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Final FA review > 3/7 endo > Flashcards

3/7 endo Flashcards

1
Q

A drug is virtually eliminated after how many half lives?

A

-5

t1/2 = Vd (.7)/Cl

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2
Q

Acute viral hepatitis

-do you see necrosis or apoptosis?

A

-both

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3
Q

Councilman body

A
  • apoptotic hepatocytes

- acidophillic

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4
Q

IV drug user w/hepatitis

-which hepatitis most likely?

A

-Hep C

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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.
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6
Q

Progesterone & gallstones

A
  • slows gallbladder emptying
  • reduces bile acid secretion
  • gallbladder hypomotility => stones
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7
Q

Why are pregnant or OCP using women more at risk for gallstones?

A
  • inc cholesterol synth via estrogen.

- gallbladder hypomotility via progesterone.

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8
Q

Bimodal distribution of plasma drug levels

  • think of what?
  • most drugs = unimodal
A

-fast v slow acetylators.

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9
Q

What is the most common benign liver tumor?

A
  • cavernous hemangioma.

* do NOT biopsy these! risk of hemorrhage!

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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.
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11
Q

pyramidal lobe of thyroid

-persistence of what?

A

thyroglossal duct

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12
Q

Normal remnant of thyroglossal duct

A

Foramen cecum

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13
Q

Foramen cecum

A

Normal remnant of thyroglossal duct

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14
Q

Most common ectopic thyroid tissue site?

A

Tongue

-presents as mass at base of the tongue.

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15
Q

Presents as an anterior midline neck mass that moves with swallowing or protrusion of the tongue

A

Thyroglossal duct cyst

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16
Q

Adrenal cortex derived from…

A

mesoderm

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17
Q

Adrenal medulla derived from..

A

neural crest

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18
Q

Is aldo secretion controlled by ACTH?

A

NO

-AT2 and hyperkalemia.

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19
Q

adrenal medulla

-under control of what?

A

Blood pressure

-sympathetic response

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20
Q

Does LH affect steroid hormone synthesis in adrenals?

A

No

-only affects gonadal cells.

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21
Q

Neuroblastoma vs pheochromocytoma

-which one causes HTN?

A
  • pheo causes episodic HTN.

- neuroblastoma rarely causes HTN.

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22
Q

Neuroblastoma

-presentation

A
  • often presents w/abdominal distention.

- it typically crosses the midline (unlike Wilm’s tumor).

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23
Q

Hypophysis

-what is it?

A

Entire pituitary

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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.

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25
Q

Post pit. derived from what?

A

Neuroectoderm

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26
Q

Ant pit. derived from what?

A

Oral ectoderm (Rathke pouch).

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27
Q

Ant. pit hormones

-alpha or beta subunit: which determines hormone’s specificity?

A

β subunit—determines hormone specificity.

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28
Q

Ant. pit hormones:
-Same α subunit shared by which hormones?
ƒ

A

TSH, LH, FSH, and hCG.

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29
Q

Ant. pit hormones:

  • which hormones = acidophils?
  • mnemonic?
A
  • GH, prolactin.

- GPA: GH, Prolactin = Acidophils.

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30
Q

Ant. pit hormones:

  • which hormones = basophils?
  • mnemonic?
A
  • B-FLAT

- basophils - FSH, LH, ACTH, TSH

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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
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32
Q

Which GLUT transporter is the glucose sensor for liver/pancreatic beta cells?

A

GLUT2

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33
Q

glucose vs insulin

-which can cross the placenta? can both?

A
  • glucose can cross.

- insulin can not cross.

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34
Q

Insulin-independent glucose uptake:

-mnemonic:

A

BRICK-L

-Brain, RBCs, Intestine, Cornea, Kidney, Liver.

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35
Q

GH influence on insulin levels

A
  • causes insulin resistance.

- this increases insulin release.

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36
Q

beta-2 agonists

-effect on insulin release

A

-inc. insulin release

but inc. glucagon release more i believe

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37
Q

Glucose influence on GH

A

-glucose should inhibit GH release

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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

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39
Q

CRH from hypoT stimulates release of what?

A

ACTH, MSH, β-endorphin

*POMC = precursor to these 3

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40
Q

Dopamine

-effect on PRL?

A

inhibits prolactin secretion

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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.

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42
Q

Somatostatin inhibits release of which pituitary hormones?

A
  • GH, TSH

* octreotide used to treat acromegaly.

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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.

Final FA review (52 decks)

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