Essentials of Pathophysiology – Exam #2

Essentials of Pathophysiology – Exam #2 Review Sheet Covers Modules 4, 5, and 6 – Chapters 7, 8, 9, 10 1. What is gastritis? What are causes? A. Inflammation of the stomach lining B. Causes: Precipitated by ingestion of irritating substances (Ex. Alcohol and aspirin, NSAIDs, viral, bacteria, & autoimmune)  2. Review the etiology (cause) and clinical manifestations (S&S) of GERD. What are complications of GERD if left untreated? Causes Increases abdominal pressure fatty foods caffeine large amounts of alcohol, cigarette smoking pregnancy Signs & Symptoms Heartburn (usually after eating) Chest pain Difficulty swallowing Regurgitation of food or sour liquid Sensation of a lump in your throat If left untreated it can cause cellular changes leading up to esophageal cancer (Barrett esophagus) and the individual can develop pulmonary symptoms (cough, asthma, and laryngitis: from reflux in breathing passages)            3. Review the etiology and clinical manifestations of peptic ulcer disease (PUD). w Cause No relation between diet and PUD Caused by NSAIDs, stress (glucocorticoids), smoking, genetics H. pylori Key role in promoting both gastric and duodenal ulcer formation Thrives in acidic conditions Slow rate of ulcer healing High rate of recurrence Clearance of H. pylori promotes ulcer healing w Clinical Manifestations (Signs & Symptoms) Epigastric burning pains Gastric Ulcers Duodenal ulcer and GI Bleeding  4. Review the etiology and clinical manifestations for pseudomembranous colitis. Acute inflammation and necrosis of large intestine Caused by Clostridium difficile (c-diff is kept in check by other bacteria in our system but due to exposure to antibiotics the other bacteria cannot keep it in check.) w Clinical Manifestations (Signs & Symptoms) Diarrhea (often bloody), abdominal pain, fever, leukocytosis, sepsis, colonic perforation (rare) 5. Review signs and symptoms of appendicitis. Periumbilical pain, RLQ pain “McBurney’s Point”, nausea, vomiting, fever, diarrhea, RLQ tenderness, systemic signs of inflammation.   6. Review causes of bowel obstructions. Know the difference between functional bowel obstructions versus mechanical obstructions. Know examples of each type. w Causes: Previous abdominal surgery w/ adhesions, congenital abnormalities of bowel (born with), and metastatic carcinoma w Mechanical obstruction- Something is physically blocking movement of material. Ex. Adhesions (tissue cells fused and stuck), hernia, tumors, impacted feces, volvulus (twisting of intestine), and intussusception (intestines collapse into themselves). w Functional obstruction- Due to change in movement Ex. Conditions inhibiting peristalsis such as certain medications (anticholinergics; stimulate flight or fight response). Opioids and low fiber diets.     7. Review signs and symptoms of liver disease. Due to hepatocellular failure and portal hypertension w Hepatocellular failure Jaundice, decreased clotting factors, hypoalbuminemia, decreased vitamins D and K w Portal hypertension GI congestion, development of esophageal or gastric varices, hemorrhoids, splenomegaly, ascites w Hepatic Encephalopathy Pathogenesis Complex neuropsychiatric syndrome from too much ammonia Clinical manifestations        Dementia Psychotic symptoms Asterixis “liver flap” (classic sign) o Spastic jerking of hands held in forced extension Mild confusion and lethargy to stupor and coma w Cirrhosis (End stage liver disease) Irreversible end stage of many different hepatic injuries Severe acute hepatitis, chronic hepatitis, toxic hepatitis Metal storage diseases Alcoholism Liver is fibrotic, scarred, and nodular Results in permanent alteration in hepatic blood flow and liver function 8. Review the etiology and clinical manifestations of gallstones (cholecystitis). Majority of gallstones are cholesterol Three phases of gallstone formation w Supersaturation of bile with cholesterol causing precipitation of cholesterol w Nucleation of bile crystals w Hypomotility (stasis of bile) allowing stone growth Risk factors w Prolonged fasting or rapid weight loss, pregnancy, oral contraceptives, obesity        Clinical manifestations RUQ pain nausea vomiting pain that radiates to the back clay-colored stools abdominal distension fever and chills Clinical manifestations Steady, boring pain in epigastrium or LUQ Increases in intensity Severe tenderness on palpation Radiates or penetrates to back Nausea and vomiting Abdominal distention Hypoactive bowel sounds Low-grade fever                9. Review the etiology and clinical manifestations of pancreatitis. Acute Pancreatitis Etiology Inflammation of the pancreas Autodigestion of the pancreas from enzyme activation Predisposing factors Biliary tract disease, hypertriglyceridemia, ethanol-associated 2/3 of pancreatitis cases due to alcoholism 10. What are the function of the kidneys? What is CVA tenderness? What does it indicate? A. Function of the Kidneys, is to get rid of excess fluid, manage blood volumes (BP), nutrients and ion concentrations (Acid & Base). B. CVA tenderness is costovertebral angle, recorded as CVA tenderness or flank pain that results from touching the region inside of the costovertebral angle. CVA is formed by the 12th rib and the spine. C. Kidney pathology (renal disorders) 11. Review the etiology of polycystic kidney disease. Inherited disorder in which clusters of cysts develop in the kidneys.            12. Review the following terms: nephrons, hematuria, proteinuria, nephrolithiasis, pyelonephritis, cystitis Nephrons- Each of the functional units in the kidney, consisting of glomerulus and its associated tubule, through which the glomerular filtrate passes before emerging as urine. Hematuria- Blood in urine Proteinuria- Protein in the urine Nephrolithiasis (Renal calculi)- Kidney stones (crystal aggregates composed of organic and inorganic materials located within the urinary tract) Pyelonephritis- Infection of the kidney Most common cause is ascending infection from the lower urinary tract (typically due to E. coli) Clinical manifestations - CVA tenderness (classic sign) accompanied by fever, chills, N/V, anorexia, which increases fever-induced dehydration Most effective preventive measure: early removal of catheters Cystitis- Inflammation of the bladder lining 13. Review the etiology and clinical manifestations of postinfectious acute glomerulonephritis. Postinfectious acute glomerulonephritis w Most well known in children, usually seen in developing countries w Follows skin (impetigo) and throat infections caused by β-hemolytic streptococcus w Smoky or coffee-colored urine, proteinuria, edema, decreased urine output w Care is supportive Berger’s disease- Hematuria- (Blood in urine), and upper respiratory or gastrointestinal viral infection.          14. Review signs and symptoms of acute kidney injury (AKI). Review causes of AKI including prerenal, intrinsic/intrarenal, and postrenal. Know examples of each causes to each type of injury. Causes: Disruptions in fluid (fluid overload), electrolyte, and acid-base balances. Electrocytes are unable to get rid of potassium which leads up to hypertension which can escalate to further cardiac issues. Retention of nitrogenous waste products (due to waste not being able to come out) Increased serum creatinine Decreased glomerular filtration rate (GFR) Etiology and pathophysiology Three sites of disruption: Prerenal – disruption to renal perfusion Prerenal kidney injury Caused by conditions that diminish perfusion of the kidney Extremely low blood pressure (hypotension) or low blood volume (hypovolemia) Heart failure Renal artery obstruction Fever, vomiting, diarrhea          15. Review the stages of AKI presentation. What happens if AKI does not resolve? Clinical presentation of acute kidney injury Divided into four phases: Asymptomatic/Prodromal Normal or declining urine output Serum BUN and creatinine begin to rise Insult to the kidney has occurred and the duration of this phase will vary depending on: Cause of the injury Amount of the toxin ingested Duration and severity of the hypotension Oliguric May last up to 8 weeks with usual urine output 50 to 400 mL/day Characterized by oliguria, decreased GFR, hypervolemia Have signs/symptoms of fluid excess, hyperkalemia, uremic syndrome Typically may last 1 to 2 weeks Dialysis may be required Diuretic/Postoliguric Urine volume increases (diuresis) Patient at risk for dehydration, electrolyte imbalances GFR increases May last 1-week, full recovery 1 year Full recovery: creatinine and BUN normal Usually degree of renal insufficiency persists Unfortunately, not all recover, progress to chronic renal disease and failure                      Burns Drugs: ACE inhibitors, angiotensin II blockers, NSAIDs Postrenal – disruption to urine flow distal to the kidney Postrenal kidney injury Caused by obstruction within the urinary collecting system distal to the kidney *Example – stone in ureter, tumor, enlarged prostate Results in elevated pressure in Bowman’s capsule - impedes glomerular filtration Prolonged postrenal injury leads to acute tubular necrosis (intrinsic) and can lead to irreversible kidney damage Intrinsic/intrarenal – damage/disruptions within the kidney blood vessels, tubules, or glomeruli Intrinsic/intrarenal kidney injury Due to dysfunction of the nephrons and the kidney itself Damage to renal tubules resulting in acute tubular necrosis (ATN) Causes include: Reduced blood supply within the kidneys Toxic injury – certain medications, chemotherapy, amphetamines, contrast media Renal inflammation Prolonged postrenal failure Distinction between the sites of disruption helps determine appropriate therapy   Hypertension and cardiovascular disease * Hypervolemia, escalated atherosclerotic process Uremic syndrome * Retention of metabolic wastes, impaired healing, pruritusm dermatitis, uremic frost Metabolic acidosis * Retention of acidic waste products, hyperkalemia Electrolyte imbalances- Retained potassium, phosphorus, magnesium Bone and mineral disorders- Elevated phosphorus and PTH causes altered bone/mineral metabolism Kidneys unable to reabsorb calcium Malnutrition- Decreased intake, depression, dietary limitations Anemia- Lack of erythropoietin, uremia shortens RBCs life Pain- Many reasons; disease itself, treatment, comorbidities Depression- Comorbid conditions; disease itself; disruption of social interactions and relationships Risk factors Diabetes Hypertension Recurrent pyelonephritis Glomerulonephritis Polycystic kidney disease Family history of CKD History of exposure to toxins Age over 65 Ethnicity                    16. Review the causes of chronic kidney disease and the various complications of chronic kidney disease w Outcome of progressive and irrevocable loss of functional nephrons within the kidney w Progressive process: Chronic kidney disease (CKD) chronic renal failure (CRF) end-stage renal disease (ESRD) o ESRD requires dialysis w A global health problem often linked with other comorbidities, primarily hypertension and diabetes mellitus 17. Review the different types of incontinence including: urge, stress, overflow incontinence, and reflex incontinence Urge incontinence - sudden need to void with an involuntary leakage of urine w If happens at night (nocturia) it is called overactive bladder Stress incontinence - small amounts of urine are voided involuntarily when there is an increase in intraabdominal pressure w Can occur with sneezing, laughing, picking up heavy objects Common in women following child birth Reflex incontinence - this is from a disruption of nervous communication that controls micturition w This is seen in CNS disorders such as stroke, Parkinson’s, spinal cord injury w Person will have difficulty starting urination Functional incontinence - secondary to physical or environmental limitations such as not getting to the toilet in time    Overflow incontinence - when the bladder becomes full and overflows Often occurs seen when there is an obstruction in the urethra such as enlarged prostate, prolapsed uterus, and urethral stricture Dribbling of urine typically occurs Seen in patients with diabetes, multiple sclerosis, or spinal cord injury 18. What is cystitis? What is some important patient teaching to prevent cystitis? What can happen if cystitis does not resolve? Inflammation of the bladder lining Diagnosis – urinalysis (UA), culture and sensitivity Treatment w Antibiotics Patient teaching to decrease reoccurrences w Urinate before and after sexual intercourse w Toileting hygiene – wipe from front to back w Take antibiotics as prescribed w Increase fluid intake w Do not resist urge to urinate If left untreated it could become a Kidney infection. 19. Review clinical manifestations for conditions of the male genitourinary tract such as: BPH, testicular cancer, hydrocele, testicular torsion      Clinical manifestations   Benign Prostatic Hyperplasia (BPH) Urinary retention Obstruction to flow Decreased stream Hesitancy, difficulty initiating a stream Interruption of the stream Infection caused by retention Etiology and clinical manifestations   Hydrocele Fluid collection surrounding the testicle or spermatic cord Scrotum progressively swells by evening.   Testicular Torsion Twisting of the spermatic cord with compromised vascular supply and ischemia, followed by infarction Occurs primarily in prepubertal males 20. Review clinical manifestations for conditions of the female genitourinary tract such as: endometriosis, uterine prolapse, pelvic inflammatory disease, ovarian and cervical cancer       Uterine Prolapse Depend on severity of prolapse Vaginal discomfort Discomfort in walking/sitting Difficulty urinating Bleeding Ulceration of cervix from friction     Clinical manifestations Abdominal tenderness, pelvic pain Cervical/adnexa pain or tenderness on palpation Fever, elevated WBC count Purulent vaginal discharge Endometriosis     Clinical manifestations    Pelvic Inflammatory Disease Dysmenorrhea Pain in lower abdomen, vagina, posterior pelvis, back (more diffuse when compared to primary dysmenorrhea) Pain begins 5 to 7 days before menses and lasts for 2 to 3 days Pain with intercourse Pain with defecation  Excessive menstrual bleeding Clinical manifestations Preinvasive    Asymptomatic, changes in cells detected by Pap smear Early invasive      Cervical Cancer Abnormal, persistent vaginal bleeding Pain and bleeding after intercourse Progression usually beyond early stages when symptoms appear May spread to vaginal wall, pelvis, bladder, rectum, and pelvic lymph nodes Clinical manifestations None until late in disease When occur include:         Ovarian Cancer Increased abdominal girth Weight loss Abdominal pain Dysuria or urinary frequency Constipation 21. Review which organisms/viruses contribute to the following conditions: pelvic inflammatory disease, cervical cancer, UTIs, herpes, syphilis, chlamydia. What is the concern with chlamydial infection during labor/delivery? Common organisms   Pelvic Inflammatory Disease Neisseria gonorrhoeae Chlamydia trachomatis  Cervical Cancer Human papillomavirus (HPV) (certain types)  Cystitis (UTI) Syphilis Most cases are due to Escherichia coli (E. coli)  Treponema pallidum, anaerobic spirochete, contributes to syphilis  Herpesvirus Infection Typically caused by HSV-2 Transmission during birth may result in ophthalmia neonatorum Infection of eyes in newborn   Chlamydia 22. Review the stages of syphilis. What complications can occur in the final stage of disease? Incubation period Period of 10 to 90 days Primary phase Begins with formation of chancre Female - may go unnoticed Men - chancre may form on genitalia Resolve spontaneously within 3 to 6 weeks       Low-grade fever Malaise Sore throat Headache Lymphadenopathy Mucosal or cutaneous rash Occurs as T. pallidum is spread through body and lymphatic system     Latent phase   Painless, ulcerative lesion that arises at original portal of entry Secondary stage           Syphilis No symptoms are present Positive serologic assay Contagious Can last 40 years May experience infectious mucocutaneous lesions Final, destructive phase of disease    Two thirds remain asymptomatic Late phase  Develops in one third of affected people     Manifestations Depend on area of arterial lesion and extent of circulatory insufficiency Cardiovascular and CNS at risk for damage Blindness and paresis 23. Review disorders during pregnancy such as: pregnancy induced hypertension, hyperemesis gravidarum. Pregnancy-Induced Hypertension (PIH)  0.5% to 8% pregnancies  Leading cause of pregnancy-related deaths  Characterized by a rapid rise in arterial blood pressure associated with the loss of large amounts of protein in the urine (proteinuria) Hyperemesis Gravidarum  Excessive vomiting during pregnancy  0.3% to 2% pregnancies  Cause - abnormal response to large amounts of human chorionic gonadotropin from the placenta    Clinical manifestations Severe vomiting and electrolyte imbalances Hepatic/renal damage, death if not corrected o The mother could infect the infant during labor/Delivery   Treatment IV therapy to correct metabolic/nutritional deficits, antiemetics, supportive care in hospital 24. Review the etiology and clinical manifestations of pituitary disorders such as gigantism, dwarfism, and acromegaly Dwarfism Etiology o Decreased GH secretion o Defective GH action (structurally abnormal GH or defective GH receptor) Clinical manifestations o Hypoglycemia o Growth below third percentile o Dental eruption delayed o Irregular setting of permanent teeth o Thin hair, poor nail growth o Greater fat mass, decreased muscle mass and delayed bone formation o Delayed puberty Gigantism - occurs in childhood before the skeletal epiphyses close o Accelerated growth velocity (>95 percentile on pediatric growth chart) o Left untreated, may grow >8 feet tall with increased risk of cardiomegaly and heart failure 25. What is ADH? What electrolyte is most affected by disorders of ADH production?   w Antidiuretic hormone (ADH) – also called somatostatin Prevents dehydration, regulates thirst, causes kidneys cells to reabsorb water ADH inhibited by alcohol – increased urine production when drinking – can lead to dehydration High Sodium (hyponatremia)  26. Review the differences between hypothyroidism and hyperthyroidism. What labs can be drawn to determine if an individual is suffering from a thyroid disorder? w Hypothyroidism o Elevated TSH (sensitive indicator of thyroid hypoactivity) o Low levels of T3 and T4 Clinical manifestations Decreased basal metabolic rate, mild/moderate weight gain Weakness, lethargy, cold intolerance Constipation Bradycardia Elevated serum cholesterol and triglycerides Enlarged thyroid Depression, difficulties with concentration/memory Loss of eyebrow hair, dry skin Menstrual irregularities  w Hyperthyroidism o Most common cause = Graves disease - autoantibodies bind and stimulate TSH receptors o Thyromegaly o Exophthalmos – bulging of the eyes o Lid lag, vision changes, photophobia Clinical manifestations Increased basal metabolic rate leads to weight loss, although appetite and dietary intake increases Insomnia, restlessness, inability to concentrate Tremor, irritability Tachycardia, heart palpitations Heat intolerance, diaphoresis Diarrhea Amenorrhea/scant menses 27. What is parathyroid hormone (PTH)? Which electrolyte is primarily affected by PTH disorders? w Parathyroid glands lie posterior to thyroid in neck w Produces parathyroid hormone (PTH) w Increases calcium levels in blood w Causes calcium to be released from bones by activating osteoclasts o Increases Ca2+ absorption in intestine o Decreases Ca2+ excretion in urine 28. Review signs and symptoms of Cushing’s syndrome versus Addison’s disease  Cushing’s Syndrome Results in persistent hyperglycemia, loss of muscle and bone (osteoporosis), excess water and salt retention (weight gain)   o Hypertension, edema, hypernatremia Patients develop characteristic swollen “moon” face Redistribution of fat to the abdomen and the posterior neck - “buffalo hump”    Addison’s disease Caused by adrenocortical insufficiency, decreased glucocorticoid levels (usually decreased cortisol) Can be due to autoimmune condition or removal of adrenal glands Can also be caused by sudden withdrawal from corticosteroid therapy 29. Review etiology and clinical manifestations of Diabetes insipidus (DI) versus Syndrome of inappropriate ADH (SIADH) Diabetes Insipidus w Caused by decrease or lack of ADH production  Kidneys are unable to retain water in body  w Results in output of profuse amounts of dilute urine and extreme thirst w Can be caused by a blow to the head that damages the hypothalamus or the posterior pituitary, tumor w Loss of water in these individuals leads to dehydration High serum osmolality (increased concentration of solutes in blood) S/S include dizziness, disorientation, nausea, rapid heart rate, and headaches Syndrome of inappropriate w w w w Body produces too much ADH Results in retention of water in the body (water intoxication) Very little urine output (oliguria), high urine osmolality Serum dilution occurs due to retention of water (low serum osmolality) o Results in edema, weight gain, hyponatremia w Hyponatremia can lead to cerebral edema o Seizures, confusion, coma, death 30. Review differences between Type 1 diabetes versus Type II diabetes. What is the role of insulin and glucagon in regulating blood glucose?    Type 1 diabetes mellitus Typically diagnosed in young children/adolescents Autoimmune disorder – beta cells in pancreas destroyed Unable to produce insulin, resulting in hyperglycemia   Type 2 diabetes mellitus Cells become resistant to insulin, decrease insulin receptors on target cells Overtime insulin production by pancreas decreases 31. What are signs and symptoms of hyperglycemia versus hypoglycemia. What are the three Ps?    Three Ps: Polyuria - increased urination Polydipsia – increased thirst Polyphagia – increased hunger 32. Review differences between diabetic ketoacidosis and Hyperglycemia hyperosmolar nonketotic syndrome (HHNS). Diabetic ketoacidosis (DKA) S/S include: w Deep, labored respirations (Kussmaul respirations) w Acetone “fruity” breath odor w Confusion w Lethargy w Three Ps: polyuria, polydipsia, polyphagia w Dehydration and hypovolemia w Nausea w Blurred vision Nonketotic Hyperglycemic Hyperosmolar Syndrome (NHHS)   w More common in type 2 DM Severe hyperglycemia with little to no ketosis (fat metabolism) Ketoacidosis is uncommon w Hyperglycemia may go untreated for some time and result in persistent glycosuria with osmotic diuresis w Causes severe dehydration w Can be life threatening      Chronic Hyperglycemia May lead to systemic changes over time and increase the risk of other diseases Hypertension, cardiovascular disease, and stroke Retinopathy Diabetic neuropathy Nephropathy A patient has acute tubular necrosis and is in the oliguric phase. Which laboratory finding is of greatest concern to the nurse? A. Hyponatremia B. Hyperkalemia C. Hypernatremia D. Hypokalemia A patient develops kidney dysfunction from hemorrhage. Which type of kidney injury will be documented on the chart? A. Prerenal kidney injury B. Postrenal kidney injury C. Intrinsic kidney injury D. Intrarenal kidney injury Which person is most prone to develop nephrolithiasis? One with A. dehydration B. an exercise routine C. hypotension D. a nephroblastoma A patient has pain upon light palpation over the costovertebral angle. Which term should the nurse use to describe this finding? A. Chronic pain B. Referred pain C. Flank pain D. Hematuria Which information is correct regarding pseudomembranous colitis? Pseudomembranous colitis: A. develops because of overgrowth of Clostridium difficile B. does not recur following treatment C. is a major cause of diarrhea in premature infants D. may also be called regional enteritis An 83-year-old patient is confused, anxious, lethargic, and has no appetite. Which of the following conditions may be responsible? A. Bladder cancer B. Cystitis C. Nocturnal enuresis D. Ureterolithiasis A nurse is teaching about syphilis. Which information should the nurse include? A. Syphilis has two distinct stages B. Syphilis can be fatal in the final stage of the disease C. Syphilis produces a painful chancre in the latent stage D. Syphilis lesions appear as fluid-filled vesicles that appear 10 to 90 days after infection Which of the following laboratory results are consistent with diabetes insipidus? A. Hyponatremia and high serum ADH B. Hypernatremia and low serum ADH C. Elevated serum calcium, decreased serum phosphorus D. High serum GH levels A patient has a low cortisol level from autoimmune destruction of the adrenal gland. Which diagnosis will the nurse observe documented on the chart? A. SIADH B. Diabetes insipidus C. Cushing syndrome D. Addison’s disease A patient with type 1 diabetes mellitus is pale, has tremors, and is diaphoretic. What does the nurse suspect the patient is experiencing? A. Hypoglycemia B. Hyperglycemia C. Nonketotic Hyperglycemic Hyperosmolar Syndrome (NHHS) D. Diabetic ketoacidosis