Thrombosis, Embolism and Infarction Flashcards
(115 cards)
1
Q
what is thrombosis
A
pathologic formation of intravascular blood clot
2
Q
where can thrombi occur
A
in veins or arteries
3
Q
most commonly thrombi are found in and originate from
A
deep veins of lower extremities (leg)
4
Q
characteristics of thrombi
A
- Lines of Zahn (alternating layers of platelets, fibrin and red blood cells)
- attached to vessel walls
5
Q
what is Virchow’s Triad of formation
A
- Endothelial damage
- Alterations in normal blood flow
- Hypercoagulability
6
Q
Normally, thrombosis is prevented bc
A
- Intact endothelium limits exposure to subendothelial collagen and tissue factor
- Endothelial cells produce prostacyclin and nitric oxide- inhibit vasodilation and platelet aggregation
- Endothelial cells produce substances which inhibit thrombin and coagulation factors
- Secrete tissue plasminogen activator
- Secrete thrombomodulin
7
Q
endothelial damage can be defined as
A
any disturbance in dynamic balance of endothelium can lead to thrombosis
8
Q
physical loss of endothelium leads to
A
- exposure of subendithelial ECM
- aggregation of platelets
- release of TF
- local depletion of prostaglandins and plasminogen activators
9
Q
how does endothelial cell dysfunction disturb balance
A
convert procoagulant factors to anticoagulant effectors
10
Q
name 3 causes of endothelial cell damage
A
- atherosclerosis
- increased homocysteine levels
- vasculitis
11
Q
normal blood flow is
A
laminar - platelets flow centrally in vessel lumen, separated from endothelium by slower moving plasma
12
Q
what can cause alteration in blood flow
A
- turbulence
2. stasis
13
Q
what is turbulence
A
countercurrents and pockets of stasis contribute to arterial and cardiac thrombi
14
Q
what is stasis
A
contributes to venous thrombi (slow moving blood)
15
Q
ulcerated atherosclerotic plaques cause
A
turbulence and exposure to ECM
16
Q
aneurysms cause
A
local stasis
17
Q
myocardial infarctions cause
A
stasis and flow abnormalities
18
Q
mitral valve stenosis cause
A
left atrial dilation
arterial fibrillation and stasis
19
Q
hyperviscosity causes
A
- polycythemia
2. sickle cell anemia
20
Q
what is polycythemia
A
small vessel stasis and increased resistance to blood flow
21
Q
what is sickle cell anemia
A
vascular occlusion
22
Q
other clinical settings for thrombosis
A
- arterial aneurysms in myocardial infarction
- immobilization (causes DVT)
- trauma, surgery, burns associated with reduced physical activity
- cardiac failure
- malignancies associated with tumour-associated tissue thromboplastic release (called migratory trombophlebitis)
23
Q
hypercoagulability/thrombophilia due to increased
A
procoagulation or defective anticoagulation
24
Q
inherited forms of hypercoagulability/thrombophilia
A
- patients present with deep venous thrombosis at young age
- usually veins of leg are involved
25
name 4 inherited hypergoaulable diseases
1. Factor V Mutation/Leiden mutation
2. Prothrombin 20210A
3. Protein C/S deficiency
4. Antithrombin III deficiency
26
Factor V Leiden has a mutated form of factor
V therefore lack cleave site for deactivation by protein C and S
27
Factor V Mutation presents in --% of Caucasians
2-15%
28
Factor V mutation is one of the most common reasons for inherited
hypercoagulation
29
do homozygous and heterozygous pts have an increase risk of thrombosis with a factor V mutation
homozygous
30
what happens in pts with heterozygous genes for factor V mutation
propensity for thrombosis with other acquired risk factors:
- pregnancy
- prolonged best rest
- long airplane flights
31
prothrombin 20210A is what type of mutation
point mutation in prothrombin - increased gene expression
32
prothrombin 20210A increases
thrombin increases chance of thrombosis
33
Protein C/S deficiency decreases
negative feedback on coagulation cascade
34
describe Warfarin skin necrosis
Protein C/S deficiency causes skin thrombosis at onset of warfrin therapy (normally, warfarin causes temporary deficiency of protein C and S in normal individuals)
35
the drug warfarin is given to patients with
thrombosis
36
what is heparin
an anticoagulant
37
mechanism of action of heparin
- given to patients to prevent thrombosis
| - acts by binding and activating antithrombin III
38
what happens to patients with antithrombin III deficiency
heparin is unable to find to antithrombin III and anticoagulation is not achieved
39
pts with antithrombin III deficiency is given ---- insntead
Coumadin
40
Name 2 acquired hypercoaulable states
1. Heparin induced thrombocytopenia
| 2. antiphospholipid antibody syndrome/ lupus anticoagulant syndrome
41
when does heparin induced thrombocytopenia occur
following administration of unfractionated heparin
42
what happens in heparin induced thrombocytopenia
induces antibodies which recognize complexes of heparin and platelet factor 4 on the surface of platelets
43
heparin induced thrombocytopenia can lead to
thrombocytopenia
| prothrombotic state
44
what is used instead of unfractionated heparin
newer low molecular weight fractionated heparins - less incidence of HIT
45
see slide 25
see slide 25
46
clinical presentation of Antiphopholipid Antibody Syndrome/ Lupus Anticoagulant syndrome
- recurrent thrombosis
- repeated miscarriages
- cardiac valve vegetations
- thromboytopenia
- pulmonary embolism
- bowel infarction
- renovascular hypertension
47
mechanism of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome
- auto-antibodies induce a hypercoaguable state mediated by binding to epitopes on prothrombin
- activating platelets and endothelial injury
48
primary form of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome
no autoimmune disorders associated with certain drugs/infections
49
secondary form of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome
associated with lupus
50
aggressive form of antiphospholipid antibody syndrome/ lupus anticoagulant syndrome causes
widespread small vessel thrombi and multiorgan failure
51
antiphospholipid antibody syndrome/ lupus anticoagulant syndrome causes a false positive for
serologic test fr syphillis
52
what are the types of thrombi
1. mural - occur on endocardium; not occlusive
2. arterial
3. venous
4. cardiac
53
arterial and cardiac thrombi develop at sites of
turbulence or endothelial injury
54
venous thrombi develop at sites of
stasis
55
arterial and venous thrombi can both propagate towards
heart - can detach and become emboli
56
DVT occur in what veins
- popliteal
- femoral
- iliac
57
LE DVTs associated with
stasis and hypercoagulable states
58
predisposing factors of DVT
immobilization, congestive heart failure, pregnancy, tumors
59
DVTs can emobolize to
lungs and cause pulmonary infarction
60
pulmonary infarction are asymptomatic in --% cases
50% (develop collateral channels)
61
arterial thrombi may send fragments (emboli) in
systemic circulation
62
which organs are more prone to emboli
organs that get more % of cardiac output
| ex. brain, kidneys, spleen
63
what is disseminated intravascular coagulation (DIC)
-fibrin thrombi in small vessels that cause circulatory insufficiency
64
DIC is a consumptove coagulopathy, meaning
there is reduced platelets, fibrinogen, F-VIII and other consumable clotting factors
65
in what patient type is DIC seen in
- obstetric complications
- advanced malignancy
- shock
66
DIC is caused by
widespread activation of thrombin
67
what organs are affected by DIC
brain, heart, kidneys
68
DIC is initially
thrombotic, then bleeding (after clotting factors used up)
69
what is an embolus
intravascular mass carried away by blood stream to a site remote from its origin
70
emboli may consist of
- blood clots (thromboembolism- most common),
- atherosclerotic plaques (cholesterol clefts seen)
- gas / air
- amniotic fluid
- fat
- bone marrow fragments
- microorganisms
- tumor cells
71
pulmonary embolism due to
thromboemboli
72
name 4 sources of pulmonary thrombi
- Deep saphenous veins
- Periprostatic venous plexus
- Uterine venous plexus
- Right atrium
73
risk factors for pulmonary embolism
- immobility due to recent surgery, injury or obesity
- hereditary states eg. factor V leiden
- oral contracepties
- neoplasms
74
complications of pulmonary embolism
- sudden death (saddle embolus)
- pulmonary infarct
- pulmonary hypertenstion
75
pulmonary infarct
occlusion of large or medium artery obstructed in compromised lung (eg. pneumonia, congestive heart disease)
76
pulmonary hypertension
>60% obstruction by thrombus and with chronic emboli, increases work of R ventricle
77
systemic thromboembolism usually --- emboli
arterial
78
systemic thromboembolism cause
infarction and gangrene
79
80% of systemic thromboembolism arise from --- heart
left heart
80
paradoxical emobli
-emboli gaining access to systemic circulation through heart defects
81
how does air embolisms form
air enters venous circulation
81
how does air embolisms form
air enters venous circulation
82
air enters venous circulation through
- neck wounds
- thoracocentesis
- puncture of major veins during surgical procedures
- hemodialysis
82
air enters venous circulation through
- neck wounds
- thoracocentesis
- puncture of major veins during surgical procedures
- hemodialysis
83
gas bubbles within circulation can coalesce to form
frothy masses obstructing blood flow
83
gas bubbles within circulation can coalesce to form
frothy masses obstructing blood flow
84
decompression sickness affects
deep sea scuba divers
84
decompression sickness affects
deep sea scuba divers
85
how do you treat acute decompression sickness
placing individual in high pressure chamber
85
how do you treat acute decompression sickness
placing individual in high pressure chamber
86
mechanisms of fat embolism
mechanical obstruction of circulation and endothelial damage caused by fatty acids release from embolizing fat globules
86
what is caissons disease
chronic form of decompression sickness
| -persistence of gas emboli in skeletal system causing ischemic necrosis of bone
87
clinical symptoms of amniotic emboli
```
severe dyspnea
cyanosis
hypotensive shock
seizures
coma
```
88
most common risk factors for fat embolism
long bone fracture after accidents or orthopedic procedures
89
clinical consequences of fat embolism
- respiratory failure (tachypnea, dyspnea, tachcardia, petechie)
- neurologic findings (delirium, coma)
90
when do clinical symptoms of fat embolism appear
1-3 days after injury
91
mechanisms of fat embolism
mechanical obstruction of circulation and endothelial damage caused by fatty acids release from embolizing fat globules
92
amniotic fluid emboli
amniotic fluid enters venous circulation through torn veins in pts having difficult labor or immediate postpartum period
93
clinical symptoms of amniotic emboli
```
severe dyspnea
cyanosis
hypotensive shock
seizures
coma
```
94
infarct
localized area of dead cells within an organ
95
white infarcts occur in
arterial occlusions in solid organs with end-arterial circulation (heart, spleen, kidney)
96
which is more damaging: hypoxia or ischemia
ischemia - bc decreased oxygen, nutrients and decreased removal of toxic metabolites
97
causes on infarcts
1. obstruction of vessel
| 2. hyptension
98
septic infarctions
an infarct is converted into an abscess by superimposed infection
99
red (hemorrhagic) infarcts seen with
1. venous occlusions (ovary)
2. loose tissue (lung)
3. dual circulations (lung and small intestine) - blood flows form an unobstructed parallel supply into a necrotic zone
4. sluggish venous outflow
5. blood flow re-established to site of previous arterial occlusion and necrosis (e.g., following angioplasty of an arterial obstruction)
100
white (anemic) infarcts occur in organs with -- blood supply
single (ie. heart, spleen)
101
white infarcts occur in
arterial occlusions in solid organs with end-arterial circulation (heart, spleen, kidney)
102
most infarcts morphologically show
ischemic coagulative necrosis
103
Brain and CNS show what type of infarct
liquefactive necrosis
104
septic infarctions
an infarct is converted into an abscess by superimposed infection
105
--- blood supply helps against infarction
alternate (ex. liver, lung)
106
--- arterial vascular obstruction causes infarction
end (ex. spleen)
107
--- developing occlusions less likely to cause infarction
slow
108
neurons have irreversible damage in -- minutes
3-4
109
myocardial cells damage in -- minutes
20-30
