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pharm > 12. Antidiabetics > Flashcards

12. Antidiabetics Flashcards

1
Q

Criteria for OAD

A

-does not replace the regimen (diet)
-age, weight, blood insulin level
-glycemia - fasting and postprandial
-comorbidities , metabolic syndrome

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2
Q

OAD -general principles

A
  • their ability is bound to the ability of insulin secretion
  • most OADs are contraindicated in pregnancy (METFORMIN may be used )
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3
Q

indications for OADs

A

T2 DM if not properly compensated with diet
T1DM with high insulin resistance -> when insulin does not lead to a decrease in blood glucose

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4
Q

what are the groups of OADS

A

-biguanides
-sulfonylurea derivatives
-thiazolidindiones
-alpha glucosidase inhibitors
-meglitinides
-Inhibitors of DP IV
-SGLT2 inhibitors
–GLP 1 analogues- insulin alternative that is an injectable antidiabetic

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5
Q

biguanides moa

A

increase sensitivity of peripheral tissues to insulin
* increase insulin binding to its receptor
* reduce hepatic gluconeogenesis
* decrease glucose absorption from GIT

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6
Q

biguanides and insulin?

A

-does not affect insulin secretion , b- cell function->NO HYPOGLYCEMIA

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7
Q

what are other benefits of biguanides

A

-stimulates glycolysis in the periphery
-reduces hep gluconeogenesis
-delays glc absorption from GIT
-decreases plasma glucagon levels
-increases proportion of HDL chol
not metabolised -> low protein binding
excreted non metabolised in kidneys

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8
Q

what are the side effects of biguanides

A

lactic acidosis
nausea
GIT problems about 20% have diarrhoea
reduced vit b12 absorption
weight loss
disulfuram effect

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9
Q

Metformin contraindications

A

-kidney disease
-alcoholism, liver disease (higher risk of lactic acidosis )

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10
Q

Indications of metformin

A

-type 2 DM drug of choice -esp in obese patients
-non obese in combos (with insulin , glitazones, SU , incretins )

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11
Q

what are the off label indications for metformin

A

PCOS
anticancer effect

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12
Q

SU derivatives -moa

A

pancreatic - release of insulin from beta cells
extrapancreatic -
potentiation of endogenous I effect on the target tissue
- reduction of hepatal glucose production
- reduction of hepatal Insulin degradation
- reduction of serum glucagon levels

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13
Q

what are the SU derivatives

A

-glibenclamide
-gliclazide

both 2nd generation

3rd gen-glimepride

-these drugs are 2nd line treatment

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14
Q

adverse effects of su derivatives

A

-HYPOGLYCEMIA
increased appetite
metal taste in mouth
*headaches, nausea (5 %)
* fluids retention
* allergy, fotosensitivity

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15
Q

what are the CI of SU derivatives

A

DM Type 1 monotherapy
, hypoglycemia,
ketoacidosis, kidney or liver
failure
pregnancy, hypersensitivity

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16
Q

Thiazolidinones moA

A

increase the sensitivity of periphery to insulin

  • ligands of PPAR gamma (part of the steroid and thyroid superfamily
    of nuclar receptors) modulate the expression of the genes
    involved in the metabolism of lipids and glucose
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17
Q

what are the thiazolidinones

A

PIOGLITAZON

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18
Q

effects of thiazolidindiones

A
  • Lowering blood glucose by the primary effect on insulin resistance
  • in diabetic and pre-diabetic patients
  • NO HYPOGLYCAEMIA
  • Increases glycogen synthesis and glycolysis in muscles
  • Stimulating glucose oxidation and lipogenesis in adipose tissue and
    reducing gluconeogenesis in the liver … optimal metabolic effects
19
Q

therapeutic use of thiazolidindiones

A

Sensitizers of insulin receptors
The onset of effect in 4 weeks

20
Q

what are the side effects of thiazolidindiones ?

A

Hepatotoxicity
Fluid retention
Increase TAG

21
Q

what are the CI of thiazolidindiones ?

A

hypersenisitivity
predisposition of heart failure
liver damage
pregnancy
lactation

22
Q

what are the inhibitors of intestinal glucosidase ?

A

Acarbose

23
Q

what is the moa of intestinal glucosidase inhibitors

A

-reduce sacharide absorption from GIT
-competitively inhibits a glucosidase -> inhibiting the cleavage of polysaccharide from the meal

24
Q

what is the effect of intestinal glucosidase inhibitors

A
  • decrease postprandial glycemia
  • do not affect monosacharides absorption
  • acarbosis do not rech the systemic blood, miglitol does
    *
    „educative drugs“- consequences in bad compliance
25
Q

in hypogycemia and treatment with other oads - what should be given

A

monosaccharide -glucose or fructose

26
Q

what are the meglitinides

A

repaglinide

27
Q

moa of meglitinides

A

-similar to SU-derivatives:
-block ATP- sensitive K+ channel in membrane of beta-cells, depolarisation of membrane, activation of voltage-gated Ca2+ channel, influx Ca2+, insulin release through different receptor at K + channel

28
Q

pk of meglitinides

A

-good bioavailability
-extensive protein binding
-metabolised into inactive compounds
-excreted in feces

29
Q

clinical use of meglitinides (repaglinide)

A

-combined with metformin
-given as an alternative to SU derivatives when pt has a renal impairment
-take it before meals- because they have a rapid onset and fading effect
-skipping a meal -> skipping a dose -> risk of hypoglycemia if you do take it

30
Q

what is the CI of meglitinides (repaglinide)

A

-hypersensitivity
-DM 1 type
-diabetic ketoacidosis
-pregnancy
-lactation

31
Q

what are the AE of meglitinides (repaglinide)

A

hypoglycemia
nausea
diarrhoea
joint pain

32
Q

what are the SGLT2 -sodium glucose cotransporter inhibitors

A

empagliflozin
gliflozins ( dapagliflozin, canag;iflozin)
glycosurics

33
Q

moa of empagiflozin (sglt2 inhibitors)

A
  • Inhibition SGLT2 = controlled glucosuria
  • cardioprotective, renoprotective
34
Q

AE of sglt2 inhibitors

A

-thirst
genital infections
UTIs
lower limb amputations
HYPOGLYCEMIA IF GIVEN WITH INSULIN

35
Q

CI of SGLT2 inhibitors

A

-kidney pathologies
>75 year olds
loop diuretics

36
Q

what are the DPP4 inhibitors

A

LINAGLIPTIN

gliptins

37
Q

moa of DPP4 inhibitors

A

inhibit dipeptidyl peptidase 4 which is responsible for GLP-1 breakdown-> increased GLP-1
-usually no hypoglycemia -> stops progression of illness-> better glycemia control than conventional drugs

38
Q

advantages of DPP4 inhibitors

A

-no hypoglycemia
-stops progression of illness
-better glycemia control

39
Q

AE of DPP4 inhibitors

A

pancreatitis
hypoglycemia with insulin
possible increased risk of thyroid cancer

40
Q

what is an injectable antidiabetic that is not INSULIN

A

glucagon like peptide 1 and analogues

s.c. admin

41
Q

glp analogues

A

EXENATIDE

(incretin mimetics- exenatide,lixisenatid , liraglutide, semaglutide)

42
Q

moa of glp 1 analogues

A

stimulate GLP-1-> promotes insulin secretion-> inhibits glucagon secretion-> prolongs stomach emptying

-dependent on glycemia-> no effecr if PG is low/normal-> NO HYPOGLYCAEMIA

43
Q

AE of glp 1 analogues

A

nausea and diarrhoea
pancreatitis
chronic admin leads to rapid decrease of body weight

pharm (6 decks)

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