BVI, WIII

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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

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