Cardiology Flashcards
1
Q
Right dominant configuration of the heart
A
SA and AV nodes supplied by RCA. RCA supplies inferior portion of LV via PD artery (most common. In left dominant the PD arises from the CFX)
2
Q
Fick equation
A
CO = (rate of O2 consumption) / (arterial O2 content - venous O2 content)
3
Q
What is the pulse pressure proportional to?
A
Stroke Volume
4
Q
Name a classic venodilator and a classic vasodilator
A
Veno - nitroglycerin, Vaso - hydralazine
5
Q
How does nitroglycerin help in angina?
A
Venodilation, decreased preload, decreased cardiac work, decreased demand for O2
6
Q
Normal ejection fraction
A
Greater than or equal to 55 percent
7
Q
Causes of increased blood viscosity (3)
A
Polycythemia, hyperproteinemic states (eg multiple myeloma), hereditary spherocytosis
8
Q
Cardiac function curves - give the curve affected (CO or venous return) and direction the intersection moves in each of the following: pos inotropy, neg inotropy, inc blood vol, dec blood vol
A
Positive inotropy - CO, intersection moves up and left. Neg inotropy - CO, intersection moves down and right. Inc BV - venous return, intersection moves up and right. Dec BV - venous return, int moves down and left
9
Q
On a cardiac cycle graph, the slope of what curve gives contractility?
A
A line from the origin to the top left portion (where aortic valve closes) of the curve
10
Q
What causes an S3
A
Increased filling pressure (e.g. MR, CHF) and dilated ventricles. Normal in children and preggers
11
Q
What causes an S4?
A
High atrial pressure. Due to ventricular hypertrophy and stiffness
12
Q
What is going on in the right heart during each of the following: a wave, c wave, x descent, v wave, y descent
A
A wave - atrial contraction, c wave - RV contraction, x descent - atrial relaxation, v wave - RA filling, y descent - blood flow from RA to RV
13
Q
What disorders lead to wide splitting of A2 and P2?
A
Pulmonic stenosis, RBBB
14
Q
What condition leads to fixed splitting
A
ASD
15
Q
What conditions lead to paradoxical splitting?
A
Aortic stenosis, LBBB
16
Q
What kind of murmurs can be heard in an ASD?
A
Pulmonary flow murmur (inc flow through pul valve), and diastolic rumble (inc flow across tricuspid)
17
Q
Between inspiration and expiration, which increases right heart findings and which increases left?
A
Inspiration increases right heart sounds, expiration increases left
18
Q
What murmurs are louder on hand grip?
A
MR and VSD
19
Q
What murmurs are louder on valsalva (decreased venous return)
A
MVP, HOCM. (most murmurs are quieter on valsalva)
20
Q
Pulse associated with AS
A
Parvus and tardus
21
Q
Murmur associated with VSD
A
Holosystolic, harsh sounding. Loudest at tricuspid area
22
Q
Two common causes of PDA
A
Congenital rubella and prematurity
23
Q
Give the main ions flowing across the cardiac ventricular muscle membrane during each of the phases of the cycle
A
Phase 0 - Na, Phase 1 - K starts, Na stops, Phase 2 - Ca, K, Phase 3 - K, Phase 4 - K
24
Q
Why do CCBs work on heart but not on skeletal muscle?
A
Skeletal muscle has no dependence on extracellular calcium during an action potential (due to sarcoplasmic stores) unlike cardiac muscle
25
What causes rapid calcium decrease immediately before relaxation in cardiac muscle cells?
Na/Ca exchanger
26
Give the ions traversing the cardiac pacemaker cell membrane during each phase of the cardiac cycle
Phase 4 - Na (funny current, If), Phase 0 - Ca, Phase 1 and 2 absent, Phase 3 - K
27
What property of heart cell action potentials determines heart rate in normal individuals?
The slope of Phase 4 in SA nodal cells
28
How does symphathetic stimulation affect the AP in heart cells?
Increases the chance that If channels are open in pacemaker cells
29
Normal length of PR interval, QRS complex, and AV node delay
PR - less than 200 ms, QRS - less than 120 ms, AV node delay - around 100 ms
30
Torsades de pointes is related to what EKG abnormality?
Long QT
31
Jervell and Lange-Nielsen syndrome
Severe congenital sensorineural deafness and long QT (predisposes to torsades)
32
Order the following from fastest to slowest conduction: Atrial muscle, AV node, Purkinje system, Vent muscle
(fastest) Purkinje, Atrial muscle, Vent muscle, AV node (slowest)
33
Common precipitants of a-fib
Alcohol binge, increased cardiac sympathetic tone, pericarditis
34
Treatments for a-fib
B-blocker, CCB, digoxin. Also give warfarin
35
Treatment for a-flutter
Class Ia, Ic, or III antiarrhythmics or B-blockers
36
Treatment for third degree heart block
Pacemaker
37
What infectious disease can result in heart block and which type?
Lyme, third degree
38
Release of what may cause normal sodium levels even in hyperaldosterone hypertension?
Atrial natriuretic peptide
39
What effect does ANP have on renal vasculature?
Constricts efferent arterioles and dilates afferent arterioles (via cGMP)
40
Does the aortic arch baroreceptor respond to high pressure, low pressure, or both?
High pressure only
41
Where does the parasympathetic system exert its influence to slow heart rate?
By slowing conduction through the AV node
42
Give the factors that determine autoregulation in the brain and heart respectively
Brain - CO2 (via pH), Heart - CO2, adenosine, NO
43
Congenital right to left shunts (early cyanosis) (5)
Tetralogy of Fallot (most common), Transposition of great vessels, Truncus arteriosus, Tricuspid atresia, Total anomalous pulmonary venous return (TAPVR)
44
What is required for viability in tricuspid atresia?
ASD and VSD
45
Congenital left to right shunts (late cyanosis) (3)
VSD (most common), ASD, PDA
46
What effect does indomethacin have on a PDA?
Closes it
47
Eisenmenger syndrome
Reversal of L to R shunt (making it R to L), causing late cynaosis (clubbing and polycthemia)
48
4 features of tetralogy of Fallot
Pulmonary stenosis, RVH, Overiding aorta, VSD
49
In what congenital condition do patients typically squat to improve symptoms?
Tetralogy of Fallot (increased TPR reduces R-to-L shunt)
50
Where are infantile and adult type coarcations located respectively?
Infantile - preductal, Adult - postductal
51
Describe the cyanosis in each of the following conditions: aortic coarctation, PDA, septal defects and tetralogy of fallot
Coarctation - no cyanosis, PDA - late lower extremity cyanosis, Septal Defect and ToF - whole body cyanosis
52
What should you check first if you suspect aortic coarctation?
Upper and lower extremity pulses (upper will be strong, lower will be weak)
53
Cardiac defects associated with 22q11 syndromes (DiGeorge, velocardiofacial)
Truncus arteriosus, tetralogy of fallot
54
Cardiac defects associated with Down syndrome
ASD, VSD, AV septal defect (endocardial cushion defect)
55
Cardiac defects associated with congenital rubella
Septal defects, PDA, pulmonary artery stenosis
56
Cardiac defects associated with maternal diabetes
Transposition of great vessels
57
List the four signs of hyperlipidemia
Atheromas, xanthomas, tendinous xanthomas, and corneal arcus
58
In patients with visible signs of hyperlipidemia, what should you check for?
Cholestasis (eg primary or secondary biliary cirrhosis)
59
Which form of arteriosclerosis is calcific, where is it most commonly seen, and what is the prognosis.
Monckeberg. Radial and ulnar arteries especially. Benign
60
What are the keywords for arteriolosclerosis in essential hypertension, diabetes, and malignant hypertension respectively
Essential HTN and DM - hyaline, Malignant HTN - hyperplastic, onion skinning
61
In what conditions are fatty streaks seen?
EVERYONE over 10 years old
62
List the steps of atherosclerosis (7) in order
Endothelial cell dysfunction, Macrophage and LDL accumulation, Foam cells, Fatty streaks, SM migrational (PDGF and TGF-b), fibrous plaque, complex atheroma
63
Most common locations of atherosclerosis (in order starting with most common)
Abdominal aorta, coronary artery, popliteal artery, carotid artery
64
What decreases atherosclerotic plaque stability and thus increases chance of rupture
Metalloproteinases from macrophages
65
What are abdominal and thoracic aortic aneurysms respectively associated with?
Abdominal - atherosclerosis (men, smokers, over 50), Thoracic - HTN, cystic medial necrosis (Marfan)
66
What are aortic dissections associated with?
HTN and cystic medial necrosis (Marfan). Same risk factors as THORACIC aortic aneurysms
67
What is the precursor lesion in aortic aneurysm and aortic dissection respectively?
Aneurysm - intimal streak (atherosclerosis), Dissection - intimal tear
68
Where do we typically harvest vessel from for CABG?
Great saphenous vein just below the pubic tubercle
69
Give the pathology associated with each of the following precursor lesions: intimal streak, intimal tear, medial degeneration, medial inflammation, vasa vasorum obliteration
Intimal streak - atherosclerosis, intimal tear - aortic dissection, medial degeneration - aortic dissection (eg Marfan), medial inflammation - takayasu, GCA, vasa vasorum obliteration - syphillis
70
How much narrowing has to occur in coronary arteries to get angina?
75 percent or greater
71
What is seen on EKG with prinzmetals angina?
ST elevation (note that ST DEPRESSION is seen in stable and unstable angina)
72
What kills you in sudden cardiac death?
Arrhythmia (usually V-fib)
73
What prevents or slows the development of pulmonary edema in pts with MR?
Increased left atrial compliance (holds more blood in the LA rather than refluxing it to the lungs)
74
Give the light microscopy findings at various points after an MI
0-4 hrs - normal, 4-12 hrs - edema, hemorrhage, wavy fibers, 12-24 hours - contraction bands, neutrophils arrive, 2-4 days - coag necr, neutrophils leave, 5-10 days - neovascularization, gran tissue, 7 weeks - scar
75
Give the main complications post MI and the time window for each
0-4 days - Arrhythmia. 3-5 days - pericarditis and friction rub. 5-10 days - Ruptures (free wall, papillary muscle, IV septum) and tamponade. After 10 days - ventricular aneurysm. Several weeks - Desslers
76
Which cardiac enzyme peaks first?
Troponin
77
CK-MB is not the first cardiac enzyme to peak (troponin is) and is less specific. What is the value of CK-MB in addition to troponin?
CK-MB goes away sooner, so you can use it diagnose reinfarction
78
What finding would you have in a patient with pulmonary edema post-MI
S3 (also crackles from the edema). Its due to LV failure
79
Which type of cardiomyopathy is most common?
Dilated
80
Which type of dysfunction (systolic or diastolic) is each type of cardiomypoathy associated with?
Dilated - systolic, Hypertrophic - diastolic, Restrictive/Obliterative - diastolic
81
Which cardiomyopathy is concentric hypertrophy and which is eccentric?
Dilated - eccentric, Hypertrophic - concentric
82
Causes of dilated cardiomyopathy (8)
ABCCD plus 2. Alcohol, wet Beriberi, Coxsackie B, Cocaine, Chagas, Doxorubicin, hemochromatosis, peripartum cardiomyopathy
83
What is the most common cause of hypertrophic cardiomyopathy?
Familial (AD)
84
What cardiac problem is associated with Friedreichs ataxia?
Hypertrophic cardiomyopathy
85
Treatment for hypertrophic cardiomyopathy
Beta blockers or non-dihydropyridine CCBs (eg verapamil)
86
Findings in hypertrophic cardiomyopathy
Systolic murmur and syncopal episodes
87
Causes of restrictive cardiomyopathy (6)
Sarcoidosis, amyloidosis, postradiation, endocardial fibroelastosis (kids), Lofflers (eosinophils), hemochromatosis (also dilated CM)
88
What drugs reduce mortality in CHF and what are just used for symptomatic relief?
Reduce mortality - ACEi, B-blocker, ARBs, Spironolactone. Symptomatic relief - Thiazides, Loop diuretics, Nitrates
89
Presentation of bacterial endocarditis
Fever, Roths spots (retinal white spots), Oslers nodes (fingers, toes), new Murmur, Janeway lesions (palm or sole), anemia, splinter hemorrhages
90
Most common causes of acute and subacute bacterial endocarditis respectively
Acute - s aureus. Subacute - viridans strep (dental procedures)
91
Most common causes of nonbacterial endocarditis
Malignancy, hypercoagulability, lupus, colon cancer (strep bovis), prosthetic valve (staph epidermis)
92
Most common agents in tricuspid endocarditis due to IV drug use
S aureus, pseudomonas, candida
93
What organisms cause rheumatic fever?
Group A beta hemolytic strep
94
Early death in rheumatic fever
Myocarditis
95
Early and late valvular lesions of rheumatic fever
Early - MVP, late - MS
96
Aschoff bodies and anitschkow cells
Aschoff - Granuloma with giant cells, associated with rheumatic fever, Anitschkow - activated histiocytes also associated with rheumatic fever
97
What type of hypersensitivity is rheumatic fever
Type 2 (antibodies are to M protein)
98
Presentation of rheumatic fever
FEVERSS. Fever, Erythema marginatum, Valvular damage, ESR inc, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, St Vitus dance (chorea)
99
Pulses paradoxus
Associated with cardiac tamponade, asthma, OSAS, pericarditis, and croup. Decreased amplitude in sys BP by 10 or more during inspiration.
100
Most frequent cardiac tumor in children and what condition its associated with
Rhabdomyosarcoma, tuberous sclerosis
101
Complications of varicose veins
Poor wound healing and ulcers. Rarely throws emboli (as opposed to stasis in DEEP veins)
102
Causes of Raynauds phenomenon (3)
Mixed connective tissue disease, SLE, CREST
103
What vascular condition is associated with a hepatitis and which hepatitis?
Hep B with PAN
104
Fever, weight loss, malaise, headache, abdominal pain, melena, HTN, neurologic dysfunction, cutaneous eruptions
PAN
105
What vessels are typically involved in PAN?
Renal and visceral vessels. DOES NOT involve pulmonary arteries
106
Treatment for PAN
Corticosteroids, cyclophosphamide
107
Fever, lymphadenitis, conjunctivitis, oral mucosa changes, hand-foot erythema, desquamation
Kawasaki
108
Treatment for Kawaski
IVIG and aspirin
109
What finding is unique to Buergers disease?
Hypersensitivity to tobacco extract antigen
110
Give the ANCA associated with each of the following: microscopic polyangiitis, Wegners, Churg-Strauss
MP - p-ANCA, Wegener - c-ANCA, Churg-Strauss - p-ANCA
111
What is found in the kidney with Wegeners?
Necrotizing (crescentic) glomerulonephritis
112
Treatment for Wegeners
Cyclophosphamide, corticosteroids
113
Microscopy of Churg-Strauss
Granulomatous vasculitis with eosinophilia
114
Asthma, sinusitis, palpable purpura, peripheral neuropathy
Churg-Strauss (may also involve heart, GI, kidneys)
115
What does Henoch-Schonlein purpura typically follow?
Upper Respiratory Tract Infection
116
What type of immune complexes are seen in Henoch-Schonlein purpura?
IgA immune complexes
117
Palpable purpura of buttocks and legs, arthralgia, abdominal pain, melena
Henoch-Schonlein
118
What is an important difference between the lesions of PAN and Henoch-Schonlein
PAN the lesions are of different ages, Henoch-Schonlein they are all the same age
119
What size blood vessels are affected by Sturge-Weber
Capillary size
120
Findings with Sturge-Weber other than port-wine stain
Ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, early onset glaucoma
121
Best way to differentiate a strawberry from a cherry hemangioma
Strawberry in little kids (also they regress), Cherry in elderly (also they do not regress)
122
What are pyogenic granulomas associated with and what is the main complication?
Can ulcerate and bleed. Associated with trauma and preggers
123
What are cystic hygromas associated with, where are they found, and what do they look like on microscopy?
Associated with Turner. Found in neck. Appear as cystic spaces with connective tissue and lymph aggregates (they are cavernous lymphangiomas)
124
Where are glomus tumors found, what do they arise from, and what is the prognosis?
They are red-blue tumors under the fingernails, arising from smooth muscle cells of the glomus body. They are benign
125
What does a bacillary angiomatosis look like, what causes it, and what patients get them? What is the prognosis?
Look like Kaposi. Found in AIDS pts. Caused by bartonella henselae. Benign.
126
Where are angiosarcomas found, what causes them, what is their marker, and what is the prognosis?
Liver, vinyl chloride, arsenic, and thorotrast exposure, CD31 (endothelial marker), and they are highly lethal malignant
127
What are lymphangiosarcomas associated with?
Lymphedema (eg post-radical mastectomy)
128
Causal agent of Kaposi sarcoma
HHV-8
129
Hydralazine
Directly relaxes SM cells via increased cGMP. Vasodilates arterioles more than veins. Use in HTN, CHF (esp in pregnancy). AE - compensatory tachycardia, lupus like syndrome
130
What is the first line treatment for isolated systolic hypertension?
Thiazides and calcium channel blockers
131
Calcium channel blockers (4)
Nifedipine, verapamil, diltiazem, amlodipine
132
Which CCBs work mostly only vascular smooth muscle?
(most) Nifedipine, Diltiazem, Verapamil (least)
133
Which CCBs work most on heart muscle?
(most) Verapamil, Diltiazem, Nifedipine (least)
134
What agents are used to treat Prinzmetals angina and Raynauds disease?
CCBs
135
Nifedipine class
CCB (more SM than heart)
136
Verapamil class
CCB (more heart than SM)
137
Diltiazem class
CCB
138
Amlodipine class
CCB
139
Nitroprusside
Increases cGMP via NO release. Can cause cyanide toxicity. Decreases preload AND afterload
140
What do you give in a nitroprusside overdose?
Sulfur thiosulfate (prevents cyanide toxicity)
141
Fenoldopam
Dopamine D1 agonist. Relaxes renal vascular smooth muscle, use in malignant HTN
142
Diazoxide
K channel opener (hyperpolarizes vascular SM). Use in malignant HTN. AE - hyperglycemia (reduces insulin release)
143
Malignant HTN drugs (3)
Nitroprusside, fenoldopam, diazoxide
144
What drug works essentially the same as nitroglycerin?
Isosorbide dinitrate
145
Does nitroglycerine work more on arteries or veins
Much more on veins
146
Nitroglycerine is sublingual. If you wanted to give it PO, what would you give instead?
Isomononitrate
147
Symptoms of Monday morning disease (on monday morning) and what chemical it is due to.
Due to nitroglycerin. Will have tachycardia, hypotension, flushing, headache
148
What should you give when you want to lower BP and raise HR?
Nifedipine (causes vasodilation and reflex tachycardia)
149
What is it important for patients to do when taking nitrates
Have a nitrate free period every day to avoid developing tolerance
150
Nifedipine and verapamil are both CCBs but are somewhat different. For each, which other class of drugs is it most similar to?
Nifedipine is like nitrates, Verapamil is like B-blockers
151
Which beta blockers are contraindicated in angina and why?
Pindolol and Acebutolol because they are partial agonists
152
Effects of statins on lipids
LDL down, HDL up (a little), TGs down (a little)
153
Side effects of statins
Hepatotoxicity (inc LFTs), rhabdomylosis
154
Effects of niacin on blood lipids
LDL down, HDL up (quite a bit), TGs down (so all the good things)
155
What is the mechanism of niacin relative to lipids?
Inhibits lipolysis in adipose, reduces hepatic VLDL secretion
156
Side effects of niacin
Flushing (give aspirin), Hyperglycemia and acanthosis nigricans, Hyperuricemia (hope your patient doesnt have gout)
157
What mediates flushing when niacin is given?
Prostaglandins
158
What can you give when administering niacin to reduce pain associated with niacin?
Capsaicin (will decrease substance P levels)
159
List the bile acid resins (3)
Cholestyramine, Colestipol, Colesevelam
160
Effects of bile acid resins (cholestyramine, colestipol, colesevelam) on blood lipids
LDL down, HDL up (slightly), TGs up slightly
161
Mechanism and side effects of bile acid resins (cholestyramine, colestipol, colesevelam)
Prevent intestinal reabsorption of bile acids (liver must use cholesterol to make more). SEs - pts hate it, GI discomfort, GALLSTONES.
162
Ezetimibe
Cholesterol absorption blocker. Prevents cholesterol reabsorption at small intestine brush border
163
Effects of ezetimibe on blood lipids and side effects of ezetimibe
Decreases LDL, does not affect HDL or TGs. Rarely increases LFTs
164
List the fibrates (4)
Gemfibrozil, clofibrate, bezafibrate, fenofibrate
165
Effects of fibrates on blood lipids
LDL down, HDL up, TGs way down (all the good things)
166
Mechanism of fibrates and side effects
Upregulate LPL leading to increased TG clearance. AEs - myositis, hepatoxocity (inc LFTs), cholesterol GALLSTONES
167
Which lipid lowering agents lead to cholesterol gallstones?
Niacin and fibrates (also the two that do all the good things)
168
What combination of lipid lower agents gives a high risk of myopathy?
Statins and fibrates
169
What enzyme do fibrates inhibit
7a-hydroxylase (converts cholesterol to bile acid)
170
What effect does digoxin have on HR and how?
Slows it. Positive inotropy stimulates vagus nerve. This slows conduction at AV node and depresses SA node
171
Uses of digoxin
CHF and a-fib
172
What increases digoxin toxicity?
Renal failure, hypokalemia, quinidine
173
Digoxin non-EKG toxicity
Blurry yellow vision, cholinergic effects (n/v/d)
174
Digoxin EKG toxicity
Increased PR, short QT, scooping, T-wave inversion, arrhythmias, hyperkalemia
175
Antidote for digoxin
Lidocaine, anti-dig Fab, Mg, normal K, cardiac pacing
176
Nesiritide
Recombinant B-type natriuretic peptide (increases cGMP and vasodilates). Acute decompensated heart failure. AE - hypotension
177
Give the mechanism of each class of antiarrhytmic
1 - Na channel blockers, 2 - B blockers, 3 - K channel blockers, 4 - Ca channel blockers
178
List the class Ia antiarrhythmics
Quinidine, Procainamide, Disopyramide
179
Class Ic antiarrhythmics
Flecainide, propafenone, moricizine
180
What effect does each of the Class I subclasses have on AP duration?
Ia - longer, Ib - shorter, Ic - no effect
181
What is the mnemonic for class I antiarrhythmics?
Double Quarter Pounder. Lettuce Tomato Mayo. More Fries Please
182
Which antiarrythmics increase the risk of TdP?
Class Ia, and Sotalol (III)
183
Brief summary of the uses of class I antiarrhythmics
Ia - Reentrant and ectopic rhythms, Ib - Ventricular arrhytmias post-MI and digitalis toxicity arrhythmias, Ic - last resort in tachyarrhythmias
184
What increases the toxicity of all class I antiarrhythmic drugs?
Hyperkalemia
185
Class II antiarrhytmics
Beta blockers. Propanolol, esmolol, metoprolol, atenolol, timolol
186
What part of the EKG do beta blockers (class II antiarrhythmics) affect primarily?
P wave and PR interval
187
Uses of Class II antiarrhythmics
V-tach, SVT, slowing ventricular rate in a-fib and a-flutter
188
What do you treat overdose of Class II antiarrhythmics (b-blockers) with?
Glucagon
189
What class of antiarrhythmics may mask signs of hypoglycemia?
Class II (Beta blockers)
190
Class III antiarrhythmics
K blockers. Ibutilide, Sotalol, Bretylium, Amiodarone, Dofetilide
191
What drug increases the QT interval but does not increase risk of TdP?
Amiodarone
192
Effects of class III antiarrhytmics on EKG
Incrased AP duration, Increased ERP, increased QT interval
193
What do you need to check when using amiodarone?
PFTs, LFTs, and TFTs
194
Amiodarone toxicities
Pulmonary fibrosis, hepatotoxicity, hypo or hyper thyroidism, corneal deposits, skin deposits (blue or gray), photodermatitis, neurologic effects, constipation, CV effects
195
Amiodarone
A class III antiarrhythmic that has class 1, 2, 3 and 4 effects because it alters the lipid membrane
196
Class IV antiarrhythmics
Ca channel blockers. Verapamil and diltiazem
197
EKG effects of class IV antiarrhythmics
Increased ERP, Increased PR interval, decreased conduction velocity
198
What is the main use of Class IV antiarrhythmics?
Nodal arrhythmias (eg SVT)
199
What is the drug of choice in SVT?
Adenosine (for diagnosing or treating)
200
What blocks the effects of adenosine?
Theophylline
201
What arrhythmias is magnesium used to treat?
Torsades de pointes and digoxin toxicity
202
Why is the most common site of aortic aneurysm below the renal arteries?
Because in this section there is no vasa vasorum on the aorta
203
Signs and symptoms of abdominal aortic aneurysm
Severe left flank pain, hypotension, pulsatile mass
204
Most common cause of aneurysm in the arch of the aorta
Tertiary syphilis
205
Water hammer pulse
AR
206
Absent pulse on the left
Dissecting aneurysm of the aortic arch (has closed off the lumen of the subclavian)
207
Test of choice for a dissecting aortic aneurysm
Chest x-ray (look for widening of the proximal aortic knob)
208
Conditions predisposing to aortic dissection (3)
Marfan, Ehlers Danlos, Pregnancy
209
What are spider angiomas usually due to?
Hyperestrogenism
210
Typically what type of hypersensitivity is involved in all small vessel vasculitis?
Type 3
211
How can you tell polymyalgia rheumatic (eg with GCA) apart from polymyositis?
No elevation of serum CK in polymyalgia rheumatic (but will have aches and pains in muscles and joints)
212
A cause of saddle nose besides congenital syphillis
Wegners granulomatosis
213
What infection includes a rash that starts on the extremities and goes to the trunk?
Rocky Mountain Spotted Fever
214
CREST syndrome
Calcinosis (also Centromere Ab), Raynauds, Esophageal dysmotility, Sclerodactyly, Telangiectasia
215
What class of drugs can cause Raynauds?
Ergot derivatives
216
In the case of what heart murmur should you get an immediate surgical consult?
Austin flint murmur. The AR has gotten so bad that the valve needs to be replaced fairly soon
217
What is paroxysmal nocturnal dyspnea a sign of?
Left heart failure
218
Best nonpharmacologic treatment for heart failure
Restrict water and salt
219
Why are ACE inhibitors the treatment of choice in CHF
They decrease preload (decreased sodium reabsorption) and afterload (vasodilation)
220
How does thiamine deficiency lead to high output heart failure?
ATP depletion causes vascular smooth muscle to fail and dilate, causing your BP to tank
221
What impact does chronic hyperthyroidism have on the heart?
Increases synthesis of beta receptors, leading to increased force of contraction (high systolic pressure, high output heart failure eventually)
222
Brenhams sign
Heart rate slows when you press on the proximal part of an AV fistula
223
What vessels in the fetus have the highest and lowest O2 concentration respectively?
Highest - umbilical vein, Lowest - umbilical arteries (2)
224
Most common cause of a congenital ASD?
Fetal Alcohol Syndrome
225
Where is the murmur of a PDA heard best?
Between the shoulder blades
226
What is the most common cause of PDA?
Congenital rubella
227
Why are the junctions of the communicating arteries and main cerebral arteries common points for aneurysms (berry aneurysm)?
Because there is no internal elastic lamina or smooth muscle there
228
2 main ways to get around an aortic obstruction (such as a coarctation)
1) Superficial epigastric artery with internal mammary artery. 2) Intercostals (which is why you have notching of the ribs in coarctation)
229
CAD risk factors
Age (most important), Family History, Cigarette Smoking, HTN, Diabetes, LDL, HDL (negative risk factor)
230
Is tPA more effective on arterial or venous clots and why?
Arterial, they have less fibrin than venous clots
231
Thrombosis of what artery can cause MR?
RCA. It supplies the papillary muscles of the mitral valve
232
What type of an MI can present with epigastric pain?
An RCA MI
233
What type of MI is the most common antecedent to IV septum rupture?
LAD MI
234
If the patient had an LAD MI, what do you need to be sure to give to prevent a particular complication?
Warfarin or Heparin to prevent a mural thrombus from forming (most common after an LAD MI)
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How would a post MI ventricular aneurysm present?
Massive pectoralis major which bulges with the pulse
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What is the most common cause of death in ventricular aneurysm?
Heart failure (they generally do not rupture)
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What is the best predictor of survival at time of discharge from an MI?
Ejection fraction
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Reinfarction is defined by CK-MB that is still elevated after how long?
3 days
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What is seen with LDH in MI?
LDH1 becomes higher than LDH2 (called the flip)
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What is the pathology of MVP?
Myxomatous degeneration
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What GAG makes up the mitral valve?
Dermatan sulfate. Too much of it becomes redundant and you get MVP
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Which way do the murmur and click in MVP move when you increase and decrease preload respectively?
Increased preload - moves towards S2 (takes longer for all blood to get out), Decreased preload - moves towards S1
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Does the murmur of MVP move closer to S1 or S2 when one is anxious?
Closer to S1 (ventricles have less time to fill due to higher HR)
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In AS and HOCM respectively, does increased blood volume in the LV increase or decrease the intensity of the murmur?
AS - increases it, HOCM - decreases it
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Most common symptom in rheumatic fever
Polyarthritis
246
Differential for polyarthritis
Juvenile rheumatic arthritis, Henoch Schonlein, rubella, rheumatic fever
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2 genetic diseases associated with MVP
Marfans and Ehler Danlos
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Most common cause of sudden death in the Marfan
MVP and conduction defect
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Valvular lesions associated with carcinoid syndrome
Tricuspid insufficiency and pulmonic stenosis (TIPS)
250
Top two most common causes of infective endocarditis
1) Strep viridians, 2) Staph
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What defect predisposes patients to getting infective endocarditis on the aortic valve?
VSD (because membranous portion of septum is right next to the valve)
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What actually causes the visible findings in infective endocarditis (splinter hemorrhages, oslers nodes, janeway lesions, roth spots, and glomerulonephritis)?
Type 3 hypersensitivity (immune complex vasculitis)
253
Most common lesion of the heart in lupus
Pericarditis. Libman-Sacks endocarditis is associated with SLE but is less common
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Most common cause of myocarditis and pericarditis
Coxsackie virus
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Most common cause of viral menigitis
Coxsackie virus
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Cause of hand, foot, and mouth disease
Coxsackie virus
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Cause of herpangina (painful mouth blisters)
Coxsackie
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What is contraindicated in HOCM?
Digitalis (as are all positive inotropic agents)
259
Treatment for HOCM
Beta blocker, Ca channel blocker
260
Most common cause of restrictive cardiomyopathy in children
Endocardial fibroelastosis
261
What heart defect does Pompes disease cause?
Restrictive cardiomyopathy (as does Fe overload, and amyloidosis)
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First step in management of a suspected pericardial effusion
Echocardiogram (then call the surgeon to do a pericardiocentesis)
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Most common cause of pericardial effusion
Pericarditis (the most common cause of which is Coxsackie)
264
Most common cause of constrictive pericarditis
Worldwide - TB, US - previous cardiac surgery
265
Auscultatory finding in constrictive pericarditis
Pericardial knock (important because no knock present in pericardial effusion)
