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Y6 Senior Med > Haem Laz > Flashcards

Haem Laz Flashcards

1
Q

What do multipotent stem cells differentate into

A
  • common myeloid progenitor

- common lymphoid progenitor

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2
Q

what do commoon myeloid cells differentiate into

A

MYELOBLASTS (monocytes, neutrophils, basophils, oesinophils)

ERYTHROCYTES

MEGAKARYOCYTES

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3
Q

What do common lymphoid progenitor differentiate into?

A

T cells

B cells > plasma cells

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4
Q

What cells does AML affect

A

Common myeloid progenitor and myeloblast

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5
Q

What cells does CML affect

A

Monocytes, neutrophils, basophils, oesinophils

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6
Q

What cells does ALL affect

A

Common lymphoid progenitor

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7
Q

What cells does CLL affect

A

B cells, T cells

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8
Q

Summarise AML presentation

A

Adults
BM failure (pancyctopoena)
acute onset
Auer rods

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9
Q

Summarise ALL presentation

A

Children
BM failure
Failure to thrive

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10
Q

Summarise CML presentation

A

Adults
t(9,22) transolcation - PHIILADELPHIA CHROMOSOME
Often incidental finding, occasionally BM failure
Tx IMATINIB

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11
Q

Summarise CLL presentation

A

Adults
Often incidental finding, occasionally BM failure
SMUDGE CELLS

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12
Q

What does MAHA stand for

A

Microangiopathic Haemolytic Anaemia

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13
Q

WHat is MAHA

A

MECHANISM NOT DISEASE

RBC breakdown in small vessels

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14
Q

What does HUS stand for

A

Haemolytic uraemic syndrome

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15
Q

What is HUS caused by

A

E coli 0157:H7 which produces shiiga like toxins
this causes endothelial injury in glomerular vessels
leading to platelet plug formation > THROMBOCYTOPOENIA
RCs destroyed as they try to get past > MAHA
Poor kiidney perfusion > renal failure

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16
Q

What is the triad of HUS and what othher Sx may occur

A

HUS: MAHA + thrombocytopoenia + renal failur

+ diarrhoea (due to e coli)

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17
Q

What is TTP

A

Thrombotic thromobocytopoenic purpura

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18
Q

What occurs in TTP

A

ADAMTS 13 is reduced (unkown cause, cancer, pregnancy)

AdamTS13 is usually used to break dowon vWF multimers

This means that there are excessve vWF multipmers > form platelet plug > platelet consumton, RC destruction, poor end organ perfusion

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19
Q

Sx of TTP

A

MAHA + Thrombocytopoenia + renal failure

+ RASH + CONFUSION (due to reduced brain perfusion)

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20
Q

What is DIC caused by

A

increased exposure to tissue factor, such as in

  • pregnancy
  • sepsis
  • tumour
  • pancreatitis
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21
Q

What does DIC stand for, and what occurs

A

Disseminated INtravascular Coagulaton

increased exposure to tssue factor
activation of clotting cascade
- increased platelet consumption > THROMBOCYTOPOENAI
- increased coag factor consumption > decreased coagulation factors

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22
Q

What is multiple myeloma

A

Cancer of plasma cells

resulting in excessive monoclonal Ig production

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23
Q

What is the progression of monoclonal Ig disease

A
  1. MGUS
  2. Smouldering myeloma
  3. MM
  4. B cell leukaemia
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24
Q

how does MGUS present

A

NO CRAB SX

  • M protein <30g/L
  • BM plasma cells <10%
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25
Q

how does smouldering myeloma present

A

M protein >30g/L
BM plasma cells >10%

annual risk of progression to MM is 10%
no CRAB SX

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26
Q

How does mutliple myeloma present

A

CRAB SX
M protein >30g/L
>60% plasma cells in BM
>1 focal lesion on MRI

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27
Q

What symptoms occur with MM

A 
CRAB 
calcium elevared
renal failure 
anaemia 
bone lesions (lytic)
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28
Q

what Ix myst you get in MM

A
  1. FBC, UE, bone profile, ESR, serum Ca
  2. Serum / urine electrophoresis
  3. Whole body low dose CT
  4. Bone marrow aspirate and biopsy
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29
Q

What does Serum / urine electrophoresis show in MM

A

shows a single monoclonal band (MONOCLONAL GAMMOPATHY)

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30
Q

what proteins are present in MM

A

Bence Jones proteins

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31
Q

what is myelodysplasia

A

abnormal differentiation of cells along myeloid line

this causes a BM disorder with PANCYTOPOENIA and FUNCTONALLY IMMATURE CELLS

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32
Q

what is myelofibrosis

A

clonal BM disorder characterised by fibrous scar tissue deposition

overexpansion of clone in BM > fibrous scar tissue deposits in reesponse

> > PANCYTOPOENIA, TEAR DROP CELLS; DRY TAP; MASSIVE SPLENOMEG to compensate for low RBC

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33
Q

causes of MICROCYTIC anaemia

A

TAILS

Thalassaemia 
Anaemia of Chronic Disiease 
Iron Deficiency anaemia 
Lead poisoning 
Sideroblastic anaemia
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34
Q

causes of NORMOCYTIC anaemia

A 
Iron deficiency (early) 
Chronic disease (early)
Marrow failure 
Renal failure 
Aplastic anaemia, Acute blood loss 
Leukaemia, Myelofibrosis
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35
Q

causes of MACROCYTIC anaemia

A

Alcoholics May Have Liver Failure

Alcoholism 
Myelodysplastic sydrome, MM
Hypothyroid, haemolytic anaemia 
Liver Failure 
Folate / B12 def
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36
Q

what size are RBC in haemolytic anaemia and why

A

MACROCYTIC or normocytuic

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37
Q

what are causes of haemolytic anaemia

A

INHERITED: defect of RBC which cauze them to be broken down

  • membrane (hereditary spherocytosis)
  • cytoplasm / enzyme (G6PD deficiency)
  • Haemoglobin (SCD or thalassaemia)

Aquired (defect in environment the RBC are in, either immune or non immune mediated)

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38
Q

why must you be careful measuring ferritin in IDA?

A

if no illness, fair to check

if ill - be aware that FERRITIN is an ACUTE PHASE PROTEIN so check TIBF, TTF, iron instead

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39
Q

what are the two types of immune-mediated anaemia

A

AIHA (warm and cold)

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40
Q

What test can you do for AIHA

A

Coomb’s test / direct antiglobulin test

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41
Q

Explain features of WARM AIHA

A

GHANA: IgG, 37 deg
spherocytes
outside of europe: EXTRAvascular haemolysis

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42
Q

explain features of COLD AIHA

A

Mountain: IgM
under 37 deg
inside europe: INTRAvascular

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43
Q

what causes tumour lysis syndrome

A

recent chemotherapy, causing destruction of lots of cells

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44
Q

what are electroolytes like in tumour lysis syndrome

A

HIGH K+
hgh phosphate
low calcium

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45
Q

what does positive clinical TLS require

A

At least one of the following.

  • > 1.5x ULN creatinine
  • cardiac arrythmia / sudden death
  • seizure
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46
Q

Mx tumour lysis syndrome

A 
IV allopurinol (if high risk) 
PO allopurinol (if low risk) - can be given prophylactically
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47
Q

when do you ned to transfuse packed RBC

A

No ACS : for Hb <70

ACS: Hb <80

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48
Q

what level do you need to maintain platelets at for:

  • pre-procedure
  • pre-procedure if surgery at critical site
  • no active bleedsing / planned surgery
A
  • pre-procedure: >50
  • pre-procedure if surgery at critical site >100
  • no active bleedsing / planned surgery >10
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49
Q

what is a THROMBOPHILIA

A

LOVES THROMBI > propensitiy to develop clots

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50
Q

causes of thrombophilia - inherited

A

Factor V Leiden
Prothrombin gene mutation
Protein C/S deficiency
Antithrombin III deficiency

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51
Q

causes of thrombophilia - aquired

A

antiphospholippid syndrome

Drugs (COCP)

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52
Q

what is heparin inducted thrombocytopoenia (HIT)

A

a PROTHROMBOTIC condition

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53
Q

how does HIT ooccur

A

AB form against complexes of platelet factor 4 and hepatin > induce platelet activation > low platelets but LOTS OF THROMBI FORMATION

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54
Q

Classic HIT presentaton

A

> 50% reduction in platelets
Thrombosis
Skin allergy

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55
Q

How do you manage HIT

A

STOP HEPARIN, chaange to Argatroban (thrombin inhibitor)

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56
Q

what category are anti D antibodies

A

IgG (dont cause direct agglutination - cause a delayed haemolytic transfusion reaction instead)

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57
Q

what are antibodies against A, B on blood

A

IgM against normal RBC antigens

IgG against atypical RBC antigens

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58
Q

List acute transfusion reactions (<24h)

A 
Acute haemolytic reactions (ABO incompatibility) 
Allergic / anaphylactic
Infection (bacterial) 
Febriile non haemolytic reaction 
Respiratory (TACO, TRALI)
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59
Q

what occurs in sickle cell anameia

A

defective beta globin gene (glutamine to valine), which leads to abnormal folding of RBC into sickle shape

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60
Q

What is mode of inheritance of sickle cell

A

AR

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61
Q

what occurs in thalassaemiai

A

reduced haemoglobin synthesiis

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62
Q

which type of malaria is most fatal

A

Plasmodium falciparum

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63
Q

what other types of less fatal malaria exist

A

Plasmodium vivax
ovale
knowlesi

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64
Q

describe symptoms of P falciparum

A 
cyclical fevers (every 48h) 
splenomegaly 
neuro involvement (altered GCS and seizures) 
DV 
metabolic acidosis 
shock
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65
Q

how do you treat malaria falciparum

A

mild: oral MALARONE / artemisin combination therapyu
severe: IV Artesunate

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66
Q

how do you treat other types of malaria

A

chloroquine

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67
Q

classical general S/S of malaria

A 
onset 7-10 days after inoculation 
fever (cyclical or continuous with spikes) 
DV 
flu like sx 
jaundice 
anaemia 
drowsiness, confission
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68
Q

how do you investigate for malaria

A

3 thick and thin blood films (thick: presence; thin: species)
Malaria rapid antigen detection test

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69
Q

How do you prevent malaria

A

Quinine prophylaxis

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70
Q

typhoid fever cause

A

salmonella typhi / paratyphi

71
Q

how is typhoid transmitted

A

faeco oral

72
Q

sx typhus

A 
fever 
bradycardia 
headache 
dry cough 
weight loss, anorexia 
GI sx (diarrhoea or constipation)
73
Q

classical derm presentation of typhuss

A

rose spots

74
Q

Mx typhus

A

IV ceftriaxone

75
Q

where is typhus still found

A

pakistan
india
bangladesh

76
Q

organism that causes dengue fever

A

arbiirus flavivirus - aedes aegiptii mosquito

77
Q

sx dengue

A

short incubation period
Primary infection: headache, sunburn rash, fever and myalgia
Secondnary infection: DENGUE HAEMORRHAGIC FEVER, very unwell with hypotennsion and massive haemorrhages

78
Q

how do you treat dengue

A

supportive (fluids and monitoring) >ITU

79
Q

what are ‘Tear-drop’ poikilocytes found in

A

myelofibrosis

80
Q

what is ITP

A

Immune Thrombodytopoenia

essentially antibodies against GLPIIb/IIIa > thrombocytopoenia

81
Q

how does ITP present

A

petechhiae, purpura, bleeding

82
Q

how do you manage ITP

A

oral pred

IVIG

83
Q

how does acute haemolytic reaction present

A

DURING/RIGHT AFTER TRANSFUSION

  • fever
  • abdo pain
  • hypotension
84
Q

how do you confirm an acute haemolytic reaction

A

COOMBS +ve

85
Q

How do you manage acute haemolytic reaction

A
  • stop transfusion

- fluid resus

86
Q

what is the most common BLEEDING DISORDER

A

von Willenbrand isease

87
Q

mode of inheritance of vWD

A

AD

88
Q

what is the normal role of vWF

A

to promote platelet adhesion to damaged endothhelium

89
Q

types of vWD

A
  1. Reduced quantity vWF
  2. poor quality vWF
  3. total lack vWF
90
Q

mx neutropoenic sepsis

A

Tazocin

91
Q

what drughs cause haemolysis in G6PD deficiency

A

Ciprofloxacin

S drugs: sulphoonamides, sulphonylurea, sulphasalazine

92
Q

how do you confirm G6pD deficiency

A

G6PD levels now and in 3 months

93
Q

what transfusion reaction is someone with IgA deficiency more at risk of

A

ANAPHYLACTIC REACTION (because they are more likely to have anti-IgA that attack the donor blood)

94
Q

which type of vWD are AD and which are AR?

A

AD: type 1 and 2
AR: type 3 (total lack vWF)

95
Q

what do ix for vWF reveal

A

prolonged APTT

prolonged bleeding time

96
Q

how can you manage vWF

A

tranexaminc acid, desmopressin (which induces vWF release), F8 concentratee

97
Q

important ix in MM and their findinga

A
  • serum / urine electrophoresis (shows monoclonal gammopathy of IgG or IgA and Bence-Jonees protein)
  • FBC, UE, Ca, bone profile, blood film, ESR
  • bone marrow aspirate and biopsy
  • whole body CT/MRI
  • X ray head
98
Q

what does X ray head show iin MM

A

a RAINDROP SKULL (similar to pepper pot skull in 1HPTH)

99
Q

sx of polycythaemia

A

hyperviscosity: headache, light headedness, visual changes, fatigue, dyspnoea

histamine release: aquagenic pruritus, peptic ulceration, splenomegaly

100
Q

What are blood findings on polycythaemia

A

Raised Hb and Htc

101
Q

what mutation is iportant in distinguishing the cause of polycythaemia

A

JAKV617F +ve = polycythaemia vera

JAKV617F -ve = True polycythaemiia (hypoxia, renal disease, tumour) or pseudopolycythaemia (dehydration)

102
Q

what does polycythaemia vera risk progressing to

A

myelofibrosis

AML

103
Q

mx polycythaemia

A

venesection

aspirin (to reduce risk of thrombosis)

104
Q

what is the FASTEST reaction to blood transfusion that can occur

A

anaphylactic reaction (SOB, wheeze, facial oedema. IMMEDIATE)

or allergic (may be mild - just pruritic rash)

105
Q

what is the decond fastest reaction to blood transfusion that can occur

A

Acute haemolytic reaction(due to ABO incompativiliy, IgM mediagted) - within mins

106
Q

sx Acute haemolytic reaction

A
  1. Fever
  2. Abdo pain
  3. low BP
107
Q

how do you mx Acute haemolytic reaction

A

stop transfusion

fluid resus

108
Q

how does febrile non haemolytic transfusion reaction pesent

A

rise in temp by 1 degree without circulatory collapse

+- chilld and rigors

109
Q

how do you manage febrile non haemolytic transfusion reaction

A

stop or slow transfusion, give paracetamol

110
Q

what kind of transfusion is most likely to cause bacterial contamination

A

platelet transfusion

111
Q

how do you manage TACO

A

IV furosemide
slow / stop transfusion
oxygen

112
Q

how do you manage TRALI

A

stop transfusion, supportive

113
Q

how doees a delayed type haemolytic transfusion reeaction present

A

same as acute but milder

occurs within one week of transfgusion

114
Q

how does GvHD present

A

within one week of transfusion

  • rash
  • skin desquamation
  • diarrhoea
  • fever
115
Q

causes of MASSIVE SPLENOMEGALY

A 
myelofibrosis
chronic myeloid leukaemia
visceral leishmaniasis (kala-azar)
malaria
Gaucher's syndrome
116
Q

how do you remove the risk of GvHD and what patients need this adaptation

A

by IRRADIATING

patients with hodgkin /immunocompromised/neonates <28days

117
Q

what patients need CMV neg blood

A

intrauterine / neonates / preg

118
Q

what do you give in pts with IDA who cannot tolerate oral iron / time interval is too short

A

give IV iron 1g

repeat 1 week later

119
Q

how does ITP present

A

petechiae
purpura
bleeding q

120
Q

how do you manage ITP

A

Oral pred

IVIG

121
Q

what are the four types of hodgkins lymphoma

A

Nodular sclerosing
Mixed cellularity
lymphocyte predominant
lymphocyte depleted

122
Q

what cells are classical of hodgkins and what do they looi like

A 
REED STERNBERG (binucleated Owl's eye cells) 
= large multinucleate cells with prominent eosinophilic nucleoli.
123
Q

what is the staging system of hodgkins

A

ANN ARBOUR

124
Q

explain ann arbour staging

A

1: 1 site on one side of the diaphragm
2: >1 site, on one side of diaphragm
3: both sides of diaphragm
4: BM, lungs, liver involvement

125
Q

what are B symptoms in hodgkins

A

fever >38
night sweats
unintentional WL >10% body weight in 6 months

126
Q

what do B symptoms suggest in terms of prognosis

A

POOR

127
Q

how do you manage an allergic reaction to the transfusion

A

stop the transfussion

administer antihistamine

128
Q

which type of hodgkins has the best prognosis

A

Lymphocyte predoiminant

129
Q

what part of the intestine is iron absorbed in

A

in the DUODENUM

130
Q

what part of the intestine is folate absorbed in

A

JEJUNUM

131
Q

what part of the intestine is B12 absorbed in

A

ILEUM

132
Q

what vitamin will someone with al ilieocaecal resection from chrons be deficient in

A

B12

133
Q

blood findings for EBV glandular fever

A

RAISED lymphocytes, no neutrophils

134
Q

sx glandular fever

A

fatigue

recurrent tonsillitis

135
Q

how is hodgkins different to NHL

A

Hodgkin’s lymphoma has:

  • alcohol-induced pain in the node
  • ‘B’ symptoms typically occur earlier
  • Extra-nodal disease rare
136
Q

how do you invesitgate lymphoma

A
  • FBC, CRP ESR, blood film, LDH
  • exisional node biopsy
  • CT chesst abdo pelvis (staging)
  • HIV test
137
Q

what is the most aggressive NHL

A

Burkitt’s

138
Q

who does Burkitts occur in

A

young immunosuppressed

EBV and HIV associations

139
Q

what are high grade NHL

A

DLBCL and mantle cell lymphoma

140
Q

what is the MOST COMMON type of lymphoma

A

DLBCL

141
Q

what virus is DLBCL asociated with

A

EBV

142
Q

types of low grade lympha

A

follicluar
malt
SLL/CLL

143
Q

how do you treat CML

A

Imatinib (tyrosine kinase inhib)

144
Q

what lymphoma has a starry sky appearance on LN buopsy

A

Burkitts

145
Q

what findings does waldenstrom’s macroglobilinaemia have

A

monoclonal IgM paraproteinaemia
systemic upset: weight loss, lethargy
hyperviscosity syndrome e.g. visual disturbance
the pentameric configuration of IgM increases serum viscosity
hepatosplenomegaly
lymphadenopathy

146
Q

how must you manage beta thalassaemia major

A

LIFELONG BLOOD TRANSFUSIONS

+ desferroxamine to avoid iron overload

147
Q

what electrolyte abnormality may occur following transfusion of large volume RBC

A

HYPERKALAEMIA (because packed RBC have high potassium)

148
Q

what is the most common inherited thrombophilia, and what is pathophy

A

FACTOR V LEIDEN (heterozygous)

– due to resistance to Protein C

149
Q

what does the presence of band cells indicate

A

CML

150
Q

what kind of leukaemia does LOW LYMPHOCYTES point to

A

AML or CML

151
Q

what is sideroblastic anaemia

A

inability to form haem > form ring sideroblasts instead

152
Q

causes of sideroblastic anaemia

A 
congenital 
myelodysplasia 
alcohol 
lead
anti TB meds
153
Q

ix in sideroblastic anaemia

A 
FBC (hypochromic microcytic) 
iron studies (raised ferritin, raised iron, raised transferrin sat) 
blood film (Basophilic stippling) 
BM staining (ring sideroblasts)
154
Q

what is aplastic anaemia

A

pancytopoenia + hypoplastic BM

155
Q

causes of aplastic anaemia

A

congenital

  • Fanconi
  • dyskeratosis congenita

drugs

  • cytotoxics
  • chloramphenicol
  • sulphonamides
  • phenytoin

viral

  • parvovirus
  • hepatitis
156
Q

which pathway does PT measure

A

the EXTRINSIC PATHWAY (i.e. the short one, activated by tissue factor)

157
Q

which pathway does APTT measure

A

the INTRINSIC PATHWAY (long)

158
Q

what factors are involved in the INTRINSIC PATHWAY

A

12, 11, 9, 8, 10

159
Q

which factors are involved in EXTRINSIC PATHWAY B

A

tissue factor

F7

160
Q

explain the common pathway

A

PROTHROMBIN converts to THROMBIN (by F10a)
FIBRINOGEN converts to FIBRIN (by thrombin)
FIBRIN cross links the clot

161
Q

what are causes of prolonged PT only (i.e. issue is in the extrinsic pathway)

A

inherited (F7 deficiency)

Aquired (mild viit K, liver disease, warfarin, DIC)

162
Q

what are causess of prolonged APTT ONLY (issue in intrinsic pathhway)

A

deficiency of any of the factors invlved

vWD

163
Q

causes of prolonged PT AND APTT

A

deficiency of fibrinogen, prothrombin, F5, F10
liver disease
DIC
anticoagulants

164
Q

what is heparin MoA

A

inhibits antithrombin (whhich blocks thrombin)

165
Q

how many globin chains is each Hb made up of

A

4 globin chains

166
Q

what are the types of Hb and which globin chains do they contain

A 
HbF= 2 alpha, 2 gamma (foetal, drops at 3m of life) 
HbA = 2alpha, 2 beta (adult) 
HbA2 = 2alpha, 2 delta (small portion of adult)
167
Q

what occurs in beta thalassaemia

A

beta globin deficiency !! > free alpha chains form inclusions > haemolysis of RBC

haemolysis means

  • raised bilirubin > jaundice
  • raised iron > haemochromatosis

increased RBC production to compensate > HEPATOSPLENOMEGALY

168
Q

what sx do you get with beta thalassaemia then

A

jaundice, haemochromatosis

hepatosplenomegaly

169
Q

what are blood findings of thalassaemia

A

microcytic anaemia
target cells
raised iron

170
Q

what are the combinations of beta blobin mutations you can get in thalassaemia

A 
beta+ = less than normal 
beta0 = no beta chains
171
Q

what are the types of beta thalassaemia

A

beta thalassaemia major = beta0beta0
beta thal intermedia ? beta+beta+
beta thal minor = beta+beta or beta0beta

172
Q

how does beta thalaasaemia present on electrophoresis

A

low HbA

raised HbF, HbA2

173
Q

what type of thalassaemia is incompativle with life

A

alphha thalassaemia major = Hb Barts (x4 alpha globin gene deletion) > hydrops fetalis, death in utero

Y6 Senior Med (29 decks)

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