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STUDY FOR BARRIERS > Haematology > Flashcards

Haematology Flashcards

1
Q

Hb levels which define anaemia

A

Less than 120g/L in females
And less than 140g/L in males

Or less than 12.5g/dL in adults

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2
Q

Potential causes of low Hb

A

Lack of production
Destruction of RBCs
Dilution
Loss of blood

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3
Q

Causes of iron deficiency anaemia

A 
Increased loss of iron 
Reduced iron absorption
Gynaecological disorders eg menorrhagia 
Hemoglobinuria
Multiple blood donations

Anything in the GIT causing inflammation

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4
Q

Causes of loss of iron

A 
Cancer/polyp - colon, stomach, oesophagus, small bowel 
Peptic ulcer, oesophagitis 
NSAID use 
IBD- ulcerative colitis, chrons 
Intestinal parasites 
Vascular lesions: angiodysplasia
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5
Q

Reduced iron absorption causes

A 
Deficient iron intake 
Coeliac disease 
Gastrectomy and gastric atrophy 
Gut resection or bypass 
Bacterial overgrowth
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6
Q

Weight loss surgery can cause

A

Anaemia

Affects stomach absorption

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7
Q

Anaemia production problems include

A

Iron deficiency
B12 deficiency
Folate deficiency

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8
Q

Causes of b12 deficiency

A 
Low intake (vegans) 
Impaired absorption (stomach - pernicious anaemia, gastrectomy) 
Small bowel (chrons, ileal disease or resection, bacterial overgrowth, tapeworm)

B12 needs the parietal cells of the stomach to be absorbed
Anything competing with it like tapeworms

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9
Q

Causes of folate deficiency

A 
Poor intake (eg alcoholics) 
GIT disease (gastrectomy, coeliac disease, chrons) 
Increased requirement (pregnancy, lactation, malignancy) 
Anti folate drugs (methotrexate, trimethoprim)
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10
Q

What deficiency causes macrocytic RBCs ?

A

Folate?
B12

Cells arrested in G2

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11
Q

Iron deficiency anaemia is

A

Microcytic hypochromic

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12
Q

Causes of anaemia of chronic disease

A

Infection
Malignancy
Autoimmune (RA, SLE, vasculitis, sarcoidosis, IBD)
Chronic kidney disease

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13
Q

Anaemia of chronic disease leads to what type of RBCs

A

Normocytic normochromic

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14
Q

How can renal disease lead to anaemia

A

Lack of EPO

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15
Q

What protein/hormone control iron release/absorption into circulation

A

Hepsidin

Inflammatory effect raises hepsidin ?

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16
Q

Reasons for the bone marrow not making sufficient RBCs

A

Fibrosis
Infiltration
Failure
(Most common cause of acquired bone marrow failure is aplastic anaemia characterised by peripheral pancytopenia and marrow hypoplasia)

Chemo agents can cause failure or fibrosis

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17
Q

Destruction problems leading to anaemia

A

Destruction of normal RBCs eg ABO and Rh incompatibilities (Ab mediated - haemolytic)

Shortened lifespan due to abnormal RBC eg sickle cell anaemia (HbS), thalassemia (alpha or beta protein abnormality in Hb)

High uptake in splenomegaly eg malaria, EBV

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18
Q

EPO is produced by

A

Kidneys 90%

Liver 10%

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19
Q

Shortened lifespan of RBC due to

A

HbS
G6PD deficiency
Thalassemia
Anything causing haemolysis

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20
Q

Haemolytic anaemia causes

A

Inherited - hemoglobinopathy, membranopathy, enzymopathy

Acquired - drugs, transfusion reaction, immune disorders, mechanical heart valve

Rh D haemolytic disease

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21
Q

Clinical signs of haemolytic anaemia

A

Jaundice
Dark urine
Splenomegaly!!

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22
Q

Signs in blood of haemolytic anaemia

A

Reticulocytosis
Unconjugated hyperbilirubinemia
Raised LDH

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23
Q

Tests for haemolytic anaemia

A

Direct antiglobulin test (Coombs)
Blood film
Hb screen

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24
Q

What helps in hereditary spherocytosis

A

Splenectomy

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25
Q

Causes of dilution of Hb

A

Pregnancy (also causes iron deficiency)

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26
Q

Causes of microcytic anaemia

A

Iron deficiency

Thalassemias

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27
Q

Causes of normocytic anaemia

A 
Chronic disease
Acute blood loss 
Haemolysis 
Aplastic anaemia 
Bone marrow infiltration

Combined deficiencies

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28
Q

Causes of macrocytic anaemia

A 
B12 
Folate 
Alcohol excess 
Liver diseases 
Marrow disorders, myelodysplasia
Drugs
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29
Q

MCV

A

Mean corpuscular volume

Red blood cell size

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30
Q

TIBC

A

Total iron binding capacity

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31
Q

High TIBC means

A

Iron deficiency
Pregnancy
OCP

Means lots of empty transferrin

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32
Q

Low TIBC

A

Anaemia of chronic disease
Malnutrition
Inflammation
Haemochromatosis

Can be due to not enough transferrin around or some sort of malnutrition

May not be anaemic depending on TIBC as it only shows transferrin saturation!!!!!

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33
Q

Ferritin levels reflect

A

Bone marrow iron stores

Decreased = iron deficiency
*low normal (up to 100 ug/l) possible if iron deficiency when this co exists with inflammation, liver disease or malignancy (acute phase response)

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34
Q

Low reticulocyte indicates

A

Bone marrow hypoproliferation

Production problems

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35
Q

High reticulocyte count indicates

A

Bone marrow hyperproliferation

Haemolytic anaemia, acute blood loss

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36
Q

How many Hb molecules in each RBC

A

250 million

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37
Q

Quantitative changes in globin chains

A

Thalassemias

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38
Q

Qualitative changes in globin changes

Are

A

Hemoglobinopathies

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39
Q

Iron switches to which state when oxygen binds

A

Fe2+ to fe3+

Ferrous to ferric state

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40
Q

Which two types of chains make up Hb

A

A2B2

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41
Q

What does 2,3-BPG do?

A

Stabilises the low affinity state of the Hb molecule

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42
Q

Where does heme synthesis take place?

A

Mostly in RBCs in bone marrow

About 15% daily in liver for formation of heme containing enzymes

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43
Q

Heme is made from

A

Glycine and succinyl coA(made from alphaketoglutamate via succinyl Coa dehydrogenase) –> succinate

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44
Q

The first main enzyme in heme production

A

Aminolevulinate synthase

ALA synthase

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45
Q

Things that inhibit heme production

A

Heme

Low iron

Vitamin b6 deficiency (rare, precursor for ALA synthase)

Erythrocyte formation - enhances
Liver - drug induced alterations in heme synthesis through p-450 dependent oxidises (p450s are major consumers of hepatic heme)

Inhibitory feedback loop affects delta-ALA synthase and first enzymes

46
Q

Heme feedback loop

A

Inhibits activity of pre existing d ala synthase
Diminishes transport of enzyme
Repressed production of enzyme

Stimulates globin synthesis

47
Q

Symptoms of porphyria

A

Photosensitive
Hypertrichosis
Lowered levels of heme
Severe blistering and scarring
Progressive deforming ears, nose and lips
Weakness in wrist and fingers
Reddish brown teeth that fluoresce in UV light due to deposition of some types of porphyria
Garlic stimulates haem and can exacerbate symptoms

48
Q

What is CEP

A

Congenital erythropoietic porphyria
Deficiency of enzyme uroporphyrinogen III synthase

Extreme photosensitive skin blistering scarring and increased skin bacterial infections

Lower RBCs feed back to increase production and exacerbate symptoms

49
Q

Epidemic porphyria cutanea tarda

A

Porphyrinuria appeared early
Began with bullous lesions which progress to ulceration and generally healed leaving pigmented scars characterised by presence of microcysts

50
Q

Primary haemostasis in bleeding

A

Vasoconstriction and platelet activation

51
Q

Secondary haemostasis

A

Coagulation cascade

Fibrinolysis

52
Q

MCV

A

Mean corpuscular volume
Red cell size

Hematocrit/ red cell concentration

53
Q

MCH

A

Mean corpuscular hemoglobin

Hb concentration / red cell conc

54
Q

MCHC

A

Mean corpuscular hb conc

Hb conc / hematocrit

55
Q

Failure to produce reticulocyte response indicates

A

Bone marrow failure or haematinic deficiency

56
Q

Haematocrit is reduced in

A

Anaemia

57
Q

Anisocytosis

Poikilocytosis

A

Frequently associated with disease of blood

Increased variation in cell size - anisocytosis
Presence of abnormal shape - poikolocytosis

58
Q

Aniso-poikolocytosis occurs in

A

Absences of functioning spleen

59
Q

Leukoerythroblastic blood results from

A

Gross marrow disturbance such as infiltration by malignancy, or fibrous tissue (myelofibrosis) or in severe anaemia due to deficiency of vitamin b12 or folate (megaloblastic anaemia)

60
Q

Heinz bodies seen in

A

Certain haemolytic anaemia Such as g6pd deficiency (denatured Hb)

61
Q

Basophils are closely related to

A

Mast cells

Contain heparin or histamine

62
Q

Causes of reative neutrophil leukocytosis include

A 
Sepsis 
Trauma 
Infarction 
Chronic inflammatory disease 
Malignant neoplasms 
Steroid therapy 
Acute haemorrhage or haemolysis
63
Q

Monocytosis may be reactive to

A

Sepsis
Chronic infections eg tb
Malignant neoplasms

64
Q

Eosinophili leukocytosis may be reactive to

A

Allergy eg asthma
Parasites
Malignant neoplasms
Miscellaneous eg polyarteritis nodosa

65
Q

Causes of pancytopenia

A

Bone marrow failure
Megaloblastic anaemia
Hypersplenism

66
Q

Causes of selective neutropenia include

A 
Overwhelming sepsis 
Racial 
Autoimmune such as RA 
Drug induced 
Cyclical - uncommon condition
67
Q

Platelets are

A

Contractile and adhesive

68
Q

Reactive thrombocytosis may be seen in

A 
Acute or chronic blood loss
Iron deficiency 
Chronic inflammatory disease eg RA 
Neo plastic disease 
Tissue trauma 
Primary disorders of bone marrow - the myeloproliferative diseases and chronic myeloid leukaemia
69
Q

Coagulation pathway?

A

[image]

70
Q

Where are almost all of the coagulation factors (and inhibitory factors) made?

A

In the liver

71
Q

Which clotting factors require vitamin k?

A

2,7,9,10

72
Q

Which clotting factors are serine proteases?

A

2,7,9,10,11,12

Presence of serine necessary for action in hydrolysing peptide bonds

73
Q

What are the principal clotting inhibitors and what do they require for synthesis?

A

Protein C and S
require vitamin K

Tissue factor pathway inhibitor
Antithrombin III - serine protease inhibitor (and requires glycosaminoglycan ‘heparans’ present on vascular endothelial surface)
Antiplasmin

74
Q

What clotting factors does protein C inhibit

A

requires co-factor protein S for full acivity

V, VIII

75
Q

What does thrombin do?

A

Promotes fibrin formation and also has crucial role in negative feedback to inhibit clot formation

76
Q

What does protein C require for activation?

A

Thrombin bound to endothelial protein, thrombomodulin

77
Q

Plasminogen activators are released from…

A

endothelial cells

Cleave plasminogen –> plasmin which rapidly digests fibrin clot
this partially balanced by TAFI (thrombin activated firbinolytic inhibitor)

78
Q

What is the main pathway for coagulation?

A

Tissue factor pathway (extrinsic pathway)

79
Q

APTT

A

acitvated partial thromboplastin time
invovles all clotting factors other than VII and XIII
intrinsic pathway activated

80
Q

PT

A

prothrombin time
assess factors VII, V, X, II and fibrinogen only
tissue factor and phospholipid added (extrinsic pathway)

81
Q

INR

A

International normalised ratio

Pateint’s PT/normal mean PT

82
Q

ESR

A

erythrocyte sedimentation rate
increased aggregation and sedimentation occurs in the presence of high concentrations of immunoglobulin and fibrinogen

acute phase reactant

83
Q

Where are blood cells produced

A

Adult - all blood cells produced in red marrow which is restricted to bones of axial skeleton (50% adipocytes and 50% blood cells and precursors)
Fatty marrow of other bones capable of hemopoiesis when demand required

infant/young child - practically all bones

fetal life - liver and spleen (yolk sac before 6 weeks)
*extramedullary haemopoiesis typically assoc with progressive fibrosis of BM seen in myelopriliferative disorders

84
Q

growth factors that govern production of leukocytes

A

eg IL-1, 3, 6
GM-CSF - increases stem cell committment to granulocyte and monocyte production
G-CSF - granulocytes
M-CSF - monocytes

85
Q

Thrombopoietin

A

capable of stimulation of platelet production and produced mainly in liver

86
Q

Acute leukemia which cells accumulate?

A

Blast cells
mutations in haemopoietic stem cells - the luekemic clone proliferates but loses ability to mature
accumulation of blast cells in bone marrow

87
Q

ALL is common in

A

children

88
Q

AML is common in

A

adults

89
Q

hepcidin action

A

downregulates the plasma membrane transfer protein ferroportin

90
Q

when erythropoiesis is more active –>

A

increased iron uptake even if stores are high ( can lead to iron overload as seen in thalassemias)

91
Q

deficiency of iron , b12 and folate may have a misleading

A

normal MCV and MCH

92
Q

increase in TIBC means

A

iron deficiency with compensatory increase in transferrin concentration

93
Q

in chronic disorders, TIBC is usually

A

reduced

and serum ferritin is usually raised due to inflamamtion or malignancy

94
Q

chronic anaemia can lead to

A 
acute chelitis
atrophic glossitis
brittle nails 
koilonychia 
oesophageal web
95
Q

vitamin b12 metabolism

A

present in foods of animal origin –> becomes bound to intrinsic factor in parietal cells of stomach –> this complex binds to receptors in terminal ileum where only b12 is absorbed –> transported to tissues attached to transcobalamin II

deficiency takes a long time to develop

96
Q

neutrophil large and hypersegmented/exaggerated segments in b12 deficiency?

A

?

97
Q

vitamin b12 deficiency leads to

A

unconjugates hyperbili and increased LDH due to increased cell breakdown/ineffective erythropoiesis/premature removal

lesions of the nervous system:
myelin degeneration of posterior and lateral columns often assoc with peripheral neuropathy affecting sensory neurons (subactue combined degeneration of the cord)
*demyelination and axonal degeneration

optic atrophy and cerebral changes resulting in psychiatric disease less common

musosal abnormalities may be present - atrophic glossitis, weight loss due to malabsorption because of mucosal changes, sore mouth

chronic hypoxia –> cardiomyopathy (transfusion poorly tolerated due to volume overload)

thrombocytopenia (bruising and mucosal haemorrhage)

98
Q

folate is absorbed in

A

proximal jejunum

99
Q

anticonvulsants that impair folate absorption

A

phenytoin and phenobarbitone

100
Q

in myelofibrosis the marrow is replaced by

A

reticulin and collagen

101
Q

what happens to haptoglobin in haemolytic anaemia

A

absent serum haptoglobin

102
Q

Malaria and pregnancy

A

First two trimesters
Trans placental spread
Low birth weight/ premature birth

103
Q

Which genetic blood factors protect against p.falciparum

A

HbS
Thalassemia
G-6PD deficiency
HbC

104
Q

Which genetic blood factor protects against p. Ovale and vivax?

A

Duffy blood group negative

105
Q

P.falciparum

A 
Tertian (2day) cycle
Cyclical fever 
No relapse 
Cerebral malaria - fatal 
Malignant malaria 
In PNG

Multiple thing rings
Small RBC
Affects all age RBCs

106
Q

P.Vivax

A

tertian cycle
Relapse - hypnozoite liver stage

Thick rings
Enlarged RBCs
Young RBCs

107
Q

P.Ovale

A

Tertian cycle
Relapse

Comet trophozoite
Oval and large RBCs
Smiley face :)

108
Q

P.malariae

A

In west pacific
Nephrotic syndrome

Quartan cycle (3day) 
Chronic malaria

Band trophozoites
Daisy schizonts
Mature RBCs

109
Q

P.knowlesi

A

Zoonotic
Macaques- long pig tailed

Low platelets !

1d cycle

Ring and schizont

110
Q

Malaria life cycle

A

Image

111
Q

Antithrombotic effects of endothelial cells to modulate hemostasis

A

Inhibit platelet aggregation - NO and prostacyclin (PGI2)

Anticoagulant effect - thrombomodulin (activation of protein c and s) and heparin like molecules (–> antithrombin)

Fibrinolysis - t-PA

112
Q

Prothrombotic effects of endothelial cells to modulate hemostasis

A

Platelet adhesion and aggregation - vWF

Procoagulant effect - tissue factor

Anti-fibrinolytic - PA inhibitor (PAI)

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