Endocrine Flashcards

1
Q

primary damage:

A

damage to the endocrine gland

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2
Q

secondary damage

A

damage to pituitary or thalamus

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3
Q

primary glands

A

only job is hormone secretion
- pineal, hypothalamus, pituitary, parathyroid, thymus, adrenals, ovaries, testes

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4
Q

autocrine signalling

A

cell releases a hormone—> targets the same cell to make more molecules ( local)

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5
Q

paracrine signalling

A

1 cell secretes hormones that interacts w neighbouring cells to influence their activity
ex: ecosinoids

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6
Q

secondary hormones:

A

heart–> ANP
Kidneys__> bicarb, erythropoiten,

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7
Q

cortisol, ALDO, E/P/T are examples of ….

A

steroid hormones
- hydrophobic molecules
can diffuse across cells membranes to transcript MRNA

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8
Q

glycoproteins, AA derivaties, and ionated AA=

A

nonsteriodal hormones

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9
Q

upregulation

A

when there is a decreased amount of hormone in the blood the target ell will make more receptors to pick up more hormones

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10
Q

down regulations

A

when there is too much hormones in the blood and the target cells reduce its amount of receptors to take up less hormone

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11
Q

neurohypophysis secretes…..

A

vasopression, oxytocin

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12
Q

adenohypophysis secretes…

A

TRH, CRH, TSH, ACTH, LH & GNRH, prolactin, somatostatin

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13
Q

short loop feedback:

A

when the pituitary hormone changes the secretion of the hypothalamic hormone

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14
Q

long loop feedback

A

target organ changes the hormone secretion of the hypothalamic/pituitary hormones

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15
Q

circadian rhythms….

A

influences the production of CRH in blood
GH=++ secretion @ 12am–>4am

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16
Q

adrenal cortex layers

A

zona glomerulosa: outermost, secretes mineralcorticoids ex:ALDO
Zona fasiculata: middle zone which secretes glucocorticoids, ex: cortisol
ZOna reticularis: inner most layer that secretes gonadococorticoidsex:androgens

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17
Q

adrenal medulla secretes…

A

catechoalmines like norepinephrine

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18
Q

ALDO functions:

A

regulates ECF fluid vol by reabsorbing Na+ & H2O in the nephron of the kidneys
-regulates ECF K+ Na+/K+
- release stimmed by ++ANG2 when Bp= low–> travels through caps & diffuse through nephrons cells—>bids to cell receptor & alters mrna transcription to ++ expression of NA+/K+ pumps= more K+ excreted +Na+ reabsorbed

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19
Q

glucocorticoid functions:

A

+BGL, aa/FA , gluconeogenesis, anti-inflammatory

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20
Q

neg feedback loop for hypothalamic- pituitary pathway:

A

1 hypothalamus = stimmed by stress/circadian rhythm–>anteiror pituitary–> secretes acth (influencescells of zona fasiculata to secrete more cortisol
(as CRH increases—> cortisol +/as Cortisol +—> CRH decreases)

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21
Q

cushings diease

A

primary/secondary hypercortisol secretion, onset=40yrs, can be iatrogenic due to excessive use of glucocorticoids & can completely stop the production of CRH/ACTH
s/s:Fat depositions, Decreased muscle mass: muscle weakness
Bone demineralization
aldosterone(like effects)
Increased production of androgens
Hyperglycemia ( loss of sensitivity to insulin)
Poor concentration & memory

22
Q

Addisons disease

A

primary hypocortiso; secretion & low ALDO, hypovolemia, hyponatremia, hyperkalemia, decreases BGL, N/V/D/C, +pigmentation

23
Q

general adaption syndrome (GAS)

A

1) ALARM: stress activity of hypothalamus ++ cotrisol/+SNS, 2)resistance–> maintenance of alarms, allostasis, if stress not managed body compensates( counter productive) 3) exhaustation: body resources are depleted ++ risk of infection

24
Q

thyroid hormone fucntions…

A

T3/T4–> ++ SNS response
- ++BMR, +protein synthesis/degradation, glycogenolysis, gluconeogenesis, + lypolysis, +Hr/FOC/CO

25
Q

secretion regulation of t3-t4:

A

1) hypothalamus–> tonic release of TRH 2)anteiror pituitary release TSH–> TSH binds to receptors on follicular cells (thyroid) to make more T3/T4 3) T3/T4: metabolic effects & TSH secretion fro anterior pituitary ( neg feedback)

26
Q

PTH

A

+ ECF Ca2+–> +bone reabsorption Ca2+, activates osteoclasts break down matrix and reabsorb Ca2+ through the nephrons

27
Q

Vit D

A

influences Ca2+ diet & synthesis (food/skin)—> liver–>kidneys

28
Q

Calcitonin:

A

secreted when blood Ca2+= too high, secreted by the thyroid cells, osteoclasts stop break-down normal levels Ca2+

29
Q

melatonin

A

secreted by the pineal gland/ circadian cycle
-amino acid derivative

30
Q

GH

A

regulated by somtotropin pr GnRH, levels ++ at night, + muscle mass, ++ Ca2= retention, + osteoblasts, -BGL,

31
Q

pancreatic hormones

A

alpha- glucagon
beta-insulin
delta-somatostatin
episonlin- gherlin
pp cell- pancreatic polypeptide
acini: exocrine pancreas funftion

32
Q

what hormone do neonates need for proper neuro development?

A

T3/T4–> for myelin sheath/axon development

33
Q

Hypothyroidism

A
  • congenital, due to lack of precursors/non-ionated salts
    manifestations:
  • -BMR, bradycardia, -BP, weight gain despite appetitie, hyperlipidemia, lethargy, bad memory, low t3/t4, + TSH/TRH, cold intolerance
34
Q

cretinism….

A

hypothyroidism in neonates, s/s: 1 month old, thickened tongue/lips, poor muscle tone, jaundice, neuro delays, irreversible damage

35
Q

myxedema

A

ptolonged lack of t3/t4, non pitting edema, alt mental state, cold intolerance

36
Q

lack of iodine ( goiters)

A

TSH stim thyroid to make T3/T4
No iodine so no T3/T4 but thyroglobulin continues ot be produced—> colloid
No T3/T4 thus TSH remains High

37
Q

hyperthyroidism( primary/secondary)

A

primary: graves disease antibiody produced to stim TSH receptor on follicularcells produce more t3/t4
secondary: usually related to tumour of the anteriori pittuitary gland, affects the secretion of TRH/YSH by having an + secretion of both
manifestations: +BMR, +SNS, weight loss, Heat intlerance, amenorrhea, thyroidmegally

38
Q

congenital adrenal hyperplasia

A

autosomal recessive condition ( can not make enzye necessary for cortisol/ALDO production)
-turns htem into progesteron ( androgens
- enhances maleness, lack of cortisols, +CRH/ACTH, virillization of females:

39
Q

giantism

A

pituitary tumour thats benign before the epiphyseal plates stop growing, +GH/IGF secretion–> + bone growth/cartillage, extremely tall individuals, delayed puberty, excessive face bones

40
Q

hyposecretion of GH

A

congenital/can be aquired, lack of gh production, receptors dont respond/lack of IGF
- normal Birthweight tho no long bone growth

40
Q

diabetes mellitus: typ1

A

pancreas does not make insulin anymore due to beta cell destruction, (can be auto immune)
tx: insulin

40
Q

hypersecretion of GH/acromegaly

A

begnin tumour on pituitary after epipheals plate stops growing (20-40 y/o)
TSH stim thyroid to make T3/T4
No iodine so no T3/T4 but thyroglobulin continues ot be produced—> colloid
No T3/T4 thus TSH remains High

41
Q

3 p’s of hyperglycemia

A

polyphagia, polyuria, polydispia

42
Q

kussmals respirations can occur in what kind of diabetes…

A

hyperglycemia, type 1 diabetes mellitus.

43
Q

NIDDM

A

skeletal muscle cells/liver is less reactive to insulin & pancreas does not secrete enough insulin
factors: age, lifestye, obesity, genetics

44
Q

Tx for HHS

A
  • Regular exercise and healthy diet
  • Oral hypoglycemic meds
    Increased insulin secretion ( incretins, sulfonylureas, meglitinides)
    Drugs that increase receptor sensitivity ( Biguanides)
    Drugs that reduce CHO absorption ( alpha glucosidase inhibitors)
    Drugs that promote satiety ( Amylin)
  • Insulin
45
Q

NKHH?

A

non-ketoitic hyperosmolar syndrome–> DKA in NIDDM, 20% higher mortality compared to DKA

46
Q

neuropathy

A

due to glomerulosclerosis ( initial increased filtering—> damage to glomeruli through I/N/F process); hypertension

47
Q

why do diabetics have ++ risk for infection?

A

Poor circulation, increased glucose supports bacteria, poor healing due to reduced insulin

48
Q

diabetes insipidus:

A

-Central inability to make and secrete ASH- idiopathic tumor, surgery, trauma
-Nephrogenic: inability to respond to the ADH; lack of reabsorption of H2O
-Dipsogenic- constant thirst→ big water load= lots of pee
Gestational: w/ pregnancy, placenta produces enzymes that metabolize ADH

49
Q
A