Manegement of Diabetes Mellitus and it’s complications
Name- INDU HOODA
Roll no. -2338
Goals of Treatment
[Link] restore metabolism to normal, avoid symptoms due to hyperglycaemia and glucosuria.
The generally accepted criteria for adequate glycaemia control in an adult diabetic treated with
insulin or oral antidiabetics are:
Fasting (morning) blood glucose levels
90-126 mg/dl
Blood glucose levels ≤140 mg/dl 2 hours after meal
HbA1c levels <6.5%
[Link] short-term complications (infection, ketoacidosis, etc.) and long-term sequelae
(cardiovascular, retinal, neurological, renal, etc.).
• M n gement of Di betes Mellitus
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Complications of Diabetes Mellitus
[Link] Ketoacidosis
Etiology & C uses
Mostly occurs in Type 1 DM due to insuf cient or no insulin.
Rare in Type 2 DM.
Common precipitating factors:
Infections (most common)
Trauma, stroke, pancreatitis
Stressful conditions
Missed/inadequate insulin doses
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1. IV Fluids
a)Initial: Normal saline (1 L/hr)
b)Taper based on volume status (to 0.5 L/4hr)
c)Once stable: switch to ½ N saline
d)When BG < 300 mg/dL:Use 5% glucose in ½ N saline
as it prevents hypoglycemia and replenishes hepatic glycogen.
2. Insulin Ther py
.
a)Regular insulin:
Bolus: 0.1–0.2 U/kg IV
Infusion: 0.1 U/kg/hr, double if no improvement in 2 hrs
Goal: blood glucose by 10% per hour
b)When blood glucose reaches 300 mg/dL:Reduce to 2–3 U/hr
Continue until consciousness returns
Then switch to subcutaneous insulin.
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3. Pot ssium (KCl)
Despite total body K+ loss, serum K+ may appear normal during DKA
Insulin causes intracellular shift risk of hypokalemia
After 2–3 hrs: add 10–20 mEq/hr KCl to IV uids
[Link] Bic rbon te
Not routinely needed
Indicated if:Arterial pH < 7.0
Acidosis not resolving
Hyperventilation is inadequate
Dose: 50 mEq IV, stop once pH > 7.1
5. Phosph te
If low-normal serum PO₄³⁻: give 3–4 mmol/hr K phosphate
Avoid rapid infusion risk of tetany
Not routinely recommended
6. Other Me sures
Antibiotics if infection present
Treat underlying cause
Supportive care
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[Link] r (Nonketotic Hyperglycemic) Com – HHS
[Link] nition
Acute complication of Type 2 Diabetes Mellitus
Marked hyperglycemia: > 600 mg/dL
Serum osmolality: > 320 mOsm/L
Absent or minimal ketosis
Altered mental status or coma
2.P thophysiology
Insulin de ciency (partial) + increased counter-regulatory hormones
Glycosuria Osmotic diuresis
Severe dehydration and hemoconcentration
Decreased urine output further glucose accumulation
High blood osmolality impaired cerebral function coma
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[Link] tment
Similar to diabetic ketoacidosis (DKA), with key differences:
Rapid IV uid replacement (more aggressive than in DKA)
Lower insulin requirement
Less potassium replacement (K+ loss less severe)
No need for alkali therapy
Prophylactic heparin recommended (due to risk of thrombosis)
[Link]
High mortality rate despite treatment
Prompt recognition and management are critical.
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[Link] Resist nce:
[Link] nition:
Suboptimal response of liver, skeletal muscle, and fat to insulin.
[Link] ted Conditions:
Type 2 Diabetes Mellitus (T2DM) – insulin resistance is integral.
PCOD – commonly associated.
Metabolic Syndrome – includes insulin resistance with hypertension
3.P thophysiology in T2DM:
Insulin receptor number usually normal.
Faulty intracellular transducer mechanism is the main issue.
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[Link] Insulin Resist nce:
Onset: Rapid, short-term.
Causes:
Stress (infection, trauma, surgery, emotional) release of
counter-regulatory hormones.
Ketoacidosis – ketones & free fatty acids inhibit glucose uptake.
[Link] tment:
Remove precipitating cause.
Administer high doses of regular insulin
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[Link] emi in Di betes
1. De nition:
Most frequent and serious adverse e ect in diabetes, especially insulin-treated.
2.C uses:
Large insulin dose .
Skipping meals post-injection.
Vigorous physical activity.
[Link]:
Sympathetic (early warning): Sweating, anxiety, palpitation, tremor.
Neuroglucopenic (brain glucose deprivation): Dizziness, headache, visual disturbances,
behaviour changes, hunger, fatigue, muscular incoordination, hypotension.
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[Link] Hypoglyc emi (<40 mg/dl):
Mental confusion, seizures, coma.
Risk of irreversible neurological damage.
[Link] tment:
Mild cases: Oral glucose/sugar 15–20 g. Repeat after 15–20 mins if needed.
Severe cases:IV glucose 30–50 ml of 50% over 10 mins.
If IV unavailable:Glucagon 0.5–1 mg IV.
Adrenaline 0.2 mg SC (less pre ered)
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Thank you
Diabetes is all about insulin levels and
sugar levels and what you put in your body.
Glucagon
Glucagon is a single chain polypeptide containing 29 amino acids, MW 3500.
It is secreted by the a cells of the islets of Langerhans and commercially produced now by recombinant
DNA technology.
• Mech nism of ction
• Gluc gon
Activate adenylyl cyclase
Increases cAMP in liver,fat cells,heart and
Other tissues
cAMP does actions
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Regulation of Secretion
Its secretion is regulated by glucose levels, other nutrients, paracrine hormones and nervous system.
Glucose has opposite effects on insulin and glucagon release, i.e., high glucose level inhibits glucagon
secretion.
The incretin GLP-1, FFA and ketone bodies also inhibit glucagon release.
Amino acids, however, induce both insulin and glucagon secretion.
Insulin, amylin and somatostatin, elaborated by the neighbouring B and & cells, inhibit glucagon
secretion.
Sympathetic stimulation consistently and parasympathetic stimulation under certain conditions
evokes glucagon release.
Actions
Glucagon is hyperglycaemic; most of its actions are opposite to that of insulin.
Glucagon causes hyperglycaemia primarily by enhancing glycogenolysis and gluconcogenesis in liver.
Suppression of glucose utilization in muscle and fat contributes modestly.
Glucagon is considered to be the hormone of fuel mobilization. Its secretion is increased during fasting, and is largely responsible for the high
fasting blood glucose levels in type 2 diabetics.
Glucagon plays an essential role in the development of diabetic ketoacidosis.
Increased secretion of glucagon has been shown to attend all forms of severe tissue injury.
Glucagon increases the force and rate of cardiac contraction and this is not antagonized by ß blockers.
It has a relaxant action on the gut and inhibits gastric acid production.
• Ph rm cokinetics
Glucagon is inactive orally
Released from pancreas is broken down in liver, kidney, plasma and other tissues.
Its plasma t½ is 3-6 min.
USES
1. Hypoglycaemia Use of glucagon to counteract insulin/ oral hypoglycaemic drug induced hypoglycaemia is only an expedient
measure for the emergency, and must be followed by oral glucose / sugar given repeatedly till the blood glucose level stabilizes. It
may not work if hepatic glycogen is already depleted.
2. Cardiogenic shock Glucagon may be used to stimulate the heart in ß adrenergic blocker treated patients. However, action is
not very marked.
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