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Physio Exam 2 > Sweep 1 > Flashcards

Sweep 1 Flashcards

1
Q

LDLs in the circulation are endocytosed into the

A

steroidogenic cell and lysed to produce cholesterol esters which have low solubility in water, and can be stored in lipid droplets

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2
Q

. Steroidogenic cells store cholesterol esters so typically the cells will appear

A

white or fatty

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3
Q

Steroid Synthesis usually stimulated by

A

peptide hormones from other glands –

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4
Q

activate a G protein coupled receptor →

Steroidogenesis

A

activate adenyl cyclase → increase cAMP → activate PKA which stimulates activity of cholesterol esterases → release cholesterol from intracellular stores

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5
Q

Anterior pituitary –

A

adenohypophysis

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6
Q

Posterior pituitary =

A

neurohypophysis

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7
Q

hypothalamic hormones are transported in the blood within the ————- to the anterior pituitary

A

portal vessels

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8
Q

In the anterior pituitary are

A

5 different cell types that produce 6 primary hormones in response to different hypophysiotropic hormones (that were secreted by hypothalamic neurons)

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9
Q

CRH—->

A

stimulates ACTH secretion

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10
Q

Thyrotropin releasing hormone TRH —->

A

stimulates secretion of TSH

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11
Q

GHRH—>

A

stimulates GH secretion

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12
Q

Somatostatin SS—>

A

inhibits GH secretion

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13
Q

GnRH - gonadotropin releasing hormone—->

A

stimulates secretion of LH and FSH

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14
Q

Dopamine—>

A

Inhibitis prolactin

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15
Q

POMC is a

A

precursor polypeptide synthesized in corticotrophs that is cleaved to yield multiple peptides with varied actions and target tissues. Products: β - lipotropin and β- endorphin

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16
Q

Secretion of thyroid hormones is stimulated by

A

TSH (thyroid stimulating hormone) which is released from the anterior pituitary in response to TRH (thyrotropin releasing hormone) from the hypothalamus.

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17
Q

TSH receptors are on the

A

follicle cells;

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18
Q

TSH also acts to increase the

A

synthetic activity of the follicle cells and stimulates hyperplasia (and replication). Stimulation of endocytosis of colloid back into follicle cell.

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19
Q

TSH also acts to increase the

A

synthetic activity of the follicle cells and stimulates hyperplasia (and replication). Stimulation of endocytosis of colloid back into follicle cell.

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20
Q

TH can lead to

A

upregulation of β-adrenergic receptors that are critical for responses to activation of the sympathetic nervous system; increases sensitivities to catecholamines in both the endocrine and nervous systems (vasoconstriction and contraction of cardiac muscle; critical for sympathetic stimulation), also acts on the lungs and smooth muscle
regulates production of growth hormone (GH)- synthesis and interacts with effects of GH in bone; formation of skeletal bone

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21
Q

Thyroid Disorders are due to under- or overproduction of TH because of

A

disruption of the feedback mechanism that normally controls TH synthesis and secretion.

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22
Q

Without iodine, there is insufficient production of TH → lack of negative feedback increases

A

TRH and TSH secretion → growth of a goiter in response to TH stimulations

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23
Q

• The symptoms of moderate hypothyroidism are due to the effects of reduced

A

β-adrenergic receptors, and the disruption of responses to catecholaminergic stimulation

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24
Q

Graves disease is an autoimmune disease that is a common cause of hyperthyroidism. Antibodies are produced against

A

TSH, and these antibodies are able to activate the TSH receptor so there is no feedback regulation of thyroid function.

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25
Q

In graves disease, TH concentrations are

A

• TH concentrations are high even though TSH (and TRH) are low due to the feedback effects of increased TH.

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26
Q

Secondary defects causing hyperthyroidism include tumors that secrete

A

TSH without responding to feedback control by TH.

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27
Q

• Several antithyroid drugs act to inhibit iodination of

A

TYR, block the release of TH, or ameliorate the effects of TH in peripheral tissues. Can block T3 peripherally.

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28
Q

Adrenal medulla: Most of what is secreted is

A

epinephrine (E

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29
Q

Norepinephrine (NE) is secreted by other postganglionic neurons in the SNS, but the adrenal medulla contains significant amounts of

A

the enzyme phenyl-N-methyltransferase which converts NE to E.

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30
Q

There is also an effect of E and NE on organs and tssues not directly innervated by postganglionic neurons including the liver, skeletal muscle, and fat. In these tissues, epinephrine acts to increase the availability of

A

metabolic fuel by stimulating lipolysis, glycogenolysis and gluconeogenesis.

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31
Q

the cells in the zona glomerulosa contain high levels of

A

aldosterone synthase, and are deficient in the enzymes that convert corticosterone to cortisol or androgens.

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32
Q

The principle action of aldosterone is to stimulate

A

Na+ and H2O retention by the kidney in order to maintain blood volume and blood pressure.

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33
Q

The mechanisms by which aldosterone helps reabsorb Na+ and H2O in the kidney results in an increase in urinary excretion of

A

K+ and H+.

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34
Q

The aldosterone-receptor complex binds to DNA and stimulates the

A

synthesis of proteins that act to increase Na+ and H2O reabsorption from the tubular fluid back into the blood.

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35
Q

Aldosterone can lead to increased synthesis of

A

mitochondrial enzymes used in oxidative phosphorylation (electron transport system)

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36
Q

The secretion of aldosterone is regulated by multiple factors (ACTH has a minor/negligible effect).

A
  • stimulated by an increase in plasma angiotensin II – angiotensin II is a hormone produced in response to renin, a hormone released by the kidney in response to a decrease in Na+ or blood pressure.
  • stimulated by an increase in plasma K+ -
  • stimulated by a decrease in plasma pH or increase in plamsa H+ -
  • stimulated by a drop in systemic blood pressure –
  • inhibited by increased Na+ intake –
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37
Q

Glucocorticoids, cortisol and corticosterone, are secreted by the cells of the .

A

zona fasciculata

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38
Q

Glucocorticoids, cortisol and corticosterone:

A

• ↓ immune and inflammatory responses- inhibits cytokine production.

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39
Q

Glucocorticoids, cortisol and corticosterone: • permissive action on β-adrenergic receptors in vascular smooth muscle to regulate

A

blood pressure. Increases receptor expression*

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40
Q

Cortisol has a negative feedback action on both

A

CRH and ACTH.

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41
Q

Sex steroids (mostly androgens) are secreted by the

A

zona reticularis;

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42
Q

androstenedione is synthesized by enzymatic conversion of

A

DHEA

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43
Q

in females, E2 has positive feedback actions on

A

LH secretion prior to ovulation.

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44
Q
  1. Gigantism is caused by a pituitary tumor that inhibits feedback regulation and leads to a prepubertal onset of excess GH.

T or F

A

F

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45
Q
  1. This hormone stimulates prepubertal bone growth.
    a) Testosterone
    b) Estradiol
    c) Progesterone
    d) hCG
A

b

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46
Q
  1. Which endocrine defect is due a mutation in steroidogenic enzymes that presents with increased adrenal androgen syndrome. Genotype XX with a predominantly male phenotype.
    a) Congenital adrenal hyperplasia
    b) 5〈 reductase deficiency
    c) Androgen insensitivity
A

a

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47
Q
  1. During the uterine cycle, ________ from developing follicles stimulates endometrial proliferation.
    a) FSH
    b) LH
    c) Estrogen
    d) Progesterone
A

c

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48
Q
  1. During the ovarian cycle, there are increased levels of FSH and LH during follicular development. A subsequent decrease in FSH causes the dominant follicle to trigger release of increased estradiol and inhibin.
    a) Both statements are true
    b) First true second false
    c) First false second true
    d) Both statements are false
A

a

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49
Q
  1. This hormone increases mitosis in follicles, regulates oocyte development, leads to the development of secondary sex characteristics, regulates bone deposition as well as mood.
    a) Estradiol
    b) Progesterone
    c) Testosterone
    d) DHEA
A

a

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50
Q
  1. Which cells are located in the lining of the ovarian follicle and convert androstenedione to estradiol as well as secreting inhibin in response to FSH?
    a) Follicular cells
    b) Theca cells
    c) Cumulus oophorus
    d) Granulosa cells
A

b

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51
Q
  1. This disease affects the adrenal glands. It is usually due to a pituitary tumor that leads to excess catabolism and presents with diabetes-like symptoms.
    a) Addison’s disease
    b) Cushing’s syndrome
    c) Crohn’s disease
    d) Asthma
A

b

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52
Q
  1. There are two principle androgens secreted by the adrenal gland. Which one is more potent and is the main extragonadal source of testosterone and estradiol?
    a) DHEA
    b) Androstenedione
A

b

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53
Q
  1. Leydig cells or interstitial cells lie outside of the
A

seminiferous tubules.

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54
Q

Leydig cells synthesize

A

T in response to LH.

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55
Q

In the gonad, T regulates

A

spermatogenesis.

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56
Q
  1. Sertoli cells or sustentacular cells are the
A

epithelial cells lining the seminiferous tubules.

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57
Q

In response to FSH, sertoli cells regulate

A

spermatogenesis and produce the peptide hormone inhibin.

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58
Q

Sertoli cells: Inhibin has negative feedback actions on

A

FSH secretion.

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59
Q

aromatase: T → ——– OR androstenedione → ——— by aromatase in brain and bone

A

estradiol, estrone

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60
Q

There are four types of cells in the ovary with important reproductive functions.

A

oocyte, theca, granulosa, luteal

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61
Q

Shortly after birth, all oocytes are arrested in

A

prophase of meiosis I.

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62
Q
  1. Theca cells surround each
A

follicle; location and function is analogous to that of Leydig cells.

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63
Q

Theca cells =

A

leydig cells

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64
Q
  1. Granulosa cells are the
A

epithelial cells of the follicle (analogous to Sertoli cells).

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65
Q

In an early follicle, one or more layers of granulosa cells surround the

A

oocyte. Large, developing follicles become filled with fluid, and some granulosa cells continue to surround the oocyte in the cumulus oophorus.

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66
Q

Granulosa cells =

A

sertoili cells

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67
Q
  1. Luteal cells are present after ovulation when the
A

theca and granulosa cells from the ovulatory follicle are transformed into the cells of the corpus luteum.

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68
Q

Theca cells synthesize androstenedione in response to

A

LH

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69
Q

androstenedione diffuses into

A

granulosa cells

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70
Q

In response to FSH, granulosa cells

A

convert androstenedione to estrone which is converted to estradiol (E2)

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71
Q

estradiol: stimulates

A

granulosa cell function and replication

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72
Q

estradiol: regulates

A

oocyte development

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73
Q

estradiol: regulates

A

female secondary sex characteristics

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74
Q

estradiol: important regulator of

A

bone turnover and arterial function

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75
Q

estradiol: typically inhibits

A

GnRH and LH secretion

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76
Q

granulosa cells in response to FSH: secrete

A

inhibin that has a negative feedback effect on FSH secretion

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77
Q

proliferative phase: follicular E2 stimulates

A

proliferation of the endometrium

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78
Q

luteal phase: P and E2 stimulate

A

uterine secretory activity; increase glandular production of glycogen, increase angiogenesis, decrease contractility

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79
Q

Menopause consequences:

A

gonadotropin and inhibin secretion very high

increase reliance on adrenal steroids

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80
Q

Male:

genital tubercle →  urogenital fold →>  labioscrotal folds →
A

glans of penis

urethra and surrounding penis

scrotum and skin of penis

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81
Q

Female
genital tubercle →
urogenital fold →
labioscrotal fold →

A

glans of clitoris

labia minor and urethral opening

labia majora

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82
Q

Congenital adrenal hyperplasia

adrenal enzyme deficiency results in excess production of

A

adrenal androgens

caused by more than one mutation and severity varies depending on mutation

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83
Q

Congenital adrenal hyperplasia genotype is

A

XX; phenotype is virilized or more male than female depending on severity

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84
Q

Congenital adrenal hyperplasia genotype is

A

XX; phenotype is virilized or more male than female depending on severity

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85
Q

Pregnancy

There is a dramatic increase in circulating concentrations of steroid hormones during pregnancy due to

A

placental production

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86
Q

CL regresses after ~ 3 months and hCG supports

A

luteal steroidogenesis

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87
Q

placental E2 stimulates

A

growth of myometrium

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88
Q

placental P reduces

A

uterine contractility and stimulates vasodilation

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89
Q

The hormones of the growth axis —— control growth by their actions in

A

(GHRH → GH → IGF-1), somatic tissue and the liver.

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90
Q

. IGF-1 is necessary for

A

fetal growth;

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91
Q

GH becomes

A

important later in development.

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92
Q

Achondroplasia is reduced growth due to constituitive activation of the

A

fibroblast growth factor receptor.

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93
Q

FGF normally inhibits or regulates

A

bone growth, and continued activation of its receptor results in abnormally impaired development of cartilage.

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94
Q

GH insensitivity or dwarfism is due to the absence of a functional

A

GH receptor. These individuals do not suffer from diabetes or cancer, but are often obese.

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95
Q

GH insensitivity The condition can be treated with

A

exogenous IGF-1.

96
Q

There are no known defects in

A

IGF-1 synthesis or for the IGF-1 receptor

97
Q

Malnutrition impairs IGF-1 synthesis independent

A

of GH

98
Q

GH stimulates

A

maturation of chondroblasts

99
Q

IGF-1 stimulates

A

cell division

100
Q

Somatic growth is the result of interactions between

A

GH and IGF-1

101
Q

GHRH elevated during

A

sleep

102
Q

SS elevated during the

A

day

103
Q

IGF-1 and GH inhibit

A

GH and GHRH secretion, but stimulate SS secretion

104
Q

GH is a

GH acts in

A

mitogen – will stimulate cell division.

opposition to insulin

105
Q

Thyroid hormone is required for synthesis of

A

GH and manifestation of GH effects.

106
Q

Growth is also controlled by

A

glucose-regulating hormones.

107
Q

Glucocorticoids inhibit

A

GHRH secretion.

108
Q

Insulin has actions that oppose

A

GH and IGF-1

109
Q

At puberty, the epiphyseal plates ossify due to the actions of

A

E2

110
Q

This can alter the resistance and thereby flow

A

blood viscosity

111
Q

Flow =

A

volume per unit time

112
Q

F=

A

ΔP/R

113
Q

Parasymp:

A

atria- slows, muscarinic receptors

114
Q

Symp

A

beta andronergic receptors, atria and ventricles - fast.

115
Q

Bundle of His depolarizes slower than

A

AV node.

116
Q

The action potential of a myocardial ventricular cell.
The prolonged “plateau” of
depolarization is due to the

A 
The prolonged “plateau” of 
depolarization is due to the slow 
but prolonged opening of 
voltage-gated calcium channels 
          PLUS
closure of potassium channels
117
Q

Calcium influx doesn’t allow for

myocardial ventricular cell

A

repolarizing. Longer refractory period.

118
Q

The action potential of an autorhythmic cardiac cell (nodal):

Sodium ions “leaking” in through
the

A 
F-type [funny] channels 
     PLUS
calcium ions moving in through
the T [calcium] channels cause a 
threshold graded depolarization.
119
Q

The action potential of an autorhythmic cardiac cell (nodal).

Reopening of

A 
potassium channels
   PLUS
closing of calcium channels 
are responsible for the
repolarization phase.
120
Q

if you lose SA node, you get

A

diff pacemaker, but not in sinus rhythm.

121
Q

Gap junctions lead

A

SA signal onward - cardiac impulses travel through these

122
Q

Funny channels remove

A

true resting potential

123
Q

ECG: P wave

A

atria depolarization

124
Q

ECG: QRS

A

QRS complex - ventricular depolarization

125
Q

ECG: T wave

A

Ventricular repolarization

126
Q

ECG can be used to look at

A

arrhythmias

127
Q

Some people have a potentially lethal defect of ventricular muscle, in which the current through voltage-gated K+ channels is delayed and reduced. How could this defect be detected on their ECG recordings?

A

t wave is extended

128
Q

How does the electrical signal transfer to contractile force?

A

ec coupling

129
Q

EC coupling:

A

calcium enters, leads to release of more calcium (calcium binds to ryanadine receptors which releases calcium). Binds during plateau phase.

This is calcium induced calcium release.

130
Q

Calcium that enters during plateau phase in CICR

A

is trigger calcium

131
Q

Ventricular cells have

A

long refractory period to ensure that they can fill.

132
Q

The prolonged refractory period of cardiac muscle

prevents

A

tetanus, and allows time for ventricles to

fill with blood prior to pumping.

133
Q

Stenotic valve

A

narrowed - there is a murmer

134
Q

Insufficient valve

A

backflow - it cannot completely close.

135
Q

Wiggers Diagram

A

top is pressure, middle is volume

136
Q

Aortic, left atrial, left ventricular pressure

A

wigger’s diagram - top to bottom

137
Q

isovolumetric relaxing/contracting

A

rising pressure and dropping pressure of left ventricular pressure.

138
Q

Right heart and left heart is the same except for

A

pressure generated.

139
Q

Parasymp only decreases

A

HR by closing funny channels.

140
Q

Autonomics work

A

in concert - reduce one, raise other.

141
Q

Preload –

A

the volume of blood in the ventricles just before contraction. End-diastolic volume

142
Q

Afterload –

A

the pressure against which the ventricle pumps

143
Q

Symp input into venticle -

A

beta. Increases contraction, increases stroke volume.

144
Q

Symp increases

A

calcium availabiility - thus how it contracts harder and faster.

145
Q

High compliance

A

little change in pressure with more volume. Why veins don’t change.

146
Q

Pulse pressure =

A 
SP – DP
Determined by:
stoke volume
Speed of ejection of the stroke volume
Arterial compliance
147
Q

Compliance =

A

Δ volume/Δ pressure

148
Q

Mean arterial pressure =

A

DP + 1/3(SP-DP), CO*TPR

149
Q

Hypertrophic cardiomyopathy particularly in

A

IV septum

150
Q

Hypertrophic cardiomyopathy is

A

pre load dependent.

151
Q

Intrinsic tone

Controlled by:

A

Local controls - two organs - heart and brain

Extrinsic controls- everything else

152
Q

Local control - active hyperemia

A

active hyperemia - changes in metabolites, dilate arterioles.

  • Increase in metabolic activity sparks this
      • accumulation of: CO2, H+, K+, eicosanoids, adenosine, bradykinin, nitric oxide (NO)

Also happens with working skeletal muscle

153
Q

Local control - flow autoregulation

A
  • decrease in arterial pressure sparks this. Occurs in every organ
154
Q

Flow autoregulation ** myogenic responses –

A

some arteriolar smooth muscle respond to increased stretch caused by increased pressure by contracting to a greater extent (Converse is also true).

155
Q
  • Reactive hyperemia – response to
A

cessation of blood flow

156
Q

Endothelial cell monolayer

A

lining, release paracrine agents for smooth muscle.

157
Q

Sympathetic stimulation of alpha-adrenergic receptors causes

A

vasoconstriction to decrease blood flow to that location.

158
Q

▪ Sympathetic stimulation of beta-adrenergic receptors leads to

A

vasodilation to cause an increase in blood flow to that location

159
Q

Local controls will involv

A

alpha andrenergic receptors

160
Q

Extrinsic controls:

A 
Sympathetic nerves
Parasympathetic nerves
Noncholinergic, Nonadrenergic Autonomic neurons (release NO – enteric and penile)
Hormones
Epinephrine
Norepinephrine
Angiotension II
Vasopressin
Atrial natriuretic peptide
161
Q

Heart blood vessels

A

intrinsicl, local.

162
Q

Skeletal

A

restinjg == symp.

Active = local

163
Q

Gi tract

A

all symp. Splanchnic organs. Do have autoregulation, but all extrinsic.

164
Q

Kidney

A

Extrinsic symp

165
Q

Brain

A

local

166
Q

Skinb

A

symp

167
Q

lungs

A

symp - little control. Gravitational mainly.

168
Q

Paracrine effect

A

parasymp - regulator in penile blood flow.

169
Q

Endothelium derived relaxing factor (EDRF) =

A

Nitric oxide (NO) viagra.

170
Q

How can symp lead to vasodilation?

A

turn it off.

171
Q

More area

A

less velocity.

172
Q

Low molecular weight penetrating solutes =

A

crytalloids

173
Q

Non-penetrating plasma proteins =

A

colloids

174
Q

PC=

A

capillary hydrostatic pressure (favoring fluid movement out of the capillary

175
Q

PIF=

A

Interstitial hydrostatic pressure (favoring fluid movement into the capillary)

176
Q

πC=

A

Osmotic force due to plasma protein concentration (favoring movement into the capillary)

177
Q

πIF=

A

Osmotic force due to interstitial fluid protein concentration (favoring movement out of the capillary)

178
Q

Net filtration pressure =

A

PC + πIF - PIF - πC

179
Q

If an accident victim loses 1 L of blood, why would an intravenous injection of a liter of plasma be more effective for replacing the lost volume that injecting a liter of an equally concentrated crystalloid solution? –

A

increase piC

180
Q

. Sympathetically mediated venoconstriction can substantially

A

increase venous return to the heart. - Alpha receptors

181
Q

Alterations in “venous return” alter

A

end-diastolic volume (EDV); and stroke volume, cardiac output.

182
Q

Serum =

A

plasma with fibrinogen and

clotting proteins removed

183
Q

Ferritin serves as a

A

storage buffer for iron

184
Q

Bilirubin –

A

major breakdown product of hemoglobin

185
Q

Iron released from destroyed RBC is bound by

A

transferrin and delivered to bone marrow.

186
Q

Folic acid – needed for thymine –> if deficient leads to

A

impaired cell division

187
Q

B12 – required for action of

A

folic acid.

188
Q

B12 absorption requires

A

intrinsic factor.

189
Q

If no intrinsic factor —>

A

pernicious anemi

190
Q

Erythropoiesis is

hormonally regulated: decreased oxygen delivery to the kidney causes the secretion of

A

erythropoietin, which activates receptors in bone marrow, leading to an increase in the rate of erythropoiesis.

191
Q

Hemostasis – the stoppage of bleeding

Accomplished by 2 processes that occur in rapid succession:

A

Formation of a platelet plug
Blood coagulation (clotting)
Platelets are critical to both.

192
Q

Blood coagulation (clotting) is the transformation of blood into a solid gel called a clot or thrombus and consist mainly of a protein polymer –

A

fibrin

193
Q

Thrombin leads to

A

Platelet activation

194
Q

the extrinsic pathway is the more important of the two under most circumstances for

A

clotting

195
Q

Coumadin (Warfarin) –

Blocks

A

Vitamin K metabolism

196
Q

Moreover, bile salts from the liver facilitate the absorption of

A

lipids in the diet, including vitamin K,

197
Q

vitamin K,

which is required for the synthesis of .

A

prothrombin

198
Q

Vit. K dependent factors =

A

Coagulation proteins: factors II (prothrombin), VII, IX and X

199
Q

Anticoagulation proteins:

A

proteins C and S
These proteins have in common the requirement to be post-translationally modified by carboxylation of glutamic acid residues (forming gamma-carboxyglutamic acid) in order to become biologically active.

200
Q

proteins C and S

These proteins have in common the requirement to be

A

post-translationally modified by carboxylation of glutamic acid residues (forming gamma-carboxyglutamic acid) in order to become biologically active.

ANTICOAGULATION PROTEINS

201
Q

Following tissue repair, fibrin clots are dissolved in a

process mediated by

A

plasmin;

202
Q

synthetic plasminogen
activators can be used immediately after a stroke or
heart attack to help

A

dissolve clots and restore blood flow

203
Q

 The effect of norepinephrine on β1-receptors located on ventricular muscle cells is to

A

increase the amount of cytosolic (free) Ca2+ and to produce a stronger contraction and an increase in stroke volume.

204
Q

Thus, when the INCREASE in stroke volume is produced by an increase in free Ca2+ , we say that the

A

CONTRACTILITY of the ventricle is increased.

This happens during exercise.

205
Q

Therefore, deltaP, which is called the

A

perfusion pressure, is the same for all vascular beds;

206
Q

delta p =

perfusion pressure

A

MAP–VP, where MAP is the mean arterial pressure and VP is the venous pressure.

207
Q

What will the coronary vascular bed have to do if the heart muscle needs more blood flow? (Assume the MAP and the VP to be constant.)

A

Answer:
Since F = (MAP – VP) / R, it will have to decrease its resistance.

F = deltaP/R **

208
Q

MAP=

A

CO*TPR

209
Q

Dynamic changes in vasodilation/vasoconstriction due to changes in the resistance of arterioles can alter the

A

MAP

210
Q

Compensatory changes in arteriolar resistance occur to protect the

A

maintenance of mean arterial pressure

211
Q

Mean systemic arterial pressure

A

F = delta P/R

Delta P = F x R

Systemic vascular system is a series of tube….therefore delta P = mean systemic artereial pressure (MAP) – pressure in the right atrium. F = CO and R = TPR

MAP- Right atrial pressure = CO x TPR

RAP ~O mmHg…… therefore

MAP = CO x TPR

212
Q

Baroreceptor neurons deliver MAP information to the

A

medulla oblongata’s cardiovascular control center (CVCC);

the CVCC determines autonomic output to the heart.

213
Q

Increase in baroreceptor firing leads to

A

increase in psymp, decrease in symp to heart.

214
Q

Other causes of hypotension

A

Allergic response
Histamine release –> vasodilation

Emotional stress
↓Sympathetic and ↑Parasympathetic
–> vasovagal syncope

215
Q

Increase in CO during exercise

is due to large increase in

A

HR and

smaller increase in SV.

216
Q

VO2max could be limited by:

A

1- cardiac output
2- respiratory system’s ability to deliver oxygen
3- exercising muscle’s ability to use oxygen

217
Q

Except for highly trained athletes – ——- is the factor that
determines VO2max

A

CO

218
Q

Hypertension.

results from

A

increase in cardiac output or total peripheral resistance

219
Q

Renal hypertension –>

A

increased renin release –>

increased angiotension II release (this will lead to increased aldosterone release.)

220
Q

beta andrenergic blockers

A

decrease CO

221
Q

angiotensin II is a

A

vasoconstrictor

222
Q

Diastolic dysfunction –

A

reduced ventricular compliance results in an
increase end-diastolic pressure and thus a decreased end-diastolic
volume and a decreased stroke volume.

223
Q

Systolic dysfunction – a decrease in

A

cardiac contractility – a lower

Stroke volume at any given end-diastolic volume.

224
Q

It is not possible, under normal circumstances, to increase one
but not the other of these determinants of cardiac output.

A

**referringt o HR and stroke volume SV

225
Q

Heart failure leads to increased

A

fluid retention, leading to
increased blood volume and greater stroke volume;
however, the failing heart is less able to handle a large EDV

226
Q

Sudden cardiac death occurs from

A

ventricular fibrillation.

227
Q

Thrombolytic therapy

A

Streptokinase

tissue plasminogen activator

228
Q

Percutaneous coronary intervention

A

Balloon angioplasty

Stenting

229
Q

Repolarization of SA nodal cells occurs via:

A) Opening of Ca channels
B) Opening of Na channels
C) Opening of K channels
D) Closing of K channels
E) Na/K ATPase
A

c

230
Q

Funny channels are

A

sodium channels

231
Q

The length-tension relationship of cardiac muscle is responsible for the

A

Frank-Starling mechanism.

232
Q

Frank-Starling mechanism matches

A

the CO to the VENOUS RETURN

and it matches the outputs of the two VENTRICLES

233
Q

That’s what happens during exercise. The End-diastolic size of the heart doesn’t change and the SV

A

increases because of sympathetic stimulation.

234
Q

The effect of epinephrine (from the adrenal medulla) or norepinephrine (released by sympathetic fibers) on 1-receptors in heart muscle produces an increase in

A

contractility

235
Q

Increased adenosine in a metabolically controlled organ will cause:

A) vasodilation
B) vasoconstriction
C) decreased blood flow
D) increase diffusion
E) nothing
A

a - it is a metabolite, local controls kick in - active hyperemia.

Physio Exam 2 (11 decks)

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