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Flashcards in 3/7 endo Deck (105)
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1
Q
A drug is virtually eliminated after how many half lives?
A
-5

t1/2 = Vd (.7)/Cl
2
Q
Acute viral hepatitis
-do you see necrosis or apoptosis?
A
-both
3
Q
Councilman body
A
-apoptotic hepatocytes
-acidophillic
4
Q
IV drug user w/hepatitis
-which hepatitis most likely?
A
-Hep C
5
Q
beta-glucoronidase
-who releases it?
-what does it lead to?
A
-following infection of biliary tree, injured hepatocytes and bacteria release this enzyme.
-unconjugates bili = more unconjugated bili in bile = brown pigment stone.
6
Q
Progesterone & gallstones
A
-slows gallbladder emptying
-reduces bile acid secretion
*gallbladder hypomotility => stones
7
Q
Why are pregnant or OCP using women more at risk for gallstones?
A
-inc cholesterol synth via estrogen.
-gallbladder hypomotility via progesterone.
8
Q
Bimodal distribution of plasma drug levels
-think of what?
*most drugs = unimodal
A
-fast v slow acetylators.
9
Q
What is the most common benign liver tumor?
A
-cavernous hemangioma.
*do NOT biopsy these! risk of hemorrhage!
10
Q
Thyroid diverticulum
-arises from where? descends to where?
-connected to tongue via?
A
-arises from floor of primitive pharynx, and descends into neck.
-Connected to tongue by thyroglossal duct, which normally disappears but may persist as pyramidal lobe of thyroid.
11
Q
pyramidal lobe of thyroid
-persistence of what?
A
thyroglossal duct
12
Q
Normal remnant of thyroglossal duct
A
Foramen cecum
13
Q
Foramen cecum
A
Normal remnant of thyroglossal duct
14
Q
Most common ectopic thyroid tissue site?
A
Tongue
-presents as mass at base of the tongue.
15
Q
Presents as an anterior midline neck mass that moves with swallowing or protrusion of the tongue
A
Thyroglossal duct cyst
16
Q
Adrenal cortex derived from...
A
mesoderm
17
Q
Adrenal medulla derived from..
A
neural crest
18
Q
Is aldo secretion controlled by ACTH?
A
NO
-AT2 and hyperkalemia.
19
Q
adrenal medulla
-under control of what?
A
Blood pressure
-sympathetic response
20
Q
Does LH affect steroid hormone synthesis in adrenals?
A
No
-only affects gonadal cells.
21
Q
Neuroblastoma vs pheochromocytoma
-which one causes HTN?
A
-pheo causes episodic HTN.
-neuroblastoma rarely causes HTN.
22
Q
Neuroblastoma
-presentation
A
-often presents w/abdominal distention.
-it typically crosses the midline (unlike Wilm's tumor).
23
Q
Hypophysis
-what is it?
A
Entire pituitary
24
Q
What protein transfers ADH & oxytocin from hypothalamus down to post. pit?
-mutations in this protein can lead to what?
A
-neurophysins
-point mutations to neurophysin 2 underlie most cases of hereditary hypothalamic diabetes insipidus.
25
Q
Post pit. derived from what?
A
Neuroectoderm
26
Q
Ant pit. derived from what?
A
Oral ectoderm (Rathke pouch).
27
Q
Ant. pit hormones
-alpha or beta subunit: which determines hormone's specificity?
A
β subunit—determines hormone specificity.
28
Q
Ant. pit hormones:
-Same α subunit shared by which hormones?
ƒ
A
TSH, LH, FSH, and hCG.
29
Q
Ant. pit hormones:
-which hormones = acidophils?
-mnemonic?
A
-GH, prolactin.
-GPA: GH, Prolactin = Acidophils.
30
Q
Ant. pit hormones:
-which hormones = basophils?
-mnemonic?
A
-B-FLAT
-basophils - FSH, LH, ACTH, TSH
31
Q
Why is C-peptide a good marker for insulin secretion?
A
-1:1 secretion w/insulin
-does not undergo significant first pass metabolism
-not included in exogenous insulin
32
Q
Which GLUT transporter is the glucose sensor for liver/pancreatic beta cells?
A
GLUT2
33
Q
glucose vs insulin
-which can cross the placenta? can both?
A
-glucose can cross.
-insulin can not cross.
34
Q
Insulin-independent glucose uptake:
-mnemonic:
A
BRICK-L
-Brain, RBCs, Intestine, Cornea, Kidney, Liver.
35
Q
GH influence on insulin levels
A
-causes insulin resistance.
-this increases insulin release.
36
Q
beta-2 agonists
-effect on insulin release
A
-inc. insulin release
(but inc. glucagon release more i believe)
37
Q
Glucose influence on GH
A
-glucose should inhibit GH release
38
Q
Insulin
-pathway for insulin release & protein/fat/glycogen synth:
-pathway for txn alteration:
A
-insulin release + synthesis: IP3/PKC

-txn alteration: RAS/MAP kinase
39
Q
CRH from hypoT stimulates release of what?
A
ACTH, MSH, β-endorphin
*POMC = precursor to these 3
40
Q
Dopamine
-effect on PRL?
A
inhibits prolactin secretion
41
Q
What prevents lactogenesis during pregnancy?
A
-during pregnancy, the high amount of E & P made by
placenta will prevent prolactin from causing lactogenesis.
42
Q
Somatostatin inhibits release of which pituitary hormones?
A
-GH, TSH
*octreotide used to treat acromegaly.
43
Q
TRH
-causes inc in which hormone?
A
-TSH, prolactin
-All hormones are super exclusive, only act on their specific receptor, except TRH. TRH can make prolactin go up.
44
Q
If you cut pituitary stalk, which is the only hormone that will increase?
A
Prolactin
-its under tonic inhibitory control by dopamine.
-dopamine being made by hypothalamus.
45
Q
Link btwn primary hypothyroidism (ie. hashimotos) and galactorrhea.
A
-In primary hypothyroidism (ie. hashimotos) you have inc. TRH & inc. TSH.
-this can lead to inc. PRL and galactorrhea in women.
46
Q
Somatotropes =
A
cells in ant. pit. that produce GH
47
Q
Which AAs stimulate GH secretion?
A
arginine & histidine
48
Q
Somatomedin effect on GH.
A
-Somatomedin also has INDIRECT neg. feedback on GH by stimulating stomatostatin production.
49
Q
What inhibits GH secretion?
A
Somatostatin & glucose
50
Q
Glucose tolerance test
A
If GH isn't down-regulated w/glucose infusion then you could have pituitary adenoma secreting GH = acromegaly/gigantism.
51
Q
ADH
-made in which hypoT nuclei?
A
supraoptic nuclei
52
Q
Tx for central DI?
A
Desmopressin (ADH analog)
-does NOT have V1 vasoconstrictive properties of ADH.
53
Q
Where are osmoreceptors?
A
hypothalamus
*threshold to signal thirst = lower in pregnant women. One way pregnant women inc. their plasma level.
54
Q
Cholesterol => pregnenolone
-whats the enzyme?
-whats enzyme controlled by?
A
Cholesterol desmolase
-ACTH stimulates it (reticulara & fasciculata)
-AT2/potassium stimulates it (glomerulosa)

-Ketoconazole inhibits it.
55
Q
Triple test
-fetal
A
Checks for b-HCG, AFP, estriol
-btwn weeks 16 & 18.
56
Q
AFP
-what makes it?
A
-fetal liver
-fetal GI tract
-early gestational yolk sac
57
Q
Most common cause of elevated AFP levels?
A
Dating error.
-under-estimation of gestational age.
-other causes: neural tube defects, ant abdominal wall defects (omphalocele, gastroschisis), multiple gestation.
58
Q
Down's syndrome
-inc. or dec. AFP?
A
-dec. AFP.
59
Q
Dec. fetal estriol levels suggest what?
A
-placental insufficiency.
-intrauterine growth retardation.
60
Q
Inc. HCG
-associated w/what?
A
-hydatidiform mole
-multiple gestation
-choriocarcinoma
61
Q
Is Afib specific for graves?
-or can it happen in any hyperthyroid condition?
A
-not specific for graves.
-can happen in any hyperthyroid condition.
62
Q
Heat intolerance
-found in hypo or hyperthyroidism?
A
-hyperthyroidism
-you can't tolerate heat b/c you're already making so much heat in your body.
63
Q
Why would ALP be increased in hyperthyroidism?
A
-due to the increased bone resorption.
64
Q
Glitazones
-mechanism?
A
-inc. tissue sensitivity to insulin.
-binds PPAR-gamma nuclear txn regulator.
65
Q
Which DM drugs alone can cause hypoglycemia?
A
-sulfonylureas & insulin.
66
Q
Sex steroid effect on growth plate.
-how does this differ from IGF-1 affect?
A
-Initially inc. linear growth then encourage closure of epiphyseal plate (aka, fuse w/metaphysis).
-IGF-1 never encourages closure. Just growth.

*estrogen responsible for closing the epiphyseal plate.
67
Q
-Are adiponectin levels high or low in DM2?
-Which drug inc. their levels and how?
A
-adiponectin is LOW in DM2.
*secreted by adipocytes.
-glitazones inc adiponectin levels by activating their txn factor, PPAR-gamma. Inc. levels will dec. insulin resistance.
68
Q
MEN 1
-mnemonic
A
PPP
-parathyroid tumor (hypercalcemia)
-pancreatic tumor (gastrin)
-pituitary adenoma (PRL, ACTH)
69
Q
MEN 2A
A
MPP
-medullary carcinoma of thyroid (calcitonin)
-pheochromocytoma
-parathyroid tumor (
70
Q
MEN 2B
A
MPM
-medullary carcinoma of thyroid (calcitonin)
-pheochromocytoma
-marfanoid habitus/mucosal neuromas
71
Q
Where can you find 5-alpha-reductase?
A
-prostate, testes, hair follicles, adrenals
72
Q
What is lipotoxicity?
A
-too much FFAs inc. insulin resistance & reduces the amount of insulin that is released.
73
Q
Glucose => sorbitol
-but what is sorbitol converted to?
A
-fructose via sorbitol DH
*both sorbitol & fructose are osmotically active.
74
Q
Chlorthalidone
-what is it?
A
thiazide diuretic
75
Q
Long term exogenous glucocorticoid use
-effect on HPA axis?
A
-suppresses HPA axis
-reduced CRH, ACTH, cortisol.
-all 3 are decreased!
76
Q
Adrenal insufficiency
-whats the most common cause?
A
-HPA axis suppression due to exogenous glucocorticoid use.
77
Q
What type of necrosis is seen in sheehan syndrome
A
-coagulation necrosis
-not liquefactive b/c pituitary is not part of the brain.
78
Q
Atheletes/anorexic women who dont menstruate, whats the cause?
A
-hypogonadotropic amenorrhea.
79
Q
Link btwn prolactin and femoral fracture
A
-PRL inhibits GnRH = less FSH & LH = less estrogen.
-Estrogen = protective of bone.
-Reduced estrogen can lead to osteoporosis.
80
Q
17α-hydroxylase
-inc or dec aldo?
A
-dec aldo
-may seem counter-intuitive
-make so much 11-doc before getting to aldo that you get HTN and dec. renin/AT2.
81
Q
Cortisol effect on alpha-1 receptors
A
up-regulates them
-remember, cortisol is permissive on catecholamines and glucagon.
82
Q
Cortisol effect on:
-mast cells
-eosinophils
-IL-2
A
-blocks histamine release from mast cells.
-reduces eosinophils.
-blocks IL-2 production
83
Q
Exogenous corticosteroids can cause reactivation of:
A
-TB and candidiasis (blocked IL-2 production).
84
Q
Which cells make PTH?
A
Chief cells of parathyroid.
85
Q
Regulation of PTH by Mg
-inc or dec?
A
-dec. Mg => inc. PTH
-severely dec. Mg => dec. PTH

*Common causes of dec. Mg2+ include diarrhea, aminoglycosides, diuretics, and alcohol abuse.
86
Q
*Common causes of dec. Mg2+:
A
-diarrhea, aminoglycosides, diuretics, and alcohol abuse.
87
Q
Alkalosis
-effect on Ca level?
A
-Albumin deprotonated, now has even more (-) charge, binds Ca.
-free calcium decreased.
*alkalosis can lead to Sxs of hypocalcemia.
88
Q
Which cells make calcitonin?
A
-Parafollicular cells (C cells) of thyroid.
89
Q
HPA hormones that use cAMP pathway
-mnemonic?
A
FLAT ChAMP

-FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2-receptor), MSH, PTH, calcitonin, GHRH, glucagon.
90
Q
HPA hormones that use IP3 pathawy
-mnemonic?
A
GOAT HAG

-GnRH, Oxytocin, ADH (V1-receptor), TRH, Histamine (H1
-receptor), Angiotensin II, Gastrin.
91
Q
Thyroid hormones
-which signaling pathway do these use?
A
-steroid receptor.
92
Q
OCPs, pregnancy effect on sex hormone binding globulins.
A
inc. SHBG (free estrogen levels remain unchanged).
-sex hormone binding globulin.
93
Q
Thyroxine relationship w/GH
A
thyroxine is permissive on GH.
94
Q
Thyroxine sets metabolic rate for all tissues except:
A
-all tissues in the body except the brain, gonads & uterus.
-although dont forget, you need thyroxine for CNS formation in utero.
95
Q
Thyroxine effect on heart
A
-up-reg beta-1 receptors on heart.
96
Q
How does thyroxine inc. basal metabolic rate?
A
inc. Na/K ATPase activity
97
Q
Thyroxine 4 functions
A
-Brain maturation
-Bone growth
-β-adrenergic effects
-Basal metabolic rate inc.
98
Q
Wolff-Chaikoff effect:
A
excess iodine temporarily inhibits thyroid peroxidase => dec. iodine organification => dec. T3/T4 production.
99
Q
What are the only cells in the body that can absorb iodine?
A
Thyroid follicular cells
100
Q
TBG inc or dec in...
-hepatic failure
-pregnancy
-OCP use
A
-hepatic failure: dec.
-pregnancy: inc.
-OCP use: inc.

*estrogen inc. TBG production.
101
Q
-inc total T4 w/normal TSH levels =
A
-you're on estrogen.
-inc. in thyroid binding globulin.
102
Q
Waist to hip ratio
A
waist = visceral fat
hip = subQ fat
-high visceral fat = high correlation w/insulin resistance.
103
Q
LDL receptor
-mechanism of getting it into the cell?
A
Endocytosis w/clathrin coated vesicles.
104
Q
Primary hyperaldosteronism
-whats the serum sodium?
A
NORMAL serum sodium due to aldosterone escape!
105
Q
Diarrhea
-what do you lose?
A
Water, potassium, bicarb
-Get hypernatremia (cuz u lose water).
-hypokalemic
-metabolic acidosis.