Hemodynamics and Clotting Flashcards
What does normal hemostasis rely on?
maintenance of blood in a fluid, clot free state
induction of rapid and localized hemostatic plug at site of vascular injury
What regulates hemostasis?
platelets
coagulation cascade
endothelium
What is the first event in primary hemostasis?
vasoconstriction as a result of endothelin and reflex
What steps occur in platelet adhesion?
bind to ECM via von Willebrand factor (produced by endothelium)
What occurs during platelet activation?
shape changes and release secretory granules which recruit more platelets
How is secondary hemostasis activated?
tissue factor-activates coagulation cascade
thrombin-converts fibrinogen to fibrin
cross-linked fibrin forms permanent plug
What are the primary sites for the coagulation cascade to occur?
phospholipids on activated platelets, bind Ca (cofactor for cascade)
What are the important mediators in platelet aggregation?
ADP and thromboxane A2-amplify aggregation forming primary hemostatic plug
thrombin binds to protease activated receptor on platelet membrane causing further aggregation
still reversible
What does fibrinogen bind to?
GP2b3a for aggregation
What moderates the size of clot?
fibrinolytic cascade
plasmin cleaves fibrin to fibrin split products
What are the anti-thrombotic properties of endothelial cells?
PGI2 and NO vasodilators
ADPase inhibits platelet aggregation by breaking down ADP
What is the mechanism of action for thrombomodulin?
binds thrombin
activates protein C
with protein S inactivates factors 5 and 8
What is the mechanism of action for anti-thrombin III?
inhibits the activity of thrombin, 10 and 9
What is the mechanism of action for tissue factor pathway inhibitor?
inhibits the activity of 7 and 10
What is the mechanism of action for tissue type plasminogen activator?
converts plasminogen to plasmin
plasmin cleaves fibrin, degrading thrombi
What are the pro-thrombotic properties of endothelial cells?
von Willebrand factor-cofactor in binding platelets to ECM
thrombomodulin-expression down regulated by activated endothelial cells
tissue factor-activates extrinsic coagulation cascade
plasminogen activator inhibitor-limits fibrinolysis
What stimulates the synthesis of tissue factor?
stimulated by TNF, IL-1, bacterial endotoxins
activates extrinsic coagulation cascade
What is Virchow triad?
endothelial injury
abnormal blood flow
hypercoagulability
What can cause injury to the endothelium?
HTN, turbulent flow, bacterial endotoxins
increased procoagulant factors, decreased anti-coagulant effectors
What is abnormal blood flow?
disruption of laminar flow
turbulence and stasis
turbulence from plaques
stasis from aneurysms, flaccid myocardium post MI, heart chamber dilation, a-fib
What are the causes of hypercoagulability?
primary-genetic-mutation in factor V, prothrombin, MTHFR (increases homocysteine), deficiencies in antithrombin III, protein C, protein S
What is factor 5 Leiden?
mutant factor 5 is resistant to cleavage by protein C
Arg to Glu at 506
heterozygotes 5x relative risk, homozygotes 50x relative risk
What happens due to a mutation in the prothrombin gene?
mutation causes elevated prothrombin levels
3x relative risk of venous thrombosis
What happens due to the MTHFR gene?
variant in 5,10 methylenetetrahydrofolate reductase
causes modest elevation of homocysteine (inhibits antithrombin III-promotes clotting)
What are the secondary hypercoagulability states?
prolonged immobilization MI, a fib, prosthetic cardiac valves tissue damage cancer DIC heparin-induced thrombocytopenia antiphospholipid antibody syndrome
What is antiphospholipid antibody syndrome?
formerly called lupus anticoagulant syndrome
antibodies bind to protein epitopes exposed by phospholipids
clinical-recurrent thrombi and miscarriages, cardiac valve vegetations, thrombocytopenia, prolonged PTT
treatment-chronic anticoagulation, immunosuppression
What are other secondary risks (lower) for hypercoagulability?
cardiomyopathy, nephrotic syndrome, hyperestrogenic states, oral contraceptives, sickle cell anemia, advancing age (decrease PGI2), cigarette smoking, obesity
What are combined states of hypercoagulability?
homozygous mutations
concurrent inheritance of different mutations (combined heterozygosity)
mutations plus acquired risk factors
–patients under 50 with DVT should be checked for genetic risk factors even in setting of acquired risk factors
What are lines of Zahn?
pale layers are platelets
darker layers are fibrin and RBCs
more prominent in arterial thrombi
Where does a thrombus attach?
underlying heart or vessel wall
What are the characteristics of an arterial thrombus?
usually occlusive-coronary, cerebral, femoral
usually overlies atherosclerotic plaque
gray-white, friable mesh of platelets, fibrin, RBCs and WBCs
grows retrograde to blood flow (toward the heart)
What are the characteristics of a venous thrombus?
essentially always occlusive
lower extremities (90% of cases)
Red-more RBCs
grow in direction of blood flow (toward heart)
propagating tail-not well attached and prone to embolization
What are the characteristics of a post-mortem clot?
usually not attached
dependent portion is dark red
supernatant is yellow, gelatinous like chicken fat
What are the possible fates of a thrombus?
propagation
embolization
dissolution
organization and recanalization
What happens during organization and recanalization?
endothelial cells, fibroblasts, smooth muscle cells grow into clot
small channels develop through clot
clot may incorporate into vessel wall
What is the fate of a superficial venous thrombosis?
rarely embolize
cause edema distal to obstruction, predispose overlying skin to injury, infection, ulceration
What is a deep venous thrombosis?
at or above knee most likely to embolize
collateral circulation can relieve pain
diagnosis-ultrasound or angiogram
treat with anticoagulation
What does a coronary artery thrombosis cause?
MI
What does a cerebral artery thrombosis cause?
stroke, TIA
What does a femoral artery thrombosis cause?
gangrene
What does an atrial mural thrombus cause?
secondary to a-fib or mitral valve stenosis, can embolize
What does a ventricular mural thrombus cause?
secondary to MI, cardiomyopathy, can embolize
What is an embolism?
a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
What causes pulmonary thromboembolisms?
DVT in 90% of cases
often occurs as multiple emboli, sequentially or shower
What is the clinical presentation of massive occlusion of pulmonary circulation?
sudden death, right heart failure (cor pulmonale) or cardiovascular collapse
What is the clinical presentation of medium sized arterial occlusion?
hemorrhage but not infarction due to dual circulation
What is the clinical presentation of end arteriole occlusions?
infarction
What is a systemic thromboembolism?
80% come from heart (intracardiac mural thrombi)
others from aortic aneuysm, atherosclerosis, valvular vegetations
paradoxical (from R to L shunt) allows it to bypass lungs
go to lower extremities (most common) and cause ischemia or infarction-depends on extent of collateral or dual circulation
What is a fat embolus?
microscopic fat globules may be found in circulation after fracture of long bones
What is the clinical presentation of fat embolism syndrome?
1-3 days post injury
pulmonary insufficiency
neurologic effects
anemia and thrombocytopenia (see petechiae)
due to obstruction of pulmonary and cerebral microvasculature
What is an air embolus?
obstruction of circulation by large or coalesced gas bubbles
sources-neck and chest injuries, obstetric procedures, thoracentesis, hemodialysis
What is decompression sickness?
air breathed at high pressure increases amount of air that dissolves in the blood
gas bubbles out of the blood during rapid depressurization forming emboli
in muscle-the bends
treat with 100% O2, compression chamber
What is an amniotic fluid embolus?
infusion of amniotic fluid or fetal tissue into maternal circulation at delivery
initial sx-sudden severe dyspnea, cyanosis, hypotensive shock, then seizures and coma
late-pulmonary edema and DIC
anticoagulants
inhibit fibrin formation
heparin, LMW heparin, warfarin, fondaparinux, argatroban, dabigatran
antiplatelets
inhibit platelet aggregation
aspirin, dipyridamole, clopidogrel, ticlopidine, abciximab, eptifidatide
thrombolytics
dissolve formed fibrin clots
streptokinase, alteplase, anistreplase, tenecteplase
heparin
porcine unfractioned
cleaved by endo-D-glucuronidase into various fractions
MOA heparin
reversibly binds ATIII
active coagulation factors bind irreversibly to ATIII (Arg-Ser) to prevent fibrin generation
suicide substrate
heparin in pregnancy
approved because it does not cross the placenta
administration of heparin
injected sc or iv (im contraindicated induce hematoma)
monitor partial thromboplastin
increase lipoprotein lipase activity
adverse effects of heparin
bleeding HIT (type I non immune mediated, type II immune mediated based on heparin platelet factor 4 complex)
reversal of heparin induced bleeding
reverse with plasma, whole blood or protamine
do not give to NPH insulin or fish allergy for protamine
LMW heparin
too small to simultaneously bind ATIII and thrombin
specific for ATIII inactivation of X (low affinity for thrombin)
indications for LMW heparin
unstable angina or STEMI
monitor anti-X activity
advantages of LMW heparin
longer half life
outpatient
lower incidence of thrombocytopenia
predictable response
fondaparinux
administer iv or sc
inactivation of factor X
MOA warfarin
inhibits synthesis of biologically active vitamin K dependent clotting factors
clotting factors cant bind Ca (2,7,9,10,C,S)
time for action of warfarin
5-7 days for generation of coagulation factors incapable of binding Ca
oral administration
warfarin monitoring
monitor INR (prothrombin time)
measures extrinsic pathway
goal of 2-3 (2.5-3.5 for heart valve replacement)
polymorphisms for warfarin
CYP2C9*1 normal (2 and 3 decreased clearance)
VKORC1 G normal (A synthesizes less VKORC1 so less protein for warfarin to bind)
increase warfarin effect
aspirin ketoconazole and erythromycin cimetidine ibuprofen cephalosporins sulfa/trimeth
decrease warfarin effect
cholestyramine
rifampin
phenobarbital
cigarette smoking
contraindications for warfarin
not in pregnancy
causes nasal hypoplasia in first trimester
CNS, increased fetal death in second and third trimester
treatment of excessive bleeding on warfarin
whole blood or plasma viramin K (takes 24 hrs)
direct thrombin inhibitors
argatroban or dabigatran (oral)
argatroban
directly block active site on thrombin
use for patients with HIT
dabigatran
prodrug with affinity for free and fibrin bound thrombin
converted to active by plasma esterases
excretion of dabigatran
less drug interactions
substrate for p-glycoprotein
glucuronide metabolites
use with caution in diminished renal function
aspirin MOA
irrevesible inhibitor of Cox1/2
acetylates enzyme
adverse reactions aspirin
bleeding
GI irritation
GI ulcers
dipyridamole MOA
inhibits phosphodiesterase
increases platelet cAMP levels
used with warfarin
MOA clopidogrel and ticlopidine
prodrugs-metabolized to active thiol metabolite
irreversibly bind ADP P2Y12 R on platelets
inhibits ADP activation of 2b3a
ticlopidine and clopidogrel characteristics
irreversible inhibitors
Ticlo-forms dissulfide link between the drug and SH group on CYS of receptor
Ticlo longer lasting
clipidogrel less side effects
Ticlopidine and clopidogrel side effects
bleeding
agranulocytosis and thrombocytopenia
Thrombocytopenia purpura risk ticlopidine>clopidogrel
cangrelor
reversible P2Y12 receptor inhibitor administer IV (reversed in 1 hr)
abciximab
Ab binds to 2b3a receptor
more effective
longer half life
eptifibatide
peptide derivative
less effective than abciximab
good for unstable angina or angioplasty
contraindications for abciximab and eptifibatide
history of hemorrhagic stroke
surgery in past 6 weeks
thrombocytopenia
cannot use with warfarin
tPA
more rapidly activates plasminogen bound better than in circulation
binds fibrin via lysine binding sites
circulating plasmin inactivation
alpha 2 antiplasmin and PAI-1
streptokinase MOA
binds to plasminogen to form complex
complex converts second molecule of plasminogen to plasmin
adverse effects of streoptokinase
fever
bleeding
lytic state (plasmin exceeds capacity of alpha 2 antiplasmin)
highly antigenic
contraindications of strepotkinase
surgery or trauma in past 10 days
pre-existing bleeing disorder
diastolic >110
intracranial trauma
antistreplase
streptokinase and plasminogen with catalytic site acylated-removed by plasma enzymes
more specific binding to fibrin (less lytic state)
tenecteplase
more specific binding to fibrin than alteplase
more resistant to PAI-1
longer half life
adverse reactions for all thrombolytics
bleeding due to inducing hypocoagulable state
aminocaproic acid
inhibitor of fibrinolysis
lysine analog binds to lysine binding sites on plasminogen and plasmin (inhibits interaction of plasmin and fibrin)
causes of excessive bleeding
increased vessel fragility
platelet deficiency or dysfunction
derangement of coagulation
platelet function analysis
stimulates in vivo conditions
utilizes platelet agonists
prolonged with ADP and Epi-vWD; normal with ADP from aspirin
PTT partial thromboplaastin time
kaolin+cephalin+calcium
test intrinsic and common pathway
PT prothrombin time
tissue thromboplastin+Ca
test extrinsic and common pathway
mixing study
serum and pooled sera
if corrected PTT-factor deficiency
if still abnormal-inhibitor present
clotting factors
specific factor poor plasma and patient plasma
vessel abnormalities
see petechiae and purpura
drug complexes cana cause leukocytoclastic vaculitis
impaired collagen support
scurvy-vitamin C def required for hydroxylation of procollagens
Ehler-Danlos
elderly
cushing-protein wasting
Henoch-Schonlein Purpura
hypersensitivity disease complexes deposit in vessels
colicky abdominal pain, polyarthralgias, AGN
hereditary hemorrhagic telangiectasia
AD
dilated tortuous vessels with thin walls
amyloid infiltation
weakens vessel walls
thrombocytopenia
spontaneous bleeding of small vessels <20k
skin, mucus membranes, GI, GU, intracranial
etiologies of thrombocytopenia
decreased production (bone marrow)
increased peripheral destruction/decreased survival
sequestration
dilutional effect secondary to massive transfusions
neoplastic thrombocytopenia
non-hematopoietic (prostate, breast, neuroblastoma)
hematopoietic-AML, ALL, MDS, lymphoma
non neoplastic causes of thrombocytopenia
infections
drugs
EtOH, toxins
B12/folate deficiency
immune thrombocytopenic purpura
primary-idiopathic autoimmune
secondary-identifiable etiology
chronic-SLE, HIV, viruses (peripheral blood with giant platelets increased MPV)
acute-abrupt onset after viral illness, self limited
chronic ITP
IgG Ab against platelet antigens
removed by spleen but it is normal size
BM-increased megs with left shift
treatment of ITP
immunosuppression with steroids
splenectormy
IVIG
Rituximab CD20 Ab
HIT Type 1
most common
moderate thrombocytopenia
few days of heparin due to platelet aggregation
HIT Type 2
5-14 days after heparin is started
moderate to severe drop in platelets
Ab directed against heparin-platelet factor 4 complex result in direct platelet activation
risk lower with LMW (but cannot give it again)
HIV auto-immune thrombocytopenia
CD4 on surface of megs
results in dysregulation and hyperplasia of B cells
Auto Ab towards GP2b3a
TTP pentad
fever thrombocytopenia microangiopathic hemolytic anemia neurologic sx renal failure
HUS symptoms
thrombocytopenia
microangiopathic hemolytic anemia
acute renal failure
mostly kids
TTP pathogenesis
ADAMTS 13 deficiency
deficiency results in accumulation of HMW multimers can promote platelet microaggregation
presentation of TTP
hyaline thrombi (platelet aggregates) form platelet consumption leads to thrombocytopenia schistocytes and organ dysfunction
treatment of TTP
total plasma exchange to remove auto-Ab
do not give platelet transfusions
HUS presentation
bloody diarrhea and renal failure
associated with E. coli O157H7
treat with supportive care
acquired platelet abnormalities
ASA, NSAID
uremia
congenital platelet abnormaliteis
Bernard Soulier
Glanzmann
storage pool disorders
Bernard Soulier
AR deficient Gp1b
everything works but ristocetin
giant platelets
Glanzmann
AR Gp2b3a
only ristocetin works
clinical findings of clotting abnormalities
prolonged bleeding after laceration, trauma or surgery
bleeding into GI/GU
bleeding into weight bearing joints
von Willebrand Disease
prolonged bleeding from cuts, menorrhagia, mucous membrane bleeding
abnormal PFA and PTT
normal platelet count
subtypes of von Willebrand Disease
type 1-quantitaive AD DDAVP before surgery type 2-qualitative AD defective multimer assembly type 3-quantitative decrease low levels (give humate P)
Hemophilia A
8 cofactor for 9
X linked recessive
symptoms of hemophilia A
easy bruising, massive hemorrhage after surgery/trauma
hemarthrosis
no petechiae and no mucous membrane bleeding
diagnosis of hemophilia A
prolonged PTT
treat with humate P or recombinant factor
symptoms occur in hemophilia A
extrinsic is burst to get cascade moving but intrinsic pathway maintains it
inappropriate fibrinolysis not inhibited
hemophilia B
x linked recessive
deficiency in IX
acquired clotting factor abnormalities
vitamin K deficiency
liver disease
DIC
DIC
pathologic activation of coagulation cascade in microvasculature
DIC tests
prolonged PT, PTT
decreased platelets and decreasing fibrinogen
increased D-dimer
etiologies of DIC
obstetric-placental abruption, retained products of conception, septic aborption
infections-gram negative sepsis and meningococcemia
neoplasms-APL and adenocarcinoma
massive tissue injury
mechanism of DIC
tissue factor released leading to fibrin deposition in microvasculature
endothelial cell injury leads to hemorrhagic diathesis
pathologic findings for DIC
thrombi in brain, heart, lungs, kidney, adrenals, spleen, and liver
micro-infarcts and hemorrhage
Waterhouse-Friederichsen Syndrome
bilateral adrenal hemorrhage associated with meningococcus
Sheehan syndrome
postpartum pituitary necrosis
toxemia of pregnancy
microthrombi in placenta
DIC presentation
microangiopathic hemolytic anemia petechiae and purpura dyspnea convulsions oliguria, acute renal failure circulatory shock
DIC peripheral smear
schistocytes, increase reticulocytes
leukocytosis and neutrophilia, left shift
decrease in platelets
shock
final common pathway for potentially lethal clinical events-massive hemorrhage, extensive trauma and burns, massive MI, massive PE, bacterial sepsis
hypoperfusion and cellular hypoxia result in injury-initially reversible but eventually irreversible
categories of shock
cardiogenic shock hypovolemic shock spetic shock anaphylactic shock neurogenic shock
SIRS
exaggerated and generalized manifestation of a local inflammatory reaction, often fatal
massive inflammatory reaction due to cytokines (TNF, IL1, IL6, PAF)
diagnosis of SIRS
two or more signs of systemic inflammation temp >100.4, <95 HR>90 RR>20 WBC>12k or <4k >10% immature WBC
Sepsis
SIRS with culture-proven infection or obvious infection
Septic shock
clinical sepsis severe enough to lead to organ dysfunction and hypotension
epidemiology of septic shock
mortality rate 20%
number one cause of deaths in ICUs
triggers of septic shock
gram positive bacterial infections
gram negative and fungal infections
pathophysiologic factors of septic shock
inflammatory mediators endothelial cell activation and injury metabolic abnormalities immune suppression organ dysfunction
inflammatory mediators for septic shock
TLR start sepsis
TNF, IL1, IFN gamma, IL12, IL18 creates pro-inflammatory state
prostaglandins and PAF activate endothelial cells, causing adhesion molecule synthesis and pro-coagulant state
complement cascade activated by microbial components
endothelial activation in septic shock
results in thrombosis, increased vascular permeability, vasodilation
thrombosis in septic shock
inflammatory mediators stimulate tissue factor and PAI-1 production
decreased production of tissue factor pathway inhibitor, thrombomodulin and protein C
decreased blood flow producing stasis
increased vascular permeability-third spacing and edema
vasodilation due to increased NO synthesis
metabolic abnormalities in septic shock
hyperglycemia and insulin resistance
cytokines, stress hormones and catecholamines drive gluconeogenesis
pro-inflammatory creates insulin resistance
hyperglycemia decreases neutrophil function
myocardial contractility
weakened by cytokines and secondary mediators decreasing cardiac output
adult respiratory distress syndrome
decreased CO, increased vascular permeability and endothelial injury damage lungs
nonprogressive phage of septic shock
reflex mechanisms compensate and tissue perfusion is maintained (SIRS)
progressive stage
tissue hypoperfusion ensues with worsening circulatory and metabolic imbalances including acidosis
irreversible state
extent of cellular and tissue injury is so great that death is inevitable even with infection control and hemodynamic correction
treatment of septic shock
control infection fluid resuscitation and vasopressor drugs insulin therapy for hyperglycemia corticosteroids anti-inflammatory (not successful) activated protein C (controversial)
ABO grouping
difference is one sugar B-galactose A-N acetyl galactosamine O-no sugar most common is O
universal donor
group O
universal recipient
group AB
Rh+
can give Rh negative to Rh positive
can give Rh positive to Rh negative if patient has no anti-D
15% Rh-
Anti-D can cause
hemolytic disease of newborn
acute hemolytic transfusion reactions
packed red blood cells
increase blood oxygen carrying capacity increase HCT 3% give for symptomatic anemia store 1-6C can only give through IV with normal saline
frozen RBC
frozen in glycerol for 10 yrs
thaw and use within 24 hrs
give for autologous units, rare blood types, IgA def
washed RBC
washed in saline
shelf life 24 hrs
give for IgA def, allergic reactions to plasma proteins
platelets
random or platelet apheresis from single donor
stored at room temp for 5 days
6 pack will raise 30k
indications for platelets
thrombocytopenia (not actively bleeding)
bleeding without thrombocytopenia (aspirin, uremia)
massive transfusion
platelet refractory
does not increase platelets after transfusion
causes-splenomegaly, accelerated consumption from DIC, sepsis, alloimmunization
leukoreduced platelets and PRBC
reduces WBC content
decreases incidence of alloimmunization against WBC antigen, decreased risk of CMV transmission, decreased risk of febrile nonhemolytic transfusion
fresh frozen plasma
within 8 hrs of drawing
1 IU of each coagulation factor per cc/plasma
18C until needed for 1 year
indications-significant bleeding with coagulation deficiency, correction of PTT and PT, TTP, massive transfusion
inappropriate use of fresh frozen plasma
volume expansion
coagulation factor replacement
cryoprecipitate
rich in fibrinogen, vWF, factor 8 and 13
used for fibrinogen replacement
human derived products
factor 8, vWF (humateP), Rhogam, IVIG, 4 Prothrombin complex concentrate (2,7,9,10)
type and screen
blood type and antibody screen
IAT-if positive blood is cross patched
type and cross
type and screen
test donor cells against patient plasma
always protect transfused blood from antibodies in patient
DAT
test patient RBC for attached IgG or compliment
IAT
test patient serum for antibodies
done for TS and TC
positive DAT
hemolytic transfusion reaction
patient antibody on transfused RBC
negative rules out majority of autoimmune anemias and acute hemolytic transfusion reactions
positive IAT
alloantibody against foreign RBC antigens
autoantibody can also sometimes be detected
febrile reactions
acute hemolytic transfusion reaction febrile non-hemolytic transfusion reaction infection TRALI delayed hemolytic transfusion reaction GVHD infection
nonfebrile reactions
anaphylaxis urticaria TACO hypotension iron overload infection
distribution of water
intra extra interstitial intravascular (from high to low)
forces governing movement of fluid in and out of blood vessel
hydrostatic pressure
osmotic or oncotic pressure
increased intravascular oncotic pressure
venous side due to fluid loss due (from hydrostatic pressure)
exudate
protein rich due to increased vascular permeability (inflammatory edema-allows large molecules to leak out of the vessels)
transudate
non-inflammatory edema
protein poor
causes of noninflammatory edema
increased hydrostatic pressure
reduced plasma oncotic/osmotic pressure (hypoproteinemia)
lymphatic obstruction
sodium and water retention
DVT causing edema
increase hydrostatic pressure (localized)
CHF causing edema
systemic edema due to generalized increase in hydrostatic pressure
treat with salt restriction, diuretics, aldo antagonists
edema from reduced plasma oncotic pressure
albumin loss-nephrotic syndrome
reduced albumin syntehsis-liver cirrhosis, protein malnutirtion
loss of fluid from intravascualr space leads to decreased renal perfusion and activation of R/Angio/Aldo
causes of lymphatic obstruction
filariasis-inflammatory and obstructive neoplastic obstruction (peau d'orange appearance of skin from lymphvascular invasion by breast cancer) iatrogenic-axillary dissection
sodium and water retention
increases hydrostatic pressure
decrease vascular osmotic pressure (dilutes proteins)
occurs in acute renal dysfunction
diffuse edema
subq
affects all parts of body (seen in renal failure)
dependent edema
subq
legs of mobile, sacrum of bed-ridden pt
pulmonary edema
left sided heart failure, renal failure, lungs show frothy, blood-tinged fluid
from excess pre-load causing a backup
present with dyspnea, orthopnea, paroxysmal nocturnal dyspnea
causes of cerebral edema
infection
neoplasm
hypertensive crisis (causes transudate)
venous obstruction
effusions
accumulations of fluid in body cavities
hyperemia
active process
increased blood inflow into tissues due to dilation of arterioles (inflammation, blushing, exercise), appears red
congestion
passive process
stagnation of blood in capillaries due to impaired out flow, tissue appears dusky red or bluish
heart failure cells
alveolar spaces contain hemosiderin-laden macrophages
healing of ecchymoses
hemoglobin (red-blue) to bilirubin (blue-green) to hemosiderin (gold-brown)
hypovolemic shock
> 20% loss of blood
infarction color classification
red-hemorrhagic (venous occlusions, tissues with dual circulation)
white-end arterial circulation
liquefactive necrosis
CNS
