BVI, WIII
Terms
undefined, object
copy deck
- define myocarditis
- inflammation of myocardium with features NOT typical of an acute MI
- how is the definitive diagnosis of myocarditis made?
- endomyocardial biopsy
- if you see myocarditis, for practical purposes think ...?
- viral infection
- what is the most common viral pathogen causing myocarditis?
- coxsackie A and B
- which disease, carried by the Reduviid bug, causes a form of myocarditis?
- Chagas disease
- what are four toxic agents causing specific myocardial diseases?
-
1. alcohol (and acetaldehyde, it's derivative)
2. cobalt
3. catecholamines
4. doxorubicin - hyperthyroidism has what cardiovascular effects? (3)
-
1. cardiomegaly
2. direct inotropic and chronotropic effects
3. decreased PVR - hypothyroidism has what cardiovascular effects? (3)
-
1. dilated heart
2. decreased CO, HR, contractility
3. increased PVR - Beriberi heart disease is due to which deficiency?
- thiamine (B1) deficiency
- which two stereotypic lifestyles is thiamine deficiency commonly seen in?
-
1. polished rice diet
2. alcoholics -
in Beriberi what changes are seen in:
1. PVR
2. heart size -
1. decreased PVR
2. dilated heart (results in high output heart failure) - treatment for Beriberi heart disease?
- IV thiamine administration
- two neuromuscular diseases that cause cardiac disease?
-
1. Friedreichs ataxia
2. muscular dystrophies - infiltrative disorders that cause myocardial disease? (3)
-
1. sarcoidosis
2. amyloidosis
3. metastatic carcinoma - storage disease that cause myocardial disease?
-
1. hemochromatosis (iron in myocytes)
2. Pompe's disease (glycogen storage disease)
3. mucopolysaccharidosis - Three types of cardiomyopathies in order of common occurence?
-
1. dilated
2. hypertrophic
3. restrictive - which type of cardiomyopathy is sometimes seen in pregnancy (3rd trimester to postpartum period)?
-
dilated cardiomyopathy
(50% recover from this) - how does dilated cardiomyopathy affect the coronary arteries?
- it does NOT affect the coronary arteries. The coronaries are wide open!
- prognosis for dilated cardiomyopathy?
-
progression to CHF
if no heart transplant: 75% die within 5 yrs - define hypertrophic cardiomyopathy
- cardiac ventricular hypertrophy without dilitation and WITH diastolic and systolic dysfunction
- when does hypertrophic cardiomyopathy typically develop?
- in first two decades
- heredity and genetics of hypertrophic cardiomyopathy?
-
autosomal dominant with variable expression
(mutation in myosin gene on chr. 14) - gross and histologic characteristics of hypertrophic cardiomyopathy?
-
gross: LV hypertrophy (esp. septum), atrial dilation with fibrillation
histo: myocyte hypertrophy, myofiber disarray, fibrosis - define restrictive cardiomyopathy
- limitation of diastolic filling by myocardial/endocardial disease
- gross and histo characteristics of restrictive cardiomyopathy?
-
gross: ventricles normal sized to slightly enlarged, myocardium firm
histo: interstitial fibrosis present -
which type of pericardial effusion am I?
clear to straw colored
seen in CHF, nephrotic syndrome, cirrhosis? - Serous effusion
-
which type of pericardial effusion am I?
white milky color
seen in lymphatic obstruction, carcinomas - Chylous effusion
-
which type of pericardial effusion am I?
Frank blood
seen in cardiac rupture, trauma, aortic dissection - hemopericardium
- describe the cause of serous acute pericarditis
- usually non-infectious (ie. autoimmune, uremia)
- describe possible causes of Fibrinous/serofibrinous acute pericarditis
-
Acute MI
Dresslers (postmyocardial) syndrome - describe the causes of purulent/suppurative acute pericarditis
-
usually infectious
may organize and form a fibrous pericarditis - describe the causes of hemorrhagic acute pericarditis
- TB or malignant neoplastic involvement
- what type of pericarditis would pulsus paradoxus possibly be present?
- chronic pericarditis (adhesive mediastinopericarditis)
- three possible etiologies of constrictive pericarditis?
-
1. previous bacterial (or TB) pericarditis
2. radiation
3. surgery - physiological consequence of constrictive pericarditis?
- restrictive hemodynamics (due to fibrosis and calcification) - right heart failure pattern
- treatment for constrictive pericarditis?
- pericardiectomy
- two prototype large vessel vasculitis diseases?
-
1. Giant cell arteritis
2. Takayasu arteritis - two prototype medium vessel vasculitis diseases?
-
1. Polyarteritis nodosa
2. Kawasaki disease - many small vessel vasculitis diseases are associated with which antibody?
- ANCA (Anti Neutrophil Cytoplasmic Antibody)
- what are the 3 ANCA associated vasculitis diseases?
-
1. Wegener's granulomatosis
2. microscopic polyangiitis
3. Churg-Strauss - Giant Cell Arteritis (GCA) most often effects which arteries?
- temporal arteries
- age of onset of GCA?
- 70 yrs (rare before 50)
- treatment for GCA?
- corticosteroids
- why must treatment be initiated immediately in GCA?
- possibility of blindness (via involvement of opthalmic artery)
- hypothesis behind pathogenesis of GCA?
- immunologic rxn to some artery component (maybe elastin)
- which vasculitis is also known as pulseless disease?
- Takayasu arteritis
- stereotypical patient with Takayasu's arteritis
-
1. young woman under 40
2. weaking of pulses in upper extremities - which vessels are involved in Takayasu's arteritis?
-
aorta
aortic arch vessels
aortic branches - what causes the fibrosis of the aorta and aortic wall thickening seen in Takayasu's arteritis?
- inflammation of vasa vasorum
-
which vasculitis am I?
young adults
medium and small muscular arteries involved
30% of patients have a HepB infection - Polyarteritis nodosa (PAN)
- where would you see inflammation in PAN?
-
inflammation at arterial branch points
all three layers of blood vessel would be inflammed - what age patient would we see Kawasaki disease in?
- <4yrs
-
what do all these small vessel vasculitis diseases have in common?
leukocytoclastic vasculitis
Henoch-Schonlein purpura
Cryoglobulinemia - ANCA negative
- stereotypic sex and age of patient with Wegener's Granulomatosis (WG)?
-
Male
5th to 6th decade - classic involvement of WG?
-
ELK
(ENT - sinusitis
Lungs - pneumonitis
Kidney - glomerulonephritis) - Treatment for WG?
-
corticosteroids
cyclophosphamide
*high mortality if untreated* - most commonly affected organ in microscopic polyangiitis (MPA)?
- kidneys
- vessels involved with MPA?
- small vessels (arterioles, capillaries, venules)
-
between WG and MPA:
which is P-ANCA positive and which is C-ANCA positive? -
P-ANCA positive - MPA
C-ANCA positive - WG -
1. what is the antigen in P-ANCA?
2. what is the antigen in C-ANCA? -
1. myeloperoxidase
2. proteinase 3 - which vasculitis is associated with eosinophilic granulomatous inflammation?
- Churg-Strauss syndrome
- stereotypical churg-strauss patient?
-
young
allergic rhinitis
asthma
peripheral blood eosinophilia - is churg strauss ANCA positive?
- yes. it is P-ANCA positive
- characteristic of leukocytic vasculitis?
-
palpable purpura
(vasculitis that manifests on the skin) - which antibody is associated with Henoch-Schonlein purpura?
- IgA
- which vasculitis may be hepC related?
- Cryoglobulinemic vasculitis
- which disease is sometimes found in young to middle age smokers and presents with claudication and ischemic ulceration of the extremities?
- Buergers Disease (thromboangiitis obliterans)
- two major mechanisms of common arrythmias?
-
1. abnormal automaticity
2. reentrant conduction - mechanism and origin of sinus tachycardia?
-
mechanism - abnormal automaticity
origin - SA node - mechanism and origin of A fib/flutter?
-
mechanism - reentry
origin - atria - mechanism and origin of PVC?
-
mechanism - abnormal automaticity
origin - Purkinje fibers, ventricles - mechanism and origin of V tach/fib?
-
mechanism - reentry
origin - ventricles - mechanism and origin of Torsades de pointes?
-
mechanism - triggered early after depolarizations
origin - ventricles - four classes of antiarrythmics?
-
1. Sodium channel blockers
2. Beta blockers
3. Potassium channel blockers
4. Calcium channel blockers - difference in AP between slow response tissues and fast response tissues in the myocardium?
-
slow response tissues (SA and AV nodes):
shallow slope of phase 0
weak AP
Ca++ mediated upstroke
fast response tissues:
steep slope of phase 0
strong AP
Na+ mediated upstroke - five phases of action potential?
-
phase 0 - upstroke
phase 1 - early fast repolarization
phase 2 - plateau
phase 3 - repolarization
phase 4 -diastole - the ability of the cell to depolarize is known as?
- excitability
- define a supernormal refractory period.
- interval during or just after the relative refractory period. get a normal or larger than normal response with a smaller than normal stimulus.
- which type of refractory period is most susceptible to initiation of fibrillation?
- Relative refractory period
- which type of refractory period is most susceptible to initiation of arrythmias in general?
- supernormal refractory period
- antiarrythmic drugs most likely effect which two phases of the cell cycle?
- phase 0 and 3
- effect of Na+ channel blockers on AP of a fast response fiber?
- slow rate (decrease slope) and amplitude of phase 0 depolarization
- effect of Na+ channel blockers on the AP of a slow response fiber (SA and AV nodes)
-
little effect
(SA and AV nodes have few Na+ channels) - effect of K+ channel blockers on AP?
- prolongs repolarization and AP duration
- EKG changes seen as a result of K+ channel blockers?
- prolonged QT interval
- effects of Ca++ channel blockers on fast response fibers? (2)
-
1. decrease intracellular [Ca++]
2. negative inotropic effect - effects of Ca++ channel blockers on slow response fibers?
-
1. reduce phase 0
2. reduce HR and AV conduction velocity -
effect of antiarrythmics on:
1. automaticity
2. threshold
3. refractory period
4. conduction velocity of phase 0?
5. conduction velocity of AV node? -
1. decreases
2. increases
3. prolongs
4. decreases
5. decreases - type IV antiarrythmic agents are calcium channel blockers. Are all CCBs good antiarrythmics?
-
NO
Dihydropyridines are NOT included, only Pyridines are class IV antiarrythmics (Verapamil, Diltiazem) - compare and contrast class IA, B, and C antiarrythmics in regards to which channels they block and how well they block them.
-
IA - moderate Na+ channel blocker & K+ channel blocker
IB - LOW Na+ channel blocker, NO K+ channel blockage
IC - High Na+ channel blocker, little effect on the K+ channel - name two class IA antiarrythmics.
-
1. procainamide
2. quinidine - what is the prototype class IB antiarrythmic?
- lidocaine
- what is the prototype class IC antiarrythmic?
- propafenone, flecainide
- compare the effects of class IA, B and C antiarrythmics on the phase 0 slope
-
IA - moderately depresses
IB - little or no effect
IC - marked depression - indications for class IA agents?
- Not used much anymore (increases mortality). Use if patient is not tolerating other agents
- why is there a decreased max rate of depolarization seen with Class IA agents?
- because there is a decrease in Na+ entry during repolarization
- why is there a moderate delay in repolarization seen in Class IA agents?
- Class IA agents are moderate K+ channel blockers - this will prolong the refractory period
-
Regarding Class IA antiarrythmics:
what exactly is the indirect effect and direct effect seen on the AV node? -
direct effect: decrease AV conduction via stimulating vagal nerve
indirect effect: vagolytic - increase conduction velocity of AV node
*net reponse is dependant on vagal tone* - under which conditions must the dosage of class IA antiarrythmics be adjusted?
- liver or renal disease
-
ECG changes seen with quinidine treatment?
-possible consequence? -
widened QRS and QT intervals even at low doses
- could induce Torsades de pointes - which class IA antiarrythmic is known to induce SLE after 3-6 month of use?
- procainamide
- why do class IA antiarrythmics exacerbate CHF?
- they are negative inotropes
-
effects of class IB antiarrythmics on:
1. AP duration?
2. phase 0?
3. fibrillation threshold? -
1. decreases
2. little effect
3. increases -
how is lidocaine cleared from the body?
-why is this important? -
liver (100% liver clearance)
- can't give orally due to first pass effect - under what 3 conditions would you adjust the dose of lidocaine?
-
1. liver failure
2. CHF
3. elderly
(hepatic blood flow is a major factor in clearance) - what is notable about the administration of lidocaine?
- a loading dose is given
- what is a hallmark side efect of lidocaine that is dose dependant?
-
CNS toxicity
(see dizziness, parasthesias, drowsiness, tingling) - ECG effects of class IB agents?
-
small decrease in QT interval
(little to no effect on PR interval or QRS duration) - indications for class IB agents? (2)
-
1. life threatning ventricular arrythmias (currently controversial as to whether this or amiodorone is drug of choice for this indication)
2. digitalis cardiac toxicity -
effects of class IC agents on:
1. phase 0
2. conduction velocitiy
3. repolarization
4. AP duration -
1. marked decrease (potent Na+ channel blockers)
2. decrease
3. little or no effect
4. little or no effect - which class IC antiarrythmic also has beta blocking properties?
- Propafenone
- what does it mean to us if propafenone has beta blocking effects?
-
1. slowers HR and decreases AV node conduction
2. SAFEST class IC drug (least likelly to have proarrythmic effects) - ECG effects of class IC agents?
-
marked prolongation of QRS duration
prolongs PR interval - why are the class IC agents rarely used?
- the CAST trial showed that they increased mortality
- when we use class IC agents what are the indications? (2)
-
1. supraventricular arrythmias
2. suppression of ventricular arrythmias - ECG effect of beta blockers?
- prolonged PR interval
- indications for beta blockers in the use of arrythmia?
-
1. atrial fibrillation/flutter
2. arrythmias associated with pheochromocytosis or thyrotoxicosis - which beta blocker is exclusively used in acute arrythmias?
- Esmolol
- three class III antiarrythmics?
-
Sotalol
Ibutilide
Amiodarone - why is amiodarone considered safe in heart failure patients?
-
1. little negative inotropic activity
2. low proarrythmic activity -
effect of amiodarone on:
1. repolarization time
2. SA node and ectopic automaticity
3. phase 0 -
1. marked increase (blocks K+ channels)
2. decreases
3. little effect - what two things are notable about the kinetics of amiodarone?
-
1. longest 1/2 life drug known (~3/4 yr. to reach steady state)
2. 100% liver metabolism - notable side effects of amiodarone? (4)
-
1. corneal microdeposits
2. photosensitivity
3. blue-gray skin
4. pulmonary fibrosis - ECG effects of amiodarone?
-
1. prolonged PR interval
2. prolonged QRS duration
3. MARKEDLY prolonged QT interval
4. sinus bradycardia - the prolonged PR interval can be attributed to what type of action of amiodarone?
- beta blocker and calcium channel blocker effects
- the markedly prolonged QT interval can be attributed to what type of action of amiodarone?
- blockage of K+ channels
- the sinus bradycardia can be attributed to what type of action of amiodarone?
- BB and CCB effects
- IV amiodarone can convert a-fib to what rythm?
- normal sinus rythm
- other indications of amiodarone?
-
preventing recurrences of:
supraventricular a-fib
ventricular tachycardia
ventricular fibrillation
*BEST ORAL ANTIARRYTHMIC* -
effect of Sotalol on:
1. HR and AV conduction
2. repolarization and AP duration
3. Na+ channels -
1. decreases (has BB activity)
2. prolongs (has K+ blocking activity)
3. no effect on NA+ channels - ECG effects of sotalol?
-
1. sinus bradycardia
2. prolonged PR interval
3. prolonged QT interval - indications of sotalol? (2)
-
1. prevention of a-fib recurrences
2. oral tx. of life threatning ventricular arrythmias (although ICD is tx. of choice) - which class III antiarrythmic is a pure K+ channel blocker? (2)
-
Ibutilide
Dofetilide -
effects of ibutilide on:
1. repolarizaton
2. refractory period -
1. prolongs
2. increases - side effects of pure K+ channel blockers?
- prolonged QT interval - could result in Torsade de pointes
- indications for ibutilide?
- recent or new a-fib/flutter
- advantage of using dofetilide?
- safe in CHF and patients with a low EF.
- class IV agents (CCBs) are most effective in which type of cardiac fiber?
- slow fibers (SA and AVnodes)- therefore they interfere with automaticity, conduction, contractility
- inotropic effect of CCBs?
- negative inotropes
- vascular effects of CCBs?
- coronary and peripheral vasodilation
- ECG changes seen with CCB use? (2)
-
1. prolonged PR interval
2. bradycardia - two indications for CCBs in arrythmia treatment?
-
1. paroxysmal atrial tachycardia
2. rate control in a-flutter/fib - adenosine is the drug of choice for?
- paroxysmal supraventricular tachycardias (PSVT)
- what is notable about the 1/2 life of adenosine?
-
shortest (<10sec).
(advantage: side effects are short lived) - what are two ECG effects of adenosine?
-
1. prolonged PR
2. transient heart block - what is notable about the administration of adenosine?
-
rapid bolus IV followed by a saline flush
(this maximizes effectiveness) - digoxin has what effect on AV conduction?
-
reduces AV conduction
(vagal effect) - indications for digoxin?
- a-fib/flutter
- EKG effects of digoxin? (2)
-
1. prolonged PR
2. ST depression - treatment of choice for drug induced torsades de pointes?
- IV MgSO4
- which ECG change is most likely to precede development of Torsades de pointes?
- prolonged QT interval
- what happens physiologically during the QT interval?
- ventricular conduction and repolarization
- what would torsades de pointes look like on an ECG?
-
1. polymorphic ventricular tachycardia in the setting of prolonged QT intervals
2. look different in different leads (peaks are small in one and large in another) - besides prevention of CHD, what are we trying to prevent when treating a patient with very high triglyceride levels?
-
acute pancreatitis
(high TAG levels have been associated with increased pancreatitis risk) - what is the secondary target of therapy for patients with a serum TG >200mg/mL?
- Non-HDL cholesterol
- besides drug therapy, what else is recommended for lipid lowering?
-
diet
exercise
weight loss
control of CV risk factors - 4 first line lipid lowering agents?
-
1. HMG-CoA reductase inhibitors
2. Ezetimibe
3. Bile acid sequestrants
4. Niacin - fibric acids are used to alter what levels?
-
lower TG
raise HDL
(no effect on LDL) - MOA of bile acid binding resins?
-
*bind intestinal bile acids - causes increased synthesis of bile acids from liver cholesterol
*also causes upregulation of LDL receptors (compensatory) - what is notable about the adverse effects of bile acid binding resins?
- poorly tolerated: up to 50% stop because of GI side effects
- why should we advise the patient to take multivitamins while on bile sequestrants?
- these drugs decrease the absorption of fat soluble vitamins (A, D, E, K)
- effects of ezetimibe on LDL and TC?
- lowers both
- MOA of ezetimibe?
-
1. selective inhibitor of cholesterol absorption (active near brush border of small intestine/blocks absorption here)
2. decreases hepatic cholesterol stores, resulting in a compensatory upregulation of LDL receptors and increased clearance of LDL from the blood. - is ezetimibe more beneficial alone or in combination with other agents?
- more beneficial when used in combination with statins
-
effects of niacin on:
1. LDL
2. TG
3. HDL -
1. lowers
2. lowers
3. increases - MOA of niacin decreasing LDL?
- inhibits hepatic production and secretion of VLDL
- MOA of niacin decreasing TG?
- increased clearance of VLDL by lipoprotien
- niacin: MOA of increase in HDL?
- decreased cholesterol catabolism
- adverse effects of niacin?
-
high intolerance rate >50%
1. skin flushing/warmth
2. headache
3. GI
4. myopathy (increases CPK)
5. increased hepatitis risk - why should niacin never be used in pts with gout?
- niacin increases the levels of uric acid
- which two drug classes have rhabdomyolysis as an adverse effect?
-
niacin
statins - statins are the best agents to lower LDL. By how much percent can they lower it?
- 18-60%
- MOA of statins?
-
1. competitive inhibitors of HMG-CoA reductase (needed for cholesteral synthesis from HMG-CoA)
2. this decreases cholesterol synthesis in the liver
3. compensatory upregulation of hepatic LDL receptors resulting in increased clearance of LDL from blood - which statin is responsible for the highest % of LDL lowering?
- atorvastatin
-
define:
1. myopathy
2. myalgia
3. myositis
4. Rhabdomyolysis -
1. any disease of muscles
2. muscle ache or weakness w/o CPK elevation
3. muscle ache or weakness with increased CPK
4. muscle symptoms with marked CPK elevation and SCr elevation - urinary symptoms of rhabdomyolysis?
-
brown urine
urinary myoglobin - possible complication of rhabdomyolysis?
- renal failure
- which 3 statins are metabolized by the CYP3A4?
-
lovastatin
simvastatin
atorvastatin - which 3 statins have little or no CYP3A4 metabolism?
-
fluvastatin
pravastatin
rosuvastatin - which 2 drugs are combined and sold as Vytorin? (Zetia/Zocor)
-
ezetimibe and simvastatin
(can lower LDL up to 60%) - gemfibrozil and feofibrate belong to which drug class?
- fibric acids
- MOA of fibric acids?
- increase lipoprotein lipase activity (thereby increasing TG clearance)
-
effect of fibric acids on:
1. HDL
2. LDL -
1. elevates HDL
2. little or no effect on LDL - indication for fibric acid treatment?
- hypertriglyceridemia
- notable adverse effects of fibric acid? (3)
-
1. myopathy
2. increase in liver function enzymes
3. cholesterol gallstones - drug interactions with fibric acid? (2)
-
1. statins, niacin (may increase myopathy)
2. warfarin - what is the LDL treatment goal for a patient with established atherosclerosis?
- <100
- what is the treatment plan for a patient with established atherosclerosis?
-
2-3 agents
low doses
bile acid sequestrants considered the cornerstone - which bile acid sequestrant has the lowest GI side effects?
- colesevelam (Welchol)
- combining statins with either niacin or fibrates increases the risk of? (2)
-
1. hepatitis
2. myopathy - what is the LDL treatment goal for a patient that is very high risk or has DM?
- <70
- non-pharmacologic ways to increase HDL? (3)
-
1. weight loss
2. exercise
3. smoking cessation - pharmacologic ways to increase HDL?
-
1. statins
2. fibrates
3. niacin - two new therapies currently being studied that raise HDL?
-
1. CETP (cholesterol ester transfer protein)inhibitor
2. IV synthetic HDL (apoA-I Milano) - what is torcetrapib?
-
CETP inhibitor plus atorvastatin
(in clinical trials) - definition of varicose veins?
- abnormally distended, lengthened and tortuous veins that have increased intraluminal pressure
- what is the most common place varicose veins are seen?
- superficial veins of leg (saphenous)
- two other etiologies of varices?
-
hemorrhoids
esophageal varices
both due to portal hypertension - predisposing factors to varicose veins? (6)
-
1. old age (>50)
2. heredity
3. posture
4. obesity
5. obstruction
6. pregnancy - complications of varicose veins (4)
-
1. stasis dermatitis
2. ulcers (poorly healing)
3. thrombosis (or DVT if in deep veins)
4. vascular calcification - what is the triad of factors that predispose a person to thrombophlebitis?
-
1. stasis (HF, bedrest)
2. hypercoagulable state (ie. pregnancy)
3. endothelial injury (trauma, regional inflammation) - most common location of thrombophlebitis?
- deep leg and pelvic veins
- clinical sign of thrombophlebitis?
-
Homan's sign
(pain on squeezing leg or pain on forced dorsiflexion of foot) - thrombophlebitis carries a risk of?
- embolism
- what is phlegmasia alba dolens? (milk leg)
- iliofemoral venous thrombosis with lymphatic obstruction (seen in late pregnancy and early postpartum)
- what is the clinical presentation of lymphangitis?
-
subcutaneous streaks and distal lymphadenopathy
(lymph is draining bacterial and inflammatory factors) -
give an example of something that could cause the following lymphatic obstructions by the methods listed:
1. scarring
2. surgical
3. tumor obstruction
4. parasites -
1. radiation
2. post lymphadenectomy
3. Peau d'orange in breast CA
4. filariasis (leads to elephantiasis) - what is a granuloma gravidarum?
- a lobular capillary hemangioma appearing in the oral cavity during pregnancy
- describe a glomus tumor and where it would be found
- painful tumor of glomus body cells usually seen in the distal digits.
- what are telangectiasias?
- focal abnormally dilated small vessels, skin and mucous membranes
- what is Nevus flammeus (a type of telangectasia)
-
aka. birthmark
(includes port wine stains and leptominingeal angiomas) -
what is a spider telangectasia?
associations? - small arteriovenous communications associated with hyperestrinism, pregnancy, cirrhosis
- heredity of Osler-Weber-Rendu syndrome?
- autosomal dominant
- what is osler-weber-rendu syndrome?
- small aneurysmal telangectasias of skin and mucous membranes (lips, oral cavity, GI, GU, resp. tract)
- what is risky about osler-weber-rendu syndrome?
- may hemorrhage
- which disease is associated with AIDS and simulates Kaposi's sarcoma?
- Bacillary angiomatosis
- organism causing bacillary angiomatosis?
- Bartonella
-
which vascular tumor am I?
-low grade malignant
-rare
-may involve skin, lung, spleen, liver
-epithelioid and spindle cell forms present - hemangioendothelioma
-
which vascular tumor am I?
-rare
-associated with exposure to arsenic, PVCs, thorotrast
-malignancy of endothelial cells
-soft red nodules, may be ecchymosis like - angiosarcoma
- what are the four types of kaposi's sarcoma?
-
1. classic KS
2. african KS
3. transplant-associated KS
4. AIDS associated KS - the AIDS associated KS is associated with?
-
human herpesvirus-8
(HHV-8) -
three lymphatic tumors are as follows:
1. capillary lymphangioma
2. cavernous lymphangioma
3. lymphangiosarcoma
which one is malignant? -
lymphangiosarcoma is malignant
(usually arises in the setting of chronic lymphedema) - lymphatic tumor that is seen as a mass lesion in the neck or axilla of children is called?
- cavernous lymphangioma
- what is the most common primary tumor of the heart?
- cardiac myxoma
- is a cardiac myxoma benign or malignant?
- benign
- where do most cardiac myxomas occur?
- left atrium
- what makes a cardiac myxoma "serious"?
-
if it
obstructs a valve
-or-
embolizes - what is the most common benign cardiac tumor in infants and children?
- rhabdomyoma
- which disease is associated with a rhabdomyoma?
- tuberous sclerosis
- which is involved more in a rhabdomyoma: atria or ventricles?
- ventricles more than atria
- which tumor is a benign, papillary hemartoma found on cardiac valves?
- fibroelastoma
- danger of a fibroelastoma?
- may embolize
- which cancers often metastasize to the heart? (5)
-
1. lung
2. breast
3. melanoma
4. leukemia
5. lymphoma - when in fetal development would an abnormality occur to cause congenital heart disease?
- weeks 3-8
- 5% of congenital heart disease is associated with a chromosomal abnormality - what 2 have a very strong association?
-
Down's syndrome
Turner's syndrome - which congenital disease is known to cause cardiac defects?
- rubella
- which drugs are strongly linked to congenital heart disease? (5)
-
1. thalidomide
2. phenytoin
3. amphetamines
4. ETOH
5. lithium - which two congenital heart diseases make up ~50% of the total?
-
1. ventricular septal defects
2. atrial septal defects - s/s of a right to left shunt?
- initial cyanosis, polycythemia, clubbing
- s/s of a left to right shunt?
-
initially non-cyanotic
then pulmonary HTN develops and there is a late shunt reversal - which defect is associated with Turner's syndrome?
- pre-ductal aortic stenosis
- two types of aortic stenosis?
-
1. post-ductal (adult type)
2. pre-ductal (infantile type) - compensation for post ductal aortic stenosis?
-
collateral vessels develop to bypass stenosis
-internal mammary a.
- intercostals
get notching of ribs - hallmark sign of preductal aortic stenosis?
- lower 1/2 of body cyanotic
- what is ebstein's anomaly?
- tricuspid valve displacement into right ventricle - results in TV insufficiency
- which congenital defect has an association with maternal DM?
- transposition of the great arteries
-
in TGA:
1. what is the RV attached to?
2. what is the LV attached to? -
1. aorta
2. pulmonary a. -
1. what other defect is normally present with a child that has TGA?
2. why? -
1. PDA, ASD or VSD
2. without it there would be two separate circulatory systems (incompatible with life) - what can we give pharmaceutically to keep the ductus arteriosus open?
- prostaglandins
- tetrology of Fallot is a ___ to __ shunt
- Right to Left shunt