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More CP Flashcards

1
Q

What is haematocrit?

A

Vol % rbcs in blood

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2
Q

Is haematocrit higher or lower in children?

A

Higher

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3
Q

Zeta + epsilon = what sort of Hb?

A

Hb Gower-1

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4
Q

Zeta + gamma =?

A

Hb Portland

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5
Q

Alpha + epsilon

A

Hb gower-2

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6
Q

Hb gower 1 is ?

A

Zeta + epsilon

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7
Q

Hb Portland is ?

A

Zeta + gamma

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8
Q

Hb gower 2 is ?

A

Alpha + epsilon

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9
Q

When are Hbs gower1, portland and gower 2 present?

A

4-14 weeks gestation

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10
Q

When does HbF become present?

A

more than 14 weeks gestation

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11
Q

Difference in WBCs in children?

A

More lymphocytes

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12
Q

Which Ig crosses the placenta?

A

IgG

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13
Q

Which Igs in breast milk?

A

All

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14
Q

When do babies start producing their own antibodies?

A

2-3 months

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15
Q

When can babies have their own satisfactory immune responses?

A

6 months

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16
Q

When do platelets reach adult numbers?

A

18 weeks gestation

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17
Q

What are 2 features of gestational platelets?

A

Larger initially but reduce to adult size by birth

Hyperresponsive to vWF

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18
Q

Which clotting factors are normal at birth? What are the rest of them like?

A

Fibrinogen, FV, VIII, XIII

Rest are reduced

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19
Q

When do haemostatic parameters reach adult values?

A

6 months

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20
Q

What is vitamin k dependent other than factors 10, 7, 9, 2?

A

Proteins S and C

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21
Q

What does routine neonatal vit k injections prevent?

A

Haemorrhagic disease of the newborn

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22
Q

What are 5 features of neonatal haemostasis?

A 
Pro-coagulant proteins reduced (e.g. all the other factors)
Reduced conc. coagulation inhibitors
unique forms fibrinogen, plasminogen
Raised D dimers and vWF
Platelet aggregation differs
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23
Q

What is acute leukaemia?

A

Accumulation of early myeloid or lymphoid precursors in BM, blood and other tissues

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24
Q

What are the two main subgroups of acute leukaemia

A

Acute myeloid leukaemia and acute lymphoblastic leukaemia

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25
Q

How does acute leukaemia present?

A

Anaemia
Infection
Easy bruising or haemorrhage
Possibly organ infiltration by the leukaemia cells

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26
Q

FAB classification of leukaemia is ?

A

Morphological

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27
Q

WHO classification of leukaemia is ?

A

Risk adapted- takes into account prognosis

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28
Q

6 poor prognostic factors in ALL?

A 
Age
High wcc
Male
Cytogenetic abnormalities (some)
Poor response to Rx
T cell -ALL and null-ALL
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29
Q

2 tests for diagnosis?

A

MABs

Fluorescence activated cell sorting

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30
Q

Treatment for acute leukaemia that is shared with ALL and AML

A

Induction therapy to obtain remission
Consolidation cheomtherapy
Possible BM transplant

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31
Q

Additional Rx in ALL

A

Prophylaxis of meningeal leukaemia with intrathecal methotrexate and cranial irradiation

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32
Q

Siblings have a ?% change of being a bone marrow donor match?

A

25%

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33
Q

What is neutropenic sepsis?

A

All pts with acute leukaemia receiving intensive chemotherapy will become neutropenic for 10-21 days.
Overwhelming gram negative or positive infection= sepsis.

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34
Q

What is neutropenic fever?

A

Pyrexia in the presence of neutrophil count of less than 1.0/10^9/L

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35
Q

What is the management of neutropenic sepsis?

A

Immediate broad spectrum IV Abx (often Tazocin and gentamicin) given empirically- within 30 mins of temperature

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36
Q

Prevention of neutropenic sepsis?

A

Isolation
Prophylactic Abx
Granulocyte colony stimulating factors
Strict hand hygeine

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37
Q

Which element of virchow’s triad contributes to arterial thrombosis?

A

Endothelial damage

38
Q

Which elements of virchow’s triad contributes to venous thrombosis?

A

Venous stasis and hypercoagulable state

39
Q

What are arterial thrombi made of?

A

Platelets

40
Q

What are venous thrombi made of?

A

Fibrin

41
Q

Definition of a hospital acquired VTE?

A

Within 90 days discharge

42
Q

Having considered the risks of bleeding and VTE, if there is a risk of bleeding how can you still help prevent a VTE?

A

Mechanical methods eg stockings

43
Q

When must you reassess risks of bleeding and VTE?

A

Within 24hrs admission and whenever the clinical situation changes

44
Q

True of false antiplatelets are adequate prophylaxis against VTE alone?

A

False, also mobilisation and hydration

45
Q

4 pharmacological methods of prevention

A
  1. low molecular weight heparin (antithrombin and mostly anti-Xa)
  2. Fondaparinux
  3. Rivaroxaban/apixaban (direct factor Xa inhibitor)
  4. Dabigatran (direct thrombin inhibitor)
46
Q

What is the exclusion test for a VTE?

A

Use Wells score and D-dimer in an algorithm

47
Q

What are D-dimers?

A

Breakdown product of fibrin clots

48
Q

Scans for:
VTE
PE

A

VTE- US

PE- CT, VQ- compare inhaled and injected isotopes. Mismatch is diagnostic of a PE

49
Q

Advantages of Rivaroxaban/apixaban/dabigatran over heparin?

A

Dose uniform rather than done by weight so monitoring not needed
Rapid onset of action
Oral route

50
Q

Management for a first episode of DVT or PE

A

Treat for 3-6 months if there is a temporary risk factor such as pregnancy

51
Q

What is warfarin target INR?

A

2.5

52
Q

Management for recurrent episodes of cardiothoracic emboli?

A

Long term anticoagulation

53
Q

Management of a proximal DVT or PE that has occured in the absence of a reversible risk factor?

A

Consider long term anticoagulation

54
Q

Management if they have recurrent VTEs even on therapeutic anticoagulants?

A

Increase target INR to 3.5 for warfarin

55
Q

What is a thrombophilia (2 definitions)

A
  1. familial/acquired predisposition to thrombosis

2. patients who develop VTE spontaneously, extra bad or recurrently at an early age

56
Q

What is the action of protein C and what is it activated by?

A

Thrombin-thrombomodulin complex activates it (thrombomodulin is on the vessel wall), protein C-protein S complex breaks down factor Va and VIIIa resulting in coagulation.

57
Q

In factor V leiden, factor V is resistant to what?

A

Protein C

58
Q

When is factor V leiden asymptomatic?

A

Heterozygous

59
Q

Are screening tests valuable in factor V leiden?

A

Debatable as often wouldn’t change management. Doesn’t increase risk of recurrent thrombosis.

60
Q

What is prothrombin 20210A?

A

Increased prothrombin levels, 3 fold increase in VTE

61
Q

What is the dx criteria for antiphospholipid syndrome?

A

Presence of antiphospholipid antibodies on at least 2 occasions 8-12 weeks apart in assoc with VT, AT or recurrent foetal loss (more than 2)

62
Q

What might antiphospholipid syndrome be secondary to?

A

SLE, conn tissue disorders etc.

63
Q

When should you screen for thrombophilia?

A

In younger patients, positive Fhx and if management will change.

64
Q

Folate and B12 deficiency cause what type of anaemia?

A

Megaloblastic macrocytic

65
Q

Main cause and other 4 causes of folate deficiency?

A 
Dietary main cause
Alcohol
Malabsorption
Increased usage
Drugs
66
Q

What is iron transported in?

A

Transferritin

67
Q

What is iron stored in?

A

Ferritin/haemosiderin

68
Q

2 causes of microcytic anaemia

A

Fe deficiency

Hb disorders

69
Q

3 causes of iron deficiency

A 
Blood loss
Increased demand (pregnancy,growth)
Redued intake (diet, malabsorption)
70
Q

Rx for iron deficiency

A 
Oral iron (although constipation and abdo pain)
IM iron (although painful and skin colour change)
IV iron probably best
71
Q

How do B12 and folate deficiencies cause anaemia?

A

B12 required for cell folate generation, folate required for nitrogenous base synthesis which make up DNA

72
Q

What foods is B12 from?

A

Animal sources

73
Q

Describe the absorption of B12

A

Gastric parietal cells absorb
Bound to intrinsic factor
Receptors in terminal ileum

74
Q

How long are B12 stores sufficient for?

A

Years

75
Q

3 causes of B12 deficiency

A 
Nutritional (vegan)
Gastric problems (pernicious anaemia, gastrectomy)
Small intestine problems (resection, crohns, stagnant loops, jejunal diverticulitis, tropical sprue, fish tapeworm)
76
Q

Severe B12/folate deficiency can result in…?

A

pancytopenia

77
Q

What neurological problem can B12 deficiency result in?

A

Sub acute degeneration of the spinal cord

78
Q

Rx B12+/folate deficiency?

A

Give B12 and folate until B12 deficiency is excluded as folic acid in isolation can make B12 def worse.

79
Q

7 cases haemolytic anaemia

A 
Haemoglobinopathy
Enzyme defects (G6PD)
Hereditary spherocytosis/elliptocytosis
Antibodies to RBC
Drubs/toxins
Heart valves
Vascular
80
Q

What is the name of haemolytic anaemia in its own right?

A

autoimmune haemolytic anaemia (AIHA)

81
Q

Rx AIHA

A

steroids and immune suppression

82
Q

What sort of aneamia is anaemia of chronic disease?

A

Normocytic

83
Q

What is the MCV in anaemia of chronic disease?

A

Normal

84
Q

3 reasons anaemia of chronic disease happens?

A

Abnormal Fe metabolism
Poor EPO response
Poor BM response

85
Q

11 causes of thrombocytopenia

A 
drugs alcohol toxins
infection (sepsis, EBV, HIV)
Other autoimmune
DIC
Liver disease
Hypersplenism
Congenital
Pregnancy
Haematological/marrow diseases
Immune thrombocytopenic purpura
Thrombotic thrombocytopenic purpura
86
Q

Immune thrombocytopenic purpura cause in children

A

Post viral- self limiting

87
Q

Rx immune throbocytopenic purpura

A

Steroids
Thrombomimetics
IV Igs (blocks spleen)
Splenectomy

88
Q

What is the role of the spleen in terms of platelets?

A

Removes them

89
Q

How does Immune thrombocytopenic purpura present?

A

Bruising, petechiae, bleeding

Splenomegaly

90
Q

Cause of thrombotic thrombocytopenic purpura

A

Immune (ADAMTS-13, vWF)

91
Q

Presentation of thrombotic thrombocytopenic purpura

A

Thrombocytopenia +

Fever, neurological, haemolysis

92
Q

Rx thrombotic thrombocytopenic purpura

A

Plasma exchange

Steroids

AH extra cards (29 decks)

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