Atelectasis: lung collapse due to decrease amount of ...



Atelectasis: lung collapse due to decrease amount of expansion in the lung. This results in less volume, and in turn less oxygenated blood is produced. With poorly oxygenated being used in the body hypoxia will result

Asthma: is seen with bronchospams that are caused by over stimulated bronchoconstrictor response to a given stimulus.

Emphysema: permanent enlargement of the air space distal from the terminal bronchioles. This has direct effect on the acini, which are distal to the terminal bronchioles. The acini are the primary unit for gas exchange, and in emphysema that are damaged

Bronchiectasis: permanent dilation of the bronchi and bronchioles. Caused by destruction of the muscle and elastic supporting tissues. It is a secondary condition that is caused by an infection or obstuctuion

Intrinsic Asthma: (non atopic asthma) this is NOT stimulated by an immune response. Occurs later on in life. Stimulus that has no effect on a normal person but can cause a bronchospasm. Reason for hypersensitivity is unknown

Extrinsic Asthma: caused by a type-1 hypersensitivity reaction. Often found in children or earlier in life and can grow out of it. IgE, mast cells, and eosinophils all play a role in atopic (allergic) asthma.

Obstructive Lung Disease: air cannot get out of the lung easily.

-Diseases that are obstructive: asthma, emphysema, chronic bronchitis

-Total Lung Capacity = NORMAL

-Forced Vital Capacity (FVC) = NORMAL

-Forced Expiratory flow rate per second (FEV1) = DECREASED

-FEV1 / FVC ratio = DECREASED

Restrictive Lung Disease: air cannot get into the lungs easily= REDUCED CMPLIANCE

-Defects that are restrictive: extrapulmonary disorders (i.e. obesity, scoliosis)

-Total Lung Capacity= DECREASED

-Forced Vital Capacity (FVC) = DECREASED

-Forced Expiratory flow rate per second (FEV1) = NORMAL

- FEV1 / FVC ratio = NORMAL

*If you severe the phrenic nerve you will get restrictive lung disease*

Wegener’s granulomatosis – type III immune complex

Sarcoidosis is a multisystem disease of unknown cause characterized by noncaseating granulomas in many tissues and organs, but it can cause restrictive lung disease also.

Sarcoidosis is multisystem (eye and skin involvement) but the major manifestations are bilateral hilar lymphadenopathy or lung involvement or both and these can be seen on x-ray. The lymph nodes and tonsils (in one-third of cases) are affected and are enlarged and lobulated. When seen on x-ray, the bilateral hilar lymphadenopathy is referred to as “potato nodes”.

Hypersensitivity pneumonitis is an immunologically mediated lung disease that primarily affects the alveoli and is therefore often called allergic alveolitis. It is often an occupational disease resulting from heightened sensitivity to inhaled organic dusts (moldy hay). Unlike bronchial asthma where the focus of damage is to the bronchi, the damage from hypersensitivity is at the level of the alveoli.

Goodpasture’s syndrome is an uncommon, but intriguing condition, characterized by crescentic, usually rapidly progressive, glomerulonephritis and hemorrhagic pneumonitis. Antibodies to antigens common to glomerular and pulmonary basement membranes cause both renal and pulmonary lesions. This is a Type II autoimmune disorder.

Jarvis (11-20)

11.) More than 95% of all pulmonary emboli arise from thrombi within the large deep veins of the lower legs, typically originating in the popliteal vein and larger veins above it. Thromboemboli do not commonly arise from superficial or smaller leg veins.

12.) Klebsiella pneumoniae is the most common cause of gram negative bacillary pneumonia and occurs frequently on malnourished persons and chronic alcoholics. . The sputum is thick and gelatinous and the pattern of pneumonia is frequently lobar. This pneumonia carries a greater mortality rate than pneumococcal pneumonia.

13.) Pseudomonas aeruginosa is a common cause of nosocomial (hospital acquired) pneumonia and it affects persons with defective immune systems. Bacterial Pseudomonas is a progressive, necrotizing pneumonia with blood vessel invasion and high mortality rate.

14.) Mycobacterium tuberculosis usually affects the lungs but can affect any tissue or organ and the tubercular granulomas can undergo caseous necrosis.

Difference b/t Infection & Disease

• Infection implies that the person has been seeded with the organism, but does not manifest any clinical symptoms.

• Disease is w hen there is tissue damage due to M. tuberculosis.

Test for TB: Infection with M. tuberculosis typically leads to a delayed hypersensitivity detected by the Mantoux test (tuberculin test). About 2 to 4 weeks after the infection has begun, an injection of purified protein derivative (PPD) will produce a visible and palpable induration.

It does not differentiate between infection and disease.

15.) Primary tuberculosis is the form of disease that develops in a previously unexposed, and therefore, unsensitized person. Primary tuberculosis almost always begins in the lungs. Typically, the bacilli implant in the lower part of the upper lobes and upper part of the lower lobes, deep in the lungs, and close to the pleura.

Secondary tuberculosis (Reactivation tuberculosis) is the pattern of disease that arises in a previously sensitized host. Secondary tuberculosis is classically localized in the apex of one or both of the upper lobes.

16.)

Ghon focus - As sensitization to 10 TB develops, a 1.5 cm gray-white inflammatory consolidation emerges. (parenchymal lung tissue; no nodes involved)

Ghon complex - the combination of parenchymal lung tissue and lymph node involvement.

Miliary TB - In progressive primary TB, the primary focus enlarges, caseates, and cavitates, sometimes spreading through the airways or lymphatics to multiple sites in the lungs. If TB circulates it gives arise to miliary TB. (also possible in 20 TB)

:Bird seed scattered lesions in lungs:

Pott’s disease – when TB affects the vertebrae.

17.) Smokers are 10 times more likely to get bronchial carcinoma than non smokers and all patterns of bronchogenic carcinomas are associated with smoking; the strongest is with squamous cell and more so with small cell carcinomas. Bronchogenic carcinoma (bronchial carcinoma) is the number one cause of cancer-related deaths in industrialized countries.

18-19.) Involvement of the supraclavicular node (Virchow’s node) is characteristic and calls attention to an occult primary tumor.

Apical tumors (Pancoast tumors) may invade the brachial or cervical sympathetic plexus to cause pain in the distribution of the ulnar nerve or produce Horner’s syndrome (enophthalmos, ptosis, miosis, and anhydrosis).

20.) Coin Lesions - benign tumors that can be seen occasionally on x-ray are hamartomas (indigenous, but disorganized tissue) that can be 3 – 4 cm in diameter.

Pathology Test 2 # 21-30 (Jana)

Urea is formed in the liver. Ammonia from deamination of AA is toxic; hence it’s metabolized in a way that it can be excreted from the kidneys in the form of urea.

Creatinine is a protein produced by muscle and released into blood. Creatinine clearance is technically the amount of blood cleared of creatinine per time period (ml/min). Normal adult = 120ml/min. It is ~ inversely related to serum creatinine. So, if adult serum creatinine = 2, then creatinine clearance of 60 ml/min (120/2). Kidney “hyperfilters” if a kidney removed, so the creatinine level will rise to 1.8 as opposed to 2 (in other words, it works a bit harder and the fcn is not quite halved).

Azotemia is a biochemical abnormality that refers to an elevation of blood urea N (BUN) and creatinine levels and is largely related to a decreased glomerular filtration rate.

Nephrotic Syndrome = heavy proteinuria (>3.5g/day), hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria.

The glomerulus is an anastomosing network of capillaries in Bowman’s capsule. Parietal layer lines the urinary space, and visceral part is incorporated in the capillary network.

The capillary network (Inside ( Urinary space):

1. fenestrated endothelial cells- cap walls

2. glomerular basement mem. (GBM) - lamina rara interna, lamina densa, lamina rara externa. (densa: electron dense = neg charge, composed of Type IV collagen, laminin, polyanionic proteoglycans, fibronection, and glycoproteins). Water and cation permeable.

3. visceral ep. cells (podocytes) – interdigitating foot processes (pedicels) on externa with filtration slits/diaphragm in between.

4. mesangial cells – separate cap (space = mesangium), have matrix, mesenchymal origin, phagocytic, contractile, secrete bio active mediators.

Acute glomerulonephritis is an abrupt onset of hematuria and proteinuria w/ reduced GFR and renal salt/water retention, followed by full recovery of renal fcn. Caused by infectious disease (A beta-hemolytic strep, etc)

Rapidly progressive glomerulonephritis is when recovery from acute does NOT occur. Worsening renal fcn = irreversible/complete renal failure in wks to months. Eventually display all features for chronic renal failure. Caused by heterogeneous group of disorders (poststreptococcal Glomerulonephritis, systemic lupus erythematosus, Goodpasture’s syndrome, drugs, and idiopathic crescentic Glomerulonephritis)

Glomerulonephritis (chronic) – renal impairment follows acute and progresses slowly (years) to chronic renal failure. Unclear origin.

Lipoid Nephrosis (minimal change disease) – Relatively benign disease, which is most frequent, cause of nephrotic syndrome in kids. Characterized by glomeruli that have normal appearance under light microscope but disclose diffuse loss of visceral ep. foot processes under electron microscope. Develops age 2/3 and unknown cause.

Membranous Glomerulonephritis, MGN (membranous nephropathy) – slow, progressive disease, most common ages 30 – 50, characterized morphologically by the presence of subendothelial immunoglobulin-containing deposits along the GBM. 80% idiopathic and primary MGN.

Crescentic Glomerulonephritis (rapidly progressive) RPGN – clinicopathologic syndrome, no specific etiology. Histologic picture is characterized by presence of crescents in most of the glomeruli, which are produced by proliferation of the parietal cells of Bowman’s capsule and infiltration of monocytes and macrophages.90% of these pt’s become anephric and require long-term dialysis or transplant. SEVERE glomerular injury in all 3 types.

1. Type I RPGN: anti-GBM disease – linear deposits of IgG and C3 on the GBM

2. Type II RPGN: immune-complex mediated disease

3. Type III RPGN: pauci-immune type – lack of anti-GBM Ab’s or immune complexes. Most pt’s have ANCA in their serum.

IgA nephropathy (Berger’s disease) – affects young children and young adults, begins as episode of gross hematuria occurring w/in 1-2 days of non-specific respiratory tract infection. Often assoc w/ loin pain. One of the most common causes of recurrent microscopic or gross hematuria and MOST COMMON GLOMERULAR DISEASE WORLDWIDE. Pathognomic hallmark = deposition of IgA in mesangium, elevated levels of IgA, maybe genetic. 50% = chronic renal failure.

Pylonephritis – Acute: inflammation of the kidney or its pelvis, it is usually caused by a lower urinary tract infection, however all lower UTI’s do not effect the kidney. Chronic: a morphologic entity in which predominately interstitial inflammation and scarring of the renal parenchyma is associated with grossly visible scarring and deformity of the pelvicalyceal system. Chronic Obstuctive: obstruction leads to kidney infection and recurrent infections lead to recurrent renal inflammation and scarring eventually leading to chronic pyelonephritis. Reflux nephropathy or chronic reflux associated polynephritis: more common form of chronic pylonephritis scarring and results from superimposition of a UTI on congenital vesicoureteral reflux and intrarenal reflux.

Cystitis – inflammation of the urinary bladder, also caused by a urinary tract infection

Interstitial nephritis - Inflammation of the interstitium. When bacteria are not involved and the damage is due to drugs, metabolic disorders, physical injury, or immune reactions it is know as this.

Glomerulonephritis – see questions 26 – 28 concerning acute, rapidly progressive, and chronic glomerulonephritis.

Hyrdroureter – a dilated ureter

Hydronephrosis – refers to dilation of the renal pelvis and calyces, with accompanying atrophy of the parenchyma, caused by obstruction of the outflow of urine. Can be congenital or alterations in the anatomy of the area causing obstruction, or acquired via foreign bodies tumors, inflammation, neurogenic, and normal pregnancy.

Papillary necrosis – associated with analgesic nephropathy. Patients who consume large quantities of analgesics may develop chronic interstitial nephritis often associated with this phenomenon. Basically I guess it is necrosis of papillary muscles in the kidney.

Kidney stones – particular causes of stone formation are unknown, but the most important causes are by increased urine concentration of the stone’s constituents, so that is exceeds their solubility in urine. They are made up 75% of the time of calcium oxalate alone or mixed with phosphate. 15% of the time magnesium ammonium phosphate or a uric acid composition 10% of the time. Clinically: they may be present without pain or symptoms and may not cause much renal damage, especially if located in the pelvis. Small stones may pass into the ureter causing intense excruciating pain. This may cause obstruction of the ureter causing ulceration of tissues or cause bacterial infections. Prevention includes a high fluid intake to maintain daily urine volume of 2L or more. High protein diet predisposes stone formation. Some factors protective against stone formation are fluids, citrate, magnesium, and dietary fiber.

Renal cell carcinoma – cancer of the kidney and is an adenocarcinoma arising from the tubular epithelial cells. It comprises 90% of all malignant tumors of the kidney. There is a greater frequency in smokers and familial forms have been reported. Clinically: renal cell tumors are hard to diagnose. The most frequent presenting manifestation is hematuria, occurring in 50% of cases. Others with this tumor have flank pain when the tumor has gotten large and a fever. Polycythemia is present in 5-10% of patients due to increased production of erythropoietin. This tumor can invade the renal vein and extend as a solid column even into the right side of the heart.

Wilms tumor – it is an embryonal renal neoplasm, one of the most common childhood abdominal malignancies, mean age of diagnosis is 3.5 years. Approximately 5% of children infected have bilateral disease with the mean age of this illness being found at 2.5 years. Associated conditions include aniridia, hemihypertrophy, genitourinary anomalies, and beckwith-widemann syndrome. Evidence of a genetic connection is emerging. It also involves mesenchymal tissue.

Autosomal dominant (Adult) polycystic kidney disease – characterized by multiple expanding cysts of both kidneys that ultimately destroy the intervening parenchyma. It is caused by inheritance of at least two autosomal dominant genes of very high penetrance. In 90% of the cases the defective gene is on the short arm of chromosome 16. Clinical: symptoms are usually not seen until the 4th decade. The most common complaint is flank pain or a heavy, dragging sensation. Intermittent gross hematuria commonly occurs. The most important complications are hypertension and urinary infection.

Nephrolithiasis – fancy word for a kidney stone. See above information.

Chapter 15 GI tract

Aphthous ulcers – (canker sores) They are common small painful, shallow ulcers. They form singly or as a group covered with grey exudates and rimmed by erythematous tissue. They appear on the soft palate, buccolabial mucosa, floor of the mouth, and lateral sides of the tongue. They are more common before 20 and are causes by stress, fever, foods, and activation of the inflammatory bowel syndrom.

Herpesvirus infection (cold sores, fever blisters) Very common and transmited by kissing. The primary infection is assymptomatic and is dormant in trigeminal ganglia. With reactivation small vesicles appear about the lips and nasal orifices that contain a clear fluid. The rupture leaving shallow, painful ulcers that soon heal. Giant cells are known as polykaryons. Recurrences are common. Tzanck test ID’s the inclusion bodies in the polykaryons. A young child or immonocomprimised patient could have a more violent reaction, known as herpetic gingivostomatitis. The infection could even cause encephalitis.

Candida albicans – is a fungal infection and is a normal inhabitant of the oral cavity in 30-40% of the population. It causes disease when normal defenses fail. Oral candida is known as thrush. Thrush takes the form of adherent white, curd like, circumscribed plaque (psuedomembrane) anywhere in the oral cavity.

Leukoplakia – a whitish, well defined, mucosal patch or plaque caused by epidermal thickening or hyperkeratosis. Plagues are seen more in older men along the lip or soft palate. Lesion cause is unknown but there is a strong correlation with tobacco use, and less so with excessive drinking and bad dentures. 5-15% will progress to squamous cell carcinoma.

Keratoconjunctivitis – dry eyes seen in association with autoimmune sialadenitis (sjogren’s syndrome)

Xerostomia – dry mouth seen in association with autoimmune sialadenitis (sjogren’s syndrome)

46-48. Mallory-Weiss syndrome- longitudinal tears in esophagus at esophagogastric jxn, frequent in chronic alcoholics after sever retching, may involve only mucosa or penetrate the wall, if not penetrating most bleeding will cease w/out surgery

Esophageal hernias-

Hiatal hernia-segment of stomach protrudes above diaphragm, 9% of adults suffer from heartburn/regurgitation of gastric juices

Sliding hernia-95% of hiatals, esophagus is above the stomach and the diaphragm is below; usually no reflux but if reflux is present it is probably sliding hernia

Paraesophageal hernia- (rolling hiatal) greater curvature lies alongside the lower esophagus, above the diaphragm; rarely have reflux

Achalasia- “failure to relax”, incomplete relaxation of lower esophageal sphincter (LES) when swallowing, three causes: aperistalsis, incomplete relaxation of sphincter, increase sphincter resting tone; abnormal innervation of LES does not allow it to relax during peristalsis, characterized by painful swallowing, nocturnal regurgitation, aspiration of food may occur; appears in adulthood; may develop into esophageal squamous cell carcinoma (5%)

Primary alchalasia- dilation of esophagus above sphincter, hypertrophy/thinning of muscularis due to dilation

Secondary alchalasia- can be caused by Chagas’ disease destroying part of GI myenteric plexus

Varices- dilated esophageal veins, caused by cirrhosis of liver blocking portal venous flow thru the liver; 2/3 of all cirrhotic patients have these, often associated with alcoholic cirrhosis; produce no symptoms until they rupture and produce massive hemorrhage into the lumen and suffusion of blood into the esophageal wall;

49, 50. Achalasia- see above

Barrett’s esophagus-results form long standing gastroesophageal reflux; replacement of normal distal stratified squamous mucosa by abnormal metaplastic columnar epithelium containing goblet cells; clinical significance is 30-40 times greater risk of developing adenocarcinoma

Crohn’s disease- may effect any portion of the GI tract from esophagus to anus, mostly involves SI and colon; provides extraintestinal complications of immune origin making it a systemic disease with mostly GI involvement; usually occurs b/t 20-30 years old in 2/100,000 people; when fully developed it has: 1. a sharply delimited and transmural involvement of the bowel by inflammatory process wit mucosal damage 2. presence of noncaseating granulomasin 40-60% of cases 3. fissuring with formation of a fistula; in diseased segments serosa is granular with fat wrapping around the bowel, intestinal wall is rubber and thick from edema, inflammation, fibrosis, hypertrophy of muscularis propria; classic feature- sharp demarcation of diseased bowl segments from uninvolved bowel segments.

Clinical features- recurrent diarrhea, cramps, ab pain, fever for several days/weeks; sometimes appendicitis is suspected; 50% have melena; debilitating problems are: fistula formation, abdominal abscesses, intestinal stricture; renal disorders/ nephrolithiasis seen in 1/3 of patients; amyloidosis and thromboembolic disease are serious complications

51-54.Gastritis- inflammation of gastric mucosa

Chronic- presence of chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia; commonly caused by Helicobacter pylori which is gram neg. rod; Autoimmune gastritis- caused by autoantibodies against gastric parietal cells with loss of acid and intrinsic factor resulting n pernicious anemia; clinical features of chronic: few symptoms, upper abdominal discomfort, nausea, vomiting; when autoimmune achlorhydria is evident, serum gastrin levels normal/slightly high, may develop peptic ulcers (duodenal or gastric) and gastric carcinoma; Peptidic ulcers- breach in mucosa of alimentary tract that extends thru the muscularis mucosa into the submucosa or deeper; chronic, solitary, can occur anywhere in GI tract, 98% are in first portion of duodenum or in stomach; remitting/ relapsing lesions; duodenal ulcers frequent in alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, hyperparathyroidism; pathogenesis: mucosal exposure to gastric acid and pepsin, association with H. pylori infection

Acute- acute mucosal inflammatory process, usually of transient nature; severe cases produce sloughing of superficial mucosal epithelium (erosion); numerous causes: drugs, alcohol, chemotherapy, mechanical/severe stress, disruption of mucous layer, too much acid, loss of bicarbonate, reduced blood flow; endoscopic exam can reveal erosion and hemorrhage called acute erosive gastritis; clinical features: depend on severity, ranges form asymptomatic to epigastric pain with nausea/vomiting, hematemesis especially in alcoholics, melena, fatal blood loss; 25% of people taking daily aspirin for arthritis develop gastritis; Erosions- loss of superficial epithelium

55. Celiac sprue- gluten-sensitive enteropathy, B-cells/plasma cells sensitized to gliadin cross enterocytes to intestinal lumen, damage/flatten mucosal villi; disorder towards gliadin, a water-insoluable protein of wheat and related grains

Pancreatic insufficiency- from chronic pancreatitis/cystic fibrosis; is defective intraluminal digestion which features osmotic diarrhea and steatorrhea; bacterial overgrowth damages epithelium

Lactose intolerance- defective mucosal absorption, more of a problem in infants than adults

56, 57. Hereditary nonpolyposis colorectal cancer- autosomal dominant familial syndrome, characterized by increased colorectal cancer and endometrial cancer in women

Ulcerative colitis- nongranulomatous limited to colon; inflammation is final common pathway for inflammatory bowel disease (IBD), both have initial inflammatory response with neutrophiles and mononuclear cells resulting in impaired integrity of mucosal epithelial barrier, loss of surface epithelial cell absorptive fxn, activation of crypt epithelial cell secretion

Familial polyposis- uncommon autosomal dominant disorders, in familial adenomatous polyposis (FAP) patients develop 50-2500 colonic adenomas; risk of colonic cancer is virtually 100% by midlife, unless a prophylactic colectomy is performed

Crohn’s disease- see above

58, 59. Polyp- a tumorous mass that protrudes into the lumen of the gut, may be type with stalk (pedunculated) or w/out a stalk (sessile)

Diverticuli- blind pouch off alimentary tract, lined by mucosa, communicates with lumen of the gut; 2 important factors in protrusions: 1 exaggerated peristaltic contractions with abnormal elevation of intraluminal pressure 2 focal defects peculiar to the normal muscular wall; Tx : high fiber diet

60. I couldn’t find these in the notes, these definitions are from the book

Sarcoma- malignant neoplasms arising in mesenchymal tissue or its derivatives

Carcinoma- malignant neoplasms of epithelial cell origin

Hammartoma- malformation that presents as a mass of disorganized tissue indigenous to the particular site

Adenocarcinoma- lesion where the neoplastic epithelial cells grow in gland patterns

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