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MEH Diseases > Haematological Disorders > Flashcards

Haematological Disorders Flashcards

1
Q

Describe hyposplenism
-Causes
-Blood film
-Risk
-Treatment

A

Causes:
-Splenectomy
-Sickle cell disease
-GI diseases e.g. Coeliac, Crohn’s, Ulcerative Colitis
-Autoimmune disease: Rheumatoid arthritis

Blood film:
-Reveals Howell-Jolly bodies

Risk:
-Risk of sepsis from encapsulated bacteria e.g streptococcus pneumoniae, Haemophilus influenzae

Treatment:
-Patients must be immunised and given life long antibiotic prophylaxis

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2
Q

Describe neutrophilia
-What is it?
-Causes

A

-An increase in the absolute number of circulating neutrophils

Causes:
-Infection
-Smoking
-Acute inflammation
-Drugs

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3
Q

Describe neutropenia
-Neutrophil count
-Causes (reduced production, increased removal or use)
-Consequences
-Neutropenic sepsis and its treatment

A

-Neutrophil count <1.5x10^9/L (severe if <0.5x10^9/L)

Causes:
-Reduced production: B12/folate deficiency, aplastic anaemia, radiation, drugs
-Increased removal or use: Immune destruction, sepsis, splenic pooling

Consequences:
-Severe life threatening bacterial/fungal infection
-Mucosal ulceration e.g. painful mouth ulcers

Neutropenic sepsis is a medical emergency, intravenous antibiotics must be given immediately

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4
Q

Describe anaemia
-Definition
-Signs and symptoms

A

-Anaemia is when the haemoglobin concentration is lower than the normal range.

Signs and symptoms:
-Symptoms: Shortness of breath, palpitations, headaches, claudication, confusion, lethargy, angina
-Signs: Pallor, tachycardia, hypotension

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5
Q

Why might anaemia develop?
-Bone marrow
-Peirpheral RBCs
-Removal

A

Bone marrow:
-Reduced or dysfunctional erythropoiesis
-Abnormal haem synthesis
-Abnormal globin chain synthesis

Peripheral RBCs:
-Abnormal structure
-Mechanical damage
-Abnormal metabolism

Removal:
-Increased removal by reticuloendothelial system

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6
Q

Describe folate deficiency
-Causes
-Symptoms
-When do you require more folate?

A

Causes:
-Dietary deficiency
-Disease of duodenum and jejunum (coeliac, Crohn’s)
-Alcoholism
-Drugs which inhibit dihydrofolate

Symptoms:
-Diarrhoea
-Reduced sense of taste
-Numbness and tingling in hands and feet
-Muscle weakness

When do you require more folate?
-Pregnancy
-Increased erythropoiesis
-Severe skin disease

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7
Q

Vitamin B12 deficiency
-Causes
-Symptoms

A

Causes:
-Dietary deficiency
-Lack of intrinsic factor
-Crohn’s disease

Symptoms:
-Glossitis and mouth ulcers
-Diarrhoea
-Parasthesia

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8
Q

Treatment of vitamin B12 and folate deficiency
-Folate
-Pernicious anaemia
-Other B12 deficiency

A

Folate:
-Oral folic acid

Pernicious anaemia:
-Hydroxycobalamine intramuscular for life

Other causes of B12 deficiency:
-Oral cyanocobalamine

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9
Q

Appearance of megaloblastic anaemia on blood film

A

-Anisopoikilocytosis (variance in shape and size)
-Tear drop red cells
-Ovalocytes
-Hypersegmented neutrophils
-Macrocytic red cells

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10
Q

Investigation of megaloblastic anaemia:
-What levels are low?
-What levels are raised?

A

Low:
-Haemoglobin
-Erythrocyte count
-Reticulocyte count

Raised:
-MCV
-Serum ferritin
-LDH
-Bilirubin

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11
Q

Microcytic Anaemia:
-TAILS

A

-Thalassaemia
-Anaemia of chronic disease
-Iron deficiency anaemia
-Lead poisoning
-Sideroblastic anaemia

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12
Q

Anaemia of chronic disease
-What is it?
-What is released by immune cells
-Erythropoietin production
-Hepcidin production and its effects
-Overall inhibition

A

-Anaemia of chronic disease is an inflammatory condition, e.g. rheumatoid arthritis, chronic infection.

-Immune cells release cytokines, e.g. IL6

-Inhibition of erythropoietin production by kidneys

-Increased production of hepcidin by liver -> inhibition of ferroportin -> plasma iron reduced

-This all leads to inhibition of erythropoiesis in bone marrow, therefore -> anaemia

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13
Q

Iron deficiency
-Causes
-At risk groups
-Signs and symptoms
-Treatment

A

Causes:
-Insufficient iron in diet
-Malabsorption of iron
-Bleeding
-Increased requirement e.g. pregnancy

At risk groups:
-Infants
-Children
-Women of child bearing age
-Geriatric age group

Signs and symptoms:
-Physiological effects: Tiredness, pallor, increased respiratory rate, angina, reduced exercise tolerance
-Epithelial changes: Angular cheilitis, glossitis, koilonychia (spoon nails)

Treatment:
-Dietary advice
-Oral iron supplements
-IV iron
-Blood transfusion

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14
Q

FBC results in iron deficiency anaemia

A

-Low MCV
-Elevated platelet count
-Normal or elevated WBC count
-Low serum ferritin
-Low reticulocyte haemoglobin cotent (CHr)

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15
Q

Peripheral blood film results in iron deficiency anaemia

A

-RBCs are microcytic and hypochromic
-Anisopoikilocytosis
-Sometimes pencil cells and target cells

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16
Q

Hereditrary Haemochromatosis
-Mode of inheritance and what it is
-What happens?
-Treatment

A

-Autosomal recessive disease caused by mutation in HFE gene

-Too much iron enters cells and accumulates in end organs causing damage

-Treat with venesection

17
Q

Thalassaemia
-Blood smear
-Consequences
-Treatment

A

Blood smear:
-Hypochromic and microcytic red cells
-Anisopoikilocytosis with frequent target cells and circulating nucleated red blood cells and Heinz bodies

Consequences:
-Extramedullary haemopoiesis
-Reduced O2 delivery causing stimulation of EPO
-Iron overload (major cause of premature death)
-Reduced life expectancy

Treatment of thalassaemia:
-Red cell transfusion from childhood
-Folic acid
-Iron chelation

18
Q

Sickle cell disease
-Mode of inheritance and mutation
-Region most common
-Amino acid change
-3 crises
-Symptoms

A

Mode of inheritance and mutation:
-Autosomal recessive disease resulting form a mutation of B-globin gene

Region:
-Black Africans
-Arab
-Mediterranean
-South Asia

Amino acid change:
-GAG codon changed to GTG, causing glutamic acid to be replaced by valine

Crises:
-Haemolytic
-Vaso-occlusive
-Aplastic anaemia

Symptoms:
-Jaundice
-Splenic atrophy

19
Q

Haemolytic anaemia
-Key laboratory findings
-Signs and symptoms
-Severe consequences

A

Key lab findings:
-Raised reticulocytes
-Raised bilirubin
-Raised LDH

Signs and symptoms:
-Jaundice and associated risk of complications such as pigment gallstones
-Splenomegaly

Severe consequences:
-Massive sudden haemolysis can cause cardiac arrest and hyperkalaemia

20
Q

Hereditary spherocytosis
-Shape
-Defects and what they disrupt
-How are cells affected?

A

Shape:
-Many cells take on spherical shape

Defects:
-Ankyrin, spectrin, protein 4.2 or Band 3 defects disrupt membrane-cytoskeletal interactions

How are cells affected:
-Cells less flexible and more easily damaged

21
Q

Hereditary eliptocytosis
-Shape
-Defects
-Hereditary Pyropoikilocytosis

A

Shape:
-Many cells elliptical rather than biconcave disc shape

Defects:
-Spectrin most common defect
-Also defects in band 4.1, Band 3 and glycophorin C proteins

Hereditary Pyropoikilocytosis:
-Severe form of hereditary eliptocytosis

22
Q

Polycythaemia Vera
-Clinical features
-Management

A

Clinical features:
-Significant cause of arterial thrombosis
-Venous thrombosis
-Gout
-Haemorrhage into skin or GI tract
-Pruritis (itchy skin)

Management:
-Venesection
-Aspirin
-Manage CVS risk factors
-Sometimes consider drugs to reduce overproduction of cells

23
Q

Essential Thrombocythaemia
-Clinical features
-What should you screen for?
-Management

A

Clinical features:
-Excess platelets in blood
-Large and excess megakaryocytes in bone marrow
-Thrombotic events

Screening:
-Screen for Jak2 and CALR mutations

Management:
-Aspirin
-Hydroxycarbomide for >60yrs, platelet count >1500, or disease related to thrombosis/haemorrhage.

24
Q

Myelofibrosis
-Symptoms
-Treatment

A

Symptoms:
-Hepatosplenomegaly
-Bruising
-Fatigue
-Weight loss
-Fever
-Portal hypertension

Treatment:
-Supportive
-Some benefits using hydroxycarbamide, folic acid
-Advance disease: Blood transfusions, splenectomy

25
Q

Chronic myeloid leukaemia
-Presentation
-Who does it occur in?
-Treatment

A

Presentation:
-Usually a very high WCC
-May present with symptomatic splenomegaly, hyperviscosity (sticky blood) or bone pain

Who does it occur in?
-Disease of adults, v rare in children

Treatment:
-Tyrosine kinase inhibitors

26
Q

Thrombocytopenia
-Causes (acquired)
-Consequences
-Treatment

A

Acquired causes:
-Decreased platelet production (B12/folate deficiency, aplastic anaemia)
-Increased platelet consumption (Haemorrhage)
-Increased platelet destruction (Hypersplenism, Heparin)

Consequences:
-Usually not symptomatic until platelet count <30
-Easy bruising
-Petechiae

Treatment:
-Corticosteroids, other immunosuppressive drugs
-Splenectomy

27
Q

Anaemia of chronic disease
-Contributors (all caused by inflammatory cells)
-Examples of diseases
-Treatment
-Management

A

Contributors:
-Iron dysregulation
-Marrow shows a lack of response to erythropoietin
-Reduced lifespan of red cells

Examples of diseases:
-Rheumatoid arthritis
-Inflammatory bowel disease
-Chronic infections (TB)

Treatment:
-Treat underlying condition
-If associated renal failure, use recombinant human erythropoietin
-Transfuse red cells if all else fails and patient is symptomatic

Management:
-IV iron if required

28
Q

Rheumatoid arthritis:
-Treatment

A

-Pain relief, often NSAIDS
-Disease modifying agents: Corticosteroids, chemo

29
Q

Felty’s syndrome
-Triad

A

Triad:
-Neutropenia
-Splenomegaly
-RA

30
Q

Chronic liver disease
-What does it cause?
-What cells are often seen?

A

-Causes portal hypertension which causes splenomegaly

-Target cells are often seen (increased cholesterol:phospholipid ratio)

MEH Diseases (3 decks)

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