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Phase 2a Ru > Haem > Flashcards

Haem Flashcards

1
Q

What is prothrombin time

A

The coagulation speed through the extrinsic pathway (10-13.5s)

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2
Q

How do you calculate INR

A

Patient PT/ Reference PT

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3
Q

What can raise INR

A

Anticoags
Liver Disease
Vit K deficiency
Disseminated intravascular coag (DIC)

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4
Q

What is Activated partial Thrombo-plastin (APT) time

A

Coagulation speed through Intrinsic Pathway

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5
Q

Examples of microcytic anaemia

A

Fe deficiency (MC)
Thalassemia
sideroblastic anaemia
Lead poisoning
Chronic disease

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6
Q

Examples of Haemolytic normocytic anaemia

A

Sickle cell
GGPDH deficiency
Autoimmune hemolytic anaemia (AHA)
Hereditary spherocytosis (rbc are spherical instead of bi-concave)

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7
Q

Examples of non haemolytic anaemia

A

Aplastic
Chronic disease (especially CKD)
Pregnancy
Hypothyroidism

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8
Q

Examples of megaloblastic macrocytic anaemia

A

B12 Deficiency
Folate deficiency

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9
Q

Examples of non-megaloblastic macrocytic anaemia

A

Alcohol
Hypothyroidism
NALD

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10
Q

Symptoms of anaemia

A

Fatigue, pallor, chest pain, exertional dyspnoea, tachycardia, hypotension, palpitations

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11
Q

Most common cause of iron deficiency anaemia worldwide

A

Hookworm (causes GI bleeding)

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12
Q

What age is recommended for urgent endoscopy with fe deficiency

A

60+ (red flag for colon cancer)

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13
Q

What can cause malabsorption of fe

A

IBD, Coeliac

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14
Q

Other than general anaemia Sx, what do you get in fe deficiency

A

Koilonchya (spoon-shaped nails)
Angular stomatitis (ulceration @ mouth corners)
Atrophic glossitis (tongue enlarged)

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15
Q

What do you see on blood film of fe deficiency anaemia

A

Hypochromic RBC, target cells + howell Jolly bodies

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16
Q

What do fe studies show in someone with fe deficiency anaemia

A

Low serum fe
Low ferritin
Low transferrin
Raised Total iron binding capacity

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17
Q

What is the treatment for fe deficiency anaemia

A

Treat underlying causes then
Ferrous sulphate (Oral Fe)

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18
Q

What are side effects of ferrous sulphate

A

GI upset, diarrhoea/ constipation, black stool
If poorly tolerated then consider ferrous gluconate

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19
Q

What is the inheritance pattern of thalassemia

A

Autosomal resseive

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20
Q

What anaemias are protective against malaria

A

Thalassemia, sickle cell

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21
Q

What is the gold standard investigation for Thalassemia

A

Hb electrophoresis

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22
Q

Is alpha or beta thalassemia more common

A

Beta

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23
Q

What mutations cause alpha thalassemia

A

4 genes of chromosome 16 (deletions)

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24
Q

What mutations cause beta thalassemia

A

2 genes on chromosome 11

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25
Q

Which thalassemia is associated with abnormal Hb isoforms

A

Alpha (HbH isoform)

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26
Q

What are the 3 classes of beta thalassemia

A

Thalassemia minor/ intermedia/ major
Minor:- carrier
Inter:- marked anemia
Major:- severe anaemia

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27
Q

What gene abnormalities do patients have with each of the beta thalassemia classes

A

Minor:- 1 abnormal 1 normal
Inter:- 1 abnormal 1 deletion or 2 abnormal
Major:- 2 deletion

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28
Q

Other than general anaemia Sx, what do you see in beta-thalassemia major

A

Chipmunk face:- massively enlarged cheekbones and forehead due to decreased RBC needing extramedullary haematopoiesis

Hepatosplenomegaly
Failure to thrive
May see RUQ pain due to gallstones

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29
Q

What do you see on blood film in thalassemia

A

Hypochromic RBC, Target cells

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30
Q

What do you see on XR in thalassemia

A

‘Hair on end’ due to increased bone marrow activity in the skull

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31
Q

What is the treatment for thalassemia

A

Regular transfusion
Iron chelation:- to prevent Fe overload
Splenectomy after 6 y/o
Folate supplements for haemolytic
Vit C

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32
Q

What is side effecst of iron chelation

A

Deafness
Cataracts

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33
Q

Why do you wait until after 6 y/o for splenectomy in thalassemia

A

Spleen plays a defensive role against encapsulated bacteria

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34
Q

What is the definitive treatment for thalassemia

A

BM stem cell transplant:- risky

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35
Q

What is sideroblastic anaemia

A

Defective Hb synthesis

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36
Q

What is most common inheratance for sideroblastic anemia

A

X linked

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37
Q

What is a functional Fe deficiency

A

High levels of Fe but not used in Hb synthesis, becomes trapped in mitochondria

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38
Q

What do you see on blood film in sideroblastic anemia

A

Ringed sideroblasts + basophilic strupping

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39
Q

What do Fe studies show in sideroblastic anaemia

A

High Fe
High ferritin
High transferrin sats
Low Total iron binding capacity

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40
Q

Where can haemolyisis occur and what is marker to differentiate

A

Intravascular:- marked by raised haptoglobin
Extravascular @ spleen

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41
Q

What is the inheritance pattern for sickle cell anaemia

A

Autosomal recessive

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42
Q

GS investigation for sickle cell anaemia

A

Hb electrophoresis

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43
Q

What malaria is sickle cell protective against

A

Falciparum malaria

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44
Q

What is the mutation and amino acid change seen in sickle cell anaemia

A

GAG to GTG
Glutamic acid to valine

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45
Q

Which codon is affected in sickle cell anemia

A

6th

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46
Q

What are the complications of sickle cell anaemia

A

Splenic sequestration:- spleen expanding due to trapped RBC
Vaso-occlusive crisis:- sickle cells polymerise and get trapped in long bone blood vessels
Acute chest crisis:- pulmonary vaso-occlusion (emergency)

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47
Q

In patients with sickle cell disease, what organism is most likely to cause osteomyelitis

A

Salmonella

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48
Q

What do you see on the blood film in sickle cell anaemia

A

Normocytic normochromic w/ increased reticulocytes
Sickled RBC + Howell Jolly Bodies

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49
Q

How do you treat acute attacks in sickle cell

A

IV Fluid+ NSAIDS + O2

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50
Q

What is the long term treatment for sickle cell disease

A

Hydroxycarbamide + folic acid supps
Transfusion, Fe Chelation

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51
Q

What is the inheritance pattern for G6PDH Deficiency

A

X linked recessive

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52
Q

What is the pathology of G6PDH deficiency anaemia

A

Enzynompathy causes a dysfunction in the G6PDH enzyme which is involved in the synthesis of glutathione. Glutathione protects RBC against ROS. Halfs the length of RBC

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53
Q

Symptoms of G6PDH deficiency

A

Mostly aSx unless precipitated
Naphthalene:- Pesticide in mothballs
Antimalarials:- quinine
Aspirin
Fava Beans:- Contains Glucosides

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54
Q

How does a G6PDH attack present

A

Rapid anemia+ Jaundice

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55
Q

What do you see on a blood film of G6PDH between attakcs

A

Normal

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56
Q

What do you see on a blood film in a G6PDH attack

A

Normocytic normochromic w/ increased reticulocytes
Heinz bodies + bite cells

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57
Q

What is management for G6PDH deficiency

A

Avoid precipitants
Transfusions when attacks ensue

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58
Q

What is the inheritance pattern for Hereditary Spherocytosis

A

Autosomal dominant

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59
Q

Age of onset for CML, CLL, AML, ALL

A

ALL CeLLmates have CoMmon AMbitions
ALL:- under 5 over 45
CLL:- over 55
CML:- over 65
AML:- over 75

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60
Q

1st line investigation in Lueakmia

A

FBC

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61
Q

DDx of Petechiae

A

Leukaemia
Meningococcal septicaemia
Vasculitis
Non-Accidental injury

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62
Q

GS investigation for leukaemia

A

Bone marrow biopsy

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63
Q

Bone marrow aspiration vs Bone marrow trephine

A

Aspiration:- liquid sample, can be examined straight away
Trephine:- Solid core sample provides better picture, requires a few days of preparation

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64
Q

What cell is usually affected n ALL

A

Proliferation of B-Lymphocytes

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65
Q

What chromosome abnormality is ALL associated with

A

Trisomy 21 Downs

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66
Q

What does ALL show on blood film

A

Blasts

67
Q

What is the translocation that occurs in the Philadelphia chromosome

A

9:22

68
Q

What % of adults with ALL have Philidelphia chromosome

A

30%

69
Q

What is CLL

A

Chronic lymphocytic leukaemia is where there is chronic proliferation of a single type of well-differentiated lymphocyte, usually B-lymphocyte

70
Q

What is ALL

A

Acute lymphoblastic leukaemia is where there is a malignant change in one of the lymphocyte precursor cells. It causes acute proliferation of a single type of lymphocyte, usually B-lymphocytes.

71
Q

Sx of CLL

A

Often asymptomatic but can present with
Infections
Anaemia
Bleeding
Weight Loss

72
Q

What anaemia can CLL cause

A

Warm autoimmune haemolytic anaemia

73
Q

What can CLL transform into and what is this known as

A

High-grade lymphoma
Richters transformation`

74
Q

What do you see on a blood film in CLL

A

Smer/ smudge cells
These occur during preparation of blood film when aged/ fragile WBC rupture

75
Q

What are the 3 phases of CML

A

Chronic phase
Accelerated phase
Blast phase

76
Q

What occurs in the chronic phase of CML

A

Lasts around 5 years
Often Asymptomatic
Patients diagnosed initially with raised WCC

77
Q

What is the accelerated phase of CML

A

The abnormal blast cells take up 10-20% of the cells in the bone marrow.
Patients become more symptomatic
Develop anaemia and thrombocytopenia become immunocompromised

78
Q

What is the blst phase of CML

A

Blast cells take up 30% of bone marrow
More severe symtpoms
Pancytopenia
Often fatal

79
Q

What is the cytogenic gene change that is characteristic of CML

A

Philadelphia chromosome t(9:22)

80
Q

What do you see on blood film in AML

A

A high proportion of blast cells with rods inside their cytoplasm known as Auer rods

81
Q

Examples of myeloproliferative disorders AML can transform from

A

Polycythemia ruby vera
Myelofibrosis

82
Q

What are the complications of chemotherapy

A

Failure
Stunted growth
Infections
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
Tumour lysis syndrome

83
Q

What is leukaemia primarily treated with

A

Chemotherapy and steroids

84
Q

What is tumour lysis syndrome

A

Caused by the release of uric acid from cells that are being destroyed by chemotherapy. The uric acid can form crystals in the interstitial tissue and tubules of the kidneys causing AKI.

85
Q

What is tumour lysis syndrome

A

Caused by the release of uric acid from cells that are being destroyed by chemotherapy. The uric acid can form crystals in the interstitial tissue and tubules of the kidneys causing AKI.

86
Q

What is given to treat tumour lysis syndrome

A

Allopurinol or rasburicase reduce uric acid levels

87
Q

What are the general symptoms of leukaemia

A

Bone pain, Bleeding, infections, anaemia

88
Q

What Sx of AML

A

General leukaemia
Gum infiltration
Hepatosplenomegaly

89
Q

Sx of CML

A

General leukaemia
Massive hepatosplenomegaly

90
Q

Sx of CLL

A

General
Lymphadenopathy

91
Q

Treatment for CML

A

Chemo + imantinib

92
Q

Treatment for ALL

A

Chemo

93
Q

In which leukaemia do you sometimes give IVIg

A

CLL

94
Q

Which lymphoma has Reed Steinberg cells

A

Hodgkins lymphoma

95
Q

What are the B symptoms

A

Fever
Night sweats
Unintended weight loss

96
Q

What the 3 grades of non-Hodgkin lymphoma

A

Low grade:- follicular
High grade:- Diffuse
Very high grade:- Burketsts

97
Q

How would you describe the age presentation in Hodgkins lymphoma

A

Bimodal:- Teens and elderly

98
Q

What virus is EBV associated with

A

Epstein Barr virus
(Glandular fever)

99
Q

Sx of Hodgkins lymphoma

A

B symptoms
Painless rubbery lymphadenopathy
(Painful after drinking alcohol)

100
Q

GS investigation for hodgkins lymphoma

A

Lymph node biopsy
Reed-Steinberg +ve

101
Q

What is the effect of Hodgkins lymphoma on the levels of Lactate dehydrogenase, Hb and ESR

A

Raised ESR
Raised LDH
Reduced Hb

102
Q

What do you use for staging lymphoma

A

CT/MRI chest/ abdo/ pelvis
Ann Arbour staging

103
Q

What are the grades in the Ann Arbour staging

A

1:- Single lymph node
2:- 2 lymph nodes on the same side of the diaphragm
3:- Lymph odes on both sides of the diaphragm
4:- Extra nodal organ spread
(A or B if ‘B’ symptoms present)

104
Q

Treatment for Hodgkins Lymphoma

A

ABVD chemotherapy
Adriamycin, Bleomycin, Vinblastine, Dacarbazine

105
Q

What is Nodular Lymphocytic predominant Hodgkins

A

A subtype of Hodgkins that produces Popcorn Cell

106
Q

What are SE of Chemo

A

Alopecia
N+V
Myelosuppression
Infection

107
Q

What are patients whove just had high dose chemo at massive risk of

A

Febrile Neutropenia

108
Q

What are Sx of febrile Neutropenia

A

Fever, Tachycardia, Sweats, Tachypnoea

109
Q

Treatment for Febrile Neutropenia

A

Immediate broad-spec antibiotics
Amoxicillin

110
Q

Is hodgkin or non-hodgkin lymphoma more common

A

Non hodgkin

111
Q

What is the most common type of non-hodgkin lymphoma

A

Diffuse Large B cell 80%

112
Q

What are Sx of non-hodgkin lymphoma

A

B symptoms
Painless rubbery lymphadenopathy not affected by alcohol

113
Q

What is GS investigation for non Hodgkin lymphoma

A

Lymph node biopsy
Confirms subtype

114
Q

What is the treatment for non Hodgkin lymphoma

A

R-CHOP chemotherapy
Rituximab
Cyclophosphamide
Hydrodaunorubin
Vincristine (Oncon)
Prednisolone

115
Q

What does Rituximad tartget

A

CD20 on b cell

116
Q

What is multiple myeloma

A

Neoplastic monoclonal proliferation of a plasma cell. Typically leads to excess production of 1 Ig

117
Q

Sx of multiple myeloma

A

OLD CRAB
Old
HyperCalcemia
Renal failure
Anaemia
Bone lesions

118
Q

What ethnicity are risk from multiple myeloma

A

Afro-Caribbean

119
Q

What do you see on blood film in multiple myeloma

A

Normocytic normochromic anaemia
Rouleaux formation (aggregation of RBC)

120
Q

Other than FBC and blood film, what investigations may you perform in suspected multiple myeloma

A

Urine dipstick (Bence jones proteins)
U+E:- renal failure
Bone profile:- Hypocalemia+ raised ALP
Serum electrophoresis:- Ig ‘M Spike’
XR:- pepper pot skull
osteolytic lesion

121
Q

What is a precursor to multiple myeloma

A

MGUS
Mammyloid gammopathy of undetermined siginifcance

122
Q

What is the treatment for multiple myeloma

A

Chemotherapy, bisphosphonates, dialysis
Consider BM transplant

123
Q

What is polycythemia

A

Increased RBC/ Hb

124
Q

What is cause of primary and secondary polycythemia

A

Primary:- Polycythemia Vera
Secondary:- Hypoxia, Increased EPO, Dehydration (alcohol)

125
Q

What mutation is present in 95% of polycythemia vera

A

JAK2V617

126
Q

Sx of polycythemia vera

A

Itchy after a bath, burning in fingers and toes (erythromelalgia), reddish complexion, blurred vision/ headache, hepatosplenomegaly

127
Q

What does FBC show in polycythemia vera

A

Raised WCC/ platelets/ RBC

128
Q

Treatment for polycythemia vera

A

Non-curative
Venesection + aspirin
Consider chemo in high-risk patient (hydroxycarbamide)

129
Q

What is inheritance pattern of haemophilia

A

X linked recessive males more affected

130
Q

Is haemophillia A or B more comme

A

A

131
Q

Sx of haemophilia

A

Spontaneous bleeds, haemarthrosis, very easy bruising + epistaxis

132
Q

How are PT and APTT affected in haemophilia

A

Normal PT but increased APTT as only intrinsic pathway affected

133
Q

Which clotting factors are affected in haemophilia A and B

A

A:- factor 8
B:- factor 9

134
Q

Investigations in haemophilia

A

Bleeding scores, coagulation factor assays,

135
Q

Treatment for haemophilia A

A

IV factor 8 + desmopressin (releases factor 8 stored in vessel walls

136
Q

Treatment for haemophilia B

A

IV factor 9

137
Q

What is the inheritance pattern for VWF disease

A

Autosomal dominant

138
Q

What chromosome is the VWF gene located on

A

12

139
Q

What is the most common inherited bledding disorder

A

Von Willebrand Factor disease

140
Q

How are PT and APTT affetced in VWF diseases

A

Normal Pt, Increased APTT

141
Q

Treatment for von Willebrand factor diseases

A

Non-curative
Desmopressin (releases of VWF from endothelial Weibelpalade bodies

142
Q

What is DIC

A

Disseminated intravascular coagulation
Massive activation of coagulation cascade

143
Q

What can cause Disseminated intravascular coaulation

A

Trauma, sepsis (meningococcal meningitis rash), malignancy

144
Q

How can DIC lead to a bleed risk

A

Platelets unnecessarily consumed = microthrombi form in small BV
Lack of systemic platelets

145
Q

Treatment for DIC

A

Replace clotting factors, cryoprecipitate (replace fibrinogen), platelet transfusion + RBC transfusion if bleed.

146
Q

How is D-Dimer affected in DIC

A

Raised

147
Q

What is D-Dimer

A

Fibrin degradation product

148
Q

What do you see on a blood film in EBV

A

Atypical lymphocytes

149
Q

What age at risk form EBV

A

15-24

150
Q

What conditions is EBV associated with

A

Hodgkins, Burketts, Nasopharyngeal carcinoma

151
Q

What types of malaria with most common

A

Plasmodium falciparum MC
P. Ovale
P. vivax
P. malanese

152
Q

What type of mosquitoes carry malaria

A

Female anopheles mosquito

153
Q

Pathology of malaria

A

Sporozoites in mosquito salvia inoculate into human host
Mature in hepatocytes into merozoites
Then enter RBC:- merozoites to trophozoites to schizont to new merozoite
RBC rupture causing systm=emic infection

154
Q

Sx of malaria

A

Fever +exotic travel
Anemia
Blackwater fever
Massive hepatosplenomegaly

155
Q

Investigation for malaria

A

Thick and Thin blood film
3 samples sent over 3 consecutive days to exclude malaria due to 48hr cycle

156
Q

Treatment for malaria

A

Quinine+ Doxycycline
IV artesunate if severe

157
Q

What is a SE of quinine

A

Hypoglycemia

158
Q

Which is more virulent HIV-1 or HIV-2

A

HIV-1, is also more common

159
Q

Pathology of HIV

A

HIV gp120 binds to CD4 on T helper
Endocytoses RNA + enzyemes
Reverse transcriptase turns RNA into DNA
Viral DNA is integrated into host
Protein synthesis
Viral proteins + RNA exocytose + take part of CD4

160
Q

What testing do you undertake to diagnose someone with HIV

A

Anti HIV Ig
p24 Antibody

161
Q

How do you monitor the progression of HIV

A

HIV RNA copies+ CD4 count

162
Q

Treatment for HIV

A

HAAART
High active antiretroviral therapy
3 drugs

163
Q

What is the progression of HIV

A

Primary infection leads to CD4 dip
Years of clinical latency
Then Fever, diarrhoea, night sweats, minor opportunistic infection (oral infection)
AIDS when CD4 <200/mm3

164
Q

AIDS-defining conditions

A

CMV
Pneumocystis jirovecii pneumonia
Cryptosporidium (fungal)
TB
Kaposi sarcoma
Toxoplasmosis
Lymphomas

Phase 2a Ru (10 decks)

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