3. PHYSICAL OR PSYCHOLOGICAL STRESSOR ALARM REACTION (FIGHT-OR-FLIGHT RESPONSE) * Arousal of the central nervous system begins. * Epinephrine and norepinephrine, along with other hormones, are released, causing an increase in heart rate, force of heart contractions, oxygen intake, and mental activity. RESISTANCE * The body responds to the stressor and attempts to return to homeostasis. * Coping mechanisms come into play. RECOVERY * If stress ceases, the body should return to a normal state, leading to recovery. EXHAUSTION * The body can no longer produce hormones as it did in the alarm stage. * Organ damage begins.
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7. Understanding Disseminated Intravascular Coagulation and its Treatment Precipitating mechanism Tissue damage Treat the underlying problem Endothelial damage Increased tissue thromboplastin Intrinsic pathway of coagulation Extrinsic pathway of coagulation Heparin to prevent microclotting (controversial) Intravascular coagulation (production of microthrombi) Production of thrombi Activation of fibrinolytic system Digestion of fibrin clots Inhibition of platelet function Consumption of clotting factors Decreased clotting factors Cryoprecipitate factor VIII Fresh frozen plasma Platelets Occlusion of small blood vessels Tissue necrosis Thrombocytopenia Bleeding Blood Key: = treatment
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24. TREATING MYOCARDIAL INFARCTION *Aspirin *Antiplatelet Aggregates *Glycoprotein IIB/IIIA Receptor Blocking Agents *Thrombolytic Therapy *Percussions Transluminal CoronaryAngio-plasty *Nitrates *Beta- Adrenergic Blockers *Oxygen *Bed Rest *Vasodilators *Morphine *Beta –Adrenergic Blockers *Nitrates *Vasodilators Change in the condition of plaque in the coronary artery Altered depolarization of the myocardium Pathologic Q wave appears Elevated ST segment T wave changes Elevated CK-MB Elevated lactate dehydrogenase Elevated troponin and myoglobin Activation of platelets Altered repolarization of the myocardium Formation of thrombus Release of lysosomal enzymes Coronary blood supply less than demand Anaerobic glycolysis Lactic acid production Myocardial irritability Angina Ischemia of tissue in the region supplied by the artery Myocardial cell death Arrhythmias Decreased contractility Stimulation of the sympathetic nervous system Decreased left ventricular function Increased heart rate Increased afterload Increased 0 2 needs Vasoconstriction Increased preload Decreased cardiac output *Angiotensin- Converting Enzyme Inhibitors Decreased left ventricular ejection fraction *Fluid Restriction *Diuretics Increased central venous pressure Increased pulmonary artery wedge pressure Key: = treatment
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45. AVERTING RENAL FAILURE IN GLOMERULONEPHRITIS Antigen –antibody reaction Antibiotics, corticosteroids, plasmapheresis Glomerular proliferation and damage Tension builds within the rigid medullary cavity Decreased glomerular filtration rate Increased vasopressor activity Capillary damage Increased aldosterone Vasoconstriction Release of protein molecules and RBCs Sodium retention Hypertention Proteinuria or hematuria Water retention Edema Diuretics Dialysis, renal transplant Renal failure Vasolidators Key: = treatment
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54. AVERTING AN ASTHMA ATTACK Exposure to allergens and causative factors Avoidance of allergens Allergy injections Reduction of causative factors (stress-reduction classes) Corticosteroids Mast cell degranulation Immunoglobunin E stimulation Mast cell stabilizers Histamine Leukotrienes Prostaglandins Bradykinins Antihistamines Mucus secretion Inflammation Bronchospasm Wheezing and narrowing of airways Airway obstruction Bronchodilators Key: = treatment
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79. Treatment of type 1 diabetes mellitus Genetic predisposition Environmental or viral stressor Destruction of alpha and beta cells of the pancreas Pancreatic transplantation Failure to produce insulin Production of excess glucagon Production of glucose from protein and fat stores Wasting of lean body mass Chronic elevations in blood glucose levels Increased ketones Acidosis Fatigue Weight loss Acetone breath odor Increased osmolarity due to glucose Elevated blood glucose level Polydipsia Polyuria Polyphagia Weight loss Small-vessel disease Accelerated atherosclerosis Impaired immune function Diabetic retinopathy Diabetic nephropathy Diabetic retinopathy Infection Delayed wound healing Dialysis, transplantation End- stage renal failure Laser therapy Hypertension Coronary artery disease Increased low-density lipoprotein levels Loss of vision, blindness Symmetrical loss of sensation Numbness and tingling in the extremities Wasting of intrinsic muscles Charcot’s joint (neopathic joint disease) Autonomic neuropathy Diabetic and foot ulceration Insulin, meal planning, exercise Key: = treatment
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113. SYMPTOM PROGRESSION ON INTESTINAL OBSTRUCTION Obstruction Fluid, gas, and air collect behind obstruction Peristalsis temporarily increases in attempt to force contents past obstruction. Distention increases at and above obstruction site. Distention impedes blood supply to bowel, halting absorption. Bowel wall swells as water, sodium, and potassium are secreted into intestine and not absorbed from it. Gas-forming bacteria collect above obstruction, increasing distention. Dehydration results because fluids aren’t absorbed into bloodstream. With no treatment, severe hypovolemia occurs. Shock Sepsis Death
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121. TREATING PEPTIC ULCER DISEASE Bile salts, aspirin, nonsteroidal anti-inflammation, alcohol, ischema Damaged mucosal barrier Increased number of parietal and chief cells Inade q uate mucosal blood supply Decreased function of mucosal cells Decreased q uality of mucus Loss of tight junctions between cells Increased sensitivity to food and other stimuli Decreased inhibition of gastric secretions Bile or pancreatic enzyme reflux from duodenum Conversion of pepsinogen to pepsin Antimicrobials Further mucosal erosion Destruction of blood vessels Bleeding Colonization by Helicobacter pylori Ulceration Mucosal injury Dietary measures Misoprostol Sucralfate Histamine-2 blockers Antacids Formation and liberation of histamine Increased acid secretion Local Vasodilatation Anticholinergic drugs Excessive vagal stimulation Stimulation of cholinergic intramural plexus, causing muscle spasm Increased capillary permeability Loss of plasma proteins Mucosal edema Loss of plasma in gastric lumen Key = treatment
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