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USMLE step 1 > Cardiology > Flashcards

Cardiology Flashcards

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USMLE® Step 1 flashcards
1
Q

Truncus Arteriosus gives rise to…

A

Ascending Aorta and pulmonary trunk

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2
Q

Bulbus Cordis gives rise to…

A

smooth parts (outflow tract) of left and right ventricles

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3
Q

Primitive ventricle gives rise to…

A

trabeculated left and right ventricles

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4
Q

Primitive atria gives rise to…

A

trabeculated left and right atria

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5
Q

Left horn of sinus venosus gives rise to…

A

coronary sinus

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6
Q

Right horn of sinus venosus gives rise to…

A

smooth part of right atrium

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7
Q

right common cardinal vein and right anterior cardinal vein gives rise to…

A

SVC

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8
Q

Embryology of truncus arteriosus

A

1) neural crest migration
2) truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary (AP) septum
3) Ascending aorta and pulmonary trunk

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9
Q

Pathology of Truncus Arteriosus

A

1) transposition of great vessels- failure to spiral
2) tetralogy of Fallot- skewed AP septum development
3) persistent Truncus Arteriosus- partial AP septum development

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10
Q

Interventricular septum development

A

1) Muscular ventricular septum forms. Opening is called interventricular foramen.
2) AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen.
3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum

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11
Q

Pathology of interventricular septum

A

1) improper neural crest migration into the truncus arteriosus (TA) can result in transposition of the great arteries or a persistent TA
2) membranous septal defect causes an initial left to right shunt which later reverses to a right to left shunt due to the onset of pulmonary hypertension (Eisenmenger’s syndrome)

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12
Q

Interatrial Septum development

A

1) Foramen Primum narrows as septum primum grows toward endocardial cushions.
2) Perforations in septum primum form foramen secundum (foramen primum disappears)
3) Foramen secundum maintains right to left shunt as septum secundum begins to grow
4) Septum secundum contains a permanent opening (foramen ovale)
5) Foramen secundum enlarges and upper part of septum primum degenerates
6) Remaining portion of septum primum forms valve of foramen ovale.
7) Septum secundum and septum primum fuse to form the atrial septum
8) Foramen ovale usually closes soon after birth because of increased left atrial pressure.

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13
Q

Pathology of Interatrial Septum

A

Patent foramen ovale caused by failure of the septum primum and septum secundum to fuse after birth

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14
Q

Fetal Erythropoiesis

A

1) Yolk Sac: 3-10 weeks
2) Liver: 6 weeks to birth
3) Spleen: 15-30 weeks
4) Bone Marrow: 22 weeks to adult

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15
Q

Fetal Circulation (shunts)

A

1) blood entering the fetus through the umbilical vein is conducted via the ductus venosus into the IVC to bypass the hepatic circulation
2) Most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body
3) Deoxygenated blood entering the RA from the SVC enters the RV, is expelled into the pulmonary artery and then passes through the ductus arteriosus into the descending aorta.

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16
Q

Umbilical Vein

A

Ligamentum teres hepatis, contained in falciform ligament

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17
Q

Umbilical arteries

A

medial umbilical ligaments

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18
Q

ductus arteriosus

A

ligamentum arteriosum

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19
Q

ductus venosus

A

ligamentum venosum

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20
Q

foramen ovale

A

fossa ovalis

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21
Q

allantois

A

urachus-median umbilical ligament; the urachus is part of the allantoic duct between the bladder and the umbilicus. Urachal cyst or sinus is a remnant.

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22
Q

Notochord

A

Nucleus pulposus of intervertebral disc

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23
Q

SA and AV nodes are supplied by…

A

Right coronary artery (RCA)

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24
Q

Right dominant circulation

A

85%; posterior descending artery (PD) arises from RCA

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25
Q

Left dominant circulation

A

8%; PD arises from left circumflex coronary artery (LCX)

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26
Q

Codominant circulation

A

7%; PD arises from both LCX and RCA

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27
Q

Most common coronary artery occlusion?

A

Left Anterior Descending artery (LAD)

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28
Q

When do coronary arteries fill?

A

During Diastole

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29
Q

LCX supplies…

A

lateral and posterior walls of the left ventricle

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30
Q

LAD supplies…

A

anterior 2/3 of interventricular septum, anterior papillary muscle and anterior surface of left ventricle

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31
Q

PD supplies…

A

posterior 1/3 of interventricular septum and posterior walls of ventricles

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32
Q

Most posterior part of the heart?

A

Left atrium; enlargement can cause dysphagia due to compression of the esophagus or hoarseness due to compression of the left recurrent laryngeal nerve

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33
Q

Transesophageal echocardiography

A

useful for diagnosing left atrial enlargement, aortic dissection and thoracic aortic aneurysm

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34
Q

stroke volume is affected by…

A

contractility, afterload and preload. Increased SV when increased preload, decreased afterload or increased contractility

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35
Q

Contractility increases with…

A

1) catecholamines (increased activity of Ca pump in sarcoplasmic reticulum)
2) increased intracellular Ca
3) decreased extracellular Na (decreased activity of Na/Ca exchanger)
4) Digitalis (blocks Na/K pump which increases intracellular Na and decreases activity of Na/Ca exchanger which then increases intracellular Ca)

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36
Q

Contractility decreases with…

A

1) Beta 1 blockade (decreases cAMP)
2) heart failure (systolic dysfunction)
3) acidosis
4) hypoxia/hypercapnea
5) Non-dihydropyridine Ca channel blockers

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37
Q

Myocardial O2 demand is increased by ?

A

1) increased afterload
2) increased contractility
3) increased heart rate
4) increased heart size (increased wall tension)

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38
Q

Inspiration

A

increased intensity of right heart sounds

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39
Q

expiration

A

increased intensity of left heart sounds

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40
Q

Hand grip (increased systemic vascular resistance)

A

increased intensity of MR, AR, VSD, MVP murmurs; decreased intensity of AS, hypertrophic cardiomyopathy murmurs

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41
Q

Valsalva (decreased venous return)

A

decreased intensity of most murmurs; increased intensity of MVP, hypertrophic cardiomyopathy murmurs

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42
Q

Rapid Squatting (increased venous return, increased preload, increased afterload with prolonged squatting)

A

decreased intensity of MVP, hypetrophic cardiomyopathy murmurs

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43
Q

Systolic heart sounds

A

aortic/pulmonic stenosis, mitral/ tricuspid regurgitation, ventricular septal defect

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44
Q

Diastolic heart sounds

A

aortic/pulmonic regurgitation, mitral/tricuspid stenosis

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45
Q

What can you hear in aortic area?

A

1) aortic stenosis
2) flow murmur
3) aortic valve sclerosis

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46
Q

What can you hear in left sternal border?

A

1) aortic regurgitation
2) pulmonic regurgitatio
3) hypertrophic cardiomyopathy

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47
Q

what can you hear in pulmonic area?

A

1) pulmonic stenosis

2) flow murmur (atrial septal defect, patent ductus arterious)

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48
Q

What can you hear in tricuspid area?

A

1) tricuspid regurgitation
2) ventricular septal defect
3) tricuspid stenosis
4) atrial septal defect

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49
Q

What can you hear in mitral area?

A

1) mitral regurgitation

2) mitral stenosis

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50
Q

Mitral regurgitation

A

high pitched “blowing murmur”; loudest of apex and radiates toward axilla. Enhanced by maneuvers that increase TPR (squatting or hand grip) or LA return (expiration). It is often due to ischemic heart disease, mitral valve prolapse or LV dilation

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51
Q

Tricuspid regurgitation

A

It is loudest at tricuspid area and right sternal border. Enhanced by maneuvers that increase RA return (inspiration). It can be caused by RV dilation. Rheumatic fever and infective endocarditis can cause either MR or TR

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52
Q

Aortic Stenosis

A

“Pulsus Parvus et tardus” Pulses are weak with a delayed peak. Can lead to Syncope, Angina and Dyspnea on exertion. Often due to age related calcific aortic stenosis or bicuspid aortic valve.

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53
Q

VSD

A

Harsh sounding murmur. Loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload.

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54
Q

Mitral Valve Prolapse (MVP)

A

Late systolic crescendo murmur with midsystolic click due to sudden tensing of chordae tendinae. Most frequent valvular lesion, best heard over apex, loudest at S2. Usually benign, can predispose to infective endocarditis. It can be caused by myxomatous degeneration, rheumatic fever or chordae rupture. Enhanced by maneuvers that decrease venous return (standing or Valsalva).

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55
Q

Aortic Regurgitation (AR)

A

Immediate high pitched “blowing” diastolic decrescendo murmur. Wide pulse pressure when chronic; can present with bounding pulses and head bobbing. Often due to aortic root dilation, bicuspid aortic valve, endocarditis or rheumatic fever. Increased murmur during hand grip. Vasodilators decrease intensity of murmur.

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56
Q

Mitral Stenosis (MS)

A

Follows opening SNAP due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion at leaflet tips. Delayed rumbling late diastolic murmur. Often occurs secondary to rheumatic fever. Chronic MS can result in LA dilation. Enhanced by maneuvers that increase LA reurn (expiration)

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57
Q

PDA

A

Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity. Best heard at left infraclavicular area.

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58
Q

Atrial Fibrillation

A

Chaotic and erratic baseline with no discrete P waves in between irregularly placed QRS complexes. Can result in atrial stasis and lead to stroke. Treatment includes rate control, anticoagulation and possible cardioversion.

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59
Q

Atrial Flutter

A

rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves.

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60
Q

Ventricular fibrillation

A

completely erratic rhythm with no identifiable waves. Fatal Arrythmia without immediate CPR and defibrillation

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61
Q

Right to Left Shunts (early Cyanosis)- Blue babies

A

5 Ts

1) tetralogy of fallot (most common cause of early cyanosis)
2) Transposition of great vessels
3) Persistent Truncus Arteriosus
4) Tricuspid Atresia
5) Total Anomalous pulmonary venous return (TAPVR)

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62
Q

Tricuspid Atresia

A

characterized by absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability.

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63
Q

Left to right Shunts (late cyanosis)- Blue kids

A

VSD (most common congenital cardiac anomaly)
ASD
PDA

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64
Q

Eisenmenger’s syndrome

A

Uncorrected VSD, ASD or PDA causes compensatory pulmonary vascular hypertrophy which results in progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from left to right to right to left which causes late cyanosis, clubbing and polycythemia.

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65
Q

2q11 syndromes

A

truncus arteriosus, tetralogy of Fallot

66
Q

Down Syndrome

A

ASD, VSD, AV septal defect (endocardial cushion defect)

67
Q

Congenital Rubella

A

Septal defects, PDA, Pulmonary artery stenosis

68
Q

Turner Syndrome

A

Coarctation of Aorta (preductal)

69
Q

Marfan’s syndrome

A

aortic insufficiency and dissection (late complication)

70
Q

Infant of diabetic mother

A

transposition of great vessels

71
Q

atheromas

A

plaques in blood vessel walls

72
Q

xanthomas

A

plaques or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids (xanthelasma)

73
Q

tendinous xanthoma

A

lipid deposit in tendon, especially achilles

74
Q

Corneal arcus

A

lipid deposit in cornea, nonspecific (arcus senilis)

75
Q

Arteriosclerosis- Monckeberg

A

Calcification in the media of the arteries, especially radial or ulnar. Usually benign; “pipestem”arteries. Does not obstruct blood flow.

76
Q

Arteriolosclerosis

A

Two types: hyaline (thickening of small arteries in essential hypertension or diabetes mellitus) and hyperplastic (“onion skinning” in malignant hypertension)

77
Q

Atherosclerosis

A

fibrous plaques and atheromas form in intima of arteries

78
Q

Abdominal Aortic Aneurysm

A

associated with atherosclerosis. Occurs more frequently in hypertensive male smokers more than 50 years of age.

79
Q

Thoracic aortic aneurysm

A

associated with hypertension, cystic medial necrosis (Marfan’s syndrome) and historically tertiary syphilis.

80
Q

Coronary steal syndrome

A

vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion

81
Q

Symptoms of MI

A

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue.

82
Q

Most common cardiomyopathy?

A

Dilated (congestive) cardiomyopathy

83
Q

Dilated cardiomyopathy etiologies?

A

Chronic alcohol abuse, wet Beri Beri, Coxsackie B Virus myocarditis, chronic cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis and peripartum cardiomyopathy.

84
Q

Dilated cardiomyopathy Findings?

A

S3, dilated heart on ultrasound, balloon appearance on chest x-ray

85
Q

Dilated cardiomyopathy treatment?

A

Na restriction, ACE inhibitors, diuretics, digoxin, heart transplant

86
Q

Hypertrophic Cardiomyopathy?

A

Hypertrophied interventricular septum is too close to mitral valve leaflet, leading to outflow obstruction. Cause of sudden death in young athletes.

87
Q

Hypertrophic cardiomyopathy findings?

A

normal sized heart, S4, apical impulses, systolic murmur

88
Q

Hypertrophic cardiomyopathy treatment?

A

beta blocker or non-dihydropyridine calcium channel blocker (verapamil)

89
Q

Restrictive/ obliterative cardiomyopathy

A

major causes include sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children) and hemochromatosis

90
Q

Loffler’s Syndrome

A

endomyocardial fibrosis with a prominent eosinophilic infiltrate

91
Q

CHF

A

Occurs in patients with an inherited or acquired abnormality of cardiac structure or function which is characterized by a constellation of clinical symptoms (dyspnea, fatigue) and signs (edema, rales).

92
Q

cause of cardiac dilation?

A

greater ventricular end-diastolic volume

93
Q

cause of dyspnea on exertion?

A

failure of cardiac output to increase during exercise

94
Q

Left Heart Failure

A

Pulmonary edema, paroxysmal nocturnal dyspnea

Orthopnea (shortness of breath when supine)

95
Q

Right heart failure

A

hepatomegaly (nutmeg liver)
peripheral edema
jugular venous distention

96
Q

Pulmonary edema

A

increased pulmonary venous pressure that leads to pulmonary venous distention and transudation of fluid. Presence of hemosiderin-laden macrophages (“heart failure” cells) in the lungs

97
Q

Orthopnea

A

increased venous return in supine position exacerbates pulmonary vascular congestion

98
Q

Hepatomegaly

A

increased central venous pressure leads to increased resistance to portal flow. Rarely, leads to “cardiac cirrhosis”

99
Q

Peripheral edema

A

increased venous pressure which leads to fluid transudation

100
Q

jugular venous distention

A

increased venous pressure

101
Q

bacterial endocarditis symptoms

A

1) fever (most common)
2) Roth’s spots- round white spots on retina surrounded by hemorrhage
3) Osler’s nodes- tender raised lesions on finger or toe pads
4) new murmur
5) Janeway lesions- small, painless, erythematous lesions on palm or sole
6) anemia
7) splinter hemorrhages on nail bed

102
Q

Acute bacterial endocarditis

A

S. Aureus (high virulence). Large vegetations on previously normal valves. Rapid onset.

103
Q

Subacute endocarditis

A

viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. More insidious onset.

104
Q

Acute pericarditis

A

commonly presents with sharp pain, aggravated by inspiration and relieved by sitting up and leaning forward. Presents with friction rub. Widespread ST-segment elevation and/or depression.

105
Q

fibrinous acute pericarditis

A

caused by Dressler’s syndrome, uremia, radiation. Presents with loud friction rub.

106
Q

serous acute pericarditis

A

viral pericarditis (often resolves spontaneously); noninfectious inflammatory diseases (rheumatoid arthritis, SLE)

107
Q

Suppurative/purulent acute pericarditis

A

usually caused by bacterial infections (pneumococcus, streptococcus). Rare now with antibiotics.

108
Q

Cardiac tamponade

A

compression of heart by fluid in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers. Findings: hypotension, increased venous pressure, distant heart sounds, increased heart rate, pulsus parodoxus

109
Q

Pulsus parodoxus

A

decrease in amplitude of systolic blood pressure by more than 10 mm Hg during inspiration. Seen in severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis and croup.

110
Q

Myxomas

A

most common primary cardiac tumor in adults. Usually described as a ball valve obstruction in the left atrium (associated with multiple syncopal episodes).

111
Q

Rheumatic Fever

A

1) Fever
2) Erythema marginatum
3) Valvular damage (vegetation and fibrosis)
4) ESR increase
5) Red hot joints (migratory polyarthritis)
6) Subcutaneous nodules
7) St. Vitus’ dance (Sydenham’s chorea)

112
Q

Acute Pericarditis

A

presents with sharp pain, aggravated by inspiration and relieved by sitting up and leaning forward. Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression.
3 Types: fibrinous, serous, suppurative/purulent

113
Q

Fibrinous Acute pericarditis

A

caused by Dressler’s syndrome, uremia, radiation. Presents with loud friction rub.

114
Q

Serous Acute pericarditis

A

Viral pericarditis (often resolves spontaneously), noninfectious inflammatory diseases (rheumatoid arthritis, SLE)

115
Q

Cardiac Tamponade

A

compression of heart by fluid (blood, effusions) in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers.
Findings: hypotension, increased venous pressure, distant heart sounds, increased heart rate, pulsus paradoxus.

116
Q

Syphilitic heart disease

A

tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of the vessel wall and dilation of the aorta and valve ring. May see calcification of the aortic root and ascending aortic arch. Leads to tree bark appearance of the aorta. Can result in aneurysm of the ascending aorta or aortic arch and aortic insufficiency.

117
Q

Rhabdomyomas

A

most frequent primary cardiac tumor in children (associated with tuberous sclerosis)

118
Q

suppurative/purulent acute pericarditis

A

usually caused by bacterial infections (pneumococcus, streptococcus). Rare now with antibiotics.

119
Q

Kussmaul’s sign

A

increase in JVP on inspiration instead of a normal decrease. May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors, or cardiac tamponade.

120
Q

Raynaud’s phenomenon

A

decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress. Most often in the fingers and toes.

121
Q

Temporal (giant cell) arteritis epidemiology

A

generally elderly females, unilateral headache (temporal artery), jaw claudication. May lead to irreversible blindness due to ophthalmic artery occlusion. Associated with polymyalgia rheumatica.

122
Q

Temporal (giant cell) arteritis pathology

A

most commonly affects branches of carotid artery, focal granulomatous inflammation, increased ESR, treat with high dose corticosteroids.

123
Q

Takayasu’s arteritis epidemiology

A

asian females less than 40 years of age, “pulseless disease” (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances.

124
Q

Takayasu’s arteritis pathology

A

granulomatous thickening of aortic arch, proximal great vessels, increased ESR, treat with corticosteroids.

125
Q

Large vessel vasculitis

A

1) temporal (giant cell) arteritis

2) takayasu’s arteritis

126
Q

medium vessel vasculitis

A

1) polyarteritis nodosa
2) kawasaki disease
3) Buerger’s disease (thromboangiitis obliterans)

127
Q

Polyarteritis nodosa epidemiology

A

young adults, hepatitis B seropositivity in 30% of patients. Fever, weight loss, malaise, headache. GI: abdominal pain, melena. Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage.

128
Q

Polyarteritis nodosa pathology

A

Typically involves renal and visceral vessels, not pulmonary arteries. Immune complex mediated. Transmural inflammation of the arterial wall with fibrinoid necrosis. Lesions are of different ages. Many aneurysms and constrictions on arteriogram. Treat with corticosteroids, cyclophosphamide.

129
Q

Kawasaki disese epidemiology

A

Asian children less than 4 years of age. Fever, cervical lymphadenitis, conjunctival injection, changes in lips/oral mucosa (strawberry tongue), hand foot erythema and desquamating rash.

130
Q

Kawasaki disease pathology

A

may develop coronary aneurysms. Treat with IV immunoglobulin and aspirin.

131
Q

Buerger’s disease (thromboangitis obliterans) epidemiology

A

heavy smokers, males less than 40 years of age. Intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis. Raynaud’s phenomenon is often present.

132
Q

Buerger’s disease pathology

A

segmental thrombosing vasculitis, treat with smoking cessation.

133
Q

small vessel vasculitis

A

1) microscopic polyangitis
2) wegener’s granulomatosis (granulomatosis with polyangitis)
3) Churg-Strauss syndrome
4) Henoch-Schonlein purpura

134
Q

Microscopic polyangitis epidemiology

A

necrotizing vasculitis commonly involving lung, kidneys and skin with pauci-immune glomerulonephritis and palpable purpura

135
Q

Microscopic polyangitis pathology

A

no granulomas, p-ANCA, treat with cyclophosphamide and corticosteroids

136
Q

Wegener’s granulomatosis epidemiology

A

upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.
Lower respiratory tract: hemoptysis, cough, dyspnea.
Renal: hematuria, red cell casts

137
Q

Wegener’s granulomatosis pathology

A

Triad:
1) focal necrotizing vasculitis
2) necrotizing granulomas in the lung and upper airway
3) necrotizing glomerulonephritis
c-ANCA, treat with cyclophosphamide, corticosteroids.
chest x-ray: large nodular densities

138
Q

Churg-Strauss Syndrome epidemiology

A

asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop). Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis)

139
Q

Churg-Strauss Syndrome pathology

A

granulomatous, necrotizing vasculitis with eosinophilia. p-ANCA, elevated IgE level.

140
Q

Henoch-Schonlein purpura epidemiology

A

most common childhood systemic vasculitis. Often follows URI. Classic triad:

1) skin: palpable purpura on buttocks/legs
2) Arthralgia
3) GI: abdominal pain, melena, multiple lesions of same age.

141
Q

Henoch-Schonlein purpura pathology

A

vasculitis secondary to IgA complex deposition. Associated with IgA nephropathy.

142
Q

Strawberry Hemangioma

A

benign capillary hemangioma of infancy. appears in first weeks of life; grows rapidly and regresses spontaneously at 5-8 years of age.

143
Q

Cherry Hemangioma

A

Benign capillary hemangioma of the elderly. Does not regress. Frequency increases with age.

144
Q

Pyogenic Granuloma

A

Polypoid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy.

145
Q

Cystic Hygroma

A

Cavernous Lymphangioma of the neck. Associated with turner syndrome.

146
Q

Glomus Tumor

A

benign, painful, red-blue tumor under fingernails. Arises from modified smooth muscle cells of glomus body.

147
Q

Bacillary Angiomatosis

A

benign capillary skin papules found in AIDS patients. Caused by Bartonella Henselae infections. Frequently mistaken for Kaposi’s sarcoma.

148
Q

Angiosarcoma

A

Rare blood vessel malignancy typically occurring in the head, neck and breast areas. Associated with patients receiving radiation therapy, especially for Breast cancer and Hodgkin’s lymphoma. Very aggressive and difficult to resect due to delay in diagnosis.

149
Q

Lymphangiosarcoma

A

lymphatic malignancy associated with persistent lymphedema (post-radical mastectomy).

150
Q

Kaposi’s sarcoma

A

endothelial malignancy most commonly of the skin, but also mouth, GI tract and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis.

151
Q

Sturge-Weber Disease

A

congenital vascular disorder that affects capillary sized blood vessels. Manisfests with port-wine stain (nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, and early onset glaucoma. Affects small vessels.

152
Q

essential hypertension therapy

A

diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.

153
Q

CHF therapy

A

diuretics, ACE inhibitors/ARBs, beta blockers (compensated CHF), K sparing diuretics.

154
Q

Diabetes Mellitus therapy

A

ACE inhibitors/ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers.

155
Q

calcium channel blockers

A

nifedipine, verapamil, diltiazem, amlodipine

156
Q

clinical use of calcium channel blockers

A

hypertension, angina, arrhythmias (not nifedipine), Prinzmetal’s angina, Raynaud’s.

157
Q

Toxicity of calcium channel blockers

A

cardiac depression, AV block, peripheral edema, flushing, dizziness and constipation.

158
Q

Hydralazine Clinical use

A

severe hypertension, CHF, first line therapy for hypertension in therapy, with methyldopa. Frequently co-administered with a beta blocker to prevent reflex tachycardia.

159
Q

Hydralazine toxicity

A

compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, Lupus-like syndrome.

160
Q

Malignant hypertension treatment

A

commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.

161
Q

nitroprusside

A

short acting: increased cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide).

162
Q

Fenoldopam

A

dopamine D1 receptor agonist: coronary, peripheral, renal, and splanchnic vasodilation. Decreased BP and increased natriuresis.

USMLE step 1 (1 decks)

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