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Pharmocology - step > Endocrine > Flashcards

Endocrine Flashcards

1
Q

strategy for DMI

A

insulin and low carb diet

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2
Q

strategy for DMII

A

lifestyle modification, oral agents, non insulin injecatblse, insulin

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3
Q

stragey for GDM

A

dietary modifications, exercise, insulin replacement

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4
Q

what are the side effects of insulin tx

A

hypoglycemia

rare hypersensitivities

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5
Q

what MOA of insulin pelase

A

binds insulin receptor (y kinase)
liver - increase glucose sotred as glycogen
muscle - increase glycogen and protein sytne and K uptake
fat - increase TAG storage

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6
Q

what are the rapid acting insulins

A

aspart
glulisine
lispro

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7
Q

what are aspart, glulisine and lispor used for

A

DMI
DMII
GDM
POST PRANDIAL GLUCOSE CONTROL

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8
Q

what are the short acting insulins

A

regular insuline

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9
Q

what is regular insulin used for

A 
DM I
DM II
GDM
DKA iv
hyperkalemia and glucose
stress hyperglycemia
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10
Q

what are the intermediate acting insulins

A

NPH

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11
Q

what is NPH used for

A

DM I
DM II
GDM

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12
Q

what are the long acting insulins

A

detemir

glargine

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13
Q

what are detemir and glargine used for

A

DM I
DM II
GDM
BASAL GLUCOSE CONTROL

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14
Q

whats a biguanide

A

metformin

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15
Q

MOA of metformin

A

unknown
decrease gluconeogenesis
icnreass glycolysis
increase peripheral glucose uptake

*increase insulin sensitivity

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16
Q

use of metformin

A

DOC at DMII

bc weight loss

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17
Q

a/se metformin

A

bad for renal failure
lactic acidosis
gi upset

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18
Q

what drug can be used when there is no residual islet cell function

A

metformin

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19
Q

what drugs cause increased release of insulin

A

the sulfonylurea: chlorpropamide, tobutamide, glimepiride, glipizide, glyburide

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20
Q

what are the first gen sulfonylureas

A

chlorpropamide, tolbutamide

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21
Q

what are the second gen sulfonylureas

A

glimepiride, glipizide, glyburide

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22
Q

a/se of first gen sulfonyulreas

A

disulfiarm reaction

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23
Q

a/se of secnd gen sulfonylueras

A

hypoglycemia

renal insfuff espeically

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24
Q

list the glitazones/glitter zones/thiazolidinedoines

A

pioglitazone
rosiglitazone
pio and rosi glitterzone

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25
Q

MOA of glitazones

A

increased sensitivity

bind to PPAR gamma nuclear transcription regulator

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26
Q

what are two drugs famils that increase insulin sensitivity

A

metform

glitazones

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27
Q

what is function fo PPARY

A

genets activated by it regulated fatty acid sorage and glucose metabolism; activation results in increase insulin esnsitivyt and increase levels of adiponectin

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28
Q

how are glitazones used

A

as MONO THERAY or in combo for type Ii

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29
Q

a/se of glitazones

A 
weight gain
oedema
hepatoxicity
heart failure
increased risk of fractures
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30
Q

what two drugs can be used as monotherapy

A

glitazones and alpha glucosidase inhibitors

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31
Q

what are the GLP 1 analogs

A

exenatide

liraglutide

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32
Q

what is the moa of GLP1 analogs

A

increase insulin

decrease glucagon

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33
Q

what two drug families increase insulin and decreas glucagon

A

GLP1 and DDP4 inhibis

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34
Q

what is cxl use fo GLP1

A

DMII

35
Q

what are a/se of GLP1

A

nausea, vomiting

PANCREATITIS

36
Q

list the DDP4 inhibits

A

linagliptin
saXagliptin
sitagliptin
LINA-SAX’A-SITTIN

37
Q

what is the amylin analog

A

pramlintide

38
Q

what is the moa of pramlintide

A

amylin anaolog
decreases gastric emptying
decrease glucagon

39
Q

use fo pramlintide

A

DMI and DMII

40
Q

a/se of pramlintide

A

hypoglycemia

nausea diarrhoea

41
Q

what are a/se of DDp4 inhibis

A

milkd urinary or resp infections

42
Q

oral hypoglycemic that can be used in DM I

A

pramlinotide - amylin analogue

43
Q

what are the SGLT2 inhibits

A

CANAgliflozin

44
Q

function fo canagliflozin

A

block reabsorption of glucose in PCT

45
Q

a/se of canagliflozin

A

glucosuria
uti
vaginal candida infection

46
Q

use of canagliflozin

A

DM II

47
Q

what are the alpha-glucosidase inhibitors

A

acrabose miglitol

48
Q

what is the MOA of alpha glucosidase inhibitors

A

inhibit intestinal brush border alpha glucosidases - delayed carbohydrate hydrolys and glucose absrotpion - decrease post praindal hyperglycemia

49
Q

use of alpha glucosidase inhibitors

A

DMII mono or in combo

50
Q

what are a/se of alpha glucosidase inhibitors

A

gi disturbances

51
Q

what is the MOA of propylthiouracil

A

inhibits peroxidase and 5-deiodinase

52
Q

what is the MOA fo methimazole

A

inhibits peroxidase

53
Q

use of propylthiouracil

A

pregos

hyperthyroidisn

54
Q

use of methimazole

A

not in pregos - teratogen (aplastic cutis)

hyperhytoridism

55
Q

a/se of propylthiouracil

A

hepatoxic
agranulocytosis
aplastic anaemia
skin rash

56
Q

a/se of methimazole

A

agranulocytosis
aplastic anaemia
skin rash
teratogen - aplastis cutis

57
Q

what are levthyroxin and triiodothyronin used fro

A

hypothyroidis, of label weight lsoa nd myxedema

58
Q

toxo of levothyroxine and triiodothyronin

A

tachycardia
heat intolerance
tremors
arrhtymias

59
Q

conivaptan and tolvaptan

A

ADN antags
SAIDH
bloc ADH V2 receptors

60
Q

desmopression acetate

A

central DI

61
Q

Gh

A

turners and GH deficiency

62
Q

oxytocin

A

stimulates labour, uterine contractions
milk let down
controls uterine bleeding

63
Q

octreotide

A 
acromegaly
carcinoid syndrome
gastrinoma
glucagonoma
esophageal varices
64
Q

used to control beleding

A

oxytocin - uterine hemorrhage

octreotide - esophageal varices

65
Q

what is the MOA of demeclocycline

A

ADH antagonist

a tetracycline

66
Q

what is clinical use of demeclocycline

A

SIADH

67
Q

how to treat SIADH

A

conivaptain, tolvaptain, demeclocycline

68
Q

what are a/se of demeclocycline

A

photosensitivity
nephrogenic DI
abnormalities of bone and teeth

69
Q

MOA o glucocoricoids

A

metabolic, catabolic, anti inflamm, immunosupppresion by interaction with GRE, inhibit of PLA2, inhibit NfkB and other transcription factors

70
Q

uses of glucocorticoids

A

addisons disease/adrenal insufficiency
inflammation
immunosuppression asthma

71
Q

glucocorticoid with mineral and glucocorticoid actiosn pelase

A

fludrocortisone

72
Q

toxo of glucocorticoids

A 
cushing syndrome
adrenocrotcail atrophy
PUD
steroid diabetes
steroid psychosis
73
Q

PUD
steroid diabetes
steroid psychosis
what are the other a/se caused by deugs that do that?

A

cushign

adrenocortical atrophy

74
Q

what happens when you stop taking glucocorticoids abruptly

A

adrenal insufficeincy

75
Q

what is cinacalcet

A

sensitizses CA senscint receptors in parathyroid gland to circulating CA to decrease PTH

76
Q

what is cinacalcet used for

A

hypercalcenia due to primary or secndoary hyperaprthyrodism

77
Q

what is the toxo risk of cincalcet

A

hypocalcemia

78
Q

presentation of hypocalcemia

A

tetany
calcium deposits in basal ganglia
cataracts candida infectiosn

79
Q

calcium in basal ganglia
cataracts
candida infections
what do you suspect

A

tetany and hypocalcemia

80
Q

what is tesamonelin

A

GHRH antago

treat HIV associated lipodystrophy

81
Q

what is pegvisomant

A

GH receptor antag for acromegayl

82
Q

how to treat acromegaly

A

octreotide, pevisomant

83
Q

how to treat HIV associated lipodystrophy

A

tesamonelin - GHRH analogue

Pharmocology - step (16 decks)

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