BSNC 1000 Final Test Questions with Complete Solutions
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Course
BSNC 1000
Institution
BSNC 1000
BSNC 1000 Final Test Questions with Complete Solutions
Local manifestations of inflammation - Answer-following tissue injury, inflammatory mediators (histamine) are released by injured tissue cells and mast cells
Vascular phase of inflammation - Answer-in response to inflammatory mediators:
...
BSNC 1000 Final Test Questions with
Complete Solutions
Local manifestations of inflammation - Answer-following tissue injury, inflammatory
mediators (histamine) are released by injured tissue cells and mast cells
Vascular phase of inflammation - Answer-in response to inflammatory mediators:
1. vasodialation of small blood vessels around the injury site to increase blood flow
2. increased permeability dt retraction of endothelial cells
exudate exit the blood vessels and enter the injured site
Exudate - Answer-fluid containing leukocytes, proteins, inflam. mediators, and plasma
that leaks from the blood vessels out of the injury site dt increase permeability. Exudate
moving to extracellular space is the cause of edema
Cellular stage - Answer-White blood cells enter the injured tissue via recruitment and
chemotaxis and promote resolution to inflammation via phagocytosis
First step of cellular stage - Answer-recruitment or attraction
1. a. adhesion - leukocytes lie closer to the endothelial wall bc of disturbance of blood
flow
b. markers cause leukocytes to bind to the endothelium (rolling, as the connection is
weak so they fall off and reconnect)
c. firm adhesion
2. transmigration - movement of leukocytes from the endothelium to the interstitial
space
3. chemotaxis - the movement of leukocytes towards the injury site the increasing
chemoattractant gradient
Second step of cellular stage - Answer-phagocytosis
leukocytes bind to necrotic tissue or foreign bodies
engulfment
killing and degrade the engulfed substance
systemic manifestations of inflammation - Answer-fever, red blood cell stacking, muscle
catabolism, production of acute-phase proteins, increased production of leukocytes
Artherosclerosis - Answer-formation of plaque in large and medium sized arteries
two causes of artherosclerosis - Answer-endothelial injury - chronic inflammation
lipid infiltration - retention of LDLs
, causes of endothelial injury - Answer-hypertension, free radicals, high glucose,
hyperlipidemia
cause of artherosclerosis - Answer-injury to endothelium triggers an inflammatory
response, thus making the membrane permeable and vasodialates
- allows circulating LDLs in
-LDLs are oxidized which triggers macrophage phagocytosis
-foam cells secrete inflam. mediators
-mediators recruit more immune cells to the injured site
- growth factors increase division and migration of smooth muscle cells
-smooth muscle cells produce collagen which build up the fibrious cap
- Macrophages, foam cells, necrotic tissue with released cholesterol form the lipid-rich
necrotic core.
clinical manifestations of artherosclerosis - Answer-earliest is fatty streak
fatty streaks can progress to lesions called plaques
protrude into arteries
take 20-40 yrs to develop
three types of plaque - Answer-stable - plaque is build on arteries, can cause blockages
(MI)
plaque erosion - almost ruptured, but not yet
arterial wall dialation - can cause anneurism
what is stress - Answer-lifes demands, perceived events, and stimulus, with reactions to
stress being orchestrated bodily responses to keep the body at homeostasis
physiological stressors - Answer-stress associated with cell damage and illness. Ex:
htn, tissue trauma, COPD, osteoporosis, vascular dementia
what body systems does mobility involve - Answer-skeletal, muscular, nervous
under what conditions could someone have impaired mobility - Answer-bone/joint
diseases (osteoporosis/arthritis)
surgery
broken bones
disabilities
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