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NRSG 258 PATHO > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

cellular alter.

cell functions

A

movement (musc. cells), conductivity, metab. absorption, secretion/excretion, respiration, communication (ex. gap function)

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2
Q

Plasma membrane fun-

A

cell recognition, cellular mobility, mol mvmnt, storage

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3
Q

plasma mem- transportation

A

intra-extracellular mvmnt (pumps, surface markers + catalyze rxns)

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4
Q

cell to cell adhesions- 3 ways

A

extracellular matrix, plasma mem, specialized cell junctions

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5
Q

cell to cell adhesions- extracellular matrix materials

A

collagen (tensile strength), elastin (stretching), fibronectin (anchorage)

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6
Q

cell to cell adhesions- spec. cell junctions

A 
tight seal (tight jun, prevents leakage)
mechanical attach (adherence)
chem comm (gap junction, sm ion mvmnt)
cellular polarity (tight)
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7
Q

cellular comm- types

A

plasma mem receptor
intracellular recep (remote signaling)
contact signaling via gap jun.

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8
Q

passive transport

A

diffusion- (high con to low, down conc gradient)
filtration- “hydrostatic p”, (mvmt h20 and solution)
osmosis- water across selec. perm mem. (h20 potential)

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9
Q

active transport

A

requires energy

against conc. gradient

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10
Q

tonicity

A

effec. osmolarity of sol.
hypotonic sol- more diluted
hypertonic sol- more conc.
isotonic- equal to ICF and ECF

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11
Q

Atrophy

A

age related
due loss blood supply
cells shrink

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12
Q

hypertrophy

A

cells inc size

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13
Q

hyperplasia

A

cells inc in #

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14
Q

dysplasia

A

dearranged cell growth

persistent or severe

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15
Q

metaplasia

A

replace one cell type w/ another

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16
Q

necrosis- types

A

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)

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17
Q

somatic death- postmortem changes

A 
name, mortis
algor- dec temp
liver- purple color
rigor- stiffness
autolysis- brkdown endogenous substances
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18
Q

h20 mvmnt btw plasma and interstitial fluid

A

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.

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19
Q

h20 mvmnt between ICF and ECF

A

diffuses through aquaporins passively
or o/ mat w/ active transport
ICF- K dominant
ECF- Na dominant

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20
Q

edema- causes

A

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

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21
Q

edema- manifestations

A

local or general “anasarka”

dependant- functions on gravity (precursor to general)

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22
Q

Na/ Cl regulation location

A 
juxtaglomerular cells- secrete renin
hypothalamus- inc thirst
venules/ arteries- vasoconstriction
efferent arterioles- vasoconstr
adrenal gland- secrete aldosterone
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23
Q

Na/ Cl effectors

A

renin act angiotensinogen to ang. 1, ACE act. ang1 to ang2, ang2 acts on hypothal, adrenal gland, and arterioles

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24
Q

hypervolemia cause

A

inc Na conc, hyper secretion of aldosterone (dilutes o/ electrolytes)

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25
Q

hypervolemia manifestations

A

edema and heart failure

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26
Q

hypovolemia cause

A

dec water intake, hemorrhage (bleeding) and wound drainage

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27
Q

hypovolemia manifestations

A

dec urine output, tachycardia (hypotension), dry skin and weight loss

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28
Q

hypernatremia cause

A

> 145
dec free intake h2o, hypersecretion ADH
highly conc. hypertonic solution

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29
Q

hypernatremia manifestations

A

thirst, fever, seizures, hypotension, tachycardia, pulmonary edema

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30
Q

hyponatremia cause

A

<135
extrarenal loss
excess total body water (dilution) from renal failure

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31
Q

hyponatremia manifestations

A

cerebral edema (effects neurological fun.), inc intracranial P

32
Q

carbonic acid-bicarb buffer

A 
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
33
Q

hemoglobin buffer

A 
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
34
Q

protein buffer

A

intracellular
Hb and CO2Hb expelled through lungs
protein - charge
buffer H+ ions, (charges offset)

35
Q

renal buffer

A

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)

36
Q

normal pH range

A

7.35-7.45
acidic 7.35-7.4
alkaline 7.4-7.45

37
Q

metabolic buffer

A

HCO3- kidney (renal)

38
Q

respiratory buffer

A

PCO2- lungs

39
Q

innate immunity- first line defense

A

skin, o/ natural barriers and immunity

40
Q

innate imm.- second line defense

A

inflammatory response (edema, erythema, pain and exudate)

41
Q

innate imm- third line defense

A

adaptive imm. (acquired or specific)
targets specialized tissues
passive v active

42
Q

inflammation-cause

A

infection, mechanical damage, ischemia (inadeq blood supply), temp extreme and nutrient deprivation

43
Q

inflamm- reponse characteristics

A

vascular response
cellular/chem response
nonspecific
immune responce

44
Q

inflamm- plasma protein system

A

“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

45
Q

inflamm- coagulation system

A 
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 10
46
Q

inflamm- kinin system

A

product activation of F12= release bradykinin
fun- assist inflam cells
results- vasodil, pain, sm musc contraction and inc vasc perm.

47
Q

inflamm- mast cell degranulation

A

release mast cell contents and histamine/ chemotactic factors

48
Q

inflamm- histamine fun

A 
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
49
Q

inflamm- chemotactic factor fun

A

neutrophil chemotactic factor
eosinophil chemotactic factor of anaphylaxis
mvmnt cell along chem. gradient formed by cheotactic factor

50
Q

inflamm- cellular componets- pattern recognition receptor

A

fun- id and damage pathogen assoc. mol. patterns,

(found on surfac. / diss. mol)

51
Q

inflamm- cellular componets- toll-like receptor

A

single-mem spanning

fun- recogn structurally conserved mol derived from microbes

52
Q

inflamm- cellular componets- Complement receptor

A

detect pathway w/out ab mediation

triggered by antigens

53
Q

inflamm- cellular componets- scavenger receptor

A

recog. + eat bac pathogens, damaged cells and altered soluble lipoproteins

54
Q

inflamm- cellular componets- NOD like receptors (NLR’s)

A

cytoplasmic recep

recog products of microbes and damaged cells

55
Q

inflamm- phagocytosis

A

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

56
Q

acute inflamm- characteristics

A

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

57
Q

acute inflamm- exudate types

A

serous- early/mild (watery w/ few plasma p)
fibrinous- severe (thick and clotted)
purulent- Inc leukocyte #, indication of infection
hemorrhagic- has blood or erythrocytes

58
Q

chronic inflammation- characteristics

A

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

59
Q

wound healing- step 1

A

hemostasis (coagulation)

damage to capill and blood v= bleeding w/ immedi. vasoconstric, then vasodil and platelet activation (fibrin meshwork)

60
Q

wound healing- step 2

A

inflammation
vasoactive cytokinin related= inc blow flow
results= inc. neutroph and lymphocyte flow to injury

61
Q

wound healing- step 3

A

proliferation + new tissue formation
inc macroph
angiogenesis act= clearing debris, + releasing grwth factors
epithelialization, collagen syn, fibroblast proliferation

62
Q

wound healing- step 4

A

remodeling and maturation

scar formation

63
Q

wound healing- factors for abnormal healing

A

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

64
Q

adaptive immunity- hummoral

A

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

65
Q

adaptive immunity- cell mediated

A

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

66
Q

antibody functions-

A

direct- neutralization (cover antigen binding sites)
agglutination- clumping insol material together and precipitate out of sol
opsonization- binding of ab to antigen
stimulates inflammation

67
Q

hypersensitivity- allergy

A

response to environment of antigen

most common

68
Q

hypersensitivity- autoimmunity

A

altered immunologic tolerance

failure to recog. “self”

69
Q

hypersensitivity- alloimmunity

A

immune rxn to tissues w/ new introduction

ex. blood transfusion rx (Rh factor and ab)

70
Q

universal blood donor

A

o-

because has no antigens, and accepts both a and b antibodies

71
Q

microo infection factors

A

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

72
Q

stages of infection

A

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)

73
Q

diff. btw bacteria and virus

A

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

74
Q

viral transmission types

A

aerosol
infected blood
vector
sexual contact

75
Q

viral process

A

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)

76
Q

difficulties of viral replication treatment

A 
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
77
Q

treatment for infection- antibiotic resistance causes

A

microo genetic mutation
overuse of med
lack of compliance w/ prescribed recommendations

NRSG 258 PATHO (3 decks)

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