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Haematology > Revision > Flashcards

Revision Flashcards

1
Q

what is serum

A

clotted plasma

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2
Q

what is the liquid in blood

A

plasma

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3
Q

what is haematopoiesis

A

production of blood cells

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4
Q

where does haematpoiesis occur

A

embryo- yolk sac then liver then marrow
birth- bone marrow, liver and spleen when needed
adult- bones in axial skeleton: skull, ribs, sternum, pelvis, proximal ends of femur

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5
Q

what are the steps in the haematopoietic tree

A 
stem cells 
multipotent progenitors (ones that proliferate the most)
oligolineage progenitors (becomes the different types of these depending on the bodys needs) 
mature cells (RBC, platelets, granulocytes, macrophages, dendritic, T cells, B cells, NK cells)
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6
Q

what is erythopoiesis

A

formation of mature red blood cells

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7
Q

what are the stages in erythropoiesis

A

pronormoblast
(lots of others, all in bone marrow, cell and its nucleus gets smaller each differentiation)
reticulocyte (enters circulation)
mature red cell/ erythrocyte

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8
Q

what is a reticulocyte

A

immediate precursor of red blood cell, has no nucleus but some RNA which makes it appear darker in colour
is in the circulation not bone marrow

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9
Q

what do platelets originate from

A

bud off megakaryocytes (cytoplasm doesnt divide)

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10
Q

what is the role of platelets

A

stop bleeding

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11
Q

what are the types of granulocytes

A

eosinophils
basophils
neutrophils

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12
Q

what are granulocytes

A

most common type of WBC, contains granule

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13
Q

what are neutrophils

A

type of granulocyte

first white cell to respond in an infection (Q specific to bacterial infections)

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14
Q

what are polymorphs

A

different name for neutrophils (called this because segmented lobular nucleus)

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15
Q

what is the main phagocytosing cell

A

macrophage

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16
Q

what are the roles of neutrophils

A

short life in circulation- goes to tissues where it:
phagocytoses invaders
kills with granule contents (dies in process)
attracts other cells

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17
Q

what can increase neutrophils

A

body stress - infection, trauma, infarction

steroids (makes them unable to leave blood stream and get into tissues)

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18
Q

what are eosinophils

A

type of granulocyte

are bilobed, granules makes them look red-orange

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19
Q

what are the roles of eosinophils

A

fight parasitic infections

involved in hypersensitivity reactions/ allergic conditions

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20
Q

what are basophils

A

type of granulocyte w/ purple- black granules

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21
Q

what are the roles of basophils

A

mediates hypersensitivity reactions
granules contain histamine
FcReceptors bind IgE

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22
Q

what are monocytes

A

largest type of white blood cell, pale, single nucleus

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23
Q

what is the role of monocytes

A

circulate for a week then enter tissues to become macrophages
-phagocytose invaders (endocytosis, present antigen to lymphocytes)
-attract other cells
more long lived than neutrophils

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24
Q

what is the structure of lymphocytes

A

mature- small

activated (aka atypical)- large open structure

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25
Q

what is the function of lymphocytes

A

lots of diff types: B, T, NK

adaptive immune system

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26
Q

where are common sites for bone marrow aspiration/ biopsy

A

posterior iliac crests

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27
Q

what are target cells

A

In liver disease the red cell membrane is disrupted which causes change in shape of the red cell from pale bit in the middle (concave) –> dark part in the middle = target cells

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28
Q

what is the most common cause of macrocytic anaemia

A

liver disease (due to alcohol most commonly, then NAFLD)

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29
Q

what are the Hb levels below which probs means anaemia

A 
children 6mnth-6yrs = 110
6-14 120 
men 130
females 120
pregnant females 110
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30
Q

what are haematinics

A

MCV

MCH (cell Hb content)

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31
Q

what does anaemia with increased reticulocyte mean

A

caused by haemolysis or blood loss

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32
Q

what does anaemia with reduced reticulocyte mean

A

maturation abornmalty or hypoproliferative

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33
Q

what will MCV be like in hypoproliferative anaemias

A

normocytic (and normochromic)

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34
Q

what can distinguish haemolysis from blood loss causing anaemia

A

(obvs Hx and clinical picture, blood film)
if bleeding then rbcs gone, nothing to breakdown
if haemolysing:
-increased unconjugated serum bilirubin
-increased urinary urobilinogen
-work hypertrophy (splenomegaly)

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35
Q

what causes hypochromic microcytic anaemia

A

problems with haemoglobin formation:

  • iron deficiency
  • haem defects (rare, lead poisoning, congenital sideroblastic anaemia)
  • globin defects (thalassaemias)
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36
Q

what causes macrocytic anaemias

A

nuclear maturation defects (failure of cell division)

  • diet: B12, folate (megaloblastic)
  • myelodysplasia
  • drugs e.g. chemo
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37
Q

what can cause macrocytosis without significant anaemia

A

hypothyroidism
alcohol
liver disease

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38
Q

what can cause normochromic normocytic anaemia

A

hypoproliferative:
-marrow failure :drug induced, aplastic anaemia (can be mactocytic)
hypometabolic (can be macro)
marrow infiltration (mets, fibrosis)
renal impairment
chronic disease (infective. inflammatory, malignant= anaemia of chronic disease) (can be micro)

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39
Q

what is renal anaemia

A

an anaemia of chronic disease due to failure of erythropoietin production

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40
Q

what is the second most common cause of anaemia after iron deficiency

A

anaemia of chronic disease

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41
Q

what causes anaemia of chronic disease

A

inflammatory stimulus activates monocytes and T cells which releases inflammatory cytokines:

  • inhibits erythropoietin release
  • inhibits erythroid proliferation
  • augments haemophagocytosis = reduced red cell survival
  • increases hepatic syntheses of hepcidin (negative regulator of iron absorption, decreasing iron)
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42
Q

why might anaemia of chronic disease by microcytic

A

If the predominant mechanism is through hepcidin stimulation

reduced release of iron from macrophages ie failure of haemoglobin synthesis
Explains low transferrin saturation despite normal/raised ferritin
Explains why it may respond to IV iron

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43
Q

are iron def anaemias always microcytic

A

no- relative measure so many normocytic (in normal range just not normal for the individual)

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44
Q

how do you differentiate anaemia of chronic

A

serum iron:

  • ID: reduced
  • ACD: reduced

transferrin:
- ID: normal/ increased
- ACD: normal/ reduced

% transferrin sat:

  • ID: reduced
  • ACD: reduced

Ferritin:

  • ID: reduced
  • ACD: normal/ increased

MCV:

  • ID: reduced (can be normal)
  • ACD: normal (can be reduced)
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45
Q

what are the implications of the biconcave shape of ebcs

A

needed for increased gas exchange

need more room for Hb so why nucleus removed

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46
Q

what is needed to make the rbc flexible

A

lipid bi layer membrane with protein spars and anchors

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47
Q

what is enucleation

A

when the nucleus is budded off with other organelles and functional fibrous proteins (absorbed by the macrophage)

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48
Q

In what circumstances might nucleated red cells appear in the blood?

A

bone marrow damage or severe stress

  • severe anaemia
  • thalassaemia
  • hypoxia
  • myelomas
  • leukemias
  • lymphomas
  • myelofibrosis

removal of spleen can make immature cells more apparent in the blood

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49
Q

is Fe2+ or Fe3+ oxygenated- which one is blue or red

A

Fe2+ deoxygenated- blue

Fe3+ oxygenated- red

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50
Q

what does free iron cause

A

is toxic- causes inflammation

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51
Q

what can free Hb cause in the blood

A

can be life threatening

can cause DIC and other dysfunctional responses

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52
Q

what different mechanisms can cause red cell membrane damage

A

Mutations in cytoskeletal proteins resulting in the cell membrane not working well:

  • Hereditary spherocytosis (this is usually autosomal dominant)
  • RARE! Zieve’s syndrome: haemolysis related to alcoholic liver disease. Abnormalities of lipid metabolism results in red cell membrane damage

Autoimmune haemolytic anaemia: autoantibodies against red cells damage the red cell membrane

Infection

  • DIC(disseminating intravascular coagulopathy)
  • Sepsis

Mechanical damage

  • Severe burns: capillaries are damaged and as blood vessels squeeze through these they get sheared resulting in microspherocytes
  • Heart valve
  • Haemolytic Uraemic Syndrome (E.Coli)
  • Thrombotic Thrombocytopenic Purpura (TTP)
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53
Q

what virus might cause a decompensation in HS

A

parovirus

virus enters bone marrow and stops erythroid precursors from dividing

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54
Q

What are the sources of energy and reducing powers which protect the red blood cell against oxidative damage?

A

(Anaerobic) NADH and NADPH are important molecules generated by the cycle (direct or hexose monophosphate shunt)
G6PD contributes to formation of glutathione which is required for NADPH formation

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55
Q

what does a G6PD deficiency result in

A

reduced protection from oxidative damage

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56
Q

what is dapsone

A

antibiotic previously used in the treatment of leprosy

can induce oxidative stress

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57
Q

what drugs induce oxidative stress

A

dapsone, quinines, anti-malarials, fava beans

can lead to splenomegaly

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58
Q

what are the clinical manifestations of increased oxidative damage

A

tiredness, lethargy, pale gums, pallor, jaundice

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59
Q

what are heinz bodies

A

Red cells with haemoglobin exposed to oxidative stress–>Hb has been oxidised + damaged–>clumped together in a ball (Heinz body)–>red cells are contracted–>heinz body anaemia

this seen in G6PD deficiency causing haemolytic anaemia

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60
Q

what can cause a problem with Hb synthesis

A

Haem production

  • Iron deficiency
  • Porphyrin synthesis

Globin production
-Thalassaemia

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61
Q

what are the symptoms and signs of microcytic hypochromic anaemia

A

Signs: Tachycardia, tachypnoea, rising pulse or even extra heart sound, pallor
Symptoms: Palpitations, lethargic, fatigue, TATT, tinnitus, somnolence

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62
Q

how does the red cell try and improve oxygen delivery in microcytic anaemia

A

increase 2,3-DPG to increase oxygen dissociation

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63
Q

what codes for beta chains

A

1 gene on each chromo 11

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64
Q

what are the affects of beta thalassaemia major

A

Failure to thrive
General Sx of anaemia
Splenomegaly
Chronically - permanent bone marrow changes. Frontal bossing, skeletal deformities, spinal cord compression

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65
Q

what is B12 important for the production of

A

thiamine

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66
Q

what are agranulocytes

A

leukocytes and monocytes

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67
Q

what are the symptoms of megaloblastic anaemia

A

Pallor, mild jaundice (lemony tinged), red beefy tongue, reduced vibration and proprioception sense (dorsal columns): rely on proprioception in the dark (falling over in the night), lemony tinged/mild jaundice

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68
Q

what causes sickle cell anaemia

A

substitution of valine for glutamic acid at codon 6 of beta glogin gene

homozygotes produce only haemoglobin S and variable amount of haemoglobin F

sickled red cells produces microvascular obstruction and ischaemia

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69
Q 
Pale patient
 Mildly jaundiced
 No obvious bleeding
 Dark urine 
suspect what?
A

haemolysis

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70
Q

what tests to confirm haemolysis

A

Blood film: polychromasia, spherocytes
Reticulocytosis
Unconjugated hyperbilirubinaemia

if intravascular : haemoglobinuria haemosiderinuria methaemalbuminaemia

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71
Q

what are the acuired immune causes of haemolysis

A

Autoimmune: spherocytic

Alloimmune: haemolytic disease
of the newborn (non-spherocytic)
ABO mismatch transfusion

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72
Q

what are the non immune acquired causes of haemolysis

A

Mechanical: prosthetic heart valve,
disseminated intravascular coagulation

Infection: malaria, Clostridium welchii

Chemical/ physical: oxidative stress
(aspirin, dapsone, anti-malarials), burns

Membrane: liver disease

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73
Q

what are the inherited causes of haemolysis

A

red cell enzyme defects: G6PD def

red cell membrane defects: HS, hereditary elliptocytosis

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74
Q

what diagnostic tests for haemolysis

A

Direct Coombs test: detects antibody coated red cells using antisera to immunoglobulins; end point is red cell agglutination

Osmotic fragility test: incubate red cells in increasingly hypotonic solutions and measure release of haemoglobin from lysed cells. Increased fragility in hereditary spherocytosis.

G-6-PD enzyme activity screening test: quantitate fluorescence of NADPH generation by G-6-PD. Detects enzyme activity <20%

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75
Q

what are causes of macrocytosis not related to B12 or folate deficiency

A

Drugs: methotrexate/ AZT/ metformin
Alcohol abuse/ liver disease/ myelodysplasia (stem cell dysfunction) /myeloma/anaplastic anaemia/ hypothyroidism

pregnancy, neonatal, reticulocytosis

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76
Q

why would hypothyroidism be relevant in a Hx of macrocytic anaemia

A

as can cause macrocytosis but also is associated with pernicious anaemia

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77
Q

what is pernicious anaemia

A

autoimmune condition that results from atrophic gastritis and destruction of the gastric parietal cells ultimately leading to a reduction in intrinsic factor.
IF is required to bind to vitamin B12 to allow absorption in the terminal ileum.
Pernicious anaemia is also linked with other autoimmune conditions such as hypothyroidism, vitiligo and addison’s disease.

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78
Q

is macrocytosis always associated with anaemia

A

no

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79
Q

what is the most common cause of macrocytosis

A

alcohol consumption

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80
Q

what does a MCV >120 mean

A

macrocytosis usually caused by def of B12 or folate

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81
Q

what does macrocytosis with anaemia and also low neutrophils or platelets

A

Megaloblastic or myelodysplasia more likely

82
Q

macrocytosis blood film:

hypersegmented neutrophils, oval macrocytes

A

megaloblastic

83
Q

macrocytosis blood film:

uniform macrocytosis

84
Q

macrocytosis blood film:

dysplastic neutrophils

A

myelodysplasia

85
Q

macrocytosis blood film:

polychromasia

A

reticulocytosis

86
Q

macrocytosis blood film:

agglutinates

A

artefacts with cold agglutins

87
Q

what are the causes of microcytic anaemias

A

iron deficiency
anaemia of chronic disease
thalassaemia
sideroblastic anaemia

88
Q

what is the best test for diagnosing iron deficiency anaemia

A

serum ferritin (should be low showing lack of iron stores)

FBC

if symptomless: GI endoscopy, barium enema/ colonoscopy

89
Q

what happens to reticulocytes in iron deficiency

A

reduced

raised if bleeding

90
Q

how else can you measure storage iron

A

bone marrow biopsy with perls stain

91
Q

which iron in body is depleted first

A

storage iron

then transport iron

92
Q

what are the causes of iron deficiency

A 
Reduced dietary iron
Increased physiological requirements
Blood loss (menstruation, GI)
Malabsorption
jejunum
need gastric acid
93
Q

why in acute bleeding might the Hb underestimate any blood loss

A

as redistribution of body water has not yet fully allowed dilution of the remaining red cells

94
Q

what fluid is 1st line in the acutely shocked patient

A

synthetic colloids

95
Q

when is reticulocytosis maximal after a bleed

A

8-10 days after (begins days 1-2)

96
Q

what is an appropriate marrow response to marked anaemia

A

6-8 fold increase in reticulocyte count
(3-4 fold increase in amount of erythropoiesis +
earlier release of reticulocytes into blood)

97
Q

what are the signs of shock

A 
Tachycardia
Hypotension (postural)
Tachypnoea 
Peripheral vasoconstriction (pallor, delayed capillary refill)
Oliguria
98
Q

what are the causes of vasogenic shock

A

anaphylaxis

sepsis

99
Q

how is blood cross matched

A

ABO and RhD antigen grouping of patient
Screen for alloantibodies in patient:
-Antibodies in the patient to antigens that might be on the donor red cells
-If alloantibody identified in patient check donor unit is negative for that antigen
Mix donor cells and recipient plasma as a final check in wet crossmatch
Confirm historical records for an electronic crossmatch

quickest test ABO group

100
Q

what types of blood are available (maybe if not time to do all tests)

A

O RhD negative
ABO type specific
Fully crossmatched
Electronic crossmatched (if historical group and negative allo antibody screen)

101
Q

what can ABO transfusion reactions cause

A

DIC and death

102
Q

when and why do delayed transfusion reactions occur

A

IgG alloantibody to red cells antigen
Acquired following previous transfusion or pregnancy
at low level but secondary response 10 days later

103
Q

what are the immune complications of transfusion

A

febrile non-haemolytic reactions (white cell antibodies/ hypersensitivity to donor plasma proteins)

immediate (intravascular- acute haemolytic- ABO) or delayed (extravascular- IgG- red cell antigen) haemolytic reactions

urticarial reactions
taGVHD, PTP, IgA deficiency, TRALI

104
Q

what is the role of VWf

A

helps platelets stick together and to collagen in the endothelium

also binds to factor 8 to protect it from destruction, increasing its half life

105
Q

how do you screen for problems in primary haemostasis

A 
(usually results in mucosal bleeds) 
platelet count (within FBC)
106
Q

what is the extrinsic, intrinsic and final common pathway

A

parts of secondary haemostasis

Extrinsic factors= Tissue factor released first in tissue damage, this activates factor 7 (becomes CF VIIa)- when activates has a negative charge, binds to positive (calcium) platelets
TF and CF 7 activate factors 5 and 10, which then activate prothrombin to thrombin (prothrombin is CF II)
Thrombin converts the protein fibrinogen to fibrin which forms stable blood clot.

Intrinsic pathway= thrombin activating factors 8 and 9 which in turn activates factors 5 and 10, allows rapid response and quick formation of a fibrin clot
Also have factors 11 and 12 (if 12 missing no clinical consequences) (if 11 missing can get bleeding problems but not as significant as other CF)

Final common pathway= prothrombin -> thrombin and fibrinogen -> firbrin

107
Q

what tests make up a coagulation screen

A

prothrombin time
activated partial thromboplastin time

(additional tests sometimes done inc. fibrinogen assay, thrombin time (surrogate marker for fibrinogen), heparin

108
Q

what coagulation tests assess the extrinsic and intrinsic pathways

A 
extrinsic= PT 
intrinsic= APTT
109
Q

what is a normal platelet range

110
Q

19 year old with menorrhagia and easy bruising
Isolated prolonged APTT
normal platelets

A

VWF deficiency

111
Q

what can cause an isolated prolonged APTT

A

factor 8 or 9 deficiency (haemophilia)
heparin
APS

112
Q

what are the features of APS

A

autoimmune condition, that causes increased blood clots (arterial and venous and miscarriage)

113
Q

why do you get prolonged APTT in APS

A

lupus anticoagulants interfere with assay and prolong APTT. Anti body binds to antiphophospholipid which are used in tests

114
Q

why do people with VWf deficiency have a prolonged APTT

A

VWf binds to factor 8 to protect it from destruction prolonging its half life. Those with VWf def will have low factor 8 (not as much as in haemophilia) but enough to cause increase in APTT

115
Q

59 year old male with past history of thromboembolic disease
prolonged PT and APTT
normal platelets

A

warfarin therapy

116
Q

what can cause prolongation of PT and APTT

A

multiple factor deficiency, DIC, liver disease (don’t make clotting factors and increased platelet destruction due to hypersplenism), warfarin (affects 2,7,9,10 as antagonises vit K which is required for the carboxylation of these clotting factors), vit k deficiency (diet- leaf green veg, intestinal synthesis- haemorrhagic disease of the newborn (no vit k in breast milk and no gut bacterial), obstructive jaundice (is a fat soluble vitamin and bile salts are needed to absorb it)

117
Q

what is the placenta v rich in

A

tissue factor and phopsholipids- why DIC happens in placental abruption

118
Q

what is the target range for INR

119
Q

what is the target APTT for those on heparin

120
Q

what do NOACs target

A

CF Xa
thrombin
(more direct action so dont need monitoring)

121
Q

what does thrombin clotting time show

A

fibrinogen levels

122
Q

what tests can confirm DIC

A 
low platelets, markedly prolonged APTT and PT
D dimers (fibrin degradation products, will be high)
123
Q

what are the differentials for an acute onset red swollen leg

A 
DVT
cellulitis
lymphoedema 
trauma 
ruptured bakers cyst
124
Q

what tests for a DVTT

A

doppler USS

D-dimer (can exclude if low, high can be caused by lots of things)

125
Q

is smoking a risk factor for arterial or venous clots

A

arterial (provokes atherosclerosis pathophysiology)

126
Q

what can decrease anticoagulant defences

A

hereditary deficiency in proteins C and S (factor 5 leiden or heretary deficiency), antithrombin

127
Q

why does the COCP increase clot risk

A

makes body think its pregnant by increasing oestrogen

this causes increased CFs and fibrinogen

128
Q

what type of vessel damage increases the risk of a VTE

A

valve damage- age (collagen loss), previous VTE (risk massive is previous VTE was spontaneous without provoking factor)

(NOT atherosclerosis= arterial)

129
Q

factor V leiden patient (X5 risk) goes on COCP (X6 risk)

what is there new risk of a VTE

A

x30 (risks times each other dont add up= synergistic)

130
Q

what are the non inherited risk factors for VTE

A

 Age: vessel damage, stasis
 Marked obesity: stasis, hypercoagulable (fat cells secrete cytokines e.g. IL 6 that increase coagulation)
 Pregnancy (hypercoagulability, stasis)
 Puerperium (hypercoagulability, stasis)
 Oestrogen therapy (hypercoagulability)
 Previous DVT/PE (vessel damage)
 Trauma/Surgery: (highest risk surgery lower limb orthopaedic surgery) stasis and hypercoagulability
 Malignancy: tissue damages releases TF increases coagulation, immobility
 Paralysis: Immobility - stasis
 Infection (hypercoagulability)
 Thrombophilia (hypercoagulablility)

131
Q

what measures can be taken to reduce risk of VTE after surgery

A 
early mobilisation 
compression stockings
flowtron boots 
LMWH
fonaparinux sodium (inhibits CF Xa)
132
Q

what must you ensure the patient doesnt have before firring compression stockings

A

arterial disease - ensure peripheral pulses good

133
Q

what does LMWH predonminantly target

A

activated factor 10

134
Q

why would you choose LMWH over warfarin in clot prevention after surgery

A

immediate action
warfarin antagonises vit K so takes a while for CFs to decrease, however in first few days it decreases proteins c and s making the patient hypercoagulable
warfarin needs to be monitored by APTT

135
Q

why would you choose LWMH over unfractionated heparin

A

unfractionated needs to be given IV and needs more monitoring (APTT)

136
Q

what does unfractionates heparin predominantly target

A

antithrombin (protentiates it action) and then CF Xa binds to this complex

137
Q

what are acanthocytes

A

spicules (spikes) on RBCs caused by unstable membrane due to splenctomy, alcoholic liver disease, spherocytosis

138
Q

what are blasts

A

nucleated precursor cells, appear in myelofibrosis or malignancy

139
Q

what are cabot rings

A

seen in pernicious anaemia, lead poisoning and bad infections

140
Q

what are howell jolly bodies

A

DNA nuclear remnants in RBCs, normally removed by spleen, seen post splenectomy, hyposplenism (e.g. sickle cell, coeliac, crohns/uc, myeloproliferative, amyloid)

141
Q

what is rouleaux

A

stacking of red cells (chronic inflammation, myeloma)

142
Q

what are spherocytes

A

spherical cells seen in HS and autoimmune haemolytic anaemia

143
Q

what are target cells

A

RBCs with central staining, a ring of pallor and outer ring of staining
seen in liver disease, hyposplenism, thalassaemia

144
Q

what are pappenheimer bodies

A

granules of siderocytes containing iron, seen post splenectomy

145
Q

when should you vaccinate beofre splenectomy

A

2 weeks before (can give all types)

may also need lifelone Abx prophylaxis

146
Q

what is the test for EBV

A

IgM response

if this negative test for HIV

147
Q

what are pencil cells a sign of

A

iron deficiency

148
Q

what should mature red cells be the same size as

A

lymphocyte nucleus

149
Q

what do you see macrovalocytes and hypersemented (more than 5 segments) neutrophils in

A

B12 and folate def

150
Q

where do you get haemolysis in macrosytosis

A

in bone marrow as cells too big to leave

151
Q

lacking central pallor + spherical = ?

A

spherocytes

152
Q

what is the test for autoimmune haemolytic anaemia

A

direct coombs test

153
Q

what are schistocytes

A

fragmented RBCs: look for microangiopathic anaemia (anything that fragments RBCs- mechanical damage, DIC, HUS, TTP, pre-eclampsia)

154
Q

what are the signs of hyposplenism on a blood film

A

howell jolly bodies

target cells

155
Q

should you normall ahve more neutrophils or lymphcytes

A

neutrophils

156
Q

what causes lympcytosis

A

acute viral infections, chronic infections, leukaemias and lymphomas (esp chronic lymphcytic anaemia)

157
Q

62 yr old woman visiting GP generally under the weather. Feels exhausted all the time, everything is an effort the last few months. Gets very short of breath even just walking up a flight of stairs and everyone says how pale and gaunt she is looking. Has lost a fair bit of weight over the last 3 months too

blood tests: hypochromic microcytic anaemia

what test would you do to confirm the cause of the anaemia

A

serum ferritin

158
Q

62 yr old woman visiting GP generally under the weather. Feels exhausted all the time, everything is an effort the last few months. Gets very short of breath even just walking up a flight of stairs and everyone says how pale and gaunt she is looking. Has lost a fair bit of weight over the last 3 months too

blood tests: hypochromic microcytic anaemia

she also has neutrophilia and thrombocytosis- why might this be

A

reactive changes to underlying inflammatory problem

159
Q

62 yr old woman visiting GP generally under the weather. Feels exhausted all the time, everything is an effort the last few months. Gets very short of breath even just walking up a flight of stairs and everyone says how pale and gaunt she is looking. Has lost a fair bit of weight over the last 3 months too

blood tests: hypochromic microcytic anaemia

what is the most likely cause

A

malignancy of the GI tract causing occult blood loss/ anaemia of chronic disease resulting in iron deficiency anaemia

160
Q

A 52 year old woman with a past history of graves disease presented with a six month history of increasing fatigue. Family members thought she was looking jaundiced and sent her to the GP. He checked her bloods and sent her into the medical admissions ward for an urgent transfusion.

FBC: pancytopenia, macrocytic anaemia, oval macrocytes, circulating megaloblasts, macrocytic normochromic anaemia

what test would you do to establish the diagnosis

A

serum B12 and folate

161
Q

what would bone marrow look like in megaloblastic anaemia

A

hypercellular

lots of output activity but ineffective erythropoesis so increases apoptosis - jaundice

162
Q

Patient is B12 deficient and has intrinsic factor auto antibodies confirming the diagnosis of pernicious anaemia (PA).
Why is she jaundiced?

A

B12 deficiency causes premature red cell destruction in the marrow resulting in excess bilirubin production

163
Q

A 23 year old male found wandering the streets confused and aggressive. Was thought to be smelling of drink. On admission febrile, tachycardic and hypotensive.

reactive features on FBC- neutrophilia and monocytosis

what might be the causes of this

A

sepsis

alcohol wouldnt increase white cells that much

164
Q

what does it mean if a neutrophil has vacuoles

A

is angry- immune response has been initiated

165
Q

This man was seen in the haematology clinic for annual review. He is of short stature and jaundiced. His gallbladder was removed when he was 12 years old. His father is similarly affected. he has splenomegaly

blood film: polychromasia, spherocytes

what blood test would confirm haemolysis

A

reticulocyte count

166
Q

what is the test for autoimmune haemolysis

A

coombs test (direct antiglobulin)

167
Q

This man was seen in the haematology clinic for annual review. He is of short stature and jaundiced. His gallbladder was removed when he was 12 years old. His father is similarly affected. he has splenomegaly

blood film: polychromasia, spherocytes

A

hereditary spherocytosis

168
Q

do you use genetic tests to diagnose spherocytosis

A

no as not caused by one single gene

169
Q

what treatment for hereditary spherocytosis

A

if have compensated haemolysis and are fully grown= folate supplements
if still growing/ decompensated haemolysis= splenectomy

170
Q

why might someone with HS be short

A

chronic marrow hyperplasia- when growing all energy was put into making red cells

171
Q

This 59 year old woman presented two weeks following a valve replacement for bacterial endocarditis with a history of increasing shortness of breath.

normocytoic normochromic anaemic (has some large and some small cells on blood film)

why is the MCV normal

A

there are both large and small cells and the mean is normal as a result

172
Q

This 59 year old woman presented two weeks following a valve replacement for bacterial endocarditis with a history of increasing shortness of breath.

normocytoic normochromic anaemic (has some large and some small cells on blood film)

what will the small and large cell be

A

small- spherocytes

large- reticulocytes

173
Q

This 59 year old woman presented two weeks following a valve replacement for bacterial endocarditis with a history of increasing shortness of breath.

normocytoic normochromic anaemic (has some large and some small cells on blood film)

what is the diagnosis

A

microangiopathic haemolytic anaemia

(conditions that cause red cell fragmentation resulting in haemolytic anaemia- in this case mechanical damage to cells form valves)

174
Q

what tests make up a coagulation screen

A 
PT 
APTT
INT 
FBC
depending on NHS region- fibrinogen assay and thrombin time
175
Q

what are the causes of a low platelet count

A

hereditary: inherited thrombocytopenia
acquired: increased destruction (heparin induced thrombocytopenia, ITP, SLE, TTP, DIC, HELLP, HUS), reduced production (diet (b12 and folate def), myelosuppression from chemo, myeloma/ leukemia/lymphoma, aplastic anaemia, viral infection, hep A/B/C, long term alcohol use)

176
Q

what are the common causes of shock

A 
o	Hypovolaemic
	Haemorrhage 
	Burns 
	Renal disease 
o	Cardiogenic 
	MI
	Arrhythmias 
o	Distributive 
	Anaphylactic
	Sepsis 
	Neurogenic 
o	Obstructive 
	Tension pneumothorax
	Cardiac tamponade
177
Q

how is shock treated

A 
o	Fluids
o	Oxygen 
o	Treat the cause of shock; antibiotics, blood, adrenaline, stabilisation (C-spine), ionotropes, pacing, steroids (addisonian crisis, myxoedema coma)
o	Sepsis 6 
o	Stop bleeding
178
Q

when does the bone marrow start blood production

A

16 weeks, before this liver and yolk sac

179
Q

how is venous thrombosis treated

A

DOAC/ low molecular weight heparin

180
Q

which works quicker heparin or warfarin

181
Q

what factor influence warfarin control

A

drinking, drugs, liver enzymes

182
Q

what is the screening test for primary haemostasis

A

platelet count

183
Q

what can cause thrombocytopenia

A

hereditary (rare)

acquired:
- reduced production (bone marrow failure: leukaemia, lymphoma, parovirus B19 (aplastic anaemia)
- increased destruction (DIC, ITP, hypersplenism)
- drugs (aspirin, NSAIDS)
- renal failure

184
Q

what can cause failure of fibrin clot formation

A

multiple factor deficiency: DIC, liver failure, vit K def, warfarin therapy
(will have prolonged PT and APTT)
single CF deficiency: haemophilua

185
Q

what is a ‘rub’ seen in

186
Q

why is an abdo/pelvic mass a risk factor for VTE

A

might compress IVC/ causes stasis

187
Q

can you do a V/Q scan in pregnancy

188
Q

are D dimer sensitive or specific

189
Q

who should you not request D dimers in

A

people with malignancy, pregnancy, sepsis, post op (will be raised in all of these)

190
Q

what can a D dimer definitively tell you

A

(want to reduce need for imaging)

patients that are low from from a clinical scoring system and have a negative d imers = no VTE

191
Q

what is the wells score

A

calculates risk factor for a VTE

192
Q

where are vit k dependent factors synthesised

A

(CF 2,7,9,10, proteins C and S)

liver

193
Q

which work quicker to reverse warfarin vit k or clotting factors

A

clotting factors

vit k takes 6 hours

194
Q

what inheritance is haemophilia

A

X linked (usually inherited, 1/3rd spontaneous mutation)

195
Q

when does haemophilia usually present

A

as toddlers start to mobilise

196
Q

what are the bleeds link in haemophilia

A

bleeding into joints (haemoarthrosis) and muscle

197
Q

what blood test for haemophilia

A

APTT

then CF 8 and 9 assays

198
Q

why would alcohol affect blood production

A

toxic to bone marrow
liver disease
spleno and hepatomegaly

199
Q

why does liver disease affect coagulation

A

liver produces all procoagulant proteins expect VWf
will have reduced levels or naturally occuring anticoagulants
impaired utilisation of vit K

200
Q

what cell type do monocytes share a precursor with

A

granulocytes

201
Q

what is infective mononucleosis

A

when T cells are activated (usually in response to EBV but can be HIV, CMV, viral hepatitis and toxoplasma) and gain blue cytoplasm that wraps around neighbouring cells

Haematology (27 decks)

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