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BMS200 final exam > week 3 > Flashcards

week 3 Flashcards

1
Q

magnocellular vs parvocellular neurons

A

magnocellular (in PVN and SON): oxytocin, vasopression

parvocellular: CRH, TRH, GHRH, GHIH, DA, GnRH/LHRH, PRH
** IN THE HYPOTHALAMUS

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2
Q

posterior vs anterior pituatiary

A

posterior: oxytocin, vasopressin

anterior: ACTH, TSH, FSH/LH , GH , PrL

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3
Q

most loops are negative feedback but 1 is postiive

A

oxytocin

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4
Q

GH made from

and stimulates release of what

A

somatotrophs in the anterior pituitary

insulin like growth factor IGF1

stimulated by hypoglucemia, dopamine, arginine, GHRH(hypothalamus) and grhelin

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5
Q

GH is inhibited by

A

somatostatin/ GHIH
i.e. hyperglycemia

and IFG-1

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6
Q

GH receptor

A

class 1 cytokine receptor

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7
Q

GH for

A

bone growth longitudinal

acromegaly (also cancer, GNG and insulin resistance, vision if tumor big, cardio)

and

gigantism (before puberty and epiphyseal long bone fuse)

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8
Q

prolactin is made from

A

lactotrophs

make milk and mammary gland

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9
Q

stimulate prolactin

A

suckling and estrogen GnRH, serotonin, oxytocin

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10
Q

inhibit prolactin

A

dopamine, somatostatin, GABA

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11
Q

4 types of hormon

A

glucocorticoids (cortisol) (blood sugar and stress)

mineralocorticoids (aldosterone) - (water salt balance)

catecholamines (NE and E)

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12
Q

which part of adrenal glands for the hormoens

A

cortex= cortisol and aldosterone

medulla- NE And E

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13
Q

adrenal medulla is made freom vs adrenal cortex

A

medulla (NE and E) neural crest cells (“SNS”)

cortex (cortisol and aldosterone) is mesoderm

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14
Q

adnrenal medulla hormone and PNS or SNS

A

SNS and NE and E

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15
Q

hormones in adrenal cortex and what its derived freom

A

mesoderm

zona glomerulosa- aldosterone

zona fasiculata- cortisol

zona reticularis- androgens

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16
Q

adrenal medulla vs adnreal cortex derived

A

medulla- neural crest cells (SNS)

cortex- medulla

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17
Q

HPA axis

A

hypothalamus to anterior pituitary to target gland

i.e. hypothalamus has TRH to AP has TSH to target T3 T3 in thyroid

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18
Q

what in the anterior pituitary to make cortisol

A

CRH (hypthal) –> ACTH (AP)

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19
Q

mineralcortioicd regulated by

A
  • Secretion of angiotensin II
  • Serum K+ levels
20
Q

steroid hormones (cortisol, aldosterone, estrogen, testosterone) are made from

A

cholesterol (then enzymes to convert to homrone)

made on demand bc lipid soluble (hydrophobic) can cross cell membrane via simple diffusion

21
Q

how to get cholesterol

A

from LDL then use * Cholesteryl ester hydrolase (CEH) removes the fatty acid

22
Q

in the inner mitochondrial membrane what helps to get cholesterol in

A

Steroidogenic acute regulatory protein (StAR)

23
Q

what does cholesterol turn into in inner mitochondrial memrbane

A

pregnenlone

24
Q

bow to get pregnenolone to become cortsiol

A

lots of rxn via : side-chain cleavage enzyme (SCC)
* This is the rate limiting step of the synthesis pathway

25
Q

steps of make cortsiol

A

LdL to cholesterol with cholesterol ester hydorlase (CEH)

then into inner mitochondria membrane via STAR

then become pregnenolone

: side-chain cleavage enzyme (SCC) to turn into cortisol
* This is the rate limiting step of the synthesis pathway

26
Q

ACTH upregulates cortisol production (steroidogensis)

A

▪ Increased LDL receptor expression
▪ Increased activity of CEH and StAR
▪ Increased activity of the side chain cleavage enzymes

27
Q

CRH and ACTH regulation

A

via circadian and SCN and melatonin and stress

28
Q

synthesis of mineralocorticoids (aldosterone)

A

same as cortisol but when gets to corticosterone use aldosterone synthase enzyme to convert to aldosterone

this is done in zona glomerulosa

unlike cortisol in zona fasciulata

29
Q

RAAS system regulates aldosterone

A

decreased perfusion to kidney the release renin then ANGIO II to vasoconstrict and make aldosterone and absorption Na+ and secrete. K+

30
Q

aldosterone

A

▪ Decreased potassium reabsorption from the GI tract
▪ Increased activity of the sodium/potassium pump in many
cells
▪ Increased sodium reabsorption and increased potassium
secretion from the kidney

31
Q

how is cortisol carried in circulation

A

cortsiol via cortisol binding protein

aldosterone is unbound

32
Q

what needs to happen to cortsiol and aldosterone by the liver before being excreted by the kidneys

A

glucuronidation makes the hydrophobic steroid hormones more polar & therefore more easily excreted by the kidney

  • Eliminated forms of cortisol are known as 17-hydroxycorticosteroids
  • Aldosterone as 18-glucuronide
33
Q

catecholamine (NE and E) are made form

A

tyrosine –> DOPA –> dopamine –> NE–> E

34
Q

how does cortsiol convert NE to E

sympathetic stimulation

A

PMNT enzyme

35
Q

catabolism of catecholimees

A

NE –> noremetaneprhine
E –> metanephrine
via COMT

then via MAO into vanillylmandelic acid (VMA)

excrete in urine

36
Q

tertiary secondary and primary endocrine disroder

A

territory at hypothalamus
secondary at pituaitary
primary at final organ

37
Q

cushings syndrome and most common cause

A

hypercortisol (mostly from iatreogenic/ meds)

38
Q

Cushing disease

A

ACTH procucing microadenoma

secondary - high cortisol

39
Q

adrenal labs

A

dexametahaone syppresion test

40
Q

Addisons vs cushings

A

cushing- too much cortsiol form secondary

addisons- primary adrenal insufficiency

41
Q

addison

A

Chronic primary Adrenal Insufficiency

not enough cortsiol, aldosterone and androgen

42
Q

primary hyperaldosteronism/ conn syndrome

A
  • Causes sodium retention and potassium excretion * Resulting in hypertension and hypokalemia
43
Q

congenital adrenal hyperplasia

A

cant make cortisol

Most common enzyme deficiency: 21-Hydroxylase

accumulate progesterone –> ambiguous genatlia

44
Q

chromaffin cells in adnreal medulla for

A

NE and E (catecholameins)

45
Q
A

BMS200 final exam (14 decks)

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