PATHOLOGY-Gen.Principles Flashcards
(159 cards)
Key player in the intrinsic pathway of apoptosis?
What activates this pathway?
Key player= cyt c
Release of cytochrome c from the mitochondria means death (suicide) will occur.
Activated by: Signal comes from within the cell e.g toxin, radiation, hypoxia
Name 2 pro-apoptotic proteins and 1 anti-apoptotic protein in the intrinsic pathway of apoptosis?
PRO: Bax
Bak
ANTI: Bcl2….which inhibits Apaf1 which would normally activate caspases
In the extrinsic pathway, how does the binding of the Fas-Ligand to the Fas receptor lead to apoptosis?
Binding of ligand creades binding site for FADD…a death adaptor protein that then activates caspases…Caspases then activate proteases
Major differences between Necrosis and Apoptosis?
-Name 2
Necrosis is murder and Apoptosis = suicide
After necrosis, Inflammatory ensues but there is no inflammation in this “organized” way of dying
Difference in sequence of events between Coagulative Necrosis and Liquefactive Necrosis
COAG: proteins denature first, then enzymatic degradation occurs
LIQUI: Enzymatc degradation due to release of lysosomal enzymes occurs first.
Three diseases or species associated with Caseous Necrosis?
- TB
- Systemic Fungi
- Nocadia (a Gram.P.Rod)
Two pathways of activating the extrinsic pathway of apoptosis?
- Via the binding of a Fas ligand to a Fas receptor (CD95)
- Via cytotoxix release of
a. Granzymes
b. Perforin
by CD8+ cells
Two organs/disease processes associated with Fatty Necrosis?
What causes the “chalky” appearance in Fatty necrosis?
Pancreatitis (enzymatic saponification)
Breast Trauma (non-enzymatic sapofication) Nb: Saponification = binding with resulting in chalky deposit
What kind of damage is inflicted by “Fibrioid Necrosis”?
Name 2 classic diseases associated with this type of necrosis?
DEF: this is damage to a vessel wall
EXAMPLES:
- Henoch-Schonlein Pupura,
- Churg Strauss Syndrome
**Also see in malignant HTN
What is the major difference between wet gangrenous necrosis and dry?
Which two parts of the body are most susceptible to gangrenous necrosis?
DRY: regular Ischemic coagulative necrosis
WET: Same as above, but with infection superimposed on top.
COMMON SITES:
-GI Tract and limbs (think diabetes)
Which organs undergo coagulative necrosis?
Everything except the brain! Brain = liquefactive necrosis due to high fat content
What is the hallmark of reversible cellular injury? i.e. reversible with re-oxygenation
-Name at least 3 other findings in reversible damage?
HALLMARK= cellular swelling
OTHER FINDINGS:
- low Na+/K+ activity due to low ATP
- Fatty changes
- low glycogen
- Membrane Blebbing
- Ribosomal Detachment and low protein synthesis
What is the hallmark of Irreversible cellular injury?
-Name at least 3 other findings in irreversible damage?
HALLMARK: Membrane damage from degradation of phospholipid and increasing Calcium concentration
OTHER FINDINGS:
- Nuclear: Pyknosis, karyorrhexis, karyolysis
- Lysosomal rupture
- Mitochondrial permeability and vacuolization
the following organs, which areas are more susceptible to hypoxia/ischemia and infarction:
a. Brain
b. Heart
c. Colon
BRAIN:
- ACA/MCA/PCA boundary areas
HEART:
-LV Subendocardium
COLON:
- Splenic Flexure
- Rectum
In the following organs, which areas are more susceptible to hypoxia/ischemia and infarction:
a. Kidney
b. Liver
KIDNEY:
-Straight segment of the proximal tubule
-Thick ascending limb
(both are found in the medulla)
LIVER:
-Zone III…the area around the central vein
In Hypoxic Ischemic Encephalophathy (HIE), which 2 areas are most susceptible?
- Pyramidal cells of the hippocampus
- Purkinje cells of the cerebellum
What is the difference between a RED and a PALE infarct?
PALE:
- usually due to occlusion
- occurs in solid tissues with a single blood supply (heart, kidney, spleen)
RED:
- usually hemorrhagic
- occurs in loose tissue with multiple blood supply (liver, lungs, intestines, etc)
What causes reperfusion injury?
Damage by free radicals…so enzymes that quench free radicals will minimize this damage.
- Superoxide Dismutase
- Glutathione Peroxidase
- Catalase
How does the PCWP IN cardiogenic versus hypovolemic shock?
How is the PCWP (high or low) in a distributive shock e.e. one including septic, neurogenic, or anaphylactic
Increased in Cardiogenic
Decreased in Hypovolemic
Decreased in distributive
How do the vessels differ in cardiogenic (or hypovolemic) as compared to distributive shock?
How do these differences contribute to the differences in the appearance of the patients?
CARDIOGENIC/HYPOVOLEMIA:
–The vessels are constricted and the patient is cool and clammy
DISTRIBUTIVE SHOCK:
—Vessels are vasodilated and therefore, the patient is warm and has dry skin (flushing too)
Name 7 processes that could cause atrophy?
- Reduction of endogenous hormones eg post-menopausal ovaries
- Increase in exogenous hormones e.g. factitious thyrotoxicosis or steroid hormones
- Decreased innervation…e.g. muscle damage
- low blood flow or nutrients
- decreased metabolic demand e.g. inpatient
- increased pressure e.g. nephrolithiasis
- occlusion of secretory ducts e.g cystic fibrosis
Name three enzymes that lower free radicals
- Superoxide Dismutase
- Glutathione Peroxidase
- Catalase
In inflammation, which two agents cause pain and how do they accomplish this?
PGE2 and Bradykinin.
They sensitize nerve endings and that’s how they cause pain
Which 3 cells types are the key players in acute inflammation?
Which 3 cells types are the key players in chronic inflammation?
ACUTE:
- neutrophils
- eosinophils
- antibodies
CHRONIC:
- Macrophages
- T-cells
- Fibroblasts