increase in size of an organ or tissue due to an increase in the size of cells (also can have increased protein synthesis and increase in size or number of organelles).

It's a cellular adaptation to increased workload (ie skeletal mass increase assoc with exercise, enlargement of left ventricle in hyptertensive heart disease)

1) stem cells aka labile cells (ie bone marrow, & crypts of Lieberkuhm & basal cells of epidermis--these can do hyperplasia, not hypertrophy)

2) stable or resting cells (in G0 resting phase, must be stimulated to enter cell cycle ie GFs. examples: hepatocytes, astrocytes, smooth muscle cells--hyperplasia OR hypertrophy in response to cell injury).

3) permanent/non-replicating cell (highly specialized, ie neurons skeletal muscle and cardiac muscle, and of these, the muscle cells can only do hypertrophy)

1) squamous to glandular

2) glandular to other types of glandular (intestinal metaplasia: pylorus and antrum epithelium show an increase in goblet cells and panneth cells in response to H. pylori-induced chronic atrophic gastritis)

3) glandular to squamous (ie resposne to irritants from cigarette smoking; also, endocervical epithelium undergoes squamous metaplasia in response to acid pH in vagina)

4) transitional to squamous (e.g. shistomiasis, infection of urinary bladder can cause epithelium to undergo squamous metaplasia

4)

what is dysplasia?

what are the risk factors?

what do you see microscopically?

why is dysplasia worrisome?

1) disordered cell growth.

2) risk factors: hyperplasia, metaplasia, infection (ie HPV on cervix), chemicals, UV light.

3) microscopic: increased mitotic activity but normal spindles in nucleus, and increased nucleus size in chromatin.  & disorderly proliferation of cells.

4) may progress to cancer

what are two types of death?

what is necrosis?

1) apoptosis ; necrosis

2) necrosis: death of a group of cells accompanied by inflammatory infiltrate (ie PMNs).

Necrosis: death of group of cells accompanied by inflammatory infiltrate.

types: 1) Coagulative (kidney & heart)

          2) Liquefactive (CNS): 

          3) Caseous  (granulamatosis, ie TB):

          4) Enzymatic (fat) necrosis (pancreas or 

              breast tissue de

          5) Fibrinoid (artery wall)

          6) Gangrenous (lower extremity/bowel)

Name the type of infarction:

loose textured tissue prevents RBCs from diffusing through the necrotic tissue.

Liquefactive: necrotic tissue, soft and liquefied. NOT coagulative. Enzymatic liquefaction of necrotic tissue most often in the CNS due to interruption of blood supply (but also in areas of bacterial infection).

Caseous: architecture not preserved but tissue is not liquefied. Gross appearance is soft and "cheese-like". Histologically, can see amorphous cells with increased affinity for acidophilic dyes (shares features of coagulataive AND liquefaction and most often seen in TB granulomas).

Definition: necrotic fat cells, acute inflammation, hemorrhage, and calcium soap formation. Clustering of lipid laden macrophages in the pancreas, for example.

1) alcohol: excess activates lipase and causes hydrolysis of TRGs in fat cells. Fatty acids converted into soaps. Basophilic staining of calcification areas.

2) Non-enzyme mediated: fat cells necroses in breast tissue due to trauma

What type of necrosis is characterized by deposition of proteinaceous material in walls of arteries?

When is it most often seen?

What are the pathological changes that occur in fibrinoid necrosis?

It is associated with which two conditions?

fibrinoid necrosis is limited to small muscular arteries, arterioles, venules, and glomerular capillaries. pathologically: Smudgy pink appearance in vascular walls; actual necrosis may or may not be present.

associated with malignant hypertension and immune vasculitis.

Tuberculosis most commonly causes which type of necrosis?

what is its gross appearance and WHY?

Acute pancreatitis would lead to which kind of necrosis?

what is the gross appearance?

Enzymatic fat necrosis!

gross: chalky yellow-white deposits

What is apoptosis and how does it differ from necrosis?

how is apoptosis part of normal development?

Necrosis: death of GROUPS of cells, often accompanied by inflammatory INFILTRATE (PMNs or macrophages, or both)

apoptosis: PROGRAMMED cell death & enzyme mediated, of one or mroe cells.

development: destruction of mullerian structure cells during embryogenesis in a male fetus due to MIF (aka AMH--anti mullerian hormone) 

what is...

1) BAX gene?

2) BCL2 gene?

3) TP53 suppressor gene?

1) Bax gene: apoptosis gene (cytochrome c related).

2)BCL2 anti-apoptosis gene; its products prevent mitochondrial leakage of cytochrome c into the cytosol.

3) TP53: "guardian" of apoptosis. temporarily arrests in G1 phase to repair DNA damage and thus ABORT apoptosis. Or promotes it if DNA damage too great by activating BAX.

***remember, BAx the BAstard leads to death; BCL2 will save YOU! (the cell); TP53--deaths checks first with me****

Histologically, how can you identify apoptosis depending on ...

1) relation to other nearby cells

2) staining

3) nucleus features/changes

4) inflammatory cells

Apoptosis if...

1) cell detached from neighboring cells (can see a white space around cell)

2) deeply eosinophilic CTYOPLASM (red!)

3) pyknotic (shrinkage), fragmented, or absent nucleus.

4) minimal/no inflammatory cells.

The following enzymes are markers for cell necrosis in WHICH tissue(s)?

1) AST/ALT

2) Creatine kinase MB (CK-MB)

3) Amylase and lipase

1) liver  (ALT is more specific however, example of this is viral hepatitis)

2) heart: acute MI or myocarditis

3) pancreas: lipase more specific for acute pancreatitis & amylase more sensitive in MUMPS

GROSS MORPHOLOGY

A liver is enlarged (hepatomegaly) and yellowish in color, soft, and GREASY to the touch; what is wrong with it?