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ENDOCRINE > [PHARMA] ANTI-DIABETICS > Flashcards

[PHARMA] ANTI-DIABETICS Flashcards

1
Q

1st line therapy in T2DM

A

Metformin + lifestyle modifications

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2
Q

secretagogues

A

sulfonylureas
non-sulfonylureas

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3
Q

sensitizers

A

metformin
Tzds (Pioglitazone)

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4
Q

α-glucosidase inhibitor

A

acarbose

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5
Q

SGLT2 inhibitors

A

canagliflozin

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6
Q

DPP4 inhibitors

A

Sitagliptin

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7
Q

GLP1 agonists

A

Liraglutide

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8
Q

Sulfonylureas chronic use leads to

A

↓Glucagon

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9
Q

sulfonylureas mechanism of action

A

↑insulin secretion via
binds to β-cell receptors–> (-) ATP-sensitive K+channels=↓K+ efflux=depolarization=Ca++ influx via voltage gated channels= INSULIN RELEASE

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10
Q

sulfonylureas indications

A

T2DM
(if initial therapy fails/ metformin is CI)

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11
Q

sulfonylureas 1st generation disadvantage

A

↑PPB= ↑ adverse effects + drug interaction

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12
Q

sulfonylureas 2nd generation advantages

A

-↑receptor affinity= 150x more potent
-less adverse effects & interactions

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13
Q

sulfonylureas CI (5)

A

1-T1DM
2-DM w/ pregnancy & lactation
3-DM w/ stress
4-DM w/ renal or liver disease
5-past history of sulfa allergy

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14
Q

sulfonylureas CI in pregnancy & lactation because

A

cross placenta & excreted in milk—>hypoglycemia in fetus

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15
Q

sulfonylureas CI in T1DM because

A

needs functioning Beta-cells

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16
Q

sulfonylureas CI in DM w/ stress because (3)

A

-ineffective
-stress ↑ insulin requirements
-ketoacidosis liable to occur

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17
Q

sulfonylureas CI in liver & renal diseases

A

-metabolized by liver & excreted by kidney so
prolonged action—> ↑hypoglycemia risk

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18
Q

sulfonylureas adverse effects (3)

A

Hypoglycemia
Hypersensitivity (skin rash)
Heavy weight

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19
Q

hypoglycemia is increased w/ sulfonylurea use in cases of

A

-preparation w/ long t1/2
-impaired elimination (old age, renal/liver disease)

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20
Q

nonsulfonylureas mechanism of action

A

-↑ insulin secretion via:
binds to β-cell receptors= (-) ATP-sensitive K+ channels= ↓K+ efflux= depol=Ca++ influx=INSULIN RELEASE

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21
Q

nonsulfonylureas advantages (4)

A

1-rapid onset, short duration
2- ↓ early hyperglycemia
3- ↓ late hyperglycemia
4-used in patients w/ sulfa allergy

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22
Q

nonsulfonylureas disadvantages (3)

A

1-frequent dosing (3times/day)
2-mild hypoglycemia
3-weight gain

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23
Q

Nonsulfonylureas used cautiously in

A

liver impairement

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24
Q

DOC in patient w/ sulfa allergy

A

nonsulfonylurea secretagogues

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25
Q

peak effect of sulfonylureas

A

after 2-3 hours so give before main meal

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26
Q

euglycemics

A

sensitizers; metformin
Pioglitazone (Tzds)
acarbose

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27
Q

drugs causing weight gain

A

1-secretagogues; sulfonylureas & nonsulfonylureas
2- Tzds

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28
Q

drugs NOT causing weight gain

A

metformin

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29
Q

metformin mechanism of action

A

(-) Hepatic gluconeogenesis
(+) Glycolysis in SKM & adipose tissue=
↑uptake of blood glucose + ↑ lactic acid
↓intestinal absorption=mild anorectic effect

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30
Q

metformin advantages (3)

A

1-NO hypoglycemia
2-NO weight gain (so↓ insulin resistance)
3- NO drug interactions

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31
Q

metformin doesn’t lead to drug interactions due to

A

-NO PPB
-NO hepatic metabolism

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32
Q

metformin indications

A

T2DM w/ lifestyle modifications & diet

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33
Q

metformin adverse effects

A

1-GIT upset
2-Lactic acidosis

34
Q

GIT symptoms of metformin can be managed by

A

starting w/ low dose and gradually increasing it

35
Q

GIT symptoms of metformin (4)

A

1-metallic taste
2-anorexia
3-dyspepsia
4-diarrhea

36
Q

metformin CI in (3)

A

1-RF
2-Liver failure
3-HF, MI, pneumonia, alcoholics
⤷(severe hypoxia)

37
Q

Pioglitazone (Tzd) mechanism of action

A

-* (+) PPAR-γ receptors (msc,liver,fat)
(+) adipocytes synthesis & differentiation
-↑new insulin-sensitive fat cells
- ↑ FFA uptake
- (-) intracellular lipolysis= ↓FA mobilization to blood
- ↓ insulin resistance= ↑ glucose uptake
- (-) hepatic gluconeogenesis= ↓ blood glucose

38
Q

Tzd indications

A

-T2DM monotherapy (if met/sulfa are CI)
-combination

39
Q

Tzds adverse effects

A

1-fluid retention & edema
2-weight gain
3-fractures

40
Q

Tzds CI in

A

1-HF
2-Liver impairement

41
Q

Tzds must be monitored for

A

liver injury

42
Q

Acarbose mechanism of action

A

(-) α-glucosidase enzyme= ↓intestinal glucose absorption

43
Q

drugs altering gene regulation

44
Q

drug w/ insulin sparing effect

45
Q

acarbose advantages

A

1-limits postprandial glucose increase
2-NO hypoglycemia

46
Q

acarbose adverse effects

A

GIT= flatulence, abdominal pain, diarrhea
due to fermentation

47
Q

acarbose indications

A

T2DM, metformin intolerance:
adjuvant to sulfonylurea

48
Q

SGLT2 inhibitors mechanism of action

A

(-) SGLT2 in PCT
↓ glucose reabsorption
↑excretion
↓ HbA1c, weight, BP

49
Q

SGLT2 inhibitors indications

A

monotherapy/combined w/ metformin & Tzfd

50
Q

SGLT2i adverse effects (3)

A

1-genitourinary infections
2-mild hypoglycemia
3-fractures

51
Q

SGLT2i precaution

A

adequate renal function is necessary

52
Q

SGLT2 advantages

A

1-given orally once/day= compliance
2-useful in DKD

53
Q

DPP4i mechanism of action

A

(-) DPP4= ↑incretins
↑glucose-dependent insulin release
↓glucagon
↓ hyperglycemia

54
Q

DPP4i indications

A

T2DM: monotherapy/ combo w/ metformin or Tzds

55
Q

DPP4i adverse effects (3)

A

1-nasopharyngitis
2-URTI
3-joint pain

56
Q

GLP-1 agonists mechanism of action

A

↑ glucose-dependent insulin release
↑ β-cell responsiveness
↓ inappropiate postprandial glucagon
↓gastric emptying = ↓food intake

57
Q

GLP-1 agonists compared to natural GLP1

A

more stable than natural GLP1

58
Q

GLP1 agonists adverse effects

A

1-Nausea w/ high doses
2-pancreatitis
3-medullary thyroid carcinoma

59
Q

amylin analogues mechanism of action

A

↓ inappropriate postprandial glucagon
↓gastric emptying
improves satiety

60
Q

incretin mimetic

A

liraglutide

61
Q

GLP-1 route of admin? dose?

A

SC
once/day

62
Q

drug chosen in obesity

A

liraglutide

63
Q

drugs causing hypoglycemia

A

sulfa
nonsulfa
SGLT2
amylin analogues

64
Q

amylin analogue indication

A

T1DM & T2DM
Prior to meal
adjunct to insulin

65
Q

amylin analogues adverse effects

A

1-hypoglycema
2-NV
3-anorexia

66
Q

causes Na+ retention

A

insulin
Tzds

67
Q

neutral

A

metformin
Sitagliptin

68
Q

unfavorable CVS effects

A

sulfonylureas
Tzds (in HF)

69
Q

induces lactic acidosis in HF & RF

70
Q

beneficial in patients w/ DM & HF

71
Q

beneficial for patients w/ CVS events

A

GLP-1 agonists (Liraglutide )

72
Q

drugs causing bone fractures

73
Q

(+) glucose dependent insulin release

A

DPP4i
GLP-1 agonists

74
Q

drugs NOT causing hypoglycemia

A

metformin
acarbose

75
Q

DKA coma management

A

fluid replacement
Insulin
KCL
Bicarbonate
TTT of underlying cause

76
Q

most important step in management of DKA coma

A

fluid replacement

77
Q

DKA coma: fluid replacement

A

3-5L
-isotonic saline followed by half tonic solution (IF ↑Na+)
-5% glucose if glucose falls to 250mg/dl
(to prevent brain edema due to ↓plasma osmolality)

78
Q

DKA coma: insulin therapy

A

-regular insulin IV/ IM until blood acetone disappears
-↓ IV dose by half if glucose falls to 250mg/dl
-once patient is stable–> SC 4times/day

79
Q

DKA coma: K+ replacement

A

KCl according to K+ level
-20mmol if normokalemic
-40mmol if hypokalemic

80
Q

mild acidosis is corrected by

A

insulin spontaneously

81
Q

DKA coma: Bicarbonate

A

when pH <7.1
stop when pH= 7.2

82
Q

DKA coma: underlying cause

A

infections
give broad spectrum Ab

ENDOCRINE (9 decks)

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