Year 3: Haematology Flashcards
Everything you need to know to pass for Haematology in Dundee Medical School (300 cards)
1
Q
Reduced amount of Hb in blood
A
Anaemia
2
Q
Too much Hb in blood
A
Polycythaemia
3
Q
Reduced platelets in blood
A
Thrombocytopenia
4
Q
Too many platelets in blood
A
Thrombocytosis
5
Q
Too much iron in blood
A
Haemochromatosis
6
Q
Circulating iron
A
Transferrin
7
Q
Stored iron
A
Ferritin (in the liver)
8
Q
Functional iron
A
Hb
9
Q
Haematocrit
A
% of Hb in blood
10
Q
The production of cells derived from pluripotent stem cells
A
Haematopoiesis
11
Q
The two lineages of a multipotential haematopoietic stem stell (Haemocyoblast)
A
Left: Common Myeloid Progenitor
Right: Common Lymphoid Progenitor
12
Q
Extended lineage of the myeloid family
A
- Megakaryocyte
- Erythroblast
- Mast Cell
- Myeloblast
13
Q
A megakaryocyte becomes
A
Thrombocytes (Platelets)
14
Q
A myeloblast gives lineage to?
A
- Basophil
- Neutrophil
- Eosinophil
- Monocyte
15
Q
An erythroblast gives rise to an
A
Erythrocyte (RBC)
16
Q
A monocyte becomes
A
Macrophage
17
Q
Extended lineage of the lymphoid family
A
- Natural Killer cell (NK)
- Small lymphocyte
18
Q
A small lymphocyte becomes
A
- T cell lymphocyte
- B cell lymphocyte
19
Q
A B cell lymphocyte becomes
A
Plasma cell
20
Q
- Segmented nucleus
- Neutral staining granules
A
Neutrophil
21
Q
- Bi-lobed nucleus
- Bright orange granules
A
Eosinophil
22
Q
- Large deep purple granules (containing histamine)
- Associated with IgE
A
Basophil
23
Q
- Single large nucleus
- Faintly staining granules
- Vacuolated
A
Monocyte
24
Q
- Large nucleus
- Rim of cytoplasm
A
Lymphocyte
25
Neutrophils usually indicated
Bacterial infection
26
Lymphocytes usually indicate
Viral infection
27
Eosinophils usually indicate
* Allery/ Atopy
* Parasitic infection
28
Basophils can indicate
* Polycythaemia Rubra Vera
* Chronic myeloid Leukaemia
29
Granular leukocytes
WBC that contain granules
* Neutrophils
* Basophils
* Eosinophils
30
Agranular Leukocytes
WBC that contain a single nucleus and have few/no granules
* Monocytes
* Lymphocytes
31
The process of producing RBCs
Erythropoiesis
32
Haemoglobin is made out of
* Haem (porphyrin ring and Fe2+)
* Globins
33
Adult Haemoglobin: HbA
* 2 x Alpha chain globins
* 2 x beta chain globins
97% of Hb
34
Variant of adult haemoglobin: HbA2
* 2 x alpha chain globins
* 2 x delta chain globins
2.5% of Hb
35
Foetal haemoglobin: HbF
* 2 x alpha chain globins
* 2 x gamma chain globins
0.5% of Hb
However is very high in foetus and 1st year of life
36
Haemoglobin life span
120 days
37
Thrombocyte life span
7-10 days
38
Neutrophil life span
7-8 hours
39
Haematopoiesis in an embryo takes place in
* Yolk sac (until week 10)
* Liver (starts week 6)
* Bone Marrow (starts week 16)
40
Haematopoiesis at birth takes place in
* Bone marrow
* Liver
* Spleen
41
Haematopoiesis in an adult takes place in
Bone marrow of:
* Skull
* Ribs and sternum
* Pelvis
* Proximal femur
42
As you get older your bone marrow turns from red to
Yellow ( as it's more fatty)
43
What anatomical landmark do you aim for when taking a bone marrow biopsy
Posterior Superior Iliac Spine
44
Describe how erythropoiesis begins
1. Interstitial fibroblasts and the proximal tubule in the kidney sense hypoxia
2. The kidneys produce erythropoietin (EPO)
3. EPO then stimulates the bone marrow to produce more RBCs
4. The increase in O2 levels in the blood causes EPO levels to drop
45
What is needed for erythropoiesis to take place
* Globins - from amino acids
* Haem - from iron stores
* B12
* Folate
Stimulation by EPO
46
What is the end cell produced in erythropoiesis
Reticulocyte (an immature RBC)
47
What is the maturation stages of a RBC
1. Pronormoblast
2. Early normoblast
3. Intermediate normoblast
4. Late normoblast
5. Reticulocyte
6. Erythrocyte
48
Hypersegmented nucleus in a neutrophil
| (~7-9 segments)
This usually means macrocytic anaemia
(Due to an inefficient breakdown of cell)
49
An erythroblast contains
A nucleus
50
Reticulocytes contain
RNA
Hence why they are polychromatic
51
Reticulocytosis happens
In episodes of acute blood loss or haemolytic anaemia
The bone marrow produces RBCs rapidly, to compensate, hence why they are still immature reticulocytes
52
The destruction and breakdown of RBCs
Haemolysis
53
Site of haemolysis
Spleen
54
Describe Haemolysis
* RBCs are taken out of the circulation by macrophages and taken to the liver
* Iron is taken to iron stores (becoming ferritin)
* Porphyrin becomes unconjugated bilirubin and is taken to the liver to become conjugated
* Globulin chains are recycled into amino acids
55
During haemolysis, globulins are recycled as
Amino acids
56
During haemolysis, Fe2+ is
Recycled to iron stores
57
During haemolysis, the porphyrin ring is broken down into
bilirubin
58
Haemolysis causes
Haemolytic anaemia due to loss of RBC
59
Signs of haemolysis
* Spherocytes in blood film
* Reticulocytes
* Jaundice
* Fatigue
60
Two types of haemolytic anaemia
* Extravascular
* Intravascular
61
Extravascular haemolysis
happens in the liver and spleen by macrophages
62
Intravascular haemolysis
happens in the circulation
63
Examples of Extravascular haemolysis
* Liver disease
* Hypersplenism
64
Signs of extravascular disease
Bilirubinuria (dark yellow urine)
65
Examples of intravascular haemolysis
* HBO transfusion reaction
* G6PD deficiency
* Malaria
* Prosthetic valve
* Paroxysmal nocturnal haemoglobinuria
* Autoimmune Haemolytic anaemia
66
Signs of intravascular haemolysis
Haemoglobinuria
"Pink urine, black on standing"
67
2 types of autoimmune haemolytic anaemia
* Warm
* Cold
68
Warm autoimmune haemolytic anaemia is a
Delayed reaction
69
Cold autoimmune haemolytic anaemia is an
Immediate reaction
70
IgG is involved in
Warm autoimmune haemolytic anaemia
71
IgM is involved in
Cold autoimmune haemolytic anaemia
72
Causes of Warm autoimmune haemolytic anaemia
* Autoimmune disorders (SLE)
* Chronic lymphocytic leukaemia (CLL)
* Infections
* Drugs (penicillin)
73
Causes of cold autoimmune haemolytic anaemia
* Infections (EBV, mycoplasma)
74
Direct Coomb's Test
Detects antibodies on the RBC surface
Is used to narrow down the cause of haemolysis
75
Positive Direct Coomb's Test
* Autoimmune haemolytic anaemia
* Drug-induced haemolytic anaemia
* Haemolytic disease of the newborn
76
Heinz bodies indicate
G6PD Deficiency Haemolytic Anaemia
77
Pathophysiology of G6PD deficiency
a defect in glucose-6-phosphate dehydrogenase causes red blood cells to break down prematurely
78
Pathophysiology of Paroxysmal Nocturnal Haemoglobinuria
Your body thinks your blood is foreign and so it destroys it
79
Symptom of Paroxysmal Nocturnal Haemoglobinuria
Peeing blood
80
Polycythaemia Rubra Vera
A myeloproliferative neoplasm which causes the bone marrow to produce too many red blood cells
81
Polycythaemia RV is usually due to a default in
JAK 2 gene
82
Polycythaemia RV presents with
* Itch (after hot bath)
* Patient looks red
* DVT
* Splenomegaly
* Gout
* Headache
83
Treatment for Polycythaemia RV
* Hydroxycarbamide (marrow suppression)
* Venesection
84
Presentation of haemochromatosis
* Liver disease
* Heart problems
* Bronzing of the skin
* Diabetes (iron deposition kills islet cells)
* Arthritis
85
Types of Haemochromatosis
* Primary
* Secondary
86
Primary Haemochromatosis
Inherited
(decreased hepcidin, so the channels for iron release in the gut open more often, so iron is in serum)
* High Transferrin (\>50%)
* High Ferritin (\>200 (F), \>300 (M))
Gradual increase, and so present in their 40s
Causes end-organ damage
87
Secondary Haemochromatosis
More acute
Too many blood transfusions (so iron overload)
88
Iron in cells can be detected by
Perl Staining Prussian Blue
89
Treatment for Primary haemochromatosis
Weekly Venesection in aim of exhausting iron stores
90
Treatment of Secondary Haemochromatosis
Desferrioxamine (Iron-chelating drugs)
91
Erythropoiesis
The production of RBCs
92
Mechanism of Erythropoiesis
1. Hypoxia is sensed by the proximal tubule in the kidneys
2. Kidneys produce erythropoietin
3. Erythropoietin stimulates RBC production in the bone marrow
93
Role of folate
* Converts uridine to thymidine
* Needed for DNA synthesis
94
Daily requirement of Folate
Adult: 200 micrograms
Pregnant Women: 400 micrograms
Diabetic Pregnant Women: 5mg
95
Body store of Folate
4 months
96
Folate absorption takes place in
Duodenum and jejunum
"Coz DJs stay up fo-late playing music"
97
Folate deficiency is often seen in
Malnourished (e.g. alcoholics)
98
Role of B12
Is needed to make DNA, RNA, proteins due to S-adenosylmethionine synthesis
99
Daily requirement of B12
1.5 micrograms
100
B12 body stores last
2-4 years
101
B12 absorption takes place in
Ileum
"Because vegans lack B12 and they are ill"
102
Symptoms of B12 deficiency
* Sore tongue "glossitis"
* Neurological problems as B12 is associated with myelin development
103
Don't prescribe folate without
B12 (in healthy people) as it will cause spinal cord problems (due to myelin interaction)
104
Iron absorption is regulated by
Hepcidin
Inhibits iron transport, and so regulates iron
* High hepcidin: iron accumulated
* Low hepcidin: iron exported
105
Iron absorption takes place in
Duodenum
"Because you need to iron your denum jeans"
106
Daily requirement of Iron
* Men: 8.7mg
* Women: 14.8mg
107
Chronic disease and inflammation causes
Increased hepcidin (due to IL6 and macrophages)
Which causes:
* Decrease in iron absorption release, and this leads to microcytic anaemia
108
Glucose-6-phosphate dehydrogenase "G6PD" pathway is responsible for getting rid of
H2O2 free radicals
Converts NADP+ to NADPH
109
What converts Fe3+ to Fe2+
NADH
110
Microcytic anaemia
* Low Hb
* Low MCV (size of RBC)
Hypochromic RBCs
111
Causes of microcytic anaemia
* Iron related: GI bleed, Period related, Chronic disease
* Porphyria related: lead poisoning
* Globulin synthesis: Thalassaemia
112
Chromosome associated with Alpha Thalassaemias
16
113
Chromosome associated with Beta Thalassaemias
11
114
2 types of thalassaemia
* Alpha
* Beta
115
Types of Alpha thalassaemias
* a+/a (3 alpha globulin)
* a0/a+ (1 alpha globulin) = HbH (3/4 betas)
* a0/a0 (0 alpha globulin) = Major: Hb Barts (4 gammas)
116
HbH presentation
* Jaundiced
* Splenomegaly
* "Golf ball occlusions" on blood film
* Common in South East Asians
117
Presentation of Alpha thalassaemia major (Hb Barts)
* Barts Hydrops Fetalis
* Usually always stillborn
* Oedema and hypoxic tissues
118
2 types of Beta thalassaemias
* Trait (b+/b) or (b0/b) = 3 or 2 betas
* Major (b0/b+) or (b0/b0) = 1 or 0 betas
119
Beta Thalassaemia Trait
* Increased HbA2
As 2 alpha, 2 delta chains involved
120
Beta Thalassaemia Major
* HbA2 or HbF
* Presents 6-24 months (due to loss of HbF), failure to thrive
* Extramedullary haematopoiesis (large head, spinal cord compression)
121
How to investigate/diagnose Thalassaemias
High Performance Liquid Chromatography
122
Macrocytic Anaemia
* Low Hb
* Increased MCV
123
3 types of Macrocytic Anaemia
* Megaloblastic
* Non-megaloblastic
* False Megaloblastic
124
Megaloblastic Anaemia
* Due to failure of DNA synthesis (caused by B12 and Folate deficiencies)
* RBC precursors cannot break down into RBCs, hence why they stay large (high MCV) and why there is less Hb (as less of them break down)
125
Pathophysiology of Pernicious anaemia
Autoimmune condition resulting in the destruction of gastric parietal cells which leads to B12 deficiency due to malabsorption
126
Non-megaloblastic anaemia
There are no reticulocytes etc
Due to liver disease, there is increases cholesterol and so RBCs are bound to fat/cholesterol etc and this is percieved as an increased MCV
127
False megaloblastic anaemia
Due to cold agglutination- reticulocytosis occurs and therefore MCV is raised
128
Fanconi Anaemia
* Macrocytic anaemia
* Increased HbF
* Bone marrow failure
129
Inheritance of Fanconi Anaemia
Autosomal recessive
130
Fanconi Anaemia Presentation
* Child (Usually of Jewish origin)
* Undeveloped thumbs
* Eye and ear defects
* Horseshoe kidney
* Cafe au lait spots
* Short stature
131
Fanconi Anaemia sufferers are at risk of
Acute Myeloid Leukaemia
132
Types of Sickle Cell Disease
Trait or Anaemia
133
Pathophysiology of Sickle Cell Disease
Valine takes place of glutamic acid
134
Sickle Cell Trait
One normal Beta, one abnormal beta
(B/BS)
Mainly HbA (60%), HbS (40%)
135
Sickle Cell Trait are asymptomatic until
Hypoxia
136
HbS protects you against
Malaria
137
Sickle Cell Anaemia (HbSS)
Two abnormal beta genes
(BS/BS)
HbS \>80% the other 20% is HbF/HbA2
138
Inheritance pattern for Sickle Cell Anaemia
Autosomal Recessive
More commin in sub-saharan africans
139
Why are HbSS anaemic
Due to chronic haemolysis
Shortened RBC
Howell-Jolly bodies are seen on a blood screen
140
Presentation of a sickle cell crisis
* Dactylitis
* Chest pain
* A lot of pain everywhere
Due to RBCs clumping together in small veins
141
Investigation of HbSS
High performance liquid chromatography
to see HbS globin
142
Treatment of a sickle cell crisis
* Supportive
* Hydroxycarbamide (induces HbF production)
143
Haemostasis
The arrest of bleeding and the maintenance of vascular patency
4 pathways
144
4 pathways to haemostasis
Extrinsic pathway (left)
Intrinsic pathway (right)
Common pathway
Fibrinolysis
145
Extrinsic pathway (left side)
**TF \> Factor VIIa**
146
Intrinsic pathway (right side)
**Factor IXa \> Factor VIII**
Preceded by XIIa \>XIa \>IXa
147
Common pathway
**Prothrombin \> Factor Xa/V \>Thrombin**
**Thrombin then converts fibrinogen to fibrin**
148
What converts Prothrombin to thrombin
Factor Xa/V
149
What converts fibrinogen to fibrin
Thrombin
150
Fibrinolysis
Plasminogen \> Plasmin by tissue plasminogen activator (tPA)
then plasmin converts fibrin to fibrin degredation products
151
Tissue plasminogen activator converts
Plasminogen to Plasmin
152
Plasmin converts
Fibrin to fibrin degredation products
153
Describe physiology of haemostasis
Enothelial wall damage exposes collagen and releases Von Williebrand Factor (VWF), platelets then adhere to the site of injury and secrete thromboxane 2 which leads to the aggregation of more platelets
154
Another name for prothrombin
Factor II
155
All coagulation factors are synthesised in
The Liver
156
Vitamin K carboxylates factors
II, VII, IX, X
As well as proteins S and C
157
Thrombin also
Accentuates factors VIII/IXa
158
Primary Haemostasis
Platelet plug
159
Secondary haemostasis
Fibrin clot
160
Test of primary haemostasis
PLT count
161
Test for Secondary haemostasis
Prothrombin time (PTT)
Activated Partial Thromboplastin time (APTT)
162
PTT measures
Extrinsic pathway
TF and Factor VIIa
163
APTT measures
Intrinsic pathway
Factors IX/VIII
"AY PTT = factor AY-TE"
164
Inhibitions of primary haemostasis
* Inhibited thromboxane 2 (COX2)- by NSAIDs (decreases platelet aggregation)
* Decreased Collagen- elderly people (makes it easier for endothelial walls to break)
* VWF Disease (stops platelet aggregation and intrinsic pathway from working)
* Marrow disease (thrombocytopenia)
* Immune Thrombocytopenic Purpura (ITP)
165
VWF Disease
Affects platelet aggregation and Factor VIII
166
Vitamin K is absorbed in the
Dueodenum
"Wearing denum is Kool"
167
To be absorbed Vit K needs
Bile salts
168
Inhibitions of secondary haemostasis
* Vit K deficiency
* DIC (used up all of your clotting factors)
* Haemophilia
169
Disseminated Intravascular Coagulation (DIC)
* Uses up all the clotting factors leading to bleeding, purpura and bruising
* Leading to microvascular thrombus formation = end organ failure
170
Treatment for DIC
FFP
171
Two Haemophilias
Haemophilia A: Problem with Factor VIII
Haemophilia B: Problem with Factor IX
"AY = AY-TE"
"Bee=NINE, benign"
172
Haemophilia affects the
intrinsic pathway
173
Haemophilia A affects
Factor VIII
174
Haemophilia B affects factor
IX
175
Which haemophilia is more common
Haemophilia A (5 times more common)
176
Presentation of Haemophilias
* Male (X-linked)
* Swellings in elbows and knees
177
What is prolonged in VWF Disease
* APTT: prolonged (problem with Factor VIII)
* PTT: normal
* Bleeding time: increased (problem with platelets)
178
What is prolonged in Vit K deficiency
* APTT: prolonged (due to Factor IX)
* PTT: prolonged (due to Factor II and Factor VII)
* Bleeding time: normal (platelets are fine)
179
What is prolonged in Haemophilia
APTT: prolonged (due to Factors VIII/IX)
PTT: normal (extrinsic not affected)
Bleeding time: normal (platelets are fine)
180
What is prolonged in DIC
* APTT: Prolonged (Affects intrinsic factors)
* PTT: (Affects extrinsic factors)
* Bleeding time: (Affects platelets)
181
Types of Thrombosis
* Arterial
* Venous
* Thrombophilia
182
Arterial thrombosis clots are
**Platelet-rich clot** in a high-pressure system
Endothelium breaks off, exposing endothelium leading to a platelet plug quickly fixing the problem
183
Factors that increase arterial thrombosis
* Enothelial damage
* HTN/smoking
* Hypercholesterolaemia
* Diabetes
184
Arterial thrombosis lead to
* CHD
* Angina
* MIs
185
Treatments for Arterial Thrombosis
* **Aspirin**- blocks thromboxane 2 (COX2)
* **Clopidogrel** (ADP inhibitor)
COX 2 (leads to platelet aggregation)
ADP (activates platelets to find more platelets)
186
Venous thrombosis clots are
**Fibrin rich clot** in a low-pressure system
187
Factors for venous thrombosis
**Virchow's Triad**
* Stasis
* Vessel Wall damage
* Hypercoagulability
188
Venous thrombosis lead to
* DVTs
* PEs
* Strokes
189
Treatments for venous thrombosis
* Heparin
* Warfarin
* DOACs (Rivaroxaban)
* Thrombin Inhibitors (Dabigatran)
190
Two types of Heparin
* Unfractionated
* Low Molecular Weight Heparin (LMWH)
191
Mechanism of action of unfractionated heparin
Blocks thrombin
192
What should you monitor if on unfractionated heparin
APTT
193
Mechanism of action of LMWH
Blocks factor Xa
194
What reverses the effects of heparin
Protamine sulphate
195
What contraindicated protamine sulphate use
Fish allergy
as it's made from salmon semen
196
Side effects of Heparin
* Heparin-Induced Thrombocytopenia
* Osteoporosis
197
Mechanism of action of Warfarin
Vit K antagonist
198
Problem with warfarin
Takes 3 days to work
199
Warfarin is contraindicated in
CYP interactions (Grapefruit Juice etc)
200
How do you reverse Warfarin
* Acute: Beriplex/ Prothrombin complex concentrate (clotting factors)
* In 24 hours: Vitamin K
201
International Normalized Ratio (INR)
A test for how well Warfarin is working
202
What should INR be between
2 - 3
203
An INR \< 2 means
At risk of clotting
204
An INR \>3 means
At risk of bleed
205
Mechanism of action of Direct Oral Anticoagulants (DOACs)
**Directly inhibit active factor Xa:**
* **Rivaroxaban** (Ban Xa is in the name)
* Apixaban
* Edoxaban
**Direct thrombin inhibitor:**
* **Dabigatran**
206
What is the effect of thrombophilias
Deficiency of naturally occurring anticoagulants
Increased risk of clotting
207
Two types of thrombophilias
* Factor V Leiden
* Antiphospholipid Syndrome
208
Antiphospholipid Syndrome Presentation
* Multiple pregnancy losses
* Recurrent DVTs
209
Antiphospholipid syndrome pathophysiology
Autoimmune disease where antibodies change beta-2-glycoprotein which effects primary and secondary haemostasis
210
Antiphospholipid antibodies
aPL autoantibodies
Anti-cardiolipin antibodies
211
Treatment of Antiphospholipid Syndrome
Aspirin- primary haemostasis
Warfarin- secondary haemostasis
212
When would you swap warfarin therapy for LMWH
During pregnancy as Warfarin is teratogenic
213
Myeloproliferative Disorders
* BCR ABL positive
* BCR ABL negative
214
Myeloproliferative BCR ABL positive disorder
Chronic Myeloid Leukaemia (CML)
215
Myeloproliferative BCR ABL negative disorders
* Polycythaemia Rubra Vera (PVC)
* Idiopathic Myelofibrosis
* Essential Thrombocythaemia (ET)
216
Myeloproliferative disorders are
Increase in all myeloid lineages' cells
217
Myeloid disorders present with
* Weight loss
* Night sweats
* Fatigue
* Anaemia
* Splenomegaly (due to an increase in RBCs)
218
Chronic Myeloid Leukaemia (CML)
* Increased WBC (granulocytes)
* Increased basophils and eosinophils
219
Philadelphia chromosome indicates
Chronic myeloid leukaemia (9:22)
220
Treatment of CML
Imatinib (Tyrosine Kinase inhibitor)
221
Idiopathic myelofibrosis is
Fibrosis of the bone marrow leading to bad production of cells
Hence:
* Leukoerythroblastic blood film (nucleated RBCs)
* Tear-drop shaped RBCs
222
Leukoerythroblastic blood film
| (Nucleated RBCs)
Myelofibrosis
223
Tear-drop shaped RBCs
Myelofibrosis
224
Essential Thrombocythaemia
Excessive production of platelets
| (\>1000)
225
Presentation of Essential thrombocythaemia
* Headache
* Visual problems
* Sore digits
* Bleeds a lot
226
Treatment for ET
* **Hydroxyurea**
* Aspirin
227
Lymphoid Cancers
* Acute (problem with precursors)
* Chronic (problem with mature cells)
228
Acute lymphoid cancers
* Acute Lymphoblastic Leukaemia (ALL)
* Acute Myeloid Leukaemia (AML)
229
Chronic Lymphoid cancer
Chronic Lymphoid Leukaemia
230
Acute Lymphoblastic Leukaemia (ALL) pathophysiology
* An increase in lymphoid progenitors
* A decrease in myeloid progenitors (because body is so busy making lymphoid progenitors)
231
ALL occurs in
Young kids
232
An ALL blood test would show
Increased Lymphoblasts
* Decreased RBCs
* Decreased PLTs
233
Increased lymphoblasts is a diagnosis of
ALL
234
Investigations for ALL
* Gold standard: Bone marrow biopsy
* Immunophenotyping: Establish specific cells
235
Treatment for ALL
* Vaccinations against gram negatives
* Antibiotics and antifungals
* Chemotherapy
236
Acute Myeloid Leukaemia (AML)
* An increase in myeloid progenitors
* A decrease in lymphoid progenitors (due to over-production of myeloid progenitors)
237
AML occurs in
Older adults (age 60ish)
238
A blood test of AML would show
**Auer rods**
Increased Myeloblasts
* Decreased RBCs
* Decreased PLTs
239
Auer rods
AML
240
Increased myeloblasts is a diagnosis of
AML
241
Treatment of AML
A lot of chemotherapy
242
Chronic Lymphocytic Leukaemia (CLL)
Increased number of Mature B Cells
243
CLL can travel in
The blood and the lymph
244
On a CLL blood film you would see
Smudge cells
245
Smudge cells
CLL
246
CLL can sometimes transform into
a Non-Hodgkin's Lymphoma
247
CLL patients are more likely to get
Viral infections (Herpes zoster)
248
Types of Lymphoma
* Hodgkins
* Non Hodgkins
249
* Enlarged lymph nodes
* Chills
* Fatigue
* Weight loss
* Increased LDH
Symptoms of Lymphoma
250
Investigations for Lymphomas
Lymph node biopsy
251
Lymphoma is associated with
EBV
252
Hodgkins Lymphoma
* Reed-Sternberg Cells
* Painful upon drinking alcohol
* Itching
* Asymptomatic painless lymphadenopathy
253
Treatment for Hodgkins Lymphoma
Chemotherapy (Brentuximab)
Radiotherapy
254
Non-Hodgkins
* T-Cell
* B-Cell
255
Prognosis for T-Cell NHL
Bad
256
Immature B-cell NHL
Low Grade
257
Mature B-cell NHL
High grade
258
Treatment for NHL
Rituximab
259
Types of high grade B-cell NHLs
* Burkitt's Lymphoma
* Mantle Cell Lymphoma
* Waldenstorm's Macroglobinaemia
260
Burkitt's Lymphoma
* Common in Africans
* Associated with EBV
* Mandibular/Maxillary Tumours
* Sometimes intra-abdominal tumours
261
Stary Sky Appearance on blood film
Burkitt's Lymphoma
262
Treatment of Burkitt's Lymphoma
Chemotherapy
* Can cause tumour lysis syndrome so give with IV allopurinol or IV rasburicase to reduce this risk
263
Tumour Lysis Syndrome can cause
* hyperkalaemia
* hyperphosphataemia
* hypocalcaemia
* hyperuricaemia
* acute renal failure
264
What Ig is associated with Waldenstrom's Macroglobulinaemia
IgM
Hyperviscosity syndrome
265
Grade I lymphomas
1 node group
266
Grade II lymphomas
2 nodal groups on 1 side of the diaphragm
267
Grade III lymphomas
Nodes involved on both sides of the diaphragm
268
Grade IV
Extra nodal disease
269
T cells are produced in the
Paracortex
270
B cells are produced in the
Follicles
271
Myeloma
A plasma cell malignancy in the bone marrow
272
Presentation of Myeloma
* Older patient
* Bone pain
* Wedge fractures of vertebrae
* Bone lesions "Pepperpot skull"- lytic punched out lesions
* Hypercalcaemia
273
What causes hypercalcaemia in Myeloma
IL-6 increases osteoclasts and decreases osteoblasts which leads to the breakdown of bone
274
Treatment of hypercalcaemia
Biphosphonates
275
Investigations for myeloma
* Serum electrophoresis: Monoclonal antibodies (IgG/IgA)
* Urine electrophoresis: Bence-Jones protein
* Increased ESR
* X-ray: Rain-drop skull/Pepperpot skull
276
Bence-jones proteins and Monoclonal antibodies
Myeloma
277
Treatment for myeloma
* Bortezomib (proteasome inhibitor) + Steroid
* Thalidomide + Steroid
* Cyclophosphamide + Steroid
* Daratuximab + Steroid
278
Monoclonal Gammopathy of Unknown Significance (MGUS)
* Paraprotein \<30g/l
* Low plasma cells in bone marrow
279
Amyloidosis
* Amyloid is laid down everywhere (beta-pleated sheets)
* Usually associated with Myeloma
280
Muscle biopsy of amyloidosis patient
* Congo red stain
* Apple-green bifringent under polarized light
281
If a patient has Infectious Mononucleosis (EBV) never give them
Amoxicillin - causes rash
Tx: Penicillin G
282
Felty's Syndrome Triad
* Rheumatoid Arthritis
* Splenomegaly
* Neutropenia
283
Howell-Jolly bodies are seen in
* Hyposplenism (splenectomy)
* Sickle-Cell anaemia
284
Blue gums is a symptom of
Lead poisoning
285
RBCs are stored for
35 days at 4oC
286
Factors (FFP) are stored for
3 years at -30oC
287
PLTs are stored for
7 days at 22oC
288
Treatment for Neutropenic Sepsis
* 1st: Piperacillim (Tazobactam if P allergy)
* Severe: add Gentamicin
Give all patients at risk antifungals (Itraconazole)
289
Rituximab is a
Monoclonal antibody
290
Imatinib is a
Tyrosine kinase inhibitor
291
Side effects of Vinca Alkaloid (Vincristine) Chemo
Neuropathy
292
Side effect of Antracycline (Daunorubicin) Chemo
Cardio toxic
293
Side effect of Cis-Platinum Chemo
Nephrotoxicity
294
Universal blood donor
O-
As they have no antigens
295
Universal receiver
AB+
As they have all of the antigens
296
ABO system is defined on chromosome
9
297
85% of blood types are
RhD+
298
Transfusion-Associated Circulatory Overload (TACO)
* Oedema
* Respiratory distress
* HTN
* Increased JVP
Within 6 hours of blood transfusion
Tx: Diuretics
299
Transfusion-Relate Acute Lung Injury (TRALI)
* Immune-mediated lung injury
* Hypotension
* Within 6 hours of blood transfusion
300
Indications for a blood transfusion
Hb \<70 and symptomatic
Hb \<80 and has cardio disease
