Drugs Used in Diabetes Mellitus Flashcards

1
Q

what is Type 3 Diabetes Mellitus

A

Refers to multiple other specific causes of an elevated blood glucose.

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2
Q

what is Type 4 Diabetes Mellitus

A

Gestational diabetes (GDM)
- During pregnancy, the placenta and placental hormone create an insulin resistance at 3rd trimester

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3
Q

what is the treatment for Type 3 Diabetes Mellitus.

A

insulin

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4
Q

what is the treatment for Type 4 Diabetes Mellitus.

A

insulin

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5
Q

MOA of insulin

A

tyrosine kinase phosphorylation promotes entry
of glucose into the cell

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6
Q

The standard mode of insulin therapy is ________injection

A

subcutaneous (SC)

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7
Q

which drugs is categorized as rapid acting insulin

A

Lispro
Aspart
Glulisine

tallest curve

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8
Q

which drugs is categorized as short acting insulin

A

Regular (SC/IV)

subcutaneous (SC)injection.
IV: Intravenous; NPH: Neutral Protamine Hegedorn.

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9
Q

which drugs is categorized as intermediate acting insulin

A

NPH

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10
Q

which drugs is categorized as LONG acting insulin

A

Glargine
Detemir
Degludec

flatest curve

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11
Q

Afrezza is an ____ form of insulin

A

inhaled -Powdered human insulin
Insulin powder is aerosolized and delivered to the lungs .

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12
Q

what do you give to treat fruity breath odor of acetone

A

give insulin drip until acetone goes away

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13
Q

how do you treat DKA

A

IV insulin (regular)
IV fluids, Dextrose
Correct electrolytes, K+

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14
Q

symptoms of hypoglycemia (<70 mg/dL)

A

“TIREDD”
T- tachy
-i - irritability
r- restless
E- excessive hunger
d- depressed
d- diaphoresis

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15
Q

Insulin allergy is mediated via

A

anti insulin IgE-mediated
local cutaneous reactions, angioedema, urticaria

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16
Q

Immune insulin resistance is mediated via

A

IgG antibodies
neutralize the action of insulin

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17
Q

Neuroglycopenic symptoms: Difficulty in
concentrating, confusion, weakness, drowsiness, a feeling
of warmth, dizziness, blurred vision, and loss of
consciousness
is seen in what glucose levels

A

:(<40 mg/dL)

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18
Q

lipoatrophy is due to

A

Atrophy of
subcutaneous fat at the site of insulin injection

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19
Q

what is lipohypertrophy

A

lipohypertrophy (enlargement of subcutaneous fat
depots)

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20
Q

if glucose is low counter regulatory hormones kicks in to raise it . those are :

A

glucagon
growth hormone
cortisol
epnephrine

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21
Q

what is the MOA of glucagon

A

lucagon molecule bind to specific Gs protein-coupled
receptors on liver and heart → increase in cAMP → hyperglycemia & inotropic and chronotropic effect on the heart without requiring functioning beta-adrenergic receptors.

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22
Q

what are the adverse effects of glucagon

A

Nausea

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23
Q

what are the uses for glucagon

A

Severe hypoglycemia
- glucagon injection
Endocrine diagnosis
Beta adrenergic receptor blocker overdose
- Ability to increase cAMP production in the heart
Radiology of bowel
- Relaxes the intestine
- Used in radiology as an aid to X-ray visualization

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24
Q

what type of category are: sulfonylureas & Glitinides

A

Insulin secretagogues

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25
Q

what type of category are: Biguanides & Thiazolidinediones

A

insulin sensitizers

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26
Q

what type of category are: Acarbose & Miglitol

A

alpha- glucosidase inhibitors

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27
Q

what type of category are: Sitagliptin & saxagliptin

A

DPP-4 inhbitors

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28
Q

what type of category are: Exenatide & Liraglutide

A

GLP-1 analogs

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29
Q

what type of category are: Pramlintide

A

Amlyin analogs

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30
Q

what type of category are: Canagliflozin

A

SGLTT inhbitors

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31
Q

what type of category are: Canagliflozin

A

SGLTT inhbitors

32
Q

what are Sulfonylureas first generations?

A

FirsT-generation

Tolbutamide
Tolazamide
Chlorpropramide

33
Q

what are Sulfonylureas second generations?

A

second Generation

Glipizide
Glyburide
Glimepiride

34
Q

what are some use for Second Generation Sulfonylureas

A
  • To control hyperglycemia in type 2 DM patients who
    cannot achieve appropriate control with changes in
    diet alone
  • Most effective when pancreatic ß cells are functioning
  • Most appropriate in non-obese
35
Q

what are some Adverse effects of Sulfonylureas

A

Hypoglycemia
Severe hypoglycemia
 - Overdose
 - Most common with glyburide
Weight gain, Rashes, hypersensitivity

36
Q

how can you tell if someone is taking Glipizide

A
  • making more iinsulin
  • c-peptide is increased
  • antibodies are absent
37
Q

how do you test if someone is ingesting sulphonyurea

A

perform urine sulphonylurea

38
Q

MOA of Repaglinide, Nateglinide (D-phenylalanine)
(no sulfur)

A
  • Meglitinides

Binds to 2 common sites of SUR, one unique site of
meglitinides on beta cells of pancreas
– Closure of ATP-sensitive K+ channels
– Restoration of more normal insulin secretion
– Glucagon secretion & hepatic glucose production
 Rapid onset and short duration of action
 Taken just before meals

39
Q

what are some use for Repaglinide, Nateglinide (D-phenylalanine) (no sulfur)

A

Alone or with biguanides in type 2 diabetes & pts with S or SU allergy

40
Q

which drug is safe in renal insufficency

A

Nateglinide is safe in renal insufficiency & lower incidence of hypoglycemia

41
Q

MOA of metformin (biguanides)

A

**Inhibits hepatic glucose production **(through the activation of enzyme AMP-activated protein kinase (AMPK).
 Inhibits mitochondrial Glycerol-3-phosphate dehydrogenase
 Decreases renal gluconeogenisis
Direct stimulation of glycolysis in tissues,
 Converts glucose to lactate by enterocytes
 Increases removal of glucose form blood
** Increases the hepatic sensitivity **to insulin
 Reduction of plasma glucagon levels
 Slowing the glucose absorption from GIT
dec. Triglycerides

42
Q

what are some uses for metformin

A

Appropriate for obese Type 2 diabetics
Decreases Insulin resistance

43
Q

what are the side effects for metformin

A

-Anorexia, nausea, vomiting, diarrhoea
-Lactic acidosis ( inc. Blood lactate & anion gap, dec. pH, dec. HCO3)
(Anion gap= [Na+ ] – ([Cl- ] + [HCO3])
-Vitamin B 12 deficiency

44
Q

what are the contraindication in metformin

A

 Alcoholism
 Renal and hepatic disease
 Chronic cardiopulmonary dysfunction
 Radiographic contrast studies, seriously ill patients,
 Metabolic acidosis

45
Q

what are the contraindication in metformin

A

 Alcoholism
 Renal and hepatic disease
 Chronic cardiopulmonary dysfunction
 Radiographic contrast studies, seriously ill patients,
 Metabolic acidosis

46
Q

what is the MOA of Thiazolidinediones:
Pioglitazone & Rosiglitazone

A

 Pioglitazone activates PPAR-γ & PPAR-α → Upregulation of adiponectin & fatty acid uptake → Triglyceride lowering
activity (PPAR-α)

 Decreases hepatic gluconeogenesis

 Decreases insulin resistance [increases insulin sensitivity]

47
Q

what are the adverse effects of Thiazolidinediones

A
  • Fluid retention, edema, increased risk of heart
    failure.
  • Weight gain, loss of bone mineral density - atypical
    extremity bone fractures in women
  • Rosiglitazone carry more risk of Cardiovascular than Pio
  • Hepatotoxicity (Troglitazone discontinued to use by
    FDA
48
Q

what are the contraindications of Thiazolidinediones

A
  • Patients with a history of heart failure
  • Active liver disease (or elevated transaminase levels) -
    due to increased risk of hepatic injury
49
Q

what is the MOA for Acarbose, Miglitol

A
  • Inhibitor of α-glucosidase in the brush borders of
    small intestine & inhibits amylase
  • Delay carbohydrate digestion and absorption
  • Decreased demand for insulin
50
Q

what is the clinical uses for Acarbose, Miglitol

A

control postprandial hyperglycemia

51
Q

what is the adverse effects for Acarbose, Miglitol

A

GI discomfort, Flatulence, Diarrhea, &
hepatotoxicity

52
Q

what is the adverse effects for Pramlintide

A

hypoglycemia

53
Q

what is the MOA for Pramlintide

A

Suppresses glucagon release, delays gastric
emptying, and has central nervous system-mediated
anorectic effects

54
Q

what are the uses for Pramlintide

A

Modulates postprandial glucose levels →
Preprandial use in individuals with type 1 and type 2
diabetes.

55
Q

A synthetic analog of amylin given by injection is

A

pramlintide

56
Q

what is the MOA of EXENATIDE, Liraglutide

A

A synthetic analog of glucagon-like-polypeptide 1 (GLP-1)
 Adjunctive therapy with metformin or sulfonylureas
 Potentiation of glucose-mediated insulin secretion,
 Decreases glucagon release
 Slowed gastric emptying, increase satiety, loss of appetite
 Increased beta cell mass result from decreased beta cell
apoptosis

57
Q

what are the side effects of EXENATIDE, Liraglutide

A

 Nausea, hypoglycemia with sulfonylureas
 Necrotizing & hemorrhagic pancreatitis

58
Q

what is the MOA of SITAGLIPTIN, Saxagliptin

A

Inhibitor of dipeptidyl peptidase-4 (DPP-4)
 Inhibiting the inactivation of GLP-1
 Increase levels of GLP-1, GIP – increasing glucose
mediated insulin secretion and decreasing glucagon
levels

59
Q

what are the adverse effects of SITAGLIPTIN, Saxagliptin

A

Naso-pharyngitis, upper respiratory infections, head
aches, hypoglycemia, acute pancreatitis, joint pain.

60
Q

what are the MOA of Canagliflozin, Dapagliflozin, Empagliflozin

A

SGLT2- inhibitors-inhibits glucose reabsorption
in PCT → decrease blood glucose

61
Q

what are the side effects of Canagliflozin, Dapagliflozin, Empagliflozin

A

hypotension/dehydration, & genital mycotic
infections, hyperkalemia, weight loss

62
Q

what are the contraindications of Canagliflozin, Dapagliflozin, Empagliflozin

A

severe renal impairment

63
Q

what is the MOA of Colesevelam

A

decreased Farnesoid X receptor (FXR) activation
-FXR is a nuclear receptor with multiple effects
on cholesterol, glucose & bile acid metabolism.
-Decrease glucose absorption
dec. HbA1c by 0.5%, LDL by 15%

64
Q

what is the side effects of Colesevelam

A

Constipation, Indigestion & flatulance

65
Q

what is the C/I of Colesevelam

A

Hypertriglyceridemia, pacreatitis,
esophagial, gastric & duodenal disorders

66
Q

list the anti-obesity drug names

A

Orlistat, Lercaserin, Phenteramine/topiramate, Bupropionnaltrexone

67
Q

what is the MOA of Orlistat

A

Alters fat digestion by inhibiting pancreatic lipases.
 In hypertensive patients, orlistat improves blood pressure (likely
due to weight loss)

68
Q

what is the adverse effects of Orlistat

A

GI upset; cramps, flatus, fecal incontinence, oily spotting, and
flatus with discharge

Renal – Oxalate-induced acute kidney injury has also been
reported in orlistat users

69
Q

what is the contraindications of Orlistat

A

not be used during pregnancy or in patients with
chronic malabsorption, cholestasis, or a history of calcium oxalate
stones.

70
Q

what is the MOA of Phentermine, diethylpropion, benzphetamine, phendimetrazine

A

Stimulate the release of norepinephrine or inhibit its reuptake
into nerve terminals, and sympathomimetic drugs reduce food intake by causing early satiety.

71
Q

what is the adverse effects of Phentermine, diethylpropion, benzphetamine, phendimetrazine

A

All sympathomimetic drugs can increase heart rate
and blood pressure and cause insomnia, dry mouth, constipation, and nervousness.

72
Q

what is the MOA of Lorcaserin

A

is a selective agonist of the serotonin 2C receptor. It reduces appetite and thereby reduces body weight in men and women

73
Q

what is the adverse effects of Lorcaserin

A

Headache, upper respiratory infections,
nasopharyngitis, dizziness, and nausea

74
Q

what is the contraindications of Lorcaserin

A

should not be used in individuals with
CrCl <30 mL/min. It is contraindicated during pregnancy

75
Q

what are the drug interactions for Lorcaserin

A

lorcaserin should not be used with other serotonergic drugs *
(ex :SSRI’S, SNRI’S, bupropion, TCA’s, and monamine oxidase inhibitors), because of the theoretical potential for **
serotonin syndrome
*