Patho exam 4 PDF

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Here is the notes to study for exam 4 RENAL SYSTEM 1.

Acute unilateral renal obstruction and hypertension.

The reduced perfusion (kidneys require at least 20-25% cardiac output – MAP) of the affected kidney activates the renin-angiotensin-aldosterone system (RAAS), which causes constriction of peripheral arterioles. The most common type of renal stone is Calcium oxalate. Passage of kidney stones can be extremely painful and may produce “referred pain” to umbilicus area – this is due to the sensory innervation of the upper part of the ureter arising from the 10th thoracic nerve roots.

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Urinary tract infections: Clinical manifestations of a urinary tract infection in an older adult are Confusion and poorly localized abdominal discomfort. Can be very difficult diagnose due to vague symptoms.

Pyelonephritis is an infection of one or both upper urinary tracts (ureter, renal pelvis, and kidney interstitium). Urinary obstruction and reflux of urine from the bladder (vesicoureteral reflux) are the most common underlying risk factors. 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 risk of stone formation. Painful bladder syndrome/interstitial cystitis (PBS/IC) is a condition that includes nonbacterial infectious cystitis (Links to an external site.)Links to an external site. (viral, mycobacterial, chlamydial, fungal) and noninfectious cystitis (Links to an external site.)Links to an external site. (radiation, chemical, autoimmune, hypersensitivity). The cause of PBS/IC is unknown, but an 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.

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Glomerular disorders.

Reduced GFR during glomerular disease is evidenced by elevated plasma urea, creatinine concentration, or reduced renal creatinine clearance. Acute glomerulonephritis includes renal diseases in which glomerular inflammation is caused by immune mechanisms that damage the glomerular capillary filtration membrane including the endothelium, basement membrane, and epithelium (podocytes). The classic symptoms include sudden

onset of hematuria including red blood cell casts and proteinuria ( milder than nephrotic syndrome), and in more severe cases, these symptoms are also accompanied by edema, hypertension, and impaired renal function. Nephrotic syndrome (Links to an external site.)Links to an external site. is the excretion of 3.0 g or more of protein (massive proteinuria) in the urine per day, hypoalbuminemia (less than 3.0 g/dl), and peripheral edema. Nephrotic syndrome is characteristic of glomerular injury. Primary causes of nephrotic syndrome include minimal change disease (lipoid nephrosis), membranous glomerulonephritis, and focal segmental glomerulosclerosis (see Table 387 (Links to an external site.)Links to an external site.). Secondary forms of nephrotic syndrome occur in systemic diseases including diabetes mellitus, amyloidosis, and systemic lupus erythematosus. Nephrotic syndrome also is seen with certain drugs, infections, malignancies, and vascular disorders. Acute Kidney injury may be acute and rapidly progressive (within hours), and the process may be reversible. Kidney failure also can be chronic, progressing to end-stage kidney failure over a period of months or years. Renal insufficiency refers to a decline in renal function to about 25% of normal or a GFR of 25 to 30 ml/minute. Levels of serum creatinine and urea are mildly elevated. However, changes in serum creatinine level occur only if more than 50% of glomerular filtration is lost and are often delayed by more than 24 hours. Such diagnostic delays make the implementation of early therapy very difficult, contributing to disease progression and mortality.

They are prone to hyperkalemia and metabolic acidosis. Renal phosphate excretion is decreased, causing hyperphosphatemia. Fluid retention may cause edema. Symptoms of congestive heart failure develop in persons with cardiac disease. Nausea, vomiting, and fatigue accompany uremia and electrolyte imbalances. Wound healing is delayed, and the risk of infection, particularly pneumonia, is greater. Gastrointestinal System Obesity is defined as a body mass index (BMI) that exceeds 30 kg/m2 and generally develops when caloric intake exceeds caloric expenditure in genetically susceptible individuals. Obesity is a 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: cardiovascular disease, type 2 diabetes mellitus, and cancer. Visceral obesity (also known as intra-abdominal, central, or masculine obesity) occurs when the distribution of body fat is localized around the abdomen and upper body, resulting in an apple shape. Visceral obesity is associated with accelerated lipolysis and has an increased risk for inflammation, metabolic syndrome (hypertriglyceridemia, reduced highdensity lipoprotein, increased low-density lipoproteins, hypertension, and insulin resistance), type 2 diabetes mellitus, cardiovascular complications, and cancer. Peripheral obesity (also known as gluteal-femoral, feminine, or subcutaneous obesity) occurs when the distribution of body fat is extraperitoneal and distributed around the thighs and buttocks and through the muscle, resulting

in a pear shape; it is more common in women. Peripheral and subcutaneous fat is less metabolically active and less lipolytic and releases fewer adipocytokines (particularly adiponectin) than visceral fat. Risk factors are still present for the complications of obesity but they are less severe than for visceral obesity.

Gastroesophageal reflux disease (GERD) (Links to an external site.)Links to an external site. is the reflux of acid and pepsin from the stomach to the esophagus that causes esophagitis. Risk factors for GERD include obesity, hiatal hernia, and drugs or chemicals that relax the LES (anticholinergics, nitrates, calcium channel blockers, nicotine). GERD may be a trigger for asthma or chronic cough

Clinical manifestations of reflux esophagitis are heartburn from acid regurgitation, chronic cough, asthma attacks, and laryngitis. Upper abdominal pain usually occurs within 1 hour of eating and can be relapsing and remitting. Symptoms can worsen if the individual lies down or if intraabdominal pressure increases (e.g., as a result of coughing, vomiting, or straining at stool). Heartburn also may be experienced as chest pain, which requires ruling out cardiac ischemia.

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Bowel Obstruction: the most common occurring small intestinal obstruction is related to adhesions and account for 50% to 70% of small bowel obstructions.

Small bowel obstructions usually present early with abdominal distention. 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. In prolonged intestinal obstruction, the lack of circulation produces lactic acid (decreased tissue perfusion) thus metabolic acidosis.

Intussusception is the telescoping of part of the intestine into another, usually causing strangulation of the blood supply. 1.

Peptic Ulcer Disease

A peptic ulcer is a break, or ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum. Risk factors for peptic ulcer disease include genetic predisposition, H. pylori infection of the gastric mucosa, and habitual use of NSAIDs. Additional factors include excessive use of alcohol, smoking, acute pancreatitis, chronic obstructive pulmonary disease, obesity, cirrhosis, and age greater than 65 years. Psychologic stress may be a risk factor for peptic ulcer disease but the exact mechanism of causation is not known.

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 autodigestion causing erosion and ulceration. Dumping syndrome: Clinical manifestations including increased pulse, hypotension, weakness, pallor, sweating, and dizziness following a partial gastrectomy or pyloroplasty. Occurs about 20 minutes after eating. 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. Rapid distention of the intestine produces a feeling of epigastric fullness, cramping, nausea, vomiting, and diarrhea. Usually managed very well with dietary management: frequent small meals; no fluid during meals; high protein, low carbs. 2. Crohn Disease compared to UC: TABLE 41-5 1.

FEATURE

ULCERATIVE COLITIS

CROHN DISEASE

Age at onset

Any age; 10-40 years most common

Any age; 10-30 years most common

Family history

Less common

More common

Gender (prevalence)

Equal in women and men

About equal in women and men

Location of lesions

Colon and rectum, no “skip” lesions

All of GI tract: mouth to anus, “skip” lesions common

Inflammation and ulceration

Mucosal layer involved

Entire intestinal wall involved

Fistulae and abscesses

Rare

Common

Strictures and possible obstruction

Rare

Common

Occasional

Common

Incidence

Pathophysiology

Clinical Manifestations Abdominal pain

Diarrhea

Common

Common

Bloody stools

Common

Less common

Small intestinal malabsorption Rare

Common

Steatorrhea

Common

Rare

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Liver: One of the main functions of the liver is the deamination of amino acids. Any condition that disrupts the normal functioning of the liver, thus hepatocyte dysfunction, can cause hypoalbuminemia.

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Hepatitis: The pathologic 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 hepatitis B and hepatitis C. Hepatitis B is also associated with acute fulminating hepatitis, a rare form of the disease that is characterized by massive hepatic necrosis.

Prodromal (preicteric) phase of hepatitis begins about 2 weeks after exposure and ends with the appearance of jaundice. Fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, and low-grade fever are prodromal symptoms that precede the onset of jaundice. Icteric phase begins about 1 to 2 weeks after the prodromal phase and lasts 2 to 6 weeks. The urine may be dark and the stools clay colored before the onset of jaundice from conjugated hyperbilirubinemia. During the icteric phase, gastrointestinal and respiratory symptoms subside, but fatigue and abdominal pain may persist or become more severe. Mild and transient itching often accompanies jaundice. Posticteric or recovery phase begins with resolution of jaundice, about 6 to 8 weeks after exposure. Although the liver may still be enlarged and tender, symptoms diminish. In most cases, liver function test results return to normal within 2 to 12 weeks after the onset of jaundice.

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Cirrhosis (Links to an external site.)Links to an external site. is an irreversible inflammatory, fibrotic liver disease and the twelfth leading cause of death in the United States. Alcohol abuse and viral hepatitis are the most common causes. 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: esophageal varices is the most common clinical manifestation of portal hypertension. Thrombocytopenia (decreased platelet count) is the most common manifestation of congestive splenomegaly and can contribute to an increased bleeding tendency. The most common clinical manifestation of portal hypertension is esophageal bleeding. Hepatic encephalopathy results from a 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 gastrointestinal 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. Ammonia levels in hepatic encephalopathy is most important to monitor in a patient with liver failure

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Acute pancreatitis. Clinical Manifestations: Epigastric or midabdominal pain is the cardinal symptom of acute pancreatitis. The pain may radiate to the back because of the retroperitoneal location of the pancreas. Fever and leukocytosis accompany the inflammatory response. Electrolyte imbalances – hypocalemia. Hypotension and shock occur with hypovolemia and SIRS.309 (Links to an external site.)Links to an external site. Tachypnea and hypoxemia are indicative of complications (SEPSIS and ARDS). In severe cases, hypovolemia decreases renal blood flow sufficiently to impair renal function. 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.

Tachypnea related to acute pancreatitis would indicate a complication and need further investigation.

Reproductive System 1.

Primary dysmenorrhea is attributed to excessive endometrial prostaglandin production*. Women with painful periods produce 10 times as much prostaglandin F (PGF2α), a potent myometrial stimulant and vasoconstrictor, as asymptomatic women. Elevated levels of prostaglandins (especially PGF2α and PGE2α) cause uterine hypercontractility, decreased blood flow to the uterus, and increased nerve hypersensitivity, thus resulting in pain. Secondary dysmenorrhea results from disorders such as endometriosis (the most common cause), endometritis (infection), pelvic inflammatory disease, obstructive uterine or vaginal anomalies, uterine fibroids, polyps, tumors, ovarian cysts, pelvic congestion syndrome, or nonhormonal intrauterine devices (IUDs).

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Polycystic ovarian syndrome. Although the underlying cause of PCOS is unknown, a genetic basis is suspected. No single factor fully accounts for the abnormalities of PCOS. A hyperandrogenic state is a cardinal feature in

the pathogenesis of PCOS. However, glucose intolerance/insulin resistance (IR) and hyperinsulinemia often run parallel and markedly aggravate the hyperandrogenic state, thus contributing to the severity of signs and symptoms of PCOS. Obesity adds to and worsens IR. Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and enabling follicles, which would normally disintegrate, to survive.

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Benign ovarian cysts are quite common and are the fourth leading diagnosis for gynecologic hospital admissions. Benign cysts of the ovary are produced when a follicle or a number of follicles are stimulated but no dominant follicle develops and completes the maturity process. Normally, during the early follicular phase of the menstrual cycle, follicles of the ovary respond to hormonal signals from the pituitary gland. The pituitary produces FSH to mature follicles in the ovary. As the follicles enlarge, granulosa cells in the follicle multiply and secrete estradiol (a form of estrogen). As a dominant follicle develops, it secretes higher levels of estradiol, which stimulates the LH surge that comes from the pituitary. A small cyst on the ovary during the follicular phase is normal. The LH surge stimulates the follicle to rupture, releasing the ova and transforming the granulosa cells of the dominant follicle into the corpus luteum. If the dominant follicle develops properly before ovulation, the corpus luteum becomes vascularized and secretes progesterone. Progesterone arrests development of other follicles in both ovaries in that cycle. LH, proteolytic enzymes, and prostaglandins trigger follicular rupture and release of the ovum.

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Human papillomavirus (HPV). Fifty percent 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. For this reason, 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. 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. It is unknown why some women are able to clear HPV infection and others cannot. Smoking has been shown to increase the risks of persistent infection and later development of cervical cancer. 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. HPV is a is a necessary precursor for developing cervical intraepithelial carcinoma (CIN) and cervical cancer.

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Sexually transmitted infection (STI) In the past an infection transmitted through sexual intercourse was called a venereal disease. Because of its limited scope, the term venereal disease has been replaced with 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 (Links to an external site.)Links to an external site.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. Know the difference between the two!

TABLE 26-2 SIMILARITY OF CLINICAL SYNDROMES CAUSED BY NEISSERIA GONORRHOEAE AND CHLAMYDIA TRACHOMATIS

CLINICAL SYNDROME SITE OF INFECTION N. GONORRHOEAE C. TRACHOMATIS Men Urethra

Urethritis

Nongonococcal urethritis; postgonococcal urethritis

Epididymis

Epididymitis

Epididymitis

Rectum

Proctitis

Proctitis

Conjunctiva

Conjunc...