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Pathoma High Yield: Questions And Correct Answers
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Pathoma High Yield: Questions And Correct AnswersKey mediators of acute inflammation that attract neutrophils Right Ans -
LTB4, C5a, IL-8, Bacterial Products
3 ways in which Mast Cells can be activated Right Ans - Tissue Trauma, C3a
& C5a, Cross-linkage of cell surface IgE by antigen
Two major mediators of pain Right Ans - PGE2 & Bradykinin
HY mediator of acute inflammation that is most commonly tested on in
relation to Gram (-) sepsis DIC Right Ans - Hageman Factor (Factor XII)
Mechanism of fever in acute inflammation Right Ans - Macrophages release
IL-1 & TNF --> activate cyclooxygenase activity in pericytes of hypothalamus
--> increased PGE2 --> increased set point
On initial injury, mast cells are involved in acute inflammatory response by
releasing histamine granules...6 hours later, what would be the mechanism for
the delayed mast cell response? Right Ans - Release of Arachadonic Acid
Metabolites, specifically Leukotrienes
In acute inflammation, where does vasodilation occur & where does increased
vascular permeability occur? Right Ans - Vasodilation: arterioles
Increased Vascular Permeability: post-capillary venules
Name the key components of Complement & their actions Right Ans - C3a
& C5a: activate Mast Cells
C5a: attracts Neutrophils
C3b: opsonin for phagocytosis
MAC: lyses microbes by making holes in their membranes
Name a notable exception to the concept that "pathologic hyperplasia can lead
to dysplasia & eventually cancer" Right Ans - BPH does not increase your
risk for prostate cancer
In atrophy, the decrease in cell # is due to apoptosis, what accounts for the
decrease in cell size? Right Ans - Ubiquitin-Proteosome Degradation:
,cytoskeleton filaments are tagged with Ubiquitin & then degraded by
proteosomes...
Very HY example of metaplasia Right Ans - Barrett's esophagus: change
from Non-Keratinizing Squamous epithelium --> Non-ciliated, mucin-
producing columnar epithelium
Hallmark of Reversible Cell Injury Right Ans - *Cellular Swelling*, loss of
microvilli, blebbing, decreased protein synthesis (from ribosomes popping off
of the swelling RER)
Hallmark for Irreversible Cell Injury Right Ans - *Membrane Damage*
(plasma, mitochondrial, lysosomal)
Hallmark of Cell Death Right Ans - Loss of Nucleus
Necrosis characterized by ischemia to tissue, wedge-shaped/pale area, no
nuclei & preservation of cellular structure Right Ans - Coagulative Necrosis
**infarct could be red if hemorrhagic & blood re-enters, such as in the
testicle**
Necrosis characterized by enzymatic lysis of cells
Brain: via microglia
Abscess: via neutrophils
Pancreatitis: via pancreatic enzymes Right Ans - Liquefactive Necrosis
Necrosis characterized as "coagulative necrosis resembling mummified
tissue..." If dead tissue is infected it can liquefy.... Right Ans - Gangrenous
Necrosis
(if infected-->liquefy-->Wet Gangrene)
**Lower Limb Ischemia**
Necrosis characterized by soft, friable tissue with cottage-cheese like
appearance. Combination of coagulative & Liquefactive....Granulomatous
inflammation from TB or Fungi Right Ans - Caseous Necrosis
,Necrosis characterized by chalky-white appearance due to deposition of
Calcium...characteristic of trauma or pancreatic issues Right Ans - Fat
necrosis
See psammoma bodies, dystrophic calcification on dead fat tissue (psammoma
bodies)
Difference between Dystrophic Calcification & Metastatic Calcification
Right Ans - Dystrophic: Serum Ca++/Phosphate Normal
Metastatic: Serum Ca++/Phosphate HIGH
Necrosis characterized by damage to blood vessel wall, BRIGHT PINK on
histo... Right Ans - Fibrinoid Necrosis
Most common causes of Fibrinoid Necrosis Right Ans - Malignant HTN,
Vasculitis, FIBRINOID NECROSIS OF THE PLACENTA (30 y/o pregnant woman
presents with pre-eclampsia)
Breast mass, Giant Cells, Calcifications... Right Ans - Fat Necrosis, beware of
being tricked into picking breast cancer....make sure to see serum levels....also
look for trauma.
Pt has M.I., taken to cath lab, artery is opened & blood supply is re-established
however serum troponins/cardiac markers are still increasing, why? Right
Ans - Reperfusion Injury: oxygen & inflammatory cells that are circulating in
the blood return to the damaged tissue --> inflammatory cells react with the
dead tissue --> generation of free radicals & more injury!!!
Mechanisms for elimination of free radicals Right Ans - Antioxidants:
glutathione, Vit A, C, E
Enzymes: Superoxide Dismutase, Glutathione Peroxidase, Catalase
Metal Carriers: transferrin, ceruloplasmin
Primary Systemic Amyloidosis Right Ans - AL Amyloid Light Chain
deposition, associated with plasma cell dyscrasias
**Multiple Myeloma* *Kidney Most Common Site*
Secondary Systemic Amyloidosis Right Ans - AA Amyloid deposition from
SAA (acute phase reactant)
Seen in chronic inflammatory states, malignancy
, Senile Cardiac Amyloidosis Right Ans - NON-MUTATED Serum
Transthyretin Deposits
Asymptomatic
Familial Cardiomyopathy Right Ans - MUTATED Serum Transthyretin
deposits
Restrictive Cardiomyopathy
Type 2 Diabetes Amyloid Deposition Right Ans - Amylin deposits in Islets
of pancreas
Alzheimer's associated Amyloid Deposition Right Ans - A Beta Amyloid
Plaques in Brain....
Chromosome 21...associated with Down's!!
Dialysis-Associated Amyloidosis Right Ans - Beta-2 Microglobulin buildup
in joints (not filtered by dialysis!!)
MHCI
Medullary Carcinoma of the Thyroid Amyloid Deposition Right Ans -
Calcitonin deposits...
"Tumor cells in an amyloid background"
Half of Neutrophils are floating around in the blood, where is the second half?
Right Ans - Marginated Pool of Neutrophils --> hang out in the blood vessels of
the lungs like bats in a cave, waiting to be called on.....able to hang bc of their
integrins
Where does Neutrophil arrival & function occur? Right Ans - POST
CAPILLARY VENULE, Very Important
"Rolling" is the 2nd step of Neutrophil arrival & function, what cells modify
this step? Right Ans - E-Selectins: Induced by TNF & IL-1
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