medic patho Flashcards
Patho
suffering
Physio
Nature, origin
-ology
study of
communication within the body
Cellular lvl
chemical lvl
Negative feedback
“off” switch, inhibits the original stimulus. usually good
Positive feedback
intensifies signal, enhances the original stimuli. can be bad
adaption
cells exposed to adverse conditions will protect themselves from injury
atrophy
decrease in cell size
hypertrophy
increase in cell size
hyperplasia
increase in number of specific cells (cell division)
dysplasia
change in size, shape, organization
metaplasia
change type of cell
hypoxemia
most common cause of cell injury
most common cause of hypoxemia
low 02 in air
loss of hemoglobin
down number of RBC
respiratory or cardio DZ
ischemia
reversible
irreversible
necrosis
chemical injuries
poison- cyanide, pesticides
lead- brain injury
carbon monoxide- hemoglobin affinity 200x than 02
pharmacologic agent- drugs
virulence (toxicity)
measures potential of microorganism to cause DZ
invades and destroys cells
produces toxins
immunosuppressed- less able to defend
bacteria
normal flora, prokaryotic (no organized nucleus), capsule-protects rely on host - environment, nutrition gram + blue gram- red (most) antibiotics septicemia- sepsis, gram -
exotoxin
gram neg and gram pos released from inside cell during growth many types of exotoxins heat labile specific effects on host vaccines highly poisonous/ toxic (not common in people)
endotoxin
gram neg only integral part of cell wall, released during lysis one type endotoxin heat stable diverse effects on host no vaccine pyrogenic/ inflammation primary cause of sepsis, disseminated intravascular coagulation, ARDS
Virus
most common in humans
smaller, more adept than bacteria
Capsid- enclosed genetic material
replication occurs inside host cell; hides inside, from body’s defense.
no endo or exo toxins
evoke immune response; memory of virus, defense against future attacks.
host cell must die w/ virus
antiviral Rx; tgt infected cells, few available, tamiflu, relenza
vaccines; live, dead, or antigens
mutate
infectious
fungi- yeast, molds on skin, mucous membranes
protozoa- malaria
parasites- endoparasites- tape worms, pinworms, ringsworms; ectoparasites- ticks, lices, fleas
prions- protein-brain&nervous system; transmissible spongiform encephalophy (mad cow DZ); Creutzfeldt Jakob in humans (mad cow in people)
apoptosis
cant live forever normal cell death genetically programed into cell aging, early development, menses, lactating breast tissue, thymus involution, and RBC turnover damaged cell- autolysis
Abnormal cell death
necrosis irreversible cell injury always from pathological cause gangrene dry- shrivels, dries, brown or black wet-tissue liquefied gas- clostridium perfringens: food born, bubbles inside cells RBC, tissue gas in dead person
3 lines of defense
- anatomical barriers
- immune response
- inflammation responce
anatomical barriers
skin
hair
chemical; nose, lining of lower respiratory tract (cilia), acid in stomach
Immune response
response to foreign invaders
slow onset, specific
long term immunity
lymphocyte (WBC)
inflammatory response
response to tissue to irritation and injury
rapid onset, general response
lasts only as long as needed
several kinds of cells involved
immunity types
natural
acquired
antigen
immunogen
natural
genetic
immediate response against pathogens
species specific
acquired
active- tgt invader after exposure
passive- mom to child
antigen
protein on cell
self or non self?
does it “belong” to you?
( allergic reaction kicks in, tachyphylaxis)
immunogen
antigen that activates the immune response
antibody (immunoglobulins)
binds w/ antigen to destroy it induces an allergic or inflammatory response T-lymphocytes-thymus B-lymphocytes- bone marrow (both live in lymph nodes) exposure antigen chemotaxis
T-lymphocytes
direct attack on invader
cell mediated response
cell to cell combat
immune response - slow
B-lymphocytes
antigen/ antibody specific
no memory of antigen- B cells created w/ memory
humoral response- B cells live in body fluid (plasma)
ABO blood groups
blood type= antigen present in RBC
antibody= opposite of antigen present (present in plasma)
universal donor= O-
universal recipient= AB+
Rh factor; Pos (+) have antigen, Neg (-) does not
Transfusion reactions s/s
RBC ANTIGEN headache alt LOC N/V facial flushing dyspena tachy- weak thready fever, chills chest pain cynpsos
Transfusion TX
stop transfusion
prime IV line-IV boluses NS
( may need to do Epi IV, diphehydramine 25-50mg, furosemide diuresis, doapmine 2-5 mcg/kg/min
ABO compatibility
don’t give an antigen to someone who doesn’t need already own it.
type O has no antigen to give
type AB+ owns all antigen
antibodies present in the plasma
