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Spring 2015 > Block 3 Phys > Flashcards

Block 3 Phys Flashcards

1
Q

ADH V1 receptor is

A

alpha q– smooth muscle

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2
Q

ADH V2 receptor is

A

alpha s – kidney

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3
Q

90% of filtered water is reabsorbed in the _____ tubule by _______

A

proximal

AQP1

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4
Q

only AQP responsive to ADH

A

AQP2

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5
Q

How does water leave the basolateral membrane of the collecting duct?

A

AQP 3&4

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6
Q

Which is more sensitive to dehydration (leading to AVP release) baroreceptors or osmoreceptors?

A

osmoreceptors

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7
Q

which neurons sends hormones to the posterior pituitary?

A

magnocellular

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8
Q

somatostatin stimulates the release of what hormone from anterior pituitary?

A

GH

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9
Q

AVP and oxytocin are made in what hypothalamnic nuclei?

A

SON and PVN

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10
Q

Ca-calmodulin activates ________

A

MLCK

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11
Q

what is SIADH

A

syndrome of inappropriate ADH secretion

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12
Q

bad taste in mouth is a symptom of what syndrome?

A

SIADH

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13
Q

decreased ADH release is often a complication of

A

diabetes insipidus

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14
Q

anterior pituitary is derived from _____derm

A

ecto

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15
Q

the 3 glycoprotein hormones of the anterior pituitary

A

TSH FSH and LH

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16
Q

all 3 glycoprotein hormones of the anterior pituitary have similar __ subunits and dissimilar ___ subunits

A
  • alpha

- beta

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17
Q

pro-opiomelanocortin is cleaved into what hormones

A

ACTH, beta endorphin, alpha/beta/gamma melanocyte stimulating hormones

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18
Q

Growth hormone release is stimulated by _____glycemia and suppressed by ____glycemia

A
  • hypo

- hyper

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19
Q

major players in GH release

A

GHRH and ghrelin

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20
Q

minor regulators of GH release

A

acetylcholine, alpha-adrenergic agonists, dopamine, serotonin

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21
Q

GH release is inhibited by

A

somatostatin and IGF-1

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22
Q

a long term increase in GH has what effect on adipose tissue?

A

anti insulin effect

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23
Q

laron’s syndrome

A

GH resistance

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24
Q

low GH in adults is associated with

A

CV risk and muscle loss

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25
Q

Hypothalamus controls prolactin by maintaining inhibitory tone via

A

dopamine

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26
Q

Prolactin requires what other 2 things for milk production

A

insulin and cortisol

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27
Q

Long term increases in prolactin lead to

A

infertility and gonadal dysfunction

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28
Q

Increase in prolactin leads to decreases in what hormones?

A

LSH, FSH, gonadal steroidogenesis, estrogen, testosterone, progesterone

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29
Q

What inhibits release of TSH from anterior pituitary?

A

dopamine, somatostatin, and high levels of glucocorticoids

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30
Q

Thyroglobulin is made in _______. Then it’s ______ residues are iodinated in the colloid

A

thyroglobulin

tyrosine

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31
Q

How many Na+ are transported per Iodine into the basolateral membrane of the follicular cells

A

2

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32
Q

which form of thyroid hormone is very inactive

A

rT3

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33
Q

when the inner ring of T4 is deiodinated it becomes

A

rT3

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34
Q

Type 1 deiodinase converts T4 into

A

T3, rT3, and T2

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35
Q

Type 2 deiodinase converts T4 into

A

T3

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36
Q

Type 3 deiodinase converts T4 into

A

rT3 and T2

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37
Q

____ increases the expression of uncoupling proteins and mitochondria

A

TH

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38
Q

thyroid hormone _____ vascular resistance

A

decreases

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39
Q

too much Iodide intake decreases

A

TSH receptor activated pathways

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40
Q

Iodide deficiency in utero is called

A

cretinism

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41
Q

primary hypothyroidism involves

A

the thyroid gland directly

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42
Q

an increase in thyroid tissue, such as a goiter, etc leads to

A

hypothyroidism

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43
Q

Lab tests will show a decrease in both ___ and ___ in hypothyroidism

A

rT3 and T3

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44
Q

starvation and critical illness will show an increase in what form of thyroid hormone?

A

rT3

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45
Q

when using imaging, “cold spots” are usually

A

malignant

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46
Q

DLCO =

A

diffusion capacity of carbon monoxide

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47
Q

RQ =

A

respiratory quotient

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48
Q

above anabolic threshold, your RQ will go

A

above 1

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49
Q

normal body temperature range in celcius and farenheit

A

36-37.5 and 97-99

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50
Q

cutaneous circulation can range between what percent of CO?

A

0-30%

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51
Q

most abundant blood flow to the skin is via

A

venous plexus

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52
Q

what controls cutaneous circulation

A

AV anastomoses

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53
Q

epi and norepi do what to blood flow to the skin?

A

open anastomoses, decreasing flow to skin, conserving heat

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54
Q

most drastic change in capillary caliber will occur in what range of temp

A

75-110 F

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55
Q

what is the relationship btw the cooling effect of air convection to wind velocity?

A

cooling effect = the square root of wind velocity

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56
Q

what part of the hypothalamus regulates temperature?

A

anterior

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57
Q

which produce a more powerful response? heat or cold sensitive neurons?

A

cold sensitive

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58
Q

pyrogen

A

substance that produces fever by resetting the hypothalamus’s thermostat

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59
Q

where are lipid soluble vitamins stored?

A

liver

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60
Q

what is added to bilirubin to conjugate it?

A

sulfate or glucuronic acid

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61
Q

Phase 1 biotransformation is catalyzed by

A

p450

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62
Q

what is the purpose of phase 2 biotransformation

A

increase solubility

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63
Q

what is the Na+ independent transporter?

A

OATP

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64
Q

is bile salt transport to canaliculi active or passive?

A

active

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65
Q

what does bile salt transport rely on?

A

ATP

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66
Q

what pumps bile salts into canaliculi?

A

bile salt export pump

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67
Q

interference with what transporters can result in jaundice?

A

multi drug resistance proteins

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68
Q

what Ig is in bile?

A

IgA

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69
Q

what is the purpose of phospholipids in bile?

A

soulbilize cholesterol and decrease bile acid toxicity

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70
Q

cholesterol is converted to primary bile acids by

A

7a hydroxylase

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71
Q

2 principal bile acids

A

cholic acid and chenodeoxycholic acid

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72
Q

before bile acids are transported into canaliculi, they are conjugated to what?

A

glycine or taurine. This makes them bile salts

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73
Q

name 2 secondary bile acids

A

deoxycholic and lithocholic acid

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74
Q

the 2 most important components of bile

A

cholesterol and bilirubin

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75
Q

what cells reuptake glucose and amino acids from bile?

A

cholangiocytes

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76
Q

what do cholangiocytes secrete into bile?

A

bicarbonate and IgA

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77
Q

toxic damage to the brain from bilirubin is called

A

kernicterus

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78
Q

common risk factors for gallbladder disease:

A

fat forty fertility female

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79
Q

hormones that stimulate bile release from the gallbladder:

A

CCK, PSNS, gastrin, and glucagon

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80
Q

where are bile salts reabsorbed?

A

terminal ileum

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81
Q

alchoholism increases gut barrier permeability, causing an increase in bacterial activation of ____ cells

A

kupffer

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82
Q

Hepatocytes release ______ in response to high kupffer cell activity

A

C reactive proteins

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83
Q

what cells cause liver fibrosis

A

stellate cells found in the space of disse

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84
Q

why does liver failure lead to edema?

A

less albumin production

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85
Q

why does acetamionphen fuck your liver up?

A

it gets conjugated with glutathione and depletes it, leaving your liver susceptible to ROS

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86
Q

glutathione levels can be restored with

A

acetylcysteine

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87
Q

how does cholesterol get to peripheral tissues that need it?

A

the liver packages it as cholesteryl esters

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88
Q

statins inhibit

A

HMG CoA reductase

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89
Q

fast twitch oxidative fibers are what color?
have low or high myoglobin?
have low or high mitochondrial content?

A

red
high
high

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90
Q

Fick principle

A

the total amt of oxygen that someone will consume per minute depends on the amt of blood pumped by heart per minute time amt of oxygen extracted

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91
Q

arterial oxygen content doesn’t change during exercise, so the only 2 ways to increase oxygen consumption is through an increase in

A

cardiac output and oxygen extraction in tissues

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92
Q

stroke volume increases until you get to ____% of max capacity. Any increase in CO thereafter comes from ___

A

30-40

HR

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93
Q

SV is influenced by

A

preload, contractility, and afterload

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94
Q

contractility has to do with avaliability of

A

Ca++

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95
Q

MABP=

A

(systolic pressure x (2x diastolic))/3

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96
Q

changes in pulmonary ventilation have a linear increase with exercise up to _____% of maximum effort

A

60-70%

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97
Q

minute volume =

A

tidal volume x breathing frequency

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98
Q

we can increase our minute volume by how much?

A

20 fold

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99
Q

breathing frequency can increase:

A

4 fold

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100
Q

tidal volume can increase:

A

4 fold

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101
Q

how do we maintain arterial O2 content during exercise?

A

decrease the Vd/Vt ratio

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102
Q

Karvonen formula

A

used to decide how hard to exercise in order to achieve aerobic or anaerobic exercise. HR during exercise = HR at rest + .6 x (HRmax - HRrest)

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103
Q

HRmax =

A

220 - age

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104
Q

young individuals have lower stroke volumes because

A

older people have larger EDV

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105
Q

Rate pressure product-

A

HR x MABP (good indicator of myocardial O2 consump.)

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106
Q

Whipple’s triad-

A

hypoglycemia, low plasma glucose conc. and relief of symptoms after glucose is raised

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107
Q

whipple’s triad indicates-

A

hypoglycemia

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108
Q

nesidioblastosis-

A

non malignant beta cell overgrowth

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109
Q

hypoglycemia = plasma glucose <

A

45 mg/dl

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110
Q

biguanides (metformin) MOA-

A

inhibit gluconeogenesis and glycogenolysis, increase insulin sensitivity

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111
Q

Alpha-glucosidase inhibitor MOA-

A

delay intestinal carb absorption through inhib. of brush border enzymes

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112
Q

Thiazolidinedione MOA-

A

reduce insulin resistance

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113
Q

GLP-1 Agonist MOA-

A

amplify glucose induced insulin release and synthesis, suppresses glucoagon release

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114
Q

Dipeptidyl peptidase 4 inhibitors MOA-

A

inactivate DPP-4, which leads to increase in endogenous incretin levels

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115
Q

sodium glucose co-transporter 2 (SGLT2) inhibitors MOA-

A

inhibit glucose reabsorption from kidneys

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116
Q

2 things needed to cause diabetic ketoacidosis-

A

severe insulin deficiency and glucagon excess

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117
Q

Kussmaul’s respiration is associated with

A

metabolic acidosis from diabetic ketoacidosis. effort to eliminate excess CO2

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118
Q

“leaky vessel” retiopathy

A

non-proliferative

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119
Q

“too many vessels” retinopathy

A

proliferative

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120
Q

The ABCDE’s of trauma

A

airway, breathing, circulation, disability, exposure

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121
Q

what is more dire, bleeding or brain trauma?

A

bleeding. it will kill you faster

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122
Q

intubate if a pt has a GCS score of

A

8 or below

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123
Q

a T is annotated to a GCS if…

A

pt cant talk due to intubation

124
Q

GCS Eye Opening score breakdown:

A

4- spontaneous
3- only to verbal command
2- only to pain
1- not at all

125
Q

GCS verbal response breakdown:

A 
5- oriented and conversing
4- confused conversation
3- inappropriate words or mumbling
2- incomprehensible sounds
1- no sound
126
Q

GCS motor response breakdown:

A 
6- obeys commands
5- localized pain
4- withdraws to pain
3- decorticate
2- decerebrate
1- No posture at all
127
Q

give _____ to decrease ICP from brain injury

A

mannitol

128
Q

3 important variables of trauma pt instability

A

CO, Hb, and O2 satuation

129
Q

what causes trauma pt instability?

A

shock

130
Q

if a trauma pt isn’t urinating much, urine and plasma Na+ conc. are compared. a prerenal problem would be indicated if urine Na+ was _____. A renal problem would be indicated if urine Na+ was ______

A

low

high

131
Q

> 3% creatinine in urine means

A

renal failure

132
Q

> 20% Na+ in urine means

A

renal failure

133
Q

CPP=

A

MABP - ICP

134
Q

SIADH-

A

syndrome of inappropriate ADH

135
Q

SIADH presents as-

A

increased water retention

136
Q

CSW-

A

cerebral salt wasting

137
Q

CSW presents as

A

not enough water retention. treat with mineralocorticoids

138
Q

when splanchnic blood flow decreases, organs compensate by

A

increasing O2 extraction

139
Q

3 factors that regulate splanchnic blood flow during stress

A

SNS, RAS, Vasopressin

140
Q

increased plasma Ca++ binds to parathyroid calcium sensor. describe the cascade

A

phospholipase A2–> arachidonic acid–> leukotrienes–> increase in PTH degradation

141
Q

most important PTH receptor

A

PTHR1

142
Q

PTHR1 binds

A

PTH and PTHrP

143
Q

the culprit in malignant hypercalcemia

A

PTHrP

144
Q

how does Vit D enhance Ca++ reabsorption

A

stimulates calbindin synthesis and Ca++ ATPase activity

145
Q

PTH causes an increase in renal excretion of ___ in the _____ tubule

A

phosphate

proximal

146
Q

PTH also causes increase in renal excretion of Phophate by causing internalization of

A

Na+/P IIa cotransporters (degraded in lysosome)

147
Q

how doe high phosphate level cause hypocalcemia?

A

it complexes with Mg. Mg is needed for proper PTH release

148
Q

how does PTH stimulate bone resorption

A

binds PTHR1 on osteoblasts, leading to expression of RANKL. osteoclast precursors bind RANKL to mature.

149
Q

mature osteoclasts bind to bone using

A

beta-integrins

150
Q

PTH acts on intestines to increase the activity of _________, which is needed to form active vitamin D

A

1 alpha hydroxylase

151
Q

most protein bound calcium is bound to

A

albumin

152
Q

vitamin D precursors:

A

cholecalciferol (skin) and ergocalciferol (diet)

153
Q

activation steps for Vit D

A

precursors are transported to liver–> hydroxylated at C-25 to become 25-hydroxyvitamin D3–> transported to kidneys–> hydroxylated at C-1 to 1,25 dihydroxyvitamin D3 (active)

154
Q

how is vitamin D regulated?

A

increases in plasma Ca++ levels inhibit hydroxylation at C1 and stimulate hydroxylation at C24. This makes 24,25 dihydroxyvitamin D (inactive)

155
Q

sex steroids stimulate an increase in 2 things that decrease bone resorption:

A

1 alpha hydroxylase and osteoprotegrin activity

156
Q

primary hyperparathyroidism-

A

PT gland problem

157
Q

secondary hyperparathyroidism-

A

renal failure. decreased P excretion, hypocalcemia, increased PTH excretion

158
Q

pseudohypoparathyroidism-

A

defect in PTH receptor. low plasma Ca++, high P levels, and elevated PTH.

159
Q

zona fasiculata produces

A

glucocorticoids

160
Q

zona reticularis produces

A

androgens

161
Q

Corticotrophs in the pituitary make

A

proopiomelanocirtin (POMC)

162
Q

POMC is posttranslationally cleaved into

A

ACTH, beta endorphin, and MSH

163
Q

ACTH binds GPCR at the adrenal cortex, downstream activates PKA, causes activation of what 2 enzymes

A

cholesteryl ester hydrolase and STAR

164
Q

role of cholesteryl ester hydrolase-

A

frees cholesterol

165
Q

STAR role

A

moves cholesterol into inner mito. mem.

166
Q

DHEA is a precursor for-

A

testosterone and estradiol

167
Q

pregnenolone (previously synth in IMM then sent to ER) is made into 1 of 2 products:

A

progesterone or 17 alpha hydroxypregnenolone

168
Q

progesterone is a precursor for

A

mineralocorticoids and glucocorticoids

169
Q

17 alpha hydroxypregnenolone is a precursor for

A

androgens

170
Q

11 beta hydroxysteroid dehydrogenase type 2 isoform does what?

A

converts cortisol to cortisone

171
Q

11 beta hydroxysteroid dehydrogenase type 1 isoform does what?

A

converts cortisone into cortisol in adipose tissue

172
Q

increased circulating K+ causes a release of

A

aldosterone

173
Q

aldosterone is made in less amts than cotisol and mostly circulates in its ____ form

A

free

174
Q

aldosterone is excreted in the urine as:

A

acid labile metabolite (18- glucuronide), intact, or tetraglucuronide

175
Q

Type 1 corticoid receptor binds

A

aldosterone and cortisol

176
Q

Type 2 corticoid receptor binds

A

just cortisol

177
Q

How do we fix the issue of type 1 receptors binding cortisol?

A

the same tissues express 11 beta hydroxysteroid dehydrogenase

178
Q

what does cortisol do to vasculature?

A

ensures integrity/responsiveness by helping regulate blood fluid volume and Na+ retention

179
Q

principal cells-

A

respond to aldosterone to increase Na+ reabsorption

180
Q

intercalated cells-

A

respond to aldosterone to increase H+ ATPase, contributing to the Cl-/HCO3- exchanger on basolateral membrane

181
Q

2 main androgens of the adrenal gland-

A

DHEA and androstenedione

182
Q

2 enzymes act on androstenedione-

A

17 beta hydroxysteroid dehydrogenase makes testosterone and estradiol

aromatase makes estrone

183
Q

deficiency of 11b hydroxylase result-

A

impaired cortisol production, shifts precursors to aldosterone sythesis

184
Q

deficiency in 21 hydroxylase result-

A

cant convert progesterone to gluco and mineralo corticoids. leads to more DHEA

185
Q

Cushings syndrome-

A

excess in circulating levels of cortisol regardless of cause

186
Q

cushing disease-

A

pituitary tumor causes excess CRH release`

187
Q

Addison’s disease-

A

destroyed adrenal cortex, no cortisol or aldosterone. leads to increased melanin production by MSH

188
Q

secondary adrenal insufficiency-

A

decrease in ACTH release

189
Q

tertiary adrenal insufficiency-

A

decrease in hypothalamic function

190
Q

Conn’s sydrome

A

primary hyperaldosteronism

191
Q

high renin and high aldosterone leads to

A

hyperreninemic hyperaldosteronism

192
Q

Barter’s syndrome

A

tertiary hyperaldosteronism- defect in Na+ transporters in tubules

193
Q

Barter’s syndrome leads to what disease

A

sodium wasting disease

194
Q

licorice inhibits

A

11 beta hydroxysteroid dehydrogenase, leads to high cortisol–> binds type II–> hypertension

195
Q

Dexamethasone suppression test-

A

dex. will mimic glucocorticoids so you should see a decrease in CRH, ACTH, cortisol

196
Q

Pituitary ACTH tumor responds to

A

Dexamethasone and CRH

197
Q

In a Dexamethasone test a reaction indicates:

No reaction indicates:

A

normal function or if there is a tumor the tumor is in the HP axis
ectopic tumor

198
Q

does the adrenal medulla release more epi or norepi

A

more epi

199
Q

norepi is converted to epi by:

A

phenylethanolamine N-methyltransferase (PNMT)

200
Q

PNMT synthesis is increased by

A

cortisol

201
Q 
Name the kinds of catecholamine receptors on these organs
vasculature- 
heart 
lungs
kidneys
GI
liver
pancreas
fat 
SKM
A 
vasculature- a1/a2
heart- b1/a1
lungs- b2
kidneys- b1
GI- a1/b2
liver- a1/b2
pancreas- a2
fat b3
SKM b2
202
Q

2 enzymes that degrade catecholamines

A

MAO and COMT

203
Q

ne and epi are broken down into

A

metanephrine and normetanephrine. both are the broken down into Vanillylmandelic acid (VMA)

204
Q

VMA production does not occur in the

A

adrenal medulla

205
Q

NE and EPI can be broken down in what 3 tissues?

A

liver, kidney, adrenal medulla

206
Q

acute effects of hypothalamus turning on the SNS and HPA axis

A

increase in lipolysis and glycolysis

207
Q

chronic effects of hypothalamus turning on SNS and HPA axis

A

insulin resistance

208
Q

the price our body pays for constant adaptation to chronic stressors is called

A

allostatic load

209
Q

after a meal, what changes about insulin release?

A

pulsatile amplitude and frequency increase

210
Q

pulsatility of insulin is critical for

A

maintaining insulin responsiveness by giving time for receptors to regroup

211
Q

90% of insulin circulates as ____ form

A

free

212
Q

half life of insulin:

A

a few minutes

213
Q

why would an IV injection of IGF-1 cause hypoglycemia?

A

not enough time for binding proteins to be made to bind IGF-1 and it would cause a hyper-insulin like response

214
Q

what are pancreas beta cell K+ channels sensitive to?

A

ATP

215
Q

4 hormones that stimulate insulin release:

A

acetylcholine, CCK, glucagon, GLP-1

216
Q

what is GLP-1 produced by?

A

the intestines

217
Q

how do sulfonylurea drugs increase insulin release?

A

mimic ATP in pancreatic beta cells

218
Q

where is GLUT 2 expressed?

A

pancreas B cells, liver, intestine, and kidney

219
Q

the major neuronal GLUT

A

GLUT3

220
Q

insulin activates ______ which causes growth of vascular smooth muscle

A

MAPK

221
Q

pro-glucagon can be cleaved into 2 major products-

A

glucagon (pancreas) and GLP-1 (intestines)

222
Q

half life of glucagon and GLP-1

A

minutes

223
Q

GLP-1 is degraded by

A

dipeptidyl peptidase IV (DPP IV)

224
Q

what do incretins (like GLP-1) do?

A

stimulate insulin release

225
Q

GLP-1 stimulates insulin release only in the presence of

A

high glucose levels

226
Q

what doe GLP-1 do to glucaon secretion

A

decreases it

227
Q

if you are diabetic, would you want to take a drug that increased or decreased GLP-1?

A

increased

228
Q

_______ degrades DPP4 to prolong the activity of _____

A

vildagliptin

GLP-1

229
Q

somatostatin half life

A

minutes

230
Q

somatostatin is made by

A

delta cells of pancreas

231
Q

amylin is in the _____ family of hormones

A

calcitonin

232
Q

amylin suppresses ______ secretion and decreases ______

A

glucagon

gastric emptying

233
Q

Syndrome X-

A

insulin resistance syndrome characterized by hypertension, atherosclerosis, and central obesity

234
Q

defective PI3 kinase pathway can lead to

A

Type 2 diabetes

235
Q

Diabetic if:
Fasting glucose =
random plasma glucose =

A

> 126

>200

236
Q

HbA1C levels greater than ___ should be treated

A

8%

237
Q

Normal oral glucose tolerance levels:
fasting=
1 hour =
2 hour =

A

60-110

<140

238
Q

what forms blood-testis barrier?

A

sertoli cells

239
Q

what cells signal spermatogenesis?

A

sertoli

240
Q

sertoli cells produce _______

A

inhibin B

241
Q

what cells produce testosterone?

A

leydig cells

242
Q

what is used clinically to track the health of the prostate?

A

prostate specific antigen

243
Q

what does the epididymus secrete?

A

H+

244
Q

FSH stimulates what testicular cells?

A

sertoli

245
Q

what hormones inhibit the HPG axis?

A

IL-1, beta endorphins, Prl, GABA, and dopamine

246
Q

stress causes CRH release, leads to more beta endorphin, leads to suppression of ________

A

HPG axis

247
Q

FSH stimulates production of ________ which captures testosterone for spermatogenesis

A

androgen binding protein

248
Q

inhibin B correlates with:

A

sperm count and testicular volume

249
Q

most testosterone circulates in blood as ______ form

A

protein bound

250
Q

17 beta estradiol can be broken down into:

A

estriol and 2 methoxyestrone

251
Q

testosterone can be converted to _______, a much stronger androgen, via _______

A

DHT

5 alpha reductase

252
Q

DHT is broken down into

A

3 alpha andrstenediol

253
Q

in utero, testosterone stimulates ______ cell proliferation

A

leydig

254
Q

what cells secrete mullerian inhibitory factor?

A

sertoli

255
Q

DHT causes fetal development of

A

prostate and penis

256
Q

adrenarche-

A

spike in production of DHEA prparing for puberty

257
Q

spermatogonia become spermatocytes, which then undergo meiosis to become:

A

spermatids

258
Q

spermatids mature into sperm during

A

spermiogenesis

259
Q

spermiation-

A

release of mature sperm into seminiferous tubules

260
Q

5 substances that inhibit GnRH release

A

beta endorphin, IL-1, prolactin, GABA, DA

261
Q

theca cells are regulated by

A

LH

262
Q

theca cells are important in

A

follicle development and ovulation

263
Q

Granulosa cells are regulated by

A

FSH

264
Q

granulosa cells produce

A

estrogen and progesterone

265
Q

a rise in estrogen right before ovulation will cause a feed forward release of _____ and an inhibition of _____

A

LH

FSH

266
Q

rise in progesterone during menstrual cycle causes feedback inhibition of

A

LH

267
Q

inhibins released from granulosa cells decrease ___ release

A

FSH

268
Q

a released oocyte is surrounded by corona radiata, which is formed from ______ cells in the zona pellucida

A

granulosa

269
Q

LH surge peaks ____ hours before ovulation

A

12-24

270
Q

corpus luteum contains what 2 types of cells?

A

small (theca) and large (granulosa)

271
Q

proliferative phase of menstrual cycle controlled by

A

estrogen

272
Q

secretory phase of menstrual cycle controlled by

A

progesterone

273
Q

theca cells convert cholesterol into

A

androgens

274
Q

granulosa cells convert androgens into

A

estradiol

275
Q

the secretion of ______ parallels estrogen throughout the menstrual cycle

A

testosterone

276
Q

inhibin A and B are made by the ovary are regulated by

A

FSH, LH, and growth factors

277
Q

_____ is a marker of corpus luteum function

A

Inhibin A

278
Q

______ is a marker of granulosa cell function

A

Inhibin B

279
Q

Inhibin A and B have a negative feedback effect on production of

A

FSH and LH

280
Q

Activin increases:

A

graulosa cell proliferation, FSHr expression, and steroidogenesis

281
Q

Activin antagonizes ______ and increases FSH releasse

A

inhibin

282
Q

the androstenedione made in theca cells goes to _____ cells to be converted into ________

A

granulosa

17 beta estradiol

283
Q

estradiol is broken down into

A

2 methoxyestrone

284
Q

progesterone is broken down into

A

pregnandiol

285
Q

estrogen upregulates _____ receptor expression even though it antagonizes this hormone’s effects

A

progesterone

286
Q

non-genomic effects of estrogen are mediated by

A

MAPK

287
Q

what does human placental lactogen do?

A

regulates metabolism and development of fetus. STIMULATES SURFACTANT PRODUCTION

288
Q

HGH V role

A

increases availablility of fetal glucose and amino acids. ONLY ON MATERNAL SIDE OF PLACENTA

289
Q

HGH V replaces what hormone

A

maternal pituitary growth hormone

290
Q

fetoplacental unit-

A

cooperation between maternal liver, placenta, and fetal adrenal glands

291
Q

the placenta can convert cholesterol into

A

pregnenolone then progesterone

292
Q

in fetal adrenal gland, pregnenolone is converted into

A

DHEA

293
Q

in fetal liver DHEA is hydroxylated then sent

A

back to the placenta where it is converted into estriol

294
Q

what metabolite, exreted in maternal urine, can be measured as a reflection of the whole fetoplacental unit?

A

estriol

295
Q

what do these things do to developing breasts:
EGF=
thyroid hormone=
oxytocin=

A

EGF= ductal elongation and branching
thyroid hormone= ductal branching and budding
oxytocin= expansion and differentiation

296
Q

levels of what hormones will increase significantly during menopause?

A

FSH and LH

297
Q

A T score of ______ indicates osteoporosis

A

-2.5 or less

298
Q

Bisphosphonates-

A

inhibit osteoclast activity and protect osteoblasts

299
Q

anti-progestins-

A

increase expression of prostaglandins to expel embryo. “the morning after pill”

300
Q

Kallman syndrome-

A

gonadotropin deficiency

301
Q

How does the Balke protocol increase work load?

A

increases resistance

302
Q

on an EKG, what indicates ischemia?

A

severe ST depression

303
Q

what happens to the T wave during exercise?

A

decreases in height

304
Q

Vd/Vt =

A

PaCO2-PeCO2/PaCO2

305
Q

breathing reserve =

A

MVV - Ve max

306
Q

FEV x 35 gives you a rough estimate of

A

what the max ventilation per minute is

Spring 2015 (9 decks)

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