Advanced Pathophysiology HESI Exam review

Advanced Pathophysiology HESI Exam review metabolic acidosis low pH, low HCO3 metabolic alkalosis high pH, high HCO3 respiratory acidosis low pH, high CO2 respiratory alkalosis high pH, low CO2 metabolic acidosis causes Primary Cause: Addition of large amounts of fixed acids to body fluids; Contributing Causes: Lactic acidosis (circulatory failure), Ketoacidosis (diabetes, starvation), Phosphates and sulfates (Renal dz), Acid ingestion (salicylates), Secondary to respiratory alkalosis, Adrenal insufficiency metabolic alkalosis causes Primary Cause: Retention of base or removal of acid from body fluids; Contributing Causes: Excessive gastric drainage, Vomiting, Potassium depletion (diuretic therapy), Burns, Excessive Sodium Bicarb admin respiratory acidosis causes Primary Cause: Hypoventilation (causes hypercapnia); Contributing Causes: COPD, Pulmonary dz, Drugs, Obesity, Mechanical asphyxia, Sleep Apnea respiratory alkalosis causes • Primary stimulation of CNS: hyperventilation. Can be due to emotional origin (anxiety, fear, apprehension), CNS infection (encephalitis), or salicylate poisoning. • Reflex stimulation of CNS. Hypoxia stimulates hyperventilation (heart failure, pneumonia, pulmonary emboli). Can also be stimulated by fever. • Mechanical hyperventilation, resulting in "over breathing." Neuro exams include: -hand strength, limb strength -ability to follow commands -ability to move eyes in equal and uniform fashion -deep pain stimulus response -symmetrical and coordinated movement -clear, speech. Acute Bronchitis patho infection or inflammation of the bronchi. In more than 90% of individuals, this is a self-limiting disorder caused by viruses. will not have high fevers and will have only scattered coarse wheezes on examination without evidence of pulmonary consolidation. Chest X-ray examination is usually normal. Chronic Bronchitis patho sequence The chronic bronchitis pathophysiologic sequence of events is as follows: Hypersecretion of bronchial mucus, which leads to Recurrent respiratory infections, which lead to Airway inflammation, which leads to Bronchospasm and irreversible airway obstruction chronic bronchitis patho characterized by chronic inflammation with recruitment of neutrophils, macrophages, and lymphocytes to the lung, with progressive damage to airways and the lung parenchyma. hyperplasia of the mucus-producing goblet cells of the bronchial epithelium occurs, resulting in the production of large amounts of mucus in the airways. Mucus accumulation facilitates the colonization and growth of bacteria, which further contributes to airway inflammation, bronchospasm, and eventual scarring. Narrowed airways cause v/q mismatching and expiratory airway obstruction with air trapping, resulting in both hypoxemia and hypercapnia. CAD risk factors pathological Major: Advanced age Gender (men > women before age 55, women > men after age 55) Dyslipidemia Hypertension Smoking Diabetes mellitus and insulin resistance Obesity Sedentary lifestyle Metabolic syndrome Atherogenic diet Non traditional: Markers of inflammation C-reactive protein (CRP) Fibrinogen Protein C Others Troponin I Adipokines Chronic kidney disease Air pollution & ionizing radiation Medications Coronary artery calcification and carotid artery wall thickness atherosclerosis pathophysiology -Inflammatory response -Injury to endothelial lining -LDL penetrates vessel wall -inflammation/macrophage adhesion -cytokines released -release enzymes & oxygen radicals that oxidize LDL -foam cells occur that form fatty streak -collagen deposits & makes firm plaque CKD patho - lab values azotemia - increased serum urea, serum creatinine, & other nitrogenous compounds Uremia Proteinuria urine sediment elevated potassium elevated creatinine clearance anemia elevated potassium GFR < 15 mL/min = dialysis colon cancer risk factors -obesity -ETOH -Family hx -polyposis -UC -Diet: high fat, high red meat, low fruits, low fiber -Smoking Colon cancer screening Begin at 50 FOBT (fecal occult blood test) Colonoscopy q 10y -monitoring for recurrence using eval of serum levels of tumor marker carcinoembryonic antigen (CEA) colorectal cancer manifestations gradual onset of changes in bowel movements, melena or hematochezia, weight loss, abdominal pain, and bowel obstruction. decorticate posturing characterized by upper extremities flexed at the elbows and held closely to the body and lower extremities that are externally rotated and extended. occurs when the brainstem is not inhibited by the motor function of the cerebral cortex. esophageal varices swollen, twisted veins in the esophagus that are especially susceptible to ulceration and hemorrhage hematemesis with resultant severe blood loss, hypotension, and even death. risk factors for esophageal varices Elevated pressure in the portal vein is a risk factor for bleeding EVs. Red color signs are elevated red areas that are important for predicting the risk of variceal bleeding, and red wale markings, dilated venules oriented longitudinally on the mucosal surface, have been considered to be the sign with the highest risk Constipation, vomiting, severe coughing, and excessive consumption of alcohol may precipitate rupture of EVs. Scombroid fish poisoning Toxicity due to ingestion of contaminated fish in which bacterial substances convert compounds in fish tissue to histamine, more correctly called histamine fish poisoning because affected fish can come from families other than Scombroidei. Scombroid poisoning MOA: Bacterial histidine decarboxylase converts histidine to histamine (which is not degraded by cooking) AE: Acute-onset burning sensation of the mouth, flushing of the face, erythema, urticaria, pruritus, headache; may cause anaphylaxis-like presentation Misc: Caused by consumption of dark-meat fish improperly stored at warm temperature; frequently misdiagnosed as allergy to fish; treat supportively with antihistamines foodborne illness symptoms Inflammation of the gastrointestinal tract lining (gastroenteritis) Nausea Abdominal cramps Diarrhea Vomiting glomerulonephritis symptoms Two major symptoms distinctive of more severe glomerulonephritis are (1) hematuria with red blood cell casts and (2) proteinuria exceeding 3 g/day to 5 g/day with albumin (macroalbuminuria) as the major protein other s/s Proteinuria Flank or back pain Hematuria Hyperlipidemia Decreased urine output Edema General signs of inflammation: malaise, fatigue, headache, anorexia, and nausea Blood pressure increase Acute poststreptococcal glomerulonephritis Cloudy tea colored urine Decreased output Irritability Ill appearance Lethargy Anorexia Discomfort-headache, ab pain, dysuria Periorbital edema Facial edema in morning Ab edema in evening Mild to severe hypertension