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phase 2a mine > haem top tier > Flashcards

haem top tier Flashcards

1
Q

anaemia epidemoiology

A

common

esp pre-menopausal

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2
Q

different types of anaemia

A

microcytic = small rbc size

normocytic = normal

macrocytic = large

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3
Q

microcytic anaemia causes

A

iron deficiency
– microcytic hypochromic (small with less colour) = iron def until proven otherwise

chronic illness

thalassemia

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4
Q

normocytic anaemia causes

A
  • chronic illness
  • acute blood loss (trauma, periods, haemolysis, hypersplenism( increased rbc removal), rbc disorders)
  • combined micro and macro (iron and b12 def - malabsorption)
  • increase in volume (so relative low rbc conc) – pregnancy, overhydration
  • bone marrow failure - aplastic
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5
Q

name examples of haemolysis

A

sickle cell
malaria
chronic illness

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6
Q

rbc disorders

for each:

  • eg
  • presentation
  • epidemiology
A

membranopathies
- Eg spherocytosis, elliptocytosis
- Mild, benign, common
cause= decrease in red cell membrane proteins
- Presentation = neonatal jaundice, anaemia

enzymopathies

  • Inherited enzyme deficiencies so less fuel for ebc
  • Shortened rbc lifespan from oxidative damage
  • Eg - glucose-6-phosphate dehydrogenase deficiency
  • Epidemiology = men>women (x linked). African, Middle East, S Asia, mediteranian
  • Often asymptomatic , usually self limiting. Exacerbated by broad beans, infections, drugs → brown urine (so avoid broad beans, occasionally need transfusion)
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7
Q

what is another cause of normocytic anaemia (in which the causes are not actually normocytic!)

A

combined micro and macro cells - balance out

— iron and B12 def (think malabsorption

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8
Q

what is the cause of bone marrow failure

how does it present

treatment

A

infection
genetic
drugs

more bleeding, more infection

remove causative agent
blood transfusion

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9
Q

macrocytic anaemia causes

A
  • b12 / folate
  • alcohol /liver disease
  • hypothyroidism
  • haem causes (reticulocytes (immature rbc) increased)
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10
Q

b12 deficiency
aka
appears as
why might there be b12 def

A

pernicious anaemia (gradually worse)

  • macrocytic anaemia
  • hyper-segmented neutrophil (more than 5 dark blue bits - normally 3-5)

b12 absorption requires intrinsic factor (made in gastric parietal cells) for terminal ileum absoprtion
- so issue is with intrinsic factor or terminal ileum

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11
Q

differential diagnosis of anaemia

A

n third trimester of pregnancy, there is an increase in rbc number but also an increase in volume so appears anaemic

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12
Q

what is anaemia

what is the affect

pathological consequences

A

reduced red cell mass OR increased plasma volume (dilutes rbc conc)

decrease in oxygen transport --> tissue hypoxia
physiological compensation 
-- increased tissue perfusion
----- increased HR
-- increased oxygen transfer to tissues
----- oxygen saturation curve
-----  breathing rate increases?
  • Myocardial fatty charge
  • Aggravate angina /claudication
  • Fatty change in liver
  • Skin and nail atrophic changes
  • CNS cell death
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13
Q

why does iron matter in terms of anaemia

A

Iron necessary for formation of haem on each strand in haemoglobin → ineffective haemoglobin

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14
Q

surrogate marker for anaemia (low rbc) =

A

haemoglobin

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15
Q

common anaemic symptoms

A 
Fatigue, lethargy
Dyspnoea 
Short of breath on exertion
Faintness
Palpitations
Headache
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16
Q

what additional anaemia symptoms would you have if you were

iron def
B12 def
folate def
haemolytic

A

Iron def

    • Brittle nails, spooning. Brittle hair
  • -Glossitis (tongue inflammation)

B12 def
– Neurological problems

Folate def

  • -Glossitis
  • -Slow development

Haemolytic

  • -Jaundice
  • -Gallstones
  • -Leg ulcers
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17
Q

how might B12 def (Anaemia ) be picked up

A

IF (intrinsic factor) antibodies (IF needed to absorb B12)

Schilling test - measures B12 intestinal absorption (radiolabelled B12 supplement)

coeliac antibodies (may affect terminal ileum)

B12 in blood

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18
Q

anaemia investigations

A

bloods

  • haemoglobin levels
  • reticulocytes (immature rbc) rbc)
  • B12, folate, ferritin levels
  • U/E
  • LFT
  • TSH

blood film

  • see type (size )
  • colour
  • eveness
  • shape
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19
Q

hypo/normo/hyperchromic

A

this refers to rbc colour (in aneamia)

rbc colour is given by haemoglobin so it indicates haem levels

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20
Q

why are reticulocytes a useful tool for anaemia

A

Reticulocytes = immature rbcs
Marker of balance between rbc creation and removal (spleen, liver, bone marrow, blood loss)
– lots of reticulocytes = lots of creation eg short life span of sickle cells

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21
Q

microcytic hypochromic

A

= iron deficiency anaemia (until proven otherwise)

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22
Q

Hypersegmented neutrophil

A

(more than 5 dark blue clumps)

=B12 deficiency

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23
Q

anaemia treatment

A

treat the cause

  • dietary supplements (iron, B12, folate (folic acid))
  • immunosuppression if autoimmune (eg B12, some genetic haemolytic ones)
  • hypersplenism –> surgery
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24
Q

anaemia complications

A 
Worsens angina 
Worsens claudication 
Tissue ischaemia - pain, loss of sensation, loss of function
Nails brittle, spoon shape
Hair thin/receding/loss (?)
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25
Q

thalassemia and sickle cell anaemia in broad terms

A

thalassemia = decrease in QUANTITY of haemoglobin

sickle cell = decrease in QUALITY of haemoglobin

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26
Q

what is the cause of thalassaemia

different varieties=

A

Globin chain production switched off, so reduction in haemoglobin (genetic, heterogenous- carriers asymptomatic)

Varies in severity - major/intermedia/minor
alpha/beta (alpha rarer, more die)

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27
Q

where is thalassaemia most common

A

South asia, central africa, far east

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28
Q

symptoms of thalassaemia and when does it present

A 
Presents 6-12 months 
Failure to feed
Pale
Listless
crying
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29
Q

management of thalassaemia

A
  • Transfusion regularly
  • Iron chelation (to prevent iron overload that is caused by transfusion)
  • Endocrine supplementation (hormones)
  • Bone health
  • psychological
  • Fertility
  • Monitor - ferritin, endocrine, function, heart and liver MRI, bone density
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30
Q

what is iron chelation and why is it needed

A

removal of iron in body via drugs

to prevent iron overload that is caused by transfusion

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31
Q

what is normal adult and foetal haemoglobin

A 
normal = 2 alpha, 2 beta, heme group on each. 
Foetal = 2 alpha, 2 gamma
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32
Q

cause of sickle cell anaemia

A

genetic. Disease is homozygous (or heterozygous if with other haematological disorders eg thalassemia). HbS carrier symptom free + falciparum malarial protection. Spread from malarial regions to UK/USA via slave trade.

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33
Q

sickle cell anaemia symptoms

acute and chronic

A

affects multiple systems

Acute

  • Pain - sickle cell crisis = blockage of vessels in bone so bone marrow swells
  • Lungs- sickle chest syndrome = occlusion of micro-vessels –> chest pain, cough, fever, hypoxia
  • Stroke

Chronic

  • Poor circulation
  • Renal impairment
  • Joint impairment
  • Pulmonary hypertension ( → heart failure)

many effects more

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34
Q

sickle cell anaemia management

A

Treat complications

Treat disease

  • Blood transfusion
  • Stem cell transplant
  • Gene therapy (genetic information introduced to cells)
  • Gene editing (DNA modified in someone)
  • Hydroxycarbamide for sickle cell crises (suppresses bone marrow?)
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35
Q

what viral infection worsens sickle cell and why

treatment

A

if have parvovirus too, a common infection that reduces RBC production, there is a dramatic drop in Hb as short life span of sickle cells. Associated with death, need asap blood transfusion

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36
Q

deep vein thrombosis risk factors

triggers

A

older
surgery/hospital
thrombophilia
malignancy

Contraceptive pill (oes )
Pregnancy (oes)
Surgery >30min
fracture/ immobility
Long haul flights
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37
Q

deep vein thrombosis pathophysiology

A

Clot in a deep vein in leg
Disrupts circulation
Can embolise

38
Q

signs and symptoms of DVT

A

normally unilateral

SIGNS
Tenderness
Swelling
Warmth
Discolouration 
SYMPTOMS
Pain / cramping esp walking 
Throbbing
Swelling
red/darkened skin
Warm skin
Swollen veins -hard/sore
39
Q

well’s score (DVT)

A

Short survey - no= 0, yes =1. Score of 2+ means likely DVT

Questions = cancer, paralysis, recent surgery/bedridden 3+ days, swollen leg, calf 3cm+ other calf, large veins, previous DVT, pitting oedema (thumb mark compression when prodded)

40
Q

DVT investigations

A

well’s score

D dimer
= fibrin degradation product (blood test.)
Positive does not confirm (not specific) but negative (normal result) does rule it out
So if +ve then do ultrasound

ultrasound
Looks at proximal veins for DVT : popliteal fossa to groin
With probe, if can squash flat, it is fine. If not-clot

41
Q

DVT management

A

LMW (low molecular weight) Heparin injection = immediate anti-coag

Oral warfarin - longer term but takes a while to act (so hep first)

DOAC (direct oral anticoagulants)
Oral, 2xday, longterm

Compression stockings

Treat/seek underlying cause
Malignancy
Thrombophilia (genetic predisposition)

42
Q

DVT prevention

A

need to prevent around surgery/immpbility

Compression stockings (pre and post surgery)
Early mobilisation after op
Hydration
Foot pumps during theatre if high risk/ long surgery
LMW heparin for many inpatients

43
Q

PE small vs big clot effects

A

Small clot = more common

  • Chest pain, pleuritic
  • Sob
  • DVT symptoms
  • Tachycardia
  • Tachypnoea

Big clot = emergency /death

  • Hypotension
  • R sided heart strain/heart failure
  • Dyspnoea
  • Cyanosis = bluish skin
  • Hemoptysis = coughing up blood
44
Q

PE investigations

A

wells score

CXR- usually normal

ECG - sinus tachycardia (and excludes dif diagnosis

blood gases - type 1 resp failure

45
Q

well’s score (PE)

A

2-6 is medium probability, 6+high probability. (all d dimer, 2-6 consider CTPA and high sensitivity d dimer, 6 def ctpa (dont bother d dimer)

Questions : DVT symptoms, immobilisation 3d/ surgery in the last month, previous DVT/PE, tachycardia 100+, hemoptysis, cancer

46
Q

PE treatment

A

Same as DVT (LMW Heparin, Oral warfarin DOAC )
Plus IV heparin (needs monitoring)
Plus aspirin - irreversible inhibitor

47
Q

who gets leukaemia most commonly- age

A

v old or v young

48
Q

leukaemia pathophysiology and cause

A

Cancer of Blood cells residing mainly in bone marrow / blood

Due to an undetected , undestroyed mutation. then more likely for further generations to have further abnormal mutations

49
Q

leukaemia vs lymphoma

A

both cancer of blood cells (too many produced)

leukaemia - too many wbc residing mainly in bone marrow/ blood
lymphoma = too many lymphocytes residing mainly in lymph nodes

50
Q

types of leukaemia

ALL
CLL
AML
CML

A

ALL : acute lymphoblastic leukaemia

CLL : chronic lymphoblastic leukaemia

AML: acute myeloid leukaemia

CML: chronic myeloid leukaemia

51
Q

risk factor for ALL (acute lymphoblastic leukaemia)

A

Down’s syndrome
radiation
benzene

52
Q

CML (chronic myeloid leukaemia) cause

A

Philadelphia chromosome- genetic swap between chromosome 9 and 22 . makes new protein: active tyrosine kinase

also can cause AML, ALL

53
Q

CML (chronic myeloid leukaemia) treatment

A

Treatment = imatinib. Blocks tyrosine kinase activity (specific). Mutations in cancer can stop from working.

54
Q

myeloid vs lymphoid

A

both progenitor cells
they are more differentiated than hematopoietic progenitor cell

myeloid cell can differentiate into eosinophils, basophils, monocytes (macrophage), rbc, neutrophil, megakaryocytes (platelets)

lymphoid cell can differentiate into B, T lymphocytes and natural killer cells

55
Q

mast cell vs basophil

A

similar cells
NOT one is a mature version of the other as u once thought
they are different

basophil leaves bone marrow already mature
mast cell matures once it reaches tissue

56
Q

leukaemia signs and symptoms

A 
Due to anaemia
- Fatigue
- Sob on exertion
- Light headed
Due to thrombocytopenia
- Bruising
- Bleeding
Bone pain 
Palpitations
57
Q

low wbc =
high wbc=
symptoms-wise

A

If low wbc- recurrent, non-resolving infections

If high wbc- renal impairment, sob, hyperkalemia

58
Q

leukaemia investigations

A

bloods

  • FBC
  • – 20%+ blast cells (big cells, large nucleus with lots of patched nucleoli. usually less than 5%)

for acute:

  • – low platelets
  • – anaemia( low haemoglobin /rbc)
  • – WCC variable

for chronic

  • – anaemia
  • – raised WBC (if myeloid - raised non-lymphocyte wbc,if lymphoid- raised wbc)
  • blood film
  • haemolysis screen and biochem profile
  • karyotype (looking for philadelphia chromosome for chronic myeloid leukaemia - switch between 9 and 22)

bone marrow biopsy

hepatosplenomegaly

59
Q

blast cells and leukaemia

A

Blast cells = big cells with large nucleus and lots of patched nucleoli

normally make up <5% of bone marrow. In leukaemia, >20%

60
Q

leukaemia treatment

A

watch and wait

chemo

supportive measures

  • fertility cryopreservation
  • rbc and platelet transfusion
  • isolation (as they are immunosuppressed)

stem cell transplant (steroids and HRT alongside)

monoclonal antibodies

  • end in ‘mab’ (rituximab)
  • Sole target (“mono”) = CD20 protein on only B lymphocytes (so side effects low)
61
Q

monoclonal antibodies

  • called?
  • action?
  • what are they?
  • conjugates
A

-“mab” (rituximab)

Sole target (“mono”) = CD20 protein on only B lymphocytes (so side effects low)

Chimeric- mouse and human (hot/cold, allergic side effects)

immuno/radio -conjugates = stick poison (chemo) or gamma-emitting radiation on end of monoclonal antibody- extra effect

62
Q

lymphoma causes

A

Immunodeficiency

  • -Primary
    • Secondary (HIV, transplant)

Autoimmune

Infection (EBV)- commonly virus- infect B cells, proliferate autonomously

63
Q

hodgkins lymphoma

  • age
  • stage one, two, three, four
  • prognosis
A
  • two peaks! : teenagers/young adults and old 70+

1- one place
2- multiple places
3- nodes either side of diaphragm
4- disseminated to extra-lymphatic tissue

stages 1-2 = good prognosis: cure even if relapse (dont know about 3-4!)

64
Q

indolent means?

A

not aggressive, causes little pain

lymphoma can be indolent or aggressive

65
Q

non-hodgkins lymphoma

  • age
  • how does it vary from hodgkins lymphome
  • grades
A
  • rare under 40y
  • more variation in presentation, treatment and outcome
  • more extra-nodal presentation than in Hodgkins
  • low grade= slow growing, incurable, relapse, presents advanced
  • high grade= nodal presentation with poorly patient, short hisrory
66
Q

cure for follicular lymphoma

A

no cure. manageable though

67
Q

neck lump differential diagnosis

A

Infection, inflammation

    • Reactive lymph node growth
    • Tender
    • Transient - <6w

Neck lump from other - thyroid enlargement

Embryological remnant

Metastatic cancer

lymphoma

68
Q

symptoms and signs of lymphoma

A

Night sweats (distinguish from menopause)
Fatigue
Anaemic - breathless
Neck lump (lump in abdomen has to be really large to notice it)
Loss of appetite/ weight
Oedema

69
Q

lymphoma investigation

A 
1 Do they have it ?
Needle biopsy
Blood test and blood film
Bone marrow biopsy
PCR
Immunophenotyping
Cytogenetic- karyotype analysis
2 if Yes 
CT, PETscan, CXR, echo ,lung function tests PFT
--- How fit they are
--- How extensive is it- how many places
History 
bloods
70
Q

lymphoma treatments

A

chemotherapy

radiotherapy

monoclonal antibodies

  • –“Mab” eg rituximab
  • – Targets CD20 - only on B lymphocytes- minimal side effects
  • – Chimeric- mouse and human - so allergy side effects
  • – immuno/radio -conjugates = stick poison (chemo) or gamma-emitting radiation on end of monoclonal antibody- extra effect

bone marrow treatment

watch and wait

71
Q

“late effect” of lymphoma

A

= long term side effects of treatment

Infertility
Cardiomyopathy
Second cancers
Psychological issues
Peripheral neuropathy
Lung damage
72
Q

what is ITP immune thrombocytopenia

  • cause
  • pathophys
  • symptoms
  • treatment
A

a complication of lymphoma

lymphocytes attack platelets

  • bleeding
  • tired

treatment= steroid + rituximab (monoclonal antibody)

73
Q

lymphoma complications

A

bowel cancer
aneurysm
thyroid nodule
ITP immune thrombocytopenia

74
Q

myeloma =

pathophysiology

A

cancer of plasma cells in the bone marrow

Clonal proliferation→ extra plasma cells → normally <5%, myeloma >10%

More plasma cells produce more antibodies. More of these are abnormal. They also produce paraproteins (light chain only of antibodies)

Paraproteins aggregate - increase blood viscosity

75
Q

myeloma age

A

old , 60+

76
Q

myeloma cause

A

mutation

77
Q

myeloma vs multiple myeloma

A

same thang

78
Q

mgus (monoclonal gammopathy of uncertain significance )

A

benign condition
abnormal protein in the blood
paraprotein
some will go on to develop myeloma

79
Q

what is the most common type of antibodies produced in myeloma

A

IgG

then IgA

80
Q

myeloma investigations

A

blood

  • hypercalcaemia
  • raised globulins
  • serum paraprotein - seen as a band on electrophoresis
  • decrease in normal antibodies, increase in abnormal
  • FBC - high wbc, low rbc and platelet

urine

  • proteinuria (paraprotein)
  • bence jones protein

Xray/ CT/MRI : lytic bone lesions (breakdown)

bone marrow biopsy
- aspirate and see percentage of plasma cells (normally less than 5, here more than 10)

81
Q

myeloma affect on organs

A

kidney - deposition of light chains and amyloid in the distal tubule causes AKI and obstruction

bone- destruction as plasma cells cause an increase in osteoclastic activity and reduce osteoblast activity . this causes pain and osteocytic lesions. and hypercalcaemia

bone marrow - is infiltrated so there is reduced function

blood : paraproteins aggregate to greatly increase viscosity

eyes : protein aggregates –> blurred vision

82
Q

myeloma presentation

A

quite silent , presents late

CRAB
calcium : hyper
renal failure (due to paraprotein deposition)
anaemia (shift toward stem cells making plasma cells)
bone - pain and resorption

tiredness and malaise (anaemia)
back/bone pain
fractures
infections - esp resp tract
bleeding
raynauds
purpura = red/purple dots from haemorrhage of small vessles
blurred vision (from paraprotein aggregates)
gangrene
dehydration (from hypercalcaemia)
83
Q

diagnosis of myeloma

A

Plasma cells in bone marrow >10% (biopsy)

antibodies/paraproteins increase in serum/urine

1 or more of CRAB

84
Q

myeloma management

A

Cytotoxic

    • Chemotherapy
    • Radiotherapy

Supportive

    • Given extra red cells, platelets - transfusion
    • stimulate stem cells
    • Isolation - stop getting bugs when immunosuppressed/ill

Bone marrow transplant?

Some respond well. ALL will eventually relapse

85
Q

myeloma prognosis

A

Some respond well to treatment but ALL will eventually relapse

86
Q

complications of myeloma

A

infection – = major cause of death (lower normal immunoglobulins)

amyloidosis=
Amyloid is an abnormal protein produced from bone marrow. It builds up in tissues :( 
Oedema in legs
Red marks on eyelids
Yellow on tongue
Organ failure
87
Q

auer rods seen in?

A

AML

88
Q

what can be seen in AML that distinguishes it

A

auer rods

89
Q

reed sternburg cells seen in?

A

Hodgkins

90
Q

hodgkins vs nonhodgkins neck lump

A 
hodgkins = asymmetrical
non-hodg = symmetrical
91
Q

painful drinking alcohol but painless lump =

A

hodgkins

phase 2a mine (38 decks)

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