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2 - MOD > deck_605135 > Flashcards

deck_605135 Flashcards

1
Q

Why don’t you bleed to death from a minor injury?

A

Blood clotting process stop outflow of blood from damaged vessel.

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2
Q

What does successful haemostasis depend on?

A

vessel wallplateletscoagulation systemfibrinolytic system

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3
Q

Describe the haemostasis process occuring in blood vessels. When is this process more effective?

A

Vessels constrict to limit blood loss (Vascular spasm)– better when vessels are severed completely

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4
Q

Describe the heamostasis process occuring with platelets

A

Platelets adhere to the damaged vesel wall as well as each other (seals break in vessel wall). Initiated by the release of Von Willebrand FactorForms a platelet plug.

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5
Q

What chemicals are released in the platelet release reaction and what do they cause?

A

ADP and thromboxane A2 – platelet aggreagation5HT (seratonin) – causes vasoconstrictionPF3 – important in coagulation

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6
Q

Why is coagulation tightly controlled?

A

Why: very sensitive – 1ml blood can generate thrombin to convert all fibrinogen to fibrin in the body. Need a balance of procoagulant and anticoagulant forces.

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7
Q

How is coagulation controlled?

A

Thrombin inhibitors which positively feedback on factor 5, 8 and 11.e.g. anti-thrombin III*inherited deficiency may lead to thrombosis and thrombophilia

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8
Q

What is fibrinolysis?

A

The breakdown of fibrin, by Plasmin.

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9
Q

How is the process of fibrinolysis manipulated in a clinical setting?

A

Used as clot/thrombus buster– only in serious settings e.g. coronary artery occlusion or if circulation to a limb is occluded.

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10
Q

What properties do vessel walls have and what effect do they have?

A

Have an antithrombotic effect and secretes:– plasminogen activators (prevents fibrinolysis)– prostaglandin and nitric oxide (prevent adhesion and aggregation of platelets)– thrombomodulin (initiates protein C & S – destroy factor 5 and 8)– Antithrombin 3 – inactivate coagulaiton cascade proteins

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11
Q

Define thrombosis

A

Thrombosis is the formation of a solid mass of blood within the circulatory system

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12
Q

What are the three reasons that thrombosis can occur?

A
  1. Abnormality of the vessel wall2. Abnormality of blood flow3. Abnormality of blood components
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13
Q

What are abnormalities of vessel walls?

A

atheromadirect injuryinflammation

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14
Q

What are abnormalities of blood flow?

A

Stagnation and turbulencce

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15
Q

What are abnormalities of blood components?

A

smokers – are hyper coagulablepost-partumpost-op – have increased coagulability

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16
Q

List the characteristic of an arterial thrombi

A

palegranularlines of Zahnlower cell content

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17
Q

List the characteristic of a venous thrombi

A

softgelatinousdeep redhigher cell content

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18
Q

What are the outcomes of thrombi?

A

LysisPropagationOrganisationRecanalisation Embolism

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19
Q

Describe lysis of a thrombus

A

complete dissolution of thrombusfibrinolytic system activebloodflow restored to normalmost likely when thrombi are small

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20
Q

Describe propagation of a thrombus

A

progressive spread of thrombosis through the vascular systemoccurs distally in arteries and proximally in veins– usually widens due to stagnation at inflow vessel which cause an accumulation of RBCs

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21
Q

Describe organisation of a thrombus

A

is a reparative processingrowth of fibroblasts and capillaries (similar to granulation tissue)lumen remains obstructed – scar tissue forms

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22
Q

Describe recanalisation of a thrombus

A

Reforming of channel through obsruction– bloodflow re-established but usually incompletely– one or more channels formed through organising thrombus

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23
Q

Describe embolism of a thrombus

A

part of thrombus breaks off and travels through bloodstream and lodges at distant site

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24
Q

What are the effects of an arterial thrombosis?

A

Ischaemia (thinning of blood supply)Infarction – effects depend upon the site and collateral circulation of the tissuee.g. brain has good collateral circulation, retina does not so blindness occurs

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25
Q

What are the effects of a venous thrombosis?

A

CONGESTION – leads to increased hydrostatic pressure in tissue. When tissue = arterial pressure, OEDEMA occurs. ISCHAEMIA can lead to INFARCTION.

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26
Q

Define embolism. What are the origins of 90% of emboli?

A

Embolism is the blockage of a blood vessel by solid, liquid or gas at a site distant from its origin.>90% of emboli are thrombo-emboli

27
Q

What can an embolism be caused by?

A

air = most common at throat when cutamniotic fluidnitrogen - comes out of solution due to decompression (divers)medical equipment – breaks offtumour cells

28
Q

Where are the main places that thrombi-emboli can form and where do they effect?

A
  1. from systemic veins pass to the lungs = pulmonary emboli2. from the heart pass via the aorta to renal, mesenteric, and other arteries3. from atheromatous carotid arteries pass to the brain4. from atheromatous abdominal aorta pass to arteries of the legs – DVTREMEMBER – what direction is the blood flowing, where did it originate, size of capillaries
29
Q

What are some predisposing factors to DVT?

A

immobility/bed restpost-operativepregnancy and post-partumoral contraceptives – not so much oestrogen nowsevere burns cardiac failuredisseminated cancer

30
Q

What can be done to prevent DVT?

A

high risk patients must be identified and offered prophylaxis (treatment to prevent illness)

31
Q

How can DVT be prevented?

A
  1. heparin sub-cutaneously2. leg compression during surgery3. TED stocking (thrombo-embolitic deterrent)– prevents blood stagnation in legs after surgery – stimulate muscle pumping mechanism
32
Q

How can DVT be treated?

A

intravenous heparinoral warfarin

33
Q

What are the four classes of pulmonary embolism?

A
  1. Massive PE >60% reduction in blood flow. Rapidly fatal2. Major PE - medium sized vessels blocked. SOB, cough and blood stained sputum3. Minor PE - small peripheral pulmonary arteries blocked. Asymptomatic or minor SOB.4. Recurrent minor PEs lead to pulmonary hypertension
34
Q

How can yoy tell that a blood clot in the lungs is a pulmonary embolism and not from post-mortem coagulation?

A

Will be in the shape of the veins it has come from when you remove it from arteries of lungs

35
Q

What shape is a cerebral haemorrhage?

A

Wedge shaped

36
Q

How does fat enter the vascular system to cause an embolism?

A

Enters systemic circulation as it is small and pliable

37
Q

What are the three factors that contribute to a thrombus?– Virchow’s Triad

A

HypercoagulabilityEndothelial InjuryStasis of blood flow

38
Q

What is a deep vein thrombosis?

A

Formation of a blood clot in the legs, which will then travel towards the heart. The thrombus can cause a pulmonary embolus if it travels in the circulation to the lungs.

39
Q

What does heparin do?

A

Heparin is a co-factor for antithrombin III (inhibits some coagulation cascade proteins), so reduces the chance of thrombus formation.

40
Q

What does warfarin do to treat DVT?

A

It prevents the formation of coagulation factors. It inhibits Vitamin K – essential in the formation (via the addition of Gla-residues) of factors II, VII, IX, and X in the clotting cascade.

41
Q

When does a fat embolism occur?

A

Following trauma to bones or lacerations of adipose tissue, so that fragments of fat released from adipocytes enter the circulation

42
Q

What effects can a fat embolism have?

A

Fat droplets will occlude lung capillariesSome pass into the pulmonary veins and enter the systemic circulation – can affect cerebral circulation leading to coma & death. Presentation – SOB and confusion.

43
Q

What conditions increase the risk of a thrombus developing?

A

MIAtrial Fibrillation

44
Q

How does having an MI increase the risk of a thrombus forming?

A

It casues a loss of endocardium which causes the loss of anticoagulant properties being secreted. Also, the dead tissue can’t contract so there will be stagnant blood in the heart.

45
Q

What is a mural thrombus?

A

Thrombus sticks to the vessel wall and decrease the flow of blood through that vessel. They tend to occur in the heart and the aorta (large vessels)

46
Q

How does atrial fibrillation increase the risk of a thrombus forming?

A

AF = dis-coordinated contraction of the atriaIrregular contraction causes thrombus to form due to stagnant blood– Give patients with AF warfarin to minimise risk of clots forming

47
Q

What occurs in a patient whose has overcoagulative blood?

A
  1. Easily bruises2. Pale3. Blood in the urine4. Cerebral bleed – subdural haemorrhage
48
Q

What inhibits fibrinolysis?What activates fibrinolysis?

A

Plasma inhibitorsPlasminogen activators released by the endothelium which produce plasmin. Plasmin degrades fibrin.

49
Q

What normally inhibits the release of plasminogen activators?What is given following an MI to cause fibrinolysis?

A

PAI-1 – plasma inhibitors of the coagulation cascadeStreptokinase – used in plasmin production so causes fibrinolysis and reperfusion

50
Q

Define haematoma

A

n accumulation of blood within soft tissues; it is usually due to traumatic damage to vessels but occasionally follows spontaneous rupture following disease

51
Q

What is haemophilia?What are the two types of haemophilia?What is the treatment for haemophillia?

A

An X-linked disorder of the blood coagulation system meaning that blood clotting is severally limited and slow– Haemophilia A is a factor VIII deficiency– Haemophilia B is a factor X deficiencyTreatment = self-administered factor 8 replacement therapy

52
Q

What does haemophillia cause?

A

Haemorrrhage into main joints, synovial hypertrophy and painMuscle bleeding causes pressure and necrosis of nerves (painful)Can haemorrhage inte the urinary tract

53
Q

What does DIC stand for?What is it?

A

Disseminated Intravascular CoagulationResults from the activation of the coagulation system in small vessels throughout the body

54
Q

What are the main effects of DIC?

A
  • Platelets are consumed –> low platelet count- Thrombi are deposited in small vessels in various organs causing ischaemic changes- Coagulation factors are also consumedCauses dysfunction of major organs, septicaemia and increased risk of serious bleeding as coagulation cannot occur (low platelet and coagulation factors)
55
Q

What is Thrombocytopaenia?

A

The presence of a low level of platelets and can be caused by a number of disease processes (leukaemia, vitamin B12 deficiency)

56
Q

What are the symptoms of thrombocytopaenia?

A

Abnormal bleeding, nosebleeds, and a rash caused by pinpoint pricks called petechiae. COMPLICATIONS = intracranial haemorrhage & gastrointestinal bleedingwhich leads to vomiting blood or blood in the stools.

57
Q

What is thrombophillia?

A

The blood has an increased tendency to clot

58
Q

How do you confirm a diagnosis of DVT?

A

Ultrasound

59
Q

Who usually develops DIC?

A

ICU patients – disease of the severely ill

60
Q

What is the treatment for DIC?

A

Blood transfusionPlasma and platelet transfusion for coagulation factorsTreat the cause/disease in order to restore coagulation

61
Q

What does a low platelet number indicate?What is the name for bruising due to low platelets?

A

ThrombocytopaeniaThrombocytopaenic purpura

62
Q

How can you treat autoimmune thrombocytopaenic purpura?

A

Immunosuppresants e.g. steroids (pregnizalone)Remove the spleen

63
Q

What causes thrombocytopaenia?

A

Failure of platelet productionIncrease in platelet destructionSequestering of platelets– tends to be accompanied by a bone marrow dysfunction (leukaemia)

2 - MOD (18 decks)

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