ANTI-DIABETIC DRUGS Flashcards by Iseoluwa Ojo

Diabetes mellitus (DM) is defined as a ______geneous metabolic disorder characterized by (acute or chronic?) ______glycemia with relative disturbance of ————,________,________

heterogeneous

chronic

hyperglycemia

carbohydrate, fat and protein metabolism

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There are two major types of DM and a number of minor types
Major types
Type 1/ _______ Dependent DM
Type 2/ __________ Dependent DM

Minor types
•____________ DM
•_______ Onset Diabetes of the _______
•_____________ DM

Insulin

Non Insulin

Gestational DM

Maturity ; Young

Secondary DM

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PATHOPHYSIOLOGY

In a normal patient, Glucose metabolism is regulated by the hormone _________
And this is a polypeptide hormone made up of _____ amino acids

It is produced in the _________ Cells of the _________

It is secreted into circulation usually in response to _____ease in Glucose in the _________, usually (before or after?) a meal

INSULIN

51 amino acids

Beta Islet ; Pancreas

increase ; blood ; after

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Function of Insulin after release includes

Enables _________ by tissues in the body

___________ Glycogen synthesis

___________ Gluconeogenesis and Glycogenolysis

___________ Lipogenesis

___________ Lipolysis

___________ Protein ______bolism

Glucose uptake

Stimulates

Inhibits

Stimulates

Inhibits

Stimulates

Anabolism

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Hence absence or inactivity of Insulin would lead to

(Reduced or Increased ?) Uptake of Glucose by Tissues

(Reduced or Increased ?) Hepatic Glycogenosis and Gluconeogenesis

(Reduced or Increased ?) Lipolysis

(Reduced or Increased ?) Protein Catabolism

(Reduced or Increased ?) uptake of Glucose by tissues leads to accumulation of Glucose in the blood

Thus (ACUTE or CHRONIC?) HYPERGLYCEMIA

Reduced
Increased
Increased
Increased
Reduced

CHRONIC HYPERGLYCEMIA

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ETIOLOGY

Type I Insulin-dependent diabetes mellitus (IDDM)

There is ____________ in pancreatic _______;

____________ (type _____) antibodies that ___________ are detectable in blood.

_________ INSULIN DEFICIENCY from ______

β cell destruction ; islets

Autoimmune (type 1A)

destroy β cells

Absolute; start

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Type II Noninsulin-dependent diabetes mellitus (NIDDM)
Reduced ________ of ________ to ______ or ________

________ INSULIN DEFICIENCY at ______ stage

sensitivity ; peripheral tissues

insulin ; Insulin resistance

Relative ; later stage

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Classification of hypoglycemic agents

A and B

B can be divided into C and D

A can be divided into E, F , G

A parenteral
B oral
C sulfonylureas
D Biguanides
E short acting
F intermediate acting
G long acting

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INSULINS

Rapid
Insulin _______
Insulin _______
Insulin _______

Short acting
_______ Insulin

Intermediate acting
Neutral protamine Hagedorn/Insulin _______

Long acting
Insulin _______
Insulin _______

Rapid
Insulin Lipro
Insulin Aspart Insulin Glulisine

Short acting
Regular Insulin

Intermediate acting
Neutral protamine Hagedorn/Insulin isophane

Long acting
Insulin glargine
Insulin detemir

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INSULIN

SOURCE

Naturally
Extracted from ______

– Artificially
Produced by ___________ technology using special strains of ___________ or _________ that have been genetically altered to ______________________________

PIGS

recombinant DNA technology

Escherichia coli ; yeast

contain the gene for human insulin

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INSULIN

Binds to Insulin Receptor in the __________, __________ and __________

Insulin receptors are a type of __________ RECEPTOR

Activation of this receptor leads to the expression of unique glucose transporters on the membrane of the cells called __________

_______ expression causes an uptake of GLUCOSE from the blood

LIVER, SKELETAL MUSCLE and ADIPOSE TISSUE

TYROSINE KINASE RECEPTOR

GLUT; GLUT

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INSULIN: PHARMACOKINETICS

Administered _____________

Insulin preparations vary primarily based on
________ and _____________

Metabolized in the _____ and _______ by _____________ ENZYME/ _____________

SUBCUTANEOUSLY

Onset; Duration of action

Liver and Kidney

INSULIN-DEGRADING ENZYME/ INSULIN PROTEASE

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INSULIN: ADVERSE EFFECT

_____________
Weight _____
____________ at injection site
______kalemia
______/ _________ reaction
Edema
______ and _________ at Injection site

Hypoglycemia; gain

Lipodystrophy ; Hypokalemia

Allergic/ Hypersensitivity

Pain and Erythema

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NON-Insulins

Insulin Secretagogues
____________
____________

Insulin Sensitizer

____________
____________/____________

Glucosidase Inhibitors
____________
____________

Meglitinide
Sulfonylurea

Biguanides
Thiazolidinediones/Glitazone

Acarbose
Miglitol

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NON-Insulins

Insulin ________

Insulin _________

_________ Inhibitors

___________ Inhibitor

________ analogue

__________ ________

Secretagogues

Sensitizer

Glucosidase

Dipeptidyl Peptidase IV

Amylin

Incretin mimetic

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NON-INSULINS

Dipeptidyl Peptidase IV Inhibitor
___________

Amylin analogue
__________

Incretin mimetic
___________

Sitagliptin

Pramlintide

Exenatide

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Non-insulins: sulfonylureas

Examples

First Generation
___________
___________
___________

Second Generation
___________
___________
___________

Chlorpropamide
Tolbutamide
Acetohexamide

Glyburide
Glipizide
Glimepiride

Mechanism of action of SULFONYLUREAS

Insulin __________

Binds and Block ______________________________ of the pancreatic β cells

This causes _________ of the cell membrane

Leading to ___________

Eventually causing ____________

Extra-pancreatic effect: ↓ ______ ___________, ↑ peripheral ____ ___________

Insulin secretagogue

ATP- sensitive potassium channels

depolarization ; calcium influx

Insulin secretion

hepatic gluconeogenesis ; insulin sensitivity

Non-insulins : sulfonylureas

Adverse effect
________________
______ intolerance
Weight ______
______________ reaction
Granulocytopenic
_________ anemia

Hypoglycemia

Alcohol ; gain

Allergic skin

Hemolytic

NON-INSULINS: MEGLITINIDES

Examples
__________;________

Repaglinide
Nateglinide

NON-INSULINS: MEGLITINIDES

Mechanism of action

Insulin ___________
Binds and Block _______________of the pancreatic β cells
Causes _________ leading to ________________

Eventually causing Insulin _________

ATP-sensitive potassium channels

depolarization ;calcium influx

Insulin secretion

NON-INSULINS: MEGLITINIDES

Adverse effect
______________
Weight ______
________toxicity

Hypoglycemia

gain

Hepato

Non INSULINS: BIGUANIDES

Example

____________

Metformin

Non INSULINS: BIGUANIDES

Mechanism of action
Reduction in insulin __________ via modification of ______________________

–Inhibits _______________________(mGPD)

•Increases peripheral insulin _________ → ↑ peripheral _________ and glycolysis

Insulin resistance

glucose metabolic pathways

mitochondrial glycerophosphate dehydrogenase

insulin sensitivity

glucose uptake

NON-INSULINS: BIGUANIDES Adverse effect _________ ________ ________/ _______ taste in the mouth ____________ deficiency Weight ______

Lactic Acidosis Dysgeusia/ Metallic taste in the mouth Vitamin B12 deficiency Weight loss

NON-INSULINS: THIAZOLIDINEDIONES Examples List 3

Pioglitazone Troglitazone Rosiglitazone

NON-INSULINS: THIAZOLIDINEDIONES Mechanism of action Bind and activates of the _________ factor ______ (_______________________________ of _______ type in the nucleus) Lead to Increased glucose _________ and _____________ production

transcription PPARγ peroxisome proliferator-activated receptor gamma utilization hepatic glucose production

NON-INSULINS: THIAZOLIDINEDIONES Adverse effect Weight _____ Increase risk of _________ Increased risk of _________ Edema

gain; Heart failure Bone fracture

Non-INSULINS: INCRETIN MIMETICS Examples List 4

Exenatide Liraglutide Albiglutide Dulaglutide

Non-INSULINS: INCRETIN MIMETICS Mechanism of action Binds to ___________________ (______) receptor Lead to increase Insulin _______ and decrease ________ secretion

Glucagon Like Peptide-1 (GLP1) Insulin secretion Glucagon secretion

Non-INSULINS: INCRETIN MIMETICS Adverse effect Nausea Vomiting (Early or Late?) Satiety ___________ Weight ____

Early Pancreatitis Loss

Non insulins : DIPEPTIDYL PEPTIDASE INHIBITOR Examples List 3

Sitagliptin Saxagliptin Linagliptin

Non insulins : DIPEPTIDYL PEPTIDASE INHIBITOR Mechanism of action Binds and Inhibits the _____ enzymes that breaks down ______ or _______ Hence leads to ______________________ This leads to increase insulin _________ and decrease ________ secretion

DPP-4 enzymes GLP-1 or Incretin accumulation of Incretin insulin secretion glucagon secretion

DIPEPTIDYL PEPTIDASE INHIBITOR Adverse effect ___________ upset Arthralgia _____ satiety Risk of _______ infection Risk of _______itis Risk of _________ infection Risk of _______ failure Headache Dizziness

Gastrointestinal upset Early satiety Urinary infection Pancreatitis Respiratory infection Renal failure

Non-Insulins: GLUCOSIDASE INHIBITOR Example ____________ _______________

Acarbose Miglitol

Non-Insulins: GLUCOSIDASE INHIBITOR Mechanism of action Binds and inhibit _______________ (a brush border enzyme expressed by _________________ cells This causes delayed and decrease intestinal glucose _________ Hence reduces _________ after ________

alpha-glucosidase intestinal epithelial cells intestinal glucose absorption hyperglycemia food ingestion

NON-insulins: GLUCOSIDASE INHIBITOR Adverse effect __________ _________ Abdominal _________ Diarrhea

Flatulence Bloating Abdominal discomfort

Non-insulins: AMYLIN ANALGOUE Examples _______________

Pramlintide

Non-insulins: AMYLIN ANALGOUE Mechanism of action Acting as an _______________ ________ is a peptide hormone that is co-secreted with insulin Hence pramlintide delays __________, decreases ________________ secretion, and improves ________.

amylinomimetic Amylin gastric emptying postprandial glucagon satiety

AMYLIN ANALGOUE Adverse effect Nausea Anorexia Vomiting.

Lol

Miscellaneous: GESTATIONAL DIABETES __________ _____________ ____________

Insulin Glyburide Metformin