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Year 3 Conditions > Haem > Flashcards

Haem Flashcards

1
Q

What are 2 types of ITP

A

Primary- no identifiable cause

Secondary- alongside a precipitant or associated condition

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2
Q

What is priapism

A

Extended and painful erection

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3
Q

Where are petechiae most commonly found

A

Lower limbs

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4
Q

Rare treatments for SCD

A

Bone marrow transplant

Gene therapy

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5
Q

Diagnosis of ITP

A

Diagnosis of exclusion so all tests normal except for low plts
No systemic signs
No organomegaly
No lymphadenopathy

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6
Q

Complications of SCD

A 
Avascular necrosis in bones
Stroke
MI
Splenic sequestration
Chronic cholecystisis and gall stones
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7
Q

Signs on examination of ITP

A

No lymphadenopathy
No organomegaly
No other signs
Just petechiae or bruising

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8
Q

What happens when renal pupillae is occluded

A

Necrosis- presents with haematuria and proteinuria

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9
Q

What happens to haptoglobin in intravascular haemolysis

A

Goes down

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10
Q

What make up majority of splenic sequestration cases

A

6 months to 2yrs infants with SCD

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11
Q

Complications of TTP

A

Stroke, MI and any thrombo-embolic events

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12
Q

What is low haptoglobin a sign of

A

Intravascular haemolysis

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13
Q

Definitive test for TTP

A

ADAMTS- 13 activity test- takes a month

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14
Q

Acquired non immune causes of thrombocytopenia

A

Infection
Drugs
Malignancy

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15
Q

Which drugs can cause thrombocytopenia

A

Anti platelets and any blood thinning drugs
Alcohol
Sulfa drugs
Quinine

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16
Q

How does SCD affect the spleen

A

Infarct which can lead to backup of blood in spleen- splenic sequestration

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17
Q

Where is SCD commonly found

A

People of african and South asia descent due to evolutionary protection against malaria

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18
Q

Risk factors for ITP

A

Women of childbearing age- tends to be chronic

People under age of 10 and above 65- tends to be more acute so presents after a viral infection for example

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19
Q

Treatment for SCD

A 
Vaccines 
Anitbiotics to treat any underlying infections
Fluids and oxygen
Opiods for crises
Transfusions
Penicillin prophylaxis
Hydroxyurea
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20
Q

What is name given to heterozygote SCD

A

Sickle cell trait

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21
Q

How does hydroxyurea work

A

Increases production of gamma Hb which composes HbF. HbF doesnt include HbS so reduces sickling

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22
Q

What is danger of splenectomy or dysfunctional spleen

A

Susceptible to encapsulated bacteria as they are normally opsonised and phagocytosed there

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23
Q

Findings of TTP investigations

A

FBC- platelets and RBC low
Blood film- reduced platelets and schistocytes present
Reticulocyte count- raised
Urinalysis- kidney issues common so protein in urine common and U and Es will be pathological
Haptoglobin- down

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24
Q

What are some conditions assocaited with secondary ITP

A

HIV
Hep C
Lupus

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25
Q

Pathophysiology of TTP

A

Antibodies formed against enzyme that cleaves VwF meaning VwFs circulate without inhibition leading to spontaneous and excessive thrombous formation which cause ischaemia and shearing of RBCs

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26
Q

3 factors that increase sickling

A

Acidosis
Dehydration
Hypoxia

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27
Q

TTP pentad of symptoms

A 
Renal disease
Microangiopathic haemolytic anaemia
Thrombocytopenic purpura
Neurological symptoms
Fever
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28
Q

What happens to Hb after RBC breakdown

A

Binds to haptoglobin

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29
Q

Dangers of transfusions

A

Iron overload

Antibodies produced against future infections

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30
Q

What is petechiae

A

Small red or purple spots on skin or mucosal membranes that indicate small capillary bleeds

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31
Q

Risk factors for SCD

A

Family inheritance

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32
Q

What is particular SCD symptom for men

A

Priapism

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33
Q

What is result of splenic infarcts over time

A

Auto-splenectomy where it fibroses down to become very small

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34
Q

Presentation of TTP

A

Prodrome for a week
Neurological symptoms such as confusion, drowsiness, focal symptoms and coma
Digestive symptoms including vomiting, diarrorhoea and abdo pain
Bleeding signs such as bruising and purpura
Fever

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35
Q

Define TTP

A

Microangiopathic haemolytic anaemia and thrombocytopenic purpura coupled.

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36
Q

Investigations and findings for ITP

A

FBC- low platelets and no other abnormalities
Blood film- fewer platelets which can be larger in size
Bone marrow biopsy- increased megakaryocytes due to need for production, no dysplasia and normal cytogenics

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37
Q

Signs of increased inconjugated bilirubin

A

Scleral icterus
Jaundice
Gallstones

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38
Q

Dactylitis

A

Swollen joints on the back of hands and feet

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39
Q

Investigations of TTP

A 
FBC- RBC and Plt
Blood film
Reticulocyte count
Urinalysis and U and Es
Haptoglobin
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40
Q

What is TTP

A

Thrombotic thrombocytopenic purpura

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41
Q

Define sickle cell disease

A

Autosomal recessive disease in beta chain of Hb resulting in the formation of sickle cell shaped RBCs due to agglutination of Hb

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42
Q

Site of extramedullary haematopoeisis

A

Liver- hepatomegaly

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43
Q

Common symptoms of SCD

A

Painful crises anywhere from legs to chest
Swollen dorsa of hands for feet joints- dactylistis
DUE TO VASO-OCCLUSIVE CRISES

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44
Q

Risk factors for TTP

A

Black
Age 20-50
Stresses on body such as infection, pregnancy and maligancy

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45
Q

What does excessive recycling of haptoglobin bound to Hb lead to

A

Increased unconjugated bilirubin

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46
Q

Acquired immune causes of thrombocytopenia

A

ITP
TTP
AI disorder
Anti phospholipid syndrome

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47
Q

Differentials of thrombocytopenia by category

A

Hereditary
Acquired immune
Acquired non immune

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48
Q

What is living with sickle cell trait like

A

Comfortable- only have problems during hypoxia such as altitude and exercise

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49
Q

What is ITP

A

Immune thrombocytopenic purpura

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50
Q

Symptoms of ITP

A

Any sign of bleeding, normally on legs
No signs of alternative cause such as lymphadenopathy, systemic symptoms or splenomegaly
No drugs which cause thrombocytopenia

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51
Q

What happens to bone in anaemia

A

Increased production of reticulocytes resulting in new bone formation due to medullary expansion

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52
Q

How does medullary expansion appear on examination

A

Enlarged cheeks

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53
Q

What is complication when SCD RBCs occlude pulnmary arteries

A

Acute chest syndrome- blockage results in build up of deoxygenated blood which sets up negative feedback loop as pulnomary arteries constrict in hypoxia

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54
Q

Define ITP

A

Isolated thrombocytopenia in absence of identifiable cause. Involves autoimmune antibody destruction of peripheral platetels. IgG produced by spleen

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55
Q

Which encapsulated bacteria does splenectomy increase risk of

A

Strep pneumoniae
Haemophilus influenzae
Neissera meningitidis
Salmonella

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56
Q

How does medullary expansion appear on head XR

A

“hair on ends” appearance to skull- increased haematopoeisis

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57
Q

Investigations for SCD

A 
Newborn blood spot in a lot of countries
FBC
Blood smear
Protein electrophoresis
Urinalysis
LFTs
Lung function
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58
Q

3 causes of microangiopathic haemolytic anaemia

A

DIC
TTP
HUS

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59
Q

Blood features of DIC

A 
Low Plts
Anaemia
Low fibrinogen
Increased PT/APTT
Increase D-dimer
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60
Q

Blood features of HUS

A

Decreased Hb
Increased Bilirubin
Uraemia
Reduced plts

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61
Q

Hereditary cause of haemolytic anaemia

A

Red cell membrane- hereditary spherocytosis
Enzyme deficiency- G6PD deficiency
Haemoglobinopathy

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62
Q

Acquired causes of haemolytic anaemia

A

Autoimmune
Drugs
MAHA
Infection

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63
Q

What is ALP in myeloma

A

Normal- as plasma cell suppress osteoblasts

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64
Q

What is telengiecstasia

A

Condition which widened venules cause threadlike red lines or patterns on the skin

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65
Q

What is inheritance of hereditary telengiecstasia

A

Autosomal dominant

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66
Q

Where do telengiecstasia occur

A 
Skin
Mucous membranes
Lungs
Liver
Brain
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67
Q

What would most likely cause of microcytic anaemia in patient with high platelets

A

Slow GI bleed

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68
Q

What must you check if patient presents with microcytic anaemia

A

Platelets to see if evidence of bleeding

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69
Q

What does normal RDW suggest

A

There is a homgenous population of RBCs

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70
Q

What does a high RDW suggest

A

Aniscocytosis of RBCs

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71
Q

What causes pernicious anaemia

A

Malabsorption of B12 caused by failure to produce intrinsic factor

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72
Q

Blood finding of pernicious anaemia

A

Macrocytosis

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73
Q

What happens to neutrophils in pernicious anaemia

A

Hypersegmented

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74
Q

How to distinguish anaemia of chronic disease from a mixed picture of B12 and Iron deficiency

A

RDW is normal in ACD but wide in mixed picture

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75
Q

What happens in general malabsorption normally to MCV

A

Is normal as mixture of B12 and iron deficiency however RDW will be skewed as cells all different sizes

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76
Q

What would WCC be in a normal infection

A

Maybe 11-12

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77
Q

What would WCC be in pneumonia

A

15

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78
Q

What would WCC be in sepsis

A

15-25/30 depending on severity

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79
Q

What happens to WCC in malaria

A

Low/normal

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80
Q

Blood findings of malaria

A

Low/normal WCC
Anaemic
Platelet low

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81
Q

How would an immediate transfusion reaction present

A 
Fever
Rigor
Hypotenisve
Tachy
Chest pain
Dark urine
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82
Q

What would present acutely with rigor, fever, hypotenisve, tachy, chest pain and dark urine

A

Immmediate transfusion reaction

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83
Q

What can cause microcytic anaemia

A

IDA

Beta thalassaemia heterozygosity

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84
Q

What can cause IDA

A

Bleed in GI tract

Diet

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85
Q

What could ferritin be in normocytic anaemia

A

Normal or high

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86
Q

What causes normocytic anaemia

A

Chronic disease such as rheumatoid

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87
Q

When would you suspect beta thalassaemia heterozygosity

A

Normal healthy person who presents with very low MCV

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88
Q

Causes of macrocytic anaemia

A 
Alcohol
Myelodysplaisa
Hypothyroid
Liver disease
Fotale/B12 deficiency
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89
Q

Pnemoninc for causes of macrocytic anaemia

A

Alcoholics may have liver failure

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90
Q

Clues for alcoholic macrocytosis

A

History

Raised GGT

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91
Q

Clues for myelodysplasia macrocytosis

A

Pancytopenia

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92
Q

Clues for hypothyroidism macrocytosis

A

Hx

Low T4 High TSH

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93
Q

Clues for liver diseases macrocytosis

A

Hx

Exam

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94
Q

Clues for folate deficiency macrocytosis

A

Hx small bowel disease or gastrectomy

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95
Q

What is pancytopenia

A

Low platelets, WCC and RBC

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96
Q

Presentation of polycythaemia

A 
Pruritus after hot bath
Thromboses
Gangrene
Headache
Choreiform movements
Blurred vision
tinnitus
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97
Q 
What presents with
Pruritus after hot bath
Thromboses
Gangrene
Headache
Choreiform movements
Blurred vision
tinnitus
A

Polycythaemia

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98
Q

Management of SCD painful crises

A

Analgesia
Oxygen
IV fluids
Abx

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99
Q

Management of stroke SCD

A

Blood transfusion

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100
Q

Why does SCD lead to gall stone and chronic cholecystitis

A

Chronic haemolysis

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101
Q

Pnemonic for multiple myeloma

A 
CRAB
Calcium
Renal failure
Anaemia
Bone
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102
Q

Calcium presentation of multiple myeloma

A

Hypercalcaemia- polyuria, polydipsia and constipation

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103
Q

Renal presentation of multiple myeloma

A

Urea and creatinine elevated

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104
Q

Anaemia presentation of multiple myeloma

A

Breathlessness
Lethary
FBC

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105
Q

Bone presentation of multiple myeloma

A

Bone pain

Osteoporosis- fracture

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106
Q

Fractures seen in osteoporosis

A

Neck of femur
Wrist- colles fracture
Vertebral

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107
Q

What are some acute presentations of multiple myeloma

A

Infection

Cord compression

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108
Q

What causes anaemia with high reticulocytes

A

Myelodysplasia
Haemolytic crises
Haemorrhages

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109
Q

What causes anaemia with low reticulocyte count

A

Blood transfusion
Parvovirus B19 infection
Aplastic crises in SCD

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110
Q

What are patients with low reticulocytes normally presenting with

A

Aplastic crisis where not producing enough RBCs

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111
Q

What drug can cause macrocytosis

A

Azathioprine

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112
Q

How does where GI bleed is affect type of anaemia

A

Location- eg distal ileum affects B12 absorption

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113
Q

Microcytic anaemia causes

A

IDA
Thalassaemia
ACD

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114
Q

Normocytic anaemia causes

A

Acute bleed
Aplastic anaemia
Mixed anaemia from crohns

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115
Q

Investigations for microcytic anaemia

A

Haematinics

Hb electrophoresis

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116
Q

Investigations for macrocytic anaemia

A

B12
Folate
DAT test

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117
Q

Diseases that can cause B12 deficiency

A

Pernicious anaemia

Crohns

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118
Q

How can haematological malignancies be split up

A

Lymphoma
Leukaemia
Other

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119
Q

What comes under other in haem malignancies

A

Myeloma
Myelofibrosis
Myelodysplasia
Polycythaemia vera

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120
Q

How are leukaemias split up

A

Lymphoid
Myeloid
Are either acute or chronic

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121
Q

How are lymphomas split up

A

Hodgkins

Non-hodgkins

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122
Q

Similarities between lymphoma and leukaemia

A

Abnormal proliferation of lymphocytes

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123
Q

What is difference between lymphoma and leukaemia

A

The location of abnormalities

Location of leukaemia is in blood but lymphoma in the lymph nodes

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124
Q

Differences between acute and chronic leukaemia in terms of differentiation

A

Abnormal differentiation in acute but normal in chronic therefore mature cells present in chronic but immature in acute

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125
Q

Pathophysiology of hodgkins lymphoma

A

B cell abnormally differentiates within the lymph node leading to neoplasm with exact mechanism unclear but is assocaition with HIV and EBV virus infections

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126
Q

What are cells present in hodgkins lymphoma

A

Hodgkins cells- large undifferentiated B cells

Reed steenberg cells- multinucleated plasma cells joined together

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127
Q

Can hodgkins cells or reed steenberg cells produce ABs

A

No they are “crippled”

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128
Q

What happens in non-hodgkins lymphoma

A

Neoplasm of B or T cells that grow in nodes but DONT have reed steenberg cells

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129
Q

What is most common lymphoma

A

Non-hodgkins

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130
Q

Differences between non hodgkins and hodgkins lymphoma

A

H tends to just affect local nodes within tits group whereas non affects multiple groups and also other organs
H contains reed steenberg cells

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131
Q

Non lymph node effects of non-hodgkins lymphoma

A

Mets anywhere
Spinal chord compression
Bone marrow suppression as crowds out other cells there

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132
Q

What is myeloma

A

Cancer of plasma cells producing excessive monoclonal Igs

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133
Q

Investigations for myeloma

A 
ESR
Calcium
U&E
Renal
Elctrophoresis
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134
Q

Protein electrophoresis findings in myeloma

A

Normally would see polyclonal bands however in myeloma will see one large monoclonal band

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135
Q

Presentation of non-hodgkins lymphoma

A

Painless lymphadenopathy
B symptoms
Pruritus

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136
Q

Obs findings of anaemia

A

Tachypnoea

Tachycardia

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137
Q

What is angular cheilitis

A

Reddening of angles of mouth

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138
Q

Where do you see angular cheilitis in

A

IDA

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139
Q

Categories for IDA causes and examples of each

A

Increased loss- peptic ulcer, cancer, menstruation, IBD
Reduced uptake- coeliac, diet, IBD
Increased need- pregnancy, breastfeeding

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140
Q

To restore iron levels what are best foods to eat

A

Meats as plant based iron harder to absorb

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141
Q

What is most common cause of IDA worldwide

A

Parasitic infection of ascariasis or schistosomiasis

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142
Q

How does chronic disease lead to anaemia

A

Leads to release of cytokines that means hepcidin is upregulated

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143
Q

When hepcidin is upregulated what does this do

A

Reduced uptake via ferroportin
Increased storage in ferritin
Reduced transport via transferrin

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144
Q

Why is ferritin an acute phase protein

A

Logic is that in an infection the bacteria will want to use iron stores so body protects its store

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145
Q

How to differentiate between IDA and ACD

A

TIBC/ transferrin will be reduced in ACD but elevated in IDA

Ferritin will be low in IDA but elevated in ACD or normal

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146
Q

What is TIBC the same as

A

Transferrin

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147
Q

What type of anaemia is ACD

A

Microcytic or normo

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148
Q

Out of beta and alpha thalassaemia which is rarer

A

Alpha

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149
Q

Which disease is SCD and thalassaemia protective against

A

Falciprum malaria

150
Q

Which groups of people often present with thalassaemia

A

Those from malaria belt countries

Cyprus especially

151
Q

On what chromosome do alpha thalassaemias develop from

152
Q

On what chromosome do beta thalassaemias develop from

153
Q

What are the 4 alpha defects in thalassaemia

A

Alpha+
Alpha
Hb H
Hb barts

154
Q

What happens when have alpha + or alpha0

A

Mild anaemias as only missing 1 or 2 alpha genes respectively

155
Q

What happens when have Hb H

A

Missing 3 alpha genes leading to severe anaemia

156
Q

What happens when have Hb Barts

A

Death in utero- hydrops fetalis syndrome where fluid overloaded

157
Q

What are 3 types of beta thalassaemia

A

Beta minor
Beta intermedia- just know exists
Beta major

158
Q

What happens when have beta minor thalassaemia

A

Mild anaemia with very low MCV

159
Q

What happens when have beta major thalassaemia

A

Severe anaemia presenting in early life

160
Q

Difference between alpha and beta thalassaemias in their presentation

A

Beta between 3-6 months
Alpha from birth
Due to that in first few months are synthesising Beta as have lots of HbF still

161
Q

What Hb is elevated in beta thalassaemia

A

HbA2

Alpha and delta to compensate

162
Q

What predisposes to SCD events

A

Hypoxia
Dehydration
Acidosis
Infection

163
Q

Features of SC trait

A

Asymptomatic and resistant to falciprum malaria

164
Q

Mutation leading to SC trait

A

Point mutation of B globin chain Chr 11

Autosomal recessive

165
Q

Causes of microcytic anaemia

A

IDA
Thalassaemia
ACD
SCD

166
Q

Difference in life span between sickle cells and normal RBC

A

10-20 days as opposed to 100 days

167
Q

What are howell jolly bodies

A

Nuclear remnants of RBCs

168
Q

What are howell jolly bodies a marker of

A

Splenic function deteriorating

169
Q

Blood film findings of SCD

A

Sickle cells

Howll jolly bodies if splenic function affected by vaso-occlusive crises

170
Q

Management of SCD crisis

A

Oxygen
Abx
Pain relief
IV fluids

171
Q

Crises caused by SCD and how they are managed

A

Stroke-> transfusion
Splenic sequestration-> splenectomy
Chronic cholecystitis-> cholecystectomy

172
Q

What happens in splenic sequestration

A

As sickle cells need clearing the spleen does this however can remove too many leading to splenomegaly and anaemia from accumulation of cells in spleen

173
Q

Difference in spleen problems with age

A

When younger sequestration a problem however as get older due to recurrent occlusive crises leads to hyposplenism

174
Q

Problems of hyposplenism

A

Susceptibility to infection as an important immune organ- white pulp

175
Q

How is SCD diagnosed

A

Hb electrophoresis

Blood film

176
Q

Complications of SCD

A 
Priapism
Haemolytic anaemia
Aplastic crisis
Acute chest syndrome
Dactylitis
177
Q

Conservative management of SCD

A

Trigger avoidance

Vaccination

178
Q

Medical management of SCD

A

Vaccinations
Hydroxyurea
Prophylactic Abx

179
Q

Surgical management of SCD

A

Bone marrow transplant

180
Q

What ABx is given prophylactically in SCD

A

Penicillin V as gives protection against encapsulated bacteria- meningitis

181
Q

Why are vaccinations given in SCD

A

Infections can trigger crises and hyposplenism

182
Q

Which is replaced first folate or B12

A

B12 due to neurological implications

183
Q

How long do B12 stores last

184
Q

Blood film findings of folate or B12 deficiency

A

Macrocytic anaemia

Hypersegmented neutrophils

185
Q

What causes megaloblastica anemia

A

B12 or folate

186
Q

What are hypersegmented neutrophils seen on blood film of

A

Megaloblastic anaemia

187
Q

What can cause folate but not B12 deficiency

A

Anti-folate drugs

Pregnancy

188
Q

Why doesnt pregnancy cause B12 deficiency

A

B12 stores 3-4 years

189
Q

What causes B12 deficiency but not folate deficiency

A

Pernicious anaemia

Malnutrition

190
Q

Why doesnt malnutrition tend to cause foalte deficiencies

A

In vedgetarians diet there is plenty of folate but not B12 as is normally found in meat

191
Q

What causes both folate and B12 deficiency

A

Alcoholism
Crohns
Coeliac

192
Q

3 ways alcohol causes macrocytic anaemia

A
  1. alcohol itself causes non-megaloblastic anaemia
  2. alcholism leads to poor dietary intake as get calories from alcohol itself
  3. alcohol can affect gut causing malabsorption
193
Q

How long does it take folate sotres to run out

A

3-4 months

194
Q

How does B12 cause neuro sx

A

Needed for building the myelin sheath

195
Q

What is physical examination test for B12

196
Q

What is physical examination test for folate

A

Schillings

197
Q

What antibodies are made in pernicious anaemia

A

Anti parietal cell

Anti intrinsic factor

198
Q

2 ways B12 affects the nervous system

A

Subacute combined degeneration of the chord

Peripheral sensory nerves

199
Q

How does subacute degeneration of spinal chord present due to B12 deficiency

A

Corticospinal tract myopathy

Dorsal column tract- vibration, pressure

200
Q

Who does pernicious anaemia tend to affect

A

60 year olds

201
Q

What presents with bilateral myopathy, dorsal column problems

A

B12 deficiency

202
Q

In exclusively what type of haemolysis does haptoglobin get used up in

A

Intravascular- doesnt happen in extravascular

203
Q

What must be avoided in people with G6PD deficiency

A

Anything that causes oxidative stress like broad beans

204
Q

Blood features of any haemolysis

A

Anaemic
Unconjugated bilirubin high
LDH raised
*haptoglobin low in intravascular

205
Q

What is inheritance of G6PD

A

X linked recessive

206
Q

What are heinz bodies

A

Intracellular inclusions of denatured Hb that are only present during haemolytic anaemia due to oxidative stress

207
Q

Is G6PD the only predisposing enzymopathy to oxidative stress

A

No but just happens to be the most common

208
Q

What are bite cells formed from

A

Previous removal of heinz bodies by spleen

209
Q

What in inheritance of hereditary spherocytosis

A

Autosomal dominant

210
Q

What do you see heinz bodies and bite cells in

A

Oxidative stress leading to haemolysis- most commonly G6PD

211
Q

In which group of people do you see hereditary spherocytosis

A

White northern europeans

212
Q

In hereditary spherocytosis what are people deficient in

A

Beta spectrin or ankyrin which leads to weak cytoskeleton so cells cant maintain biconvex shape

213
Q

What is the osmotic fragility test

A

Give patient hypotonic saline

214
Q

What is result of osmotic fragility test in HS

A

HS cells are more likely to lyse as their cytoskeleton is much weaker

215
Q

What is an aplastic crisis

A

When you fail to only produce red cells

216
Q

What can lead to aplastic crises in HS sufferers

A

Parvovirus B19 infection- invades RBC precursors

217
Q

Why are HS sufferers more prone to aplastic crises

A

HS cells have a lifespan of only 30 days as their shape leaves them very vulnerable to damage in microcirculation

218
Q

What are schistocytes

A

Fragmented RBCs produced after after microangiopathic haemolytic anaemia

219
Q

GI features of Ecoli 0157

A

Abdo pain

Bloody diarrorhoea

220
Q

Triad of HUS

A

AHA
AKI
Thrombocytopenia

221
Q

Pathophysiology of HUS

A

Ecoli 0157 releases toxin that binds to endothelial cells within the kidney and damages them- damaged endothelium leads to platelet plug formation which leads to microthrombi production. These then shear RBCS and cause AKI

222
Q

Examination findings of HUS

A

Jaundice

Conjuctival pallor

223
Q

Pathophysiology of DIC

A

Severe inflammatory response initiated that activates clotting factors everywhere which exhausts platelets and clotting factors. These then break down and lead to MAHA. Also due to exhaustion of clotting factors this predisposes to bleeding

224
Q

Some triggers for DIC

A 
Pancreatitis
Sepsis
Obstetric problems
Cancers
Trauma
Transfusion reaction
225
Q

Signs on examination of DIC

A

Petechiae
Haematuria
Ecchymoses
Jaundice

226
Q

What are ecchymoses

A

Discolouration of skin due to underlying bleeding

227
Q

Examination findings of DIC

A

Jaundice
Conjunctival pallor
Petechiae
Ecchymoses

228
Q

What is main difference between ITP and TTP

A

Autoimmune reaction against platelets in ITP

229
Q

Is TTP coombs positive or neg

230
Q

What is DAT test and what does it show

A

Direct Antiglobulin Test

Shows whether haemolytic anaemia is autoimmune or not

231
Q

What happens in DAT/coombs test

A

Anti-human globulin antibodies are given to blood sample- if antibodies are present against RBC globulin antigen then the RBCs will agglutinate and be postive for autoimmune haemolytic anaemia

232
Q

What drugs cant be used in G6PD

A

Anti-malarials (e.g. primaquine and chloroquine)
Nitrofurantoin
Quinolone antimicrobials (e.g. ciprofloxacin)
Rasburicase
Sulphonamides (e.g. co-trimoxazole)

233
Q

What are risk factors for myelofibrosis

A

Old age

Radiation exposure

234
Q

Physiologically what happens in myelofibrosis

A

Fibroblasts in bone marrow become overactive and proliferate in response to BM cancer which causes a crowding out effect that reduces out put of blood cells

235
Q

What is myelofibrosis classed as

A

Philadelphia chr negative myelodysplasia

236
Q

What are typical cells seen in myelofibrosis on blood film

A

Tear cells also known as dacrocytes

237
Q

What are tear cells seen in

A

Myelofibrosis- could imagine as bm fibrosis squeezes out the cells affecting their shape as they leave

238
Q

What do you see dry tap on aspirate in

A

Myelofibrosis

239
Q

Which 2 conditions classically do you see massive splenomegaly in

A

CML

Myelofibrosis

240
Q

Blood findnigs of myelofibrosis

A

Low WCC, RBC, Hb

High plts

241
Q

How is polycythaemia classified

A

Into secondary and primary

Secondary is in response to a trigger than can either be appropriate or inappropriate

242
Q

How is inappropriate polycythaemia classified

A

Into appropriate and inappropriate

243
Q

Examples of appropriate secondary polycythaemia

A

Response to hypoxia- cyanotic heart disease, altitude, hypoxic lung disease like COPD

244
Q

Example of inappropiate secondary polycythaemias

A

EPO secreting tumour

245
Q

What is primary polycythaemia also called

A

Polycythaemia rubra vera

246
Q

What condition is always JAK 2 positive

A

Polycythaemia rubra vera

247
Q

Physiology of JAK 2 mutation

A

Leads to Polycythaemia rubra vera
EPO is secreted in kidney and binds to JAK 2 receptor on haematopoietic cells which stimuluates red cell production. When its mutated it activates itself rather than by EPO meaning it is a true primary polycythaemia

248
Q

What is polycythaemia rubra vera classed as

A

Philadelphia chr negative myelodysplasia

249
Q

What is an essential thrombocytosis

A

When exclusively platelets are raised

250
Q

What is aquagenic pruritis

A

Skin itching in absence of skin lesions particularly when make contact with water

251
Q

How can polycythaemia rubra vera typically present

A

Asymptomatically but then in older people around 60 get symptoms

252
Q

What are symptoms of polycythaemia rubra vera

A

Due to hyperviscosity of blood

  • stroke
  • headaches
  • lightheadedness
  • gangrene
  • eye problems
  • aquagenic pruritus
253
Q

What leads to aquagenic pruritis in PCV

A

overproduction of histamine

254
Q

Blood findings of PCV

A

High Hb
High haematocrit
Can be thrombocytosis

255
Q

What does electrophoresis show in beta thalassaemia

A

Increase HbA2

256
Q

What does haemoglobin H present with on examination

A

Signs of extreme anaemia

Splenomegaly

257
Q

Blood film findings of haemoglobin H

A

Target cells

Heinz bodies

258
Q

Best test for IDA

A

Serum ferritin (CRP must be normal to be accurate)

259
Q

What do you see schistocytes in

A

Haemolytic anaemia

DIC

260
Q

What do you see spheorcytes in

A

Haemolytic anaemia

HS

261
Q

What do you see target cells in

A

Obstructive jaundice
Liver disease
Haemoglobinopathies
Hyposplenism

262
Q

How do you get target cells in obstructive jaundice

A

Ratio of cholesterol in RBC influenced by bile salts

263
Q

Possible blood transfusion reactions

A 
Tissue related lung injury
Immediate haemolytic anemia
Delayed haemolytic anaemia
IgA deficiency
Febrile non-haemolytic transfusion reaction
264
Q

What happens in tissue related lung injury

A

2-6hrs after transfusion inflammatory process causes sequestration of neutrophils within the lungs and antibodies form against donor white cells which then attack cells in lungs with HLA antigens

265
Q

How does tissue realted lung injury post transfusion present

A

Fever
Hypotension
Cyanosis
Pulmonary oedema

266
Q

In haemolytic reactions to transfusions how does that present

A 
Hyoptension
Tachycardia
N and V
Abdo pain
Loin pain
267
Q

How to differentiate between delayed and immediate haemolytic reaction

A

Within 24 hours or not

268
Q

How does IgA deficiency present after transfusions

A

Bronchospasm
Laryngeal oedema
Hypotension

269
Q

How does febrile non haemolytic anaemia present

A

Fever
RIgors
Discomfort

270
Q

What is von willebrand factor important in

A

Platelet adhesion and factor VIII function

271
Q

Which pathway does von willebrand deficiency affect

272
Q

What is von willebrand disease

A

Deficiency of von willebrand factor

273
Q

Blood findings of VwB

A

Normal PT
PTT longer
Total bleeding time longer
Plt count normal

274
Q

In pernicious anaemia what tends to be MCV

A

Very high- over 120

275
Q

How can blood cancers present

A

Sign of failure of bone marrow- bleeding, infections, anaemia
Recurrent or severe infections
Accumulation of malignant cells
Systemic signs

276
Q

How can blood cancers present in terms of recurrent or severe infections

A

Gram negative septicaemia from neutropenia

Lympoid infections of herpes

277
Q

Examination findings of cml

A

Hepatosplenomegaly

278
Q

Examination findings of CLL

A

Hepatosplenomegaly

Lymphadenopathy

279
Q

How can blood cancers present where pressure obstructs something

A

Lymphoid hyperplasia- liver, appendix, brain, bowel

280
Q

Causes of pancytopenia

A 
B12 deficiency
Aplastic anaemia
Drug toxicity
Radiation
Blood cancer
Mets to bone marrow
281
Q

Difference between core biopsy and excisional biopsy in process

A 
Core
- per cutaneous US guided
- day case
- no wound
Excision
- GA with surgery
- excision scar
282
Q

Uses of core biopsy vs excision biopsy

A

Core is good for non lymphoid matter so can see TB and mets

Excisional can do that as well as lymphoma diagnosis

283
Q

Limitation of core biopsy

A

Can’t use it for lymphatic architecture so limited in lymphoma diagnosis

284
Q

What can myeloma plasma cells do at bone sites

A

Cause bone expansile
Infiltrate the bone marrow
Form soft tissue tumours called plasmacytomas

285
Q

What is name of soft tissue tumours formed in myeloma

A

Plasmacytomas

286
Q

What can myeloma plasma cells produce

A

Monoclonal IgA and IgG

Monoclonal kappa and lamda light chains

287
Q

What is found in urine of myeloma

A

Urine monoclonal light chains called bence jones protein

288
Q

What are bence jones proteins

A

Monoclonal light chains in the urine or blood of myeloma

289
Q

What is a paraprotein

A

Intact monoclonal antibody

290
Q

What does SFLC stand for

A

Serum free light chain

291
Q

What is immune paresis

A

When due to mass production of paraprotein in myeloma the other Igs are decimated

292
Q

Bone presentation of myeloma

A 
Normally proximal bones affected 
Pain
Osteolytic lesions
Osteopenia
Easy fractures
293
Q

Difference between prostate met and myeloma lesion

A

Prostate mets will have osteosclerosis in area around the lesion but myeloma lesions just a punched out lesion

294
Q

Risk factors for myeloma

A

Black
Male
Elderly

295
Q

Two types of bone biopsy

A

Aspirate- liquid bone marrow

Trephine- whole cut

296
Q

Common sources of mets to bone marrow

A

Melanoma

Stomach adenocarcinoma

297
Q

What is diaphoresis

A

Xs sweating

298
Q

Sx of malaria

A

Cyclical fevers
Diaphoresis
Chills
Headache

299
Q

How does malaria present on blood film

A

Ring form of parasite within blood cell

300
Q

What are 4 main forms of plasmodium parasite

A

Falciparum
Malariae
Ovale
Vivax

301
Q

Which plasmodiums are relapsing

A

Ovale

Vivax

302
Q

Management plan for someone with IDA

A

Oral iron supplementation

If Hb doesnt improve move to IV supplement in forms of ferrous sulphate/fumarate

303
Q

What is initial blood cell in process

A

Pluripotent haematopoeitic stem cell

304
Q

Products of pluripotent haematopoeitic stem cell

A

Common myeloid progenitor

Common lymphoid progenitor

305
Q

Products of small lymphocyte

A

T lymphocyte

B lymphocyte

306
Q

Products of common lymphoid progenitor

A

Small lymphocyte

NK cell

307
Q

What do B cells divide into

A

Plasma cells

308
Q

Products of common myeloid progenitor

A

Myeloblast
Eryhtocytes
Megakaryocytes
Mast cells

309
Q

What do myeloblasts differentiate into

A

Neutorophils
Basophils
Eosinophils
Monocytes

310
Q

What cells are AML and CML neoplasms from

A

Myeloblasts

Myeloid progenitor cell

311
Q

What cells are ALL neoplasms from

A

Common lymphoid progenitor cell

312
Q

What cells are CLL neoplasms from

A

Small lymphocytes

313
Q

Where do essential thrombocytopenias arise from

A

Megakaryocytes or thrombocytes

314
Q

Blood findings of myeloma

A 
Raised ESR
Anaemia
Hypercalcaemia
Raised creatinine
Pancytopenia
315
Q

What does raised ESR suggest physiologically

A

Increased proteins in the blood

316
Q

How can you get headaches, blurred vision and SOB in myeloma

A

Due to hyperviscosity of blood from increased proteins

317
Q

What can cause spinal chord compression in myeloma

A

Plasmacytoma

Vertebral body collapse

318
Q

Differential to consider when have renal impairment and hypercalcaemia

A

Prostate mets

Myeloma

319
Q

What is a myeloproliferative disorder

A

Where is neoplasm of myeloid pathway where all cells tend to elevated- name determined by what cell line predominates

320
Q

Name of myeloproliferative disorder when RBC line predominates

A

Polycythaemia vera

321
Q

Name of myeloproliferative disorder when plt line predominates

A

Essential thrombocytosis

322
Q

Name of myeloproliferative disorder when granulocyte line predominates

A

CML

Can be divided further if one cell predominates- ie eosinophilic leukaemia

323
Q

FBC findings of myelofibrosis

A

Anaemia

Can be panctopenic or all elevated

324
Q

What is Hct in polycythaemia vera

325
Q

How can polycythaemia vera present with low MCV

A

Become iron deficient as use it all up

326
Q

Weird causes of PCV

A

Polycystic kidney disease

Hepatocellular carcinoma

327
Q

What would exclude a peptic ulcer from IDA cause on gastroscopy

A

Clean based

No vessel present in the ulcer

328
Q

What infection in children can give marked lymphocytosis

A

Whooping cough- bordetella pertussis

329
Q

Who is CLL very common in

A

Elderly- normally picked up incidentally

330
Q

Signs on examination of CLL

A

Lymphadenopathy

Hepatosplenomegaly

331
Q

Presentation of CLL

A

Weight loss
Lymphocytosis
Lymphadenopathy
Hepatosplenomegaly

332
Q

Difference between warm and cold AIHA in terms of COOMBS

A

In warm COOMBs is positive at temp eaual to or above 37C(body temp)
Cold COOMBs happens at temps below that

333
Q

Difference between warm and cold AIHA in terms of physiology

A

Warm- IgG, complement cant be activated, extravascular

Cold- IgM, complement activated, intravascular

334
Q

What are the proportions of AIHA

A

Extravascular- 70
Intravascular- 20
Drug- 10

335
Q

How can warm AIHA be classified

A

Primary

Secondary- SLE, CLL

336
Q

Causes of cold AIHA

A

Post infection

Lymphoproliferative conditions

337
Q

Common post infection causes of AIHA

A

CMV
Mycoplasma
EBV

338
Q

What condition are auer rods seen in

339
Q

What is the translocation in APML

340
Q

What is APML

A

A subtype of AML which results in proliferation of promyelocytes

341
Q

What is most worrisome complication of APML

342
Q

What is translocation of CML

A

9;22 -> philadelphia chromosome

Present in 95% of CML cases

343
Q

Blood count findings of CML

A

Elevated WCC
Basophils
Neutrophils
Hypercellular bone marrow

344
Q

What cancer does a latent EBV infection lead to

A

Burkitts lymphoma

345
Q

How to describe splenomegaly in EBV

346
Q

Thalassaemia on examination

A

Massive splenomegaly

347
Q

What are elliptocytes

A

Oval shaped red cells

348
Q

What are pencil cells

A

Hypochromic elliptocytes

349
Q

What do pencil cells occur in

350
Q

What do elliptocytes occur in

A

IDA

Hereditary elliptocytosis

351
Q

What happens if take anti malarial in G6PD

A

Oxidative stress- SOB, pallor and bloody urine

352
Q

What is stain used to differentiate between AML and ALL

A

Sudan black

353
Q

Test used to diagnose SCD

A

Sodium metabisulphate

354
Q

How to differentiate depressive dementia and frontotemporal dementia if has change in hobbies

A

With this could be either but fronto temporal will have speech changes too

355
Q

Symptoms of frontotemporal dementia

A

Change in personality

Dysphasia

356
Q

Step wise decline in cogntion

A

Vascular dementia

357
Q

Which clotting factors are made by the liver

A

II. VII, IX, X- all Vit K dependant

358
Q

Why when on warfarin does patient go through initial pro thrombotic stage

A

Because protein S and C are also vit K dependant and get affected first

359
Q

Which pathway does heparin affect

360
Q

Which pathway do haemophilias affect

361
Q

When are packed red cell transfusions indicated

A

Catastrophic haemorrhage
Hb less than 70 with signs of compromise- syncope, dyspnoea, tachy
Hb less than 80 with known ischaemic heart disease and severe resp disease

362
Q

What is target Hb for transfusions

A

Above 70 as risk of complications from too many is too great

363
Q

What is most common coagulopathy causing DVTs in young people

A

Factor V leiden

364
Q

What are coagulopathys causing prothrombotic states

A

Factor V leiden
Protein S deficiency
Protein C deficiency
Antithrombin deficiency

365
Q

Symptoms of VwB disease

A

Easy brusing

Epistaxis

366
Q

Triad for B12 deficiency

A

Weakness
Glossitis
Fatigue

367
Q

How much does 1 unit of packed red cells increase Hb

368
Q

What is FFP used for

A

Corrects clotting factors- DIC eg

369
Q

Early complications of transfusion

A 
Anaphylaxis
Transfusion association lung injury
Febrile non-haemolytic reaction
Acute haemolytic reaction
Bacterial infection
370
Q

Late complications of transfusion

A

Delayed haemolytic reaction
Infection
Iron overload

371
Q

What is paroxysmal cold haemoglobinuria

A

Haemolysis triggered by cold such as washing hands and drinking cold water

Year 3 Conditions (33 decks)

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