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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
fate of sulfonylurea
hepatic and renal
25
mechanism of action of sulfonylurea
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.
26
sulphonylurea treat Hypothalamo-pituitary Diabetes insipidus.
Chlorpropamide
27
indications of sulphonylurea
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.
28
Contraindications of sulfonylureas
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.
29
sulphonylurea most likely accumulate during renal dysfunction and cause hypoglycemia
glyburide (glibenclamide)
30
sulfonylurea preferred in renal and hepatic diseases
Glipizide and glimepiride
31
common adverse effects of sulphonylurea
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.
32
uncommon adverse effects of sulfonylurea
a- Cholestatic jaundice b- Hematological: agranulocytosis, aplastic and hemolytic anemias:
33
Non-specific Adverse Effects of sulphonylurea
Generalized and dermatological Hypersensitivity & cross-allergy
34
effect of taking Aspirin, Phenylbutazone & sulfa with sulphonylurea
Displace sulfonylureas —>> Hypoglycemia.
35
effect of taking oral anticoagulants with sulfonylurea
Sulfonylureas displace Oral anticoagulants —>> bleeding.
36
effect of taking Phenobarbitone, Phenytoin & Rifampicin with sulphonylurea
induce HME >> increase Metabolism of Sulfonylureas.
36
mask sympathetic manifestation of hypoglycemia caused by sulphonylurea
b blockers as propranolol
36
effect of taking dicoumarol with sulphonylurea
decrease excretion of chloropropamide
36
drug interactions of sulphonylurea
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
# what drug? They Block ATP-sensitive K*-channel (Karp-Channels) of B-Cells of Pancreas — Depolarization — Influx of Ca?*— Excocytosis — /' Release of Insulin.
sulphonylurea
37
effect of taking MAO-I, Allopurinol, Cimetidine & Chioramphenicol with sulphonylurea
decrease metabolism of Sulfonylureas.
38
the meglitinidaeses
repaglinide, mitglinide, nateglinide
39
route of administration of metformin
orally
40
fate of metformin
renal excretion as the active drug without hepatic mechanism
41
mechanism of action of metformin
1. reduce hepatic glucose production by activating the enzyme AMP dependent protein kinase (AMPK) >>> 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
DM drug that increases lactic acid production
metformin
43
DM drug that antgonizes the effects of glucagon
metformin
44
DM drug delays the intestinal glucose absorption
metformin
45
DM drug that activates the enzyme AMP dependent protein kinase
metformin
46
therapeutic uses of metformin
type 2 (Non insulin dependent diabetes) particulary in overweight
47
Adverse Effects of Biguanides (metformin)
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
DM drug causes fatal lactic acidosis
metformin
49
contraindication of metformin
a- Hepato-cellular failure & Chronic alcoholism >> Cannot metabolize lactic acid. b- Renal insufficiency >> Cannot excrete lactic acid. c- Hypoxic states e.g. Cardiac & pulmonary diseases ( increase lactic acid production)
50
the thiazolidinediones (glitazones)
Rosiglitazone pioglitazone
51
fate of Thiazolidinediones
hepatic metabolism
52
mechanism of action of glitazones
-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
receptor of thiazolidinediones
PPAR gamma
53
therapeutic uses of glitazones
Type 2 DM (NIDD)
54
adverse effects of glitazones
1. weight gain and edema 2. heart failure after long use 3. osteoporosis and fracture 4. hepatotoxicity 5. teratogenic
54
how to avoid hepatotoxicity caused by glitazones
Liver enzyme levels should be measured jnitially, then every 2 months for a year, and periodically thereafter
55
The Alpha-Glucosidase Inhibitors
Acarbose and miglitol
55
MoA of acarbose and miglitol
Inhibit o-Glucosidase on brush border of intestinal mucosa — Absorption of complex Carbohydrates>\ Postprandial hyperglycemia.
56
use of acarbose
Type-2 N.I.D.D.
57
Adverse Effects of acarbose and miglitol
* Flatulence, diarrhea & abdominal cramping. » Hypoglycemia with sulfonylurea + Decrease the bioavailability of metformin so concurrent use should be AVOIDED
58
how to treat hypoglycemia caused by acarbose
Give oral glucose (not sucrose) in hypoglycemia, as they impair digestion and absorption of sucrose
58
what are Glucagon-like peptide-1 (GLP-1) analogs
Exenatide (Byetta) Liraglutide Albiglutide
59
MoA of Glucagon-like peptide-1 (GLP-1) analogs
Bind to GLP-1 receptors — reduce postprandial glucose elevation and glucagon levels, delay gastric emptying, © insulin release & and suppress appetite
60
what are the incretin mimetics & enhancers
Glucagon-like peptide-1 (GLP-1) analogs Di-Peptidyl Peptidase-4 inhibitors
61
route of administration of
62
adverse effect of sexagliptin
increase risk of heart failure
63
what is the amylin analog
Pramlintide
63
the Di-Peptidyl Peptidase-4 inhibitors
a- Sitagliptin b- Vildagliptin c- Saxagliptin d- Alogliptin
64
actions of pramlintide
- Reduces glucagon secretion - Delays gastric emptying (mediated by vagus) - Decreases appetite - Reduces postprandial glucose elevation
65
adverse effects of Di-Peptidyl Peptidase-4 inhibitors
pancreatitis sexaglibtin increase risk of heart failure
65
MoA of Di-Peptidyl Peptidase 4 inhibitors
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
MoA of SGLT 2
result in glucose excretion of only 30— 50% of the amount filtered causing glycosuria and lowers glucose levels
67
clinical indications of SGLT2 inhibitors
-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
The most common adverse effects with SGLT2 inhibitors:
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
what are SODIUM GLUCOSE COTRANSPORTER 2 (SGLT2) INHIBITORS
Canagliflozin Dapagliflozin Empagliflozin

Pharma (7 decks)

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