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41 Cards in this Set

  • Front
  • Back
-Does apoptosis require energy?
-Inflammation present?
-Histo characteristics?
-Yes, ATP
-No inflammation!
-Cell shrinkage, nuc pyknosis (small, dark), karyorrhexis (frag), karyolysis (fading), membrane blebbing, apoptotic bodies.
Intrinsic pathway of apoptosis
-physio example?
-nonphysio example?
-What happens inside cell to activate?
-Embryogenesis, hormone (menses), atrophy (menopause)
-Injury (xrt, toxin, hypoxia)
-Increase Bax, decrease Bcl2. Then mito release cyto c, which activates caspasaces.
Extrinsic pathway of apoptosis
-example?
-FasL binding to Fas (CD95)
-Killer T cell release perforin and granzyme B
Types of Necrosis - causes
-Coagulative?
-Liquefactive?
-Caseous?
-Fat?
-Fibrinoid?
-ischemia/infarct
-brain, abscess, pleural effusion
-TB, fungal
-enzymes, trauma
-immunologic
-When does hemorrhagic infarct happen?
-Jiggly tissue with dual blood supply
-Reperfusion injury
-Define atrophy
-Name 6 causes of atrophy
-Decline in size OR number of cells.
1. decrease hormones
2. decrease innervation
3. decrease blood flow
4. decrease nutrients
5. increase pressure (stones)
6. occlusion of ducts (CF)
-Which markers of cell injury are reversible with O2?
Cell swelling (no ATP for Na/K)
Chromatin clumping
Low glycogen/ATP
Ribosomal detachment
Fatty change
-Which markers of cell injury are NOT reversible with O2?
Pyknosis, karyolysis, karyorrhexis
Ca influx (activate caspasace)
PM, lysosomal, mito damage
What chemical mediator causes:
-Rubor?
-Calor?
-Tumor?
-Dolor?
-histamine, arteriole dilation
-histamine, arteriole dilation
-histamine, contracted endothelial cells of venules
-bradykinin, PGE2
-How does a granuloma form?
-What type hypersen?
-Alveolar mac eats TB, takes trip around body, present to Th1 cell. Th1 releases IFNgamma to activate mac into epitheliod mac, and several of these fuse into giant cells. Then mac secretes TNFalpha to maintain granuloma formation.
-Type IV hypersen
-What are the 4 steps of leukocyte extravasation? (leuk-endothelial cell)
1. Rolling: Sialyl Lewis x- E/P selection
2. Tight Binding: LFA1-ICAM1
3. Diapedesis: PECAM1 (both)
4. Migration (chemotactic factors-CILK)
-What chemotactic signals cause migration of leukocytes thru tissue interstitium?
"CILK"
C5a, IL-8, LFTB4, kallikrein
-How do free rads cause damage? (3 ways)
1. Membrane lipid peroxidation
2. Protein modification
3. DNA breakage
-How does acetaminophen tox cause free rad damage?
-Name some other causes free rad damage?
-Depletes glutathione stores. (Mucomyst repletes)
-Fe overload, CCl4 (liver necrosis), reperfusion, ROP, BPD
-Name 8 granulomatous diseases
TB
Fungal infxn
Leprosy
Syphilis
Cat scratch fever
Sarcoid
Berryliosis
Crohn's
Takayasu, temporal arteritis, Wegener's, Churg-Strauss
Visceral larva migrans (toxocara canis)
-What do anti-TNF drugs do to granulomatous diseases?
-Reactivation! TNFalpha from macs helps keep granuloma sealed off. Without it, infxn can run rampant again!
-What is ESR?
-Erythrocyte sedimentation rate. Products of inflam coat RBC and make aggregate, fall at a faster rate.
-What elevates ESR?
-What decreases ESR?
-Infxn/inflam, preg, malig, SLE
-Sicke cell, CHF, polycythemia
-How does Fe poisoning kill?
-Acute and chronic sx?
-Lipid peroxidation of membranes, free rad damage
-Acute: gastric bleed
-Chronic: met acidosis, scarring causing GI obstruction
-What is amyloidosis?
-What does affected tissue look like grossly?
-Mutation in a protein causes misfolding to beta-pleated sheets that accumulate in various organs and cause trouble.
-Waxy tissue
Type of amyloidosis, original, and amyloid protein?
-Primary
-Secondary
-Senile Cardiac
Primary: Ig light chains-->AL (light)
Secondary: Serum amyloid assoc protein (SAA)-->AA (acute phase)
Senile Cardiac: transthyretin-->AF (fogie)
Type of amyloidosis, original, and amyloid protein?
-DM2
-Medullary thyroid carcinoma
-Alzheimer's
-Dialysis-associated
DM2: Amylin-->AE (endocrine)
Med Thyroid Ca: Calcitonin-->A-CAL
Alzheimer's: Amyloid precursor protein (APP)-->beta-amyloid
Dialysis: MHC Class I-->beta-microglobulin
-How do cancer cells become invasive and break thru BM?
-How do they metastasize to lymph/blood vessels?
-collagenases and hydrolases
-decrease cadherin, increase laminin, integrin receptors
-What is desmoplasia?
-Fibrous tissue proliferation in response to neoplasm
-What cancer(s) is assoc with Paget's disease?
-Autoimmune dz (Hashimoto, Sjogren's, MG)
-Acanthosis Nigricans
-Radiation
Paget: secondary osteosarcoma, fibrosarcoma
Autoimmune: NHL
Acanthosis: Solid tumors of breast, lung, uterus, stomach
Radiation: leukemia, papillary thyroid carcinoma, sarcoma
Which cancers produce CEA?
Colon and pancreas (70% of all of these)
Breast, med thyroid, gastric
Which tumors produce CA-125?
Ovarian, malig epithelial tumors
Which tumors produce S-100?
Melanoma
Neural tumors
Astrocytomas
Langerhans cell histiocytosis
Which tumors produce bombesin (GRP)?
Neuroblastoma
Lung
Gastric

**n-myc, l-myc, c-myc
TRAP (Tartrate resistant acid phosphatase) is marker for what?
Hairy cell leukemia ("TRAP the hairy animal")
Which cancers can EBV cause?
Burkitt's lymphoma
Nasopharyngeal carcinoma
HL
Which cancers can HHV8 cause?
Kaposi's sarcoma
Body cavity fluid Bcell lymphoma
-What cancer can vinyl chloride cause?
Angiosarcoma of liver
What cancer can arsenic cause?
SCC, angiosarcoma of liver
What cancer can alkylating chemo agents cause?
Leukemia
Which tumors can cause EPO paraneoplastic syndrome?
RCC, Pheochromocytoma
HCC, Hemangioblastoma
Which tumors can cause Eaton-Lambert?
thymoma
small cell lung cancer
-Which tumors can cause hyperCa?
-Due to release of what?
Squamous cell carcinoma of lung
RCC
Breast
-PTHrp, TGF-beta, IL-1, TNF
In what tumors can you find psammoma bodies?
"PSaMMoma"
Papillary thyroid
Serous ovarian
Meningioma
Mesothelioma
Mets to brain
-which tumors?
-where do they go?
"Lots of Bad Stuff Kills Glia"
Lung, breast, skin (melanoma), kidney (RCC), GI
**Go to gray-white matter jxn
Mets to liver
"Cancer Sometimes Penetrates Benign Liver"
Colon, stomach, panc, breast, lung.