PATHOPHYSIOLOGY

PREDISPOSING FACTORS FOR DM & MI:

1. Genetics (familial history of DM both sides) 2. Family history of hypertension 3. Age (68 years old) 4. Gender (female) 5. Race

PRECIPITATING FACTORS:
1. Sedentary Lifestyle 2. Fluctuating Increase of Blood sugar Level 3. Hypertension (130-150 systolic blood pressure)

TYPE 1 DIABETES MELLITUS Autoimmune Disorder

Beta Cells in the pancreas are gradually destroyed

Insulin deficiency is absolute

Decreased insulin production causing decreased insulin transport into cells

Polyphagia

262mgdl

Blood glucose levels become excessively high in intravascular spaces (HYPERGLYCEMIA)

Polydipsia Polyuria

*8units insulin subcutaneously *Sitagliptin

Increased Blood Viscosity volume

Sluggish Blood flow

*Clopidogrel *Heparin

Hyperosmolarity

Decreased Myocardium Myocardial Perfusion

Decreased perfusion to the kidneys

Progression of tissue ischemia

RAAS stimulation

Inferior Infarction

A>35mS, flat T, II, III aVF

Anterolateral Infarction

Oliguria (150cc) T negative, Q 35mS & >.10mV, V3V6

Retention of water and sodium

Vasoconstriction Atorvastatin Carvedilol Amlodipine Telmisartan

Increased BP 150/90 Upper Peripheral edema

Destruction of the myocardial tissue

Anaerobic Metabolism

Decreased Glomerular Filtration

Decreased myocardial contractility

Production of Lactic Acid

Increased Creatinine in the blood and BUN, and retention of Potassium

BUN: 96mg/dl CREA: 3.76mg/dl

Severe reduction on cardiac output

Stimulates Pain nerve endings

Tramadol + Paracetamol = Dolcet

CHEST PAIN
Trimitazine Isosorbide Mononitrate Amlodipine

Lactulose

LEGEND:

PATHOPHYSIOLOGIC PROCESS

MEDICATION GIVEN

LABORATORY RESULTS

CLINICAL MANIFESTATIONS