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
steps of make cortsiol
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
ACTH upregulates cortisol production (steroidogensis)
▪ Increased LDL receptor expression ▪ Increased activity of CEH and StAR ▪ Increased activity of the side chain cleavage enzymes
27
CRH and ACTH regulation
via circadian and SCN and melatonin and stress
28
synthesis of mineralocorticoids (aldosterone)
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
RAAS system regulates aldosterone
decreased perfusion to kidney the release renin then ANGIO II to vasoconstrict and make aldosterone and absorption Na+ and secrete. K+
30
aldosterone
▪ 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
how is cortisol carried in circulation
cortsiol via cortisol binding protein aldosterone is unbound
32
what needs to happen to cortsiol and aldosterone by the liver before being excreted by the kidneys
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
catecholamine (NE and E) are made form
tyrosine --> DOPA --> dopamine --> NE--> E
34
how does cortsiol convert NE to E sympathetic stimulation
PMNT enzyme
35
catabolism of catecholimees
NE --> noremetaneprhine E --> metanephrine via COMT then via MAO into vanillylmandelic acid (VMA) excrete in urine
36
tertiary secondary and primary endocrine disroder
territory at hypothalamus secondary at pituaitary primary at final organ
37
cushings syndrome and most common cause
hypercortisol (mostly from iatreogenic/ meds)
38
Cushing disease
ACTH procucing microadenoma secondary - high cortisol
39
adrenal labs
dexametahaone syppresion test
40
Addisons vs cushings
cushing- too much cortsiol form secondary addisons- primary adrenal insufficiency
41
addison
Chronic primary Adrenal Insufficiency not enough cortsiol, aldosterone and androgen
42
primary hyperaldosteronism/ conn syndrome
* Causes sodium retention and potassium excretion * Resulting in hypertension and hypokalemia
43
congenital adrenal hyperplasia
cant make cortisol Most common enzyme deficiency: 21-Hydroxylase accumulate progesterone --> ambiguous genatlia
44
chromaffin cells in adnreal medulla for
NE and E (catecholameins)
45