Brainscape's Knowledge GenomeTM

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


See full index

Step 1 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Drugs that are selective vasodilators of coronary vessels (aka coronary steal)?

A

Adenosine and dipyridamole (coronary perfusion studies therefore pretty precise)

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

VSD murmur

A

Holosystolic murmur over L mid-sternal border

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

Mucosal cyanosis and fingernail clubbing found in what defects?

A

Cyanotic congenital heart diseases (like Tetralogy) or late features 2/2 Eisenmengers

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

Fixed, wide splitting of S2?

A

ASD! L-to-R shunt –> delayed closure of the pulmonary valve all the time.

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

Pulsus paradoxus

A

Dec. in systolic pressure of > 10 mmHg w/ inspiration. Conditions that impair expansion of pericardial space (tamponade, constrictive pericarditis, obstructive lung disease, restrictive cardiomyopathy), causes the inter ventricular septum to move into the left and reduce SV during inspiration.

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

Cardiac tamponade exam?

A

Beck’s triad - hypotension, JVD, distant/muffled heart sounds; tachycardia

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

Fick principle?

A

CO = rate of O2 consumption/arteriovenous O2 difference. Derived from the idea that flow * concentration difference = amount of substance consumed.

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

Concentric LV hypertrophy associated with?

A

Chronic HTN, aortic stenosis

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

Extended consumption of appetite suppressants leading to?

A

Pulmonary hypertension

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

Aortic regurgitation murmur

A

Diastolic decrescendo, heard loudest in early diastole (increased pressure gradient). Left sternal border w/ pt leaning forward at END-expiration.

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

Perivascular infiltrate with abundant eosinophils in cardiac tissue?

A

Hypersensitivity myocarditis

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

Light micro path after MI

A

Minimal change < 4h. Up to day 5 becomes coagulation necrosis (edema, wave fibers -> band necrosis -> neurophils). Days 5-10 = macrophage. Days 10-14 = granulation tissue and neovasc. 2 wk-2mo = collagen deposition/scar

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

Selective beta-blockers?

A

Metoprolol, atenolol, acebutolol, and esmolol. Preferred in patients with COPD or asthma b/c won’t B2 blockade -> bronchoconstriction

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

How does nitroglycerin relieve angina?

A

DECREASED cardiac preload (LV diastolic volume) via venodilation leading to retention of blood in venous system. Modest coronary arteriolar dilation, but high doses -> coronary steal

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

Phase 0 pacemaker?

A

Upstroke. Opening of L-type (long-lasting dihydropyridine-sensitive Ca2+ channels leading to slow influx

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

Phase 3 pacemaker?

A

Repolarization. Opening of K+ channels and efflux. Closure of L-type Ca2+ channels.

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

Phase 4 pacemaker?

A

Pacemaker potential. Slow influx of Na+ occurring at end of 3. Also slow decrease in K+ efflux. At -50 mV, T-type (Transient) Ca+ opens leading to depolarization. At -40, L-types open until we get AP.

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

Effects of adenosine on cardiac pacemakers?

A

Adenosine activates K+ channels and prolongs K+ efflux leading to longer time NEGative, while also inhibiting L-type Ca+ channels prolonging time to reach threshold -> decreased HR.

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

Digoxin toxicity treatment

A

Oral activated charcoal, mgmt of K+ w/ insulin, kayexelate, or dialysis (avoid Ca gluconate), digoxin-specific Ab fragments

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

Digoxin toxicity

A

AV nodal block -> brady -> junctional escape -> ventricular tachyarrhythmias. HyperK leads to increased susceptibility. Anorexia, n/v, abdominal pain, fatigue, confusion, weakness, COLOR VISION change

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

Effects of an arteriovenous shunt on preload and after load?

A

Decreased after load but increased preload.

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

ADP-mediated drugs?

A

Clopidogrel and ticlopidine

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

Two QT prolongation congenital syndromes?

A

Romano-Ward (AD, no defaness) and “Jervell and LAnge-Nielsen syndrome” (AR, neurosensory deafness) —> torsades at young age. K+ channel mutations -> delayed rectifier current

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

Paradoxical embolism

A

Cerebrovascular event in setting of known thromboembolic disease is suspicious for an intracardiac or intrapulmonary shunt (patent foramen ovale, ASD, VSD, plum AV malformations). Even if L-R shunt, transient reversal during elevated R-sided pressure periods –> embolization

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

Phase 0 myocyte

A

SODIUM (not Ca+ as in pacemaker) inward (voltage-gated)

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

Phase 1 myocyte

A

Initial rapid repol b/c of Na+ channel closure

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

Phase 2 myocyte

A

Plateau (only seen here). Opening of L-type Ca+ channels and closure of some K+ channel.

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

Phase 3 myocyte

A

Late rapid depolarization b/c of closure of Ca+ channel and OPENING of K+ channels

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

Phase 4 myocyte

A

Resting potential. Mostly b/c of K+ permeability.

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

Inspiration affecting murmurs

A

Intrathroacic pressure drops, increased blood flow to right heart. Inc. RV SV, decreased LV return. Increased TR murmur.

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

Myxomatous degeneration

A

Often seen in connective tissue disease for the MV –> prolapse.

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

Pulsus alternans

A

Beat to beat variation in magnitude of pulse pressure. LV dysf(x)

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

Pulsus paradoxus

A

Decrease in systolic > 10 mmHg upon inspiration vs. expiration. Associated with cardiac tamponade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Dicrotic pulse?

A

Pulse w/ two distance peaks - one in systole, the other in diastole. Best palpated in CAROTIDs and associated with severe SYSTOLIC dysf(x)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Pulsus parvus et tardus

A

Aortic stenosis. Low magnitude w/ delayed peak.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Most reliable auscultatory indicator of degree of mitral stenosis?

A

A2-OS interval. Shorter = more SEVERE b/c increased LA pressures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Degree of cyanosis in TOF determined by?

A

Degree of pulmonic stenosis. (TOF = pulmonic stenosis, VSD, RVH, overriding aorta). If severe, blood goes across the VSD and does not oxygenate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Post-MI pericarditis

A

Early-onset pericarditis develops in 10-20% of patients between days 2-4 following STEMI b/c of inflammation overlying necrotic segment. Short-lived, 1-3 days with ASA. Late-onset post-MI pericarditis = Dressler’s syndrome = autoimmune reaction starting 1 week to few months after MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Atrial myxoma

A

Most common primary cardiac neoplasm. Constitutional symptoms, mid-diastolic rumble at apex, positional dyspnea, large pedunculated mass of LA. Path - scattered cells within mucopolysaccharide stroma, normal blood vessels (VEGF) and hemorrhaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Antihypertensive that has minimal effect on AV conduction?

A

Nifedipine. Vasodilator. a CCB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What part of the cardiac electrical conduction system is the slowest and why?

A

The AV node. B/c after P-wave fires from SA node, want to give time for ventricles to fill before firing off for systole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Fastest to slowest cardiac tissue conduction?

A

Purkinje, Atrial tissue, Ventricular Tissue, AV node. Purk At Ventricle Ave.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Nitroglycerin’s effect

A

Venodilates>arteriodilates -> decreasing PRELOAD. Reflexive increased HR NOT overcome by overall decreased volumes -> decrease O2 consumption by cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Atrial septation

A

First the septum primum forms superiorly to inferiorly. At some point, a foramen secundum forms in the septum primum before the foramen primum is obliterated. The septum secundum then forms superiorly to partially cover the foramen secundum allowing a R-L shunt. When LA increases at birth, the septa will fuse to form the atrial septum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Fetal erythropoiesis

A

Young Liver Synthesizes Blood. Yolk sac (3-8wk), Liver (6 wk-birth), spleen (10-28 weeks), bone marrow (18 weeks to adult)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

The three major shunts in fetal circulation

A

Ductus venosus bypasses the liver form umbilical vein to IVC. Patent foramen ovale allows said oxygenated blood to R-L shunt into the aorta. Finally, deoxygenated blood moving into RV go mostly into the aorta via ductus arteriosus instead of going into the pulmonary vasculature, which has high resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What keeps PDA open (and what can close it?)

A

Prostaglandins E1 and E2. Indomethacin can help close it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ductus arteriosus and ductus venosus turn into?

A

Ligamentum arteriosum and ligamentum venosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Umbilical vein and umbilical arteries turn into?

A

Ligamentem teres hepatis and mediaL umbilical ligaments. MediaL for umbiLical.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Median vs medial umbilical ligament?

A

ONE median umbilical ligament from the allantois. TWO medial umbilical ligaments from umbiLical arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Interventricular septum perfusion?

A

PDA/posterior interventricular artery supplies the posterior 1/3. LAD supplies anterior 2/3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

MAP equations (2)

A

MAP = 2/3 diastolic + 1/3 systolic = CO x TPR; (V=IR w/ V ~ Pa b/c Pv ~ 0)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Pulse pressure equation; what does it mean?

A

Pulse pressure = Psystolic - Pdiastolic ~ Stroke volume / arterial compliance (b/c difference in pressure ~ change in volume / compliance). Therefore, pulse pressure is proportional to SV but INVERSELY proportional to arterial compliance. (Inc. pulse pressure in athersclerosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Pulse pressure increased when?

A

Atherosclerosis, hyperthyroidism, AR (inc. SV), OSA (sympathetic tone), exercise (Transient)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Pulse pressure is decreased when?

A

Aortic stenosis (dec. SV), cardiogenic shock, cardiac tamponade, HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Digoxin mechanism

A

Blocks the Na+/K+ channel, which increases intracellular Na+, which prevents Na+/Ca2+ exchanger -> INC. intracellular Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Approximaters for preload and afterload?

A

Preload ~ EDV. Afterload ~ MAP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How relate LV structural parameters with afterload?

A

LaPlace’s law. Wall tension = pressure x radius / (2 x wall thickness). LV seeks to decrease wall tension in HTN by increasing wall thickness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Ejection fraction equation

A

SV / EDV = (EDV - ESV) / EDV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which way does the Starling curve go with increased contractility?

A

Y axis = SV. X axis = pre-load. Soooo, left-shift the curve with increased contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Vascular resistance components (equation)

A

R ~ viscosity x length / r^4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Jugular venous pulsations?

A

a wave (atrial kick), c wave (RV Contraction), x descent (atrial relaXation), v wave (RA pressure due to filling against closed tricuspid Valve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Wide split S2?

A

P2 comes after A1 b/c of delayed RV emptying (e.g. pulmonic stenosis, RBBB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Fixed split S2?

A

Seen in ASD b/c the Left-Right shunt delays RV emptying constantly regardless of breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Paradoxical split S2?

A

P2 comes before A2 b/c of delayed LV emptying (aortic stenosis, LBBB). On inspiration, no split, but split on EXPiration!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Hand grip maneuver increases intensity of what murmurs?

A

Hand grip increases SVR. Increased - MR, AR, VSD. Catch the regurgitation w/ your hand! Decreased - AS, HCOM.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Valsalva or standing increases intensity of what murmurs?

A

Decreased venous return. Increased HOCM.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Rapid squatting increases intensity of what murmur?

A

AS

69
Q

Where do you hear the HOCM murmur?

A

Left sternal border

70
Q

Mitral valve prolapse murmur?

A

Late systolic crescendo murmur with mid systolic click (sudden tensing of chordae tendinae).

71
Q

MS vs. AR murmurs?

A

MS follows an opening snap with “rumbling” late diastolic murmur. AR is high-pitched early diastolic decrecending.

72
Q

What does U wave look like and what does it signify?

A

A small positive deflection following T-wave that may indicate hyPOkalemia or bradycardia

73
Q

Meds that can prolong QT?

A

Some Risky Meds Can Prolong QT: Sotalol, Risperidone (antipsychs), Macrolides, Chloroquime, Protease inhibitors (-navirs), Quinidine (Ia AND III), Thiazides

74
Q

Two congenital long QT syndromes

A

Romano-Ward (AD, pure cardiac phenotype) and Jervell and Lange-Nielsen syndrome (AR w/ sensorinueral deafness)

75
Q

WPW can lead to what?

A

A re-entery circuit -> supraventricular tachycardia; Delta wave

76
Q

Atrial-flutter sinus conversion with what and rate-control with what?

A

IA, IC, III anti-arrhythmics; Rate-control with beta-blocker or CCB

77
Q

Mobitz type I vs. type II

A

Type I is lengthening PR until dropped whereas type II is dropped QRS. Both are 2nd degree AV blocks. II must be treated.

78
Q

ANP vs. BNP

A

Atrial release vs. ventricular release. Increased blood volume and atrial pressure vs. increased tension. BNP used for negative predictive value for HF.

79
Q

ANP/BNP physiological effects

A

Vasodilation, decreased Na+ resorption, dilates afferent and constricts efferent via cGMP to promote diuresis.

80
Q

Nerve transmission differences between aortic arch and carotid sinus baroreceptors?

A

Aortic arch receptor via vagus nerve (to solitary nucleus) and only reports on INCreased pressure. (The aorta is above hypotension apparently). Carotid sinus baroceptors via CN IX to solitary and reports both increased and decreased blood pressure.

81
Q

Peripheral vs. central chemoreceptors

A

Peripherals (carotid and aortic) stimulated by low PO2, high PCO2, low pH BUT central only responds to PCO2 and pH.

82
Q

Organs that rely on local metabolites for auto-regulation of perfusion?

A

Heart (CO2, adenosine, NO), brain (CO2 via pH), and skeletal muscle (lactate, adenosine, K+, H+, CO2)

83
Q

Tetralogy of Fallot

A

RVOT stenosis, VSD, aorta dextropositin (over-riding aorta), and RV hypertrophy. “Tet” spells (episodes of blush pale skin during crying or feeding. Harsh systolic ejection murmur.

84
Q

Neural crest cell abnormal migration cyanotic diseases?

A

ToF, transposition, truncus arteriosus (namely aorticopulmonary septation).

85
Q

Cardiac effects of carcinoid syndrome.

A

Overproduction of serotonin -> endocardial fibrosis on the RIGHT heart (b/c pulmonary system inactivates serotonin and bradykinin). Pulmonic stenosis and restrictive cardiomyopathy. Corelated with urinary excretion of 5-hydroindoleacetic acid (serotonin-metbaolite)

86
Q

Right to left shunts?

A

Truncus arteriosus, Transposition, Tricuspid atresia, Tetralogy of Fallot, Total anomalous pulmonary venous return (TAPVR)

87
Q

Tetralogy of Fallot

A

Abnormal anterior and cephalic displacement of infundibular portion of inter ventricular septum: VSD, pulmonic stenosis, overriding aorta (receiving blood flow from both ventricles), and RV hypertrophy. “Tet” spells following exertion b/c systemic VASOdilation -> increased right to left shunt. Associated with diGeorge.

88
Q

Transposition of great vessels

A

Aorta is ANT and leaves RV while pulmonary artery is POSTerior and leaves LV. Requires shunt to support life. Failure of aorticopulmonary septum to spiral. Most common cause of cyanosis in NEONATE period. Associated with diabetic mother.

89
Q

VSD

A

Left to right shunt. Asymptomatic at birth. Most self resolve but large lesion -> LV overload and HF

90
Q

ASD

A

Wide, fixed split S2 (2/2 constant P2 late). Usu. septum secundum. NOT patent foramen ovale b/c septa are missing not unfused.

91
Q

Patent ductus arteriosus

A

Indomethicin closes, PGE2 keeps open. Machine-like continuous murmur. Differential cyanosis.

92
Q

Eisenmenger syndrome

A

An uncorrected Left-to-right shunt can cause pulmonary vasculature to be remodeled and increased resistance eventually leading to a REVERSAL to a R-L shunt -> cyanosis (clubbing, and polycythemia)

93
Q

TAPVR

A

Total anomalous pulmonary venous return. Pulmonary veins drain into Right heart circulation. Associated with ASD +/- PDA.

94
Q

Coarctation of the aorta

A

Infantile type is PRE-ductal (before ductus arteriosus) and is associated with XO Turner’s. PGE2 to prevent closure. Adult type is post-ductal (after ligamentem arteriosum), associated with rib notching (collateral circulation), HTN of UPPER limbs and weak pulses in lower extremities, cerebral aneurysms and circle of Willis deformities

95
Q

Truncus arteriosus

A

No septation. Often associated with a VSD. Seen in diGeorge

96
Q

Congenital rubella is associated with what cardiac defects?

A

Septal, PDA, pulmonary artery stenosis

97
Q

Turner syndrom is associated with what cardiac defects?

A

Bicuspid valve, coarctation of the aorta

98
Q

Monckeberg arteriosclerosis

A

Medial calcific sclerosis. Calcification of then media NOT intima of blood vessels. Usu. benign. X-rays of radial or ulnar arteries.

99
Q

What type of people would you expect to get an abdominal aortic aneurysm vs. a thoracic aortic aneurysm?

A

Abdominal - 50’s smoker. Thoracic - Marfan syndrome, tertiary syphilis. Associated with cystic medial degeneration in the older population

100
Q

Aortic dissection Sanford type A vs. B?

A

A involves ascending aorta (+/- descending) while B does not.

101
Q

Prinzmetal angina

A

2/2 to coronary spasm. Triggers include tobacco, cocaine, triptans, ergot alkaloids (ergonovine - an abortifacent/placental delivery drug). Tx = CCB, nitrates, smoking sessation

102
Q

MI days 3-14: what do I need to know?

A

Macrophages doing their thing. Granulation tissue. Hyperemic border with central yellow-brown softening on gross. Free wall rupture, papillary muscle rupture, IV septal rupture (macrophage-mediated structural degradation). LV pseudoaneurysm = mural thrombus plugs hole = a time bomb

103
Q

How long after occlusion does it take for histological or gross changes to occur in a MI?

A

FOUR hours. Coincedentally (or not), it takes four hours for troponin I to start rising (most specific cardiac marker)

104
Q

Why use CK-MB?

A

Found in myocardium and skeletal muscle (less specific). BUT, it goes back to normal after 48 hours (troponins rise for 7-10 days). Therefore , it’s used for diagnosing re-infarction

105
Q

Anteroseptal vs. Anterolateral leads?

A

V1-V2 vs. V4-V6

106
Q

Dressler syndrome

A

autoimmune, takes several weeks to months (true ventricular aneurysm timeline)

107
Q

Etios of dilated cardiomyopathy

A

Alcohol, wet Beriberi, Coxsackie B myocarditis, chronic Cocaine, Chagas, Doxorubicin toxicitiy, hemochromatosis, peripartum cardiomyopathy. Idiopathic and congenital.

108
Q

Hypertrophic cardiomyopathy

A

LV ONLY. Most are familial and AD (Beta-myosin heavy chain mutation) although rarely associated with Friedreich ataxia. Can syncopize if septum to close to mitralm leaflet. Diastolic dysfunction. S4. Myofibrillar disarray and fibrosis. Tx = Cessation of high-intesnsity, Beta-block or non-di CCB.

109
Q

Explain night symptoms of HF?

A

Orthopnea and PND are due to increased venous return 2/2 to the gradual reabsorption of pooled blood toward the lungs.

110
Q

Physical signs of bacterial endocarditis

A

Fever, new murmur, Roth spots, Osler nodes, Janeway lesions, splinter hemorrhages on nail bed

111
Q

Acute vs. subacute etios of endocarditis?

A

Acute - Staph aureus. Subacute - Viridians strep.

112
Q

Culture negative bacterial endocarditis?

A

Coxiella burnetii, Bartonella. Or 2/2 malignancy, hpercoagulable state, lupus

113
Q

Rheumatic fever histo findings

A

Aschoff bodies (granuloma with giant cells), Anitschkow cells (enlarged macrophages w/ ovoid nucleus).

114
Q

Fibrinous vs. serous pericarditis?

A

Fibrinous is usu. Dressler, uremia, radiation. Serous is usually viral or inflammatory/auto-immune

115
Q

Findings in cardiac tamponade

A

Beck’s triad (hypotension, distended neck veins, distant hear sounds). Tachy. Pulsus paradoxes, Kussmaul sign (rise of JVP on inspiration), ECG electrical alternans

116
Q

Pathogenesis of syphilitic heart disease

A

In tertiary syphilis, disruption of the vasa vasorum of the aorta -> atrophy of wall and dilation. “Tree bark” aorta. Aneurysm.

117
Q

Myxoma vs. rhabdomyoma

A

Myxoma - most common primary. LA. Associated with syncopal episodes associated with obstruction of valve. Rhabdo - mostly in children (i.e. tuberous sclerosis)

118
Q

Cherry vs. strawberry hemangiomas?

A

Strawberries are for kids! Regress by 5-8. Cherries are for old people. Don’t regress.

119
Q

Pyogenic granuloma

A

Hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy.

120
Q

Glomus tumor

A

Benign, PAINful, red-blue tumor under fingernails. From mod SMC’s of glomus body (temp. regulation)

121
Q

Bacillary angiomatosis

A

Like Kaposi, associated with AIDS. But looks uglier and caused by Bartonella henselae.

122
Q

Angiosarcoma

A

Rare blood vessel malignanty of the H&N and breast. Eldelry, sun-exposed. Radiation and arsenic. Agressive

123
Q

Lymphangiosarcoma

A

Lymphatic malignancy associated with too much lymph (e.g. post-mastectomy)

124
Q

Large vessel vasculitis

A

Temporal (Giant cell) and Takayasu

125
Q

Medium-vessel vasculitides

A

Polyarteritis nodosa, Kawasaki disease, Buerger disease

126
Q

Small-vessel vasculitides

A

Granulomatosis with polyangiitis, microscopic polyangiitis, Churg-Strauss syndrome, Henoch-Schonlein purpura

127
Q

Temporal arteritis

A

Elderly women with unilateral HA and jaw claudication. Treat with corticosteroids before temporal a. biopsy to prevent irreversible blindness 2/2 opthalmic artery occlusion. Associated with polymyalgia rheumatic. Path - focal granulomatous inflammation.

128
Q

Takayasu arteritis

A

Asian women < 40. “Pulseless disease.” Weak upper extremity PULSE, fever, night sweats, arthritis, myalgias, skin nodules, ocular. Path - granulomatous thickening and narrowing of aortic arch and great vessels. Tx = steroids

129
Q

Polyarteritis nodosa

A

Young adults with abdominal pain, melena, HTN, neuro, cut. eruptions, renal damage w/ Hep B seropositivity in 30%. IC-mediated. Transmural inflammation of wall w/ fibrinoid necrosis. MICROaneurysms. Renal and visceral vessels. Tx = steroids, cyclophosphomide

130
Q

Kawasaki disease

A

Asian children < 4 w/ fever, cervical nymphs, RED (conjuctiva, strawberry tongue, hand-foot), desquamating rash. Comps include coronary artery ANEURYSM -> MI,rupture. Tx = IVIG and ASA

131
Q

Buerger disease

A

Smoking men < 40 w/ claudication that can lead to gangrene and autoamputation.

132
Q

Granulomatosis with polyangitis

A

Perf’d nasal septum, chronic sinusitis, hemoptysis, cough, hematuria. Necrotizing vascultisi, granulomas of lung, glomerulonephritis. PR3-ANCA/c-ANCA. Tx - cyclophosamide, corticosteroids.

133
Q

Microscopic polyangitis

A

Kidney, lung, skin. Hemoptysis, cough, hematuria. NO granulomas. MPO-ANCA/p-ANCA. Tx = cyclophosphamide, corticosteroids

134
Q

Churg-Strauss

A

Asthma, sinusitis, palpable purpura, peripheral neuropathy. Granulomatous, necrotizing vasculitis with EOSinophilia. MPO-ANCA/p-ANCA.

135
Q

Henoch-Schonlein purpura

A

IgA complex deposition often following a URI. Palpable purport, arthralgia, GI.

136
Q

Dihydropyridine CCBs?

A

Amlodopine, nimodipine, nifedipine. HTN, angina, Raynauds. Nimodipine in particular used to decrease vasospasm following SAH.

137
Q

Non-dihydropyridine CCB’s?

A

Verapamil, Diltiazem. Used for HTN, angina, AFIB/FLUTTER.

138
Q

Vascular smooth muscle vs. heart effects by CCBs?

A

For smooth muscle: amlodopine = nifedipine > dilt > verp. For heart, Verapamil > dilt > amlodopine = nifedipine.

139
Q

CCB toxicities?

A

Cardiac depression, AV block, peripheral edema, flusshing, dizziness, hyperprolactinemia, constiation

140
Q

Hydralazine mech and use?

A

Increases cyclic GMP -> vasodilating arterioles > veins. Used fo rsevere HTN, CHF. 1st line for pregnancy with methyldopa. Often administered with Beta-blockers to prevent reflex tachy. B/c of reflex tachy, contra’d in angina/CAD

141
Q

Nitroprusside

A

Increases cGMP via direct NO release. But releases cyanide. Used for hypertensive emergencies. Balanced veno and arteriodilator.

142
Q

Fenoldopam

A

A D1 receptor agonist -> coronary, peropheral, renal, splanchnic vasodilation.

143
Q

Nitrates

A

Venodilation > arteriolardilation via increased cGMP. Decreased preload is mechanism as anti-anginal. Isosorbide mono nitrate has best oral availability. Nitroglycerin is given SL. Sodium nitroprusside is the only one given IV.

144
Q

Bile acid resins

A

Cholestyramine, colestipol, colesevelam. Prevents intestinal reabsorption of bile forcing the liver to use more cholesterol. Decreases LDL. GI discomfort, decreased absorption of fat-soluble vitamins. Cholesterol gallstones.

145
Q

Cholesterol absorption blockers

A

Ezetimibe. Only affects LDL (lowers)

146
Q

Niacin mech and side effecst

A

Inhibits lipolysis in adipose tissue and reduces hepatic VLDL synthesis. SE include flushing (dec. by aspirin), hyperglycemia, and hyperuricemia.

147
Q

Fibrates

A

Upregulate lipoprotein lipase to increase triglyceride clearance. (Suppresses cholesterol 7alpha-hydroxylase activity). Activates PPAR-alpha to induce HDL synthesis. Best TG lowering drug. Myositis (inc. with statins), hepatotoxicity, cholesterol gallstones (inc. with resins)

148
Q

Important digoxin pharmacokinetics

A

RENAL excretion. 75% bio. 20-40% protein bound. t1/2 of 40 hours.

149
Q

Digoxin mech?

A

Inhibits Na/K ATPase -> indirect inhibition of Na/Ca exchanger -> increased Ca intracellular -> positive isotropy. Also stimulates vagus nerve -> bradycardia.

150
Q

Digoxin Tox and Tx?

A

Cholinergic tox, increased PR, decreased QT, ST scooping, TWI, arrhythmia, AV block. HyperKalemia. Renal failure, hypokalemia, verapamil, amiodarone, quinidine all predispose. Tx = fix K+ slowly, pacer, anti-digoxin Fab-fragments, Mg2+

151
Q

Class IV antiarrhythmics

A

Non-dihydropyridine CCBs = verapamil and diltiazem. Decrease conduction velocity, increase effective refractory period, increase PR. Slowed rise of AP, prolonged depolarization. Used for nodal arrhythmias and rate control in AFib.

152
Q

Class III anti-arrhythmic names

A

Amiodarone (all class effects), Ibutilide, Dofetilide, Sotalol. AIDS is Potassium on Three.

153
Q

Class III anti-arrhythmics mechanism and usage

A

K+ channel blocker -> markedly prolong depolarization. Increased AP duration, increased refractory period. Increased QT. Used for Afib, A-flutter, ventriclear tachy

154
Q

Amiodarone toxicities

A

pulmonary fibrosis, hepatotoxicity, hypothyroidism/ hyperthyroidism, corneal depositis, skin deposits (blue/gray), neurological, constipation, brady, heart block, CHF. Therefore, must check PFTs, LFTs, TFTs.

155
Q

Class II antiarrhythmics mechanism and usage

A

Decreased cAMP -> dec. nodal activity. Decrease the phase 4 depolarization slope AND prolong repoarlization. Used for SVTs, rate control

156
Q

Class II antiarrhythmics tox

A

Impotence, exacerbate COPD/asthma, brady, AV block, CNS. Metoprolol can cause DLD. Propanolol can exacerbate vasopasm. Contra’d in COCAINE (b/c of risk of unopposed alpha-adrenergic receptor). Tx with glucagon.

157
Q

Class IA antiarrhythmics mech and usage

A

Quinidine, Procainamide, Disopyramide. Na+ channel bicker that decreases rate of depolarization -> inc. AP duration, inc. refractory, inc. QT. Used of atrial and ventricular arrhythmias.

158
Q

Class IB mech and usage

A

Lidocaine, Mexiletine. Decreased AP duration. Preferentially affects ischemic or depolarized tissue. Used for acute ventricular arrhythmias (post-MI), digitalis-induced.

159
Q

Class IC mech and usage

A

Flecainide, Propafenone. Significantly prolongs refractory period in AV node. Used for SVTs, AFib. “Use-dependence” - Na+ blocking gets more prominent as HR increases b/c medication has less time to dissociate from receptor

160
Q

Adenosine mech

A

K+ out of cells -> hyper polarizing and decreased Ca2+ current. Used to abolish and dx SVTs. Flushing, hypotension, CP. Blocked by theophylline and caffeine.

161
Q

Fatty streak composition

A

Composed of intimal lipid-filled foam cells derived from macrophages and SMCs that have engulfed LDL’s.

162
Q

Drug-induced lupus drugs

A

Procainamide, Hydralazine, INH. (Quinidine and minocycline). ANA and anti-histone Ab’s present in > 95% of cases

163
Q

Supine hypotension?

A

Aortocaval compression syndrome. Pregnant woman lies supine - sweating, nausea, dizziness.

164
Q

Isolated atrial amyloidosis

A

Due to deposition of ANP-derived peptides. Senile cardiac amyloidosis -> inc. risk of A-fib.

165
Q

Isolated systolic hypertension

A

Frequent among people > age 50. Thought to be due to decreased compliance of the aorta.

166
Q

Cardiac defects associated with down syndrome?

A

Endocardial cushion defects (ostium primum ASD [lower down], regurgitant AV valves)

167
Q

Mitral valve prolapse?

A

Mid-systolic click with short late-systolic murmur. Diminishes on squatting b/c increased preload and rise in afterload -> increased LV volume, which helps close the valve. Etio - connective tissue defects -> myxomatous degeneration

168
Q

Ebstein’s anomaly

A

Atrialization of R ventricle, atrial displacement of the tricuspid valve, and decreased RV volume.

169
Q

Mechanism of statins

A

HMC-CoA reductase inhibitors. Decreased hepatic cholesterol synthesis -> increased expression of hepatic LDL receptor -> receptor-mediated endocytosis of more LDL particles –> lowered LDL. (Also helps to lower TG’s and increase HDL).

Step 1 (19 decks)

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