thrombosis embolism Flashcards
- A thrombus is an aggregate of — blood containing —, — and — blood cells that occurs in — blood, i.e. a blood clot within a blood vessel.
- A thrombus is adherent to the — but can —
- sites of thrombus formation:
coagulated blood
platelet fibrin and red blood cells
flowing
vascular endothelium
separate
sites:
* Arteries
* Veins
* Heart
* Capillaries
THROMBUS AETIOLOGY
* Virchow, a German Pathologist, described the factors which predispose to thrombosis. These are known as Virchow’s triad:
1. — damage
2. Abnormal — (stasis/turbulence)
3. —
- the causes and consequences of thrombosis are often different in — and —
endothelial damage
blood flow
hypercoagulability
arteries n veins
1- endothelial damage:
* Normal endothelial cells produce substances that — thrombi formation. These substances prevent — inhibit — and encourage —
* When the endothelial cell is damaged, vessels are —
- endothelial damage prothrombotic:
Normal Cell
* — ( — inhibitor)
* — ( — )
* — activator
* NO
Damaged Cell
* — factor
* — – inhibitors
* Platelets produce — , which causes further platelet —
- different mechanism in:
reduce
platelt aggregation
coagulation
encourages fibrinolysis
prothrombotic
prostacyclin ( platelt inhibitor )
theombodulin ( antithrombin )
plasminogen activator
NO
platelt aggregating factor
plasminogen activator inhibtirs
thromboxane
aggregation
arteries , veins , heart
endothelial damage mainly affects —
- causes:
* Ulcerated — in atherosclerotic arteries
* —
* Endothelial — due to —- stresses
of – or — flow over scarred valves
* — may initiate endothelial injury
arteries
plaque
vasculrties
dysfunction
haemodynamic
hypertension
turbulent flow
ciggeratte smoke
2- abnormal blood flow:
* Normal blood flow –
* Platelets flow — in the vessel lumen
* Abnormal blood flow is —:
1. Disrupts – flow and bring platelets into contact with the –
2. Prevents — of activated clotting factors by – flowing blood
3. — inflow of clotting factor inhibitors and permits the — of thrombi
4. Promotes — activation
causes:
* Arterial and Venous not the same
* — mainly in —
* — mainly in
1- abnormal blood flow turbulence of artries n heart:
* — injury or —
* Counter-currents and local pockets of stasis, e.g.
— atherosclerotic plaques
—
Sites of arterial –
* These cause arterial and cardiac –
2- abornmal blood flow more commonly veins:
* – venous thrombi
* General:
Prolonged — in bed
— Failure
—
* Local:
— pressure
–
Eddy –
lamiar
centrally
prothromobotic
laminar flow
endothelium
dilution
fresh
slows
build ip
endothelial cells
turbulence in artries
stasis in veins
endothelial injury or dysfunction
ulcerated
aneurysm
bifurcation
thrombosis
stasis
immobilisation
heart failure
shock
external
aneurysm
eddy currents
3- increased coagulability:
* Alteration of the coagulation pathways that predispose
to thrombosis (“ —- ”)
* The causes may be inherited (genetic) or acquired
1- inherited ( primary ) as:
- factor v leiden mutation
- prothrombin gene mutation
- antithrombin deficneyc
- protein c definceyc
- protein s deficiency
2- acquired (2ndary)
- tissue damage as surgery fractures burn
- cancer
- DIC
- anti phospholipid syndrome
- High oestrogen states (e.g. pregnancy, combined oral contraceptive pill, hormone replacement therapy)
- Nephrotic Syndrome
-Myeloproliferative disorders (e.g.
polycythaemia vera)
-Paroxysmal nocturnal haemoglobinuria
(PNH)
thrombophilias
what are the clinical consequences:
* Arterial thrombi : — / — and— into other arteries/arterioles
* Venous Thrombi – — into venous side of circulation e.g. pulmonary arteries → lungs → –
summary :
* Causes of Thrombosis different in arteries and veins
Arteries: Atherosclerotic — , — , — , — , counter —
Veins: — , –
ishcaemia / infraction
emboli
emboli
infraction
-plaque , turbulence stasis hypertension and counter currents
- stasis and hpercoagubiltiy
fate of thrombus:
1. — : enlarges leading to vessel obstruction
2. — : dislodges, travelling to a different site
3. — : degraded by fibrinolytic system
4. — and — of blood vessels
summary of clinical effects of arterial thrombosis:
* — (Definition: Injury or death of tissue resulting from inadequate blood supply, especially as a result of obstruction of the
local circulation by a thrombus or embolus)
Myocardial infarction
Cerebral infarction
Acute limb ischaemia
* Embolise peripherally through — → –
Brain, kidneys, spleen
- summary of venous thrombosis and the obstruction of the vein :
* Localised:
May be —
— , —
If sudden and extensive, may cause — and —
* Distant
— embolism
—- embolism, e.g. stroke
(paradoxical embolus, rare)
propagation
embolism
dissolution
organisation ad recanelisation
infractions
arteries —> infracts
asymptomatic
odema n pain
necrosis n gangrene
pulmonary
systemic
1- thrombosis - capillaries ( small print) :
* —
* —
* Thrombotic — (e.g. DIC, TTP, HUS)
* — crisis
* Capillary thrombosis causes — and sometimes —
2- covid associated coagulopathy:
* Clinically Disseminated Intravascular Coagulation picture- D dimers
elevated: renal, cardiac, CNS symptoms stroke, DVT, Pulmonary emboli
* Autopsy- platelet-rich micro thrombi in lung, kidneys, heart, CNS, liver-
large vessel thrombosis, pulmonary arteries
* Why? Unknown- ?cytokine storm endothelial cell damage-Role of RA
System, Virus bind to ACE2 enzyme reduced angiotensin 1-7
* Rarely seen now with less pathogenic variants & a vaccinated
population
frost bites
burns
micro angiopathies
sickle cell
necrosis , ulceration
thrombosis - cardiac thrombi:
* Mural thrombus post —
* Thrombotic vegetation’s on cardiac valves in —
* In the left atrium, especially atrial appendix, in —
- consequences:
* Thrombi in the heart are a source of — emboli e.g.—
myocardial infractions
infective endocarditis
artial fibirllation
systemic
stroke
- An embolus is a detached — — mass that arises from one part of the — and travels to another part of the circulation
- types:
Thrombi ( — )
May be pulmonary or systemic
—
Air or gas
Fat
– fluid
— bodies
Tumour
intravasular physical mass
pulmonary and systemic
thrombolisem
septic
amniotic
forgein
( can be solid liquid or gas)
pulmonary embolism:
* Arise mainly in the — of the – limbs, but occasionally can arise in the – side of the –
* Part of a — detaches and is carried in the circulation along the inferior vena cava through the right side of the heart and lodges in the pulmonary circulation
* Pulmonary emboli are a –
- diagnosis:
* Clinical assessment
* —:
– non specific
– Needs to be used in conjunction with a clinical risk predication
model (e.g. the — criteria)
* CT Pulmonary Angiogram (CT-PA)
* Ventilation Perfusion (V/Q) scan
deep vein
lower
right
heart
venous thrombus
medical emergency
d dimers
wells
pulmonary embolism ESC classification :
* Most useful to classify based on — — risk (ESC criteria):
* High Risk– — instability
* — Risk– Evidence of right ventricle dysfunction
– — – Imaging* and biochemical**
– — – Imaging or biochemical
* – Risk– No evidence RV dysfunction and low clinical – score
(e.g. PESI)
*Imaging = CT-PA and/or Echocardiogram
**Biochemical = Raised Troponin and/or NT-proBNP
- pulmonary complications:
* Cardiogenic Shock
* Death
* Pulmonary Infarction
* Recurrent PE
* Chronic Thromboembolic Pulmonary
Hypertension (CTEPH)
* Chronic dyspnoea
* Anxiety / Depression
early mortality risk
haemodyamic
intermediate risk
intermediate high
intermediate low
low risk
1- rare evet paradoxixal emboli:
* Rarely, an embolus may pass through an – or — defect to gain access to the – circulation (paradoxical embolism).
2- systemic emboli:
* The majority of systemic emboli arise in the – side of the – , some in the aorta (e.g. abdominal aneurysm)
or in the carotids
* They may lodge anywhere in the systemic circulation
(brain, lower limbs, intestine, kidneys or spleen)
* What are the consequences of this?
* — or – e.g. – in brain
iterartial or intraventicular
systemic
left side of the heart
ischaemia or infraction as stroke
3- gas / air embolism:
* Damage to the — of the – and —
* During — , the – pressure from the – is transmitted to the head and neck veins. If these veins are cut, air is – in during inspiration
* Lots of air required to be significant – mls
* – mass – obstruct – flow
- decompression sickness:
* When the body is subjected to — pressure, as occurs in – divers, increased amounts of – go into solution in the blood and
body fluids
* If the pressure is reduced rapidly, bubbles of — form
— : – within skeletal muscles and joints
— : – oedema and haemorrhages in lungs causing respiratory
distress
— : of different tissues, esp brain
veins pf head n neck
inspiration
-ve
thyroid?
sucked in
100 mls
frothy
vascular
high pressure in deep sea
nitrogen
bubbles of nitoroge
Bends
chocks
ishcaemia
4- fat embolism ( rare) :
* Fat embolism occurs when — of fat get into the circulation
* It is a — embolism
* Follows – of long bones, which contain —
When the bone is fractured, blood vessels in marrow are — and — leaks into the –
Signs and Symptoms:
Dyspnoea and cyanosis (– hours)
Mental —- , — , convulsions ( — hours)
Petechial — around the neck and the front of the chest — )
* Mortality rate is about 30%
tiny globules
liquid micro
fractures
fatty marrow
torn
blood
24 hours
confusion n uncosnituosuness 24-48
haemorrhage
2-3 days
other emboli :
* — embolism – this allows tumours spread/metastasis
* – emboli – clusters of micro organisms spread via the blood
stream causing distant abscesses or septicaemia
* — embolism - fragments of catheters may become dislodged during cardiac catheterisation or intravenous therapy
* – embolism – extremely rare
tumour
septic
forge in body
amniotic fluid.
( check the questions from last slides)
