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223 Cards in this Set
- Front
- Back
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Fanconi's
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expired tetracycline
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inside carotid sheath
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VAN
internal jugular commmon carotid artery vagus nerve (posterior) |
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artery for the posterior left ventricle
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circumflex
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artery for the apex
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LAD
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artery for anterior interventricular septum
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LAD
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supply to SA and AV nodes
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RCA
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right dominant heart means
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PD supplies the inferior left ventricle from teh RCA (left would be CFX)
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most common site of coronary artery occlusion
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LAD
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effect of multiple myeloma on viscosity
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increases it
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a wave
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atrial contraction
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c wave
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RV contraction (with triCuspid valve bulging into atrium)
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v wave
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increased atrial pressuredue to filling against closed tricuspid valve
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wide splitting
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pulmonic stenosis
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fixed splitting
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ASD
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paradoxical splitting
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aortic stenosis
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harsh holocystolic murmure
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VSD
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phase O in SA/AV vs ventricular
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SA/AV: Calcium
V: Sodium |
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pleateau phase in SA/AV
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absent
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what accounts for the automaticity of the SA/AV nodes
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phase 4 If Na channles
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what about the SA/AV node determiens rate
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slope of phase 4
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U wave causes
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hypokalemia
bradycardia |
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delta wave
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WPW
reentrant supraventricular tachycardy accessory conduction pathway from atria to ventricle |
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sawtooth ECG
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atrial flutter
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no discrete P waves
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a fib
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prolonged PR
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1st degree AV block
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P wave not followed by QRS
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Mobitz type I 2nd degree block
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dropped beats not preceded by a change int he length of the PR interval
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Mobitz II 2nd degree block
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atria and ventricles beat independently
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3rd degree, complete block
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right to left shunt etiologies
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"blue babies"
the 5 Ts TOF Transposition of the great vessels Truncus arteriosus Tricuspid atresia Total anomalous pulmonary venous return |
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clubbing and polycythemia
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Eisenmenger's
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Tetralogy of Fallot
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PROVe
Pulmonary stenosis RVH Overriding aorta VSD |
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boot shaped heart
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TOF, due to RVH
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anterosuperior desplacement of the infundibular septum
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TOF
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med to keep a shunt open
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alprostadil
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med to close a shunt
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indomethacin
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22q11
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TOF
truncus arteriosis |
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cardiac anomalies associated with downs
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ASD, VSD, AV septal
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congenitals associated with rubella
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Septal
PDA pulmonary artery stenosis |
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congenital anomaly in offspring of diabetic mother
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transposition of great vessels
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calcification in the media of the arteries, especially radial or ulnar
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Monckeberg arteriosclerosis
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hyaline thickening of small arteries in essential hypertension
onion skinning in malignant hypertension |
Arteriolosclerosis
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fibrous plaques and atheromas in teh intima of arteries
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atherosclerosis
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angina on exertion
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stable angina
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angina at rest
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Prinzmetl's
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angina secondary to coronary artery spasm
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Prinzmetl's
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worsening chest pain
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unstable angina
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organs that get pale infarcts
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heart
kidney (single blood supply) |
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stage after MI when there are a lot of neutrophils
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5-10 days
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how long after MI does troponin go up
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4 hours
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ST elevation
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transmural infarct
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ST depression
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subendocardial infarct
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pathological Q waves
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transmural infarct
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when does Dressler's happen
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several weeks after MI
autoimmune phenomenon resulting in fibriinous pericarditis |
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cardiomyopathy associated wtih alcohol abuse
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dilated
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cardiomyopathy associated with beriberi
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dilated
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cardiomyopathy associated wtih Coxsackie B
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dilated
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cardiomyopathy associated wtih cocaine
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dilated
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cardiomyopathy associated wtih chagas
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dilated
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cardiomyopathy associated wtih doxorubicin
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dilated
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cardiomyopathy associated wtih genetic cause
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hypertrophic
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cardiomyopathy associated wtih genetic cause
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hypertrophic
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verrucous vegetations on both sides of heart valve
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Libman-Sacks endocarditis
associated with lupus |
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endocarditis in lupus
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libman sacks
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erythema marginatum
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rheumatic heart disease
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granuloma with giant cell
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Aschoff bodies
rheumatic heart disease |
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activated histiocytes
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Anitschkow's cells in rheumatic heart disease
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migratory polyarthritis
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rheumatic heart disease
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electrical alternans (beat to beat alternation fo QRS complex height)
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cardiac tamponade
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pulsus paradoxus/ Kussmauls' pulse
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TACO P
severe cardiac tambonade asthma obstructive sleep apnea pericarditis croup |
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serous pricarditis
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Very SeRioUs
SLE RA viral infetion uremia |
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Fibrinous pericarditis
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a fibrinous RUM
uremia Dressler's syndrome post MI rheumatic fever |
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hemorrhagic pericarditis
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TB
malignancy (e.g., melanoma) |
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dilatation of aorta nd valve ring
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syphilis
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"ball valve" obstruction in left atrium
associated with multiple syncopal episodes |
cardiac myxoma
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most frequent cardiac tumor in adults
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myxoma
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most frequent cardiac tumor in kids
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rhabdomyoma
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rhabdomyoma associated with
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tuberous sclerosis
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most common mets in heart
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melanoma lymphoma
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nosebleeds and skin discolorations
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Osler Weber Rendu (hereditary hemorrhagic telangiectasia)
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Raynaud's associations
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SLE
CREST mised connective tissue disease |
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necrotizing vasculitis with necrotizing granulomas (lung and kidney)
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Wegeners
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performation fo nasal septum
chronic sinusitis, otitis media, mastoiditis, cough, dyspena hemoptysis hematuria |
Wegeners
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tx for Wegeners
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cyclophosphamide and corticosteroids
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necrotizing vaslulitis without granulomas
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microscopic polyangiitis
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granulomatous vasculitis with eosinophilia
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Churg Strauss
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pANCA
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microscopic polyangitis and
Churg-Strauss |
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leptomeningeal angiomatosis
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Sturge-Weber
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childhood systemic vasculitis following URI
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Henoch Schonlein
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intermittend claudication
superficial nodular phlebitis Raynaud's |
Buerger
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treatment for Buergers
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stop smoking
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vessels affected in Kawasaki
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small and medium
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necrotizing arteritis of medium arteries vs small
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PAN is medium; Wegeners (Wee Wegners) is small.
PAN has no ANCA association. Wegeners has c-ANCA |
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granulomatous thickening of aortic arch
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Takayasu
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arthritis
night sweats myalgia skin nodules ocular distrubances weak pulses |
Takayasu
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unilateral headache
jaw claudication imparied vision |
temporal arteritis
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rx with severe rebound hypertension
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clonidine
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rx with positive coomb's test
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methyldopa
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rx with ototoxicity
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loop diuretics
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rx with orthostatic and exercise hypotension
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guanethidine
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rx with first dose orthostatic hypotension
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prazosin
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heart meds that can cause impotence
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beta blockers
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drug that can cause lupus like syndrome
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hydralazine
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vasodilater that can cause hypertrichosis
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minoxidil
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vasodilatro that can cause AV block
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verapamil
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vasodilatr that can cause cyanide toxicity
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nitroprusside
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antihypertensive that can ause fetal renal toxicity
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losartan
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rx for Prinzmetal
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calcium channel blockers
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among Calcium channel blockers, which is most effective on vasculature vs heart
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vascular smooth muscle:
nifedibpin>diltiazem> verapamil (opposite for heart) |
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Monday disease with a vasodilator
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nitroglycerin, isorbidide dinaitrate
workers get used to the effects during their work week, lose that tolerance over the weekend, and then get tachycardia, dizziness, headache on Monday |
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tx for malignant htn
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Drugs For Nefarious HTN
Nitroprusside fenoldapam diazoxide (opens K+) |
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combo for antianginal therapy
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nitrate
beta blocker |
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what drug tastes really really bade
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bile acid resins
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lipid lowering drug that can cause red flushed face
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niacin
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MOA of niacin
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inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation |
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blurry yellow vision
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digoxin
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quinidine decreases its clearance
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digoxin
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causes cinchonism
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quinidine
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causes a reversible SLE-like syndrome
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procainamide
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increases AP duration
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Class IA (papa bear)
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decreases AP duration
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class 1B (mama bear)
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no effect on AP duration
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Class IC (just right)
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check PFTs LFTs and TFTs when using this drug
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amiodarone
pulmonary fibrosis hepatotoxicity hypo/hyper thyroidism |
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side effect of metoprolol
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dyslipidemia
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antiarrhythmic that can be used in WFW
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amiodarone
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rx that increase the QT inteval
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potassium channel blockers
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side effect of sotalol
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torsades
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action of adenosine
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K+ out of cells
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what is adenosine the DOC for
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diagnosing/abolisin AV nodal arrhythmias
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what do Ca channel blockers affect primarily
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AV nodal cells
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pregnant woman in 3rd trimester has orthostatic hypotension
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IVC compression
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patient with history of HTN has sudden sharp, tearin pain radiation ot the back
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mediastinal widening
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heard on right sternal border/aortic area
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systolic murmurs
- aortic stenosis - flow mumur |
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heard in pulmonic area
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systolic ejection murmur
- pulmonic stenosis - flow mumur (eg ASD) |
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heard in tricuspid area
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Tricuspid area
Pansystolic murmur - tricuspid regurg - VSD Diastolic murmur -tricuspid stenosis -ASD |
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heard in mitral area
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Systolic mumur
- mitral regurg Diastolic - mitral stenosis |
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what sustains increased cardiac output ininitial exercise? after prolonged?
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first, increased stroke volume
then, increased HR |
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effect of catecholamines on heart
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increased contractility by acting on Ca++ pump in SR
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mechanism of Digitalis' increase of contractility
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increases intracellular Na, resulting in increased Ca
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effect of acisdosis on contractility
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reduces it
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an effect of anxiety, exercise and pregnancy on the heart
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increased SV
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effect of increased blood volume on venous return curve
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up and to right
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effect of increased inotropy on CO curve curve
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up and steeper
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effect of increase TPR on cardiac function curves
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lowers the X, directly below intersection point
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where is mean systemic pressure on cardiac function curves
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where venous return crosses x axis
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what is it and where is it loudest: S1
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mitral and tricuspid valve closure
loudest at mitral area |
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what is it and where is it loudest: S2
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aortic and pulmonary valve closure
left sternal border |
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what is it and where is it loudest: S3
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increased filling pressures
more common in dilated ventricles |
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what is it and where is it loudest: S4
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atrial kick
high atrial pressure ventricular hypertrophy |
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why does S2 split
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aortic closes bfore pulmonic
(alphabetical order) |
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holosystolic, high pitched blowing murmur
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Mitral or tricuspid regurg
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late systolic murmur with midsystolic click? when is it loudest
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MP
loudest at S2 |
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blowing diastolic mumur
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aortic regurg
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what widesn pulse pressur
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chronic aortic regurg
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late diastolic rumbling murmur
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Mitral stenosis
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late diastolic murmur that gets louder with inspiration
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tricuspid stenosis
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continuous machine like murmur? when is it loudest
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PDA
S2 |
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holosystolic harsh sounding murmur. Where is it loudest
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VSD
tricuspid area |
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delta wave
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WPW
looks like an opening up of the QR, so that Q no longer dips below line and leans up towards R |
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What can WPW lead to
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supraventricular tachycardia
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progressive lengthening of the PR until a beat is dropped
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2nd degree block
Mobitz I |
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dropped beats not preceded by a change in length of PR interval
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2nd degree block
Mobitz II |
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effect of stimulation of alpha 1 receptors
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venous constriction, increasing CO
arteriolar constriction, increasing TPR |
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what do vagus and IX transmit to re increased BP
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medulla
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what do aortic arch and carotid sinus sense?
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carotid sinus senses increases and decreases in BP;
aortic responds only to increases in BP |
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when the afferets coming to the medulla fire less, what happens to the firing by the sympathetics? parasympathetics?
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increase sympathetics
decrease parasympathetics |
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how does carotid massage work?
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pressure on carotid artery
increaeses stretch increases afferent firing decreases efferent firing |
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what do peripheral chemoreceptors respond to
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decreases in oxygen
increases in carbon dioxide decreased pH |
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what do central chemoreceptors respond to
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changes in pH and PCO2 (not O2)
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What is responsible for the Cushing reaction
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central chemoreceptors
reaction: increased intracranial pressure constricts arterioles cerebral ischemia hypertension (sympathetic) and reflex bradycardia |
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Cusing triad
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hypertenion
bradycardia respiratory depression |
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which organ has a large arteriovenous O2 difference
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heart
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which organ gets the most CO
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liver
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causes of left to right shunts
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VSD
ASD PDA (which is in order of frequency) |
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which malformations, uncorrected, lead to Eisenmengers
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VSD, ASD, PDA
shunt gost to being a R-L shunt |
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notching of ribs
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coarctation of aorta
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what can keep a PDA open
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PGE
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what does corneual arcus indicated
|
hyperlipidemia
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what does a xanthoma indicate
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hyperlipidemia
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what does an atheroma indicate
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hyperlipidemia
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ipiestem arteries with calcification
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Monckeberg arteriolosclerosis
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hyaline thickining in essential HTN
onion skinning in malignant HTN |
arteriolosclerosis
|
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cystic medial necrosis
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Marfan's
aortic dissection |
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mediastinal widening
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emerginc aortic dissection
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what is diseases in atherosclerosis
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elastic arteries
large and medium sized muscular arteries |
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what initiates atherosclerosis
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endothelial cell dysfunction
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timeing of coagulative necrosis post MI
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18-24 hours
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when does neutrophil emigration
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4 hours, and goes on thru day 4
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when is risk for ventricular aneyrysm
|
7 weeks
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granulation tissue post MI
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5-10 days
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gross heart - when is there central yellow-brown softening post MI
|
10 days
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gross heart - when is there hyperemia post MI
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2-4 days
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gross heart - when is there dark mottling post MI? What stain is used
|
first day
tetrazolium |
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how long after MI does fibrinous pericarditis tend to happen
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3-5 days
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how long after MI does Dresslers tend to happen
|
several weeks
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what heart sound is loud in hypertrophic cardiomyopathy
|
S4
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tx for hypertrophic cardiomyopathy
|
beta blocker
verapamil |
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endomyocardial fibrosis with a prominent eosinophilic infiltrate
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Loffler's syndrome
restrictive cardiomyopathy |
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what kind of cardiomyopathy does hemochromatosis cause
|
restrictive or dilated
|
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what is the most reliable marker for HF
|
3rd heart sound!
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|
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hemosiderin laden macrophages in the lungs
|
LV failure
|
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what does dyspnea on exertion indicate
|
failure of LV output to increase during exercise
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what does PND indicate
|
LV failure
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what does pulmonary edema indicate
|
LV failure
|
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what does orthopnia indicate
|
exacerbated pulmonary vascular congestion
|
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what does ankle, sacral edema indicate
|
RV failure
|
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cardiac tumor in atria
obstruction in the LA multiple syncopal episodes |
myxoma
|
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arteriovenous malformation in small vessels.
looks like dilated capillary |
telangiectasi
|
|
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like Wegeners but lacks granulomas
pANCA |
Microscopic polyangiitis
|
|
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pANCA
|
Wegeners
Microscopic polyangiitis Churg STrauss |
|
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mechanism of Hydralazine
|
increases cGMP to induce smooth muscle rlaxation
A>V |
|
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mechanism of Minoxidil
|
K+ channel opener
|
|
|
mechanism of Nifedipien, verapamil, diltiazem
|
L type Calcium channel blockers
reduce muscle contractility |
|
|
mechanism of nitrolycerin, isosorbide dinitrate
|
release NO in smoth muscle, increase cGMP and smooth muslce relaxation
V>A |
|
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mechanism of diazoxide
|
K+ channel opener
|
|
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effect of Nitrates and beta-blockers on end diastolic volume
|
nitrates decrease
beta blockers increase |
|
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what are statins most effective at reducing
|
LDL
|
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what is Niacin most effective at doing
|
lowering LDLincreasing HDL
|
|
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which lipid lower agents can increase HDL
|
Niacin>statins and fibrates >bile acid resins
|
|
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which meds best lower triglycerides
|
fibrates
|
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toxicity of statins
|
increase LFTs
|
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toxicity of bile acid resins
|
tastes bad
decreased absorption of fat-soluble vitamins |
|
|
toxicity of fibrates
|
myositis
increased LFTs |
|
|
mechanism of cardiac glycosides
|
that is, Digoxin...
direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger/antiport so that the Ca++ levels rise |
