Exam 1 Flashcards
cellular alter.
cell functions
movement (musc. cells), conductivity, metab. absorption, secretion/excretion, respiration, communication (ex. gap function)
Plasma membrane fun-
cell recognition, cellular mobility, mol mvmnt, storage
plasma mem- transportation
intra-extracellular mvmnt (pumps, surface markers + catalyze rxns)
cell to cell adhesions- 3 ways
extracellular matrix, plasma mem, specialized cell junctions
cell to cell adhesions- extracellular matrix materials
collagen (tensile strength), elastin (stretching), fibronectin (anchorage)
cell to cell adhesions- spec. cell junctions
tight seal (tight jun, prevents leakage) mechanical attach (adherence) chem comm (gap junction, sm ion mvmnt) cellular polarity (tight)
cellular comm- types
plasma mem receptor
intracellular recep (remote signaling)
contact signaling via gap jun.
passive transport
diffusion- (high con to low, down conc gradient)
filtration- “hydrostatic p”, (mvmt h20 and solution)
osmosis- water across selec. perm mem. (h20 potential)
active transport
requires energy
against conc. gradient
tonicity
effec. osmolarity of sol.
hypotonic sol- more diluted
hypertonic sol- more conc.
isotonic- equal to ICF and ECF
Atrophy
age related
due loss blood supply
cells shrink
hypertrophy
cells inc size
hyperplasia
cells inc in #
dysplasia
dearranged cell growth
persistent or severe
metaplasia
replace one cell type w/ another
necrosis- types
cell death
breakdown of cell (autolysis)
coagulative (acciden. , frm hypoxia)
liquefactive (bac/fungal infec., puss)
caseous (soft white appear., pink surr by grey)
fatty (cell dissolution from lipids)
gangrenous ( potenti. deadly, can be dry, wet or gas related)
somatic death- postmortem changes
name, mortis algor- dec temp liver- purple color rigor- stiffness autolysis- brkdown endogenous substances
h20 mvmnt btw plasma and interstitial fluid
cap hydrostatic p (blood p)- cap outward to interst.
cap. (plasma) oncotic p- intersit back to cap
interstit. HP- intersist inward to cap
interst. oncon. P- cap to interstit.
h20 mvmnt between ICF and ECF
diffuses through aquaporins passively
or o/ mat w/ active transport
ICF- K dominant
ECF- Na dominant
edema- causes
Na or h20 retention + venous obstruction= inc cap Hydro p
loss plasma p (mvmnt proteins into tissue)= dec oncotic P
proteins into interstit from vasc= inc capill perm
lymphatic blockage, not absorb fluid= lymphedema
edema- manifestations
local or general “anasarka”
dependant- functions on gravity (precursor to general)
Na/ Cl regulation location
juxtaglomerular cells- secrete renin hypothalamus- inc thirst venules/ arteries- vasoconstriction efferent arterioles- vasoconstr adrenal gland- secrete aldosterone
Na/ Cl effectors
renin act angiotensinogen to ang. 1, ACE act. ang1 to ang2, ang2 acts on hypothal, adrenal gland, and arterioles
hypervolemia cause
inc Na conc, hyper secretion of aldosterone (dilutes o/ electrolytes)
hypervolemia manifestations
edema and heart failure
hypovolemia cause
dec water intake, hemorrhage (bleeding) and wound drainage
hypovolemia manifestations
dec urine output, tachycardia (hypotension), dry skin and weight loss
hypernatremia cause
> 145
dec free intake h2o, hypersecretion ADH
highly conc. hypertonic solution
hypernatremia manifestations
thirst, fever, seizures, hypotension, tachycardia, pulmonary edema
hyponatremia cause
<135
extrarenal loss
excess total body water (dilution) from renal failure
hyponatremia manifestations
cerebral edema (effects neurological fun.), inc intracranial P
carbonic acid-bicarb buffer
carbonic acid (PCO2 respir) bicarb (HCO3 metab)
location - lungs and kidney
lungs- exhale co2
kidney- reabsorb/regen. extra bicarb HCO3
function- 20:1 w/ pH 7.4 co2 and carbonic a inc= pH dec co2 conserved + combines w/ h2o high co2= respir acidosis low co2 respir alkalosis
hemoglobin buffer
prominant in ICF (not plasma) high pH= Hb lose H+ low pH= Hb adds H+ (taken out of sol)= HHb carbonic acid dissoc into H and HCO3 co2 and RBC combine w/ H2o
protein buffer
intracellular
Hb and CO2Hb expelled through lungs
protein - charge
buffer H+ ions, (charges offset)
renal buffer
H secretion or HCO3 reabsorption
location- distal tubule of glomerulus
ratio 1:20 (bicarb/ base)
low pH- (acidic, HCO3 reab)
high pH- (alkalotic, H+ reab)
normal pH range
7.35-7.45
acidic 7.35-7.4
alkaline 7.4-7.45
metabolic buffer
HCO3- kidney (renal)
respiratory buffer
PCO2- lungs
innate immunity- first line defense
skin, o/ natural barriers and immunity
innate imm.- second line defense
inflammatory response (edema, erythema, pain and exudate)
innate imm- third line defense
adaptive imm. (acquired or specific)
targets specialized tissues
passive v active
inflammation-cause
infection, mechanical damage, ischemia (inadeq blood supply), temp extreme and nutrient deprivation
inflamm- reponse characteristics
vascular response
cellular/chem response
nonspecific
immune responce
inflamm- plasma protein system
“complement system”
local inflam= histamine responce
antigen breakdown w/ mem. brkdwn= c3b (coat surface bac)
attraction macrophages= c5a (attract leuk)
classical path- need ab and antigen binding (c 1,c3,c5)
altern path- direct surface mol binding
inflamm- coagulation system
mesh-like fibrin net made
fun- stop bleeding, prevent spread infection and makes grndwork for healing
extrinsic- act. by damaged epith cells
tissues release thromboplastin
intrinsic- act w/ exposure collagen
factor 12
* pathways converge w/ factor 10inflamm- kinin system
product activation of F12= release bradykinin
fun- assist inflam cells
results- vasodil, pain, sm musc contraction and inc vasc perm.
inflamm- mast cell degranulation
release mast cell contents and histamine/ chemotactic factors
inflamm- histamine fun
binds H1 (pro inflammatory) and H2 (anti-inflamm) causes temporary capill. constriction and venule dilation fun- inc blood flow and cap perm w/ retraction endo cells
inflamm- chemotactic factor fun
neutrophil chemotactic factor
eosinophil chemotactic factor of anaphylaxis
mvmnt cell along chem. gradient formed by cheotactic factor
inflamm- cellular componets- pattern recognition receptor
fun- id and damage pathogen assoc. mol. patterns,
(found on surfac. / diss. mol)
inflamm- cellular componets- toll-like receptor
single-mem spanning
fun- recogn structurally conserved mol derived from microbes
inflamm- cellular componets- Complement receptor
detect pathway w/out ab mediation
triggered by antigens
inflamm- cellular componets- scavenger receptor
recog. + eat bac pathogens, damaged cells and altered soluble lipoproteins
inflamm- cellular componets- NOD like receptors (NLR’s)
cytoplasmic recep
recog products of microbes and damaged cells
inflamm- phagocytosis
cell eating
remove cells out of vascular space= produc. adhesion mol through margination or diapedesis
margination- neutrophil adhering to endoth wall
diapedesis- mvmnt cells thru endothel junction
steps: recog+ adherence thru opsonization
engulfment
fusion phagosome
target destruction
acute inflamm- characteristics
self limiting
inc vasc perm (bradykinin and histamine)
heat
swelling (protein mvmnt into interstitial)
redness- inc blood flow to damaged tissue
pain- inc P of fluid on nerves
acute inflamm- exudate types
serous- early/mild (watery w/ few plasma p)
fibrinous- severe (thick and clotted)
purulent- Inc leukocyte #, indication of infection
hemorrhagic- has blood or erythrocytes
chronic inflammation- characteristics
indicated w/ purulent exudate + incomplete wound healing
lasts >2 weeks
cellular signs: lympho and macrophage # inc
granuloma formation (raised bump)
includes:
epithelia cell formation (accum of debris)
giant cell formation
wound healing- step 1
hemostasis (coagulation)
damage to capill and blood v= bleeding w/ immedi. vasoconstric, then vasodil and platelet activation (fibrin meshwork)
wound healing- step 2
inflammation
vasoactive cytokinin related= inc blow flow
results= inc. neutroph and lymphocyte flow to injury
wound healing- step 3
proliferation + new tissue formation
inc macroph
angiogenesis act= clearing debris, + releasing grwth factors
epithelialization, collagen syn, fibroblast proliferation
wound healing- step 4
remodeling and maturation
scar formation
wound healing- factors for abnormal healing
impaired collagen matrix (keloid)
impaired epithelial oxygen (hypoxemia)
impaired contraction (tightening skin)
dehiscence (would pulls aprt at suture line)
infection, nutrition deficiency, + chronic illness
obesity, excessive fibrin, diabetes, medications
adaptive immunity- hummoral
antibody mediated!!
b- cell receptor for path (antigen)
differentiates into memory or effector
effector fun- produces specific ab to path that are mem bound)
activation: presents antigen, attracts T-cell, T- cells binds and B cell releases Interleukin
adaptive immunity- cell mediated
T-cell production and differentiation
types: memory t, cytotoxic c and T helper
T-helper– MHCII, act. after antigen presentation
activation:
tcell binds to MHCII protein on surface B cell
differentiates into effector or memory
effector fun- initiate response, recruit o/ cells, remove debris and promote regen/repair
t cytotoxic– MHC I, kills o/ cells
directly attacks, not need antigen presentation
differentiates into memory and effector
effector fun- release perforin and granzymes
antibody functions-
direct- neutralization (cover antigen binding sites)
agglutination- clumping insol material together and precipitate out of sol
opsonization- binding of ab to antigen
stimulates inflammation
hypersensitivity- allergy
response to environment of antigen
most common
hypersensitivity- autoimmunity
altered immunologic tolerance
failure to recog. “self”
hypersensitivity- alloimmunity
immune rxn to tissues w/ new introduction
ex. blood transfusion rx (Rh factor and ab)
universal blood donor
o-
because has no antigens, and accepts both a and b antibodies
microo infection factors
immunogenicity- ability to provoke imm system
infectivity- abilt. est. infection
mech of action- kind of recep
pathogenicity- ability microo cause disease
portal of entry
toxicity- lvl of toxin
virulence- severity of microo
stages of infection
incubation- infection till appearance of sympt
prodromal- onset initial sympt
invasion “acute illness”- start of immune response
convalescence- removal of infectious agent
(if not = latency phase)
diff. btw bacteria and virus
bac- gram - or +, asexual reproduc, produced toxins (endo and exo), aerobic and anerobic
virus- needs host for reproduc., directly infects/ damages cell, has multiple transmissions and own viral process
viral transmission types
aerosol
infected blood
vector
sexual contact
viral process
attachment- specific to certain cell types
penetration- endocytosis
uncoating- release viral DNA
replication- injecting DNA in host cells
assembly- dev new viron
release- shedding via lysis (rupture of cell wall/mem)
difficulties of viral replication treatment
virus can hide in cells (away from inflamm) highly sensitive to neutralizing ab not touched by infection ab genes mutate and adapt new defense mech. Ex- dev. new surface antigens
treatment for infection- antibiotic resistance causes
microo genetic mutation
overuse of med
lack of compliance w/ prescribed recommendations
