What we need to know for Patho Exam 3 + Practice Test PDF

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Intrarenal Disorders (12) ● Azotemia – abnormal elevation of nitrogenous waste ● Anasarca – generalized edema in patients with hypoalbuminemia - seen in patients with nephrotic syndrome ● Uremia – syndrome that involves elevation of nitrogenous wastes, fatigue, anorexia, nausea, vomiting ● Osmolality – concentration of a solution in terms of solutes to solvents ● GFR – glomerular filtration rate – volume of filtrate entering Bowman’s capsule per unit of time. In adult, it is 135 mL/min. ● Renin – hormone released by the kidney that responds to a decrease in BP ● Erythropoietin – secreted by kidney, stimulates bone marrow to produce RBC in response to tissue hypoxia. ● Glomerulonephritis - This is an inflammatory problem whereas pyelonephritis is an infectious problem (pye is infectious!) ● Pathology of acute glomerulonephritis: ○ Increase in membrane permeability because of inflammation (or the swelling)– leads to proteinuria and hematuria ○ Decrease in GFR leads to increase in serum creatinine, azotemia, oliguria, edema ● Glomerulonephritis clinical manifestations in kids: ○ Kids the presenting clinical manifestations is smoky or cocoa colored urine (hematuria) ● Nephrotic syndrome pathophysiology ○ Loss of large amounts of proteins in urine ○ Proteinuria leads to hypoalbuminemia and generalized edema as a result of decreased colloid osmotic pressure ● Why would someone with kidney disease have a low hematocrit level ○ He does not have enough erythropoietin ○ Also hyperkalemic ■ Lose sodium, retain potassium ● During acute tubular necrosis, what could happen to the specific gravity of urine? ○ Sometimes 1 which is the specific gravity of water ○ Not being able to concentrate anything ● Patients with kidney disease are also anemic because they are not making enough erythropoietin ● Know the difference between nephrotic and uremic syndrome ○ Slide 85 Alterations in GU (14 questions) ● Stress incontinence

○ Due to weakening of pelvic muscles ● Urge incontinence ○ Due to overactive detrusor muscle ● Know all the different types of incontinence ● Enuresis

○ ● Powerpoint in red of what you have to know ● Etiology, pathophysiology, and clinical manifestations of BPH ● Know the abnormal uterine bleeding patterns ○ Metorrhagia ○ Hypomenorrhea ○ Oligomenorrhea ○ Polymenorrhea ○ Menorrhagia ○ Dysfunctional uterine bleeding ○ Dysmenorrhea ■ Know etiology and pathophysiology ● Ovarian cancer ○ Most common of all these types of cancers ○ Cancer of AGING where the other two previously were of younger women ○ Usually asymptomatic so carries a high mortality rate ● Fibrocystic breast disease versus breast cancer ○ Disease: tender, mobile, firm, regular in shape ○ Breast cancer: painless, hard, and fixed ● Clinical manifestations of breast cancer ○ Painless, hard, poorly moveable lump ○ •Dimpling of the skin ○ •Nipple retraction ○ •Changes in breast contour ○ •Bloody discharge from nipple ● Organisms of certain diseases ○ Syphilis ○ Nongonococcal urethritis ○ Gonococcal ○ Bacterial prostatitis ○ Vulvovaginitis ○ HPV af

○ Cystitis ○ Yeast vaginitis ○ Epididymitis Alterations in GI (16 questions) ● Types of dysphagia - know the difference between them ○ Type 1 ■ Problems in delivery of food/fluid into esophagus ■ Causes ● R/T neuromuscular incoordination/disorders – USUALLY A PATIENT WITH A STROKE ● Normal sequence is altered or absent ■ –Clinical manifestations ● May cough and expel the ingested food/fluids ● Aspirate when attempting to swallow ● Worse with liquids than solids ○ Type 2 ■ Problems in transport of bolus down esophagus (toward the LES, in the middle) ■ Causes ● Outpouchings of one or more layers (diverticula) ● Disorder of smooth muscle function (achalasia) ● Structural interference of esophageal peristaltic activity (neoplasms, strictures) ● Abnormal peristaltic activity ■ –Clinical manifestations ● Sensation food is “stuck” behind sternum ● Initially with solid food, may progress to liquids ○ Type 3 ■ Problems in bolus entry into stomach ■ Causes ● Lower esophageal dysfunction or lesion obstruction ■ Clinical manifestations ● Tightness or pain in substernal area during swallowing process – they talk about their heart burn right below the sternum ● Vomiting ○ •Associated with alterations in integrity of the GI tract wall (what has happened to the lining of the GI tract) or alterations in motility of the GI tract – food stays there because peristalsis stops ● Complication of constipation

○ Fecal impaction ○ Seen a lot in elderly ● Stomatitis ○ Common cause: candida albicans ○ Breast feeding infants and people on chemotherapy - open sores ● GERD ○ •Backflow of highly acidic gastric contents through the LES----inflammation caused by reflux of highly acidic material. ○ Persistence may result in esophagitis ○ Progression can lead to barrett esophagus ○ An etiology: Gastroparesis---delayed emptying of something due to decreased peristalsis. Food sits there. More irritation. Can lead to stomach contents spilling back up into esophagus ○ Pathophysiology: an imbalance between defensive factors protecting the esophagus and aggressive factors from the stomach contents. Mr. Sander is 67 years old with a long history of knee osteoarthritis for which he selfmedicates regularly with over-the-counter (OTC) naproxen. He is in the clinic today complaining of a swallowing difficulty that has progressively worsened over the past several months.. He denies significant past medical history. A review of systems is negative except for arthritic symptoms and swallowing difficulty. He denies noticing blood in his stool or vomiting blood. He denies history of gastroesophageal reflux disease (GERD) or ulcer. He does not drink alcohol, although he drank heavily many years ago. He does not smoke. The dysphagia is described as “food gets stuck in my throat and I can't get it down.” The feeling occurs only after he has ingested solid food; liquids are not a problem. There is burning chest pain associated with meals. ■ Dysphagia ■ Burning chest pain GERD ● H. pylori is usually a factor of gastritis ● Peptic ulcer disease ○ Upper GI tract ○ Ulcers located in esophagus, stomach, or duodenum ○ Most are associated with NSAID use or H pylori infection ○ Gastric peptic ulcer disease ■ Due to breakdown of protective mucous layer that normally prevents diffusion of acids into gastric epithelia due to chronic irritations---Aspirin , NSAIDs, alcohol, and bile acids ■ has no correlation to food intake. Food does not take away the pain ○ Duodenal peptic ulcer disease ■ Inappropriate excess secretion of acid that spills through the pylorus into the duodenum ■ eating makes the pain go away. Taking a lot of antacids. Eating small frequent meals. ● Crohn’s disease (know the difference between this and ulcerative colitis) ○ Affects proximal portion of the colon or terminal ileum ○ Inflammation of ALL layers - full thickness of bowel wall ○ Cobblestone or skip lesions

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○ Inflammatory lesions can occur anywhere from mouth to anus ○ Weight loss or malnutrition ○ Get melena ■ Black tarry stools because of breakdown of RBCs Ulcerative colitis ○ Chronic inflammatory disease of the mucosa of rectum and colon (not whole GI tract) - affects inner lining only ○ Large ulcers found in the mucosal layer of colon and rectum (not ALL layers) ○ Bloody diarrhea and lower abdominal pain ○ No skip lesions ○ Associated with increased cancer risk Pseudomembranous enterocolitis ○ C dif Diverticulosis ○ Lower left sided abdominal pain Appendicitis ○ Right sided pain IBS ○ No identifiable pathology Intestinal obstruction ○ •Classified as mechanical caused by condition that decrease the patency of the bowel---adhesions, hernia, tumors, volvulus, intussusception or functional caused by neurogenic or muscular impairment that hinders peristalsis – opioids ○ 1.Mechanical obstructions: increased bowel sounds initially, accompanied by abdominal pain, nausea, and vomiting ○ 2.Functional obstructions: absence of bowel sounds Intussusception ○ Most often in infants as they start to walk ○ More often in males than females ○ Small intestine goes into large intestine Volvulus ○ Tight twisting of bowel causing intestinal obstruction and blood vessel compression Celiac disease ○ •Familial intolerance to gluten. ○ •Malabsorption due to immunologic response in genetically susceptible people or an intramucosal enzyme defect. ○ •Leads to inflammation and atrophy of intestine with severe malnutrition. Dumping syndrome ○ Dump stomach contents into small intestine ○ •Elevated blood glucose levels---rapid absorption of large amount of glucose leads to an excessive rise in plasma insulin and rebound hypoglycemia (jitteriness, fainting, etc) Barrett esophagus is a risk factor for esophageal cancer H. pylori infection is a risk factor for gastric carcinomas Colon cancer clinical manifestations ○ –Right side: black, tarry stools (melena) (ascending, transverse) ○ –Left side (descending colon, cecum, rectum : intermittent abdominal cramping and fullness; “ribbon” or pencil-shaped stools; blood or mucus in stool ○ –Rectum: change in bowel habits; urgent need to defecate on awakening; alternating constipation and diarrhea; sensation of rectal fullness; dull ache in rectum/sacral region Cholecystitis clinical manifestations

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○ •Colicky pain that radiates to the subscapular area and back---steadily increases for minutes and lasts several hours. – referred type of pain ○ Clay colored stools L.B. is a 45-year-old woman with three children ages 4, 6, and 10 years. She works long hours as an instructor at a local college to support her three children and husband, who is chronically unemployed. She has had a 6-month history of severe bouts of abdominal pain associated with indigestion, gas, and steatorrhea. Fatty foods seem to exacerbate the symptoms. L.B. is about 40 pounds overweight. An ultrasound of L.B.'s abdomen revealed multiple stones in her gallbladder. She was scheduled for a cholecystectomy. Pancreatitis patients put on NPO, pain in back Cause and effect of manifestations of liver dysfunction ○ •Impaired protein synthesis ■ Bleeding (clotting factor deficiency) ■ Edema (hypoproteinemia) ■ Immune deficiency (substrate for antibody) ○ •Accumulation of toxins and hormones ■ Feminization (excess estrogens) ■ Poor metabolism of drugs ■ Spider nevi (estrogen) ○ •Inadequate bile synthesis ■ Increased bilirubin level ■ Jaundice ○ •Inadequate urea synthesis ■ Increased blood ammonia level (NH3) ■ Hepatic encephalopathy ○ •Release of marker enzymes into blood ■ AST (SGOT) ■ ALT (SGPT) How do you get jaundice ○ LIVER CAN NOT BIND OR CONJUGATE THE BILLIRUBIN TO EXCRETE IT Hepatic encephalopathy ○ Damage to the brain tissue, which occurs as a complication of cirrhosis of the liver due to much ammonia in brain tissue. ■ Asterixis liver flap is a classic sign Esophageal varices ○ •Increased pressure in portal veins causes development of collateral vessels to develop between the portal veins and systemic veins and then carried to the esophagus, stomach, rectum. For appendicitis, white blood cells would be elevated People who have had lots of C sections or lots of abdominal surgeries would be more prone to developing adhesions later in life

Diabetes (10 questions including diabetes mellitus) ● Question on metabolic syndrome ● Type 1 ○ Etiology: autoimmune pathology ○ Patho: destruction of B cells ○ Clinical manifestations: ■ Polyuria

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● Glucose spills into the urine causing osmotic diuresis which leads to excessive amounts of urine ■ Polydipsia ● Loss of fluids leads to excessive thirst ■ Polyphagia ● Breakdown of nutritional stores leads to excessive hunger ■ Weight loss ■ Glycosuria ■ Ketoacidosis ○ Prone to developing ketoacidosis ■ Blood glucose above 400 Type 2 ○ Etiology: unknown but obesity is a huge risk factor ○ Patho: Tissue resistance to insulin with high insulin secretion is at the root of disorder ○ Clinical manifestations ■ Polyuria ■ Polydipsia ■ Blurred vision ■ Weight gain ○ Prone to developing nonketotic hyperglycemic hyperosmolar coma Protein in urine is earliest precipitating factor of diabetic nephropathy Glycemic control improves nerve function Clinical manifestations of hypoglycemia ○ cold sweats ○ headache ○ trembling ○ pounding heart ○ sleepiness ○ personality change ○ Hunger Clinical manifestations of hyperglycemia ○ increased thirst and urination ○ ketones in urine ○ aching, weak ○ heavy breathing ○ nausea, vomiting ○ Fatigue Types of fractures ○ Greenstick fracture ■ Incomplete break ○ Comminuted fracture ■ More than one fracture line and more than two bone fragments ○ Impacted fracture

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■ Caused by excessive force that drives one fragment into another Avulsion fracture ■ Separation of small fragments of bone at site of attachment of a ligament or tendon Nondisplaced fracture ■ Fragments remain aligned and in position Open or compound ■ When skin has been penetrated Closed or simple ■ When skin has not been broken

● In the healing process, callus formation leads to new bone formation at the edges of the periosteum ○ Callus formation would tell you if you have broken a bone as a little kid ● Compartment syndrome ○ Complication of frature ○ 6 P’s of arterial insufficiency ● Dislocation versus subluxation ○ Dislocation is complete separation of a joint articulating surfaces ○ Subluxation is a partial separation ● Strain versus sprain ○ Strain is a tear in tendon ○ Sprain is a tear in ligament ● Scoliosis ○ Lateral curvature of spine resulting in a C or S shaped spinal column with vertebral column ● Osteoporosis ○ •The most common metabolic disease that occurs when the rate of bone resorption is greater than that of bone formation

● Pathophysiology of osteoporosis ○ Rate of Bone absorption is greater than bone formation ● Possibly myasthenia gravis?? ○ Chronic autoimmune disease ○ Pathophysiology ■ Defect in nerve impulse transmission at NM junction ■ Destruction of acetylcholine receptor sites so nerve impulse cannot move on ○ Ptosis ● Fibromyalgia ○ Diagnosis of exclusion ● Infections of bone can happen in different ways (osteomyelitis) ○ •May occur due to burns, sinus disease, trauma, malignant tumor necrosis, periodontal infection or an infected pressure ulcer (if it isn’t due to compound fracture) ○ •Direct infection can occur due to open fracture, penetrating wounds, surgical contamination, or insertion of prostheses, metal plates, or screws

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○ Staph aureus is most common pathogen Ligaments ○ Connect bone to bone Possibly?? Ligament injuries normally during physical activity Tendinitis possibly? ○ Inflammation of tendon ○ Repetitive motion Osteoarthritis versus rheumatoid arthritis ○ Osteoarthritis ■ Local degenerative joint disorder associated with aging and wear and tear from repetitive stress ■ Noninflammatory ■ Characterized by loss of articular cartilage, wear of underlying bone, and the formation of bone spurs ■ Nodules ■ Progressive noninflammatory disease of weight bearing joints ○ Rheumatoid arthritis ■ Systemic ■ Inflammatory ■ First exacerbation is normally in childhood ■ •Joint destruction is inflammatory and involves synovial membranes, cartilage, joint capsule, and surrounding ligaments and tendons. (in OA, it was just the joint and the loss of cartilage)

■ •May be related to infectious processes, or have an autoimmune or genetic etiology. ■ May run in families Etiology of gouty arthritis ● Lack of enzyme uricase - lack of ability to oxidize uric acid

Practice Test ● Abnormal elevation of nitrogenous waste? ● Generalized edema in patients with hypoalbuminemia ● Syndrome that involves elevation of nitrogenous wastes, fatigue, anorexia, nausea, vomiting ● Concentration of a solution in terms of solutes to solvents ● Volume of filtrate entering Bowman’s capsule per unit of time. In adult, it is 135 mL/min. ● Hormone released by the kidney that responds to a decrease in BP ● Secreted by kidney, stimulates bone marrow to produce RBC in response to tissue hypoxia. ● This is an inflammatory problem whereas pyelonephritis is an infectious problem ● Pathology of acute glomerulonephritis? ● Glomerulonephritis clinical manifestations in kids? ● Nephrotic syndrome pathophysiology ● Why would someone with kidney disease have a low hematocrit level ● During acute tubular necrosis, what could happen to the specific gravity of urine? ● Why are patients with kidney disease also anemic? ● Which incontinence is due to weakening of pelvic muscles ● Which incontinence is due to overactive detrusor muscle ● What is nephroblastoma ● Occurs when urine is involuntarily lost with increases in intra-abdominal pressure ● Involuntary sudden leakage of urine along with or immediately following the sensation of a need to urinate (urgency) ● urgency is associated with increased daytime frequency and nocturia though not necessarily with incontinence ● due to a combination of stress and urge incontinence – MOST COMMON ● broad classification of voiding dysfunction in which the specific cause is a pathology that produces a disruption of nervous communication governing micturition. – anything neuro, MS, spinal cord injury – impulse to void is not communicated to CNS

● bladder becomes so full that it leaks urine, or “overflows”---causes include obstruction of the urethra and underactive/inactive detrusor muscle ● related to physical or environmental limitations resulting in an inability to access a toilet in time ● What is enuresis ● Etiology of BPH ● Pathophysiology of BPH ● Clinical manifestations of BPH ● Metorrhagia ● Hypomenorrhea ● Oligomenorrhea ● Polymenorrhea ● Menorrhagia ● Dysfunctional uterine bleeding ● Dysmenorrhea ○ Etiology? ○ Pathophysiology? ● Ovarian cancer - cancer of ________? Mortality rate? ● Fibrocystic breast disease masses versus breast cancer ● Clinical manifestations of breast cancer ● Organisms of certain diseases ○ Syphilis ○ Nongonococcal urethritis ○ Gonococcal ○ Bacterial prostatitis ○ Vulvovaginitis ○ HPV ○ Cystitis ○ Yeast vaginitis ○ Epididymitis ● Type 1 dysphagia ○ What is it ○ Cause ○ Clinical manifestations ● Type 2 dysphagia ○ What is it ○ Cause ○ Clinical manifestations ● Type 3 dysphagia ○ What is it ○ Cause

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○ Clinical manifestations Vomiting Complication of constipation; seen a lot in who? Stomatitis - common cause? Seen a lot in who? GERD ○ What is it ○ Persistence may result in? ○ Progression can lead to? ○ Etiology ○ Pathophysiology ○ Mr. Sander is 67 years old with a long history of knee osteoarthritis for which he self-medicates regularly with over-the-counter (OTC) naproxen. He is in the clinic today complaining of a swallowing difficulty that has progressively worsened over the past several months.. He denies significant past medical history. A review of systems is negative except for arthritic symptoms and swallowing difficulty. He denies noticing blood in his stool or vomiting blood. He denies history of gastroesophageal reflux disease (GERD) or ulcer. He does not drink alcohol, although he drank heavily many years ago. He does not smoke. The dysphagia is described as “food gets stuck in my throat and I can't get it down.” The feeling occurs only after he has ingested solid food; liquids are not a problem. There is burning chest pain associated with meals.

● __________ is usually a factor of gastritis ● Peptic ulcer disease ○ Where? ○ Ulcers located where? ○ Most are associated with ______ use or _____ infection ○ Gastric peptic ulcer disease is due to? ○ Duodenal peptic ulcer disease is due to? ○ For which of these peptic ulcer diseases does eating relieve the pain? ● Crohn’s disease ○ Where does this affect ○ Inflammation of how many layers of the bowel wall? ○ Clinical manifestations ● Ulcerative colitis ○ What is it ○ What part of the bowel does it affect ○ Clinical manifestations ● What organism is associated with Pseudomembranous enterocolitis ● Where is the pain in di...