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Haroon Phase 2A > Haematology > Flashcards

Haematology Flashcards

1
Q

Treatment for glandular fever?

A
  • Supportive therapy (fluids, analgesia) - Avoid contact sports for 6 months eels to prevent splenic rupture
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2
Q

What does full blood count check for

A

RBCs - Neutrophils - Lymphocytes - - Platelets - Eosinophils - Monocytes

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3
Q

Abnormal FBC for neutrophils

A

High = neutrophilia, caused by acute bacterial infection Low = neutropenia, caused by myeloma and lymphoma

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4
Q

Abnormal FBC for lymphocytes

A

High = lymphocytosis, caused by chronic infection Low = lymphocytopenia

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5
Q

Abnormal FBC for platelets

A

High = thrombocytosis Low = thrombocytopenia

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6
Q

FBC values for eosinophils and monocytes

A

Eosinophils - elevated in parasitic infection - Monocytes - elevated in myelodysplastic syndrome

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7
Q

Ideal haemoglobin and mean corpuscular volume values

A

Haemoglobin: - Women: 120-165g/L - Men: 130-180g/L anything less than the lower value is classed as anaemia MCV: - 80-100 femtolitres

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8
Q

MCV for different types of anaemia

A

<80 = microcytic 80-95 = normocytic >95 = macrocytic

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9
Q

When would you consider transfusions for anaemia?

A

Hb <70g/L or Hb <80g/L + cardiac comorbidity

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10
Q

General symptoms of anaemia

A

Fatigue - Headache - Dizziness - Dyspnoea (especially on exertion) - Chest pain

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11
Q

General signs of anaemia

A

Tachycardia + hypotension - Skin pallor - Conjunctiva pallor - Intermittent claudication

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12
Q

Signs specific to iron deficiency anaemia

A

Koilonchia - Angular stomatitis - Atrophic glossitis - Brittle hair and nails - Subconjunctival pallor

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13
Q

Signs specific to thalassaemia

A

Bone deformities

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14
Q

Signs specific to B12 deficiency anaemia

A

Angular stomatitis + glossitis - Lemon-yellow Skin - Neurological symptoms

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15
Q

Signs specific to haemolytic anaemia

A

Prehepatic jaundice - Dark urine

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16
Q

Signs specific to CKD

A

Oedema - Hypertension - Excoriations on the Skin

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17
Q

Iron deficiency anaemia

A

Non-inherited Fe deficiency, impairing Hb synthesis - Most common anaemia worldwide - More common in females

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18
Q

Aetiology of iron deficiency anaemia

A
  • Infants: malnutrition, prolonged breastfeeding - Children: malnutrition, malabsorption - Alults: malnutrition, malabsorption, menorrhagia, pregnancy, hookworm - Elderly (60+): rare, red flag for colon cancer bleeding
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19
Q

NICE recommendation for iron deficiency anaemia age 60+

A

Urgent endoscopy

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20
Q

What causes malabsorption of iron?

A

Conditions that result in inflammation of the duodenum and jejunum - Coeliac - IBD - Crohn’s disease Medications that reduce stomach acid (eg: PPI) - Because acid is needed to keep iron as the soluble Fe2+

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21
Q

Hookworm as a cause of iron deficiency anaemia

A

Most common cause worldwide - Results in GI blood loss

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22
Q

Normal iron function

A

Absorbed - Circulated bound to transferrin - Stored as ferritin or incorporated into Hb

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23
Q

Diagnosis of iron deficiency anaemia

A

FBC = microcytic - blood film - pencil cells (smol) platelet aggregates - Iron studies

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24
Q

What would a blood film of iron deficiency anaemia show?

A
  • Small, hypochromic (pale) RBCs - Target cells - non-specific Bull’s eye pattern - Howell Jolly bodies - non-specific nucleated RBCs
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25
Q

Fe studies in iron deficiency anaemia

A

Serum Fe: Low - ferritin: Low - transferrin saturation: Low - Total Iron binding capacity (and transferrin): High

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26
Q

Treatment for iron deficiency anaemia

A

blood transfusion - immediate correction but need to treat underlying cause - Iron infusion - Oral Iron

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27
Q

Iron infusion

A

eg: cosmofer - Small risk of anaphylaxis - CI during sepsis

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28
Q

Oral iron

A
  • Ferrous sulphate 200mg 3x a day - SE: constipation, black stools, GI upset - If poorly tolerated, consider ferrous gluconate - Unsuitable where malabsorption is the cause of the deficiency
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29
Q

What is thalassaemia?

A

Autosomal recessive haemoglobinopathy - A type of haemolytic anaemia - Defective alpha-globin chain = alpha thalassaemia - Defective beta-globin chain = beta thalassaemia

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30
Q

Pathophysiology of thalassaemia

A
  • RBCs are more fragile and break down more easily - Spleen collect all the destroyed RBCs, resulting in splenomegaly - Bone marrow expands to produce extra RBCs -> susceptibility to fractures, pronounced forehead and molar eminence
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31
Q

Where is thalassaemia prevalent?

A

Where malaria is as it is protective from it (like sickle cell)

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32
Q

Alpha thalassaemia

A
  • Less common - 4 gene deletions on chromosome 16 - Associated with HbH - Can cause death in utero if severe
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33
Q

Beta thalassaemia

A
  • More common - 2 gene mutations in chromosome 2 - Normal Hb isoforms, just depletion of beta chains
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34
Q

Presentation of thalassaemia

A

Failure to thrive - Hepatospenomegaly - Gallstones - Chipmunk face

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35
Q

Diagnosis of thalassaemia

A
  • FBC + blood film - Hb electrophoresis - diagnostic - Xr - “hair on end” skull
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36
Q

FBC and blood film in thalassaemia

A

hypochromic (pale) RBCs - Target cells - microcytic anaemia with High reticulocytes

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37
Q

Treatment for thalassaemia

A
  • Regular transfusion - Iron chelation - Splenectomy - Ascorbic acid (vit C) - Bone marrow transplant (curative)
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38
Q

Iron chelation

A

Prevents Fe overload from transfusions - Desfemoxamine - SE: deafness, cataracts

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39
Q

Splenectomy

A
  • Wait till after 6 y/o - Spleen plays defensive role vs encapsulated bacteria - So wait due to risk of sepsis
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40
Q

What is sideroblastic aneamia?

A
  • Defective Hb synthesis within mitochondria - Often X inherited ALA synthetase deficiency - High Fe but not used in Hb synthesis, trapped in mitochondria!
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41
Q

Diagnosis of sideroblastic anaemia

A

FBC + blood film - Fe studies

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42
Q

Fe studies for sideroblastic anaemia

A

Serum Fe: High - ferritin: High - transferrin saturation: High - Total Iron binding capacity (and transferrin): Low

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43
Q

FBC and blood film for sideroblastic anaemia

A

microcytic - Ringed sideroblasts (immature RBC) - Basophilic stippling (increased Basophilic granules)

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44
Q

Haemolytic vs non-haemolytic anaemia

A

Failing bone marrow in non-haemolytic

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45
Q

Types of haemolysis

A

Intravascular - marked by haptoglobin - Extravascular - @ Spleen - Can be both

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46
Q

What is sickle cell anaemia?

A

Autosomal recessive haemoglobinopathy affecting beta-globin chains - Commonest in africa for antimalarial properties (vs plasmoduium falciparum) - HbS variant

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47
Q

Pathophysiology of sickle cell anaemia

A
  • Glutamic acid -> valine on 6th codon of beta-globin on chromosome 11 - Causes irreversible RBC sickling - RBC more fragile so less efficient - Bone marrow focuses more on reticulocytes, decreasing other cell lines (eg: causes neutropaenia) - Intra+extravascular haemolysis
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48
Q

Presentation of sickle cell anaemia

A

General anaemia symptoms + prehepatic jaundice

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49
Q

What are sickle cell complications (crises) precipitated by?

A

Cold - Hypoxia - Acidosis - Dehydration - exertion - Stress

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50
Q

Types of sickle cell crises

A

Vaso-occlusive (aka painful crisis) - Splenic sequestration - Acute Chest syndrome - Aplastic crisis (from parvovirus) - Osteomyelitis

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51
Q

Another common complication of sickle cell anaemia

A

Osteomyelitis - Usually due to s.aureus, but in those patients = salmonella

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52
Q

Diagnosis of sickle cell anaemia

A
  • Sickle solubility test- Newborn heel prick test - Antenatal: Molecular genetics - Hb electrophoresis - diagnostic when above 90% HbS (number 4 has sickle cell)
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53
Q

FBC and blood film in sickle cell anaemia

A

Normocytic normochromic - increased reticulocytes - Sickled RBC - Howell Jolly bodies

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54
Q

Last resort treatment for sickle cell anaemia

A

Bone marrow transplant

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55
Q

Long term treatment for sickle cell anaemia

A

Avoid precipitants - Drugs - hydroxycarbamide (aka hydroxyurea) to increase HbF levels, folic acid supplements - transfusion + Fe chelation

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56
Q

Vaso-occlusive crisis

A

Sicke shaped RBCs clog capillaries, causing distal ischaemia - Dehydration and raised haematocrit - Can cause priapism in men (treated with aspiration of blood from the penis)

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57
Q

Treatment for acute complicated attacks

A

Low threshold for hospital admission - treat any infection - Keep warm - IV fluids - Simple analgeisa

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58
Q

Splenic sequestration crisis

A

RBCs block blood flow within the Spleen - Can cause autosplenectomy - splenomegaly - Can lead to severe anaemia and circulatory collapse (hypovolaemic shock) - Splenectomy used in cases of recurrent crisis

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59
Q

Aplastic crisis

A

Temporary loss of the creation of new RBCs - Most commonly triggered by infection with parvovirus B19 - Management is Supportive with blood transfusions - Usually resolves spontaneously within A week

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60
Q

Acute chest syndrome sickle cell crisis

A

Caused by pulmonary vessel Vaso-occlusion - Fever or resp symptoms with new infiltrates seen on Xr - Can be due to infection or Non-infective causes - Medical emergency with High mortality

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61
Q

Treatment for acute chest syndrome

A

Exchange blood transfusion - sickle cell blood replaced w healthy blood

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62
Q

What is G6PDH deficiency

A
  • X linked recessive enzymopathy - Causes 1/2 lifespan + RBC degeneration
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63
Q

What is G6PDH?

A

Glucose-6-phosphate dehydrogenase - Protects RBCs from vasoxidative damage - Involved in glutathione synthesis (Protects from ROS like H2O2)

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64
Q

Factors that can precipitate G6PDH deficiency

A

Naphthelene (in moth balls (pesticide)) - Antimalarials, eg: quinine - Aspirin - Fava beans (contain glucosides that Can be oxidised into ROS) - Nitrofurantoin

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65
Q

G6PDH attack

A

Rapid anaemia + jaundice (intravascular haemolysis)

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66
Q

Diagnosis of G6PDH deficiency

A

FBC + blood film - Normal inbetween attacks - Attack: normocytic, normochromic, increased reticulocytes, heinz bodies and bite cells Low G6PDH levels

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67
Q

Treatment for G6PDH deficiency

A

Avoid precipitants - blood transfusions when attacks ensue

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68
Q

What is hereditary spherocytosis?

A

Autosomal dominant membranopathy - common in Northern Europe and America

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69
Q

Pathophysiology of hereditary spherocytosis

A

deficiency in structural membrane protein spectrin - increased Splenic recycling (Extravascular haemolysis) - Makes RBCs More spherical and rigid

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70
Q

Presentation of hereditary spherocytosis

A
  • General anaemia - Neonatal jaundice - Splenomegaly - Gall stones (50%)
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71
Q

Treatment for hereditory spherocytosis

A

Splenectomy

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72
Q

Treatment of neonatal jaundice in hereditory spherocytosis

A

treated with phototherapy - risk of kernicterus if untreated (bilirubin accumulates in basal ganglia, CNS dysfunction, death)

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73
Q

What is autoimmune haemolytic anaemia precipiated by

A

Precipitated by temperature (warm most common but idiopathic)

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74
Q

Pathophysiology of autoimmune haemolytic anaemia

A

IgM autoantibodies activate compliment system by binding to cell surface of RBCs - Intra/Extravascular haemolysis

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75
Q

Special test for autoimmune haemolytic anaemia

A

Direct coombs +ve - Agglutination of RBCs with coombs reagent

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76
Q

Diagnosis of hereditary spherocytosis

A

FBC and blood film: Normocytic, normochromic, spherocytes, increased reticulocytes - Direct coombs -ve - Eosin-5-maleimide (EMA) test - Cryohaemolysis

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77
Q

Myelophthisic process in non-haemolytic anaemia

A

Bone marrow replaced with something else (eg: malignancy)

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78
Q

Signs of G6PDH deficiency

A

Neonatal or Intermittent jaundice - anaemia - Gallstones - splenomegaly

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79
Q

Types of malaria

A
  • Plasmodium falciparum (most severe and dangerous, 75% in the UK) - Plasmodium vivax - Plasmodium ovale - Plasmodium malariae
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80
Q

Pathophysiology of malaria

A
  • Spread by female anopheles mosquitos - When mosquito bites human, sporozoites are injected - Travel to liver - Mature into merozoites which enter blood and infect RBCs - Merozoites replicate and RBCs rupture after 48 hours, cause a systemic infection
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81
Q

In what forms of malaria can sporozoites lie dormant in the liver for years?

A

P.vivax and P.ovale - Lie dormant as hypnozoites

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82
Q

Presentation of malaria

A

Blackwater Fever (malarial haemoglobinuria) - Massive hepatosplenomegaly - pallor - jaundice - Myalgia - Headache - Vomiting

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83
Q

Diagnosis of malaria

A
  • Malaria blood film - 3 samples over 3 consecutive days
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84
Q

Oral treatments for malaria

A

quinine sulphate - Doxycycline

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85
Q

IV treatment for malaria

A

Artesunate (Most effective but not licensed) - quinine dihydrochloride

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86
Q

Complications of P.Falciparum

A

Cerebral malaria Reduced GCS AKI Seizures Haemolytic anaemia (severe) DIC Oedema Multi-organ failure and death

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87
Q

Antimalarials

A
  • 90% effective at preventing infections Options: - Proguanil nad atovaquone (malarone) - Mefloquine - Doxycycline
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88
Q

Proguanil nad atovaquone (malarone) antimalarial

A

Most expensive - Best side effect profile

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89
Q

Mefloquinne antimalarial side effects

A

Bad dreams - Rarely psychotic disorders or seizures

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90
Q

Doxycycline antimalarial side effects

A
  • Diarrhoea and thrush (as it’s a broad spectrum antibiotic) - Makes patients sensitive to the sun, causing a rash and sunburn
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91
Q

Pathophysiology of CKD anaemia

A

Occurs in chronic diseases - Decreased Bone marrow stimulation for production of erythropoetin

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92
Q

Diagnosis of CKD anaemia

A

Normocytic and normochromic - Decreased reticulocytes due to Low erythropoetin

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93
Q

Pathophysiology of aplastic anaemia

A

Pancytopenia where bone marrow fails and stops making haematopoetic stem cells

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94
Q

Cause of aplastic anaemia

A

Idiopathic - Could be infection (EBV, parovirus B19) or congenital

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95
Q

Diagnosis of aplastic anaemia

A

FBC = Normocytic anaemia with Decreased reticulocytes - Bone marrow biopsy = hypocellularity

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96
Q

Complication of aplastic anaemia

A

increased infection risk (neutropenia) - treat with broad spectrum antibiotic and Bone marrow transplant

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97
Q

Causes of B12 deficiency anaemia

A
  • Pernicious anaemia (autoimmune, most common) - Gastrectomy - Malnutrition - Intestinal problems such as Crohn’s and celiac disease - Chronic nitrous oxide use - Oral contraceptives - Vegan (cool people basically😎)
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98
Q

Normal metabolism of B12

A
  • B12 binds to transcobalamin 1 in saliva (protects against stomach acid) - Bind to intrinsic factor in duodenum - Absorbed as B12-IF complex in terminal ileum
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99
Q

Pathophysiology of pernicious anaemia

A

Anti parietal and intrinsic factor antibodies = Low if - Low B12-if complexes - Less B12 absorption

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100
Q

Neurological symptoms of B12 deficiency

A

Demyelination (DDx for folate deficiency) - Symmetrical parathesia - Muscle weakness - Altered mental state

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101
Q

What are haematinimics?

A

Nutrients needed for haematopoesis (B12, folate, Fe) - Deficiencies cause Angular stomatitis and glossitis

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102
Q

Diagnosis of B12 deficiency

A

FBC + blood film (Macrocytic and megaloblasts present) - Low Serum B12 - Anti parietal and Anti if antibodies (specific in Pernicious anaemia)

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103
Q

What are megaloblasts?

A
  • Hypersegmented nucleated neutrophils with 6+ lobes - Less mature DNA = less compacted around histones - So more lobes = more immature
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104
Q

Treatment for B12 deficiency

A

Dietary advice - B12 supplements (PO hydroxycobalamin)

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105
Q

How long do folate and B12 deficiency anaemia take to develop?

A

folate: months - B12 : years (More common in older patients)

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106
Q

Aetiology of folate deficiency anaemia

A

malnutrition - malabsorption - pregnancy - Trimethoprim + methotrexate (dihydrofolate reductase inhibitors) - Alcohol - Bacterial overgrowth

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107
Q

Symptom of folate deficiency anaemia

A

Angular stomatitis

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108
Q

Diagnosis of folate deficiency anaemia

A

FBC + blood film = Macrocytic + megaloblasts - Low Serum folate - Could have concomitant B12 deficiency

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109
Q

Treatment for folate deficiency

A

Dietary advice (leafy greans, brown rice) - Don’t replace folate without checking B12 - folate supplements (if concomitant with B12 def., replace B12 first as giving folate first depleted B12)

110
Q

Treatment for folate deficiency during pregnancy

A
  • Prophylactic folate 400mg for first 12 weeks - Ensure baby develops ok
111
Q

Main complication of folate deficiency

A

CKD

112
Q

Causes of non-megaloblastic anaemia

A

Alcohol - toxic to RBC and depletes folate and B1 - Hypothyroidism - inteference w/ EPO, multifactorial - liver disease - liver decompensated cirrhosis - NAFLD - CKD

113
Q

Pathophysiology of leukaemia

A

Neoplastic proliferation of WBC line (myeloblasts or lymphoblasts) - Lose ability to differentiate but maintain ability to replicate - Decreased production of other haematopoetic cells (functional pancytopaenia)

114
Q

General signs of leukaemia

A

Thrombocytopaenia - bleeding and bruising - Leukopaenia - infections - anaemia symptoms - hepatosplenomegaly - Fatigue - Failure to thrive (Children)

115
Q

Acute lymphoblastic anaemia (ALL)

A
  • Neoplastic proliferation of lymphoblasts, mostly B - Terminal deoxynucleotidyl transferase expressed - Patients typically under 6 (75%) and over 50 - Associated with Down’s syndrome
116
Q

Presentation of ALL

A
  • General leukaemia symptoms - Lymphadenopathy - CNS infiltration -> headaches, CNS palsies
117
Q

Testing for leukaemia

A
  • FBC (shows pancytopaenia) - Blood film - Bone marrow biopsy - diagnostic - Imaging (CT/CxR) - Genetic testing
118
Q

Blood films for leukaemia

A
  • ALL - increased lymphoblasts - AML - increased lymphoblasts with auer rods, myeloperoxidase positive - CLL - smudge cells (Richter’s transformation)
119
Q

Presentation of AML

A

General leukaemia symptoms - Gum hypertrophy

120
Q

Acute myelogenous leukaemia (AML)

A
  • Neoblastic proliferation of myeloblasts - Present mostly in the elderly (over 65) - Rapid progression if not treated asap - 3 year survival 20%, 5 year survival 15%
121
Q

Leukaemia bone marrow biopsies

A

ALL - lymphoblasts ≥20% AML - myeloblasts ≥20% CLL - pancytopaenia (except lymphocytosis) CML - increased granulocytes, blast cell percentage shows severity (diff card)

122
Q

Chromosomal translocations in leukaemia

A

ALL - mostly t(12:21) AML - t(15:17) CLL - multifactorial CML - t(9:22) (Philadelphia chromosome)

123
Q

Philadelphia chromosome in ALL

A
  • 30% in adults 3-5% in children - Worse prognosis
124
Q

AML + DIC

A

common subtype of AML - Acute premyelocytic leukaemia (APML)

125
Q

Chronic myelogenous leukaemia (CML)

A
  • Neoplastic myelocyte proliferation - mainly neutrophils - Adults around 60 - BCR - ABL gene fusion causing tyrosine kinase to be irreversibly switched on
126
Q

What do tyrosine kinases do

A

Increase cell proliferation

127
Q

Chronic lymphocytic leukaemia (CLL)

A
  • Neoplastic proliferation of lymphocytes, mostly B - Most common leukaemia in adults - Over 70 year olds, men typically - 5 year survival of 75%
128
Q

Blast vs cyte

A

Blast - immature cell, eg: myeloblast Cyte - mature cell, eg: myelocyte

129
Q

Presentation of CML

A

General leukaemia - Massive hepatosplenomegaly when with Malaria

130
Q

Presentation of CLL

A

General anaemia symptoms - Often asymptomatic - Rubbery Non-tender Lymphadenopathy - Might have night sweats and weight loss

131
Q

What is hypogammaglobulinaemia

A
  • Low conc. of immunoglobulins present in CLL - This is because B cells proliferate but don’t differentiate to plasma cells (which are responsible for producing Igs)
132
Q

Treatment of ALL

A

Chemotherapy - typically good prognosis

133
Q

Treatment of AML

A

Chemo + tretinoin (used for APML) - transfusion for anemia - Abx prophylaxis for neutropaenia - Last resort: Bone marrow transplant

134
Q

What to give with chemo

A

✨allopurinol✨ - Chemo releases uric acid from cells which can accumulate in kidneys - This would cause tumour lysis syndrome - Allopurinol prevents it

135
Q

Treatment for CML

A

Chemo + imantinib (tyrosine kinase inhibitor)

136
Q

Severity of CML based on blast cell % in bone marrow biopsy

A
  1. <10% - Chronic (best) 2. 10-19% - Accelerated 3. ≥20% - Blast crisis (worst, could progress to AML, poorer prognosis - often happens when CML is untreated or diagnosed late)
137
Q

Treatment of CLL

A

Watch and Wait in early stages - Monoclonal antibodies (rituximab) - Bruton kinase inhibitors (ibrutinib)- Palliative (if v old) - IV Ig for hypogammaglobulinaemia

138
Q

Complicaton of CLL

A

Richter transformations🥲 - B cells massively accumulate in lymph nodes - Mahoosive lymphadenopathy and transformation from CLL to aggressive lymphoma - #oops

139
Q

What are B symptoms

A

Fever - night sweats - Unintentional weight loss

140
Q

Ages susceptible to lymphomas

A

Hodgkin: Bimodal distribution, with peaks in early 20s and in 70s Non-Hodkin: Over the age of 40

141
Q

Pathophysiology of Hodgkin lymphoma

A

Proliferation of lymphocytes in lymph nodes, typically in the cervical, axillary or inguinal lymph nodes

142
Q

Risk factors of Hodgkin lymphoma

A

HIV - EBV (gladular Fever) - autoimmune conditions - Family history

143
Q

Presentation of Hodgkin lymphoma?

A

B symptoms (Hodgkin is A High grade B cell lymphoma) - Non-tender Rubbery Lymphadenopathy which becomes painful after drinking Alcohol

144
Q

Other possible symptoms of Hodgkin lymphoma

A

Fatigue - Itching - Cough - Dyspnoea - Abdo pain - recurrent infections

145
Q

Diagnosis of lymphoma

A

Lymph node biopsy - PET-CT/MRI Chest/Abdo/pelvis for staging - Performance status score to establish treatment

146
Q

How to distinguish between Hodgkin and non-Hodgkin lymphoma?

A

Lymph node biopsy (core needle/excision needle) - Hodgkin’s shows Reed-Sternberg cells🦉 - Abnormally large B cells with multiple nuclei and nucleoli - These aren’t present in Non-Hodgkin lymphoma, but you can still use the biopsy to determine NHL subtype, eg: Burkitt’s shows starry sky🌌

147
Q

Popcorn cells🍿

A
  • Seen in nodular lymphocyte predominant Hodgkin’s - (a subtype of Hodgkin lymphoma) - They are a variant of Reed-Sternberg cells
148
Q

Ann Arbor staging in both types of lymphoma

A
  1. One region of lymph nodes 2. 2 or more lymph nodes on same side of the diaphragm 3. Lymph nodes on both sides of the diaphragm 4. Extranodal organ spread also: a - no B symptoms b - B symptoms
149
Q

Treatment of Hodgkin lymphoma

A
  • ABVD immunochemotherapy (adriamycin, bleomycin, vinblastine, dacarbazine) - +/- radiotherapy - Marrow transplant
150
Q

Side effects of chemo for Hodgkin lymphoma

A

Alopecia - N+v - Myelosuppression - BM Failure - infection - Infertility - leukaemia

151
Q

Side effects of radiotherapy for Hodgkin lymphoma treatment

A

Cancer - damage to tissues - Hypothyroidism

152
Q

Types of Non-Hodgkin lymphoma

A
  • Low grade - Follicular - High grade - Diffuse large B cells - Very high grade - Burkitt’s
153
Q

Febrile neutropaenia

A

Massive risk in patients with recent/High dose Chemo (or on carbimazole) - Fever, Tachycardia, swears, rigors, tachypnoea - treated with immediate broad spectrum antibiotics

154
Q

Cells affected in Non-Hodgkin lymphoma

A
  • B cells (90%) - T cells (10%) - NK cells (<1%)
155
Q

MALT lymphoma

A

Affects mucosal-associated lymphoid tissue - associated with H.pylori infection or eye chlamydia infection

156
Q

Burkitt lymphoma

A

associated with EBV, Malaria and HIV - Often causes Massive jaw Lymphadenopathy in Children

157
Q

Other risk factors for Non-Hodgkin lymphoma

A
  • Hep B or C infection - Exposure to trichloroethyline (pesticide) - Immunosuppression
158
Q

Presentation of Non-Hodgkin lymphoma

A

B symptoms - Non-tender Rubbery Lymphadenopathy, not affected by Alcohol - Can get hepatosplenomegaly

159
Q

Treatment of low-grade lymphoma

A
  • Radiotherapy - R-CHOP Chemotherapy Rituximab (targets CD20 on B-cells) Cyclophosphamide Hydroxy-daunorubicin Oncovin (brand name for vincristine) Prednisolone
160
Q

Malaria in children

A
  • Convulsions (60-80%) - High ICP, hypoglycaemia - Rule out meningitis (examination and CSF analysis if no high ICP)
161
Q

Chronic complications of sickle cell anaemia

A

Avasular necrosis of joints - Silent CNS infarcts - Nephropathy - ED

162
Q

Pathophysiology of multiple myeloma

A
  • Neoplastic monoclonal proliferation of a plasma cell - Results in large quantities of a single type of antibody/monoclonal paraprotein being produced (55% IgG, 20% IgA)
163
Q

Monoclonal gammopathy of undetermined significance (MGUS)

A
  • Too much Ig released by abnormal plasma cells - <10% BM plasma cells - Asymptomatic - 1% of cases develop into myeloma
164
Q

Smouldering myeloma

A
  • Progression of MGUS with higher levels of antibodies - Premalignant, more likely to progress to myeloma than MGUS - Waldenstrom’s macroglobulinaemia is a type of smouldering myeloma with excessive IgM specifically
165
Q

Epidemiology of myeloma

A
  • Around 70 years old - Afro-Carribeans - Male - Obesity - 1% of cancers are myeloma
166
Q

Presentation of multiple myeloma (🦀)

A

HyperCalcaemia Renal failure Anaemia Bone lesions

167
Q

What are anaemia and bone lesions caused by in multiple myeloma?

A

Bone marrow failure

168
Q

What are hypercalcaemia and bone lesions caused by in multiple myeloma?

A

Increased osteoclast bone resorption due to cytokines released by plasma and stromal cells

169
Q

What is renal failure caused by in multiple myeloma?

A
  • Hypercalcaemia -> calcium oxalase renal stones - Immunoglobulin light chain deposition - Bence Jones protein in pee
170
Q

Testing for multiple myeloma

A

FBC and blood film - U+E = renal Failure - Bone profile = hypocalcaemia and increased ALP - Serum electrophoresis - urine dipstick - Bence Jones protein - Xr

171
Q

FBC and blood film for multiple myeloma

A

Normocytic normochromic anaemia - raised ESR - Rouleaux formation in blood film (aggregation of RBCs)

172
Q

Serum electrophorisis in multiple myeloma

A
  • Ig paraprotein ‘M spike’ - Hypergammaglobulaemia for that specific Ig
173
Q

X-ray for multiple myeloma

A
  • Pepper pot skull - Osteolytic lesions -> “punched out holes”
174
Q

Confirmatory diagnosis of multiple myeloma

A
  • Bone marrow biopsy required - >10% plasma cells - NICE recommends full body MRI (if not, then CT or Xray in that order of preference)
175
Q

Treatment of multiple myeloma

A
  • Bisphosphonates (eg: alendronate) to decrease octeoclastic activit and increase osteoblastic activity - protects bones Older patients: - Anti-myeloma chemotherapy - Consider BM stem cell transplant
176
Q

Plasma viscocity in multiple myeloma

A
  • Increased due to large amounts of immunoglobulins in blood Complications: - Easy bruising and bleeding - Reduced or loss of sight due to vascular disease in the eye - Purple discolouration of extremities - Heart failure
177
Q

Pathophysiology of polycythaemia vera

A

A High concentration of erythrocytes in the blood - due to JAK2V617 mutation - the affected Bone marrow Can also produce excessive Platelets and white blood cells

178
Q

Relative vs absolute polycythaemia

A

Relative: - Normal number of erythrocytes, reduction in plasma - Causes include obesity, dehydration execessive alcohol and increased erythropoetin Absolute: - Increased number of erythrocytes - Primary and secondary

179
Q

Primary vs secondary polycythaemia

A

Primary: Polycythaemia vera - abnormality in the bone marrow Secondary: Disease outside the bone marrow causing overstimulation of the bone marrow

180
Q

General symptoms of polycythaemia

A
  • Erythromalagia (fig 1) - Reddish plethoric complexion - Blurred vision - Headache + dizziness (features nonspeifically related to hyperviscosity)
181
Q

Symptoms unique to polycythaemia vera

A
  • Itchy after a bath (contact with warm water) 🛁 - Hepatosplenomegaly
182
Q

Diagnosis of polycythaemia vera

A

FBC = High WCC, High Platelets, High RBCs - High Hb - Genetic tests JAK2V617 positive

183
Q

Treatment of polycythaemia vera

A

Non-curative, main aim is to maintain a normal blood count Low-risk: - Venesection regularly (often used solely) - Low dose aspirin High risk: - Consider chemotherapy (hydroxycarbamide) for patients at high risk of thrombus (60+, background of thrombosis)

184
Q

Thrombosis chart

A

img

185
Q

Differential diagnoses of abnormal or prolonged bleeding

A

Thrombocytopaenia (Low Platelets) - Haemophilia A and B - Von Willebrand disease - Disseminated Intravascular coagulation (secondary to sepsis)

186
Q

Pathophysiology of ITP

A

autoimmune - antibodies (Usually IgG) created against platelet, causing platelet destruction - Specifically, Gpiib/iiia on Platelets are destroyed

187
Q

Types of ITP

A

Type 1: Children 2-6, post viral infection, acute + severe Type 2: Adult women w malignancy, HIV or other autoimmune condition. Chronic + mild

188
Q

Ge symptoms of thrombocytopaenia (all of the symptoms of ITP)

A

Purpuric rash - Easy bleeds - Mennhoragia Fig1. shows A Purpuric rash

189
Q

Diagnosis of ITP

A

FBC - raised WCC, Low Hb, Low Platelets - increased Bone marrow megakaryocytes (due to negative feedback)

190
Q

Treatment of ITP

A

First line: Prednisolone + IV IgG this decreases splenic platelet destruction Second line: Splenoctomy

191
Q

Pathophysiology of TTP

A
  • ADAMTS13 (VWF cleaving protein) deficiency - VWF remain as multimers and aggregate at endothelial injury sites - Incidence same as Type 2 ITP
192
Q

Symptoms unique to TTP

A

AKI - Fever - haemolytic anaemia - Neurologicla symptoms

193
Q

Diagnosis of TTP

A
  • Same FBC as ITP - Raised billirubin and creatinine - Blood smear: schistocytes - RBCs; microangiopathic haemolytic anaemia - Genetic testing shows low ADAMTS13
194
Q

Treatment of TTP

A

First line: Plasmapharesis Second line: Prednisolone + rituximab

195
Q

What’s EBV associated with?

A

Many conditions inc: - Hodgkin’s lymphoma - Burkitt’s lymphoma - Nasopharyngeal carcinoma

196
Q

Incidence and spread of EBV

A
  • 15-24 years old - Spread via saliva or bodily fluids
197
Q

Symptoms of EBV

A

Varied mild symptoms: - Fever - Tonsilitis - Hepatosplenomegaly - Cough Self limiting 2-4 weeks

198
Q

Diagnosis of EBV

A

(Not with a green viral swab like most viruses) - FBC = Atyptical lymphocytes on blood film - Serology = EBV Igs with clotted sample - ELISA TEST

199
Q

Types of HIV

A

HIV-1 - More common, Most virulent - HIV-2 - Less common, Less virulent

200
Q

Transmission of HIV

A

Retrovirus - Sexual transmission - Sharing needles

201
Q

Risk factors of HIV

A

Sharing needles, needle stick injury - MSM - unprotected anal sex

202
Q

Pathophysiology of HIV

A
  • HIB gp120 binds to CD4 on TH - Endocytoses RNA + enzymes - Reverse transcriptase RNA -> DNA - Integrase; viras DNA integrated into host’s - Protein synthesis - Viral proteins + RNA exocytose and take part of CD4+ cell CSM - Increased viral copies, decreased CD4+ (TH cells)
203
Q

img

A
  1. CD4+ dip then ‘set point’ 2. Clinical latency (years) 3. Symptoms 4. AIDS (CD4+ <200/mm3)
204
Q

AIDS definining conditions

A
  • CMV (eg: collitis -> owl eyes) - Pneomocystis jirovecci pneumonia - Kaposi sarcoma (fig1) - Cryptosporadium (fungal) infection - TB - Toxiplasmosis - Lymphomas
205
Q

Diagnosis of HIV

A

history + Anti HIV Ig, P24 Ab (Elisa testing) - Monitor Progression - HIV RNA copies + CD4 count

206
Q

Treatment for HIV

A

HAART - highly active antiretroviral therapy - 3 drugs <, reverse transciptase inhibitors - Aim is to maintain CD4 count and decrease HIV RNA copies

207
Q

Epidemiology of haemophilia?

A

X linked recessive clotting factor deficiency so way more common in males

208
Q

Types of haemophilia

A

A - Factor 8 deficiency, most common B - Factor 9 deficiency, also known as Christmas disease🎄 C - Factor 11 deficiency, very rare

209
Q

Presentation of haemophilia

A

Spontaneous bleeds - Haemarthrosis (bleeding into joint) - V. Easy bruising - Epistaxis🤧

210
Q

When do most cases of haemophilia present?

A

in neonates or early childhood - Intercranial haemorrhage, haematomas, cord bleeding

211
Q

Diagnosis of haemophilia

A

Normal PT, long APTT (as only intrinsic pathway is affected) - Low CF assay (which factor depends on type)

212
Q

Treatment for haemophilia A and B

A

A - high intensity IV factor 8 + desmopressin (releases F8 stored in vessel walls) every two days B - IV factor 9

213
Q

Pathophysiology of Von Willebrand disease

A
  • Autosomal dominant mutation of VWF gene on chromosome 12 - Defect in quality or quantity of VWF - VWF is responsible for the basis of the platelet plus -> more spontaneous bleeding and bruising - Most common inherited bleeding disorder
214
Q

Presentation of Von Willebrand disease

A

Mucocutaneous bleeding: - Epistaxis - GI bleeds - Mennhoragia - Bleeding gums with brushing 🪥 - Heavy bleeding during surgery

215
Q

Diagnosis of Von Willebrand disease

A
  • Normal PT, long APTT - Normal factor 8/9 assay - Low VWF
216
Q

Treatment of Von Willebrand disease

A
  • Desmopressin (releases VWF from endothelial Weibel palade bodies) - IV factor 8 can also be infused for 2 weeks in severe cases - Tranexemic acid (antifibrinolytic)
217
Q

Pathophysiology of DIC

A
  • Tissue damage causes release and activation of tissue factor - Widespread activation of coagulation cascade and therefore platelet activation (crisis) - Platelets unnecessarily consumed + microthrombose in small blood vessels - Tissue plasminogen activator activated, leads to increased fibrinolysis - clotting removed - Lack of systemic platelets -> increased bleed risk
218
Q

Aetiology of DIC

A

Trauma - sepsis (eg: meningococcal meningitis) - Malignancy

219
Q

Diagnosis of DIC

A

Low Platelets - Low fibrinogen - increased D-dimer - long PT and APTT

220
Q

Presentation of DIC

A

bleeding (epistaxis, bruising, rash, GI bleeding) - Acute resp distress syndrome

221
Q

Treatment for DIC

A

treat underlying cause - Fresh frozen plasma to replace clotting factor - Cryoprecipitate to replace fibrinogen - platelet transfusion

222
Q

Risk factors for G6PDH deficiency

A

X-linked recessive (men) - West African, Mediterranean, Asian

223
Q

Heparin-induced thrombocytopenia

A
  • Antibodies bind to heparin after administration -> prothrombotic state - Onset of emboli - Platelets <50%, D-dimer high - Treatment: stop heparin, anticoagulate
224
Q

Pathophysiology of haemolytics uraemic syndrome

A
  • Paediatric condition - Following infection with shiga-toxin producing bacteria like E.Coli/Shigella (typically 5 days after gastroenteritis) - Microvascular clot formation, deposition of platelets and fibrin in small vessels
225
Q

Presentation of haemolytic uraemic syndrome

A
  • Mostly self limiting but presents as medical emergency - AKI (oliguria, haematuria, hypertension) -> uraemia - Hameolytic anaemia - Thrombocytopaenia
226
Q

Diagnosis of haemolytic uraemic syndrome

A

FBC - blood smear - differentiate from TTP with ADAMTS13 testing

227
Q

FBC in haemolytic uraemic syndrome

A

Thrombocytopaenia - anaemia - High reticulocytes - High LDH - High bilirubin

228
Q

Pathophysiology of tumour lysis syndrome

A

Collection of metabolic disturbances occuring with rapid destruction of Neoplastic cells Following Chemotherapy - More common in aggressive treatment of haem malignancies

229
Q

Signs of tumour lysis syndrome

A

Hyperuricaemia, hyperkalaemia, hyperphosphataemia - hypocalcaemia - AKI

230
Q

Types of haemostasis

A

Primary: Initiation and formation of platelet plug - platelet activation Secondary: Formation of the fibrin clot - coagulation cascade

231
Q

PT/INR

A
  • Work out INR using equation: Patient PT/Reference PT - Normal INR: 0.8 - 1.2 INR could be high due to: - Anticoagulants (eg: warfarin usually INR of 2-3) - Liver disease - Vit K deficiency - DIC
232
Q

What is prothrombin time? (PT)

A
  • Coagulation speed through extrinsic pathway - Normally 10-13.5s
233
Q

What is activated partial thromboplastin time? (APTT)

A
  • Coagulation speed through intrinsic pathway - Usually 35-45s - Patient on heparin may be 60-80
234
Q

Other values measured for coagulation

A
  • Bleeding time - Thrombin time - Fibrinogen -> fibrin time (usually 12-14s)
235
Q

Treatment of haemolytic uraemic syndrome

A

Supportive fluids - antibiotics

236
Q

Supportive treatment for multiple myeloma

A

Bisphosphonates - blood transfusion/EPO injection - antibiotics and pain-killers as needed - GCSF to boost Neutrophils - Radiotherapy - Kyphoplasty occasionslly indicated - Psychological support

237
Q

What to give patients with sickle cell painful crisis?

A

IV fluids - Analagaesia - NSAIDs - Oxygen if Low - broad spectrum antibiotics due to neutropaenia

238
Q

Two types of non-Hodgkin lymphomas

A

aggressive - quick onset but Can be treated - Indolent - worse prognosis

239
Q

Indolent lymphoma

A
  • Slow growing and advanced on presentation - “Incurable” - High on Ann Arbour scale - Median survival 9-12 years variable across and within subtypes
240
Q

B symptoms of lymphomas

A

Fevers - night sweats - weight loss

241
Q

Aetiology of indolent lymphoma

A

Primary and secondary immunodeficiency - infection - autoimmune disease

242
Q

What are myelodysplastic syndromes?

A

Bone marrow cells fail to make adequate numbers of healthy blood cells - abnormal cells crowd out healthy Normal cells

243
Q

What haematocrit is concerning in polycythaemia vera?

A

> 45%

244
Q

Diagnostic pathway for thrombocytosis

A

img

245
Q

Diagnosis of thrombocytosis

A
  • Ferritin 221, Serum iron 15, % iron saturation 23% - Blood film: Platelet anisocytosis (Platelets with size variation)- BCR::ABL1 no rearrangement on FISH - JAK2V617F mutated
246
Q

Most common causes of splenomegaly

A

infection - liver disease - autoimmune conditions (eg: SLE, rheumatoid arthritis) Once excluded these: myeloproliferative neoplasms and lymphomas

247
Q

What is bud chiari

A

Thrombus in hepatic artery - Increasing pressure - Leading to enlarged Spleen

248
Q

What is multiple myeloma characterised by?

A

Monoclonal protein in Serum or urine - Lytic Bone lesions/ CRAB end organ damage - Excess plasma cells in Bone marrow

249
Q

Reasons for decrease in RBCs

A

Decreased production - Iron, folate or B12 deficiency - Bone marrow failure Increased loss - Bleeding - Haemolysis

250
Q

Causes of macrocytosis

A

folate or B12 deficiency - Reticulocytosis - raised Igs - Hypothyroidism - Alcohol - Bone marrow Failure, esp. myelodysplastic syndromes - Drugs, eg: methotrexate (inhibits folate metabolism), hydroxyurea

251
Q

How much folate is needed daily?

A

0.1-0.2mg/day Isn’t stored

252
Q

Where is folate absorbed?

A

In the proximal jejunum

253
Q

Aetiology of AML

A
  • Down’s syndrome - Radiation
254
Q

Diagnosis of Hodgkin lymphoma

A

FBC: anaemia, High ESR - High LDH - CxR - Wide mediastinum - blood film - Reed Sternberg cells

255
Q

Symptoms of G6PDH deficiency

A

Fatigue - Palpitations - Dyspnoea - pallor

256
Q

Classic features of myeloma

A

Osteoporosis - Nephrotic syndrome - Hypercalcaemia - Thrombocytopaenia

257
Q

What is the precursor condition to developing multiple myeloma?

A

Mammyloid gammopathy of undetermined significance

258
Q

Symptoms of post thrombotic syndrome

A

Skin hyperpigmentation - Venous ulcers due to poor circulation in the leg - leg swelling

259
Q

What percentage of patients with DVT get post-thrombotic syndrome?

A

30%

260
Q

What to do if someone is at high risk for DVT

A

Ultrasound scan and give anticoags while waiting for results

261
Q

What is antithrombin 3 deficiency

A
  • Inherited (or aquired in nephrotic syndrome) - Antithrombin 3 inhibits factor Xa by binding to its co-factor heparin
262
Q

HB structures

A

95% - HbA - 2x alpha - 2x beta 5% - HbA2 - 2x alpha - 2x delta Fetal - Fetal - 2x alpha - 2x gamma Sickle cell - 2x alpha - 2x HbS HbH - 4 x beta

263
Q

What to give in suspected neutropaenic sepsis

A

One of the piperacillin (broad spec antibiotics) with tazobactam - Do blood cultures - IV fluids and Oxygen

264
Q

Affects of warfarin and heparin on APTT and PT

A

heparin increases APTT - Warfarin increases PT

265
Q

How does DIC cause infection

A

High clotting factors uses up platelets so systemic defences are down

266
Q

What does ferritin increase in?

A

Infection - as it is an acute phase reactant

267
Q

What conditions is autoimmune haemolytic anaemia secondary to?

A

leukaemia - lymphomas - SLE - any sort of infections (eg: EBV)

268
Q

What is aplastic anaemia?

A

Pancytopaenia with hypocellular bone marrow

269
Q

Signs of essential thrombocytosis

A

splenomegaly - Erythromelalgia (red or blue discolouration in peripheries with burning sensation) - Livedoreticularis

270
Q

Risk factors for aquired haemophilia

A

Age >60 - IBD - Diabetes - pregnancy/ postnatal - Malignancy

271
Q

Types of microcytic anaemia

A

Thalassaemia Anaemia of chronic disease Iron deficiency Lead poisoning Sideroblastic 🐒

Haroon Phase 2A (14 decks)

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