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Pharma Flashcards

1
Q

signs of DM

A

1- Glycogenolysis, Gluconeogenesis &V Uptake of glucose by tissues - Hyperglycemia - Glucosuria = Polyuria - Polydipsia.
2- Polyphagia BUT loss of weight.
3- Lipolysis &decrease Lipogenesis = Hyperlipidemia = Ketonemia (Ketosis) Ketonuria.
4- Increased protein Catabolism - Azotemia - Azoturia
5- Weakness, Vv Immunity & Recurrent infections.

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2
Q

Insulin Secretagogues:

A

1-Sulphonylureas 2-Meglitinides (glinides

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3
Q

Insulin Sensitizers:

A

1-Biguanides (metformin)
2-thiazolindinediones (Glitazones)

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4
Q

Inhibitors of Glucose Absorption:

A

Alpha-glucosidase inhibitor
1-Acarbose 2-Miglitol

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5
Q

Newer Anti-diabetic drugs:

A

a- Glucagon Like Peptide-1 (GLP-1) receptor agonist: Exenatide.
b- Di-Peptidyl Peptidase IV (DPP-IV) inhibitor: Sitagliptin.
c- Amylin analogue: Pramlintide
d- Sodium-glucose co-transporter 2 (SGLT2) inhibitors

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6
Q

Mechanism of Action:

Mechanism of Actions of insulin

A

1- Insulin binds to the a subunit of tyrosine kinase receptors, — Activation of tyrosine kinase activity of B subunit — Phosphorylation of intracellular proteins — Change in enzyme activity, gene expression and translocation of Glut-4 transporter — Glucose
uptake by adipose tissue & Sk.m.
2-The insulin/receptor complex is then rapidly internalized into the cell - Metabolism of insulin and recycling of the receptor.

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7
Q

Insulin Administration Routes

A
  • Subcutaneous: All insulin preparations
  • Intravenous: Only regular soluble insulin
  • Inhaled aerosol insulin preparation (to eliminate the need for injections)
  • Intranasal insulin: some studies suggest benefit in Alzheimer’s diseas
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8
Q

Rapid Acting (ultrashort acting) insulin

A

Insulin Aspart
Insulin Lispro

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9
Q

Short Acting insulin

A

regular insulin (soluble insulin)

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10
Q

insulin can taken intravenous

A

Regular

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11
Q

Intermediate Acting insulin

A

Isophane insulin (NPH)

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12
Q

Long Acting (basal insulin )

A

Insulin Glargine
Insulin Detemir

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13
Q

insulin has no peak

A

Glargine

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14
Q

indication of insulin

A

1- Type-1 diabetics, all cases of Insulin Dependent Diabetes Mellitus (IDDM):
2- Type 2 (NIDDM)
a- Temporary in N.I.D.D. during STRESS periods e.g. Infection, Operation & Pregnancy.
b- Permanently in N.I.D.D. with
-Failed Diet regulation + Exercise + Oral hypoglycemics.
Renal impairment.
3- Emergency treatment of Diabetic Ketoacidosis& Non-ketotic Hyperosmolar Diabetic coma.
B) Other Indications: Hyperkalemia due to renal failure.

type 2 temporary permanent emergency

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15
Q

receptor of insulin

A

tyrosine kinase

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16
Q

adverse effects on insulin

A

1- Hypoglycemia: (the most common and most important)
2. Hypersensitivity reactions:
3. Hypocalemia
4. subcutaneous lipodystrophy avoided by changing injection site
5. secondary infection due injection
6. Somogyi Effect: rebound mourning hyperglycemia
7. weight gain
8. insulin resistance

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17
Q

causes of hypoglycemia result of insulin

A

1- Too much or bad timing of insulin — True Hyper-insulinism.
2- Too little food intake or missing meal.
3- Too much muscular exercise.

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18
Q

manifestation of hypoglycemia

A

1- Sympathetic — Sweating, pallor, tachycardia & tremors.
2- Neuro-glyco-penia — Hunger, headache, irritability, weakness, blurring of vision, confusion, convulsions & coma. If prolonged Permanent brain damage & Death.
3- Laboratory — Low blood sugar & Urine is —ve for glucose.

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19
Q

treatment of hypoglycemia caused by insulin

A

a- If patient is conscious— Oral glucose or sweets.
b- If patient in Coma = Unconscious—
i) IV. Glucose Lifesaving. Then flush the vein with saline to avoid thrombosis & sclerosis.
ii) Glucagon S.C.
iii) Adrenaline 1 mg S.C.

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20
Q

why to flush the vein after iv glucose injection

A

to avoid thrombosis & sclerosis.

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21
Q

first generation of sulfonylurea

A

short acting: tolbutamide
intermediate acting: acetohexamide
long acting: chlorpropamide

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21
Q

what is somogyi effect and its causes

A

Rebound morning hyperglycemia (due to excess release of counterregulating hormones) that follows insulin-induced hypoglycemia during night. Avoided by
reducing the evening dose of insulin.

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22
Q

Second Generation of sulfonylurea

A

Gliclazide
Glipizide
Glibenclamide
Glimepiride

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23
Q

administration of sulfonylurea

A

Absorbed orally

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24
Q

fate of sulfonylurea

A

hepatic and renal

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25
Q

mechanism of action of sulfonylurea

A

1- Increase the insulin release from the pancreas:
a- It is the main action of sulfonylureas, so their action depends on presence of preformed endogenous insulin (about 30% functioning B-cells)
b- They Block ATP-sensitive K-channel (Karp-Channels) of B-Cells of Pancreas — Depolarization — Influx of Ca?— Excocytosis — /’ Release of Insulin.
2- Other actions (Extra-pancreatic): sulfonylureas may reduce hepatic glucose production and increase peripheral insulin sensitivity.

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26
Q

sulphonylurea treat Hypothalamo-pituitary Diabetes insipidus.

A

Chlorpropamide

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27
Q

indications of sulphonylurea

A

1- Type-2 Diabetes (NIDD) after failure of Diet regulation & exercise.
2- Chlorpropamide potentiates anti-diuretic hormone (ADH) effect on Nephron - Treat Hypothalamo-pituitary Diabetes insipidus.

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28
Q

Contraindications of sulfonylureas

A

1- Type-1 Insulin Dependent Diabetes (1.D.D.).
2-N.1.D.D. during stress periods e.g. Infection, operation & trauma.
3- Pregnancy & Lactation: Sulphonylureas pass placental barrier — Teratogenic & hypoglycemia of neonate.
4- History of diabetic ketoacidosis (type 1 diabetic is converted into type 2).
5- Severe hepatic or renal diseases.

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29
Q

sulphonylurea most likely accumulate during renal dysfunction and cause hypoglycemia

A

glyburide (glibenclamide)

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30
Q

sulfonylurea preferred in renal and hepatic diseases

A

Glipizide and glimepiride

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31
Q

common adverse effects of sulphonylurea

A

a- Hypoglycemia
b- Weight gain
c- Failure: - Primary failure in 10 - 15 % of N.I.D.D.
- Secondary failure after long use (years) due to exhaustion -Cells.

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32
Q

uncommon adverse effects of sulfonylurea

A

a- Cholestatic jaundice
b- Hematological: agranulocytosis, aplastic and hemolytic anemias:

33
Q

Non-specific Adverse Effects of sulphonylurea

A

Generalized and dermatological Hypersensitivity & cross-allergy

34
Q

effect of taking Aspirin, Phenylbutazone & sulfa with sulphonylurea

A

Displace sulfonylureas —» Hypoglycemia.

35
Q

effect of taking oral anticoagulants with sulfonylurea

A

Sulfonylureas displace Oral anticoagulants —» bleeding.

36
Q

effect of taking Phenobarbitone, Phenytoin & Rifampicin with sulphonylurea

A

induce HME&raquo_space; increase Metabolism of Sulfonylureas.

36
Q

mask sympathetic manifestation of hypoglycemia caused by sulphonylurea

A

b blockers as propranolol

36
Q

effect of taking dicoumarol with sulphonylurea

A

decrease excretion of chloropropamide

36
Q

drug interactions of sulphonylurea

A

1- Aspirin, Phenylbutazone & sulfa — Displace sulfonylureas — Hypoglycemia.
2- Sulfonylureas — Displace Oral anticoagulants — bleeding.
Dicoumarol —{ Excretion of Chlorpropamide.
3- Phenobarbitone, Phenytoin & Rifampicin —1 HME —T Metabolism of Sulfonylureas.
4- MAO-I, Allopurinol, Cimetidine & Chioramphenicol —»{ Metabolism of Sulfonylureas.
5- B-Blockers e.g. Propranolol:
a- Augment their hypoglycemia &) compensatory hepatic glycogenolysis.
b- Mask sympathetic manifestation of hypoglycemia — Silent coma.
6- Alcohol— hypoglycemia.
7- Thiazides, Corticosteroids & Contraceptives decrease the action of sulfonylureas.

37
Q

what drug?

They Block ATP-sensitive K-channel (Karp-Channels) of B-Cells of Pancreas — Depolarization — Influx of Ca?— Excocytosis — /’ Release of Insulin.

A

sulphonylurea

37
Q

effect of taking MAO-I, Allopurinol, Cimetidine & Chioramphenicol with sulphonylurea

A

decrease metabolism of Sulfonylureas.

38
Q

the meglitinidaeses

A

repaglinide, mitglinide, nateglinide

39
Q

route of administration of metformin

A

orally

40
Q

fate of metformin

A

renal excretion as the active drug without hepatic mechanism

41
Q

mechanism of action of metformin

A
  1. reduce hepatic glucose production by activating the enzyme AMP dependent protein kinase (AMPK)&raquo_space;> stimulation of hepatic fatty acid oxidation, glucode uptake, and nonoxidative glucose metabolism and reduction of lipogenesis and gluconeogenesis
  2. other effect
    a- increases insulin sensitivity in muscle, improving peripheral glucose uptake and utilization
    b- delays intestinal glucose absorption
    c- increases anaerobic glycolysis in peripheral tissues
    d- antagonises the effect of glucagon
42
Q

DM drug that increases lactic acid production

A

metformin

43
Q

DM drug that antgonizes the effects of glucagon

A

metformin

44
Q

DM drug delays the intestinal glucose absorption

A

metformin

45
Q

DM drug that activates the enzyme AMP dependent protein kinase

A

metformin

46
Q

therapeutic uses of metformin

A

type 2 (Non insulin dependent diabetes) particulary in overweight

47
Q

Adverse Effects of Biguanides (metformin)

A

1- GIT: Anorexia, nausea, vomiting, abdominal discomfort, and diarrhea:
2- long use of metformin decrease absorption of vit B12
3- Rarely fatal Lactic Acidosis

48
Q

DM drug causes fatal lactic acidosis

A

metformin

49
Q

contraindication of metformin

A

a- Hepato-cellular failure & Chronic alcoholism&raquo_space; Cannot metabolize lactic acid.
b- Renal insufficiency&raquo_space; Cannot excrete lactic acid.
c- Hypoxic states e.g. Cardiac & pulmonary diseases ( increase lactic acid production)

50
Q

the thiazolidinediones (glitazones)

A

Rosiglitazone
pioglitazone

51
Q

fate of Thiazolidinediones

A

hepatic metabolism

52
Q

mechanism of action of glitazones

A

-glitazones decrease insulin resistance. they bind to specific nuclear receptor (PPAR-gamma) that responsible for expresseion of genes involved in synthesis of cellular molecules important for lipid and glucose metablism as lipoprotein lipase enzyme and GLUT-4
-Increase insulin-mediated glucose uptake by adipose tissue and muscles
-Reduce hepatic glucose production and increase hepatic glucose uptake
-Reduces plasma levels of fatty acids by increasing clearance and reducing lipolysis.

52
Q

receptor of thiazolidinediones

A

PPAR gamma

53
Q

therapeutic uses of glitazones

A

Type 2 DM (NIDD)

54
Q

adverse effects of glitazones

A
  1. weight gain and edema
  2. heart failure after long use
  3. osteoporosis and fracture
  4. hepatotoxicity
  5. teratogenic
54
Q

how to avoid hepatotoxicity caused by glitazones

A

Liver enzyme levels should be measured jnitially, then every 2
months for a year, and periodically thereafter

55
Q

The Alpha-Glucosidase Inhibitors

A

Acarbose and miglitol

55
Q

MoA of acarbose and miglitol

A

Inhibit o-Glucosidase on brush border of intestinal mucosa — Absorption of complex Carbohydrates>\ Postprandial hyperglycemia.

56
Q

use of acarbose

A

Type-2 N.I.D.D.

57
Q

Adverse Effects of acarbose and miglitol

A
  • Flatulence, diarrhea & abdominal cramping.
    » Hypoglycemia with sulfonylurea
    + Decrease the bioavailability of metformin so concurrent use should be AVOIDED
58
Q

how to treat hypoglycemia caused by acarbose

A

Give oral glucose (not sucrose) in hypoglycemia, as they impair
digestion and absorption of sucrose

58
Q

what are Glucagon-like peptide-1 (GLP-1) analogs

A

Exenatide (Byetta)
Liraglutide
Albiglutide

59
Q

MoA of Glucagon-like peptide-1 (GLP-1) analogs

A

Bind to GLP-1 receptors — reduce postprandial glucose elevation and glucagon levels, delay gastric emptying, © insulin release & and suppress appetite

60
Q

what are the incretin mimetics & enhancers

A

Glucagon-like peptide-1 (GLP-1) analogs
Di-Peptidyl Peptidase-4 inhibitors

61
Q

route of administration of

A
62
Q

adverse effect of sexagliptin

A

increase risk of heart failure

63
Q

what is the amylin analog

A

Pramlintide

63
Q

the Di-Peptidyl Peptidase-4 inhibitors

A

a- Sitagliptin
b- Vildagliptin
c- Saxagliptin
d- Alogliptin

64
Q

actions of pramlintide

A
  • Reduces glucagon secretion
  • Delays gastric emptying (mediated by vagus)
  • Decreases appetite
  • Reduces postprandial glucose elevation
65
Q

adverse effects of Di-Peptidyl Peptidase-4 inhibitors

A

pancreatitis
sexaglibtin increase risk of heart failure

65
Q

MoA of Di-Peptidyl Peptidase 4 inhibitors

A

Inhibit Di-Peptidyl Peptidase 4 (DPP-4) enzyme (DPP-4 is an enzyme that breaks down incretin hormones e.g. GLP-1) leading to prolongation of the action of endogenously released GLP-1 and GIP

66
Q

MoA of SGLT 2

A

result in glucose excretion of only 30— 50% of the amount filtered causing glycosuria and lowers glucose levels

67
Q

clinical indications of SGLT2 inhibitors

A

-Used as 3” line therapy for type 2 DM
- Recently, gliflozins are used in the treatment of heart failure as it improves cardiac contractility

68
Q

The most common adverse effects with SGLT2 inhibitors:

A
  1. Genital & urinary tract infections
  2. Hypotension has also occurred, particularly in the elderly or patients on diuretics.
  3. Decrease mineral bone density-> risk of fractures
  4. Low incidence of hypoglycemia
69
Q

what are SODIUM GLUCOSE COTRANSPORTER 2 (SGLT2) INHIBITORS

A

Canagliflozin
Dapagliflozin
Empagliflozin

Pharma (7 decks)

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