Path II Exam II Review
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-
Tim & Friends
Fall 05 – Dr. Gray
1
Path II Exam II Review
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.
Tim & Friends
Fall 05 – Dr. Gray
2
Path II Exam II Review
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
Tim & Friends
Fall 05 – Dr. Gray
3
Path II Exam II Review
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.
Tim & Friends
Fall 05 – Dr. Gray
4
Path II Exam II Review
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.
Tim & Friends
Fall 05 – Dr. Gray
5
Path II Exam II Review
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
Tim & Friends
Fall 05 – Dr. Gray
6
Path II Exam II Review
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 herniasHiatal 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
Tim & Friends
Fall 05 – Dr. Gray
7
Path II Exam II Review
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
Tim & Friends
Fall 05 – Dr. Gray
8
Path II Exam II Review
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
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
60.
Tim & Friends
Fall 05 – Dr. Gray
9