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Endo II > Phys review > Flashcards

Phys review Flashcards

1
Q

hormones secreted from hypothalamus

A 
TRH
CRH
GnRH
somatostatin
dopamine
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2
Q

ant pituitary hormones

A 
released from portal circulation
TSH
FSH
LH
ACTH
MSH
GH
Prolactin
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3
Q

post pituitary hormones

A

released directly from neurons
oxytocin
ADH

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4
Q

thyroid hormones

A

T3
T4
calcitonin

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5
Q

parathyroid hormones

A

PTH

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6
Q

pancreas hormones

A

insulin

glucagon

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7
Q

adrenal medulla hormones

A

NE

Epi

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8
Q

kidney hormones

A

renin

vit D

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9
Q

adrenal Cx hromones

A

cortisol
aldosterone
adrenal androgens

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10
Q

testes hormones

A

testosterone

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11
Q

ovaries hormones

A

E2

progesterone

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12
Q

corpus luteum

A

estradiol

progesterone

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13
Q

Placenta

A

HCG
E3
progesterone
HPL

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14
Q

example of positive feedback loop

A

E2 on anterior pituitary midcycle

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15
Q

lipid soluble hormone receptors

A

inside cell

usually in nucleus

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16
Q

lipid soluble hormone action

A

TF -> new proteins

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17
Q

lipid soluble hormone storage

A

synthesized as needed

exception T3 and T4

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18
Q

lipid soluble hormone plasma transport

A

attached to proteins

exception adrenal androgens

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19
Q

lipid soluble hormone half life

A

long due tprportional to affinity for carrier

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20
Q

water soluble hormone receptor

A

outer surface of cell

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21
Q

water soluble hormone action

A

second messangers

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22
Q

water soluble hormone storage

A

stored in vesicles

sometimes prohormone stored

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23
Q

water soluble hormone plasma transport

A

dissolved unbound

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24
Q

water soluble hormone half life

A

short proportional to MW

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25
Q

tertiary condition ex

A

hypothalamic failure

TRH, TSH, and T3/4 ALL low

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26
Q

secondary condition ex

A

pituitary failure

high TRH low TSH and T3/4

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27
Q

primary thyroid conditions ex

A

thyroiditis

graves

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28
Q

thyroiditis

A

TRH and TSH high

T3/4 low

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29
Q

graves

A

low TRH and TSH

high T3/4

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30
Q

mutation in hormone receptor

A

all preceding signaling molecules will be elevated

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31
Q

nuclei of post pituitary

A

SON (supraoptic nuclei)

PVN (paraventricular nuclei)

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32
Q

ADH

A

maintain normal osmolality of body fluids
releases in response to increased serum osmolality (and decreased BP)
increases number of aquaporins in distal tubule to increase water resorption
induces contraction of vascular smooth mm

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33
Q

Oxytocin

A

milk letdown

uterine contraction

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34
Q

receptor for ADH

A

V2 on basolateral membrane of collecting duct

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35
Q

DI

A

Dx confirmed by dehydration stimulus with inability to concentrate urine

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36
Q

plasma osmolality in DI

A

neurogenic normal/high

nephrogenic normal/high

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37
Q

urine osmolality in DI

A

neurogenic low

nephrogenic low

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38
Q

plasma ADH

A

neurogenic low

nephrogenic normal-high

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39
Q

urine osmolality after water deprivation

A

no change

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40
Q

plasma ASH after water deprivation

A

neurogenic no change

nephrogenic high

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41
Q

urine osmolality after ADH administation

A

neurogenic high

nephrogenic no change

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42
Q

factors which stimulate GH

A 
decrease glucose concentration
decreased FFAs
arginine
fasting/starvation
hormones of puberty (E,T)
EXERCISE
STRESS
STAGE III/IV sleep
alpha-adrenergic agonisits
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43
Q

factors which inhibit GH

A 
increased glucose concentration
increased FFAs
obesity
senesence
somatostatin
somatomedins
GH
beta-adrenerigc agonists
pregnancy
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44
Q

overall affects of GH

A

diabetogenic effect
increased protein synthesis and organ growth (IGF-I)
increased linear growth (IGF-I)

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45
Q

diabetogenic effect of GH

A 
causes insulin resistance
decreased glucose uptake
increased blood glucose
increased lipolysis
increased blood insulin levels
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46
Q

increased protein synthesis and organ growth

A

IGF-I
increased aa uptake
increased DNA, RNA, and protein synthesis
increased lean body mass and organ size

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47
Q

increased linear growth

A

IGF-I

altered cartilage metabolism

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48
Q

factors which stimulate prolactin

A 
pregnancy (due to estrogen)
breast-feeding
sleep
stress
TRH
Dopamine antagonists
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49
Q

factors which inhibit prolactin

A

dopamine
bromocriptine (dopamine agonist)
somatostatin
prolactin

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50
Q

GnRH

A

pulsatile release prevents downregulation of its receptors

constant infusion will cause a decrease in LH and FSH

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51
Q

T3/4 synthesis

A
  • synthesis of TG and exocytosis to follicular lumen
  • transport of I into cell via Na cotransport
  • oxidation of I via peroxidase
  • organification of I into MIT and DIT ( inhibited by PTU)
  • coupling rxn (DIT+DIT = T4 DIT + MIT = T3)
    endocytosis of TG
    -proteolysis of iodinated TG -> T3/4
  • MIT and DIT and TG recycled
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52
Q

transport of T3/4

A

circulate bound to TBG and to lesser extend albumin and TTR

  1. 98% of T4 bound
  2. 5% of T3 bound
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53
Q

T3

A

more active thyroid hormone b/c 10x higher affinity for TR
ratio of T4:T3 is 10:1
tissues contain deiodinases to convert T4 -> T3
people without

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54
Q

normal TH levels

A

T4 5-12ug/dL

T3 70-190ng/dL

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55
Q

factors which stimulate TH

A

TSH
Thyroid stimulating immunoglobulins
increased TBG levels (pregnancy)

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56
Q

factors which inhibit TH

A

I deficiency
deiodinase deficiency
excessive I intake (Wolff-Cahikoff effect)
Perchlorate (thiocyanate) inhibit NA/I cotransporter
PTU (inhibits peroxidase)
decreased TGB levels (liver disease)

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57
Q

TH effects on growth

A

growth formation

bone maturation

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58
Q

TH effects on CNS

A

maturation of CNS

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59
Q

TH effects on BMR

A

increased Na/K ATPase
increased O2 consumption
increased heat production

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60
Q

TH effects on metabolism

A

increased glucose absorption
increased glycogenolysis
increased gluconeogenesis

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61
Q

TH effects on CV

A

increased CO

62
Q

thyrotoxicosis

A 
graves disease
factitious thyrotoxicosis
toxic adenoma
toxic nodular goiter
pituitary overproduction of TSH
granulomatous thyroiditis
subacute lymphocytic thyroiditis
63
Q

graves disease

A

autoimmune thyroid disease

.5% of population

64
Q

factitious thryotoxicosis

A

exogenous thyroid hormone with gland atrophy and low TG

65
Q

toxic adeoma

A

aka hot nodule

overproduction of TH by nodule with low TSH and gland atrophy surrounding nodule

66
Q

toxic nodular goiter

A

multiple nodules

67
Q

pituitary overproduction of TSH

A

rare

68
Q

granulomatous thyroidtiis

A

aka subacutre thyroiditis
viral etiology with painful gland
hyperthyroidism -> euthyroidism -> hypothyrodism -> euthyroidism

69
Q

subacute lymphocytic thyroiditis

A

aka silent thyroiditis
believed to be autoimmune
non-tender gland transient
example is postpartum thyroiditis

70
Q

primary hypothyroidsim

A

hashimotos 5-10% of population
T cell mediated, but Abs can also be present
radioactive ablation of thyroid

71
Q

zona glomerulosa

A

aldosterone

controlled by Ang II and K

72
Q

zona fasciulata

A

cortisol

controlled by ACTH

73
Q

zona reticularis

A

androgens

controlled by ACTH

74
Q

medulla

A

Epi

controlled by ANS

75
Q

factors which stimulate cortisol

A 
decreased blood cortisol 
sleep-wake transition
stress, surgery, trauma
hypoglacemia
psychiatric disturbances
ADH
alpha-adrenergic agonists 
beta-adrenergic antagonisits
serotonin
76
Q

factors which inhibit cortisol secretion

A

increased cortisol
opioids
somatostatin

77
Q

factors which stimulate aldosterone secretion

A

angiotensin II
ACTH
high plasma K

78
Q

actions of glucocorticoids

A 
increased gluconeogenesis
increased proteolysis
increased lipolysis 
decrease glucose utilization
decrease insulin sensitivity
79
Q

actions of mineralcortiocoids

A

increased Na reabsoprtion
increased K secretion
increased H secretion

80
Q

actions of adrenal androgens

A

females: stimulate growth of pubic and axillary hair and stimulate libido
males: same as testosterone

81
Q

acute cortisol effects

A

mobilize glucose
optimize adrenergic R fnx to increase CO
helps provide energy for inflammatory and immune response, but also protects from damage of unregulated inflammation

82
Q

acute cortisol on liver

A

increased glycogenolysis

increased gluconeogenesis

83
Q

acute cortisol on skeletal mm

A

increased proteolysis
decreased protein synthesis
increased glycogenolysis
decreased glut-4 mediated glucose uptake

84
Q

acute cortisol on adipose tissue

A

increase lipolysis
decreased lipogeneis
decreaed glut-4 mediated glucose uptake

85
Q

chronic cortisol on CNS

A

increased appetite

86
Q

chronic cortisol on liver

A

increased hepatic glycogen synthesis

87
Q

chronic cortisol on skeletal m

A

increased proteolysis

decreaed GLUT-4 mediated glucose uptake

88
Q

chronic cortisol in adipose tissue

A

decrease lipolysis
increased TG synthesis
increased preadipocyte to adipocyte differentiation
decreased GLUT 4 mediated glucose uptake

89
Q

chronic cortisol effects

A

promote localized obesity (abdominal, neck, face)
mm wasting and weakness
glucose intolerance

90
Q

acute cortisol and other hormones

A

decreased insulin/glucagon ratio

increased Epi and NE

91
Q

chronic cortisol and other hormones

A

increased insulin/glucagon ratio

decreased epi and NE

92
Q

addison disease

A

primary adrenocortical insufficiency

93
Q

addisons clinical

A 
hypoglycemia
anorexia, weight loss, nausea
vomiting
weakness
hypotension
hyperkalemia
metabolic acidosis
decreaed pubic and axillary hair in females
hyperpigmentation
94
Q

addisons ACTH

A

increased sue to decreased cortisol

95
Q

addisons Tx

A

replacement of glucocorticoids and mineralcorticoids

96
Q

cushings syndrome

A

primary adrenal hyperplasia

97
Q

cushings syndrome clinical

A

hyperglycemia
mm wasting
central obesity
round face, supraclavicular fat, buffalo hump
striae
virilzation and menstrual disorders in females
HTN

98
Q

cushings syndrome ACTH

A

decreased due to neg feedback of increased cortisol

99
Q

cushings syndrome Tx

A

ketoconazole

metyrapone

100
Q

cushings disease

A

excess ACTH

101
Q

cushings diseases ACTH

A

increased

102
Q

cushings diseases clinical

A

same as cushing syndrome

103
Q

cushings diseases Tx

A

surgical removal or ACTH secreting tumor

104
Q

Conn syndrome

A

aldosterone secreting tumor

105
Q

Conn clinical

A

HTN
hypokalemia
metabolic alkalosis
decreased renin levels

106
Q

conn Tx

A

aldosterone antagonists

surgery

107
Q

21 beta-hydroxylase deficiency clincal

A

virilization of femailes
early acceleration of linear growth
early appearance of pubic hair and axillary hair
symptoms of deficiency of glucocorticioids and mineralcorticoids

108
Q

21 beta-hydroxylase deficiency ACTH

A

increased due decreased cortisol

109
Q

21 beta-hydroxylase deficiency Tx

A

replacement of glucocortiocoids and mineralcorticoids

110
Q

17 alpha hyroxylase deficiency clinical

A

lack of pubic and axillary hair in females
symptoms of deficiency of glucocortiocoids
symptoms of deficiency of glucocorticoids
symptoms of excess mineralcorticoids

111
Q

17 alpha hyroxylase deficiency ACTH

A

increased

112
Q

17 alpha hyroxylase deficiency Tx

A 
replacement of glucocorticoids 
aldosterone antagonists  (spironolactone)
113
Q

Glucose R on brain

A

GLUT3

114
Q

glucose R on liver

A

GLUT2

115
Q

glucose R on mm

A

GLUT4

116
Q

Glucose R on adipose tissue

A

GLUT4

117
Q

beta cells of pancreas

A

insulin

118
Q

alpha cells of pancreas

A

glucagon

119
Q

delta cells of pancreas

A

somatostatin

120
Q

actions of insulin

A 
increase glucose uptake
increase glycogen formation
decrease glycogenolysis
decrease gluconeogenesis
increases protein synthesis
increases fat deposition
decreases lipolysis
increases K uptake
121
Q

factors which stimulate insulin

A 
increased glucose
increased aa 
increased FA and ketoacids
glucagon
cortisol
GIP
K
vagal stimulation Ach
sulfonylurea drugs
obesity
122
Q

factors which inhibit insulin

A 
decreased glucose
fasting
exercise
somatostatin
alpha-adrenergic agonists
diazoxide
123
Q

actions of glucagon

A

increased glycogenolysis
increases gluconeogenesis
increased lipolysis
increased ketoacid formation

124
Q

factors which stimulate glucagon

A 
fasting
decreased glucose concentration
increased aa concentration
beta-adrenergic agonists
Ach
125
Q

factors which inhibit glucagon

A

insulin
somatostatin
increased FA and ketoacid concentration

126
Q

effects of glucagon on blood

A

increases glucose, FA, and ketoacids concentrations

127
Q

high insulin:glucagon ratio

A

favors anabolic rxns

128
Q

low insulin: glucagon ratio

A

favors catabolic rxns

129
Q

normal Ca levels

A

8.5-10.5 mg/dL

130
Q

symptoms of hypocalcemia

A

twitching, mm cramps, tingling, numbness

131
Q

symptoms of hypercalcemia

A

constipation, polyuria, polydipsia, lethargy, coma, death

132
Q

Free Ca

A

50%
45% bound to albumin (kicked off by H)
5% complexed

133
Q

free PO4

A

84%

134
Q

hormones which control Ca

A

PTH
vit D
calcitonin

135
Q

organs which control C

A

skeleton
kidney
intestines

136
Q

CaSR

A

Ca sensor R
7 membrnae G-protein coupled R
senses extracellular Ca-ionized Ca
R found on parathyroid cells, parafollicular cells, and renal tubular cells

137
Q

fnx of PTH

A
  • triggers Ca and PO4 resopriton from bone
  • promotes Ca resorption from kidney
  • promotes PO4 excretion from kidney
  • increases vit D production in kidney
138
Q

functions of vit D

A

bone remodeling
Ca absorption from gut
renal resorption of Ca and PO4

139
Q

PTH binds to osteoblasts

A

osteoblasts release RANKL (IL6) which binds to RANK on osteoclasts to stimulate bone resorption

140
Q

OPG

A

soluble receptor for RANKL to inhibit activation of osteoclasts

141
Q

loss of RANKL

A

increases bone density

osteopetrosis

142
Q

loss of OPG

A

decreases bone density

osteoporosis

143
Q

severe vit D deficiency

A

0-10

144
Q

moderate vit D deficiency

A

10-20

145
Q

mild vit D deficiency

A

20-30

146
Q

normal vit D

A

> 30

147
Q

90% of hypercalcemias due to

A

primary hyperparathyroidism (increased PTH)
or
hypercalcemia of malignancy

148
Q

other causes of hypercalcemia

A 
granulomatous disease
vit D toxicity
vit A toxicity
hyperthyroidism
thiazide diuretics
milk-alkali syndrome
immobilization
adrenal insufficiency
adrenal insufficiency
acute renal failure 
familial hypocalciuric hypercalcemia
149
Q

familial hypocalciuric hypercalcemia

A

heteozygous inactivating mutation in CaSR

increased PTH and serum Ca

150
Q

causes of hypocalcemia

A 
vit D deficiency
hypoparathyroidism
pseudohypoparathyroidism 
hypomagnesmia
renal failure
liver failure
acute pancreatitis
hypoporteinemia
151
Q

pseudohypoparathyroidism

A

genetic condition causing resistance to PTH

Endo II (15 decks)

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