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Medical Studies 1 > Week 12 Haematology > Flashcards

Week 12 Haematology Flashcards

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USMLE® Step 1 flashcards
1
Q

Describe the structure of platelets

A

-nucleus lacking cells (cell fragments)
-packed with granules that contain chemicals
-contains mitochondria and microtubules
-also contains many surface membrane surface receptors

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2
Q

function of platelets

A

participate in hemostasis by
forming a plug at a vessel defect

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3
Q

list the steps of haemostasis

A

vasoconstriction
primary haemostasis
coagulation

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4
Q

Outline an overview of hemostasis

A

-endothelial damage with exposed collagen fibres
-vasoconstriction
-circulating platelets (via vWF) adheres to the exposed collagen beginning the formation of platelet plug
-ADP and TXA2 are released promoting adhesion, activation and aggregation enhancing the plug
-prostacyclins and NO are released to prevent excess clotting for uninjured endothelium (confining the plug)

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5
Q

describe how the clot specifically forms

A

-prothrombin activator, activates prothrombin
-prothrombin (inactive) is converted into thrombin via vitamin K and factor 10
-thrombin converts fibrinogen into fibrin
-fibrin molecules adhere to the damaged vessel surface, forming a loose, netlike meshwork that traps blood cells,
including aggregating platelets, resulting is a clot

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6
Q
A

l

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7
Q

role of the mechanical barrier in platelet adhesion

A

anticoagulant - prevents platelets from binding to suboendothelial proteins

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8
Q

role of anti aggregation in platelet adhesion

A

anticoagulant- secretes small anti aggregation molecules that prevent clotting

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9
Q

role of expression in platelet adhesion

A

anticoagulant- expresses surface anticoagulant proteins

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10
Q

role of fibrinolysis in platelets adhesion

A

anticoagulant: enables the breakdown of blood clots

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11
Q

role of von willebrand factor in platelet adhesion

A

procoagulant: vWF promotes coagulation during infections or inflammation

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12
Q

role of glycoprotein 1b

A

GP1b complex binds von Willebrand factor, allowing platelet adhesion and platelet plug formation at sites of vascular injury

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13
Q

list the stages of platelet plug formation

A

adhesion
activation
aggregation
plug

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14
Q

describe adhesion phase of platelet plug formation

A

reversible adhesion to exposed ECM; certain receptors bind to certain subendothelial factors eg vWF

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15
Q

describe activation phase of platelet plug formation

A

platelet binding to collagen triggers platelet activation,
-resulting in a conformational shape change (protrusions to increase SA),
-granule secretion
-receptor activation

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16
Q

describe aggregation phase of platelet plug formation

A

GP2b/2a on platelets bind to fibrinogen irreversibly; fibrinogen acts as a molecular glue

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17
Q

describe plug phase of platelet plug formation

A

forms a plug of degranulated platelets, trapped by fibrinogen, with entrapped blood cells

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18
Q

what factors trigger platelet activation

A

ADP
Thromboxane A2
thrombin

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19
Q

role of ADP in platelet activation

A

secreted by activated platelets, activates itself and platelets in the vicinity

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20
Q

role of thromboxane A2 in platelet activation

A

TXA2 diffused out of activated platelets, activating itself and other platelets

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21
Q

role of thrombin in platelet activation

A

formed from the coagulation cascade, enables coagulation to occur

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22
Q

role of GP 1a/2a and GP 6

A

binds to collagen -> adhesion

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23
Q

role of GP 1b/5/9

A

bind to vWF–> adhesion

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24
Q

role of GP 2b/3a

A

bind to fibrinogen–> aggregation

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25
Q

Features (roles of molecules) in platelet aggregation

A

-Release reaction (ADP):Activated platelets release ADP, a signalling molecule that attracts more platelets to the injury site
-Thromboxane synthesis: Activated platelets also synthesise thromboxane, which further promotes platelet activation and aggregation.
-ADP and thromboxane receptors: Platelets have specific receptors for ADP and thromboxane, which, when bound, enhance platelet activation and aggregation
-GP 2b/3a: GP 2b/3a receptors on the platelet surface play a crucial role in platelet aggregation by binding to fibrinogen and other platelets.
-Fibrinogen: Fibrinogen is a plasma protein that bridges platelets via their GP2b/3a receptors, facilitating the
formation of stable platelet aggregates.

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26
Q

brief mechanism of COX inhibitor

A

blocks cyclooxygenase enzymes 1,2 to reduce the synthesise of prostaglandins, which play a key role in inflammation and pain

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27
Q

brief mechanism for ADP receptor antagonist

A

Blocks adenosine diphosphate (ADP) receptors on platelets, preventing platelet activation and aggregation.

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28
Q

brief mechanism for phosphodiesterase inhibitor

A

inhibits phosphodiesterase enzymes to increase cyclic AMP levels, leading to vasodilation and reduced platelet aggregation

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29
Q

brief mechanism for GP2b/GP3a inhibitor

A

Blocks the GP2b/3a receptors on platelets, preventing fibrinogen binding and
inhibiting platelet aggregation.

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30
Q

list the contraindications for anti platelet medications

A

active bleeding
thrombocytopenia
bleeding disorders

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31
Q

why’s active bleeding a contradiction for anti platelets meds

A

Contraindicated in individuals with ongoing, uncontrolled bleeding as antiplatelet
drugs may exacerbate the haemorrhage.

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32
Q

why’s thrombocytopenia a contraindication for anti platelet medication

A

Contraindicated in patients with low platelet counts, as further reducing platelet function can increase the risk of bleeding

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33
Q

why are bleeding disorders a contraindication for anti platelet medication

A

Contraindicated in those with known bleeding disorders, as antiplatelet drugs may
worsen their condition

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34
Q

what is a thrombus

A

A blood clot that forms and remains within a blood vessel.

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35
Q

what is an embolus

A

A dislodged or traveling mass, often a blood clot, that can obstruct a blood vessel in
a different location.

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36
Q

what is a thromboembolus

A

blood clot (thrombus) that has broken free and is carried though the bloodstream (embolus) potentially causing blockages in distant blood vessels

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37
Q

list the pathways for coagulation

A

intrinsic
extrinsic
common

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38
Q

describe the intrinsic pathway for coagulation

A

-EXPOSED COLLAGEN at surface of damaged vessel
-inactivated factor 12 is converted into active factor 12 when it is exposed to collagen
-active factor 11 is formed
-active factor 9 is formed via Ca2+ (factor 4)
-active factor 10 is formed via Ca2+ (factor4), PF3, factor 8
-prothrombin (factor 2) is converted into thrombin via Ca2+ (factor 4), PF3 and factor 5
-in addition to converting fibrinogen into fibrin, thrombin activates factor 13 to
stabilise the resultant fibrin mesh
-clot forms

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39
Q

what is the extrinsic pathway for coagulation

A

-TISSUE DAMAGE (blood leaks out of tissue)
-tissue thromboplastin (factor 3) produced
-tissue thromboplastin produces
factor 10 via Ca2+ (factor4), PF3, factor 8
-prothrombin (factor 2) is converted into thrombin via Ca2+ (factor 4), PF3 and factor 5
-in addition to
converting fibrinogen into fibrin, thrombin activates factor 13 to stabilise the resultant fibrin mesh
-clot forms

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40
Q

what is the common pathway for coagulation

A

active factor 10 contributes to the activation of fibrinogen to form fibrin

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41
Q

what additional factors are involved in the common pathway

A

1,2,5,10,13

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42
Q

mechanism of activated C protein

A

anticoagulant that inactivates coagulation factor 5a and 8a by cleaving them

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43
Q

mechanism of antithrombin

A

inhibits multiple coagulation factors, including factors 2a (thrombin), 9a and 10a and 11a

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44
Q

mechanism of vitamin K antagonist eg warfarin

A

interferes with the synthesis of vitamin-k dependent coagulation factors (2,7,9,10) and proteins c and s, decreasing clotting

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45
Q

mechanism for heparin

A

Enhances the activity of antithrombin, which inhibits multiple coagulation factors, including Factors 2a (thrombin), 9a,10a,11a,12a

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46
Q

mechanism for LMW heparin

A

Acts similarly to heparin, but it has a greater effect on Factor 10a and less on Factor 2a (thrombin).

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47
Q

mechanism for direct-acting oral anticoagulants (DOAC)

A

inhibits specific coagulation factors directly. DOACs include:
-Factor 10a inhibitors
(e.g., apixaban, rivaroxaban)
-direct thrombin (2a) inhibitors (e.g., dabigatran).

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48
Q

features of fibronlysis

A

-process by which body dissolves blood clots
-enzyme plasmin plays a key role in promoting fibrinolysis, cleaves fibrin, into soluble fragments thereby dissolving clots
-balanced process that involves delicate interplay between clot coagulation and fibronlysis

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49
Q

describe the role of tranexamic acid in inhibiting fibrinolysis

A

-TXA is an antifibrinolytic medication
-TXA works by blocking the enzymatic activity of plasmin, which is responsible for degrading fibrin, the protein
that forms the mesh-like structure of blood clots
-TXA exerts its inhibitory effect on plasmin by binding to the lysine-binding sites on plasminogen, preventing
the conversion of plasminogen to its active form, plasmin
-used in controlling bleeding in surgeries, trauma or medical conditions eg menorrhagia

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50
Q

what are the components of virchows triad

A

endothelial damage
blood stasis
hypercoagulabilty

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51
Q

what is endothelial damage in virchows triad

A

Injury to the inner lining of blood vessels

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52
Q

what is blood stasis in virchows triad

A

Slow or turbulent blood flow, which can promote clot formation.

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53
Q

what is hypercoagulabilty in virchows triad

A

Increased tendency of the blood to clot due to various factors, such as genetic predisposition or certain medical conditions.

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54
Q

list the inherited causes of hypercoagulopathy

A

-factor 5 leiden mutation
-activated protein C resistance
-protein c or s deficiency
-antithrombin deficiency

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55
Q

what is factor 5 Leiden mutation

A

A genetic mutation that makes it difficult for the body to deactivate factor 5, leading to excess clotting

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56
Q

what is activated protein c resistance

A

Reduced sensitivity to the anticoagulant effects of activated protein C, often due to the Factor V Leiden mutation.

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57
Q

what is protein c or s deficiency

A

Inherited deficiencies of natural anticoagulant proteins, Protein C or Protein S.

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58
Q

what is antithrombin defiency

A

Genetic deficiency of antithrombin, a protein that regulates blood clot formation.

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59
Q

list the inherited causes of hyper coagulability

A

thrombophillic conditions

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60
Q

list the acquired causes of hyper coagulability

A

-pregnancy
-hormone replacement therapy
-COVID 19
-long distance travel
-carcinoma

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61
Q

describe how pregnancy can cause hyper coagulability

A

Increased risk of clot formation due to changes in hormone levels, blood flow, and clotting factors during pregnancy.

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62
Q

describe how HRT can lead to hyper coagulability

A

Elevated risk of clots associated with estrogen-based hormone therapies,
particularly in postmenopausal women.

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63
Q

describe how COVID 19 can lead to hyper coagulation

A

Viral infection may lead to an inflammatory and prothrombotic state,
increasing the risk of blood clot formation

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64
Q

describe how long distance travel can lead to hyper coagulation

A

Prolonged sitting during travel or immobility can slow blood flow, leading to
deep vein thrombosis (DVT).

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65
Q

describe how carcinoma can cause hyper coagulation

A

cancer related hyper coagulability can be triggered by tumour cell interactions with blood components, cytokine release and treatment related factors

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66
Q

incidence of coagulopathies

A

-For inherited coagulopathies like haemophilia, the incidence is relatively low, occurring in approximately 1 in 5,000 to 1 in 10,000 male births for haemophilia A.
-Acquired coagulopathies may have a higher incidence in certain situations, such as during surgeries or trauma.

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67
Q

prevalence of coagulopathies

A

Haemophilia, an inherited coagulopathy, has a relatively low prevalence because it is a rare genetic condition,
affecting about 1 in 5,000 to 1 in 10,000 males for haemophilia A and less frequently for haemophilia B

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68
Q

list the risk factors for coagulopathies

A

increased age
sex
obesity
recent surgery
malignancy
pregnancy

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69
Q

describe increased age as a risk factor for coagulopathies

A

Aging can lead to a higher risk of coagulopathy due to factors like decreased mobility and changes in blood vessel function.

70
Q

describe sex as a risk factor for coagulopathies

A

-Men and women have different risks;
-women may experience coagulopathy during pregnancy or with hormonal changes,
-while men might face increased risk due to
factors like lifestyle choices.

71
Q

describe obesity as a risk factor for coagulopathies

A

Obesity is associated with coagulopathy risk due to inflammation, changes in clotting factors, and altered blood vessel function.

72
Q

describe recent surgery as a risk factor for coagulopathies

A

Surgery can trigger coagulopathy risk due to factors like immobilisation, anaesthesia, and surgical trauma, which can activate the clotting process

73
Q

describe malignancy as a risk factor for coagulopathies

A

Cancer can lead to coagulopathy risk because some tumours release procoagulant substances, and treatment may affect blood clotting.

74
Q

describe pregnancy as a risk factor for coagulopathies

A

Pregnancy increases coagulopathy risk due to hormonal changes and compression of pelvic veins, which can lead to venous thromboembolism.

75
Q

Describe how a DVT can result in a PE

A

1.thrombus forms: blood clot forms in deep veins of legs (thrombus) who can obstruct blood flow into affected vein
2.embolus forms: thrombus dislodges from deep vein and travels through blood
3.Migration to lungs: embolus migrates through circulatory system to heart, whereafter it enters pulmonary circulation
4.PE: embolus blocks blood flow into pulmonary arteries –> PE

76
Q

list the investigations for diagnosis of coagulopathies

A

-prothrombin time
-activated partial thromboplastin time
-fibrinogen level
-thrombin time
-CBE
-genetic testing
-antithrombin activity
-protein C activity
-antibody screening
-blood film
-VWD and FVIII if personal or family bleeding history

77
Q

describe the use of prothrombin time (PT) in dx coagulopathies

A

Measures the time it takes for blood to clot, used to assess blood clotting ability and monitor the effects of anticoagulant medications, with results often reported as an International Normalised Ratio (INR)

(tennis (outside) extrinsic)

78
Q

describe the use of activated partial thromboplastin time (APTT) in dx coagulopathies

A

Evaluates the clotting function of the intrinsic and common coagulation
pathways, helping diagnose bleeding disorders and monitor heparin therapy

(table tennis (Inside) intrinsic)

79
Q

describe the use of fibrinogen level in dx coagulopathies

A

Measures the concentration of fibrinogen in the blood, which is essential for
blood clot formation.

80
Q

describe the use of thrombin time in dx coagulopathies

A

assesses the ability of blood to form fibrin clots by measuring the time it takes
for a clot to form after the addition of thrombin.

81
Q

describe the use of CBE in dx coagulopathies

A

routine blood test that provides information about the number and types of
blood cells in the body, including red blood cells, white blood cells, and
platelets

82
Q

describe the use of genetic testing for dx coagulopathies

A

Analyses an individual’s DNA to identify genetic mutations or variations that may affect their risk of clotting disorders or bleeding disorders.

83
Q

describe the use of antithrombin activity in dx coagulopathies

A

Measures the activity of antithrombin, a natural anticoagulant in the blood that inhibits blood clot formation.

84
Q

describe use of protein C activity in dx coagulopathies

A

Evaluates the activity of protein C, a natural anticoagulant, to assess the risk of developing blood clots.

85
Q

describe the use of antibody screening in dx coagulopathies

A

Detects the presence of specific antibodies in the blood, which can be
associated with autoimmune or coagulation disorders.

86
Q

describe the use of blood films for dx coagulopathies

A

Microscopic examination of a blood smear to assess the size, shape, and
appearance of platelets, helping diagnose platelet disorders and assess their
function.

87
Q

describe the use of VWD in dx coagulopathies

A

Specialised tests to assess the levels and function of von Willebrand factor and Factor 8 in individuals with a designated risk

88
Q

list the clinical features of venous thrombosis

A

unilateral chest pain
peripheral oedema
erythema
tenderness

89
Q

list the clinical features of PE

A

dyspnoea
pleuritic chest pain
tachycardia
haemopytsis
syncope

90
Q

what is haemophillia

A

A genetic bleeding disorder characterized by a deficiency of clotting factors,
leading to prolonged bleeding and easy bruising

91
Q

what is disseminated intravascular coagulation

A

A complex and life-threatening condition where the body’s coagulation
system is excessively activated, causing both excessive clotting and
bleeding.

92
Q

what is von willebrand disease

A

A hereditary bleeding disorder resulting from a deficiency or dysfunction of
von Willebrand factor, which plays a crucial role in blood clotting

93
Q

list the risk factors for bleeding disorders

A

FHx
gender
age
medications
trauma/surgery

94
Q

how is FHx a risk factor for bleeding disorders

A

A family history of bleeding disorders, such as haemophilia or von Willebrand disease,
can increase the risk of these conditions in offspring.

95
Q

how is gender a risk factor for bleeding disorders

A

Haemophilia, for example, is more common in males. While females can be carriers,
males are more likely to experience symptoms.

96
Q

how is age a risk factor for bleeding disorders

A

Some bleeding disorders, like von Willebrand disease, may not become apparent until
later in life.

97
Q

how are meds a risk factor for bleeding disorders

A

Certain medications, such as blood thinners (anticoagulants) and nonsteroidal antiinflammatory drugs (NSAIDs), can increase the risk of bleeding.

98
Q

how is trauma/surgery a risk factor for bleeding disorders

A

Recent surgery or significant injury can lead to bleeding disorders due to a loss of blood components.

99
Q

what is clot dissolution

A

The controlled dissolution of the fibrin mesh within a blood clot to restore normal
blood flow.

100
Q

classify thrombocytopenia

A

primary platelet disorder

101
Q

classify von willebrands disease

A

primary platelet disorder

102
Q

classify haemophilia

A

secondary platelet disorder

103
Q

classify factor 5 Leiden

A

secondary platelet disorder

104
Q

classify disseminated intravascular coagulation

A

secondary platelet disorder

105
Q

classify fibrinolytic disorders

A

fibrinolytic platelet disorder

106
Q

pathogenesis of metastatic carcinoma formation

A

*tumour development -> cancer cells invade nearby tissue/vasculature
*intravasation of lymph and blood
*extravasation of lymph and bloodstream–> secondary tumour at new site

107
Q

pathogenesis of disseminated intravascular coagulation

A

-underlying cause (sepsis or trauma)
-activation of coagulation cascade
-widespread microthrombi formation
-consumption of coagulation factors
-fibrinolysis and plasmin over-activation
-increased bleeding
-end organ damage

108
Q

how do anticoagulants cause bleeding disorders

A

Inhibit clot formation by interfering with blood coagulation factors, increasing the risk of bleeding

109
Q

how do fibrinolytics cause bleeding disorders

A

Promote the breakdown of blood clots, potentially leading to excessive bleeding

110
Q

how does aspirin cause bleeding disorders

A

Inhibits platelet aggregation, reducing the ability to form stable blood clots and
increasing the risk of bleeding

111
Q

how do NSAIDs cause bleeding disorders

A

Interfere with platelet function and can cause gastrointestinal bleeding by damaging the stomach lining.

112
Q

pathophysiology of thrombocytopenia

A

-reduced platelet production at bone marrow
AND
-increased platelet destruction (in Immune thrombocytopenic purpura)

–>low levels of platelets in blood

113
Q

pathophysiology of bleeding disorder secondary to renal failure

A

renal failure–> uraemia toxin buildup–> platelet dysfunction and increased vWF cleavage –> reduced vWF

114
Q

pathophysiology of bleeding disorders secondary to malignancy

A

-myeloma/lymphoma

leads to anaemia, thrombocytopenia and DIC

115
Q

pathophysiology of vWD

A

vWF dysfunction and vWF deficiency

leads to impaired platelet adhesion–> prolonged bleeding (bleeding disorder)

116
Q

haemophilia pathogenesis

A

-X linked genetic mutation
-factor 8 deficiency
-factor 9 deficiency
-clotting cascade impairment
-increased risk of bleeding

117
Q

list the clinical features of bleeding disorders

A

bruising
purpura
postoperative bleeding
menorrhagia
haematuria
epistaxis

118
Q

describe bruising in bleeding disorders

A

Result from impaired clotting due to a bleeding disorder, leading to blood leaking into the skin’s tissues after minor trauma.

119
Q

describe purpura in bleeding disorders

A

Widespread, small red or purple skin spots caused by bleeding under the skin, often
due to blood vessel fragility associated with bleeding disorders.

120
Q

describe postoperative bleeding in bleeding disorders

A

Excessive bleeding following surgery can occur if clotting factors are deficient,
impairing the body’s ability to form stable blood clots.

121
Q

describe menorrhagia in bleeding disorders

A

Heavy menstrual bleeding in women is often linked to bleeding disorders, as inadequate clot formation can lead to prolonged and heavy periods

122
Q

describe haematuria in bleeding disorders

A

Blood in the urine can result from bleeding disorders, affecting the urinary tract’s ability to prevent blood from entering the urine.

123
Q

describe epitaxis in bleeding disorders

A

Frequent nosebleeds can occur due to fragile blood vessels in the nasal mucosa, often
linked to bleeding disorders

124
Q

list some anti platelets

A

aspirin
clopidogrel and ticagrelor (P2Y12 blockers)

125
Q

how does aspirin work

A

An antiplatelet medication that inhibits blood clot formation by reducing platelet aggregation (decreases TXA2)

126
Q

how does clopidogrel work

A

Another antiplatelet agent that inhibits platelet activation by binding to P2Y12, reducing the risk of clot formation.

127
Q

how does ticagrelol work

A

Another antiplatelet agent that inhibits platelet activation by binding to P2Y12, reducing the risk of clot formation.

128
Q

how does apixaban work

A

A direct oral anticoagulant (DOAC) that inhibits a specific clotting factor, factor Xa, to
prevent blood clot formation.

129
Q

how does dabigatran work

A

Another DOAC that targets thrombin, a key enzyme in the blood clotting cascade, to
prevent thrombus formation.

130
Q

how do tissue plasminogen activators work

A

thrombolytic agent (has enzymes) that promote the conversion of plasminogen into plasminogen, which dissolves blood clots

131
Q

list the factor replacement therapies

A

vWF
Factor 13
Factor 9

132
Q

how does vWF replacement therapy

A

replacement therapy involving vWF for individuals with vWD, a bleeding disorder, to correct clotting abnormalities

133
Q

how does factor 13 FRT work

A

Replacement therapy with Factor 13 for individuals with a deficiency of this clot stabilising factor to improve clot formation and stability

134
Q

how does factor 9 FRT work

A

Replacement therapy with Factor 9 for individuals with haemophilia B to restore blood clotting and prevent bleeding episodes.

135
Q

indications for anti platelets meds

A

CVD
Cerebrovascular disease
PVD

136
Q

contraindications for anti platelets

A

-active/recent haemorrhage
-upcoming recent surgery
-severe thrombocytopenia

137
Q

side effects of anti platelet meds

A

blood loss
dyspnoea (ticagrelor)
bradycardia (ticagrelor)
GI irritation/ulceration
gout (ticagrelor)

138
Q

indications of unfractioned heparin

A

renal impairment

139
Q

indications of LMWH

A

cases when monitoring is difficult

140
Q

contraindications of heparins

A

active/recent haemorrhages
severe thrombocytopenia

141
Q

side effects of heparins

A

-Heparin-induced Thrombotic Thrombocytopaenia
Syndrome (HITTS)
-liver enzyme elevation
-bleeding
-alopecia

142
Q

indications for vitamin K antagonists

A

mechanical heart valves
renal disease
arterial thrombi

143
Q

contraindications for vitamin K antagonists

A

active/recent haemorrhage
severe thrombocytopenia
pregnancy

144
Q

side effects of vitamin K antagonists

A

-Heparin-induced Thrombotic Thrombocytopaenia
Syndrome (HITTS)
-bleeding
-alopecia
-liver enzyme elevation

145
Q

indications for DOAC’s

A

-Venous thromboembolism
-prophylactic VTE treatment
-atrial fibrillation

146
Q

contraindications for DOAC’s

A

active/recent haemorrhage
severe thrombocytopenia
severe renal impairment

147
Q

side effects for DOAC’s

A

bleeding
indigestion
livre function abnormality
nausea
skin rashes
headache

148
Q

Outline transfusion of blood products in treating blood disorders

A

-Fresh frozen plasma (FFP): FFP contains clotting factors and is used to treat bleeding disorders
-Platelet transfusion: platelet transfusions are administered to individuals who are diagnosed with relatively low platelet counts
-Packed red blood cells: given when anaemia or severe blood loss has occurred to increase O2 carrying capacity

149
Q

describe antifibrinolytic use for bleeding disorders

A

Antifibrinolytic drugs like tranexamic acid are used to prevent the breakdown of blood clots and are effective in treating bleeding disorders, they are often given before surgeries

150
Q

describe desmopressin use in treating blood disorders

A

-used in certain bleeding disorders, such as mild haemophilia A and von Willebrand disease
-It helps release von Willebrand factor and factor 8 from storage sites in the body, temporarily increasing their levels in the blood.

151
Q

components vs products of blood

A

-components are individual parts of blood separated though blood fractionation (RBC’s,platelets, plasma and cryoprecipitate)
-products are prepared blood derivatives designed for therapeutic purposes eg Ig, albumin and clotting factors

152
Q

why are red cells used transfusion

A

Oxygen-carrying components of blood used to treat anaemia and increase oxygen delivery to tissues.

153
Q

why are pooled platelets used for transfusion

A

Fragments of blood cells essential for clot formation in patients with bleeding disorders

154
Q

why is plasma used for transfusion

A

The liquid portion of blood containing clotting factors and proteins, often used for
patients with coagulation disorders or massive blood loss.

155
Q

why is immunoglobulins used for transfusion

A

antibodies for immune support

156
Q

why is albumin used for transfusion

A

clotting factors

157
Q

features of blood donor selection process

A

testing for
-HIV
-Hepatitis C
-Human T-lymphotropic virus (type II)
-syphillis
-hepatitis B
-Human T-lymphotropic virus (type I)

158
Q

list the major blood types

A

A
B
AB
O

159
Q

what is ABO/Rhesus incompatibility

A

-Rh incompatibility is a condition that develops when a pregnant woman has Rh-negative blood and the baby in her womb has Rh-positive blood
-During pregnancy, red blood cells from the unborn baby can cross into the mother’s blood through the placenta.
-If the mother is Rh-negative, her immune system treats Rh-positive foetal cells as foreign substances; the
mother’s body makes antibodies against the foetal blood cells.
-These antibodies may cross back through the placenta into the developing baby; they thereafter destroy the baby’s circulating red blood cells.

160
Q

list the risks/complications associated with blood transfusion

A

haemolytic reaction
allergic reaction
febrile non-haemolytic reaction
infection transmission
iron overload
volume overload

161
Q

describe haemolytic reaction as a side effect of blood transfusion

A

Occurs when there is a mismatch between the donor and recipient blood, leading to the destruction of the recipient’s red blood cells. Can be life-threatening

162
Q

describe allergic reaction as side effect to blood transfusion

A

May cause itching, hives, and, in severe cases, anaphylaxis. Typically, due to allergies to components of the transfused blood or additives.

163
Q

describe febrile non haemolytic reaction as complication of blood transfusion

A

Results in fever and chills but is generally not life-threatening. Caused by an immune response to white blood cells in the transfused blood

164
Q

describe infection transmissions as a side effect of blood transfusion

A

Extremely rare but possible. Bloodborne infections such as HIV, hepatitis, and other pathogens could be transmitted if the donated blood is contaminated.

165
Q

describe iron overload as a side effect of blood transfusion

A

Frequent transfusions can lead to an accumulation of excess iron in the recipient’s body, potentially damaging organs, and tissues. Requires iron-chelation therapy

166
Q

describe volume overload as a side effect of blood transfusions

A

Rapid infusion of a large volume of blood can lead to fluid overload, congestive heart failure, and pulmonary oedema

167
Q

how to minimise risk of haemolytic reactions in blood transfusion

A

Stringent blood typing and cross-matching procedures to ensure compatibility between donor and recipient blood.

168
Q

how to minimise risk of febrile non haemolytic reaction in blood transfusions

A

Leukoreduction, which removes white blood cells from donated blood to reduce the risk of immune reactions.

169
Q

how to minimise infection transmission in blood transfusions

A

Rigorous screening of donated blood for infectious diseases

170
Q

how to minimise iron overload risk in blood transfusions

A

limiting unnecessary blood transfusions and using alternative therapy when possible

171
Q

outline the three pillars of patient blood management

A

optimising Hb-proactively improve Hb levels to reduce need for transfusion
minimising blood loss-minimal invasive surgery, careful tissue handling
appropriate transfusion-focus on clinical indications before deciding

Medical Studies 1 (15 decks)

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