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UWORLD Q REVIEWS > Cardio Block Wk 1 > Flashcards

Cardio Block Wk 1 Flashcards

1
Q

What is the order for the femoral structures in the femoral triangle from medial to lateral?

A

VAN Vein Artery Nerve Deep to the vein -> lymph nodes

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2
Q

What are the borders of the femoral triangle?

A

Inguinal ligament (superiorly) Sartorius (lat) Adductor lungus (med)

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3
Q

Where should cannulation of the femoral vein occur?

A

1 cm below the inguinal ligament and medial to the femoral artery pulsation.

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4
Q

What pathological finding can be seen in lung tissue due to heart failure?

A

Hemosiderin laden macrophages.

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5
Q

How would a patient with a TIA (transient ischemic attack) present?

A

HTN, hypercholesterolemia and sudden onset neuro deficits (UE weakness, difficulty speaking)

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6
Q

In addition to optimal BP control and statin therapy, what else is added to prevent ischemic stroke (TIA)?

A

NSAIDs

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7
Q

What is the adverse effect of using NSAIDs?

A

Risk of upper GI bleeds.

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8
Q

What is the process behind NSAID induced GI bleeds?

A

COX 1 inhibition. 1) Inhibition of platelet aggregation 2) Impairment of prostaglandin dependent GI mucosal protection (prostaglandin inhibit stomach acid secretion).

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9
Q

What is myocardial hibernation?

A

State of chronic myocardial ischemia where myocardial metabolism and function are reduced to match reduction in coronary blood flow to prevent myocardial necrosis. Px as L. ventricular systolic dysfunction.

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10
Q

What is ischemic preconditioning?

A

Brief episodes of MI followed by reperfusion protect the myocardium from subsequent prolonged episodes of ischemia. In order words (previous anginas help delay cell death after coronary occlusion allowing for more time for salvage)

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11
Q

What are the symptoms of digoxin toxicity?

A

Cardiac - life threatening arrhythmia. GI: anorexia, N/V. Abd pain Neuro: Fatigue confusion, **Color vision alterations.

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12
Q

Does digoxin have a narrow or wide therapeutic index?

A

Narrow So toxicity is common.

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13
Q

How are patients with digoxin toxicity treated?

A

Anti-digoxin antibody fragments.

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14
Q

What are precipitating causes of digoxin toxicity?

A

Hypokalemia, hypovolemia and renal failure.

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15
Q

A wide fixed splitting of heart sound is found in pts with what heart condition?

A

ASD

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16
Q

A wide fixed splitting can lead to what chronic condition?

A
  1. Pulmonary HTN (from increased in volume from L->R shunt) 2. Eisenmenger syndrome (reversal of shunt)
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17
Q

Rapid infusion of vancomysin can lead to?

A

Red man syndrome (non allergic drug reaction) Px: flushing, erythema, pruritus. NOT A TRUE ALLERGIC REACTION and can be resumed at slower rate when symptoms resolve.

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18
Q

RMS (red man syndrome) occurs due to ?

A

Direct activation of mast cells (histamine release) by vancomycin.

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19
Q

Which class of antiarrhythmic drug blocks sodium channels and inhibits phase 0 depol of action potential?

A

Class I ** these also have moderate potassium channel blocking activity -> slow rate of repol.

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20
Q

What is the difference between papillary muscle dysfunction and muscle rupture?

A

Muscle rupture occurs 3-5 after an MI, is mechanical and is not resolved with reperfusion of coronary artery.

21
Q

Which population does enterococci majorly affect?

A

Older male that have undergone GU/GI tract manipulation.

22
Q

When can fenoldopam be used? MOA?

A

HTN emergency. D1 agonist. Leads to vasodilation of renal, coronary, peripheral and splanchnic vasodilation -> Decreased BP and natureisis.

23
Q

Difference between HTN urgency and emergency?

A

HTN emergency has features of end organ damage.

24
Q

What differentiates skeletal muscle functioning from smooth and cardiac muscle?

A

Skeletal muscle does NOT require extracellular calcium for the coupling of RYR to sarcoplasmic reticulum for release of calcium.

25
Q

What is niacin used for?

A

Treatment of hyperlipidemia

26
Q

Major side effect for Niacin? Due to release of what chemical?

A

Flushing, warmth and itching due to release of prostaglandin

27
Q

What can be given with Niacin to prevent its adverse effect of flushing? And why?

A

NSAIDs (Aspirin). ** inhibits prostaglandin release.

28
Q

Which part of the aorta is most likely to be injured in a blunt aortic injury (rapid decelleration in MVA)? Why? What do most patients die from? What is seen on XRay?

A

The aortic isthmus. The isthmus is tethered by the ligamentum arteriosum and is fixed and immobile. Aortic rupture. A widened mediastinum.

29
Q

What is congenital long QT syndrome?

A

Inherited disorder of myocardial repolarization due to channel defects (K+ channels) -> decrease outward K+ flow -> prolongation of QT -> life threatening ventricular arrhythmias -> torsades de pointes. Px: syncope, seizures or sudden cardiac death.

30
Q

What are janeway lesions?

A

Septic embolization from valvular vegetations. Composed of bacteria, neutrophils, necrotic material and subq hemorrhage.

31
Q

Which of the following are painless manifestation of infective endocarditis: Vascular or immunologic phenomena

A

Vascular Immunologic phenomena are painful and tender.

32
Q

Immunologic phenomena of infective endocarditis?

A

Osler nodes and Roth spots

33
Q

Vascular phenomenon of infective endocarditis?

A

Systemic emboli, mycotic aneurysm, janeway lesions.

34
Q

What is the presentation of kawasaki disease?

A

CRASH and burn C- onjuctivitivial injection R- ash A- denopathy S- trawberry tongue H- and & foot changes (edema/erythema) & burn (Fever)

35
Q

What is a serious complication of Kawasaki disease?

A

Coronary artery aneurysms.

36
Q

In which patients will the addition of mineralocorticoid receptor antagonist be useful?

A

Patients with CHF and decreased ejection fraction

37
Q

Why are mineralocorticoid receptor antagonist helpful in CHF?

A

Cause regression of myocardial fibrosis and improvement in ventricular modelling.

38
Q

What artery does the inferior epigastric artery branch off? In what direction does this artery run? What does it supply?

A

External illiac artery Superiorly and medially Lower ant. abdominal wall.

39
Q

In addition to hypertension what can ACE inhibitors also treat?

A

Early Diabetic nephropathy

40
Q

When ACE inhibitors are used in combination with this medication, significant hypotension can occur.

A

Thiazides

41
Q

When ACE inhibitors are used in combination with this medication, significant hypotension can occur.

A

Thiazides **On its own ACE inhibitors can cause hypotension. But is worse when combined with thiazides.

42
Q

What artery supplies the SA, AV nodes & most of the bundle of His?

A

The RCA (supplies the inferior wall).

43
Q

Conduction impairments is common with acute ____ wall MI?

A

Inferior wall **Sinus brady, AV block

44
Q

What are two possible reasons for bradycardia?

A

Nodal ischemia Enhanced vagal tone (**Treat with atropine).

45
Q

On jugular venous pressure tracing, which peak is absent in patients with atrial fibrillation?

A

A wave.

46
Q

The SVC is derived from ?

A

The common cardinal veins

47
Q

What are some causes for QT prolongation?

A

Macrolides & fluoroquinolones Antiemetics Azoles Antipsychotics, TCAs & methadone Class IA and III antiarrhythmics

48
Q

Elevated levels of plasma homocysteine are independent risk factors for?

A

Thrombotic events.

49
Q

Hyperhomocysteinemia is most commonly due to what reasons?

A

Enzymes or deficiencies of Vitamin B12, 6 or folate.

UWORLD Q REVIEWS (13 decks)

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