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GNUR 293 Pathophysiology FINAL EXAM.
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- Anatomy Condensed Final Exam Review - GNUR 155
GNUR 293 Pathophysiology FINAL EXAM.
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GNUR 293 Pathophysiology FINAL EXAMLiquefactive necrosis - ANS-From bacterial infection, ischemia
Affects brain tissue
Coagulative necrosis - ANS-From hypoxia
Causes proteins to degranulate and become gelatinous
Affects kidneys, heart, adrenal system
Caseous necrosis - ANS-From TB
Combination of coagulative + liquefactive
Affects lungs
Walled off by granuloma
Fat necrosis - ANS-From enzymes that dissolves cells
Affects breasts, pancreas, any organs with fat
Gangrenous necrosis - ANS-From severe ischemia/hypoxia
Dry = coagulative necrosis
Wet = liquefactive necrosis (causes internal organs to be black, cool, swollen, and foul
smelling)
Gas = clostridium infection
Reperfusion injury - ANS-Sudden restoration of blood supply creates ROS
Lines of defense - ANS-Barriers, inflammation, adaptive immunity
Phagocytes originate in - ANS-bone marrow
Monocytes originate in - ANS-bone marrow
When do neutrophils arrive on site? - ANS-6-12hrs
When do macrophages arrive on site? - ANS-3-7 days
May proliferate on site
Live for a long time
Mast cells - ANS-initiate inflammation
,Mast cells release - ANS-histamine
NK cells - ANS-Adaptive immunity
Can recognize and eliminate cells infected by viruses
Acute inflammatory response - ANS-Mast cells release histamine
Vasodilation causes redness and heat
Vascular permeability
Stimulation of nerve endings = pain
Cytokines - ANS-Call in the troops!
TNF - induces fever and muscle weakness
Chemokines - ANS-Induce WBC chemotaxis
Produced by macrophages and endothelial cells
Tell the cells where to go
Leukotrienes - ANS-Similar to histamines
Produce a longer-acting response
Prostaglandins - ANS-Released by mast cells
FEVER AND PAIN
Complement system - ANS-Destroys pathogens
Osponization
Increases phagocytosis
Osponization - ANS-Paints bad cells so phagocytes know to eat it
Coagulation system - ANS-Forms fibrous mesh
Thrombin, fibrinogen, fibrin
Begins with vessel injury
Kinin system - ANS-Activates and assists inflammatory cells
Bradykinin
Bradykinin - ANS-Causes blood vessel dilation and pain
Events in inflammation - ANS-Vascular permeability
Emigration of leukocytes
, Phagocytosis
Diapedesis - ANS-Neutrophils and monocytes migrate through wall to site
Left shift - ANS-Acute inflammation
Right shift - ANS-Chronic inflammation
At risk for anemia (pernicious anemia)
Lower the ANC number means - ANS-higher risk of infection
Chronic inflammation - ANS-Lymphocyte activation
Formation of scar tissue
May develop without prior acute inflammation
Hydrostatic - ANS-Push
Osmotic/oncotic - ANS-Pull
Capillary hydrostatic pressure - ANS-Water pushed out of capillaries
Interstitial hydrostatic pressure - ANS-Water pushed out of interstitial space
Capillary osmotic pressure - ANS-Water pulled into capillaries
Interstitial osmotic pressure - ANS-Water pulled into interstitial spaces
Forces favoring filtration - ANS-Capillary hydrostatic pressure
Interstitial osmotic pressure
Forces against filtration - ANS-Capillary osmotic pressure
Interstitial hydrostatic pressure
Hypoalbuminemia - ANS-Decreased osmolality
Water leaves blood/capillary and goes into interstitial space = edema
Hyperalbuminemia - ANS-Increased osmolality
Caused by dehydration + accompanying symptoms
Isotonic solution - ANS-0.9% saline
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