Pathology 2 exam 1 notes
Pathology 2 exam 1 notes BSC-80228-001-201605
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Path 2 Exam 1 Renal Function Studies Nitrogen waste clearance-Urea. 80% of protein/AA filtered through this process, measured as BUN. Freely filtered by glomerulus, partially reabsorbed by the tubules, no secretion. Liver converts ammonia to urea. Creatinine-function of lean body mass, derived from non-enzymatic interconversion of creatine in skeletal muscle. No reabsorption. Measure in serum and urine, is better measurement than BUN. Also increases with decreased renal function. Influenced by less non-renal factors, lean body mass, muscle integrity, and pregnancy. Clearance equals Urine creatinine/ (serum/plasma creatinine) x (urine volume/min). Reference range is 125ml/min. Requires 24 hour urine collection (as does protein collection). Can correct value based on weight. Uric acid- from oxidation of purines. BUN relies on fact that serum/plasma concentration of nitrogen are proportional to urea levels. Crude measurement, is indirect and can be influenced by a lot of non-renal factor, dietary protein intake, anabolic/catabolic states, hydration, and pregnancy. Levels increase with decreasing renal functions. Estimated GFR- uses creatinine, age, race and gender. Different for pediatrics and creatinine methods using mass spec. Lupus loves to destroy kidneys. Analgesics can affect kidneys too. Urine protein detection is reliable indicator of disease. 24 hour collection is best to indicate this. Nephrotic Syndrome; Very heavy proteinuria, low serum albumin, general edema, and increased serum lipids (lipid urea too). Protein excretion typically 3.5g/24hr. Interesting Observations. Normal BUN to Cr is 10-12:1. Ratio stays same with renal parenchymal damage. Altered ratio suggests other abnormalities like GI bleeding, fever or catabolic drugs (chemotherapy). Decreased urine flow increases urea reabsorption. Pregnancy increases ratio because GFR is increased. In hemodialysis urea more effectively dialyzed, increases ratio. Azotemia; increased serum/plasma urea and/or creatinine. Symptoms not implied. Pre-renal form- trauma, hemorrhage, dehydration, cardiac decompensation, infection (septic shock), increased protein intake or protein breakdown. Renal form- glomerulonephritis, pyelonephritis, acute tubular necrosis, acute glomerular damage. Post renal- obstruction, congenital defects. Uremia; azotemia with symptoms. Fatigue, lassitude, decreased mental vigor, can progress to stupor and coma, psychosis, peripheral neuropathy, cardiovascular (uremic fibrinous pericarditis). Water Balance Antidiuretic hormone plays a big role in this, concentrates urine. Osmole; total number of moles of solute in solution after dissociation. Osmolality: number of osmoles for every kilogram of solution. Osmolarity is number of osmoles per liter. Osmolality measure water balance. 2NA + glucose/20 + BUN/3, simplified form. Diabetes Insipidus; Central = pituitary, renal = kidney. Deficiency, high serum osmolality, continued production for dilute urine, further increase in serum osmolality. SIADH (Syndrome for Inappropriate Secretion of ADH); can be paraneoplastic syndrome, CNS disorder, and pulmonary disorder. Low serum osmolality. Continued production for concentrated urine. Renal Calculi- Kidney stones. 75% with Calcium, triple phosphate 10-15%, Uric Acid 6%, cystine 1-2%, Others 10%. Cause obstruction, hematuria, can predispose the patient to infection. May cause renal colic (very painful, or be asymptomatic). Some stones don’t show up on radiographs. Urinalysis/Acid Base Disorders To monitor disturbances when renal function is normal, like diabetes. Color can be affected by a lot of things. Fruity odor, ketones. But odor is not diagnostically significant. Clarity, cloudiness not uncommon in normal people. Reagent strip methodology is most often used. PH normally 4.6-8, can vary from diet or disease. Specific gravity; Normal is 1.005-1.130. Increased with dehydration, decreases with too much water, diabetes insipidus, stays fixed with damage to medulla. Protein up to 150mg in 24 hrs. Glomerular damage will give marked levels of increase, tubular damage more mild. In general test strips measure albumin, not Bence Jones proteins (multiple myeloma, light chains). False positive with alkaline urine. Glucose in urine, occurs with blood glucoses and tubules not reabsorbing it well. With diabetes, there is a threshold that is overwhelmed in tubules. Other disease states can cause this too, Cushing’s, acromegaly, pancreatic disease, liver disease, CNS disorder and others. Ketones show up with increased fat utilization. 3 types; B-hydroxybuterate (most used by brain if needed) is 78%, acetoacetic acid 20% and acetones 2%. Test strips measure acetoacetic acid. Causes: Vomiting with pregnancy, Cachexia, acute fever in children, nausea, vomiting and diarrhea in kids, inherited metabolic disorders. Blood- we measure hemoglobin (strips also positive for myoglobin). Asymptomatic hematuria can be seen in 16% of people, causes by kidney stones, malignancies, or trauma. Statins can cause myglobinuria. Nitrite- detects certain asymptomatic bacteria, specific for gram negative, best used in office. Not all organisms form nitrite. Leukocyte esterase; detects pyuria, not infection. Azurophilic granules. Bilirubin; conjugated form is water soluble. Urine Sediment- Done on a random specimen. Occasionally see red cells, but if increase in RBC and casts bleeding is renal, if casts are absent bleeding is downstream from kidney. Leukocytes increase with fever and exercise, if casts are present consider renal infection (pyelonephritis). Tubule cells constantly being shed, increased number means tubular damage. Hyaline and fine granular casts, may be seen with exercise, dehydration and fevers. Waxy casts; oliguria. Fatty casts; lipiduria. Crystals; some are present normally. Some are always pathologic, cystine, cholesterol, tyrosine, leucine, and bilirubin. Normal urine is sterile, but some can show up. Fungal UTI’s more common in diabetics and immunosuppressed. Acid-Base Disturbances Henderson-Hasselbach = H2CO3 goes to H + HCO3. CO2 and pH can be measures, which can determine HCO3. We use pKa + log (HCO3/CO2). Buffering Mechanisms: Carbonic Acid-Bicarbonate buffer system, tied to respiration, greatly expands its ability. Hemoglobin, has 38 histadines, can bind H. Phosphate has lowest capacity. Proteins in system can buffer too. Anion Gap: Sodium must be balanced by anions. But HCO3 and Cl do not equal Na, so unmeasured anions fill this role. Na – (Cl + HCO3). K is negligible in calculation. Metabolic acidosis does not increase gap initially, increase in H causes increase in Cl. If acidosis cause by something whose counter ion is not Cl (lactic acid) anion gap increases, Cl can’t keep up. Decreased Gap, abnormal cations, decreased albumin. Acid Base Imbalances Metabolic Acidosis; increased organic acid, correct by hyperventilation. Decreased pH and bicarb. P (CO2) will drop with compensation. Metabolic Alkalosis, loss of acid, hypoventilation, excretion of bicarb will increase. Alkaline urine, increase P (CO2). Respiratory Acidosis, can’t get rid of CO2, smaller increase in HCO3. Respiratory Alkalosis/hyperventilation, kidneys excrete bicarb. Pregnancy can cause, excessive crying, aspirin intoxication. Renal Diseases Renal cortex- where most of the work is happening. Glomerulus has thick basement. Type 4 Collagen forms the scaffold. Only certain things get through. Albumin too big (most of them). Nephritic syndrome- glomerular syndrome with acute renal failure (acute kidney injury), and oliguria. Hematuria (red or brown if present), proteinuria and hypertension. Chronic kidney disease- GFR less than 60mL/mL for at least 3 months and/or persistent albumuria. Can’t keep albumin in. Acute kidney injury- most severe as oliguria or anuria, result from glomerular, interstitial or tubular. Renal tubular injury- electrolyte loss. Chronic kidney disease (renal failure) - End stage GFR is < 5%. Dehydration, edema, uremia, bleeding issues, hypertension, mimic uremia, skin problems. Glomerular damage- hypercellularity, form crescents (bad sign), leukocytes come in, basement thickens, increase protein synth, hyalinosis (result of wall injury), sclerosis. Pathogenesis of glomerulus injury- commonly immune complex mechanism. 2 ways: injury of antibodies in situ, and deposition of antibody-antigen complexes. In situ formation- to intrinsic antigens or antigens (DNA, aggregated products, and proteins) planted into glomerulus. Anti-GBM Nephritis, diffuse linear immunofluorescent staining, antibodies to NC1 domain of type 4 collagen. Deposition pattern is granular with circulating complex deposition. With circulating depositions, glomerulus is innocent bystander, complex formed in circulation. Epithelial cells can be injured by toxins and other things, changes to foot processes. Mechanism of progression- Renal Ablation Glomerulopathy, once GFR goes down below 30-50% end stage failure is inevitable. Major histological characteristics of progressive renal damage are focal segmental glomerulosclerosis (leads to proteinuria and functional impairment, glomerular hypertrophy too) and tubular fibrosis. TGF-B plays a role inducing sclerosis. Proteinuria can cause direct injury. Nephrotic Syndrome- Massive proteinuria, 3.5g or more/day. Hypoalbuminemia, generalized edema and hyperlipidemia with lipiduria. Almost always a primary renal lesion in children under 15. Adults with systemic disease (Diabetes, amyloidosis, lupus, drugs, infections, malignancies, miscellaneous things like bee stings). Membranous Nephropathy- slow progressing, 75% primary, secondary to lupus and other disorders. Diffuse thickening of glomerular capillary wall from Ig accumulation along the sub-epithelium. Primary linked to HLA antigens or renal autoantigens (PLA2R). Complement plays big role in leaky capillaries. Spike and dome pattern, granular Ig complement. Loss of foot processes. Clinically insidious nephrotic syndrome. 15% have proteinuria, 13- 35% hematuria and HTN. Resistant to steroids. High risk of disease coming back even with new kidney. Highest incidence of renal vein thrombosis and other thrombosis. Minimal Change Disease- most common in children 2-6 years. Commonly associated with atopy (also seen with asthma). Proteinuria. No deposits. Diffuse effacement of foot processes. Selective proteinuria, primarily albumin, great response to steroids. Focal Segmental GS- only involves segments of glom. Secondary associated with heroin use, component of ablation. Degeneration and focal disruption of visceral epithelial cells, loss of foot, and mechanism of epithelia damage unknown (genetics?). Collapse of BM, detachment of cells. Only certain areas get hurt, and only parts of the glomeruli. Membranoproliferative Glomerulonephritis- is immune-mediated injury instead of disease. 2 groups. Both types look similar, proliferation of cells, double contour of membrane (train tracks). Type 1- deposition of IgG and complement. 2/3 of cases, granular deposits of IgG and C3. Clinical course; in younger people, hematuria, proteinuria, high incidence of recurrence with transplants. Type 2- activation of complement most important. Dense deposit disease, lamina densa is transformed into electron dense structure. More common in adults with immune disorders, decrease C3 normal C4, and complement system always on. Primary type 2 hits children and young adults, lead to end stage renal disease. Nephritic syndrome; inflammatory alterations to glomerulus Acute Post-infectious GN- diffuse proliferation of Gm cells. Classic in children or adults. Typically after certain strains of strep (pharyngitis and skin, honey- crust and impetigo). Mostly children 6-10. Increased cells, might see thrombi, crescents if bad. What cells = neutrophils, and all types of others. Deposits everywhere. IgG and complement. Usually clears in a few months. Abrupt onset, malaise, fever, nausea, oliguria, red cells and red cell casts in urine (red to brown color). Complete recovery in 95% especially in epidemics. Sporadic and adult cases more likely to go end stage. Rapidly progressive crescentic GN- Not specific etiologic form, associated with severe injury, rapid and progressive loss of function, severe oliguria, death if untreated. Most causes is immune mediated. Type 1 is anti- glomerular basement membrane disease, linear staining, cross reactivity with lung (coughing up blood). Type 2 is also immune mediated, lumpy bumpy deposits, treat underlying disease. Type 3, Pauci-immune type, lack of basement antibodies, most have ANCAs in serum. Clinical course pronounced oliguria and azotemia, if crescents in less than 80% prognosis in better. IgA Nephropathy (Berger disease): IgA deposits in mesangial, worldwide most common cause of GN. Dense deposits. Chronic GN, end stage of many entities. Tubulointerstitial Nephritis: Acute Pyelonephritis- bacterial infection of kidney and renal pelvis (ascending route most common). Obstruction can aid in causing this. Patchy interstitial inflammation and necrosis. Papillary necrosis more common with diabetics. Abscess formation, lots of little holes. Obstruction, diabetes and immune issues predisposes. Sudden onset of pain at costovertebral angle and evidence of infection, pyuria, WBC casts in urine, papillary necrosis is poorer prognosis. Chronic Pyelonephritis- pelvis and calyces, due to obstruction, reflux nephropathy most common, scarring of kidney. Maybe be insidious or acute recurrent, polyuria and nocturia, may develop focal sclerosis. Acute tubular injury/necrosis. From ischemia or toxin, reversible in most people. Tubules are very sensitive to oxygen and toxins. Disturbance in blood flow further reduces blood flow to medulla. Ischemic form- patchy tubule necrosis, rupture of basement. Nephrotoxic- extensive necrosis mostly proximal tubule, no rupture of basement. Can be caused by dyes in vascular studies. Initiating (36hrs) – slight decline in urine output, increasing BUN. Maintenance- oliguric or non-oliguric (better outcome), BUN rises, hyperkalemia, salt and water overload. Recovery- steady increase in urine volume, hypokalemia, may need dialysis. Eventually tubules restored and function improves. 95% who don’t succumb to cause recover. Shock related to sepsis can have high mortality as can burns. Cause of death infection, worsening of disease. Drug induced interstitial nephritis. Acute Drug Induced form- common with antibiotics, diuretics, NSAIDs, and others, 15 days after exposure, fever, rash (25%), eosinophilia, renal abnormalities. Drug acts as hapten, becomes immunogenic, IgE. Hematuria, mild proteinuria. Edema, mononuclear cells, tubulitis. Hard to make out tubules. Withdrawal leads to recovery, important to recognize. Analgesic Nephropathy- excessive intake of analgesics. Low incidence in US. Aspirin, caffeine, acetaminophen, codeine. Papillary necrosis is first, raised and depressed areas, fibrosis and inflammation. More in women, and patients with headaches. Early finding, can’t concentrate urine, stones, infection can occur too. Disease of blood vessels Nephrosclerosis- strongly associated with HTN. Hyaline deposition, increased basement, diabetic patients have this too. Slightly smaller kidney, granular surface, narrowing of wall, hyaline in walls. Patchy ischemic atrophy. Malignant form is really bad, associated with malignant hypertension. Can arise as first sign of HTN. Some form of vascular damage to kidneys, markedly elevated renin. Morphology: fibrinoid necrosis of arterioles, hyperplastic arteriosclerosis (arteriolitis). Hypertensive encephalopathy can be seen with this too. Systolic above 200, diastolic above 120, is an emergency. May have CNS signs, can go into renal failure. Big chunk survive but still have disease. Hyaline atherosclerosis associated with benign form. Renal Artery stenosis is very treatable, can be caused by plaques are fibromuscular dysplasia. Hydronephrosis- dilation of pelvis, caused by obstruction, bilateral if in ureters. Can be sudden or insidious, unilateral or bilateral (obstruction below ureters). Congenital- atresia of the urethra, valve formation in ureter or urethra, aberrant renal artery, kinking of ureter. Acquired, foreign bodies, stones, lesions, inflammation, neurogenic (spinal cord injury with paralysis, diabetes), pregnancy. Kidneys may or may not be enlarged. Bilateral leads to renal failure. Bilateral leads to anuria with complete obstruction. Unilateral can be silent for a long time, repeated infection. Renal Cell Carcinoma: older males, smoking, pipe and cigar, obesity, HTN. Carcinogens in blood get concentrated in urine. Comes from tubular epithelial cells. Clear cell is most common form. Yellowish, spherical, areas of hemorrhage or necrosis, and tendency to invade renal vein. Costovertebral pain, palpable mass, hematuria, but often remain silent. 45% 5 year survival rate, better when found early. Male Genitourinary Diseases: Bladder Unique epithelium, transitional cells. At the base more cuboidal and glandular, near surface flatter and squamous. Diverticulum more often secondary, outpouching of bladder. Rarely congenital. Site of urinary stasis, predisposition to infection and formation of stones, as well as backwash. Exstrophy; failure of abdominal wall to close, bladder on the outside, urine goes out into the abdominal opening. Chronic UTI, increased risk for adenocarcinoma of the bladder. Inflammatory disorder; acute cystitis- infection, hemorrhage, radiation. Chronic- interstitial cystitis, malakoplakia. Symptoms (important) - urinary frequency, lower abdominal pain, pain/burning on urination (dysuria). Acute infectious cystitis, usually from colonic bacteria (E. coli, Klebsiella, proteus, Enterobacter). Middle Eastern countries, notably Egypt get Schistosoma haematobium. Hemorrhagic, common with chemotherapy. Radiation cystitis not as common anymore. Chronic cystitis- petechial hemorrhages, localized ulceration, shrunken bladder. Middle age females, extreme urinary frequency, urgency and dysuria. Wall gets thickened. Malakoplakia- defect killing bacteria (commonly E. coli) by macrophages. Associated with immunosuppression. Macrophages form lumps and bumps. Soft, yellow, slightly raised plaques. Large, pink, foamy macrophages. Metaplastic disorders; caused by inflammation, exstrophy, stones, infection. Shoving things up your wiener, like gum and tie tacks. Neoplasms; 90% are transitional cell carcinoma. Transitional papilloma; rare, finger-like, benign. Prone to recur, but rarely progress to cancers. Inverted papilloma, grows into the wall, rare and benign. On the surface looks flat. Malignant carcinomas; more common in males 3:1, age 50-80. Presentation, painless hematuria, frequency, urgency, dysuria. Risk factors; smoking, chemical exposure, Schistosoma infection, chemotherapy. Transitional carcinomas can be papillary (more common) or flat (more aggressive). In situ or non-invasive- haven’t broken through basement membrane. 60% are singular and 70% are localized to bladder, so treatment usually good. Squamous cell carcinoma most common in Egypt because of Schistosoma infection. Adenocarcinoma, associated with bladder exstrophy and very rare. From urachal remnants. Urethra Shorter in women, more pathology potential. Most common disorder is inflammatory disorders, gonorrhoeae, E. coli, Chlamydia, and Mycoplasma. Transitional cell carcinoma again. All inflammatory disorders results in urethral obstruction. Penis Congenital anomalies, most common is malformation of urethral groove. Epispadias on dorsal surface, hypospadias on the ventral surface. Associated with malformed bladder and undescended testicle. Can lead to UTI and sterility. Phimosis: abnormally small opening in prepuce (opening of foreskin). Primary developmental defect, secondary to infection. Chronic accumulation of secretions and debris, can lead to carcinoma. Paraphimosis, abnormal painful swelling of the glans penis. Underlying swelling, things get stretched, chronic urethral obstruction. Inflammation disorders, sexually transmitted diseases. Syphilis (not painful), Gonorrhea, Chancroid, Herpes (little vesicles). Balanopthitis, nonspecific infection of glans and prepuce. Associated with phimosis or redundant prepuce, chronic accumulation of debris. Yeast more common with diabetes. Staph and Coliforms in others. May lead to ulcerations and scarring. Neoplasms: benign ones pretty common. Squamous cancer is slow growing (important). Condyloma acuminatum= warts. Small but multinodular. Most remain benign, are recurrent. Carcinoma in situ, pre-cancer. Diagnosed by biopsy. Usually a whiter plaque like growth. If left alone, will eventually become invasive squamous, but slow growing process. Squamous cell carcinoma, almost always on uncircumcised men. Slow growing tumors, easy to treat! Distant metastases are uncommon. Testis and Epididymis Cryptorchidism: failure to descend into scrotum, 75% unilateral. Most are idiopathic, linked to trisomy 13, or deficiency of luteinizing hormone- releasing hormone. Grossly are small and firm. High prevalence of inguinal hernias and sterility, 10x risk for neoplasms. Orchiopexy to treat (less sterility but cancer risk the same), or give LHRH agonist. Marijuana can elevate female hormones and lead to this. Orchitis and epididymitis = inflammation. Most infections are ascending, so epididymitis is more common. Specific inflammation; Mumps is common for Orchitis, Tb and syphilis are rare but can happen. Inflammatory disorders not as common. Granulomatous, cause enlargement which mimic tumors (more common). Mumps orchitis uncommon in children, usually not associated with sterility. Tb goes from epididymis to testis, syphilis begins in testis. All associated with swelling. Torsion: twisting of the spermatic cord. Venous obstruction but arteries remain patent. Caused by trauma or other violent movement, incompletely descended testicle, absence of ligaments, testicular atrophy. Also causes swelling. Extensive hemorrhagic necrosis. Tunica Vaginalis: sac around the testis and epididymis. Conditions based on what gets into that space in between. All can cause enlargement of scrotal sac, and may cause infertility. Hydrocele is serous fluid, often with chronic edema. Hematocele, blood accumulation from trauma, tumor, generalized bleeding disorder. Chylocele, lymphatic fluid, obstruction often from tumor. Spermatocele is descended spermatic cord. Varicocele is veins being engorged, venous stasis, more on left than right, bag of worms. Neoplasms; Often in younger population. 10% of all cancer deaths. Risk factors; undescended testis, genetic factors (African blacks much less likely than American blacks), feminization, Klinefelter. Are generally painless. 95% are germ cell tumors, seminoma most common of these. 5% are sex-cord stromal. Seminoma; middle age 30-40. Fairly benign, respond very well to treatment. Grey-white mass. Most common tumor in young adult males. Spermatocytic seminoma; same process, slow growing, not as common 5% of seminomas. Embryonal carcinoma; 20-30 years old. Considered highly aggressive, poorly demarcated. Areas of necrosis means outgrowing blood supply. Yolk Sac tumor; 3 years and less. Adults can get them too, but very uncommon. Very good prognosis up to 3 years of age. More aggressive in adults. Choriocarcinoma; ugly cancer, extensive hemorrhage and necrosis, very aggressive. Don’t buy green bananas, you won’t live long enough to eat them. Teratoma; has cells from all three germ layer of embryo. 2nd most common tumor in children. Hair and teeth and heterogeneous layers. Can form into a carcinoma. Mixed tumors; 50% of all germ cell tumors. Commonly we see teratoma with embryonal and yolk sac. Whatever the most aggressive tissue is present is what determines prognosis. All tumors treated with radiation and chemotherapy. Sex-cord stromal tumors- usually small masses, secrete hormones. Leydig cells lead to accelerated puberty, man boobs. Sertoli cells rarely induce precocious puberty, occasionally see male boobs. Lymphomas very uncommon; often in 60 years older patients. Looks like a big lymph node. Homogenous tan process. Prostate About the size of a walnut, normally. Lots of little holes, representing glands (where pathology occurs). If it feels hard it’s bad. Should feel like nose or ear, spongy. Inflammation not as common. Similar organism as bladder and testis, direct extension from these infections. Soft and enlarged from edema, tender. Abacterial, no positive culture, etiology uncertain. Benign nodular enlargement, incidence increases with age. Nodular hyperplasia is benign, no interest in becoming cancer. Usually enlargement of stromal cells. Are peri-urethral, well circumscribed nodule, rubbery and yellow, and obstruct urethra. Adenocarcinoma; most common cancer in men. Second leading cause of cancer death. Age greater than 50 years. Rare in Asians, more common in blacks than white. Pathogenesis unknown. 70% are in periphery of the gland. Poorly demarcated, firm, gritty yellow nodule. Gleason scale is 2-10, higher score is bad. Central area of prostate, growths usually benign. Metastasize to local lymph nodes. Stage A is least common because it’s non-palpable. Stage B is 60% because palpable. Most don’t have symptoms yet. Chief diagnosis is rectal digital examination. Trans-rectal sonography, needle biopsy, prostatic acid phosphatase. Prostate-specific antigen, can be elevated from other things, better for follow ups. Treatment and prognosis based on stage. Female Urogenital diseases Infections- wide variety of organisms, some cause discomfort, others infertility, or even spontaneous abortion. Candidiasis, most common female genital pathogen, since it is a normal GI flora. Risk for= pregnant, diabetes, antibiotic. Pseudohyphae in yeast forms. Chlamydia- most common STD in world, majority are asymptomatic, affect cervix but most women can’t see that. Can cause ascending infection resulting in Pelvic Inflammatory Disease. Pelvic Inflammatory Disease- common, results from ascending infection, gonococcus, chlamydia, Enterobacter. Can spread to fallopian tubes. When you look inside all you see in inflammation. Pain, tenderness, fever, discharge. Can lead to infertility and other infections. Surgery and antibiotics. Vulva Lichen Sclerosis and squamous hyperplasia; non-neoplastic, cause white scaly plaque (leukoplakia). Lichen Sclerosis, may be linked to estrogen, inflammation, band like infiltrate in dermis. Thinned whitened epithelium, constriction of opening. Commonly see with chronic inflammation. Squamous Hyperplasia, women 30-60, focal vulvar puritis and focal grey-white plaques. Neoplasms of Vulva Condyloma Acuminatum, genital warts. HPV 6 and 11, vulva less common than cervix. Verrucous gross appearance, koilocytosis (nuclear atypia, perinuclear vacuole). May regress or progress. Interepithelial epiplasia; presents as white plaque often over 60 years. Shift in incidence with women under 40 years of age, from venereal warts. Multi- centric, look like basaloid cells, flatten out and keratinize. May persist for years before invading. Squamous cell carcinoma; associated with HPV, when not involved the lesions are more defined. Lesions less than 2 cm have much better prognosis. Extramammary Paget’s disease; uncommon in this location, labia majora most common site. Malignant Melanoma can occur as well, always capable of wide metastasis, prognosis poor. Vagina Squamous cell carcinoma; 90% of vaginal malignancies, most associated with HPV. Lower 2/3 lesions drain to inguinal nodes, upper 1/3 to region iliac nodes. Painless vaginal bleeding, discharge. Some may remain silent until it burrows through. Clear Cell adenocarcinomas; much less common, increased with exposed to diethylstilbestrol in utero (exposed as fetus). Vaginal adenosis is probably precursor. Most see signs at 10-20. Difficult to cure. Cervix Polyps; benign, cause regular bleeding. Soft mucoid masses, inflammation and metaplasia are common. Intraepithelial and invasive squamous cancers of the cervix (a must know); Cervical pathology starts often in transition zone. Squamous metaplasia. HPV- DNA detected in greater than 80% of cervical cancers, especially high risk strains 16, 18, 31, 33. Have specific viral oncogenes E6 and E7. Viral integration disrupts regulatory proteins. E6 binds p53 and accelerates its proteolytic degeneration. E7 displaces t factors it normally sequesters, cells are pushed into mitosis. HPV not only factor, but is most common. Can also invade glandular tissue. CIN 1 to 3 depending on severity, which sent to squamous interepithelial lesion, low or high grade. Likelihood of progression is based on where it’s at in its course, what type of HPV. Invasive cervical carcinoma; squamous is most common type, occurring in younger women, vaginal bleeding, and painful coitus. Spreads by direct extension. Endometrium Endometriosis; Presence of glands in abnormal location, infertility, pain. During reproductive period. Adenomyosis when in the wall. Regurgitation theory, metaplastic theory, vascular dissemination theory. Ovary can get “chocolate cyst”. To make diagnosis need 2/3: Endometrial glands, endometrial stroma, or hemosiderin pigment. Dysmenorrhea, dysuria. Endometrial Hyperplasia; Relate to high levels of prolonged estrogenic stimulation with little or absent progesterone activity. Occurs around menopause, or with anovulation. Abnormal uterine bleeding (won’t get true menstruation). Increased risk of endometrial carcinoma. Inactivation of PTEN is common, among other risk factors. Non-atypical- low risk, increased gland to stroma ratio, response to persistent estrogen. Atypical- complex glands, higher risk. Endometrial Carcinoma; most common invasive cancer of female genital tract. Most common in glands, post-menopause, dysfunctional uterine bleeding (DUB). Higher frequency with diabetes, fat tissue makes estrogen. Type 1, estrogen stimulation hyperplasia, PTEN mutation, not high risk, go right into endometrium. Type 2, no increased estrogen, poorly differentiated, endometrial atrophy, poorer prognosis, mutation in TP53, all are grade 3. Uncommon in women under 40, no screening test, abnormal bleeding (leads to diagnosis often). Leiomyoma; fibroid tumor, estrogen responsive, most are asymptomatic, can cause pain, bleeding, pregnancy issues. Ovary Follicular and luteal cysts are common, and immediately sealed. Polycystic ovary syndrome- complex endocrine disorder. Menstrual abnormalities, cysts, anovulation, decreased fertility. Associated with obesity. Ovarian tumors; numerous types majority are benign, malignant more in older women. Mild symptoms until large size 25-30 kilograms. Malignant tumors have often spread outside by time of diagnosis. Epithelial tumors are often bilateral. Vague symptoms. Ovarian carcinoma is relatively common, not found early. Not having children is a risk. BRCA1 mutation is risk as is other oncogenes, high levels of HER2/neu. Divided by tissue of origin. Germ Cell tumors are 15-20%, 3-5% are malignant. Serous epithelial tumors; benign are 60%, malignant 25%. More in younger women. Two types; low grade endometriosis mucinous. Type 2, inclusion cysts, high grade features, serous tubule. Can be 1040cm, borderline had more projections. Malignant have more nodules. Classification relevant to prognosis and treatment, high survival rate if only in ovary, but malignant does a lot worse. Mucinous tumors; KRAS mutation, middle aged women, more cysts than their counter part. Pseudomyxoma Peritonei; associated with mucinous ovarian tumors. Implants and adhesions on surface, can cause death. Germ Cell tumor- teratoma. Mature- ectodermal differentiation (dermoid cysts). 90% unilateral, usually on the left. Hair bearing epidermal lining. Other tissues often present. 1% undergo malignant transformation, one of the tissue type become a carcinoma, commonly squamous cell carcinoma. Immature = malignant, found in prepurbertal women, resembles embryonal and fetal tissue. Nondermal or specialized teratomas are very rare, may be functional. Must be differentiated from metastatic disease. GI disorders: Esophagus Cricoid cartilage, left bronchus and diaphragm, narrowing areas of esophagus. Vast majority is squamous epithelium. Dysphagia (difficulty in swallowing). Pyrosis (heartburn). Congenital; Atresia, part is not canalized, blind pouches. Fistula, pouch joins into another structure. Are uncommon, found soon after birth, incompatible with life, associated with heart disease. Stenosis is non-neoplastic narrowing. May arise as congenital defect, though not common, more common in adult life after esophageal injury, reflux commonly, radiation, scleroderma, caustic injury. Achalasia- failure of innervation for relaxation around esophageal sphincter, bird’s beak narrowing. Secondary from invasive organisms. Proximal becomes relaxed and over-dilated. Hiatal hernia; may also affect infants and children. Retro-sternal chest pain related to regurgitation of gastric juices. Dilation of stomach above the diaphragm. More common type is sliding/axial hernia, bell shaped dilatation, short esophagus. Other type is rolling hernia, normal esophagus length, stomach pops up next to esophagus, vulnerable to strangulation and infarction. Can ulcerate and bleed, more often with rolling type. Diverticulum- very common so it’s important, also common in colon. Outpouching of one or more layers of esophageal wall, “lump in the throat”, bad breath, regurgitation, gurgling sensation or sound. Zenker’s type, pharyngeal from motor dysfunction, upper esophagus. Traction type is also motor dysfunction, but often with an area of stenosis that pushes through weak spot. Laceration (Mallory-Weis Syndrome) - lower esophageal, tears in the mucosa, result in catastrophic bleeding, commonly seen in alcoholics, usually nonfatal bleeding, prompt healing. Results from excessive vomiting, in the setting of toxic gastritis. Can be potentially massive bleeding, more commonly inflames and forms scar tissue which can form a stenosis. Mucosal lesion. Varices- submucosal, distal esophagus, tortuous dilated veins, in 90% of cirrhotic patients, common in alcoholics again. Clinically silent until rupture, catastrophic bleeding. Result in severe portal hypertension from stenosis (scar tissue). 90% chance for recurrence within a year, 40% fatality. Urgent surgery required. Inflammatory disorders Reflux esophagitis- most common esophagitis, usually in adults. Injury to mucosal from reflux. Can get a little bleeding (hematemesis), when passed into feces (Melena). Hiatal hernia can cause, relaxed emptying, and reduced reparative ability. Key feature is formation of Barret esophagus - replacement of squamous with columnar cells, response to prolonged injury. More of a dull velvety look, can form scars, 30 times increased risk for adenocarcinoma. Neoplasms Benign are more commonly intramural. Mucosal: Squamous papillomas, fibrovascular polyp (may be quite large), inflammatory polyp (less common). Intramural or Submucosal; Leiomyoma and fibroma most common ones. Malignant are largely mucosal. 6% of cancers in GI tract. Squamous is 50% and adeno is 50% (more distal in location). Age greater than 50, black men, northern china, Iran, Russia and South Africa (cold environments from foods they eat, nitrates, alcohol, and tobacco). Anything that causes long standing esophagitis. Insidious onset. Obstruction, weight loss, maybe some bleeding, acquired fistula formation. 50% in the middle, equal numbers upper and lower. Metastasize quickly, can locally invade, not a good diagnosis. Adenocarcinoma is a little earlier age, 40. Similar symptoms, GI reflux in less than 50%. Usually in distal third, better survival, but not great. Stomach Most pathology will be glandular. Congenital anomalies; Diaphragmatic hernia- failure to form diaphragm, more common on left, does not involve hiatal orifice, protrusion of abdominal organs into thorax, usually in utero, respiratory impairment. Pyloric stenosis is more common, secondary to muscular hypertrophy, more in little boys. Regurgitation and vomiting by 3 week of life (important), peristalsis is visible, palpable firm, ovoid mass in epigastric region. Secondary swelling and edema formation. Fix by cutting out a segment, making it more c-shaped and less like a donut. It can also be acquired, long term chronic inflammation, peptic ulcers, or malignancies. Inflammatory disorders. Acute gastritis, usually transient, may be some minor pain and bleeding. Results from increased acid, decreased bicarbonate, reduced blood flow (shock), disruption of mucus layer, and direct damage. Chronic NSAID use, particularly aspirin, heavy alcohol consumption, heavy smoking, chemotherapy. Little bit of edema and reddening, superficial erosion, hemorrhage, black and tarry stool. Chronic gastritis- may lead to mucosal atrophy and cancer. Usually few vague symptoms, nausea, vomiting, upper abdominal discomfort. H. pylori overgrow especially prominent. Risk for cancer is 2-4%. Gastric ulcers- peptic or stress. Mucosal defect that extends into submucosa. Peptic ulcer, usually solitary, start with mucosal defect, duodenum and stomach account for 98%, may involve any portion of tracts, more in men, middle aged to older. Burning, aching pain, more when you lie down and after meals (1-2hrs). Cirrhosis, pulmonary disease, renal failure, hyperparathyroidism are risk factors. Caused by imbalance between defense and damaging forces. H. pylori again is a culprit. Look like a nice punched out hole. Raised margins would be a sign of cancer. Once they break through, they get to blood vessels or cause catastrophic bleeding or leakage of gastric contents. Acute gastric ulcer- stress ulcer. More likely with stressed out people, intensive care unit. Can result in GI hemorrhage. Are superficial hemorrhages that are staring to break down, often are multiple. Key factor is treatment, treat underlying cause. Hypertrophic gastropathy- rugal folds exaggerated, giant cerbreform folds, hyperplasia of epithelial cells, increased risk for peptic ulcers and adenocarcinomas. Patients often malnourished. Neoplasms- same process as cancers in lower GI tract. Polyps are common in stomach, mostly in large intestine. Benign forms- hyperplastic/inflammatory polyps 90% always stay benign, gastric adenoma 10% is pre-cancer. Exuberance of normal mucosa. Gastric adenomas are usually single while hyperplastic ones are multiple. Malignant; 90-95% are carcinomas, lymphoma, carcinoid and sarcomas are rare. Not common is U.S. Usually asymptomatic until near pyloris or have metastasized. Risk factors are bad foods, nitrated, smoked foods, pickled vegetables, lack of fresh fruits and vegetables. H. pylori because it causes inflammation and peptic ulcers. Big polypoid masses or spreading flat masses. Linitis plasticus; rigid diffuse thickening when it infiltrates the wall, white color. Pylorus and antrum 50-60% usually better because we see signs earlier, on lesser curvature more than greater. Signet ring cells mean worse prognosis, Krukenberg’s tumor metastasizes to ovaries. Prognosis is poor because usually not found early. Nutrition Primary deficiencies are dietary inadequacies. Secondary has other causes, like a tapeworm. Anorexia Nervosa- self-imposed, do not believe they are thin or starving, intense fear of weight gain. Severe protein calorie malnutrition, amenorrhea from lack of adipose tissue, decreased GnRH, LH and FSH. Hypoalbunemia may or may not be present, lymphopenia, decreased thyroid hormone, dehydration. Increased risk of sudden death, cardiac arrhythmias, hypokalemia. Bulimia; binging followed by vomiting. More normal height to weight ratio. Still see menstrual irregularities, electrolyte abnormalities, aspirate gastric contents, esophageal and cardiac rupture, dental issues. Obesity- common problem, 20% increase in weight is health risk, 20% of men 40% of women, childhood obesity is increasing. BMI is correlated with body fat, but not always. Distribution of fat; Central Obesity- it accumulates in trunk and abdomen, cortisol causes, higher risk for certain disease. LEP gene is a key gene in energy homeostasis, Leptin is its product. Arcuate nucleus in hypothalamus- process and integrate peripheral signals, generates new signals. Protein-energy malnutrition; inadequate intake of protein and calories. Somatic protein compartment- skeletal muscle, look at mid-arm. Visceral compartment- stores in visceral organs, serum albumin, total protein and transferring. Marasmus: deficiency in total calories (protein, carb and fat). Weight falls to 60%, catabolism of somatic compartment, but sparing of visceral. Loss of muscles and fat, stunted growth, classically co edema (hybrid forms exists), serum albumin is normal or slightly decreased, are alert and hungry. Thymic and lymphoid atrophy, immune issues. Kwashiorkor: “disease the child gets when the next one is born”, deficiency of protein with high carbohydrates. More severe than marasmus, loss of protein in visceral compartment. Hypoalbuminemia gives edema. Apathy, general edema, flag sign; alternating pigment and depigmented areas, dermatosis, fatty liver (need lipoprotein to get fat off liver), weight near normal, as low as 60%. Visceral and thymic atrophy. Secondary PEM- commonly with chronic illness or hospitalized patients. Vitamin Deficiency; Fat Soluble- A, D, E and K. Must have intact fat digestion and absorption. Vitamin A- next to protein malnutrition, is most prevalent nutritional disease. From leafy and yellow vegetables. Active in vision, rhodopsin, iodopsins. Photosensitive pigment of visual system. Also important role in cell differentiation and immune system. Problem with epithelial differentiation- xeropthalmia- keratinization on conjunctiva. Keratomalacia- corneal stiffened and ulcering. Metaplasia especially in mucus-secreting epithelium. Night blindness. Respiratory infections, renal stones, higher infection rates. Toxic when taken in excess. Acute- headache, dizziness, vomiting, blurred speech. Chronic- weight loss, anorexia, nausea, vomiting, bone and joint pain. Stimulates osteoclast production and activated, risk for fractures. Synthetic retinoid toxicity, used to treat acne. Avoid using in pregnancy, teratogenic effect of retinoid. Vitamin D- leads to bone problems. Synthesis in the skin, from exposure to sunlight. In fish, plants and grains. Stimulates intestinal absorption of Calcium, and helps pull it back in from the urine. Deficiency leads to Rickets in children, legs bow out, lumbar lordosis, rosary, Harrison’s groove, and pigeon breast. We see un-calcified bone matrix. Osteomalacia in adults; osteopenia. Lab measure 25 OH, Blacks, Hispanics, and Asians are at higher risk of deficiency from more melanin. Give supplements. Vitamin E: vegetables, grain and buts. Active as a-tocopherol, is an antioxidant. Deficiency- loss of proprioception and vibration, impaired eye movements and muscle weakness, degeneration of axons in posterior column. Vitamin K; gut flora make it, but inadequate as a sole source. Cofactor for carboxylation of glutamate, important for coagulation, and osteocalcin. 2, 7, 9 and 10, C and S. Petechial hemorrhages, joint bleeding, hemorrhagic disease of newborn. Water Soluble Vitamins B1: Thiamine, helps synthesis ATP, maintain neural membranes. Deficiency = Beriberi- wet or dry. Wet is flabby heart with four chamber dilatation. Dry has peripheral neuropathy, foot drop. Wernicke-Korsakoff syndrome; Grayish discoloration and softening of mammillary bodies, changes in thalamus, 4 th ventricle, cerebellum. Opthalmoplesia (paralysis of eye muscles) can occur, goes away quick if thiamine given. Will have memory problems, and make stuff up (Korsakoff Psychosis). Neuropathy is symmetric. Riboflavin (B2); changes at angles of mouth, tongue, ocular and skin changes. Tongue becomes atrophic and magenta, greasy, scaly skin. Niacin deficiency is pellagra; similar to riboflavin, but tongue swells and is red. Also with diarrhea from atrophy of columnar cells. Glove and stocking distribution, necklace formation. B6, Pyridoxine; 3 forms, important for AA and protein metabolism. Similar to last 2 deficiencies. Vitamin C; Scurvy. Important to know, involved in bone formation and wound healing. L-ascorbic acid. Growing child, hemorrhages (can’t make collagen in blood vessels). Bleeding into joint spaces, can’t make osteoid matrix, scorbutic rosary- depression of sternum and projection out of ends of ribs. Poor wound healing, gingival swelling and hemorrhages. Bone pain, pretty bad, periosteum gets stretched. In excess, there’s no support they protect against cold or cancer. Zinc deficiency; Co enzyme for over 200 systems, in lots of things. Acrodermatitis enteropahica, loss of appetite to anorexia, growth retardation, hypogonadism. Lower GI Pathology Small Intestine, 3 distinct regions; DJ ill. Absorptive cells, mucin secreting goblet cells, and endocrine cells. Congenital; Omphalocele (musculature fail to form, prune belly), and Gastroschisis (wall fails to form, guts on the outside). Both rare and life threatening. Meckel’s diverticulum- mucosa-lined blind pouch whose lumen communicate with lumen of ileum, dead end, in 2% of population. Food gets trapped and inflamed, mimics other disorders. Around 30cm of ileocecal valve. Might be a sight for perforation. Atresia and stenosis; Atresia = blind pouches, stenosis = narrowing (more commonly acquired). Ischemic bowel disease; fairly common, due to vascular compromise. Not a lymphatic process. Classification based on thickness. Anything that causes vascular compromise, thrombi, embolism, venous collapse, tumors, blunt trauma, cardiac failure, shock, dehydration. Transmural is full thickness necrosis of all bowel layers, can cause spillage of content. Mural and mucosal; incomplete and patchy, usually lots of small blood vessels far downstream. Chronic are typically segmental, over time can scar and constrict, prolonged period. Severe pain and tenderness, bloody diarrhea or melena, nausea, vomiting, bloating, rigidity. Typically occurs in severe ill patients (vascular compromise, tumors). 50-75% death rate with transmural infarction. Malabsorption syndromes; disturbance of digestion in lumen, or inability to pass nutrients into bloodstream. Diarrhea, flatus, pain, weight loss, bulky, frothy, greasy stools, anemia, bleeding. 3 major diseases that cause; Celiac sprue, chronic pancreatitis, Crohn’s disease. Celiac sprue; gluten sensitive enteropathy, largely in whites, fairly common, infants to adults, no understanding why or what starts. Immunologic sensitivity to gluten. Can’t see grossly, need microscope, sheets of lymphocytes in lamina propria. Diarrhea, farts, weight loss, fatigue. Complications of vitamin and iron deficiencies, 10-15% risk of GI lymphoma, treatment is don’t eat gluten. Obstructive disorders; something preventing flow of food, fairly common diagnosis. Commonly see hernia as obstruction typically involves small or large intestine. Weakness of defect in peritoneal wall, permits protrusion of peritoneal sac (hernia sac). Since it bulges through, viscera gets stuck in sac. Typically in inguinal and femoral canals, umbilicus, surgical scars, retroperitoneal space. May lead to ischemia and perforation. Incarcerated means it’s stuck in that area. Strangulation = vascular compromise, pending infarction. Adhesions may act like a hernia, scar tissue form inflammation, surgery. Intussusception- one section of intestine telescope into itself, snake eating its own tale. Common with pediatrics (usually reversible), may be symptom of colic. Bad in adults, almost always from a tumor. Volvulus- twisting of mesentery, obstruction or pseudo-obstruction from dead tissue. Neoplasms; benign 60%. Duodenum around Ampulla of Vader often. Adenocarcinoma- napkin ring Carcinoid tumor- from endocrine cells, when they happen in the GI, strong affinity for terminal ileum, appendix, right colon (lower right quadrant). Because of location don’t often cause big symptoms, but do secrete hormones causing effects. Breast enlargement in men. Have yellowish, tan hue, solid, up to 50% of small intestinal tumors. Small bowel obstruction can occur. Appendix No known function, maybe mucosal immunity. Worm off of cecum, terminal ileum nearby. Inflammatory disorders much more common, appendicitis. Acute form requires surgery, any age group, peri-umbilical pain, goes right lower quadrant, mild fever, elevated WBC, abdominal guarding. Don’t know how it occurs, may be obstruction, fecalith (petrified piece of poop), stone, tumor, parasites (pin worm). Red and swollen, necrosis. Up to 25% false positive rate. Can be 2% perforation and mortality. Neoplasms; benign are not common, mucocele, mucinous cytadenoma. Carcinoid tumor is most common (mimics appendicitis), adenocarcinoma also occurs. Large Intestines Cecum is the beginning, where the appendix is. Widely spaced mucosal folds (haustra). Rectum is only part that is retroperitoneal. Lined by columnar cells, absorb water and electrolytes, move and store stool. Congenital; Hirschprung’s disease, similar to achalasia. Aganglionic segment of distal colon, poop stops moving, gets distended, boy 4 times more than girls. Fail to pass meconium. May lead to perforation, sepsis. Acquired anomalies; Megacolon, overdistension, from bowel obstruction. Typically from inflammatory bowel disease or psychosomatic disorders (people don’t like to crap). Diverticular disease (very common). Same definition as before, blind sacular pouch, most common in colon. Lined by normal epithelium, but wall is thin. Often no symptoms (-otis), which can accumulate something and get inflamed (-itis). Usually get more than one, down near sigmoid where poop is more solid. Obstruction or perforation, abscess, peritonitis. Vascular disorders; Angiodysplasia, blood vessels wear out, thinning of tissue. Blood in stool. Hemorrhoids, fairly common, variceal dilation of anal and perianal submucosal venous plexus. Can be caused by constipation, straining, pregnancy, cirrhosis. Engorged veins, blood can form thrombi, get more formation, bulge into lumen, can break blood vessels, blood in stool, opening that can get infected. Fairly common for the internal blood vessels to engorge, and prolapse, mimic warts. Inflammatory disorders; Inflammatory bowel- Crohn’s (has granulomas, can be in multiple places), and ulcerative colitis (no granulomas, only in large intestine). Crohn’s presents usually in teens, white people, process waxes and wanes, pain and discomfort. “Skip lesions”, segmental distribution. “Bear claw”, deep fissuring ulcers. Wall can thicken, and for strictures/fistulas. Non-caseating granulomas are key for diagnosis. Ulcerative colitis, similar process, different etiology. Similar demographics and presentation, different is where it occurs, only in the colon. Starts in rectum and works backwards. No skip lesions, diffuse process, may see pseudo-polyps when it heals (looks like a shag carpet), don’t function properly, overgrowth of surface. No granulomas, risk for adenocarcinoma (with healing). Necrotizing enterocolitis- death of small intestine and colon, acutely, abruptly and often in premature/low birth weight neonates (important, lack of flora). Anti-biotic associated colitis (Pseudomembranous colitis); normal flora killed, except for c. diff. Watery or foamy diarrhea. Polyps- very common. Tumorous masses, protrude into lumen of the gut. Pedunculated- with stalk, sessile- flat. Non-neoplastic ones have no malignant potential, from abnormal maturation, inflammation. In neoplasms, adenomas are precursors to carcinomas (important). Non-neoplastic polyps. Hyperplastic are most common, rarely shown symptoms, usually seen with endoscope and can’t determine if malignant without biopsy. Often are multiple and recur. Adenomas are often solitary. Juvenile polyp (hamartoma malformation- too much of normal tissue). Usually children under 5, rectal bleeding, prolapse/protrusion. Can break off. Multiple polyposis syndrome, slight risk for adenomas. Peutz-Jeghers (hamartoma), often with pigment disorder in skin, not common at all. Dozens of polyps, no malignant potential, but can get other cancers. 100% involvement of small intestine. Neoplasms- Adenomas = benign, polyps that result in proliferative dysplasia, gone to the bad side, and may go to the worse side, are most common neoplasms of humans. 90% will arise in large intestine, also in stomach and small intestine. Majority are tubular 95%, can be villous (fingerlike) or a combination of the two. Usually smooth, pedunculated, can pull off, but villous one are broad and harder to cure with a biopsy, have to take out segment of intestine. Can and will evolve into adenocarcinoma. Approximately 10years to double in size, resection is only good treatment. FAP, innumerable adenomas polyps, only way to cure is take out intestines. Malignant neoplasms; Adenocarcinoma 98% of colon cancers, 3 leadingd cause of death. Generally in older population as they are slow growing. Can be asymptomatic for years, arise from adenomas. Occur typically in cecum and ascending colon, and recto sigmoid colon, proximal and distal areas. Right sided= Cauliflower-like. Left sided- lumen narrows, napkin ring on barium ring, grows into wall. Prognosis based on extent of invasion, surgery is only hope for cure, not radiation sensitive. Environmental Diseases Outdoor Air Pollution: Gas and particles, worse in industrial areas. Limits on sulfur dioxide, CO, O3, NO2, Pb, particulates. Lungs are involved, but others can be too. Ozone- toxicity from free radical formation, even low levels detrimental to those with pulmonary disease, injure lining cells. CO- from auto engines, using fossil fuels, cigarette smoke, important cause of suicide and accidental death, hemoglobin has 200 fold affinity for it than Oxygen, insidious CNS depression, hypoxia at 20-30% saturation, unconsciousness and death at 60-70%. Chronically can slowly accumulate to life threatening condition. Changes is basal ganglia and lenticular nuclei, permanent damage can occur. Acute poisoning- generalized cherry-red color of skin and mucous membrane with lighter skinned people, with longer survival you get brain edema, those who survive may recover but could lose memory, vision hearing and speech. Sulfur Dioxide, particles and acid aerosols- emitted by coal and oil burning. Particles less than 10 microns are worst, phagocytized by macrophages and neutrophils, release inflammation mediators. Indoor Air Pollution: Most common is cigarette smoke. Radon often tested for. Increased insulation of houses increases potential for pollution. Metals as pollutants: Lead- now in older homes and soil contamination, major hazard for children (absorption is 50% as opposed to 15% in adults). Most is taken up by the bone, has a half-life of 20-30 years. Encephalopathy and mental degeneration. Anemia is one of the earliest sign of lead accumulation, elevated levels of zinc protoporphyrin or free erythrocyte protoporphyrin. Lead lines in bones. 5 is the limit now, now 10 micrograms. Tobacco- most common exogenous cause of human cancers. Increases risk of cancers other than lung cancer too. Risk goes up the more you smoke. 43 known carcinogens. Cessation is followed by a slow reduction in excess mortality. Former smoker will always have a slight increased risk for cancer. Children of smokers have increased risk of respiratory and ear infection, exacerbation of asthma. Pneumoconiosis- non-neoplastic lung reaction from organic and inorganic particulates. Amount of dust retained in the lung is important in risk, as is size, shape and buoyancy of particles. 1 to 5 microns are most dangerous. Fibrosis is particularly bad when it happens in the lung, prevent expansion. Coal Worker’s form- from coal dust, anthracosis is most minimal (asymptomatic, black coloring in lungs). One up is simple coal workers, start to get macrophages coming in, with minimal or no pulmonary dysfunction, and could have small macules. Complicated form (progressive massive fibrosis), extensive fibrosis, lung function compromised, blackened scars. Silica in coal favors fibrosis, but mostly carbon dust causes. Caplan syndrome- also have RA, distinctive nodular pulmonary lesions, develop rapidly. In minority causes with pulmonary fibrosis, increased pulmonary dysfunction, and cor pulmonale. Silicosis; more prevalent than coal, sandblasting and mine workers. Occurs after decades of exposure, acute onset much less common. Crystalline forms are more fibrogenic. Tiny discrete nodule at first, may coalesce into hard scars, may cavitate or calcify (eggshell). Disease is slow to kill, but restricts activity. Asbestos: Insulation, can be brought home on workers clothes. Linked to plaques, effusions, carcinomas, and other cancers. Two forms: Serpentine- curly and flexible (Chrysotile). Amphibole- straight and stiff, more pathogenic. Mesothelioma linked to amphiboles. Both forms are fibrogenic. Asbestos is a complete carcinogen. Asbestos bodies- golden brown, fusiform or beaded rods with translucent center. Ferruginous body is if you can’t find the asbestos. Pleural plaques, well circumscribed of dense collagen, rarely occur without asbestos exposure. Malignant mesothelioma- very long latent period. Extensive pleural effusion, mixture of two cells: Mesenchymal stromal cells (fibroscarcoma) and epithelial-like cells (adenocarcinoma). Berylliosis: Just look over. Very rare. Aerospace and nuclear industries. Non- casseating granulomas. Chemical and Drug injury: Acetaminophen – toxic as 12-25g. Increased overdosing in children. Large amounts cause hepatic necrosis, NVD, sometimes shock, jaundice, and renal damage may also occur to compensate for liver. Aspirin- respiratory alkalosis followed by metabolic acidosis which can be fatal, chronic toxicity with 3g or more daily, headache, dizziness, NVD, can lead to coma and convulsions. Alcohol: most widely abused drug in the world. Amount exhaled in breath is proportional to blood level. Affects inhibitory neurons first, than cortical and medullary. Chronic abuse affect multiple organs, liver most of all. Can see Cardiomyopathy, gastritis and Wernicke syndrome. Physical Injuries: Mechanical injuries, blunt and soft trauma. Know the terms. Laceration is rough edged tear, incised wound is smooth edged cut. Thermal Injuries: Local or systemic. Salt concentration goes up when liquid freezes in the cell with local hypothermia. Trench Foot, slow chilling, induces vasoconstriction, paralysis, increased permeability and edema from endothelial cell injury. Frostbite is more sudden, ischemic changes, vasoconstriction and localized hyperviscocity, edema comes with warming. Generalized hypothermia- prolonged exposure, cold wet clothing, and ingestion of alcohol which causes vasodilation, bradycardia and AF. Pass out at 90F. Treat with internal warming. Ischemic brain, heart, kidney and liver damage. You are never cold and dead, only warm and dead. Hyperthermia; Burns- severity is related to % body involved, depth involved, internal injuries present, and promptness of therapy. More than 50% is often fatal, infection. Rule of 9s to determine % body burnt. Internal thermal injury from inhaling hot fumes. Can get down to tracheobronchial tree. Generalized form: Heat cramps, then heat exhaustion, failure for CV to compensate for hypovolemia. Heat stroke, failure to sweat. 106F is grave sign, 50% mortality. Electrical injuries: current magnitude, duration and path (how it goes through body). Radiation: DNA is most vulnerable. Indirectly forms free “hot” radicals from water. G2 and mitotic phase are most sensitive. Hematopoietic and lymphoid systems are particularly sensitive. Lungs can be sensitive, all parts of GI. Heart damage possible. Urinary bladder is sensitive, kidney not as much. Whole body exposure is potentially lethal, LD50 is 250-400 rad for 60 days. Basophilic stippling- ribosomes, arsenic poisoning, thalassemia. Abrasion- scrape, loss of outer layer of skin. Contusion- bruise, contained hemorrhage.
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