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Step 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

When do you see granulation tissue form after an MI? How about a scar?

A

Granulation tissue- 1 week (type III collagen)

Scar- 1 month (type I collagen)

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2
Q

Dressler syndrome

A

A pericarditis that arises 6-8 weeks after an MI due to production of auto-antibodies against your own pericardium

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3
Q

55 year old woman presents with headache, fever, muscle pain, and jaw claudication. ESR is elevated. What do you suspect?

A

Temporal (Giant cell) arteritis

Need to biopsy! But remember that a negative biopsy does not rule out disease, due to segmental pathology

Tx with corticosteroids

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4
Q

What is the most feared complication of temporal (giant cell) arteritis?

A

Irreversible blindness due to occlusion of the ophthalmic artery

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5
Q

What patients is Takayasu Arteritis seen most often in?

A

Young asian females

Just like temporal giant cell arteritis but is at the aortic branch points

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6
Q

Patient presents with HTN, abdominal pain and melena, and muscle pain (myopathy). Muscle biopsy shows transmural inflammation of mid sized arteries with areas of necrosis. What do you suspect? What is this associated with?

A

Polyarteritis nodosa

Associated with Hep B infection

The lungs are classically spared

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7
Q

Kawasaki disease

A

medium vessel vasculitis (coronary artery) that affects children.

S/S: CRASH and burn: conjunctival injection, rash, adenopathy (cervical), strawberry tongue, hand and foot rash/edema, and fever

→ can cause MI or aneurysm of coronary artery, leading to death

Tx: Aspirin and IVIG

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8
Q

Patient with a longstanding hx of smoking presents with gangrene of the fingers/toes and autoamputation of one of the fingers. What is the disease and how is the pathology?

A

Buerger disease:

Segmental thrombosing vasculitis that extends into contiguous veins and nerves—due to direct endothelial toxicity from tobacco or from hypersensitivity to them

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9
Q

55 year old male presents with sinusitis, hemoptysis and hematuria. What does this constellation of symptoms suggest?

A

Wegeners Granulomatosis (Granulomatosis with polyangiitis)

Small vessel vasculitis that involves nose, lungs, and kidneys

Tx with cyclophosphamide and steroids

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10
Q

Churg Strauss syndrome

A

Necrotizing granulomatous inflammation with eosinophils, involving the heart and lungs

Often associated with asthma and peripheral eosinophilia

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11
Q

p-ANCA or C-ANCA

  • Wegener’s granulomatosis
  • Microscopic granulomatosis
  • Churg Strauss syndrome
A
  • Wegener’s granulomatosis: c-ANCA
  • Microscopic granulomatosis: p-ANCA
  • Churg Strauss syndrome: p-ANCA
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12
Q

What is the most common vasculitis in children?

A

Henoch-Schonlein Purpura

Palpable purpura (patches) on buttocks and legs, GI pain, and hematuria following an upper respiratory tract infection (source of the IgA)

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13
Q

What usually precedes Henoch-Schonlein Purpura

A

An upper respiratory infection (source of the IgA deposits)

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14
Q

Kaposi Sarcoma

A

Vascular tumor associated with HHV-8
Purple patches, plaques and nodules on skin
Seen in HIV, immunocompromised patients

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15
Q

What valve disorder is seen in syphilis?

A

Aortic valve regurg- caused by dilation of the aortic valve root

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16
Q

What is the most common location of AAA?

A

Below the renal arteries and above the aortic bifurcation

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17
Q

What two medical problems lead to hyaline arteriolosclerosis?

A

Benign HTN and diabetes

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18
Q

What congenital heart defect is associated with fetal alcohol syndrome?

A

Ventricular septal defect
Atrial septal defect
Tetralogy of fallot
Patent ductus arteriosus

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19
Q

What are the consequences of a left to right shunt?

A

inc flow through the pulmonary circulation causes hypertrophy of pulmonary vessels and pulmonary HTN → eventually leads to reversal of shunt and causes late cyanosis (Eisenmenger syndrome)

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20
Q

Patient presents with Down syndrome and S2 splitting on auscultation

A

They have an atrial septal defect, which causes a left to right shunt.

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21
Q

What is a PDA associated with? What is the treatment for PDA?

A

Congenital rubella

Tx: indomethacin: decreases PGE and causes closure of the ductus arteriosus

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22
Q

When is it necessary to keep the ductus arteriosus patent?

A

In transposition of the great arteries - allows the two circulations to mix between pulmonary artery and aorta

Do this by giving the patient prostaglandin E (PGE)

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23
Q

CXR shows a boot shaped heart

A

Tetralogy of Fallot

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24
Q

Findings in tetralogy of fallot

A

1) stenosis of the RV outflow tract
2) RV hypertrophy
3) VSD
4) Aorta overriding the VSD

Causes a right to left shunt

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25
Q

What is transposition of the great arteries associated with?

A

Maternal diabetes

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26
Q

What cardiac finding is common in Turner syndrome?

A

Preductal coarctation of the aorta (causes lower extremity cyanosis in infants)

Also see aortic bicuspid valve

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27
Q

30 year old male presents with HTN of the upper extremities and hypotension of the lower extremities. You get a CXR and there is notching of the ribs. What do you suspect?

A

Coarctation of the aorta

Notching seen on CXR is due to engorgement of the intercosal arteries

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28
Q

What are some causes of dilated cardiomyopathy?

A 
Usually idiopathic
Coxsackie virus
Autosomal dominant genetic condition
Cocaine
Alcohol abuse
Pregnancy (usually late term)
Drugs (Doxorubicin)
Hemachromatosis
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29
Q

What is the genetic cause of hypertrophic cardiomyopathy?\

What disease can it be associated with?

A

usually due to genetic mutations in sarcomere proteins (myosin heavy chain)→ causes hypertrophy and stiffness of the LV

Associated with Friedrich Ataxia

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30
Q

What type of cardiomyopathy is seen in sudden death of young athletes?

A

Hypertrophic cardiomyopathy- causes a ventricular arrhythmia

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31
Q

What type of cardiomyopathy does amyloidosis cause?

A

Restrictive cardiomyopathy- abnormal deposition of amyloid makes the myocardium stiff and waxy

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32
Q

Systolic or diastolic dysfunction?:
Hypertrophic cardiomyopathy:
Restrictive cardiomyopathy:
Dilated cardiomyopathy:

A

Hypertrophic cardiomyopathy: diastolic
Restrictive cardiomyopathy: diastolic
Dilated cardiomyopathy: systolic

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33
Q

Most common cause of endocarditis in previously damaged valves (rheumatic heart disease and mitral valve prolapse)

A

Strep viridans

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34
Q

Most common cause of endocarditis in IVDA? What valve is effected most commonly?

A

Staph aureus

Right sided heart valves: tricuspid

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35
Q

Most common cause of endocarditis in prosthetic valves

A

staph epidermidis

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36
Q

Most common cause of endocarditis in patients with underlying colorectal carcinoma

A

strep bovis

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37
Q

Patient presents with erythematous nontender lesion on palms and soles, tender lesions on fingers, and splinter hemorrhages

A

endocarditis, due to microembolization of septic vegetations to skin vessels

  • Janeway lesions: erythematous nontender lesions on palms and soles
  • Osler nodes: tender lesions on fingers and toes (ouch osler)
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38
Q

Histology of the myocardium shows Aschoff bodies and Anitschkow cells

A

Characteristic of rheumatic fever

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39
Q

What valve is most commonly involved in rheumatic fever?

A

The mitral valve (less commonly involves the aortic valve)

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40
Q

Patient has stenotic aortic valve with fusion of the commissures as well as mitral stenosis… What likely caused this?

A

Rheumatic fever (not likely due to normal wear and tear seen in aortic stenosis)

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41
Q

What do you hear in someone with aortic stenosis?

A

A systolic ejection click and a crescendo-decrescendo murmur

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42
Q

What drug can cause dilated cardiomyopathy?

A

Doxorubicin (chemo drug)

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43
Q

Loffler syndrome

A

Restrictive cardiomyopathy

Endomyocardial fibrosis with a prominent eosinophilic infiltrate

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44
Q

What congenital heart disease is associated with a continuous “machine like” murmur?

A

PDA

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45
Q 
Role of different vessels
o	Arteries= 
o	Arterioles= 
o	Capillaries= 
o	Veins=
A

o Arteries= pressure vessels
o Arterioles= resistance vessels
o Capillaries= exchange vessels
o Veins= volume/capacitance vessels

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46
Q

Where in circulation is velocity the slowest? Why is this ideal?

Where is velocity to highest?

A

Capillaries- Has the greatest total cross sectional area
this is ideal because it optimizes conditions for exchange of substances across the capillary wall

The highest velocity is in the aorta- smallest cross sectional area

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47
Q

Which vessels have the greatest compliance? Where is there the biggest loss of compliance over time?

A

Veins have the greatest compliance. Arteries have the biggest loss of compliance over time.

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48
Q 
Capillary fluid exchange
o	Pc: 
o	Pi: 
o	πc: 
o	πi:
A

Pc: pushes fluid out of capillary
Pi: pushes fluid into capillary
πc: pulls fluid into capillary
πi: pulls fluid out of capillary

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49
Q

What forces cause edema

A

inc Pc, inc πi, inc capillary permeability, dec πc (dec plasma proteins)

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50
Q

Effect of CO2 on vessels

A

vasodilation (in patient with brain injury, have them hyperventilate to blow off CO2, cause vasoconstriction and dec blood flow)

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51
Q

When is blood flow through the coronary arteries increased?

A

During diastole – the heart is relaxed, there isn’t any pressure on the coronary arteries and there is increased flow

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52
Q

S1 heart sound

A

mitral and tricuspid valve closure

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53
Q

S2 heart sound

A

Aortic and pulmonic valve closure

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54
Q

S3 heart sound

A

In early diastole during rapid ventricular filling phase –> rapid flow from the atria into the ventricles

Normal in kids
Disease in adults: Associated with inc filling pressures and in dilated ventricles

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55
Q

S4 heart sound

A

In late diastole, associated with ventricular hypertrophy

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56
Q

What closes first, the pulmonic or aortic valve? Why?

A

The aortic valve closes first because pressure in the LV falls below aortic pressure before RV pressure falls below pulmonary pressure

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57
Q

Systolic murmurs

A

Aortic, pulmonic stenosis
Mitral, tricuspid regurg
Mitral prolapse

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58
Q

Diastolic murmurs

A

Mitral, tricuspid stenosis

Aortic, pulmonic regurg

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59
Q

Preload

A

End diastolic volume - the pressure in the left ventricle just before it ejects blood during systole

60
Q

Afterload

A

The pressure the heart must overcome in order to open the aortic valve

61
Q

What causes the normal splitting of the S2 heart sound during inspiration?

A

Inspiration causes a drop in intrathoracic pressure, which increases the venous return, increasing the RV filling (volume and time), and leads to the delayed closure of the pulmonic valve

62
Q

Most common sites of atherosclerosis

A

abdominal aorta>coronary artery>popliteal artery> carotid artery

63
Q

Virchow’s triad

A

1) venous trauma 2) stasis 3) hypercoagulability

64
Q

What is the significance of the plateau in the ventricular action potential?

A

Opening of Ica channels with influx of Ca balances the K+ efflux

Myocyte contraction

65
Q

What accounts for the automaticity of the SA and AV nodes?

A

I funny channels

(Na and K), slow spontaneous depolarization

66
Q

What is the cause of aortic stenosis in people younger than 60?

A

Congenital bicuspid aortic valve (more susceptible to calcifications)

67
Q

Patient presents with angina, syncope, and dyspnea. What do you suspect?

A

Severe aortic stenosis. Patient likely requires a valve replacement.

68
Q

What lab value is used to diagnose heart failure? What does this do? What drug is the synthetic form of this?

A

BNP
Acts via cGMP to cause vasodilation, dec Na absorption at the collecting duct, and promotes diuresis

Nesiritide is a synthetic form of this and is used to treat acute HF

69
Q

What types of patients is thiazide therapy contraindicated in?

A

People with sulfa allergies and people with gout (hyperuricemia)

70
Q

Effect of thiazides on calcium levels?

A

Increase calcium reabsorption – can lead to hypercalcemia

71
Q

Ingestion of meats and cheese (contain tyramine) while on MAO inhibitors can cause what?

What is this treated with?

A

Hypertensive crisis

Treat this with Phentolamine (a1 and a2 reversible blocker)

72
Q

Blunt aortic injury: mechanism and most common location

A
  • mechanism of injury involves a sudden deceleration that results in extreme stretching and torsional forces affecting the heart and aorta
  • most common at the aortic isthmus (right after the branches off the aorta) which is tethered by the ligamentum arteriosum and is immobile compared to the rest of the aorta
73
Q

Child with a heart defect that causes cyanosis and dyspnea that is improved with squatting

A

Tetralogy of Fallot (Caused by deviation of the infundibular septum)
The squatting increases SVR which decreases the R to L shunt and improves cyanosis

74
Q

Patient develops endocarditis after a dental procedure. It is likely from which bacteria?

A

Strep viridans

75
Q

Beck’s triad

A

Hypotension, distended neck veins, and muffled heart sounds = cardiac tamponade

76
Q

Why do people become hypotensive when supine or in the right lateral decubitus position?

A

Compression of IVC decreases venous return → reduced preload → dec cardiac output → hypotension

“Supine hypotension syndrome”

77
Q

Carotid baroreceptors/chemoreceptors are innervated by what nerve?
Aortic chemoreceptors/baroreceptors are innervated by which nerve?

A

Carotid = Glossopharyngeal IX

Aortic = vagus X

78
Q

Order of Speed of conduction through the heart

A

Purkinje>Atrial Muscle> Ventricular Muscle>AV node

79
Q

Involuntary head bobbing

A

Sign of a widened pulse pressure (usually due to aortic regurg)

o Pulse pressure is proportional to stroke volume and is inversely proportional to arterial compliance

80
Q

VSD produces what heart sound?

A

Holosystolic murmur over the left sternal border

81
Q

Most common cause of death after an MI

A

Ventricular fibrillation

82
Q

Delta waves are seen in

A

Wolff Parkinson White

Ventricular pre-excitation syndrome

83
Q

What does a schwann ganz catheter measure?

A

Pulmonary capillary wedge pressure – approximates left atrial pressure

84
Q

Where is the most deoxygenated blood in the body?

A

The coronary sinus: because myocardial oxygen extraction is very high

85
Q

What does the loss of the dicrotic notch on the cardiac pressure graph (of aortic pressure) indicate?

A

Aortic regurg

86
Q

What is the most common cause of coronary sinus dilation?

A

Inc R sided heart pressure due to pulmonary HTN

87
Q

Adenosine

A

Tx of supraventricular tachycardia- slows AV conduction
Very short acting (15 secs)
Can cause sense of impending doom, chest pain, and bronchospams

Dec effectiveness with caffeine and theophylline

88
Q

Digoxin

A

Inhibits the Na/K ATPase in myocardial cells which increases intracellular Na –> this indirectly inhibits the Na-Ca exchanger and increases intracellular Ca

Inc calcium in the myocyte improves contractility and left ventricular systolic function

89
Q

What drugs selectively vasodilate the coronary vessels?

A

Adenosine

Dipyridamole

90
Q

What drug is the treatment of choice for a Pheochromocytoma?

A

Phenoxybenzamine (Tx pheo with pheoxy!)

Irreversible a1 and a2 antagonist and blocks the vasoconstrictive actions of NE

91
Q

What drug(s) improve survival in heart failure patients?

A

B blockers
ACE-inhibitors
Ang II blockers
Spironolactone

92
Q

What drug should you use in a person with Aspirin allergy that needs to prevent cardiovascular events?

A

Clopidogrel: prevents platelet aggregation

93
Q

Cardiac auscultation: Opening snap with a mid diastolic murmur

A

Mitral stenosis

94
Q

What drugs selectively vasodilate veins?

A

Nitrates like nitroglycerin and isosorbide dinitrate *there is some arteriole dilation

95
Q

Congenital long QT is caused by?

A

A defect in ion channels

96
Q

Patient has an MI and develops a pericardial friction rub after 3 days. What caused this?

A

Post-infarction fibrinoid pericarditis

97
Q

Patient dies 1 week after an MI. What caused this?

A

Ventricular free wall rupture –> tamponade

Likely due to a LV pseudoaneurysm

98
Q

Where does most fetal blood go?

A

Through the foramen ovale to the LA (a small portion goes RA → RV → pulm artery → ductus arteriorsus → aorta)

99
Q

What is a complication of a patent foramen ovale:

A

paradoxical emboli – venous thromboemboli that enter systemic arterial circulation

100
Q

Where do you see the highest decrease in pressure?

A

Across the arterioles – because they are the site of highest resistance

101
Q

What is nitric oxide synthesized from?

A

Arginine and O2 (via endothelial nitric oxide synthase)

102
Q

What drugs inc the risk of statin myopathy?

A

Fibrates
Niacin
Any drug that inhibits CYP450 (since statins are metabolized by this)

103
Q

Aortic arch derivatives

A

1st Maxillary artery 1st arch is maximal

2nd Stapedial artery and hyoid artery Second = stapedial

3rd Common carotid and proximal part of internal carotid C is the 3rd letter of the alphabet

4th Aortic arch, right subclavian “Four = aor-ta”
“Fours” right subclavian

6th Pulmonary arteries and ductus arterious 66 looks like a pair of lungs

104
Q

How does digoxin decrease HR?

A

By stimulating the vagus nerve (parasympathetics), causing dec in HR

105
Q

Patient presents with blue gray discoloration and photodermatitis – what drug is he on and what labs need to be monitored?

A

Amiodarone:

Monitor LFTs, thyroid levels (can cause hyper/hypothyroidism) and pulmonary function tests (can cause pulmonary fibrosis)

106
Q

What does the middle meningeal artery branch off of?

A

The maxillary artery (which branches off the external carotid artery)

107
Q

Prostacyclin vs Thromboxane

A

Products of the arachidonic acid cascade (formed by COX)

  • Prostacyclin: dec platelet aggregation, dec vascular tone
  • Thromboxane (A2): inc platelet aggregation, inc vascular tone

Normally exist in balance of each other to maintain capillary patency and normal blood flow

108
Q

In what organ are infarcts rare? Why?

A

The liver because it has dual blood supply (hepatic artery and portal vein)

109
Q

What is pulsus paradoxus and when do you see it?

A

Pulsus paradoxus: dec in amplitude of systolic BO by >10 mmHG during inspiration

Pericarditis, *cardiac tamponade, asthma, COPD, croup

110
Q

Hereditary pulmonary HTN

What is increased?
Treatment?

A

Hereditary PAH is due to an inactivating mutation in BMPR2 (AD with variable penetrance)

Increased endothelin (antagonize endothelin with Bosentan)

Causes dysfunctional endothelial and vascular smooth muscle cell proliferation → thickening and fibrosis and inc resistance → pulmonary HTN

Can progress to R heart failure (cor pulmonale)

111
Q

How can there be near total occlusion of a coronary artery with no myocardial necrosis or scarring?

A

Slow growth rate of the occlusion allows for development of compensation via arterial collaterals around the point of occlusion

112
Q

In an aortic dissection, where is the defect?

A

A tear in the aortic intima

Usually due to chronic HTN

113
Q

Which drug can prolong the QT but has little risk of progressing to torsades?

A

Amiodarone

114
Q

Phenoxybenzamine vs Phentolamine

A

Phenoxybenzamine: IRREVERSIBLE a1 and a2 blocker

Phentolamine: REVERSIBLE a1 and a2 blocker

115
Q

Histo findings of giant cell arteritis

A

Granulomatous inflammation of the media

116
Q

Patient presents with multiple telangiectasias on the skin and recurrent nosebleeds. What do they have and what is the inheritance of this?

A

Osler-Weber-Rendu Syndrome

AD: hereditary hemorrhagic telangiectasia – can rupture and cause hemorrhage

117
Q

What cells are responsible for the formation of a fibrous cap in atherosclerosis?

A

Smooth muscle cells

118
Q

What cells are responsible for forming fatty streaks?

A

Lipid laden macrophages

119
Q

Young woman presents with excertional dyspnea

A

Think pulmonary HTN! mutation in BMPR2 leading to vascular smooth muscle proliferation

120
Q

MI complications:

Day 1:
Day 1-3:
Day 3-14:
2 weeks-months:

A

Day 1: ventricular arrhythmia
Day 1-3: fibrinous pericarditis
Day 3-14: free wall rupture. tamponade, LV pseudoaneurysm
2 weeks-months: dressler syndrome, true ventricular aneurysm

121
Q

What drug should be used to increase HDL levels?

A

Niacin B3 (blocks VLDL secretion and prevents lipolysis)

122
Q

What drug should NOT be used in a patient with triglyceridemia?

A

Cholestyramine

123
Q

What drug should be used to decrease LDL levels

A

Statins are first line

124
Q

What drug should be used to decrease triglyceride levels?

A

Fibrates

Upregulation of lipoprotein lipase cause increase removal of triglycerides from the blood

125
Q

Noninfectious causes of endocarditis? What will the pathology look like

A

Malignancy, hypercoagulable states, lupus

Sterile, platelet rich thrombi seen on valve

126
Q

Patient presents with migratory thrombophlebitis. What do you suspect?

A

Visceral malignancy (pancreas, colon, lung)

127
Q

Fenoldopam

A

Used in HTN emergency

o selective dopamine receptor agonist that increases cAMP and causes arterial dilation
o Increases renal perfusion by dilating renal arteriole and causes natiruesis

128
Q

What electrolyte change do you see in myocardial ischemia? How will this look histologically?

A

Inc intracellular Calcium (lack of O2 means that ATP isn’t being formed, so Na/K ATPase and Na/Ca ATPase can’t work)
Histo: visualization of bands under the microscope: hypercontraction of the sarcomeres due to massive calcium influx

129
Q

EKG shows ST elevation in leads II, III, and aVF. Where is the infarct?

A

The inferior heart – the right coronary artery

130
Q

Ortner syndrome

A

when an enlarged left atrium compresses the left recurrent laryngeal nerve and causes horseness

131
Q

Mediastinal widening on CXR

A

Aortic dissection

132
Q

How long does it take for loss of cardiomyocyte contractility after the onset of ischemia?

A

60 seconds due to loss of ATP

133
Q

When do atherosclerotic plaques in the coronary arteries become symptomatic and cause angina?

A

When they obstruct at least 75% of the luminal cross sectional area

134
Q

Carcinoid syndrome effects on the heart

A

Can cause valvular fibrous plaques (R>L)

135
Q

Libman-Sacks Endocarditis:

A

seen in SLE – nonbacterial, verrucous thrombi usually on mitral or aortic valve (LSE in SLE)

136
Q

How does nitroprusside work and what is a significant side effect?

A

used for HTN emergency, causes release of nitric oxide to increase cGMP in smooth muscle to promote venous and arteriolar vasodilation
o Can cause cyanide toxicity!!

137
Q

Coronary steal phenomenon

A

Adenosine and dipyridamole (phosphodiesterase inhibitor) are selective vasodilators of coronary vessels. When myocardial ischemia is present, these drugs cause a redistribution of blood flow to normal areas and bypass the collateral circulations → can allow for detection of ischemic areas because there is less blood flow to these areas

138
Q

Eccentric Hypertrophy

A

Sarcomeres added in series

Seen in dilated cardiomyopathy

139
Q

Concentric Hypertrophy

A

Sarcomeres added in parallel

Seen in pressure-overload hypertrophy (due to HTN or aortic stenosis)

140
Q

When do you see Q waves?

A

In a transmural STEMI (usually develops over several hours)

141
Q

When do you start to see histologic changes in an MI?

A

After 4 hours
0-4 hours: tissue looks normal
4-12 hours: early coagulation necrosis, edema, hemorrhage, wavy fibers
12-24 hours: coag necrosis and marginal contraction band necrosis
1-5 days: neutrophilic infiltrate
5-10 days: macrophages phagocytose dead cells
10-14 days: granulation tissue and neovascularization
2 weeks to 2 months: collagen deposition and scar formation

142
Q

How to assess the severity of mitral stenosis

A

The best indicator of mitral stenosis severity is the length of time between S2 (the A2 component) and the opening snap of the stenotic valve: as mitral stenosis worsens, left atrial pressure increases due to impaired movement of blood into the left ventricle. Higher pressure causes the valve to open more forefully and as a result, the A2-O2 interval becomes shorter

143
Q

What type of arteriolosclerosis do you see in severe HTN?

A

Hyperplastic: onion skinning with proliferation of smooth muscle cells

144
Q

Dopamine receptors

A

D1: Gs
D2: Gi

145
Q

Dopamine doses and effects

A

Low dose: D1 receptors – inc renal blood flow
Med dose: B1 receptors – cardiac activation
High dose: a1 receptors – pressor effects

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