PATHOPHYSIOLOGY OF DM type 2, HPN and HACVD not in failure

Host
N.F.C. 68y.o., Female HFD: HPN, DM type 2

Agent
Insulin resistance sensitivity to glucose levels glucose utilization of cells Cell hunger

Environment

Pancreas secretes more insulin Insulin levels in the blood Induction of HMG-CoA Reductase activity Cholesterol synthesis in the liver Gluconeogenesis Liver cholesterol levels

Signals hypothalamus Appetite Polyphagia Carbohydrate Metabolism

Glycogenolysis Breakdown of glycogen to glucose

Protein Metabolism Muscle wasting Weakness and fatigue

Fat Metabolism circulating fats Fats adhere to blood vessel wall

LDL receptor synthesis is inhibited LDL uptake blood LDL cholesterol levels Plaque formation in blood vessels Atherosclerosis

Ketone production Blood ph Metabolic Acidosis Diabetic Ketoacidosis

Blood Glucose Levels

6/12/11Lipid Panel 169 mg/dl N =75-115

Fruity Breath

Kussmauls Respiration

Blood vessel lumen Peripheral Resistance Blood Pressure HACVD

Hyperglycemia

Excretion of excess glucose by kidney Osmotic diuresis

bloodosmolarity Fluid shifts from interstitial space to blood

blood viscosity

Blood vessel endothelial cells take in more glucose Increase Surface Glycoprotein formation Thickening of the wall and basement membrane of blood vessels Accelerated Atherosclerosis Decreased Tissue Perfusion Sequel II

Glycation of ion pumps Osmotic stress disrupts the cells of the eye Cataract formation Sequel III

Polyuria Sequel I

Sequel I

Sequel II Inability to meet oxygen demands of the body

Weight Loss

Dehydration

Polydypsia

Electrolyte Imbalance
6/13/11 Sodium = 143 mg/dl N = 136-142 6/13/11 Potassium = 3.3 mg/dl N = 4.0-5.6 See at Lab Results

Organ becomes hypoxic

Poor wound healing Risk for infection

Macrovascular

Organ failure Death

Microvascular

Kidneys Conserve fluid when water is limited in the body

Hypovolemia

Weakness

Coronary Artery DIsease Myocardial Infarction

Stroke

Peripheral Vascular Disease

Neuropathy Nerve Conduction disrupted Decreased sensation in extremities

Nephropathy Kidney Function Impaired

Retinopathy Angiogenesis Rupture of fragile blood vessels Vitreous Hemorrhage

Hypovolemic Shock

Sequel II

Fibrous Scar Tissue Formation Retinal Detachment

Light unable to pass through

Sequel III Diminished Vision Loss of Vision

PATHOPHYSIOLOGY OF Ruptured Appendicitis

Host

Agent
Obstruction of the appendix by (fecalith, lymph node, tumor , foreign object) Increase in pressure inside the appendix Distention of the lumen of the appendix Impaired venous return causing hypermia (improper O2 and nutrient supply) Invasion of bacteria from the normal flora of the appendix in the wall lining Distention of the lumen of the appendix Inflammatory response Inc Immune Complex Medical Mgt. Appendectomy Swelling of the tissue of the appendix Death of tissue Perforation of Appendix due to increase pressure Exit of fecal matter to peritoneal cavity Forming of abscess and spreading of infection Bacterial invasion of Peritoneal cavity Inflammation of the peritoneum (peritonitis) Sepsis Abdominal Pain at RLQ Fever

Environment
Risk Factors: Constipation Diet: low fiber Postponing defecation GI Infections

N.F.C. 68y.o., Female HFD: HPN, DM type 2

Untreated Septic Shock: dec. BP and dec. BV coma DEATH

Treated Antibiotic and Fluid Volume Replacement Therapy Recovery