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CICM > Heamatology > Flashcards

Heamatology Flashcards

1
Q

Macrocytosis causes

A 
Alcohol
B12/folate deficiency
Myelsdysplastic syndrome
Hypothyroidism
MM
Acute leukaemia
Drugs - valproate, phenytoin, metformin, chemo agents, antiretroviral
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2
Q

Microcytosis

A

Iron deficiency, thalassaemia, anaesmia of chronic disease, vit b deficiency, sideroblastic anaemia

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3
Q

Nucleated red cell

A

An immature subtype
Due to; BM struggling to keep up with losses or insufficient resources to complete maturation process

Causes-
Asplenua
Anaemia
Hypoxia
Sepsis
DKA
Renal Tx
Liver disease
Uraemia
Thermal injury
BM invasion by malignancy
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4
Q

Rouleaux formation of RBC

A 
Form of reversible RBC aggregation
Seen with anything that increases ESR
Causes-
Infection
Inflammatory disease of any sort
Hyperviscisity stndromes
MM
Malignancy dehydration
Diabetes
Chronic liver disease
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5
Q

Target cells (codocytes)

A

Lots Seen in thalassaemia
Hepatic disease with jaundice
Hb-C disorders
Post splenectomy

Less target cells seen in;
Iron deficiency
Sickle cell
Lead intoxification

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6
Q

Polychromasia

A

Many colours - immature cells in circulation
A non specific marker of bone marrow stress
A marker of impaired erythrocyte control (like Howell-jolly bodies)
Causes-
Haemorrhage, haemolysis
Recovery of normal BM function eg iron infusion, EPO injection
Failure of BM to sustain normal function eg myelofibrosis, BM infiltration
Failure of RBC control - splenectomy

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7
Q

Howell jolly bodies

A

Bits of leftover DNA in erythrocytes

Seen post splenectomy

Also - pernicious anaemia, steroid use

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8
Q

Heinz bodies

A

Lumps of denatured Hb within red cells
Indicate oxidative stress
Causes -
Toxins - solvents, quinidine
Unstable haemoglonins - chronic liver disease, alpha thalassaemia, methylene blue methaemoglobinqemia
Deranged RBC metabolism - dapsone toxicity, Bactrim
Decreased clearance defective RBC - post splenectomy

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9
Q

Blister cells

A

Blebs on surface of RBCs

Suggestive of oxidative damage

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10
Q

Leukemoid reaction

A

Hyperproliferation of leukocytes (typically neutrophils)

Usually only lasts 24 hours
Most important aetiology is myeloid leukaemia

Causes -
Infection
Drugs - steroids, GCSF
Increased neutrophil release - stress, trauma, exercise, sepsis
Inflammatory conditions - organ necrosis, empyaema, DKA
Malignancy - myeloproliferative disorders, lymphoma, solid tumours
Decreased neutrophil clearance - splenectomy

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11
Q

Schostocytes

A

Haemolysis

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12
Q

Cryoprecipitate contains

A

Fibrinogen
Factor 8, 13
VWF

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13
Q

TRALI diagnostic criteria

A 
Onset within 6 hours of transfusion
Hypoxia
Bilateral CXR infiltration
No other cause identified
No preexisting lung injury
Absence of risk factors for other causes of ALI
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14
Q

Clinical features of TRALI

A 
Hypoxia
Dyspnoea
Fever
Pulmonary oedema
Hypotension
Cyanosis
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15
Q

Pathophysiology ofTRALI

A

Neutrophils sequestered in lung parenchyma

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16
Q

Risk factors for TRALI

A 
Critical illnsee
Chronic alcoholism
Shock states
Smoking
High ventilatory pressures
Positive fluid balance
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17
Q

Risks of massive transfusion

A

Usually risks of transfusion (TRALI, reactions, infection, storage lesions)
Risks and complications of large volume resuscitation with blood; overload, overtramafusion, hypothermia. ALI, citrate toxicity)
If o neg used - difficulty cross matchcing in future. Difficulty with matching solid organs

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18
Q

Ghost cells

A

Clostridium perfingens

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19
Q

Underlying causes of TTP

A

Infection
Surgery
Pancreatitis
Pregnancy

All lead to endothelial activation

There is low activity of ADAMTS13 - a vWF cleaving protein
Then allows large vWF multimers to accumulate

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20
Q

Plasma exchange removes

A 
Autoantibody
Immune complexes
Myeloma light chains
Cryoglobulins
Endotoxins
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21
Q

Indications for plasma exchange

A 
GBS
MG
NMDA antibody encephalitis
TTP
Hyperviscpsity syndrome
Antiphospholipid syndrome
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22
Q

IVIg action and indications

A

Actions;
Multiple immunomodulatory and anti inflammatory activities
- modulates complement
- suppression of idiotype antibodies
- neutralisation of super antigens
- suppression of various mediators; cytokines, chemokines, adhesion molecules

Indications;
GVHD
ITP
APLS
toxic shock
Nec fasc
Wegners
Pempigus
SJS/TEN
GBS
MG
MS
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23
Q

COAG changes in pregnancy

A

Low platelets
Low factor 9
Low protein s

Increase factors 5 7 8 9 10 12 vWF
Increased fibrinogen

No change factor 2 and 5
Unchanged protein c

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24
Q

Ferritin

A

Gold standard for assessment of iron stores
Only cause of low level is iron deficiency
High levels -
- acute phase reactant
- pregnancy
- malignancy
- iron overload
- chronically transfused disease states (sickle cell, thalassaemia)
- haemophagocytic syndrome; VERY high levels; may be congenital or acquired (infections eg EBV CMV HIV, neoplastic eg lymphoma, autoimmune eg SLE

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25
Q

Transferrin

A

Binding protein and part of innate immune system
Decreased in inflammatory states
May rise in response to iron deficiency state

Transferrin saturation -
If less than 20% there is iron deficiency state, if over 45% there is iron overload state

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26
Q

Causes of thrombocytopaenia

A

Decreased production
- BM suppression due to alcohol, chemo, myelofibrosis, virus, nutritional deficiency, liver disease

Pseudothrobocytopaenia - improper sampling and clumping

Dilution - MBT, massive resus

Increased destruction
SLE, ITP. DIC, drugs, TTP, APLS, HELLP, circuits

Sequestration - hypersplenism, hepatic sequestration, extremes of temp

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27
Q

Management of thrombocytopaenia

A

Minimise destruction - withhold heparin, manage sepsis, address specific aetiologies (TTP, HELLP)

Maximise production -
Nutrition, rationalise drugs that are BM toxic, correct BM failure if possible

Protect from complications -
Postpone non essential invasive procedures
Cover essential procedures with platelets

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28
Q

Storage lesions

A

occur after 2-3 weeks
RBCs unergo a structural and function change
Changes include -
- reduced deformability
- reduced 23DPG -> left shift and decreased O2 delivery
- increased adhesiveness
- decreased concentration of NO
- reduced ATP
- accumulation of pro-inflammaory bioactive substances

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29
Q

Is it better to use newest blood?

A

NEJM 2017 - transfusion of freshest blood vs standard care (mean 22 days)

  • no difference in death at 90 days or secondary outcomes
  • subgroup analysis - higher APACHE group had higher 90 day mortality with fresher blood

Bottom line - no need to use newest blood, no harm from using older blood

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30
Q

Plasmacytosis

A

Increased plasma cells -
due to;
plasma cell disorder - MM, Waldenstroms macroglobulinaemia, solitary plasmacytoma

Other causes - pulmonary TB, cirrhosis, adenoCa of colon, syphillis

31
Q

Hyperviscosity syndrome

A

Often due to waldenstroms (IgM) but can be due to any plasmcytosis

Clinical presentation -

  • severe headaches (due to increased ICP from venous occlusion)
  • fluctuating level of consciousness
  • stroke
  • seizures
  • coma
  • constitutional symptoms - fatigue, malaise, letheragy
  • haemorrhagic symptoms - epistaxis, mucosal bleeding
  • blurred vision (retinal vein occlusion)
  • renal failure
  • aggravated heart failure

Lab -

  • leucocytosis (suggestive of malignancy)
  • high plasma count
  • high globulin level

Mx - plasmaaphesesis

32
Q

Smudge cells

A

deformed lmyphocytes associated with CLL

33
Q

Pathogenesis of anaemia of chronic disease

A

inflammation -> cytokine release -> increase hepcidin -> reduced iron release from BM and macrophages and reduced absorption of iron

34
Q

Findings in iron deficieny anaemia

A 
Low MCV
low iron
low ferritin (only cause)
high transferrin (a binding protein - increases as a reaction)
tranferrin saturation <<20%
35
Q

Findings in anaemia of chronic disease

A 
may be microcytic or normocytic
low iron
normal ferritin
low transferrin
normal transferrin saturation
36
Q

Causes of high ferritin

A

acute phase protein
pregnancy
malignancy
iron overload
chronically transfused states - sickle cell
chronic inflammatory states - chronic liver/renal disease, HIV

haemophagocytic lymthohistiocytosis

  • causes a VERY high ferritin
  • may be congenital or acquired; infection (|eBV, CV, HIV), neoplastic (lymphoma), autoimmune (SLE)
37
Q

Types of leukaemias

A

AML -

  • acute proliferation of immature myeloid precursor cells
  • acute promyelocytic anaemia is characterised by dense cytoplasmic granules and Auer rods

ALL - childhood, good prognosis

CLL -

  • presents with B symptoms, BM failure, splenomegaly and autoimmune haemolytic anamia
  • richters transformation -> diffuse large B cell lymphoma associated with poor prognosis

CML - linked to philadelphia chromosome

  • typically beings with chronic phase -> accelerated phase -> blast crisis
  • presents with wt loss, splenomegaly, fever, night sweats
38
Q

Classification of lymphoma

A

Hodkins - seen in young
- reed-sternberg cells are characteristic on hisology

Non-hodgkins -
- heterogeneous group with 30 different subtypes
- may be low grade or high grade
Low - follicular (most common), waldenstrom macroglobulinaema, mantle cell lymphoma
High - most common is diffuse b cell lymphoma
- Burkitts - fast growing, high risk of TLS

39
Q

Multiple myeloma

A

plasma cell malignancy

present with bone pain, fractures, BM faliure, renal failure

40
Q

Types of haematopoietic stem cell transplant

A

Source of stem cells -

  • peripheral
  • bone marrow
  • umbilical cord blood

Donor of cells -

  • autologous - re-infusing peripheral blood of patient from during time of remission
  • allogenic - donor; more intensive myeloablative regimens and immunosuppresion
41
Q

Patterns of infection following HSCT

A

Pre-engraftment - <30days
- at risk of bacterial infections due to neutropenia

Early post-engraftment - 30-100days

  • cell mediated immunity impaired
  • risk of fungal and viral infections (CMV, PJP, aspergillus)

Late post-engraftment -

  • impaired reticuloendothelial, cell medicated and humoral factors
  • at risk of mycobacteria and viruses
42
Q

Problems following HSCT -

A 
INfection
GVHD
Graft failure
Diffuse alveolar haemorrhage
Idiopathic pneumonia syndrome
Engraftment syndrome
cryptogenic organising pneumonia
veno-occlusive disease
Posterior reversible encephalopathy syndrome
post transplant lymphoproliferative disorder
TTP
43
Q

GVHD

A

incidence 30-50% post allogenic Tx
- increases with advancing age of donor and recipient, inadequate immunosuppresion, HLA mismatch, use of peripheral blood as stem cell source

Acute - presents 7-28days after Tx with rash (esp on palms and soles), dirrhoea and intrahepatic cholestasis

Is staged and graded -

  • each system staged 0-4
  • then combined to give clinical grade

Prophylaxis is with immunosuppressants
treatment is high dose methyl pred

44
Q

Chronic GVHD

A

multi-organ syndrome which occurs >100 days after Tx
May be limited or extensive

Can involve - skin, eyes, lungs, salivary glands, neuromuscular system, liver

Treatment is difficult as need to increase immunosuppresion but try to avoid infections

45
Q

idiopathic pneumonia syndrome

A

usually seen 3/52 after Tx
diffuse infiltrates on CXR
high mortality

46
Q

Engraftment syndrome

A

also known as capillary leak syndrome
- presents 4-5 days after autologous Tx with fever, rash, non-cardiac pulm oedema

Use of GCSF increases prevalence and must be stopped

47
Q

cryptogenic organising pneumonia (or bronciolotis obliterans organising pneumonia)

A

occurs 1-3/12 after Tx
Presents with SOB, fever, cough

Treatment is with steroids and response usually good

Other causes -

  • follow on from many types of pneumonia
  • drugs
  • connective tissue disordrs
  • organ tx (BM and lung)
  • malignancies
  • radiotherapy

Is an important cause of peripheral consolidation on HRCT

  • presents with flu-like illness

Definitive Dx is with lung biopsy and negative mirco
- PFT will show reduced DLCO

NB - it is DIFFERENT to bronchiolitis obliterans - non reversible due to fibrosis and inflammation

48
Q

Veno-occlusive disease (sinusoidal obstruction syndrome)

A

Triad of -

  • painful hepatomegaly
  • jaundice
  • ascites

Presents 3/52 after Tx

Other features - wt gain, encephalopathy, bleedings, hepato-renal sydrome

Doppler will show reduced or reversed portal flow

49
Q

Posterior reversible encephalopathy syndrome

A

Characterised by headache, seizures, visual loss

T2 MRI (CSF bright) shows diffuse hyperintensity in parieto-occipital white matter

50
Q

Acute oncological emergencies

A

Neutropenic sepsis - Abx in1 hours, consider antigungals if no improvement in 4-7days
- start with anti-pseudomonal beta-lactam with addition of vanc/aminoglycoside or fluroquinolone if resistance suspected

Neutropenic enterocolitis (typhlitis) - abdo pain, fever and diarrhoea due to mucosal wall damage
 - usually  needs conservative Mx (TPN)

Respiratory failure - many causes

AKI - many causes

TLS

51
Q

Causes of respiratory failure in a haem onc patient

A

Non infectious - general

  • ARDS
  • aspiration
  • pulmonary oedema
  • chemo-induced toxicity
  • cryptogenic organising pneumonia
  • pulmonary infiltration - leukaemia or thumour

Non infectious specific to HSCT -

  • diffuse alveolar haemorrahge
  • idiopathic pnemonia syndrome
  • engraftment syndrome

Infectious -

  • bacterial - psuedomonas, klebsiella, acinetobacter, staph, enterococcus, strep, leigonella, mycoplasma
  • viral - flu, adenovirus, parainfluenza, RSV, CMV, HSV, VZV
  • fungal - candida, aspergillus, PJP
  • mycobacterium - TB
52
Q

Tumour lysis syndrome

  • definition
  • characteristics
  • risk factors
A

oncological emergency
caused by rapid lysis on tumour cells -> release of intracellular contents into circulation

Characterised by -
raised K, PO4, urate, LDH
low Ca

Increased risk with - (can be divided into patient and tumour factors)

  • large tumour mass
  • organ infiltration by tumour
  • bone marrow involvement
  • pre-existing renal disease or dehydration
  • tumours sensitivity to chemo
  • high intensitiy of chemo
  • acidic urine
  • nephrotoxin exposure
  • unchecked K and PO4 replacement
  • pre-exisiting gout
53
Q

TLS - prevention and treatment

A

Prevention -
Hydration to achieve u/o 1-1.5ml/kg/hr to reduce chance of uric acid precipitating in renal tubules

Avoid K containing fluids

Allopurinol - 300-600mg/day
- decreases uric acid formation by blocking xanthine oxidase enzyme

Rasburicase - a recombinant urate oxidase enzyme that converts uric acid to allantoin (10x more soluble that uric acid)

Alkalinization of urine - not common - aim is to reduce the liklihood of uric acid precipitating in the tubules

54
Q

Treatment of TLS

A

repeated dose of rasburicase
Careful management of fluids and electrolyes
Specific Mx of hyperK, HypoCa and hyper PO4
Haemodilysis for standard indications

55
Q

Causes of hepatosplenomegaly

A 
malaria
myelofibrosis
sarcoidosis
amyloidosis
CML
chronic liver disease
kala-azar (viscaeral leischmaniasis)

the above list also cause massive splenomegaly

pernicious anamia
acromegaly
thyrotoxicosis
SLE
obesity
viral infections eg EBV
metabolic storage diseases
56
Q

Massive splenomegaly

A 
malaria
myelofobrosis
sarcoid
amyloid
CML
chronic TB
thalassaemia major
polycythehmia
Waldenstroms macrogolobulinaemia
57
Q

abnormal bleeding

normal PT normal APTT

A

vWB disease
platelet dysfunctoin
fibrinolysis disorder

SHould order platelet function studies

58
Q

normal APTT, abnormal PT

A

Exrinsic pathway failure

warfarin
vit K def
liver diease
isolated factor VII def

59
Q

Abnormal APTT, normal PT

A

Intrinsic pathway failure
?factor deficiency or anticoagulant factor - answered by mixing studies

factor deficiency fixes with mixing

  • vWB disease - de factro factor 8 deficiency
  • factor 8 (haemophilia A)
  • factor 9 (haem B)
  • factor 11 (hame C - 8% ashkenazi jews)
  • factor 12 - very rare

Doesnt fix; presence of anticoagulant factor -
NOrmal TT and RT - antiphospholipid antiodies
High TT, normal RT -heparin
High TT, high RT -low fibrinogen, abnormal fibrinogen, amyloid

60
Q

Thrombophilia screen

A 
antithrombin
protein c
protein s
factor 5 leiden
lupus anticoagulant - antiphospholipid syndrome
anti Beta 2 glycoprotein antibody (APS)
anticardiolipin antibody (APS)
prothrombin gene mutation
61
Q

Antithrombin III deficiency

A

consequences are thrombosis and loss of heparin effect
management is supplementation of ATIII with purified factor or FFP

Causes -
inherited ATIII defects
Acquired -
- reduced production - liver disease, oral contraceptive, eclampsia
- loss of protein - nephrotic syndrome, plasmapheresis with albumin, extnesive blood loss
- increased consumption - DIC, acute thrombosis, extra-corporeal circuits

62
Q

TEG values

A

R value = reaction time (s); time of latency from start of test to initial fibrin formation (amplitude of 2mm); i.e. initiation
K = kinetics (s); time taken to achieve a certain level of clot strength (amplitude of 20mm); i.e. amplification
alpha = angle (slope between R and K); measures the speed at which fibrin build up and cross linking takes place, hence assesses the rate of clot formation; i.e. thrombin burst
TMA = time to maximum amplitude(s)
MA = maximum amplitude (mm); represents the ultimate strength of the fibrin clot; i.e. overall stability of the clot
A30 or LY30 = amplitude at 30 minutes; percentage decrease in amplitude at 30 minutes post-MA and gives measure of degree of fibrinolysis
CLT = clot lysis time (s)

63
Q

TEG response to changes

A

Increased R time => FFP
Decreased angle => cryopreciptate
Decreased MA => platelets (consider DDAVP)
Fibrinolysis => tranexamic acid (or aprotinin or aminocaproic acid)

64
Q

Heparin - pharmacology

A

heterogeneous mix of mucopolysaccharides
subcut dose take 1-2hours to reach peak effect

Mechanism -

  • enhances activity of ATIII by factor of 1000
  • ATIII inactivates several factors - Xa and thrombin

LMWH vs UFH -

  • inactivation of thrombin depends on heparin molecule lenght - clexane does not affect it
  • inactivation of Xa is independent of length so both effect it
65
Q

interactions with heparin

A

potentiated by -

  • sodium valproate
  • hyroxycholoroquine

Effects of heparin antagonised by -

  • antihistamines
  • digoxin
  • nicotine
  • tetracyclines
66
Q

chronic complications of heparin

A

HITS - occurs 5-10days after start of heparin

  • mostly associated with UFH, more frequent in elderly
  • type 1 - mild, reversed by cessation of heparin, occurs in 10% patients
  • type 2 - severe, associted with thrombosis in 30% cases, due to formation of antibodies to the complex made up of platelet factor 4 (PF4) and heparin

osteopaenia
mineralocorticoid
alopecia
elevation of AST and ALT

67
Q

Protamine

A

1mg reverses 100units
given slowly

Side effects -

  • catastrophic hypotension due to vasodilatation
  • pulmonary hypertension
  • anaphylaxis
68
Q

Resistance to heparin therapy

A

due to -

  • increased heparin-binding protein levels (all of them are acute phase reactants)
  • low antithrombin III levels
  • increased heparin clearance
  • high factor VII levels

Management -

  • change to LMWH
  • give FFP or cryo
  • given ATIII concentrate
69
Q

tirofiban

A

reversible inhibition of P2Y12 ADP receptor -> inhibition of cAMP dependent platelet activation
Biliary clearane
duration of action 3-5 days

70
Q

Dabigatran/rivaoroxiban

A 
Dabigatran - direct thrombin inhibitor
 - renally excreted 
can use dialysis to clear
lower bleeding risk than warfarin
new antidote - praxbind (monoclonal antibody)

Rivaroxiban -

  • factor Xa inhibitor
  • prevents thrombin generation
  • bad in both liver and kidney disease
  • not able to dialyse
71
Q

Drugs that increase bleeding risk with Xa inhibitors

A 
ca channel blockers
fluconazole
immunosuppresants
macrolides (clarithro, erythro)
amioderone
tamoxifen
72
Q

INdications for IVC filter

A

Absolute contraindication to anticoagulation in patient with high risk DVT/PE
COmplication of anticoag -> needs to be reversed
Inability to achieve full anticoagulation
PE while fully anticoagulated

Extended indications - no evidence, but may get placed – trauma, burns, cancer pt, clot induced pulmoary HTN

73
Q

IVIg actions

A

modulates; B and T cells, macrophages, cytokines networks and complement

Regulates cell growth

74
Q

IVIg indications

A

Haematological

  • idiopathic thrombocytopenic purpura (ITP)
  • post plasma exchange course completion
  • antiphospholipid syndrome (APLS)
  • chronic graft versus host disease (hypogammaglobulinaemia)

Infections
- toxic shock syndromes (staphyloccocal and streptococcal)

Vasculidities

  • Kawasaki disease
  • Wegener’s granulomatosis
  • Microscopic polyangiitis

Dermatological

  • pemphigus vulgaris
  • bullous pemphigoid
  • SJS/TEN (controversial)

Neuromuscular

  • GBS (AIDP)
  • dermatomyositis
  • myasthenia gravis
  • chronic inflammatory demyelinating peripheral neuropathy (CIDP)
  • Eaton-Lambert syndrome
  • Stiff Person Syndrome
  • Multiple sclerosis

Renal transplant rejection (controversial)

CICM (20 decks)

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