Disease Processes Final

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What are some lesions of the oral cavity?: - Acute ulcerations-caused by friction or trauma (resolve quickly, painful)
- Aphtha (cancer sores)-hyperkeratosis
- Leukoplakia â€“ white raised patch, not easily removed (hairy leukoplakia, associated with HIV or EB virus infection â€“ on lateral surface of the tongue)
- Oral candidiasis (thrush) â€“ a white plaque, readily removed and bleeds
- Squamous cell carcinoma-lesion with persistent bleeding and/or enlarges
What are some esophageal diseases?: - Dysphagia-interruption of bolus transport
- Achalasia-lower esophagus does not dilate properly
- Odynophagia-painful sensation during swallowing.
- Hiatal hernia â€“protrusion of the stomach above the diaphramatic esophageal opening
What are some ulcerations of the upper GI tract?: - GERD (gastroesophageal reflux disease)
- GU/DU (gastric and duodenal ulcers)
- SRMD (stress-related mucosal damage)
- NSAID-induced ulcerations
What are the symptoms of GERD?: - Epigastric, burning pain (â€œheartburnâ€) resulting from transient LES relaxation
- Most common postprandial
- Atypical symptoms
-- Coughing, hoarseness
-- Chest pain, pain upon swallowing
-- Weight loss, anemia
What factors can aggrivate GERD?: - Overeating
- Alcohol and smoking
- Spices and carminatives
- Caffeine and other xanthines
- Fatty foods
What drugs have adverse interactions with GERD?: - Anticholinergics
- Opiates
- Benzodiazepines
- Oral contraceptives
- Glucocorticoids
What lifestyle changes can be made to manage GERD?: - Weight loss
- Reduce alcohol and cigarette smoking
- Raise the head of the bed to increase esophageal clearance
- Not eating within 3 h of bedtime
What are the characteristics of duodenal ulcers vs. gastric ulcers?: see table
What is the pathogenesis of peptic ulcer disease?: - Most forms dependent upon H. pylori, but <10% due to systemic disease.
- Characterized by discrete ulcerative lesions which may spontaneously heal or rupture (with increased mortality).
What is SRMD?: - Stress-related mucosal damage
- A systemic response to stress (an intensive care unit disorder)
- May resolve upon treatment of primary disease, but requires aggressive treatment to prevent blood loss, mucosal damage, and reduce mortality.
What can induce SRMD?: - CNS injury
- Mechanical ventillation
- Coagulopathy
- Extensive burns
- Sepsis, trauma, shock
What are the differences between SRMD and peptic ulcers?: **SRMD:
- Asymptomatic
- Diffuse lesions
- Located in acid producing regions
- Perforation rare
- Bleeding from superficial capillaries
**PEPTIC ULCER
- Superficial
- Discrete lesions
- Located in the duodenum and antrum
- Perforation common
- Bleeding from major arteries and veins
What is NSAID-induced gastric disease?: - Characterized as a mix between SRMD and PU disease
- Tx involves decreased reliance upon NSAID, steroid use and trials of COX-II inhibitors.
- Misoprostol restores prostaglandins decreased by NSAIDs, may reverse damage.
What is the basis of motility disorders of the small intestine?: - Transit time â€“ normally 40-180 min
- Uncoordinated contractions, obstruction or herniations have serious consequences:
-- Nausea and vomiting
-- Cramping or sharp pain
Peritonitis
-- Fever and sepsis
What are the classes of diarrhea?: **Osmotic
- Poorly absorbed solutes
Decreased digestive capacity
**Secretory
- Usually indicates a infectious or parasitic agent, but may be chemically induced (laxative, etc.)
**Infectious
- May be viral, bacterial or parasitic. Most often self-limiting, but may be lethal in very old, young or immunosuppressed.
What is viral gastroenteritis?: Rotovirus damage to villae, replacement cells are immature, dysfunctional. May spontaneously resolve, but severe in neonates.
What is sprue?: An immune reaction toward wheat gluten protein, resulting in villus atrophy, diarrhea and malabsorption. Special diets necessary to avoid atrophic changes.
How can AIDS affect bowel function?: Infections and Kaposiâ€™s sarcoma can result in malabsorption syndrome â€“ AIDS enteropathy.
What are some diagnostic tests used to determine malabsorbtion?: - Lactose intolerance
- Quantitative stool fat
- D-xylose
What is IBD?: - Genetic and immune-based factors involved in T-cell hyperreactivity toward colonic tissue.
- Both are characterized by bleeding and pain upon eating/defecation.
What are the differences between chron's disease and ulcerative colitis?: **Chron's
- Regional Enteritis
- Fistulas Common
**Ulcerative colitis
- Diffuse Bleeding
- Fistulas Uncommon
What are the characteristics of bowel infarction?: - Mesenteric artery occlusion
- May result from atherosclerosis (geriatric) or embolism (pediatric/geriatric)
- Symptoms include severe abdominal pain, hypotension, acidosis, fever, blood loss.
- Leads to ischemia, necrosis and peritonitis⬦lethal if untreated.
- Treatment involves supportive measures and bowel resection.
What are adenomatous polyps?: - Painless, pre-malignant growths into the lumen of the colon.
- Most common in men/women > 40 yoa
- Screening by endoscopy important (esp. > 50 yoa)
- Polyps always removed, since they are pre-malignant lesions and ulceration may indicate malignant transformation.
What are the characteristics of diverticulitis?: - Often exhibits as left-sided pain (sigmoid), fever and constipation, with feeling of fullness and lack of appetite.
- Antibiotics and a bland liquid diet (with watchful waiting) useful for mild exacerbations.
- Repeated episodes may lead to abcesses, ulceration, scarring transmural adhesions and fistulas.
- Avoidance of triggers, increase in fiber and regular bowel movements may decrease incidence.
What are the types of appendicitis?: **Acute â€“ inflammation, ulceration and perforation a medical emergency. Nausea and vomiting common. Diarrhea is rare. Reflexive pain upon abdominal compression and release.
** Chronic â€“ an inflammatory process with increasing pain (other symptoms may be present or absent).
What is IBS?: - Irritable bowel syndrome
- Abdominal pain, commonly with either decreased or increased GI motility and spasm.
- Associated with changes in dietary, emotional or environmental status.
- A wide range of therapeutic agents, including antidepressants and anticholinergics may be useful, but not curative.
What are the characteristics of hemorrhoids?: - Masses of areolar rectal tissue with numerous arteries and veins, may become inflammed, bleed and are extremely painful.
- Associated with pregnancy, aging, heavy lifting and changes in bowel habits.
- If not transient, may be occluded by laser or removed surgically.
What are the types of diabetes?: ** Type 1 - insulin deficiency, induced by an autoimmune reaction.
** Type 2 - insulin resistance, genetic and age-related factors, may include a defect in insulin release.
What are the acute complications of diabetes?: ** Hyperglycemia - inability to normalize blood glucose, a natural consequence of diabetes
** Ketoacidosis - insulin deficiency and increased glucagon leads to increased ketogenesis (more common in Type 1).
** Hypoglycemia - usually due to improper management of antidiabetic therapy.
What is the pathogenesis of hyperglycemia?: - Due to insufficient insulin or insulin resistance.
- Reduced ability to move glucose into cells.
- Reduced ability to metabolize glucose.
- Increased gluconeogenesis
What are the effects of hyperglycemia?: - Hyperosmolality â€“ > 320-330 mosm/L
- Polyuria, polydipsia, N&V
- Marked fatigue and mental stupor
- Coma, if untreated
What are the characteristics of ketoacidosis?: - Results from increased peripheral lipolysis and hepatic ketogenesis due to insulin deficiency (primarily Type 1).
- Associated with hyperglycemia (>250 mg/dL)
- Acidosis - pH < 7.3
- Serum bicarbonate - < 15 meq/L
- Serum positive for ketones
What are the symptoms of diabetic ketoacidotic coma?: - Comatose
- Rapid deep breathing
- â€œFruityâ€ breath
- Hypotension
- Tachycardia
What are the symptoms of hypoglycemia?: - Mental confusion, behavioral disorders
- Tachycardia, palpitations, sweating, tremors
- Nausea and hunger
- Coma and convulsions
What are the causes of chronic complications of diabetes?: - Related to glycosylation of membrane proteins over time (assessment of glycosylated; hemoglobin A1c over time is indirect index of glycemic control).
- Interference with membrane function through alterations in myoinositol disposition in neurons.
- Excessive gluconeogenesis and interference with cellular metabolism.
What are diabetic cataracts?: - A clouding of the lens (cortical or subcapsular) with impairment of vision.
- Linked closely with uncontrolled diabetes and hyperglycemia /hyperlipidemia
- Requires surgical intervention
What is diabetic retinopathy?: - A leading cause of blindness in diabetes
- Usually due to vascular problems associated with the retina (microaneurysms, edema hemorrhages, infarction, and proliferation of new vessels).
- In addition to proper glucose control, laser surgery, smoking cessation, and control of hypertension are essential therapeutic elements.
What type of glaucoma occurs as a result of diabetes complications?: - Usually tx as the open-angle type.
- Neovascularization after cataract removal may convert to closed-angle type.
What are the characteristics of diabetic neuropathy?: - Results in End-stage renal disease; a major cause of death in Type 1 and 2.
- Hyperglycemia and increased vascular pressure damage the glomerulus and nephron.
- Initially exhibited as microalbuminuria (>20 ug/min).
- Progressive proteinuria with increased renal failure (even with decreased creatinine clearance), a unique form of renal failure.
- ACE inhibitors/angiotensin antagonists and dietary protein restriction is beneficial - in later stages more so than normoglycemic control. Angiotensin increases the accumulation of extracellular matrix proteins in the glomerulus, resulting in glomerular damage.
What are the 5 stages of diabetic neuropathy?: 1. Above normal GFR
2. Microalbuminuria
3. Albuminuria and hypertension
4. Increase in serum creatinine, BUN and reduction in GFR
5. ESRD GFR < 10 ml/min
What are the characteristics of foot ulcerations associated with diabetes?: - Etiology includes neuropathy as well as vascular disease.
- In addition to glycemic control, increased attention to foot care is absolutely essential for prevention and treatment.
- Smoking cessation required for prevention and tx, as well as platelet-derived growth factor for ulcers refractory to debridement and antibiotics.
What are the two types of diabetic neuropathy?: ** Peripheral neuropathy- includes polyneuropathy with desensitization, isolated neuropathy, and painful diabetic neuropathy.
** Autonomic neuropathy - gastroparesis, diarrhea, postural hypotension, urinary retention
What are the characteristics of peripheral neuropathy?: - Impaired sensory perception (pain, temperature, vibration) increases chances of unnoticed trauma.
- May be isolated and associated with vascular ischemia.
- Hypersensitivity to touch and burning pain in the evening
What are the characteristics of autonomic neuropathy?: - Gastroparesis - damage to vagus leading to inadequate gastric emptying.
- Diarrhea - damage to ganglia leads to unopposed residual vagal tone and increased intestinal secretions and motility.
- Postural hypotension - decreased vascular responsiveness.
- Urinary retention - inadequate voiding pressure and increased sphincter tone.
How does diabetes cause erectile dysfunction?: - Combination of a neuropathy and vascular disease
- Decreased parasympathetic tone - a neuropathic feature occurs early.
- Vascular occlusion - decreased ability of blood to fill the corpus.
How does diabetes cause skin and mucous membrane lesions?: - Increased fragility of the vasculature, (in part due to hyperglycosylation) leading to increased damage and bleeding.
- Decreased perfusion due to vascular occlusion, impaired wound healing response.
- Increased glucose as substrate for bacterial and fungal infections.
How does diabetes affect cardiovascular disease?: - Hyperlipidemia and coronary artery disease - results from peripheral hepatic impairment of cholesterol extraction and increased peripheral deposition (related to hyperglycemia).
- Hypertension - may be related to alterations in peripheral and central control mechanisms and membrane structures.
What can urinalysis by dipstick evaluation detect?: Specific gravity
pH
Protein
Hemoglobin
Glucose
Ketones
Bilirubin
Nitrites
leukocyte esterase
What can urinalysis by microscopic evaluation detect?: Crystals
Casts
Cells
Infectious Organisms
What is GFR?: - Usually determined from Creatinine Clearance
C=UV/P more precise, but technically difficult.
- Ccr=(140-Age) X Weight (kg)/Pcr X 72
- Decrease in Ccr is an important index of renal disease.
What are the characteristics of BUN?: - End product of protein catabolism, reabsorbed appreciably in the renal tubule.
- Normal BUN : serum creatinine is 10:1
- Increased ratio can be seen in dehydration.
- Increased BUN results from bleeding, cell lysis, increased dietary protein decreased renal perfusion, etc.
- A buildup of nitrogenous wastes in the blood is known as uremia or azotemia.
What is the equation for fractional excretion of Na+?: see equation
What is acute renal failure?: - Defined as worsening renal function over hours to several days.
- Inability to maintain fluid and electrolyte balance and excrete nitrogenous wastes.
- Classification:
-- Prerenal azotemia
-- Intrinsic renal failure
-- Postrenal azotemia
What are the characteristics of renal failure?: *Signs and Symptoms
- Azotemia produces N&V, malaise, altered sensorium.
- Arrythmias and seizures may occur if electrolyte imbalance is severe.
- Diffuse abdominal pain
* Laboratory Findings
- Azotemia
- Hyperkalemia, Hyperphosphatemia, Hypocalcemia
- Anemia and platelet dysfunction
What is prerenal azotemia?: - Most common, due to renal hypoperfusion.
- Results from decreased intravascular volume, change in vascular resistance or low cardiac output.
- GFR will decrease.
- BUN and Na is reabsorbed effectively
- BUN:Cr > 20 and UNa < 20
- Fractional excretion of Na+ less than 1%
- Correction of GFR can prevent conversion to intrinsic failure.
What is postrenal azotemia?: - Most commonly due to a bilateral obstruction of the ureters (most commonly prostatic hypertrophy).
- In this case, fractional excretion of Na may be variable, depending upon the degree of obstruction.
What are the characteristics of acute tubular necrosis in intrinsic renal disease?: - Caused by ischemia (thrombosis, hypoperfusion) and nephrotoxins (drugs and endogenous agents).
- Tubular damage reduces absorption of BUN relative to excreted creatinine (BUN:Cr < 20) and sodium (UNa > 20).
- Ability to concentrate urine is decreased (reduced urinary osmolality).
- Casts of tubular cells are found in the urine.
What drugs can cause acute tubular necrosis?: - Aminoglycosides
- Amphotericin B
- Vancomycin
- Acyclovir
- Cephalosporins
- Radiographic contrast media
- Cyclosporine
- Cisplatin
- Heavy metals
What are endogenous nephrotoxins that can lead to acute tubular necrosis?: - Myoglobin (rhabdomyolysis)
- Hemoglobin
- Hyperuricemia
- Bence Jones protein (multiple myeloma)
What are the characteristics of interstitial nephritis in intrinsic renal disease?: - An interstitial inflammatory response caused by drugs (70%), infectious diseases, immunologic disorders.
- Characterized by fever, rash and arthralgia, hematuria, proteinuria, and urinary WBCs.
- Better prognosis than acute tubular necrosis.
What drugs can cause interstitial nephritis?: - Penicillins and cephalosporins
- sulfonamides and sulfa-based diuretics
- NSAIDS
- Rifampin
- Phenytoin
- Allopurinol
What are some infection/immune based causes of interstitial nephritis?: - Streptococcal
- leptospirosis
- CMV
- Histoplasmosis
- Rocky Mountain spotted fever
- Intrinsic autoimmune disorders
What are the characteristics of glomerulonephritis in intrinsic renal disease?: - Autoimmune complexes, especially GBM resulting in destruction of glomeruli.
- Characterized by hematuria, edema and hypertension.
- Associated with several autoimmune phenomena, including Goodpastureâ€™s syndrome, Wegenerâ€™s granulomatosis, etc.
What are the general characteristics of chronic renal failure?: - Diabetes is the primary cause (50%)
- Azotemia over many years
- Symptoms and signs of uremia
- Hypertension as disease progresses
- Extended casts in urine
- Bilateral small kidneys
- Renal osteodystrophy
What are the signs and symptoms of uremia in chronic renal disease?: - Fatigue, weakness
- Bruises easily
- Metallic taste, breath odor
- shortness of breath
- anorexia, nausea
- nocturia, impotence
- numbness, leg cramps
- irritability, inability to concentrate
What are the laboratory findings in chronic renal disease?: - Progressive elevation in BUN and Cr
- Isosthenuria; inability to concentrate urine above isotonicity.
- GFR progressively falls.
- Hyperkalemia if GFR less than 10 ml/min
- Metabolic acidosis (inability to excrete acids)
What are the complications of chronic renal failure?: - Hyperkalemia if GFR less than 10 ml/min
- Metabolic acidosis (inability to excrete acids)
- Hypertension
- Pericarditis
- CHF
- Anemia
- Coagulopathy - platelet dysfunction
- Renal osteodystrophy
What are the 3 major stages of alcoholic liver disease?: 1. Fatty liver â€“ fatty acid oxidation is impaired, triglycerides are increased.
2. Alcoholic hepatitis â€“ a hepatocellular necrosis with hepatomegaly, jaundice and fever.
3. Alcoholic cirrhosis â€“ hepatic scarring, collagen formation and diffuse connective tissue replacement. Liver is firm in consistency.
What are the sequelae of liver cirrhosis?: **Portal Hypertension
- Splenomegaly and varices: due to increased back pressure due to obstruction.
- Ascites: resulting from increased back pressure increases passage of fluid from the hepatic circulation into the intercellular space and peritoneal cavity.
- Peritonitis: stasis of blood flow may allow bacteria to gain entry into the peritoneum and circulation.
** Liver Failure
What are the characteristics of liver failure?: - Fatigue due to inability of liver to process waste products and other nutrients systemically.
- Nausea and vomiting: inability to process nutrients, the body rejects enteric nutrition.
- Jaundice: inability to metabolize heme and bilirubin
- Bleeding: lack of clotting factor synthesis.
- Edema and ascites: decreased production of plasma proteins necessary to sustain proper colloid osmotic pressure.
- Hepatic encephalopathy: ranging from mild confusion to coma, resulting from inability to process intestinal ammonia and mercaptans
- Progressive and fatal, requiring liver transplantation.
- Occurs over many years (as in alcoholic liver disease)
- Fluminant hepatic failure can occur with acetaminophen overdose (over an 8 week period)
What is cholelithiasis?: - Gallstones
- Formed in gallbladder due to precipitation of cholesterol and other bile tract components (bilirubinates, calcium, etc)
- May grow to large size stones, over years to decades, with or without symptoms (pain after meals, most common).
What are cholesterol stones?: - > 50% cholesterol
- Greater prevalence in women
- Excess biliary cholesterol in relationship to bile acid solubilization.
- Gallbladder is primary focus of the disease.
What are pigment stones?: ** Black pigment (calcium bilirubinate) â€“ hemolysis and cirrhosis may be predisposing factors.
** Brown pigment (calcium bilirubinate with salts of fatty acids) higher incidence in Asia, pathogenesis is highly debated.
What is the pathology of cholelithiasis?: - Obstruction (pain, nausea and vomiting) due to increased contraction pressure of the gallbladder after meals.
- If obstruction blocks the opening to the pancreas, pancreatitis may result (flank pain, nausea, increase in serum amylase and lipase).
- A variety of surgical methods may be employed to treat these conditions.
What are hepatic neoplasms?: ** Hepatocellular adenoma
- Female prevalence
- Most commonly associated with oral contraceptive use
- Usually benign, may present a liver function problem if progressive
** Hepatocellular carcinoma
- Male prevalence
- In US, commonly alcohol and androgen abuse
- May be associated with hepatitis in other countries
What is innate immunity?: Innate immunity is a resistance to a pathogen that is present at birth; it does not require prior exposure to the pathogen and it is not modified by repeated exposures over a lifetime.
What is acquired immunity?: Acquired immunity is resistance that is weak or absent when a pathogen is encountered for the first time, but increases with repeated exposures to the pathogen over time.
What is lysozyme?: Lysozyme is an endoglycosidase that attacks bacterial cell walls. It acts by digesting peptidoglycan in the wall, cleaving linkages between carbohydrate residues. This weakens the cell wall, leaving the bacteria susceptible to osmotic lysis, causing cell death.
Describe the mechanism of action of mannose-binding protein and serum amyloid protein P and C-reactive protein.: Mannose-binding protein, serum amyloid protein P and C-reactive protein are proteins that bind to sugar, carbohydrate, or lipid side chains present on bacterial cell walls. These proteins do not have a direct effect on the bacterial cell, but they target the cell for destruction by other humoral or cell-mediated processes. When these proteins are bound a pathogen, they can trigger opsonization and/or the complement cascade.
Describe the mechanism of action of gram negative bacteria-associated lipopolysaccharide (LPS).: LPS a target for immune recognition; it is found on the outer lipid bilayer surrounding the cell walls of gram-negative bacteria. Two of the humoral proteins that recognize LPS are LBP and CD14. These proteins form complexes with LPS on the bacterial surface, which are then recognized by surface receptors on cell types such as endothelial cells, neutrophils, and monocytes.
What are the two major cell types of the innate immune system?: Neutrophil and macrophage.

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