BSNC ACTUAL REVIEW QUESTIONS AND
ANSWERS SURE A+
✔✔Second step of cellular stage - ✔✔phagocytosis
leukocytes bind to necrotic tissue or foreign bodies
engulfment
killing and degrade the engulfed substance
✔✔systemic manifestations of inflammation - ✔✔fever, red blood cell stacking, muscle
catabolism, production of acute-phase proteins, increased production of leukocytes
✔✔Artherosclerosis - ✔✔formation of plaque in large and medium sized arteries
✔✔two causes of artherosclerosis - ✔✔endothelial injury - chronic inflammation
lipid infiltration - retention of LDLs
✔✔causes of endothelial injury - ✔✔hypertension, free radicals, high glucose,
hyperlipidemia
✔✔cause of artherosclerosis - ✔✔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.
✔✔risk factors for atherosclerosis (non modifiable) - ✔✔Obesity
hypertension
smoking
, drinking
inactivity
diabetes
stress
dyslipidemia
✔✔clinical manifestations of artherosclerosis - ✔✔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 - ✔✔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 - ✔✔lifes demands, perceived events, and stimulus, with reactions to
stress being orchestrated bodily responses to keep the body at homeostasis
✔✔physiological stressors - ✔✔stress associated with cell damage and illness. Ex: htn,
tissue trauma, COPD, osteoporosis, vascular dementia
✔✔psychological stressors - ✔✔stress from work, environment, financial, family
struggle
✔✔scope of stress - ✔✔no stress ---> manageable stress---> unmanageable stress
✔✔General Adaptation Syndrome - ✔✔the body responds to stress with alarm,
resistance and exhaustion
✔✔Phase one of GAS - ✔✔Alarm reaction: sympathetic nervous system activation,
reversal of shock and increase in resistance
✔✔shock - ✔✔initial decrease in resistance to stress (influx of stress and worry)
✔✔what resources are mobilized during the alarm stage - ✔✔increased r\cardiovascular
and respiratory fx (increase HR/BP, increase breathing rate)
Sharpening of senses
release of glucose and fatty acids from storage sites (liver and adipose tissue)
Suppression of digestion, growth and reproduction
✔✔Neuroendocrine response in alarm stage - ✔✔immediate response is aided by
catecholamines (epi/norepinepherine released by SNS and adrenal medulla)
slow and long lived response is controlled by cortisol
ANSWERS SURE A+
✔✔Second step of cellular stage - ✔✔phagocytosis
leukocytes bind to necrotic tissue or foreign bodies
engulfment
killing and degrade the engulfed substance
✔✔systemic manifestations of inflammation - ✔✔fever, red blood cell stacking, muscle
catabolism, production of acute-phase proteins, increased production of leukocytes
✔✔Artherosclerosis - ✔✔formation of plaque in large and medium sized arteries
✔✔two causes of artherosclerosis - ✔✔endothelial injury - chronic inflammation
lipid infiltration - retention of LDLs
✔✔causes of endothelial injury - ✔✔hypertension, free radicals, high glucose,
hyperlipidemia
✔✔cause of artherosclerosis - ✔✔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.
✔✔risk factors for atherosclerosis (non modifiable) - ✔✔Obesity
hypertension
smoking
, drinking
inactivity
diabetes
stress
dyslipidemia
✔✔clinical manifestations of artherosclerosis - ✔✔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 - ✔✔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 - ✔✔lifes demands, perceived events, and stimulus, with reactions to
stress being orchestrated bodily responses to keep the body at homeostasis
✔✔physiological stressors - ✔✔stress associated with cell damage and illness. Ex: htn,
tissue trauma, COPD, osteoporosis, vascular dementia
✔✔psychological stressors - ✔✔stress from work, environment, financial, family
struggle
✔✔scope of stress - ✔✔no stress ---> manageable stress---> unmanageable stress
✔✔General Adaptation Syndrome - ✔✔the body responds to stress with alarm,
resistance and exhaustion
✔✔Phase one of GAS - ✔✔Alarm reaction: sympathetic nervous system activation,
reversal of shock and increase in resistance
✔✔shock - ✔✔initial decrease in resistance to stress (influx of stress and worry)
✔✔what resources are mobilized during the alarm stage - ✔✔increased r\cardiovascular
and respiratory fx (increase HR/BP, increase breathing rate)
Sharpening of senses
release of glucose and fatty acids from storage sites (liver and adipose tissue)
Suppression of digestion, growth and reproduction
✔✔Neuroendocrine response in alarm stage - ✔✔immediate response is aided by
catecholamines (epi/norepinepherine released by SNS and adrenal medulla)
slow and long lived response is controlled by cortisol
