Physiology Flashcards

1
Q

Multi-unit vs unitary smooth muscle

A

multi-unit - fiber operate individually (have nerve fiber running between them)
Unitary - smooth muscle cells adhere and contain gap junctions to allow simultaneous contraction

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2
Q

What excites skeletal muscle vs smooth muscle?

A

Skeletal muscle - ACh

Smooth muscle - ACh (excitatory/inhibitory), NE/Epi (inhibit GI, excite vasculature), NO (inhibitory)

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3
Q

How do neurotransmitters reach smooth muscle?

A

through varicosities - swelling along the axon that release NTs

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4
Q

Describe differences in contraction between skeletal muscle and smooth muscle?

A

Skeletal muscle has faster cycling and myosin/actin attached for less time; high ATP demand
Smooth muscle has slower cycling and myosin/actin attached for more time; less ATP demand

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5
Q

How does Ca enter smooth muscle cytosol?

A

through plasma membrane (Ca L type channels or ligand activated Ca channels) or through SR

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6
Q

Describe how Ca is released from the SR

A

incoming Ca triggers ryanodine receptors (RYRs) on SR or NT/hormone can trigger PLC to convert PIP2 to IP3 which will react w/ receptor on SR

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7
Q

What does Ca in the cytosol do?

A

It binds reversibly to calmodulin (CaM)

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8
Q

What steps are involved in smooth muscle contraction?

A

CaM-Ca complex activates MLCK; phosphorylated MLCK allows myosin and actin to bind

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9
Q

What is smooth muscle contractile strength proportional to?

A

Intracellular Ca levels

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10
Q

What is responsible for smooth muscle relaxation?

A

myosin phosphatase -> removes phosphate from myosin to make it inactive

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11
Q

Describe the latch mechanism?

A

actin and myosin still latched after removal of phosphate; cell continues to generate active tension without use of ATP

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12
Q

What is RMP of smooth muscle?

A

-50 to -60 mv

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13
Q

Slow waves vs spike potentials

A

Slow waves - waves of partial depolarization that sweet along smooth muscle
Spike potentials - true APs that elicit muscle contraction; found on tope of slow waves

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14
Q

What can cause smooth muscle activity?

A

hormones, NT, mechanical stretch

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15
Q

Active tension vs passive tension

A

Active tension = muscle contraction

Passive tension = stretching of the muscle cell membrane

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16
Q

What allows smooth muscle to have longer active tension and less passive tension?

A

Dense bodies (aka adheren junctions) attached to myosin/actin fibers and rearrange to reduce passive tension

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17
Q

What is considered normal HDL?

A

< 40 mg/dL in men; < 50 mg/dL in women

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18
Q

What is considered normal LDL?

A

< 100 mg/dl in people w/ low CV risk

< 70 mg/dl in people w/ high CV risk

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19
Q

What are the criteria for metabolic syndrome?

A

3 or more of the following:
Waist circumference > 102 cm in men (40 inches) and >88 cm in women (35 inches)
Serum triglycerides > 1.7 mmol/l
Blood pressure > 130/85
HDL cholesterol < 40 mg/dl in men; < 50 mg/dl in women
Serum glucose > 115 mg/dl

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20
Q

What are 3 things that people should avoid eating?

A

foods that contain trans fats, processed meats, and sugar sweetened beverages (SSBs)

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21
Q

What does dietary approaches to stop HTN (DASH) recommend for daily Na intake?

A

< 2300 mg/day; recommends < 1500 mg/day

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22
Q

What is the recommended amount of exercise?

A

150 minutes per week of moderate aerobic exercise

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23
Q

What is normal MAP?

A

93.3 mmHg (approximately 100 mmHg)

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24
Q

MAP is regulated by what to things?

A

baroreceptor reflex and renin-angiotensin-aldosterone system (RAAS)

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25
Q

What are the detectors for the baroreceptor reflex?

A

mechanoreceptors - respond to changes in arterial pressure (through stretch receptors on vessel wall)
chemoreceptors - respond to changes in PO2, PCO2, and pH

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26
Q

What are the afferent neural pathways for the baroreceptor reflex?

A

carotid sinus through the glossopharyngeal nerve (CN IX)

aortic sinus through the vagus nerve (CN X)

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27
Q

Describe each of the following: nucleus of tractus solitarius (NTS); Dorsal motor nucleus of vagus & nucleus ambiguous; Rostral ventrolateral medulla

A

nucleus of tractus solitarius (NTS - receives and coordinates afferent signals from carotid and aortic sinuses
Dorsal motor nucleus of vagus & nucleus ambiguous - parasympathetic activity w/ CV function (inhibitory)
Rostral ventrolateral medulla - sympathetic activity w/ CV function

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28
Q

What is the control center for the baroreceptor reflex?

A

the medulla

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29
Q

Which sinus has a higher threshold for activation?

A

Aortic sinus; carotid bodies will fire up to 200mmHg and not below 40-60mmHg

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30
Q

What is the relationship between stretch and firing rate?

A
decreased stretch (MAP) = decreased firing
increased stretch (MAP) = increased firing rate
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31
Q

What effect does the firing of baroreceptors have on the nervous system?

A
parasympathetics = increased firing rate (decrease HR and indirect vasodilation through NO release)
sympathetics = decreased firing rate (constriction of arterioles and veins, increased HR and contractility)
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32
Q

What is renin secreted by and in response to what?

A

secreted by juxtaglomerular (JG) cells in response to drop in BP; release stimulated by B1 receptor

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33
Q

What is the function of renin?

A

causes angiotensinogen (from liver) to covert to angiotensin I (inactive)

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34
Q

What coverts angiotensin I to angiotensin II?

A

angiotensin converting enzyme (ACE) in the lungs and kidneys; angiotensin II is active

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35
Q

What is the function of angiotensin II?

A

causes secretion of aldosterone from adrenal cortex; leads to Na and H20 retention and increased blood volume; stimulates secretion of antidiuretic hormone (vasopressin)

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36
Q

What receptors does angiotensin II bind?

A

AT1 receptors on arterioles; causes global vasoconstriction

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37
Q

What receptors does vasopressin bind to?

A

V1 receptors (smooth muscle) and V2 receptors (collecting ducts); increases TPR and water retention

38
Q

What secretes ANP, BNP, and CNP? What is their function?

A

secreted by heart by excessive preload of atria and ventricles; protects against over dilation or overstretching of cardiac chambers

39
Q

In what way will the vascular function curve shift during hemorrhage?

A

shifts to the left; CO and RA pressure both decrease

40
Q

Describe the body’s reaction to hemorrhage

A

carotid sinus firing (baroreceptor) decreases; HR and contractility increase; unstressed volume (veins) decreases; TPR increases; production of renin, angiotensin II, aldosterone, Epi, and ADH increase

41
Q

Describe the body’s reaction to increased blood volume

A

increased preload; increased secretion of ANP; decrease ADH secretion and renal vasodilation

42
Q

Describe the body’s reaction to exercise

A

increased sympathetics (B1); increased HR and contractility; increased venous return

43
Q

In what type of vessels would you find alpha 1 adrenergic receptors?

A

arterioles

44
Q

What affects velocity of flow?

A

cross sectional area

larger diameter = slower velocity; velocity is slowest at capillaries to allow gas exchange

45
Q

In which vessels in compliance the greatest?

A

greatest in veins compared to arteries; compliance = how far vessel will distend (opposite of elasticity)

46
Q

How does arteriosclerosis affect MAP?

A

plaques in arterial wall decrease diameter and compliance (increase SBP, pulse pressure, and MAP)

47
Q

How does aortic stenosis affect MAP?

A

narrowing of aortic valve (SBP, pulse pressure, and MAP all decrease)

48
Q

What is autoregulation?

A

maintenance of constant blood flow in face of changing arterial pressure

49
Q

What is active hyperemia?

A

blood flow to organ proportional to metabolic activity (flow increases to exercising muscles)

50
Q

What is reactive hyperemia?

A

increased blood flow in reaction to period of decreased blood flow (heart after ischemic event)

51
Q

Describe each of the following as natural constrictors/dilators: histamine, bradykinin, 5-HT, prostacyclin, thromboxane A2, Angiotensin II, vasopressin, NO

A
histamine - dilation
bradykinin - dilation
5-HT - constrictor
Prostacyclin - dilation
thromboxane A2 - constrictor
Angiotensin II - constrictor
vasopressin - constrictor
NO - dilator
52
Q

What is an important factor in coronary circulation?

A

metabolic control -> using vasoactive metabolites from hypoxia

53
Q

What is an important factor in cerebral circulation?

A

metabolic control -> uses vasoactive metabolites CO2 and H+ for active and reactive hyperemia

54
Q

What is an important factor in renal circulation?

A

metabolic control -> myogenic, tubuloglomerular feedback)

55
Q

What is an important factor in skeletal muscle circulation?

A

metabolic control during exercise; sympathetics during rest

56
Q

What is an important factor in skin circulation?

A

sympathetics -> temperature regulation via alpha 1 during vasoconstriction

57
Q

Factors that affect Ca release from SR

A

size of inward Ca current during phase 2 and amount of Ca previously stored in SR

58
Q

What type of inotropic effect does the sympathetic nervous system have? Which receptors?

A

positive (increased contractility); faster rate of relaxation (twitch is shorter allowing for more time refilling); B1 receptors

59
Q

What is phospholamban?

A

protein that regulates SERCA in SR -> when phosphorylated, stimulates SERCA resulting in greater uptake of Ca into SR

60
Q

What type of inotropic effect does the parasympathetic nervous system have? Which receptors?

A

negative (decreased contractility); ACh decreases inward Ca during plateau phase; muscarinic receptors

61
Q

What is the relationship between HR and contractility?

A

increased HR = increased contractility -> less time between contractions means less Ca released from cell

62
Q

What effect do cardiac glycosides have on contractility? What is an example?

A

positive inotropic effect; Digoxin (increases contractility but not HR)

63
Q

Why is there a relationship between CO and right atrial pressure?

A

EDV depends on venous return which determines RA pressure

64
Q

Describe the cardiac function curve

A

as venous return increases, RA pressure increases; volume of blood LV ejects as CO equals volume it receives as venous return (up to certain point)

65
Q

Describe vascular function curve

A

inverse relationship between venous return and RA pressure -> the lower pressure gradient in RA, the higher the gradient between systemic arteries and RA and greater venous return

66
Q

What is the length-tension relationship in cardiac muscle? What is the sweet spot of sarcomeric length? Is it usually reached?

A

as pressure/filling of LV increases, greater tension is generated; sweet spot is 2.2-2.3 micrometers; resting beats don’t reach sweet spot (heart greatly resists stretch)

67
Q

Relationship between venous return and contractility

A

increased venous return = more filling = greater contraction

68
Q

What is preload?

A

left ventricular end-diastolic volume

69
Q

What is afterload?

A

pressure required to eject blood (open aortic valve); generally equal to aortic artery pressure (increases w/ increased systemic pressure)

70
Q

What is stroke volume? What is the normal value?

A

volume of blood ejected by ventricle w/ each beat; usually about 70 ml

71
Q

What is end diastolic volume (EDV)?

A

ventricular volume right before contraction

72
Q

What is end systolic volume (ESV)?

A

ventricular volume right after contraction

73
Q

What is ejection fraction?

What is the normal value?

A

fraction of EDV ejected in each stroke volume (how much blood is left in ventricle w/ each contraction); usually about 55%

74
Q

What is cardiac output? What is the normal value?

A

total volume of blood ejected by ventricle per minute; usually about 5 L/min

75
Q

Describe the Frank-Starling Relationship

A

volume of blood ejected by ventricle depends on volume present at end of diastole (more blood present, the harder the heart will contract)

76
Q

What happens to pressure volume loop if preload increases?

A

more venous return = more blood volume; greater EDV; after load and contractility remain the same

77
Q

What happens to pressure volume loop if afterload increases? When would you see this occur?

A

greater pressure is needed to open aortic valve; reduced SV and reduced EF%; would see w/ aortic stenosis or HTN

78
Q

What would happen to pressure volume loop if contractility increases? When would you see this occur?

A

increased SV and increased EF% (less blood left in the heart); would see w/ adrenergic stimulation

79
Q

Sympathetic influence on troponin I

A

phosphorylation of troponin I is inhibitory - when inhibited, troponin C (opening up actin and myosin) is more efficient; increased CO

80
Q

Define each of the following: volume work, pressure work, minute work, stroke work

A

volume work = CO
pressure work = aortic pressure
minute work = CO x aortic pressure
stroke work = area within pressure volume loop (performed by LV)

81
Q

Which requires more O2 consumption: pressure work or volume work?

A

pressure work -> LV must work harder than RV b/c systemic pressure greater than pulmonary pressure

82
Q

What does it mean when the cardiac function curve moves left?

A

increased isotropy, increased HR, decreased afterload

83
Q

What does it mean when the cardiac function curve moves right?

A

decreased isotropy, decreased HR, increased afterload

84
Q

What will shift the vascular function curve right (up)?

A

increased blood volume or decreased compliance

85
Q

What will shift the vascular function curve left (down)?

A

decreased blood volume or increased compliance

86
Q

What does increased TPR do to the cardiac/vascular function curve?

A

shifts both curves down; cardiac to the right and vascular to the left

87
Q

What does decreased TPR do to the cardiac/vascular function curve?

A

shifts both curves up; cardiac to the left and vascular to the right

88
Q

What will occur to the relationship between CO and venous return w/ heart failure?

A

decreased inotropy; decreased vascular compliance; increased blood volume; increased systemic vascular resistance (SVR)

89
Q

What does a (+) and (-) force mean w/ the Starling forces?

A

(+) means fluid is flowing out of the capillary; (-) means fluid is flowing into the capillary

90
Q

How do capillary beds in series and parallel contribute to resistance?

A

Capillaries in series increase resistance

Capillaries in parallel decrease resistance