Atchley Objectives Flashcards
Differentiate necrosis from apoptosis in terms of how controlled and mess each is
- necrosis: irreversible, often uncontrolled death of many cells. May produce exudate-mess, high protein fluid filled with neutrophils. May be aseptic due to blood loss
- apoptosis: programmed cell death, well organized self-destruction of cells. Apoptosis is critical in fine tuning the developing retina
Identify the 4 types of necrosis discussed in class
Coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis
Recognize the gross morphological features and general cause for each of the types of necrosis
a. Coagulative necrosis: the structural boundary of a coagulated cell, tissue or vessel is maintained by internal proteins are denatured. Due to ischemia or infarction: heart attack
b. Liquefactive necrosis: structural transformation of the tissue into a liquid viscous mass. Leave spurs and fluid remains, forms abscess. Associated with bacterial or fungal infections. EXCEPTION: in the brain, liquefactive necrosis is aseptic and due to ischemia.
c. Caseous necrosis: Cheesy proteinaceous dead cell mass. Most often observed in TB infections
d. Fat necrosis: death of adipose tissue, small white lesions formed. Usually in subcutaneous tissue because of trauma
Identify the type of necrosis that occurs in the brain due to ischemia vs other organs in the body.
In most places in the body, ischemia leads to coagulative necrosis, but in the brain it leads to aseptic liquefactive necrosis.
Identify the enzyme that initiates the arachidonic acid pathway and predict the impact of steroids on the COX and LOX pathways
a. Pal-2
b. Steroids hit PAL-2 and stops the whole cascade
Name the two arms of the COX pathway and explain why aspirin blocks one arm, but not the other.
a. COX goes into PGI2 and Thromboxane A2
b. Aspirin blocks thromboxane A2. It actually works on cyclooxygenase, but causes platelets to not regenerate TXA2. This is a way for it to work on the platelets without shutting down PGI2
How does the action of aspirin differ from that of other NSAIDS?
a. Aspirin is irreversible. It acetylates the platelets and neutralizes them. Other NSAIDs are reversible
List the cardinal signs of inflammation
Rubor, tumor, dolor, calor, functio laesa
Determine which of the signs are driven by histamine and which is activated by another facto
a. Histamine drives rubber, tumor, calor.
b. Dolor is from PGE2 and bradykinin
Recall which cell types play the leading role in a true inflammation vs chronic inflammation
a. Acute: neutrophils
b. Chronic: macrophages and lymphocytes, eosinophils, basophils/mast cell
Explain how circulating neutrophils can double in numbers without activating bone marrow.
- 50% aim circulating pool and 50% in marinating pool.
- When taking CBC, you are only getting a reading of the circulating pool, if trauma happens, the marginating neutrophils become detached and now you get a higher reading
Describe the cellular composition of a granuloma
Epithelioid macrophages (sometimes forming multinucleated giant cells) surrounded by lymphocytes, central necrosis commonly occurs in TB
Decipher the acronym ‘ACID’ as it pertains to the four types of hypersensitivities
a. Anaphylactic/atopic-type I
b. Cytotoxic-type II
c. Immune Complex-type III
d. Delayed (cell mediated)-type IV
Anaphylactic (type I)
i. Allergen activates B cells, IgM class switches to IgE, preformed IgE docks on mast cells (basophils). Subsequent allergen exposure crosslinks IgEs and causes degranulation.
ii. Late phase: infiltration of tissues with eso and segs (major basic protein). Splits arachidonic acid from cell membrane. Releases leukotrienes and prostaglandins
Cytotoxic type II
i. Ab bind to cell membrane causing cellular destruction, inflammation, or cellular dysfunction
ii. Opsonization leads to complement, NK cell killing, and inflammation
iii. Ab bind and cause abnormal blockade or activation
Immune complex type III
Circulating Ag-Ab (IgG/IgM) complexes lodge in vessels and on tissues and activate complement, producing tissue damage
Delayed type IV
i. Antigens bind to sensitized CD4 cells
ii. CD 4 cells release cytokines that activate macrophages and CD8 cells and cause tissue damage
iii. AB not involved