Charts...hormones...mbbs

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Pharmacological applications Of drugs ‘mimic or block’

•Replacement therapy •Antagonists for diseases of excess •Diagnostic tool

GROWTH HORMONE (SOMATOTROPIN)

Mediation of Its effects: IGF-1, IGF-2 Pituitaries of human cadavers. Contaminated with prions -cause Creutzfeldt-

Jakob disease GH has a half-life of 20-25 minutes

Somatropin Somatrem rhGH----36 hours. 4-6/week Uses: 1. GH Def----- 2. Idiopathic short stature????? 3. Catabolic

states 4. Anti aging 5. Banned drug-sports 6. Cattle-Milk production ADE↑ICT MECASERMINrhIGF-1 & rhIGFBP-3

GROWTH HORMONE ANTAGONISTS Somatostatin

USES

Octreotide-analog

Acromegaly

Bromocriptine-DA ago Pegvisomant-GH Rec.Anta

Gigantism

? MOA

Hormone secreting

tumors-Carcinoid ADE Gallstones Bradycardia

Answer:

Q.

•Octreotide, 50200 mcg given s.c 8th hourly

•Octreotide acetate injectable long-acting suspension -slow-release microsphere formulation [After effect is established by short acting]

Q.

Answer:

•Somatrem •Somatropin

GONADOTROPIN-RELEASING HORMONE & ITS ANALOGS

Gonadorelin

-acetate salt of synthetic human GnRH. Synthetic analogs  Goserelin, Histrelin, Leuprolide, Nafarelin Triptorelin. Route; I.v, i.m, s.c. Nasal

PD; Pulsatile i.v: Stim.-FSH &

Lh Continuous Biphasic respones 7-10 daysStimulation

GnRH-Uses Inhibition

Controlled ovarian Hyperstimulation To ↓ LH surge

Stimulation-Not common use Female infertility Male infertility Diagnosis of LH

responsiveness

Endometriosis Uterine fibroids Prostate cancer Central precocious puberty

GnRH Rec. Antagonists

Ganirelix and cetrorelix Competitive antagonists of

GnRH receptors Used to Prevent the LH surge during controlled ovarian hyperstimulation Advantages and disadvantages over GnRH agonists????????

Answer: •Endometriosis •Assisted reproduction •Central precocious puberty

Q:

Diabetes mellitus Types 1, 2, 3, 4 Insulin Oral anti-diabetic drugs

Endocrine secretions of pancreas Alpha Beta

Glucagon, proglucagon Insulin, C-peptide, proinsulin, amylin Somatostatin

Delta F(PP)

Pancreatic polypeptide (PP)

Control of insulin release from the pancreatic B cell by Glucose [Chemical][Hormonal, Neural are other stimuli]

Oral>i.v

First phase- Within 2 minutes Delayed phase

Insulin Degradation Endogenous

Liver[60%]

Kidney[40%]

s.c

Liver?? [40 %]

Kidney?? [60%]

Glut 1

All tissues

Glut 2

Pancreas

Glut 3

Brain, kidney

Glut 4

Muscle, adipose [Insulinmediated uptake of glucose] Gut, kidney

Glut 5

The Insulin Receptor

TRANSLOCATION

Phosphorylation of tyrosine residues on the β subunits and tyrosine kinase activity directed at cytoplasmic proteins

Gluconeogenes is IN LIVER Glycogenolysis In su Insulin [-] lin

Absorption

[-]

No actio n

Blood

Processes add glucose [Hyperglycemia] Processes utilize glucose [Hypoglycemia]

in l u

In

su

l in

[+ ] Protein Synth. In Muscles

[+ ]

s In

Insuli [+ n ]

Peripheral utilization

Lipogenesis

Sources and insulin preperations Species

A Chain

B Chain

8th AA

10th AA

30th AA

Human

THR

ILEU

THR

Pork

THR

ILEU

ALA

Beef

ALA

VAL

ALA

1. Highly purified pork Insulins • Monocomponent insulins

Conventional prep. •Impurities •Antigenic •Less expensive

•Replaced by 2.Highly purified pork Insulins 1. Human insulins 4.Human insulins • Recombninant DNA 5.Insulin analogs Technology[E.Coli, porcine, Yeast] 3. Insulin analogs Changing or replacing AA sequences 3. Lispro 4. Aspart 5. Glulisine 6. Glargine 5. Detemir

Principal Types and Duration of Action of Insulin Preparations Type

Duration]

Onset

Peak

Appearance

Rapid acting I.Lispro

3-5

Clear

I.Aspart

3-5

Clear

I.Glulisine

2-4

Clear

6-8

Clear

Short acting Regular[Soluble ] Intermediate acting I.Zinc[Lente]

20-24

Cloudy

Isophane.I [NPH]

20-24

Cloudy

24-36

Cloudy

Long acting Protamine zinc I. [Ultra lente] I.Glargine

24

Clear

Complications of insulin therapy Hypoglycemia

Lipodystroph y

Diagnosi Atrop

s Treatme nt

hy Hypertrop

hy

Immunopathology

•Insulin allergy •Insulin resistance

Q Answer:

•Regular human insulin •NPH Human insulin •70/30 Human insulin

Q

Answer: •Non-antigenic, less allergenic •Less lipodystrophy, •Preferred in insulin resistance

Why? •Infection •DKA •Chronic tt with conventional Q

Answer:

What to do? •Treat the cause •Use newer preparations

When insulin requirement is > 200 i.u

Q

Answer: •Regular insulin •Intravenous •Bolus [0.1-0.2u/kg] →Infusion [0.1u/kg/hr.]

Q Why shoud serum potassium be monitored with Insulin therapy in diabetic ketoacidosis? Answer:

+

•Though K is lost in urine in DKA + serum K is normal [Intracellular exchange] •Insulin→ DKA subsides → + K is driven intracellular →Hypokalemia •So, after 4 hrs →10-20mEq/hr KCL to i.v.fluid

ORAL ANTIDIABETIC [ Insulin Biguanide secretagog s Metformin ues 1.

HYPOGLYCAEMIC

Sulfonylureas

I Gen •Tolbutamide, •Chlorpropamide •Tolazamide II Gen •Glibenclamide •Glipizide •Gliclazide •Glimepiride

2. Meglinitides •Repaglinide

3. Dphenylalanine derivative

] AGENTS

Thiazolidinedion es •Rosiglitazone •Pioglitazone •aglucosidase inhibitors. •Acarbose •Miglitol

Sulfonylureas :Mechanism of Action ACUTE ADMINISTRATION: INSULIN RELEASE FROM PANCREATIC Beta CELLS↑

CHRONIC ADMINISTRATION:

1. Down regulation of sulf.receptors on pancreas

Insulinaemia decreased But antidiabetic action maintained?????????

Increase in the insulin receptors in target tissues 2.Reduction of serum glucagon concentrations…. [Minor action]

Biguanides :Metformin [-]

mi n

or

Glycogenolysis

M et fo rm in

[-]

Me

tfo r

s Ab

on i t p

Gluconeogenesis

Processes add glucose [Hyperglycemia]

Blood

Processes utilize glucose [Hypoglycemia]

o

f t e

in rm

[+ ]

M

Blood sugar reduced

Peripheral utilization Protein Synth.

Lipogenesis

Pio Glitazon es

THIAZOLIDINEDIONES (Tzds) Bind to nuclear PPAR-γ Rec.

Reduce blood glucose by • Increasing Glu tpt into muscles and adipose tissues • Inhibiting hepatic gluconeogenesis • Promoting lipogenesis

Peroxisome ProliferatorActivated Receptor-gamma (PPAR-γ),

ALPHA-GLUCOSIDASE INHIBITORS Oligosaccharides and Disaccharides

Monosaccharide [Glucose Fructose ]

Acarbos e Miglitol

Not Absorbe d

Uses: Add on drugs in Type 2 ADE: Flatulence, diarrhea, and abdominal pain

Q: Answ er

•Fewer adverse effects and drug interactions •More potent •Longer acting

Q:

Answer:

Anorexic-Clinical relevance???? Does not promote weight gain Reduces plasma triglycerides . nsulin sensitizer-Obesity + Insulin resistance

Q:

Answer:

•Reduces postprandial glycemic elevations •Fewer episodes of hypoglycemia

Q:

Answer: •Increase in weight-edema •Expansion of plasma volume •Reduction in renal sodium excretion •↑ Vascular permeability

Q:

Answer:

Unacceptable levels of hyperglycemia n who respond initially to a sulfonylurea hange in drug metabolism, rogression of β-cell failure, hange in dietary compliance, Misdiagnosis of a patient with slow-onset type 1 DM.

Q:

Answer:

•Levothyroxine of 10 to 15 µg/kg •Life long

Q:

Answer: •Carbimazole •Radioactive iodine

Grave’s disease ↓ Hyperthyroidism ↓ Thyrotoxicosis ↑ Thyrotoxicosis Without Hyperthyroidism ↑ Thyroiditis