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195 Cards in this Set

  • Front
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3 general features of apoptosis:
1. *requires* ATP

2. => activation of cytosolic caspases

3. NO inflam. (unlike necrosis)
what do caspases do?
7 steps of the apoptotic process:
1. deeply-eosinophilic cytoplasm

2. cell shrinks

3. pyknosis (nuclear shrinkage)

4. membrane blebbing

5. karyorrhexis (nuclear fragmentation)

6. => formation of apoptotic bodies

7. => phagocytosed
what is a sensitive indicator of cell apoptosis?
DNA laddering
DNA laddering:
*during karyorrhexis,* endonucleases cleave at internucleosomal regions,

yielding 180-bp fragments
radx therapy causes apoptosis of:
tumors and *surrounding* tissue

via free radical formation and dsDNA breakage

=> rapidly-dividing cells (e.g. skin, GI mucosa) are very susceptible to radx therapy-induced apoptosis
intrinsic pathway of apoptosis occurs in:
tissue remodeling following embryogenesis
the intrinsic pathway of apoptosis is employed when:

(2 cases)
1. a regulating factor is withdrawn from a proliferating cell population

2. after exposure to injurious stimuli (toxins, radx, hypoxia)
the intrinsic pathway of apoptosis includes pro- and anti-apoptotic factors;

2 pro-apoptotic prots =

1 anti-apoptotic prot. =

Bcl-2 is anti-apoptotic
intrinsic pathway: changes in proportions of pro- and anti-apoptotic factors =>
increased mitochondrial permeability => cytochrome c release
Bcl-2 prevents cytochrome c release by:
binding to and inhibiting Apaf-1

(Apaf-1 nly induces the activation of caspases)
if Bcl-2 is overly expressed (as in follicular lymphoma), Apaf-1 is overly:

resulting in a decreased caspase activation

=> tumorigenesis (formation of tumor)
2 extrinsic pathways of apoptosis:
1. ligand-r' interactions
(FasL binding to Fas/CD95)

2. immune cell-mediated
(cytotoxic T-cell release of perforin and granzyme B)
the Fas-FasL interaction is necessary in thymic medullary negative selection - it stops defective/excess T cells from being expressed. but mutations in Fas increase the numbers of:
circulating self-reacting lymphocytes

=> AI disorders

(defective Fas-FasL interaction is the basis for AI disorders)
normal Fas-FasL interaction: after Fas crosslinks with FasL, multiple Fas mlcls coalesce, forming a binding site for:
a death domain-containing adaptor protein, FADD
what does FADD do?
binds inactive caspases,

activating them

=> apoptosis
5 characteristics of necrosis in general:
1. ~~exogenous injury

2. prot. denaturation

3. enzymatic degradation

4. intracellular components leak

5. **an INFLAMMATORY process**
(unlike apop)
coagulative necrosis:

1. occurs in tissue supplied by end arteries

2. m.c. in heart, liver, kidney

3. prots denature first, then enzymatic degradation

4. cytoplasms bind acidophilic dye

5. cytoskeleton remains
liquefactive necrosis:

1. occurs in CNS due to high fat content

2. m.c. in brain, due to bacterial abscesses

3. enzymatic degradation due to release of lysosomal enzymes occurs first

4. => cell shape NOT retained
caseous necrosis is caused by:

1. TB

2. systemic fungi

3. Nocardia (bact)
fatty necrosis:

1. enzymatic (pancreatitis/saponification)

2. or nonenzymatic (e.g. breast trauma)

3. **Ca2+ deposits appear DARK blue on stain
fibrinoid necrosis

1. vasculitides (plural of vasculitis)

2. => Henoch-Schonlein purpura, Chaug-Strauss syndrome

3. malignant HTN

4. amorphous and PINK on H/E
gangrenous necrosis

1. dry (if ischemic coagulative)

2. or wet (if inf)

3. common in limbs, GI tract
7 facets of REVERSIBLE cell injury:

(i.e. if O2 was returned, these could be undone)
1. ATP depletion

2. cellular/mitochondrial swelling

3. nuclear chromatin clumping

4. dec. glycogen

5. fatty change

6. ribosomal/polysomal detachment

7. membrane blebbing
4 signs of IRREVERSIBLE cell injury:
1. pyknosis, karyorrhexis, karyolysis

2. deg. of P memb.

3. lysosomal rupture

4. mitochondrial permeability/vacuolization
=>=> P-containing, amorphous, densities within mitochondria
specific areas of Brain susceptible to hypoxia/ischemia/infarction:
watershed areas

(places where ACA, PCA, MCA meet)
specific area of Heart susceptible to hypoxia/ischemia/infarction:

subendocardium of LV
2 specific areas of Kidney susceptible to hypoxia/ischemia/infarction:
1. straight segment of proximal tubule (medulla)

2. thick ascending limb (medulla)
1 specific area of Liver susceptible to hypoxia/ischemia/infarction:
zone III (area around central vein)
specific areas of Colon susceptible to hypoxia/ischemia/infarction:

1. splenic flexure

2. rectum
red infarct:

1. aka hemorrhagic infarct

2. ~~loose tissues with multiple blood supplies (liver, lungs, intestines)

3. ~~emboli

4. ~~**reperfusion**
pale infarcts:
1. ~~solid organs with single blood supply

2. e.g. heart, kidney, spleen
the first sign of shock is:
distributive shock = shock due to poor distribution of blood flow; includes these 3 types:
1. septic

2. neurogenic

3. anaphylactic
features of distributive shock:

1. high-output failure
(TPR is low, CO is high, venous return is high)

2. PCWP is low

3. ~vasodilation

4. BP fails to rise with fluids
4 features of hypovolemic/cardiogenic shock:
1. ~~ low-output failure
(TPR is high, CO and venous return are low)

2. PCWP is inc. in cardiogenic, dec. in hypovolemic

3. vasoconstriction

4. BP is increased with fluids
granuloma =
nodular collection of epithelioid mP's and giant cells

("epithelioid mP's" = mP's resembling epithelial cells: finely granular, pale eosinophilic cytoplasm and central, ovoid nucleus)
chromatolysis =
increased protein synthesis in axon following damage
chromatolysis is characterized by:

1. round cellular swelling

2. displacement of the nucleus to the periphery

3. dispersion of Nissl substance throughout cytoplasm
(Nissl substance/body =
large granular body of RER with free ribosomes, found in neurons)
2 types of calcification:
1. dystrophic calcification

2. mets calcification
3 features of dystrophic calcification:
1. deposition is secondary to necrosis

2. localized

3. **pts NORMOcalcemic** (NOT hypercalcemic)
4 features of mets calcification:
1. widespread deposition

2. secondary to hypercalcemia or high calcium-P product (as in CRF)

3. ~~ most to interstitial tissues of kidney, lungs, and gastric mucosa
(these tissues lose acid quickly - inc. pH favors deposition)

4. pts are NOT normocalcemic
leukocyte extravasation occurs predominantly at:
postcapillary venules
4 stages of leukocyte extravasation:

(extravasation = exit from blood vessel toward site of injury/inflammation)
1. margination/rolling

2. tight-binding

3. diapedesis
(squeezing between endothelial cells)

4. migration
(travel to site of inflam.)
5 chemotactic factors of leukocytes that are released in response to bact:
1. C5a

2. IL-8

3. LTB4

4. kallikrein

5. plat-activation factor
inhalation injury =
m.c. pulmonary complication after exposure to fire

- inhalation of combustion products => tracheobronchitis, edema, and pneumonia
2 types of scars:
1. hypertrophic

2. keloid
5 features of keloid scarring:
1. production of scar tissue is WAY out of proportion to wound

2. ~~ type III collagen (vs. type I in hypertrophic)

3. more common in blacks

4. *frequently recur* after resections

5. ~~ ear lobes, face, UE's
3 phases of wound-healing:
1. inlammatory

2. proliferative
(2-3 days after wound)

3. remodeling
(7 days after)
granulation tissue =
new CT + blood vessel

(fibroblasts, myofibroblasts, and caps)
Th1 cells secrete IFN-y, activating mP's; mP's release TNF-a, which induces and MAINTAINS:
granuloma formation

- **anti-TNF-a drugs can cause granulomas to break down**

=> disseminated dz

=> ALWAYS test for latent TB before starting anti-TNF therapy
3 features of exudate:
1. (hyper)cellular

2. protein-rich

3. sg > 1.020
specific gravity =
ratio of a density of a substance to a standard
exudate occurs due to:

1. lymphatic obstruction

2. inflam/inf

3. malignancy
3 features of transudate:
1. hypocellular

2. protein-poor

3. sg < 1.012
transudate occurs due to:

1. inc. hydrostatic P (as in CHF)

2. dec. oncotic P (as in cirrhosis)

3. Na+ retention
m. of inflam

- higher ESR = more inflammation going on
3 causes of dec. ESR:
1. sickled cell
(due to altered shape)

2. polycythemia
(due to inc. RBC's diluting the inflammatory aggregation factors)

3. CHF
pathophys of iron poisoning =
cell death due to peroxidation of membrane lipids
3 acute symps of iron poisoning:
1. n/v

2. gastric bleeding

3. lethargy
2 chronic symps of iron poisoning:
1. inc. AG met. acidosis

2. scarring leading to GI obstruction
treatment for iron poisoning =

1. chelation
(IV deferoxamine, oral deferasirox)

2. dialysis
lipofuscin =
yellow-brown "wear and tear" pigment associated with nl aging

- widespread deposition in elderly
P-glycoprotein =
multidrug R protein 1 (aka MDR1)

- expressed by some CA cells, it pumps out toxins, including chemotherapeutic agents

=> one mechanism of dec. responsiveness or R to chemotherapy over time
3 REVERSIBLE _____plasias:
1. hyperplasia

2. metaplasia

3. dysplasia
metaplasia =

(+ features)
change in cell type

- mc.ly involves surface epithelium

- can progress to dysplasia if stress not removed
dysplasia =
disordered cell growth

~~ proliferation of PRE-cancerous cells
3 IRREVERSIBLE ____plasias:
1. anaplasia

2. neoplasia

3. desmoplasia
anaplasia =
loss of structural differentiation and function of cells, causing them to resemble primitive cells of the same tissue
neoplasia =
uncontrolled, excessive, clonal proliferation of cells

- benign OR malignant
desmoplasia =
fibrous tissue formation in response to neoplasm
difference between tumor grade and tumor stage:
grade ~~ degree of cellular differentiation

1 = low grade, well-differentiated

4 = high grade, poorly-differentiated, anaplastic

stage ~~ spread
stage, which consists of TMN, has more:
prognostic value than grade

- each component of TMN has an independent prognostic value

Tumor size, Node involvement, Mets
"carcinoma" implies:
epithelial origin

- sarcoma implies mesenchymal origin

- both imply malignancy
mesenchymal =
bone, blood vessels, blood cells, SM, striated muscle, fat, CT
most carcinomas spread:
most sarcomas spread:
4 exceptions of carcinoma spreading lymphatically

(i.e. these 4 spread hematogenously):
1. RCC
(often invades renal vein)

2. HCC
(invades hepatic vein)

3. Follicular CA of the thyroid

4. Choriocarcinoma
hemangioma =
benign tumor of blood vessel
leiomyoma =
benign tumor of SM

- vs. rhabdomyoma (striated muscle)
fibroma =
benign tumor of CT
leukemia and lymphoma are both:
malignant tumors of blood CELLS
angiosarcoma =
malignant tumor of blood vessels
cachexia =

wt loss, muscle atrophy, fatigue that occur in chronic dz's

(e.g. CA, AIDS, TB)
cachexia is mediated by:

1. TNF-a

2. IFN-y

3. IL-6
neoplasm associated with acanthosis nigricans:
GI malignancy (esp. stomach)
neoplasm associated with actinic keratosis:
SCC (squamous cell carcinoma) of skin
neoplasms associated with AIDS:

1. aggressive malignant lymphomas (non-Hodge)

2. Kaposi sarcoma
neoplasm associated with AI dz's:
B-cell lymphoma
neoplasm associated with Barret Esophagus:
esophageal adenocarcinoma
gastric adenocarcinoma is associated with these 3 conditions:
1. chronic atrophic gastritis

2. pernicious anemia

3. postsurgical gastric remnants
neoplasm associated with cirrhosis:
neoplasm associated with Cushing Syndrome:
small cell CA of lung
neoplasm associated with dermatomyositis:
lung CA
2 neoplasms associated with Down Syndrome:
1. ALL,
(ALL fall Down)

2. AML
neoplasm associated with dysplastic nevus:
malignant melanoma
neoplasm associated with hypercalcemia:
SCC of lung
neoplasms associated with immunodeficiency states:
malignant lymphomas
neoplasm associated with Lambert-Eaton myasthenic syndrome:
small cell CA
thymoma is associated with 2 conditions:
1. MG

2. pure RBC aplasia
2 neoplasms associated with Paget dz of the bone:
1. secondary osteosarcoma

2. fibrosarcoma
neoplasm associated with Plummer-Vinson Syndrome (dec. iron):
SCC of the esophagus
2 neoplasms associated with polycythemia:
1. RCC

2. HCC
4 neoplasms associated with radx exposure:
1. leukemias

2. sarcomas

3. Papillary CA of the thyroid

4. BC
neoplasm associated with SIADH:
small cell CA
3 neoplasms associated with tuberous sclerosis:
1. Giant cell Astrocytoma

2. renal Angiomyolipoma

3. cardiac rhabdomyoma
neoplasm associated with UC:

3 neoplasms associated with both xeroderma pigmentosum AND albinism:
1. **SCC of skin**

2. melanoma

3. BCC
tumor markers are NOT used as:
primary CA diagnostic tools

- instead, they monitor tumor recurrence and response to therapy

- definitive dx only made by biopsy
11 tumor markers:
1. AP
(alkaline phosphatase)

2. a-FTP

3. Beta-hCG

4. CA-15-3/CA-27-29

5. CA-19-9

6. CA-125

7. calcitonin

8. CEA

9. PSA

10. S-100

11. TRAP
Alkaline Phosphatase is a tumor marker for:

1. mets to bone

2. mets to liver

3. Paget dz of bone

4. seminoma (placental AP)
a-FP is a tumor marker for:

1. HCC

2. hepatoblastoma

3. yolk sac tumor

4. testicular CA

5. mixed germ cell tumor
(co-secreted with B-hCG)
B-hCG is a tumor marker for:

1. Hydatidiform moles

2. choriocarcinomas
(gestational trophoblastic dz)

3. testicular CA
CA-15-3/CA-27-29 is a tumor marker for:

Breast Cancer
CA-19-9 is a tumor marker for:

pancreatic adenoCA
CA-125 is a tumor marker for:

ovarian CA
calcitonin is a tumor marker for:


(Medullary CA of thyroid)
CEA is a tumor marker for:


(CarcinoEmbryonic Antigen)
(very nonspecific but produced by about 70% of)

CRC and pancreatic CA's
PSA is a tumor marker for:

prostate adenoCA

- but also elevated in BPH and prostatitis
S-100 is a tumor marker for:
CA's of neural crest origin

(e.g. melanomas, schwannomas)
TRAP is a tumor marker for:

hairy-cell leukemia

- largely replaced by cytology now
oncogene =
a gene that can transform a regular cell into a tumor cell

~~ GAIN of function

***need to damage only ONE allele to make an oncogene***
oncogene BCR-ABL:

gene product =

associated tumors =
tyrosine kinase;

oncogene bcl-2:

gene product =

associated tumor =
anti-apoptotic mlcl;

follicular lymphoma
oncogene BRAF:

gene product =

associated tumor =
serine/threonine kinase;

oncogene c-kit:

gene product =

associated tumor =
cytokine r' (for stem cell factor);

GIST (GI stromal tumor)
oncogene c-myc:

gene product =

associated tumor =

Burkitt lymphoma
oncogene HER2/neu (c-erbB2):

gene product =

associated tumors =
tyrosine kinase;

Breast, Ovarian, and gastric CA's
oncogene L-myc:

gene product =

associated tumor =

Lung tumor
oncogene N-myc:

gene product =

associated tumor =

(m.c.ly found in the adrenal gland)
oncogene ras:

gene product =

associated tumors =

CRC, lung, and pancreatic CA
oncogene RET:

gene product =

associated tumors =

tumor suppressor gene in cancer ~~
LOSS of function

- no suppression => tumor growth

***BOTH alleles must be lost in order for tumor suppressor gene problem to result in cancer***
tumor suppressor APC: associated tumor =

(inherited knocked out in FAP)
tumor suppressor BRCA1:

gene product =

associated tumors =
DNA repair prot;

BC and Ovarian cancer

(same for BRCA2)
tumor suppressor CPD4/SMAD4:

gene product =

associated tumor =
DPC (Deleted in Pancreatic Cancer);

pancreatic CA
tumor suppressor DCC:

gene product =

associated tumor =
DCC (Deleted in Colon Cancer);

tumor suppressor MEN1: associated tumor =
MEN type 1

(pituitary tumor, pancreatic (endocrine) tumor, PT gland tumor
tumor suppressor NF1:

gene product =

associated tumor =
RAS GTPase activating prot. (neurofibromin);

NeuroFibromatosis type 1
tumor suppressor NF2:

gene product =

associated tumor =
Merlin (schwannomin) protein;

NeuroFibromatosis type 2
tumor suppressor p16:

gene product =

associated tumor =
cyclin-dependent kinase inhibitor 2A;

tumor suppressor p53:

gene product =

associated tumors =
TF for p21, which blocks G1 to S phase;

most human cancers, esp. of Li-Fraumeni syndrome
tumor suppressor PTEN: associated tumors =

BC, prostate CA, endometrial CA
tumor suppressor Rb:

associated tumors =
inhibits E2F; blocks G1 to S phase

RetinoBlastoma, osteosarcoma
tumor suppressor TSC1:

gene product =

associated tumor =
hamartin prot;

Tuberous Sclerosis
tumor suppressor TSC2:

gene product =

associated tumor =
tuberin prot;

Tuberous sclerosis
tumor suppressor VHL:

gene product =

associated dz =
inhibits hypoxia-inducible factor 1a;

VHL dz
tumor suppressor WT1:

gene product =

associated tumor =
Wilms Tumor (nephroblastoma)

(same for WT2)
9 oncogenic microbes:
1. EBV

2. HBV

3. HCV

4. HHV-8 (Kaposi sarcoma-associated herpesvirus)

5. HPV

6. H. pylori

7. HTLV-1

8. Liver fluke (Clonorchis sinensis)

9. Schistosoma haematobium
cancers associated with EBV:

1. Burkitt lymphoma

2. Hodgkin lymphoma

3. nasopharyngeal CA

4. Primary CNS lymphoma (in imm-comp)
cancer associated with HBV, HCV:

cancers associated with HHV-8:

1. Kaposi sarcoma

2. body cavity fluid B-cell lymphoma
cancers associated with HPV:

1. cervical and penile/anal CA (16,18)

2. head and neck/throat cancer
cancers associated with H. pylori:

1. gastric adenoCA

cancers associated with HTLV-1:

1. adult T-cell leukemia

2. adult T-cell lymphoma
cancer associated with liver fluke (Clonorchis sinensis):

cancer associated with Schistosoma haematobium:

bladder cancer (SCC)
12 carcinogens:
1. aflatoxins (from Aspergillus)

2. alkylating agents

3. aromatic amines

4. arsenic

5. asbestos

6. CCL4

7. cigarette smoke

8. ethanol

9. ionizing radx

10. nitrosamines (smoked food)

11. radon

12. vinyl chloride
target organ and resulting cancer due to aflatoxins (from Aspergillus):

target organ and resulting cancer due to alkylating agents:

target organ and resulting cancer due to aromatic amines (eg. benzidine, 2-naphthylamine):

transitional cell CA
3 target organs and 3 resulting cancers due to arsenic:
liver, lung, skin;

angiosarcoma, lung cancer, SCC
target organ and resulting cancer due to asbestos:

bronchogenic CA > mesothelioma
target organ and 2 results due to CCL4:

centrilobular necrosis, fatty change
6 target organs of cig smoke:
1. bladder

2. esophagus

3. kidney

4. larynx

5. lung

6. pancreas
6 resulting cancers from cig smoke:
1. transitional cell carcinoma of bladder

2. SCC *or* adenoCA of esophagus

3. RCC

4. SCC of larynx

5. SCC and small cell CA of lung

6. pancreatic adenoCA
target organ and resulting cancer due to ethanol (alcohol):

target organ and resulting cancer due to ionizing radx:

Papillary Thyroid CA
target organ and resulting cancer due to nitrosamines (smoked foods):

gastric cancer
target organ and resulting cancer due to radon:

lung cancer (2nd leading cause after smoking)
target organ and resulting cancer due to vinyl chloride:

6 hormones/agents associated with paraneoplastic syndrome:
1. 1,25-OH (Vit. D)


3. ADH

4. AB's against presynaptic Ca2+ channels at NMJ

5. EPO

6. PTHrp
effect and 2 associated neoplasms of Vit. D in paraneoplastic syndrome:

Hodgkin lymphoma, some non-Hodgkin lymphomas
effect and associated neoplasms of ACTH in paraneoplastic syndrome:
Cushing Syndrome;

small cell CA
effect and 2 associated neoplasms of ADH in paraneoplastic syndrome:

small cell CA, intracranial neoplasms
effect and associated neoplasms of AB's against presynaptic Ca2+ channels at NMJ in paraneoplastic syndrome:
Lambert-Eaton myasthenic syndrome
(muscle weakness);

small cell CA
effect and 6 associated neoplasms of EPO in paraneoplastic syndrome:

1. RCC

2. thymoma

3. hemangioblastoma
(tumor of CNS, MA adult)

4. HCC

5. leiomyoma

6. Pheo
effect and 3 associated neoplasms of PTHrp in paraneoplastic syndrome:

1. SCC of lung

2. RCC

3. BC
psammoma bodies =
concentric, calcific spherules
PSaMMoma bodies are seen in:

1. Papillary CA of thyroid

2. Serous cystadenoCA of ovary

3. Meningioma

4. Mesothelioma
6 m.c. primary tumors that mets to brain, in order:
lung > breast > GU > osteosarcoma > melanoma > GI
half of all brain tumors are:

- well-circumscribed, at junction of gray/white matter
3 m.c. primary tumors that mets to liver, in order:
colon >> stomach > pancreas
after the regional LN's, ____________ and __________ are the m.c. sites of mets
liver and lung
4 m.c. primary tumors that mets to bone, in order:
prostate and breast > lung > thyroid
bone mets are MUCH m.c. than:
primary bone tumors
mets to bone have predilection for:
AXIAL skeleton
bone cancer that mets to prostate is:

- that mets to breast, = lytic and blastic
3 permanent tissues that have NO stem cells and so CANNOT have hyperplasia:
1. cardiac myocytes

2. skeletal muscle

3. nerves

(=> only hypertrophy)
BPH does NOT increase the risk of:
what's the only kind of metaplasia that doesn't increase risk of cancer?
apocrine metaplasia
deficiency in ________ can result in metaplasia:
Vit A

- nec. to maintain squamous epithelium in surface of the eye

- deficiency => metaplasia => thickening of the corneal layer (keratomalacia)
example of mesenchymal tissue undergoing metaplasia:
myositis ossificans

= presence of bone within skeletal muscle

**NOT osteosarcoma** - bone of myositis ossificans is distinct from nl bone
dysplasia is reversible, but if stress persists, it progresses to:
carcinoma (irreversible)

(the irreversibility is the biggest difference between CA with dysplasia and a carcinoma)