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Pathology exam III review > Review > Flashcards

Review Flashcards

1
Q

Aphthous Ulcers ( Canker Sores)

A

Small, painful, shallow ulcers

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2
Q

Canker sores triggers

A

stress, fever, ingestion of certain foods, activation of inflammatory disease

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3
Q

Canker Sores clinical course

A

self-limiting, usually heals without scarring but may recur in same/different location

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4
Q

What are canker sores covered by?

A

covered by fibrinopurulent exudate with underlaying infiltrate with mononuclear and polymorphonuclear leukocytes

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5
Q

Leukoplakia what is it? where is it found? How does it look like?

A

preneoplastic epithelial lesion— well-defined, demarcated.

Found on buccal mucosa, tongue, floor

A white plaque that cannot be scrapped off or identified as other disease

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6
Q

leukoplakia association

A

tobacco, pipe smoking, smokeless tobacco

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7
Q

Banal hyperkeratosis

A

varies from leukoplakia ( no underlying dysplasia to mild/sever dysplasia, potential carcinoma in situ)

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8
Q

Can leukoplakia go through malignant transformation?

A

Yea, to squamous cell carcinoma in 3-25%

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9
Q

Erythroplakia

A

red-equivalent to leukoplakia.

less common

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10
Q

Erythroplakia can go through malignant transformation?

A

Yea, greater than 50%

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11
Q

how does eythroplakia looks like?

A

red, velvety, often granular, circumscribed

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12
Q

Pleomorphic Adenoma

A

Most common salivary gland tumor esp. in superficial parotid gland

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13
Q

can pleomorphic adenoma be surgically removed?

Can a malignant mixed tumor arise?

A

yea, but may recur

yea, it has a 30-50% year mortality rate

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14
Q

Pleomorphic Adenoma characteristics

A

admixture of epithelial and stromal elements (heterogeneity)

Forms slowly growing, painless, movable, encapsulated firm mass with smooth surface

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15
Q

Mucuoepidermoid Carcinoma

A

most common primary malignant tumor of the salivary glands

malignant salivary gland tumor with neoplastic epidermal cells, mucus secreting cells, and epithelial cells of the intermediate type

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16
Q

Where does the mucuoepidermoid carcinoma originates? How is the differentiation?

What are the ‘nests’ composed of?

A

originates in the ductal epithelium
differentiation variable and clinical course depends on grades

‘Nests’ composed of squamous cells as well as clear vacuolated cells with mucin.

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17
Q

Esophageal varices: causes? clinical?

A

dilation of esophageal and periumbilical veins dues to portal hypertension

causes cirrhosis and portal hypertension, often diue to alcohol abuse.

Hepatic schistosomiasis is the second most common cause of varices

varices greater than 5mm prone to rupture, leading to life-threatening hemorrhage

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18
Q

what are esophageal varices?

A

dilated veins beneath the mucosa with a tendency to rupture and hemorrhage due to extra blood volume, connecting the intra-abdominal and systemic venous circulation

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19
Q

cancers of the esophagus?

A

1) adenocarcinoma

2) squamous cell carcinoma

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20
Q

adenocarcinoma of the esophagus

A

occurs in the Distal end!

  • Risk with dysplasia, tobacco use, obesity, radiation, therapy.
  • Fresh fruits/veggies lower risk
  • Pain/difficulty, progressive weight loss, hematemesis, chest pain, vomiting.
  • usually has spread to submucosal lymphatics upon discovery
  • 5 year survival rate is less than 25%
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21
Q

Squamous cell Carcinoma of the esophagus

A
  • occurs in MIddle Third where it commonly causes strictures
  • Risk from alcohol and tobacco, esophageal injury, achalasia, radiation therapy.
  • Begins as squamous dysplasia
  • ranges from well-differentiated with epithelial pears to poorly differentiated tumors
  • presents with dysphasia (difficulty in swallowing), but by time of discovery, tumors are unresectable
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22
Q

Gastric cancer

A
  • mainly adenocarcinomas
  • many environmental/dietary factors are associated
  • loss of E-cadherin function seems to be a key step
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23
Q

what are the the two types of Adenocarcinomas of gastric cancer?

A

1) Intestinal type

2) Diffuse (Infiltrating) type

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24
Q

intestinal Type gastric cancer

A

Bulky tumor composed of glandular structures, elevated mass with heaped-up borders and central ulcerations.
predominant in high risk area and develops from precursor lesions including dysplasia and adenomas.
Depth of invasion and extent of metastasis (staging) most powerful prognostic indicator for gastric cancers.
Remarkable decrease in gastric cancer only applies to intestinal type

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25
Q

Diffuse (Infiltrating) Type gastric cancer

A

no true tumor seen— Do not form glands
Large mucin vacuoles that expand cytoplasm and push nucleus to the edge, looking like a “signet-ring”
evoke desmoplastic reaction that stiffens gastric wall. Rigid thickening of wall of the whole stomach creating the appearance of a water bottle —Litinis plastic

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26
Q

Barrett Esophagus: cause? clinical?

A

metaplastic replacement of squamous epithelium by columnar epithelium

cause: results from gastroesophageal reflux— involves lower third of esophagus
clinical: increases risk of esophageal adenocarcinoma– 30-100x greater risk

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27
Q

barret esophagus morphology

A

“intestinal metaplastic epithelium” goblet cells with gastric foveolar cells
Dysplasia classified low or high grade

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28
Q

Sialadenitis: what? cause? clinical tx?

A

inflammation of the salivary gland
cause: mucocele (blockage/rupture of salivary gland duct often due to trauma)
clinical tx: excision of cyst with the minor salivary gland

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29
Q

Sialadenitis Morphology

A

cyst-like space with inflammatory granulation tissue filled with mucin and macrophages

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30
Q

Acute gastritis: what? cause? associated with? clinical?

A

acute mucosal inflammatory process, usually transient with mucosal necrosis

cause: disruption of mucosal layer, stimulation of acid secretion, decreased bicarbonate production, reduced mucosal blood flow, direct epithelial damage

Associated with: NSAID, aspirin, alcohol, smoking, chemo, ischemic injury

clinical: complete restitution if stimulus removed

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31
Q

Acute gastritis morphology

A

localized or diffuse superficial inflammation—concurrent erosion and hemorrhage. mucosal edema and inflammatory infiltrate of neutrophils and chronic inflammatory cell

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32
Q

Celiac Disease: what? characterized by? diagnosis based on?

A

immune response to Gluten. Gliadin particles interact with immune system leading to killing of eneterocytes and damage to mucosal epithelium

characterized by: generalized malabsorption mucosal lesions

Diagnosis based on: prompt clinical/histological response withdrawal of gluten containing foods.

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33
Q

Celiac Disease histology

A

atrophy/loss of villi. eosinophils in lamina propria but not deeper

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34
Q

Pseudomembranous colitis: what? causes(4)?

A

classic example of infectious enterocolitus
caused by: C. difficile–following administration of antibiotics, resulting in cytotoxin release.= causes
(1) disruption of epithelial cytoskeleton,
(2) tight junction loss,
(3) cytokine production, and
(4) apoptosis

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35
Q

what is pseudomembrane?

A

is adhesion of fibrinopurulent debris and mucus to damaged superficial mucosa

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36
Q

Pseudomembranous colitis histology

A

denuded with an infiltrate of neutrophils– superficially damaged crypts with exudate released resembles a “volcano”

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37
Q

Crohn diseases Vs Ulcerative colitis

A

Crohn: chronic, segmental, transmural inflammation of the intestine

Ulcerative colitis: chronic, superficial inflammation of the colon and rectum

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38
Q

Crohn disease vs ulcerative disease? location?

A

Crohn: principally in distal small intestine but can be anywhere in digestive tract and discontinuous “skip lesions”—colon particularly the right one can be affected

ulcerative colitis: continuos colonic involvement beginning on the rectum—limited to the colon and rectum

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39
Q

Crohn’s disease histology

A

affects all wall layers (transmural inflammatory disease.) Granulomas in 40-60% of cases
early lesions as aphthous ulcers which later become deeper and look like fissures

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40
Q

ulcerative colitis histology: name and describe the 3 stages.

A

Early: mucosal surface raw, red, granular, crypt abscesses dilated with crypt filled neutrophils

Progressive: mucosal folds are lost. Fragments of mucosa between ulcers form pseudopolyps – granulation tissue is denuded areas but no stricture.

Advanced: large bowel shortened. Mucosal folds indistinct. mucosa atrophied

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41
Q

Crohn vs Ulcerative colitis: clinical

A

Crohn: abdominal pain and diarrhea, colonic bleeding and intestinal obstruction and fistulas

Ulcerative colitis: diarrhea, rectal bleeding (risk of moderate anemia) with intermittent attacks.– Severe colitis occurs with 20 bloody bowl movement daily with massive hemorrhage being life threatening

Toxic megacolon– extreme dilation of colon and risk of perforation (dangerous complication)

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42
Q

Crohn vs Ulcerative colitis: neoplastic pottnial

A

Crohn: predisposition to colorectal cancer

ulcerative colitis: higher risk of colorectal cancer than general population

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43
Q

Colorectal cancer: what? risk? clinical?

A

mostly adenocarcinomas– A classical example of neoplastic progression with multistep carcinogenesis
two possible mechanisms involved
risk factors: age, chronic inflammatory bowel disease, diet, genetics
clinical: occult blood in the stool, iron deficiency anemia, obstruction.— Metastasis through direct extension or vascular/lymphatics invasion (particularly for liver)

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44
Q

polyps of the small and large intestines

A

non neoplastic or premalignant lesions within the mucosa

neoplastic potential: some hyperplastic polyps on the right side of the colon are precursors to colorectal cancer

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45
Q

villous adenoma (polyps)

A

a) large, broad based elevated lesions made of thin, tall finger like processes that superficially look like villi.
b) Variable degrees of dysplasia.
c) Foci of carcinomas occur more often than tubular type
d) >1/3 resected villous adenomas contain invasive carcinomas

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46
Q

Tubular Adenomas (polyps)

A

a) smooth surface lesions with as stalk covered by normal colonic mucosa
b) Head has neoplastic epithelium with branching glands
c) All degrees of dysplasia can be encountered from contained cancer in mucosa to invasive carcinoma in submucosa
d) Cancer risk correlates to size

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47
Q

Histogenesis of the polyps

A

non-neoplastic type occurs sporadically and increase in frequency with age. Most are hyperplastic polyps… adenomatous type arises from mucosa

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48
Q

jaundice: what? possible causes?

A

retention of bile results from abnormal processing of bilirubin and its retention (bilirubin metabolism:production, uptake, conjugation and transport.)

possible causes of hepatocellular jaundice: anything that interferes with uptake, conjugation, and transport
other plausible causes: excessive production, impaired excretion, obstruction

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49
Q

Cholestasis: cuases?

A

systemic retention of bilirubin and other solutes eliminated in the bile due to decreased bile flow through canaculi, reducing secretion of water, bilirubin, and bile acids

causes: intrinsic liver disease (intrahepatic cholestasis), obstruction of bile ducts (extrahepatic cholestasis)

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50
Q

Cholestasis histological changes

A

presence of brownish pigment within dilated canaliculi and hepatocytes ot “bile lakes”

bile ductular proliferation,edema, bile pigment retention, inflammatory infiltrate

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51
Q

what is the diagnosis of cholestasis?

A

elevated serum alkaline phosphatase

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52
Q

Portal hypertension

A

often caused by cirrhosis; severely compromises ability to deliver blood, leading to blood flow to other locations. causes esophageal varices, ascites, and splenomegaly among other factors.

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53
Q

esophageal varices

A

“caput- Medusae” collateral veins of lower esophagus and upper stomach used and dilated. Rupture can lead to death

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54
Q

Ascites

A

accumulation of fluid from not enough albumin produced by liver leading to decreased oncotic pressure. Liver “weeps” lymph into abdomen. Renal retention of sodium and water.

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55
Q

Splenomegaly

A

hypertrophy of spleen- decreased life span and reduction of red/white cells. Spleen is firm, large. uniformly deep red with inapparent white pulp

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56
Q

what are the result of hypodonagium in women?

A

oligomenorrhea, amenorrhea, and sterility are frequent

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57
Q

Acute/ Chronic hepatitis

A

infection of hepatocytes by hepatotropic viruses named from A to G that produce necrosis and inflammation

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58
Q

Acute Hepatitis morphology (4)

A

(1) Scattered necrosis of single cells.
(2) ballooned hepatocytes (degeneration involving diffuse swelling of cells).
(3) Councilman bodies (apoptotic liver cells that are small, deeply, eosinophilic.)
(4) Infiltration of macrophages.

Cholestasis is common.
Regenerative changes

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59
Q

Chronic Hepatitis morphology (4)

A

(1) Piecemeal periportal necrosis (fragmented necrosis that looks like it was “moth-eaten”,
(2) intralobular and portal tract inflammation,
(3) bridging necrosis (formation of connective tissue septa between adjacent portal tracts),
(4) ground-glass hepatocytes (have large granular cytoplasm with HBsAg)

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60
Q

Alcoholic hepatitis: name the three morphologic and clinical entities

A

alcoholic liver disease

1) Fatty change: acculumulation of fat in hepatocytes steatosis
2) Hepatitis: necrosis of hepatocytes in the central zone, cytoplasms hyaline inclusions hepatocytes
3) Mallory bodies” alcoholic hyaline, collagen deposition around central vein

Cirrhosis

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61
Q

Hepatocellular Carcinomas

A

malignant primary tumor derived from hepatocytes. one of the most common worldwide tumors which appears as a soft, hemorrhagic mass in the liver

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62
Q

Hepatocellular Carcinoma association? histology?

A
  • Associated with HBC, HCV, metabolic conditions (hemochromatosis dues to iron helping with free radical production, cirrhosis) and environmental agents (alpha-toxin B1)
  • Histology variable–will try to invade vascular channels

-Alpha-fetoprotein is a tumor marker
prognosis is dismal

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63
Q

Cholelithiasis

A
  • Gall stones

- presence of stones within lumen of gall bladder or extra-hepatic biliary tree

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64
Q

composition of Gall stones

A

1) most gallstones are composed of cholesterol

2) pigmented gallstones are composed of calcium bilirubinate or other calcium salts

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65
Q

Cholecystitis

A
  • Gall bladder inflammation

- Usually secondary to obstruction by gall stones

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66
Q

Cholecystitis chronic (3)

A
  1. thickening of muscular wall,
  2. presence of chronic inflammatory cells.
  3. mucosa ulcerated and atrophic or may be intact
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67
Q

Cholecystitis Acute (2)

A
  1. neutrophils in epithelium and lamina propia,

2. mucosa fiery red to purple

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68
Q

Ischemic Bowel disease

A
  • injury from decreased intestinal blood flow.

- Acute intestinal ischemia is the most common type

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69
Q

three levels of severity of IBD

A

1) mucosal
2) mural
mucosal/mural secondary to acute/chronic hypo-perfusion

3) transmural infarcts- due to acute occlusion

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70
Q

IBD predisposing conditions

A

a) Obstruction: atherosclerosis, aortic aneurysm, hypercoagulable states, oral contraceptive use, embolization of cardia vegetations, aortic atheromas
b) Hypoperfusion: Cardiac failure, shock, dehydration, vasoconstrictive drugs, systemic vasculitides, portal hypertension, compression by masses

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71
Q

IBD results

A
  • a range from mucosal necrosis to transmural bowel infarction.
  • Occlusion of one of the three major vessels may lead to extensive infarction, although rich anastomoses may prevent affect
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72
Q

Cirrhosis

A

End stage of chronic liver disease characterized by bridging fibrous septa, parenchymal nodules, and disruption of the normal architecture of the entire liver

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73
Q

What happens in Cirrhosis (3)

A
  1. death of hepatocytes,
  2. extracellular matrix deposition,
  3. vascular reorganization
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74
Q

Clinical Cirrhosis

A

silent, but symptoms may be anorexia, weight loss, weakness, and in advanced disease, frank debilitation.
Ultimately leads to death through liver failure, portal hypertension complication, or hepatocarcinoma

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75
Q

Cirrhosis morphology

A

a) type I and III collagen deposited in space of disse, vascular architecture disruption leading to scarring, shunting of blood, loss of fenestration, impairment of exchange.
b) Fibrosis due to proliferation of hepatic stellate cells activated to become myofibroblasts
c) Nodule formation from surviving hepatocytes stimulated to regenerate rather than normal “pineapple” shape

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76
Q

Pancreatitis

A

injury to acini cells in the exocrine portion of the pancreas leading to an inflammatory reaction

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77
Q

Acute pancreatitis

A

varies from mild. self-limited with inflammation and stromal edema to severe, acute hemorrhagic disorder . dystrophic calcification

will return to normal if cause is removed

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78
Q

Chronic pancreatitis

A

results from repeated acute pancreatitis leading to recurrent attacks of severe abdominal pain, progressive fibrosis, and pancreatic insufficiency

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79
Q

Causes of pancreatitis

A

1) inappropriate activation of pancreatic enzymes- injuries to acinar cells lead to trypsin activation leading to proteolytic enzyme activation. tissue destruction and fat necrosis
2) overwhelmed anti-activation mechanisms
3) secretion against obstruction: any condition that narrows the pancreatic duct or prevents outflow of enzymes (ex. neoplasms, anatomical anomalies) leading to inappropriate activation
4) gallstones: 45% pts with pancreatitis have them, sick 25x higher than general population—not always seen though
5) alcohol consumption: 1/3 cases associated in acute, ethanol possibly causing spasm or acute edema. may stimulate secretion from intestine, triggering release of pancreatic juice
6) other: viral infection, drugs, trauma
7) unknown causes: 10-20%

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80
Q

pancreatitis: macroscopic changes

A

fat necrosis, chalky calcium deposits, hemorrhage

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81
Q

Pancreatitis: Microscopic changes

A

Acute: fat necrosis, calcium deposits, saponification, destruction of blood vessels leading to hemorrhage, parenchymal destruction, inflammatory response, edema, acini cell necrosis
Chronic: fibrosis, reduction in functional parenchyma (endo-exocrine components reduced in number/size, acinar and islet size) ducts dilated

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82
Q

pancreatitis clinical

A

acute: severe upper back pain, nausea and vomiting, vascular collapse/shock, elevated serum amylase/lipase. Gram-negative bacteria infection. Usually mild/self-limiting, but 20% severe and a medical emergency
Chronic : repeated episodes of acute pancreatitis in 5% of pts. Continuos/intermittent pain wight loss, jaundice , calcification is visible in radiographs
1/5 pts die

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83
Q

Serous Cystadenomas

A

1/4 of all pancreatic cystic adenomas

  • Glycogen rich cuboidal cells surrounding cysts with clear, straw-colored fluid.
  • Begins in 7th decade of life: female/male ration of 2:1
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84
Q

Mucinous Cystic adenomas

A

cystic tumor with thick mucin — almost always in women

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85
Q

mucin. cystic adenomas found in?

A

in body or tail

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86
Q

Mucin. cystic adenomas tumor

A

is a cystic space filled with thick, tenacious mucin. lined by columnar mucinous epithelium with dense cellular stroma

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87
Q

can Mucin cystic adenomas be benign, borderline malignant or malignant ?

A

Yea

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88
Q

Insulinomas

A

most common islet cell neoplasm–most are benign lesions in the body/tail

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89
Q

describe the clinical aspect of insulinomas

A

severe hypoglycemia, sweating, nervousness, hunger eventually becoming confusion, lethargy, and coma— high levels of insulin in blood and tumor cells

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90
Q

morphology of insulinomas

A

resemble normal beta cells but form trabecular and solid patterns—- amyloid found in stroma

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91
Q

islet cell tumors name (5)

A

account of 10% of pancreatic neoplasms

(1) gastrinomas (2) Glucagonomas (3) somatostatinomas (3) vasointestinal (5) insulinomas

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92
Q

gastrinomas

A

G cells— intractable gastric hypersecretion leading to peptic ulceration of duodenum and jejunum–most more malignant

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93
Q

glucagonomas

A

Alpha cells— mild diabetes, necrotizing migratory, erythematous rash, anemia, venous thrombosis
Glucagon levels 30x higher than normal 2/3 malignant

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94
Q

Somatostatinomas

A

delta cella— mild diabetes, gallstones, steatorrhea— most malignant

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95
Q

Vasointestinal polypeptide secreting tumors (VIPoma)

A

elevated levels of VIP. Explosive diarrhea

Most malignant

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96
Q

Pancreatic Cancer

A

4th most common cause of cancer death– 5 year survival rate of 5%— occurs later in life

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97
Q

90% of all pancreatic cancers

A

Ductal adenocarcinoma

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98
Q

Pancreatic cancer: Where is it found? give me %?

A

1) head- 60%
2) body- 10%
3) tail- 5%

rest is diffused

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99
Q

do cancers of the body and tail impinge on the biliary tract?

A

nope

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100
Q

pancreatic cancers association?

A

a) smoking- 25% of cases

b) 80% of patients with pancreatic, evidence of DM (increased risk)

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101
Q

Pancreatic cancer: classical neoplastic progression name (4)

A 
accumulation of mutations:
i) K-RAS
ii) p16 gene
iiI) SMAD4
iv) p53
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102
Q

p53 (PC)

A

tumor suppressor gene inactivated in 50-70% of cases

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103
Q

SMAD4 (PC)

A
  • tumor suppressor gene inactivated in 55% of cases
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104
Q

p16 (PC)

A

most frequently inactivated tumor supressor gene

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105
Q

K-RAS (PC)

A

most frequent altered oncogenes

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106
Q

Pancreatic cancer clinical (4)

A
  1. jaundice,
  2. migratory thrombophlebitis especially in body/tail adenocarcinoma (paraneoplastic syndrome related to hyper-coagulability)
  3. early metastasis: by the time of diagnosis.
  4. Courvoisier sign– acute, painless gallbladder dilation accompanied by jaundice due to bile duct obstruction by tumor
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107
Q

Oral thrush

A

a fungal infection of the oral cavity resulting in a scrapable, white plaque

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108
Q

what causes oral thrush?

A

Caused by candida albicans in combination with some impairments of usual protection such as diabetes mellitus, anemia, antibiotic/glucocorticoid therapy, HIV infection, disseminated cancer

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109
Q

how does it oral thrush looks like?

A

white, circumscribed plaque– pseudomembrane of fungal organisms superficially attached (and thus can be scrapped off)

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110
Q

Can oral thrush spread to esophagus?

A

Yea, life threatening if disseminated

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111
Q

xenobiotic metabolism

A

intake of chemicals which further become metabolized either to safe or unsafe forms

112
Q

how are exogenous chemicals absorbed?

A

through inhalation, ingestion, skin contact

113
Q

chemicals

A

can be excreted or can accumulate

114
Q

most solvents and drugs are

A

lipophilic

115
Q

cys p450

A

the most !. detoxifies or activates xenobiotics in phase I.

Variations in individuals can be due to induces or genetic polymorphisms

116
Q

What does grapefruit do?

A

it inactivates Cyp3A4 in intestines reducing metabolism of some oral drugs and increase bioavailability

117
Q

Phase I of xenobiotic metabolism

A

hydrolysis, oxidation and reduction resulting in “primary metabolite”

118
Q

Phase II of xenobiotic metabolism

A

conversion into water soluble compounds by glucoronidation, sulfuration, methylation, conjugation with glutathione

readily excreted

119
Q

lead

A

chemical which interferes greatly with skeletal, blood, renal system, and especially neuro system

120
Q

is air pollution classified a carcinogen?

A

yep

121
Q

lead in children

A

major hazard

causes central effects: low IQ, behavioral problems, generally irreversible.

122
Q

what is the maximum allowable for lead?

A

10 ug/dL but subclinical lead poison may happen in children with less than 10

123
Q

in adults with lead poisoning

A

peripheral neuropathies predominante

124
Q

effects in lead poisoning in skeletal system

A

interferes with normal remodeling, resulting in “lead lines” along the epiphyses, cartilage mineralization delayed

125
Q

effects in lead poisoning in hematopoietic

A

microcytic, hypo-chromic anemia. Basophilic stippling (dotting of RBC). hemolytic anemia due to increased fragility of cell membranes

126
Q

effects in lead poisoning in Nervous system

A

brain damage, especially in children—peripheral neuropathies

127
Q

effects in lead poisoning in kidneys

A

tubular damage

128
Q

Tx. for lead poisoning?

A

Nope, only tx is to remove from source and chelation therapy for severe symptoms

129
Q

alcohol

A

it is the cause and solution to all of life’s problems

130
Q

what happens to the liver with drinking alcohol?

A

fatty liver, alcoholic hepatitis, cirrhosis, portal hypertension, increased risk of hepatocellular carcinoma

131
Q

alcohol can also result in

A

gastritis, gastric ulcers, peripheral neuropathies. cardiomyopathies, acute/chronic pancreatitis

132
Q

alcohol increases risk of

A

cancers of the oral cavity, pharynx, larynx, esophagus

risk is greatly increased by concurrent smoking or use of smokeless tobacco

133
Q

exogenous estrogens

A

administered for post-menopausal and for birth control

134
Q

Oral contraceptives

A

major complications include thromboembolism, cardiovascular diseases, and hepatic adenoma

135
Q

Hormone replacement therapy

A

used for distressing menopausal symptoms or to prevent/slow osteoporosis

increases risk of: endometrial carcinoma (mainly estrogen, less with estrogen and progesterone together) and breast cancer (estrogen and progesterone together) as well as thromboembolism

little evidence that it protects against MI

136
Q

do burns depend on the depth of penetration in the dermis?

A

yea! there are three!

137
Q

First degree burn

A

only epidermis is injured

138
Q

second degree burn

A

necrosis extends to upper dermis but skin appendages such as hair follicle and sebaceous gland are spared

139
Q

Third degree burns

A

necrosis extends to deep dermis, subcutis may be involved, skin appendages are destroyed

140
Q

marasmus

A

calorie deficiency

141
Q

what do you see in marasmus?

A

growth retardation
somatic protein affected result in muscle loss while visceral protein is barely reduced
serum albumin is normal
subcutaneous fat is mobilized

142
Q

marasmus leads to

A

extremities thin and weak while head is disproportionately larger
anemia, multivitamin deficiencies, immun deficiency, concurrent infection

143
Q

kwashiorkor

A

protein reduction rather than just total caloric reduction

144
Q

in kwashiorkor

A

there is muscle mass and subcutaneous fat spared, visceral protein affected, resulting in hypoalbuminemia and consequent edema

145
Q

we see in kwashiorkor

A

zones of hyperpigmentation in skin and hypopigmentation “flaky paint”
Hair changes: loss of color or pattern of pale and dark hair
loss of firm attachment to skull, straightened, fine texture

146
Q

kwashiorkor results in

A

fatty liver, apathy, listlessness, loss of appetite— sequelae are multivitamin D efficiency, immune deficiency, secondary infections

147
Q

vitamin D deficiency

A

basic derangements for rickets and osteomalacia

148
Q

rickets

A

children “bowing of legs”

149
Q

osteomalacia

A

adults “ unmineralized matrix”

150
Q

Atelectasis

A

pulmonary collapse, inadequate expansion of airspaces

Hypoxemia- low arterial oxygen sue to shunting of the oxygenated blood from pulmonary arteries into veins

151
Q

Resorption Atelectasis

A

obstruction of airway, collapse of alveoli distal to obstruction

152
Q

Which atelectasis are reversible? which are not?

A

Reversible : Resorption and compression

Irreversible: Contraction

153
Q

Resorption atelectasis: causes and involves?

A

Causes: Mucus (CF), tumor (Mass Effect), foreign bodies (aspiration)

Involves: the entire lung, complete lobe, or one or more segments

154
Q

Compression Atelectasis

A

external pressure leads to mechanical collapse

155
Q

Compression atelectasis causes?

A

pneumothorax (air); hemothorax (blood); effusion (fluid); mass effect (neoplasm); Basal (posture)

156
Q

Contraction Atelectasis

A

interstitial fibrosis interferes with expansion— low compliance indicates a stiff lung

157
Q

ARDS

A

progressive respiratory insufficiency caused by diffused alveolar damages in the setting of sepsis, severe trauma,and diffused pulmonary infections

“Shock lung”

158
Q

Causes of ARDS

A

Shock, pneumonia with sepsis, endotoxins, near drowning, ischemia, aspiration

159
Q

ARDS pathogenesis

A
  • diffuse alveolar damage with endothelial/epithelial cell injury
  • more pro than anti-inflammatory mediators activated
  • Neutrophils
160
Q

What are the two steps of ARDS progression?

A

1) Acute

2) Organizing

161
Q

Acute ARDS

A

lungs dark red, airless, heavy

Necrosis, edema, collection of neutrophils with alveolar ducts lined with hyaline membranes

162
Q

Organizing ARDS

A

proliferation of type II pneumocytes and fibroblasts, removal hyaline membrane by macrophages

Resolution is unusual, and fibrin organizes leading to fibrosis

163
Q

ARDS clinical

A

arterial hypoxemia, cyanosis, mult. organ failure
scarred lung–sequelae
Tx methods: mechanical ventilation for hypoxemia

164
Q

obstructive airway disease

A

limitation of airflow – increase in resistance by partial or complete obstruction

165
Q

Obstructive disease examples

A

emphysema, chronic bronchitis, bronchiectasis and asthma

166
Q

Obstructive disease characteristics

A

total lung capacity is normal

decreased maximal airflow rates during forced expiration

167
Q

Restrictive disease

A

reduced expansion of lung parenchyma accompanied by decreased total lung capacity

168
Q

restrictive disease examples

A

1) chest wall disorder in the presence of normal lungs– severe obesity, diseases of the pleura, neuromuscular disorders
2) acute or chronic interstitial lung diseases — ARD, pneumoconioses, sarcoidosis

169
Q

restrictive diseases characteristics

A

reduced total lung capacity

expiratory flow rate is normal or reduced proportionately

170
Q

emphysema

A

a form of COPD with irreversible airflow obstruction— permanent dilation

alveolar wall destruction w/out fibrosis

overinflation

171
Q

lobule

A

terminal bronchiole and distal structures

172
Q

acinus

A

respiratory bronchiole and distal structures

173
Q

what are the two types of emphysema

A

1) centriacinar

2) Panlobular

174
Q

Centriacinar

A

most common, seen in smokers, upper lobes, and apical segments

distal alveoli spared!!

175
Q

Panlobular

A

non-smokers, alpha-1-antrypsin deficiency, affects lower lung zones

176
Q

emphysema pathogenesis

A

insufficient tissue repair—- inflammation because of cytokines, elstases, MMOs, oxidants

homeostasis imbalance between pro/anti- inflammatory mediators

177
Q

Emphysema diagnosis

A

-expiratory airflow limitations
-“pink puffer”
barrel chested, pursed lips, hunched over

178
Q

Emphysema complications

A

bullous formation, pulmonary hypertension, CHD, cor pulmonale

death due respiratory acidosis, right- side heart failure

179
Q

Chronic Bronchitis

A

form of COPD with irreversible airflow obstruction

persistent cough

180
Q

Chronic Bronchitis (4) morphology

A

(1) hyper-secretion of mucous
(2) hyperplasia/ hypertrophy of goblet cells
(3) Reid index increases
(4) inflammatory cells : mononuclear and neutrophils

181
Q

Chronic bronchitis clinical

A

Productive cough
blue bloater- combination of cyanosis and edema
cor pulmonale

may be seen with emphysema

182
Q

Asthma

A

form of Obstructive pulmonary disease with reversible airflow obstruction

183
Q

asthma caused by?

A

reversible bronchoconstriction caused by airway hyper-responsiveness

184
Q

Main features of asthma? (4)

A

1- intermittent/reversible
2- eosinophils
3- SMC hypertrophy/hyperactivity
4- airway remodeling

185
Q

Differences between extrinsic and intrinsic asthma?

A

extrinsic- majority asthma cases, caused by Th2 and IgE

intrinsic- non-immune stimuli (aspirin, cold, stress…)

186
Q

Asthma Morphology (5)

A
  1. Mucus plugs
  2. cellular infiltrate- eosinophils
  3. curshmann spirals
  4. charcot-leyden crystals
  5. airway remodeling:
    • thickening of BM
    • edema
    • increase of submucosal glands
    • hypertrophy of walls
187
Q

Asthma clinical

A

dyspenia w/ wheezing

difficulty in expiration

188
Q

Bronchiectasis

A

permanent dilation of branchi and bronchiole— destruction of SMC and elastic supporting tissues

189
Q

Causes of bronchiectasis

A

bronchial obstruction such as tumors and foreign bodies
pneumonia- S. aureus
congenital/ hereditary conditions like cystic fibrosis

190
Q

Morphology of bronchiectasis (5)

A

1) lower lobes
2) airways dilated
3) intense acute and chronic inflammatory
4) chronic cases lead to fibrosis
5) lung abscess may form

191
Q

Bronchiectasis clinical

A

severe, persistent cough, expectoration, infection

192
Q

restrictive lung diseases of diffuse interstitial (4)

A

restrictive disorders which affect lung movement during respiration

  1. usual interstitial pneumonia
  2. pneumoconioses
  3. Asbestosis
  4. sarcoidosis
193
Q

usual interstitial pneumonia

A

idiopathic pulmonary fibrosis

pleura has cobblestones appearance

fibroblastic foci, honeycomb fibrosis

heterogeneity of both early and late lesions

clinical: dsypenia, cyanosis.. lung transplant only therapy

194
Q

pneumoconioses

A

chronic interstitial restrictive pulmonary diseases caused by particle inhalation
reactivity depends on size, shape, solubility, reactivity

particles that are 1-5 um are the most dangerous b/c they get lodged at bifurcation of airways

most particles removed by mucociliary clearance

tobacco smoking worsens the effects of all inhaled mineral dusts

195
Q

Asbestosis

A

classical example of pneumoconiosis:

very fibrogenic particles

196
Q

Morphology of asbestosis

A

diffuse interstitial fibrosis, asbestos bodies in the lungs— iron-protein coat

golden brown stains w/ prussian blue

197
Q

Asbestosis clinical

A

pleural plaques: well circumscribed of dense collagen
mesotheliomas: bronchogenic carcinomas, fibrosis, pleural effusions

cigarette smoking increases risk of lung cancer in comb. with this

worsening dspenia

198
Q

sarcoidosis

A

non-caseating granulomatous diseases of type IV hypersensitivity: steroid bodies and shaumann bodies

199
Q

in diffuse interstitial lung disease the ________ ________ ___ is involved

A

pulmonary connective tissue

200
Q

Diffuse interstitial lung disease

A
  • reduced compliance
  • fibrosis may or may not see honeycombing
  • presence of macrophages
  • alveolitis is the initial manisfetation
201
Q

Pneumonia name the two clasess

A

infection of the lungs

1) bronchopneumonia
2) lobar pneumonia

202
Q

Morphology of lobar pneumonia (4) steps if not stopped with antibiotics

A

affects the entire lobe:

(1) congestion- lobes red, heavy and soggy. vascular congestion w/ proteinaceous fluid, neutrophils
(2) red hepatization- liver like consistency– alveoli have neutrophils, red cells, fibrin
(3) gray hepatization- dry, gray, firm due to red cell lysing—- fibrinosuppurative exudate in the alveoli
(4) resolution- happens in uncomlicated cases— exudate that was digested produced granular, semifluid debris that is reabsorbed and ingested by MQ or coughed up

203
Q

Morphology of Bronchopneumonia (4)

A

(1) distributed in patches
(2) focal suppurative exudate
(3) complete restitution of tx properly
(4) complications: abscess, emphysema, organization, bacteremic dissemination

204
Q

pulmonary neoplasms

A

lung is frequent site of metastasis—

primary tumors are a leading cause of death

205
Q

Bronchial epi. is site of ____ of lung carcinomas

A

95%

206
Q

___ are miscellaneous bronchial carcinoids

A

5%

207
Q

what are the four types of Carcinomas of the lung? name also the two therapies?

A

(1) squamous cell
(2) Adenocarcinomas
(3) large cell
(4) small cell

i. SCLC– small cell, likely have already metastasized and it is treated with chemo
ii. NSCLC– non-small cell, responds poorly to chemo and it better tx with surgery

208
Q

Squamous cell carcinoma

A

3-% of lung cancers, arises in major bronchi and associated smoking

smoking forces regeneration in the form of squamous metaplasia and it follows same sequence of dysplasia (carcinoma in situ)– metaplastic mucosa

209
Q

Adenocarcinomas

A

1/3 of lung cancer and most common form of cancer in women and non-smokers

210
Q

adenocarcinomas appears in the _____ and associated w/ ___ ____ and ___ ___, resulting in pleural ____

A

occurs in the periphery
ass. w/ pleural fibrosis and pleural scars
pleural puckering

211
Q

adenocarcinomas characterized

A

moderate to well differentiated tumors— mucin droplets in tumor cytoplasm

212
Q

precursor of adenocarcarcinomas

A

atypical adenomatous hyperplasia – prolif. of cuboidal to low columnar cells resembling clara/type 2 cells

213
Q

small cell carcinoma

A

20% of lung cancers and strong assoc. w/ smoking
small cells w/ neuroendocrine features
highly malignant– 70%

214
Q

small cell carcinoma are assoc. with paraneopladtic syndromes except

A

hypercalcemia and hematologic type

215
Q

Large cell carcinoma

A

10% of lung cancer, evolves from poorly differentiated adenocarcinomas/ squamous cell carcinomas

216
Q

Bronchial carcinoids

A

low- grade malignant tumors (centrally located) composed of neuroendocrine cells though to arise from kulchitsky cells that line bronchial mucosa and resemble intestinal carcinoids

often resectable and curable

217
Q

Large cell carcinoma have

A

large nuclei, prominent nucleoli and moderate cytoplasm

218
Q

______ _______ epithelial tumors w/out cytologic features of small-cell and glandular or squamous differentiation

A

undifferentiated malignant

219
Q

bronchial carcinoids appear at an ____ ____ and represent about ____ of pulmonary tumors

A

early age, 5%

220
Q

bronchial carcinoids show no gender predilection? what about assoc, with smoking?

A

no gender p. and no assoc. with smoking

221
Q

Bronchial carcinoids tumor cells

A

contain dense- core neurosecretory granules in the cytoplasm

test positive for : synaptophysin

most of the mare endocrinologically silent and rarely secrete hormonally active polypeptides

222
Q

hypercalcemia most often encountered with

A

squamous cell neoplasams

secrete PTH

223
Q

hematologic syndromes encountered w/

A

adenocarcinomas

224
Q

malignant mesothelioma

A

neoplasm of mesothelial cells in the pleura

combination w/ cigarette smoking does not increase meo but does carci

225
Q

malignant mesothelioma assoc. w/

A

asbestos exposure

226
Q

malignant mesothelioma have a ____ latency. The tumor cells often ______ and ______ the lung

A

latency, encase and compress “pleural rind’ looks like an orange peel

227
Q

malignant mesothelioma have

A

extensive pleural fibrosis and plaque formation and tx is largely ineffective and prognosis is poor

228
Q

signs of cholestasis

A

jaundice, pruritus due to deposition of bile acid on skin

229
Q

portal hypertension causes

A

Esophageal varices, ascites, splenomegaly

230
Q

pseudocysts are a common aftermath of pancreatitis

A

they are delimited by Connective tissue with degraded blood, debris, necrotic pancreatic tissue

has no epithelial lining and may become infected

75% of all pancreatic cysts

231
Q

Vitamin A is important for

A

vision, cell growt/ differentiation, metabolism, resistance to infection, photo-protection and antioxidation

232
Q

Vit. A deficiency

A

leads to night blindness, dry eye, Bitot’s spots (keratin debris plaques and keratomalacia (cornea erosion)

233
Q

Vit. A def. principally results in _____ ______

A

Squamous metaplasia– hyperkeratinization immune dificiency

234
Q

Vitamin C

A

normally helps out with hydroxylation and amidation (collagen)

w/out, collagen is more vulnerable to enzymatic degradation– functions as an oxidant

235
Q

vit. C deficiency

A

impaired collagen formation leading to bleeding (poor vascular support), inadequate osteoid matrix formation and impaired wound healing

236
Q

Malnutrition

A

inability/ insufficient intake of energy, amino acids, vitamins and minerals

237
Q

protein compartments in the body are regulated separately name them and explain

A
  1. somatic: proteins in skeletal muscles

2. Visceral: proteins in the viscera, primarily in liver

238
Q

primary malnutrition

A

missing some component of appropriate diet

239
Q

Secondary malnutrition

A

from nutrient supply sufficient but malabsorbed, impaired utilization or storage, excess nutrient loss or need for nutrients

240
Q

hyperthermia

A

prolonged exposure to elevated ambient temperature can have detrimental effects on the body

241
Q

Heat cramps

A

loss of electrolytes via sweating – normal core temp, cramping of voluntary muscles during exercise

242
Q

Heat exhaustion

A

sudden onset and collapse— CV cannot compensate for loss of fluid—- equilibrium spont. reestablished

can progress to heat stroke

243
Q

Heat stroke

A

heat regulation fails, sweating ceases, core temperature rises,

peripheral vasodilation, pooling of blood, decreased effective circulating blood volume

244
Q

with hyperthermia can you have a change in mental status, arrhythmias, intravascular coagulation?

A

yep

245
Q

hyperthermia can be a risk for

A

the elderly, people with CV disease, and healthy people doing stressful things

246
Q

sialadenitis assoc. with

A

viral infection- paramyxovirus, mumps
bacterial infection- ductual obstruction
sjogren syndrome- dry eyes/ mouth; immunological destruction

247
Q

colorectal cancer

A

mostly adenocarcinomas– classical examples of neoplastic progression with multistep carcinogenesis

248
Q

what are the two possible pathways involved in colorectal cancer

A
  1. beta catenin

2. microsatellite instability

249
Q

risk factors of colorectal cancer

A

age, chronic inflammatory bowel disease, diet, genetics

250
Q

colorectal cancer clinical

A

occult blood in stool, iron deficiency anemia, obstruction– metastasis through direct extension or vascular lymphatic invasion (part. in liver)

his friend that walks in boston commons got this!

251
Q

acetaminophen

A

normally taken as a pain reliever, if overdoses metabolism can lead to toxicity

252
Q

what is the antidote for acetaminophen?

A

N- Acetylcysteine which restores GSH

253
Q

acetaminophen although generally detoxified by phase ___ enzymes, it is also metabolized by ____ which produces ____ which can be conjugated with _______

A

II, CYP2E1, NAPQ, glutathione- GSH

254
Q

Depletion of reduced GSH results in

A

free radical damage and cell death leading to centrilobular necrosis of hepatic lobules

255
Q

chronic gastritis

A

H. Pylori gastritis– chronic inflammatory changes

256
Q

what are the chronic inflammatory changes assoc. w/

A

mucosa leading to mucosal atrophy and epithelial metaplasia– results from imbalance btw. gastroduodenal mucosal defenses and damaging forces tat overcome these defenses

257
Q

cellular infiltrate of chronic gastritis

A

intraepithelial neutrophils and subepithelial plasma cells

258
Q

over time in chronic gastritis, will extend to involve the bosy and funsus of the stomach and bc. ____. Assoc. w/ ____ with germinal centers can transform into ______

A

atrophic, MALT, lymphomas

259
Q

Clinical Chronic Gastritis

A

combination Tx of antibiotic eliminate H.Pylori and proton pump inhibitors– less acid

260
Q

peptic ulcer disease

A

ulcers penetrate the mucosa, often as a result of H. pylory and NSAIDs

261
Q

Peptic Ulcer dis. is seen in the ______ and _______ ( more common in later)

A

stomach and duodenum

262
Q

peptic ulcer dis. gross

A

round to oval “punched- out” defect. Mucosal margin level w/ surrounding mucosa. base of ulcer smooth and clean, blood vessels may be evident

263
Q

Peptic ulcer dis. histological

A

thin layer of fibrinoid debris w/ neutrophil infiltrate.
granulation tissue infiltrated with mononuclear lymphocytes and fibrous/ collagenous scar. vessels walls in the scar are thickened and thrombosed

264
Q

Peptic ulcer dis. clinical

A

bleeding– potentially life-threatening- perforation

265
Q

herpetic stomatitis

A

common viral infection of the oral cavity

266
Q

herpetic stomatitis caused by

A

HSV1 or HSV2

267
Q

herpetic stomatitis mprphology

A

inclusion and polykaryons detected with Tzanck test—- vesicles filled with exudate

268
Q

Cancers of the oral cavity and tongue

A

are mostly squamous cell carcinomas risk factors included tobacco

they are moderately to well- differentiated keratinizing tumors
“keratin pearls”— early lesions
may progress to dysplasia

269
Q

ionizing radiation

A

DNA damage through a direct/indirect effect with indirect effect creating free radicals

270
Q

What can happen in ionizing radiation?

A

Damage DNA: rapidly dividing cells such as germ cell, bone marrow, GI sensitive to radiation.

inadequate repair of DNA can lead to neoplastic transformation

271
Q

ionizing radiation factors influencing effects (5)

A
  1. higher rate of cell turnover
  2. vascular damage– late manifestation— replacement of fibrous tissue
  3. rate of delivery– single/fractional doses
  4. hypoxic tissues more resistant
  5. large/small doses more potent than small/large
272
Q

Acute radiation syndrome

A

different modes of death dependent on radiation dosage

273
Q

acute radiation syndrome- small dosage

A

hemopoietic– 2 week latency, death in 3 weeks

kills bone marrow, resultant leukopenia,

274
Q

acute radiation syndrome- medium dosage

A

intestinal- 3 day latency— death in 2 weeks

GI epithelium necrosis and ulceration, infection, and diarrhea

275
Q

acute radiation syndrome- large dosage

A

Cerebral- 1 hour latency– death in 1 day

cerebral edema, neuronal necrosis, vasculitis, coma

Pathology exam III review (1 decks)

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