Endocrine Flashcards
(163 cards)
1
Q
which adrenergic receptors increase hepatic glucose output
A
beta 2 and 3
2
Q
alpha 1 receptor works by which second messanger
A
IP3, Ca (Gq)
3
Q
alpha 2 receptor works by which second messanger
A
Gi : decrease cAMP
4
Q
beta1 receptor works by which second messanger
A
Gs increase cAMP
5
Q
beta2 receptor works by which second messanger
A
Gs increase cAMP
6
Q
alpha 1 prefers which adrenergic ligand
A
NE
7
Q
alpha 2 prefers which adrenergic ligand
A
NE
8
Q
which adrenergic receptor inhibits insulin release
A
alpha 2
9
Q
beta 1 prefers which adrenergic ligand
A
NE=E
10
Q
beta 2 prefers which adrenergic ligand
A
E
11
Q
beta 3 prefers which adrenergic ligand
A
NE
12
Q
where do you find beta 2 receptors
A
GI, urinary, adipose, liver, skeletal muscle, alpha cells in pancreas, bronchiole
13
Q
where do you find beta 1 receptors
A
heart
14
Q
where do you find alpha receptors
A
veins, lymph, beta cells in pancreas
15
Q
beta3 receptor works by which second messanger
A
Gs increase cAMP
16
Q
disease: high circulating catecholamines causing headache, palpitations, HTN, sweat, tachycardia
A
pheochromocytoma
17
Q
disease: high cortisol, low ACTH
A
cushing syndrome (spontaneous or drug induced cortisol excess)
18
Q
disease: high cortisol, high ACTH
A
cushing disease (pituitary adenoma)
19
Q
how to distinguish cushing disease from syndrome
A
dexamethasone suppression test
20
Q
osteoporosis, poor wound healing, virilization, HTN, round face, buffalo torso
A
cushing
21
Q
treatment for cushings
A
ketoconozole, metyrapone
22
Q
why do we get HTN with high cholesterol
A
alpha 1 stimulation causes vasoconstriction
23
Q
disease: hypoglycemia, hypotension, hyperkalemia, acidosis, decreased hair and libido, hyperpigmentation
A
addisons
24
Q
what will cortisol, CRH, ACTH look like in secondary adrenocortical insufficiency
A
low cortisol, high CRH, low ACTH
25
disease: primary adrenocortical insufficiency
addisons
26
why do we get hyper pigmentation with addisons
increased ACTH with alphaMSH can't stimulate adrenal cortex (cuz its messed up) but the MSH produces discoloration
27
disease: primary hyperaldosteronism
conn syndrome
28
disease: hypervolemic, hypernatremic, HTN, low K, low H (alkalosis)
Conn syndrome
29
how do you treat conn syndrome
spironolactone (aldosterone antagonist)
30
disease: overproduction of mineral corticoids can occur when we have deficiency in which enzyme
17alpha hydroxylase
31
disease: cannot synthesize gluco or mineral corticoids so we get excess androgens leading to urinary ketosteroids and sterility
21 beta hydroxylase deficiency
32
a deficiency in which enzyme along the steroid hormone synthesis pathway would lead to HTN
11 beta hydroxylase
33
a deficiency in which enzyme along the steroid hormone synthesis pathway would lead to Hypotension
21 beta hydroxylase
34
angiotensin II stimulates what enzyme
aldosterone synthase
35
what regulates secretion of cholesterol desmolase
ACTH
36
what enzyme is needed to convert cortisol to the less active corticosterone after binding mineral corticoid receptors
beta hydroxysteroid dehydrogenase
37
who secretes PTH
chief cells
38
who secretes calcitonin
C parafollicular cells
39
oxytocin and ADH are stored in these enlarged axon terminals
herring bodies
40
glial cells of neurohypophysis
pituicytes
41
pineal gland secretory function is mediated by what type of receptor
beta adrenergic
42
what do F cells in pancreas secrete
pancreatic polypeptide
43
what do delta cells secrete in pancreas
somatostatin and gastrin
44
what do catecholamines and thyroid hormones have in common
derived from tyrosine (amine hormones)
45
POMC neurons make what kind of hormone
ACTH, MSH
46
what stimulates GH release
low glucose, GHRH, estrogen, testosterone, exercise, stress, sleep, alpha adrenergic agonist
47
Somatomedin C is also called
IGF1
48
GH directly affects what organs
skeletal muscle, adipose, liver
49
what does GnRH do
stimulates anterior pituitary to make LH and FSH
50
GH has indirect anabolic affect via what mediator
somatomedins made in liver
51
the hypothalamus releases what product that inhibits GH secretion from anterior pituitary
somatostatin
52
what test is performed to confirm diagnosis of GH excess (acromegaly)
administer oral glucose-- should suppress GH levels and if they remain high we know there is exogenous GH secretion
53
how does prolactin suppress ovulation
inhibit GnRH
54
what stimulates prolactin release
TRH
55
what inhibits prolactin release
dopamine
56
3 sources of dopamine which inhibits release of prolactin
posterior pituitary, hypothalamus, non lactotroph cells of anterior pituitary
57
how does ADH increase peripheral resistance
binds V1 receptors increasing intracellular ca++ and contraction of SM in arterioles
58
disease: large volume of dilute urine excreted and high osmolarity of body fluids-- fixed with ADH analogue
central DI
59
disease: large volume dilute urine excreted and high osmolarity of body fluids and high ADH
nephrogenic DI
60
MOA for nephrogenic DI
V2 defect
61
nephrogenic DI can occur secondary to what
lithium use, polycystic kidney disease, sickle cell anemia
62
how to treat nephrogenic DI
thiazide diuretics: inhibit Na reabsorb from PCT
63
disease: dilute body fluids, hyponatremia, high concentration of urine
SIADH
64
disease: enlargement of pituitary during pregnancy leads to infarction and hypopituitism
sheehan syndrome
65
what enzyme activates a GPCR by making the GDP GTP
GEF
66
what enzyme deactivates GPCR by hydrolyzing GTP
GAP
67
what are the ligands for RTKs
growth factors
68
inactive versus active form of insulin
hexamer: inactive
monomer: active
69
end result of RAS dependent insulin action
upreg glucokinase
70
end result of RAS independent insulin action
move GLUT4 to membrane (and activate glycogen synthase)
71
insulin resistance may happen because PKB does not activate to insert GLUT4 into PM's. this could be because ___ gets phosphorylated at the wrong spot (ser/thr instead of tyr)
IRS1 and IRS2
72
epinephrine encourages what pancreatic secretion
glucagon (stress can cause DKA because E also inh insulin)
73
when we have no more glycogen, ___ stimulates gluconeogenesis
cortisol
74
estrogen binds ___ which is a HAT loosening DNA allowing transcription
SRC1
75
estrogen antagonists like ___ are going to activate HDAC to tighten chromatin
tamoxifen
76
conversion from T4 to T3 requires what enzyme
deiodinase
77
what enzyme hydrolyzes bonds to release MIT and DIT from TG allowing them to combine and form thyroid hormones
lysosomal proteases
78
MIT and DIT interact with ___ in the thyroid epithelial cell to produce tyrosine and thyroglobulin
intrathyroidal deiodinase
79
deficiency in intrathyroid deiodinase mimics what other condition
I- deficiency
80
who does I- get to lumen
pendrin + peroxidase
81
drug that blocks NIS
perchlorate and thiocynate
82
drug that blocks peroxidase
PTU
83
high levels of I- inhibit organification and synthesis of thyroid hormones (peroxidase aint working)
wolff chaikoff effect
84
what causes high TBG
pregnancy
85
thyroid hormone encourages synthesis of
NaK ATPase, beta adrenergic receptors, lysosome enzymes
86
to convert carotene to vitamine A we need what hormone
thyroid hormone
87
disease: antibodies destroy or block thyroid hormone synthesis by blocking peroxidase resulting in hypothyroid with goiter
autoimmune thyroiditis
88
disease: hypothyroidism in mother during pregnancy leads to this in baby
cretinism
89
disease: antibody stimulates TSH receptors
graves disease
90
disease: protruding eyeballs, periorbital edema, elevated thyroid hormone, goiter
graves
91
disease: impaired synthesis of thyroid hormones due to TG or TPO antibodies
hashimoto disease
92
disease: iodide deficiency in developing baby
cretinism
93
most common hyperthyroidism cause
graves
94
can you have goiter with i deficiency
yes- low T3/T4 stimulates TSH release
95
disease: new bones fail to mineralize so we get bending and softening
osteomalacia
96
disease: hyperreflexia, muscle twitching, tingling
hypocalcemia
97
disease: decrease QT interval, constipation, lack apetite, hyporeflexive, coma
hypercalcemia
98
academia leads to what ca++ related condition
H displaces Ca from albumin and you get increase in free ionized ca
99
chromic hypomagnesemia in alcoholics inhibits synthesis storage and secretion of what
PTH
100
how does vitamin D increase calcium reabsorption in GI tract
synthesis of calbindin which increases the absorptive capacity of GI epithelial cells so we can bring more into blood
100
how does PTH increase Pi excretion
inhibits NPT (NaPi cotrasport) in PCT
101
whats the job of osteoprotegrin
bone formation (inactivate osteoclast)
102
where does ca reabsorption take place in a kidney stimulated by PTH
TAL, distal tubule
103
what does estrogen do to [ca]
stimulate intestinal and renal absorbtion
105
what regulates activity of 1alpha hydroxylase
activated by PTH
| inhibited by Ca
105
disease: stones, bones, groans
primary hyperparathyroidism
106
what are vitamin D levels like in someone with parathyroid adenoma
increased PTH causes lots of vitamin D activation so levels are HIGH
107
disease: renal failure or vitamin D deficiency leads to low ca
secondary hyperparathyroidism
108
in secondary hyperparathyroidism what are the Pi levels like
DEPENDS on the cause
vitamin D deficient: low Pi levels
renal failure: high Pi levels (cannot excrete)
109
disease: low ca, low vitamin D, high serum Pi, muscle cramping, seizure, poor tooth development, mental deficit, intestinal malabsorbtion
hypoparathyroidism
110
disease: autosomal dominant inherited, Gs of PTH-R is broken leading to hypocalcemia and hyperphosphatemia
pseudohypoparathyroidism
112
what do glucocorticoids do to [ca]
inhibit absorption from kidney and intestine
113
disease: high PTH, low vitamin D, low ca, high Pi
pseudohypoparathyroidism
114
disease: PTHrp
humoral hypercalcemia of malignancy
115
what are vitamin D levels in humoral hypercalcemia of malignancy
low (this is the only difference from hyperparathyroid symptoms)
116
how to treat humoral hypercalcemia of malignancy
furosimide (increase ca excretion)
| etidronate (inhibit bone resorbtion)
117
disease: autosomal dominant mistake in CaSR
hypocalcuric hypercalcemia
118
disease: deficiency in 1alpha hydroxylase
rickets type I
119
disease: deficiency in vitamin D receptor
rickets type II
120
disease: bone mass decreases
osteoporosis
121
treat for osteoporosis
PTH, estrogen, calcitonin, RANKL inhibitor
122
treat for rickets/osteomalacia
vitamin D, ca, sunlight
123
what brings glucose into beta cell to initiate insulin release
GLUT2
124
high levels of ATP in pancreatic beta cell causes what to happen
K channels close (depolarization)
125
an increase in intracellular ___ causes clathrin coated vesicles containing insulin to be released from beta cell
Ca
126
drugs that promote closure of ATP dependent K channels to increase insulin secretions in T2D
sulfonurea (tolbutamide, glyburide)
127
which tissues require insulin for effective glucose uptake (via GLUT4)
muscle, adipose, liver
128
insulin activates SREBP1c for what purpose
uptake more LDL's (to build more TAG's not break them down)
129
what does insulin release do to blood [k]
decrease
130
disease: autoimmune destruction of beta cells
type I diabetes
131
disease: progressive exhaustion of beta cells leading to insulin resistance
type II diabetes
132
medication for type II diabetics that sensitizes them to insulin
metformin
133
disease: patient has antibodies to GAD65, IA2, insulin autoantibody
type i diabetes
134
disease: patient has antibody that is antagonist against insulin
type ii diabetes (blocks insulin at target tissue)
135
while auto Ab's are found in type i diabetic patients, who is actually doing the most harm to beta cells
CTL's
136
what is the most common genotype mutation in type i diabetes patients
HLA: DQ2 or DQ8
| DR3 or DR4
137
if you have this genotype you are said to have "protective" factor from developing type i diabetes
HLA DR2 DQ6
138
what viruses can cause direct or indirect (via molecular mimicry) development of T1D
mumps, rubella, CMV
139
what bacteria can cause harm to beta cells
streptozocin, bafilomycin a1
140
cell markers for treg
CD4+25+FOXP3+
141
disease: messed up FOXP3
IPEX
142
what kind of cell infiltrates adipose tissue in obese patients causing inflammation and eventually leading to insulin resistance
M1 macrophages (TNFalpha and IL1beta)
143
excess palmitate induces expression of TLR4 in beta cells which will release cytokines to attract ___ which are cells that cause harm to these cells
M1 macrophages
144
what gets released (at normal term birth) in order to stimulate surfactant production in newborn babies-- otherwise they get IRDS
glucocorticoids
145
enzyme that turns cortisol into cortisone so it doesn't overstimulate mineral corticoid receptors
11 beta hydroxysteroid dehydrogenase
146
why does real licorice give us HTN
it blocks 11 beta hydroxysteroid dehydrogenase allowing mineral corticoids AND glucocorticoids to raise BP
147
how does cortisol suppress immune function
inhibit NFKB by sequestering it
reduce IL2 synthesis
promote T cell apoptosis
148
enzyme required to make estradiol in the ovaries
aromatase
149
estradiol that gets circulated to the brain has what effect
down regulation of FSH and LH
150
gives breath a fruity smell in T1D
acetoacetate
151
disease: headache, weakness, diarrhea, arrhythmia, increase HR, vomitting, SOB with kussmaul
DKA
152
disease: parathyroid, pituitary, pancreas tumors
MEN1
153
disease: L dopa decarboxylase deficiency
this is in APUD cells -- MEN syndromes
154
most common parathyroid abnormality with MEN 1
hyper-- hyperplasia of all 4 glands
155
most common pancreas abnormality with MEN 1
gastrinoma
156
most common pituitary abnormality with MEN 1
prolactinoma
157
whats RET
protooncogene-- MEN2
158
whats menin protein
product of MEN1 gene (tumor suppressor)
159
disease: MTC and pheochromocytoma
MEN2
160
disease: MTC, pheochromocytoma, hyperparathyroidism
MEN 2a
161
what is unique to MEN2a
hyperparathyroid, cutaneous lichen amyloidosis
162
what is unique to MEN2b
mucosal neuroma, marfanoid habitus
163
disease: high E, high calcitonin, normal PTH
MEN 2b
