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248 Cards in this Set

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Where is pericardial pain referred?
C3-C5
Where is cardiac visceral pain referred?
T1-T5
At what vertebral level is the aortic arch?
T4
At what vertebral level is the aortic hiatus?
T12
At what vertebral level is the aortic bifurcation?
L4
SA and AV nodes are supplied by which coronary artery?
RCA (via the posterior descending artery)
If someone is "left dominant" in terms of coronary arteries, what does that mean?
It means the posterior descending artery comes off of the circumflex artery, which comes off of the LMCA.
Which artery supplies the anterior intraventricular septum?
LAD
During which part of the heart beat cycle? do the coronary arteries fill?
During diastole
What's the most posterior part of the heart?
The left atrium
What's the equation for the Ficke principle?
CO = Rate of O2 consumption / (arterial O2 content - venous O2 content)
What can enlargement of the left atrium cause?
Dysphagia (due to compression of esophageal nerve) or hoarseness (due to compression of recurrent laryngeal nerve)
Whats the formula for mean arterial pressure when given systolic/diastolic?
MAP = 2/3 diastolic + 1/3 systolic pressure
Pulse pressure is equivalent to what other value?
Stroke volume
What is the mechanism of action of digoxin?
Blocks the Na/K+ ATPase, which leads to increased intracellular sodium, which prevents the Na/Ca2+ exchanger from working and keeps Ca2+ inside the cell
How do catecholamines increase contractility?
They increase the activity of the Ca2+ pump in the sarcoplasmic reticulum
Does nitroglycerin affect preload or afterload?
preload (dilates veins)
Does hydralazine affect preload or afterload?
Afterload (dilates Arteries)
Describe what happens to CO during exercise and during extremely increased HR (like vtach)
CO increases during exercise, but decreases during vtach bc diastolic filling is incomplete
What is a normal ejection fraction?
> 55%
What is the equation for resistance given viscosity/radius?
R = 8 (viscosity) * length / ( pi * r ^4)
Name three disease states in which you would see increased viscosity.
Polycythemia, hyperproteinemic states (multiple myeloma), and hereditary spherocytosis
In which vessels is most of the blood in your body?
Veins
Which vessels contribute the most to TPR?
arterioles
Are vessels within an organ considered to be in series or in parallel? how about organs in the body?
In organ- series

In body- parallel
What is the period in the cardiac cycle that has the highest O2 consumption?
Isovolumetric contraction
If someone has increased preload, would they be more likely to have an S3 or an S4 gallop?
S3, bc increased preload could be from something like mitral regurg, leading to dilation, etc.
What is the sound at S1?
Mitral and tricuspid valves closing
What is the sound at S2?
Aortic and pulmonary valves closing
S4 means what?
Stiffened ventricle, could be caused by hypertension or aortic stenosis
JVP a wave represents?
atrial contraction (at the end of atrial emptying into ventricle)
JVP c wave represents?
RV contraction (it bulges into the RA and creates increased pressure)
JVP x descent represents?
atrium relaxing as RV pushes out blood during systole, atrium is filling at this point
JVP v wave represents?
atrial pressure increase as it continues to fill against the closed tricuspid valve
JVP y descent represents?
atrial emptying at the beginning of diastole, before the atrium contracts
What causes a split S2 and when does it happen in a normal person?
The aortic valve closes before the pulmonic, leading to a split S2

In a normal person, it happens during inspiration because you have more blood volume through the right side of the heart on inspiration due to decreased intrathoracic pressure.
What is wide splitting and when would you see it?
A more exaggerated normal splitting (that increases on inspiration)

You would see it with pulmonic stenosis or right bundle branch block (delayed pulmonary emptying)
What is fixed splitting and when would you see it?
S2 is also split the same amount on inspiration and expiration

It's associated with ASD; overall increased flow through pulmonic valve
What is paradoxical splitting and when would you see it?
It's when you hear a split S2 that is worse on EXPIRATION, not inspiration like normal, and the Pulm. valve is actually closing sooner than the aortic.

You would see it with aortic stenosis or LBBB - the problem is preventing the aortic valve from closing so the pulmonic valve actually closes first. This gets BETTER on inspiration because it slows down the closing of the pulmonic valve due to the increased pulmonary blood flow.
Where would you listen for a murmur of aortic stenosis?
aortic area - right upper sternal border
Where could you look for an aortic stenosis, flow murmur, or aortic valve sclerosis murmur?
Aortic area (right upper sternal border)
Where would you listen for pulmonic stenosis or a flow murmur?
Pulmonic area (left upper sternal border)
Where would you listen for aortic regurgitation, pulmonic regurgitation, and hypertrophic cardiomyopathy?
Left sternal border (NOT tricuspid or mitral area)
Where would you listen for tricuspid regurgiation, a VSD, tricuspid stenosis, or an ASD?
Tricuspid area (left lower sternal border)
Where would you listen for mitral regurgitation or mitral stenosis?
Mitral area (PMI/apex)
Sounds on which side of the heart increase in intensity with inspiration?
Right side
Sounds on which side of the heart increase in intensity with expiration?
Left side
Patient has holosystolic, high-pitched, blowing murmur. Loudest at apex and radiates toward axilla. Enhanced by squatting. Murmur?
Mitral regurgitation
Patient has holosystolic, high-pitched, blowing murmur. Loudest at tricuspid area and radiates to right sternal border. Enhanced by inspiration. Murmur?
Tricuspid regurgitation
Patient has crescendo-decrescendo systolic ejection murmur following an ejection click. Radiates to carotids/apex. Pulses weak compared to heart sounds. Murmur?
Aortic stenosis
Patient has a holosystolic, harsh-sounding murmur, loudest at the tricuspid area. Two options for the murmur?
VSD or tricuspid regurgitation
Patient has a late systolic crescendo decrescendo murmur with a midsystolic click. Loudest at S2. Enhanced by squatting. Murmur?
Mitral prolapse
Patient has an immediate, high-pitched, blowing, diastolic murmur. Wide pulse pressure with bounding pulses and head-bobbing. Murmur?
Aortic regurgitation
Patient has a delayed rumbling, late diastolic murmur. LA > LV pressure during diastole. Murmur?
Mitral stenosis
Patient has a continuous, machine-like murmur, loudest at S2. Murmur?
PDA
Patient has a systolic ejection murmur in the pulmonic area and along the LSB, fixed split S2. Murmur?
ASD

You get the systolic ejection murmur (aka flow murmur) bc of increased flow through the pulmonary valve, but it can later turn into a diastolic rumble of tricuspid regurgitation
What kinds of movements increase total peripheral resistance?
squatting, hand-grip, valsalva* (double check this)
What maneuver would increase LA return?
expiration
Contraction of which types of muscle requires extracellular calcium?
cardiac, smooth (only sometimes)
Name three things that are different about cardiac muscle than about skeletal muscle?
1) Cardiac muscle action potential has a plateau (due to Ca2+ influx)
2) Cardiac nodal cells spontaneously depolarize during diastole, so firing is automatic
3) Cardiac myocytes are electrically coupled to each other by gap junctions
Describe what happens in each phase of the ventricular action potential.
Phase 0 - rapid upstroke, voltage-gated Na+ channels open
Phase 1- initial repolarization- K+ channels open, K+ goes out, Na+ channels close
Phase 2- plateau- Ca2+influx, which actually triggers myocyte contraction
Phase 3- rapid depolarization, massive K+ efflux
Phase 4- resting, dominated by K+ efflux
Describe what happens in each phase of the pacemaker action potential.
Phase 0 - upstroke- opening of voltage gated Ca2+ channels
Phase 3- Inactivation of Ca2+ channels and K+ efflux
Phase 4- slow, diastolic depolarization, via sodium channels. These are NOT the same as the fast Na+ channels in the regular myocytes.
What represents atrial depolarization on the EKG?
P wave
What represents conduction delay through AV node on the EKG?
PR interval
What represents ventricular depolarization on the EKG?
QRS complex
What represents mechanical contraction of the ventricles on EKG?
QT interval
What represents ventricular repolarization on EKG?
T wave
What is the primary pacemaker?
the SA node
How long is a normal PR interval?
< 200 milliseconds (.2 secs) (1 big box on EKG)
How long is a big box on EKG?
200 milliseconds
What can peaked T waves indicate (re K+)?
high K+
What can flattened T waves indicate (re K+)?
low K+
What are congenital long QT syndromes normally due to?
defects in cardiac sodium or potassium channels
What could be a sign of a congenital long QT syndrome?
severe, congenital, sensorineural deafness
V5, V6, I, and avL leads show which part of the heart?
lateral
V1-V4 leads show which part of the heart?
anterior
II, III, and avF show which part of the heart?
inferior
What is Wolff-Parkinson White syndrome?
accessory conduction pathway from atria to ventricle, bypassing AV node
What is the risk in WPW wyndrome
?
reentry current, leading to supraventricular tachycardia
Why do you get a delta wave in WPW?
Because ventricles start to depolarize early because the the impulse bypasses the AV node
How could you treat SVT in WPW?
procainamide (class IA) or amiodarone (K+ blocker)
What would you use to treat atrial fibrillation?
beta blocker or calcium channel blocker + warfarin prophylaxis against thromboembolism
In atrial fibrillation, what controls ventricular contraction?
The AV node, bc there are lots of "rogue" SA nodes firing all over the atrium.
What (classes) of drugs could you use to treat atrial flutter?
class IA, IC, or III anti-arrhythmics
What would you see in first degree AV block on EKG?
Prolonged PR interval
Which bacteria can cause AV block?
B. burgderfori
What would you see on EKG in 2nd degree, Mobitz type I AV block?
longer and longer PR interval followed eventually by a dropped beat
What would you see on EKG in 2nd degree, Mobitz type II AV block?
dropped beats, not preceeded by a change in the length of the PR interval
Which kind of 2nd degree AV block is dangerous?
Type II
What would you see on EKG in third degree AV block?
P wave and QRS complex are both present, but independent of each other; atrial rate is faster than ventricular rate
What is the body's short-term response to low mean arterial pressure?
baroreceptors decrease firing, and medullary vasomotor center then increases sympathetic activity
What is the body's long-term response to low mean arterial BP?
the juxtaglomerular apparatus senses decreased MAP (based on volume) and activates the renin/angiotensin system
What two things (related to blood pressure) are the outcome of activating the RAA system?
Angiotensin II --> increased vasoconstriction

Aldosterone --> inc. blood volume, increased CO
What does ANP do at the renal arteries?
Constricts the efferent and dilates the afferent; "escape from aldosterone" mechanism
Name two chemical mediators that act via cGMP.
ANP and NO
Where in the brain to the baroreceptors signal to?
the solitary nucleus (medulla)
Where are peripheral chemoreceptors located?
carotid & aortic arteries
What do peripheral chemoreceptors respond to?
decreased pO2, increased pCO2, and decreased pH
What do central chemoreceptors respond to?
changes in pH and pCO2; do NOT directly respond to changes in pO2
What is the Cushing reaction?
Increased intracranial pressure --> constricted arterioles --> cerebral ischemia --> hypertension --> reflex bradycardia
What part of the brain is responsible for the Cushing reaction?
The central chemoreceptors
What is the Cushing triad?
hypertension, bradycardia, respiratory depression
Which organ gets the largest share of systemic cardiac output?
liver
Which organ gets the highest blood flow/gram of tissue?
kidney
How is increased demand for oxygen met in the heart?
By increasing coronary blood flow; you can't extract more oxygen from the same amt. of blood bc O2 extraction is always near 100%.
Normal right atrial pressure?
less that 5 mmHg
Normal LA pressures?
Sytolic- <25, diastolic- <5
Normal PA pressure?
Systolic- <25
Diastolic- <10
Normal LA pressure?
<12
Normal LV pressure?
Systolic- <130, Diastolic- <10
Normal aortic pressure?
Systolic- <130, Diastolic- <90
What factors determine autoregulation in this organ:
heart
O2, adenosine, NO (local metabolites)
What factors determine autoregulation in this organ:
brain
local metabolites - CO2 (pH)
What factors determine autoregulation in this organ:
kidneys
myogenic, tubuloglomerular feedback
What factors determine autoregulation in this organ:
lungs
hypoxia causes vasoconstriction!
What factors determine autoregulation in this organ:
skeletal muscle
local metabolites like lactate, adenosine, and K+
What factors determine autoregulation in this organ:
skin
sympathetic stimulation --> vasoconstriction in skin
Why does pulmonary vasculature constrict in hypoxia?
It's so only well-ventilated areas (the ones that are getting oxygen) get perfused, so the most oxygen actually gets out into the body
What is the difference between things that cause pitting and things that cause non-pitting edema?
Pitting- caused by exudate (fluid without protein)- so in heart failure or sepsis

Non-pitting- protein/fluid level is equal. So liver failure (less protein in blood) or lymphatic blockage (MORE protein in interstitium)
What are the 5 causes of blue baby syndrome?
1- persistent truncus arteriosus
2- transposition of the great vessels
3- tricuspid atresia
4- tetrallogy of fallot
5- total anomalous pulmonary venous return
What are the heart defects associated with congenital rubella?
PDA, pulmonary artery stenosis
What other defect is seen along with persistent truncus arteriosus?
VSD
What other defects are seen with tricuspid atresia?
ASD and VSD
What happens in total anomalous pulmonary venous return?
The pulmonary veins drain into the rt. heart circulation, rather than the left. So ox/deox blood mix in the rt atrium and then travel the rest of the way through the circulation togethe
What other defect would you have to see in total anomalous pulmonary venous return?
an ASD
What's the most common congenital cardiac anomaly?
VSD
What's Eisenmenger's syndrome?
When an ASD, VSD, or PDA uncorrected goes from L to R shunt --> pulmonary hypertension --> R to L shunt --> late cyanosis
What are the 4 defects in tetralogy of fallot?
pulmonary stenosis, right ventricular hypertrophy, overriding aorta, and VSD
Why does the VSD start off as a R to L shunt in tetralogy of fallot?
bc of the pulmonary stenosis leading to increased RV pressure
What is the embryological cause of tetralogy of fallot?
anterosuperior displacement of the infundibular septum
Coarctation of the aorta can lead to what type of murmur?
Aortic regurgitation
What keeps a PDA open and what closes it?
Indomethacin closes it, PGE keeps it open
What does the body do to compensate for coarctation of the aorta?
So in coarctation, the body wants to keep flow the same everywhere. Pressure in distal extremities is reduced, so to compensate, body must decrease resistance to keep flow even. Remember P = Q * R
What heart defects is 22q11 syndrome associated with?
truncus arteriosus, tetralogy of fallot
What heart defects is marfan syndrome associated with?
aortic insufficiency (late complication)
What heart defect is an infant of a diabetic mother likely to have?
transposition of great vessels
How is high BP defined?
Greater than or equal to 140/90
Plaques in blood vessel walls are called?
atheromas
Plaques or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids are called?
xanthomas
lipid deposit in the tendon, esp. Achilles is called?
tendinous xanthoma
lipid deposit in the cornea, nonspecific, is called?
corneal arcus
calcification in the media of the arteries, esp. radial or ulnar. "Pipestem" arteries. Diagnosis?
Monkeberg arteriosclerosis
Hyaline thickening of the small arteries secondary to essential hypertension or diabetes.

Also described as "onion-skinning" in malignant hypertension. Diagnosis?
Arteriosclerosis
What's the difference between hypertensive urgency and hypertensive emergency?
- urgency- high BP, no symptoms or end-organ damage

- emergency- high BP + symptoms & end-organ damage
What types of arteries are affected in atherosclerosis?
large and medium-sized muscular arteries
What is pathophysiology of atherosclerosis?
endothelial cell dysfunction --> macrophages & oxidized LDL accumulate --> macrophages eat the lipid and become foam cells --> fatty streaks --> smooth muscle migration to form fibrous cap
What does oxidized LDL have to do with atherosclerosis?
It's the type of LDL that the macrophages take up to become foam cells
Where is the most common location for atherosclerosis?
abdominal aorta
Which type of aortic dissection involves the ascending aorta?
Type A- must be fixed immediately
Why would you give antioxidants to someone with atherosclerosis?
to prevent the formation of oxidized LDL and reduce plaque formation
What would be the ECG findings in stable angina vs. Prinzmetal's angina?
Stable- ST depression, Prinzmetal's- ST elevation
How would you treat prinzmetal's variant angina?
Dihydropiridine calcium channel blockers (bc you want to decrease the vasospasm)
What is actually narrowing in angina?
coronary arteries
How would you tell the difference between unstable/crescendo angina and prinzmetal's?
Unstable would have ST depression like stable angina, Prinzmetal's would have ST elevation
How can you provoke prinzmetal's angina to test if you have it?
with ergonovine
What is the mechanism of action of ergonovine?
it stimulates alpha adrenergic and serotonergic receptors --> smooth muscle constriction
dyspnea related to cardiac cause (worse when lying down) = ?
orthopnea
When do you start to see early coagulative necrosis after MI?
4 hours
When do you start to see contraction bands after MI?
12-24 hours
Acute inflammation, dilated vessels, neutrophil emigration, extensive coagulative necrosis. How long after MI?
2-4 days
2-4 days after MI, you are at risk of what additional pathology?
arrhythmias
Heart shows hyperemic border, central yellow-brown softening, macrophages have degraded structural components. How long after MI?
5-10 days
5-10 days after MI you are at most risk for?
ruptures (free wall, interventricular septum, etc.) + tamponade
How long after MI would you see a contracted scar?
>10 days (FA says 7 weeks)
What are you at risk for 10 days + out from an MI?
Ventricular aneurysm, which is NOT likely to burst bc it's made of scar tissue
What is the #1 modifiable risk factor for AAA?
smoking
What is NOT a risk factor for AAA that you might think is?
diabetes
How long does it take troponin to rise and how long does it stay elevated after MI?
4 hours to rise, stays elevated for 7-10 days
Why is CK-MB useful in diagnosing reinfarction?
Bc levels decrease around two days, so a re-infarction past 2 days out would show a new rise in CK-MB
What type of MI does ST elevation indicate?
transmural infarct
What type of MI does ST depression indicate?
subendocardial infarct (same ECG findings as angina)
What type of MI do pathological Q waves indicate?
transmural infarct
Q waves in V1-V4 would indicate ?
anterior wall MI
Q waves in V1- V2 would indicate?
anteroseptal MI
Q waves in V4-V6 would indicate?
anterolateral MI
Q waves in I, aVL would indicate?
lateral wall MI
Q waves in II, III, and avF would indicated?
inferior wall MI
Patient presents with pericardial friction rub 3-5 days post MI. Diagnosis?
Postinfarctious fibrinous pericarditis
Patient presents with pericardial friction rub several weeks post-MI. Diagnosis?
Dressler's syndrome
What's the most common type of cardiomyopathy?
Dilated
Name some (7) etiologies of dilated cardiomyopathy.
Alcohol abuse/thiamine deficiency --> wet beri beri, coxsackie B virus & other viruses, cocaine, chagas' disease, doxorubicin, hematochromatosis, and peripartum, cardiomyopathy
dilated cardiomyopathy --> (systolic/diastolic) dysfunction?
systolic
What neural pathology is hypertrophic cardiomyopathy related to?
Friedrich's ataxia
What would you treat hypertrophic cardiomyopathy with?
beta blocker or non-dihydropyridine calcium channel blocker
What type of cardiomyopathy is Loffler's syndrome associated with?
restrictive
Which type of cardiomyopathy would have the greatest increase in filling pressure?
Restrictive, followed by hypertrophic
What kind of cardiac infiltrate do you see in Loffler's syndrome?
eosinophilic
Why does hypertrophic cardiomyopathy have a systolic murmur?
Still don't completely understand but I think basically the mitral valve leaflets get in the way of ejection during systole, leading to a murmur & also mitral regurg because the valve leaflets are messed up.
What is the difference between concentric and eccentric hypertrophy and when do you see them?
eccentric = sarcomeres added in series, seen in dilated cardiomyopathy

Concentrtic= sarcomeres added in parallel; seen in hypertrophic cardiomyopathy
Where is aortic rupture most likely to occur?
At the aortic isthmus, right after the left subclavian artery branches off.
Why do you see hemosiderin-laden macrophages in lungs in heart failure?
Due to microhemorrhages from increased pulmonary capillary pressure
What valve is most commonly involved in bacterial endocarditis?
mitral
What is the most likely causative organism of acute (highly virulent) bacterial endocarditis?
staph. aureus
What bacteria would you suspect in a subacute case post-dental procedure?
strep viridans
What organism would you suspect in bacterial endocarditis in someone with prosthetic valve?
staph epidermidis
What three organisms could cause bacterial endocarditis in IV drug user?
S. aureus, pseudomonas, candida
What are the HACEK organisms that might cause culture-negative bacterial endocarditis?
H-haemophilus, A-actinobacillus, C-cardiobacterium, E-ekinella, K-kingella
Patient presents with culture-negative endocarditis with verrucous, sterile vegetations on both sides of valve. What disease do they have and what other disease might they have?
Libman Sacks endocarditis, might also have SLE
What bacteria causes rheumatic heart disease?
Group A beta hemolytic strep
If you die early from rheumatic heart disease, what do you die of?
myocarditis
What are the two common murmurs seen in late rheumatic heart disease?
mitral prolapse and mitral regurgitation
Which valve is most commonly affected in rhematic fever? second?
mitral, followed by aortic
What is an aschoff body and when is it seen?
It's a granulomatous thing with lymphocytes & some plasma cells and abnormal macrophages (giant cells); seen in rheumatic fever
What could you check with a blood test in rheumatic heart disease?
elevated ASO titers
What type of hypersensitivity is rheumatic heart disease?
type II
What specific protein are Abs against in rheumatic heart disease?
M protein
What is erythema marginatum?
red, faint, circular rash on trunk, can be seen in acute rheumatic fever
What are the signs/sx of acute rheumatic fever?
Think FEVERSS

f- fever, e- erythema marginatum, v-valvular damage, E-esr, R-red hot joints, S-subcutaneous nodules, S-st. vitus' dance (chorea)
When you see equilibration of diastolic pressures in all four chambers, that is a sign of?
cardiac tamponade
What is pulsus paradoxus and what causes it?
pulsus paradoxus is when your systolic bp drops by more than 10 mmHg on inspiration. Normally, that doesn't happen bc more blood comes back into the rt heart on inspiration but the right heart can expand. In pulsus paradoxus, the rt. heart can't expand so it pushes into the left heart and decreases the systolic BP on inspiration. Seen in cardiac tamponade and pericarditis.
What would you see on EKG in cardiac tamponade?
electrical alternans- beat to beat variation in QRS complex
What structure of the aorta gets disrupted in tertiary syphilis?
vasa vasorum (small network of vessels providing blood supply to aorta)
What types of aortic pathology might you see in tertiary syphilis?
calcification of aortic root, aneurysm of ascending aorta or aortic arch, aortic valve problems like aortic regurgitation or stenosis
What ECG finding would you see in pericarditis?
ST elevation in multiple leads
What is kussmal's sign and when would you see it?
increased JVD on inspiration, seen in pericarditis
What's the most common primary cardiac tumor in adults?
myxoma
Where are myxomas usually seen?
In left atrium, attached to septum
Child presents with multiple cardiac tumors projecting into the ventricular cavity. Most likely type of tumor & what is it associated wtih?
Rhabdomyoma, associated with tuberous sclerosis
What "sign" would you see in cardiac tumors, potentially?
Kussmaul's sign
What pathology might you see secondary to mixed connective tissue disease, SLE, CREST syndrome, and Buerger's disease?
Raynaud's phenomenon
What would you use to treat raynaud's (4)?
Ca2+ channel blockers (dihydropiridine), alpha 1 blockers, nitrates, or surgery to cut sympathetic nerves
What is the triad seen in Wegener's granulomatosis?
Necrotizing vasculitis, necrotizing granulomas in lung & upper airway, and necrotizing glomerulonephritis
What would you see in urine in Wegener's?
red urine, red cell casts
What's the treatment for Wegener's granulomatosis?
cyclophosphamides + corticosteroids
Patient presents with granulomatous vasculitis with eosinophilia; asthma, sinusitis, skin lesions, and peripheral neuropathy. p-ANCA positive. Diagnosis?
Churg-Strauss syndrome
Henoch schonlein purpura is associated with which nephropathy?
IgA nephropathy
Henoch schonlein purpura follows what type of infection?
upper respiratory
What is the triad associated with henoch schonlenin purpura?
skin, joints, GI
Child presents with necrotizing vasculitis, fever, conjunctivitis, strawberry tongue, lymphadenitis, desquamative skin rash on hands/feet. Diagnosis?
kawasaki disease
What is the treatment for kawasaki disease?
aspirin, IVIg
Immune complex-mediated transmural vasculitis with fibrinoid necrosis = ?
polyarteritis nodosa
Patient presents with fever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension, peripheral neuropathy, and cutaneous eruptions; no pulmonary involvement. Dx?
polyarteritis nodosa
Polyarteritis nodosa is associated with which other disease?
Hep. B (30% of cases)
Weakened pulses in upper extremities in Asian female. Dx?
Takayasu's arteritis
What is the histological finding in takayasu's arteritis?
granulomatous thickening of the MEDIA of the aortic arch/proximal great vessels
What is the finding in temporal arteritis that isn't in the head/face area?
polymyalgia rheumatica (joint pain)
What's the name for a polypoid capillary hemangioma that can ulcerate and bleed; associated with trauma and pregnancy?
pyogenic granuloma
Cavernous lymphangioma of the neck =
cystic hygroma
Benign, painful, red-blue tumor under the fingernails; arises from modified smooth muscle cells of the glomus body.
Glomus tumor
Benign capillary skin papules found in AIDS patients; frequently mistaken for kaposi sarcoma
Bacillary angiomatosis
What's the causative organism of bacillary antiomatosis?
Bartonella henselae
highly lethal malignancy of the liver associated with vinyl chloride, arsenic, and ThO2 (thorotrast) exposure.
Angiosarcoma
What are the three risk factors for angiosarcoma?
vinyl chloride, arsenic, and thorotrast
lymphatic malignancy associated with persistent lymphedema (eg after radical mastectomy)
Lymphangiosarcoma
What is marantic endocarditis?
It's a paraneoplastic syndrome caused by circulating mucin from mucin-producing tumors of colon/pancreas that form sterile vegetations on the mitral valve
Name three pathogens that might cause myocarditis
Coxsackievirus, T. cruzi, B. burgdorferi
Most common overall known cause of pericarditis?
coxsackievirus
What chromosome does hypertrophic cardiomyopathy map to?
14 (think of Jenna- athlete- wearing #14)