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Bioscience Emily Clipston > quiz #idk > Flashcards

quiz #idk Flashcards

1
Q

amines

A

derivatives of tyrasine or triptophan

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2
Q

tyrasine

A

epi, norepi, T3, T4

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3
Q

tryptophan

A

serotonin, very short, 1-2 AA long

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4
Q

peptides

A

most hormones including all hypothalamic and pituitary hormones

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5
Q

steroids

A

all derivatives of cholesterol

includes sex hormones and hormones of the adrenal cortex

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6
Q

eicosanoids and retanoids

A

derivatives of fat

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7
Q

peptide class synthesis

A

synthesized as prohormone (with extra AAs stores on it) then packaged and stored in vesicles
rapid release following signal
blood levels rise quickly

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8
Q

steroid class synthesis

A 
not stored (precursor may be) need to be synthesized from precursor in response to signal
release not instantaneous and blood levels rise more slowly
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9
Q

peptide circulation

A

water soluble, circulate free
more rapidly degraded in plasma
short circulating half lives

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10
Q

steroid class circulation

A

water insoluble, circulate bound to a plasma protein
free fraction can interact with receptors
longer half lives, many minutes to hours

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11
Q

peptide interaction with target cells

A

lipid insoluble, cant enter
binds to receptors on cell membrane
biological effect via second messengers
alters activity of existing proteins

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12
Q

steroid interaction with target cells

A

diffuses into target cell (lipid soluble)
binds to receptors in cytoplasm or nucleus
biological effect via effects on DNA
increases synthesis of proteins

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13
Q

cAMP

A

acts on kinases
an increase in [] makes kinases active
modulate activity via modulation
changes protein activity

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14
Q

calmodulin

A

calcium influx makes Ca++, activates kinase, makes proteins

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15
Q

anterior pituitary

A

middle tier in the hypothalamic pituitary peripheral hormone axis
controlled by hypothalamus

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16
Q

posterior pituitary

A

neural extension of the hypothalamus
ADH
oxytocin

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17
Q

oxytocin

A

causes uterine contractions

pressure receptors –>positive feedback

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18
Q

ADH

A

prevents you from losing water in urine and retains H2O in kidney
decrease in plasmaosmolarity and increase in plasma volume
negative feedback on post pituitary

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19
Q

what determines whether a hormone has a biological effect on a cell?

A

if it has a receptor or not

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20
Q

what determines the magnitude of the biological effect?

A

amount of circulating hormone

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21
Q

tropic hormone

A

stimulates the release of another hormone

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22
Q

primary defect

A

peripheral endocrine gland

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23
Q

secondary defect

A

ant pituitary

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24
Q

tertiary defect

A

hypothalamus

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25
Q

hypopituitarism

A

post partum necrosis (not enough blood flow during delivery)
non-functioning tumor
surgery or radiation
infarction

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26
Q

order of hormone loss

A 
GH
LH
FSH
TH
ACTH
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27
Q

hyperpituitarism

A

usually due to a hormone secreting adenoma
if
a. pituitary high, hormone low: primary defect (peripheral endocrine gland)
b. pituitary low, hormone low: secondary (ant pituitary)
c. pituitary low, hormone high: negative feedback, primary

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28
Q

GH

A 
ant pituitary
normal growth dependent on many factors
-genetic: highly implicated
-hormonal
-nutritional
-other: skeletal, abnormalities, etc

systemic circulation
insulin like growth factor
direct effect on target cells

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29
Q

GH secretion

A 
starts with a lack of availability of nutrients, exercise, fasting, low BG, sleep
GHRH secreted by hypothalamus
causes ant pit. to secrete GH
increases plasma IGF-I
negative feedback mechanisms
30
Q

GH and sleep

A

much higher secretion during sleep, peaks get smaller as you age

31
Q

IGF-1 secretion effects

A

growth of long bones

growth of sk m, skin, visceral organs, endocrine organs, connective tissue

32
Q

direct metabolic GH effects

A

inc protein synthesis
inc BG
breaks down fat

33
Q

GH decrease

A

congenital or with age

results in loss of muscle mass, inc in body fat, dec in BG

34
Q

GH excess

A

nose, chin, hands, ears grow a lot
much taller possibly
inc BG, can cause diabetes
abnomalities of lipid metabolism

35
Q

follicular cells

A

make hormones

36
Q

thyroglobulin (TG)

A 
long chains of tyrosine residues, moves into colloid
then traps dietary iodide
oxidizes it, turns into iodine
enzymes iodinate TG
into T3 or T4
37
Q

T4

A

less biologically active, more of it circulating

38
Q

TH secretion

A 
just before you sleep, cold temp, stress
hypothalamus-> TRH
ant pit--> TSH
thyroid--> T3 and T4 (- feedback of TRH)
-->target organs
39
Q

effects of TH

A 
normal basal metabolic rate
thermogenesis
CV system
GI system
NM system
growth and development
40
Q

hypothyroidism types

A

congenital: growth very stunted, congenital defects
acquired
-iodide def
-hashimotos: immune attack against thyroid cells

41
Q

hypothyroidism symptoms

A 
weight gain despite normal intake
always cold
dec BP dec HR
dec digestion
constipation
sluggish
fatigue
42
Q

myxedema

A

non-pitting, firm tissue, with a lot of collagen and protein

43
Q

goiter

A

enlarged thyroid gland, hypo or hyper

44
Q

hyperthyroidism types

A

primary (grave’s disease): adenoma/carcinoma

secondary (increased TSH)

45
Q

hyperthyroidism symptoms

A 
weight loss
too hot
inc HR, BP
diarrhea
bloating
inc energy
edgy
insomnia
fatigue
brittle hair/nails
46
Q

hyperthyroidism treatment

A

propyl-thyrocil: prevents oxidation of iodide, slows converstion of T3 and T4
radiation
surgery

47
Q

amioderone

A

iodine in it, can produce hypo or hyper

48
Q

control of cortisol secretion

A

infection, pain, stress, hypoglycemia, sleep, trauma—>
hypothalamus->CRH->ant pit->ACTH->adrenal cortex->cortisol->target organs
pathway is dampened if youve been on corticosteroids
controls its own rate of release (-feedback to hypothalamus)

49
Q

cortisol effects

A 
acts on DNA, synthesis of enzymes
inc BG
catabolic protein
catabolic fat
anti infammatory effects
immunosuppressive effects: inhibits hypersensitivity
50
Q

addisons disease

A

hyposecretion of cortisol, androgens, aldosterone

51
Q

Cushings characteristics

A

muscle wasting in arms/legs
pot belly
loss of fat deposits except in adominal
thinner/fragile skin

moon face, buffalo hump, inc facial hair, thinning of scalp in women

52
Q

cushings symptoms

A 
adrenocortical excess
ligs and tendons more fragile
osteoporosis
diabetes
hypokalemia
HTN
hirsuitism: excess hair growth
acne
inhibited inflammatory and immune

caused by tumors, excess intake of corticosteroids

53
Q

corticosteroids are used to treat

A 
lupus (conective tissue)
crohns (GI)
MS, myasthenia gravis (NM)
asthma
osteo and RA
bursitis tenosynovitis
eczema (skin)
for anti imflammatory and immunosuppressive effects
54
Q

adverse effects of long term use

A 
suppression of normal adrenal functin
drug induced cushings
breakdown of bone, ligs, tendons, skin
edema, weight gain
peptic ulcers, HTN, mood changes
might induce type II diabetes
55
Q

relationship btw the medulla and adrenal cortex

A

release hormones in response to stress
ACTH stims synthesis of dopa and norepi
cortisol upregulates PNMT to convert norepi to epi
catecholamines released quickly and have short half life
cortisol release slower and longer half life
corisol permissive for catecholamines

56
Q

alpha cells

A

glucagon

57
Q

beta cells

A

insulin

58
Q

insulin

A 
mediates fate of ingested nutrients in absorptive state, handles influx of nutrients
anabolic
CHO's preferred fuel
glucose uptake
fat storage
protein uptake/synthesis
59
Q

preabsorptive vs absorptive and post

A
  1. 50/50 CHO fat
  2. > CHO
  3. > fat
60
Q

mechanism action of insulin

A

when insulin binds, signals GLUT4 to be inserted into membrane so glucose can get transported into cell

61
Q

glucagon

A

mediates mobilization of stored fuels in post absorptive state

decrease in plasma glucose causes pancreatic alpha cells to inc secretion

62
Q

glucagon effects on liver

A

glycogenolysis, AA uptake and gluconeogenesis

63
Q

glucagon effects on adipose tissue

A

lipolysis

64
Q

AIC

A

better indication of what average BG is like, more stable

65
Q

type I diabetes

A

lack of insulin production
10% of cases
95% of type I’s are autoimmune

66
Q

Type I diabetes symptoms

A

polyuria, polydipsia, polyphagia
hyperglycemia
katoacidosis
fat loss, muscle wasting

67
Q

type I treatment

A

insulin, lifestyle

68
Q

type II diabetes

A

receptor or post receptor problems
80% are obese
down regulation of receptor pop
capable of producing insulin, not taking it up
may become insulin dependent, lose the ability to produce it

69
Q

type II symptoms

A

similar to type I without weight loss and ketoacidosis

70
Q

type II treatment

A

diet and exercise: helps promote insertion of transporters into fat cell membranes

Bioscience Emily Clipston (9 decks)

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