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Phase 1c - Written > Haematology > Flashcards

Haematology Flashcards

1
Q

What is DIC

A

coagulation in blood walls → organ ischaemia.
Other blood vessels bleed -> cosumption of clotting factors

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2
Q

What organs are affected by DIC ischaemia?

A

-Brain
-Liver
-Lung
-Kidney

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3
Q

Clinical signs of DIC

A

-Bleeding
-bruising
-Confusion
-drop in bp

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4
Q

Investigations of DIC:

A

Bloods: high D Dimer, Long PT and APTT, low platlets & fibrinogen, schistocytes.

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5
Q

How to manage DIC

A

treat cause + tranfuse FFP

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6
Q

What is haemochromatosis?

A

Depositation of iron on organs.

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7
Q

What is the precursor of haemachromatosis?

A

haemosiderosis- no organ involvement

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8
Q

symptoms (organ-involvement)

A

skin->melatonin
hands-> arthritis
liver-> cirrohsis
heart-> cardiomyopathy
pancreas-> diabetes

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9
Q

What is the worst organ involvement in haemochromatosis?

A

heart

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10
Q

Causes of haemochromatosis?

A

primary-> HFE mutation
Secondary-> transfusion

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11
Q

Investigations for haemochromatosis:

A

FBC: Transferrin^ (transporter) , ferritin^ (cells holding iron) ,iron^,low TIBC (binding capacity)
LFTs
Cell microbiology: iron seen in blood
genetic testing: HFE
full body MRI: organ involvement

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12
Q

First line tx haemochromatosis

A

Venesection

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13
Q

second line tx for haemochromatosis

A

desferrioxamine (iron cheltion therapy)

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14
Q

What does heparin inhibit?

A

thrombin and antithrombin

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15
Q

Why is LMWH easier? (3)

A

longer halflife
no monitroing
better bioavailability

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16
Q

LMWH vs HMWH

A

LM: binds to just thrombin helping it inactivate factor 10
HM: binds to antithrombin and thrombin (potentiating antithrombin)

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17
Q

What is heparin used for?

A

actue coag problems (pe/dvt/ surgery)

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18
Q

APTT and PT time with heparin

A

increased (factor 10 is in both)

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19
Q

Risks of heparin

A

bleeding
osteoporosis
HIT

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20
Q

How to reverse heparin

A

Protamine sulfate

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21
Q

What is HIT and when does it occur?

A

heparin induced thrombocytopenia?
5-14 days after

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22
Q

What is warfarin and what is it given for?

A

anticoag inhibits glycoslyation of vit k so factors 2,7,9,10 inhibited.
chronic coag problems

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23
Q

How is warfarin administered vs heparin

A

W: oral
H: IV

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24
Q

APTT and PT in warfarin

A

prolonged in both

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25
Q

Monitor warfarin?

A

INR

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26
Q

Reverse Warfarin

A

INR 8+ and bleed: PTC and vit K and stop W
everything else: stop W and vit K
iNR 5-8 no Bleed: withhold W

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27
Q

Risks with Warfarin?

A

tetrogenicity
skin necrosis
interactions
bleeding

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28
Q

Protein C depletion with Warfarin

A

skin necrosis

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29
Q

drug interactions with Warfarin

A

p450 inducers: reduce INR: SCARS: (smoking,alcohol,anti epi, st johns wort)
p450 inhbiitors: increase INR: ASS-ZOLES ( antibiotics, SSRIs, sodium valoporate, -zoles)

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30
Q

What is the heparin bridge?

A

give heparin before warfarin to stop skin necrosis+ warfarin takes time

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31
Q

What anti coag should you NOT give to pregnant women?

A

Warfarin

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32
Q

What are DOACS? (stand for)

A

Direct oral anticoagulants
inhibit factor 2 or 10

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33
Q

When is it used?

A

home therapy
second line to heparin: DVT, arrythmias

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33
Q

APTT and PT time in DOACs

A

prolonged both

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34
Q

Risk

A

Bleeding, hypersenitivity

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35
Q

reverse DOACS?

A

antibodies that bind to them:
Idarucizumab → anibody binds to factor2DOAcs

andexanet alpha → anitbody factor 10 doacs

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36
Q

What is polycythaemia?

A

increased haemtocrit/blood volume (psuedo or true)

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37
Q

primary vs secondary polycythaemia?

A

primary: polycythaemia vera JAK2 mutation
Secondary: increased EPO secreted -> hypoxia, kidney disease, hormone meds(test,steroids)
pseudo: decreased plasma: dehydration

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38
Q

What hormones medications increase EPO

A

Testosterone, steroids

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38
Q

signs/symptoms of pv

A
  • plethoric (red face esp nose)
  • itchy after shower
  • headache
  • fatigue
  • -splenomegly
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39
Q

Risks for polcythaemia

A

thrombosis!!!!

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39
Q

polcythaemia is a sign of….

A

malignancy, JAK2 mut, meds

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40
Q

Invest of pv

A

Bloods: RBC, Haemtocrit, Hb
EPO serum ^
JAK2 mutation screen

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40
Q

1st line treatment of polcy

A

Venesection + aspirin,

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41
Q

second line treatment

A

add hydroxycarbiamide if not working OR high risk of thrombosis

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41
Q

How to detect Haem ?

A

genectic testing
Bloods: APTT prolonged, PT normal, Bleeding time normal, VWF low

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42
Q

What is Haemophilia A?

A

deficiency in factor 8

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43
Q

How to treat Haem ?

A

infuse lost clotting factor, sometimes desmopressin to stimulate VWF (only in A)

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43
Q

Signs of Haem ?

A

sustained bleeding, intramuscular and in joint bleeding, epistaxis.

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44
Q

Is mucosal bleeding in Haemophilia?

A

No

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45
Q

What is more common Haem A or B

A

Haem A

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46
Q

How is haemophilia passed down?

A

x LINKED Recessive

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47
Q

What is sustained haemophilia?

A

clotting factor 8/9 reduced by soemthing else eg DIC, autoimmune

48
Q

What is 50:50 mixing and how does it relate to haem

A

after 50:50 mix there is NO correction (corrects in VWF)

49
Q

How to confirm Haem A or b

A

Factor 8 & 9 assay

50
Q

Treat

A

Desmopresin

50
Q

How is VWD passed down?

A

Autosomal dominant

50
Q

What is VWF?

A

deficiency in VWD

50
Q

What deficiency is Haem b?

A

FACTOR 9 DEFIC

51
Q

Signs of VWD?

A

Mucosal bleeding + mennorhagia + intramsucualr bleeding

52
Q

Signs of bloods?

A

Factor 8 activity low, APTT prolonged, BLEEDING TIME LONG, PT normal

53
Q

Is mucosal bleeding seen in VWD, haem or both?

A

only VWD

54
Q

What is a Coombes/DAT test?

A

+ve if there is autoantibodies

55
Q

What is Sickle Cell disease?

A

Inherited condition causing a defect in the beta chain of HbS whereby red blood cells change shape and can occlude blood vessels.

56
Q

Signs of SCD?

A
  • Unprovoked persistent pain
  • Splenomegly
  • anaemia symp (lethargy, pallor)
  • bone pain
  • ## high temp
57
Q

When does scd present?

A

Typically 6 months, when HbF starts to decrease

58
Q

What can increase risk of scd crises?

A

-infection
-dehydration
-hypoxia
-acidosis
-cold

58
Q

different types of scd crises (3+1)?

A
  • Sequestration
  • Vaso-occlusive -> acute chest syndrome
  • ## Aplastic
59
Q

How is SCD passed down?

A

Autosomal recessive

60
Q

Investi

A

FBC -> haemolytic anaemia, reticulocytes
blood film-> sickle shape
Chest x ray - acute chest syndrome
confirm: haem electrophoresis (HbF ^ HbS)

61
Q

What is squestration crises + management?

A

pooling in spleen , sudden drop in haem, signs of shock.
fluid resus, splenectomy?

61
Q

What is acute chest syndrome?

A

Type of vaso occulsive in the pulmonary vasculature. chest pain, resp symtoms

62
Q

What is aplastic syndrome?

A

sudden reduction in bone marrow production. Hb drops below 10, no pain + parovirus infection

63
Q

4 types of transfusion reactions?

A
  • Delayed Haemolytic tranfusion reactions
  • Acute Haemolytic
  • Transfusion-Related Acute Lung Injury (TRALI)
  • Autoimmune haemolytic Anaemia (AIHA)
  • ## Transfusion overload
63
Q

management for acute + chronic SCD?

A

acute: IV opiate, fluid, oxygen, antibx IF infection, transfusion
chronic: hydroxycarbidamide/hydroxyurea, Vaccinates

63
Q

What virus is associated with aplastic syndrome?

A

Parovirus B19

64
Q

splenomegly and massive splenomegly measurements

A

11-20 cm
>20cm

65
Q

When does delayed Haemolytic reactions occur?

A

non-prevenatble, 3-10 days after

65
Q

When does acute Haemolytic reactions occur?managemnt?

A

ABO incompatibilty, IgM antibodies, 24 hours -> STOP transfusion + recus

66
Q

What is TRALI?sign? manag? x ray? treat?

A

activation in pulmonary vasculature -> increased perm -> pul odemea, fever, hypo. White out on CXR. tx w furosemide

67
Q

What can cuase pancytopenia? (2 need to know + …)

A

-B12 or folate def
-methotrexate
-chemo
-cancer
-BM disease

67
Q

What is transfusion associated circulatory overload?

A

Too much fluid in circulation -> HYPERtension

67
Q

target INR: Valve replace,VTE, AF

A

INR 2-3: AF, aortic VR, following VTE
2.5-3.5: mitral VR
3.-4: recurrent VTE

68
Q

What do schistocytes mean?

A

haemolytic anaemia

68
Q

What are reed sternberg cells seen in?

A

only Hodgkins Lymphoma

69
Q

When are Tear Drop poikilocytes seen?

A

Myelofibrosis

70
Q

When are howell Jolly bodies seen?

A

hyposplenism

71
Q

target cells seen in?

A

SCD, thalassemia, liver disease

72
Q

When are ringed sideroblasts seen?

A

Myelodysplasia

73
Q

megaloblastic vs non megaloblastic anaemia

A

meg: b12 or folate defi (diet, malabsorp, pregn, pernious anaemia)
non-meg: alcohol, leauk

73
Q

What are two kinds of anti-platlet therapy?

A

-P2Y12 inhib
-Aspirin

74
Q

How does aspirin work?

A

Blocks cox 1+2, no thromboxane A2, no platelet agregg

75
Q

How does clopidogerol work?

A

PY212 inhib. blocks platelet agregg

76
Q

What is Aplatic Anaemia?

A
76
Q

What is myelodysplasia?

A

precancer to CML

77
Q

Investigations +results:

A

Bloods: pancytopenia, macro/normocytic anaemia, CRP high
BM analysis: ringed sideroblasts, blast cells less than 10%

78
Q

Why does myelodysplasia have blast cells of less than 10%?

A

BC 10+ = CML

79
Q

Myelodysplasia typical patient

A

Old w/ infections

80
Q

Mangement of myelodysplasia D+S

A

direct: chemo
supportive: transfusion + iron chelation therapy

81
Q

What is myelofibrosis?

A

BM fibrosis -> failure

82
Q

examination and blood signs of myelofibrosis (3)

A

splenomegaly, pancytopenia, **TEAR DROP POIKILOCYTES

82
Q

BM analysis and aspirate for myelofibrosis

A

fibroblasts on analysis and dry tap on aspirate.

83
Q

Who is MM most likely in?

A

Older patients

84
Q

1.

signs of MM?

A

bone pain + FRACTURES
Anaemia
Hypercalcaemia
renal impairment
infections

85
Q

Blood film finding for MM? (1 SPECIAL)

A

Roleaux formation, pancytopenia, urea and creatinine up

86
Q

BM analysis for MM

A

Plasma cells 10+%

87
Q

Other tests for MM

A

U&E
whole body MRI for staging

88
Q

Main treatment for MM?

A

Stem cell transplant

89
Q

Tumour lysis syndrome tx and biochemical chnages

A

PUKE CALCIUM
Allopurinol

90
Q

Which leukaemia is seen in kids?

A

ALL

90
Q

Which leukaemias have massive splenomegly?

A

CML, CLL

91
Q

BM analysis of CLL?

A

Hypercellularity

91
Q

Which cancers have lymphadenopathy?

A

CLL, Lymphomas

91
Q

What is found on blood film in CLL?

A

Smudge cells

91
Q

CML management?

A

Tyrosine kinase inhib -> Imitimab

92
Q

Abnormal mutation in CML

A

BCR-ABL t(9:22)

93
Q

Blood film difference in ALL and AML

A

AML had aurer rods

93
Q

HL vs NHL

A

H: Reed-sternberg cells

94
Q

What are cabot rings seen in?

A

lead poinsoning

95
Q

What blood film is seen with hyposplenism

A

Howell-Jolly boides and sideroblasts

96
Q

What do you give with methotrexate and why?

A

Folate - inhibit dihydroxide reductase

97
Q

What nuero issues does vit b12 defi cause

A

hands and foot pins and needles

98
Q

3 things to give with sickle cell crisis

A

-iv opiate
-oxygen
-fluids

99
Q

lymphoma that has dysphagia with alcohol

A

Hodgkins lymphoma

100
Q

1st line tx of VWD

A

Desmopressin

101
Q

target INR for mitral valve

A

2.5-3.5

102
Q

target INR for aortic valve

A

2-3

103
Q

febrile transfusion recation tx?

A

1st: slow (with minor temp) stop (with major temp) + paracetemol

104
Q

how to diagnose MM + staging

A

Protein electrophoresis
Whole body MRI

105
Q

lymphoma Ann Arbour staging

A

(A) (B)- B symptoms
stage 1: one node
stage 2: 2 or more nodes on the sameside
stage 3:nodes on both sides of the diagphrm
stage 4: organ involvement far away

Phase 1c - Written (2 decks)

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