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Patho Exam 2 Study Guide
Week 4
Chapter 9: Gastrointestinal Function Dysphagia o Pathogenesis: o Difficulty swallowing o Etiology: o Mechanical obstruction (stenosis/stricture, diverticula, tumors) o Neurological disorders (stroke, TBI, Parkinson’s, Alzheimer’s, CP, Huntington’s, Guillain- Barre, ALS) o Iatrogenic (head/neck surgeries, intubation, radiation) o Medications that relax muscles/suppress nervous system o Clinical Manifestations: o Sensation of stuck food, choking, coughing, delayed/painful swallowing, RISK FOR ASPIRATION o Diagnostics: H&P. barium swallow, chest/neck x-ray, FEEST, VFSS, EGD o Treatment Implications: o Underlying cause, speech therapy o Maintain nutrition, prevent aspiration (sitting up while eating, thickening foods/liquids) Vomiting/emesis o Pathogenesis: o Medulla (vomiting center) stimulated and coordinates reflex response through cranial nerves o Glottis closes, soft palate rises to close airway o Deep inspiration, diaphragm contracts o Gastroesophageal sphincter and fundus of stomach relax o Abdominal muscles contract forcefully o Anti-peristaltic waves o Etiology: o Protective (drug/ETOH overdose, infection), obstructions, pain associated w/ other pathogens o Clinical Manifestations: o Nausea/retching o Color/quality: hematemesis, yellow/green, deep brown, undigested, force? o Diagnosis: H&P, labs, ABGs, causative agent o Treatment: o Treat underlying cause o Fluid/electrolyte/acid-base balance, IV fluids, antiemetics
Hiatal Hernia o Pathogenesis: o Weakened diaphragm allows stomach to protrude through opening o Inflammation of esophagus o Etiology: o Increased intrathoracic pressure (vomiting, straining w/ BM) o Increased intraabdominal pressure (pregnancy, obesity) o Clinical Manifestations: o Indigestion, heartburn (pyrosis), belching, nausea, chest pain, strictures, dysphagia o WORSE after meals, when sitting/lying o Diagnosis: H&P, barium swallowing, x-ray, manometry, EDG o Treatment Implications: o Strategies to reduce regurgitation (small meals, positioning), lose weight, don’t smoke, stress management, meds, surgery if severe Gastroesophageal Reflux Disease (GERD) o Pathogenesis: o Incompetent LES (decreased LES pressure of increased stomach pressure) allows gastric content to flow into and irritate esophagus o Etiology: o Food (chocolate, ETOH, nicotine, caffeine, citrus, spicy/fatty foods, peppermint), pregnancy/obesity, medications, NG tube, delayed gastric emptying o Clinical Manifestations o Varies- heartburn, epigastric pain, dysphagia, nausea, dry cough, regurgitation, sensation of lump in throat o Can lead to bigger problems: strictures, ulcerations, esophageal cancer, asthma o Diagnosis: H&P, barium swallow, EGD, esophageal pH monitoring, manometry o Treatment Implications: o Avoid triggers!!! Address modifiable risk factors o Medications for symptoms, surgery if severe Gastritis/Gastroenteritis o Pathogenesis: o Inflammation of mucosal lining in stomach o Acute or chronic o Erosive or non-erosive o Etiology: o H. pylori or allergic reaction, NSAIDs, ETOH, stress, genetic, other autoimmune disorders o Gastroenteritis: inflammation in stomach and intestines caused by infection/ a reaction o Clinical Manifestations: o Indigestion, heartburn, abdominal cramping, n/v, anorexia, fever, malaise
Type Acute Chronic Fulminant Pathogenesis Inflammation of liver leading to degeneration of necrosis of liver cells Inflammation of liver > 6months Inflammation of liver Etiology Viral (contagious) Advancing age, ETOH, medication Liver failure and hepatic encephalopathy Clinical Manifestations Four Stages:
1. Asymptomatic s/s vary by degree of damage Can lead to death w/in 2 **weeks of onset
- Prodromal: 2 weeks** post-exposure, nausea, vomiting, malaise, anorexia, low-grade fever, headache Muscle/joint pain, rash, angioedema, cirrhosis, pancreatitis, myocarditis, aplastic anemia, or **peripheral neuropathy
- Icteric: 1-2 weeks post-** exposure; 6 weeks: jaundice, dark tea- colored urine, clay stools, hepatomegaly, **RUQ pain
- Recovery: resolution 6-** weeks Diagnostics: H&P, serum hepatitis profile, LFTs, clotting studies, liver biopsy, ultrasound Treatment Implications Preventative (vaccines), interferon injections (some types), antivirals, rest, adequate nutrition (high carb, protein, and vitamin), increase hydration, paracentesis, liver transplant Hepatitis (A, B, C only)
Cirrhosis (make sure to review the complications associated with liver problems) o Pathogenesis: o Destruction of functional liver cells that leads to fibrosis, nodule formation, impaired blood flow and bile obstruction o Etiology: o HEPATITIS, infections, ETOH, medications and autoimmune disease o Clinical Manifestations: o Portal hypertension, esophageal varices/bleeding, ascites, changes in protein and glucose metabolism, jaundice/clay-colored stools, pruritis, buildup of toxins (ammonia- confusion), increased protein= encephalopathy, peritonitis o Diagnostics: H&P, liver biopsy, x-ray, ultrasound, MRI, CBC, liver panel, EGD, clotting studies, occult stool, endoscopy o Treatment Implications: o Complex, based on underlying cause, AVOID hepatoxic meds/ETOH, treat nutritional imbalance, shunt for portal hypertension, fluid restriction, low sodium diet, diuretics, paracentesis, treat varices, lactulose for ammonia, ABX, liver transplant Pancreatitis o Pathogenesis: o Pancreatic enzymes leak into pancreatic tissue and initiate autodigestion. Tissue and cell membranes are broken down leading to edema, vascular damage, hemorrhage, and necrosis. Tissue is replaced by fibrosis causing endocrine/exocrine problems o Can be chronic or acute (acute is medical emergency) o Etiology: o Cholelithiasis, EROH abuse, biliary dysfunction, hepatoxic drugs, metabolic disorders, trauma, renal failure, endocrine disorders, pancreatic tumors, penetrating peptic ulcers o Clinical Manifestations: o Complications: ARDS, DM, infection, shock, DIC, renal failure, malnutrition, pancreatic cancer, pseudocyst o Acute: upper abdominal pain radiating to back, n/v, mild jaundice, low grade fever, BP/pulse changes o Chronic: upper abdominal pain, indigestion, losing weight w/o trying, steatorrhea, constipation, flatulence o Diagnostics: H&P, serum amylase/lipase, CBC, liver enzymes, bilirubin, ABGs, stool analysis, x-ray, CT, MRI, ultrasound, ERCP o Treatment Implications: o Watch for complications, GI rest (NG tube to suction), TPN, slowly advancing diet, enzyme replacement, medications, insulin, hydration Diarrhea
o Abdominal distention, abdominal cramping colic, n/v, constipation, diarrhea, borborygmi, intestinal rushes, decreased/absent bowel sounds, restlessness, diaphoresis, tachycardia, weakness, confusion, shock o Diagnosis: H&P, blood chemistry, ABGs, CBC, CT, x-ray, ultrasound, barium edema, sigmoidoscopy, and colonoscopy o Treatment implications: o Correct fluid/electrolyte/acid-base imbalance, decompress the bowel (NG tube to suction), NPO, TPN, encourage ambulation, surgery (NO LAXATIVES) Paralytic ileus o Pathogenesis: o Lack of peristalsis o Etiology: o Neurologic impairment, abdominal surgeries, chemical/electrolyte/mineral disturbances, abdominal infections, decreased abdominal blood flow, medications o Clinical Manifestations: o Same as mechanical obstruction o Treatment Implications: o Same as mechanical obstruction Appendicitis o Pathogenesis: o Inflammation of variform appendix. Edema obstructs small organ causing fluid buildup and microorganism proliferation. Purulent exudate fills and stretches walls of appendix leading to ischemia and necrosis. Toxins and bacteria leak out to surround tissue. Pressure may build to rupture/perforation (in hours!) o Etiology: o Infection, IBD, constipation o Clinical Manifestations: o Pain around umbilicus that might migrate to LRQ (McBurry point) and intensifies, guarding, n/v, distention, bowel pattern changes o Pain may temporarily subside if ruptured o Diagnostics: H&P, CBC, ultrasounds, x-ray, CT, laparoscopy o Treatment implications: o Surgery, ABX, analgesics, and increasing intraabdominal pressure Peritonitis o Pathogenesis: o Inflammation of the peritoneum increases intestinal wall permeability and allows enteric bacteria in o Progression slowed by abscess formation, thick/sticky exudate, slowed peristalsis o Etiology: o Chemical irritants, direct organism invasion
o Clinical Manifestations: o Rigid, board-like abdomen, tenderness/pain, hypovolemic shock (hypotension, restlessness, diaphoresis), n/v, decreased peristalsis, fever, malaise, leukocytosis o Diagnosis: H&P, CBC, xray, CT, paracentesis w/ analysis, laparotomy o Treatment Implications: o Surgical repair of chemical leak, fluid/electrolyte imbalance, NG tube w/ suction, TPN Celiac Disease o Pathogenesis: o Defect in intestinal enzymes preventing digestion of gliadin leads to atrophy of intestinal villi w/ reduced surface area for absorption o Leads to many complications: anemia, arthralgia, myalgia, bone disease, dental abnormalities, cancers, hair loss, depression, hypoglycemia, vitamin/mineral deficiencies, endocrine disorders o Etiology: o Autoimmune response to environmental factor and genetic predisposition o Common in Caucasians and females o Clinical Manifestations: o Abdominal pain and distention, anorexia, constipation/diarrhea, change in appetite, lactose intolerance, n/v, steatorrhea, weight loss, s/s of vitamin deficiencies o Diagnosis: H&P, celiac blood panel, EGD, duodenal biopsy o Treatment implications: o Dietary management! ELIMINATE GLUTEN, supplements, medications, stress management, support groups Crohn’s o Pathogenesis: o T-cell activation leading to tissue damage with full thickness inflammation in patched of the GI tract o Ulcers can combine forming fissures divided by nodules (cobblestone appearance) o Intestinal wall thickens and narrows lumen o Absorption and motility decreased o Etiology: o Autoimmune, genetic o Clinical Manifestations: o RLQ pain and cramping, diarrhea, steatorrhea, constipation, palpable mass, melena, anorexia, mouth ulcers, weight loss, inflammatory indicators (fever, fatigue, arthralgia, malaise) o Diagnostics: H&P, stool analysis, CBC, blood chemistry, CRP, ESR, x-ray, MRI, barium (swallow and enema), sigmoidoscopy, colonoscopy, biopsy o Treatment Implications: o Nutritional support o Symptoms relief
Colorectal cancer o Pathogenesis: o Adenomatous polyps in large intestine o Etiology: o Diet- fat/calories/red meat/ETOH/ <fiber o Family hx, age, obesity, tobacco use, obesity o Men, African Americans o Clinical manifestations: o Lower abdominal pain/tenderness, blood in stool, diarrhea, constipation, intestinal obstruction, anemia, weight loss o Screening: occult blood test (annual), fecal immunochemical test (annual), flexibly sigmoidoscopy (5 years), colonoscopy (10 years) o Treatment Implications: o Removal of cells, chemo, radiation, colostomy o Ensure follow up screening Chapter 7: Urinary Function Incontinence (stress, urge, overflow, functional) o Pathogenesis: o Varies, based on type o Etiology: o Females, older age, overweight, smoking, other diseases o Clinical Manifestations: o Depends on type o Complications: skin problems, UTIs, psychological health o Diagnostics: H&P, bladder diary, urinalysis, UC, cystourethrogram, cystoscopy, pelvic ultrasound, postvoid residual measurement, urodynamic testing o Treatment Implications: o Bladder training, scheduled toileting, fluid/diet management, pelvic floor muscle exercises, electric stimulation, medications, urethral inserts, pessary, radiofrequency therapy, Botox, bulking material injections, sacral nerve stimulator, sling procedure, bladder neck suspension, absorbent pads, urinary catherization, increased perineal hygiene, acupuncture, safety measures, barrier crams, hypnotherapy, coping strategies o Stress Incontinence: o Weakened sphincter muscle leads to small amounts of urine loss w/ increased pressure (stress) o Ex. pregnant women o Urge Incontinence: o Sudden, intense urger to urinate, followed by involuntary loss of urine o Overflow Incontinence: o Cannot empty bladder completely (retention) o Dribbling urine and weak stream
o “Nurse’s bladder” o Functional Incontinence: o Physical or mental impairment prevents toileting in time Neurogenic bladder o Pathogenesis: o Disruption of innervation of the bladder nerve o Etiology: o Brain/spinal cord injury, nervous system tumors, dementia, Parkinson’s, Spina Bifida, DM, stroke, medications, vaginal childbirth, MS, ETOH abuse, SLE, Herpes Zoster o Clinical Manifestations: o Similar to overactive bladder- frequency and urgency, and underactive bladder (hesitancy and retention) o Diagnostics: H&P, bladder diary, urinalysis, UC, cystourethrogram, cystoscopy, pelvic ultrasound, postvoid residual measurement, urodynamic testing o Treatment Implications: o Depends on etiology, similar to incontinence Urinary Tract Infections o Pathogenesis: o Any infection beginning in urinary tract by direct invasion and growth of bacteria (bacteria love protein) o Most common in lower (bladder and urethra) o Etiology: o E. coli from GI, women have higher risk, immobility, incontinence, renal calculi, decreased cognition, pregnancy, impaired immune response, impaired nerve innervation, urinary catherization, improper personal hygiene, diaphragm or spermicide, unlubricated condoms o Clinical Manifestations: o Urgency, dysuria, frequency, hematuria, bacteriuria, cloudy-foul smelling urine, infection (fever, chills, fatigue) o Diagnostics: H&P, UA/UC, cystoscopy, cystourethrogram, CBC, ultrasound, x-ray, CT, MRI, of KUB o Treatment Implications: o Education: hydration, avoid irritants, stay hygienic, cotton underwear, loose fitting clothing, don’t delay urination, adequately empty the bladder (after intercourse), provide catheter care, probiotics o Medications/ABX Cystitis/Bladder Pain Syndrome o Pathogenesis: o Inflammation of the bladder o Etiology:
o Colicky flank pain/pressure, blood/foul/cloudy urine, dysuria, decreased urine output, frequency, urgency, n/v, abdominal distention, UTIs o Diagnosis: H&P, UA, ultrasound, CT, IV pyelogram, MRI o Treatment Implications: o Resolve underlying cause, facilitate urine flow Cancer renal cell carcinoma o Pathogenesis: o Primary tumor in renal tubule o Etiology: o Exact cause unknown, male, dialysis hx, family hx, age (50-70), other kidney diseases o Clinical Manifestations: o Asymptomatic (early), hematuria, abnormal urine color, palpable mass over kidney, anemia, weight loss, polycythemia, THN, fever, hypercalcemia o Diagnosis: H&P, ultrasound, BUN, creatinine, CBC, CT, UA, biopsy, PT, MRI, bone scan, x- ray, IV pyelogram, cystoscopy, renal arteriogram, biopsy, LF, CBC, blood chemistry o Treatment Implications: o Radiation, chemo, surgical removal, hormone therapy, immunotherapy Benign Prostatic Hyperplasia (BPH) o Pathogenesis: o Non-malignant enlargement of prostate gland due to increased proliferation of prostatic stromal cells or possibly lack of apoptosis leading to tissue growth o Obstructs urine flow as urethra is clamped o Bladder walls thicken and irritated w/ urine overflow, over contracts, loses ability to empty completely o Etiology: o Advancing age (over 50) o Clinical Manifestations: o Frequency, urgency, urinary retention, difficulty initiating stream, weak stream, dribbling urine, nocturia, bladder distention, overflow incontinence, ED o Diagnosis: H&P, urine flow measures, UA, PSA, rectal ultrasound, biopsy, cystoscopy, BUN, creatinine o Treatment Implications: o Relieve urinary obstruction (medications), laser therapy, TUNA, TURP, hyperthermia, HIFU, intraurethral stents, transurethral balloon dilation, partial/complete removal of prostate gland Polycystic Kidney Disease (PKD) o Pathogenesis: o Grape-like cysts enlarge size of kidneys and compress/replace kidney tissue
o Etiology: o Inherited o Clinical Manifestations: o Kids: potter facies, large, bilateral masses on flanks, respiratory distress, uremia o Adults: HTN, lumbar pain, increased abdominal girth, swollen/tender abdomen, enlarged palpable kidneys o Treatment Implications: o Control symptoms w/ meds (ABX, analgesics), hydration, low-salt, surgical draining of cysts, dialysis, kidney transplant) Glomerulonephritis o Pathogenesis: o Bilateral inflammation of glomeruli leads to inability of kidney to excrete wastes/fluids o Etiology: o Follows streptococcal infection, immunodeficiency, presence of chronic inflammatory conditions o Nephrotic and nephritic syndromes most prevalent Nephrotic Syndrome: o Pathogenesis: o Antibody-antigen complexes lodge in the glomerular membrane triggering complement system activation leading to collagen deposits/membrane thickening. Leads to increased glomerular capillary permeability and impaired glomerular filtration o Loss of protein leads to increased production of albumin, triglycerides, and cholesterol (increased risk of atherosclerosis) o Loss of protein decreases colloidal pressure = massive edema o Etiology: o Diseases that damage the kidneys (SLE, Hep B, DM), meds and infection o Clinical Manifestations: o Elevated proteins in urine, dark/cloudy urine, immunoglobulins secreted in urine o Edema, fatigue o Diagnostics: H&P, UA, blood chemistry, serum antibody levels, ESR, CT, renal biopsy o Treatment Implications: o Prompt treatment of infection, monitoring associated w/ chronic conditions Nephritic Syndrome: o Pathogenesis: o Antibody-antigen reaction leading to initiation of inflammatory response in the kidneys o RBCs lost in urine changes circulatory pressures (low GFR) and impaired renal function o Etiology:
o Diabetes mellitus, hypertension, urine obstructions, renal disease, ongoing exposure to toxins, sickle cell disease, SLE, smoking, aging 5 Stages/GFR o Stage 1: kidney damage present, GFR normal or high (>90) o Stage 2: GFR 60- o Stage 3: GFR 30- o Stage 4: GFR 15- o Stage 5: < 15 or dialysis initiated Dialysis/lifestyle modifications (diet) o Stops/slows progression (if possibly, control underlying cause) o Treat/prevent complications o Medications o Dialysis o hemodialysis
Week 5
Chapter 7: Urinary Function See above Chapter 8: Reproductive Function Epispadias o Pathogenesis/Etiology: o Exstrophy of bladder o Starts during 6 th^ week of fetal development o Clinical Manifestations: o Incontinence o Treatments: o Surgical repair (in stages) Hypospadias o Pathogenesis/Etiology: o Incomplete fusion of urethral folds o Urethral opening under the penis, or perineum o Starts during 8 th^ week of fetal development o Clinical Manifestations: o Dependent f location (range from poor aim to incontinence) o Curvature of penile shaft o Treatments:
o Surgical repair Amenorrhea o Pathogenesis/Etiology: o Absence or suppression of menstruation in women 16+ ▪ Primary- women who have not had menses ▪ Secondary- women who have had period > 6 months o Interruption of normal sequence of events causing endometrial tissues lining the uterus to proliferate and slough (dependent on progesterone, estrogen, FSH, LH) o Can be caused by anorexia nervosa, hypothyroidism, and adenomas and carcinomas o Clinical Manifestations: o Absence of menses o Treatments: o Correct the underlying cause Dysmenorrhea o Pathogenesis/Etiology: o Affects women of all ages (highschool- perimenopausal) o Primary: 1-2 years after menarche. Endometrium releases prostaglandins which cause contractions o Secondary: related to other disorders like endometriosis, leiomyoma, or pelvic adhesions- increases w/ age o Clinical Manifestations: o Primary: severe sharp pain in pelvic region and upper thighs, limits activity o Secondary: dull pain o Treatments: o Prostaglandin inhibitors (ibuprofen, naproxen) o Steroids (estrogen w/o progesterone) Uterine Prolapse o Pathogenesis/Etiology: Support structures of the uterus (uterosacral and cardinal ligaments) relax and if vaginal wall support is compromised abdominal organs push uterus down through vagina o Can occur at any age (congenital) or after childbirth (trauma to ligaments) o Three degrees- based on where uterus sits o Clinical Manifestations: o Depends on degree of severity ranging from sensation of bearing down (1st^ degree) to discomfort when walking, sitting (2nd^ degree) and friction/bleeding/ulceration from protruding uterus (3rd^ degree) o Treatments: o Hysterectomy o Pessary (supportive device to hold uterus in place)
o Treatments: o Treat the offending agent (antifungals or antibiotics) o Cool compress/sitz bath o Avoid drying soaps, non-absorptive underwear and tight clothing Pelvic Inflammatory Disease (PID) o Pathogenesis/Etiology: o Impairments in cervical mucosa allows bacteria to move from cervix/vagina into uterus (most often N. gonorrhea and C. trachomatis) o Can be r/t IUD insertion, pelvic surgery, abortion, infections, bloodstream or through the abdomen (ruptured appendix, diverticulitis) o Can lead to significant health problems (tubal scarring, infertility, ectopic pregnancy, chronic pelvic pain) o Clinical Manifestations: o Abdominal tenderness, pain of the cervix o Temp > 38 C/100.4 F, WBC > 10,000/mm o Abscess or mass may be palpable o Treatments: o ABX (early and aggressive treatment), oral or IV o Surgical draining o Total abdominal hysterectomy w/ bilateral salpingo-oophorectomy (removal of uterus, oviducts and ovaries) for rupture Chlamydia Nongonoccal Infection o Pathogenesis/Etiology: o Caused by Chlamydia trachomatis which targets and infects squamocolumnar epithelial cells o Can spread to oviducts and lead to pelvic inflammatory disease and infertility in women o Spreads from mom to infant during childbirth (ophthalmia neonatorum) o Clinical Manifestations: o Often asymptomatic- when present less severe than gonorrhea o Men- epididymitis (scrotal pain), urethritis (clear discharge from urethra) o Women- pelvic inflammatory disease (sterility), cervicitis, urethritis (dysuria, urinary frequency) o Diagnosis: urine test, nucleic-acid amplification tests o Treatments: o Antibiotic Lymphogranuloma Venereum (LGV) o Pathogenesis/Etiology: o Caused by Chlamydia trachomatis which invades mucosa during sexual contact o More common in tropical climates and MSM
o Clinical Manifestations: o Stage 1- painless lesions (slight) o Stage 2- inguinal lymph node swelling, fever, malaise o Stage 3- abscesses turn into fistulas o Treatments: o ABX (doxycycline) o Surgery (aspiration of lymph nodes, rectal strictures and fistulas) Gonorrhea o Pathogenesis/Etiology: o Gonorrhea is associated w/ the gram negative diplococcus Neisseria gonorrhaea o Contact w/ exudates from mucus membranes transmits the bacteria as it attaches and penetrates columnar epithelium and leads to a patchy inflammatory response in the submucosa o The lymphatic system extends infection in person causing localized infection, cysts, and formation of fibrous tissue leading to sterility in females o Newborns can be affected during birth causing severe eye disease o Clinical Manifestations: o Men- urethritis (most common), dysuria purulent urethral discharge, redness, swelling o Women- usually asymptomatic, but can affect endocervical canal can cause purulent vaginal discharge, dysuria, abnormal vaginal bleeding and pelvic inflammatory disease in women o Treatments: o Antibiotics o Many strains have become resistant to penicillin and tetracycline Syphilis (know difference between stages, tx) o Pathogenesis/Etiology o Systemic infection of the vascular system starting w/ inflammation and endothelial swelling, obliteration of terminal arterioles and small arteries o Caused by anaerobic spirochete Treponema pallidum getting in through mucus membranes or abraded skin during sexual contact o Includes 5 stages (incubation, primary, secondary, latency, and late) o Clinical Manifestations: o Primary phase- chancre at portal of entry o Secondary phase- spread through blood and lymph, low grade fever, malaise, sore throat, headache, lymphadenopathy, mucosal/cutaneous rash o Latent phase- asymptomatic, can last 40 years o Late phase- cause problems w/ cardiovascular system and aortic necrosis, damages central nervous system, causes blindness, paresis and mental deterioration o Treatments: o Benzathine penicillin G (given to people who test positive and those who have had contact w/ them)
