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110 Cards in this Set

  • Front
  • Back
Apoptosis is characterized by what cell changes
cell shrinkage, nuclear shrinkage (pyknosis), basophilia, membrane blebbing, nuclear fragmentation (karyorrhexis), forming apoptotic bodies
Apoptosis: Intrinsic pathway
involved in tissue remodeling, embryogenesis. Growth factor is withdrawn from proliferating cells: ↑ Bax ↓ Bcl-2 -> Cytochrome C -> Cytosolic caspases
Apoptosis: Extrinsic pathway (2 pathways)
1) Fas-L binding Fas 2) Cytotoxic T cell releases Granzyme B & Perforin
CD95 =
Fas-Receptor
Coagulative necrosis
heart, liver, kidney
Liquefactive necrosis
brain, abscess, pleural effusion
Caseous necrosis
TB, systemic fungi
Fatty necrosis
saponification, peripancreatic fat
Fibrinoid necrosis
BVs
Gangrenous necrosis 1) dry 2) wet
1) dry ischemic coagulative 2) wet has bacteria. Limbs & GI tract
Reversible cell injury
↓ ATP, cellular swelling, nuclear chromatin clumping, ribosomal detachment, ↓glycogen, fatty change
Irreversible cell injury
Ca++ influx activates caspases, PM damage, Mitochondrial permeability, lysosome rupture, nuclear pyknosis, karyolysis, karryorhexis
Hypoxia in brain
ACA/MCA/PCA watershed
Hypoxia in heart
subendocardium of LV
Hypoxia in kidney
straight segment of PT (medulla), TAL (medulla)
Hypoxia in Liver
zone III (around central vein)
Hypoxia in colon
splenic flexure, rectum
Hypoxic ischemic encephalopathy affects
pyramidal cells of hippocampus & purkinje cells
Red infarct
hemorrhagic. Red = reperfusion injury. Loose tissues with collaterals. (liver, lung, intestine)
Pale infarct
ischemia: solid tissues with single blood supply: heart, kidney, spleen
↑ TPR, low CO, cold, clammy patient = what kind of shock?
hypovolemic
↓ TPR, dilated arterioles, high VR, hot patient = what kind of shock?
septic
Acute inflammation
neutrophils, eosinophils, antibodies. Rapid. Abscess.
Chronic inflammation
mononuclear cells: persistent destruction & repair. BV proliferation & fibrosis: Scar, amyloidosis
Granuloma
nodular collections of epithelioid macrophages and giant cells.
Leukocyte rolling
E&P selectin + Sialyl Lewis
Leukocyte tight binding
ICAM-1 & integrin (LFA-1)
Leukocyte diapedesis
PECAM1
Leukocyte migration
C5a, IL-8, LTB4, Kallikrein
Mechanism of injury caused by carbon tetrachloride?
Free radical injury -> necrosis & fatty change
Free radical pathologies
Retinopathy of prematurity, bronchopulmonary dysplasia, CCL4, Acetaminophen overdose, hemochromatosis, repurfusion after anoxia
Free radicals eliminated by what enzymes
superoxide dismutase, catalase, glutathione peroxidase
antioxidant vitamins
A, C, E
Wound healing: INFLAMMATORY STAGE
Plts, NΦ, MΦs: Clot, vessel perm, NΦ migration, MΦ clear debris
Wound healing: PROLIFERATIVE STAGE
Day 2-3. Fibroblasts, myofbs, endoth cells, keratinocytes, MΦs. GT & Collagen, angiogenesis, epith cell proliferation, clot dissolution, WOUND CONTRACTION
Wound healing: REMODELING STAGE
FIBROBLASTS: Replace Type III collagen with Type I collagen for tensile strength
wound contraction mediated by
myofibroblasts
Cells that mediate granuloma formation
Th1 secrete gammaINF -> Macrophages -> TNFa
Specific gravity of transudate vs exudate
transudate < 1.012, exudate > 1.012
cellularity & protein content of transudate vs exudate
transudate: hypocellular, protein poor exudate: hypercellular, protein rich
Transudate caused by:
↑ hydrostatic P ↓ oncotic P, Na+ retention
Exudate caused by:
lymphatic obstruction & inflammation
ESR
when aggregated from products of inflammation coating RBCs, they fall at a faster rate in the test tube
↑ESR
infection, inflammation, cancer, pregnancy SLE
↓ESR
Sickle cell (altered shape), Polycythemia (too many), CHF (who the hell knows)
Cell death by peroxidation of membrane lipids from poisoning by:
Iron
Waxy appearance due to beta pleated sheet structure aggregations:
amyloidosis (oh ya and apple green birefringence)
Primary amyloidosis due to what protein
AL = Ig Light chain deposits. Plasma cell disorder or multiple myeloma
Secondary amyloidosis due to what protein
AA = Fibrils of serum Amyloid A. Chronic diseases like RA, IBD, spondyloarthropathy, chronic infections
Dialysis related amyloidosis
beta2microglobulin fibrils. Presents as carpal tunnel syndrome
Heritable amyloidosis
Transthyretin gene mutation -> ATTR neuro/cardiac amyloidosis
Age related amyloidosis
deposition of normal TTR in myocardium
Organ specific amyloidosis
ex: APP into amyloid beta in Alzheimers
Metalloproteinases secreted by cancer cells indicate they are now:
INVADING
Metaplasia
One adult cell type replaced by another
Dysplasia
abnormal growth with loss of orientation size and shape compared to normal tissue
Anaplasia
abnormal cells lacking differentiation: primitive cells of same tissue
Neoplasia
clonal proliferation of cells, excessive, uncontrolled
desmoplasia
fibrous tissue formation in response to neoplasm
Tumor Grade
Degree of differentiation
Tumor Stage
Stage = Spread
Cachexia mediated by
TNFalpha, INFgamma, IL-6
Tyrosine Kinase oncogenes:
"though still ABLe, ERB was Tyred, so he RETired" abl, c-erbB2 (HER2neu), ret
abl
CML, tyrosine kinase
HER2/neu
breast, ovarian, gastric, tyrosine kinase
Ret
MEN 2A & 2B (Tyrosine kinase)
Transcription factor oncogenes
"mycs" c-myc, l-myc, n-myc
c-myc
burkitt's..duh. TF
L-myc
L=Lung tumor. TF
N-myc
N=Neuroblastoma. TF
bcl2
antiapoptotic oncogene, follicular lymphoma
Ras
oncogene: colon CA (GTPase)
c-kit
Gastrointestinal stromal tumor (GIST), CytoKIe receptor oncogene
Rb
RetinoBlastoma, osteosarcoma. Rb = chrom 13. Inhibits E2F GI->S phase
p53
TSG. Li fraumeni syndrome (17p), TF for p21
BRCA1, BRCA 2
TSG: breast & ovarian cancer. DNA repair proteins [chrom 17, 13]
p16 & BRAF
melanoma
APC
TSG: coloectal cancer. Polyp = 5 letters, chrom 5
WT1
TSG: wilm's tumor (nephroblastoma)chrom 11
NF1
NF type 1, TSG, chrom 17. RAS GTPase activating protein
NF2
NF type 2, Chrom 22, merlin schwannomin protein
DPC4
TSG: "Deleted in Pancreatic Cancer"
DCC
TSG: "Deleted in Colon Cancer"
CEA
CarcinoEmbryonic Antigen. Colorectal and pancreatic cancers
alphaFP
HCC, GCTs
CA-125
Ovarian cancer
s100
melanoma, neural, schwannomas
alkaline phosphatase
mets to bone, liver, paget's
calcitonin
medullary thyroid carcinoma
keratin+
epithelial surfaces
Aflatoxin
HCC
vinyl chloride
liver, angiosarcoma
CCL4
liver, fatty change, centrilobular necrosis
Nitrosamines
gastric cancer
cigarette smoke LAWL
SCC of larynx, lung, small cell, RCC, transitional cell, pancreatic
Asbestos
bronchogenic CA > mesothelioma!!!
arsenic
SCC skin Angiosarcoma of liver
Naphthalene (aniline) dyes
Transitional cell carcinoma (bladder)
aklylating agents
leukemia
PSaMMoma bodies
papillary (thyroid) Serous (ovary) meningioma mesothelioma
male cancer incidence
prostate > lung > colon
male cancer mortality
lung > prostate
female cancer incidence
breast > lung > colon
female cancer mortality
lung > breast
ACTH or ACTH like peptide Paraneoplastic syndrome
cushing's syndrome effect. Small cell
paraneoplastic syndrome: ADH
SIADH effect from small cell lung carcinoma & intracranial neoplasms
paraneoplastic syndrome: PTHrP
hypercalcemia. Squamous cell lung CA, RCC, breast
paraneoplastic syndrome: calcitriol
hypercalcemia. Hodgkins
paraneoplastic syndrome: EPO
polycythemia effect from RCC, hemangioblastoma, HCC, pheochromocytoma
paraneoplastic syndrome: antibodies against presynaptic Ca++
lambert eaton syndrome, small cell