Gopal's Lectures Flashcards
1
Q
role of bromocriptine
A
d2 selective agonist that reduces prolactin (increased dopamine=decreased prolactin)
2
Q
acth is for
A
cortisol production
3
Q
fsh is for
A
spermatogenesis, estradiol and follicular development
4
Q
lh is for
A
progesterone secretion ovulation and testosterone
5
Q
site of release of releasing hormones
A
HT
6
Q
SOR (site of release) of somatostatin (GH-RIH)
A
HT
7
Q
SOR of dopamine
A
Ant pit
8
Q
SOR “_____hormone”
A
ant pit
9
Q
SOR ADH/vasopressin (AVP)
A
post pit
10
Q
SOR oxytocin
A
post pit
11
Q
2 hypothalamic hormones that act under positive neural feedback
A
oxytocin and dopamine
12
Q
cosyntropin
A
synthetic form of truncated human , fewer allergic reactions
13
Q
diagnostic tests cosyntropin is used for
A
1) to differentiate between congenital adrenal hyperplasia and ovarian hyperandrogenism
2) diagnose adrenal insufficiency
14
Q
corticorelin ovine triflutate
A
recombonant ovine CRH (–> ACTH –>cortisol)
15
Q
corticorelin use
A
differentiate between pituitary adenoma and arenal tumers
16
Q
GH=somatotropin
somatotrem (GH analogue)
A
recombinant human GH
-treat GH deficiency or growth failure in children. Management of AIDS wasting syndrome
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
18
Q
prolactin action
A
promotes lactogenesis (lactose, casein and lactalbumin in mammary alveoli), released from ant pit and increases milk production.
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
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)
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
22
Q
dopamine agonists (l dopa, non selective DA agonists,D2 selectie agonists like bomocriptine and cabergoline)
A
decrease prolactin
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)
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
25
fall in estrogen and progesterone during delivery
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
26
AVP (arginine vasopressin) aka
ADH (antidiuretic hormone) aka
27
AVP/ADH=structurally related to oxytocin therefore, and both 9aa peptides
both exert antidiuretic and vasopressor effects, oxytocin is more mild and has lower efficacy
28
oxytocin MOA
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)
29
therapeutic uses of oxytocin
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
30
therapeutic uses of oxytocin
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
31
role of AVP aka ADh
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
absence of ADH leads to
increased water loss=Diabetes Insipidus (DI)
33
causes ADH/AVP release
increased plasma osmolality (Na) and decreased plasma volume
34
DDAVP (desmopressin acetate)
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
hydroclorothiazide
drug of choice for nephrogenic diabetes insipidus
36
use of AVP
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
DDAVP (desmopressin acetate)
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
use of AVP
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
dilutional hyponatremia
endocrine abnormality; increased AVP/ADH production or Syndrome of inappropriate antidiuretic hormone (SIADH). Leads to increased water reabsorption and expansion of plasma volume.
40
Treat dilution hyponatreia
ADH antagonists (Tolvaptan*), demeclocylcine
41
Treat dilution hyponatreia
ADH antagonists (Tolvaptan*), demeclocylcine
42
testosterone
synthesized in testis by leydig cells, converted by 5 alpha reductase to dihydrotestosterone. Orally ineffective
43
weak androgens secreted by adrenal gland
androstenedione, dehydroepiandrosterone
44
synthetic androgen
17 alpha methyl testosterone; oral or subing
45
testosterone preparations
testosterone propionate (ester, stanozolol (synthetic anabolic steroid derived from dihydrotestosterone with less androgenic and more anabolic activity)
46
actions of testosterone
```
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
therapeutic uses testosterone
- hypogonadism; secondary sex characteristics
- osteoporosis
- trauma to decrease protein loss and promote positive nitrogen balance
- post operative convalescence
- manage intractable anaemia
48
adverse effects testosterone
- 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
insulin sensitizers
enhance insulin action
- biguanide (metformin)
- thiazolidine diones (TZD) (ex pioglitazone, rosiglitazone)
50
insuiln secretagogues
- KATP blockers (sulfonylureas like glyburide and metglinides like repaglinide)
- GLP1 analogs: incretins, exanatide, liraglutide
- DPP4 inhibitor- sitagliptinm saxagliptin
51
insulin and its analogs
fast acting: lispro, aspart, glulisine
short acting: regular
intermediate: NPH
long: ; glargine, ; detemir
52
insulin and its analogs
fast acting: lispro, aspart, glulisine
short acting: regular
intermediate: NPH
long: ; glargine, ; detemir
53
acarbose
alpha glucosidase inhibitor
54
dapagliflozin
SGLT2 inh (renal sodium glucose co transporter 2 inhibitor)
55
WHO essential medicine status for diabetes
metformin, glyburide NPH insulin
56
insulin and its analogs
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
WHO essential medicine status for diabetes
metformin, glyburide NPH insulin
58
type 1 diabetes treatment
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
conventional insulin therapy
no longer used; bid short acting and inter acting insulin
60
hazards of insulin
- 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
inhaled insulin withdrawn because
high lung concentration activates IGF receptor and possible lung cancer incidence
62
sulfonyl urea role and mechanism
stimulate release of endogenous insulin; inhibit kATP channels to decrease glucagon. May also increase number of functional insulin receptors in peripheral tissues.
63
Sufonyl urea generations
1st- not used
2nd- glyburide, glipizide
3rd- glimepiride
2nd and 3rd are more potent, longer acting, better PK, decreased AE
64
sulfonyl urea role and mechanism
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
Sufonyl urea generations
1st- not used
2nd- glyburide, glipizide
3rd- glimepiride
2nd and 3rd are more potent, longer acting, better PK, decreased AE
66
AE sulfonylureas
hypoglycemia*
rash, allergic, nausea, vomit, cholestatic jaundice.
not helpful in advanced stages of type 2; must use at start
67
miglitinides
- 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
metformin (a biguanide)
- 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
adverse effects metformin
gi distress, **lactic acidosis (esp in patients with renal or liver disease-
70
metformin (a biguanide)
- 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
adverse effects metformin
gi distress, **lactic acidosis (esp in patients with renal or liver disease, or with predisposition to tissue anoxia)
72
metformin uses
- type 2 diabetes
- treat insulin resistance and polycystic ovarian syndrome, gestational diabetes
- **in hypoxic condition use may promote lactic acidosis
73
acarbose
alpha glucosidase inhibitor' slows carb absorption, reduce postprandial hyperglycemia, *no effect on fasting blood sugar
-AE flatulance, diarrhea, cramping
74
metformin uses
- type 2 diabetes
- treat insulin resistance and polycystic ovarian syndrome, gestational diabetes
- **in hypoxic condition use may promote lactic acidosis
75
thiazolidinediones (TZD)
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
thiazolidinediones (TZD)
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
