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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
what do AV valves do? when do they open vs close?
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
what semilunar valves do in systole vs diastole?
open d/t intraventricular pressure > aortic & pulm pressure vs ventricles relax -> intraventricular pressure falls. R pulm valve, L aortic valve
27
s1 vs s2 heart sounds
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
Law of LaPlace + eqn. concentric vs eccentric hypertrophy
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
systolic vs diastolic failure
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
1st vs 2nd vs 3rd degree heart block. afib vs vfib
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
factors that cause vasoconstrict vs vasodil
symph, adrenal NE, angiotensin II, vasopressin vs metabolites, adrenal epi, nitric oxide, autoreg
32
shear stress. when is it highest vs lowest?
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
what's compliance?
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
where does pulsatile vs nonpulsatile happen? which area corresponds to transition? where does small vs lg pressure drop occur?
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
pulse pressure vs MAP eqns. how do they change in arteriosclerosis vs aortic stenosis?
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
what are baroreceptors? know Lec 8-9, slides 24-25
change in arterial BP --> change in stretch --> mechanoreceptors detect & fire AP in aff nn to brainstem --> eff changes in heart
37
what happens in orthostatic hypotension?
dec in arterial bp when supine to upright --> malfxn autonomic nervous system --> compensatory symph activation --> vasoconstrict --> inc ctx, CO, HR
38
RAAS
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
chemoreceptors? central vs periph?
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
atrial and brain natriuretic peptide. cardiopulm low pressure baroreceptors
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
what kind of motion does blood flow have?
vasomotion: intermittent flow from intermittent ctx of arterioles & precapillary sphincters dictated by local O2 & metab needs (prevents nutritional defic & promotes heart effic)
42
cont vs fenestrated vs sinusoidal/discont capillaries
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
main capillary anatomy? - intercellular cleft: - plasmalemmal vesicles: - fenestrations:
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
hydrostatic pressure vs colloid osmotic/oncotic pressure vs interstitial oncotic pressure
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
what are starling forces?
relationship b/w hydrostatic & osmotic pressure. pos Jv = filtration, neg Jv = absorption. water moves toward higher osmolarity
46
kidney has high pressure > interstitium --> favoring? lungs have low pressure favoring?
filtration. water absorption --> no fluid in interstitium
47
general lymphatic system pathway. R lymphatic duct vs L thoracic duct. how permeable are lymph capillaries?
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
when does edema form? vasogenic vs hypoproteinemic vs permeability vs lymph edema
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
L vs R heart failure
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
when moving from Supine to Standin?
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
what happens if you dec diameter/constrict artery?
inc R -> dec Q & P (like bp), vol, conductance -> dec capillary filtration

Block 4 (18 decks)

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