Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/67

Click to flip

67 Cards in this Set

  • Front
  • Back
5 signs of inflammation
rubor
calor
dolor
tumor
loss of function
purpose of inflammation
protective response with ultimate goal of ridding the organism of the initial cause of cell injury and its consequences, such as necrotic cells & tissues
four major functions of inflammation
brings phagocytic cells to the area to engulf foreign material
brings in antibodies
walls off area
prevents systemic spread
exudate
high protein, inflammatory extravascular fluid (sp grav >1.020)
4 types of exudate
fibrinous
sanginous
purulent (suppurative)
serous
fibrinous exudate
lining of body cavities; fibrous strands seen (pericardium)
serous exudate
outpouring of thin fluid, der from either serum or mesothelial cells (effusion)
purulant/suppurative exudate
large amounts of pus and/or neutrophils, necrotic cells and edema fluid (abcesses, appendicitis)
sanguinous
Blood in exudate (more often purulosanginous - pus & blood - eww)
Stages of Inflammation
acute
chronic
acute inflammation - definition, mechanisms
immediate & early response to an injurious agent; short duration (minutes-days); exudation of fluid & plasma proteins (edema); emigration of leukocytes esp neutrophils
Chronic inflammation
prolonged duration (weeks/months); monocyte/macrophage dominant
What three things are present simultaneously in chronic inflammation
Active INFLAMMATION
Tissue DESTRUCTION
Attempts at REPAIR
resolution
go back to normal cells
When do we get scars?
when resolution fails in acute inflammation
ongoing necrosis/chronic inflammation
when cell necrosis can't be repaired
5 Stages of scar formation
PREPARATION (remove debris)
GRANULATION tissues (highly vascularized; fibronectin)
COLLAGENATION (tensile strength)
MATURATION (pale, lacks circulation)
CONTRACTING/STRENGTHENING (type III to type I collagen)
cells in stages of scar formation
preparation - phagocytes
granulation - fibroblasts
collagenatin - fibroblasts
maturation -
contraction/strengthening - myofibroblasts
3 possible results of an injury
Regeneration (normal returns)
Healing (scar formation/organization of exudate)
Fibrosis (tissue scar) (persistent damage)
Cirrhosis is a form of what type of wound repair?
Fibrosis (altered architecture, persistent damage)
Healing by first intention (wounds with opposed edges) (Primary Union)
edges are approximated (no gap)
eschar (scab)
epidermal cells proliferate under scab
dermis - scarred; epithelium not
Healing by Second Intention (wounds with separated edges)
poor apposition (dehiscence); foreign material; extensive necrosis; infection
more fibrin/more granulation tissue/scarring of both epidermis and dermis; wound contraction c/b disfiguring
dehisence
rupture or pulling apart of a wound
What do vitamin B2, Vit C bioflavinoids, zinc and sulfur have to do with wound repair?
deficiencies can cause defective wound healing
What are two conditions that would lead to defective collagen?
Ehlers-Danlos; Marfan syndrome
what is a keloid?
excess collagen formation
Three factors in defective wound healing?
Diabetes
Radiation/Chemo
Exogenous steroids
angiogenesis
formation of new blood vessels (neo-vascularization) in healing; branching of adjacent vessels
recruitment of EPC (endothelial progenitor cells from bone marrow)
(new bv not as strong, removed by apoptosis)
when would you see angiogenesis?
cancer, healing, regeneration
Pathological fracture
bone not healthy, so breaks
Greenstick fracture
periosteum intact, inside broken
comminuted fracture
shattered (lots of little broken parts)
compound fracture
breaks skin too (osteomyelitis poss)
non-union fracture
motion of the bony ends & incomplete healing more than 6 months
3 stages of fracture healing
PROCALLUS - anchorage, no stability
FIBROCARTILAGENOUS CALLOUS
OSSEOUS CALLOUS & remodeling
etiology of auto-immune dz
many theories - cross-reactivity w/ common epitopes & HLA antigens; self-tolerance lost (micro organisms act as triggers)
some microorganisms that can act as triggers for auto-immune dz
Coxsackie B - myocarditus
Klebsiella - ankylosing spondylitis
Virus - Type I Diabetes
Yersinia Pestis - Graves Dz, Reiders sy
Strep A-Beta - rheumatic fever, endocarditis
Vit D and autoimmune
UV-B radiation & Vit D reduce risk of viral infex, reducing sequelae (autoimmune dz, some cancers)
central tolerance - T cells - where
thymus
peripheral tolerance mechanisms
anergy - stimulated, no costim
suppression - Treg
Activation induced cell death
SLE
Systemic lupus erythmatosis
silicone implants
trigger "Lupus-like" illness
ubiquitin
"stress protein" - flag that says "kill me" assoc with autoimmune
SLE anti-histone antibodies
seen in drug-induced lupus
symptoms of Lupus
chronic exacerbations and remissions of immune injury to SKIN, JOINTS, KIDNEYS, SEROSA; characteristic red "mask" on face
Etiology of lupus
Failure of self tolerance (Ab to nuclear proteins - ANA)
SLE - ANA
Anti-nuclear antibodies
anti ds-DNA; anti-sm are close to diagnostic
SLE - dogs?
dogs of lupus pts more likely to have ANA
SLE - genetics?
20% concordace in twins;
SLE - Environmetal, drug, dietary fax
alfalfa
Hydralazine, procainamide, D-pennicillamine, Isoniazid
Steroids
UV exposure
SLE - Solvents & UCTB
paint thinner/petroleum - 3x
perfume/cosmetic mfg - 7x
furniture refinishing - 9x
SLE - sulfur metabolism
sulfur - phase II detox (also estrogen)
abnormal - more sens to xenobiotics, steroids
exacerbations - sulfur, pregnancy, menstruation
UCTD
Undifferentiated Connective Tissue Dz - more than one autoimmune dz in same pt (aka M(ixed)CTD
SLE - incidence
10:1 childbearing women:men
2:1 post-menopausal:men

1:1000 US women
1:2500 worldwide women
1:700 childbearing
1:245 AfroAmerican
SLE - L.E. cell
any phagocyte that contains coagulated nucleus of an injured cell (used to be diagnostic, now blood test)
SLE - vasculitis
occurs most often in SKIN, muscle, spleen
SLE - fibrinoid necrosis
in vessel walls.
aka "onion skin lesions"
fibrin laid down in wall; Ab to phospholipids stick to wall
SLE - glomerulonephritis
4 types of Lupus nephritis - common
SLE - skin lesions
butterfly rash - 50% of cases
atrophic lesions (destruction & loss of cell substance) on trunk & extremities
ERYTHEMA & SCALING
SLE - joints
non-erosive synovitis without deformity (polyarthritis)
SLE - CNS
occlusion of small vessels by intimal proliferatin or arteritis; Ab to synaptic membrane; increased hypercoagulability
depression/psychosis/strokes
SLE - Heart
serousitis, pericarditis (fibrinous exudate); endocarditis (warty deposits on both sides of valves); atheroslerosis
SLE - spleen
splenomegaly (tho not giant)
SLE - lymph
lymphadenopathy - generalized
SLE - lungs
pleuritis, effusio, interstitial fibrosis (exercise intolerant)
SLE - liver
Lupoid hepatitis - vasculitis of portal tracts with lymphocytic infiltration
SLE - 11 criteria
Malar rash
Discoid rash
photosensitivity
oral ulcers
arthritis
serositis
renal d/o
neruological d/o (seizures/psychosis)
hematological d/o
immunological d/o (anti-dsDNA, anti-Sm, anti-phospholipid
ANA
SLE - clinical
Protean (highly variable, unpredictable)