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2A content- Sameera > 7. HAEMOTOLOGY > Flashcards

7. HAEMOTOLOGY Flashcards

1
Q

what is anaemia and what is its value in men and women

A

low concentration of haemoglobin
Hb <130 in men, <120 in women

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2
Q

what is the most common cause of anaemia

A

iron deficiency

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3
Q

what r the 5 types of anaemia

A

haemolytic, aplastic, microcytic, macrocytic, normocytic

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4
Q

what is haemolytic anaemia

A

anaemia caused by RBC destruction rate being faster than RBC production

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5
Q

what type of jaundice does haemolytic anaemia always cause

A

pre hepatic jaundice

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6
Q

what is aplastic anaemia

A

anaemia caused by decreased RBC production

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7
Q

what is microcytic anaemia 2

A

MCV of less than 80
small hypochromic (lighter coloured due to reduced haemoglobin) RBCs

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8
Q

what is normocytic anaemia 2

A

MCV of 80-100
normal sized RBC but fewer RBC than normal

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9
Q

what is macrocytic anaemia 2

A

MCV of more than 100
bone marrow produces abnormally large RBCs

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10
Q

compare symptoms and signs

A

symptoms= what patient tells u
signs= medical observations u make as a doctor

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11
Q

general symptoms of anaemia (4)

A

fatigue
headache
dizziness
dyspnoea on exertion

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12
Q

give signs specific to deficiency anaemia and mention which type of anaemia this is (4)

A

Koillonychia (iron)
angular stomatitis (iron/b12)
lemon-yellow skin (b12)
leukonychia (iron)

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13
Q

what r GENERAL (NON SPECIFIC) SIGNS NOT SYMPTOMS of anaemia (5)

A

TACHYCARDIA
skin pallor
conjunctiva pallor
intermittent claudication
brittle hair

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14
Q

what is conjunctiva pallor

A

pale appearance of conjunctiva in eye that indicates anaemia

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15
Q

what is intermittent claudication and why does this happen

A

muscle pain during exercise due to ischaemia occurring

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16
Q

what is Koillonychia

A

spoon shaped nails

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17
Q

what is leukonychia

A

white marks of nails

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18
Q

what is angular stomatitis

A

inflammation of corners of mouth

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19
Q

what is a sign of haemolytic anaemia (3)

A

jaundice/ dark urine/ pale stools

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20
Q

what is ferratin

A

main protein that stores iron intracellularly

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21
Q

where is majority of iron storage

A

liver

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22
Q

what happens to ferritin levels during acute inflammation and why (1,1)

A

increases as ferritin is a acute phase reactant

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23
Q

what is transferrin

A

protein mediating iron transport in the blood

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24
Q

when r transferrin saturation levels low

A

iron deficiency: as not much iron bound to i

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25
Q

when r there raised transferrin levels

A

iron deficiency
due to body trying to compensate for reduced iron levels by producing more transferrin

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26
Q

what r the causes of microcytic anaemia (4) and what is the acronym to remember this

A

iron deficiency, anaemia of chronic disease, thalassemia, sideroblastic anaemia
(TAIS: thalassaemia, anaemia of chronic disease, iron deficiency, sideroblastic anaemia)

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27
Q

what r the three causes of iron deficiency anaemia and give two examples of each

A
  1. reduced absorption of iron (low in diet, malabsorption at SI)
  2. increased iron utilisation (pregnancy, children)
  3. blood loss (menstruation and trauma)
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28
Q

can iron deficiency be inherited and what gender is it more prevalent in

A

no
females

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29
Q

how does iron deficiency cause microcytic anaemia

A

reduces haemoglobin synthesis which causes microcytic anaemia

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30
Q

what r the 2 signs of iron deficiency anaemia

A
  1. plummer vinson syndrome
  2. atrophic glossitis (enlarged tongue)
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31
Q

what is plummer vinson syndrome and when does it present

A

typical triad presentation: dysphagia, iron deficiency, oesophageal webs
iron deficiency anaemia

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32
Q

what r the two things seen on a blood film test of iron deficiency anaemia and what is the general appearance of the cells 2

A
  1. target cells (non specific bullseye pattern)
  2. howell jolly bodies (non specific nucleated RBCs)
    small, hypochromic cells
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33
Q

what r the FBC results for iron deficiency anaemia (2)

A

low haemoglobin levels
low iron

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34
Q

what are the iron studies results for iron deficiency anaemia (5)

A

low ferritin (unless active inflammation)
low serum iron
low transferrin saturation
high transferrin
high TIBC

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35
Q

what is TIBC and what does it stand for

A

(total iron binding capacity test)- affinity for iron to bind to a protein

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36
Q

treatment for iron deficiency anaemia (1)

A

ferrous sulphate

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37
Q

what r the causes of anaemia of chronic disease (3)

A

chronic infection
chronic inflammation (in connective tissue diseases)
neoplasia

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38
Q

FBC results for anaemia of chronic disease (3)

A

low haemoglobin
low/ normal MCV

high ESR

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39
Q

iron studies results for anaemia of chronic disease (5)

explain the odd one out 1
explain why iron is low 1

A

normal or raised ferritin
low serum iron
low transferrin
low transferrin saturation
low TIBC

(everything is low except ferratin- which is an acute phase reactant)
(iron is low because macrophages trap iron within it so it can’t be reused in the iron cycle)

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40
Q

what is thalassaemia 1, its inheritence 1 and what does this cause 1

A

inherited autosomal recessive alpha or beta globin mutations
which causes haemoglobin chain abnormalities

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41
Q

where is thalassaemia prevalent and why

A

areas where malaria is because it is protective

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42
Q

presentation for thalassemia (1)

A

microcytosis disproportionate to haemoglobin levels

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43
Q

iron studies results for thalassemia (anaemia) (5)

A

normal/ raised ferritin
normal/ raised serum iron
normal/ low transferrin
normal/ raised transferring saturation
normal/ low TIBC

transferrin and TIBC is normal/ low
everything else is normal/ raised

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44
Q

blood film results for thalassemia (anaemia) (1)

A

generally microcytic, hypochromic cells

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45
Q

investigations for thalassaemia 4

A

blood film
iron studies
Hb electrophoresis
X ray- increase bone marrow activity looks like a hair on end appearance (increase in activity due to poor erythropoiesis)

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46
Q

specific test for thalassemia 1 (anaemia) and expected results 3

A

Haemoglobin electrophoresis
high HbA2 and HbF
low HbA

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47
Q

treatment for thalassemia causing anaemia (3)

A

blood transfusions
venesection
splenectomy

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48
Q

what is the definitive treatment for thalassaemia and why is this not used more often

A

bone marrow stem cell transplant
risky

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49
Q

compare blood transfusion and splenectomy for treating thalassemia (1, 2)

A

blood transfusions (can have complications- risk of side effects from too much iron)
splenectomy (reduces mass RBCs destruction and reduces transfusion complications)

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50
Q

how is the excess iron counteracted during blood transfusion, give an example and 2 side effects

A

iron chelation eg desfemoxamine (des fem ox amine)
deafness, cataracts

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51
Q

complication of thalassemia (1) and why 1

A

organ failure (heart and liver)

not enough oxygen carried to these organs

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52
Q

compare how common alpha and beta thalassaemia r compared to each other

A

beta is more common than alpha

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53
Q

what is alpha and what is beta thalassaemia

A

alpha= genetic disorder with a deficiency in alpha globin chains of Hb
beta= genetic disorder with a partial/ complete deficiency in beta globin chains of Hb

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54
Q

what r the types of alpha thalassaemia based on and what chromosome

A

based on deletions of the 4 alleles on chromosome 16 responsible for alpha globin

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55
Q

symptoms for alpha thalassaemia 3

A

usually asymptomatic
jaundice
fatigue

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56
Q

what r the 4 types of alpha thalassaemia

A
  1. silent carrier
  2. mild anaemia
  3. marked anaemia
  4. HbH Barts
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57
Q

what is the silent carrier type 1 alpha thalassaemia’s gene mutation and what symptoms r there

A

one gene deletion
asymptomatic

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58
Q

what is the mild anaemia type 2 alpha thalassaemia’s gene mutation

A

2 gene deletions

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59
Q

what is the marked anaemia type 3 alpha thalassaemia’s gene mutation and how is damage caused in this type (1)

A

3 gene deletions
beta chains form tetramers known as HbH which cause damage due to their high affinity to oxygen and by causing haemolysis

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60
Q

what is the HbH Barts type 4 alpha thalassaemia’s gene mutation and what damage caused in this type (3)

A

4 gene deletions (gamma chains form tetramers called Hb Barts which causes sever hypoxia and high carbon monoxide levels, leading to heart failure and hepatosplenomegaly and oedema)

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61
Q

what is hydrops fetalis and what causes this

A

heart failure in utero due to HbH Barts alpha thalassaemia mutation

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62
Q

what mutation determine the types of beta thalassaemia 3

A

based on point mutations at 2 gene points on chromosome 11

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63
Q

what r the types of beta thalassaemia 3 and explain their gene mutations (reduced/ absent… what?)

A

thalassaemia minor= 1 normal alleles and reduces/ absent beta chain allele
thalassaemia intermedia= 2 reduces beta chain alleles
thalassaemia major= 2 absent beta chain alleles

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64
Q

what is the pathophysiology of beta thalassaemia 3
what can it potentially lead to 1

A

beta deficiency causes alpha chain accumulation in RBCs which forms inclusions which damages RBCs, leading to haemolysis and potentially hypoxia

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65
Q

when do symptoms develop in beta thalassaemia

A

develop within 5 months of life

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66
Q

signs of beta thalassaemia 4

A
  1. chipmunk facies (enlarged forehead and cheekbones due to ineffective erythropoiesis causing bone changes )
  2. failure to thrive
  3. hepatospenomegaly
  4. gall stones (presenting feature may have right upper quadrant pain)
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67
Q

what is sideroblastic anaemia 1 and what happens to this iron 1

A

body unable to insert iron into haemoglobin
iron accumulates in mitochondria

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68
Q

causes of sideroblastic anaemia (3)

A

excess alcohol
metal poisoning
vitamin B deficiency

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69
Q

what three things r seen on a blood film for sideroblastic anaemia

A

microcytic CMV
ringed sideroblasts on blood film
basophillic stippling

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70
Q

iron studies results for sideroblastic anaemia (5)

A

increased ferritin
high serum iron levels
low transferrin
high transferrin sat
low TIBC

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71
Q

what r the two categories of normocytic anaemia and what value defines each

A

NON HAEMOLYTIC:
-reduced reticulocyte count due to failing BM-
HAEMOLYTIC:
-high reticulocyte to make up for RBC death which shows the BM has a good response-

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72
Q

name 3 non haemolytic causes and 4 haemolytic causes of normocytic anaemia

A

NON HAEMOLYTIC:
chronic kidney disease
Aplastic anaemia
pregnancy
CAP (BM is capping)

HAEMOLYTIC:
sickle cell
G6PDH deficiency
autoimmune haemolytic anaemia
hereditary spherocytosis
SAGH (sagging BM- struggling but still functional)

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73
Q

3 markers and values of normocytic anaemia

A

high LDH
high unconjugated bilirubin
low haptoglobin in haemolytic anaemia

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74
Q

what is LDH marker

A

marker of cell damage in body
indicates haemolysis

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75
Q

what is haptoglobin a marker of

A

acute phase marker of RBC destruction

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76
Q

3 investigations for haemolytic anaemia and results (3)

A

FBC: high reticulocytes (chronic)
urine: high urobilinogen and high bilirubin
blood film: schistocytes on blood film

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77
Q

what r schistocytes

A

fragments of RBCs which r jagged and can cause endothelial damage

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78
Q

what r the 5 causes of macrocytic anaemia, split into two subcategories

A

megoblastic
B12 deficiency
folate deficiency
nonmegablastic
liver disease (non alcoholic)
hypothyroidism
alcohol excess

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79
Q

what r codocytes 1 and what type of anaemia r they formed in 3

A

codocytes= ‘target cells’ on blood film
sickle cell, thalassaemia, iron deficiency
STI

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80
Q

causes of B12 deficiency macrocytic anaemia (4)

A
  1. Pernicious anaemia
  2. malabsorption (coeliac, IBD, ileostomy, bowel resection)
  3. decreased dietary intake (found in meat, fish, eggs and milk)
  4. chronic nitrous oxide use (laughing gas)
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81
Q

FBC results for B12 deficiency macrocytic anaemia (2)

A

low Hb
low B12

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82
Q

blood film results for B12 deficiency macrocytic anaemia (3)

A

megaloblasts
oval RBCs
hypersegmented neutrophils

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83
Q

symptoms of B12 deficiency macrocytic anaemia (1, 3)

A

general anaemia presentation
neurological signs: paraesthesia in extremities, muscle weakness, reduces sense of taste

PMS

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84
Q

treatment for B12 deficiency 2

A

dietary advice (increase eggs and salmon)
take B12 supplements (eg oral hydroxycolbamin)

hydroxy col ba min

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85
Q

why is there increased bone marrow activity in certain types of anaemias

A

due to poor erythropoeisis

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86
Q

6 abnormal cell counts

A

neutrophilia
neutropenia
thrombocytopenia
thrombocytosis
lymphocytosis
lymphocytopenia

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87
Q

what is neutrophillia and causes of neutrophillia (3)

A

high neutrophil count
infection, inflammation, chronic myeloid leukaemia

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88
Q

what is neutropenia and causes of neutropenia (4)

A

low neutrophil count
antibiotics, marrow failure, chemo, LIVER DISEASE

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89
Q

what is pernicious anaemia

A

autoimmune condition where autoantibodies produced against parietal cells and intrinsic factor= where body cannot absorb B12

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90
Q

what is thrombocytosis and causes 5

A

high platelet count (secondary to a condition)
infection, inflammation, tissue injury, splenectomy, essential thrombocythemia (BM makes too many platelets)

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91
Q

what is thrombocytopenia and causes (2 and 2 eg for each)

A

low platelet count
causes= low production (bone marrow failure or congenital) or increased removal (SLE, DIC)

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92
Q

what is lymphocytosis and causes (7)

A

high lymphocytes
EBV, HEPATITIS, CLL, ALL, lymphoma, ITP, TTP

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93
Q

what is lymphocytopenia and causes (4)

A

low lymphocytes
steroids, HIV, marrow failure, chemo

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94
Q

what is primary and secondary haemostasis

A

1: initiation and formation of platelet plug
2: formation of fibrin clot

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95
Q

what does primary haemostasis involve (1)

A

involves platelet activation

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96
Q

what does secondary haemostasis involve (1)

A

involves intrinsic and extrinsic coagulation cascade

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97
Q

what r the 2 main things that occur in platelet activation

A
  1. initial activation
  2. amplification
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98
Q

explain initial activation in platelet activation

A

collagen binds to GP2b and 3a via VWF

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99
Q

explain amplification in platelet activation (4)

A

thromboxane binds to TPa receptors
ADP binds to P2Y12 receptors
other platelets form GP2a/b crossbridges
thrombin binds to PAR1/4 receptors

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100
Q

how do NSAIDs, clopidogrel and dabigatran inhibit platelet plug formation

A

NSAIDs inhibit thromboxane formation
clopidogrel inhibits P2Y12 binding
dabigatran inhibits thrombin binding

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101
Q

3 changes to platelets during activation

A
  1. platelets change shape (to pseudopodia)
  2. dense granule release (contains more ADP for further P2Y12 activation)
  3. alpha granule release (inflammatory mediators and clotting factors)
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102
Q

what initiates the intrinsic pathways and what is the factor number pathway

A

initiated by endothelial collagen
12-> 11-> 9-> 8-> 10-> 10a

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103
Q

what initiates and expresses the extrinsic pathways and what is the factor number pathway

A

initiated by tissue factor
expressed by immune cells and endothelium
3->7-> 10-> 10a

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104
Q

state the common pathway (5)

A

10a-> prothrombin (II)-> thrombin (IIa)-> fibrinogen-> fibrin (factor 13 reinforces fibrin)

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105
Q

how does warfarin block the clotting cascade

A

warfarin blockers vitamin K so it prevent factors 10, 9, 7 and 2 being formed

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106
Q

how does heparin block the clotting cascade

A

heparin is an unselective antithrombin III inhibitor which blocks factor 10 and 2 in the common pathway

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107
Q

how does rivaroxiban block the clotting cascade

A

rivaroxiban directly inhibits factor 10a

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108
Q

what is APTT stand for and what does it measure (1,1(

A

activated partial thromboplastin time (measure of intrinsic and common pathway)

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109
Q

what is PT stand for and what does it measure

A

prothrombin time (measure of extrinsic pathway)

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110
Q

what is the inheritance type of sickle cell disease and what is the expression in hetero/homozygotes and what is the genotype for homozygous

A

autosomal recessive (heterozytes get the traits, homocytes get the disease)
genotype for homozygous= HbS HbS

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111
Q

what is the gene mutation for sickle cell disease, what chromosome and what is the effect of this mutation (3)

A

gene on Cr11: glutamic acid substitution with valine which causes B-globin polymerisation

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112
Q

what r the 4 consequences of sickle shaped cells

A

reduced oxygen carrying capacity
cause endothelial damage
RBC sequestration (build up of RBC in spleen)
reduced lifespan

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113
Q

exacerbators of sickle cell (4)

A

hypoxia
cold weather
parvovirus B19
physical exertion

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114
Q

acute presentation of sickle cell (6- broken up into 3 organ systems)

A

GI: sequestration crisis
RESP: dyspnoea, cough, hypoxia
MSK: bone pain, joint pain

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115
Q

what is sequestration crisis

A

blood outflow from the spleen is blocked which causes accumulation of blood in the spleen= splenomegaly

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116
Q

complications of chronic sickle cell disease (5)

A

avascular necrosis of joints
silent CNS infarcts
retinopathy
nephropathy
osteomyelitis
CROANS (c= chronic complications)

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117
Q

4 investigations for sickle cell disease

A

FBC
blood film
sickle solubility test
haemoglobin electrophoresis

118
Q

results for FBC in sickle cell disease (2)

A

low MCV, low haemoglobin levels

119
Q

results for blood film in sickle cell disease (2)

A

shows sickled erythrocytes and howell jolly bodies

120
Q

results for sickle solubility test in sickle cell disease (1) and what is a limitation of this test (1)

A

HbS presences
only detects HbS presence- doesn’t differentiate between heterozygous and homozygous

121
Q

results for Hb electrophoresis in sickle cell disease (1)

A

band of HbS

122
Q

acute management for sickle cell (4)

A

morphine, oxygen, IV fluids, transfusion exchange
MOIT

123
Q

chronic management for sickle cell (2)

A

hydroxycarbamide and folic acid supplements in combination with each other

hydroxy- car - baa mide
hydroxy in a car with a sheep that goes baa whos name is mide

124
Q

what does hydroxycarbamide do (3)

A

inhibits ribonucleotide reductase, decreases DNA synthesis and raised HbF (foetal) levels in the sickle cell

125
Q

what is the last resort treatment for sickle cell disease 1

A

bone marrow stem cell transplant

126
Q

what is G6PDH deficiency (inheritence) and what 1 thing does this cause
what is the normal function of G6PDH

A

x linked recessive enzymopathy causing shortened RBC lifespan (G6DPH is usually protective against oxidative damage)

127
Q

what is the presentation of G6PH deficiency 2

A

mostly asymptomatic
unless precipitated= presents in a form of a attack

128
Q

what r the triggers for a G6PDH deficiency attack 4

A

Fava beans, antimalarials, nitrofurantoin, naphthalene (in presticide)

129
Q

what are the symptoms of a G6PDH attack 2 and what occurs in an attack

A

rapid anaemia and jaundice
intravascular haemolysis occurs

130
Q

what r the investigations 1 for a G6PDH deficiency and what are the results 6

A

FBC and blood film:
-normal in between attacks
-during attack: normocytic with increased reticulocytes and Heinze bodies and bite cells
-low G6DPH levels

131
Q

what is the treatment for G6PDH deficiency 2

A

avoid precipitants
blood transfusions when there is an attack

132
Q

what is hereditary spherocytosis and its inheritence, 1, 1

A

autosomal dominant
sphere shaped RBC

133
Q

what is the pathophysiology of hereditory spherocytosis 5

A
  1. loss of proteins of RBC cell membrane
  2. causes SA to be disproportionate to volume of RBC
    3.= spherical shaped RBCs
  3. this increases splenic recycling
  4. RBCs get stuck in spleen= splenomegaly
134
Q

symptoms of Hereditary Spherocytosis 4

A

general anaemia
neonatal jaundice
splenomegaly
gall stones (in 50%)

135
Q

investigations and results for hereditary spherocytosis (2-> 3, 1-> 1)

A

FBC and blood film:
normocytic with increased reticulocytes, sphreocytes (also seen in acquired haemophilia A)

direct coombs test: negative, if + then autoimmune haemolytic anaemia (spherocytes commonly seen in AHA)

136
Q

treatment of Hereditary Spherocytosis 4

A

folate supplements
splenectomy (to decrease extravascular haemolysis)
for neonatal jaundice give phototherapy
transfusions in an acute crisis

137
Q

what r the types of autoimmune haemolytic anaemia, which is more common and what precipitates this (pathophys) 2

A

-warm and cold subtypes (warm is most common)
1. precipitated by autoantibodies
2. these bind to RBCs, causing intra and extravascular haemolysis

138
Q

investigation 1 for autoimmune haemolytic anaemia and result

A

direct coombs positive (agglutination) of RBCs with coombs agent

139
Q

what is aplastic anaemia pathophysiology 2

A
  1. bone marrow failure means it stops making haematopoeitic stem cells
  2. this leads to deficiency of all red, white cells and platelets= pancytopenia)
140
Q

2 causes for aplastic anaemia

A

idiopathic acquired
infectious (EBV/ parvovirus B19)

141
Q

investigations 2 and results for aplastic anaemia (1->2, 1->1)

A

RBC= normocytic anaemia with low reticulocytes
BM biopsy exam= hypocellularity

142
Q

how long does pernicious anaemia take to present

A

presentation at a later point in life

143
Q

what is the presentation characteristic of folate deficiency and how can it be linked to B12 deficiency 1,1

A

takes months to develop (unlike years for B12)
can be concomitant with B12 deficiency

144
Q

causes of folate deficiency 5

A

malnutrition
malabsorption
pregnancy
trimethoprim and methotrexate
alcohol

145
Q

symptoms of folate deficiency 3

A

general anaemia symptoms
angular stomatitis
glossitis

146
Q

investigations for folate deficiency 2->2

A

FBC and blood film:
megaloblasts
low serum folate

147
Q

treatment for folate deficiency 2, what about if concomitant with B12 def 1 and what about in cases of pregnancy 1

A

dietary advice (have leafy greens, brown rice etc)
folate supplements
if concomitant with B12 deficiency, replace B12 first
pregnant: prophylactic folate 100mg for first 12 weeks for healthy development

148
Q

how does alcohol cause non megaloblastic anaemia 2 pathophys

A
  1. toxic to RBCs
  2. also depletes folate
149
Q

how does hypothyroidism cause non megaloblastic anaemia 1

A

interferes with erythropoeisis

150
Q

how does liver disease cause non megaloblastic anaemia 1

A

increases cholesterol deposition on the RBCs which means it cant carry as much Hb

151
Q

what r the bleeding dysfunctions 4

A
  1. over anticoagulation eg overdose heparin
  2. DIC
  3. haemophillia A and B
  4. von willebrands disease
152
Q

what does TTP stand for and what is this an issue with (in terms of thrombosis formation)

A

Thrombotic thrombocytopenia purpura
primary haemostasis

153
Q

what is TTP 3

A
  1. ADAM TS13 protein deficiency which normally cleaves VWF
  2. so body is unable to break clumps of VWF
  3. these accumulate as microvascular clots in small blood vessels
154
Q

risk factors for TTP 3

A

adults
female
familial inheritence

155
Q

symptoms for TTP 5

A

fatigue
fever
jaundice
petechiae
purpuric rash

156
Q

what is purpuric rash

A

rash of purple spots on skin due to small bleeding from small BVs under the skin

157
Q

what is petechiae

A

red spots on skin due to small bleeding from small BVs under the skin

158
Q

what investigations r done for TTP (4)

A

blood smear, genetic test, FBC, bloods

159
Q

FBC results for TTP(3)

A

high WCC
low Hb
low platelets

160
Q

bloods results for TTP (4)

A

normal PT
normal APTT
raised bilirubin
raised creatinine

161
Q

blood smear results for TTP (1) and ADAM t513 test result

A

schistocytes present
low ADAM t513 result

162
Q

why r PT and APTT test results normal in TTP (1)

A

because there is an issue with primary haemostasis not with secondary haemostasis

163
Q

what is the treatment for TTP (2)

A
  1. plasmapheresis
  2. prednisolone and rituximab
164
Q

what does ITP stand for

A

Immune thrombocytopenia purpura

165
Q

what is more common ITP or TTP

A

ITP

166
Q

what is ITP 1 and why is this an issue with primary haemostasis 1

A
  1. autoimmune IgG destruction of GP2b/3a platelets
  2. platelets cant be activated= issue with primary haemostasis
167
Q

2 types of people/ presentations that can have ITP

A
  1. children post viral infection
  2. adult females with autoimmune condition eg HIV
168
Q

presentation of ITP (2)

A

same as TTP
BUT no systemic signs

169
Q

investigations (3) and results for ITP (3,2,1)

A

FBC: raised WCC, low Hb, low platelets
bloods: normal PT and APTT
blood smear: normal RBC appearance

170
Q

treatment for ITP (3)

A
  1. prednisolone and IV IgG
  2. splenectomy
171
Q

what does DIC stand for and what is it usually triggered by (2)

A

Disseminated intravascular coagulation
systemic inflammation or infection

172
Q

what is DIC 1, what does this cause 2 and what increased risk does this lead to 1 and what type of disorder is it? 1

A

widespread activation of coagulation cascade and platelet activation
this causes microvascular thrombosis and unnecessary consumption of clotting factors
increased risk of bleeding
disorder of primary and secondary haemostasis

173
Q

what r the causes for DIC (3)

A

sepsis
trauma
malignancy

174
Q

what is the presentation for DIC (2)

A

bleeding (epistaxis, bruising, rash, GI bleeds)
ARDS-an acute respiratory distress syndrome

175
Q

what are the 2 investigations for DIC

A

blood tests
blood smear

176
Q

results of blood tests in DIC (5)

A

low platelets
low fibrinogen
high d-dimer
long PT
long APTT

177
Q

what does the blood smear in DIC show (1)

A

schistocytes

178
Q

treatment for DIC (3)

A
  1. fresh frozen plasma to replace clotting factors
  2. cryoprecipitate to replace fibrinogen
  3. if bleeding then give platelet/ RBC transfusion
179
Q

what r the two types of haemophilia, which is more common and what part of the coagulation do they affect, how r they inherited

A

A and B
A (b is rare)
intrinsic pathway
x-linked

180
Q

what is haemophilia A and what type of disorder is it

A

factor 8 deficiency
secondary haemostasis disorder

181
Q

how is haemophilia A inherited

A

recessive
x-linked

182
Q

what is haemophilia B and what type of disorder is it

A

factor 9 deficiency
secondary haemostasis disorder

183
Q

presentation of haemophilia (4)

A

spontaneous bleeds
easy bruising
epistaxis (nose bleeds)
haemarthrosis (bleeding into joint spaces)

EESH

184
Q

2 investigations and results for haemophilia (1-> 2, 1-> 1)

A

bloods: high APTT, normal PT
low F8 (A) or F9 (B) assay

185
Q

what is the treatment for haemophilia (2,1)

A

A= IV F 8 plus desmopressin (releases F8 stored in vessel walls)
B= IV F9

186
Q

what type of disorder is von willibrands disease and what is the inheritance and location of the mutation

A

a primary haemostasis disorder
auto dom mutation of VWF gene on chromosome 12

187
Q

what is von willebrands disease and what types does it include

A

decreased functional VWF in blood
type 1,2,3

188
Q

what is the most common type of VW disease

A

type 1

189
Q

what is a consequence of VW disease and explain how this comes about

A

vwf protects factor 8 from liver protein C destruction so lack of vwf can caused factor 8 deficiency

190
Q

presentation of VW disease (4)

A

epistaxis
GI bleeding
menorrhagia
easy bruising

191
Q

investigation and results for VW disease (1:2)

A

bloods: low plasma vWF measurement and prolonged APTT if factor 8 is low

192
Q

treatment for VW disease (2)

A

type 1 is treated with desmopressin
tranexamic acid can reduce acute bleeding

193
Q

how does desmopressin treat VW disease 1

A

increases VWF release from endothelial Weibel Palade bodies

194
Q

what r the 3 main types of blood cancer

A

leukaemias
lymphomas
others

195
Q

what 4 examples of leukaemias r there

A

myeloid (acute myleloid leukaemia, chronic myeloid leukaemia), lymphoid (acute lymphoblastic leukaemia, chronic lymphoblastic leukaemia)

196
Q

what 2 examples of lymphomas r there

A

hodgkin, non-hodgkin

197
Q

what r the 3 other blood cancers in the other category of blood cancer

A

myelodysplasia, multiple myeloma, polycythaemia vera

198
Q

what is leukaemia

A

cancer of white blood cells

199
Q

explain the pathophysiology of leukaemia 3

A
  1. immature blast cells uncontrollable proliferate
  2. this take up space in bone marrow
  3. the lack of space in the bone marrow means fewer healthy cells can mature and be released into the blood
200
Q

what cells in the haematopoeitic pathways does each type of leukaemia affect (4)

A

CML: myeloid stem cell
AML: myeloblast
ALL: lymphoblast
CLL: B lymphocytes

201
Q

what is the key characteristic for each leukaemia? (4)

A

(ALL): children younger than 6
(AML): auer rods
(CLL): smudge cells
(CML): philadelphia chromosome

202
Q

what is ALL, what is the mutation

A

rapid proliferation of immature lymphoblasts
t(12:21)

203
Q

risk factor for ALL 1

A

downs

204
Q

presentation for ALL (5)

A

B SYMPTOMS (fever, night sweats, weight loss)
swollen testicles
hepatosplenomegaly
lymphadenopathy
HEADACHES/CN PALSIES (if infiltration of CNS)

205
Q

investigations for ALL (4) including the diagnostic

A
  1. FBC: anaemia, thrombocytopenia, neutropenia
  2. imagery (CXR/CT) which shows lymphadenopathy
  3. > 20% lymphoblasts on bone marrow biopsy (diagnosis)
  4. can do a lumbar puncture in cases of CNS involvement
206
Q

what is treatment for ALL (4)

A
  1. chemotherapy + allopurinol
  2. blood/ platelet transfusion
  3. antibiotics
  4. bone marrow transplant

CABAB (like kebab)

207
Q

what is the most common leukaemia in children under 4

A

ALL

208
Q

what is AML and what is the mutation

A

rapid proliferation of immature myoleblasts
t(15:17)

209
Q

compare the prognosis/ mortality/ progression of AML and ALL

A

ALL- good prognosis
AML- high mortality if not treated ASAP due to fast progression

210
Q

risk factors for AML (2)

A

age (mostly presents in elderly)
chemotherapy

211
Q

presentation for AML (6)

A

bone marrow failure: thrombocytopenia, neutropenia, anaemia
infections
hepatosplenomegaly
gum hypertrophy

212
Q

2 investigations and results for AML

A

FBC= anaemia, thrombocytopenia
bone marrow biopsy-> auer rods in cytology (diagnosis) and >20% myeloblasts

213
Q

what r auer rods

A

MPO aggregrates in neutrophils cytoplasm

214
Q

treatment for AML (4)

A
  1. chemotherapy + allopurinol
  2. blood/ platelet transfusion
  3. antibiotics
  4. bone marrow transplant
215
Q

why is allopurinol always given with chemo in AML and ALL

A

prevent tumour lysis syndrome-
where chemo releases uric acid form cells which accumulates in the kidneys

216
Q

what is CLL and what happens to the cells

A

proliferation of B lymphocytes
accumulation of incompetent lymphocytes due to failure of cell apoptosis

217
Q

risk factors for CLL 2

A

male
elderly

218
Q

presentation of CLL (4)

A

often asymptomatic
lymphadenopathy
might have night sweats and weight loss (due to bone marrow failure)

219
Q

what is the most common leukaemia in adults

A

CLL

220
Q

investigations and results for CLL (2)

A

FBC= anaemia, thrombocytopenia, leukocytosis
blood film= smudge cells

221
Q

treatment for CLL (3)

A

watch and wait in early stages
chemotherapy (rituximab)
stem cell/ bone marrow transplant

222
Q

complication for CLL and multiple myeloma (and what is it)

A

Richter transformation- cancer becomes more aggressive

223
Q

what is CML from what cell

A

uncontrollable proliferation of myeloblasts from the myeloid stem cell

224
Q

what age is CML most common in

A

most common in adults over 40

225
Q

what gene mutation is CML associated with

A

philadelphia chromosome translocation gene mutation (BCR-ABL gene)

226
Q

presentation of CML (8)

A

hepatosplenomegaly
hyper viscosity: headaches, thrombotic events
bone marrow failure: thrombocytopenia, neutropenia, anaemia
B symptoms
gout

227
Q

investigations for CML (2)- what is diagnostic

A

FBC= anaemia, thrombocytopenia, leukocytosis
genetic testing for BCR ABL (diagnostic)

228
Q

treatment for CML (3)

A
  1. tyrosin kinase inhibitors (imantinib)
  2. chemotherapy
  3. stem cell/ bone marrow transplant
229
Q

what is a lymphoma and what cell does it involve

A

cancer of lymph nodes
proliferation of lymphocytes in lymph nodes

230
Q

risk factors for lymphoma (6)

A

EBV virus
SLE
HIV
Sjorgens
Age
immunosupression

(2 infectious, 2 about u and 2 conditions)

231
Q

presentation of lymphoma (2)

A

lymph tissue enlargement: hepatomegaly/ splenomegaly/ lymphadenopathy
B symptoms: fever, night sweats, weight loss

232
Q

which type of lymphoma is more common and which is more predictable in its progression

A

non-hodgkin= more common
hodgkin= more predictable

233
Q

compare where hodgkin and non-hodgkin lymphomas arise

A

non-hodgkin: arise in any lymph node
hodgkin: typically start in upper body eg neck/ chest

234
Q

compare the presentation of hodgkin and non-hodgkin lymphoma

A

both have B symptoms but non-hodgkin has painless lymphadenopathy and hodgkin has painful lymphodenopathy upon alcohol consumption

235
Q

investigations for hodgkin and non-hodgkins

A

ESR is raised
imaging (CXR/CT) for staging
lymph node biopsy= Reed Sternburg cells in hodgkin, no RS cells in non-hodgkin

236
Q

what are the 3 types of non hodgkin lymphoma and their grades

A

low grade= follicular
high grade= diffuse B cell
very high grade= Burkitt’s

237
Q

compare age incidence for hodgkin and non-hodgkin

A

hodgkin= bimodal distribution (peaks in early 20s and then in 70s)
non-hodgkin= predominately affects adults over 40

238
Q

treatment for hodgkin lymphoma (4)

A

ABVD chemotherapy
adriamycin, bleomycin, vinblastine, dacarbazine)

239
Q

treatment for non-hodgkin lymphoma (6)

A

R-CHOP chemotherapy
(rituximab, cyclophosphamide, hydroxy-daunorubicin
vincristine (oncovin=brand name) , prednisolone)

240
Q

compare skin changes in hodgkin and non-hodgkin

A

H= skin excoriations
NH= skin rashes eg mycocis fungoides

241
Q

compare neutrophil levels in hodgkin and non-hodgkin

A

H= neutrophilia
NH= nuetropenia

242
Q

what staging scale is used for lymphomas

A

Ann Arbor staging

243
Q

explain the 4 stages of Ann Arbor staging

A

Stage 1: disease in one area only
Stage 2: disease in 2 or more areas on the same side of the diaphragm
Stage 3: disease in 2 or more areas on both sides of diaphragm
Stage 4: disease spread beyond the lymph nodes

244
Q

what is multiple myeloma

A

too much immunoglobulin released by abnormal plasma cells usually either IgA or IgG

245
Q

what is the precursor of multiple myeloma

A

close link to monoclonal gammopathy of undetermined significant (MGUS)
MGUS is a precursor to multiple myeloma

246
Q

what age does MM usually occur in 1

A

predominately occurs over the age of 40 years old

247
Q

complication (and stats) for MM (2)

A

1% of cases undergo richter transformation

248
Q

risk factors for MM (2)

A

age
African/Caribbean origin

249
Q

presentation of MM (5)

A

OLD CRAB
old= 70+
hypercalacemia (increase osteoblast bone resorption= bones, stones, moans and groans)
renal failure
anaemia (BM failure)
bone lesions (BM failure= painful new onset back pain in elderly)

250
Q

5 investigations for MM (6)

A

FBC – high Ca
Blood Film – Rouleaux Formation
BM biopsy – Plasma Cells > 10%
serum/ urine electrophoresis- bence jones protein in urine and hypergammaglobulinaemia for specific raised Ig and IgM spike

251
Q

treatment for MM 3)

A

chemotherapy
bisphosphonates (zoledrenic acid)
BM transplant

252
Q

what is polycythemia, what does this lead to and what r the 2 types

A

high concentration of erythrocytes in blood which causes hyper-viscosity of the blood
relative and absolute

253
Q

what is relative polycytheamia

A

normal number of erythrocytes but reduction in plasma

254
Q

what r the causes of relative polycytheamia (3)

A

obesity, dehydration and excessive alcohol consumption

255
Q

what is absolute polycythaemia and what r the two types

A

increased number of erythrocytes
primary and secondary polycytheamia

256
Q

what is primary polycythaemia and what is the alternative name to this

A

abnormality in the bone marrow
called polycythaemia vera

257
Q

what is secondary polycythaemia

A

disease outside bone marrow causing overstimulation of bone marrow

258
Q

causes of secondary polycythaemia (5)

A

COPD, sleep apnoea, polycystic kidney disease, renal artery stenosis, kidney cancer

259
Q

what type of condition is polycythaemia vera

A

myeloproliferative neoplasm (BM makes too many of RBCs)

260
Q

what mutation is polycythaemia and polycythaemia vera linked with

A

most people with this condition have a JAK2 mutation

261
Q

presentation of polycythaemia vera (6)

A

headaches
blurred vision
red skin (hands, face and feet)
hypertension
indicate polycythaemia vera as the cause: itching especially after contact with warm water, hepatosplenomegaly

3 high ribs

262
Q

2 investigations for polycythaemia vera and results (4:3, 1)

A

FBC: high RBCs, high platelets, low serum erythropoietin (can be normal or increased in other types of polycythaemia)
genetic testing- JAK2

263
Q

treatment for polycythaemia vera (3) and what is the general aim

A
  1. venesection AND low dose aspirin daily
  2. hydroxycardamide: for those at high risk of thrombus
    aim: to maintain a normal blood count
264
Q

what two things does EBV cause 2

A

glandular fever
infectious mononucleosis

265
Q

how does EBV spread 1

A

bodily fluids

266
Q

associations of EBV 3

A

hodgkins, burkitts, nasopharngeal carcinoma

267
Q

investigations of EBV 1

A

atypical lymphocytes on blood film

268
Q

what is significant about malaria 1

A

notifiable protozoal infection

269
Q

what is malaria a differential for 2

A

feverish patients with recent travel history

270
Q

symptoms of malaria 3

A

fever, haemolytic anaemia, hepatosplenomegaly

271
Q

investigations for malaria 1, positive result and what is the procedure for someone to test negative 1 (who was previously positive)

A

thick and thin blood smears- + result is identifying the pathogen under the microscope
3 separate negative reading required for a negative declaration

272
Q

treatment for malaria 2 and if severe 1 (side effect of first treatment

A

quinine (SE= hypoglycaemia) and doxycycline (antimalarials)
severe= IV artesunate

273
Q

investigations for HIV 3

A
  1. history
  2. antiHIV immunoglobulins (ELISA)
  3. p24 antigens (ELISA)
274
Q

investigation to monitor progression of HIV 2

A

CD4 count and HIV RNA copies

275
Q

treatment aim for HIV 2

A

maintain CD 4 count and reduce number of HIV RNA copies

276
Q

what value defines AIDs

A

CD4+ <200 cells/mm3

277
Q

name the 4 steps of HIV progression (with CD4 count trend)

A
  1. primary infection: CD4 dip then up set point
  2. clinical latency: CD4 peak (lower than pre-infection)
  3. symptoms and reduction in CD4 count
  4. AIDS- lowest CD4 count
278
Q

what test is needed for specifically haemolytic anaemia and what r the two results

A

urine test-
high urobilinogen and high bilirubin

279
Q

what puts u at a higher risk of developing autoimmune haemolytic anaemia 1

A

any other autoimmune condition eg SLE

280
Q

how does hydroxycarbamide help in sickle cell 2

A

makes your RBCs bigger and less sickled shape

281
Q

appearance of beta thalassaemia major erythrocytes under blood film 2

A

large and small irregular hypochromic RBCs

282
Q

what pathogen has the highest rate of human death from all malarias 1

A

plasmodium falciparum

283
Q

treatment for beta thalassaemias

A

all require lifelong transfusions except beta thalassaemia minor

284
Q

compare how alpha and beta thalassaemia r diagnosed 1, 1

A

alpha thalasaemia diagnosed with HB electrophoresis and beta with blood film

285
Q

what is the major risk factor for thyroid eye disease in patients that have graves

A

smoking

286
Q

what does presenting with a fever 1-2 weeks after chemo indicate and what is the treatment for this

A

neutropenic sepsis- treat immediately with IV piperacillin with tazobactam

287
Q

what two things indicate von willebrands disease

A

personal and family history of prolonged bleeding

288
Q

what indicates DIC specifically 1

A

bleeding from lots of different areas eg eyes, mouth, ears ets

289
Q

what doe beta thalassaemia show on blood film

A

target cells

290
Q

what is rituximab specific to 2 and what does it do 1

A

specific to CD20 on b lymphocytes and causes their death

291
Q

what two things that present together in a child indicate sickle cell disease

A

dactylitis (inflammation of finger/ toe) and fever

2A content- Sameera (21 decks)

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