Exam 3 Study Guide PDF

Summary

This document is a medical study guide, likely for a course on human anatomy, that covers various topics related to diseases. It's a comprehensive overview of diseases including renal and GI ailments, and other medical conditions like diabetes, but it does not contain exam questions.

Full Transcript

***Renal*** ***Nephrolithiasis (kidney stones)\ **Stones along the urinary tract* ***Patho*** *Supersaturation of one or more salts;* *Precipitation of the salts from a liquid to solid state;* *temperature and pH changes;* *growth of stone through crystallization or aggregation* ***Etiology**...

***Renal*** ***Nephrolithiasis (kidney stones)\ **Stones along the urinary tract* ***Patho*** *Supersaturation of one or more salts;* *Precipitation of the salts from a liquid to solid state;* *temperature and pH changes;* *growth of stone through crystallization or aggregation* ***Etiology*** *Gender* *Age* *Geographic location* *Dehydration* *Diet* *Occupation* ***Clinical Manifestations*** *Pain in flank and abdomen* *Nausea* *Vomitting* *Cool, clammy skin* *Hematuria* ***Most common stones*** *Calcium* *Struvite* *Uric Acid* ***Acute cystitis\ **Inflammation of the bladder* ***Patho*** *exposure to pathogen;* *pathogen travels upward;* *causing inflammation* ***Etiology*** *Escherichia coli (Most Common)* *VUR* *Catheter indwelling* *Obstruction* ***Clinical Manifestations*** *Frequency* *Dysuria* *Urgency* *Lower abdominal and/or suprapubic pain* *Low back pain* *Elderly may experience confusion & lower abdominal pain* ***Pyelonephritis**\ Infection of the ureter, renal pelvis, and interstitial tissue* ***Patho*** *exposure to pathogen; Pathogen ascends from lower urinary tract or bloodstream; inflammatory process develops; WBC infiltration; inflammation of renal parenchyma* ***Etiology*** *Bladder infection* *Indwelling catheter* *Renal Stones* *VUR* ***Clinical Manifestations*** *Fever* *Flank pain* *Chills* *Dysuria* *WBC's in urine* *CVA tenderness* *Urgency* *Frequency* ***Glomerulonephritis\ **An autoimmune inflammatory process in the glomerulus* ***Patho*** *Glomerulus injured from antigen-antibody complexes; Precipitates inflammatory process; Inflammatory mediators damage basement membrane of glomerulus; Degenerative changes affect all renal tissue* ***Etiology*** *Immunologic ( most common)* *Drugs/toxins* *Vascular disorders* *Systemic disease* *Viral causes* ***Clinical Manifestations*** *H/A* *Malaise* *Weight gain* *HTN* *Facial edema* *Proteinuria* *Hematuria* *Oliguria* *dysuria* ***Acute Kidney Injury (AKI)**\ Characterized by rapid and progressive loss of renal function considered reversible* ***Patho*** *Initial phase: injury to kidney* *Oliguria phase: Decreased GFR; Decreased urine formation; Increase in serum creatinine and BUN* *Recovery phase: glomerular function returns; Urine output high but not concentrated (Diuresis); Healthy nephrons begin to compensate* ***Etiology*** *Pre-renal: impaired renal blood flow* *Intrarenal: acute tubular necrosis* *Post-renal: urinary duct obstruction* ***Clinical Manifestations*** *Oliguria* *Anuria* *FVE (edema)* *HTN* *Elevated creatinine/BUN* *Hyperkalemia* ***Chronic Kidney Disease (CKD)**\ Progressive and irreversible destruction of nephrons in both kidneys characterized by stages* ***Patho*** *renal injury; increased release of angiotensin II; increased glomerular capillary HTN; increase in glomerular permeability; proteinuria; tubulointerstitial injury; renal scarring* ***Etiology*** *Diabetes mellitus (Most common)* *Intrinsic kidney disease* *HTN* *Cystic kidney disease* *Atherosclerosis* *SLE* ***Clinical Manifestations*** *Oliguria* *Anuria* *Anemia* *Pruritus* *Uremic frost* *HTN* ***5 Stages*** *Normal (GFR \>90 mL/min)* *Mild (GFR 60-89 mL/min)* *Moderate (GFR 30-59 mL/min)* *Severe (GFR 15-29 mL/min)* *End stage (GFR less than 15)* ***GI*** ***Gastroesophageal Reflux Disease (GERD)**\ The reflux of chime from the stomach to the esophagus* *\ **Patho:*** *Weakened LES (lower esophageal sphincter)/ increased intra-abd pressure; Stomach contents reflux up into esophagus; Acidic juices irritate epithelium and erosion; repeat injury causes metaplasia of epithelial cells; Barrett's esophagus* ***Etiology*** *Older age* *Medications* *Nicotine* *obesity* *Hiatal hernia* ***Clinical Manifestations*** *Dysphagia* *Heartburn* *Epigastric pain* *Dry cough* *Water brash* *Laryngitis* *Asthma attacks* ***Peptic Ulcer Disease**\ A break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum* ***Patho*** *hypersecretion of HCL; erosion in the mucosal lining of stomach or duodenum; HCL diffuses into the stomach wall and blood vessels; parietal cells are damaged; Inflammatory response initiated* ***Etiology*** *H. Pylori* *NSAIDS* *Alcohol* *Increased stress* *Smoking* ***Clinical Manifestations*** *Gastric: pain during or immediately after eating* *Duodenal: pain 2-3 hours after eating* *Intense gnawing, burning* *Nausea* *Melenas* ***Ulcerative Colitis**\ (Sigmoid colon and rectum)\ Chronic inflammatory disease that causes ulcerations of the colonic* ***Patho*** *Inflammation at the base of the **crypts of Lieberkuhn;** leads to shallow ulcerations and bleeding; edema and thickening of muscle layer w/narrow bowel lumen; abscesses are **formed pseudo polyps**; necrosis* *Etiology* *Environmental factors* *Genetics* *Altered immune response to intestinal infection* ***Clinical Manifestations*** *Diarrhea* *Bloody stools* *Abdominal cramping* *Weakness* *Anemia* *Low grade fever* *Dehydration* *anorexia* ***Crohn Disease\ **(Terminal ileum and ascending right colon)\ Chronic, transmural inflammatory process; affects any part of the digestive tract from mouth to anus rectum rarely involved.* *Patho :Chronically inflamed intestinal wall; Increased tissue damage leads to formation of lesions and ulcers; skip lesions (reddish purple areas); fissures and fistulae* ***Etiology*** *Same as UC* ***Clinical Manifestations*** *Diarreha* *Abdominal pain* *Weightloss* *Fatigue* *Vit B12 anemia* ***Endocrine*** ***SIADH\ Syndrome of Inappropriate Antidiuretic Hormone**\ * *Excessive secretion of antidiuretic hormone (ADH) from the pituitary gland* ***Patho*** *excessive ADH secretion; fluid retention by kidneys; dilutional hyponatremia* ***Etiology*** *Head trauma* *Tumors* *Infection* *Stroke* *Emphysema* *Meningitis* ***Clinical Manifestations*** *Weight gain* *JVD* *Crackles* *Decreased urine output* *Edema* *Hyponatremia* *Hypoosmolality* *HTN* ***Diabetes insipidus**\ Disorder caused by antidiuretic hormone (ADH) insufficiency, results in excess fluid excretion* ***Patho*** *decreased ADH secretion or insensitive ADH receptor in kidney; nephron does not reabsorb water; body loses high amounts of water in the urine; dehydration and hypernatremia* ***Etiology*** *neurogenic: head surgery; brain tumors* *Nephrogenic: renal tubular defect; genetic; drugs* ***Clinical Manifestations*** *Polyuria* *Polydipsia* *Poor skin turgor* *Dry mucous membranes* *Hypotension* *FVD* *Hypernatremia* *Hyperosmolality* ***Hyperthyroidism (Thyrotoxicosis)**\ Increase secretion of thyroid hormone\ * ***Patho*** *body produces TSI or gland enlarges; elevated T3 and T4; negative feedback inhibition of pituitary TSH; low TSH more hormone secreted; high basal metabolic rate* ***Etiology*** *Graves disease: Autoimmune disorder/Type II hypersensitivity* *Autoimmune disorder/ type II hypersensitivity* *Toxic adenoma* *Toxic multinodular goiter* ***Clinical Manifestations*** *Nervousness* *Weight loss* *Hyperactive reflexes* *Diaphoresis* *Tachycardia* *Increased systolic* *BP* *Expothalmos* ***Hypothyroidism\ **Decrease in the secretion of thyroid hormone* ***Patho*** *loss of thyroid function; decreased production of thyroid hormone; increased production of TSH; slows basal metabolic rate* ***Etiology*** *Congenital thyroid defects* *Autoimmune: hashimoto disease* *Surgical removal* *thyroiditis* ***Clinical Manifestations*** *Fatigue* *Weight gain* *Constipation* *Delayed reflexes* *Feeling cold* *Sluggishness* ***Hyperparathyroidism**\ Increase in secretion of parathyroid hormone (PTH)* ***Patho*** *excess secretion of PTH; increased bone resorption and GI absorption of Ca2+; feedback system fails so Ca2+ continues to increase; elevated Ca2+* ***Etiology*** *Primary: adenoma; gland hyperplasia* *Secondary: chronic hypocalcemia* ***Clinical Manifestations*** *Deep bone pain* *Pathological fractures* *Renal damage* *Hypercalcemia* *Hypophosphatemia* *Kidney stones* *Cardiac dysrhythmias* ***Hypoparathyroidism**\ Decrease in secretion of parathyroid gland* *\ **Patho*** *destruction of gland; insufficient PTH secretion; decreased in Ca2+ levels; low Ca2+* ***Etiology*** *Damage or removal of parathyroid gland* ***Clinical Manifestations*** *Muscle cramps* *Irritability* *Tetany* *+Trousseau Sign* *+ Chvostek's Sign* ***Type 1 Diabetes Mellitus**\ Results from destruction of pancreatic beta cells which leads to NO production of insulin* ***Patho*** *activation of macrophages, T cytotoxic cells, and autoantibodies toward beta cells; destruction of beta cells with decreased insulin secretion* ***Etiology*** *Genetic* *Environmental* *Immunological* ***Clinical Manifestations*** *Polydipsia* *Polyuria* *Polyphagia* *Weight loss* *Fatigue* *Hyperglycemia* ***Type 2 Diabetes Mellitus**\ Results from a decrease in beta cell number or insulin resistance* ***Patho*** *Genetic: decreased activity of amylin; decreased beta cell mass and function; hypoinsulinemia; increased glucagon; high BS* *Obesity: decrease activity of ghrelin; insulin resistance; increased demand for insulin synthesis leads to hyperinsulinemia; high BS* ***Etiology*** *Exact unknown* ***Risk factors*** *obesity; genetics* ***Clinical Manifestations*** *Polyuria* *Polydipsia* *Polyphagia* *Fatigue* *Pruritus* *Recurrent infections* ***Acute Complications of\ Diabetes Mellitus*** ***Hypoglycemia*** *Abnormally low blood glucose* *More common inT1DM* *Too much or incorrectly timed insulin or exercise or not enough food* ***Diabetic ketoacidosis (DKA)*** *High blood glucose with serum ketones (metabolic acidosis)* *More common in T1DM* *Acute complication that develops quickly* *Precipitated by illness, stress, noncompliance with insulin administration* ***Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)*** *High blood glucose without serum ketones* *More common inT2DM* *Develops slower* *Precipitated by infection, MI, stroke, acute illness which stresses the already weak functioning beta cells* ***Chronic Complications of Diabetes Mellitus*** *Microvascular disease -- diseased capillaries (angiopathy)* *Diabetic retinopathy - blindness* *Diabetic nephropathy -- kidney failure* *Diabetic neuropathies -- nerve damage/loss of sensation* ***Cushing disease**\ Hypersecretion of glucocorticoids (cortisol)* ***Patho*** *loss of feedback control of ACTH secretion; constant secretion of ACTH; increase secretion of cortisol* ***Etiology*** *ACTH dependent: Pituitary adenoma; Ectopic secreting non pituitary tumor (small cell in lung* *Administration of exogenous steroids (syndrome)* ***Clinical Manifestations*** *Obese trunk* *Moon face* *Bufflo hump* *Hirsutism* *Ecchymotic areas* *Purple striae* *Hyperglycemia* ***Addison disease\ **Adrenocortical hypofunction* ***Patho*** *autoimmune destruction of adrenal cortical cells; adrenal atrophy; decreased cortisol causes increased ACTH; Inadequate corticosteroid and mineralocorticoid synthesis* ***Etiology*** *Autoimmune destruction of adrenal cortical cells* ***Clinical Manifestations*** *Bronze pigmentation* *GI disturbances* *Weakness* *Weight loss* *Postural hypotension* ***Pheochromocytoma\ **Tumor of the adrenal medulla resulting in excessive secretion of catecholamines* ***Patho*** *Excess stimulation of alpha & beta adrenergic receptors; Increased secretion of epinephrine and norepinephrine; Increased peripheral vascular resistance* ***Etiology*** *Catecholamine secreting tumor of the adrenal medulla* ***Clinical Manifestations*** *Hypertension* *Headache* *Tachycardia* *Palpitations* *Diaphoresis* ***Musculoskeletal*** ***Compartment Syndrome*** *Result of increased pressure within a muscle compartment* *Can be caused by any condition that disrupts the vascular supply to an extremity* *Muscle ischemia causes edema, rising compartment pressure, and tamponade that lead to muscle infarction and neural injury* ***"6 Ps" of compartment syndrome*** *Pain* *Paralysis* *Paresthesia* *Pallor* *Pulselessness* *Polar* ***Osteoporosis**\ A metabolic bone disease resulting in a reduction in density or mass of bone* ***Patho*** *decreased estrogen; increase in RANKL; bone resorption greater than bone deposition; alterations in bone microarchitecture; loss of bone mineralization; diminished bone mass and porous bone* ***Etiology*** *Primary: postmenopausal* *Secondary: other conditions* ***Clinical Manifestations*** *Decreased height* *Compression spinal fx* *Kyphosis* *Decreased bone mass measurements* *Pathologic fx* ***Osteomyelitis**\ infection of the bone* ***Patho*** *Entry of pathogen (most common Staphylococcus aureus); Pus accumulation in bone; Bone cells become ischemic; Sequestra forms (dead bone tissue); Involucrum: new bone formation; Allows sinus tracts to develop and spread disease* ***Etiology*** *Post-trauma* *Vascular insufficiency* *MVA* *Orthopedic hardware* *Puncture wound of foot* ***Clinical Manifestations*** *Bone pain* *Malaise* *HA (headache)* *Fever* *Edema* *Erythema over bone* *Brodie abscess* ***Osteoarthritis\ **A progressive destruction of cartilage in both synovial joints and vertebrae* ***Patho*** *Loss of articular cartilage; Inflammatory response; New bone formation of joint margins (bone spurs); Subchondral bone changes; Synovitis and thickening of joint capsule* ***Etiology*** *Risk Factors 2ndry: Age; obesity; injury; repetitive trauma* *Primary is idiopathic* ***Clinical Manifestations*** *Asymmetric joint pain increases w/activity* *Relieved by rest* *Heberden's Nodes (DIP)* *Bouchard\'s Nodes (PIP)* ***Rheumatoid Arthritis**\ A chronic, progressive, systemic, autoimmune disease with inflammation of joints and deformity\ **Patho*** *T lymph activation; RANKL Increases; Forms pannus; Destruction of cartilage and bone* *B lymph activation; Rheumatoid factor is formed and binds with IgG; Inflammatory response; Enzymes destroy collagen; Forms pannus; Destruction of cartilage and bone* ***Etiology*** *Unclear* *Higher in women* *autoimmune* ***Clinical Manifestations*** *Symmetrical pain in small joints* *Swelling* *Warmth* *Erythema* *Anorexia/fatigue* *Ulnar drift* *Swan neck deformity* *Boutonniere deformity* ***Gout**\ What is it?* ***Patho*** *Body unable to metabolize purine; Leads to Increased uric acid in blood; Uric acid crystals form; Deposit into joints; inflammatory response* ***Etiology*** *Familial* *diet* ***Clinical Manifestations*** *Sudden onset of asymmetric joint pain usually great toe* *Edema* *Warmth* *Erythema* *Elevated uric acid* *Fever*

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