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GI P2a > Haem > Flashcards

Haem Flashcards

1
Q

what is multiple myeloma?

A

neoplastic proliferation of bone marrow plasma cells. Excess immunoglobulins (paraprotein) produced, leading to organ dysfunction

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2
Q

When are Rouleaux formations seen? What are they?

A

Multiple myeloma. Aggregation of RBC

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3
Q

What is the presentation of multiple myeloma?

A

OLD CRAB

  • old age
  • calcium increase (bones, stones, groan, psychic moans)
  • renal impairment (light chain deposition –> bence jones proteins in urine)
  • anaemia (normocytic normochromic anaemia)
  • bone lytic lesions (due to immunoglobulins activitating osteoclasts)
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4
Q

Dx of multiple myeloma?

A
  • FBC: anaemia
  • Films: rouleaux formation
  • U and Es: increased calcium, urea, creatinine
  • xray: lytic punched out lesions. Salt and pepper skull
  • serum/urine electrophoresis: Bence Jones Proteins
  • bone marrow biopsy: increased plasma cells
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5
Q

what do most cases of multiple myeloma develop from?

A

MGUS (pre malignant stage)

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6
Q

what are causes of microcytic anaemia? (low MCV)

A

Iron deficiency, anaemia of chronic disease, thalassemia

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7
Q

What are causes of normochromic anaemia?

A

Acute blood loss, anaemia of chronic disease, haemolytic anaemia

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8
Q

What are causes of macrocytic anaemia?

A

Megaloblastic, vitamin B12 deficiency, alcohol, liver disease, hypothyroidism

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9
Q

What do reticulocytes indicate?

A
  • reticulocytes are young RBCs recently released from bone marrow
  • reticulocyte count: guide to erythroid activity.
  • increases after haemorrhage, haemolysis
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10
Q

Where is most of the body’s iron absorbed? What factors promote iron absorption?

A

duodenum. Factors that promote iron absorption: gastric acid, iron deficiency, increased EPO activity

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11
Q

How is B12 absorbed?

A

liberated from protein complexes y gastric acid and pepsin, then binds to intrinsic factor, formed by parietal cells

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12
Q

What is the presentation of iron deficiency anaemia?

A
  • microcytic - brittle hair and nails -atrophic glossitis (tongue papillae worn down) -angular stomatitis (ulcers)
  • HIGH total iron binding capacity in blood
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13
Q

What is the causes of iron deficiency anaemia?

A

blood loss, increased demands (growth and pregnancy), decreased absorption, poor dietary intake

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14
Q

What is pernicious anaemia, causes and its presentation?

A
  • low B12, macrocytic anaemia
  • causes: autoimmune conditions can mean destruction of parietal cells. Also impaired absorption and low B12 in the diet
  • presentation: neurological defects (peripheral neuropathy, but spinothalamic tract intact). Lethargy, fatigue, dyspnoea, faintness.
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15
Q

What is the treatment of pernicious anaemia?

A

B12 injection: hydroxocalamin (IM)

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16
Q

What is the presentation of folate deficiency, and how long does it take to develop?

A
  • general anaemia presentation, and glossitis and depression. Macrocytic anaemia (folate needed for Hb DNA maturation)
  • takes 4 months to develop, as body has 4 month reserve
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17
Q

What are the causes of folate deficiency?

A

poor intake (old age, poverty, alcohol excess), malabsorption (coeliac disease, Crohn’s), excess utilisation (pregnancy, malignant and inflammatory disease). Some drugs

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18
Q

What are general anaemia symptoms:

A

fatigue, lethargy, dyspnoea, palpitations, headache, pallour

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19
Q

What is the presentation of haemolytic anaemia, and what are examples of it?

A
  • examples: sickle cell anaemia, thalaessmia

- presentation: jaundice, gallstones, leg ulcers

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20
Q

What is the pathophysiology/aetiology of haemolytic anaemia?

A

RBC destroyed before normal 120 day lifespan. Destruction can be intravascular or extravascular

  • aetiology: inherited –> red cell membrane fect (sphereocytosis), haemaglobin abnormalities, metabolic defects
  • -> acquired: autoimmune, infections (eg, malaria), systemic failure (liver failure)
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21
Q

What is the dx for haemolytic anaemia?

A

Reduced Hb, increased MCV, increased reticulocytes, spherocytes

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22
Q

What is the tx for haemolytic anaemia?

A

folate acid and iron supplement. Immunosuppression if immune cause. splenectomy if all else fails

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23
Q

What is aplastic anaemia? what is the presentation?

A
  • bone marrow failure, due to reduction in number of pluripotent stem cells, leads to lack of haemopoesis
  • presentation: increased susceptibility to infection and bleeding gums and nosebleeds
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24
Q

What is pancytopenia?

A

low red blood cells, white blood cells and platelets

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25
Q

What is the dx of aplastic anaemia? Tx?

A
  • FBC: pancytopenia, low reticulocytes
  • biopsy of bone marrow: hypocellular marrow with increased fat spaces
  • Tx: blood and platelet transfusion. immunosuppression., bone marrow transplant
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26
Q

What is sickle cell anaemia?

A

inherited haemolytic anaemia. Deformation of faulty Hb molecule. Leads to HbS. In deoxygenated state, HbS are insoluble and polymerise, leading to sickling. Can lead to haemolysis and vaso-occlusion
- autosomal recessive, more common in africa

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27
Q

What is the presentation of sickle cell anaemia?

A
  • foetal haemaglobin is normal, so presents when this is out of circulation at 6 months
  • vaso-occlusion: early childhood acute pain in feet and hands due to occlusion of small vessels. Avascular necrosis of bone marrow. Affects (in adults) long bones, ribs, spine, pelvis
  • retinal ischaemia
  • often symptoms of anaemia as HbS release oxygen early
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28
Q

What is the treatment of SCA?

A
  • avoid precipitating factors
  • folic acid supplements
  • NSAIDs
  • BMT from HLA matched siblings
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29
Q

What is thalassemia?

A

One or multiple gene defects leading to reduced rate of production of globin chains. Can be alpha or beta thalassemia depending on which is affected. Unbalanced Hb synthesis, so unmatched globins precipitate, damaging RBC membranes, causing damage

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30
Q

What is the presentation of thalassemia?

A
  • alpha presents in utero. excess beta chains
  • beta presents in infancy. excess alpha chains
  • asymptomatic if heterozygote
  • severe anaemia in homozygotes
  • failure to thrive, bone deformities
  • iron overload
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31
Q

How is thalassemia diagnosed? What is the tx?

A
  • dx: Hb electrophoresis
  • tx: blood transfusion to avoid compx. Iron chelating agent for overload. Ascorbic acid increases iron excretion in urine, to offset overload
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32
Q

What is glucose-6-phosphate dehydrogenase deficiency?

A

G6PD is an enzyme that maintains glutathione in a reduced state. This protects against oxidant injuries in the RBC. Thus, increased G6DP leads to increased haemolysis.

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33
Q

What is the presentation of G6PD deficiency? what is the tx?

A

neonatal jaundice, haemolytic anaemia, acute haemolysis (precipitated by fava beans)
- tx: avoid fava beans. Transfusion if necessary

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34
Q

What is the inheritance of G6PD deficiency?

A

x-linked recessive

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35
Q

What is polycythaemia Rubra Vera?

A

most common myeloproliferative disorder. Type of blood cancer. Excess production of RBC, WBC and platelets: increased viscosity of the blood.

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36
Q

What is a myeloproliferative disorder?

A

uncontrolled clonal proliferation of cell lines: namely erythroid, myeloid, megakaryocyte lines. Differentiation from leukemia as there is no accumulation of abnormal product.

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37
Q

What is the genetic mutation in myeloproliferative disorders?

A

Group of stem cell disorders that share mutations to JAK2, which leads to prolonged survival of RBC

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38
Q

What is the presentation of polycythaemia rubra vera?

A

Signs and symptoms due to hypervolaemia and hyperviscosity.

  • pruritus (urge to itch), especially after exposure to warm water. Headaches. Dizziness. Sweating.
  • thrombotic compx: MI, stroke, DVT
  • sometimes erythromelalgia (sudden, severe burning in hands and feet with red/blue discolouration)
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39
Q

What is the dx and tx of polycythaemia rubra vera?

A
  • dx: blood count showing increased WBC, platelets and red cell volume. Gain of function JAK-2 mutation. Decreased serum EPO
  • Tx: low dose aspirin. Myelosuppression (hydroxycarbamide). Venesection
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40
Q

What can polycythaemia rubra vera transform to?

A

acute myeloid leukaemia

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41
Q

What is the composition of a DVT?

A

RBC and few platelets. Forms in direction of blood flow

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42
Q

What is the Dx of DVT?

A

USS, d-dimers, contrast venography

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43
Q

What is disseminated intravascular coagulation?

A

acquired coagulation disorder, alongside vitamin K deficiency. Leads to widespread intravascular deposition of fibrin with consumption of coagulation factors and platelets. Then associated haemorrhagic or thrombotic syndromes as platelets used up

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44
Q

What is the aetiology of DIC?

A

secondary to many things that cause cytokine release: systemic inflammatory response syndrome, sepsis, septic shock, multiple organ dysfunction, malignancy, trauma. Major trigger: exposure of blood to a potent tissue factor: eg, brain tumour, placental rupture

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45
Q

What is the presentation of DIC?

A

bleeding from unrelated sites (ENT, GI, resp, site of venipuncture). Confusion, fever. Skin: purpura, localised infarction

46
Q

What is the dx of DIC?

A
  • increased prothromin time, increased activated partial thromboplastin time, decreased platelets and fibrinogen
47
Q

What is the treatment of DIC?

A

treat underlying cause. Consider platelet transfusion and FFP.

48
Q

what is haemophilia? Presentation? Treatment?

A

x-linked recessived. Lack of factor VIII.

  • presentation: recurrent joint and tissue bleeds. Can lead to bleeds into joint cavities.
  • tx: desmopressin raises VIII levels
49
Q

What drugs can cause overcoagulation:

A

excess warfarin and heparin

50
Q

What is Von Willebran disease? Dx? Tx?

A

reduced or abnormal VWF. Signs: bleeding, bruising, epistaxis. Dominant inheritance

  • Dx: increased APTT, increased bleeding time, decreased factor VIII
  • Tx: desmopressin
51
Q

What is ITP? (immune thrombocytopenic purpura)

A

immune destruction of platelets. Formation of auto antibodies against platelets in the spleen

52
Q

What is the cause of ITP?

A
  • children: preceding viral infection

- adults: with other autoimmune condition

53
Q

What is the treatment of ITP?

A

oral corticosteroids. Second line: splenectomy

54
Q

What is TTP (thrombotic thrombocytopenic purpura)?

A

widespread adhesion and aggregation of platelets, due to deficiency of ADAMS-13/autoantibody (the protease that degrades vWF). Leads to microvascular thrombosis.

55
Q

What is the Dx of TTP and the tx?

A
  • Dx: increased LDH levels (from ischaemic/necrotic cells)

- Tx: steroids, immunosuppression, splenectomy (spleen makes the autoantibodies). Plasma exchange (urgent)

56
Q

What is malaria?

A

Infection by plasmodium (vector) transmitted by a mosquito

57
Q

What is the most common causative pathogens of malaria?

A

1) P. falciparum: 80% cases worldwide, highest mortality

2) P. vivax and 3)P. ovale cause clinically similar, milder infections. they can be relapsing over many years.

58
Q

What is the pathogenesis of malaria?

A

-Humans acquire malaria from sporozoites transmitted by the bite of the mosquito→ Sporozoites travel through the bloodstream and enter hepatocytes→They mature into tissue schizonts which rupture and release merozoites into the bloodstream→Invade RBCs and release more
merozoites

59
Q

What is the clinical presentation of malaria?

A

fever, sweats, anaemia, hepatosplenomegaly. No specific symptoms. Severe: impaired consciousness, dyspnoea, bleeding, fits, hypovolaemia

60
Q

What is the diagnosis of malaria?

A

Thick and thin blood smears, stained with Field’s stain or Giemsa stain
-Laboratory findings: hemolytic anemia, thrombocytopenia (common), uremia, hyperbilirubinemia, abnormal LFTs, coagulopathy

61
Q

What is the treatment of malaria?

A

Quinoline derivatives (chloroquine, quinine)

62
Q

What is AML?

A

acute transformation of a clone of myeloid progenitor cells. Accumulation of leukaemic cells in bone marrow, peripheral blood and tissues. Reduction in RBC, neutrophils,etc.

63
Q

What is the presentation of AML?

A

fatigue, anaemia, bleeding. Prone to infection. Gum issues!! (identifier). DIC

64
Q

What is the dx of AML?

A
  • increased WCC (but can also be low)
  • blast cells may be low
  • blood film: anaemia, thrombocytopenia, auer rods
  • leukaemic cells in bone marrow aspirate
65
Q

What is the adetiology and epidemiology of AML?

A
  • can be a long term complication of chemotherapy.
  • associated with myelodysplastic states, radiation and Downs
  • commonest acute leukaemia of adults
66
Q

What is CML?

A

chronic malignant transformation of a clone of myeloid cells. Due to uncontrolled proliferation of clonal cells.

67
Q

What are the three phases of CML?

A
  1. chronic: lasts a few years, no symptoms
  2. accelerated phase: increased symptoms and spleen size. fever, weightloss, night sweating, gout
  3. blast cell transformation: features of acute leukaemia and death
68
Q

What is the aetiology of CML?

A
  • philadelphia chromosome (alters tyrosine kinase activity)
69
Q

What chromosomes are the translocations between with the Philadelphia chromosome?

A

9 and 22

70
Q

What is the dx of CML?

A
  • ^^ WCC, ^neutrophils, monocytes, basophils. Platelets variable. ^ urate. Bone marrow hypercellular
71
Q

What is the tx for CML?

A

imatinib (tyrosine kinase inhibitor)

72
Q

What is ALL? who is it most common in?

A

CHILDHOOD LEUKAEMIA!
- acute malignancy of lymphoid cells. Affects B or T cell lineages. Arrests maturation, and their is uncontrolled proliferation of immature blasts. May have bone marrow failure and tissue infiltration by blasts

73
Q

What is the presentation of ALL?

A

fatigue, dizziness, palpitations, anaemia, bleeding, infection. bone pain. CNS involvement: cranial nerve palsies

74
Q

What is the aetiology of ALL?

A

genetic risk: strong association with down’s syndrome Related to chemicals, drugs, radiation

75
Q

What is the dx of ALL?

A
  • characteristic blast cells on blood film and marrow. Anaemia and thrombocytopenia.
  • Lumbar puncture to look for lymphadenopathy
76
Q

What is the tx of ALL?

A
  • remission induction: vincristine, dexamethasone, asparginase
77
Q

What is CLL?

A

chronic malignant transformation of a clone of mature lymphoid cells. Progressive accumulation. Can lead to auto-immune haemolysis. Progressive accumulation

78
Q

Presn of CLL?

A

Often none, incidental finding. When symptoms start: anaemia, infection prone, decreased weight, sweats, anorexia

79
Q

What is the dx of CLL?

A

blood film: smudge cells (lymphocyte looks exploded). Increased lymphocytes, anaemia. Later, autoimmune haemolysis, marrow infiltration

80
Q

Tx of CLL

A

Tx when reaches a certain point. Chlorambucil: with or without prednisolone

81
Q

What is Hodgkins lymphoma?

A

Malignant tumour of the lymphatic system, with reed Sternberg cells. Malignant transformation of normal B or T lymphocytes.

82
Q

What is the presenation of hodgkins lymphoma?

A

painless rubbery lymph nodes, but pain induced when drinking. Systemic symptoms sometimes. (b classification). more common in the upper body.

83
Q

What is the aetiology of hodgkins lymphoma

A

previous EBV, affecting sibling, SLE

84
Q

What is the dx of lymphoma?

A

tissue biopsy, reed sternberg cells (mirror image nuclei)

  • increased LDH due to high cell turnover
  • high ESr and low Hb: worse prognosis
  • CT for staging
85
Q

What is the treatment for lymphoma?

A

ABVD chemo

86
Q

What is non hodgkins lymphoma?

A

malignant tumour of lymphatic system WITHOUT reed Sternberg cells. Wide range of possible tumour locations.

87
Q

what is the aetiology of non hodgkins lymphoma?

A

immunodeficiency; drugs, HIV,

H.pylori, toxins, congenital

88
Q

What has worse prognosis: low or high grade? what is tx for each?

A
  • low grade: indolent, incurable and widely dissemintated. Radiotherapy
  • high grade: cyclical combination of chemo and fieldirradation
89
Q

What is a myeoblast a precursor of?

A

neutrophil, eosinophil and basophil

90
Q

What are auer rodes?

A

large crystalline cytoplasmic inclusion bodies

91
Q

What is Wells score?

A

DVT risk

92
Q

What are the s/e of chemo?

A

cytopenia, infertility, nausea and GI disturbance, secondary malignancies

93
Q

What is complicated malaria?

A

specific symptoms rather than just systemic

94
Q

What are the classes of polycythaemia rubra vera?

A
  • relative: appears to increase haematocrit but actually reduction in plasma vol
  • absolute: primary (eg,polycythaemia rubra vera), and secondary (increased EPO; neoplasms, high altitude)
95
Q

What is direct coombs test?

A

test for autoimmune haemolytic anaemia

96
Q

What do Heinz bodies indicate?

A

G6PD deficiency

97
Q

What is tumour lysis syndrome?

A

group of metabolic conditions that occurs as a complication of cancer treatment, when large parts of tumour are lysed off into the circulation. presn: nausea, vomiting, diarrhoea. hyperuricemia, hyperkalemia, hyperphosphatemia, HYPOcalcaemia

98
Q

what drug prevents tumour lysis syndrome?

A

allopurinol

99
Q

When are raised eosinophils seen?

A

parasitic infection

100
Q

What drugs can cause low platelets?

A

NSAIDs, heparin, digoxin, PPIs

101
Q

What drugs interact with G6DP?

A
  • malaria tx
  • nitrofurantoin: UTIs
  • sulphonamides
102
Q

What is the diagnosis of alpha thalassemia?

A

microcytic anaemia, increased serum iron. Hb electrophoresis

103
Q

What is the dx for beta thalassemia?

A

blood film. Anaemia. nucleate red blood cells in circulation

104
Q

What confirms dx of SCA?

A

haemaglobin electrophoresis

105
Q

What is seen in a blood smear in TTP and what tx is CI?

A
  • fragmented erythrocytes seen

- platelet transfusion CI

106
Q

What is R-CHOP the treatment for?

A

non hodgkins lymphoma

107
Q

What does rutiximab treat, and what is it?

A
  • monoclonal antibody. Targets CD20 receptors on B cells.

- hodgkins

108
Q

How can ITP and TTP be differentiated clinically?

A
  • TTP: classic pentad of fever, haemolytic anemia, thrombocytopenia, acute renal failure, and neurological symptoms
  • ITP: It presents with purpura or gingival bleeding and is not associated with fever, neurological symptoms, or splenomegaly
109
Q

What is hepcidin?

A

Hepcidin is a protein synthesized by the liver, and is a regulator of iron metabolism. Associated with anaemia of chronic disease

110
Q

What is Richter’s syndrome?

A

when CLL transforms into a aggressive lymphoma

GI P2a (12 decks)

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