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Year 4 > Haematology > Flashcards

Haematology Flashcards

1
Q

Plasma vs Serum

A

Plasma contains clotting factors, WBCs and RBCs

Serum is when these have been removed, containing glucose, electrolytes and proteins

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2
Q

What condition contains target cells on blood film finding

A

Iron deficiency anaemia
Post-splenectomy

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3
Q

In what condition are Heinz bodies seen in

A

G6PD and alpha-thalassaemia

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4
Q

In what condition are Howell-Jolly Bodies seen in

A

Post-splenectomy
Severe Anaemia (sickle cell disease)

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5
Q

What are reticulocytes

A

Immature red blood cells

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6
Q

What causes reticulocyte counts to go up

A

Rapid turnover of red blood cells (e.g., haemolytic anaemia

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7
Q

What are sideroblasts

A

Immature red blood cells containing LOTS of iron

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8
Q

In what condition are smudge cells found in

A

Chronic Lymphocytic leukaemia

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9
Q

Name two conditions in which spherocytes are found

A

Autoimmune haemolytic anaemia
Hereditary spherocytosis

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10
Q

Where is iron mainly basorbed

A

Duodenum and jejunum

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11
Q

What causes the reduction of Fe2+ to Fe3+

A

When acid levels drop

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12
Q

What is the issue of Fe2+ to Fe3+ reduction

A

It becomes insoluble

So anything that can reduce acid levels (e.g., PPIs) can cause iron deficiency

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13
Q

Why can coeliac and crohn’s cause iron-deificency

A

Inflammation of the jejunum and duodenum

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14
Q

What is the most common cause of iron deficiency anaemia

A

Blood loss

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15
Q

What are the most common causes of GI tract bleeding

A

Oesophagitis and gastritis

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16
Q

What protein is Fe3+ bound to in th eblood

A

Transferrin

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17
Q

What is TIBC

A

Total space on the transferrin to bind to iron molecules

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18
Q

How does Total iron binding capacity and transferrin levels relate

A

They directly correlate to the number of transferrin molecules in t heblood

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19
Q

What is ferritin

A

Iron that is stored inside cells

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20
Q

What causes ferritin to be eleveated in the blood

A

Released from cells during inflammatory conditions (e..g, infections or cancer)

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21
Q

What serum ferritin level indicates Iron deficiency

A

Low

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22
Q

What happens to the level of TIBC and transferrin levels in iron deficiency

A

Increase

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23
Q

What happens to TIBC and transferrin levels in iron overload

A

Decrease

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24
Q

What is a normal transferrin saturation level

A

30%

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25
Q

If there is new iron deficiency without a clear underlying cause, what should be done

A

Oesophago-gastroduodenoscopy + colonscopy to look for cancer

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26
Q

Management of iron deficiency anaemia

A

Blood transfusion

Iron infusion (cosmofer)

Oral Iron (furous sulphate) 200mg three times a day

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27
Q

What type of MCV anaemia is iron deficiency anaemia

A

Microcytic anaemia

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28
Q

What cells produce intrinsic factor

A

Parietal cells

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29
Q

What is intrinsic factor needed for

A

B12 absorption in the ileum

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30
Q

Name four symptoms of B12 deficiency

A

Peripheral neuropathy (paraesthesia)
Loss of virbation and proprioception
Visual changes
Mood or cognitive changes

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31
Q

What is the first line investigation for pernicious anaemia

A

Intrinsic factor antibodies

Gastric parietal cell antibodies (second line)

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32
Q

Management of pernicious anaemia

A

Cyanocobalamin (dietray replacement)

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33
Q

If dietary replacement is insufficient for pernicious anaemia, what should be done

A

IM Hydroxycobalamin 3 times a week for 2 weeks, then every 3 months

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34
Q

If there is folate deficiency alongside pernisious anaemia, what should be treated FIRST, B12 or folate deficiency

A

B12 FIRST, otherwise folic acid correction can cause subacute degenertaion of the cord

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35
Q

What type of anaemia is haemolytic anaemia

A

Normocytic anaemia

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36
Q

What test should be done to diagnose autoimmune haemolytic anaemia

A

Direct coombs test

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37
Q

Describe the genetic inheritance of Hereditary spherocytosis

A

Autosomal Dominant

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38
Q

What virus causes hereditary spherocytosis

A

Parvovirus

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39
Q

What crisis is seen in hereditary spherocytosis

A

Aplastic crisis (parvovirus infection)

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40
Q

How is spherocytosis treated

A

Folate supplementation and splenectomy

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41
Q

In what population is G6PD deficiency common

A

Neonates with meditteranean and African background

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42
Q

How is G6PD inherited

A

X linked recessive

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43
Q

What causes G6PD crises

A

Infections
Medications
Broad Beans

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44
Q

Symptoms of G6PD deficiency

A

Gallstones
Anaemia
Splenomegaly

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45
Q

How is G6PD deficiency diagnosed

A

G6PD enzyme assay

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46
Q

What medications can trigger G6PD deficiency

A

Primaquine
Ciprofloxacin
Sulfonylureas
Sulfsalazine

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47
Q

What is autoimmune haemoltic anaemia

A

Antibodies created against the patient’s red blood cells

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48
Q

What causes warm autoimmune haemoltic anaemia

A

Idiopathic

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49
Q

At what temperatures does cold haemolytic anaemia occur at

A

less tahn 10 degrees

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50
Q

What happens in autoimmune haemolytic anaemia

A

Agglutination

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51
Q

What conditions can cause cold autoimmune haemolytic anaemia

A

Lymphoma
Leukaemia
SLE
EBV, CMV and HIV

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52
Q

Management of autoimmune haemolytic anaemia

A

Blood transfusion
Prednisolone
Rituximab
Splenectomy

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53
Q

What is characteristic of paroxysmal nocturnal haemoglubinuria

A

Red urine in the morning (contains haemoglobin and haemosiderin)

Anaemia

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54
Q

Management of Paroxysmal nocturnal haemoglobinuria

A

Eculizumab and bone marrow transplant

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55
Q

Name three conditions which has microangiopathic haemolytic anaemia

A

HUS
SIC
TTP
SLE

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56
Q

What are normal haemoglobin consisted of

A

2 alpha
2 beta gloobin chains

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57
Q

How are thalassaemia inherited

A

Autosomal recessive

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58
Q

What type of anaemia is seen in thalassaemia

A

Low mean corpucular volume

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59
Q

What phsyical features change in thalassaemia

A

Pronounced forehead and cheekbones

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60
Q

GOLD standard diagnosis of thalassaemia

A

Haemoglobin electrophoresis

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61
Q

How are serum levels affected in thalassaemia

A

Serum feritin levels increase due to iron overload

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62
Q

How is iron overload in thalassaemia corrected

A

Iron chelation

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63
Q

What gene is affected in alpha thalassamia

A

16

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64
Q

How is alpha thalassaemia managed

A

Monitoring FBC
Monitoring complications
Blood transfusions
Splenectomy

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65
Q

How can alpha thalassaemia be cured

A

Bone marrow transplant

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66
Q

What gene is affected in beta thalassaemia

A

11

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67
Q

What is thalassaemia minor trait

A

Beta thalassaemia where there is one abnormal and one normal gene

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68
Q

Beta thalassaemia trait vs major

A

Slightly anaemic (low MCV and MCH) and ASYMPTOMATIC

vs

SEVERE haemolytic anaemia: hepatosplenomegaly, VERY low MCV and MCH

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69
Q

Management of thalassaemia minor

A

Monitoring

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70
Q

Management of thalassaemia major

A

Transfusions, iron chelation and splenectomy

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71
Q

At what age is feotal haemoglobin replaced by Haemoglobin A

A

6 weeks of age

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72
Q

What gene causes SCA

A

11

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73
Q

What type of inheritance is SCA

A

Autosomal recessive

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74
Q

What condition does SCA protect people against

A

Malaria

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75
Q

How is SCA diganosed

A

Electrophoresis

Neowborn screening heel prick test at 5 days

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76
Q

Name som ecomplictaions of SCA

A

Stroke
Avascular necrosis of the hip
Pulmonary Hypertension
Priapism
CKD
Sickle cell crisis
Acute Chest Syndrome

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77
Q

Management of SCA

A

Rehydration
Vaccine check
Penicillin V
Hydroxycarbamide to increase foetal Heamoglobin

Blood transfusion for severe anaemia

Bone marrow transplant

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78
Q

What pain relief should be avoided in SCA with CKD

A

NSAIDs

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79
Q

What triggers SCA crises

A

Infections
Hypoxia
Acidosis

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80
Q

How is pripism treated in SCA

A

Emergency: Aspiration of blood from penis

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81
Q

What is indicative of splenic sequestration

A

SEVERE anaemia

Hypovolaemic shock

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82
Q

How is splenic sequestration crisis managed

A

Blood transfusion and fluid resus

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83
Q

What can prevent a splenic sequestration crisis

A

Splenectomy

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84
Q

What infection commonly triggers an aplastic crisis

A

Parvovirus B19

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85
Q

How do we diagnose Acute Chest Syndrome

A

Fever or respiratory symptoms

New infiltrates seen on a chest X-Ray

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86
Q

What HbA2 level is diagnostic for thalassaemia

A

> 3,5%

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87
Q

Name trhee lymphocytes

A

Bcells
T-Cells
NK cells

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88
Q

Lymph node appearance in infetcions vs lymphoma

A

Lymphoma is hard and fixed (cannot move)

+ B symptoms

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89
Q

Is a fine needle aspiration of lymph node diagnostic for lymphoma?

A

No

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90
Q

What is needed to diagnose a lymphoma

A

Excisional biopsy

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91
Q

Hodgkin vs non-hodgkin lymphoma

A

The presence of reed-sternberg cells = hodgkin’s

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92
Q

How can we stage a lymphoma

A

PET/CT scan

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93
Q

Describe the ann arbour staging system for lymphoma

A

Stage 1 - One lymph node on one side of the diaphgram

Stage 2 - Multiple lymph nodes on one side of the diaphgram

Stage 3 - Multiple lymph node involvement on both sides of the diaphrragm

Stage 4 - Distant metastases

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94
Q

What does A stage mean in lymphoma

A

Absence of additional symptoms

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95
Q

What does B substage mean in lymphoma

A

Presence of B-Symptoms

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96
Q

What does X subclass mean in lymphoma

A

Bulky disease (lymph node >10 cm diameter)

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97
Q

What does E subclass mean in lymphoma

A

Involvement of a single organ (e..g, lung inovlvement in mediastinal lymphadenopathy)

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98
Q

What does S mean in subclass of lymphoma

A

Spleen involvement

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99
Q

What cells do hodgkin lymphoma airse from

A

B-cells

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100
Q

Age onset of hodgkin lymphoma

A

15-30

50+

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101
Q

What antigens are positive in hodgkin’s classical lymphoma

A

CD15 and 30

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102
Q

What cells are seen in non-classical hodgkin’s lymphoma

A

Popcorn cells

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103
Q

What antigens are seen in popcorn cells

A

CD20 + 45

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104
Q

Where are hodgkin lymphoma commonly found

A

Cervical
Axillary
Mediastinal

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105
Q

Symptoms of Mediastinal lymphadenopathy

A

itchy rash
Pel Ebstein Fevers

COUGH + SOB
Hoarseness
Superior vena cava syndrome
Pleural effusion

Minimal Change Disease

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106
Q

Blood test results in Lymphoma

A

Increased ESR and LDH

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107
Q

Treatment of hodgkin Lymphoma (stage 1 and 2)

108
Q

Treatment of Hodgkin Lymphoma Stage III + IV

A

BEACOPP

Bleomycin
Etoposide
Adramycin
Cyclophosphomaide
Oncovin
Procarbazine
Prednisolone

109
Q

How can non-classical hodgkin lymphoma be treated

110
Q

Side-effect of Doxorubicin

A

Cardiotoxicity

111
Q

Side effect of Vincristine

A

Peirpheral Neuropathy

112
Q

Side-effect of bleomycin

A

Pulmonary Toxicity

113
Q

Side-effect of Cyclophosphomaide

A

Haemorrhagic cystitis

114
Q

Most common type of non-hodgkin lymphoma

A

Diffuse Large B-Cell Lymphoma

115
Q

What is Richetr Syndrome

A

Where CLL -> Diffuse large B-Cell LYmphoma

116
Q

What lymphoma is seen in HIV patients

A

Primary CNS Lymphoma

117
Q

What is Burkitt’s Lymphoma

A

8:14 translocation

Associated with EBV or HIV

118
Q

Symptom of Burkitt Lymphoma

A

Ileocaecal abdominal mass

or Jaw mass in a CHILD

119
Q

What causes marginal zone lymphoma

A

11:18 chromosomal translocation

120
Q

What Rheumatological condition can cause marginal zone lymphoma

A

Sjogren’s Syndrome

121
Q

What other condition than Sjogren’s syndrome can give rise to marginal zone lymphoma

A

H.Pylori infection (MALToma)

122
Q

Treatment of Non-Hodgkin Lymphoma

A

R-CHOP

Rituximab

Cyclophohsphomade

Hydroxydaunorubicin
Oncovin
prednicolone

123
Q

What threshold defines Leukaemia

A

WCC >11 x 10^9

124
Q

What is laeukaemia

A

Cancer of bone marrow progenitor cells

125
Q

Name 4 myeloid cells

A

basophils
Eosinophils
neutrophils
Mast Cells

126
Q

Acute vs Chronic leukaemia

A

Acute: Immature blast cells

Chronic:

127
Q

Describe the symptoms of CML

A

EFFECTS OLD people:

  1. Chronic Phase: Asymptomatic

Symptoms: Anaemia
Early Satiety
Frequent infections + Bleeding

From abnormal cells

  1. Accelerated phase
  2. Blast Crisis: Becomes Acute laeukaemia (ALL or AML)
128
Q

Onset of CLL

129
Q

Onset of CML

130
Q

Onset of AML

131
Q

Name some differentials of thrombocytopenia petechiae

A

Meningococcal septicaemia
Vasculitis
HSP
ITP
Non-accidental injury

132
Q

What is the initial invetsigation for leukaemia

A

FBC within 48 hours

133
Q

If a child or young adult present with petechiae or hepatosplenomegaly at GP and have suspected laeukaemia, what is the first line management

A

Urgent refrral to haemotolgy

134
Q

Wher eis a bone marrow biopsy typically taken

A

Iliac Crest

135
Q

What condition is ALL associated with

A

Downs Syndrome

136
Q

What does a blood film show in ALL

A

Blast cells

137
Q

What translocation is associated with ALL

A

Philadelphia chromosome (9:22)

138
Q

What other leukaemia has a philalephia chromsome phenomenon

139
Q

What blood film finding is seen in CLL

A

Smear or Smudge cells

140
Q

How long does the chornic phase in CML last for

141
Q

Symptoms of the blast phase in CML

A

Severe pancytopenia

142
Q

What does a blood film show in AML

A

Blast cells with auer rods

143
Q

What anaemia is associated with CML

A

Haemolytic anaemia

144
Q

Symptoms in chronic phase CML

A

Asymptomatic

145
Q

What conditions can progress onto AML

A

Polycythaemia ruby vera or Myelofibrosis

146
Q

Treatment of CML caused by translocation

A

Tyrosine Kinase inhibitors
Imatinib

147
Q

What genes are switched in the 9:22 translocation

A

Tyrosine Kinase ABL and BCR

148
Q

How is a blast crisis treated in CML

A

Allogeneic hematopoietic stem cell transplanttaion

149
Q

Name the two types of ALL

A

T-cell

B-cell

150
Q

Signs of pre t_cell ALL

A

Superior vena cava syndrome (mediastinal mass

151
Q

What is superior vena cava syndrome

A

Facial Swelling
SOB
Venous distention

152
Q

Signs of Pre B -Cell ALL

A

Fatigue
Infections
Bleeding
Leukostasis

153
Q

Complication of ALL (pre B-Cell

A

CNS:
Headaches
Meningitis
Cranial nerve palsies

154
Q

Name the chemotherapy phases for ALL

A

Induction: Kills most leukaemia cells

(4-6 weeks)

Consolidation: Kill remaining cells not detected by tests

Maintenance: 2 years

155
Q

What is Myeloma

A

Cancer of the plasma cells (make lots of one type of antibody)

156
Q

What chromosome is affected in myeloma

157
Q

What is monoclonal gammopathy of undetermined significance

A

Where there is an excess of one type of antibody without features of myeloma or cancer (may progress to myeloma)

158
Q

What is smouldering Myeloma

A

Progression of MGUS with higher levels of antibodies - more likely to porgress to myeloma than MGUS

159
Q

What is the main type of immunoglobulin seen in myeloma

160
Q

What is a monoclonal paraprotein

A

Abnormal protein derivative of an antibody

161
Q

Why do we get anaemia in myeloma

A

As cancerous plasma cells inflitrate the bone marrow causing anaemia, neutropenia and thrombocytopenia

162
Q

Name the four key features of myeloma

A

CRAB

Calcium (elevated)
Renal Failure
Anaemia (normocytic)
Bone lesions/pain

163
Q

Risk Factors for multiple myeloma

A

Older Age
Male
Black African history
Family HIstory
Obesity

164
Q

Why do we get hypercalcaemia in myeloma

A

Myeloma bone disease: Increased osteoclastic activity and suppression of osteoblasts

Causes the release of calcium into the blod

165
Q

What would be seen on an X-Ray in myeloma

A

Osteolytic lesions

166
Q

What tumours are usually seen in myeloma bone disease

A

Plasmacytomas (tumours made of plasma cells)

167
Q

Why do we get hyperviscocity in myeloma

A

Due to increase of proteins in th eblood: causes easy bruising, bleeding, reduced sight, heart failure

168
Q

What initial investigations would we do in suspected myeloma cases

A

FBC
Calcium
ESR
Plasma Viscocity

169
Q

Name the four specific tests used for myeloma after initial investigation

A

B - Bence-Jence protiene (urine electrophoresis)
L - Serum-free Light-chain assay
I - Serum Immunoglobulins
P - Serum Protein Electrophoresis

Then a bone marrow biopsy to confirm

170
Q

How do we check for bone lesions in multiple myeloma

A

Whole body MRI

171
Q

X-Ray signs in Myeloma

A

Raindrop skull appearance

172
Q

What is the first line treatment of myeloma

A

Bortexomid
Thalidomide
Dexamethasone

Stem cell transplantation

173
Q

Why do patients with myeloma need venous thromboembolism prophylaxis with aspirin

A

During chemotherapy regimes as they can cause thrombuses

174
Q

How can myeloma bone disease be improved/supplemented

A

Bisphosphonates

175
Q

If someone complains of bone pain, what adjuvant can be used

A

Radiotherapy

176
Q

How should fractures in multipl emyeloma be supported

A

Sabilise bones (prophylactic intramedullary rod)

177
Q

What is cement augmentation

A

Injecting cement into vertebral fractures to improve spine stability

178
Q

What gene is involved in polycythaemia vera

A

JAK2 gene: continues differentiation of stem cells into red cells (remain active without erythropoietin)

179
Q

What cells are affected in Polycythaemia Vera

A

Haematopoietic stem cells

180
Q

How does erythropoietin increase RBC production

A

Binds to JAK2 receptors on hematopoietic stem cells causing them to divide and differentiate

181
Q

What happens in Polycythaemia vera to cause anaemia, thrombocytopenia and leukopenia (spent phase)

A

Stem cells start to die out from exhaustion

Bone marrow cannot produce any more blood cells, leading to myelofibrosis

182
Q

What rheumatological condition can be seen in polycythaemia vera

A

Build up of uric acid -> Gout and kidney stones

183
Q

What Hb level indicates polycythaemia vera

A

Hb > 18.5 in men or 16.5 in women

184
Q

Define relative polycythaemia

A

Decrease in plasma volume which causes increase in RBC percentage:

Fluid loss from dehydration and burns

185
Q

Define primary polycythaemia

A

Genetic condition in which there is excessive responsiveness to reythropoietin

186
Q

Define secondary polycythaemia

A

Due to hypoxia stimulating erythropoetin release such as COPD, smoking and Eisenmenger’s, cancers (e.g, WILM’s)

187
Q

FBC findings in polycythaemia vera

A

Elevated Hb and WCC and platelets

LOW ferritin

188
Q

Erythropoietin levels in PV

189
Q

First line management of polycythaemia

A

Hydroxycarbamide and interforn alpha

190
Q

How is itching in PV managed

A

Antihistamines or SSRIs

191
Q

What cytokine causes fibrosis of the bone marrow

A

Cytokines (fibroblast growth factor) released by proliferating cells

192
Q

Define extramedullary hematopoeisis

A

When the bone marrow is scarred, the liver and spleen try to make RBCs insread

193
Q

Complication of extramedullary haematopoeisis

A

Hepatosplenomegaly or portal hypertension

194
Q

What key signs are seen in someone with polycythaemia vera

A

Conjunctival plethora (redness)
ruddy complexion
Splenomegaly

195
Q

Managemnt of primary myelofibrosis

A

Stem cell transplant

196
Q

What defines thrombocytopenia

A

<50 x 10^9 count

197
Q

Management of ITP

A

Prednisolone
IV Immunoglobulins
Rituximab (a monoclonal antibody against B cells)
Splenectomy

198
Q

Name four fat soluble vitamins

A

Vit D, E, A and K

199
Q

What is a left shift

A

Presence of immature cells

Right shift is hypermature, multisegmented cells

200
Q

In what condition is a left shift seen in

A

Acute infections, fibrosis or leukaemia

201
Q

Define anisocytosis

A

Variation in RBC size

202
Q

Diagnosis of paroxysmal nocturnal haemoglobinuria

A

Flow cytometry

203
Q

What blood test finding is seen in vWD

A

Abnormal APTT

204
Q

How to treat acute haemolytic transfusion reactions

A

Stop transfusion + Give Saline

205
Q

How to treat febrile non-haemolytic transfusion reactions

A

Slow transfusion and give paracetamol

206
Q

How to treat transfusion associated circulatory overload

A

Slow transfusion + give Furosemide

207
Q

Define the Wells criteria for a DVT

A

Active cancer
Paralysis
Bedridden for 3 days or more or major surgery within 12 weeks requiring anaesthesia
Localised tenderness along deep venous system
Entire leg swollen
Calf swelling >3cm than the other
Pitting Oedema
Collateral superficial veins
Previous DVT
Alternative diagnosis is at least as liekly as DVT

208
Q

What Well’s score indicates likely DVT

209
Q

Investigations for DVT

A

Doppler USS

210
Q

What is the problem with D-Dimer in diagnosing DVT

A

It can only exclude VTE not confirm it

211
Q

What else can increase a D-dimer (false positive)

A

Malignancy
Infection
Pregnancy
Stroke
MI
AOrtic Dissection

212
Q

Management of a DVT

A

DOAC, LMWH (Apixaban) or Warfarin

213
Q

How long is Anticoagulation given for a DVT

A

3 months at least

Unprovoked DVT: 6 months

214
Q

What is an IVC filter used for in managing DVTs

A

Reduce thr isk of DVT emboli into the pulmonary arteries (reduces risk of PE)

215
Q

Clinical features of a DIC

A

Epixstasis
Gingival Bleeding
Haematuria
Bleeding from cannula sites

Petechiae
Hypotension

216
Q

What type of leukaemia is commonly associated with DICs

A

Acute Promyelocytic leukaemia

217
Q

Blood findings in DIC

A

Increased Prothrombin AND APTT

Decreased fibrinogen

Thrombocytopenia

218
Q

How long shohuld a patient with. a DVT/PE be treated on DOAC if they have an active cancer

A

3-6 months

219
Q

In what patients would a PE/DVT be an indication for lifelong warfarin use

A

Those with ongoing risk factors (e.g., antiphospholipid syndrome)

220
Q

How do we manage a high INR

A

Stop antigoagulants
Administer IV Vit K
Administer fresh frozen plasma or prothrombin complex

Repeat INR in 24 hours

221
Q

Define some causes for non-megaloblastic marcocytic anaemia

A

Chronic liver disease
Hyposplenism
Chronic inflammation
Alcoholism
Hypothyroidism

222
Q

What is the antidote for methotrexate overdose

A

Folinic acid (NOT folic acid)

223
Q

What is Gaisbock’s Syndrome

A

Pseudopolycythaemia in people who smoke (reduces plasma volume) - relative polycythaemia cause

224
Q

What post-splenectomy prophylaxis should be given

A

Pneumococcal vaccination
Seasonal influenza vaccination
Haemophilus type b vaccination
Men C vaccination

Low dose penecillin V life long

225
Q

What is th etarget INR for AF

226
Q

What is the target INR for metallic valve replacement

227
Q

What is the typical target INR for VTE

228
Q

What should be the target INR for patients with recurrent VTE while on warfarin

229
Q

What is Factor V Leiden

A

Mutation in clotting factor 5 which stops factor S and C from deactivating it -> causes lots of clots

230
Q

What is the role of Protein C and S

A

Inactivates clotting factors V and VIII

231
Q

What factors are inhibited by antithrombin III

A

IIa, Xa, IXa and XIa

232
Q

What condition usually causes vWD manifesttaion

A

CHildbirth

233
Q

TIBC and serum ferritin levels in thalassamia minor

A

NORMAL

NOTE: Gets mistaken for iron deficiency easily, but iron deficiency, TIBC and ferritin INCREASES

234
Q

Define thalassaemia intermedia by HB levels

A

70-100 g/L (mild anaemia)

235
Q

Define pulmonary hypertension

A

MAP >25 mmHg

236
Q

When should Anti-D be given during pregnancy (criteria)

A
  • Mother is RhD-negative
    -Baby is RH-D positive

500IU if IgG Anti D IM within 72 hours

237
Q

What is the role of the Kleihauer test

A

TO determine whether more Anti-D is required beyond the first dose

238
Q

First line management of PV

A

Venesection THEN hydroxycarbamide + Interforn alpha

239
Q

What blood is given in an emergency (needs immediately)

A

O - negative

240
Q

How long does it take to cross-match blood

A

45 minutes

241
Q

What is given first in major bleeding from anticoagulants, prothrombin or vet K

A

Prothrombin Complex

242
Q

If PT >1.5, what should be done

A

Give Fresh Frozen Plasma

243
Q

If Fibrinogen levels <1.5, what should be done

A

Give Cryoprecipitate

244
Q

If Platelets < 75 x 10^9, what should be done

A

Give PLatelets

245
Q

What is fresh frozen plasma

A

Contains factors to replace for coagulation

246
Q

Under what Hb level should blood transfusion be given

247
Q

First line management of neutropenic sepsis

A

IV Tazocin first (do not need to order WBCs)

248
Q

Signs of TTP

A

Altered Mental State
Microcytic anaemia
Fever
Renal Failure
Thrombocytopenia

249
Q

First line management of ITP

A

Oral prednisolone

250
Q

Neurological signs distinctive of B12 deficiency

A

Symmetrical paraesthesia or ataxia in the lower limbs

251
Q

When can MCV be normal in B12 and folate deficiency

A

If iron deficiency is co-present

252
Q

What specific test can be used to check for B12 deficiency

A

Serum cobalamin levels

253
Q

When is hydroxycobalamin indicated over oral cyanocobalamin

A

IM = if not thought to be diet related

Oral = thought to be diet related

254
Q

What are good sources of B12

A

Eggs
Meat
Milk
Salmon

255
Q

Management of folate deficiency

A

B12 FIRST (check if deficiency)

Then 5mg folic acid daily

256
Q

What should be monitored in B12 or folate replacement therapy

A

Reticulocyte count and FBC

257
Q

What Hb level is okay in pregnant women

A

> 110 in first trimester

> 105 in second or third trimester

258
Q

IN what people is a trial of oral iron considered a first line diagnostic test for iron deficiency

A

Pregnant women (as ferritin levels are not accurate - main cause is usually anaemia)

DO NOT do this with postmenopausal or men

259
Q

What is the main cause of siderblastic anaemia

A

Alcoholism

260
Q

Ferritin levels in thalassaemia

A

Raised ferritin
Low TIBC

261
Q

What is a positive test to show improvement of iron supplements

A

Increase in Hb by 20 in a month

262
Q

When should someone with iron deficiency be referred to the 2 week pathway

A

60 years or older

50 and under + rectal bleeding

263
Q

Management of iron deficiency anaemia in men and postmenopausal women

A

Refer to gastroenterology

Also people whop are coeliac need to be referred

264
Q

In what conditions are DOACs contraindicated in

A

A prosthetic heart valve

Oesophageal varices

265
Q

When is warfarin contraindicated

A

Within 72 hours of major surgery

Within 48 hours postpartum

266
Q

Stepwise invetsigation for a DVT

A

USS of the leg

If not available: then do a D-dimer first

267
Q

First line management iof polycythaemia in pregnancy

A

Interferon alfa = high risk

Venesection = low risk

Year 4 (16 decks)

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