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Semester 2 Case Studies > Case 8 > Flashcards

Case 8 Flashcards

1
Q

what are the two clotting pathways

A

internal and external

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2
Q

what are risk factors for a DVT

A 
alteration in the blood flow 
immobilisation 
obesity 
pregnancy 
cancer
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3
Q

what are hyper coagulable states

A
  1. OCP (oestrogen containing)
  2. Genetic thrombophilia
    • factor V lieden deficiency
    • Portein S and C deficency
    • antithrombin deficiency
  3. acquired thrombophilia
    • antiphospholipid syndrome
    • nephrotic syndrome
    • paroxysmal nocturnal haemogloburnia
    • cancer/preganacy
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4
Q

blood flow from leg back to heart

A

popliteal veins

greater saphenous vein

femoral vein

inferior vena cava

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5
Q

what is the normal value of the alveolar arterial oxygen gradient

A

normal =2 for <40 but increases with age

A-a gradient = 3.9 (1.6)

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6
Q

What is PERC

A

pulmonary embolism rule out criteria

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7
Q

what is the criteria in PERC

A
  • age>50
  • HR>100
  • SaO2 on room air >95%
  • unilateral leg swelling
  • haemophysis
  • recent trauma or surgery
  • prior DVT or PE
  • hormone use - oestrogen hormone
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8
Q

NICE guidelines for a suspected DVT

A
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9
Q

NICE guidelines for PE

A
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10
Q

what do lungs that are not perfused but still ventilated look like

A
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11
Q

What is CTPA

A

computerised tomography pulmonary angiogram

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12
Q

what is a perfusion scan called

A

a Q scan

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13
Q

ECG examples of a PE and DVT

A
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14
Q

Confirmed PE therapies

A
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15
Q

why is option C there

A

because all heparins are made from pork and therefore not suitable for vegetarians and muslims

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16
Q

what is thrombosis

A

the formation of a solid or semi-solid mass from the constituents of the blood while moving within the vascular system during life

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17
Q

what is an embolism

A

the transport of abnormal material by the blood stream and its impact on a blood vessel

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18
Q

what is a clot

A

a solid mass formed from the constituents of the blood that no longer moves

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19
Q

where may thrombi form in the heart

A

the lumen of the heart

echocardiogram shows thrombi attached to walls of left ventricle after MI

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20
Q

What can an arterial thrombi cause

A

ischaemia and embolism to the leg

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21
Q

what are the lines of Zahn in veins

A

alternating laters of platelets and erythrocytes

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22
Q

what is virchows triad

A

factors that promote thrombosis

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23
Q

what are the three constituents of VT

A
  1. abnormalities to the vessel wall
  2. abnormalities of the blood flow
    3, abnormalities of the blood constituents
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24
Q

what causes abnormalities of the vessel wall in arteries

A

atheroma
inflammation
atherosclerotic plague

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25
Q

what causes abnormalities of the vessel wall in the heart

A

myocardial infarction - scarring and sites of immobility

rheumatic endocarditis

contribution of breakdown of dead muscle

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26
Q

what causes abnormalities of the vessel wall in the veins

A

trauma
inflammation
chemicals

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27
Q

what chemicals can disrupt the vessel wall in veins

A

scelerosants: irritant substances injected to induce thrombophlebitis and hence obliterate varicose veins
glucose: atheroma in diabetes mellitus

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28
Q

abnormalities of blood flow in the arteries

A

turbulence

aneurysms, plaques and spasm

(aneurysms are filled with thrombus)

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29
Q

What are abnormalities of blood flow in the heart

A

arterial fibrillation - becomes dilated and flow is limited

aneurysms

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30
Q

what causes abnormalities of blood flow in veins

A
  • compression from plaster casts
  • inactivity, postoperative bed rest
  • economy class syndrome from airplanes
  • heart failure
  • circulatory shock
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31
Q

abnormalities of blood constituents

A
  • increased viscosity
  • polycythemia
    • dehydration
    • chronic hypoxia
    • polycythemia ruba vera
  • hyperproteinaemia
    • multiple myeloma (tumour is plasma cells in bone marrow with accumulation of immunoglobulins in plasma)
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32
Q

abnormalities in clotting

A
  • pregnancy (mother does not bleed when placenta detaches)
  • some contraceptive pills
  • following trauma
  • thrombocythemia
  • tumours
  • inherited
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33
Q

most common fate of thrombi

A

resolution - fibrinolysis

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34
Q

what is the organisation fate of thrombi

A
  • incorporation into a scar by macrophages and fibroblasts. vessel lumen remains narrowed or occulded
  • intimal cell proliferation, capillary invasion and recanlisation which may restore patency
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35
Q

what is the detachment fate of thrombi

A

thromboembolism

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36
Q

what is a fat emboli

A

patients with multiple bone fractures get a fat emboli in pulmonary alveolar capillaries

petechial haemorrhages in the brain die to fat emboli following bone fracutres

when fat enters the blood stream

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37
Q

what is a gas emboli due to

A
  • infusions
  • vascular surgery
  • Caisson disease: on ascending too rapidly bubbles of N2 form in the blood stream and cause the pain known as ‘the bends’ - divers
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38
Q

what are the pathological consequences of pulmonary embolism

A 
nothing 
pain that is often pleuritic 
haemoptysis 
breathlessness 
right sided heart failure 
pulmonary hypertension
sudden death
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39
Q

What are the 5 main components of haemostasis

A
  1. blood vessels - vascular spasm
  2. platelets - platelet plug formation
  3. coagulation factors - coagulation phase
  4. coagulation inhibitors - coagulation phase
  5. fibrinolysis - breakdown of the clot
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40
Q

what is secreted to prevent thrombus formation

A
  • nitric oxide - vasodilator and inhibits platelet activation and aggregation
  • endothelia - vasoconstrictor
  • prostacyclin - inhibits platelet activation
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41
Q

what is expressed to prevent thrombus formation

A
  • heparin sulfate - activates antithrombin

- thrombomodulin - changes thrombin affinity from pro clotting to anticoagulant factors

42
Q

vessel injury diagram

A
43
Q

what is the most immediate protection against blood loss

A

vasoconstriction

44
Q

how long do effects of vasoconstriction last for as first defence

A

few seconds - minute

45
Q

what is a chemical vasoconstrictor

A

serotonin - activated platelets release chemical vasoconstrictors for example serotonin

46
Q

where are platelets produced

A

in the bone marrow

47
Q

what are platelets fragments of

A

megakaryocytic cytoplasm

48
Q

how many platelets can 1 megakaryocyte produce

A

4000 platelets

49
Q

how large are platelets

A

2-4um

50
Q

what is production of platelets stimulated by

A

thrombopoietin

51
Q

where is thrombopoietin produced

A

in the liver

52
Q

what does thrombopoetien do

A

helps to control platelet numbers

53
Q

what is the lifespan of platelets

A

8-9 days

54
Q

how long does platelet production take

A

around 7 days

55
Q

how many times a year can you donate platelets

A

24 times a year

56
Q

diagram on platelet production

A
57
Q

what is the ratio of RBC:PLATELETS:WBC

A

700:40:1

58
Q

platelet plug formation

A
  1. normal platelets flowing in blood
  2. platelets adhere to damaged endothelium and undergo activation
  3. aggregation of platelets into a thrombus
59
Q

what is in the cytoplasm of an activated platelet

A
  1. contractile proteins: actin and myosin and thrombosthenin
  2. residuals of both the endoplasmic reticulum and the Golgi apparatus that synthesis various enzymes and especially store large quantities of calcium ions
  3. mitochondria capable of forming ATP and ADP
  4. enzyme xystemsn that synthesise prostaglandins
  5. fibrin stabilising factor
  6. a growth factor that causes cell growth
60
Q

what does the cell membrane of activated platelets contain

A
  1. glycoproteins
    - these repulse adherence to normal endothelium
    - instead they cause adherence to injured areas of the vessel wall, especially to injured endothelial cells and even more to exposed collagen from deep within the vessel wall
  2. phospholipids
    - these are present in large amounts
    - these activate multiple stages in the blood clotting process
61
Q

what are the three stages of platelet plug formation

A
  1. adhesion and activation
  2. secretion and release
  3. aggregation
62
Q

characteristics of platelets when they come into contract with damaged vascular surface

A
  • they begin to swell
  • they assume irregular forms with numerous irritating pseudopods protruding from their surface
  • their contractile proteins contract forcefully and cause the release of granules that contain multiple active factord
63
Q

what do platelets adhere to in tissues

A

adhere to collagen and to protein called von Willebrand factor that leaks into the tissue from the plasma

64
Q

what is the protein found on cell membrane of platelets that adheres to the collagen

A

Glycoprotein Ib

65
Q

what does glycoprotein Ib bind to

A

vWF

66
Q

what also binds to vWF

A

glycoproteins IIb and IIIa adhere

67
Q

what does the vWF act as

A

a bridge between platelet surface receptors and exposed collagen

68
Q

how does glyocportein Ia bind to collagen

A

directly no vWF

69
Q

Platelet adhesion diagram

A
70
Q

what does prostaglandin synthesis activate

A

production of thromboxane A2

71
Q

what do ADP and thromboxane A2 induce

A

additional platelet aggregation through

  • activated platelets secrete serotonin which increase vasoconstriction
  • activated and damaged endothelial cells secrete endothelin causing vasoconstriction
  • this cascade effect of activated platelets forms the platelet plug
72
Q

what is a blood clot composed of

A
  • a meshwork of fibrin fibres ruling in all directions and entrapping blood cells
  • platelets
  • plasma
73
Q

what are the two courses a clot can follow

A
  1. it can be invaded by fibroblasts which will subsequently form connective tissue through the clot
  2. it can dissolve
74
Q

what breaks down a clot

A
  1. prostacyclin acts as an enzyme to dissolve the clot

2. the breakdown product of fibrinolysis - D dimer

75
Q

what substances cause or affect blood coagulation in the blood and tissues

A
  1. procoagulant factors: promote coagulation

2, anticoagulant factors: inhibit coagulation

  1. co-factors: these aid blood coagulation
76
Q

what does the blood coagulating depend on

A

the balance between the coagulate and anticoagulant factors

77
Q

examples of a coagulation factors known by their description name :

A
  1. tissue factor - TF/FIII

2. prothrombin - FII

78
Q

examples of coagulation factors known by their factor number:

A
  • Factor VIIII (FVIII is associated with haemophilia A)

- Factor IX (FIX associated with haemophilia B)

79
Q

where are most coagulation/anticoagulation/co-factors produced

A

the liver

80
Q

2 substances that play a minor role in blood coagulation

A
  • high molecular weight kiniogen (HMWK)

- prekallikrein

81
Q

what are these substances active to

A

kininogen and kvllikrein

82
Q

general mechanism of blood coagulation

A
  1. prothrombin activator is formed from the extrinsic/intrinsic pathway
  2. prothrombin activator, in the presence of Ca2+ converts prothrombin to thrombin
  3. thrombin causes polymerisation of fibrinogen molecules into fibrin fibres
83
Q

what do platelets convert prothrombin into

A

thrombin because much of the prothrombin first attaches to prothrombin receptors on the platelets already bound to the damaged tissue

84
Q

what is required by the liver for normal formation of prothrombin

A

Vitamin K

85
Q

steps of the extrinsic pathway

A
  1. traumatised tissue released tissue factor TF - a complex of phospholipids and a lipoprotein
  2. TF activates FVII into FVIIa
  3. TF and FVIIa together under the influence of Ca2+ ions activate FX to form FXa
  4. FXa combines with phospholipids and FV under the influence of Ca2+ to form prothrombin activator
86
Q

what activates Factor V

A

in the precedes of Ca2+, prothrombin spilts to from thrombin.
At first, the Factor V in the prothrombin activator complex is inactive, but once clotting begins and thrombin begins to form, the proteolytic action of the thrombin activates Factor V

87
Q

what is the final prothrombin activator complex:

A
  • FXa and FV
88
Q

what causes the splitting of prothrombin to form thrombin

A

FXa

89
Q

what does FV do

A

greatly accelerates the splitting of prothrombin

90
Q

extrinsic pathway diagram

A
91
Q

Step 1 of the intrinsic pathway

A

trauma to the blood alters two important clotting factors in the blood

92
Q

what are the two clotting factors In blood in intrinsic pathway

A

XII and the platelets

93
Q

what happens when XII is disturbed

A

forms XIIa

94
Q

what lipoprotein does platelet phosopholid contain

A

platelet factor 3

95
Q

step 2 the intrinsic pathway

A

the XIIa acts enzymatically activating factor XI to form XIa

  • this reaction also requires HMWK and is accelerated by prekalikrein
96
Q

step 3 of intrinsic pathway

A

XIa then activates Factor IX to IXa under influence of Ca2+

97
Q

step 4 in intrinsic pathway

A

IXa acting with VIIIIa and with the platelet phospholipids and factor 3 active factor X into Xa under influence of Ca2+

  • when either Factor VIII or platelets are short in supply, this step is defiecnt
98
Q

step 5 of intrinsic pathway

A

Xa combines with V and phospholipids to form prothrombin activator under the influence of Ca2+

99
Q

intrinsic pathway diagram

A
100
Q

what is thrombin

A

protein enzyme that removes four peptides from each molecule of fibrinogen forming a molecule of fibrinogen monomer which under the influence of Ca2+ polymerises with other fibrin monomers forming fibrin fibres

101
Q

what does the fibrin stabilising factor activated by thrombin in the platelets do

A

acts as an enzyme forming covalent bonds between the fibrin monomers as well as cross linkage between adjacent fibrin fibres

102
Q

diagram of whole coagulation cascade

A

Semester 2 Case Studies (11 decks)

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