Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Endo II > Phys review > Flashcards

Phys review Flashcards

(151 cards)

Start Studying
1
Q

hormones secreted from hypothalamus

A 
TRH
CRH
GnRH
somatostatin
dopamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ant pituitary hormones

A 
released from portal circulation
TSH
FSH
LH
ACTH
MSH
GH
Prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

post pituitary hormones

A

released directly from neurons
oxytocin
ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

thyroid hormones

A

T3
T4
calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

parathyroid hormones

A

PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pancreas hormones

A

insulin

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

adrenal medulla hormones

A

NE

Epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

kidney hormones

A

renin

vit D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

adrenal Cx hromones

A

cortisol
aldosterone
adrenal androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

testes hormones

A

testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ovaries hormones

A

E2

progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

corpus luteum

A

estradiol

progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Placenta

A

HCG
E3
progesterone
HPL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

example of positive feedback loop

A

E2 on anterior pituitary midcycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

lipid soluble hormone receptors

A

inside cell

usually in nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

lipid soluble hormone action

A

TF -> new proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

lipid soluble hormone storage

A

synthesized as needed

exception T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

lipid soluble hormone plasma transport

A

attached to proteins

exception adrenal androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

lipid soluble hormone half life

A

long due tprportional to affinity for carrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

water soluble hormone receptor

A

outer surface of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

water soluble hormone action

A

second messangers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

water soluble hormone storage

A

stored in vesicles

sometimes prohormone stored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

water soluble hormone plasma transport

A

dissolved unbound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

water soluble hormone half life

A

short proportional to MW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
tertiary condition ex
hypothalamic failure | TRH, TSH, and T3/4 ALL low
26
secondary condition ex
pituitary failure | high TRH low TSH and T3/4
27
primary thyroid conditions ex
thyroiditis | graves
28
thyroiditis
TRH and TSH high | T3/4 low
29
graves
low TRH and TSH | high T3/4
30
mutation in hormone receptor
all preceding signaling molecules will be elevated
31
nuclei of post pituitary
SON (supraoptic nuclei) | PVN (paraventricular nuclei)
32
ADH
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
33
Oxytocin
milk letdown | uterine contraction
34
receptor for ADH
V2 on basolateral membrane of collecting duct
35
DI
Dx confirmed by dehydration stimulus with inability to concentrate urine
36
plasma osmolality in DI
neurogenic normal/high | nephrogenic normal/high
37
urine osmolality in DI
neurogenic low | nephrogenic low
38
plasma ADH
neurogenic low | nephrogenic normal-high
39
urine osmolality after water deprivation
no change
40
plasma ASH after water deprivation
neurogenic no change | nephrogenic high
41
urine osmolality after ADH administation
neurogenic high | nephrogenic no change
42
factors which stimulate GH
``` decrease glucose concentration decreased FFAs arginine fasting/starvation hormones of puberty (E,T) EXERCISE STRESS STAGE III/IV sleep alpha-adrenergic agonisits ```
43
factors which inhibit GH
``` increased glucose concentration increased FFAs obesity senesence somatostatin somatomedins GH beta-adrenerigc agonists pregnancy ```
44
overall affects of GH
diabetogenic effect increased protein synthesis and organ growth (IGF-I) increased linear growth (IGF-I)
45
diabetogenic effect of GH
``` causes insulin resistance decreased glucose uptake increased blood glucose increased lipolysis increased blood insulin levels ```
46
increased protein synthesis and organ growth
IGF-I increased aa uptake increased DNA, RNA, and protein synthesis increased lean body mass and organ size
47
increased linear growth
IGF-I | altered cartilage metabolism
48
factors which stimulate prolactin
``` pregnancy (due to estrogen) breast-feeding sleep stress TRH Dopamine antagonists ```
49
factors which inhibit prolactin
dopamine bromocriptine (dopamine agonist) somatostatin prolactin
50
GnRH
pulsatile release prevents downregulation of its receptors | constant infusion will cause a decrease in LH and FSH
51
T3/4 synthesis
- 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
52
transport of T3/4
circulate bound to TBG and to lesser extend albumin and TTR 99. 98% of T4 bound 99. 5% of T3 bound
53
T3
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
54
normal TH levels
T4 5-12ug/dL | T3 70-190ng/dL
55
factors which stimulate TH
TSH Thyroid stimulating immunoglobulins increased TBG levels (pregnancy)
56
factors which inhibit TH
I deficiency deiodinase deficiency excessive I intake (Wolff-Cahikoff effect) Perchlorate (thiocyanate) inhibit NA/I cotransporter PTU (inhibits peroxidase) decreased TGB levels (liver disease)
57
TH effects on growth
growth formation | bone maturation
58
TH effects on CNS
maturation of CNS
59
TH effects on BMR
increased Na/K ATPase increased O2 consumption increased heat production
60
TH effects on metabolism
increased glucose absorption increased glycogenolysis increased gluconeogenesis
61
TH effects on CV
increased CO
62
thyrotoxicosis
``` graves disease factitious thyrotoxicosis toxic adenoma toxic nodular goiter pituitary overproduction of TSH granulomatous thyroiditis subacute lymphocytic thyroiditis ```
63
graves disease
autoimmune thyroid disease | .5% of population
64
factitious thryotoxicosis
exogenous thyroid hormone with gland atrophy and low TG
65
toxic adeoma
aka hot nodule | overproduction of TH by nodule with low TSH and gland atrophy surrounding nodule
66
toxic nodular goiter
multiple nodules
67
pituitary overproduction of TSH
rare
68
granulomatous thyroidtiis
aka subacutre thyroiditis viral etiology with painful gland hyperthyroidism -> euthyroidism -> hypothyrodism -> euthyroidism
69
subacute lymphocytic thyroiditis
aka silent thyroiditis believed to be autoimmune non-tender gland transient example is postpartum thyroiditis
70
primary hypothyroidsim
hashimotos 5-10% of population T cell mediated, but Abs can also be present radioactive ablation of thyroid
71
zona glomerulosa
aldosterone | controlled by Ang II and K
72
zona fasciulata
cortisol | controlled by ACTH
73
zona reticularis
androgens | controlled by ACTH
74
medulla
Epi | controlled by ANS
75
factors which stimulate cortisol
``` decreased blood cortisol sleep-wake transition stress, surgery, trauma hypoglacemia psychiatric disturbances ADH alpha-adrenergic agonists beta-adrenergic antagonisits serotonin ```
76
factors which inhibit cortisol secretion
increased cortisol opioids somatostatin
77
factors which stimulate aldosterone secretion
angiotensin II ACTH high plasma K
78
actions of glucocorticoids
``` increased gluconeogenesis increased proteolysis increased lipolysis decrease glucose utilization decrease insulin sensitivity ```
79
actions of mineralcortiocoids
increased Na reabsoprtion increased K secretion increased H secretion
80
actions of adrenal androgens
females: stimulate growth of pubic and axillary hair and stimulate libido males: same as testosterone
81
acute cortisol effects
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
acute cortisol on liver
increased glycogenolysis | increased gluconeogenesis
83
acute cortisol on skeletal mm
increased proteolysis decreased protein synthesis increased glycogenolysis decreased glut-4 mediated glucose uptake
84
acute cortisol on adipose tissue
increase lipolysis decreased lipogeneis decreaed glut-4 mediated glucose uptake
85
chronic cortisol on CNS
increased appetite
86
chronic cortisol on liver
increased hepatic glycogen synthesis
87
chronic cortisol on skeletal m
increased proteolysis | decreaed GLUT-4 mediated glucose uptake
88
chronic cortisol in adipose tissue
decrease lipolysis increased TG synthesis increased preadipocyte to adipocyte differentiation decreased GLUT 4 mediated glucose uptake
89
chronic cortisol effects
promote localized obesity (abdominal, neck, face) mm wasting and weakness glucose intolerance
90
acute cortisol and other hormones
decreased insulin/glucagon ratio | increased Epi and NE
91
chronic cortisol and other hormones
increased insulin/glucagon ratio | decreased epi and NE
92
addison disease
primary adrenocortical insufficiency
93
addisons clinical
``` hypoglycemia anorexia, weight loss, nausea vomiting weakness hypotension hyperkalemia metabolic acidosis decreaed pubic and axillary hair in females hyperpigmentation ```
94
addisons ACTH
increased sue to decreased cortisol
95
addisons Tx
replacement of glucocorticoids and mineralcorticoids
96
cushings syndrome
primary adrenal hyperplasia
97
cushings syndrome clinical
hyperglycemia mm wasting central obesity round face, supraclavicular fat, buffalo hump striae virilzation and menstrual disorders in females HTN
98
cushings syndrome ACTH
decreased due to neg feedback of increased cortisol
99
cushings syndrome Tx
ketoconazole | metyrapone
100
cushings disease
excess ACTH
101
cushings diseases ACTH
increased
102
cushings diseases clinical
same as cushing syndrome
103
cushings diseases Tx
surgical removal or ACTH secreting tumor
104
Conn syndrome
aldosterone secreting tumor
105
Conn clinical
HTN hypokalemia metabolic alkalosis decreased renin levels
106
conn Tx
aldosterone antagonists | surgery
107
21 beta-hydroxylase deficiency clincal
virilization of femailes early acceleration of linear growth early appearance of pubic hair and axillary hair symptoms of deficiency of glucocorticioids and mineralcorticoids
108
21 beta-hydroxylase deficiency ACTH
increased due decreased cortisol
109
21 beta-hydroxylase deficiency Tx
replacement of glucocortiocoids and mineralcorticoids
110
17 alpha hyroxylase deficiency clinical
lack of pubic and axillary hair in females symptoms of deficiency of glucocortiocoids symptoms of deficiency of glucocorticoids symptoms of excess mineralcorticoids
111
17 alpha hyroxylase deficiency ACTH
increased
112
17 alpha hyroxylase deficiency Tx
``` replacement of glucocorticoids aldosterone antagonists (spironolactone) ```
113
Glucose R on brain
GLUT3
114
glucose R on liver
GLUT2
115
glucose R on mm
GLUT4
116
Glucose R on adipose tissue
GLUT4
117
beta cells of pancreas
insulin
118
alpha cells of pancreas
glucagon
119
delta cells of pancreas
somatostatin
120
actions of insulin
``` increase glucose uptake increase glycogen formation decrease glycogenolysis decrease gluconeogenesis increases protein synthesis increases fat deposition decreases lipolysis increases K uptake ```
121
factors which stimulate insulin
``` increased glucose increased aa increased FA and ketoacids glucagon cortisol GIP K vagal stimulation Ach sulfonylurea drugs obesity ```
122
factors which inhibit insulin
``` decreased glucose fasting exercise somatostatin alpha-adrenergic agonists diazoxide ```
123
actions of glucagon
increased glycogenolysis increases gluconeogenesis increased lipolysis increased ketoacid formation
124
factors which stimulate glucagon
``` fasting decreased glucose concentration increased aa concentration beta-adrenergic agonists Ach ```
125
factors which inhibit glucagon
insulin somatostatin increased FA and ketoacid concentration
126
effects of glucagon on blood
increases glucose, FA, and ketoacids concentrations
127
high insulin:glucagon ratio
favors anabolic rxns
128
low insulin: glucagon ratio
favors catabolic rxns
129
normal Ca levels
8.5-10.5 mg/dL
130
symptoms of hypocalcemia
twitching, mm cramps, tingling, numbness
131
symptoms of hypercalcemia
constipation, polyuria, polydipsia, lethargy, coma, death
132
Free Ca
50% 45% bound to albumin (kicked off by H) 5% complexed
133
free PO4
84%
134
hormones which control Ca
PTH vit D calcitonin
135
organs which control C
skeleton kidney intestines
136
CaSR
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
fnx of PTH
- triggers Ca and PO4 resopriton from bone - promotes Ca resorption from kidney - promotes PO4 excretion from kidney - increases vit D production in kidney
138
functions of vit D
bone remodeling Ca absorption from gut renal resorption of Ca and PO4
139
PTH binds to osteoblasts
osteoblasts release RANKL (IL6) which binds to RANK on osteoclasts to stimulate bone resorption
140
OPG
soluble receptor for RANKL to inhibit activation of osteoclasts
141
loss of RANKL
increases bone density | osteopetrosis
142
loss of OPG
decreases bone density | osteoporosis
143
severe vit D deficiency
0-10
144
moderate vit D deficiency
10-20
145
mild vit D deficiency
20-30
146
normal vit D
>30
147
90% of hypercalcemias due to
primary hyperparathyroidism (increased PTH) or hypercalcemia of malignancy
148
other causes of hypercalcemia
``` 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
familial hypocalciuric hypercalcemia
heteozygous inactivating mutation in CaSR | increased PTH and serum Ca
150
causes of hypocalcemia
``` vit D deficiency hypoparathyroidism pseudohypoparathyroidism hypomagnesmia renal failure liver failure acute pancreatitis hypoporteinemia ```
151
pseudohypoparathyroidism
genetic condition causing resistance to PTH

Endo II (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions