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Block 4 > Cell Bio > Flashcards

Cell Bio Flashcards

1
Q

heart vs aa vs arterioles vs capillaries vs venules & vv

A

pump generating pressure to drive blood thru vessels vs thick walled elastic & sm mm carrying O2-blood away from heart w/ high pressure & Q vs autonomic sm mm w/ highest resistance, a1 adrenergic receptors on skin/renal circ, B2 adrenergic receptors on skel mm vs thin single layered endothel vessels w/ largest cross sectional/surface area b/w aa/vv to exchange nutrients & waste vs thin walled carry deO2-blood to heart w/ low pressure & Q, highest blood vol; a1 adrenergic receptors for symph

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2
Q

pulm vs systemic circ. how do lipid vs water soluble substances cross capillaries?

A

RV pumps blood thru lungs for C/O2 exchange to LV vs LV pumps O2-blood to body & pumps deO2-blood to RV. C/O2 diffuse across vs ions go thru clefts or pores/fenestrated capillaries

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3
Q

myocardium = b/w endo/epicardium & contains contractile & conducting cells. what fibers & energy does it use?

A

Type I fibers –> [O] metab, mod ctx vel, low fatiguability; aerobic metab = main energy src but can use anaerobic glycolysis

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4
Q

which macromolec = used to make ATP in normoxia vs hypoxia vs fasting? when does ATP lvls dec?

A

fat > carb (pyru from glycolysis) > protein vs glycogen vs ketone bodies. insuff O2, ATP use/demand = unbal

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5
Q

FA B[O] vs glu [O] energy requirements

A

gives 60-90% of nrg, require more O2, make lots of ATP vs gives 20-40% of nrg, more O2 efficient, make modest amt of ATP

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6
Q

describe GLUT4

A

for adipose, skel, cardiac mm. insulin & myocardial ischemia stim GLUT4 –> inc glu uptake. no insulin –> heart takes fat, other mm don’t take glu & leave it for other tissue w/ high affinity uptake

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7
Q

how does heart use lactate to make ATP?

A

from RBC b/c no mito –> pyru converted to lac via LDH. from skel mm undergoing intense exer –> glu [O] –> pyru > mito –> pyru converted to lac via LDH. heart takes lac –> pyru –> acetyl CoA –> TCA –> [O] phosphorylation –> ATP

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8
Q

how does heart use ketone bodies to make ATP?

A

from excess acetyl CoA d/t liver’s FA [O]; when carbs or insulin = low –> no glu uptake –> blood pH dec –> ketoacidosis. heart still prefers fat –> leaves ketone bodies for brain

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9
Q

how does angina pectoris/myocardial ischemia/CAD affect ATP?

A

less O2 –> ischemia –> greater reliance in anaerobic glycolysis –> inc GLUT4 –> lots of glu to pyru to lac –> lactic acidosis

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10
Q

how does MI affect ATP?

A

dec blood flow to regions of heart –> slow & ineffic O2 diffusion to affected area –> ischemia –> inc GLUT4 –> glycolysis –> AMP converted to adenosine that leaves cardiac myocyte –> coronary artery vasodil

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11
Q

seq of cardiac AP

A

SA node initiates AP –> atrial internodal tracts & atria carry AP from R to LA –> AP conducts to AV node, slow conduxn vel –> AP conducts to His-Purkinje of ventricles, fast conduxn vel

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12
Q

what’s conduxn vel and why is it impt for heart?

A

speed at which AP propagate. slowest at AV node (1/2 of total conduxn time) to ensure ventricles don’t activate too early & ctx little blood to atria; fastest at Purkinje to ensure ventricles activate quickly to fully eject blood

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13
Q

describe latent pacemakers. overdrive suppression? what happens if AV node can’t generate?

A

SA node = THE pacemaker cells w/ fastest rate of phase 4 depol => ctrls HR. AV node/His/Purkinje = latent pacemakers –> only ctrl HR when SA node fails (but slower HR) –> become THE pacemaker => ectopic focus. suppress latent pacemakers; respond to SA node in nml conditions. heart beat slows or skips -> can’t ctx all blood out of chambers

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14
Q

ARP vs ERP vs RRP vs SNP. what’s excitability?

A

can’t make more AP vs can’t make more conducted AP but some Na+ channels recovered vs can make 2nd AP but greater-than-nml stimulus required, more Na+ channels recovered; abnl config & short plateau vs cells = more excitable than nml. amt of inward current required to bring myocardiocytes to threshold potential

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15
Q

symph vs parasymph effects on HR

A

cardiac symph nn release NE –> inc HR/ctx, vasoconstrict. R cardiac n dominates SA node affecting HR/chronotropicity. L cardiac n dominates LV –> affecting ctx/inotropicity vs vagus nn release Ach –> dec HR. R vagus n dominates SA node affecting HR/chronotropicity. L vagus n dominates AV node affecting condxn vel/dromotropicity

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16
Q

quick summary of excitation/ctx coupling. when catecholamines bind to B receptors -> phosphorylation of L type Ca2+ channels vs RYR vs PLN vs TnI do what?

A

depol -> Ca2+ release for SR -> myocyte ctx (systole) -> ca2+ uptake into SR -> myocyte relax (diastole). stim CICR vs inc Ca2+ release from sR vs stim sERCA -> inc Ca2+ uptake -> faster relaxation vs dec sensitivity to ctx -> inc relax

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17
Q

sarcomeres = basic contractile unit of myocardiocytes. what filaments do they contain? which are responsible for active vs passive tension?

A

actin, myosin, troponin (T/I/C), tropomyosin. contractile components/actin & myosin vs elastic springy titin that ctrls the Z disc

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18
Q

quick summary of sliding filament model

A
  1. myosin = attached to actin => cross bridge
  2. ATP binds to myosin head –> myosin unbinds to actin => released state
  3. ATP hydrolyzed –> myosin head in resting position
  4. myosin has high affinity for actin again & binds to new actin => cross bridge
  5. P released –> myosin head does power stroke & slide against actin => power stroke state
  6. ADP released –> myosin still bound to actin => cross bridge
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19
Q

ultracellular structure of myocardiocyte: mito vs T tubule vs SR

A

lots of em b/c aerob [O] phosphorylation vs invagination at Z line carrying AP into cell interior; in ventricle > atria vs smaller tubules closer to contractile elements to store & release Ca2+ for excit/ctx coupling; form dyads w/ T tubules

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20
Q

Ca2+ stimulates crossbridge formation and force generation. More Ca2+ more force. what’s preload?

A

blood fills in ventricles in diastole –> stretches mm fiber like a spring passively (connective tissue) –> inc mm fiber/sarc length –> inc PE. total force of ctx + preload PE gives greater pumping power than just ctx alone –> inc SV –> inc CO. preload depends on indirect LVEDV/P

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21
Q

strength of myocardial ctx = determined by?

A

EC coupling & initial length of sarcomeres -> determines extent of actin/myosin cross bridges but intracell Ca2+/ctxility & preload determine how many crossbridges actually form

22
Q

def & eqn for SV vs ejection frxn vs CO. pos ino cause what to ctx & ejection frxn?

A

vol of blood ejected by ventricle ea beat; EDV-ESV vs frxn of EDV eject in ea SV; SV/EDV vs total vol of blood ejected ea time; SV*HR. inc ctxility -> inc ejection frxn; neg ino dec both

23
Q

Frank starling relationship of heart. what does steady state indicate? know how to read starling curves

A

inc venous return/blood filling ventricle –> more preload –> more SV –> more CO. CO = venous return. Lec 4, slides 10-11

24
Q

what’s afterload?

A

force ventricles must use to eject blood out; more afterload –> more aortic pressure –> less SV/CO –> more ESV leftover

25
Q

what do AV valves do? when do they open vs close?

A

prevent backflow into atria when ventricles ctx; in diastole when blood fills ventricle then atrial systole pushes in additional blood to ventricles vs when ventricles pump blood out

26
Q

what semilunar valves do in systole vs diastole?

A

open d/t intraventricular pressure > aortic & pulm pressure vs ventricles relax -> intraventricular pressure falls. R pulm valve, L aortic valve

27
Q

s1 vs s2 heart sounds

A

LUB dub; low rumble, mitral & tricuspid valves close; start of ventricular systole; longest & loudest vs lub DUB; high pitch/freq, semilunar valves close; end of ventricular systole; pulm or systemic HTN

28
Q

Law of LaPlace + eqn. concentric vs eccentric hypertrophy

A

pressure directly related to tension & wall thickness, inversely related to radius –> P = 2HT/r. HTN of aortic stenosis –> more afterload –> stiff/thicker wall + small chamber –> small preload vs mitral regurg –> less blood outflow/SV –> thin wall, big chamber –> more preload

29
Q

systolic vs diastolic failure

A

impaired ventricular ctxility –> dec SV & ejection frxn –> inc ESV, dec EDV, inc LV/AP b/c dil ventricle can’t push out all blood SV vs impaired ventricular filling –> inc LAP –> inc pulm venous pressure –> pulm edema –> inc RV afterload –> inc RAP –> periph edema

30
Q

1st vs 2nd vs 3rd degree heart block. afib vs vfib

A

prolonged PR –> longer AV conduxn vs dropped QRs –> frxn of AV conduxn vs no atrial impulses to ventricle. no P waves, irreg f waves vs irreg, continuous, uncoordinated twitching of ventricles, LOC in seconds

31
Q

factors that cause vasoconstrict vs vasodil

A

symph, adrenal NE, angiotensin II, vasopressin vs metabolites, adrenal epi, nitric oxide, autoreg

32
Q

shear stress. when is it highest vs lowest?

A

rubbing force fluid exerts on inner wall; when adjacent blood layers travel at diff vel. at blood vessel wall where vel = lowest –> less likely for RBC aggregates –> less viscosity –> sl greater flow vs center of blood vessel where vel = highest

33
Q

what’s compliance?

A

ability of blood vessel to hold blood vol; inverse related to elastance/stiffness & pressure, directly related to vol; in 20x vv > aa; dec w/ age

34
Q

where does pulsatile vs nonpulsatile happen? which area corresponds to transition? where does small vs lg pressure drop occur?

A

systolic & diastolic pressure at aorta/aa/arterioles vs capillaries thru venules. capillaries = transition. in major aa –> lowest resistance vs in arterioles –> highest resistance; pressure drop = proportional to resistance of that seg

35
Q

pulse pressure vs MAP eqns. how do they change in arteriosclerosis vs aortic stenosis?

A

systolic - diastolic pressure vs DP + 1/3(pulse pressure). narrow radius –> higher pulse pressure & MAP vs valve can’t open –> can’t deliver enough blood to systemic circ –> dec systolic pressure –> dec pulse pressure & MAP

36
Q

what are baroreceptors? know Lec 8-9, slides 24-25

A

change in arterial BP –> change in stretch –> mechanoreceptors detect & fire AP in aff nn to brainstem –> eff changes in heart

37
Q

what happens in orthostatic hypotension?

A

dec in arterial bp when supine to upright –> malfxn autonomic nervous system –> compensatory symph activation –> vasoconstrict –> inc ctx, CO, HR

38
Q

RAAS

A

dec in arterial bp –> dec in reenal perfusion pressure –> angiotensinogen in liver –> angiotensin via renin proteolytic enzyme –> angiotensin II via ACE –> adrenal gland to make aldosterone, hypothal/pit gland to inc thirst & make ADH, constrict arterioles –> inc water & salt retention, TPR –> inc ECF vol & blood vol –> inc bp –> inc CO

39
Q

chemoreceptors? central vs periph?

A

bind to chem stimuli & convert to AP to activate reflexes. CO2 & pH in brain/medullary cardiovasc centers vs O2 in carotid & aorta. ischemic brain -> high CO2/low pH, low O2 -> inc symph outflow -> vasoconstrict/inc HR, inc vent/RR -> inc arterial bp

40
Q

atrial and brain natriuretic peptide. cardiopulm low pressure baroreceptors

A

short term peptide secreted by heart for atrial stretch & high bp –> vasodil, dec ADH –> inc glomerular filtration –> inc HR, CO, renal perfusion –> Na+/water renal excretion. distended vessels -> aff CN10 -> vasomotor center -> reg blood vol in lg vv, pulm aa, RA/V -> reflex inhib of eff symph outflow to kid -> inc Na+ and H2O retention

41
Q

what kind of motion does blood flow have?

A

vasomotion: intermittent flow from intermittent ctx of arterioles & precapillary sphincters dictated by local O2 & metab needs (prevents nutritional defic & promotes heart effic)

42
Q

cont vs fenestrated vs sinusoidal/discont capillaries

A

most common, least permeable; tight jxns, muscle/neural/connective tissue vs pores thru endothel cells→ high rate of exchange of small molecules and fluid vol; kidneys and intestines vs big fenestrations, wide intercellular clefts, few tight jxns, incomplete basement membrane; most permeable –> blood cells & plasma proteins enter blood via endothelium; bone marrow, liver, spleen

43
Q

main capillary anatomy?
- intercellular cleft:
- plasmalemmal vesicles:
- fenestrations:

A

unicellular layer of endothelial cells surrounded by basement membrane. b/w endothelial cells –> passage of water, aqueous ions, small solutes vs w/in endothelial cells, vesicular channels –> passage of small proteins vs membrane-lined cylindrical channels –> large fluid and solute fluxes

44
Q

hydrostatic pressure vs colloid osmotic/oncotic pressure vs interstitial oncotic pressure

A

pressure against arteriole wall; inc when arterial pressure & venous resistance, dec arterial resistance; filtration > absorption; H2O out vs pressure on vessel by albumin/protein conc; restrains filtration; H2O in vs pressure by interstitial protein conc favoring filtration

45
Q

what are starling forces?

A

relationship b/w hydrostatic & osmotic pressure. pos Jv = filtration, neg Jv = absorption. water moves toward higher osmolarity

46
Q

kidney has high pressure > interstitium –> favoring? lungs have low pressure favoring?

A

filtration. water absorption –> no fluid in interstitium

47
Q

general lymphatic system pathway. R lymphatic duct vs L thoracic duct. how permeable are lymph capillaries?

A

lymph vessels pick up lymph fluid from tissue –> LN –> blood circ. right thorax, right upper limb, right head and neck → R subclavian vein vs left head, left upper limb and lower half of the body, chyle from small intest –> L subclavian vein. highly permeable but lack tight jxns –> fine filaments –> lg particles & protein enter interstitial fluid

48
Q

when does edema form? vasogenic vs hypoproteinemic vs permeability vs lymph edema

A

vol interstitial fluid > return to blood circ; inc filtration or impaired lymph drainage. disturbance in vasc component -> inc Pc (HTN, ortho HoTN, DM, CHF) vs dec albumin -> dec Pp (kidney/liver dz, malnutrition) vs disrupted physical membrane or pores in membrane -> dec Pp (inc tension of cytoskel -> pulls endothel cells apart) vs excess lymph fluid from impaired drainage, lymph obstruction, lymph permeability, LN removal

49
Q

L vs R heart failure

A

Blood backs into the LA and pulmonary capillaries→ inc pulmonary capillary pressure → pulmonary edema vs Blood backs up into systemic veins → inc central venous pressure → inc cap pressure in LE and abdominal viscera → Ascites

50
Q

when moving from Supine to Standin?

A

inc symph –> inc venous hydrostatic pressure; inc renin -> dec glom filt -> inc Na/H2O retention -> bp/ctx/HR; constrict renal vessels -> dec renal flow

51
Q

what happens if you dec diameter/constrict artery?

A

inc R -> dec Q & P (like bp), vol, conductance -> dec capillary filtration

Block 4 (18 decks)

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