INSULIN

1. Diabetics Mellitus - Insulin
 Diabetics Mellitus definition : - Metabolic disorders
characterized by
a. Hyperglycemia
b. Glycosuria
c. Hyperlipemia
d. Negative nitrogen balance and
e. Ketonemia.

2.  Types of Diabetes : -
 Type I :-
a) Insulin dependent diabetics Mellitus (IDDM) Juvenile
onset.
b) β - Cells are destroyed in pancreatic islets.
c) Genetic predisposition - less
d) In all Type 1 cases circulating insulin levels are very low,
and patients more prone to ketoses.
e) Autoimmune

3.  Type 2 : -
a) Non insulin dependent DM (NIDDM) maturity onset
DM.
b) β Cells are not destroyed but moderate reduction in β
cell mass.
c) Insulin may be low, normal or even high.
d) High degree of Genetic predisposition.
e) Late onset.

4.  Causes: -
a. Abnormality in gluco receptor of β cells so that they
respond at higher glucose concentrations.
b. Reduced Sensitivity of peripheral tissues to insulin
c. Reduction in the number of insulin receptors.
Eg: - many hypertensives are hyper insulinemic but
normoglycemic (exhibit insulin resistance) Hyper
insulinemia - causes angiopathy.
d. Excess of hyper glycemic hormones (glucagon etc
obesity) cause relative insulin deficiency – the β cells lag
behind.

5.  Islets of Langerhans contains 4 types of cells: -
1. Alpha – 20% of Islet mass - Secrete glucagon - 
blood sugar.
2. β cells – 75% of Islet mass - Secrete insulin blood
sugar
3. Delta cells – D cells – 3% of Islet mass – Secrete growth
hormone release inhibiting hormone or somatostatin.
4. F cells – 2% Islet mass - Secrete pancreatic
polypeptide – regulates pancreatic digestive enzymes.

6.  Insulin :-
 Pharmacological actions of insulin : -
1. Promotes the uptake and storage of glucose, fats and
proteins – effects are on liver, muscles and adipose tissues.
2. Influences the cell growth and metabolic functions
of various tissues.
3. Excess secretion of insulin – Hypoglycemia lack of
insulin release (as in DM) leads hyperglycemia.

7.  Rapid effects : - Insulin  the blood glucose levels by
affecting both the glucose utilization and production.
 carbohydrate metabolism.
1. In liver cells : -
a.  glycogenolysis by inhibiting glycogen
phosphoylase.
b.  glycogenolysis
c.  conversion of glycogen to glucose
d.  glycogen synthesis
e.  Gluconeogenesis

8. 2. Muscle : -
a. Facilitates glucose uptake by promoting translocation of
the intra cellular glucose transporter – 4 (GLUT -4) on to the
cell surface.
b. Promotes glycogenesis.
c.  glycolysis – conversion of glucose and ADP to lactate
and ATP. - source of energy for voluntary and cardiac
muscle.

9. 3. In adipose tissue : -
a. Facilitates glucose uptake
(through GLUT – 4)
b.  Intracellular glucose oxidative metabolism Glycerol
produced is esterified with fatty acids to form
triglycerides.  the synthesis of triglycerides.
 Protein Metabolism : -
1. In liver cells : -  protein break down and  oxidation
of A A.
2. In Muscles : -  protein synthesis  amino acid
uptake my muscle cells  positive nitrogen balances.

10.  Fat Metabolism : -
a. In liver cells: -  Lipogenesis
b. In adipose tissues : -  fatty acid synthesis and
triglycerides formation.  Lipolysis.
c. Blunts lipolysis action of adrenaline, growth hormone
and glucagons.
 Thus plasma free fatty acid and glycerol levels remain
suppressed under the influence of insulin.

11.  Other Metabolic effects :- Stimulates lipoprotein lipase and
thus increases clearance of VLDL and chlyomicrons.
 Long term effects : -
a. Insulin regulates gene transcription and stimulates cell
proliferation and differentiation.
b. It governs protein synthesis, growth regulation
c. DNA mediated synthesis of glucose transporters
(GLUTH – GLUT – 5).

12.  Mechanism of action : -
a. Acts on Insulin receptor
b. Large transmembarne glycoprotein.
c. Consists of 2 α subunits and 2 β – subunits linked by disulfide
bonds to constitute a β –a-a- β hetero tetramer.
d. β units contain tyrosine kinase residues
e. When insulin binds to α submits at the outside of the cell,
surface, the tyrosine kinase activity in β subunits is
stimulated.
f. Results in autoposphorylation of the adjutant β subunit
and Phosphorylation of the Tyrosine residues present
on cytoplasmic protein called insulin receptor substrate - 1

13. g. Initiates a series of events that lead to a cascade of
phosphorylation and dephosphorylation reactions.

14. IRS-1 IRS-1
↑ Glucose
uptake
↑ Glucose
utilisation
↑ Stores-glycogen,
fat & proteins
↓ Glycogen
breakdown
Phosphorylation cascade
IPG, DAG

15. Types of Insulin

17. Hypoglycemia Protocol
 Risk factors for hypoglycemia
 Nutritional status
 Missed meals, delayed meals
 Heart failure, renal or liver disease
 Malignancy
 Sudden reduction of steroid dose
 Altered ability of patient to report symptoms
 Vomiting

18.  Risk factors for hypoglycemia
 New NPO status
 Reduction in IV dextrose
 Unexpected interruption of feeds/TPN
 Altered consciousness from anesthesia
 Advanced age
 Previous history of severe hypoglycemia

19. Symptoms
 Variable from patient to patient
 Assess patient for his/her individual symptoms
 Trembling
 Palpitations
 Sweating
 Anxiety
 Nausea
 Hunger
 Tingling

20.  Confusion
 Difficulty concentrating
 Weakness
 Drowsiness
 Vision changes
 Difficulty speaking
 Headache
 Dizziness
 Tiredness

21. Newer Insulin Delivery system

22. Insulin Syringes
 Sizes – 30, 50, 100
units
 Disposal-

23. Syringe & Vial: Preparation
1. Get Supplies
 Insulin (Verify)
 Syringe
 Alcohol wipe
 Disposable gloves
 Sharps container

24. Syringe & Vial: Preparation
2. Wash hands;
apply gloves
3. Clean the insulin vial

25. Syringe & Vial: Preparation
4. Have student select injection site.
5. Clean the injection site

26. Syringe & Vial: Preparation
6. Check the insulin dose
7. Remove the cap from syringe.

27. Syringe & Vial: Dosing
8. Pull the plunger down to number
of units to be administered.
9. Inject air into bottle.

28. Check Dose
Syringe & Vial: Dosing
10. Draw out prescribed number
of units of insulin as per
DMMP.

29. Syringe & Vial: Injecting
11. Pinch up the skin.
12. Push needle into skin at 90.
13. Release pinch.
14. Push the plunger in.
15. Count to “5”.
16. Remove needle and dispose of syringe.
17. Document time, dosage, site, and blood
glucose value.

30. On Target!

31. Insulin Pen: Devices
Prefilled pens
Reusable (cartridge) pens
Techniques for dose preparation and insulin
delivery are similar for both types of pen devices.

32. Insulin Pen: Preparation
1. Gather supplies. Verify insulin type.
 pen device (with cartridge)
 pen needle
 alcohol wipe
 sharps container
2. Wash hands.
3. Chose injection site
4. Clean injection site
5. Screw on pen needle

33. Insulin Pen: Dosing
6. Prime: Dial “2” units.
7. Hold upright. Remove air by pressing
the plunger. Repeat “Prime” if no
insulin shows at end of needle.
8. Dial number of units to be
administered as per DMMP.

34. Insulin Pen: Injecting
9. Choose and clean injection site.
10. Pinch up the skin.
11. Push the needle into the skin at 90
12. Release pinched skin.
13. Push down on the plunger.
14. Count to “5”.
15. Remove and dispose of pen needle.
16. Document time, dose, site, and blood glucose
value.

35. Insulin Pump Therapy
 Based on what body does naturally
- Small amounts of insulin all the time
(basal insulin)
- Extra doses to cover each meal or snack
(bolus insulin)
 Rapid or Short-Acting Insulin
 Precision, micro-drop insulin delivery
 Flexibility

36.  Therapeutic Uses : -
1. Type 1 diabetics – NPH insulin combined with short acting
regular insulin – SC before meals.
2. Type 2 diabetes – Insulin Therapy
3. Gestational diabetes
4. Emergency treatment of Diabetic coma
5. Non – ketotic hyperglycemic coma
6. Short term treatment of patients with impaired glucose
tolerance (MI), (surgery).
7. Emergency treatment of hyperkalaemia.

37.  Adverse effects : -
1. Hypoglycaemia
2. Lipodystrophy at the site of S.C
3. Allergic Manifestations.
4. Insulin Resistance.