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PATHO EXAM 4 STUDY GUIDE REVIEW
RENAL SYSTEM
Acute unilateral renal obstruction and
hypertension.
- The reduced perfusion of the affected kidney activates the (RAAS), which causes constriction of peripheral arterioles.
- Kidneys require at least 20-25% cardiac output – MAP
- Most common type of renal stone: Calcium oxalate.
- Passage of kidney stones can be extremely painful and may produce “referred pain” to umbilicus area – this is d/t sensory innervation of the upper part of the ureter arising from the 10 th thoracic nerve roots.
Urinary tract infections:
- Clinical manifestations in an older adult o Confusion o Poorly localized abdominal discomfort o Can be very difficult to diagnose due to vague symptoms.
Pyelonephritis
o Infection of one or both upper urinary tracts (ureter, renal pelvis, and kidney interstitium). o Most common underlying risk factors: Urinary obstruction and reflux of urine from the bladder (vesicoureteral reflux) o Microorganisms usually associated with acute pyelonephritis include
E. coli, Proteus, or Pseudomonas. These microorganisms also split
urea into ammonia, making alkaline urine that increases the r/o stone formation.
Painful bladder syndrome/interstitial cystitis
(PBS/IC)
o Nonbacterial infectious cystitis (viral, mycobacterial, chlamydial, fungal) o Noninfectious cystitis (radiation, chemical, autoimmune, hypersensitivity). o Cause is unknown, autoimmune reaction may be responsible for the inflammatory response, which includes mast cell activation, altered
epithelial permeability, neuroinflammation, and increased sensory nerve sensitivity. Differentiating symptoms of cystitis from those of pyelonephritis by clinical assessment alone is difficult. The specific diagnosis is established by urine culture, urinalysis, and clinical signs and symptoms. White blood cell casts indicate pyelonephritis, but they are not always present in the urine.
o Can be chronic, progressing to end-stage kidney failure over a period of months or years. o Renal insufficiency refers to a decline in renal function to about 25% of normal or a GFR of 25 to 30 ml/minute. o Levels of serum Cr and urea are mildly elevated; changes in serum Cr level occur only if more than 50% of GFR is lost and are often delayed by more than 24 hours. o Such diagnostic delays make the implementation of early therapy very difficult, contributing to disease progression and mortality. o Prone to hyperkalemia and metabolic acidosis. o Renal phosphate excretion is decreased, causing hyperphosphatemia. o Fluid retention may cause edema. o Symptoms of CHF develop in persons with cardiac disease. o N/V, and fatigue accompany uremia and electrolyte imbalances. o Wound healing is delayed, and the risk of infection, particularly pneumonia, is greater.
Gastrointestinal System
Obesity
- BMI > 30 kg/m^2
- Develops when caloric intake > caloric expenditure in genetically susceptible individuals
- Major risk factor for morbidity, death, and high healthcare cost in the United States and worldwide.
- Three leading causes of death in the United States are associated with obesity o Cardiovascular disease o Type 2 DM o Cancer.
Visceral obesity
- AKA intra-abdominal, central, or masculine obesity
- Distribution of body fat is localized around the abdomen and upper body, resulting in an apple shape.
o Symptoms o Abdominal distention. o If the obstruction is at the pylorus or high in the small intestine,
metabolic alkalosis develops initially as a result of excessive loss
of hydrogen ions that normally would be reabsorbed from the gastric juice.
o In prolonged intestinal obstruction, the lack of circulation produces
lactic acid (decreased tissue perfusion) thus metabolic acidosis. Intussusception: telescoping of part of the intestine into another, usually causing strangulation of the blood supply. Peptic Ulcer Disease o Break, or ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum. o Risk factors o Genetic predisposition
o H. pylori infection of the gastric mucosa
o Habitual use of NSAIDs. o Additional factors include excessive use of alcohol, smoking, acute pancreatitis, chronic obstructive pulmonary disease, obesity, cirrhosis, and age greater than 65 years. o Psychologic stress may be a risk factor for peptic ulcer disease, but the exact mechanism of causation is not known. o Chronic use of NSAIDs suppresses mucosal prostaglandin synthesis, resulting in decreased bicarbonate secretion and mucin (a component of the gut barrier) production and increased secretion
of hydrochloric acid. The interaction of NSAIDs and H. pylori can
contribute to the pathogenesis of peptic ulcer. Disruption of the mucosa exposes submucosal areas to gastric secretions and auto digestion causing erosion and ulceration. Dumping syndrome:
- Clinical manifestations following a partial gastrectomy or pyloroplasty o Tachycardia o Hypotension o Weakness o Pallor o Sweating o Dizziness
- Occurs about 20 minutes after eating. o Rapid gastric emptying and creation of a high osmotic gradient within the small intestine cause a sudden shift of fluid from the vascular compartment to the intestinal lumen. o Rapid distention of the intestine produces a feeling of epigastric fullness, cramping, N/V, and diarrhea.
Hepatitis:
- Lesions of hepatitis are similar to those caused by other viral infection.
- Hepatic cell necrosis, scarring, Kupffer cell hyperplasia, and infiltration by mononuclear phagocytes occur with varying severity.
- Damage tends to be most severe in cases of hep B and hep C.
- Hep B is also associated with acute fulminating hepatitis, a rare form of the disease that is characterized by massive hepatic necrosis. - Prodromal (preicteric) phase o 2 weeks after exposure and ends with the appearance of jaundice. o Fatigue, anorexia, malaise, N/V, HA, hyperalgia, cough, and low- grade fever are prodromal symptoms that precede the onset of jaundice.
- Icteric phase o 1 to 2 weeks after the prodromal phase and lasts 2 to 6 weeks. o Urine may be dark, and the stools clay colored before the onset of jaundice from conjugated hyperbilirubinemia. o GI and respiratory symptoms subside, but fatigue and abdominal pain may persist or become more severe. o Mild and transient itching often accompanies jaundice.
- Posticteric or recovery phase o Begins with Resolution of jaundice o 6 to 8 weeks after exposure. o Although the liver may still be enlarged and tender, symptoms diminish. o In most cases, LFT results return to normal within 2 to 12 weeks after the onset of jaundice. Cirrhosis
- Irreversible inflammatory, fibrotic liver disease and the 12th leading cause of death in the US.
- Most Common Cause: Alcohol abuse and viral hepatitis
- Chaotic fibrosis alters or obstructs biliary channels and blood flow, producing jaundice and portal hypertension.
- New vascular channels form shunts, and blood from the portal vein bypasses the liver, contributing to portal hypertension, metabolic alterations, and toxin accumulation. Portal hypertension:
- Most common Clinical Manifestation o Esophageal Varices.
Hepatic encephalopathy
- Combination of biochemical alterations that affect neurotransmission.
- Liver dysfunction and collateral vessels that shunt blood around the liver to the systemic circulation permit neurotoxins and other harmful substances absorbed from the GI tract to accumulate and circulate freely to the brain.
- The most hazardous substances are end-products of intestinal protein digestion, particularly ammonia, which cannot be converted to urea by the diseased liver. Acute pancreatitis.
- Clinical Manifestations o Epigastric or mid-abdominal pain is the cardinal symptom of acute pancreatitis. ▪ Pain may radiate to the back because of the retroperitoneal location of the pancreas. o Fever and leukocytosis accompany the inflammatory response. o Electrolyte imbalances – hypocalcemia. o Hypotension and shock occur with hypovolemia and SIRS. o Tachypnea and hypoxemia are indicative of complications (SEPSIS and ARDS). o In severe cases, hypovolemia decreases renal blood flow sufficiently to impair renal function. o Transient hyperglycemia also can occur if glucagon is released from damaged A cells in the pancreatic islets. SIRS and multiple organ failure account for most deaths with severe pancreatitis. Reproductive System Primary dysmenorrhea
- Caused by excessive endometrial prostaglandin production.
- Women^ with^ painful^ periods^ produce^10 times^ as^ much^ prostaglandin F (PGF 2 α), a (^) potent myometrial stimulant and vasoconstrictor, as asymptomatic women.
- Elevated^ levels^ of^ prostaglandins^ (especially^ PGF 2 α^ and^ PGE 2 α)^ cause
uterine hyper contractility, decreased blood flow to the uterus, and increased nerve hypersensitivity, thus resulting in pain.
that cycle. LH, proteolytic enzymes, and prostaglandins trigger follicular rupture and release of the ovum. Human papillomavirus (HPV)
- 50% of adolescents and young women acquire HPV (predominantly high-risk types) within 3 years of initiation of sexual intercourse, and it is estimated that 8.8% of all women ages 14 to 59 have persistent infection with high-risk HPV strains.
- Most HPV infections are cleared by the immune system; the vast majority of infections do not cause cervical cancer.
- Screening for cervical cancer prior to age 21 is not recommended.
- Previous efforts at early screening resulted in many young women receiving treatments on their cervix. o These treatments destroyed or removed cervical cells and in many cases altered the structural integrity of the cervix, resulting in an increase in preterm births in women treated without substantially decreasing the later rates of cervical cancer. o It is unknown why some women are able to clear HPV infection and others cannot. o Smoking has been shown to increase the risks of persistent infection and later development of cervical cancer. o Infection with “high-risk” (oncogenic) types of HPV is a necessary precursor to development of the precancerous dysplasia of the cervix that leads to invasive cancer. Sexually transmitted infection (STI)
- Many infected individuals do not seek treatment because symptoms are absent, minor, or transient or because health services are inaccessible, unaffordable, or culturally insensitive.
- Urogenital infections caused by Chlamydia closely parallel those caused by gonorrhea. Both microorganisms infect superficial genital tract tissues, such as mucosa of the urethra and cervix, and both can invade the epididymides, fallopian/uterine tubes, and (rarely) the hepatic.
TABLE 26-2 SIMILARITY OF CLINICAL SYNDROMES CAUSED
BY NEISSERIA GONORRHOEAE AND CHLAMYDIA TRACHOMATIS CLINICAL SYNDROME SITE OF INFECTION Men
N. GONORRHOEAE C. TRACHOMATIS
Urethra Urethritis Nongonococcal urethritis; post gonococcal urethritis Epididymis Epididymitis Epididymitis
SITE OF INFECTION
CLINICAL SYNDROME
N. GONORRHOEAE C. TRACHOMATIS
Women Bartholin gland Bartholinitis Bartholinitis Cervix Cervicitis Cervicitis; cervical atypia Fallopian tube Salpingitis Salpingitis Conjunctiva Conjunctivitis Conjunctivitis Liver capsule Perihepatitis Perihepatitis Cystocele
- Descent of a portion of the posterior bladder wall and trigone into the vaginal canal and usually is caused by the trauma of childbirth.
- Symptoms: insignificant in mild to moderate cases.
- Increased bulging and descent of the anterior vaginal wall and urethra can be aggravated by vigorous activity, prolonged standing, sneezing, coughing, or straining and can be relieved by rest or assumption of a recumbent or prone position. Rectocele
- Bulging of the rectum and posterior vaginal wall into the vaginal canal.
- During childbirth women may sustain damage that can lead to a rectocele, but symptoms usually do not occur until several years after menopause.
- Lifelong chronic constipation and straining may produce or aggravate a rectocele.
- Most rectoceles are asymptomatic, larger ones cause vaginal pressure, rectal fullness, and incomplete bowel evacuation. Enterocele
- Herniation of the rectouterine pouch into the rectovaginal septum (between the rectum and posterior vaginal wall).
- Most large enteroceles are found in grossly obese and older adults and can be complicated by rupture or complete eversion of the vagina with trophic ulceration, edema, and fibrosis.
- Treatment is surgical.
Spermatoceles (epididymal cysts)
