Thrombosis Embolism and Infarction Flashcards

1
Q

What is a thrombus?

A

A solidification of blood contents that forms in the vascular system during life. (Blood clots at wounds do not count)

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2
Q

Name the three pathological features that lead to the development of a thrombus?

A

Endothelial Injury, Abnormal blood flow and hypercoagulation

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3
Q

Endothelial damage in important formation of thrombi where? and name some examples

A
  • In heart and aorta.
  • Some examples are thrombi developed of the left ventricle at sites of myocardial infarction and on ulcerated plaques in advanced atherosclerosis.
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4
Q

How can the endothelial become damaged?

A
Radiation Injury,
Both endogenous and exogenous chemical agents,
Bacterial toxins/endotoxins,
Immunological Injuries,
Neoplastic involvement (tumours)
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5
Q

Describe the role of platelets after injury to vessel

A
  • Adhesion (to exposed collagen with help of von Williebrand’s factor)
  • Secretion (of granules such as ADP, thromboxane A2 and Pf4 which recruits more platelets)
  • Aggregation (fibrin helps adhesion)
    WBC’s and RBC’s can become trapped in thrombus causing occlusion
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6
Q

Name some disorders that occur with deficiency of GpIIb-IIIa and GpIb

A

GpIIb-IIIa - Glanzmann’s Thromboasthenia
GpIb - Bernard-Soulier Syndrome
Results in inability to form clots

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7
Q

What are the two abnormal types of blood flow and what to they contribute to?

A

Turbulence (blood flow in all directions, not linear) - development of arterial and cardiac thrombi
Stasis (low blood flow) - venous thrombosis

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8
Q

Describe how the turbulence and stasis blood flow contribute to formation of thrombi

A
  • Disrupt laminar flow
  • Prevent dilution of coagulation factors
  • Retard the inflow of inhibitors of clotting factors
  • Promote endothelial cell activation
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9
Q

Define hypercoagulation

A

Alternation of the blood coagulation mechanism that in some way predisposes thrombosis

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10
Q

What is primary hypercoagulation?

A

Its genetic and can be because of;

  • Mutation in factor V gene
  • Antithrombin III deficiency
  • Protein C and S deficiency
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11
Q

What is secondary hypercoagulation?

A

It is acquired and can be;
High risk - Result of bed rest, myocardial infarction, tissue damage, DIC
Lower risk - AF, cardiomyopathy, oral contraceptive, sickle cell anaemia and smoking.

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12
Q

What are the three different morphology of thrombi?

A
Mural thrombi (chambers of heart or aorta),
Arterial Thrombi,
Venous Thrombosis (Phlebothrombosis
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13
Q

Describe some of the features of arterial thrombi

A
  • Usually occlusive, may be mural and are frequently seen (in order of commonality) Coronary, cerebral and femoral. Grey-white
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14
Q

Describe the histological appearance of a thrombus

A

Key - Lamination’s called lines of Zahn. These are pale bands of fibrin and platelets with red bands of RBC’s

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15
Q

Describe some of the features of venous thrombosis (Phlebothrombosis)

A
  • Can be occlusive and are dark red.

- 90% of time effect veins of lower limbs (deep calf, femoral, popliteal and illiac)

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16
Q

What is Thrombophelbitis

A

When a vein becomes very inflamed and then thrombosed

17
Q

Describe the fate of thrombi

A
  • Resolved (using drugs)
  • Embolization to lungs
  • Incorporated into wall, narrowing lumen
  • Organisation and recanalization
18
Q

Describe the clinical appearance of arterial thrombosis

A

Importance - Obstruction and sources of emboli
Presentation - Lose of pulses distal to thrombus, 5P’s (pulseless, perishing cold, pale, painful and parasthesia) and tissue eventually dies and gangrene results

19
Q

Describe the clinical correlations of venous thrombosis

A

Superficial - Congestion, swelling, pain and tenderness but rarely embolise.
Deep - Foot and ankle oedema, Homans’ sign but also could be asymptomatic until it embolised.

20
Q

Describe some of the treatments for thrombosis

A

Prevention - Stockings (squeeze deep veins)
Anticoagulant drugs - Warferin (oral) or Heparin (i.v or s.c). Warfarin takes a day to start working so given as after treatment, heparin used for quick effects.

21
Q

What is an embolus? What percent arise from thrombi?

A

The detachment of intravascular solid, liquid or gaseous mass carried by blood to a site distant from origin. 99% arise from thrombi so unless otherwise stated, it usually means thromboembolism.

22
Q

Rare forms of emboli include fragments of what?

A
Bone/bone marrow
Atheromatous debris
Fat
Bits of tumour
Bubbles of air/nitrogen
23
Q

Describe the classifications of embolism

A
Pulmonary embolism,
Systemic embolism
Amniotic fluid embolism
Air embolism
Fat embolism
24
Q

Describe some of the features of a pulmonary embolism

A

Occlusion of a large/medium pulmonary artery is embolic until proven otherwise. Over 95% of pulmonary emboli arise from thrombi from large deep leg veins.

25
Q

What is a saddle embolus?

A

A large embolism that bifurcation of the main pulmonary artery - causes instant death.

26
Q

Pulmonary embolism results in what?

A

Respiratory compromise and haemodynamic compromise. It is one of the few things that cause instantaneous death.

27
Q

Smaller pulmonary emboli may cause?

A

Acute respiratory and cardiac problems;

Chest pain, dyspnoea (difficulty breathing), shock, increased LDH and haemoptysis (coughing up blood)

28
Q

How can you diagnose pulmonary emboli?

A

X-ray, X-ray with radionucleotides and some occlusion can put strain on the heart which is picked up on ECG

29
Q

Describe some of the features of Systemic Embolism

A
  • Emboli that travels through arterial circulation.
  • 80%ish arise from thrombi within heart
  • Less common sources include ulcerated atherosclerotic plaque and aortic aneurysm etc
  • Most common sites of lodgement are lower extremities (70-75%), brain (10%), viscera and then upper limb
30
Q

Describe some of the features of air embolism

A
  • Presence of bubbles within circulation that obstruct vascular flow and damage tissue (barotrauma)
  • Can occur; In delivery or abortion, performance of a pneumothorax, injury to chest wall or decompression sickness (Caisson disease)
31
Q

Describe some of the features of Caisson disease

A
  • Rapid decompression causes helium and nitrogen to persist and form a gaseous emboli. Effects scuba divers.
    Treatment - Recompression chamber
32
Q

Describe some features of fat embolism

A
  • Small globules of fat in circulation
  • Can occur with long bone fractures and less common soft tissue trauma and burns.
    Pathenogenesis - Mechanical obstruction (microagregates of neutral fat causing occlusion) and chemical injury (free fatty acids released from fat cause toxic injury to endothelium)
33
Q

Describe some of the clinical features of fat embolisms

A

Characterised by; Pulmonary insufficency, neurological symptoms (irritability, restlessness which progresses to delerium and coma) and anaemia and thrombocytopenia.
Symptoms only appear 24-72hrs after injury.

34
Q

Describe some of the features of amniotic fluid embolism

A

Rare complication but cause of maternal mortality. Caused by infusion of amniotic fluid into mother’s circulation.
Patients pulmonary micocirculation at postmortem contains - Epithelial squames, lanugo hair, fat from vernix caseosa and mucin from baby respiratory/GI

35
Q

what is the clinical presentation of amniotic fluid embolism

A

Resp difficulty (deep cyanosis and cardiovascular shock), followed by convulsions and the coma.

36
Q

What is infarction and what are the main causes and some other causes

A

Occlusion of vascular supply to tissue causing cell death. Main causes are thrombosis or embolism (99%). Other causes can be vasospasm, expansion of atheroma, compression of vessel etc

37
Q

What are some of the factors that influence development of an infarct?

A

Nature of vascular supple (kidneys and spleen have single blood supply)
Rate of development of occlusion
Vulnerability to hypoxia (brain can only last 3-4mins without air, where are myocardial cells are up to 30mins)
Oxygen content of blood

38
Q

Describe the different types of infarct

A

Red (haemorrhagic) - venous occlusion
White (anaemic) - arterial occlusions
Septic/bland - collection of bacteria causing blockage of BV.

39
Q

Describe the histology of infarction

A

Ischaemic coagulation necrosis (mins-days)
Inflammatory response (hours-7 days)
Reparative response (1-2 weeks)
Scaring (2weeks-2 months)