Diabetic drugs is a very important topic for pg entrance.....so all about it has been discussed in detail as required for pg entrance....do make use of it...
3. Starch/Saccharides
In diet
Decreases gastric
emptying
Alpha glucosidase
Release of Insulin
Increases Ca entry
Depolarisation
ATP formed from
glucose inhibits
ATP-K+ channels
Stimulates GLUT-2 receptors
On Beta islet cells
Glucose enters
circulation
Releases Insulin
& amylin
Stimulates Pancreas
Increases release of
Incretin or GLP-1
Enters intestinal
epithelial cells
Glucose
Increases GLUT-4 on
surface of cells
Metabolised by DPP-4
Enzyme
-
Gliptins
-Acarbose
voglibose
+
Exenatide
Liraglutide -
Meglitinides
Sulfonylureas
Amylin analogue: Pramlinitide
4. -This drugs inhibits conversion of starch into glucose
accumulation of starch
S/E:Flatulence>Diarrhoea Prevents rise in glucose levels
During both prandial and post-
Prandial levels (But not pre-
Prandial)
Acarbose reduces fibrinogen levels but also several other markers
of inflammation are reduced.
9. Smooth and peakless effect is caused by : Glargine & Detemir
Insulin increases K+ and Glucose uptake by cells and thus leads
To Hypokalemia
10.
11. Glargine has a acidic pH. So not mixed with other insulins
Other all Insulins are Neutral Insulins.
12.
13.
14.
15.
16. 1st Generation 2nd Generation
Chlorpropamide Glybenclamide
Tolbutamide Gliclizide
Acetohexamide Glyburide
Causes Hepatotoxicity ( Mnemonic; T for tolbutamide and there are
3Ts in hepatotoxicity)
Causes SIADH and Disulfiram like reaction
18. -Insulin Secretagogues i.e they stimulate Insulin Release.
-Max. potency among sulfonylureas = Glyburide
-C.I. in = Liver disease
Renal Disease
Pregnancy/Lactation
-S/E: Hypoglycemia
Weight Gain
-Causes maximum decrease in HbA1C levels ( 2nd : Biguanides) and increases
C-peptide values
-Long acting(Max.; Chlorpropamide) and hence increases insulin for long time
whereas meglitinides are short acting.
19. -Short acting Insulin secretagogues.
-Hence used for Post-prandial Hyperglucemia
-Metabolised in liver and excreted in Kidney. Hence, dose to be reduced
in both liver and renal failure.
-Rapeglinide
-Nateglinide
27. Stimulates PPAR-@
Increase transcription factors for GLUT-4 Production
Increase GLUT-4 receptors on tissue cells
But still requires Insulin to bring glucose to cells so that glucose can be taken
up by cells.
- They decreases Insulin Resistance
-Metabolised in Liver
-Safe in Renal Failure
28.
29. 1) Weight gain
2) Sodium and water retention
3) Macular edema
4) Increase risk of bone fracture in childrens.
35. Group Main Side Effect
Alpha glucosidase
Inhibitor
Flatulence/Dyspepsia
SGLT-2 Inhibitors UTI & Vaginal infections
Gliptins Steven Johnson Sx
Thiazolidinediones Water retention/Macular
edema
Insulin Hypoglycemia/
Lipodystrophy
Chlorpropamide SIADH/Disulfiram like
reaction
Tolbutamide Hepatotoxicity
Metformin Vit. B12 deficiency
Phenformin Lactic acidosis
Meglitinides Hypoglycemia
36. 1)Q. A 45-year-old woman presents to your office with a serum glucose
of 250 mg/dL and you diagnose diabetes mellitus type II. You intend to
prescribe the patient metformin, but you decide to order laboratory
tests before proceeding. Which of the following basic metabolic panel
values would serve as a contraindication to the use of metformin?
A. K+ > 4.0
B. Na+ > 140
C. HCO3- > 30
D. Creatinine > 2.0
37. Metformin is absolutely contraindicated in patients with renal failure
due to the risk of lactic acidosis.
An elevated serum creatinine suggests a decrease in GFR and the presence
of renal failure.
Metformin is a drug in the biguanide class used to treat diabetes mellitus
type II.
Metformin treats hyperglycemia by inhibiting gluconeogenesis.
Metformin carries no risk of hypoglycemia, but is known to occasionally
cause lactic acidosis in patients with renal failure, liver dysfunction, CHF,
alcoholism, and sepsis.
D. Creatinine > 2.0
38. 2.Q.A 45-year-old African-American male presents to the family medicine
physician to assess the status of his diabetes. After reviewing the laboratory
tests, the physician decides to write the patient a prescription for miglitol and
states that it must be taken with the first bite of the meal.
Which of the following bonds will be most likely affected by taking miglitol?
1. Phosphodiester bonds
2. Glycosidic bonds
3. Peptide bonds
4. Cystine bonds
5. Hydrogen bonds
39. The bonds that will be most likely affected by taking miglitol are
glycosidic bonds.
Miglitol is an alpha-glucosidase inhibitor that prevents the breakdown
of disaccharides/polysaccharides into monomers by alpha-glucosidases
located along the intestinal brush border.
Miglitol prevents these bonds from being hydrolyzed.
This delays sugar hydrolysis, resulting in a delayed glucose absorption.
This is advantageous for patients with type II diabetes mellitus as it
decreases postprandial hyperglycemia, thereby reducing insulin demand.
Common side effects of these inhibitors are upset stomach, diarrhea, and
flatulence.
2. Glycosidic bonds
40. 3.Q. A 60-year-old African-American female presents to your office
complaining of dysuria, paresthesias, and blurry vision. Her body mass
index is 37.2 kg/m2. Which of the following drugs would most
significantly increase the levels of C-peptide in the blood when
administered to this patient?
1. Metformin
2. Insulin
3. Glipizide
4. Acarbose
41. Glipizide is a second generation sulfonylurea that triggers release of insulin
from pancreatic beta cells. Increased release of endogenous insulin results in
elevated levels of C-peptide in the blood.
This patient's presentation is consistent with type II diabetes mellitus.
Dysuria due to a urinary tract infection (the presence of glucosuria creates a
good growth media for bacteria with subsequent increased risk of UTI),
paresthesia due to diabetic neuropathy, blurry vision due to osmotic damage
of the lens of the eye, and obesity are all associated with diabetes.
Glipizide is used in the treatment of diabetes type II only.
3. Glipizide
42. 4.Q. A patient presents to the emergency room in an obtunded state.
The patient is a known nurse within the hospital system and has no
history of any medical problems. A finger stick blood glucose is drawn
showing a blood glucose of 25 mg/dL.
The patient's daughter immediately arrives at the hospital stating that her
mother has been depressed recently and that she found empty syringes
in the bathroom at the mother's home. Which of the following is the test
that will likely reveal the diagnosis?
A. C-peptide level
B. 24 hr cortisol
C. Fasting blood glucose
D. Urine metanephrines
43. This patient is presenting with severe hypoglycemia likely secondary to
exogenous administration of insulin.
C-peptide is the portion of pro-insulin that is cleaved away within the
pancreatic beta cell.
In normal physiology, c-peptide is present within the circulation in equimolar
concentrations with insulin.
With the exogenous use of insulin, additional c-peptide is not present within
the circulation.
This scenario of hypoglycemia often occurs in individuals failing to
administer insulin correctly or in healthcare workers wishing to harm
themselves.
An insulin producing tumor should also be on the differential diagnosis for
these patients.
A. C-peptide level
44. 5.Q. A simple experiment is performed to measure the breakdown of sucrose
into glucose and fructose by a gut enzyme that catalyzes this reaction.
A glucose meter is used to follow the breakdown of sucrose into glucose.
When no enzyme is added to the sucrose solution, the glucose meter will
have a reading of 0 mg/dL; but when the enzyme is added, the glucose
meter will start to show readings indicative of glucose being formed.
Which of the following diabetic pharmacological agents, when added
before the addition of the gut enzyme to the sucrose solution, will maintain
a reading of 0 mg/dL?
1. Insulin
2. Glyburide
3. Metformin
4. Acarbose
45. The gut enzyme that is added to the solution is most likely alpha-glucosidase.
The only agent that will inhibit the enzyme from breaking down sucrose
into glucose and fructose thus showing a 0 mg/dL reading on the glucose
meter is acarbose.
Acarbose and miglitol are alpha-glucosidase inhibitors that prevent the
breakdown of disaccharides and polysaccharides into monomers by
alpha-glucosidase located along the intestinal brush border.
This delays sugar hydrolysis resulting in a delayed glucose absorption.
This is advantageous for patients with type II diabetes mellitus as it
decreases postprandial hyperglycemia, thereby reducing insulin demand.
Common side effects of these inhibitors are upset stomach, diarrhea, and
flatulence.
4. Acarbose
46. 6.Q. A 55-year-old male is hospitalized for acute heart failure. The patient
has a 20-year history of alcoholism and was diagnosed with diabetes mellitus
type 2 (DM2) 5 years ago. Physical examination reveals ascites and engorged
paraumbilical veins as well as 3+ pitting edema around both ankles.
Liver function tests show elevations in gamma glutamyl transferase and
aspartate transaminase (AST). Of the following medication, which most likely
contributed to this patient's presentation?
1. Glargine
2. Glipizide
3. Metformin
4. Pioglitazone
5. Pramlintide
47. Weight gain, edema (fluid retention), hepatotoxicity, and heart failure are
toxicities associated with pioglitazone. The drug should not be
administered to patients with heart failure or liver disease.
Pioglitazone and rosiglitazone are thiazolidinedione derivatives that
reduce insulin resistance in patients with DM2. They are occasionally used
as monotherapy for DM2 but are most often combined with other
hypoglycemics. The drugs are also used to treat polycystic ovarian
syndrome.
4. Pioglitazone
48. 7.Q. A 53-year-old male presents to your office for a regularly scheduled
check-up. The patient was diagnosed with type II diabetes mellitus two years
ago. To date, diet, exercise, and metformin have failed to control his elevated
blood glucose. Past medical history is also significant for hypertension.
The patient does not smoke or use cigarettes. Laboratory values show a
hemoglobin A1c (HbA1c) of 8.5%. You decide to add sitagliptin to the
patient’s medication regimen. Which of the following is the mechanism of
action of sitagliptin?
1. Inhibits degradation of endogenous incretins
2. Inhibits alpha-glucosidases at the intestinal brush border
3. Activates transcription of PPARs to increase peripheral sensitivity to insulin
4. Depolarizes potassium channels in pancreatic beta cells
5. Increases secretion of insulin in response to oral glucose loads and delays
gastric emptying
49. Sitagliptin is a dipeptidyl peptidase 4 (DPP-4) inhibitor. This class of
drugs acts to inhibit degradation of the endogenous incretins GLP-1 and
GIP.
Incretins are a group of gastrointestinal hormones that increase the
amount of insulin released from the beta cells of the islets of Langerhans
after eating.
They begin to act before blood glucose levels become elevated.
Incretins also inhibit glucagon release from alpha cells of the islets of
Langerhans.
DPP-4 inhibitors block degradation of incretins and promote enhanced
insulin secretion.
1. Inhibits degradation of endogenous
incretins
