jdlevenson's version from 2015-06-21 03:00


Question Answer
Calcium efflux prior to relaxation is accomplished by(1) Ca ATPase (into SER), which re-sequesters Ca into the SR and (2) Na/Ca exchanger, a transmembrane protein (3:1) that does not require ATP.
Steps in cardiac muscle contraction
Depolarizaton of cell allows Ca+ in from extracellular fluid via voltage dependent Ca channels
Calcium that enters stimulates the RyR which then allows the release of Ca from the SR which is stored there (and gets put back there Ca ATPase) (Calcium mediated calcium release?)
Now a lot of calcium in cytoplasm diffuses through myofilament network and binds to Troponin C; tropomyosin is moved out of the way so that actin and myosin can interact and the myocardial cell then contracts
Calmodulin binds and activates Ca/ATPas whch removes Ca from.... (REVIEW in FA or elsewhere)
Question Answer
Pacemaking cells, how does AP happenDiastolic depolarization (during phase 4) due to sodium channels (slow, inward current) and then transient inward calcium current; once reaches threshold, opening of additional Ca is triggered and resulting increase in Ca influx begins phase 0.
Verapamil thus acts on which two parts of pace-making cellsPhase 0 and end of phase 4. Real decrease SA node firing and AV node conduction.
SA node has what stages4, 0, 3 vs. Ventricles has 4, 0, 1, 2, 3, 4
SA/ AV node, what are roles of Ca channelsT-type during Phase 4 open at -50 or so and allow Ca to enter cell which contributes to depolarization and then when it nears -40 or so L-type open which causes even more Ca to enter until threshold for Ap is reached, ie. Upstroke of Phase 0.
Cardiac myocytes differ from skeletal muscles in thatThey are electrically coupled to each other by gap junctions; Cardiac muscle AP has a plateau which is due to Ca influx and K efflux; myocyte contraction occurs due to Ca induced Ca release from SR; cardiac nodal cells fire spontaneously during diastole resulting in automaticity
In SA and AV node which channels confer automaticity?Na channels conductance increasing and with K+ make up funny current
How does sympathetic stimulation change funny currentIncreases chance that If channels are open
What increases HR at SA node? Decreases?Increased by sympathetic stimlation, cAMP, and catecholamines; decreased by adenosine and Ach
How do Adenosine and ACh slow automaticityAdenosine activates K+ channels and prolongs flow (countering Na+), making cell remain negative longer and also inhibits L-type Ca channels whereas ACh similarly opens specific K+ channels and delay Ca channels


Question Answer
Why does MAP remain fairly stable during exerciseAdaptive decrease in SVR from exercising muscle releasing local vasodilatory factors including adenosine, potassium, ATP, CO2 and lactate.
Exercise stimulates sympathetics and leads to what changesA. Increased CO, B. Contraction of the venous system leading to increased VR to the heart, C. Contraction of arterioles in all tissues except the actively working muscles, shunting blood towards exercising muscle** (receives up to 85% of cardiac output during peridods of strenuous activity but that’s also due to vasodilation)


Question Answer
Skeletal muscleDepolarization of cell membrane triggers opening of L-type Ca channels within the myocyte’s T-Tubule system; this directly results – direct, ie through physical interactions – in the opening of RyR1 calcium channels present within the SR which then leads to a subsequent release in Ca from the intracellular stores of SR; “L-Type channel RyR mechanical coupling”; no significant flux of calcium across the L-type Ca channel; skeletal muscle does NOT require Ca to enter from the extracellular space to cause calcium release within the cell; so CCBs would have no effect; calcium released from SR then binds troponin C allowing actin and myosin to bind; ATP bound to myosin is then hydrolyzed and contraction occurs (REVIEW)
Cardiac muscleL-type Channel RyR mechanical coupling does NOT exist; instead—depolarization causes L-type Ca channels to open and allow influx of extracellular Ca; this Ca binds to and activates RyR2 channels by a mechanism known as Calcium induced Calcium release when then moves Ca out of SR; contraction then occurs just as in skeletal muscle (binds troponin, actin and myosin then bind, myosin ATP release and contraction)
Smooth muscleCa enters cell from extracellular space during depolarization through voltage gated L-type Ca channels and then causes a release of Ca from SR via a calcium dependent RyR calcium channel in SR; Calcium then binds CALMODULIN (no troponin in smooth muscle cells) which activates myosin light chain kinase and that leads to phosphorylation of myosin which allows it to bind to actin and cause muscle contraction


Question Answer
Isovolumetric contractionMitral valve closed; LV contracting and increasing its pressure to point over superseding pressusre in aorta (at which point aortic valve will open)
Isovolumetric relaxationAortic valve now closed and mitral valve still closed and so ventricle just relaxes.
When left ventricular pressure equals systolic maximum blood pressureAortic valve closes.


Question Answer
IDA caused by overt or occult blood loss. Menorrhagia + epitaxis (recurrent) -> VWD, since evidence of qualitative defect in PLT binding and aggregation.
VWD diseaseEasy bleeding from skin and mucosal sites including gingiva, nasal mucosa, GI and endometrium.
Why does antiphospholipid syndrome cause spontaneous abortionsHypercoagulable state increasing risk of thrombosis.
VWD travels withHemophilia A. Since vWF protects Factor 8 from degradation.
Mucocutaneous pleadingThrombocytopenia, caused by things like immune-mediated thrombocytopenia which produces isolated thrombocyte and episodic bleeding.
Normal PLT levels but prolonged bleeding timeVWD.
Prostacyclin is synthesized fromProstglandin H2 by prostacyclin synthase in vascular endothelial cells. It vasodilates, inhibits PLT aggregation and increases vascular permeability as well as stimulates leukocyte chemotaxis.
Prostacyclin opposesTXA2. Lost when endothelial injury predisposing to thrombi and hemostasis.
Kalilkrein actionConverts Kininogen to Bradykinin
Migratory thrombophlebitis/hypercoagulability is associated with adenocarcinomas of pancreas, colon and lung becauseCancers produce thromboplastin like substance capable of causing chronic intravascular coagulations, disseminated and migrate.
Raynaud’s phenomenon does or does not occur in presence of coagulable stateDOES NOT.
Raynaud’s phenomenon treatmentCCB


Question Answer
Basket weaveFragmented elastic tissue due to medial degeneration
Cystic medial degenerationBasket weave/ fragemented elastic tissue + separation of elastic and fibromuscular components of tunica media by small, cleft-like spaces that become filled with amorphous matrix
Extracellular matrix microfibrils formed mainly fromFibrillin-1, scaffolding for elastic fibers
Cystic medial degeneration a/wMarfans and aortic aneurysms and dissections
Medial degeneration seen inYounger patients with Marfan
B-amino...chemical in sweet peas causes angiolathyrism, change in elasticity of aorta, mimicsMyxomatous degeneration of cystial medial deg in marfan by inhibiting lysyl oxidase.
What maintains elsastic lamina and integrity of aortaLysyl oxidase which cross links Elastic and Collagen
Marfan leads to 2 cardiovascular lesionsMVP and cystic medial degeneration of the aorta. Aortic dissection is cause of death in 30-45% of patients with Marfan followed by cardiac failure. Average age of death is 30-40 years.
Hereditary hemorrhagic telangiectasia presentationSkin and mucosal telangiectasias and recurrent severe nosebleeds*** and sometimes GI bleed and hematuria. Also knowns as Osler-Weber-Rendu, AD*. Mucosal may mean lips, oronasopharynx, resp tract, GI, urinary tract.
Tuberous sclerosis manofests not as angiomatous lesion butCortical and subependymal HAMARTOMAS. Cutaneous angiofibromas, visceral cysts and cardiac renal angiomyolipoma, rhabdomyomas and then cysts – kidney, liver, pancreas, CNS.
Major complication of Tuberous sclerosisSeizures.
Capillary hemangioblastomas in retina and or cerebellum and or neoplasms in kidney liver and pancreas and increased risk of RCC** bilaterally**VHL
Sturge-WeberCutaneous facial angiomas + leptomeningeal anigiomas + mental retardation, seizures, hemiplegia, skull radiopacities, tram-track calcifications**
Bilatearl cranial nerve 8 schwannomas and multiple meningiomasNF2
Peripheral, not central, nervous system tumor syndrome with neurofibromas, optic nerve gliomas, lisch nodules (pigmented noduels of iris) and café au lait spotsNF1 Von Reckling.