Haematology conditions Flashcards

1
Q

What are the normal values for an MCV (mean corpuscular volume) blood test?

3 types of microcytic anaemia
normocytic
macrocytic

A
Female = 80-98.1
Male = 81.8-96.3
Micro: 
Fe deficiency
Chronic disease
Thalassaemia
Normo:
Acute blood loss
Chronic disease
Combined haematinic: B12+Folate+Fe deficiency
Macro:
B12/Folate deficiency
Alcoho excessl/liver disease
Haematological: chemo, haemolysis, bone marrow failure
Hypothyroid(rare - neonate heel prick)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why is the reticulocyte count useful in diagnosing anaemia?

A

Bone marrow responds to anaemia by producing and releasing reticulocytes, if the count is LOW it signifies a problem with production (bone marrow) and HIGH signifies a problem with removal (spleen, liver, blood loss, bone marrow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is meant by megaloblastic anaemia?

A

Type of macrocytic anaemia that results from inhibition of DNA synthesis during red blood cell production - B12 or folate deficiency anaemia. Erythroblasts = immature red blood cells, larger than normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
Iron deficiency anaemia:
cause
symptoms 
diagnose
treat
A

Low intake, blood loss, malabsorption.
Pale, fatigue, dizzy, SOB, palpitations.
FBC: low ferritin, low MCV, low reticulocytes
Treat with oral or IV iron supplementation, treat underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Anaemia of chronic disease - commonly associated with?

A

TB, SLE, Crohn’s, RA, malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thalassaemia - types, symptoms, treatment

A
alpha and beta chains can be affected.
alpha thalassaemia
1 deletion = mormal blood picture
2 deletions = carrier
3 = moderate anaemia
4 = stillborn
beta thalassaemia
major = transfusion dependent from birth, abnormal bone growth/delayed puberty, iron chelation therapy to remove excess iron depositions
intermedia = less severe anaemia, not dependent on transfusions
minor = carrier, asymptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

B12/folate deficiency anaemia

cause, symptoms, treatment

A

B12:
autoimmune condition pernicious anaemia (body attacks parietal cells) is most common cause, also vegan diet/poor diet/maabsorption- ileal resection/medication
folate:
lack broccoli/green leafy veg, greater demands due to pregnancy
symptoms:
fatigue, pale, palpitations, dizzy, SOB (general anaemia)
B12 specific: parasthesia, mood changes, mouth ulcers, red tongue, yellow skin
Treat:
B12: if caused by pernicious anaemia, injection of hydroxocobalamin every three months for life. If dietary, supplements/advice. Folate = diet change/supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Haemolytic anaemia
what is it?
diagnosis?
common causes?

A

Early haemolysis of red blood cells. Shortened survival leads to increased production in bone marrow, large reticulocytes are released prematurely.
TESTS: increased reticulocyte count, serum unconjugated bilirubin, urinary urobilinogen, faecal stercobilinogen.
Splenomegaly, jaundice.
Cause: autoimmune - hereditary spherocytosis, enzyme defects, thalassaemias, sickle cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is hereditary spherocytosis?

sickle cell anaemia?

A

most common autoimmune anaemia, haemolytic, macrocytic.
Defect in rbc membrane makes cell spherical, unable to pass through splenic microcirculation so become trapped and are haemolysed = shortened lifespan.
Sickle cell: autosomal recessive, abnormal beta globin chains = rigid, sickel shaped cells give up O2 more readily. Haemolysed early. Heterozygous is protective against malaria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Malaria
Different types
which have long incubation? which is most common/deadly?

A
Plasmodium...
falciparum (75%, worst infections)
vivax (long incubation - formation of hypnozoites)
malariae
ovale (hypnozoites)
knowlesi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

briefly describe the general lifecycle of malaria-causing plasmodium

A
  • live as immature sporozoites in salivary glands of female anopheles mosquito
  • mosquito bites, transfered to bloodstread where sporozoites go straight to liver
  • vivax and ovale go dormant as hypnozoites, rest reproduce to form merozoites and invade RBCs where they further reproduce and develop into gametocytes.
  • haemolysis of these cells occurs and gametocytes released into blood stream
  • mosquito may pick them up and sexual reproduction occurs to form zygote in mosquito, –> new sporozoites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

who is at risk of malaria?

protective factors?

symptoms of malaria (remember incubation period = time lag infection and symptoms)diagnosis of malaria

A
People in tropics/sub tropics
2yr history of travel
pregnant
young children
immunosupppressed

Sickle cell anaemia, thalassaemia and G6PD deficiency are protective, infected cells die easily from oxidative stress
- cyclical fever, pattern depends on species of plasmodium
- haemolytic fever: fatigue, jaundice, splenomegaly, headache
complicated -> haemolysis of non-infected cells, black water urine
history: recent travel + cyclical fever
- blood film: thick and thin
- FBC shows thrombocytopenia, normocytic anaemia, increased lactate dehydrogenase from haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the process by which plasmodium falciparum may result in complicated malaria
treatment?

A

Produces sticky coating around infected RBCs, which clump together and can’t flow to spleen for destruction, also blood flow to organs blocked –> haemolytic anaemia + ischaemic damage = organ failure.
Cerebral malaria: seizure, confusion, coma, altered mental state
Bilious malaria: (liver) jaundice, diarrhoea, vomiting, liver failure
+ sepsis-like picture, ARDS, renal impairment, haemaglobinuria, parasite infected cells = >2%
Treat: IV artesunate (or quinine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treat:

  1. non-falciparum malaria
  2. uncomplicated falciparum malaria
  3. complicated
  4. vivax / ovale
A
  1. Chloroquinine
  2. oral riamet (or quinine)
  3. artesunate (or quinine)
  4. add primaquinine to clear hypnozoites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

chronic leukaemia

  • what is it?
  • cause?
  • types: how do they differ?
  • symptoms?
A

Chromosomal abnormality causes partial maturation of blast cells (precursor to WBCs), impairing their function.

Chronic myeloid leukaemia: ‘philadelphia chromosome’ translocation affects granulocytes, they divide too quickly

Chronic lymphocytic leukaemia: lymphocytes affected, especially B lymphocytes - they avoid apoptosis and accumulate.
Both –> accumulation of immature cells in the bone marrow, which spill out into the blood and crowd out healthy cells/settle in organs.
Crowding out = thrombocytopenia (easy bleeding), anaemia(fatigue), leukopenia(increased infections)
Settle in organs = CML: hepatosplenomegaly. CLL: lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

diagnosis of CML?

treat?

A

FBC:
high WCC > 100,
low Hb, normocytic anaemia
Blood film:
all types of white cell at all stages of development
increased uric acid
Bone marrow aspiration shows high cell count.
Treat: biological therapy, tyrosine kinase inhibitor imatinib. Chemo, stem cell transplant, bone marrow transplant.

17
Q

diagnosis of CLL?
treat?
prognosis?

A

FBC:
high WCC 20-40 high in lymphocytes
Blood film:
smudge cells
Treat: Blood transfusion - IV immunoglobulins. chemo, transplants.
1/3 never progress, 1/3 slow progression, 1/3 active, progress to aggressive non-hodgkin lymphoma (Richter’s syndrome)

18
Q

what is acute leukaemia? how does it differ from chronic?
subcategories
when the proliferated cells end up in the bloodstream, what effects may that have?

A

mutation causes uncontrolled proliferation of blast cells (as opposed to partially matured in chronic).
Myeloid: myeloblasts affected (usually –> erthrocytes, leukocytes - granulocytes and monocytes, thrombocytes).
Lymphoblastic: lymphoblasts affected, T or B lymphoblasts proliferate (precursor to B/T lymphocytes)
They build up in the blood over a short period of time, crowd out other bone marrow cells and use nutrition.
This leads to anaemia, thrombocytopaenia, leukopenia..
In bloodstream…
ACute myeloid - may activate clotting process, causing disseminated intravascular coagulation
Acute lymphoblastic - settles in liver, spleen, thyroid, lymph - enlarge.

19
Q

diagnosis of acute lymphoblastic leukaemia
acute myeloid

treat ALL and AML

A
ALL:
blood smear shows lymphoblasts
AML:
blood smear shows myeloblasts
both:
>20% blast cells in bone marrow
high WCC, low Hb, low platelets
 - Blood and platelet transfusions
- Neutropenia may lead to deadly infections - treat with prophylactic antivirals, antibacterial and antifungals
- ALLOPURINOL (prevents tumour lysis syndrome)
- IV fluids - insert Hickman line (permanent cannula into main vessel, tunnelled under sub-cutaneous fat so harder for infection to arise) so can easily take blood for testing and administer drugs and fluids
- Chemotherapy
- Marrow transplantation
20
Q

what age group is ALL mainly seen in? CLL?

AML?

A

ALL is mainly seen in childhood and CLL is a disease of the elderly (most common leukaemia)
AML elderly

21
Q

what are lymphomas? how are they subdivided?

A

Malignant proliferation of lymphoid cells - mostly B lymphocytes, can be T
Classified histologically into Hodgkin’s and non-hodgkin’s lymphoma.
Hodgkin’s has characteristic Reed-Sternberg cells, non-hodgkins does not.

22
Q

HODGKIN’S lymphoma
who?
presentation?
diagnose?

A

Hodgkins = teens and elderly
rubbery lymphadenopathy, worse with alcohol
Stage A: itching only systemic symptom
Stage B: systemic general: fever, night sweats, weight loss
hepatosplenomegaly

CT for ann arbor staging
lymph node excision/bone marrow biopsy shows RS cells

  • Bloods:
    • High ESR or Low Hb - indicate worse prognosis
    • High serum lactate dehydrogenase
23
Q

Risk factors for lymphoma?

A
EBV/CMV infection
Genetic
H pylori
Autoimmune conditions
Primary or secondary immunodeficiency
24
Q

presentation of non-hodgkin’s
diagnosis
treatment

A

lymphadenopathy
in 25% - extranodal symptoms
+ general systemic B symptoms

pancytopenia
lactate dehydrogenase
biopsy/bone marrow aspiration
CT for Ann Arbor staging

Treatment depends on grade/type/aggressiveness
R-CHOP regime…
R = rituximab, monoclonal antibody

25
Q

how does lactate dehydrogenase reflect the prognosis for lymphoma?

A

more = more cell turnover (produced in haemolysis) = worse prognosis

26
Q

types of non-hodgkin lymphoma

A

MOST diffuse large B cell. High grade, aggressive.

Follicular lymphoma is low grade.
Burkitt lumphoma is highly aggressive, strong ass with EBV in africa, extranodal involvement.

27
Q

myeloma:
what is it?
Presentation of myeloma

A
Malignant proliferation of plasma cells (differentiated B lymphocytes). They produce excessive amounts of only one type of IgG where they usually produce a range - 'monoclonal paraproteins'. 
Other IgG levels are low leading to susceptibilty to infections
OLD CRAB
old
Calcium elevated 
Renal failure
Anaemia - neutropenia, thrombocytopenia
Bone lytic lesions
28
Q

Diagnosis of myeloma

Treatment

A

Bone marrow biopsy reveals malignant plasma cells
Monoclonal protein band from serum/urine
Hypercalcaemia/renal failure/anaemia
Bone lesions on skeletal survey

Treat:
If unfit… CTD cyclophosphamide, thalidomide, dexamethasone
If fit… VAD vancristine, adriamycine, dexamethasone

stem cell transplant

+ treatment for bone pain, renal failure, anaemia, infections, fracture prevention