Cardiovascular Flashcards

1
Q

Patients with systolic
dysfunction, have lower than normal cardiac ejection fractions
(EF < 40%).

A

due to stroke volume reductions along with increases in end diastolic volumes.

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2
Q

Frank–Starling mechanism

A

increased fiber dilation heightens

the contractile force, which then increases the energy released

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3
Q

beta-adrenergic blockers interfere with the sympathetic nervous system. In what all ways?

A

norepinephrine induced (all the below list)-
peripheral vasoconstriction,
sodium excretion by the kidney,
cardiac hypertrophy
arrhythmia generation,
hypokalemia, or cell death (apoptosis) How cell death????????
through increased stress owing to norepinephrine stimulation.

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4
Q

blockers should not be taken without diuretics in patients with a current or recent history of fl uid
retention

A

to avoid its development and to maintain sodium balance.

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5
Q

Patients should be monitored for signs of fl uid retention & report any significant increases,

A

which might warrant increases in diuretic doses or reductions
in the dose of the beta-adrenergic blocker

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6
Q

fatigue, hypotension, bradycardia,

and heart block are reported side eff ects that

A

should be monitored to ensure appropriate attention

and management.

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7
Q

beta-Adrenergic blockers are generally used in conjunction with

A

diuretics, ACEIs, or ARBs

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8
Q

ACEIs contraindications include:

A

H/Ointolerance or adverse reactions
serum potassium >5.5 mEq/L
serum creatinine levels >3 mg/dL, symptomatic hypotension,
severe renal artery stenosis, pregnancy.

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9
Q

ACEIs: 1st method: They inhibit the ACE and this action significantly decreases total peripheral resistance(as Ang II is potent vasoconstrictor), which aids in reducing afterload.

A

2nd method: Inhibiting the production of angiotensin II interferes with stimulation of aldosterone release, thus indirectly reducing retention of sodium and water, which decreases venous return and preload.

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10
Q

ACEIs side effects to be monitored include

A

hypotension (patients should be well hydrated before initiation of ACEIs), dizziness,
reduced renal function (increased serum creatinine of 0.5 mg/dL or more requires reassessment),
cough
potassium retention (if potassium levels
are high without supplementation, discontinue the ACEI for several days and then try to restart at lower dose)
Angioedema is a life-threatening S.E
May elevate Li+ levels (monitor Li+ levels, adjust dose).

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11
Q

It is critical to wait______ hours between the administration of an ACE inhibitor and
valsartan/sacubitril (or switching back to an ACE inhibitor), to minimize the risk of
angioedema.

A

36

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12
Q

Patients who experience diuretic resistance or tolerance to their effects

A

might need intravenous administration, a combination of two DIURETIC agents with differing mechanisms or the addition of agents, such as dopamine or dobutamine VASODILATOR, which increase renal blood flow.

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13
Q

THIAZIDE
agents are relatively weak because they are able to increase the fractional excretion of sodium to only 5% to 10% of the filtered load. and lose their effectiveness with moderately impaired renal function (creatinine clearance <30 mL/min).

A

LOOP diuretics
ability to increase sodium excretion to 20% to 25% of the filtered load and to maintain their efficacy until renal function is severely impaired (creatinine clearance < 5 mL/min) plus have the added advantage of reducing venous return independent of diuresis.

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14
Q

SAR of statins

A

https://youtu.be/U_f7E5C7d1M

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15
Q

CYP3A4 inhibitor and so avoid with grape fruit juice

A

SAL

Simvastatin, Atorvastatin, Lovastatin

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16
Q

CYP2C9

A

Fluvastatin, Rosuvastatin

17
Q

Statin with least drug interaction

A

Pravastatin

18
Q

Statin that must be used With food or after food

A

Fluvastatin, Lovastatin. Lovastatin with food INCREASES the drug’s bioavailability by 50%

19
Q

Statin that must be taken at bedtime

A

FLS- BEdtime

Fluvastatin, Lovastatin, Simvastatin

20
Q

Statin that must be taken anytime of the day? WHy

A

Atorvastatin and Rosuvastatin. Longer half life

21
Q

Side Effects of HMG CoA reductase inhibtor/Statins

A

mnemonic “HMG”
1) Hepatotoxicity( ↑Transaminases in 3-12 months)
2) Myopathy ( triad : Muscle weakness, Muscle pain, Dark urine-cola-colored urine)
Gastrointestinal
( Diarrhea (4.5%), abdominal cramps (3.3%), constipation (2.7%).
CNS: Q.) Headache (7.7%), insomnia, dizziness.
Skin: rash.

22
Q

Statin that has low penetration into peripheral tissue and less side effects. WHy?

A

Pravastatin is the ring opened dihydroxy acid with 6-hydroxyl group is more hydrophobic than lovastatin

23
Q

Antihyperlipidemic Drug of choice in pregnancy.

A

Resins (Bile acid sequestrant)

24
Q

Antihyperlipidemic Drug avoid in patient with high triglycerides.

A

Resins

25
Q

Gemfibrozil is contraindicated with statins

A

myopathies, or rhabdomyolysis
Another fibrate,Bezafibrate : Combined with statins to reduce triglyerides in patient with high triglycerines ( statin is good in decreasing LDL, but not good in decreasing, TG)

26
Q

Lithiasis predispose gallstone formation. If tested discontinue the drug. Which is the antihyperlipidemic

A

Fibrates

27
Q

Antihyperlipidemic Drug which inhibits tubular secretion of uric acid, causes gout or hyperuricemia.

A

Niacin

28
Q

Niacin Side effect

A
skin flushing(Administration of ASA 325 mg prior) accompanied by uncomfortable feeling warm and pruritic, dry skin
Hyperglycemia ( not used in Diabetes, Fibrate is drug of choice), hyperuricemia, GI distress like reactivation of peptic ulcer, flatulance, nausea and diarrhea:minimized by taking with food or immediately after food.
29
Q

Fibrates mechanism of action

A

Activate or agonist peroxysome profilator activating receptors alpha (PPAR alpha)

30
Q

Severe hepatic an renal dysfunction potentiate warfarin activity, in which antihyperlipidemic drug?

A

Fibrates

31
Q

Which antihyperlipidemic drug have uricosuric effect?

A

Fibrates

32
Q

More CO2 in blood

A

Metabolic acidosis: Acetazolamide ( ACIDzolamide