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Mattias - Hemotology > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Which cell modulate hypersensitivity and destroys parasites

A

Eosinophils

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2
Q

Which cell modulate immune response, phagocytic clearance and have regulatory functions

A

Monocytes –> Macrophages

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3
Q

Which cells are involved in phagocytosis and acute inflammation

A

Neutrophils

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4
Q

Lifespan of Neutrophils, Platelets and Red cels

A

Neutrophils - 7-8h
Platelets - 7-10days
Red cells - 120days

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5
Q

What is a Myelocyte

A

Nucleated precursor between neutrophils and neutroblast

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6
Q

What is the precursor of platelets

A

Megakaryocytes

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7
Q

Define Differentiation

A

Descendent commits to one or more lineages

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8
Q

Define Maturation

A

Descendants acquire functional properties and may stop proliferating

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9
Q

What germ layer is the Hemopoietic stem cells derived from

A

The mesoderm

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10
Q

When does the Bone marrow start being the site of hemopoiesis

A

Week 16 of development

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11
Q

Major hemopoiesis site after 30

A

Vertebra, sternum and rib bone marrow

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12
Q

Describe the -physises of a long bone

A

Epiphysis is at the very end.
Diaphysis is the long middle.
Metaphysis is between the Epi and the Dia.
The physis is the growth plate, between the Metaphysis and Epiphysis

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13
Q

What is the interface between bone and bone marrow called

A

Endosteum

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14
Q

Name a few regulators of hemopoeisis

A

C/EBPalpha, G-CSF, M-CSF, PU1 - Monocyte and Granulocyte

GATA1 and EPO - Erythroid

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15
Q

Describe immunophenotyping

A

Antibodies with Fluorochromes are bound to CD proteins on cells. Different cells express different CD proteins.
Fluoresence study is done to determine what cell it is

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16
Q

Where does T-cells and B-cells mature

A

T-cells - Thymus

B-cells - Bone marrow

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17
Q

What are the Peripheral (secondary) lymphoid tissues

A

Lymph nodes
Spleen
Tonsils (Waldeyer’s ring)
Epithelio-lymphoid tissues

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18
Q

What is Chylous Ascites

A

Accumulation of lipid-rich lymph in the peritoneal cavity, due to disruption of the lymphatic system secondary to trauma or obstruction

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19
Q

How is lymph filtered in the lymph node

A

Enters through the capsule into the peripheral sinus

Filters through the node and exits through the efferent lymphatic vessel at the hilum

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20
Q

Types of Lymphocytes

A

B cells
T cells (Helper and Cytotoxic)
NK cells

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21
Q

What is a plasma cell

A

A fully differentiated B cell that only produces one type of antibodies

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22
Q

What is red lines extending from a superficial inflamed lesion on the skin called

A

Lymphangitis

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23
Q

Triad of Hyperslpenism

A

Spleomegaly
Fall in one or more cellular components of blood
Correction of cytopenias by splenectomy

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24
Q

Features of Splenic enlargements

A

Dragging sensation in LUQ
Discomfort while eating
Pain if infarction

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25
Q

What is Niemann-Pick disease

A

Lipid storage disorder affecting Spleen, liver, brain, bone marrow and lungs.

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26
Q

Common causes of Hyposplenism

A 
Splenectomy
Celiac disease
Sickle Cell disease
Sarcoidosis
Iatorgenic
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27
Q

What is a Howell-Jolly Body

A

Small purple dot inside a red cell. Remnant of basophilic nuclear remnant. Usually a sign of damage or absent spleen

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28
Q

Glycophorin A is seen on

A

Red blood cells

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29
Q

What happens in Malignant Hemopoiesis

A 
One or more of:
Increased proliferation
Lack of differentiation
Lack of maturation
Lack of apoptosis
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30
Q

Types of hemotological malignancies are based on three things

A

Speed of presentation (Actue or Chronic)
Site of malignancy (Medullary, Blood or Lymph-nodes)
Lineage (Myeloid, Lymphoid)
High grade or Low grade

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31
Q

What is blood and lymp-node malignancies called

A

Blood - Leukemia

Lymph-node - Lymphoma

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32
Q

Plasma cell malignancy in marrow is called

A

Myeloma

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33
Q

What is Acute Leukemia

A

Rapidly progressive clonal malignancy of the marrow/blood with maturation defects

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34
Q

What is the definition of Acute Leukemia

A

20% or more blasts in either the peripheral blood or bone marrow

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35
Q

What are the types of Acute Leukemia

A

Acute Lymphoblastic Leukemia (ALL)

Acute Myeloid Leukemia (AML)

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36
Q

Acute Lymphoblastic Leukemia is a malignant disease of

A

Lymphocytes

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37
Q

Most common childhood cancer

A

Acute Lymphoblastic Leukemia

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38
Q

Presentation of Acute Lymphoblastic Leukemia

A

Due to marrow failure (anemia, infections, bleeding)
Bone pain
Leukemic effects: High WCC and involvement of extra-medullary areas ie CNS, lymph nodes sometimes causing venus obstruction

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39
Q

Who gets Acute Myeloid Leukemia

A

Elderly

Median age 70

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40
Q

Presentation of Acute Myeloid Leukemia

A

Similar to ALL
Marrow failure
Sub groups may present with DIC or gum infiltration

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41
Q

What is Disseminated Intravascular Coagulation

A

Widespread activation of the clotting cascade. This uses up all the platelets so bleeding may occur at other places.
May be caused by immature red blood cells in Acute Promyeloid Leukemia

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42
Q

Investigation for Acute Leukemia

A

Blood count and film
Coagultion screen
Bone marrow aspirate

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43
Q

What is seen on Blood film in acute leukemia

A

Reduction in normal
Presence of abnormal
Abnormal cells (Blasts) with a high nuclear:cytoplasmic ratio
Auer Rods

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44
Q

What is looked at on Bone marrow aspirate in Acute Leukemia

A

Morphology
Immunophenotype
Cytogenetics

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45
Q

How is AML and ALL bone marrow cells differentiated

A

By immuniphenotyping

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46
Q

What is Trephine

A

A surgical tool used to take a piece of bone out for investigation. Better assessment of cellularity achieved than marrow aspirate

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47
Q

Treatment of Acute Lympoblastic Leukemia

A

Multi-agent chemotherapy
Can last up to 2-3years
Varying phases and intensity of treatment
Target treatments depending on subset

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48
Q

Treatment of Acute Myeloid Leukemia

A

Multi-agent Chemotherapy
2-4 cycles of chemo (5-10 days of chemo followed by 2-4 weeks of recovery)
Prolonged hospitalisation

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49
Q

What is a Hickman-Line

A

Central venous catheter used for administration of chemotherapy.
Normally enter the jugular vein and the line travels under the body further down on the chest

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50
Q

What problems arise with chemotherapy in AML and ALL suppressing the bone marrow

A

Anemia
Neutropenia (infections more likely)
Thrombocytopenia (Bleeding, purpura or Petechiae)

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51
Q

How is Infection post chemotherapy dealt with

A

Give broad spectrum antibiotics as soon as neutropenic fever occur
(Particulary cover Gram negative organism)

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52
Q

What is Tumor lysis syndrome

A 
Complication of Chemo
Elevated uric acid levels
Elevated serum potassium
Elevated serum phosphorous levels
Decreased Calcium
Potentially life-threatning
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53
Q

What is the cure rate in ALL and AML

A

Child ALL >85-90%
Adult ALL >30-40%
60y AML

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54
Q

Acute promyelocytic leukemia is associated with what

A

Specific chomosomal translocation t(15;17) and DIC coagulopathy
Treatable with VitA analogue and arsenic derivatives

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55
Q

What is the consistency of Lymphnodes in Lymphoma

A

Rubbery/soft

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56
Q

What is the surface of lymphnodes in Lymphoma vs Metastatic Carcinoma

A

Lymphoma - Smooth

Metastatic carcinoma - Irregular

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57
Q

Are lymphnodes tethered in Lymphoma and Metastatic carcinoma

A

Lymphoma - No

Metastatic carcinoma - Yes

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58
Q

What type of sample is needed if lymphoma or other malignancy is suspected

A

Not FNA or Core

Need a big sample to assess architecture of the lesion

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59
Q

Can you diagnose Lymphoma with CT

A

No

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60
Q

Nodular sclerosing on histology is diagnostic of

A

Hodgkin’s disease

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61
Q

How is Immunohistochemistry done in Lymphoma

A

Antibodies against surface proteins of lymphoma cells and enzyme reaction. Brown=positive

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62
Q

CD30 +ve Reed Sternberg cells is seen in

A

Hodgkin’s disease

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63
Q

T(14:18) is seen in

A

Follicular Non-hodgkins lymphoma

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64
Q

T(11:14) is seen in

A

Mantle cell Non-hodgkins lymphoma

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65
Q

Lymphomas can be divided into three main categorize

A

Hodgkin’s
T cell Non-Hodgkin’s Lymphoma
B cell Non-Hodgkins lymphoma

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66
Q

What is Pancytopenia

A

A deficiency of blood cells of all lineages

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67
Q

Causes of Pancytopenia - reduced production

A

Bone Marrow Failure

Can be inherited or aquired

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68
Q

What is Fanconi’s anemia

A

Rare genetic disease damaging the DNA repair system. Causes Inherited marrow failure syndrome.

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69
Q

Signs of Fanconi’s anemia

A

Short stature, Skeletal abnormalities, skin pigmentation such as Cafe au lait spots

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70
Q

When are the onset of Fanconi’s anemia, what order to abnormalities occur

A

Median age: 7years
Macrocytosis –>Thrombocytopenia –> Neutropenia
Bone marrow failure - 20y
Lekuemia risk 52% by 40y

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71
Q

What is aplastic anemia

A

Autoimmune attack against hemopoietic stem cells

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72
Q

What is Myelodysplastic syndrome

A

Increased apopotosis of progenitor and mature cells (ineffective hemopoiesis)

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73
Q

Types of Acquired Primary Bone Marrow Failure

A

Aplastic anemia
Myelodysplastic syndromes
Acute Leukemia

74
Q

How does histology of Aplastic anemia look

A

Very empty bone marrow

75
Q

Causes of secondary bone marrow failure

A

Drug incuced (chemo, chloramphenicaul, alcohol)
B12/Folate deficiency
Malignancy
Others (HIV/storage disease)

76
Q

Causes of increased destruction of blood componenets causing cytopenia

A

Hypersplenism

Autoimmune

77
Q

Causes of Hypersplenism

A 
Splenic congestion (Portal hypertension or Congestive cardiac failure)
Systemic disease (RA)
Hematological disease (Myelofibrosis)
78
Q

Rheumatoid Arthritis + Splenomegaly + Low WBC with recurrent infections. Diagnosis

A

Felty’s

79
Q

Is the Bone marrow hyper or hypo cellular in Pancytopenia

A

Can be either. Depends on the underlying cause

80
Q

Treatment of Pancytopenia

A

Treat underlying cause
Give RBC, Platelet
Antibiotic treatment aggressively and prophylactic

81
Q

Treatment of Idiopathic Aplastic Anemia

A

Immunosuppression

82
Q

Ig variable element is generated from

A

V-D-J region recombination early in development

83
Q

What happens to the B cell in the periphery

A

Travel to the follicle germinal centre of the lymph node
Identify the antigen and improve the fit by somatic mutation or be deleted
May return to the marrow as plasma cell or circulate as memory cell

84
Q

Features of a Plasma cell

A

Clock face nucleus on histology
Open chromatin (Synthesizing mRNA)
Plentiful blue cytoplasm (Laden with protein)
Pale perinuclear area (Golgi apparatus)

85
Q

What is a paraprotein

A

Monoclonal immunoglobin
Identical antibody all derived from clonal expansion of a single B-cell
Marker of underlying clonal B-cell disorder

86
Q

Serum electrophoresis: What’s in the Alpha-1 band

A

90% alpha-1 antitrypsin

87
Q

What does alpha-1 antitrypsin indeficiency cause

A

Emphesema and COPD in young non smoking person

88
Q

Serum electrophoresis: What’s in the Alpha-2 band

A

Alpha-2 macroglobulin, caeruloplasmin, haptoglobin

89
Q

Serum electrophoresis: What’s in the Beta band

A

Transferrin, low density lipoprotein, C3

90
Q

Serum electrophoresis: What’s in the Gamma band

A

Immunoglobulins

91
Q

What are Bence-Jones Protein

A

Immunoglobin light chains

92
Q

How is Kappa light cahins and Lambada light chains present in the blood

A

Kappa - monomers

Lambada - Dimers

93
Q

What is MGUS

A

Monoclonal gammaopathy of undetermined significance

94
Q

Causes of Paraproteinemia

A

MGUS
Myeloma
Amyloidosis
Lymphoma – Asymptomatic myeloma – Solitary or extramedullary plasmacytoma – Chronic lymphocytic leukemia – Waldenstrom’s macroglobulinemia

95
Q

How does Myeloma affect the body, 2 main groups

A

Direct tumor cell effects

Paraprotein mediated effects

96
Q

Myeloma: Direct tumor cell effects

A

Bone lesions
Increased calcium
Bone pain
Replace normal bone marrow –> Marrow failure

97
Q

Myeloma: Paraprotein mediated effects

A

Renal failure
Immune suppression
Hyperviscosity
Amyloid

98
Q

How is Myeloma classified

A

By the paraprotein (antibody) they produce

99
Q

X-ray features of myeloma

A

Lytic Bone disease
Punched out lesions
Major cause of bone pain

100
Q

Most common types of Myeloma

A

IgG myeloma - 59%
IgA myeloma - 21%
Bence Jones myeloma - 15%

101
Q

How does Myeloma cause Lytic bone lesions

A

Myeloma cells act on stromal cells and release IL-6

IL-6 activates Osteoclasts

102
Q

How does Myeloma cause Hypercalcemia

A

Due to the increased activation of osteoclasts the bone matrix is broken down and release Ca2+

103
Q

What does Hypercalcemia cause

A 
Stones
Bones
Abdominal groans
Psychiatric moans
Thirst -- Dehydration -- Renal impairment
104
Q

How does Myeloma affect the kidney

A 
Tubular cell damage by light chains
Ligh chain deposition - Cast nephropathy
Sepsis
Hypercalcemia and dehydration
Drugs: NSAIDs
Amyloids
Hyperuricemia
105
Q

How does Cast injury occur in Myeloma

A

Light chains is filtered through the Glomerulus. Normally it is reabsorbed in the proximal tubules but if there’s too much it continous to the loop of Henle
In the Thick ascending limb it bounds with the native protein Tamm-Horsfall proteins and this produce insoluble casts which blocks the nephron

106
Q

Onset and survival of Myeloma

A

Median age at diagnosis 65

Survival 5-8years

107
Q

Treatment of Myeloma

A 
Corticosteroids (dexamethasone or prednisolone)
Alkylating agents (Cyclophosphamid, melphalan)
Novel agents (Thalidomide, bortezomib, Lanalidomide)
High dose chemo/autologous stem cell transplants in fit patients
108
Q

Symptom control of Myeloma

A 
Opiates (avoid NSAIDs)
Local radiotherapy (Pain relief or spinal cord compression)
Bisphosphonates (corrects hypercalcemia and bone pain
Vertebroplasty - inject sterile cement into fractured bone to stabilize
109
Q

Features of MGUS

A

Paraprotein

110
Q

What is AL Amyloidosis

A

Amyloid Light-chain Amyloidosis
Small plasma cell clone
Mutation in the light chain –>altered structures
Precipitates in tissue as an insoluble beta pleated sheet

111
Q

Organ damage in AL amyloid

A 
Kidney (nephrotic syndrome)
Heart (Cardiomyopathy)
Liver (Organomegaly and deranged LFTs)
Neuropathy (Autonomic and Peripheral)
GI tract (Malabsorption)
112
Q

How is AL Amyloidosis diagnosed

A

Organ biopsy and Congo red stain to confirm deposits

113
Q

IgM paraprotein is linked to

A

Waldenstrom’s Macroglobulinemia

114
Q

Tumor effects of Waldenstrom’s macroglobulinemia

A

Lymphadenopathy
Splenomegaly
Marrow failure

115
Q

Paraprotein effects of Waldenstrom’s Macroglobulinemia

A

Hyperviscosity

Neuropathy

116
Q

What does Waldenstrom’s macroglobulinemia Hyperviscosity syndrome present as

A

Faitgue, visual disturbance, confusion, coma
Bleeding
Cardiac failure
Also, night sweats and weight loss

117
Q

Treatment of Waldenstroms Macroglobulinemia

A 
Chemo
Plasmapheresis (removes paraprotein from the circulation)
118
Q

What are Myeloproliferative disorders

A

Clonal hemopoietic stem cell disorders with an increased production of one or more types of hemopoietic cells
Maturation is relatively preserved

119
Q

Two subtypes of Myeloproliferative disorders

A

BCR-ABL1 Negative

BCR-ABL1 Positive

120
Q

What Myeloproliferative disorders are BCR-ABL1 Negative

A

Idiopathic myelofibrosis
Polychyhemia Rubra Vera
Essential Throbocytemia

121
Q

What Myeloproliferative disorders are BCR-ABL1 Positive

A

Chronic Myeloid Leukemia

122
Q

What is the BCR-ABL1 Gene associated chromosome

A

Philadelphia chromosome

Reciprocal translocation between chromosome 22 and 9

123
Q

When should Myeloproliferative disorders be considered

A

When there’s no other explanation to a high blood count (of any or more type) Splenomegaly or Thrombosis in an unusual place

124
Q

What is Chronic Myeloid Leukemia (CML)

A

Proliferation of myeloid cells (Granulocytes and their precursors, Other lineages, platelets)
Chronic phase followed by Accelerated phase followed by Blast crisis

125
Q

Clinic features of Chronic myeloid Leukemia

A 
Asymptomatic
Splenomegaly
Hypermetabolic symptoms
Gout
Priapism (not common)
126
Q

Lab features of Chronic Myeloid Leukemia

A

Normal/redued Hb
Leucocytosis w/ neutrophilia and myeloid precursors, eosinophilia, basophilia
Thrombocytosis
Bone Marrow - Increase in myelocytes and eosinophils

127
Q

What is the hall mark of Chronic Myeloid Leukemia

A

Philadelphia chromosome
A philadelphia chromosome is the BCR and ABL gene are next to each other on chromosome 22. (ABL normally on chromosome 9)

128
Q

What is Imatinib

A

Tyrosine kinase inhibitor drug. Used in ie Chronic Myeloid Leukemia

129
Q

Features common to MPD

A

Asymptomaic – Increased cellular turnover (Gout, fatigue, weight loss, sweats)
Splenomegaly
Marrow failure
Thrombosis (TIA, MI, Abdominal vessel thrombosis, claudication, erythromelalgia)

130
Q

What is Polycythemia rubra vera

A

High hemoglobing/hematocrit accompanied by erythrocytosis (a true increase in red cell mass) but can have exessive production of other lineages

131
Q

Polycythemia rubra vera needs to be distinguished from two other conditions

A 
Secondary polycythemia (Chronic hypoxia, smoking, erythropoietin-secreting tumor etc)
Pseudopolycythemia (Dehydration, diuretic, therapy, obestiy)
132
Q

Clinical features of Polycythemia Rubra vera

A

Headaches, fatigue (Blood viscosity is up but not plasma viscosity)
Itch (aquagenic puritis)

133
Q

What is aquagenic puritis

A

Intense Itching sensation without any visible lesions and is made worse by water

134
Q

What is the mutations in Polycythemia Rubra vera that is most common

A

JAK2 mutation

95% of patients has the mutation

135
Q

Investigations for polycythemia

A

CXR
O2 saturation and ABGs
Others

136
Q

Treatment of Polycythemia Rubra Vera

A

Venesect (Hematocrit

137
Q

What is Essential Thrombocytopenia

A

Type of Myeloproliferative disorder

Uncontroled production of Abnormal platelets

138
Q

What can Essential Thrombocytopenia lead to

A

Thrombosis

Bleeding due to acquired von Willebrand disease

139
Q

What needs to be excluded when Essential Thrombocytopenia is suspected

A

Reactive Thrombocytosis

CML

140
Q

Which mutations are seen in Essential Thrombocytopenia

A

JAK2 mutation (50%)
CALR (Carlreticulin)
MPL mutation

141
Q

Treatment of Essential Thrombocytopenia

A

None in low risk cases
Anti-platelet agents (Aspirin)
Cytoreductive therapy to control proliferation

142
Q

Dacrocytes (Teardrop-shaped RBCs) in peripheral blood is linked with

A

Beta Thalassemia major Idiopathic myelofibrosis

143
Q

Features of Idiopathic myelofibrosis

A

Leukoerythroblastosis
Marrow failure
Bone marrow fibrosis
Extramedullary hematopoiesis (liver and spleen)

144
Q

What is Leukoerythroblastosis

A

Anemia caused by a space occupying lesion in the bone marrow

145
Q

Typical blood film for Myelofibrosis

A

Tear-drop shaped RBC and Leycoerythrocytoblastosis

146
Q

Lab featrues of Myelofibrosis

A

Dry bone marrow aspirate
Fibrosis on trephine biopsy
JAK2 or CALR mutation
Typical blood film (tear drop and leuoerythroblastic)

147
Q

What causes Leucoerythroblastic blood film

A

Reactive (sepsis)
Marrow infiltration
Myelofibrosis

148
Q

Treatment of Myelofibrosis

A 
Supportive care (blood transfusions, platelets, antibiotics)
Ruxolitib (JAK 2 inhibitor)
149
Q

Cytotoxic drugs: Antimetabolites act by

A

Impair nucleotide synthesis/incorporation

150
Q

Cytotoxic drugs: Examples of Antimetaboltites

A

Methotrexate
6-Mercaptopurine/Cytosine arabinoside/ Fludarabine
Hydroxyurea

151
Q

How does Methotrexate act

A

Inhibits dihyrofolate reductase
Blocks nucleoside synthesis (Thymidine specific)
Also blocks purine and pyridine side ring synthesis

152
Q

Cytotoxic drugs: Mitotic spindle inhibitors

A 
Vinca Alkaloids (Vincristine/Vinblastine)
Taxotere (Taxol)
153
Q

Cytotoxic drugs: Non-cell cycle specific agents

A

Alkalating agents
Platinum derivatives
Cytotoxic antibiotics

154
Q

What is the negative about Non-cell cycle specific agents

A

Damage healthy cells as well as tumor cells

155
Q

Immediate side effects of Cytotoxic drugs

A

Bone marrow suppression
Gut mucosal damage
Hair loss (Alopecia)

156
Q

Side effects of Vinca alkaloids, Anthracyclines and Cis-platinum

A

Vinca alkaloids - neuropathy
Anthracyclines - cardiotoxicity
Cis-platinum - Nephrotoxicity

157
Q

Long term side effects of Alkylating agents

A

Infertility

Secondary malignancy

158
Q

Long term side effects of Anthracyclines

A

Cardiomyopathy

159
Q

How can some types of tumors escape systemic chemotherapy

A

Evade into the CNS. drugs do not cross the blood brain barrier

160
Q

Where are stem cells taken from for a transplantation

A

Mainly blood

161
Q

High vs Low dose of chemo kills cells by what mechanism

A

Low dose - Apoptosis

High Dose - Necrosis

162
Q

What is Neutropenic Sepsis

A

Sepsis + Neutrophil count

163
Q

Whai is given to treat fungal infections in chemo patiets

A

Prophylactic antifungal drugs

Itraconazole OR Posaconazole

164
Q

What is found in Hodgkin’s lymphoma on microscopy

A

Reed-Sternberg cells

165
Q

Rituximab is what type of drug, binds to what

A

Monoclonal antibody
Binds specifically to CD20 B cells.
IgG Fc domain works in synergy with human immunesystem

166
Q

What hematological cancers is Rituximab used for

A

High grade B cell NHL
Chronic Lymphocytic Leukemia
Low grade and Mantle cell NHL

167
Q

Anti-B cell antiboidies

A

Rituximab
Ofatumunab
Obinutumab

168
Q

What drug is used in Hodgkin’s disease and what is the target

A

Brentuximab Vedotin

CD30

169
Q

What hematological cancer is Biological treatments used in

A

Multiple Myeloma

170
Q

What is Bortezomib

A

Protesome inhibitors

Blocks breakdown of old proteins, therefore build up of toxins occur

171
Q

What are IMIDs

A

Immunomodulatory drugs
Derivatives of Thalidomide (Lenalidomide)
Used in Low grade NHL and CLL when chemo doesn’t work anymore
Used in combo with chemo in mantle cell NHL

172
Q

Treatment of Chronic Myeloid Leukemia

A

Tyrosine kinase inhibitor
Imatinib
Nilotinib – Dasatinib – Ponatinib

173
Q

What are Ibrutinib and Idelalisib

A

Drugs affecting B cell signaling pathway

Effective in low grade NHL and B cell CLL that don’t respond to Rituximab and chemotherapy

174
Q

What is Nivolumab

A

Binds to tumor cells “evasion” protein. Normally this allows the tumor to evade the immune system but this drug block the evasion and the immune system attacks the tumor

175
Q

What happens if you give Amoxycillin to EBV tonsillar lymphadenopathy

A

Induced rash

Diagnostic of EBV

176
Q

How are the lymphnodes in viral infection

A

Painful/tender
Hard and regular
Not tethered

177
Q

Hodgkin’s disease vs NHL

A

Suspect in young patient esp female
Disease above diaphragm more common
B symptoms and itch, alcohol induced pain more common than with NHL
Node biopsy is the real way to differentiate

178
Q

What is seen on biopsy of lymphnode in Hodgkins disease

A

Nodular sclerosing

Reed Sternberg cells

179
Q

How is Hodgkin’s Disease staged

A

CT and PET scan

180
Q

Done week 2 lectures

A

Yes

Mattias - Hemotology (3 decks)

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