Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M:1 year > deck_716979 > Flashcards

deck_716979 Flashcards

2
Q

protein/peptide hormones

A

syn as preprohormone or pre hormonesstored in granulespolarusually in blood unboundplasma membrane receptorsnot administered orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

steroid hormone

A

derived from cholesterolintracellular receptorsin blood boundstored inendocrine glandsnonpolaroften orally administered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Throid hormones

A

derived from tyrosinecross cell membranesin blood boundintracellular receptorsstored in folliclescan be administered orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

catecholamines

A

derived from tyrosinecell surface receptorsstored in membrane bound granulesin blood free or loosely bound to protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

hormones via phospholipase C

A

GnRH, TRH, Angiotensin II, ADH, oxytocin, alpha 1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hormones via steroid hormone mech.

A

glucocorticoids, estrogen, progesterone, testosterone, aldosterone, vit D, Thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ADH action (V1 and V2)

A

V2 receptor - collecting ducts more permeable to water - high affinity for ADH -> sensitive to small changes in blood osmolarityV1: mesangial cell contraction in glomerulus; suppress renin release from JG’s; arteriole constriction; increase ACTH release from ant. pit. - low affinity for ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Oxytocin action

A

contraction of smooth mm via V1 receptor- contraction of mammary myoepithelium -> milk ejection- contraction of myometrium of uterus during labor- released during orgasm -> contracts uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pituitary blood supply

A

allows deliver of releasing and inhibitory factors selectively to anterior pituitary in high concentration.long portal vessels - median eminence, down pituitary stalk -> ant. pitshort portal vessels - post. pit -> ant. pit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

6 major ant. pit hormones

A
  1. FSH - gonadotrophs - promotes gamete development in both sexes. 2. LH - gonadotrophs - promotes sex steroid synthesis in both sexes. 3. TSH - thyrotrophs, stimulates growth and hormone production of thyroid gland. 4. GH - somatotrophs, promotes the overall growth of the body - both bones and soft tissue. 5. PRL - mammotrophs, is responsible for milk production in females and normal levels enhance LH action in males (note that high PRL levels are inhibitory). 6. ACTH stimulates the growth and steroid production of the adrenal cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

hypothalamic releasing hormones

A

GnRH -> LH and FSH (LH is more sensitive to GnRH than is FSH)GHRH -> GH (inhibited by somatostatin (GHIH)) TRH -> TSH and PRL (inhibited by somatostatin (GHIH)) dopamine (PIH) -> inhibits PRL (stimulated by various factors (TRH, VIP, oxytocin & vasopressin).CRH -> ACTHact via G protein -> increase IP3 -> increase intracellular Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

iodothyronines

A

formed by coupling of two iodinated thyroglobulins (via thyroid peroxidase)T4 - most abundant, acts as prohormoneT3 - active (shorter half life)rT3 - inactive (high in fetus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thyroid Hormone Syn

A
  1. iodine trap; Na-Cl pump (stim via TSH)2. thyroglobulin syn in thyroid RER3. Thyroglobulin and Iodide pumped into lumen4. Iodide -> Iodine (TP)5. iodination of thyroglobulin (TP)6. coupling of MIT’s and DIT’s (TP) -> thyroid hormone bound to thyroglobulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

TH release

A
  1. stim via TSH2. Endocytose colloid3. lysosomal proteases hydrolized thyroglobulin -> AA’s, T3, T4, DIT and MIT4. T3 and T4 released5. DIT, MIT and AA’s recycled into thyroglobulin and Iodide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Wolf-Chaikoff effect

A

excess idodine -> decrease thyroid sensitivity to TSH -> decrease TH synthesis -> hypothyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T4 -> T3 enzyme

A

5’ deiodinaseT4->rT3 - 5’ monodeiodinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TH action

A

enters cell -> binds thyroid response element on target gene -> removes gene co-repressors -> gene transcriptionReceptor has higher affinity for T3target tissues have 5’ deiodinaseTarget tissues increase oxygen consumption in response except testes, brain, spleen, pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Graves disease

A

hyperthyroid w/ low levels of TSHTSI mimics TSH action -> increase TH syn and secretion -> goiter -> negative feedback decreases TSH levels, but TSI remain high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

“Hashimoto’s thyroiditis

A

most common hypothyroid in USantibodies against follicular cells and TSH receptors destroy thyroid functioninitially blood work shows high TSH but normal levels of T4 (compensation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cretinism

A

caused by hypothyroidism in fetus till 2 yrsCretins are dwarfed, have pot-bellies, protruding tongues and are severely retarded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hypothyroid as child

A

stunts growth (further exasperated by low GH)often no pubertysevere mental issuesgrowth can catch up w/ TH replacement therapy, but mental issues can’t be reversed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Thyroid actions

A

increase BMR (O2 and fuel consumption)gluconeogenesisglycogenolysislipogenesislipolysisincreases LDL receptors -> decrease serum cholesterolprotein sythesisproteolysis -> muscle wasting (hyper)increase heat productionincrease Beta adrenoreceptors -> increase sympathetic responseincrease HR and Contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

hypothyroid symptoms

A

Decreased basal metabolic rate, high cholesterole and atherosclerosis, Thick tongue, Myxedema, Weakness, fatigue, lethargy, Goiter, Somnolence, Slow speech, Mental slowness, Hoarseness, Muscle aches, Amenorrhea, Cold intolerance, Psychosis, Dry cold skin, Electrocardiogram changes, Prolonged reflex times, Constipation, Decreased sweating, Thin, brittle hair Weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hyperthyroid symptoms

A

Nervousness, Bruit over thyroid, Anxiety, Pretibial myxedema, Insomnia (Graves’ disease), Heat intolerance, Fatigue, Palpitations, Eye problems (Graves’ disease), Muscle weakness, Exophthalmos, Diarrhea, Lid retraction, Increased appetite, Extraocular muscle weakness, Moist, warm skin, Eye irritation, Goiter Tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

primary, secondary, tertiary hypothyroid

A

primary: issue in thyroid; response to TSH low, response to TRH highsecondary: issue in pituistary; response to TSH normal, response to TRH lowtertiary: issue in hypothalamus; response to TSH normal, response to TRH normal, but secretion of TRH is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

amylin

A

cosecreted w/ insulinsupports insulin action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

C-peptide

A

plasma level index of insulin secretioncleaved from insulin in activation

29
Q

Insulin biochem action on target tissue

A

binds receptor -> autophosphorylation -> activates tyrosine kinase -> phosporylation cascade.. PI3 kinase -> PKB -> activates GLUT 4 and glyocogen synthaseRAS and MAP kinase -> activate transcription factorsPLCgamma -> influx of K+, etc

30
Q

insulin stimulators

A

GLUCOSEK+, AA’s, FFA’s, GI hormones, Beta adrenergics, Parasympathetics, glucagon

31
Q

glucagon action

A

Liver is major target -> glycogenolysis, gluconeogenesis -> glucose generationProteolysis -> AA’s -> glucoseLipolysis -> ketoacidsALL action via cAMP

32
Q

cortisol action

A

increasing glycogenolysis, gluconeogenesis, glycogenesis, lipolysis, and proteolysis -> hyperglycemicGlucose: glucose production (short term E); Glycogen synthesis (long term E); promotes glucagon release while inhibiting insulin actionProtein: increase proteolysis -> AA’s -> glucoseFat: lyposis in extremeties; lypogenesis in trunk and face; inhibits LDL uptakeBone: inhibits bone formation via - osteoblast; - collagen; - Vit D; + resorptionKidney: water excretion via - ADH; + GFRGI: Peptic ulcer’s via + HCL; - prolifImmune system: decreases lymphocytes; anti-inflamvascular: maintains BP

33
Q

Aldosterone Synthesis

A

Zona GlomerulusCholesterole -> pregnolone -> progesterone (3B OH steroid dehydrogenase) -> DOC (21-hydroxylation) -> corticosterone (11-hydroxylation) -> aldosterone (aldosterone synthase)

34
Q

Cortisol synthesis

A

Zona Fasiculata: 17-hydroxylase is uniquepregnolone -> 17 hydroxypregnolone (17-hydroxylase) -> 17-hydroxypregnolone (3B-OH SD) -> 11-deoxycortisol (21-hydroxylase) -> cortisol (11-hydroxylase)1 extra step w/ 17 hydroxylase

35
Q

DHEA synthesis

A

Zona Reticularis: C17-20 lyase is unique17-hydroxypregnolone (from Fasiculata) -> DHEA (C17-20 lyase)

36
Q

ACTH action on adrenal cortex

A

trophic via IGF-IIpromotes steroid syn:- increases cholesterol availability (uptake, synthesis, mobilizes stored)- increases side chain cleavages and hydroxylases activity

37
Q

cushings syndrome

A

Hypercortisolcentripetal obesity, hypertension, hyperglycemia, amenorrhea or impotence, hirsutism, purple striae, “moon” facies, osteoporosis, easy bruisability, and personality change

38
Q

cushings causes

A

Cushings Disease: pituitary tumor -> high ACTH -> high cortisoladrenal tumor -> high cortisol -> low ACTHectopic tumor -> high ACTH -> high cortisol

39
Q

cortisol antinflammatory response

A

inhibits formation of arachidonic acidinhibits neutrophil functioninhibits COX2inhibits PAF productioninhibits NO production

40
Q

cortisol as immunosuppresent

A

inhibits IL-1 -> decrease T-lymphocytesinhibits IL-2Inhibits macrophage fnct.

41
Q

stress and cortisol

A

stress over rides negative feedback of cortisol on CRH and ACTH -> increased cortisol

42
Q

aldosterone stimulators

A
  1. angiotensin II in response to low plasma osmolarity2. hyperkalemia3. stress
43
Q

addisons disease

A

primary adrenal insufficiencyhyponatremia, hypotension, weakness (due to hyperkalemia), hyperkalemia, weight loss (anorexia, nausea, vomiting), and hyper-pigmentation

44
Q

21-Hydroxylase deficiency

A

↓ Cortisol ,↓ Aldosterone, ↑ Androgens Masculinization, Salt loss

45
Q

11β-Hydroxylase deficiency

A

↓ Cortisol, ↓ Aldosterone, ↑ Androgens, ↑ DOC Masculinization (mild), Hypertension

46
Q

17α-Hydroxylase deficiency

A

↓ Cortisol, ↓ Androgens & estrogens, ↑ DOC & corticosterone, ↑ AldosteroneHypertension, Hypokalemic, alkalosis, Sexual infantilism

47
Q

Conn’s Syndrome

A

primary hyperaldosteronism -> aldosterone-secreting tumor. increased ECF volume, hypertension, hypokalemia, and metabolic alkalosis.

48
Q

catecholamine biosynthesis

A

Tyrosine → DOPA → DA → NE → E- Tyrosine hydroxylase(tyr→ DOPA) = rate limiting enzyme (negative feedback inhibited; neuroligically stimulated)- Dopamine β-hydroxylase (DA → NE) is the only enzyme located in the granules – the rest of the enzymes are cytosolic.- PNMT (NE → E) is found only in epinephrine producing cells (stim via cortisol)

49
Q

catecholamine metabolism product

A

2 pathways - both result in VMA -> excreted in urine

50
Q

fight of flight response

A

Adrenal Cortex and Medulla work togethermedulla epinephrine -> immediate and intense responseCortical cortisol -> takes hours for response to take place

51
Q

catecholamine receptors

A

Alpha 1: equal affin for nor and epi; post synaptic terminals -> excitatory (+ IP3, DAG)Alpha 2: equal affin for nor and epi; pre synaptic terminal; inhibitory (-cAMP)Beta 1: equal affin; heart; excitatory (+cAMP_Beta 2: greater affin for epi; liver; excitatory (+cAMP)

52
Q

epi on cardiovascular

A

heart: + HR and Contractility via B1 Arterioles: constrict splanchnic, renal, cutaneous via alpha 1 and dilate muscle arterioles via B2norepi decreases heart rate

53
Q

epi on metabolism

A

Epi is antiinsulin, diabetogenic, ketogenicGets glucose and fuel into blood stream

54
Q

Symptoms of Pheochromocytoma

A

Hypertension 90 Severe headache 80 Excessive perspiration 70 Palpitations with or without tachycardia 65 Nausea 40 Tremor 30 Weakness, exhaustion, fatigue 30 Anxiety, nervousness 25 Abdominal pain 20 Blurred vision 10

55
Q

fetal growth

A
  • directly controlled by GF mediated by IGF-II- independent of hormonal control w/ exception of Insulin -> increases growth- peaks mid gestation
56
Q

postnatal growth (0-2)

A

RapidGH rises -> IGF-II risesIGF-I levels are lowThyroid Hormone very important

57
Q

3-4 yrs growth

A

IGF-I increases and peaks at puberty - plays central role in childhood growth

58
Q

puberty growth

A

Gonadal hormones play important role

59
Q

GH action

A

increases lean body massdirect action on adipose (decreases), muscle (increases), liverindirect action via IGFs (somatomedins) from liveradipose: + lipolysis; - glucose uptakemuscle: + AA transport, + protein syn, - glucose uptakeLiver: + glucose output, + FA ox, + ketogenesis, + IGF’s

60
Q

GH regulation

A

From hypthalamus:- GHRH stimulates- Somatostatin inhibitsNegative feedback from GH and somatomedin stimulate somatostatin releasestimulated by: Sleep, exercise, hypoglycemia, high AA’s, estrogeninhibits: high FFA (obesity), hyperglycemia

61
Q

hypocalcemia

A

muscle tetany -> increases permeability of Na -> depolarizes -> twitching

62
Q

hypercalcemia

A

lethargytissue calcificationdiuresis

63
Q

PTHrp

A

mimics PTH-> increases plasma Ca -> not effected by the - feedback - feedback decreases PTH levels

64
Q

PTH action

A

Bone resorptionrenal reabsorption of Carenal excretion of Phosphateactivates Vit D -> increase gut resorption of Caaction via cAMP

65
Q

calcitonin

A

defense against sudden Ca load -> slight bone depostion of Ca

66
Q

Vit. D

A

2 sources: diet, 7-dehydrocholesterolUV light changes 7-deh. -> cholecalciferol (dietary Vit D) Liver: Cholecal. -> 25-OH chole.Kidney: activates+ blood Ca, + phosphate

M:1 year (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions