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Path Exam 2

Terms

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Hyperplasia
- direct response to stimulus
- involves parenchymal and stroma
- diffuse
- organized
- typical morphology
- regresses if stimulus is removed




Neoplasia
- independent of extracellular stimulus
- involves parenchymal component only
- focal
- disorganized
- cellular atypia
- continues to grow




Mechanism of type I hypersensitivity reactions
allergen presentation by dendritic cells to CD4+ T cells --> differentiation to TH2 cells --> secretion of IL-4, IL-5, and IL-13

IL-4: activation of IgE-secreting B lymphocytes
IL-5: activation of eosinophils
IL-13: promotes IgE secretion and mucus secretion

*IgE binds to mast cells (and basophils) on first exposure* ---> mast cell degranulation





Antibody mediated (type II) hypersensitivity
- opsonization & phagocytosis: c3b

- opsonization and cell lysis w/o phagocytosis: IgG recognized by Fc receptors

- complement and Fc receptor mediated inflammation: IgM & IgG antibodies bound to ECM proteins, generate C5a

- antibody mediated cellular dysfunction





Cell-mediated (type IV) hypersensitivity
Delayed type hypersensitivity
- CD4+ T cells --> TH1 cells --> produce INF-gamma --> macro activated

ie. Tb

T cell-mediated cytotoxicity
- CD8+ T cells kill by perforin-granzyme dependent killing and Fas-FasL depedent killing

**important in killing viral-infected cells







epitope spreading
initial autoimmune response may damage self-antigens and expose new epitopes of the antigens that are normally concealed from the immune system..

this can lead to activation of new auto-reactive lympohtocytes and "spreading" of the disease

Amyloid
insoluble deposits (proteins) that may cause pressure atrophy or degeneration of surrounding cells, which can lead to organ dysfunction

- commonly found in kidney, spleen, liver



AL
amyloid light chain

- composed of immunoglobin light chains synthesized by plasma cells

AA
amyloid associated

- derived from serum amyloid associated (SAA) protein, an acute phase protein synthesized by hepatocytes

AB
beta amyloid protein

core of cerebral plaques and in cerebelar blood vessel walls in Alzheimer's disease

- transthyretin (less common amyloid protein) --> binds and transports thyroxine and retinol: deposited in heart of old people



Edema
- dropsy
- anasarca

excessive accumulation of fluid in the CT spaces and serous sacs.. ie. the interstitial compartment

- dropsy: lay term for generalized edema
- anasarca: edema of subcutaneous tissue


characteristics of edema
- transudate
- clear, straw colored (low prtoein, low coagulation)
- hydropericardium
- hydrothroax
- ascites (hydroperitoneum



characteristics of inflammation
exudate (high protein)
turbid, purulent, etc.
pericarditis
pleurisy, pleuritis,
peritonitis



Effusion
non-specific term which refers to an accumulation of fluid, which can be transudate, lymph, exudates or blood...

removal of fluid is know as PARACENTESIS (tapping, draining of fluid)

common causes of lymphatic obstruction
*causes lymphedema -- "brawny edema" or elephantiasis (in the case of filariasis)

- malignant neoplasms
- chronic granulomatous disease (Tb & bunholderia mallei)
- parasitic disease (filariasis)
- iatrogenic (post surgical or post irradiation)
- compression from the outside





Urticaria
cutaneous --> nodular swellings, or "hives"

causes an increase permeability of the vessel wall following the degranulation of mast cells

Causes of generalized edema
- cardiac
- hypoproteinemia
- increased retention of sodium
- renal edema (nephritic/nephrotic)


Hyperemia aka congestion!!
active: increase inflow of blood pumped actively into the tissue from the Arterial side
- acute - scalding water
- delayed - sunglight

passive: local acute (starving); local chronic ( pitting edema) & left-sided heart failure; generalized chronic (pulmonary stenosis) & right-sided heart failure



Hemorrhage
blood that is lost from the intravascular compartment due to:
- rupture or erosion of the vessel wall - rhexis
- diapedisis - due to increased permeability of the vessel or defects of the coagulation mechanism

Shock
inadequate blood flow to vital organs or the inability of these organs to use oxygen and other nutrients

- decreased CO
- widespread vasodilation
- loss of fluid

*primary shock is only seen in humans because of our upright posture





Thrombosis
formation of a solid mass from the constiutents of the blood within the vascular tree, during life!

(coagulation or clotting can occur outside the vascular system, in vitro, and post-mortem

Tissue factor pathway
inhibits factor III, VII, and IX
thrombomodulin
protein C combines with protein S and they inactivate factor V and VIII
Plasminogen activator
activates plasminogen to plasmin

(stimulated by NE, thrombin, bradykinin, vasporessin, stasis, and shear stress)

- plasmin lysis fibrin (is fibrolytic)



Nitric oxide
inhibits platelet aggregation and adhesion
Prostacyclin
- vasodilation
- inhibits protein aggregation
Von Willebrand factor + GpIb IX
is the carrier protein for VIII (vwf)

- promotes platelet ADHESION

Intrinsic pathway
activated *intra*vasculary

Endothelial damage --> Factor XII --> Factor XI --> IX --> X --> common pathway

Extrinsic pathway
activated in tissues!

Tissue damage --> Tissue factor III (thromboplastin) --> VII --> X --> common pathway

pathological inhibition of coagulation
systemic lupus erythematosus

rheumatoid arthritis

ulcerative colitis



conditions predisposing to thrombus formation
*Virchow triad*

- alteration in the vascular lining
- stasis (alteration is flow)
- alteration in the constituents of blood with excessive amounts of procoagulatent constituents or decrease of anticoagulant factors



infaction
a localized area of an organ or tissue which has been depreived of its vascular supply

mechanisms of occlusion:
- factor within the lumen (thrombus or embolus)
- factor from the vascular wall (artherosclerosis)
- compression from the outside by contiguous structures






Red infarct
blood filled infarct

* seen in organs with DOUBLE blood supply* after arterial occlusion (LUNg or LIVER) or where venous occlusion was the cause

Anemic infarct
Or pale

seen in **arterial occlusion in organs with a single blood supply having orgainzed stromal tissue

Embolus
any collection of solid, liquid, or gas traveling in the vascular system

venous embolisum (thromboembolism is most common cause of pulmonary embolism, which is responsible for 20% of ALL hospital deaths)
arterial side of venous embolism
- brain, kiddneys, spleen and lower legs are most common occlusion
- mural thrombus, arterial appendage are most common origin

pulmonary emboli** sudden death! (saddle emoblism)






Aspirin
blockage of the synthesis of thromboxane A2
Ticlopidine
inhibits plately aggregation by ADP, collagen, arachidonic acid, thrombin and platelet aggregating factor

(superior to aspirin)

Hirudin
direct inhibitor of thrombin

- "leech"

*anticoagulant*



Teratoma
cells represenative of more than one germ layer
Hamartoma
aberrant differentiation of mature specialized cells or tissue indigenous to the particular site
Choristoma
heterotropic rest of cells in an unrelated organ
4 characteristics of malignant tumors
- malignant change in the target cell
- growth of the transformed cells
- local invasion
- distant metastases


Anaplasia
lack of differentiation

*benign tumors are generally well-differentiated

dysplasia
disordered growth
found in epithelia, espcially metaplastic

- loss in uniformity, architectural orientation, and pleomorphism, hyperchromatic/large nuclei, mitotic figures in abnormal locations and more abundant than usual


RAS
chemically induced tumors
P53
viral-associated cancers
Mechanism and clinical syndrome of *small cell lung cancer*
- ACTH: Cushing syndrome

- ADH: SIADH

Mechanism and clinical syndrome of *non-small cell lung cancer*
- PTHRP: hypercalcemia
Mechanism and clinical syndrome of *cerebellar hemangioma renal cell carcinoma
- erythropoietin: erythrocytosis
Mechanism and clinical syndrome of *lung cancer*
- AC receptor ABs: myasthenia

- unknown: hypertrophic osteoarthropathy (clubbing)

TNM staging does not apply to..
- acute or chronic leukemia
- multiple myeloma
- lymphoma

HPV E6
- inhibits P53
HPV E7
- inhibits p53, p21, and pRB
How do HBV and HCV cause HCC?
Both viruses induce injury to liver cells (inflammation, cell death) and extensive regeneration

Deck Info

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