Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Cardiovascular UWorld > Flashcards

Cardiovascular UWorld Flashcards

1
Q

A 78 year old man dies and autopsy of his heart reveals cardiac myocytes with intracytoplasmic inclusions of yellow-brown granules. What causes this?

A

This is lipofuscin, it forms with age due to long term free radical injury and lipid peroxidation. Very common in heart and liver in aged, malnourished and cachectic patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why do patients with B12 deficiency get posterior column and other neurologic symptoms?

A

B12 deficiency results in accumulation of methyl-malonly CoA due to inability to convert it to succinyl CoA. This results in incorporation of non-physiologic fatty acids into neurons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can folic acid and B12 supplementation decrease levels of homocysteine in an attempt to minimize thrombosis?

A

Folic acid and B12 make it possible for methionine synthetase to function and convert homocysteine to methionine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What bugs might be involved in a patient with suspect endocarditis and labs that show gram-positive cocci that can synthesize dextran from sucrose?

A

Strep viridians (mutans and sanguinis). Dextran is insoluble which allows them to adhere to teeth and prosthetic heart valves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Most important mediators in auto regulation of coronary blood flow? Where do they come from?

A

NO and adenosine. NO and citrulline are synthesized from arginine and oxygen by eNOS in the coronary endothelium. NO then activates guanylate cyclase, increasing cGMP levels, causing vasodilation. Adenosine comes from ATP metabolisms and vasodilates the small coronary vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Treatment for niacin-related flushing and pruritus?

A

Aspirin 30-60 minutes prior to administration will inhibit the prostaglandins (PGD2 and PGE2) that mediate the reaction to niacin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Only class III anti-arrhythmic with additional beta-blocking properties?

A

Sotalol. You’ll know to pick this because the patient will have long QT and bradycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cardiac medication that can cause gingival hyperplasia and hyperprolactinemia?

A

Verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Treatment of a patient with endocarditis and labs showing gram positive, catalase positive, coagulase negative cocci? What if cultures come back methicillin-sensitive?

A

80% of coagulase negative staph are methicillin resistant and should be treated with vancomycin. If cultures return methicillin sensitive, you may treat with a beta-lactamase resistant PCN like nafcillin or oxacillin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When can the Purkinje system assume a pacemaker role?

A

Severe bradycardia less than 40 beats per minute.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is it that a patient with aortic stenosis has a steady state of flow through the capillary beds, which have a much smaller diameter than the aorta?

A

The steady state velocity of blood flow at any given point in the vasculature is inversely proportional to the diameter of the vessel through which the blood flows:
Vol(in) = A1V1 = Vol(out) = A2V2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Artery likely lacerated in a patient with a skull fracture at the junction of the frontal, temporal, parietal and sphenoid bones?

A

This location is the “pterion”, which is where the middle meningeal artery lies. This is a branch of the maxillary artery, from the external carotid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Coagulation labs used to monitor Warfarin and Heparin?

A

Warfarin = PT/INR. Heparin = aPTT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is calcium efflux prior to myocardial relaxation accomplished?

A

Sarcoplasmic reticulum’s Ca ATPase pump and sarcolemmal 3Na/Ca exchanger.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why do CCBs only work in cardiac and smooth muscle and not skeletal muscle.

A

The L-type Ca channels in skeletal muscle causes mechanical opening of the RyR receptor of the sarcoplasmic reticulum and no Ca influx is required to open the sarcoplasmic reticulum as is necessary in cardiac and smooth muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where does Ca go in the cardiac, skeletal and smooth muscle myocytes after it is release from the sarcoplasmic reticulum?

A

Cardiac and skeletal = troponin C, then allowing actin and myosin to bind. Smooth muscle = calmodulin -> myosin light chain kinase phosphorylation -> myosin phosphorylation -> myosin binds to actin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What makes an atheroma more prone to rupture than other atheromas?

A

Progressive plaque enlargement leads to vascular smooth muscle cell death. These cells secrete collagen and fibrin to form the fibrous cap of the atheroma, and when they die the atheroma becomes unstable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Collagen subtypes. Which types are deposited after a patient has an MI?

A

1) Dermis, bone, tendons, ligaments, dentin, cornea, blood vessels and scar tissue
2) Cartilage, vitreous humor and nucleus pulposus
3) Skin, lungs, intestines, blood vessels, bone marrow, lymphatics and granulation tissue (7 days after MI, eventually replaced by type I scar tissue)
4) Basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Conditions that cause pulsus paradoxus?

A

Those that impair the RV ability to expand in the pericardial space (tamponade, asthma, COPD and constrictive pericarditis) leading the inter ventricular septal shift towards the LV, reducing SBP during inspiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do beta-agonists cause bronchial wall dilation?

A

They bind to Gs -> adenylate cyclase activation -> increased cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Heart sound in a non-stenotic bicuspid aorta?

A

Early systolic, high pitched click in the RUSB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cause of fluid overload and cardiac remodeling in patients with CHF

A

Compensatory activation of the RAAS and sympathetic nervous system increase after load and cause cardiac remodeling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does milrinone increase cardiac contractility?

A

It is a PDE3 inhibitor, which increases cAMP concentrations. This results in increased Ca efflux from the sarcoplasmic reticulum, allowing for stronger myocyte contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does NE cause vasoconstriction?

A

Alpha-1 stimulation results in IP3 pathway mediated vasoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does NE cause increased heart rate and contractility?

A

Beta-1 stimulation results in Gs pathway mediated increased cAMP. Note that the heart rate typically remains unchanged due to reflex bradycardia after NE induces alpha-1 mediated vasoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens when you stimulate an alpha-2 receptor?

A

There is decreased cAMP and release of NE and insulin is inhibited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Statin side effects

A

Hepatotoxicity and myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Fibrate side effects

A

Gallstones and myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Bile acid sequestrant side effects

A

GI upset and malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Niacin side effects

A

Flushing, pruritus and hepatotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Ezetimibe side effects

A

Hepatotoxicity when combined with statin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Dopamine effect on cardiovascular system

A

Low dose: increases mesenteric and renal blood flow and stimulates beta-1 receptors. High dose: stimulates alpha-1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does ANP induce peripheral vasodilation?

A

It activates guanylyl cyclase and increases levels of cGMP which causes vasodilation (same mechanism as NO).

34
Q

Mechanism of TCA overdose symptoms

A

Inhibition of fast cardiac Na channels and inhibition of muscarinic, histamine and alpha-1 receptors is responsible for the arrhythmias, anti-cholinergic toxicity and orthostatic hypotension.

35
Q

When to give a patient who overdosed on TCA sodium bicarbonate.

A

When the QRS widens and the patient develops a ventricular arrhythmina. NaHCO3 increases the pH and raises Na concentration, alleviating blockade of Na fast channels.

36
Q

Mutation that causes congenital long QT syndrome

A

Decreased outward K+ currents. This results in prolongation of phase 3 of the cardiac action potential, prolonging the QT interval.

37
Q

Class IA antiarrhythmics

A

They prolong the action potential duration (long QT) and conduction velocity by blocking fast Na channels. Quinidine, procainamide and disopyramide.

38
Q

Class IB antiarrhythmics

A

They shorten action potential duration and have no effect on conduction velocity by blocking fast Na channels. Lidocaine, mexilitene, phenytoin.

39
Q

Class IC antiarrhythmics

A

They slow action potential conduction velocity and have minimal effect on duration. Flecainide and propafenone.

40
Q

Class II antiarrhythmics

A

Slows SA node discharge rate AV node conduction rate and prolongs refractory period. Beta-blockers.

41
Q

Class III antiarrhythmics

A

Prolongs action potential duration (long QT), no effect on conduction velocity. Amiodarone (minimal QT prolongation), Ibutilide, Dofetilide, Dronedarone and Sotalol (also class II)

42
Q

Class IV antiarrhythmics

A

Slows SA node discharge, AV node conduction and prolongs refractory period. Non-dihydropyridine calcium channel blockers: verapamil and diltiazam.

43
Q

Tumor cell markers in angiosarcoma

A

CD31

44
Q

WPW ECG findings

A

Shortened PR, upsloping delta wave and widened QRS (converts to narrow during PSVT)

45
Q

Carotid body baroreceptor nerve that conducts to the solitary medullary nucleus? Aortic arch?

A

Carotid body = glossopharyngeal (CN IX). Aortic arch = vagus (CN X)

46
Q

Vascular derivatives of the aortic arch

A 
1st = maxillary artery
2nd = hyoid and stapedial arteries
3rd = common carotid and proximal ICA
4th = left: aortic arch, right: proximal right subclavian
5th = none
6th = proximal pulmonary arteries, left: ductus arteriosus
47
Q

Closure of PDA in older patients

A

Can’t use indomethacin, need to close surgically

48
Q

Why does tyramine predispose patients on MAO-I to hypertensive crisis?

A

The tyramine-rich foods cannot be detoxified by MOA-A in the GI tract. They then enter nerve endings and the monoamine transport vesicles. This causes displacement of NE and increased NE back flow into circulation, elevating sympathetic tone and blood pressure.

49
Q

Great anti-hypertensive medication for patients with hypotension and long PR interval?

A

Nifedipine. It does not affect AV conduction and causes peripheral vasodilation with subsequent reflex tachycardia.

50
Q

How does EPI affect blood pressure?

A

It always raises systolic pressure due to beta-1 and alpha-1 stimulation. At low doses, it stimulates beta-2 > alpha-1 causing decreased diastolic pressure. At higher doses, it stimulates alpha-1 > beta-2 and causes increased diastolic pressure.

51
Q

How does EPI affect heart rate?

A

Dose-dependent increase in response to beta-1 stimulation. If the HR does not increase with addition of EPI, you know there is another drug on board blocking beta-1 receptors.

52
Q

Propranolol mechanism of action

A

Non-selective beta-blocker

53
Q

Phentolamine mechanism of action

A

Non-selective alpha-blocker with reversible effects (can be overcome by high dose NE infusion)

54
Q

Phenylephrine mechanism of action

A

Alpha-1 selective agonist

55
Q

Isoproterenol mechanism of action

A

Non-selective beta-agonist

56
Q

A child presents with differential cyanosis and clubbing of his lower extremities, but not his upper extremities. What is likely causing his condition?

A

PDA complicated by Eisenmeger syndrome and increased delivery of deoxygenated blood to the descending aorta. This is not coarctation because coarctation would present with differential cyanosis at infancy, not in childhood.

57
Q

Pressure volume loop in patients with an AV fistula?

A

Since the fistula increases the velocity of blood returning to the heart, end diastolic volume increases. Since the fistula allows bypassing of the arterioles (most resistance in the circuit), the pressure decreases.

58
Q

Action potential in cardiac pacemaker cells

A

Phase 0: voltage gated L-type Ca channels open at -40mV. Phase 3: L-type Ca channels close and K+ channels open for repolarization. Phase 4: funny Na channels open and slowly and the T-type Ca channels open around -50mV, then the L-type channels open and start phase 0 all over again.

59
Q

How does adenosine work to control patients with PSVT? What neurotransmitter works in a similar fashion?

A

It increases K+ conductance during phase 4, further depolarizing the membrane. It also blocks L-type Ca channels. Note that acetylcholine has a similar mechanism of action.

60
Q

Cause of familial primary pulmonary hypertension?

A

Mutation in BMPR2 that causes smooth muscle proliferation

61
Q

Common location of aortic injury in rapid deceleration injury?

A

Aortic isthmus, where the ligamentum arteriosum attaches to the descending aorta.

62
Q

Most reliable indicator of mitral stenosis severity?

A

Time from P2 to opening snap on auscultation. Severity worsens as the interval shortens.

63
Q

Mechanism of action of diphtheria toxin

A

It is an AB toxin that inhibits protein synthesis via ADP-ribosylation of EF-2.

64
Q

Mechanism of action of c. perfingens toxin

A

Lecithinase (aka phospholipase C) causes cellular death via membrane degradation

65
Q

Mechanism of action of Shigella and EHEC toxin?

A

Shiga toxin inactivates the ribosomal 60S subunit

66
Q

Mechanism of action of b. pertussis toxin?

A

AB toxin that catalyzes ribosylation of Ga subunit that causes activation and increased cAMP production. This results in increased sensitivity to histamine, leukocyte dysfunction and increased insulin production.

67
Q

Why is cardioversion indicated for patients with severe aortic stenosis and acute atrial fibrillation?

A

Left ventricular hypertrophy in AS makes the heart highly dependent on atrial contraction to have adequate LV filling during diastole. In a-fib, patients don’t have the atrial kick and are at risk for severe hypotension.

68
Q

How does cortisol have a “permissive” effect when combined with other hormones?

A

Although it doesn’t directly vasoconstrict, it up regulates peripheral alpha-1 receptors, increasing the response of ATII and NE.

69
Q

Calculating true positives

A

sensitivity x # who actually had disease

70
Q

Calculating false negatives

A

(1 - sensitivity) x # who actually had disease

71
Q

Phenoxybenzamine mechanism of action

A

Non-selective irreversible alpha antagonist

72
Q

Labetalol mechanism of action

A

Beta-1, beta-2 and alpha-1 antagonist. This is reversible and high doses of NE can overcome its effects.

73
Q

Only statin not metabolized by CYP 3A4. Why is this clinically significant?

A

Pravastatin. In patients taking drugs that inhibit CYP 3A4 metabolism (cyclosporine, HIV protease inhibitors, macrocodes, azoles and grapefruit juice) they should be on pravastatin to minimize risk of myopathy due to increased statin concentration.

74
Q

Pathophysiology of AAA vs. thoracic aortic aneurisms?

A

AAA = chronic transmural inflammation secondary to atherosclerosis.
Thoracic aneurisms = cystic medial necrosis.

75
Q

Medication of choice for claudicators

A

Cilostazol inhibits platelet PDE, leading to increased levels of cAMP. cAMP activates protein kinase A, which inhibits platelet aggregation. Additionally, cilostazol causes vasodilation and improves claudication symptoms. Of note, since PAD is a CAD equivalent, patients should also be on ASA and/or clopidogrel.

76
Q

% of coronary artery occlusion necessary to cause stable angina

A

> 75%

77
Q

Digoxin mechanism of action

A

Inhibition of Na/K ATPase increases intracellular Na. This leads to decreased Ca excretion from the cell via the 3Na/Ca exchanger. Increased intracellular Ca causes increased contractility. Digoxin also stimulates the parasympathetic nervous system and decreases heart rate.

78
Q

Signs of digoxin toxicity

A

Elevated K from inhibition of the Na/K ATPase, GI symptoms, arrhythmias, vision changes, confusion and weakness.

79
Q

Pathologic process involved in thromboangiitis obliterans?

A

Segmental thrombosing vasculitis extending into contiguous veins and nerves, encasing them in fibrous tissue.

80
Q

Side effects of thiazides

A

HYPER: uricemia, calcemia, glycemia, lipemia. HYPO: kalemia and tension

81
Q

Most common cause of native valve bacterial endocarditis among 15-60 year olds in the US

A

Mitral valve prolapse. High velocity jets striking the endothelium and turbulent flow causes injury, platelet and fibrin deposition that result in non-infectious vegetations. These vegetations can serve as a nidus for future infection and risk for embolic stroke.

Step 1 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions