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Belle Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

Describe the common pathway of the coagulation cascade

A

Intrinsic and extrinsic: Factor X > Factor Xa

Factor II (Prothrombin) > (Xa) > Factor IIa (Thrombin)

Fibrinogen > (IIa) > Fibrin

Factor XIII > Factor XIIIa

Fibrin > (XIIIa) > Fibrin clot

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2
Q

Name four causes of neutropenia

A

Infection e.g. EBV
Drugs e.g. phenytoin
Autoimmune
Myeloma

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3
Q

Name four causes of lymphocytopenia

A

Drugs e.g. steroids
Infection (post viral is common)
Renal impairment
Rheumatoid e.g. SLE, RA

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4
Q

Name four causes of neutrophilia

A

Infection e.g. bacterial
Drugs e.g. steroids
Leukaemia
Inflammation e.g. rheumatoid arthritis

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5
Q

Name four causes of lymphocytosis

A

Infection e.g. EBV
Stress
Vigourous exercise
Malignancy (CLL/ALL)

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6
Q

Name four causes of monocytosis

A

Malaria
Typhoid
TB
Myelodysplastic syndromes

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7
Q

Name four causes of eosinophilia

A

Asthma
Parasitic infections
Drugs e.g. peniciloin
Smoking

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8
Q

Name four causes of thrombocytopenia

A

Problems with production:
Viral infection e.g. EBV
Sepsis
B12/folate deficiency

Problems with destruction:
Drugs e.g. NSAIDs
Alcohol
ITP

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9
Q

Name four causes of thrombocytosis

A

Inflammation
Haemorrhage
Splenectomy
Iron deficiency

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10
Q

Name four things that cause PT/INR levels to change

A

Warfarin
Vitamin K deficiency
Liver disease
Disseminated intravascular coagulation

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11
Q

What does PT/INR measure?

A

The time taken for a blood clot to form via the EXTRINSIC pathway

Overall clotting factor synthesis/consumption

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12
Q

What does APTT measure?

A

(Activated partial thromboplastin time)

The time taken for blood to clot via the INTRINSIC pathway

Indicates issues with factors VIII, IX and XI:

  • Haemophilia A (VIII)
  • Haemophilia B (IX)
  • Haemophilia C (XI)
  • Von Willebrand’s disease (vWF pairs with factor VIII)
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13
Q

What does bleeding time measure?

A

Overall platelet function and levels
Measure of how long it takes a patient to stop bleeding from a wound

Platelet specific disorders increase bleeding time e.g. vWF disease, ITP, DIC, thrombocytopaenia

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14
Q

What does thrombin time measure?

A

How fast fibrinogen is converted to fibrin (by thrombin)

Prolonged by DIC, liver failure, malnutrition, and abnormal fibrinolysis

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15
Q

Name four causes of microcytic anaemia

A

TAILS:

Thalassaemia
Anaemia of chronic disease 
Iron deficiency anaemia (most common cause) 
Lead poisoning
Sideroblastic anaemia
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16
Q

Name four causes of normocytic anaemia

A

Acute blood loss
Anaemia of chronic disease

Haemolytic anaemia
Hypothyroidism

Pregnancy

Bone marrow failure
Renal failure

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17
Q

Two types of macrocytic anaemia

A

Megaloblastic

Normoblastic

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18
Q

Name two causes of megaloblastic macrocytic anaemia

A

B12 deficiency

Folate deficiency

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19
Q

Name four causes of normoblastic macrocytic anaemia

A 
Alcohol excess (affects bone marrow) 
Liver disease  
Iatrogenic e.g. azathioprine
Reticulocytosis
Hypothyroidism
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20
Q

Name four symptoms of anaemia

A 
Fatigue 
Shortness of breath (dyspnoea) 
Palpitations 
Anorexia 
Headache
Faintness
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21
Q

Name four signs of anaemia

A

Pallor e.g. conjunctival
Tachycardia
Hyperdynamic circulation e.g. systolic flow murmur
Raised respiratory rate

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22
Q

Name four causes of iron deficiency anaemia

A

Blood loss (most common cause in adults) e.g. GI bleed
Insufficient dietary iron (most common cause in children)
Increased requirements e.g. pregnancy
Inadequate iron absorption e.g. coeliac disease, IBD

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23
Q

Name three specific signs of iron deficiency anaemia

A

Koilonychia
Angular cheilosis
Atrophic glossitis

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24
Q

Blood film signs of megaloblastic macrocytic anaemia

A

Hypersegmented neutrophils and oval macrocytes

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25
Mediastinal lymphadenopathy
Hodgkin lymphoma (85%)
26
Primary haemostasis
Initiation and formation of the platelet plug (platelet activation)
27
Secondary haemostasis
Formation of fibrin clot (coagulation cascades)
28
Dabigatran
Inhibits thrombin (DIRECT/DOAC)
29
Initial activation of platelets
Collagen binding to GPIIb/IIIa via vWF
30
Two hallmarks of AML
Gym hypertrophy | Auer rods
31
Most common leukaemia in children
ALL
32
Multiple myeloma features
``` Old CRAB Age (>65) Calcium (hypercalcaemia) Renal Anaemia Bone lesions ```
33
Multiple myeloma protein found in urine
Bence-Jones protein
34
Hodgkin lymphoma hallmark features
Lymphadenopathy painful after drinking alcohol Reed-Sternberg cells Bimodal distribution (early 20s and then 70s)
35
Ann Arbor staging for lymphoma
Stage 1: single lymph node Stage 2: 2 or more (same side of diaphragm) Stage 3: 2 or more (both sides of diaphragm) Stage 4: extralymphatic
36
Blood test results for DIC
``` Thrombocytopenia Long PT Long APTT Low fibrinogen Raised D-dimer ```
37
Mutation in polycythaemia vera
JAK2
38
Polycythaemia definition
High concentration of erythrocytes in the blood
39
Monoclonal gammopathy of undetermined significance (MGUS)
Close link to multiple myeloma (1% of cases develop into myeloma)
40
Philadelphia chromosome association
Chronic myeloid leukaemia | t (9;22)
41
Most common type of leukaemia in adults
AML
42
Blood film CLL
Smudge cells (abnormally fragile lymphocytes)
43
Bone marrow biopsy AML
Auer rods
44
ALL Px
``` Anaemia Bleeding/bruising (thrombocytopenia) Infections (neutropenia) Hepatosplenomegaly Lymphadenopathy CNS infiltration > headaches, CN palsies Associated with Downs Syndrome ```
45
Leukaemia associated with warm haemolytic anaemia
CLL
46
Richters transformation
Complication of CLL where the cancer transforms into Non-Hodgkin lymphoma
47
Smudge cells on blood film
CLL
48
Three phases including a 5 year asymptomatic chronic phase
Chronic myeloid leukaemia
49
Multiple myeloma blood film
Rouleaux formation
50
Relative polycythaemia
Normal number of erythrocytes but reduction in plasma | - obesity, dehydration, excessive alcohol consumption
51
Absolute polycythaemia
Increased number of erythrocytes Primary: bone barrow abnormality (polycythaemia vera) Secondary: overstimulation of bone marrow (renal cancer, PKD, COPD)
52
Myeloproliferative neoplasms (disorders)
Disorder of the bone marrow that causes abnormal growth of blood cells (platelets, WBCs, RBCs)
53
2 types of myeloproliferative neoplasms
Chronic myeloid leukaemia | Polycythaemia vera
54
Polycythaemia vera Px
Headaches, dizziness, fatigue, blurred vision Erythema - hands, face, feet Itching (especially after contact with warm water) Hepatosplenomegaly
55
Polycythaemia vera Tx
Venesection Low dose aspirin daily Hydroxycarbamide for those at risk of thrombus
56
Leukaemia pathophysiology
Immature blast cells uncontrollably proliferate, taking up space within the bone marrow, and then infiltrating into other tissues Lack of space within the bone marrow = fewer healthy cells can mature and be released into the blood (anaemia, thrombocytopenia)
57
Thalassaemia
Autosomal recessive disorder causes less production of Hb | Alpha globin or Beta globin
58
FBC: anaemia, thrombocytopenia, neutropenia | Type of leukaemia?
Acute lymphoblastic leukaemia
59
Autosomal recessive (% inheritance)
Two carriers: 25% One carrier, one disease: 50% Two disease: 100%
60
Sequestration crisis
Occurs in acute sickle cell crisis Blood outflow from the spleen is blocked Splenomegaly (due to blood accumulation)
61
Aplastic anaemia
Pancytopenia
62
General anaemia symptoms
Fatigue, headache, dizziness, dyspnoea
63
General anaemia signs
Tachycardia, skin pallor, conjunctiva pallor, intermittent claudication
64
Sign of iron deficiency anaemia
Koilonychia (spoon shaped nails) | Angular stomatitis
65
Signs of B12 deficiency
Angular stomatitis | Lemon-yellow skin
66
Signs of haemolytic anaemia
``` Jaundice Dark urine (due to presence of Hb in urine) ```
67
``` FBC: low Hb, low MCV <95fl Ferratin: low Transferrin: raised Transferrin saturation: low Blood film: small, hypochromic cells ```
Iron deficiency anaemia
68
Transferrin vs Transferrin saturation
Transferrin saturation is the ratio of serum iron to the TIBC (total iron binding capacity) Transferrin is the main iron transport protein; its synthesis is inversely proportional to body iron stores. Hence, levels increase in iron deficiency to facilitate iron absorption. Transferrin levels are often low in inflammatory anaemia as transferrin expression is negatively affected by cytokines.
69
``` FBC: low Hb, low or normal MCV, high ESR Ferratin: normal Serum iron: low Transferrin: low Transferrin saturation: low ```
= AOCD Chronic infection Chronic inflammation (connective tissue diseases) Neoplasia
70
MCV: low Serum iron: increased Transferrin: increased Ferratin: increased
Sideroblastic anaemia: Iron levels normal but the body can’t insert the iron into Hb Blood film shows ringed sideroblasts
71
Reticulocytes: raised Bilirubin: raised Urobilinogen: raised Blood film: schistocytes
Haemolytic anaemia (normocytic)
72
Causes of haemolytic anaemia
Sickle cell Thalassaemia Sepsis/DIC Autoimmune
73
Causes of B12 deficiency
Pernicious anaemia Malabsorption (coeliac, IBD, ileostomy) Decreased intake Chronic nitrous oxide use
74
Pernicious anaemia
Lack of intrinsic factor (usually produced by parietal cells in the stomach and allows B12 absorption in the terminal ileum) = causes B12 deficiency anaemia
75
B12 foods
Meat, fish, eggs, milk
76
Why does severe B12 deficiency cause neurological signs and symptoms
demyelination of the spinal cord
77
Sickle cell genetics
Autosomal recessive, gene on cr11 Disease = Homozygous Trait = Heterozygous
78
Sickle cell pathophysiology
Glutamic acid substitution with valine = Beta globin polymerisation = sickled cells, endothelial damage, reduced O2 carrying capacity
79
Acute sickle cell presentation (crisis)
``` MSK: bone pain, joint pain Infection Respiratory: dyspnoea, cough, hypoxia CNS: stroke Sequestration crisis ```
80
Risk factors for sickle crisis
Low O2 Cold weather Parvovirus B19 Exertion
81
Chronic complications of sickle cell disease
Avacular necrosis of joints Silent CNS infarcts Retinopathy Nephropathy
82
Sickle cell Ix
FBC: low MCV, low Hb Blood smear: sickled erythrocytes Sickle solubility test (does not distinguish trait from disease) Hb electrophoresis = HbS band
83
Sickle cell crisis Tx
Morphine/O2/IV fluids/Transfusion exchange
84
Chronic sickle cell disease Tx
Hydroxycarbamide (inhibits ribonucleotide reductase, decreases DNA synthesis, raises HbF levels)
85
ADAM TS13 protein deficiency
Thrombotic thrombocytopenic purpura
86
Thrombotic thrombocytopenic purpura pathophysiology
PRIMARY HAEMOSTASIS PROBLEM: Deficiency in ADAM TS13 protein (vWF cleaving protease) = can’t breakdown clumps of vWF into useful monomers = microvascular clots form
87
TTP Px
Adult female | Fatigue, fever, jaundice, petechiae, purpura, neurological deficit
88
TTP Ix
FBC: raised WCC, low Hb, low platelets Other: raised bilirubin (haemolytic anaemia), raised creatinine (renal damage from clots) Blood smear: schistocytes Clotting: normal PT and APTT (primary not secondary problem)
89
TTP Tx
Plasma exchange IV methylprednisolone Monoclonal Abs Contraindicated: platelet transfusion
90
Immune thrombocytopenic purpura
Autoimmune Primary haemostasis (GPIIb/IIIa) Risk factors: paediatric, post-viral
91
DIC Ix
Bloods: low platelets, low fibrinogen, high D-dimer, long PT, long APTT Blood smear: schistocytes
92
DIC Tx
Treat underlying cause (e.g. sepsis) Low fibrinogen = cryoprecipitate Low platelets = platelet transfusion
93
Haemophilia A
Intrinsic pathway: Factor VIII deficiency X-linked recessive Male > Female
94
Haemophilia Px
Soft tissue bleeding pattern: muscles, joints, haematoma formation
95
Haemophilia A Ix
APTT: long PT may be normal Genetic testing + factor VIII testing
96
Haemophilia A Tx
Recombinant factor VIII
97
Type 1 Von Willebrands disease
Autosomal dominant Defect in QUANTITY of vWF - Primary haemostasis disorder
98
Why can vWF disease result in factor VIII deficiency
vWF protects VIII from liver protein C destruction
99
Presentation of vWF disease
Mucocutaneous bleeding (epistaxis, GI bleeds, menorrhagia, easy bruising)
100
vWF disease Ix
Plasma vWF measurement | APTT can be prolonged if factor VIII low
101
Type 1 vWF Tx
Desmopressin | Tranexamic acid can reduce acute bleeding
102
ALL/AML treatment
Blood and platelet transfusions Chemotherapy Stem cell/bone marrow transplant Antibiotics
103
CLL Tx
Chemo (Rituximab)
104
CML Tx
Chemo Stem cell/bone marrow transplant Tyrosine kinase inhibitors (Imatinib)
105
ABVD Chemotherapy used in which cancer
Hodgkin lymphoma Tx
106
RCHOP chemotherapy
Non-Hodgkin lymphoma | Rituximab, cyclophosphamide, prednisolone
107
G6PD deficiency features
X-linked West Africa, Middle East Haemolytic anaemia + Splenomegaly Heinz bodies/bite cells on blood smear
108
Haemolytic uraemic syndrome
Triad: Haemolytic anaemia AKI (e.g. oliguria, haematuria) Thrombocytopenia Differentiate from TTP with ADAMTS13 testing
109
A 50-year-old woman weight loss anaemia splenomegaly Haemoglobin: LOW Platelets: VERY HIGH White cell count: VERY HIGH Blood film: Leucocytosis with all stages of granulocyte maturation
CML = increased turnover of MYELOBLAST cells (further differentiate into basophils, neutrophils and eosinophils)
110
Reduced reflexes | Type of anaemia?
Macrocytic anaemia caused by hypothyroidism OR B12 deficiency

Belle Phase 2a (14 decks)

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