Week 12 Haematology Flashcards
(171 cards)
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
2
Q
function of platelets
A
participate in hemostasis by
forming a plug at a vessel defect
3
Q
list the steps of haemostasis
A
vasoconstriction
primary haemostasis
coagulation
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)
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
6
Q
A
l
7
Q
role of the mechanical barrier in platelet adhesion
A
anticoagulant - prevents platelets from binding to suboendothelial proteins
8
Q
role of anti aggregation in platelet adhesion
A
anticoagulant- secretes small anti aggregation molecules that prevent clotting
9
Q
role of expression in platelet adhesion
A
anticoagulant- expresses surface anticoagulant proteins
10
Q
role of fibrinolysis in platelets adhesion
A
anticoagulant: enables the breakdown of blood clots
11
Q
role of von willebrand factor in platelet adhesion
A
procoagulant: vWF promotes coagulation during infections or inflammation
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
13
Q
list the stages of platelet plug formation
A
adhesion
activation
aggregation
plug
14
Q
describe adhesion phase of platelet plug formation
A
reversible adhesion to exposed ECM; certain receptors bind to certain subendothelial factors eg vWF
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
16
Q
describe aggregation phase of platelet plug formation
A
GP2b/2a on platelets bind to fibrinogen irreversibly; fibrinogen acts as a molecular glue
17
Q
describe plug phase of platelet plug formation
A
forms a plug of degranulated platelets, trapped by fibrinogen, with entrapped blood cells
18
Q
what factors trigger platelet activation
A
ADP
Thromboxane A2
thrombin
19
Q
role of ADP in platelet activation
A
secreted by activated platelets, activates itself and platelets in the vicinity
20
Q
role of thromboxane A2 in platelet activation
A
TXA2 diffused out of activated platelets, activating itself and other platelets
21
Q
role of thrombin in platelet activation
A
formed from the coagulation cascade, enables coagulation to occur
22
Q
role of GP 1a/2a and GP 6
A
binds to collagen -> adhesion
23
Q
role of GP 1b/5/9
A
bind to vWF–> adhesion
24
Q
role of GP 2b/3a
A
bind to fibrinogen–> aggregation
25
Features (roles of molecules) in platelet aggregation
-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.
26
brief mechanism of COX inhibitor
blocks cyclooxygenase enzymes 1,2 to reduce the synthesise of prostaglandins, which play a key role in inflammation and pain
27
brief mechanism for ADP receptor antagonist
Blocks adenosine diphosphate (ADP) receptors on platelets, preventing platelet activation and aggregation.
28
brief mechanism for phosphodiesterase inhibitor
inhibits phosphodiesterase enzymes to increase cyclic AMP levels, leading to vasodilation and reduced platelet aggregation
29
brief mechanism for GP2b/GP3a inhibitor
Blocks the GP2b/3a receptors on platelets, preventing fibrinogen binding and
inhibiting platelet aggregation.
30
list the contraindications for anti platelet medications
active bleeding
thrombocytopenia
bleeding disorders
31
why's active bleeding a contradiction for anti platelets meds
Contraindicated in individuals with ongoing, uncontrolled bleeding as antiplatelet
drugs may exacerbate the haemorrhage.
32
why's thrombocytopenia a contraindication for anti platelet medication
Contraindicated in patients with low platelet counts, as further reducing platelet function can increase the risk of bleeding
33
why are bleeding disorders a contraindication for anti platelet medication
Contraindicated in those with known bleeding disorders, as antiplatelet drugs may
worsen their condition
34
what is a thrombus
A blood clot that forms and remains within a blood vessel.
35
what is an embolus
A dislodged or traveling mass, often a blood clot, that can obstruct a blood vessel in
a different location.
36
what is a thromboembolus
blood clot (thrombus) that has broken free and is carried though the bloodstream (embolus) potentially causing blockages in distant blood vessels
37
list the pathways for coagulation
intrinsic
extrinsic
common
38
describe the intrinsic pathway for coagulation
-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
39
what is the extrinsic pathway for coagulation
-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
40
what is the common pathway for coagulation
active factor 10 contributes to the activation of fibrinogen to form fibrin
41
what additional factors are involved in the common pathway
1,2,5,10,13
42
mechanism of activated C protein
anticoagulant that inactivates coagulation factor 5a and 8a by cleaving them
43
mechanism of antithrombin
inhibits multiple coagulation factors, including factors 2a (thrombin), 9a and 10a and 11a
44
mechanism of vitamin K antagonist eg warfarin
interferes with the synthesis of vitamin-k dependent coagulation factors (2,7,9,10) and proteins c and s, decreasing clotting
45
mechanism for heparin
Enhances the activity of antithrombin, which inhibits multiple coagulation factors, including Factors 2a (thrombin), 9a,10a,11a,12a
46
mechanism for LMW heparin
Acts similarly to heparin, but it has a greater effect on Factor 10a and less on Factor 2a (thrombin).
47
mechanism for direct-acting oral anticoagulants (DOAC)
inhibits specific coagulation factors directly. DOACs include:
-Factor 10a inhibitors
(e.g., apixaban, rivaroxaban)
-direct thrombin (2a) inhibitors (e.g., dabigatran).
48
features of fibronlysis
-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
49
describe the role of tranexamic acid in inhibiting fibrinolysis
-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
50
what are the components of virchows triad
endothelial damage
blood stasis
hypercoagulabilty
51
what is endothelial damage in virchows triad
Injury to the inner lining of blood vessels
52
what is blood stasis in virchows triad
Slow or turbulent blood flow, which can promote clot formation.
53
what is hypercoagulabilty in virchows triad
Increased tendency of the blood to clot due to various factors, such as genetic predisposition or certain medical conditions.
54
list the inherited causes of hypercoagulopathy
-factor 5 leiden mutation
-activated protein C resistance
-protein c or s deficiency
-antithrombin deficiency
55
what is factor 5 Leiden mutation
A genetic mutation that makes it difficult for the body to deactivate factor 5, leading to excess clotting
56
what is activated protein c resistance
Reduced sensitivity to the anticoagulant effects of activated protein C, often due to the Factor V Leiden mutation.
57
what is protein c or s deficiency
Inherited deficiencies of natural anticoagulant proteins, Protein C or Protein S.
58
what is antithrombin defiency
Genetic deficiency of antithrombin, a protein that regulates blood clot formation.
59
list the inherited causes of hyper coagulability
thrombophillic conditions
60
list the acquired causes of hyper coagulability
-pregnancy
-hormone replacement therapy
-COVID 19
-long distance travel
-carcinoma
61
describe how pregnancy can cause hyper coagulability
Increased risk of clot formation due to changes in hormone levels, blood flow, and clotting factors during pregnancy.
62
describe how HRT can lead to hyper coagulability
Elevated risk of clots associated with estrogen-based hormone therapies,
particularly in postmenopausal women.
63
describe how COVID 19 can lead to hyper coagulation
Viral infection may lead to an inflammatory and prothrombotic state,
increasing the risk of blood clot formation
64
describe how long distance travel can lead to hyper coagulation
Prolonged sitting during travel or immobility can slow blood flow, leading to
deep vein thrombosis (DVT).
65
describe how carcinoma can cause hyper coagulation
cancer related hyper coagulability can be triggered by tumour cell interactions with blood components, cytokine release and treatment related factors
66
incidence of coagulopathies
-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.
67
prevalence of coagulopathies
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
68
list the risk factors for coagulopathies
increased age
sex
obesity
recent surgery
malignancy
pregnancy
69
describe increased age as a risk factor for coagulopathies
Aging can lead to a higher risk of coagulopathy due to factors like decreased mobility and changes in blood vessel function.
70
describe sex as a risk factor for coagulopathies
-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
describe obesity as a risk factor for coagulopathies
Obesity is associated with coagulopathy risk due to inflammation, changes in clotting factors, and altered blood vessel function.
72
describe recent surgery as a risk factor for coagulopathies
Surgery can trigger coagulopathy risk due to factors like immobilisation, anaesthesia, and surgical trauma, which can activate the clotting process
73
describe malignancy as a risk factor for coagulopathies
Cancer can lead to coagulopathy risk because some tumours release procoagulant substances, and treatment may affect blood clotting.
74
describe pregnancy as a risk factor for coagulopathies
Pregnancy increases coagulopathy risk due to hormonal changes and compression of pelvic veins, which can lead to venous thromboembolism.
75
Describe how a DVT can result in a PE
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
list the investigations for diagnosis of coagulopathies
-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
describe the use of prothrombin time (PT) in dx coagulopathies
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
describe the use of activated partial thromboplastin time (APTT) in dx coagulopathies
Evaluates the clotting function of the intrinsic and common coagulation
pathways, helping diagnose bleeding disorders and monitor heparin therapy
(table tennis (Inside) intrinsic)
79
describe the use of fibrinogen level in dx coagulopathies
Measures the concentration of fibrinogen in the blood, which is essential for
blood clot formation.
80
describe the use of thrombin time in dx coagulopathies
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
describe the use of CBE in dx coagulopathies
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
describe the use of genetic testing for dx coagulopathies
Analyses an individual's DNA to identify genetic mutations or variations that may affect their risk of clotting disorders or bleeding disorders.
83
describe the use of antithrombin activity in dx coagulopathies
Measures the activity of antithrombin, a natural anticoagulant in the blood that inhibits blood clot formation.
84
describe use of protein C activity in dx coagulopathies
Evaluates the activity of protein C, a natural anticoagulant, to assess the risk of developing blood clots.
85
describe the use of antibody screening in dx coagulopathies
Detects the presence of specific antibodies in the blood, which can be
associated with autoimmune or coagulation disorders.
86
describe the use of blood films for dx coagulopathies
Microscopic examination of a blood smear to assess the size, shape, and
appearance of platelets, helping diagnose platelet disorders and assess their
function.
87
describe the use of VWD in dx coagulopathies
Specialised tests to assess the levels and function of von Willebrand factor and Factor 8 in individuals with a designated risk
88
list the clinical features of venous thrombosis
unilateral chest pain
peripheral oedema
erythema
tenderness
89
list the clinical features of PE
dyspnoea
pleuritic chest pain
tachycardia
haemopytsis
syncope
90
what is haemophillia
A genetic bleeding disorder characterized by a deficiency of clotting factors,
leading to prolonged bleeding and easy bruising
91
what is disseminated intravascular coagulation
A complex and life-threatening condition where the body's coagulation
system is excessively activated, causing both excessive clotting and
bleeding.
92
what is von willebrand disease
A hereditary bleeding disorder resulting from a deficiency or dysfunction of
von Willebrand factor, which plays a crucial role in blood clotting
93
list the risk factors for bleeding disorders
FHx
gender
age
medications
trauma/surgery
94
how is FHx a risk factor for bleeding disorders
A family history of bleeding disorders, such as haemophilia or von Willebrand disease,
can increase the risk of these conditions in offspring.
95
how is gender a risk factor for bleeding disorders
Haemophilia, for example, is more common in males. While females can be carriers,
males are more likely to experience symptoms.
96
how is age a risk factor for bleeding disorders
Some bleeding disorders, like von Willebrand disease, may not become apparent until
later in life.
97
how are meds a risk factor for bleeding disorders
Certain medications, such as blood thinners (anticoagulants) and nonsteroidal antiinflammatory drugs (NSAIDs), can increase the risk of bleeding.
98
how is trauma/surgery a risk factor for bleeding disorders
Recent surgery or significant injury can lead to bleeding disorders due to a loss of blood components.
99
what is clot dissolution
The controlled dissolution of the fibrin mesh within a blood clot to restore normal
blood flow.
100
classify thrombocytopenia
primary platelet disorder
101
classify von willebrands disease
primary platelet disorder
102
classify haemophilia
secondary platelet disorder
103
classify factor 5 Leiden
secondary platelet disorder
104
classify disseminated intravascular coagulation
secondary platelet disorder
105
classify fibrinolytic disorders
fibrinolytic platelet disorder
106
pathogenesis of metastatic carcinoma formation
*tumour development -> cancer cells invade nearby tissue/vasculature
*intravasation of lymph and blood
*extravasation of lymph and bloodstream--> secondary tumour at new site
107
pathogenesis of disseminated intravascular coagulation
-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
how do anticoagulants cause bleeding disorders
Inhibit clot formation by interfering with blood coagulation factors, increasing the risk of bleeding
109
how do fibrinolytics cause bleeding disorders
Promote the breakdown of blood clots, potentially leading to excessive bleeding
110
how does aspirin cause bleeding disorders
Inhibits platelet aggregation, reducing the ability to form stable blood clots and
increasing the risk of bleeding
111
how do NSAIDs cause bleeding disorders
Interfere with platelet function and can cause gastrointestinal bleeding by damaging the stomach lining.
112
pathophysiology of thrombocytopenia
-reduced platelet production at bone marrow
AND
-increased platelet destruction (in Immune thrombocytopenic purpura)
-->low levels of platelets in blood
113
pathophysiology of bleeding disorder secondary to renal failure
renal failure--> uraemia toxin buildup--> platelet dysfunction and increased vWF cleavage --> reduced vWF
114
pathophysiology of bleeding disorders secondary to malignancy
-myeloma/lymphoma
leads to anaemia, thrombocytopenia and DIC
115
pathophysiology of vWD
vWF dysfunction and vWF deficiency
leads to impaired platelet adhesion--> prolonged bleeding (bleeding disorder)
116
haemophilia pathogenesis
-X linked genetic mutation
-factor 8 deficiency
-factor 9 deficiency
-clotting cascade impairment
-increased risk of bleeding
117
list the clinical features of bleeding disorders
bruising
purpura
postoperative bleeding
menorrhagia
haematuria
epistaxis
118
describe bruising in bleeding disorders
Result from impaired clotting due to a bleeding disorder, leading to blood leaking into the skin's tissues after minor trauma.
119
describe purpura in bleeding disorders
Widespread, small red or purple skin spots caused by bleeding under the skin, often
due to blood vessel fragility associated with bleeding disorders.
120
describe postoperative bleeding in bleeding disorders
Excessive bleeding following surgery can occur if clotting factors are deficient,
impairing the body's ability to form stable blood clots.
121
describe menorrhagia in bleeding disorders
Heavy menstrual bleeding in women is often linked to bleeding disorders, as inadequate clot formation can lead to prolonged and heavy periods
122
describe haematuria in bleeding disorders
Blood in the urine can result from bleeding disorders, affecting the urinary tract's ability to prevent blood from entering the urine.
123
describe epitaxis in bleeding disorders
Frequent nosebleeds can occur due to fragile blood vessels in the nasal mucosa, often
linked to bleeding disorders
124
list some anti platelets
aspirin
clopidogrel and ticagrelor (P2Y12 blockers)
125
how does aspirin work
An antiplatelet medication that inhibits blood clot formation by reducing platelet aggregation (decreases TXA2)
126
how does clopidogrel work
Another antiplatelet agent that inhibits platelet activation by binding to P2Y12, reducing the risk of clot formation.
127
how does ticagrelol work
Another antiplatelet agent that inhibits platelet activation by binding to P2Y12, reducing the risk of clot formation.
128
how does apixaban work
A direct oral anticoagulant (DOAC) that inhibits a specific clotting factor, factor Xa, to
prevent blood clot formation.
129
how does dabigatran work
Another DOAC that targets thrombin, a key enzyme in the blood clotting cascade, to
prevent thrombus formation.
130
how do tissue plasminogen activators work
thrombolytic agent (has enzymes) that promote the conversion of plasminogen into plasminogen, which dissolves blood clots
131
list the factor replacement therapies
vWF
Factor 13
Factor 9
132
how does vWF replacement therapy
replacement therapy involving vWF for individuals with vWD, a bleeding disorder, to correct clotting abnormalities
133
how does factor 13 FRT work
Replacement therapy with Factor 13 for individuals with a deficiency of this clot stabilising factor to improve clot formation and stability
134
how does factor 9 FRT work
Replacement therapy with Factor 9 for individuals with haemophilia B to restore blood clotting and prevent bleeding episodes.
135
indications for anti platelets meds
CVD
Cerebrovascular disease
PVD
136
contraindications for anti platelets
-active/recent haemorrhage
-upcoming recent surgery
-severe thrombocytopenia
137
side effects of anti platelet meds
blood loss
dyspnoea (ticagrelor)
bradycardia (ticagrelor)
GI irritation/ulceration
gout (ticagrelor)
138
indications of unfractioned heparin
renal impairment
139
indications of LMWH
cases when monitoring is difficult
140
contraindications of heparins
active/recent haemorrhages
severe thrombocytopenia
141
side effects of heparins
-Heparin-induced Thrombotic Thrombocytopaenia
Syndrome (HITTS)
-liver enzyme elevation
-bleeding
-alopecia
142
indications for vitamin K antagonists
mechanical heart valves
renal disease
arterial thrombi
143
contraindications for vitamin K antagonists
active/recent haemorrhage
severe thrombocytopenia
pregnancy
144
side effects of vitamin K antagonists
-Heparin-induced Thrombotic Thrombocytopaenia
Syndrome (HITTS)
-bleeding
-alopecia
-liver enzyme elevation
145
indications for DOAC's
-Venous thromboembolism
-prophylactic VTE treatment
-atrial fibrillation
146
contraindications for DOAC's
active/recent haemorrhage
severe thrombocytopenia
severe renal impairment
147
side effects for DOAC's
bleeding
indigestion
livre function abnormality
nausea
skin rashes
headache
148
Outline transfusion of blood products in treating blood disorders
-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
describe antifibrinolytic use for bleeding disorders
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
describe desmopressin use in treating blood disorders
-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
components vs products of blood
-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
why are red cells used transfusion
Oxygen-carrying components of blood used to treat anaemia and increase oxygen delivery to tissues.
153
why are pooled platelets used for transfusion
Fragments of blood cells essential for clot formation in patients with bleeding disorders
154
why is plasma used for transfusion
The liquid portion of blood containing clotting factors and proteins, often used for
patients with coagulation disorders or massive blood loss.
155
why is immunoglobulins used for transfusion
antibodies for immune support
156
why is albumin used for transfusion
clotting factors
157
features of blood donor selection process
testing for
-HIV
-Hepatitis C
-Human T-lymphotropic virus (type II)
-syphillis
-hepatitis B
-Human T-lymphotropic virus (type I)
158
list the major blood types
A
B
AB
O
159
what is ABO/Rhesus incompatibility
-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
list the risks/complications associated with blood transfusion
haemolytic reaction
allergic reaction
febrile non-haemolytic reaction
infection transmission
iron overload
volume overload
161
describe haemolytic reaction as a side effect of blood transfusion
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
describe allergic reaction as side effect to blood transfusion
May cause itching, hives, and, in severe cases, anaphylaxis. Typically, due to allergies to components of the transfused blood or additives.
163
describe febrile non haemolytic reaction as complication of blood transfusion
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
describe infection transmissions as a side effect of blood transfusion
Extremely rare but possible. Bloodborne infections such as HIV, hepatitis, and other pathogens could be transmitted if the donated blood is contaminated.
165
describe iron overload as a side effect of blood transfusion
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
describe volume overload as a side effect of blood transfusions
Rapid infusion of a large volume of blood can lead to fluid overload, congestive heart failure, and pulmonary oedema
167
how to minimise risk of haemolytic reactions in blood transfusion
Stringent blood typing and cross-matching procedures to ensure compatibility between donor and recipient blood.
168
how to minimise risk of febrile non haemolytic reaction in blood transfusions
Leukoreduction, which removes white blood cells from donated blood to reduce the risk of immune reactions.
169
how to minimise infection transmission in blood transfusions
Rigorous screening of donated blood for infectious diseases
170
how to minimise iron overload risk in blood transfusions
limiting unnecessary blood transfusions and using alternative therapy when possible
171
outline the three pillars of patient blood management
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
