Haematology Flashcards

(144 cards)

1
Q

What causes urticaria?

A

IgE reacting with foreign material

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2
Q

Approaching urticaria reaction to blood transfusion

A

Slow transfusion rate and give antihistamine

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3
Q

Approaching anaphylactic reaction to blood transfusion

A
ABCDE 
Stop infusion 
Oxygen 
IM adrenaline 
IV hydrocortisone 
IV fluids
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4
Q

Microcytic anaemia causes

Stop Those Incy Little Cells

A
Sideroblastic 
Thalasaemia 
Iron deficiency 
Lead poisoning 
Chronic disease
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5
Q

Normocytic anaemia causes

Medium Red Blood Cells

A

Marrow failure
Renal failure
Blood loss
Chronic disease

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6
Q

Macrocytic anaemia causes

FAT RBCs

A
Folate deficiency 
Alcohol 
Thaimine deficiency 
Reticulocytosis 
B12 deficiency
Cytotoxic drugs and Cirrhosis  
Smoking
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7
Q

Symptoms of anaemia

A
Lethargy 
Headaches 
SOB 
Palpitations 
Angina
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8
Q

Blood tests in anaemia

A
FBC
U&E
LFTs
CRP 
Blood film 
Haematimics
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9
Q

Further tests in anaemia

A

BMB

GI endoscopy

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10
Q

Three causes of iron deficiency anaemia

A

Lack of intake
Malabs
Loss

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11
Q

Causes of lack of iron intake

A

Diet

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12
Q

Causes of malabsorption of iron

A

Coeliac disease

Gastrectomy

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13
Q

Causes of iron loss

A

GI bleed - upper / lower - Ca / Inflam / Infection / Ulcer

Menstruation

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14
Q

Specific clinical signs of iron deficiency anaemia

A

Spooning of nails
Angular stomatitis
Glossitis

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15
Q

Side effects of iron therapy

A

Black stools, change in bowel habits, abdo pain, nausea

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16
Q

Iron replacement therapy - aim for rise in Hn

A

2g/dl every 3 weeks

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17
Q

3 causes of B12 deficiency anaemia

A

Lack of intake - diet

Malabsorption - pernicious anaemia, gastrectomy

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18
Q

Neurological complications of B12 deficiency

A

Subacute combined degeneration of the cord - weakness, ataxia and paraplegia

Peripheral neuropathy

Parasthesia

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19
Q

Treatment of B12 deficiency

A

Injections of B12 - will not fix the cord degeneration

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20
Q

4 cause of folate deficiency

A

Increased requirement - preganancy
Insufficient intake - diet
Malabsorption - crohns, coeliac
Drugs - methotrexate

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21
Q

Extra tests if suspect folate deficiency

A

Jejunal biopsy - look for coeliac disease

BM aspirate

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22
Q

What does folate deficiency often come with?

A

Vit B12 deficiency

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23
Q

Where are RBC destroyed extravascularly in haemolytic anaemia (4)

A

Spleen
Marrow
Liver
Phagocytes

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24
Q

Two classifications of reticulocytosis

A

Intravascular and extravascular

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25
3 types of cellular defects causing haemolytic anaemia
Metabolic - pyruvate kinase Cell membrane - hereditary spherocytosis Hb dysfunction - thalassaemia, sickle cell
26
Immune causes of haemolytic anaemia (2)
autoimmune | drug induced
27
Non immune causes of heamolytic anaemia
``` heart valves DIC Drugs Toxins Infections Renal / Liver disease ```
28
target cell may indicate
thalassaemia
29
Heiz bodies are
fragments of Hb
30
Clinical features of haemolytic anaemia (5)
``` Splenomegaly Jaundice Dark urine Pallor Pigment gallstones ```
31
Hereditary spherocytosis inheritance type
autosomal dominant
32
Thalassaemia inheritance type
autosomal recessive
33
How many genes affected in hydrop fatalis?
4
34
How long does beta thalassaemia major take to become symptomatic from birth? and why does it take that long?
3-6 months as the fetal Hb is no longer made
35
What can be currative in beta thalassaemia?
bone marrow transplant
36
main way thalassaemia is treated?
blood transfusions
37
inheritance of sickle cell
autosomal recessive
38
4 types of sick cell crisis
Vaso occlusive Aplastic Haemolytic Visceral sequestration
39
Blood test in suspected sick cell crisis
``` RBC U&E LFTs Bilirubin LDH ABG ```
40
Bed side tests in suspected sick cell crisis
Urine analysis Sputum analysis Blood culture
41
Further test in sickle cell crisis
Blood film
42
Acute treatment of sick cell crisis
``` ABCDE Fluids Pain relief Antibiotics if infection +/- blood transfusion ```
43
Prevention of a sickcell crisis
Vaccinations Penicillin Avoid triggers
44
Test to detect antibodies again RBC
Indirect Coombs
45
In Acute thrombocytopenic purpura what do the autoantibodies target?
antigens on platelet surface
46
Clinical features of Acute thrombocytopenic purpura
Epistaxis Brusing under the skin Menorrhagia Gingivitis
47
At what platelet level should Acute thrombocytopenic purpura be treated?
<30
48
How should Acute thrombocytopenic purpura be treated?
Steroids and immunoglobulin infusion
49
Haemophilia A is due to a deficiency in? Haemophilia B is due to a deficiency in?
factor 8 factor 9
50
In haemophilia - blood result APTT PT vWF
elongated normal normal
51
Treatment of: Haemophilia A Haemophilia B
desmopressin and factor 8 factor 9
52
vWD - blood results APTT PT Factor 8 vW factor
Elongated Normal reduced decreased
53
Treatment of VWD
vWF concentrate vasopressin infusions cyroprecipitate FFP
54
DIC =
pathological activation of coagulation results in bleeding and microvascular thrombosis
55
Causes of DIC
``` Infection Malignancy Obstetrics Anaphylaxis Liver disease ```
56
Blood results in DIC APTT PT TT Fibrinogen
Raised Raised Raised Lower
57
Why is there bleeding in DIC ?
Depletion of platelets and clotting factors due to lots of clots being made systemically
58
DVT For those likely to have a DVT (Wells >2), what test should be done? For those unlikely to have a DVT (Wells >2), what test should be done?
Duplex scan D dimer
59
Minimum length of anticoagultant treatment after DVT
3 months 6 months if unprovoked
60
Primary causes of thrombophilia
Protein S/ C deficiency Antithrombin III deficiency Factor V leiden
61
Secondary causes of thrombophilia
``` Malignancy Immobility Major surgery OCP Smoking Pregnancy APS ```
62
Two types of lymphoma
Non hodgkins lymphoma | Hodgkins lymphoma
63
3 places lymphadenopathy can be found in lymphoma
Cervical Axilla Inguinal
64
Types of cells found in Hodgkins lymphoma
Reed-Sternberg cell
65
Which virus is associated with Hodgkins lymphoma
EBV
66
Main presentation of NHL
Painless lymphadenopathy
67
Leukaemia pathophysiology
Increase in no. of non functional haemopoietic blood cells produced by bone marrow
68
Action of leukaemia cells on the bone marrow
Suppress production of normal cells
69
Common leukaemia in children
ALL
70
Symptoms in leukaemia due to BM supression
Anaemia Bruising / bleeding Susceptible to infections
71
White blood cells raised in CLL
lymphocytes
72
WBC cells raised in CML
Neutrophils and metamyelocytes
73
ALL predominant cell type
immature lymphoblastic cells
74
Chromosomal defect associated with ALL
Philidelphia
75
Pathology of CLL
Uncontrolled poliferation and accumulation of mature non-functional peripheral lymphocytes
76
What is seen on a CLL film
Smudge cells (mature lymphocytes which are fragile)
77
Which WBC cells are class as "myeloid"
Eosinophils, neutrophils and basophils
78
In AML what do the blasts infiltrate
Mainly bone marrow Also liver, spleen, skin and gums
79
Main causes of AML
``` Radiation Chemo Transformation from myelodysplastic syndromes Down's syndrome Fanconi anaemia ```
80
Presentation of AML
Splenomegaly Hepatomegaly Lymphadenopathy Bone pain
81
Type of anaemia in AML
Normocytic and normochromic
82
Blood test results in AML ``` RBC WBC Platelets Urate LDH Calcium ```
Decreased Decreased (increase blasts) Platelets - decrease Urate / LDH / Calcium - increase
83
Other tests than bloods in AML
Blood film Bone marrow Cytogenic / molecular analysis
84
CML =
chronic accumulation of basophils, eosinophls and neutrophils
85
CML can transform to?
AML - 60% | ALL - 60%
86
90% with CML have?
Philadelphia chromosome
87
Blood test results in CML ``` FBC WBC Platelets Urate LDH Vit B12 ```
``` Decrease Increase Increase Increase Increase Increase ```
88
other tests than blood tests in CML
Bone marrow
89
Main lifelong treatment in CML
Imatinib
90
Paraproteinaemias =
presence of monoclonal immunoglobulins in the blood
91
Bence jones =
monoclonal light chains
92
Paraproteins can be three things
Whole immunoglobulins Heavy chains Light chains (bence jones)
93
Light chains can be found in?
the urine (filtered out by the kidneys)
94
Multiple myeloma =
malignant proliferation of plasma cells of the bone marrow.
95
What do the multiple myeloma cells release? As a result what is suppressed?
monoclonal immunoglobulins normal immunoglobulin function suppressed
96
Presentation of patients with multiple myeloma
``` gets regular infections pathological fractures renal failure hyperviscosity symptoms - epistaxis, visual disturbances, headaches and confusion hypercalcaemia pancytopenia SCC? ```
97
how is bone weakened in multiple myeloma
neoplastic cells produce osteoclastic activating factors, increases osteoclast activity, weakening bone
98
What is found on blood film in multiple myeloma
rouleaux formation
99
Other tests in multiple myeloma
electrophoresis - monoclonal paraprotein band bone marrow - can qualify the paraprotein
100
What is found on x-ray in multiple myeloma
pepper pot skull - osteolytic lesions in skull
101
treatment for myeloma
Supportive - bisphosphonates - AB - pain relief - watch out for cord compression - plasmapheresis - chemo - radio for bone pain
102
how to treat hyperviscosity in myeloma
plasmapheresis
103
myelopoliferative disorders =
overproduction of one or more of the early cell lines in the bone marrow
104
essential thrombocytosis =
increase in the number of platelets | often abnormal platelets so don't work properly
105
Clinical features of thrombocytosis
Asymptomatic BUT - VTE - Bleeding - esp GI - Bruising - CV symptoms - weight loss - puritis - sweats
106
Causes of secondary thrombocytosis
Iron deficiency Chronic bleeding trauma Inflammation
107
Polycythaemia =
increase in RBCs in the blood
108
cause of primary polycythaemia =
Due to a malignant myelopoliferative disorder
109
another name for primary polycythaemia =
polycythaemia rubra vers
110
cause of secondary polycythaemia =
increased erythropoietin production - chronic hypoxia - lung / heart disease, high altitude - inappropriate erythropoietin production - renal / lung disease
111
Presentation of polycythaemia ruba vera
``` erythemaa facial plethora tiredness gout arterial / venous occulsive event hyperviscosity symptoms ```
112
mutation in 92% of polycythaemia ruba vera
JAK2
113
Blood test results in PRV ``` Hb Packed cell vol RBC WBC Platelets ```
All increased
114
tests in PRV
FBC ABG CXR Renal US
115
Treatment of PRV
Venesection Aspirin Reduce risk factors for arterial / venous thromboembolism
116
myelofibrosis
fibrosis of the marrow due to hyperplasia of megakaryocytes (platelet precursor). leads to bone marrow failure.
117
what typically causes purpura?
low platelets
118
Two differentials to investigate in children with purpura?
meningococcal septicaemia or acute lymphoblastic leukaemia
119
Henoch-schonlein purpura is what type of vasculitis?
IgA mediated small vessel vasculitis
120
Hb level for transfusion in most patients
< 70 g/L aim (70 - 90)
121
Hb level for patients with ACS
< 80 aim (80 - 100)
122
Platelet transfusion should be | given?
Patient is actively bleeding and thrombocytopenia < 30 x10(9)/ L
123
What is in the first blood pack in the massive haemorrhage protocol
4 x blood | 4 x FFP
124
products to be given in initial ressus of a major haemorrhage
1:1 | FFP and blood
125
Non urgent blood transfusion given over?
2-3 hrs
126
When should observations be done on a patient who's having a blood transfusion?
0, 15mins and 30 mins
127
Factor V leiden =
activated protein c resistance - Factor V is inactivated much more slowly by protein C
128
Treatment of venous reflux disease
Conservative - compression stockings | Surgical - ligation and striping
129
Virchow's triad
Venous stasis Hypercoagulation Vascular injury
130
Thrombotic risk reduces peri surgery
compression stockings early mobalisation LMWH
131
define varicose viens
dilated subcut vein with reversed blood flow
132
Risk factors for venous valve reflux
FH Pregnancy Obesity Occupation
133
Cause of lipodermatosclerosis
chronic venous hypertension leads to subcut fat becoming fibrotic
134
saphina varix =
dilation of saphenous vein at its junction with the femoral vein in the groin
135
What does heparin activate and what does it inhibit?
Antithrombin III Forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa
136
What does LMWH activate and what does it inhibit?
Antithrombin III Factor Xa only
137
Monitor 1) heparin with? 2) LMWH with?
Activated partial thromboplastin time (APTT) Anti-Factor Xa (although routine monitoring is not required)
138
How often are Vit B12 injections given?
every 3 months
139
Venous thromoboembolism - length of warfarin treatment
provoked (e.g. recent surgery): 3 months | unprovoked: 6 months
140
antidote for dabigatran
Idarucizumab is a reversal agent for dabigatran
141
Types of Hodgkins Lymphoma
Nodular schlerosing - most common, "fibrotic bands" present Lymphocyte rich - Reed-Steinburg cells and small lymphocytes Mixed cellularity - Reed-Steinburg cells, mixed infiltrate
142
Investigations in Lymphoma
FBC Blood film Chest x-ray Lymph node BIOPSY
143
Follow up investigations in unprovoked DVT
May be concerned about cancer - Full hx and physical - chest x-ray - set of bloods including calcium Consider Abdo-pelvis CT (and mammogram in women) if >40 If concerned about thrombophillia ie first degree relative with unprovoked DVT/PE too - could check for this then as well
144
Wells score in PE meaning a CTPA is done straight away
4 or more