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FINALS > Haematology & Electrolytes > Flashcards

Haematology & Electrolytes Flashcards

1
Q

ECG findings hypocalacemia

A

QT interval prolongation secondary to a prolonged ST segment

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2
Q

ECG findings hypercalacemia

A

QT interval shortened due to a shortened ST segment

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3
Q

Pathophysiology of sickle cell disease

A

Autosomal recessive
Mutation in Beta-globin gene - chromosome 11
Produces an abnormal HbS (rather than HbA)
Causes Hb to be “sickle” shaped –> decreased lifespan & get stuck and occlude vessels

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4
Q

Sickle cell and its relation to malaria

A

More common in pt from areas traditionally affected by malaria (Africa, India, middle east, Caribbean)

One copy of gene (sickle cell trait) reduces severity of malaria –> selective advantage of having the gene

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5
Q

What is Sickle cell Trait?

Sickle cell anaemia (HbSS), HbSC disease, Sickle beta-thalassaemia (HbSA), sickle cell trait

A

1 Hb gene + 1 normal HbA gene
Carrier
Asymptomatic

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6
Q

What is sickle cell anaemia HbSS?

Sickle cell anaemia (HbSS), HbSC disease, Sickle beta-thalassaemia (HbSA), sickle cell trait

A

Homozygous for abnormal HbS
Symptomatic - most severe form

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7
Q

With relation to sickle cell

What is HbSC disease?

Sickle cell anaemia (HbSS), HbSC disease, Sickle beta-thalassaemia (HbSA), sickle cell trait

A

1 HbS gene + 1 abnormal HbC gene
Symptomatic (but less severe than HbSS)
“mild” form of sickle cell anemia

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8
Q

What is sickle beta-thalassaemia ?

Sickle cell anaemia (HbSS), HbSC disease, Sickle beta-thalassaemia (HbSA), sickle cell trait

A

1 HbS gene + Beta-thalasaemia trait
Symptomatic - more mild form of sickle cell anemia

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9
Q

Why does sickel cell cause hyposplenism?

A
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10
Q

Sickle cell

What preciptates sickling?

A

Dehydration, infection cold, acidosis, hypoxia

Causes polymerisation of the HbS, initally reversible but with repeated sickling becomes irriversible

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11
Q

Diagnosis of sickle cell disease

A
  1. Screening pregnant women who are carriers
  2. Newborn screening heel prick test @ day 5 of age
  3. Blood film - sickle cells and target cells
  4. FBC - Hb and iron studies
  5. LFTs & Bilirubin raised
  6. Hb electrophoresis by HPLC
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12
Q

General managment of sickle cell disease

A
  • Avoid dehydrayion and other triggers of crises
  • Ensure vaccines up to date
  • Antibiotic prophylaxis with penicillin V daily lifelong (because of hypospenism)
  • Daily folate supplementation
  • Hydroxycarbamide - used to stimualte production of fetal haemoglobin, used if repeat sickle cell crises / acute chest syndrome
  • Blood transfusion for severe anaemia
  • bone marrow transplant is the only cure
  • New treatments: crizanlizumab antibody that stops RBCs sickling
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13
Q

Management of vaso-occlusive crises

A
  1. A-E assessment
  2. Analgesia - IV/SC morphine/paracetamol/ibuprofen
  3. Septic screen
  4. Cross-match & transfusion
  5. FBC, reticulocytes
  6. rehydrate, keep warm
  7. Oxygen
  8. +/- antibiotics
  9. exhcange transfusion - severe cases
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14
Q

Sickle cell crises

What is a vaso-occlusive ‘painful’ crisis?

A

Common, due to microvascular occlusion, causing distal ischaemia
Sx: Pain, fever, and sx of what has caused crisis

Affected areas:
* Often affects the marrow, causing severe pain
* Hands/feet affected in young children –> dactylitis
* Mesenteric ischaemia
* CNS –> stroke, seizures, congitive deficits
* Avascular necoriss (e.g. femoral head)
* Priapism (urological emergency)
* Acute chest syndrome (emergency)

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15
Q

Types of sickle cell crises

A

Vaso-occlusive crises
Acute chest syndrome
Alpastic crisis - due to parvovirus
Sequestration crisis - in children

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16
Q

What is sequestration crisis and why does it only affect children?

A

= emergency
* Caused by rbc blocking blood flow within the sleep –> acutely enlarged and painful spleen
* Pooling of blood in spleen can lead to severe anaemia and hypovolaemia shock
* Only children because in adult the spleen becomes atrophic

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17
Q

Sickle cell disease

What is acute chest syndrome?

A

= Fever or respiratory symptoms with mew infiltrates seen on a chest xray

Causes:
* infection (pneumonia, bronchiolitis)
* fat embolism (from bone marrow)
* pulmonary vaso-occlusion

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18
Q

Sickle cell disease

What is an Aplastic crisis?

A

Caused by parvovirus B19
Sudden reduction in marrow production, especially RBCs
+/- hepatosplenomegaly +/- abdo pain

Usually self limiting

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19
Q

Sickle cell: what is seen on blood film?

A

Sickle cells and target cells

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20
Q

FAT RBC

Causes of macrocytic anaemia

A

F - folate deficiency
A - Autoimmune
T - Thyrotoxicosis
R - Reticulocytosis - compentatory from blood loss
B - B12 deficiency
C - Chemotherapy/cytotoxics

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21
Q

AAAHH

Causes of normocytic anaemia

A

Acute blood loss
Anaemia of chronic disease
Aplastic anaemia
Haemolytic anaemia
Hypothyroidism

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22
Q

TAILS

Causes of microcytic anaemia

A

T - Thalasaemia
A - Anaemia of chronic disease
I - Iron deficiency anaemia
L - Lead poisoning
A - Sideroblastic anaemia

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23
Q

Intravascular haemolytic anaemia - blood test results

A

Decreased Hb
Increased Reticulocytes (haemolysis stimulate erythopoeisis)
Increased unconjugated bilirubin (From Hb Breakdown)
Increased LDH (eznyme in RBC)
Increased Iron (from Hb breakdown)
Decreased haptoglobin (mop up free Hb - used up)

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24
Q

Extravascular haemolytic anaemia - blood test results

A
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25
Q

Intrinsic (to RBC) causes of haemolytic anaemia - causes

A

Thalassaemias
Sickle cell disease
Hereditary spherocytosis
Enzyme defectis (G6PD, Pyruvate kinase)

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26
Q

Extrinstic (to RBC) haemolytic anaemia - causes

A

Immune mediated (cold & warm autoimmune haemolytic anaemia)
Drugs (nitrofurantoin, penicillin, quinine)
Infection
Microangiopathic

27
Q

Causes of Intravascular haemolytic anaemia

A

Microangiopathic haemolysis (= physical trauma to RBC in circulation)
Osmotic lysis (from IV fluids)
Acute tranfusion reactions (ABO incompatability)

28
Q

Causes of extravascular haemolytic anaemia

A

abnormal RBC cleared in reticuloendothelial system (phagocytosis in the spleen)

  • Warm automimmune haemolytic anaemia
  • Hypersplenism
  • Malaria
  • Haemoglobinopathies (Thalassaemia, sickle cell)
  • Hereditary spherocytosis
  • Enzyme deficiency (G6PD, pyruvate kinase)
29
Q

What type of haemolytic anaemia causes brown urine (haemosiderin)

A

Intravascular haemolysis - due to increased iron from breakdown of Haem

30
Q

Causes of Microangiopathic haemolysis

A
  • Haemolytic uraemic syndrome
  • Thrombotic thrombocytopenia purpura (TTP)
  • Prosthetic heart valves
  • Pre-eclampsia / Eclampsia
  • maligant HTN
  • DIC
  • Vasculitis
31
Q

What is cold autoimmune haemolytic anaemia

A

Less common
IgM antibodies predominate
Mainly intravascular haemolysis
Spherocytosis is present as a result of red cell damage.
Haemolysis occurs at <4 degrees
May experience raynauds pnenomenon
Causes: Idiopathic, Infections (mycoplasma, EBV),
Lymphoproliferative disorders

32
Q

What is warm autoimmune haemolytic anaemia

A

IgG antibodies predominate
Mainly extravascular haemolysis
Spherocytosis is present as a result of red cell damage.
Haemolyisis occurs at body temperature
Causes: Primary (idiopathic), Secondary (SLE, lymphoma, or chronic lymphocytic leukemia)

33
Q

Causes of Drug-induced immune haemolytic anaemia

A
34
Q

Management of warm autoimmune haemolytic anaemia

A
  1. Folate
  2. Steroids +/- mycophenolate
  3. Rituximab or splenectomy
35
Q

Management of cold autoimmune haemolytic anaemia

A
  1. Folate and cold avoidance! mainly KEEP WARM
  2. Severe anaemia - give warmed blood
  3. Rituximab +/- chemotherapy
36
Q

Sickle cell

Blood test to differentiate between aplastic crisis and sequestration crisis

A

Reticulocytes
- Reduced in aplastic crisis
- Increased in sequestration crisis

37
Q

Types of thalasaemia

A

Beta thalassaemia
- major
- minior

Alpha thalassaemia
- Major (death in utero)
- HbH disease
- Alpha thalassaemia trait

38
Q

Which conditions show target cells on blood film

A

thalassemia
hepatic disease with jaundice
hemoglobin C disorders
postsplenectomy state

Lesser numbers in:
sickle cell anemia
iron deficiency

39
Q

What is Thalassaemia ?

A

Autosomal recessive
Disorders of Alpha-(x4) or beta- globin (x2) genes
Causing decreased HbA

40
Q

What is Beta-thalasaemia major

A
  • Both genes abnormal - no HbA
  • presents in the first year of life with failure to thrive and hepatosplenomegaly
  • microcytic anaemia
  • Severe anaemia when HbF runs out –> tranfusion dependent
41
Q

What is beta thalasaemia minor

A
  • 1 gene abnormal - almost normal Hb with low MCV (in the 60s)
  • mild anaemia with a disproportionate microcytosis and a raised haemoglobin A2
42
Q

What is alpha thalasaemia

A
43
Q

Management of beta-thalasaemia major

A
  1. Life long monthly blood transfusions
  2. Iron chelation (to prevent iron overload from repeated transfusion) (e.g. desferrioxamine)
  3. Bone marrow transplant is the only cure
44
Q

Blood film of chronic lymphocytic leukaemia

A

Smudge cells

45
Q

Blood film of acute lymphoblastic leukaemia

A

Blast cells

46
Q

Blood film of acute myeloid leukaemia

A

Blast cells + Auer rods

47
Q

Differenitals for petechiae

A
  • Leukaemia
  • Meningococcal septicaemia
  • Vasculitis
  • Henoch-Schonlein Purpura (HSP)
  • Idiopathic Thrombocytopenia Purpura (ITP)
  • Non-accidental injury
48
Q

What condition can myelodysplastic disorder transform into?

A

Acute myeloid Leukaemia

49
Q

CRABBI

Features of Myeloma

A

C - HyperCalcaemia
R - Renal dysfunction (light chain deposition within the renal tubules)
A - Anaemia (Decreased erythropoeisis)
B - Bleeding (decreased platelets)
B - Bone pain/lesions (osteoclast overactivity creates lytic bone lesions)
I - Infection (reduced production of normal immunoglobulins)

50
Q

What are Howell-Jolly bodies

A

nuclear remnants that are found in the RBCs of patients with reduced or absent splenic function

51
Q

Universal donor

A

O neg

52
Q

Universal receptient

A

AB positive

53
Q

Key difference between TACO and TRALI

A

Trali –> hypotension

Taco –> hypertension

54
Q

Components of haemolysis screen

A

LDH
Unconjugated bilirubin
Haptoglobin

55
Q

Chronic Lymphocytic leukaemia

What is Richter’s transformation?

A

CLL can transform into high-grade lymphoma - making patients suddenly unwell

When leukaemia cells enter lymph nodes and change into a high-grade fast growing Non-Hodgkin’s Lymphoma

56
Q

Which coagulation disorders is desmopressin used for and why?

A

Haemophilia
Von Willebrands disease

It is an antidiuretic that causes secretion of factor VIII and vWF into plasma

56
Q

Which coagulation disorders is desmopressin used for and why?

A

Haemophilia
Von Willebrands disease

It is an antidiuretic that causes secretion of factor VIII and vWF into plasma

57
Q

Lymphoma

Where are reed-sternberg cells seen?

A

Hodgkin lymphoma
They are mutated B cells
lymph node biopsy

58
Q

Staging system for lymphoma

A

Ann Arbor staging system

Stage 1: Confined to one region of lymph nodes.
Stage 2: In more than one region but on the same side of the diaphragm (either above or below).
Stage 3: Affects lymph nodes both above and below the diaphragm.
Stage 4: Widespread involvement including non-lymphatic organs such as the lungs or liver.

59
Q

Blood transfusion threshold for a patient with ACS

A

80 g/l

70 g/L in most people

60
Q

What are myeloproliferative disorders?

A

Overproduction of cells in bone marrow - but maturation still occurs
Differenitated myeloid cell subtype expasion

Maturation arrest can occur –> acute myeloid leukaemia (all of the different types can become AML)

61
Q

Types of myeloproliferative disorders

A

Chronic myeloid Leukaemia (High WBCs)
Polycythaemia rubra vera (High RBC +/- platelets)
Essential thrombocythaemia (High platelets)
Primary myelofibrosis (fibrosis of bone marrow)

62
Q

JAK2 associated myeloproliferative disorders

A

Polycythaemia rubra vera (High RBC +/- platelets)
Essential thrombocythaemia (high platelets)

63
Q

What bllod cancer is associated with BCR-ABL

A

Chronic myeloid leukaemia

FINALS (19 decks)

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