Hemodynamics and Clotting Flashcards
(213 cards)
1
Q
What does normal hemostasis rely on?
A
maintenance of blood in a fluid, clot free state
induction of rapid and localized hemostatic plug at site of vascular injury
2
Q
What regulates hemostasis?
A
platelets
coagulation cascade
endothelium
3
Q
What is the first event in primary hemostasis?
A
vasoconstriction as a result of endothelin and reflex
4
Q
What steps occur in platelet adhesion?
A
bind to ECM via von Willebrand factor (produced by endothelium)
5
Q
What occurs during platelet activation?
A
shape changes and release secretory granules which recruit more platelets
6
Q
How is secondary hemostasis activated?
A
tissue factor-activates coagulation cascade
thrombin-converts fibrinogen to fibrin
cross-linked fibrin forms permanent plug
7
Q
What are the primary sites for the coagulation cascade to occur?
A
phospholipids on activated platelets, bind Ca (cofactor for cascade)
8
Q
What are the important mediators in platelet aggregation?
A
ADP and thromboxane A2-amplify aggregation forming primary hemostatic plug
thrombin binds to protease activated receptor on platelet membrane causing further aggregation
still reversible
9
Q
What does fibrinogen bind to?
A
GP2b3a for aggregation
10
Q
What moderates the size of clot?
A
fibrinolytic cascade
plasmin cleaves fibrin to fibrin split products
11
Q
What are the anti-thrombotic properties of endothelial cells?
A
PGI2 and NO vasodilators
ADPase inhibits platelet aggregation by breaking down ADP
12
Q
What is the mechanism of action for thrombomodulin?
A
binds thrombin
activates protein C
with protein S inactivates factors 5 and 8
13
Q
What is the mechanism of action for anti-thrombin III?
A
inhibits the activity of thrombin, 10 and 9
14
Q
What is the mechanism of action for tissue factor pathway inhibitor?
A
inhibits the activity of 7 and 10
15
Q
What is the mechanism of action for tissue type plasminogen activator?
A
converts plasminogen to plasmin
plasmin cleaves fibrin, degrading thrombi
16
Q
What are the pro-thrombotic properties of endothelial cells?
A
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
17
Q
What stimulates the synthesis of tissue factor?
A
stimulated by TNF, IL-1, bacterial endotoxins
activates extrinsic coagulation cascade
18
Q
What is Virchow triad?
A
endothelial injury
abnormal blood flow
hypercoagulability
19
Q
What can cause injury to the endothelium?
A
HTN, turbulent flow, bacterial endotoxins
increased procoagulant factors, decreased anti-coagulant effectors
20
Q
What is abnormal blood flow?
A
disruption of laminar flow
turbulence and stasis
turbulence from plaques
stasis from aneurysms, flaccid myocardium post MI, heart chamber dilation, a-fib
21
Q
What are the causes of hypercoagulability?
A
primary-genetic-mutation in factor V, prothrombin, MTHFR (increases homocysteine), deficiencies in antithrombin III, protein C, protein S
22
Q
What is factor 5 Leiden?
A
mutant factor 5 is resistant to cleavage by protein C
Arg to Glu at 506
heterozygotes 5x relative risk, homozygotes 50x relative risk
23
Q
What happens due to a mutation in the prothrombin gene?
A
mutation causes elevated prothrombin levels
3x relative risk of venous thrombosis
24
Q
What happens due to the MTHFR gene?
A
variant in 5,10 methylenetetrahydrofolate reductase
causes modest elevation of homocysteine (inhibits antithrombin III-promotes clotting)
25
What are the secondary hypercoagulability states?
```
prolonged immobilization
MI, a fib, prosthetic cardiac valves
tissue damage
cancer
DIC
heparin-induced thrombocytopenia
antiphospholipid antibody syndrome
```
26
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
27
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
28
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
29
What are lines of Zahn?
pale layers are platelets
darker layers are fibrin and RBCs
more prominent in arterial thrombi
30
Where does a thrombus attach?
underlying heart or vessel wall
31
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)
32
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
33
What are the characteristics of a post-mortem clot?
usually not attached
dependent portion is dark red
supernatant is yellow, gelatinous like chicken fat
34
What are the possible fates of a thrombus?
propagation
embolization
dissolution
organization and recanalization
35
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
36
What is the fate of a superficial venous thrombosis?
rarely embolize
| cause edema distal to obstruction, predispose overlying skin to injury, infection, ulceration
37
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
38
What does a coronary artery thrombosis cause?
MI
39
What does a cerebral artery thrombosis cause?
stroke, TIA
40
What does a femoral artery thrombosis cause?
gangrene
41
What does an atrial mural thrombus cause?
secondary to a-fib or mitral valve stenosis, can embolize
42
What does a ventricular mural thrombus cause?
secondary to MI, cardiomyopathy, can embolize
43
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
44
What causes pulmonary thromboembolisms?
DVT in 90% of cases
| often occurs as multiple emboli, sequentially or shower
45
What is the clinical presentation of massive occlusion of pulmonary circulation?
sudden death, right heart failure (cor pulmonale) or cardiovascular collapse
46
What is the clinical presentation of medium sized arterial occlusion?
hemorrhage but not infarction due to dual circulation
47
What is the clinical presentation of end arteriole occlusions?
infarction
48
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
49
What is a fat embolus?
microscopic fat globules may be found in circulation after fracture of long bones
50
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
51
What is an air embolus?
obstruction of circulation by large or coalesced gas bubbles
sources-neck and chest injuries, obstetric procedures, thoracentesis, hemodialysis
52
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
53
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
54
anticoagulants
inhibit fibrin formation
| heparin, LMW heparin, warfarin, fondaparinux, argatroban, dabigatran
55
antiplatelets
inhibit platelet aggregation
| aspirin, dipyridamole, clopidogrel, ticlopidine, abciximab, eptifidatide
56
thrombolytics
dissolve formed fibrin clots
| streptokinase, alteplase, anistreplase, tenecteplase
57
heparin
porcine unfractioned
| cleaved by endo-D-glucuronidase into various fractions
58
MOA heparin
reversibly binds ATIII
active coagulation factors bind irreversibly to ATIII (Arg-Ser) to prevent fibrin generation
suicide substrate
59
heparin in pregnancy
approved because it does not cross the placenta
60
administration of heparin
injected sc or iv (im contraindicated induce hematoma)
monitor partial thromboplastin
increase lipoprotein lipase activity
61
adverse effects of heparin
```
bleeding
HIT (type I non immune mediated, type II immune mediated based on heparin platelet factor 4 complex)
```
62
reversal of heparin induced bleeding
reverse with plasma, whole blood or protamine
| do not give to NPH insulin or fish allergy for protamine
63
LMW heparin
too small to simultaneously bind ATIII and thrombin
| specific for ATIII inactivation of X (low affinity for thrombin)
64
indications for LMW heparin
unstable angina or STEMI
monitor anti-X activity
65
advantages of LMW heparin
longer half life
outpatient
lower incidence of thrombocytopenia
predictable response
66
fondaparinux
administer iv or sc
| inactivation of factor X
67
MOA warfarin
inhibits synthesis of biologically active vitamin K dependent clotting factors
clotting factors cant bind Ca (2,7,9,10,C,S)
68
time for action of warfarin
5-7 days for generation of coagulation factors incapable of binding Ca
oral administration
69
warfarin monitoring
monitor INR (prothrombin time)
measures extrinsic pathway
goal of 2-3 (2.5-3.5 for heart valve replacement)
70
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)
71
increase warfarin effect
```
aspirin
ketoconazole and erythromycin
cimetidine
ibuprofen
cephalosporins
sulfa/trimeth
```
72
decrease warfarin effect
cholestyramine
rifampin
phenobarbital
cigarette smoking
73
contraindications for warfarin
not in pregnancy
causes nasal hypoplasia in first trimester
CNS, increased fetal death in second and third trimester
74
treatment of excessive bleeding on warfarin
```
whole blood or plasma
viramin K (takes 24 hrs)
```
75
direct thrombin inhibitors
argatroban or dabigatran (oral)
76
argatroban
directly block active site on thrombin
| use for patients with HIT
77
dabigatran
prodrug with affinity for free and fibrin bound thrombin
| converted to active by plasma esterases
78
excretion of dabigatran
less drug interactions
substrate for p-glycoprotein
glucuronide metabolites
use with caution in diminished renal function
79
aspirin MOA
irrevesible inhibitor of Cox1/2
| acetylates enzyme
80
adverse reactions aspirin
bleeding
GI irritation
GI ulcers
81
dipyridamole MOA
inhibits phosphodiesterase
increases platelet cAMP levels
used with warfarin
82
MOA clopidogrel and ticlopidine
prodrugs-metabolized to active thiol metabolite
irreversibly bind ADP P2Y12 R on platelets
inhibits ADP activation of 2b3a
83
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
84
Ticlopidine and clopidogrel side effects
bleeding
agranulocytosis and thrombocytopenia
Thrombocytopenia purpura risk ticlopidine>clopidogrel
85
cangrelor
```
reversible P2Y12 receptor inhibitor
administer IV (reversed in 1 hr)
```
86
abciximab
Ab binds to 2b3a receptor
more effective
longer half life
87
eptifibatide
peptide derivative
less effective than abciximab
good for unstable angina or angioplasty
88
contraindications for abciximab and eptifibatide
history of hemorrhagic stroke
surgery in past 6 weeks
thrombocytopenia
cannot use with warfarin
89
tPA
more rapidly activates plasminogen bound better than in circulation
binds fibrin via lysine binding sites
90
circulating plasmin inactivation
alpha 2 antiplasmin and PAI-1
91
streptokinase MOA
binds to plasminogen to form complex
| complex converts second molecule of plasminogen to plasmin
92
adverse effects of streoptokinase
fever
bleeding
lytic state (plasmin exceeds capacity of alpha 2 antiplasmin)
highly antigenic
93
contraindications of strepotkinase
surgery or trauma in past 10 days
pre-existing bleeing disorder
diastolic >110
intracranial trauma
94
antistreplase
streptokinase and plasminogen with catalytic site acylated-removed by plasma enzymes
more specific binding to fibrin (less lytic state)
95
tenecteplase
more specific binding to fibrin than alteplase
more resistant to PAI-1
longer half life
96
adverse reactions for all thrombolytics
bleeding due to inducing hypocoagulable state
97
aminocaproic acid
inhibitor of fibrinolysis
| lysine analog binds to lysine binding sites on plasminogen and plasmin (inhibits interaction of plasmin and fibrin)
98
causes of excessive bleeding
increased vessel fragility
platelet deficiency or dysfunction
derangement of coagulation
99
platelet function analysis
stimulates in vivo conditions
utilizes platelet agonists
prolonged with ADP and Epi-vWD; normal with ADP from aspirin
100
PTT partial thromboplaastin time
kaolin+cephalin+calcium
| test intrinsic and common pathway
101
PT prothrombin time
tissue thromboplastin+Ca
| test extrinsic and common pathway
102
mixing study
serum and pooled sera
if corrected PTT-factor deficiency
if still abnormal-inhibitor present
103
clotting factors
specific factor poor plasma and patient plasma
104
vessel abnormalities
see petechiae and purpura
| drug complexes cana cause leukocytoclastic vaculitis
105
impaired collagen support
scurvy-vitamin C def required for hydroxylation of procollagens
Ehler-Danlos
elderly
cushing-protein wasting
106
Henoch-Schonlein Purpura
hypersensitivity disease complexes deposit in vessels
| colicky abdominal pain, polyarthralgias, AGN
107
hereditary hemorrhagic telangiectasia
AD
| dilated tortuous vessels with thin walls
108
amyloid infiltation
weakens vessel walls
109
thrombocytopenia
spontaneous bleeding of small vessels <20k
| skin, mucus membranes, GI, GU, intracranial
110
etiologies of thrombocytopenia
decreased production (bone marrow)
increased peripheral destruction/decreased survival
sequestration
dilutional effect secondary to massive transfusions
111
neoplastic thrombocytopenia
non-hematopoietic (prostate, breast, neuroblastoma)
| hematopoietic-AML, ALL, MDS, lymphoma
112
non neoplastic causes of thrombocytopenia
infections
drugs
EtOH, toxins
B12/folate deficiency
113
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
114
chronic ITP
IgG Ab against platelet antigens
removed by spleen but it is normal size
BM-increased megs with left shift
115
treatment of ITP
immunosuppression with steroids
splenectormy
IVIG
Rituximab CD20 Ab
116
HIT Type 1
most common
moderate thrombocytopenia
few days of heparin due to platelet aggregation
117
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)
118
HIV auto-immune thrombocytopenia
CD4 on surface of megs
results in dysregulation and hyperplasia of B cells
Auto Ab towards GP2b3a
119
TTP pentad
```
fever
thrombocytopenia
microangiopathic hemolytic anemia
neurologic sx
renal failure
```
120
HUS symptoms
thrombocytopenia
microangiopathic hemolytic anemia
acute renal failure
mostly kids
121
TTP pathogenesis
ADAMTS 13 deficiency
| deficiency results in accumulation of HMW multimers can promote platelet microaggregation
122
presentation of TTP
```
hyaline thrombi (platelet aggregates) form
platelet consumption leads to thrombocytopenia
schistocytes and organ dysfunction
```
123
treatment of TTP
total plasma exchange to remove auto-Ab
| do not give platelet transfusions
124
HUS presentation
bloody diarrhea and renal failure
associated with E. coli O157H7
treat with supportive care
125
acquired platelet abnormalities
ASA, NSAID
| uremia
126
congenital platelet abnormaliteis
Bernard Soulier
Glanzmann
storage pool disorders
127
Bernard Soulier
AR deficient Gp1b
everything works but ristocetin
giant platelets
128
Glanzmann
AR Gp2b3a
| only ristocetin works
129
clinical findings of clotting abnormalities
prolonged bleeding after laceration, trauma or surgery
bleeding into GI/GU
bleeding into weight bearing joints
130
von Willebrand Disease
prolonged bleeding from cuts, menorrhagia, mucous membrane bleeding
abnormal PFA and PTT
normal platelet count
131
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)
```
132
Hemophilia A
8 cofactor for 9
| X linked recessive
133
symptoms of hemophilia A
easy bruising, massive hemorrhage after surgery/trauma
hemarthrosis
no petechiae and no mucous membrane bleeding
134
diagnosis of hemophilia A
prolonged PTT
| treat with humate P or recombinant factor
135
symptoms occur in hemophilia A
extrinsic is burst to get cascade moving but intrinsic pathway maintains it
inappropriate fibrinolysis not inhibited
136
hemophilia B
x linked recessive
| deficiency in IX
137
acquired clotting factor abnormalities
vitamin K deficiency
liver disease
DIC
138
DIC
pathologic activation of coagulation cascade in microvasculature
139
DIC tests
prolonged PT, PTT
decreased platelets and decreasing fibrinogen
increased D-dimer
140
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
141
mechanism of DIC
tissue factor released leading to fibrin deposition in microvasculature
endothelial cell injury leads to hemorrhagic diathesis
142
pathologic findings for DIC
thrombi in brain, heart, lungs, kidney, adrenals, spleen, and liver
micro-infarcts and hemorrhage
143
Waterhouse-Friederichsen Syndrome
bilateral adrenal hemorrhage associated with meningococcus
144
Sheehan syndrome
postpartum pituitary necrosis
145
toxemia of pregnancy
microthrombi in placenta
146
DIC presentation
```
microangiopathic hemolytic anemia
petechiae and purpura
dyspnea
convulsions
oliguria, acute renal failure
circulatory shock
```
147
DIC peripheral smear
schistocytes, increase reticulocytes
leukocytosis and neutrophilia, left shift
decrease in platelets
148
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
149
categories of shock
```
cardiogenic shock
hypovolemic shock
spetic shock
anaphylactic shock
neurogenic shock
```
150
SIRS
exaggerated and generalized manifestation of a local inflammatory reaction, often fatal
massive inflammatory reaction due to cytokines (TNF, IL1, IL6, PAF)
151
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
```
152
Sepsis
SIRS with culture-proven infection or obvious infection
153
Septic shock
clinical sepsis severe enough to lead to organ dysfunction and hypotension
154
epidemiology of septic shock
mortality rate 20%
| number one cause of deaths in ICUs
155
triggers of septic shock
gram positive bacterial infections
| gram negative and fungal infections
156
pathophysiologic factors of septic shock
```
inflammatory mediators
endothelial cell activation and injury
metabolic abnormalities
immune suppression
organ dysfunction
```
157
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
158
endothelial activation in septic shock
results in thrombosis, increased vascular permeability, vasodilation
159
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
160
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
161
myocardial contractility
weakened by cytokines and secondary mediators decreasing cardiac output
162
adult respiratory distress syndrome
decreased CO, increased vascular permeability and endothelial injury damage lungs
163
nonprogressive phage of septic shock
reflex mechanisms compensate and tissue perfusion is maintained (SIRS)
164
progressive stage
tissue hypoperfusion ensues with worsening circulatory and metabolic imbalances including acidosis
165
irreversible state
extent of cellular and tissue injury is so great that death is inevitable even with infection control and hemodynamic correction
166
treatment of septic shock
```
control infection
fluid resuscitation and vasopressor drugs
insulin therapy for hyperglycemia
corticosteroids
anti-inflammatory (not successful)
activated protein C (controversial)
```
167
ABO grouping
```
difference is one sugar
B-galactose
A-N acetyl galactosamine
O-no sugar
most common is O
```
168
universal donor
group O
169
universal recipient
group AB
170
Rh+
can give Rh negative to Rh positive
can give Rh positive to Rh negative if patient has no anti-D
15% Rh-
171
Anti-D can cause
hemolytic disease of newborn
| acute hemolytic transfusion reactions
172
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
```
173
frozen RBC
frozen in glycerol for 10 yrs
thaw and use within 24 hrs
give for autologous units, rare blood types, IgA def
174
washed RBC
washed in saline
shelf life 24 hrs
give for IgA def, allergic reactions to plasma proteins
175
platelets
random or platelet apheresis from single donor
stored at room temp for 5 days
6 pack will raise 30k
176
indications for platelets
thrombocytopenia (not actively bleeding)
bleeding without thrombocytopenia (aspirin, uremia)
massive transfusion
177
platelet refractory
does not increase platelets after transfusion
| causes-splenomegaly, accelerated consumption from DIC, sepsis, alloimmunization
178
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
179
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
180
inappropriate use of fresh frozen plasma
volume expansion
| coagulation factor replacement
181
cryoprecipitate
rich in fibrinogen, vWF, factor 8 and 13
| used for fibrinogen replacement
182
human derived products
factor 8, vWF (humateP), Rhogam, IVIG, 4 Prothrombin complex concentrate (2,7,9,10)
183
type and screen
blood type and antibody screen
| IAT-if positive blood is cross patched
184
type and cross
type and screen
test donor cells against patient plasma
always protect transfused blood from antibodies in patient
185
DAT
test patient RBC for attached IgG or compliment
186
IAT
test patient serum for antibodies
| done for TS and TC
187
positive DAT
hemolytic transfusion reaction
patient antibody on transfused RBC
negative rules out majority of autoimmune anemias and acute hemolytic transfusion reactions
188
positive IAT
alloantibody against foreign RBC antigens
| autoantibody can also sometimes be detected
189
febrile reactions
```
acute hemolytic transfusion reaction
febrile non-hemolytic transfusion reaction
infection
TRALI
delayed hemolytic transfusion reaction
GVHD
infection
```
190
nonfebrile reactions
```
anaphylaxis
urticaria
TACO
hypotension
iron overload
infection
```
191
distribution of water
```
intra
extra
interstitial
intravascular
(from high to low)
```
192
forces governing movement of fluid in and out of blood vessel
hydrostatic pressure
| osmotic or oncotic pressure
193
increased intravascular oncotic pressure
venous side due to fluid loss due (from hydrostatic pressure)
194
exudate
protein rich due to increased vascular permeability (inflammatory edema-allows large molecules to leak out of the vessels)
195
transudate
non-inflammatory edema
| protein poor
196
causes of noninflammatory edema
increased hydrostatic pressure
reduced plasma oncotic/osmotic pressure (hypoproteinemia)
lymphatic obstruction
sodium and water retention
197
DVT causing edema
increase hydrostatic pressure (localized)
198
CHF causing edema
systemic edema due to generalized increase in hydrostatic pressure
treat with salt restriction, diuretics, aldo antagonists
199
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
200
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
```
201
sodium and water retention
increases hydrostatic pressure
decrease vascular osmotic pressure (dilutes proteins)
occurs in acute renal dysfunction
202
diffuse edema
subq
| affects all parts of body (seen in renal failure)
203
dependent edema
subq
| legs of mobile, sacrum of bed-ridden pt
204
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
205
causes of cerebral edema
infection
neoplasm
hypertensive crisis (causes transudate)
venous obstruction
206
effusions
accumulations of fluid in body cavities
207
hyperemia
active process
| increased blood inflow into tissues due to dilation of arterioles (inflammation, blushing, exercise), appears red
208
congestion
passive process
| stagnation of blood in capillaries due to impaired out flow, tissue appears dusky red or bluish
209
heart failure cells
alveolar spaces contain hemosiderin-laden macrophages
210
healing of ecchymoses
hemoglobin (red-blue) to bilirubin (blue-green) to hemosiderin (gold-brown)
211
hypovolemic shock
>20% loss of blood
212
infarction color classification
red-hemorrhagic (venous occlusions, tissues with dual circulation)
white-end arterial circulation
213
liquefactive necrosis
CNS
