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BMS 450 > final exam > Flashcards

final exam Flashcards

1
Q

somatotropin

A

-growth hormone
-released by the anterior pituitary in response to ghrh produced by hypothalamus
-released at max during sleep
-decreases with age as well as decreasing lean muscle mass
-promotes cell proliferation and bone growth
- moa is directly acted at targets (except for some that work through somatomedins like igf1 and igf 2)

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2
Q

somatropin

A

-synthetic hgh
-produced using recombinant dna
-indicates dwarfism, turner syndrome, prader willi syndrome, and aids wasting syndrome
-daily doses
-“anti aging” hormone because it increases lean body mass, bone density and skin thickness and decrease adipose tissue (shit be sold on the black market to old bitches and athletes)
-short half life, but induces igf1 from liver which has gh action
-adv eff include increased risk of diabetes. do not use in pt with closed epiphyses, diabetic retinopathies, or fatsos with prader willi
-prodrug lonapegsomatropin(skytrofa) can be used pediatrically once weekly

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3
Q

whats the deal with laron syndrome

A
  • dwarfism caused by an insensitivity to gh (mutation on gh receptor)
    -therefore somatropin is ineffective
    -exceptionally low levels of igf1 and igf3
  • treatment has to be done by biosynthetic igf1
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4
Q

somatostatin

A

-ghih (gh inhibitor)
- isolated from the hypothalamus, it is found in neurons, intestine, stomach, and pancreas
-in pituitary it binds to receptors that suppress hp and tsh(thyroid stimulating). also inhibits insulin glucagon and gastrin
- indicates gigantism(kids) and acromegaly(post epiphyseal closure) and acrogigantism(mix of the two)

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5
Q

synthetic somatostatin analogs

A

-synthetic analogs like octreotide and lanreotide are longer than the endogenous somatostatin
-can aid in diarrhea associated with carcinoid tumors and esophageal varices
-adv eff abdominal pain, farts, puke, steatorrhea, gallstones (delayed gallbladder emptying)

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6
Q

Dopamine receptor agonists and hgh excess

A

-bromocriptine and cabergoline
-inibit gh
-indicate acromegaly and pituitary microadenomas
-important note is that dop actually increases ghrh and somatostatin so kinda depends

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7
Q

synthetic Gh receptor antagonists

A

-pegvisomant
- indicates acromegaly that is refractory to other modes of therapy

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8
Q

thyroid shit you should probably know

A

-t4 and t3
-t4 20x amount of t3
- t4 is less potent but has longer half life
- t3 is more rapid (3days) while t4(11 days)
-t4 is converted into active t3 by 5’monodeiodinase
-t3 binds to nuclear receptors and initiates transcription this causes high metabolic rate and o2 consumption, wide spectrum of effects
-hyper: nervousness weight loss poopin tachycardia insomnia goiter bulging eyes
-hypo: lazy wieght gain no poopin tired not hungry weak goiter

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9
Q

hyperthyroidism

A

-nervousness weight loss poopin tachycardia insomnia goiter bulging eyes
-mostly caused by graves, which is where thyroid stimulating immunoglobins work against tsh receptors
- goiter or solitary hyperfunctioning adenoma in thyroid or pituitary
-sequelae(caused by?) is increased metabolic rate and physiological functions
-thyroid storm can happen, this is basically when metabolism and physiological functions go berserk it can lead to heart failure
-thyroid storm can be prevented by suppressing thyroid function with anti thyroid drugs
-b blockers can be useful too
-can remove the thyroid surgically or by killing it with radioactive iodine(can lead to hypo)
-

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10
Q

Methimazole vs PTU (thiamides

A
  • these are both treatments for hyperthyroid that inhibit hormone synthesis
  • methimazole is better due to longer half life, but methimazole can only be used during the first trimester of pregnancy because it has teratogenic effects
    -ptu can cause hepatotoxicity and agranulocytosis, therefore ptu should be a last resort
    -ptu blocks peripheral t4 from converting into t3
    -thioamides are concentrated in the thyroid and inhibit the oxidative processes for iodination and condensation of iodotyrosines to form t3 and t4
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11
Q

iodide

A

-blocks hormone release to treat hyperthyroid
- inhibits iodination of tyrosines but only lasts a few days
- inhibits the release of thyroid hormones from thyroglobulin by mechanisms not known
-treats thyroid storm or prior to surgery because it decreases the vascularity of the thyroid
-adv effects include throat swelling, rashes, ulcerations due to oral administration

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12
Q

hypothyroidism

A

-caused by hashimotos which is autoimmune destruction of the gland
-high tsh=goiter
-can be caused by surgery, radioactive treatment, or lithium
-can be caused by diet iodine deficiency (goitrogen veggies) though this is rare because we have a lot of iodine in salt
-slows down metabolism can cause :
-cretinism (dwarfism and retardation) which is during fetal development caused by maternal hypothyroidism
-myxedema which is deficiency in adulthood

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13
Q

hypothyroidism treatment

A

-levothyroxine(t4) is preferrable to liothyronine(t3) or liotrix(combo)
-t4 is better tolerated and has a longer half life
-levo is dosed once daily and reaches steady state in 6-8 weeks
-levo toxicity is nervousness tachycardia weight loss and such
-desiccated thyroid extract from farm animals can be generic med
-drugs that induce cytP450 like phenytoin rifampin and phenobarbitol accelerate metabolism of thyroid hormones and decrease effectiveness

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14
Q

extracellular calcium sensing receptor(casr)

A

-enables tissues involved in ca homeostasis to monitor blood calcium
-these tissues are pth secreting parathyroid glands(big one), calcitonin secreting thyroid c cells, intestines, bone, kidney
-calcium flux is regulated by pth calcitonin and 1,25dihidroxyvitamin d3 whose renal synthesis is homeostatically regulated

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15
Q

pth(parathyroid hormone)

A

-acts directly on bone and kidney to increase ca influx into plasma
-indirectly increases ca absorption from gut by stimulating 1,25oh2d in the kidney increasing blood calcium
-inhibits renal tubular reabsorption of pi increasing excretion

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16
Q

hypoparathyroidism

A

-hypocalcemia basically leaves too much na which depolarizes too much causing muscle spasms. this is hypocalcemic tetany
-can be caused by digeorge syndrome(born wo it)
-can be caused by genetic mutations of casr where chief cells assume serum ca is elevated when its not leading to lower pth
-can be autoimmune where casr is targeted, activating it, lowering pth
-latrogenic cause can be accidental removal during thyroidectomy
-idiopathic cause can be failure of tissues to respond to pth
-treated with teriparatide(acts like pth v effective in removing tetany) or calcium plus calcitriol(standard treatment)

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17
Q

osteoporosis

A

-bone resoption exceeds depostion
- estrogen normally inhibits osteoclasts and enhances osteoblasts, deficiency will do the opposite (can be postmenopausal which is primary)
-hypercortisolism (secondary)can do this because it increases rankl but decreases osteoprotegerin thereby increasing osteroclastogenesis
-also renal disease can cause it its secondary
-most common bone disease
-loss of bone and its minerals
-more common in women(WHO CARES BRUH FUCK THIS CLASS)
-can be prevented with calcium and vit d
-

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18
Q

bisphosphonates

A

-inhibit bone resorption to treat osteoporosis
-alendronate ibandronate risedronate and zoledronic acid
-preferred agents for postmenopausal osteoporosis
-moa biphosphonates decrease osteoclastic bone resorption through increasing ostroclastic apoptosis and inhibition of the cholesterol biosynthetic pathway

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19
Q

salmon calcitonin

A

-for osteoporosis in women who are at least 5 years postmenopausal
-reduces bone resorption less effective than biphosphonates, but causes relief of pain

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20
Q

rankl antibodies

A

-inhibit osteoclastogenesis to treat osteoperosis

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21
Q

selective estrogen receptor modulators

A

-treat osteoperosis duh inhibit osteoclasts
-estrogen replacement is effective but can increase risk of endometrial cancer breast cancer stroke and cardiovascular shit so it aint used too much no more
-raloxifene has estrogen like effects on bone and estrogen antagonist effects on breast and endometrial tissue

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22
Q

sclerostin (sost)

A
  • in animals, if sost is inhibited by monoclonal antibodies osteoblasts fuck off and new bones form.
    -sost is a glycoprotein secreted by osteocytes and chondrocytes that has antianabolic effects that inhibit osteoblasts
    -mutations in sost genes can create high bone mass (sclerosteosis)
    -binds to lrp5/6 and inhibits wnt signaling leading to decreased bone form
    -sost is inhibited by pth and estrogen
    -shit is increased by calcitonin
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23
Q

Denosumab(prolia amgen)

A

-this is a monoclonal antibody that targets rankl and inhibits octeoclastogensis
-this ones all good in postmenopausal osteoporosis
-subcutaneous administration every 6 months
-risk of infection and osteonecrosis in the jaw(should be a last resort)
-soluble osteoprotegerin and denosumab have been effective in cancer patients with hypercalcemia of malignancy (prostate )
-this is due to cancers secreting pth related protein which promotes rankl and inhibits osteoprotegerin (denosumab targets rankl and fakes being osteoprotegerin preventin pthrp induced osteoclastogenisis

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24
Q

romosozumab (evenity)

A

-monoclonal antibody that inhibits sost resulting in increased bone formation to aid in osteoporosis
-specifically for osteoporosis in postmenopausal women or a last resort for other patients
-subcutaneous injection whose anabolic effects wane after 12 monthly doses
-adv eff are stroke myocardial infarction and death

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25
Q

teriparatide

A

-for osteoporosis, it actually stimulates bone formation
-recombinant pth
-subcutaneous daily
-stimulates osteoblasts
-reserved for pt with high risk of fractures

26
Q

renal hyperparathyroidism

A

-results in osteoporosis and calcifications
- nephropathy results in failure of reabsorption of calcium resulting in hypocalcemia= increased pth=osteoclastogenesis-
-failing kidneys in end stage renal disease dont excrete phosphate enough and dont convert vit d to its active form= insoluble calcium phosphate forms= hypocalcemia=osteoporosis

27
Q

nutritional hyperparathyroidism

A

-inadequate vit d3 or excess phosphorous=calcum= increased pth
-skeletal demineralization and maxillary anomalies

28
Q

targeting casr to manage secondary hyperparathyroidism due to nephropathy

A

-type 1 agonists activate the receptor even without ca being present
-type 2 agonists (calcimimetics) allosterically acticivate the receptor. A good example is cinacalcet (sensipar) which is used for hyperparathyroidism in patients receiving hemodialysis for chronic kidney disease

29
Q

calcilytics

A

casr blocking drugs that can help with osteoporosis

30
Q

glucocorticoid shit

A

-genomic actions slow changes in gene expression that alter cellular function (transactivation through pgre and transrepression through ngre)
-nongenomic actions are rapid changes in cellular function with no change in gene expression including transmembrane currents phosphorylation and calcium changes

31
Q

adrenocortical insufficiency

A

-primary(hyposecretion of adrenal cortex like addison disease)
-secondary (inadequate secretion of acth, latrogenic;prolonged exogenous corticosteroid therapy)
-tertiary(lacck of crh as well as injury or disease)

32
Q

hyrdocortisone

A

-corticosteroid for adrenocortical insufficiency
- side note addison disease is diagnosed by lack of response to acth administration
- this is identical to natural cortisol and corrects the deficiency, failure to do so results in death
-for addison, 2/3 given in mornin and 1/3 at night
-works in secondary or tertiary insufficiency as well

33
Q

fludrocortisone

A

-synthetic mineralocorticoid that can supplement for primary adrenocortical insufficiency such as addison disease

34
Q

adrenocortical excess (hypercortisolism)

A

-primary is hyperfunciton of adrenal cortex
-secondary is hyperfunction of acth secreting cells (cushings disease)
-tertiary is hypothalamic crh hypersecretion

-can be excess acth, paraneoplastic or adrenal cortical tumor

35
Q

cushings disease

A

-can be diagnosed through pee tests
-low dose dexamethasone suppression test: dexamethasone (cortisol analogue) is injected at a low dose that should suppress the normal morning rise of cortisol, in cushings this wont happen
-high dose dexanethasone suppression test: dexamethasone is injected and if cushings acth will suppress, if not its a maligant non pituitary tumor

36
Q

aminogluthemide

A

-cytadren
-cushings drug
-blocks steroid production derived from cholesterol
-also used as a 2nd or 3rd line choice for hromone sensitive breast cancer because it blocks pregnelone and aromatase

37
Q

ketoconazole

A

-antifungal that treats cushings
-inhibits all gonadal and adrenal steroid hormone synthesis

38
Q

metyrapone

A

-used in diagnosis and treatment of cushing
-tests functionality of hypothalamic pituitary feedback mechanism
-normally inhibits metabolism of 11-deocycortisol to cortisol. if 11deoxycortisol levels no rise and acth rise its adrenal insufficiency, if neither rise it is an impaired hpa axis, if it faisl its an adrenal tumor
-can treat by inhibiting adrenal steroidogenesis but in women can cause hirsutism (not long term treatment)

39
Q

hyperaldosteronism

A

causes sodium and water retention and potassium excretion

40
Q

spironolactone

A

-hyperaldosteronism therapy
- antihypertensive that competes for mineralocorticoid receptor and inhibits sodium reabsorption
-can antagonize aldosterone and testosterone synthesis
-treats hirsutism in women due to interference at the androgen receptor in the hair follicle
-can cause hyperkalemia, gynecomastia, menstrual irregularities and skin rashes

41
Q

eplerenone

A

-treats hyperaldoseronism
-binds to mineralocorticoid receptor and acts as aldosterone antagonist
- avoids gynecomastia that is associated with spironolactone

42
Q

congenital adrenal hyperplasia

A

-21 hydroxylase deficiency is most common cause
-salt wasters=salt loss=vomiting weight loss adrenal crisis and failure to thrive (hyponatremic encephalopathy)
-virulizers (adrenogenital syndrome). in females resultes in pseudohermaphrodites and in males somatic and sexual precocity but appear normal at birth

43
Q

nsaids

A

-work on cox1(tissues) and coz 2(inflammaroty sites and kidney bone and brain)
-because of this many prostaglandins are inhibited and cause upregulation of leukotrienes which bronchoconstrict(dont use in asthmatics)
-this leukotriene thing can also lead to reyes syndrome which involves hepatotoxicity and encephalopathy and can be lethal in kids
- can cause heart failure in kids cuz of PDA closure (prostaglandins keep this open)
-

44
Q

aspirin

A

non selective and irriversibly inhibits both forms of cox

45
Q

acetominophen

A

not an nsaid

46
Q

estrogen progestin combination

A

-hormonal contraceptive
-can be oral transdermal(ethinyl estradiol as estrogen and norelgestromin as progestin) or vaginal ring(same as transdermal)
-

47
Q

progestin

A

hormonal contraceptive that is useful when estrogen is contradicted . does not affect milk production. no rx needed for opill(norgestrel)

48
Q

nonhormonal contraception

A

essure is permanent birth control that is a soft flexible insert that makes a barrier of scar tissue in the fallopian tubes

49
Q

morning after pills

A

high dose estrogen twice daily for 5 days or 2 doses followed by 2 doses. Can also be synthetic progestin.
-ulipristal acetate is a progesterone receptor modulator
-copper tiud induces inflammation response
-all associated with nausea

50
Q

mifepristone

A

abortion pill through 49 days of pregnancy. interferes with progesterone causing a decline in gonadotropin. sensetizes endometrium to prostaglandins . can be used with misoprostol(synthetic prostaglandin).

51
Q

danazol

A

-synthetic androgen that suppresses estrogen by inhibiting midcycle lh and fsh to aid in endometriosis.
- pt should use nonhormonal contraception
- adv eff include estrogen deficiency (headache flushing) and atrophic vaginitis
-androgenic side effects include acne edema hirsutism deep voice weight gain

52
Q

gonadotropin releasing hormone agonists

A

-temporary medical oophorectomy, initial stimulation of lh and fsh release and then inhibition of hormone release. leads to reduced sec hormone levels and regression of endometriosis related lesions
-because of concerns about osteopenia add back low dose estrogen therapy

53
Q

oral contraceptives and progestin combine

A

supress lh and fsh. render endometrial tissue thin and compact thus alleciating endo sympoms . progestins have adv eff

54
Q

polycistic ovary syndrome

A

bith control can help

anti androgen can help but is not approved by fda

metformin can help but also not approved. improves insulins ability to lower blood sugar and can lower both insulin and androgen

55
Q

clomiphene citrate

A

-clomid or serophene
-anti estrogen
-binds competitively to estrogen receptors and decreases the sites available to endogenous estrogen
-this inhibition disrupts negative feedack of estrogens on the hypothalamus and pituitary leading to an increase in gnrh and gonadotropins which leads to ovulation and spermatogenesis
-treats infertility associated with anovulatory menstrual cycles but is only effective in women with a functional hypothalamus and adequate estrogen production
-can also boost test in men to treat male factor infertility
-can cause ovarian hyperstimulation syndrome which causes swelling of hands and legs ab pain short breath weight gain and nausea. can be fatal

56
Q

hyperprolactinemia

A

-too much prolactin
-typically prolactin stimulates lactation and is inhibited by dopa at d2, so anything that is disrupting dopa to the anterior pituitary can cause this
-supresses gonadotropin secretion which diminishes reproductive function and sex drive (hypogonadotropic hypogonadism)
-most common cause is drug induced (metoclopramide and risperidone are d2 antagonists) (also antidepressants cause this as well as amenorrhea and galactorrhoea )
-can occur during pregnancy and lactation
-pathologically can be caused by pituitary adenomas and hypothyroidism(more trh=more prolactin)

57
Q

trt

A

-testosterone replacement therapy for hypogonadism and andropause
- stimulates secondary sex characteristics but does not improve fertility in men with testicular failure
-can also just help old dudes with andropause
- adv eff gynecomastia, testicular atrophy, and progression of prostatic hpertrophy to prostate cancer, also hepatic injury

58
Q

erectile dysfunction

A
  • erection is mediated by pelvic parasympathic nerves, specifically nonadrenergic noncholinergic(nanc) nerves
    -both nanc and ach stimulate no to put blood in the dick
    -sexual stimulation=no=cgmp. so erections are cgmp dependent
59
Q

tadalafil

A

-Pde5 inhibitor for ED
-works by preventing catabolism of cgmp and extends duration of erections
-no effect in the absence of sexual stimulation
-has a longer duration therefore more side effects like priapism
-can relieve benign prostatic hypertrophy because pde5 is in the prostate and its vasodilation can ease pain
-contraindicated in patients who use nitrates like alpha blockers because risk of hypotension and dizziness

60
Q

flibanserin

A

-addyi
-female viagra for premenopausal women with hypoactive sexual esire disorder
- postsynaptic 5ht1 receptor agonist and 5ht2a antagonist.
moa unknown
-supposed to correct dopa and ne while lowering serotonin

61
Q

antiandrogens

A

-prevent test and dihydrotest from doing stuff to aid in benign prostatic hyperplasia and prostate cancer
-androgen receptor antagonists (flutamide) block androgen action
-5alspha reductase inhibitors (finasteride) reduce production of dht
-gnrh agonists(leuprolide) rown regulate and inhibit the pituitary gonadal axis
-gnrh antagonists (cetrorelix) competitive occupancy of gnrh receptor and rapid reversibel suppression of gonadotropin secretion
-androgen synthesis inhibitors inhibit enzymatic biosynthesis of androgens like ketoconazole(cyp17a1 inhibitor) aminoglutethiide(cyp11a1 p450scc inhibitor)`and finasteride(5 a reductase inhibitor)
-bifluranol weakly inhibits

BMS 450 (3 decks)

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