Pathology Flashcards
What are the 2 types of edema and their differences?
- Transudate - NO endothelium dmg; clear, yellow fluid; prot poor
- Exudate - can have endothelium dmg; can be pink/red fluid; prot rich
recognition and attachment of phagocytes is enhanced by what?
opsonins
what are the 2 types of digestion?
- O2-dependent (oxidative burst method)
2. O2-independent (lysosome method)
what is the life span of PMNs?
24 hrs
What type of receptors do PMNs and mac’s have for phagocytosis?
c3b & Fc receptors - these mediate phagocytosis & aid in recognition of molecules to be digested
what do mac’s secrete?
- enzymes: collagenases, proteases, lipases, phosphatases
- plasma proteins: complement components, coagulation factors, fibronectin, a2-macroglobulin
- monokines: mediate inflamm and healing
- arachidonic acid metabolites
- ROS & NO
what are the cells of chronic inflamm?
mac’s, lymphocytes, eosinophils, mast cells/basophils, plasma cells
what cell secretes histamine?
mast cells
what cell(s) is associated with chronic granulomatous inflamm?
multinucleated giant cells, epitheloid histocytes
types of chronic granulomatous inflamm?
foreign body & immune granulomas
difference? foreign body = non-infectious etiology; immune = intracellular pathogen
cell associated w/ immune granulomas?
Langhans-type giant cell
what plasma derived mediators does hageman factor (factor XIIa) activate?
coagulation & fibrinolytic systems, complement, and kinin system
what are the 3 pathways for complement?
lectin binding pathway (bact), classical (Ab-ag complex), and alternate (bact, IgA, C3)
what does thrombin do?
converts fibrinogen to fibrin; also activates endothelial cells & platelets
source of arachidonic acid?
released from phospholipid cell memb via phospholipase A2
how is arachadonic acid activated?
by COS or 5-lipooxygenase
PG encourage platelet aggregation. T/F?
false, they inhibit it.
thromboxane induces platelet aggregation. T/F?
true
what does aspirin do for clotting?
it competes for thromboxane receptors, so it prevents platelet aggregation/clotting
what are the products of cyclooxygenase pathway?
PGs & thromboxanes
what are the products of lipooxygenase pathway?
leukotrienes & lipoxins
vasodilation = role of which mediators?
PGs, NO, histamine
increased vascular permeability = role of which mediators?
vasoactive amines, PAF, substance P, c3a & c5a, bradykinin, leukotrienes c4, d4, e4, c5a, leukotriene b4, chemokines
Chemotaxis, leukocyte recruitment & activation = role of what mediators?
c5a, leukotriene B4, chemokines, IL-1, TNF, bacterial products
fever = role of which mediators?
IL-1, TNF, PGs
pain = role of which mediators?
PGs, bradykinin
tissue dmg= role of which mediators?
neutrophil & mac lysosomal enzymes, O2 metabolites, NO
tissues are divided into 3 types in wound healing based on regenerative capacity… what are they?
labile, stable, permanent
activated mac’s synthesize and secrete what enzyme to remodel the ECM?
matrix zinc metalloproteinases
what is angiogenesis?
formation of new capillaries from existing blood vessels
proud flesh?
exuberant amounts of granulation tissue
pyogenic granuloma?
tumor-like mass of excessive granulation tissue
elastin?
core protein glycine & proline random coils
fibrillin?
peripheral microfibrils w/ unknown function
fibronectin?
binds to ECM, cell surface integrins, bacteria, and DNA; type of glycoprotein
what is the order of remodeling of ECM?
fibrin/fibronectin > PGs & GAGs > collagen III > collagen I
Tensile strength of a wound will return. T/F?
Tensile strength will NEVER return to original! only 80% of original tensile strength returns in 3 months.
mechanisms of edema formation?
- inc hydrostatic pressure
- lymphatic obstruction
- decreased plasma oncotic pressure
- increased vascular permeability
- sodium & water retention
ascites?
fluid accumulation in the anterior peritoneal cavity
anasarca?
generalized subcutaneous edema
shock is systemic hyperperfusion of the tissue. t/f?
FALSE, shock is systemic HYPOperfusion of the tissue.
types of shock?
- cardiogenic - heart failure
- hypovolemic - loss of fluid vol
- neurogenic - spinal injury; anesthesia
- septic - infection
- anaphylactic - allergy
where is renin made? angiotensin? ACE? aldosterone?
kidney, liver, lungs, adrenal gland
if initial changes in nonprogressive shock continues, what happens?
go into progressive shock where tissue becomes hypoxic, anaerobic metabolism inc, inc in lactic acid, metabolic acidosis
what type of shock involves disseminated intravascular coagulation (DIC)?
irreversible shock
what do hyperemia and congestion suggest?
local inc in blood volume in particular tissue
diff betw hyperemia and congestion?
hyperemia: active; fresh blood; red/flushed tissue
congestion: passive; older blood; blue-red tissue color
ex of hyperemia?
erythema - inc flow; due to exercise or inflamm
ex of congestion?
cyanosis/hypoxia; dec outflow; due to local obstruction, congestive heart failure
telangiectasia?
widened venules that cause red lines or patterns on the skin–not a hemorrhage (unlike petechiae); blanches w/ pressure
purpura (peliosis)?
bluish or purplish discolration of skin or mucous memb due to extravasation of blood.
ecchymosis?
larger subcutaneous hemorrhages
types of hermorrhage?
petechiae, purpura, ecchymosis
diff sources of hemorrhaging?
- hematoma -localized blood pooling
- epistaxis - nosebleed
- hematemesis -vomit blood
- hemoptysis - blood from resp tract
- melena - older bloody poo
- hematochezia - fresh bloody poo
- hemorrhagic diathesis - deficiency of vit C, platelets, clotting ffacotrs
- body cavity hemorrhage
heparin acts by?
accelerating antithrombin III rxn.
antithrombin does what?
neutralizes clotting factors
neutralizes thrombin (IIa) and factor Xa
which clotting cascade pathway is sensitive to heparin?
intrinsic (dmg to platelets)
extrinsic pathway is characterized by trauma to…?
a tissue other than blood, hence extrinsic (to blood)
factor 2 aka?
prothrombin; activated = thrombin
factor 1 aka?
fibrinogen; activated = fibrin
heparin cofactor II?
neutralizes thrombin (IIa)
c-1-esterase inhibitor?
neutralizes XIIa and kallikrein
protein C system?
inactivates active factor V and VIII in presece of cofactor Protein S
tissue factor pathway inhibitor?
binds to factor Xa & VIIa, thereby inhibiting enzymatic activity of factor VIIa
deficiency of tissue plasminogen results in accumulation of excessive amounts of fibrin aka..?
ligneous conjunctivitis
DIC is…?
overactivation of coagulation in the whole body; exceeds regulatory mechanisms; uses up all platelets and clotting factors; followed by massive fibrinolysis resulting in a massive hemorrhage
to diagnose for DIC what should we look for in blood?
d-dimers!
diff betw white thrombi and red thrombi?
white: in arterial circ; mostly of platelets & fibrin
red: in venous circ; mostly of platelets, fibrin, and trapped RBCs; due to slower blood flow
lines of zahn?
laminations in thrombus produced by alternating pale layers of platelets admixed w/ fibrin & darker layers containing more red cells; signify thrombosis at a site of pulsatile blood flow (contraction, relaxation, contraction, etc)
recanalization of a thrombus?
holes will form in the clot for blood to flow
what does factor VLeiden do?
it is a mutated factor V that cannot be inactivated by protein C, so inc in clot formation
most common type of emboli?
thromboemboli; mostly arise in deep vv of legs
coagulation necrosis?
replacement of necrotic tissue by a scar
liquefaction necrosis?
necrotic area liquefies and forms a cystic area (i.e. brain)
septic infact?
abscess formation; presence of bacteria
