Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Human Disease > Haematology > Flashcards

Haematology Flashcards

1
Q

Definition of haematology

A

-Branch of medicine concerned with the study of the cause, pathology, treatment and prevention of diseases related to the blood

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

Definition of haematopoiesis and where it can occur

A
  • Process through which all blood cells are derived
  • Haematopoietic system is composed of the bone marrow, spleen, liver, lymph nodes and thymus
  • Occurs in different sites depending on the individual age
  • In childhood, it occurs in the bone marrow of nearly all bones
  • In adults, it occurs in the bone marrow of the axial skeleton and the proximal parts of the long bones (for example, the pelvis, cranium, vertebrae and sternum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Go through the haematapoeisis system

A
  • Begins with a pluripotent stem cell, capable of both self renewal and differentiation
  • Look at a picture for this
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe how the location where haematopoesis changes as you grow from a foetus to an adult

A
  • As a young foetus, predominantly your liver and spleen make blood cells
  • As an older foetus, bone marrow (more) and lymph nodes (less) take over
  • Bone marrow produces the most when the baby is born and this decreases slowly over time
  • Lymph node is considerably less than bone marrow

-If there is an infection, or pathological cause, there is a spurt in haematopoeisis occuring in the liver or spleen

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

RBCs function and path of haematopoiesis

A
  • Transport oxygen from lungs to the tissues

- Multipotent Haematopoetic Stem Cell > Common Myeloid Progenitor Cell > Reticulocyte > Erythrocyte

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

Neutrophils function and path of haematopoiesis

A
  • Chemotaxis, phagocytosis and killing of phagocytosed cells
  • Multipotent Haematopoetic Stem Cell > Common Myeloid Progenitor > Myeloblast > Neutrophil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Eosinophils function and path of haematopoiesis

A
  • Neutrophil functions and antibody-dependent damage to parasites
  • Immediate hypersensitivity

-Multipotent Haematopoetic Stem Cell > Common Myeloid Progenitor > Myeloblast > Eosiophil

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

Basophil function and path of haematopoiesis

A
  • Immediate hypersensitivity
  • Modulate inflammatory response via proteases and heparin

-Multipotent Haematopoetic Stem Cell > Common Myeloid Progenitor > Myeloblast > Basophil

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

Monocytes and macrophages function and path of haematopoiesis

A
  • Chemotaxis
  • Phagocytosis
  • Killing of microorganisms
  • Antigen presenting
  • Release of Il-1 and TNF

Multipotent Haematopoetic Stem Cell > Myeloid Progenitor > Myeloblast > Monocyte > Macrophage

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

Platelet function and path of haematopoiesis

A

-Primary haemostasis

Multipotent haematopoetic stem cell > common myeloid progenitor > megakaryocyte > platelet

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

Lymphocytes function and path of haematopoiesis

A

-Immune response and haemopoietic growth factors

Multipotent haematopoetic stem cell> common Lymphoid Progenitor > Small lymphocyte > pre t cell and naive b cell

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

Average Haemoglobin levels for children, adult males, adult females and pregs females

Conversion of units

A
  • Children 110-155 g/L (more as older)
  • Adult males 130-170 g/L
  • Adult females 120-155 g/L
  • Pregs Females 110-150 g/L

1L= 10dL

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

What is MCV and how is it measured. Average number and conversion

A
  • Mean corpuscle volume or Mean cell Volume
  • Measure of the average volume of a red blood cell
  • A volume of blood * Proportion of blood that is cellular / Number of erythrocytes in that volume of blood
  • Normally 80-95 fL
  • 10^15 fL = 1 L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anaemia Definition and s/s

A
  • Reduction in the oxygen-carrying capacity of the blood
  • Defined by a low value for haemoglobin
  • Rate at which anaemia develops detects its signs and symptoms
  • Symptoms include lassitude (physical/mental weakness), fatigue, dyspnoea on exertion, palpitations, headache and chest pain
  • Signs include pallor, tachycardia, wide pulse pressures, flow murmurs and congestive cardiac failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanisms of anaemia

A

Blood loss (trauma or GI bleeding)

Haemolytic (increased red blood cell breakdown)
-Decreased red blood cell lifespan 
-Either:
Congenital (sickle cell anaemia)
Acquired (malaria, drugs)

Impairment of red blood cell formation

  • Insufficient erythropoiesis
  • Ineffective erytropoiesis

Pooling and destruction of the spleen

Increased plasma volume

  • Pregnancy
  • Decrease in haemoglobin concentration so apparent anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Classification of anaemia and on what is it based

Examples of each category

A

-Classified by MCV

-Microcytic Anaemia (<80fL):
Iron Deficiency
Thalassaemia

-Normocytic Anaemia (80-100fL)
Acute blood loss
Anaemia of chronic disease
Chronic renal failure

-Macrocytic Anaemia (>100fL)
Alcoholism
Folate deficiency
Vitamin B12 deficiency

  • Microcytic anaemia is primarily a result of haemoglobin synthesis failure/insufficiency
  • Macrocytic anaemia is primarily caused by a failure of DNA synthesis
  • Normocytic anaemia occurs when the overall haemglobin levels are decreased, but the erythrocyte size remains normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Definition, type and mechanisms of iron-deficiency anaemia

A
  • Most common cause of anaemia worldwide
  • Microcytic anaemia
  • Excess iron potentially toxic so body tightly controls absorption
  • Develops via 3 mechanisms:
    1) Poor dietary intake (vegetarians and vegans)
    2) Malabsorption (duodenum- Coeliac disease)
    3) Increased loss (Peptic ulceration, inflammatory bowel disease, malignancy or hookwork infestation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Manifestations of iron deficiency anaemia

A

-Mild deficiency typically asymptomatic

  • Koilonychia (spoon nails)
  • Angular Cheilitis
  • Atrophic glossitis (smooth, glossy tongue often painful and tender)
  • Recurrent oral ulceration (small mouth ulcers)
  • Burning mouth
  • Oesophageal web
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Investigations and management of iron-deficiency anaemia

A
  • Identify cause
  • Red flags include men and post-menopausal women
  • Investigations include blood film and iron studies
  • Address underlying cause
  • Oral supplementation (ferrous sulphate 200mg times day for 3 months)
  • Parenteral available
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Examples of normocytic anaemia

A
  • 80-100fL
  • Anaemia’s of chronic disease
  • Acute blood loss
  • Chronic inflammatory conditions (rheumatoid arthritis)
  • Chronic infections (tuberculosis)
  • Malignancies
  • Chronic Renal Disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Classification of macrocytic anaemia

A
  • Divided into
    1) Megaloblastic erythropoiesis- abnormal rbc development due to disordered DNA synthesis
    2) Normoblastic erythropoiesis- normal red cell maturation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Definition and causes of megaloblastic folate anaemia

A
  • Folate is essential for DNA synthesis
  • Derived from many food sources, especially green leafy vegetables

-Causes of deficiency include:
Inadequate intake (elderly, alcoholism)
Malabsorption (Coeliac disease, jejunal resection)
Increased requirement (pregnancy, haemolytic anaemias)
Increased loss (dialysis, liver disease, congestive heart failure)
Drugs (methotrexate, phenytoin)

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

How to make a diagnosis of anaemia and distinguish between all the different types

A
  • Do a FBC
  • Check Haemoglobin levels
  • <130g/L in male, <120g/L in females suggests some sort of anaemia

-Then check Mean Corpuscle Volume

  • Microcytic anaemia occurs in patients with MCV <80fL
  • Then you can do iron studies +/- Mentzer Index (helps distinguish if iron deficiency or thalassaemia)
  • Examples include iron deficiency and thalassaemia
  • Normocytic anaemia if 80-100fL
  • If there is an increased reticulocyte count, suggests either haemolytic anaemia or blood loss as the body is trying to compensate and replenish the lost blood cells
  • If reticulocyte count is down, it suggests there may be a bone marrow disorder as the bone marrow is unable to produce adequate RBCs
  • Macrocytic Anaemia (>100fL)
  • Megoloblastic if blood film shows large immature RBCs
  • Also shows hypersegmented neutrophils
  • Vitamin B12 deficiency, Folate deficiency or Drug induced
  • Non megaloblastic if blood film only shows large, mature RBCs suggesting alcoholism, hypothyroidism and pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Definitions and causes of megaloblastic Vitamin B12 anaemiaRB

A
  • Vitamin B12 is required in a number of enzymatic reactions
  • Found only in foods of animal origin
  • Deficiency impacts of DNA synthesis

-Causes of deficiency include:
Inadequate intake
Inadequate secretion of intrinsic factor (gastrectomy, pernicious anaemia)
Inadequate release from food (gastritis, PPI, EtOH abuse)
Diversion of dietary B12 (bacterial overgrowth, small intestinal strictures)
Malabsorption (Crohn’s Disease, ileal resection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Clinical features of folate and B12 deficiencies

A 
-Folate and Vitamin 12 Deficiencies 
Generic symptoms and signs of anaemia 
Occasionally mild jaundice 
Glossitis 
Oral ulceration

-Vitamin B12
Peripheral neuropathy (loss of proprioception and vibration sense)
Demyelination with subacute combined degeneration of spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Investigations and Management of folate and B12 deficiencies

A

-Identify the cause

  • Investigations will include a blood film
  • Megaloblastic anaemia if blood film shows large, immature RBCs
  • Non-megaloblastic anaemia if blood film shows large, mature, RBCs

-Check serum folate and B12 levels (low B12 can lead to low folate so must always be tested together)

  • Address underlying cause
  • Oral supplementation (never folate only if B12 level is not known)
  • Parenteral Vitamin B12 (IM) is required in pernicious anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes of normoblastic macrocytosis

A
  • Alcohol excess
  • Liver dysfunction
  • Hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Classification of haemolytic anaemias

A

-Either congenital or acquired

-Congenital
Membrane Defects
Enzyme Defects
Globin Defects

-Acquired
Immune (autoimmune or alloimmune)
Non-immune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Congenital haemolytic anaemia classification and examples

A

-Membrane Defects
Number of proteins essential to maintain cell membrane integrity
Any mutation leads to increased fragility and haemolysis
Hereditary spherocytosis most common congenital

-Enzyme defects
Glucose 6 phosphate dehydrogenase deficiency
Involved in glucose metabolism
Deficiency results in increased sensitivity to oxidative stress

-Globin defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Acquired haemolytic anaemias classification

A

Immune

  • IgG coated red cells interacting with macrophages resulting in phagocytosis
  • Autoimmune process with antibodies against RBCs (including idiopathic or secondary to infections, drugs, SLE)
  • Alloimmune results from transfusion and production of antibodies to transfused red cell

Non-immune
-Mechanical trauma (metallic valves), burns, infections or drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical features of haemolytic anaemias

A

-Vary depending on the cause

  • Pallor
  • Jaundice (due to elevated bilirubin)
  • Splenomegaly
  • Expansion of erythropoiesis leading to bone deformities and pathological fractures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Haemoglobin definition structure and function

A
  • Fundamental role of oxygen transportation
  • Normal Hb comprises of 2 alpha and 2 beta chains
  • Each globin (protein) group is associated with a haem group (protoporphyrin ring and iron)
  • 4 globin subunits (2a, 2b), 4 haem groups
  • Hb undergoes a conformational change between oxygen bound and unbound states
  • Altering affinity for oxygen (loads o2 in high o2 tension environment and releases it in low environments)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Types of adult haemoglobin

A
  • Mainly HbA (97%) A2B2
  • Some HbA2 (2%) A2 S 2
  • HbF (fetal haemoglobin) (<1%) A2Y2
34
Q

Thalassaemia definition, classification and diagnosis

A
  • Common genetic disorder with significant associated morbidity and mortality
  • Geographic variation
  • 2 main groups, depending on whether an a or B chain defect
    1) A-Thalassaemia
    2) B-Thalassaemia
  • Chains accumulate in precursor red blood cells, leading to premature death
  • Precipitated chains also result in oxidative damage to the cell membrane, leading to haemolysis
  • Severity depends on degree of globin chain imbalance

-Diagnosis made on Hb electrophoresis

35
Q

A Thalassaemia epidemiology and classification dependent on genes

A
  • Most common in South-East Asia (Thailand, Indonesia) and West Africa
  • There are 4 a globin genes on 2 chromosomes
  • 1 missing gene: Silent carrier with no symptoms. Normal Hb and reduced MCV
  • 2 missing genes: Slight reduction in Hb and reduced MCV. Minor anaemic
  • 3 missing genes: Haemoglobin H Disease. Chronic Haemolytic anaemia however transfusion independent. Can lead a normal life
  • 4 missing genes: Haemoglobin Bart’s Hydrops fetalis syndrome: Neonatal death
36
Q

What does the severity of thalassaemia depend on

A

-Depends on how many of the 4 genes coding for the alpha globin or 2 genes coding for the beta globin are missing

37
Q

Difference between thalassaemia and iron deficiency in terms of iron levels, ferritin levels, Hb types, RBC count and iron supplementation

A
  • Iron is low in iron deficient anaemia but normal in thalassaemia
  • Ferritin is low in IDA but normal in T
  • HbA in IDA, HbA2 and HbF is higher in T
  • RBC is reduced in IDA, but increased in T
  • Benefit of iron supplementation in IDA but no benefit in T
38
Q

B Thalassaemia definition, epidemiology and causes

A
  • Southern europe especially greece
  • Due to a mutation rather than deletion affecting the B-gene

Either

  • Heterozygous B-thalassaemia (trait): Asymptomatic
  • Homozygous B-thalassaemia- moderate to marked anaemia developing within 1st 2 years (may be transfusion dependent)
39
Q

Clinical classification of thalassaemia

A

-Thalalassaemia minima:
presence of mutation without clinical consequence

-Thalassaemia minor:
Microcytosis and hypochromic red blood cells

-Thalassaemia intermedia:
Microcytic hypochromic anaemia
Extramedullary haematopoiesis with splenomegaly

-Thalassaemia major:
As above with severe anaemia and transfusion dependent

40
Q

Clinical presentation of Thalassaemia, radiographic changes and major concern

A
  • Typicall those of anaemia unless severe
  • If untreated, leads to growth retardation, splenomegaly and bony deformities due to marrow expansion
  • Enlargement of maxilla (chipmunk facies)
  • Migration and spacing of upper anterior teeth
  • Skull X ray hair on head and delayed pneumatization of maxillary sinuses with chickenwire appearance of alveolar bone
  • Major concern= iron overload due to transfusion leading to iron accummulation in myocardium (cardiac failure), liver (cirrhosis), pancreas (DM) and salivary glands
41
Q

HbS definition, formation, epidemiology

A
  • Most common structural variant of Hb is HbS
  • Due to a mutation in the B-globin gene
  • Interaction of sickle B globin chains with normal a globin chains leads to HbS
  • Results in deformation of cell into the sickle shape
  • Prevalence greatest in tropical Africa, Middle East and southern india
  • Areas in which falciparum malaria is endemic
42
Q

Sickle Cell anaemia v trait

A
  • Sickle cell trait occurs in heterozygotes (20-40% HbS and remaining HbA)
  • Usually asymptomatic
  • Rarely experience spontaneous haematuria

Sickle Cell Anaemia:
-Homozygotes

43
Q

Definition of sickle cell anaemia and clinical manifestations

A

-Sickling leads to shortened erythrocyte survival and microcirculation obstruction

Clinical manifestations:

  • Chronic haemolytic anaemia (60-90g/L)
  • Hyposplenism (increased risk of infection)
  • Acute chest syndrome
  • CVA/TIA
  • Bone infarction and subsequent infections
  • Chronic leg ulcers
  • Haematuria and chronic renal disease
44
Q

Diagnosis and management of Sickle Cell Anaemia

A
  • Diagnosed with Hb electrophoresis
  • Transfusion when necessary
  • Pneumococcal, Hib and meningococcal vaccinations
  • Prophylactic penicillin
-In a crisis, 
Acute, vaso occlusive painful episodes 
Precipitated by infection, dehydration and hypoxia 
Oral and IV fluids 
Analgesics
45
Q

Types of blood group systems and importance

A
  • 30 major blood group systems
  • Most important are the ABO and Rh systems
  • Variation in surface constituents of RBCs can lead to immunological reaction between donor and recipient
  • Compatibility or cross-matching essential
46
Q

ABO system explained

A
  • H antigen is always attacked to the cell membrane
  • Presence of an A or B allele leads to H antigen modification
  • O encodes for no modification
6 possible genotypes include:
AA
AB
AO
BB
BO
OO
4 possible phenotypes include:
A (can receive A or O)
AB (can receive A, B or O)
B (can receive B or O)
O (can only receive O)
47
Q

Rh system explained

A
  • More complex than ABO
  • Encoded by 2 genetic loci on one chromosome (RHD and RHCE)
  • D antigen in most clinically relevant
  • RhD-negative person is at significant risk of developing anti-D antibodies after transfusion of RHD-positive blood
  • Main relevance is to pregnant RhD-negative mothers
  • Fetus may be RhD-positive and placental transfer may lead to an adverse reaction
  • Pregnant women have Rh tested and antenatal anti-D prophylaxis given if necessary
48
Q

Transfusion reactions classification

A

Acute Reactions
-Occur within 24h of transfusion and include acute haemolytic, febrile non-haemolytic, allergic and transfusion-related acute lung injury

Delayed reactions
-Occur days to weeks after the transfusion and include delayed haemolytic transfusion reactions, transfusion-associated graft-versus-host disease and post-transfusion purpura

49
Q

Clinical features and management of transfusion reactions

A

-Clinical features include fever, agitation/anxiety, rigor, rash, flushing and sweating, chest/abdominal pain, profound hypotension, bleeding and diarrhoea

-Management:
Stop transfusion 
Check patient identity against donor blood product unit 
Replace giving set
Paracetamol 
IV fluids 
Contact Haematology
50
Q

Dental Relevance of an anaemic patient

A
  • May present with oral features suggestive of anaemia
  • For example, Iron, vitamin B12 and folate deficiencies may manifest with angular cheilitis, glossitis, oral ulceration and peripheral neuropathies
  • Sickle cell anaemias may experience oral pain due to infarction, osteomyelitis, trigeminal neuropathy and hypomineralised dentition
  • Radiographic features may include a dense lamina dura, hypercementosis and radio-opacities due to previous infarcts
  • Anaemias may complicate tx
  • May be sensible to delay tx
  • Avoid prilocaine anaesthesia
  • Thalassaemia and sickle cell anaemia can complicate procedures under GA
  • If bone marrow infiltration, may be failure of other cells including platelets with increased risk of bleeding
  • Liver disease may result in anaemia leading to increased risk of bleeding due to impact on clotting factors synthesis
51
Q

Definition of leukaemias

A

-Uncontrolled proliferation of partially developed WBCs/Blast cells. Build-up in the blood

  • Malignant neoplasms of haemopoietic stem cells
  • Result in diffuse replacement of bone marrow and normal blood precursor cells by neoplastic cells
  • Bone marrow failure leads to anaemia, neutropenia and thrombocytopenia
  • May lead to anaemia, neutropenia and thrombocytopenia
  • Leukaemia cells spill over into blood and may infiltrate the organs
52
Q

Classification of leukaemias

A

-Classified on the basis of cell type involved and its maturity

Cell Type

  • Myeloid cell line
  • Lymphoid cell line

Maturity

  • Acute >50% myeloblasts or lymphoblasts in bone marrow at clinical presentation
  • Chronic cells are more differentiated
53
Q

Diagnosis of Leukaemias

A

Blood Film

  • Increased myeloblasts/lymphoblasts
  • Abnormal WCC

Bone Marrow Biopsy

  • Hypercellular
  • Numerous blast cells
54
Q

Prognostic indicators of leukaemia

A
  • Leukaemia type
  • Cell phenotype
  • Chromosomal abnormalities
55
Q

Aetiology of leukaemia

A
  • Genetic and Environmental factors
  • Downs syndrome (genetic)
  • Ionizing radiation
  • Chemicals eg benzene
  • Viruses eg HTLV (human T-cell leukaemic virus)
  • Genetic factors (eg. Downs syndrome)
  • Acquired haematological disorders such as aplastic anaemia
56
Q

General clinical features of infiltration and classify each

A

Marrow Infiltration

  • Bleeding (thrombocytopenia)
  • Bruising/petechiae
  • Pallor (anaemia)
  • Malaise (anaemia)
  • Fever and Infection (neutropenia)

Tissue Infiltration

  • Lymphadenopathy
  • Hepatosplenomegaly
  • Bone and Joint pain (ALL)
  • Testicular swelling (ALL)
  • Gingival Hypertrophy (AML)
57
Q

Acute Lymphoblastic Leukaemia, common in, clinical features, definition and management

A
  • Large numbers of immature lymphocytes
  • Peak incidence in 4-5yos

-Pallor, anaemia, easy bleeding and bruising, fever, lymphaenopathy, bone joint pain and testicular swelling

Management directed at control of bone marrow and systemic disease. Tx must also prevent leukaemic cells spreading to other sites

  • Remission induced with non-myelosuppressive chemotherapy
  • Combination chemotherapy to induce remission
  • CNS treatmnent must be performed prophylactically
  • Maintenance therapy for up to 2 years increases disease-free survival
58
Q

Acute Myeloid Leukaemia common in, definition, management

A
  • Young adults
  • High levels of myeloblasts in the blood cell
  • > 30% cure rate with chemotherapy
  • 4-5 courses of intensive chemo
  • No maintenance therapy
  • Autologous and allogenic stem cell therapy
59
Q

Chronic lymphocytic leukamia epidemiology, clinical features and treatment

A
  • Elderly
  • 25% of all leukaemias
  • M:F 2:1
  • Wide range of symptoms
  • Lymphadenopathy
  • Splenomegaly
  • Recurrent infections
  • Abnormal FBC (anaemia, thrombocytopenia)
  • Hypogammaglobinaemia
  • Asymptomatic patients do not require treatment (monitoring only)
  • Tx depends on stage and symptoms of the individual patient
  • Incurable so tx revolved around suppressing disease for as long as possible
  • Chemotherapy
  • Mortality usually due to infection or bone marrow failure
  • Bone marrow transplant occasioally attempted in younger patients with poor prognostic disease
60
Q

Chronic Myeloid Leukaemia definition and clinical features

A
  • <20% of all leukaemias
  • 40-50yo
  • Relatively benign

Bone marrow failure (anaemia, thrombocytopenia)
Hypermetabolism (anorexia, weight loss and night sweats)
Splenomegaly
Leucostasis (visual disturbances, priapism)
Hyperuricaemia (gout, renal failure)

61
Q

Significance of the philadelphia chromosome

A
  • > 90% of CML have this philadelphia chromosome
  • Balanced translocation between 9 and 22
  • Resultant oncogene with tyrosine kinase activity
  • Lead to first targeted therapy for leukaemia- imatinib (tyrosine kinase inhibitor)
62
Q

Definition and classification of lymphomas

A
  • Group of blood cancers that can develop from lymphocytes

- Hodgkins Lymphoma and Non Hodgkins Lymphoma are the 2 most common types

63
Q

Difference between HL and NHL

A

HL:

  • Nodal (lymph node related)
  • Contagious
  • Good outcome
  • Not associated with immunodeficiency

NHL:

  • Extra-nodal (skin GI tract and brain)
  • Non-contagious
  • Variable outcome
  • Associated with immunodeficiency
64
Q

Hodgkin’s Lymphoma epidemiology, aetiology and clinical features

A

-Peak incidence in the 3rd decade

  • Caused by Epstein-Barr virus from infectious mononucleosis
  • Familial tendencies (HLA related)
  • Benzene
  • Lymphadenopathy (painless, non tender and rubbery. Can be alcohol induced)
  • ‘B symptoms’= fever, night sweats and weight loss
  • Anorexia, fatigue
  • Pruiritus and erythematous rash
  • Hilar lymphadenopathy
  • Bronchial compression
  • SVC obstruction
  • Hepatosplenomegaly
65
Q

Staging of NHL and HL

A
  • Ann-Arbor Staging System
  • Mainly used for HL as nodal, but also can be used for NHL

Stage I: Single LN region
Stage II: Two LN regions
Stage III: Groups on both sides of the diaphragm
Stage IV: Widespread disease outside the lymphatic tissues
B symptoms= weight loss, fever and night sweats

66
Q

Investigations of HL

A
  • FBC (normocytic anaemia)
  • Increased ESR
  • CXR/CT
  • Lymph node biopsy
  • Bone marrow investigation
67
Q

Treatment of HL

A
  • Radiotherapy curative in early stage disease
  • In advanced stage disease, combination therapy. Complete remission in 60-90%
  • Prognosis related to stage of disease
  • B symptoms worsen the prognosis
68
Q

NHL epidemiology, aetiology and clinical features

A
  • Rare <40
  • Varied presentation
  • Immunodeficiency
  • Infection
  • Inherited disorders
  • Ionizing radiation
  • Carcinogenic chemicals
  • Generalized lymphadenopathy
  • Oropharyngeal involvement (Waldeyer’s ring)
  • Bone marrow infiltration (anaemia, recurrent infections and haemorrhage)
  • Bone marrow infiltration can lead to anaemia, recurrent infections and haemorrhage
69
Q

Tx of NHL

A
  • Low grade disease
  • Asymptomatic requiring no tx
  • Intermittent oral chemo
  • High grade disease
  • Combination chemo
  • 30% cure
70
Q

Definition and pathogenesis of multiple myeloma

A
  • Cancer of the plasma cells
  • No symptoms initially
  • Aetiology unknown
  • Malignant transformation of terminally deferentiated B cells
  • monoclonal expansion leads to secretion of monoclonal Ig or light chains (paraproteins)
71
Q

Clinical features of multiple myeloma

A

Bone destruction
-Myeloma cells stimulate osteoclasts causing bone destruction and classic well-defined osteolytic lesions and raised serum calcium

Bone marrow failure
-Marrow infiltration leads to anaemia, thrombocytopenia and neutropenia

Renal failure
-Due to deposition and accumulation of these paraproteins

72
Q

Investigations of multiple myeloma

A
  • FBC= bone marrow failure
  • Raised ESR and Ca levels
  • Protein electrophoresis to demonstrate monoclonal paraprotein
73
Q

Management of multiple myeloma

A
  • Only if evidence of organ damage
  • Chemo if evidence bone marrow failure or bone lesions
  • Most pts respond however relapse if common
  • Radiotherapy useful if bone pain
74
Q

Secondary oral manifestations of haemotological diseases

A
  • Anaemia manifestations
  • Haemorrhagic tendencies
  • Increases susceptibiity to infections
  • Neutropenic ulcerations
75
Q

Laeukaemic oral manifestations

A
  • Typically gingival infiltration however also bone infiltration
  • 3-6% of dentate patients
  • 18.5% in AML
  • Friable and haemorrhagic
  • Increased tooth mobility
76
Q

Intra-oral lymphomas and tx

A
  • Typically NHL
  • Associated w HIV
  • Commonly gingiva and fauces affected
  • Rapidly enlarging masses with bone destruction

-Management:
Chemo and radio

77
Q

Most common oral complications of tx

A
  • Mucositis
  • Infection including candidosis and viral (HSV and VZV)
  • Mucosal bleeding
  • Xerostomia
78
Q

Most common adverse affect of chemo and radio therapy

A

-Mucositis

eg. 
5-fluurouracil
Methotrexate
Bleomycin 
Daunorubicin 
Doxorubicin
  • Rapid onset and good recovery following cessation of chemo
  • Severity depends on white cell depletion
  • Increases risk of infection and may limit chemotherapy
79
Q

Common oral complications of radiotherapy

A
  • Mucositis
  • Xerostomia
  • Caries
  • Candidasis
  • Loss of taste
  • Trismus
  • Osteoradionecrosis and osteomyelitis
80
Q

Oral care before and after radiotherapy

A

Before

  • Assesement and tx of disease
  • Meticulous OH and preventive care
  • Minimum 2 week interval between extracting and commensing radiotherapy (no bone left exposed)
After:
-Reinforcement of OH and preventive dental care
-Palliation for dry mouth 
-Dental extractins 
Minimal trauma with careful suturing 
Prophylatic antibiotics?
81
Q

Graft v Host Disease

A

-Check slides

Human Disease (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions