Cardio Flashcards
1
Q
Four cardiac defects associated with maternal alcohol consumption
A
ASD, VSD, PDA, tetrology of Fallot
2
Q
3 Cardiac defects associated with congenital rubella
A
PDA, pulmonary artery stenosis, septal defects
3
Q
3 cardiac defects associated with Down Syndrome
A
AV septal defect, ASD, VSD
4
Q
Cardiac defect associated with diabetic mother
A
Transposition of great vessels (failure of aorticopulmonary septum to rotate)
5
Q
Cardiac defects associated with marfan syndrome
A
MVP, aortic dissection, aortic regurg
6
Q
Cardiac defect associated with prenatal lithium exposure (bipolar mother)
A
Ebstein anomaly
7
Q
2 cardiac defects associated with 22q11 syndromes
A
Truncus arteriosis, tetrology of Fallot
8
Q
2 cardiac defects associated with Turner Syndrome
A
Coarctation of Aorta, bicuspid aortic valve
9
Q
List 3 nitrates used in angina
A
Nitroglycerin, Isosorbide dinitrate, isosorbide mononitrate
10
Q
What is the mechanism of Nitrates
A
increase NO in smooth muscle cells, increase cGMP to vasodilate blood vessels (veins > arteries)
11
Q
What are 3 conditions Nitrates are used to treat?
A
Angina, acute coronary syndrome, pulmonary edema
12
Q
What effect do nitrates have on EDV, BP, contractility, HR, ejection time and myocardial oxygen demand, respectively?
A
decrease, decrease, none, increase (reflex), decrease and decrease
13
Q
What are the side effects of nitrates?
A
reflex tachycardia, throbbing headache, hypotension, flushing; “Monday disease” (tolerance during weekdays but not weekend)
14
Q
Which beta blockers are contraindicated in treating angina?
A
Pindolol and Acebutolol
15
Q
Which therapy is used when standard angina medications are not effective?
A
Ranolazine
16
Q
What is Ranolazine’s mechanism?
A
Blocks late-phase inward sodium flow of cardiomyocyte–> decreases inward flow of Ca+2 and decreases diastolic wall tension, thus decreasing myocardial oxygen demand
17
Q
How does Ranolazine prolong the QT interval?
A
Inhibits outward flow of K+ in phase 3 of cardiomyocyte potential
18
Q
What adverse effects associated with Ranolazine use?
A
constipation, headache, nausea, dizziness and prolonged QT (risk of Vfib)
19
Q
Which enzyme do statins inhibit?
A
HMG CoA reductase
20
Q
What is the mechanism of statin function?
A
Decrease cholesterol production by inhibiting HMG CoA reductase, increase LDLR expression, decrease overall cholesterol
21
Q
which medication is most potent in reducing cardiac related mortality?
A
Statins
22
Q
How do Statins influence LDL, HDL and TG levels?
A
Decrease a lot, increase and decrease
23
Q
Adverse effects of statins
A
Slight increase in LFTs, myopathy (especially when used with fibrates and niacin)
24
Q
Name 3 bile acid resins
A
Cholestyramine, colestipol, colesevelam
25
How do bile acid resins function?
Inhibit bile acid reabsorption in terminal ileum and dietary cholesterol absorption; causes increase in LDLR on hepatocytes and causes liver to use more of body's cholesterol
26
How do bile acid resins affect LDL, HDL and TG levels?
Decrease, slightly increase and slightly increase
27
What are the side effects of bile acid resins (cholestyramine, colestipol, colesevelam)
GI upset, hypertriglyceridemia, decrease absorption of ADEK vitamins (contraindicated in pts with diverticulitis or blood thinners), gallstones
28
How does ezetimibe function?
Binds dietary cholesterol in GI and prevents its absorption, increases liver production of endogenous cholesterol and LDLR to decrease LDL
29
Side effects of Ezetimibe
rare increase in LFT, diarrhea
30
How does Ezetimibe affect LDL, HDL and TG levels?
Decrease, no effect, no effect
31
Name 3 Fibrates
Gemfibrozill, Bezafibrate, Fenofibrate
32
How do fibrates function?
Target VLDL, decrease VLDL by activating PPAR alpha and increasing activity of LPL to increase TG clearance
33
How do fibrates increase HDL levels?
Induce increase in APOA1 and APOA2 to bind HDL
34
How do fibrates affect LDL, HDL and TG levels?
Decrease, increase, substantially decrease
35
Adverse effects of fibrates?
Myopathy (esp with statins), gallstones
36
How does Niacin (B3) influence LDL, HDL and TG levels?
Decrease, increase, decrease
37
How does niacin function in controlling cholesterol?
At liver, decrease VLDL secretion, in tissues, decrease TG release; inhibit lipolysis and increase HDL
38
Side effects of niacin?
Red, flushed face (decrease with NSAID use), Hyperglycemia, Hyperuricemia, can cause increased LFT (monitor liver)
39
How do omega 3 fatty acids (fish oil) decrease TGs?
decrease production of ApoB and VLDL
40
Name a common cardiac glycoside
Digoxin
41
From where is digoxin derived?
Foxglove plant
42
What is Digoxin's inotropic mechanism?
Directly inhibit cardiomyocyte Na+/K+ ATPase, indirectly inhibit Na+/Ca+2 pump, leading to increased intracellular Ca+2 and stimulating contraction
43
What is Digoxin's antiarrhythmic mechanism?
Stimulate vagus nerve, acts on muscarinic receptor of AV node, decrease AV node conduction
44
What are two major uses for Digoxin?
Heart Failure and Atrial Fibrillation
45
What are the cholinergic adverse effects of Digoxin?
nausea, vomiting, diarrhea, blurry yellow vision, arrhythmia, AV block, bradycardia
46
What are the ionic adverse effects of Digoxin?
Can lead to hypekalemia
47
How do verapaimil, amiodarone and quinidine worse digoxin toxicity?
Displace digoxin from tissue-binding sites and decrease its clearance
48
How does hypokalemia worsen digoxin toxicity?
Allows Digoxin to bind more avidly to Na+/K+ ATPase
49
What EKG changes do you see in chronic Digoxin use?
T wave changes, QT shortening, ST scooping
50
Antidote for Digoxin toxicity?
Slowly normalize K+, anti-digoxin Fab, Mg+2, cardiac pacer
51
Which antiarrhythmics act primarily on cardiomyocyte potentials?
Class I and III
52
Which antiarrhythmics primarily act on SA/AV Node potentials?
Class II and IV
53
Which antiarrhythmics are primarily important for rate control?
II and IV (act on AV and SA nodes)
54
Which anitarrhythmics are important for rhythm control?
Class I and III
55
List the Class IA antiarrhythmics
Quinidine, Procainamide, Disopyramide
56
What is the mechanism of Class IA antiarrhythmics?
Bind and inhibit depolarized (open or inactive) Na+ channels, slow AP conduction by slowing phase 0
57
What does it mean when Class I drugs are state dependent
Selectively bind to receptors that are frequently depolarized (like in tachycardia)
58
How do Class IA drugs affect the effective refractory period of an action potential?
Prolong it (prolong QT), increase risk of Torsades des pointes
59
What is the clinical use for Class IA drugs?
Atrial and ventricular arrhythmias, especially re-entrant, ectopic SVTs and VTs (like WPW)
60
Describe the side effects of quinidine
cinchonism (tinnitus, headache)
61
Describe the adverse effects of procainamide
SLE-like syndrome due to production of ANA
62
Describe the adverse effects of disopyramide
Heart failure
63
How avidly do class IA, IB, and IC antiarrhythmics bind Na+ channels? (decrease slope)
IC > IA > IB
64
List three major Class IB antiarrhythmics
Lidocaine, Phenytoin, Mexiletine
65
What is the primary clinical use of Class IB antiarrhythmics?
Treatment of post-MI ventricular arrhythmias (best for ischemic tissue) and digitalis-induced arrhythmias
66
How do Class IB drugs affects AP duration?
Decrease it
67
Adverse effects of Class IB drugs?
CNS effects (slurred speech, tremors, parasthesias), CV depression
68
List 2 Class IC drugs
Flecainide, Propafenone
69
Mechanism of Class IC drugs?
Bind INa+ channels. Prolong ERP in AV node and bypass tracts. No effect on ERP in purkinje and ventricular tissue. Minimal effect on AP duration
70
Clinical use of Class IC drugs?
SVTs, Atrial fibrillation rhythm control
71
Adverse effects of Class IC drugs
Pro-arrhythmic, especially post-MI (contraindicated in structural and ischemic heart disease)
72
Structural and ischemic heart disease is a contraindication for which antiarrhythmic?
IC
73
Which antiarrhythmic class are beta blockers?
Class II
74
Which beta blockers are nonselective beta2 antagonists?
Propanolol and timolol
75
Which beta blocker has partial alpha antagonist properties?
Carvedilol
76
What is the mechanism of beta blockers?
Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca+2 currents and thus suppress abnormal pacemakers
77
Which slope of nodal conduction do beta blockers affect?
Phase 4 (decrease slope-- prolong it)
78
How do beta blockers prolong PR interval?
AV node is more sensitive, delay conduction from SA to AV nodee
79
What are class II antiarrhythmics (beta blockers) clinically used for?
Rate control of SVTs, atrial fibrillation and flutter
80
Adverse effects of beta blockers?
Impotence, worsens COPD/asthma, bradycardia, AV block, CNS effects; may mask hypoglycemic signs
81
What is an adverse effect of metoprolol?
Dyslipidemia
82
What is an adverse effect of Propanolol?
can exacerbate vasospam in Prinzmetal angina
83
Antidote for beta blocker overdose?
Saline, atropin, glucagon
84
Why are carvedilol and labetalol okay to use for pheochromocytomas or cocaine toxicity?
Do not cause unopposed alpha1-agoonism (bc block both alpha and beta receptors)
85
List four Class III antiarrhythmics
Amiodarone, Ibutilide, Dofetilide, Sotalol
86
What is the mechanism of Class III antiarrhythhnmics?
Block K+ channels in cardiomyocytes, prolong phase 2 and 3 (effective refractory period, QT interval, AP duration)
87
What are Class III drugs primarily used to treat?
Rhythm control in atrial fibrillation and flutter. Amiodarone and sotalol for ventricular tachycardia
88
Adverse effects of sotalol
torsades des points, excessive beta blockade
89
Adverse effects of amiodarone
pulmonary fibrosis, corneal deposits, hyper and hypothyroidism (40% iodine by weight), neurologic effects, constipation, bradycardia, heart block, heart failure
90
Adverse effects of ibutilide
Torsades des pointes
91
What affect does Amiodorone have on CYP450?
Inhibits it
92
How is Amiodarone different from other Class III antiarrhythmics?
Has Class I, II, III and IV effects
93
What should be monitored while using amiodarone?
LFTs, PFTs, TFTs
94
List two major Class IV antiarrhythmics
Verapamil and Dilitiazem
95
What class of antiarrhythmics are calcium channel blockers?
Class IV
96
Which Ca+2 channels are Class IV antiarrhythmics specific for?
L-Type (phase 4 and 0)
97
Which part of the heart do class IV antiarrhythmics primarily work on?
SA and AV nodes
98
What is the mechanism of Class IV antiarrhythmics?
Decrease conduction velocity, prolong effective refractory period and increase PR interval by blocking Ca+2 channels
99
What are the two main clinical functions of Class IV antiarrhythmics?
Rate control for atrial fibrillation and prevential of nodal arrhythmias (SVTs)
100
What are the adverse effects of Class IV antiarrhythmics?
Constipation, flushing, edema, AV block (prolong PR interval), sinus node depression, heart failure
101
List three Class V antiarrhythmics
Digoxin, Mg+2, Adenosine
102
What is the clinical use of Magnesium?
Torsades des pointes and digoxin toxicity
103
What is the clinical use of Adenosine?
Diagnose/terminate certain SVTs
104
Which substances blunt effects of Adenosine?
Caffeine, Theophylline, methylxanthines
105
Adverse effects of adenosine?
Flushing, hypotension, chest pain, "sense of doom," bronchospasm
106
How does Digoxin function as an antiarrhythmic?
Stimulates vagus nerve, suppresses SA and especially AV node to dampen AP conduction
107
Which receptor does Dobutamine bind to?
Beta1, minimally on beta2 and alpha1
108
What is dobutamine used for?
Management of refractory heart failure associated with severe LV systolic dysfunction and cardiogenic shock
109
What affects on inotropy, chronotropy and vasodilation does dobutamine have?
positive inotrope (increase contractility), weakly positive chronotrope (increase heart rate a bit and thus oxygen consumption), mild vasodilation (decreased filling time)
110
Define myocardial hibernation
State of chronic ischemia in which both myocardial metabolism and function are reduced to match the reduction in coronary blood flow-- prevents myocardial necrosis
Function is restored upon restoration of blood flow
111
What type of heart failure can restrictive cardiomyopathy lead to/
Diastolic heart failure
112
Describe the presentation of diastolic heart failure
progressive exertional dyspnea, ascites, edema, elevated JVP, LV hypertrophy with LA enlargement
113
What is the histological appearance of cardiac amyloidosis?
Acellular and amorphous pink material in cardiac muscle tissue
114
What is the histologic appearance of cardiac sarcoidosis?
Noncaseating granulomas containing giant cells in myocardium
115
Signs of embolism following an invasive vascular procedure in a pt with atheroembolic disease?
Blue toe, livedo reticularis with normal peripheral pulses
116
Histo findings in pt with atheroembolic disease would show
Cholesterol clefts in arterial lumen
117
Kidney biopsy of pts with poorly controlled hypertension would show
Hyperplastic arteriola changes (intimal fibroelastosis)
118
What are the signs of left heart failure?
Bibasilar crackles, dyspnea on exertion, progressive fatigue
119
Signs of right heart failure
Jugular venous distention , peripheral edema
120
Viral myocarditis can lead to which cardiac condition
Dilated cardiomyopathy
121
6 Causes of dilated cardiomyopathy
Viral infection, genetics, toxicity, alcholism, pregnancy, hemochromatosis
122
Causes of concentric LVH
Long-standing hypertension, aortic stenosis
123
Two characteristics of hypertrophic cardiomyopathy
Asymmetric septal hypertrophy and systolic anterior motion of mitral valve
124
Which two conditions can cause cryptogenic stroke
PFO and ASD
125
What causes a PFO
Incomplete fusion of septum primum and septum secundum
126
What devo defect causes ASD
Aplasia of septum primum or secundum
127
Holosystolic murmur at lower left sternal border is significant for
Ventricular septal defect
128
Which coronary artery supplies posterior 1/3 of IV septum and most of inferior wall of left ventricle?
Posterior descending artery (branch of right coronary artery)
129
Which coronary artery supplies anterior 2/3 of IV septum and anterior wall of left ventricle and part of anterior papillary muscle?
LAD
130
Which part of the heart does the left circumflex coronary artery supply
Lateral and posterior superior walls of left ventricle
131
Which coronary artery supplies wall of right ventricle and provides collateral circulation for LAD occlusion?
Right marginal branch of RCA
132
Which anticoagulant drug targets GpIIb/IIIa?
Abciximab
133
What condition does Abciximab treat?
Unstable angina, acute coronary syndrome (pts undergoing percutaneous coronary interventions)
134
Which condition does Argatroban treat?
Heparin-induced thrombocytopenia
135
What condition does Dabigatran treat
Afib and venous thromboembolism
136
How do argatroban and dabigatran work?
Direct thrombin inhibitors
137
How does heparin work?
Potentiates antithrombin III activity to inactivate thrombin (II) and Xa
138
How does Clopidogrel inhibit platelet aggregation?
Blocks P2Y12 on platelet ADP receptors
139
Severe coarctation of the aorta with a closed ductus arteriosis can present in a neonate as
signs of heart failure (dyspnea, fatigue) and shock
140
Which cardiac condition is associated with Friedrich ataxia?
Hypertrophic cardiomyopathy
141
Which proteins are deposited in cardiomyocytes in AL amyloidosis?
Monoclonal light chains
142
Which proteins are deposited in cardiomyocytes in senile systemic amyloidosis?
wild-type transthyretin
143
Which part of the heart are most cardaiac myxomas found?
Left atrium
144
What is a common cause of dilated cardiomyopathy in Latin America?
Chagas disease (Trypanosoma cruzi infection)
145
Abnormal electrical impulses in which part of the heart usually leads to AF?
Pulmonary veins
146
How does AF beget AF?
Abnormal conduction causes remodeling of heart with shortened refractory periods and heightened excitability, forming ectopic foci and re-entrant impusles in atria
147
In AF, which factor determines the ventricular contraction rate?
AV node refractory period
148
In which cases does the Purkinje system assume pacemaker activity?
severe bradycardia (<40bmp)
149
What is the mechanism of Alteplase?
Activates plasminogen to plasmin to cause clot lysis
150
What is the most common adverse effect of fibrinolytic therapy and what are symptoms?
Intracerebral hemorrhage (abrupt onset decreased consciousness, asymmetric pupils, irregular breathing)
151
Transesophageal echocardiography probe lies within closest proximity to which part of heart?
left atrium
152
Which part of heart comprises most of posterior surface of heart?
Left atrium
153
Which part of the heart comprises apex and left border of heart on frontal CXR?
Left ventricle
154
Which part of the heart forms the right lateral cardiac border on CXR?
right atrium and SVC
155
Which part of heart forms anterior surface and majority of inferior border?
Right ventricle
156
Which part of the heart lies posterior and to the right of the main pulmonary artery?
Ascending aorta
157
Which part of the heart travels above the right pulmonary artery and left bronchus?
Aortic arch
158
Which structures originate from aortich arch?
Braciocephaic, left common carotid and left subclavian
159
Which part of the heart lies posterior to esophagus and left atrium?
Descending aorta
160
The combination of which two lipid-lowering agents increases myopathy?
Fibrates and statins
161
Which 3 hypertensive medications cause vasodilation and reflex tachycardia
ACE inhibitors, nitrates, and peripheral alpha-1 selective adrenergic blockers (prazosin)
162
Which 5 medications have negative chronotropic effects?
beta blockers, non-dihydropyridine CCBs (diltiazem, verapamil), cardiac glycosides (digoxin), amiodarone and sotalol and cholinergic agonists (pilocarpine, rivastigmine)
163
Combined use of which drugs can lead to negative chronotropic effects with severe bradycardia and hypotension?
Beta blockers and non-dihydropyridine CCBs
164
In cardiac catheterization, an excessive rise in left atrial systolic pressure is indicative of
Mitral regurgitation
165
In cardiac catheterization, elevated LV diastolic pressure and decreased aortic diastolic pressure indicates
Aortic regurge
166
In cardiac catheterization, a large pressure difference between LV and aorta indicates
Aortic stenosis
167
In cardiac catheterization, increased LAP during diastole indicates
Mitral stenosis
168
Patients with benign prostatic hyperplasia and hypertension would benefit with treatment from
allpha-1 blockers (prazosin, Doxazosin, Terazosin)
169
Patients with coronary artery disease and heart failure with hypertension will benefit from therapy with
cardioselective beta blockers
170
Patients with essential hypertension first-line therapy
HCTZ
171
Patients with evidence of vasospasm like Raynaud or Prinzmetal angina benefit with therapy from
CCBs
172
Difference between dihydropyridine (-dipines) CCB and non-dihydropyridine CCB (verapamil, dilitiazem)
-Dipines are selective for vascular smooth muscle (vasodilation) and do not affect heart as much as non-DPs
173
Endocardial thickening and fibrosis of tricuspid and pulmonary valves is a characteristic finding of
Carcinoid heart disease (elevated 5-HIAA)
174
Which two antiarrhythmics lead to QT prolongation?
Class IA and Class III
175
Mechanism of Class IB antiarrhythmicss
block Na+ channels and inhibit phase 0; does not prolong QT
176
Mechanism of Class III antiarrhythmics
Block K+ channel (phase 3)
177
Which two vascular beds are particularly susceptible to atherosclerosis?
Lower abdominal aorta and coronary arteries
178
What is the primary risk factor for aortic dissection/?
Hypertension
179
What is Monckeberg sclerosis
Sclerosis of medial layer of muscular arteries. Seen in >50 yos, generlaly leads to systolic hypertension
180
Aortitis characterized by obliterative endarteritis of vasa vasorum signifies
Tertiary syphilis
181
4 signs of a normal aging heart
Decreased LV chamber size, sigmoid-shaped ventricular septum, increased interstitial connective tissue with amyloid deposition; accumulation of lipofuscin in myocardiocytes (brownish pigment)
182
Prussian blue stain on cardiomyocytes used to identify
Hemosiderosis due to chronic hemolytic anemia or hemochromatosis
183
Asymmetric septal hypertrophy with disproportionate thickening of ventricular septum compared to LV free wall signifies
Hypertrophic cardiomyopathy
184
Subendocardial vacuolization and fibrosis signify
Chronic ischemic heart disease
185
What is Kussmaul sign and what does it signify
Paradoxical increase in JVP during inspiration,
| chronic constrictive pericarditis, RHF, cardiac tamponade and restrictive cardiomyopathy
186
Three conditions that can cause pulsus paradoxus
Cardiac tamponade, constrictive pericardial disease, cor pulmonale
187
What does a pericardial knock (after S2) signify
Cosntrictive (chronic) pericarditis
188
What is the EKG WPW triad?
Delta wave, shortened PR interval, widened QRS
189
Describe the vagal maneuver pathway
Baroreceptors on carotid sinus stimulated by massage --> afferent limb via CN IX carries signal to vagal nucleus and medullary centers--> efferent limb via CN X synapses on SA and AV nodes to slow conduction through AV node and prolong AV refractory period
190
Vagal maneuver is useful for which arryhtmia
Paroxysmal supraventricular tachycardia
191
Why is the liver not that vulnerable to infarcts?
Has dual blood supply from portal vein and hepatic artery
192
Explain reflex bradycardia upon administration of alpha1-receptor agonists (phenylephrine, methoxamine)
Increased SVR causes increased pressure on baroreceptors in carotid sinus--> stimulation of vagal response--> decreased AV nodal conduction velocity
193
Kussmaul sign, increased JVP, pulsus paradoxus and pericardial knock are findings consistent with
Constrictive pericarditis
194
What is the morphological finding of constrictive pericarditis?
Thick fibrous tissue in pericardial space between visceral and parietal pericardium
195
first-line and second-line tx for ventricular arrhythmia during MI
Amiodarone, Lidocaine
196
Why is Lidocaine preferred for tx of MI ventricular arrhythmias
Ischemic tissue has higher RMP, so more inactivated Na+ channels. Lidocaine preferentially binds to inactivated Na+ channels and has negligible effect on QRS due to short duration of action
197
Acute kidney injury, hyperuricemia and acute gout, hyponatremia, hypokalemia and hyperglycemia and high cholesterol are side effects of
Thiazide diuretics
198
Cough, angioedema and hyperkalemia are side effects of
ACE inhibitors
199
Peripheral edema, dizziness or light headedness are side effects of
CCBs (amlodipine, nifedipine)
200
Bronchospasm, bradycardia, fatigue and sexual dysfunction are side effects of
beta blockers
201
Patients with bicuspid aortic valve have increased risk of which condition in their 50s?
Aortic stenosis (accelerated atherosclerosis and calcification of valve)
202
Harsh, holosystolic murmur at mid to lower left sternal border that may not be detectable at birth but becomes audible 4-10 days of age suggests
Small VSD
203
Why do large VSDs not have murmur and how do they present
Large VSD leads to relatively equal pressure between right and left ventricles, so no murmur. Present as heart failure, failure to thrive and diaphoresis with feeding; can result in cyanosis and pulm hypertension later in life
204
Cyanosis and heart failure with Tricuspid regurg is suggestive of
Ebstein's anomaly
205
Immediate treatment/antidote for heparin overdose
Protamine sulfate (binds heparin and inactivates it)
206
Immediate treatment/antidote for Warfarin overdose
Fresh frozen plasma
207
Why is FFP not useful for heparin overdose?
contains ATIII, which can exacerbate effects of heparin
208
Long term treatment for warfarin overdose
Vitamin K (takes days)
209
All types of necrosis have which type of hallmark of cell injury? (seen in aging, stiffened aortic valves)
Dystrophic calcification
210
Best spot to hear S3?
Cardiac apex with patient in left lateral decubitus position
211
Which murmur is commonly associated with hypertrophic cardiomyopathy?
Mitral regurgitation
212
How does phenylephrine (/NE) increase total peripheral resistance and decrease heart rate
selective alpha-1 agonist causes systemic vascular constriction and induces baroreceptor response to decrease SV and slow heart rate
213
Which agent is a beta-receptor agonist that decreases TPR and diastolic pressure and increases cardiac rate, CO and pulse pressure?
Isoproterenol
214
How does clonidine decrease blood pressure
alpha-2 receptor agonist that decreases central sympathetic outflow
215
Single most important risk factor for developing aortic dissection
Hypertension
216
Which anti-inflammatory irreversibly inhibits COX1 and COX2 via acetylation?
Aspiriin
217
Which anti-inflammmatory reversibly inhibits COX enzymes
Acetaminophen
218
Best alternative for patients with aspirin allergy
Clopidogrel
219
Blocks P2Y12 component of ADP receptors on platelet surface and prevents aggregation
Clopidogrel
220
Name two arteriolar vasodilators
Hydralazine and Minoxidil
221
Side effect of arteriolar dilators
reflex SNS activation and RAAS response (increased HR, CO, Na+ and fluid retention)
222
Persistent cough and angioedema are side effects of which medications
ACE inhibitors
223
Peripheral vasoconstriction and cold extremities are side effects of which medication
Beta blockers
224
How do cardiac myxomas produce constitutional symptoms (weight loss, fever) and hemorrhage?
Produce IL-6 and VEGF
225
Histology of this condition shows scattered cells within mucopolysaccharide stroma, abnormal blood vessels and hemorrhaging. Typically found in left atria (80%)
Myxoma
226
Which subunits between hemoglobin and myoglobin are nearly identical?
beta subunits
227
Is myoglobin left-shifted or right-shifted?
Left-shifted (holds onto oxygen more tightly in muscle)
228
Monomeric protein that binds oxygen in muscle
Myoglobin
229
Two most common causes of death after lightning injury
Cardiac arrhythmias, respiratory arrest
230
Drug of choice for treating paroxysmal supraventricular tachyardia (PSVTS)
ADENOSINE
231
What causes wide and fixed splitting
Atrial septal defects
232
A cerebrovascular event in the setting of a known venous thromboembolic disease raises suspicions for
paradoxical embolism and septal defects (ASD, PFO, VSD)
233
Portal system is a derivative of which embryological structure?
Vitteline veins
234
SVC is derived from which embryologic structure?
Common cardinal veins
235
Fastest to slowest cardiac tissue conduction velocity
Purkinje system --> Atrial muscle --> ventricular muscle --> AV node (PAVA)
236
Intracytoplasmic granules that are tinged yellowish-brown in myocardial cells represent (sign of aging or "wear and tear")
Lipofuscin (product of free radical injury and lipid peroxidation)
237
Virchow's triad for developing venous thrombosis
Endothelial injury, venous stasis, and hypercoagulable state
238
Risk factor for arterial thromboembolism
Atherosclerosis
239
Which arteries are spared in polyarteritis nodosa (medium vessel vasculitis)?
Pulmonary (and bronchial sometimes)
240
PDE-3 inhibitor that causes systemic vasodilation, increases cAMP and thus inotropy
Milrinone
241
How does Digoxin primarily lower ventricular heart rate in afib?
Enhances efferent parasympathetic ganglionic transmission and potentiates end-organ responses to acetylcholine, leading to increased vagal output
242
Most common cause of sudden cardiac death
Malignant ventricular arrhythmias (fibrillation)
243
Claudication is due to
Atherosclerosis of large arteries
244
Which venous vessel is the most deoxygenate?
Coronary
245
Why is Heparin safer to use in pregnant women than Warfarin?
Heparin is hydrophilic and cannot cross the placenta while Warfarin is lipophilic and can cross placenta
246
Wide fixed split S2 is suggestive of
Atrial septal defect
247
This murmur presents with dyspnea, pulmonary congestion and right sided heart failure
Mitral stenosis
248
Do not treat patients with hypertrophic cadriomyopathy, RV infarction, and those on phosphodiesterase inhibitors with
Nitrates
