PATHOPHYS - essay 8

DIABETES 3 TYPES

🧠 Diabetes Mellitus – Etiology, Pathogenesis, Pathobiochemistry, Complications

Diabetes mellitus is a heterogeneous group of disorders of carbohydrate metabolism involving absolute or relative insulin deficiency. The common feature is hyperglycemia.

🔹 Classification

• Type 1 diabetes mellitus (including LADA)

• Type 2 diabetes mellitus

• Gestational diabetes mellitus

• Other specific types: drug-induced, endocrinopathies, pancreatic destruction, MODY

DEP!!

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🧬 Type 1 Diabetes Mellitus (T1DM)

Insulin-dependent diabetes, usually onset in childhood (except LADA).

Etiology

• Autoimmune destruction of pancreatic β-cells

• Genetic predisposition

• Environmental triggers (e.g. viral infections)

Pathogenesis

• β-cell destruction → absolute insulin deficiency - DESTROYED

• ↓ insulin → inability to lower blood glucose + ↑ glucagon

• ↑ glucagon → ↑ gluconeogenesis + glycogenolysis → severe hyperglycemia

• ↑ lipolysis → ketone body formation → risk of ketoacidosis

Consequences

• Weight loss

• Fatigue

• Polyuria

• Polydipsia

• Polyphagia

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🧬 Type 2 Diabetes Mellitus (T2DM)

Usually adult onset; due to insulin resistance.

Etiology / Risk factors

• Genetic predisposition

• Obesity

• Sedentary lifestyle

• Unhealthy diet

Pathogenesis

• Insulin resistance in target tissues (muscle, liver, adipose)

• β-cells compensate → hyperinsulinemia

• Progressive β-cell exhaustion → relative insulin deficiency (Always after EXHASUTION+

• Persistent insulin resistance + ↓ insulin → progressive hyperglycemia (INS RESIT AT START AND END)

Consequences

• Polyuria, polydipsia, fatigue

• Long-term: microvascular + macrovascular complications

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🤰 Gestational Diabetes Mellitus (GDM)

Glucose intolerance first recognized in pregnancy.

Pathogenesis

• Placental hormones → icause insulin resistance PHIR

• Pancreas increases insulin secretion to compensate (PIS)

• β-cells fail → relative insulin deficiency

• Maternal hyperglycemia → glucose transfer to fetus → fetal hyperinsulinemia

Consequences

Mother:

• Increased risk of preeclampsia

• Increased cesarean section risk

Fetus:

• Macrosomia (excessive growth)

• Increased risk of obesity

• Increased risk of type 2 diabetes later in life

BIG L - FOR TYPE 1, DOWN, UP UP FROM I TO L (INSULIN LOWERED ABILITY TO BIND LIKE HOW U GOT CONFUSED)

II

B

P = PER (PERSISTENT EXHAUSTION, RELATIVE DEFIENCY

P

IBPP (IVE BEEN POO POO) = TYPE 2 (RHYMES)INSULIN RESIST IN SAL!! U KNOW, B CELLS COMPENSATE, PROGRESSIVE, THEN PERSISTENT, THEN PROGRESSIVE AGAIN)

PPBM (PLACENTA, PANC, B FAIL, MATERNAL)
POO POO BABY MAMA

AFTER BOTH EXHASUTION AND FIALURE OF B CELLS, RELATIVE INSUFFICIENCY

carb lipid protein metabolsim , acute complications, chronic complications , idabetes foot ulcer

🧠Pathobiochemistry Carbohydrate metabolism

• ↓ cellular glucose uptake

• ↑ hepatic gluconeogenesis

• ↑ glycogenolysis

Lipid metabolism

• ↑ lipolysis

• Type 1 → ketone body accumulation → ketoacidosis risk

• Type 2 → dyslipidemia → atherosclerosis risk

Protein metabolism

• ↑ proteolysis

• Muscle wasting

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⚠ Acute Complications

• Diabetic ketoacidosis (mainly Type 1)

• Hyperglycemic hyperosmolar nonketotic syndrome (mainly Type 2) - GONK SYNDROME (HYPER HYPER)

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⚠ Chronic Complications

Microvascular - KINDEYS/EYES

• Retinopathy

• Nephropathy

• Peripheral neuropathy

Macrovascular - CAD/ PVD

• Coronary artery disease

• Peripheral vascular disease

• Cerebrovascular disease

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🦶 Diabetic Foot Ulcer (important complication) N ISH P, GANG

• Combination of neuropathy + ischemia + infection risk → NISH + inf

• Leads to poor wound healing

• Can progress to gangrene and amputation if untreated

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