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pcol350 final > Gopal's Lectures > Flashcards

Gopal's Lectures Flashcards

1
Q

role of bromocriptine

A

d2 selective agonist that reduces prolactin (increased dopamine=decreased prolactin)

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2
Q

acth is for

A

cortisol production

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3
Q

fsh is for

A

spermatogenesis, estradiol and follicular development

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4
Q

lh is for

A

progesterone secretion ovulation and testosterone

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5
Q

site of release of releasing hormones

A

HT

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6
Q

SOR (site of release) of somatostatin (GH-RIH)

A

HT

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7
Q

SOR of dopamine

A

Ant pit

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8
Q

SOR “_____hormone”

A

ant pit

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9
Q

SOR ADH/vasopressin (AVP)

A

post pit

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10
Q

SOR oxytocin

A

post pit

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11
Q

2 hypothalamic hormones that act under positive neural feedback

A

oxytocin and dopamine

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12
Q

cosyntropin

A

synthetic form of truncated human , fewer allergic reactions

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13
Q

diagnostic tests cosyntropin is used for

A

1) to differentiate between congenital adrenal hyperplasia and ovarian hyperandrogenism
2) diagnose adrenal insufficiency

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14
Q

corticorelin ovine triflutate

A

recombonant ovine CRH (–> ACTH –>cortisol)

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15
Q

corticorelin use

A

differentiate between pituitary adenoma and arenal tumers

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16
Q

GH=somatotropin

somatotrem (GH analogue)

A

recombinant human GH

-treat GH deficiency or growth failure in children. Management of AIDS wasting syndrome

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17
Q

GH-RIH= somatostatin

  • otreotide
  • pegvisomant
A
  • 8 AA peptide, short analog of somatostatin that maintains all its functions that suppresses GH and IGF (insulin growth factor). Use= acromegaly and GI secretory diarrhea
  • GH receptor antagonist=used for acromegaly and normalizes IGF level
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18
Q

prolactin action

A

promotes lactogenesis (lactose, casein and lactalbumin in mammary alveoli), released from ant pit and increases milk production.

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19
Q

High prolactin: (GnRH, SEs, DA)

A

decreases GnRH secretion due to feedback inhibition; causes secondary amenorrhea in females during lactation, and infertility in males. During lactation=less dopamine release causing the increased prolactin

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20
Q

site of action prolactin

A

breast (milk synthesis), hypothalamus (decreased GnRH leading to infertility), testes and ovaries (less gonadotropins-FSH and LH- leading to secondary amenorrhea in females, infertility in males)

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21
Q

dopamine antagonists (antipsychotics ex phenothiazines, all non deflective DA antagonists, D2 select antagonists ex domperidone metoclopromide, pro kinetic agents)

A

increase prolactin; cause drug induced i.e. iatrogenic hyperprolactinemia

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22
Q

dopamine agonists (l dopa, non selective DA agonists,D2 selectie agonists like bomocriptine and cabergoline)

A

decrease prolactin

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23
Q

reasons to decrease prolactin

A
  • loss of newborn to stop puerperal lactation
  • decrease abnormal lactation (galactorrhea amenorrhea)
  • decrease hyperprolactinemic amennorrhea
  • treat infertile males with hyperprolactinemia
  • parkinsonsism
  • acromegaly (increased GH levels after adulthood)
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24
Q

AE bromocriptine

A

orthostatic hypotension, digital vasospasm, nausea; cabergoline is more effective and has EDS for patients who don’t respond well to bromo

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25
Q

fall in estrogen and progesterone during delivery

A

developed breast converted to secretory by increased prolactin; get lactogenesis that is maintained by breast feeding. oxytocin helps with milk let down and ejection (contracts myoepithelial cells) Both OT and PRL are synergistic through positive feedback

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26
Q

AVP (arginine vasopressin) aka

A

ADH (antidiuretic hormone) aka

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27
Q

AVP/ADH=structurally related to oxytocin therefore, and both 9aa peptides

A

both exert antidiuretic and vasopressor effects, oxytocin is more mild and has lower efficacy

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28
Q

oxytocin MOA

A

increased Ca influx, IP3 generation leading to contraction of myoepithelial cells (breast) and myometrial cells (uterus-sustained titanic contractions at term after estrogen ad progesterone levels recede at end of pregnancy)

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29
Q

therapeutic uses of oxytocin

A

NOT galactopoeisis (that is prolactin)

  • induction and reinforcement of labor at term
  • uterine inertia and incomplete abortion
  • postpartum haemorrhage (promotes contraction and blood vessels shrink to stop bleeding)
  • postpartum uterine atony
  • induction of lactation to enhance milk letdown
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30
Q

therapeutic uses of oxytocin

A

NOT galactopoeisis (that is prolactin)

  • induction and reinforcement of labor at term
  • uterine inertia and incomplete abortion
  • postpartum haemorrhage (promotes contraction and blood vessels shrink to stop bleeding)
  • postpartum uterine atony
  • induction of lactation to enhance milk letdown
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31
Q

role of AVP aka ADh

A

reabsorb water from renal collecting ducts to maintain plasma volume, through activity of adenylate cyclase on renal V2 receptor to increase cAMP. In pharmacological doses it is a vasoconstrictor/vasopressor (via V1 receptors), and can activate via V1 over causing glygogenolysis and increased glucose release

32
Q

absence of ADH leads to

A

increased water loss=Diabetes Insipidus (DI)

33
Q

causes ADH/AVP release

A

increased plasma osmolality (Na) and decreased plasma volume

34
Q

DDAVP (desmopressin acetate)

A

synthetic selective V2 agonist of vasopressin is 4000x more potent and longer acting, can control central and neurogenic DI with no V1 mediated adverse effects of vasoconstriction of hepatic glycogenolysis. ineffective in nephrogenic DI due to defects at renal V2 level.

35
Q

hydroclorothiazide

A

drug of choice for nephrogenic diabetes insipidus

36
Q

use of AVP

A

only 1 situation; sea colonic and esophageal varies (bleeding) after surgery; a potent arteriolar vasoconstrictor agonist. DDAVP is ineffective since it is selectove V2 agonist.

37
Q

DDAVP (desmopressin acetate)

A

synthetic selective V2 agonist of vasopressin is 4000x more potent and longer acting

  • can control central and neurogenic DI with no V1 mediated adverse effects of vasoconstriction of hepatic glycogenolysis. ineffective in nephrogenic DI due to defects at renal V2 level.
  • for hemophilia A (clotting 8 deficiency) and von willebrands disease (factor 8 deficiency); this is unrelated to its V2 pharmacology. Increases factor 8 level
  • nocturnal enuresis in children and elderly
38
Q

use of AVP

A

only 1 situation; sea colonic and esophageal varies (bleeding) after surgery; a potent arteriolar vasoconstrictor agonist. DDAVP is ineffective since it is selectove V2 agonist.

39
Q

dilutional hyponatremia

A

endocrine abnormality; increased AVP/ADH production or Syndrome of inappropriate antidiuretic hormone (SIADH). Leads to increased water reabsorption and expansion of plasma volume.

40
Q

Treat dilution hyponatreia

A

ADH antagonists (Tolvaptan*), demeclocylcine

41
Q

Treat dilution hyponatreia

A

ADH antagonists (Tolvaptan*), demeclocylcine

42
Q

testosterone

A

synthesized in testis by leydig cells, converted by 5 alpha reductase to dihydrotestosterone. Orally ineffective

43
Q

weak androgens secreted by adrenal gland

A

androstenedione, dehydroepiandrosterone

44
Q

synthetic androgen

A

17 alpha methyl testosterone; oral or subing

45
Q

testosterone preparations

A

testosterone propionate (ester, stanozolol (synthetic anabolic steroid derived from dihydrotestosterone with less androgenic and more anabolic activity)

46
Q

actions of testosterone

A 
androgenic:
-maturation fo testis, prostate, seminal vsicle, scrotum, penis
-increase sebaceous gland secretion
-thickening on skin
-acne
-increased body hair
anabolic:
-increased muscle mass
-increase protein anabolism
-give in cachectic patients, prolonged illness
47
Q

therapeutic uses testosterone

A
  • hypogonadism; secondary sex characteristics
  • osteoporosis
  • trauma to decrease protein loss and promote positive nitrogen balance
  • post operative convalescence
  • manage intractable anaemia
48
Q

adverse effects testosterone

A
  • acne
  • prostatic hyperplasia*
  • hypertrophy
  • behaviour change
  • aggressiveness
  • psychotic symptoms
  • hepatic dysfunction; cholestatic jaundice (esp with 17 alpha methyl substituted synthetic steroids; anabolic, androgens and progestins)
49
Q

insulin sensitizers

A

enhance insulin action

  • biguanide (metformin)
  • thiazolidine diones (TZD) (ex pioglitazone, rosiglitazone)
50
Q

insuiln secretagogues

A
  • KATP blockers (sulfonylureas like glyburide and metglinides like repaglinide)
  • GLP1 analogs: incretins, exanatide, liraglutide
  • DPP4 inhibitor- sitagliptinm saxagliptin
51
Q

insulin and its analogs

A

fast acting: lispro, aspart, glulisine
short acting: regular
intermediate: NPH
long: ; glargine, ; detemir

52
Q

insulin and its analogs

A

fast acting: lispro, aspart, glulisine
short acting: regular
intermediate: NPH
long: ; glargine, ; detemir

53
Q

acarbose

A

alpha glucosidase inhibitor

54
Q

dapagliflozin

A

SGLT2 inh (renal sodium glucose co transporter 2 inhibitor)

55
Q

WHO essential medicine status for diabetes

A

metformin, glyburide NPH insulin

56
Q

insulin and its analogs

A

fast acting: lispro, aspart, glulisine (DO NOT use IV- rapid action is result of rapid release from subcutaneous)
short acting: regular
intermediate: NPH
long: ; glargine, ; detemir, degludec (slow onset but longest acting)

57
Q

WHO essential medicine status for diabetes

A

metformin, glyburide NPH insulin

58
Q

type 1 diabetes treatment

A

give insulin; intensive therapy; give long acting (glargine, detemir, degludec) plus an adjustable dose of pre meal quick onset short and rapid acting analog (lispro, aspart, glulisine) =best approach to maintain steady state plasma levels and decrease incidence on diabetic complications

59
Q

conventional insulin therapy

A

no longer used; bid short acting and inter acting insulin

60
Q

hazards of insulin

A
  • hypoglycemia (insulin shock)= tachycardia, confusion, vertigo, diaphoresis, brain damage; give glucose or glucagon
  • insulin induced immunologic complications: form insuin antibodies and get resistance
  • painful, daily admin, lipodystrophy, edema/weight gain
61
Q

inhaled insulin withdrawn because

A

high lung concentration activates IGF receptor and possible lung cancer incidence

62
Q

sulfonyl urea role and mechanism

A

stimulate release of endogenous insulin; inhibit kATP channels to decrease glucagon. May also increase number of functional insulin receptors in peripheral tissues.

63
Q

Sufonyl urea generations

A

1st- not used
2nd- glyburide, glipizide
3rd- glimepiride
2nd and 3rd are more potent, longer acting, better PK, decreased AE

64
Q

sulfonyl urea role and mechanism

A

stimulate release of endogenous insulin; inhibit kATP channels on beta cells to decrease glucagon. May also increase number of functional insulin receptors in peripheral tissues.

65
Q

Sufonyl urea generations

A

1st- not used
2nd- glyburide, glipizide
3rd- glimepiride
2nd and 3rd are more potent, longer acting, better PK, decreased AE

66
Q

AE sulfonylureas

A

hypoglycemia*
rash, allergic, nausea, vomit, cholestatic jaundice.
not helpful in advanced stages of type 2; must use at start

67
Q

miglitinides

A
  • repaglinide
  • effect and mechanism same as sulfonylureas
  • stimulate release of endogenous insulin by inhibiting kATP channels on beta cells and decreasing glucagon
  • ineffective for patients who lack functional beta cells or advanced stages of type 2
  • rapid onset and short action so must be taken before meals
68
Q

metformin (a biguanide)

A
  • reduce postprandial and fasting glucose in type 2 diabetes (best agent)
  • reduces hepatic gluoneogenesis
  • stimulate glycolysis in peripheral tissues; AMPK activation mimics causes glucose utilization during exercise
  • reduce glucose absorbed from GI
69
Q

adverse effects metformin

A

gi distress, **lactic acidosis (esp in patients with renal or liver disease-

70
Q

metformin (a biguanide)

A
  • reduce postprandial and fasting glucose in type 2 diabetes (best agent)
  • reduces hepatic gluoneogenesis
  • stimulate glycolysis in peripheral tissues; AMP activated protein kinase activation mimics causes glucose utilization during exercise
  • reduce glucose absorbed from GI
  • *decrease plasma glucose by decreasing hepatic glucose production and improving insulin sensitivity
  • *decrease gluconeogenesis and glycogenolysis, increase glycogen synthesis
71
Q

adverse effects metformin

A

gi distress, **lactic acidosis (esp in patients with renal or liver disease, or with predisposition to tissue anoxia)

72
Q

metformin uses

A
  • type 2 diabetes
  • treat insulin resistance and polycystic ovarian syndrome, gestational diabetes
  • **in hypoxic condition use may promote lactic acidosis
73
Q

acarbose

A

alpha glucosidase inhibitor’ slows carb absorption, reduce postprandial hyperglycemia, *no effect on fasting blood sugar
-AE flatulance, diarrhea, cramping

74
Q

metformin uses

A
  • type 2 diabetes
  • treat insulin resistance and polycystic ovarian syndrome, gestational diabetes
  • **in hypoxic condition use may promote lactic acidosis
75
Q

thiazolidinediones (TZD)

A

rosiglitazone, pioglitazone

  • not popular anymore
  • effective in HbA1C control; activate PPAR gamma to regulate gene transcription
  • CI in congestive heart failure
  • increased MI, CV risk, hip fracture, anemia, edam, redistribution of fat
76
Q

thiazolidinediones (TZD)

A

rosiglitazone, pioglitazone

  • not popular anymore
  • effective in HbA1C control; activate PPAR gamma to regulate gene transcription
  • CI in congestive heart failure
  • increased MI, CV risk, hip fracture, anemia, edam, redistribution of fat

pcol350 final (3 decks)

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