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Block 3: Cardio, Renal, Pulm > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

why are people with CVD given aspirin?

A

aspirin is COX inhibitor

PGH2 –> TXA2 (constrictor - produced by platelets) and PGI2 (dilator - produced by ECs)

PGI2 effects not taken out because ECs have nuclei

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2
Q

caldesmon

A

binds to actin filaments at low Ca conc. to prevent actin and muosin from interacting (preventing contraction)

doesn’t do it’s job when phosphorylated (is phosphorylated by MAPK)

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3
Q

what causes the water loss in the thin descending LOH?

A

the neighboring salt loss in the thick ascending LOH pulls water out of TDL into interstitum

(saltier the fluid means more Na is pumped out of the tubule)

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4
Q

systolic right heart failure (HFrEF)

A

myocardium can’t generate enough force to eject blood. breathlessness, large diliated heart

heart sound 3

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5
Q

2

A

interlobular artery

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6
Q

which diuretic spares K loss?

A

amiloride (acts at collecting tubules)

channel is only Na so K not affected

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7
Q

autoregulation

A

how we maintain constant blood flow despite changes in pressure

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8
Q

what is the difference in generating activity induced flow in the brain vs everywhere else

A

neurotransmitters (espec. glutamate) rather than energy are the principal agents in generating activity induced flow

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9
Q

what is excitation coupling? what are the two types?

A

the process where excitation triggers an increase in calcium

  1. electromechanical coupling: contraction WITH a change in membrane potential
    1. AP dependent - Ca channels open slower in SM
    2. graded depolarization - no AP generated/is resting potential
  2. pharmacomechanical coupling: contraction WITHOUT a change in membrane depolarization - usually caused by local tissue factors that open Ca ion channel or GPCR and depolarize membrane without AP
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10
Q

calsequestrin

A

Ca buffering molecule in the junctional SR

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11
Q

what does countercurrent mean?

A

fluid flows in opposite directions - down descending limb, up ascending limb

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12
Q

what are the steps of calcium excitation contraction?

A
  1. increase in calcium concentration (from AP)
  2. Ca binds to calmodulin (like troponin)
  3. Ca/calmodulin activates MLCK (myosin light chain kinase)
  4. MLCK phosphorylates and activates the myosin head ATPase activtiy
  5. ATP is cleaved and Pi is released resulting in confirmational changes
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13
Q

eccentric hypertrophy/dilation

A

HF thinning of wall; increases wall stress

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14
Q

heart sound 3

A

rapid blood flow from atria to ventricles (in kids). indicates CHF/Mitral regurg.

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15
Q

3

A

Collecting Duct

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16
Q

resitance compliance filter

A

what lets blood move through the CC even during diastole - guaruntees steady flow in capillaries

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17
Q

where does most of the Ca influx come from?

A

25% influx thru plasma membrane

75% Sarcomplasmic reticulum

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18
Q

pericyte

A

tight communication with ECs via gap junctions (in the brain). impacts phenotype to influence tightness of BBB - controls angiogenesis/vasculogenesis

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19
Q

whats the BFD about convective transport?

A

its the movement of blood around the body so diffusion can occur over short distances

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20
Q

1

A

PCT

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21
Q

how is the Ca transient increased?

A

by increased TIME to bind to troponin

NOT BY SUMMATION!

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22
Q

1

A

Macula Densa

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23
Q

=GFR

A

creatinine (inulin)

all of it is eliminated in the urine

  1. freely filtered at the glomerulus
  2. not reabsorbed
  3. not secreted
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24
Q

where is urea reabsorbed?

A

the collecting duct by vasopressin - puts VTA1 channels in the CT

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25
Q

1

A

arcuate artery

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26
Q

type III CRS

A

acute RCS

abrupt kidney worsening (ischemia/glomerulonephritis–> heart dysfunction)

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27
Q

what is GFR?

A

volume of filtrate kidneys produce each minute (avg 125 ml/min)

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28
Q

in the cardiac action potential, what is responsible for:

phase 4?

phase 0?

A

4: I k1 (resting potential)

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29
Q

what is the significance of the equilibrium point of a guyton curve?

A

this is where venous return equals the cardiac output

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30
Q

what does increasing TPR do to CO? to CVP?

A

reduces CO - heart has to overcome a higher pressure to eject

reduces CVP - have to translocate more blood from venous to arterial side

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31
Q

endothelin effects

A

causes vasoconstriction, induces hypertrophy of cardiac myocytes. stimulates and potentiates noradrenaline, AII and aldosterone

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32
Q

what is margination?

A

the process of leukocyte redistribution - WBC assume more peripheral position

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33
Q

pressure in the system when CO = 0

A

mean circulatory pressure (~7mmHg)

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34
Q

what happens at the thin descending LOH

A

constitutive water reabsorption - “concentrating segment”

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35
Q

cardiorenal syndrome

A

acute/chronic dysfunction in one may induce such dysfuntion in the other

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36
Q

what are the parasympathetic cholinergic nerves?

A

cranial nerves 3, 7, 9, 10

sacral 2-4

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37
Q

coronary steal syndrome

A

dipyrimidole: affects small (not large) vessels - blood flow to normal area increased, blood flow to ischemic area decreased
nitrate: collateral vessel dilated; bf to ischemic area increased

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38
Q

where would you find:

  1. continuous capillary
  2. fenestrated capillary
  3. discontinuous
A
  1. continious: BBB, muscle, lung
  2. fenestrated: kidney, endocrine glands, GI, gall bladder
  3. liver, bone marrow, spleen (RBC things)
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39
Q

what does the EDPVR determine?

A

compliance a decrease in EDPVR means an upward shift in the diastolic PVR. could be caused by scar tissue froman MI or calcified pericardium

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40
Q

unmyelinated mechanoreceptors

A

respond to distention of heart; ventricular ones during systole, atrial ones during inspiration

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41
Q

when insulin binds to receptor, what happens? (good and bad)

A

good: IRS –> PI3K –> increase glucose transport/NO production (GOOD for CV system to maintain bf, less thrombotic events)
bad: ras –> raf –> MEK –> MAPK –> VSMC growth and migration (atherosclerosis) and endothelian (thrombotic events)

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42
Q

ID #3

What is this space continuous with?

A

Urinary space

continuous with PCT

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43
Q

adenosine on vasoactivity of BV

A

released by heart, can dilate arteries. most important humoral agent in controlling BV vasoactivity!

increases bf in cerebral and coronary circulations

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44
Q

how long is the…

PR interval

QRS interval

A

PR = 120-200 ms

QRS = <100 ms (AP fast)

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45
Q

ectopic atrial rhythm

A

different P waves (but present)

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46
Q

cardiac output

A

the volume of blood pumped by the heart per minute CO=SV*HR

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47
Q

Blue arrow

A

Simple squamous epithelium of the parietal layer

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48
Q

what is a distinguishing feature histologically between elastic and muscular arteries?

A

muscular arteries have a very well defined IEL and EEL

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49
Q

exudation

A

the escape of fluids, proteins and blood cells from vascular system to interstitial tissue/body cavities

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50
Q

hypertensive heart disease on EKG

A

QRS amplitude is abnormally high and wide (high suggests heart enlarged with thickened walls, long because heart walls take longer for depolarization)

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51
Q

what happens to blood when temperature decreases

A

blood viscosity increases two fold

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52
Q

is water reabsorbed at the thick ascending LOH?

A

no!!!! impermeable to water

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53
Q

what is the breakdown of % of Na resorption along the nephron?

A

67% - PCT

20% - thick ascending LOH

6% DCT

2% Collecting tubules

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54
Q

major components of extracellular fluid

A

Na and Cl

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55
Q

Cushing Reaction

A

increased intracranial pressure, TPR, MBP (HTN, brady, resp. depression)

baroreceptor induced bradycardia

(due to hematoma/tumor/cerebral edema)

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56
Q

within each segment the vessels are arranged how?

A

in parallel decreases resitance because 1/R=…

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57
Q

tonus contraction

A

steady state contraction that smooth muscle can maintain

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58
Q

excretion

A

removal of organic wastes or drug metabolites from the blood into urine

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59
Q

phospholamban

A

protein - natural SERCA modulator (quickens SERCA pump when phosphorylated - disinhibition event)

increases calcium stored in SR for faster and greater uptake

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60
Q

AV fistula

A

extra flow back to the heart (preload pathology)

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61
Q

Frank starling mechanism

A

the intrinsic capability of the heart to change its SV in response to changes in preload

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62
Q

which is more concentrated, renal cortex or medulla?

A

medulla! (400-1200 mosm/L)

cortex is 300 mosm/L

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63
Q

valve disease

A

preload pathology

aortic/mitral regurgitation

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64
Q

atrial a wave atrial c wave atrial v wave

A

a: contraction of the atrium c: bulging of mitral valve leaflets into the LA during IVC v: filling of atria during ventricular systole

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65
Q

3

A

Interlobular artery

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66
Q

4

A

RBC

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67
Q

heart chemosensors

A

cause pain in repsonse to ischemia (K, lactic acid, bradykinin, PG’s)

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68
Q

NADPH oxidase

A

CRS activates NADPH oxidase in end stage HF through angiotensin II resulting in ROS formation

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69
Q

neovascularization

A

necessary vascular repair mechanism to preserve tissue and organ viability in response to ischemia most common form: critical limb ischemia

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70
Q

mitral regurgitation

A

during systole when mitral valve is normally closed

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71
Q

type II CRS

A

chronic CRS

chronic HF –> progressive CKD

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72
Q

transcellular pathway

A

(permeability maintenance in BVs) transports plasma proteins (size of albumin or greater) between cells

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73
Q

calcitriol

A

steroid hormone activated by kidneys in response to presence of PTH - stimulates Ca absorption along the digestive dract

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74
Q

list the steps of the CC in order

A

IVC ejection IVR relaxation atrial systole - small additional amount of blood into ventricles

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75
Q

preferred fuel of the heart

A
  1. LCFA (80%)
  2. lactate (18%)
  3. glucose (2%)
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76
Q

the property of endothelial cells to change shape in the direction of flow is? what molecule mediates this?

A

mechanotransduction achieved by integrins: transmembrane linkers that connect ECM to actin filaments

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77
Q

how does aldosterone increase Na reabsorption and K secretion?

A

aldosterone binds to cytosolic receptor in tubular cell of CT and binds translocates to nucleus to activate increases in Na and K channels being made

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78
Q

countercurrent exchange system

A

maintains the gradient - involves vasa recta (surrounds juxtamedullary capillaries)

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79
Q

3

A

CT

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80
Q

2

A

afferent arteriole

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81
Q

type 1 CRS

A

acute CRS

abrupt worsening of heart –> acute kidney injury

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82
Q

1

A

PCT

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83
Q

what is the dicrotic notch?

A

the end of left ventricular systole - when the aortic valve closes and IVR begins. there is a transient change upon closure

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84
Q

is blood a newtonian fluid?

A

no! non-newtonian because it has anomolous viscosity

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85
Q

in doppler, you see an increase in velocity. what does this mean?

A

means decrease in area (because flow has to stay constant)

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86
Q

what are those blobs

A

vasa recta

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87
Q

what is voltage dependent (depolarization induced) Ca release?

A

it is in skeletal msucle where the extra transmembrane segment makes physical contact with RYR –> during AP channel changes shape, pulling on RYR for it to open

results in most of the Ca comes from SR in skeletal muscle

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88
Q

5 abilities of pericytes

A
  1. regulation of TJ and GJ and bulk flow fluid for transcytosis
  2. regulation of vascular stability (pro/anti angiogenic)
  3. regulation of ECM protein secretion/levels
  4. regulation of capillary diameter/blood flow
  5. Phagocytosis
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89
Q

in exercise, which receptors mediate local/systemic responses?

A
  • local:
    • B2: leads to dec. TPR and dilation of skeletal muscle arterioles
  • systemic:
    • A1: constriction of veins
    • B1: inc. HR, contractility, CO
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90
Q

what is a retrospective (nonconcurrent) study

A

past exposure statys from prvious data. disease has long induction/latent period. save time and money through historical data

BUT CAN NEVER SAY COHORT STUDY DESIGN IS RETRO - ONLY EVEN PROSPECTIVE!

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91
Q

type V CRS

A

secondary CRS

systemic disorders (DM/sepsis) leads to heart and kidney disease

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92
Q

atrial natriuretic peptide

A

increases salt excretion by kidneys but reducing water reabsoprtion in collecting ducts; relaxes renal arterioles, inhibits Na reabsorption in DCT

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93
Q

diastolic heart failure (HFpEF)

A

EF at rest is normal. ventricle has to relax to permit filling of blood - lose compliance, becomes stiffer, cavity is reduced and can’t fill with blood so reduced CO

heart sound 4

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94
Q

what is cold vasodilation?

A

with continued cold exposure, blood flow in the cold hand increases

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95
Q

heart sound 4

A

heard in hypertrophy - atria trying to fill stiffened ventricle

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96
Q

where do sympathetic vasodilator fibers come from/go to?

A

come from: motor cortex (cholinergic)

go to: vascular beds of skeletal muscle

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97
Q

function of the vasa recta

A

prevents dissipation of vertical osmotic gradient in medullary interstitum (prevents hyperosmolarity) - site of countercurrent exchange

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98
Q

what is a cell with stem cell/contracting capabilities but can also repair damage in blood vessels?

A

pericyte

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99
Q

stroke volume

A

the volume of blood ejected from the ventricle SV=EDV-ESV

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100
Q

what are two ways that Ca is lowered in the cell?

A
  1. sequestration: Ca pumped from cytoplasm back to SR
  2. Na:Ca exchange
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101
Q

lung stretch receptors

A

cause tachycardia during inspiration-

102
Q

extravasation steps

A
  1. rolling: P-selectin and E-selectin appear on EC surfaces from exposure to inflammatory cytokines 2. tight binding: interaction between LFA-1 and MAC-1 and ICAM-1 - stops rolling 3. diapedesis: leukocytes extravasates endotheliam well - involves PECAM 4. migration: of leukocytes guided by chemokine gradient
103
Q

where do lasix diuretics act?

A

the thick ascending LOH

to quickly remove sodium

104
Q

how do pericytes regulate capillary diameter/blood flow?

A

they act by Ca influx - contract to occlude capillary lumen - no reflow phenomenon - post stroke no flow through capillaries

105
Q

how do Ca and Mg get into the blood? (thru resabsorption)

A

paracellular pathway - transports divalent cations

increase in positive charge from K into the lumen pushes through between the cells to the blood

106
Q

why is injecting urself with EPO (like lance armstrong) a bad idea?

A

viscosity is proportional to hematocrit people have died from this from strokes

107
Q

Green arrow

A

Glomerular capillary tuft

108
Q

how does an adherens junction open?

A

phosphorylation of tyr residues on VE-cadherin

109
Q

if RR=1

if RR>1

if RR<1

A

RR=1: risk in exposed equal to risk in unexposed

RR>1: risk in exposed greater than risk in unexposed (pos. association) ex. 3 is 3x risk of… or 1.6 60% increase in…

RR<1: risk less in exposed than risk in unexposed (neg. association) ex. 0.8 is 20% reduction of risk in…

110
Q

what type of cells release renin?

A

juxtaglomerular cells

111
Q

what is the most potent vasoconstrictor?

A

angiotensin II

112
Q

two types of enzyme that makes NO

A

eNOS: constitutively active in ECs iNOS: inducible by cytokines and vascular injury

113
Q

atrial fibrillation

A

lack of P waves, regular F waves instead

114
Q

isotonic contraction

A

muscle develops force equivalent to load (afterload) that it wants to move - when it does, the muscle shortens

115
Q

what is vasopressin’s effects on vascular smooth muscle? (V1A receptors)

A

smooth muscle contraciton

vasoconstricton: increase TPR, increase BP

116
Q

what is in the pars radiata?

A

LOH and collecting duct - aka the medullary ray

117
Q

plasma clearance

A

volume of plasma that is completely cleared of a substance in 1 min

118
Q

aortic stenosis

A

murmur between S1 and S2 during systole - greater pressure gradient due to stenosis makes turbulent flow/murmur

119
Q

caveolae

A

lipid rafts - small invaginations of plasma membrane. acts as signaling hubs in ECs

120
Q

left sided heart failure

A

fluid congestion in the lung (pulmonary edema), fluids leak out into interstitum

121
Q

what is the afterload?

A

the pressure that ventricle must overcome in order to open the valve and eject blood during the entire ejection phase

122
Q

junction rhythm

A

no P waves or atrial activity, regular QRS complexes at a slower rate

123
Q

transcytosis

A

(permeability maintenance in BVs) transports smaller molecules in vesicle carriers thru the ell originating from caveolae

124
Q

principal cells

A

nonmotile cilia and moderate infoldings and mito. respond to aldosterone - resorb Na and water and secrete K. cilium as mechanosensor of fluid flow/fluid content

125
Q

Yellow arrow

A

PCT

126
Q

BNP effects

A

inhibits RAAS, endothelin-1 and other vasoconstrictors

promotes diuresis, enhances Na excretion and GFR

127
Q

where does most material in vessels get exchanged?

A

capillaries and post capillary venules

128
Q

whats the BFD about astrocytes?

A

influence cerebral blood flow: change in flow with change in activtiy faster than in any other area - tight communincation between astrocytes and BVs

secrete vasodilators (NO, adenosine, EETs, PGs, K) or vasoconstrictors (AA) to incluence cerebral vascular resistance

129
Q

cardiac contractility what is an index for it?

A

the intrinsic ability of the ventricle to develop pressure (independent of preload and afterload) closely related to intracellular Ca concentrations regulated by the sympathetic nervous system index for contractility is ESPVR/Emax

130
Q

in clinical practice, what are indices of: left ventricular afterload right ventricular afterload contractility

A

LV: aortic pressure RV: pulmonary artery contractility: ejection fraction

131
Q

filtration

A

transfer of water, ions and small soluble compounds from blood to urine

132
Q

what is diastasis?

A

reduced ventricular filling (before the atrial kick)

133
Q

eccentric CH

A

increase in both cardiomyocyte length and width

134
Q

three ways that the body prevents too much stretch in the heart:

A
  1. titin: goes from Z line to Z line (intracellular)
  2. collagen/elastin: can’t stretch past 2.2 (extracellular)
  3. pericardium
135
Q
A
136
Q

1

A

parietal layer of BC (SSE)

137
Q

when does IVC begin? when does IVC end?

A

begins: when the mitral valve closes ends: when the aortic valve opens

138
Q

processes involved with HCM

A
  1. left ventricular outlfow obstruction
  2. diastolic dysfunciton
  3. myocardial ischemia
  4. mitral regurgitation
139
Q

juxtaglomerular cells

A

renin producing cells, stimulated to produce renin by NE and dopamine secretion. derived from SM cells, sit on afferent arteriole and secrete renin when BP falls.

140
Q

what is the glomerular basement membrane made of?

A

type IV collagen, laminin, fibronectin, heparin sulfate containing proteoglycan

141
Q

what are the final effects of RAAS

A

Na reabsorption

water reabsorption

K secretion

142
Q

5 (yellow box)

A

pedicles

143
Q

what is shear stress?

A

the force of blood flowing on endothelial cells sigma=(4viscosityQ)/pi*r^3

144
Q

2

A

vasa recta

145
Q

a failing ventricle needs a higher _____ to achieve the same improvement of CO that a normal ventricle can achieve

A

EDV

146
Q

what is Ca induced Ca release?

A

influx of Ca thru LTCC triggers Ca release from SR –> Ca goes across junctional space and binds to RYR to open up.

in cardiac muscle

147
Q

how does bicarbonate get reabsorbed, and where does it occur?

A

occurs at PCT

  1. Na/H exchanger pumps H into lumen
  2. H combines with HCO3 to make H2CO3
  3. H2CO3 becomes water (excreted) and CO2 (diffuses into cell)
  4. carbonic anhydrase combines CO2 and H2O in cell to make H2CO3
  5. HCO3- pumped back into blood stream with Na
148
Q

what is the osmolarity of isotonic ECF?

A

300 mosm/L

149
Q

speed of conduction fibers in the heart (fastest to slowest)

A

purkinje fibers > atria > ventricles > AV node > SA node

150
Q

in high CO2, how do coronary bv repsond?

A

they dilate

151
Q

how are hypokalemia and exercise related?

A

exercise leads to water loss (inc. ADH) and sympathetic activation (RAAS activity from B1 and A2 receptors) (inc. aldosterone)

aldosterone leads to K secretion

152
Q

how do parasympathetics slow the HR?

A

they activate K conductance; more K open means harder to depolarize the membrane

153
Q

What is the arrow pointing to?

A

transitional epithelium

154
Q

when is the AV shunt open/closed

A

open: heat
closed: cold

155
Q

what is the calcium transient?

A

the increase and then decrease of cytosolic free Ca

156
Q

1

A

pars convoluta

157
Q

what happens to SV during exercise?

A

it increases due to increase in contractility and venous return (diastolic filling)

158
Q

osmotic pressure

A

force that must be applied to a solution to block the movemnt of water into that solution

159
Q

how is a portal system unique from normal vascular arrangement?

A

blood drains from capillaries into artery/vein, and then into a second set of capillaries

160
Q

major components of intracellular fluid

A

K and proteins

161
Q

where do thiazide diruetics act?

A

DCT

162
Q

what is cardiac hypertrophy

A

thickening of interventricular wall/septum characterized by increment in cardiomyocyte size with increase protein synthesis and changes in organization of sarcomeric structure

163
Q

nested case control study

A

case control study within a cohort study

has efficiency of nonconcurrent study with strengths of concurrent study

164
Q

how do endothelial cells have adaptable permeability? what molecule mediates this?

A

thru the opening/closure of adherens junctions composed of VE-cadherin

165
Q

what channel is responsible for SA node phase 4 depolarization?

A

funny channel

unusual in that it opens with repolarization (phase 3) - a Na conducting channel; gets depolarization started

166
Q

concentrations of Na, K and Ca in and out of the cell:

A
  1. Na
    1. in: 10
    2. out: 140
  2. K
    1. in: 140
    2. out: 4
  3. Ca
    1. in: 100 nM
    2. out: 1 mM
167
Q

latch state

A

low energy/high tension state to avoid burning thru ATP

unique to smooth muscle

168
Q

albuminuria (proteinuria)

A

excess albumin (protein) in urine caused by disruption of the negative charges within the glomerular membrane. glomerular membrane becomes more permeable to negatively charged proteins despite capillary pore size remaining constant

169
Q

3

A

pars radiata (medullary ray)

170
Q

what is bachmann’s bundle?

A

takes electrical impulse from SA node to right atrium

171
Q

arterial chemosensors

A

stimulated in response to hypoxaemia, hypercapnia (too much CO2), acidosis, hyperkalemia), regulate breathing

172
Q

what does NO do thats so good for us?

A
  1. inhibits leukocyte adhesion to endothelium 2. inhibits platelet aggregation 3. inhibits SM cell migration ***decreases blood pressure!
173
Q

congestive heart failure

A

pathophysiologic state where heart is unable to pump blood at a rate that is equal to what the tissues need, or can only do so from an elevated filling pressure

(symptoms of increase venous pressure often prominent)

174
Q

what is the BFD about glomerular shared basement membrane?

A

fused BM (from podocyte pedicles on one side, then endothelium on the other side)

175
Q

adenosine hypothesis

A

whenever myocardial O2 consumption increases or O2 delivery decreases, ATP is metabolized to adenosine which diffuses across the cell membrane –> dilation, reduced resistance, increased blood flow/O2 delivery

176
Q

what is the difference between short and long term BP measurement?

A

short term: baroreceptors

long term: kidney RAAS, humoral mediators

177
Q

epinephrine and cardiac contractility

A

binds to B adrengergic receptor and inc. Ca peak/shortens duration/stronger contraction as HR increased duration of CC is matched to increase in CO can occur

178
Q

0<gfr>
</gfr>

A

urea

half is eliminated in the urine, half is reabsorbed

  1. freely filtered at glomerulus
  2. partially reabsorbed
  3. not secreted
179
Q
A
180
Q

concentric CH

A

increase in cardiomyocyte thickness more than length

181
Q

>GFR

A

H ions

non is reabsorbed and additional ions are secreted

  1. freely filtered at glomerulus
  2. not reabsorbed
  3. secreted
182
Q

P wave (PR interval) on ECG stands for

A

atrial systole (atrial depolarization)

183
Q

how do catecholamines regulate contractility?

A
  1. NE binds to B receptors (GPCR) activate cAMP/PKA
  2. PKA phosphorylates LTCC which opens more Ca channels
  3. PKA phosphorylates phospholamban to move off of SERCA (increases rate of decay of Ca transient)
184
Q

assumptions in cohort study

A
  1. exposed and non-exposed groups define the true population
  2. absence of exposure maintained in non-exposed group
  3. participants didn’t have outcome of interest before beginning
185
Q

how is NO produced in an EC?

A

arginine dependent eNOS produces NO which diffuses across thru paracrine signaling to the smooth muscle cell guanylate cyclase activated, converts GTP to cGMP which vasodilates

186
Q

cardiac contraction is proprtional to the amount of Ca…

A

bound to troponin

187
Q

veno-atrial mechanoreceptors

A

respond to changes in central blood volume

188
Q

what is mechanotransduction?

A

the conversion of mechanical forces into biochemical signals

189
Q

where is the major site of K secretion?

A

collecting tubules

190
Q

2 ways that afterload can be assessed:

A
  1. ventricular pressure during ejection (upper boundary of PV loop) 2. systolic ventricular wall stress: force within the myocardium during ejection that must be overcome for a sarcomere to shorten
191
Q

site of different flavors of capillaries:

A
  1. continuous - BBB 2. fenestrated - glomerulus and GI 3. discontinuous - lines sinusoids of liver and BM (deals with RBC
192
Q

MLCP (myosin light chain phosphatase)

A

constitutively active phosphatase

removes phosphate from MLC preventing reattachment to actin –> relaxation

193
Q

aortic regurgitation

A

murmur in relaxation and filling. blood flows from aorta back into ventricle

194
Q

what is the ultrafiltrate made of?

A

proteins and RBC

195
Q

how does glucose get from the lumen into the tubular cell to be resorbed?

A

secondary active transport by Na

196
Q

heart sound 2

A

end of systole occurs because of the vibrations from the closure of the aortic and pulmonic valves A precedes P can hear in inspiration

197
Q

2 factors affecting MABP

A

blood volume

CO

198
Q

where is aldosterone released from?

A

adrenal cortex

199
Q

what is compliance?

A

the stretchiness of a vessel/structure C=dV/dP

200
Q

autoregulatory escape

A

sympathetic stimulation produces decrease in BF which is not maintained - in response to vasoconstriction to override NE - once you remove the stimulus causing the change in BP

followed by reactive hyperemia

201
Q

angiogenesis (steps too) vs. vasculogenesis

A

angiogenesis: sprouting from pre existing vessels caused in response to HIF-1 (hypoxia inducible factor), stops when VEGF is shut off 1. gf/hypoxia 2. ECs make proteases 3. ECs migrate to chemoattractant 4. ECs proliferate 5. ECs form tubes and differentiate 6. pericytes urround the new vessels vasculogenesis: using EPCs (endothelial precursor cells) from bone marrow and circulation to form new vessels

202
Q

countercurrent multiplication system

A

involves juxtamedullary nephrons and surrounding medullary interstitum to establish the vertical osmotic gradient enabling concentration of dilute urine

203
Q

2

A

renal lobule

204
Q

perfusion pressure

A

differnce in pressure between aorta and right atrium

205
Q

type IV CRS

A

chronic RCS

CDK –> heart dysfunction, risk of CV events

206
Q

secretion

A

releasing or transferring an endogenous substance from one body compartment to another; unlike excretion, a secreted substance has a physiological or pharmalogical function

ex. NE needed by body

207
Q

where do sympathetic vasoconstrictor (efferent) fibers come from and go to?

A

come from: T1-L3/sympathetic ganglia

go to: artery, arterioles, veins NOT CAPILLARIES

208
Q

what is a lacteal?

A

a blind ending lymphatic capillary

209
Q

mitral stenosis

A

during diastole

210
Q

reactive hyperemia

A

transient increase in blood flow to an area following ischemia

ischemia - a decrease in blood flow / less removal of metabolic byproducts –> dilation of resistance vessels

211
Q

what are actin filaments in SM cells attached to?

A

dense bodies in the cytoplasm, attachment plaques on the inside surface of the cell membrane allows for contraction

212
Q

what is the difference between a case control study and a cohort study?

A

case control: sapling with regard to disease/effect

case control: sampling with regard to exposure, characteristic or suspected cause

213
Q

for a substance to be reabsorbed it has to pass through 5 layers. what are they?

A
  1. luminal membrane of tubular cell
  2. cytosol of tubular cell
  3. basolateral membrane of tubular cell
  4. ECF separating tubular cell and blood
  5. capillary wall
214
Q

what is filtration at the glomerulus based on?

A

size

215
Q

macula densa

A

specialized cells of the DCT wall - sensitive to NaCl and affects renin release from JCGs. in response to high sodium, triggers contraction of afferent arteriole reducing blood flow to glomerulus/decreases GFR

216
Q

what are 4 things that IRS-1 activation leads to?

A
  1. anti-apoptosis
  2. vasodilation
  3. anti-inflammation
  4. anti-oxidative stress
217
Q

how does ADH work?

A

activates V2 receptor (on basolateral membrane of CT cell) and causes synthesis and insertion of pre-existing water channels into luminal membrane of collecting ducts.

increases cAMP leavels –> PKA activation, phosphorylates cytoskeletal proteins that transport aquaporins from the cytosol to luminal membrane surface

218
Q

what is a prospective (concurrent) study

A

exposure status collected in present, subject followed forward into the future. disease has short induction/latency with current/recent exposure

219
Q

what is the diff between multiunit and single unit SM?

A

multi unit: composed of discrete, independently innervated fibers, controlled by nerve signals single unit: (in walls of gut and most arteries) gap junctions allow electrical activity to spread over a large area in unison - arranged in sheets so cell membranes touch

220
Q

right sided heart failure

A

tissue congestion including jugular venous distention, peripheral edema, ascites, abdominal organ engorgement. impairment of ventricular systolic performance.

can be caused by severe left sided HF, severe lung disease, pulmonary HTN, RV MI, congenital abnormalities of the heart

221
Q

pulmonary embolism EKG

A

inverted T wave due to increased myocardial O2 demand and strain on RV

222
Q

what is the difference between diffusion and filtration? who’s laws describe each?

A

diffusion: movement of material down concentration gradient (Fick’s law)

J=-PA(Cin-Cout)

filiration: convective transport due to energy differences on each side of barrier (Starling Landis equation)

223
Q

how are the various segments of the vasculature arranged in respect to one another?

A

in series means more resistance because additive!

224
Q

concentric hypertrophy

A

HTN higher MAP - ventricle has to develop more pressure to overcome to eject the blood. can’t optimize filling

225
Q

what is the law of laplace?

A

wall tension: T=Pr wall stress: Pr/Th the force that makes structure open up

226
Q

intercalated cells

A

microvilli and abundant mitochondria. secrete H or HCO3- and resorb K regulating acid base balance

227
Q

sieve plates

A

fenestrae organized in large planar clusters

228
Q

2

A

DCT

229
Q

three molecular hallmarks of pathological hypertrophy

A
  1. GPCRs
    1. neuroendocrine activation of ET-1 and AII
    2. chronic elevated catecholamines/beta receptor activation
  2. Ca homeostasis
    1. increase Ca influx and activation of Ca signaling pathways
  3. fetal gene program
    1. fetal cardiac proteins and natriuretic receptors
230
Q

when is coronary blood flow the lowest/highest?

A

lowest: IVC
highest: IVR

231
Q

what are the steps of the cross bridge cycle?

A
  1. myosin head is phosphorylated by MLCK and pivots to 45 degrees and reattaches - this is a cross bridge
  2. myosin head is an ATPase - when Pi is released causes myosin head to pivot back to 90 degrees but stays attached - this is the power stroke (myosin head pivot)
  3. myosin head is dephosphorylated by a phosphatase, releasing actin/set for another cycle
232
Q

what type of exercise is accompanied by a dramatic increase in blood pressure?

A

isometric! (dynamic slow)

233
Q

what is the organic acid/base secretory system and where is it?

A

transports organic acids/bases from the blood to the tubular fluid

occurs at the PCT

234
Q

heart sound 1

A

start of systole (IVC) occurs because of the vibrations of the blood, myocardium, and mitral valve (closing) from cardiac contraction

235
Q

elimination/detoxification

A

discharge of organic wastes from urine into exterior

236
Q

mesangial cells

A

in the renal corpuscle; make matrix, cells in between the afferent/efferent arterioles filled with stroma in the VASCULAR POLE

237
Q

what are the goals of local and systemic control in regulation of blood flow?

A

local: couple blood flow and tissue need of each organ (metabolic: ion changes, myogenic: pressure changes, endothelial: paracrine substance secretion)
systemic: maintain blood pressure (neuronal, hormonal)

238
Q

hemodynamic changes in isometric exercise

A

huge increase in TPR because squeezing msucle fibers so tight + metaboreflex sense inc. in stiffness; activate SNS and release NE

bad for people with HTN! want dynamic to lower TPR over time

239
Q

PTH regulates what type of Ca channel? How does it work?

A

TRPV5 - puts into the DCT, then once in cell Ca is coupled to Na gradient to go into the blood

240
Q

do SM cells have tropinin?

A

NO! they have calmodulin instead

241
Q

GFR=0

A

glucose

all of it is returned to plasma

  1. freely filtered at glomerulus
  2. reabsorbed
  3. not secreted
242
Q

What is the yellow arrow pointing to?

A

renal corpuscle

243
Q

five functions of endothelial cells:

A
  1. secretion: of factors like NO or VWF 2. surface expression: of binding proteins like adhesion molecules linked to thrombogenicity 3. contraction involved in hyperpermeability: maintenance of permeability barrier 4. mechanotransducers: mediate changes in flow 5. angiogenesis: generation of new BV
244
Q

what is a renal lobule?

A

in between interlobular arteries; consists of collecting duct and surrounding nephrons that drain into it

(1/2 pars convoluta on each side)

245
Q

does the portal vein autoregulate?

A

no!!!

hepatic artery does though

246
Q

What is the blue arrow pointing to?

A

PCTs and DCTs

247
Q

where is vasopressin made/released?

A

made in hypothalamus, released by posterior pituitary

248
Q

1

A

minor calyx

249
Q

2

A

podocyte cell body

250
Q

glomerulonephritis

A

STREP INDUCED

inflammation of glomerulus disrupts filtration mechanisms develops after an infection. Ag-Ab complexes pass through capillary EC pores and clog the filtration slits so filtrate production declines

251
Q

2

A

DCT

252
Q

does loop or thiazide diuretics have greater efficiency?

A

loop

has greater capacity to reabsorb Na ions (25% vs 6%) so blocking Na reabsorption there means more Na in tubule which creates osmotic gradient to pull water into tubular fluid at water permeable segments of the nephron

Block 3: Cardio, Renal, Pulm (5 decks)

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