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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
hypopituitarism
post partum necrosis (not enough blood flow during delivery) non-functioning tumor surgery or radiation infarction
26
order of hormone loss
``` GH LH FSH TH ACTH ```
27
hyperpituitarism
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
28
GH
``` 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
29
GH secretion
``` 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
GH and sleep
much higher secretion during sleep, peaks get smaller as you age
31
IGF-1 secretion effects
growth of long bones | growth of sk m, skin, visceral organs, endocrine organs, connective tissue
32
direct metabolic GH effects
inc protein synthesis inc BG breaks down fat
33
GH decrease
congenital or with age | results in loss of muscle mass, inc in body fat, dec in BG
34
GH excess
nose, chin, hands, ears grow a lot much taller possibly inc BG, can cause diabetes abnomalities of lipid metabolism
35
follicular cells
make hormones
36
thyroglobulin (TG)
``` 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
T4
less biologically active, more of it circulating
38
TH secretion
``` just before you sleep, cold temp, stress hypothalamus-> TRH ant pit--> TSH thyroid--> T3 and T4 (- feedback of TRH) -->target organs ```
39
effects of TH
``` normal basal metabolic rate thermogenesis CV system GI system NM system growth and development ```
40
hypothyroidism types
congenital: growth very stunted, congenital defects acquired -iodide def -hashimotos: immune attack against thyroid cells
41
hypothyroidism symptoms
``` weight gain despite normal intake always cold dec BP dec HR dec digestion constipation sluggish fatigue ```
42
myxedema
non-pitting, firm tissue, with a lot of collagen and protein
43
goiter
enlarged thyroid gland, hypo or hyper
44
hyperthyroidism types
primary (grave's disease): adenoma/carcinoma | secondary (increased TSH)
45
hyperthyroidism symptoms
``` weight loss too hot inc HR, BP diarrhea bloating inc energy edgy insomnia fatigue brittle hair/nails ```
46
hyperthyroidism treatment
propyl-thyrocil: prevents oxidation of iodide, slows converstion of T3 and T4 radiation surgery
47
amioderone
iodine in it, can produce hypo or hyper
48
control of cortisol secretion
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
cortisol effects
``` acts on DNA, synthesis of enzymes inc BG catabolic protein catabolic fat anti infammatory effects immunosuppressive effects: inhibits hypersensitivity ```
50
addisons disease
hyposecretion of cortisol, androgens, aldosterone
51
Cushings characteristics
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
cushings symptoms
``` 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
corticosteroids are used to treat
``` lupus (conective tissue) crohns (GI) MS, myasthenia gravis (NM) asthma osteo and RA bursitis tenosynovitis eczema (skin) for anti imflammatory and immunosuppressive effects ```
54
adverse effects of long term use
``` 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
relationship btw the medulla and adrenal cortex
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
alpha cells
glucagon
57
beta cells
insulin
58
insulin
``` 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
preabsorptive vs absorptive and post
1. 50/50 CHO fat 2. >CHO 3. >fat
60
mechanism action of insulin
when insulin binds, signals GLUT4 to be inserted into membrane so glucose can get transported into cell
61
glucagon
mediates mobilization of stored fuels in post absorptive state decrease in plasma glucose causes pancreatic alpha cells to inc secretion
62
glucagon effects on liver
glycogenolysis, AA uptake and gluconeogenesis
63
glucagon effects on adipose tissue
lipolysis
64
AIC
better indication of what average BG is like, more stable
65
type I diabetes
lack of insulin production 10% of cases 95% of type I's are autoimmune
66
Type I diabetes symptoms
polyuria, polydipsia, polyphagia hyperglycemia katoacidosis fat loss, muscle wasting
67
type I treatment
insulin, lifestyle
68
type II diabetes
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
type II symptoms
similar to type I without weight loss and ketoacidosis
70
type II treatment
diet and exercise: helps promote insertion of transporters into fat cell membranes

Bioscience Emily Clipston (9 decks)

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