Name: Pathophysiology Unit III Exam Review Define: homeostasis

advertisement
Name: ____________________________________________
Pathophysiology Unit III Exam Review
1.
Define:
homeostasis
pathophysiology
pathogenesis
acute disease
chronic disease
exogenous
endogenous
neoplasm
metabolic disease
congenital disease
trauma
manifestation
auscultation
palpation
percussion
olfaction
etiology
idiopathic
iatrogenic
communicable disease
epidemic
endemic
Localized disease
systemic disease
asymptomatic
self-limiting disease
naturally acquired immunity
passive immunity
phagocytosis
pathogens
acute inflammation
carbuncles & furuncle
abscess
empyema
decubitus ulcer
cellulitis
abscess
gangrene
inflammation
serous transudate, serous exudate, purulent exudate
dialysis
diabetic coma
insulin shock
hemodialysis
peritoneal dialysis
2.
3.
4.
What happens when homeostasis is not maintained?
disease will ensue
What is the difference between anatomical pathology and clinical pathology?
Anatomic: pathologist performs autopsies to determine cause of death
Clinical: pathologist who reviews lab specimens to determine evidence of an abnormal tissue or the presence of chemicals
What are the sequence in which an even leads from the cause of a disease to structural and functional abnormalities? (1-4
sequence)
I. Cause (exposure and inoculation of the cold virus)
II. Incubation time (virus multiplies)
III. Manifestation (host begins to have signs & symptoms)
IV. Recovery (body returns to previous state of health)
Structural disease is: physical and biochemical changes within the cells (exogenous / endogenous), hallmark characteristic is
a lesion
Functional Disease is: onset without presence of lesion, basic change is physiological, examples: tension headache, mental
illness
5.
What are predisposing factors for a disease? (List and explain the 8 we discussed.)
Age, sex, genetic makeup, stress, lifestyle, occupation, preexisting illness, environmental exposure
6.
The difference between sign and symptom.
Sign: physical observation noted by the person examining patient
Symptoms: patient’s awareness of abnormalities or discomfort, not measurable and are subjective
7.
Understand the types of artificially acquired immunity
Vaccines:
Live organism – nonvirulent for humans or treated in lab to weaken to make nonpathogenic
Attenuated – organism that is weakened
Killed – vaccine with toxoid occurs when the toxin produced by an organism is altered with heat or
chemicals to render it harmless, but still allows body to make antibodies against it.
8.
Purpose of inflammation? Goal of inflammation? Limiting factor? (Can inflammation occur at a site of gangrene?)
Purpose- to contain or destroy offending agent
Goal- to set stage for wound healing and repair by removing cellular debris from area
Limiting factor- cannot occur if there is not a blood supply (ex: infected with gangrene)
9.
The three major events in the inflammatory process.
I. Congestion phase
II. Leakage phase
III. Phagocytosis process
10. Differentiate between the two types of tissue repair: regeneration & fibrous connective.
Regeneration: replacement of dead tissue with new tissue, looks brand new
Fibrous connective tissue: tissue that has undergone necrosis is replaced with dense, tough mass of connective tissue (scar)
11. What is the point of an artificial kidney? Explain the three ways molecules move: diffusion, osmosis, & filtration.
Device used to separate large particles, such as blood cells, from small ones, such as urea/waste when the kidney cannot
diffusion: movement of molecules from higher to low concentration
osmosis: allows water to move through selectively permeable membrane from high to low concentration
filtration: removes particles by allowing liquid to pass through membrane, controlled by gravity or hydrostatic pressure
12. What are the parameters that affect kidney function?
Blood pressure, blood volume, hormones, caffeine, trauma, nutritional status, disease
13. Difference between Type I diabetes & Type II diabetes. Symptoms of diabetes.
Type I: insulin dependent, rapid onset, juvenile, hereditary predisposition, viral destruction of beta cells, body lacks ability
to produce insulin, uses insulin injections.
Type II: non-insulin dependent, slow onset, adult/maturity, obesity causes beta cells to overreact and they become less
responsive  decreasing insulin secretion, treat with diet or oral replacements
Symptoms: polydipsia, polyuria, glycosuria,
Download