CRASH (and fever)
1. Conjuctival injection 2. Rash (polymorphous–> desquamating) 3. Adenopathy (cervical) 4. Strawberry tongue (oral mucositis) 5. Hand foot changes (edema, erythema) 6. fever

20
Q

MC childhood systemic vasculitis (often follows)

A

Henoch-Schonlein purpura / URI

21
Q

Henoch-Schonlein purpura - classic triad

A
  1. Skin: palpable purpura on buttocks/legs
  2. Arthralgias
  3. GI: abdominal pain
22
Q

strauss) - labs

A
  1. biopsy granoulomatous, necrotizing vaculitis with eosinophilia
  2. increased IgE level
  3. MPO-ANCA/p-ANCA
23
Q

eosinophilic granulomatosis with polyangiitis (Churg strauss) - clinical manifestation

A
  1. Asthma 2. sinusitis 3. skin nobules or purpura
  2. periperal neuropathy (wrist/foot drop) 5. heart 6. GI
  3. kidneys (pauci-immune glomerulonephritis)
24
Q

microscopic polyangiitis - labs

A
  1. MPO-ANCA/p-ANCA (anti-myeloperoxidase)

2. histology: a. NO GRANULOMAS b. necrotizing vasculitis

25
Q

microscopic polyangiitis - manifestation - involve

A
  1. lung 2. kidneys 3. skin (palpable purpura) 4. pauci-immune glomerulonephritis
26
Q

microscopic polyangiitis vs wegener

A

similar but without nasopharyngeal involvement in microscopic polyangitis

27
Q

granulomatosis with polyangitis (wegener) - characteristic lab

A

PR3-ANCA/c-ANCA (anti-proteinase 3)

28
Q

granulomatosis with polyangitis (wegener) - upper respiratory tract

A
  1. perforation of nasal septum
  2. chronic sinusitis
  3. otitis media
  4. mastoiditis
29
Q

granulomatosis with polyangitis (wegener) - labs

A
  1. CXR: large nodular densities
  2. PR3-ANCA/c-ANCA (anti-proteinase 3)
  3. histological appearance: a. focal necrotizing vasculitis
    b. necrotizing vasculitis in the lung and upper airway
    c. necrotizing glomerulonephritis
30
Q

medium size vasculitis - epidimiology and treatments

A

Buerger disease –> male smoker under 40 –> stop smoking
Kawasaki –> asian under 4 –> IV immunogl + aspirin
Pol nodosa –> young adults (HBV in 30%) –> corticosteroids + cyclophosp

31
Q

initial management of GERD

A
  • fewer than 2 episodes of symptoms per week: lifestyle changes and antihistamines as needed
  • patients with more frequent or severe symptoms, evidence of erosive esophagitis, or laryngopharyngeal involvement should be managed with an 8-week course of a PPI
32
Q

β-blockers intoxication - treatment

A
  • IV fluids and atropine are the first line options

- if profound or refractory hypotension –> glucagon

33
Q

hypertensive emergencies - target (if fast decreasing?)

A

target: lowering 10-20% in the first hour and by another 5-15% in the next 23 hours
excessive drop can cause cerebral iscemia (mental status + seizures)

34
Q

HOCM - ECG

A

LV hypertrofy: tall R in aVL + Depp S in V3 (Cornell criteria)
2. Repolarization changes in anterolateral leads (I, aVL, V4, V5, V6)

35
Q

Approximate decrease in BP with life style modification

A
  1. Weight loss: 5-20 per 10 kg loss
  2. Diet with fruit + vegetables + low fat: 8-14
  3. Exercise: 30 min / d 5 days per week: 4-8
  4. Less than 3 g sodium /day: 2-8
    Less than 2 drinks in men and 1 in women : 2-4
36
Q

Medication withhold prior to cardiac stress

A

Hold for 2 days: b-blockers, CCB, nitrates
Hold 2 days prior to vasodilatory test: dypirodamole
Hold 12 h prior to vasodilatory test: caffeine
Continue: ACEi, digoxin, diuretics,statins

37
Q

HyperTG - management

A
  • evaluation of 2ry causes
  • if less 150-500: lifestyle modification (and statin in cardiovascular risk)
  • if more than 1000: pancreatitis prevention (fibrates, fish oil, no alcohol) –> if drop more than 500 -> lifestyle modif
38
Q

Guidelines for lipid-lowering therapy (general)

A
  1. LDL more than 190
  2. Clinically significant atherosc disease (ASC, angina, mi, stoke, TIA, PAD: if younger than 75: high intenisity, moderate for older than 75
  3. age 40-75 with DM 40-75
  4. estimated 10 years ASCVD risk 7.5% or more: moderate to high

Cardiovascular FA (8 decks)

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