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UWorld Incorrects > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Cardiovascular Pathology:
What patient populations are more affected by hypertension?

A

Blacks > Whites > Asian

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2
Q

Cardiovascular Pathology:
What is the most common risk factor for Atrial fibrillation?

A

Hypertension

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3
Q

Cardiovascular Pathology:
What is the correlation between blood pressure and Cardiovascular disease?

A

For every 20 mmHg increase in systolic or every 10 mmHg increase in diastolic, the risk for cardiovascular disease doubles.

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4
Q

Cardiovascular Pharmacology:
What is the initial drug of choice for primary hypertension?

A

Thiazide diuretics

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5
Q

Cardiovascular Pharmacology:
How do ACE inhibitors lower renal hypertension?

A

Decrease vasoconstriction of the efferent arteriole

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6
Q

Cardiovascular Pharmacology:
How do you slow down the progression of Renal parenchymal disease?

A

ACE inhibitors

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7
Q

Cardiovascular Pharmacology:
What drugs/ drug classes can cause drug induced HTN?
4 points

A
  • oral contraceptives
  • glucocorticoids
  • Phenylephrine
  • NSAIDs (preferentially constrict the afferent arteriole)
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8
Q

Cardiovascular Pathology/ Endocrinology Pathology:
What is the triad to be aware of with a Pheochromocytoma?

A
  • hypertension
  • diaphoresis
  • tachycardia
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9
Q

Cardiovascular Pathology/ Endocrinology Pathology:
What is the triad to be aware of with Primary Aldosteronism (Conn Syndrome)?

A

Aldosterone producing tumor causing
- hypertension
- hypokalemia
- metabolic alkalosis

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10
Q

Cardiovascular Pathology/ Endocrinology Pathology:
How can hyperthyroidism cause secondary HTN?

A

increase stimulation of beta-adrenergic receptors

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11
Q

Cardiovascular Pathology/ Endocrinology Pathology:
How can Cushing syndrome cause secondary HTN?

A

Excess cortisol up regulates alpha 1 receptors on arterioles leading to increased sensitivity to NE and E

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12
Q

Cardiovascular Pathology:
What must be present for an infant to have differential cyanosis in the setting of a Coarctation?

A

Patent ductus Arteriosus

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13
Q

Cardiovascular Pathology:
What diagnosis can you make in a patient with ongoing drug resistant hypertension?
3 points

A
  • Dx: Unilateral Renal Artery Stenosis
  • Grossly the kidney appears shrunken
  • Bx: showed crowding with tubulointerstitial atrophy, fibrosis, and focal inflammation
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14
Q

Cardiovascular Pharmacology:
What is the best treatment for fibromuscular dysplasia?

A

Percutaneous transluminal angioplasty with or without stenting.

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15
Q

Cardiovascular Pathology:
How can you distruingish primary hyperaldosteronism from conditions causing high renin?

A

Aldosterone to renin ratio (ARR)
ARR > 20:1 is suggestive of Primary hyperaldosteronism

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16
Q

Cardiovascular Pathology:
How is malignant hypertension classified?

A

Severe, rapid increase in BP, usually >240/120 mmHg associated with end organ damage

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17
Q

Cardiovascular Pathology:
Which metabolic syndromes increases the risk for CVD?
5 points

A

Insulin resistance, hypertension, abdominal obesity, dyslipidemia, and prothrombotic states

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18
Q

Cardiovascular Pathology:
How many different types of arteriolosclerosis are there?
Name them

A

2; Hyaline arteriolosclerosis and Hyperplasticity’s arteriolosclerosis

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19
Q

Cardiovascular Pathology:
Which type of arteriolosclerosis is associate with malignant hypertension?

A

Hyperplastic arteriolosclerosis ‘onion skinning” of the tunica intima

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20
Q

Cardiovascular Pathology:
Describe Mönckeberg Arteriosclerosis:
4 points

A
  • Benign calcification affecting the elastic lamina of the tunica Media, leading to stiffening WITHOUT obstruction.
  • Affects medium sized arteries like the radial, ulnar, tibial, uterine, or femoral arteries in the elderly.
  • Has a “pipestem appearance on X-ray.
  • Risk factors include increase in age, DM, CKD, SLE, increase in vitamin D
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21
Q

Cardiovascular Pathology:
List the arteries most often affected by atherosclerosis listed from most to least likely?

A

Abdominal aorta > coronary artery > popliteal artery > internal carotid artery > circle of willis

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22
Q

Cardiovascular Pathology:
What are the non modifiable risk factors associated with Atherosclerosis?
4 points

A

Age, gender (men and postmenopausal women), homocystinuria, family history

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23
Q

Cardiovascular Pathology:
Explain the 5 steps of the pathogenesis of Atherosclerosis:

A
  1. Endothelial cell injury causes monocyte emigration into intima
  2. Activated macrophages release cytokines causing smooth muscle cells to migrate into intima
  3. macrophages form foam cells into a fatty streak and a fibrous cap develops
  4. as intimal muscles cells become old and die, fibrous matrix degrades
  5. Fibrous cap (plaque) calcifies and ulcerates, causing vessel thrombosis
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24
Q

Cardiovascular Pathology:
What is the most common cause of myocarditis in developed countries?

A

Viral infectionL
- Coxsackie B virus
- Rubella virus
- Cytomegalovirus

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25
Q

Cardiovascular Pathology:
What is the most common cause of myocarditis worldwide?

A

Chagas disease
- Trypanosoma cruzi (protozoan parasite)

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26
Q

Cardiovascular Pathology:
Which bacteria are well known to cause myocarditis?

A
  • staphylococcus aureus
  • corynebacterium diphtheria
  • haemophilus influenzae
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27
Q

Cardiovascular Pathology:
What are some causes of Myocarditis in patients with HIV?

A
  • toxoplasmosis
  • kaposi sarcoma metastases
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28
Q

Cardiovascular Pathology:
How does myocarditis present?
4 points

A
  • symptoms of CHF: chest pain*, peripheral edema, dyspnea
  • palpitations* from arrhythmias
  • viral sequelae: fever, diarrhea, and fatigue
  • PE: muffled S1 and S3 and/or mitral regurgitation murmur
29
Q

Cardiovascular Pathology:
How can you diagnose myocarditis?
3 points

A
  • ECG shows diffuse T wave inversions and ST segment elevations* (mimics an MI or pericarditis
  • cardiac biopsy is the gold standard: shows edematous myocardial interstitial with lymphocytic infiltrate (neutrophilic or mononuclear)
  • Creatine kinase-myocardial bound fractions (CK-MB) and troponin may be elevated
30
Q

Cardiovascular Pathology:
What is right-sided endocarditis suggestive of?

A

IVDA

31
Q

Cardiovascular Pathology:
What îș the definition of Endocarditis?

A

Inflammation of the lining of the heart and heart valves

32
Q

Cardiovascular Pathology:
Why is infective endocarditis so dangerous?

A

There is no blood supply to the heart valves so leukocytes cannot be recruited if bacteria attach.

33
Q

Cardiovascular Pathology:
When can you suspect subacute infective endocarditis?

A

Hx of previously damaged or abnormally developed valve in the setting of oral surgery or poor dentition as is associated with Strep Viradins

34
Q

Cardiovascular Pathology:
How does Infective endocarditis present?

A
  • Janeway lesions: small, painless erythematous lesions on the palms and soles
  • Osler nodes (painful raised lesions on the finger and toe pads
  • splinter hemorrhages
  • Roth spots (round white spots on the retina surrounded by hemorrhage)
  • valvular involvement: (mitral > aortic > tricuspid)
35
Q

Cardiovascular Pathology:
How would you diagnose infective endocarditis?
6 points

A

Duke criteria:
- positive serial blood cultures
- hx of infective endocarditis
- IVDA
- fever
- vascular or immune phenomena
- valvular lesions on echocardiography

36
Q

Cardiovascular Pathology:
How would you treat infective endocarditis?
3 points

A
  • Acute endocarditis empirical antibiotics: nafcillin and gentamicin for good coverage
    Subacute endocarditis obtain blood cultures before abx:
  • ampicillin + gentamicin for native valves
  • vancomycin, gentamicin, and rifampin for prosthetic valves
37
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + prosthetic device?

A

Staphylococcus epidermidis

38
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + colon cancer?

A

Streptococcus bovis

39
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + dental procedure?

A

Streptococci viridans

40
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + GI surgery?

A

Enterococcus

41
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + total parenteral nutrition?

A

Fungal

42
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + alcoholics or the homeless?

A

Bartonella henselae

43
Q

Cardiovascular Pathology:
What bacteria is considered with endocarditis + fastidious and culture negative?

A

HACEK organisms:
- Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella

44
Q

Cardiovascular Pathology:
How does Strep Viridans adhere to enamel and valves to cause endocarditis?

A

Converts glucose to dextrans

45
Q

Cardiovascular Pathology:
How do Janeway lesions differ from Osler nodes?

A

Janeway lesions are caused by micro abscesses of the dermis surrounding septic emboli, whereas Osler nodes are caused by deposition of immune complexes

46
Q

Cardiovascular Pathology:
What is the mnemonic for endocarditis?

A

FROM JANE
- fever
- roth spots
- Osler nodes
- murmur
- Janeway lesions
- anemia
- nailbed hemorrhage
- Emboli

47
Q

Cardiovascular Pathology:
What are the complications of endocarditis?

A
  • Septic emboli
  • chordae rupture
  • glomerulonephritis
  • suppurative pericarditis
48
Q

Cardiovascular Pathology:
Explain Marantic Endocarditis:

A

Nonbacterial endocarditis/ NBTE
- small, sterile fibrin vegetations deposit on the heart valves of pts with debilitating disease
- can occur as a paraneoplastic syndrome of mucin-secreting tumors (usually colon or pancreatic), platelets aggregate and become infected
- can occur with hyper coagulable state and lupus

49
Q

Cardiovascular Pathology:
What is the complication of Marantic Endocarditis?

A

Sterile embolus leading to cerebral infarction

50
Q

Cardiovascular Pathology:
Describe Libman-Sacks endocarditis:

A

Sequela of SLE where autoantibodies target and damage the heart valves. Steril vegetations (fibrin, neutrophils, lymphocytes, and histiocytes) form on both sides of the heart valve. Asymptomatic but can be detected via murmur on the mitral valve (holosystolic ‘blowing’ murmur)

51
Q

Cardiovascular Pathology:
Why are carcinoid tumors related to cardiovascular pathology?

A

Increased serotonin leads to systemic vasodilation as well as thickening, contraction, and decreased mobility of right-sided heart valves. Results in reduced preload and end-diastolic volume.

52
Q

Cardiovascular Pathology:
Describe Rheumatic fever:

A

Multisystem involvement
- typically occurs after a pharyngeal infection with GAS (Beta hemolytic)
- symptoms referred to as JONES criteria

53
Q

Cardiovascular Pathology:
Describe the Mneumonic to remember the symptoms for Rheumatic Fever:

A

JONES PEACE:
Major criteria:
- Joints: Migratory arthritis
- Carditis: now-Onset murmur
- Nodules, subcutaneous: extensor surfaces
- Erythema marginatum
- Sydenham chorea
Minor criteria:
- PR interval, prolonged
- ESR elevated
- Arthralgias
- CRP elevated
- Elevated temperature (fever)

54
Q

Cardiovascular Pathology:
How can you show evidence of streptococcal infection:

A
  • Antistreptolysin O titers (ASO)
  • Positive throat culture for streptococci group A
55
Q

Cardiovascular Pathology:
What is the most serious complication of rheumatic fever?

A

Acute Rheumatic Heart Disease, affecting all 3 layer of the heart.
Divided into Fibrinous pericarditis, Myocarditis, Endocarditis.

56
Q

Cardiovascular Pathology:
Describe Fibrinous pericarditis:

A

Presents with chest pain and friction rub

57
Q

Cardiovascular Pathology:
Describe Myocarditis:

A

Collagen and fibrinoid material form nodule call Aschoff bodies and are surrounded by macrophages (Anitschkow cells), lymphocytes, plasma cells, and multinucleate giant cells (Aschoff cells)

58
Q

Cardiovascular Pathology:
Describe Endocarditis as a complication of Rheumatic Fever:

A

Valves become inflamed and small verrucae (rubber fibrin vegetations) form along the line of closure. Valves thicken and calcify, leading to insufficiency or stenosis. Mitral and Aortic valve commonly affected because of high pressure gradient.

59
Q

Cardiovascular Pathology:
What is the cause of death of acute rheumatic fever?

A

Myocarditis leading to cardiac failure

60
Q

Cardiovascular Pathology:
What is Sydenham chorea?

A

Involuntary, purposeless contraction of the trunk muscles and extremeties

61
Q

Cardiovascular Pharmacology:
What is the treatment for chronic rheumatic heart failure?
5 points

A
  • high dose PCN for GAS
  • symptomatic treatment
  • Steroids and salicylates to reduce pain and inflammation
  • Digitalis to reduce the symptoms of heart failure
  • Haloperidol to treat Sydenham chorea if present
62
Q

Cardiovascular Pathology:
What are the causes of Dilated Cardiomyopathy?
14 points

A
  • idiopathic
  • alcohol abuse
  • wet beri beri (thiamine deficiency)
  • coxsackie B virus myocarditis
  • Chronic cocaine use
  • Chagas disease
  • doxorubicin toxicity
  • hemochromatosis
  • HIV
  • Lyme disease
  • sarcoidosis
  • hypothyroidism
  • acromegaly
  • peripartum cardiomyopathy
63
Q

Cardiovascular Pathology:
What are the complication of dilated cardiomyopathy?
5 points

A
  • cardiac arrhythmias
  • mural thrombi
  • CHF
  • bundle-branch blocks
  • death
64
Q

Cardiovascular Pathology:
How does dilated cardiomyopathy present?

A

Right or left heart failure
- decreased ejection fraction
- JVD
- edema
- orthopnea
- hepatomegaly
- cardiomegaly
- arrhythmias
- S3
- systolic regurgitant murmur

65
Q

Cardiovascular Pathology:
How can you diagnose dilated cardiomyopathy?
3 points

A
  • radiography showing an enlarged cardiac silhouette with pulmonary congestion
  • Echocardiography showing dilated LV with decreased EF
  • Lymphocytic infiltrate with myocyte necrosis if caused by coxsackie B virus myocarditis
66
Q

Cardiovascular Pathology:
How is T Cruzi transmitted?q

A

Bite of the reduviid bug

67
Q

Cardiovascular Pathology:
What is the strategy to treat dilated cardiomyopathy?

A

Improve the symptoms of CHF
If EF < 35% despite therapy consider ICD placement to control arrhythmias or heart transplant

68
Q
A

UWorld Incorrects (5 decks)

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