Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

TAS > Haematology > Flashcards

Haematology Flashcards

(98 cards)

Start Studying
1
Q

Haematopoeisis

A

Process through which all types of mature blood cells are produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do Erythroid / megakaryocytic lineage cells give rise to?

A

Red cells and platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do granulocyte/ macrophage lineage give rise to?

A

Granulocytes and monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do lymphoid lineage give rise to?

A

T cells, B cells and NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Primitive haematopoeisis

A

Started in yolk sac
Give rise to red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When is primitive haematopoeissi replaced by definitive haematopoiesis at?

A

5-6 weeks gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is definitive haematopoiesis?

A

Produces all blood cell types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are definitive heamtopoietic stem cells created?

A

Develop in the aorta-gonad mesonephros region of the dorsal aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When do HSC’s migrate to AGM to fetal liver and spleen?

A

6-7 weeks gestation
Liver is then the primary site of haematopoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is main site of heamtopoiesis at 3rd trimester and at birth?

A

Bone marrow
Originally occurs in all areas of bone marrow - restricted to axial skeleton and proximal ends of long bones later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does metal Hb consist of? When does it start getting produced in gestation?

A

2 alpha chains, 2 gamma chains
Produced from 3-4 weeks of fatal life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does the binding and releasing of oxygen cause?

A

Causes small configuration of globin chains in Hb molecule
Oxygen is unloaded, Hb molecule opens up allowing 2,3-diphosphoglcyerate (2-3 DPG) to enter reducing oxygen affinity and ensuring Hb molecule does not take up oxygen from tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is average life span of RBC?

A

120 days in older children and adults
90 days in neonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Iron absorption

A

Iron in diet is absorbed by enterocytes in duodenum either in Fe2+ form or as haem
Ferroportin, iron transporter protein, transports iron across basolatereal membrane of enterocyte into the blood stream
Iron binds to transferrin and transported to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Transferrin

A

Transferrin can bind to 2 molecules of iron and deliver this to cells that express transferrin receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ferritin

A

Storage of iron
Shows total body iron levels (in absence of inflammation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why are Hb values higher in utero? What are the values?

A

Higher oxygen affinity of HbF and fall during first few months of life
Neonate - <130
1-12 months <100
1- 12 years <110

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of Reduced MCV - microcytosis

A

Iron deficiency
Thalassaemia major or thalassaemia trait
Anaemia of chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of increased MCV - macrocytosis

A

Folate deficiency
Vit B12 deficiency
Diamond-Blackfan anemia
Liver Disease
Hypothroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diamon-Blackfan Aneamia

A

Genetic disorder
Presents with anaemia at birth or during infancy
50% physical abnormalaties - craniofacial abnormalities, thumb and growth restrictions
Autosomal dominant
Mutations in ribosomal protein genes - RPS19
Bone marrow biopsy
Treatment - steroids and regular blood transfusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Transient erythroblastopenia

A

Parvovirus-induced red cell aplasia
TEC - presents 2 year olds
Transient red cell aplasia triggered by unknown infective agent
Recovery occurs spontaneously within 4-8 weeks
Normocytic with neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Blood tests for Haemolytic Anaemia

A

Reduced Hb
Raised reticulocytes - immature red blood cells
Raised unconjugated bilirubin
Raised LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Intravascular haemolysis

A

Occur in circulation
Depletion of haptoglobin
Increase LDH
Large numbers of fragmented RBCs (schisocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Extravascular haemolysis

A

Takes place in spleen or liver - can occur in lung
Spleen or liver macrophage Fc receptors bind immunoglobulin attached to RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Inherited haemolytic disorders
Red cell membrane defects - hereditary spherocytosis, hereditary ellipocytosis Red cell enzyme defects - G6PD deficiency and pyruvate kinase deficiency Haemoglobinopathies - sickle cell disorders, thalassaemias
26
Acquired Haemolytic disorders
Autoimmune - idiopathic, SLE, JIA Microangiopathic - HUS, TTP, haemangiomas Infection - Malaria, septicaemia Other - burns, lead poisoning
27
What conditions cause Positive DAT's
Haemolytic disease of newborn Autoimmune haemolytic anaemia Drug-induced anaemia Haemolytic transfusion reactions
28
Red cell enzyme defects
Glucose-6-phosphate dehydrogenase deficiency Pyruvate kinase deficiency
29
What does G6PD do?
Protects cell from oxidative damage Catalyses first step of pentose phosphate pathway
30
How is G6PD deficiency inherited?
X-linked disorder
31
What causes an acute haemolytic crisis in G6PD deficiency
Infection Medications - co-trimoxazole, dapsone, nitrofurantoin, chloramphenicol, chloroquine, aspirin
32
Blood results in acute haemolytic crisis
Reduced Hb Raised reticulocytes Hyperbilibuinaemia Increased LDH
33
Blood film in G6PD deficiency
fragmented red cells 'bite' cells and polychromasia Heinz bodies (denatured hB) Not in crises - blood film normal
34
Pyruvate kinase deficiency
Results in sufficient ATP production Causes rigid cells and haemolysis
35
How is pyruvate kinase deficiency inherited?
Autosomal recessive
36
Pyruvate kinase deficiency blood film
Prickle red cells
37
Autoimmune haemolytic anaemia - what it is and types
Produce antibody against their own red cells Types - warm and cold (depends if antibody binds most strongly at 37 degrees or 4 degrees)
38
Warm AIHA
usually IgG antibodies
39
Cold AIHA
usually IgM antibodies
40
Blood results in AIHA
unconjugates hyperbilirubinaemia Raised LDH Increased retidulocytes Reduced heptoglobin levels Postive DAT
41
Treatment in AIHA
Immunosuppressive treatment - steroids, azathioprine, cyclosporin
42
Lead poisoning - bloods and blood film
Microcytic anaemia Blood film - basophilic strippling (basophilic granules seen in RBC)
43
Thalassaemias
Genetic defect that results in reduced rate of synthesis of alpha-globin or beta-globin chains
44
alpha thalassaemia
Gene deletion of a-globin Normally inherit 4 (each copy of chromosome 16 has 2 copies) Deletion of one or two = trait, asymptomatic Loss of all 4 = a-thalassaemia major = death in utero or hydrops fetalis = death in few hours of birth
45
haemoglobin H disease
Deletion of 3 alpha globin genes = HbH disease Microcytic hypo chromic Splenomegaly Excess of B-globin chain forms an abnormal Hb called HbH - consists of only B-globin chains Detected - high-performance liquid chromatogaphy HPLC
46
Beta thalassaemia
mutations in B-globin gene (2 copies chromosome 11) excess of a-globin as result - precipitate in erythrocytes = anaemia 2nd to ineffective erythropoiesis and haemolysis Blood film - target cells, nucleated red blood cells and basophilic stippling
47
What age dose beta thalassaemia present?
3-6 months Hb production switched from HbF to HbA HbF = a-globin and gama globo HbA = a-globin and beta-globing 6 month roughly 95% HbA
48
Treatment for B-thalassaemia major
Regular blood transfusions Careful iron overload - iron chelation therapy started 10-15 RBC transfusions given or serum ferritin increases above 1000 - desferrioxamine
49
What causes Sickle Cell disease
Point mutation in b-globin gene= single amino acid change (valine for glutamine) HbS is relatively insoluble and polymereizes when exposed to low oxygen tension Creates sickle cells - dehydrated, rigid and less deformed = obstruct blood flow
50
Types of sickle cell disease
Sickle cell anaemia - homozygous for B-globin mutations HbSS HbSC disease - single b-globin mutation in combination wit hHbC mutation HbSC S B-thalassaemia - B-thalassaemia mutation in combination with B-globin
51
Types of sickle cell crisis
Veno-occlusive crisis (painful) Sickle chest crisis Splenic/ hepatic sequestration Aplastic crisis - 2nd to parvovirus B19 Cerebral infarction
52
Management of sickle cell disease
- Avoid factors that may precipitate a crisis - cold, dehydration, over-strenuous exercise - Twice daily penicillin proph. and vaccination - Folic acid
53
What dose Bone marrow failure cause
Pancytopenia
54
Fanconi's anaemia
Physical abnormalities - short stature, microcephaly, skin hyperpigmentation Affected gene FANC genes BRCA 2
55
Triad of Shwachman-Diamond syndrome
-Bone marrow failure -Pancreatic insufficiency -Skeletal abnormalities
56
What is DIC
intravascular deposition of fibrinogen and consumption of coagulation factors and platelets
57
What triggers DIC
Infection Malignancy Blood transfusion Liver failure Widespread tissue damage
58
Coagulation screen - what does PT measure
II, V, VII, X Extrinsic + common
59
What clotting factors does APTT test for
II, V, VIII, IX, X, XI, XII Intrinsic and common
60
What clotting factors does thrombin time or fibrinogen test for
Fibrinogen
61
Steps of heamostatis
1. Vasconstriction 2. Temporary platelet plugging 3. Coagulation cascade 4. Fibrinolysis 5. Regeneration
62
How do you test for 1st haemostatis (temporary platelet plugging(
Bleeding Tim e PLT count PLT aggregation ANTI-PLATLETS
63
What test do you use ?for testing coagulation
PT aPTT TT
64
What is haemophilia A a factor defieicny of?
Factor 8
65
What prolongs pt
Vit K defiency warfarin liver disease factor VIII, III, x defiency APS heparin DIC
66
What prolongs aPTT
heparin Haemophillia Liver disase aPS warfarin DIC
67
What prolongs TT
Hypofibrinogen Thombin inhibitor Heparin DIC liver disease warfarin
68
Where do DOACs act?
Antirhombin and X
69
MoA of heparin
Increased antithrombin
70
How does haemophilia present
Presents with joint and soft tissue bleeding
71
What are test results in haemophilia And B
Long aPTT, normal PT
72
Treatment for haemophilia
Recombinant sources of clotting factors
73
Complication of factor treatment
Development of inhibit antibodies that block efficacy of the factor Most commonly ass. with factor 8
74
What else can be used as an alternative to factor concentrate in mild haemophilia A
Desmopressin Stimulates release of factor VIII and von Willebrand factor
75
What is Von Willebrand factor
Large glcyoprotein present in endothelial cells and platelets
76
What are the two main functions of VWF
- Promote platelet adhesion to damaged endothelium - To bind and stables factor VIII, protecting It from proteolytic degradation
77
Presentation fVWF disease
Mucosal bleeding Menorrhagia Easy brushing
78
How do you diagnose VWF disease
- prolonged APTT - Factor VIII: C will be reduced - VWF ristocetin cofactor assay
79
How do antifibrinolytics work? (Tranexamic acid)
Prevent plasminogen to plasmin Plasmin breaks down strands in fibrongen
80
Which clotting factors are low at birth
Vitamin K dependent clotting factors
81
What is immune thrombocytopenia purpura
Diagnosis of exclusion
82
Treatment of ITP
Self-limiting If fails to respond within 6 months (chronic iTP) - short course of steroids With bone marrow sample prior to treatment IV immunoglobulins can be used
83
How does rituximab work
Anti-CD20 monoclonal antibody B cells involved in pathogenesis of ITP
84
Why is chicken pox an important cause of stroke in childhood
Reduction in anticoagulant Protein S - increases hisk of thrombosis
85
What does Protein C do?
Inhibits factors V and VIII
85
What does protein S do?
Enhances action sof protein C
86
What is the most common inherited thrombophillia
Factor V leiden Mutation Prevents protein C bind to and inhibiting factor V
86
What are inherited risk factors of thrombosis
Defiencies of - Antithrombin Protein C Protein S
87
Aquired risk factors of thrombosis?
Presence of central venous line Malignancy DIC SLE Trauma Polycythaemia
88
ABO blood group system - group a
Antigens - A Antibodies - Anti-B Compatible groups - A, O
89
ABO blood group systems - group B
Antigens - B Antibodies - Anti-A Compatible groups - B, O
90
ABO blood groups - AB group
Anitgens - AB Antibodies - none Compatible group s- A, b, ab, O
91
ABO groups - O group s
Antigen - none Antibodies s- Anti - A, anti -B Compatible O
92
How to present RhD haemolytic disease of newborn?
Mum's have blood group and antibody screen at booking If were RhD negative - 28 weeks - another antibody screening to see if sensitisation If lack anti-d antibodies in 2nd trimester - given anti-D prop 28- 34 weeks If anti-D antibody detected - antibody levels need to be measured to predict risk of developing HDN
93
How to calculate volume of red cell transfusions
Volume to be transfused = weight x Hb increment x 4
94
95
96

TAS (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions