BLOOD Flashcards

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1
Q

**Anaemia- Iron Deficiency

MICROcytic HYPOchromic

A

Insufficient iron to support Hb production causing a microcytic, hypochromic anaemia (Fe is absorbed in the duodenum) → ↓Ferritin (iron stores used up)

Causes: blood loss, poor diet, malabsorption, excess fe requirement e.g pregnancy

Signs: SOBOE, fatigue, spoon nails (koilonychia), atrophic glossitis, angular chelitis (ulcer corner mouth), pale eyes, palpitations, dizzy

IVX: FBC = low ferritin confirms, low MCV and MCH and low HB

Coeliac screen, urine dip all patients for bladder cancer, endoscopy and h.pylori urea breath test

TX: Ferrous sulphate 200mg TDS for 3 months and Fe rich food

blood transfusion if Hb <80

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2
Q

**Acute non-haemolytic reactions during transfusion

  1. febrile reactions
  2. bacterial contamination
  3. fluid overload
  4. Transfusion related acute lung injury
  5. Anaphylaxis
A
  • Adverse reactions to blood products
  • Early Reactions (1/1000) within 24hours (SEVERE):
  1. Febrile Reactions (1-2% of patients)
    - From HLA Abs, Multiparous women/Pts w/ multiple Hx of transfusions most @ risk
    - Fever, chills, pruritis, urticaria ~ 1/1.5 hrs from transfusion
    TX: Slow the transfusion & give Paracetamol
  2. Bacterial Contamination
    - ↑Temp, Hypotension, Rigors
    - More common in Platelets (stored @ higher temp)
    TX: Stop transfusion, call haematologist, take blood cultures, start broad spec Abx
  3. Fluid overload TACO (pulmonary oedema)
    - SOB, hypoxia, tachy, Basal creps
    TX: 02 and diuretics
  4. Transfusion Related Acute Lung Injury (TRALI)
    (acute, noncardiogenic pulmonary Oedema )
    ARDS - dyspnoea and cough- CPAP
    - White out lung CXR
    TX: STOP transfusion
  5. Anaphylaxis - ig E
    TX Adrenaline, salbutamol and Chlorphenamine
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3
Q
Macrocytic anaemia
(megaloblastic = large rbc)

CF?

Caused by what deficient?

Management:

A
  • Fall in Hb (MCV > 96fL) due to problems of RBC production (Folate = jejunum, B12 = ileum)

a) Megaloblastic = poor DNA synthesis =
● B12 (due to CD, Addison’s) or Folate (diet, malabsorp, leukaemia, hepatitis) deficiency

b) Non-Megaloblastic =
● Alcohol, liver disease, hypothyroid (sev), pregn., reticulocytosis, myelodysplasia, cytotoxic drugs (e.g. azathioprine)

CF: SOBOE, Fatigue, glossitis, angular stomatitis, dizzy

IVX: bloods HB, MCV, Ferritin, LFTS, coeliac screen

Management:
–> Folate deficient: Diet, folic acid 5mg 5 months

B12 def: B12 injections 1mg alternative days 2 weeks then 1mg every 3 months for life
(avoid peripheral neuropathy and sub acute degeneration of spinal cord = SCDSC)

X- Pernicious anaemia - lemon tingue due to pallor and jaundice, IF auto-Ab

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4
Q

Haemolytic anaemias

= Premature breakdown of RBCs before their natural lifespan (120 d)

A

Can be intravascular (leading to jaundice) or extravascular (due to immune complex formation or RBC defect spleen)

ACQUIRED (Coombs +ve)
- drug induced- penicillin or infective e.g malaria

HEREDITARY

  • –> Enzyme defects = G6PD, pyruvate kinase deficiency
  • –> membrane defect = spherocytosis or eliptocytosis

CF: dark urine, fatigue + palpitations, splenomegaly, fever (malaria), jaundice

FHx of jaundice or anaemia may instantly point to a hereditary cause,

IVX: Bloods, blood film, urine and coombs test, USS spleen

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5
Q
  • Hodgkin’s Lymphomas

M>F

A

Malignant proliferation of lymphocytes → + Reed-Sternberg cells

RF: young, EBV, SLE, obesity

CF: lymphadenopathy, painful non tender rubbery typically cervial + painful with alcohol
SYX: Pruritis

B syx: Three B symptoms – weight loss > 10% (6 months), fever > 38, night sweats (needing to change clothes)

IVX: Tissue biopsy via LN excision, histology Reed cells.
- Bloods + staging CXT, marrow biopsy.

TX: CHEMO = ABVD
Adrimycin, Bleomycin, Vinblastine, Decarbazine

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6
Q

Myeloma

plasme cell cancer

A
  • Plasma cell dyscrasia (PCD) due to malignant proliferation of plasma cells i.e. neoplasm of bone marrow plasma cells
  • a) Diffuse bone marrow infiltration → bone destruction (↑osteoclast/ ↓osteoblast → ↑Ca2+) + marrow failure
    b) Secretion of Ig or paraprotein (detectable in urine) → organ dysfunction esp. renal disease

RF: Afrocarribean

SYX:

  • -> Bone disease = backache, fractures, vertebral collapse, hypercalacemia
  • -> Blood = Anaemia, neutropenia, thrombocytopenia
  • -> Renal imparitment

IVX: Blood, FBC, Raised ESR, U+E = ↑Urea ↑Creat ↑Ca2+, Bence-Jones protein urine test

Management: Blood, fluids, abx

Compliations: MSSC and amyloidosis

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7
Q

2 -Disseminated intravascular coagulation

A

Dysregulation of coagulation + fibrinolysis → widespread clotting → all coagulation factors used up → resultant massive haemorrhages

Causes: malignancy, sepsis, trauma, HELLP Hamolysis Elevated Liver enzymes, Low platelets,

CF: Large bruising, bleeding, petechiae, renal infection, ARDS

IVX: Bloods, prolonged PT and APPT (Bleeding time)

Management: FFP replace clotting factors. Activated protein C

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8
Q

2- Sickle Cell

A
  • RF: afrocarribean
    HbSS (homozygous) or HbAS (trait)

CF: presents children 3-6 months
Anaemia + pallor, jaundice + gall stones
Lethargy and growth restrictions

VASO-OCCULSIVE CRISIS = pain
(triggered by cold, infection, dehydration)

tx: fluids and paracetemol

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9
Q

2- Haemophilia

A = 8 = COMMON  - severe
B = 9 = RARE - Mild
A

Deficiency of clotting factor 8 or factor 9
X LINKED RECESSIVE

CF:
A- massive bleed into joints and muscles
B - minor bleeds + bruising

IVX: APPT, PT, Thrombin,
Clotting factors

Management: Clotting factors replacement + desmopressin

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10
Q

2- Thalassaemia

A = Chr 16
B = Chr 11 - major or minor
A
  • mutation of either α or β globin chains of Hb

CF: Anaemia + Fatigue
Hepato-splenomegaly Osteopenia + Skull bossing (B-thal majority)

IVX: Bloods - ↑Bilirubin ↑Reticulocytes
FBC: High HbF = β Major, U&Es, LFTs,
Film: Microcytic, Hypochromic cells +/- Target or Multinucleated RBCs Hb Electrophoresis
–> Imaging
-Skull X-ray – may show “hair on end” appearance of skull due to increased bone marrow activity = B-thal major

Management:

  1. 2-4 weekly Transfusions for anaemia to maintain Hb > 90
  2. Fe chelation therapy – minimise Fe overload (excess Fe causes hypothyroidism, hypoCa2+, hypogonad)
  3. Ascorbic acid – increases urinary excretion of iron
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11
Q

2- Thrombophilia

pro-clotting

A
  • Often presents with unprovoked DVT or PE
    e. g Factor V leiden, Prothrombin gene mutation, protein C+S def, Antithrombin def, antiphospholipid syndrome.

TX: LMWH or warfarin

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12
Q

2- Thrombocytopenia
2- Pancytopenia
2- Neutropenia

A
T = a low platelet count < 150  e.g. lots of bruising and bleeding
P = low red, white and platelets 
N = low neutrophils (WBC)
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13
Q

2- Bone marrow replacement

Conditions its used for?

A

Conditions used for:

  • Severe aplastic anaemia (bone marrow failure)
  • Leukaemia – a type of cancer affecting white blood cells
  • Lymphoma
  • Myeloma – plasma cells
  • Disorders –sickle cell anaemia, thalassaemia, severe combined immunodeficiency (SCID) and Hurler syndrome
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14
Q

2- Acute lymphoblastc leukaemia

age group?

symptoms?

rapid onset what?

A
  • Always Little people (children)

●Most common malignancy affecting children – peak 2-5 yo
●↑No of Lymphoid Blast cells push other cells out of bone marrow acutely → rapid onset of Anaemic, Neutropenic, thrombocytopenic Sx
●Can progress from CML

Rapid onset marrow failure:
Anaemia – dyspnoea, pallor, lethargy 
Thrombocytopenia – bruising, purpura 
Neutropenia – recurrent infections 
●	Systemic Sx: weight loss, fever, malaise 
●	Bone pain + splenomegaly
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15
Q

2- Chronic myeloid leukaemia

A

●MATURE Elderly pts. 60-70yo
●Typically granulocytes (basophils, eosinophils, neutrophils)
●Philadelphia chromosome (95%) due to translocation T( 9:22)
●POOR PROGNOSIS
●Can cause AML (80%), ALL (20%)

↓Weight, LoA
Splenomegaly (significant

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16
Q

2- Chronic lymphocytic leukaemia

A

-● Almost always B Lymphocytes (99%)
- ● Often no unique features
↓Weight, LoA
Bleeding + infections Lymphadenopathy

17
Q

Blood product types

  • Packed Red Cells
  • Platelets
  • Fresh Frozen Plasma
  • Cryoprecipitate
  • Whole Bloods
A

▪ Packed Red Cells – for severe anaemia, should ↑Hb by ~1.25/dL
▪ Platelets – only used when count v low <50
▪ Fresh Frozen Plasma – for clotting disorders, Vit K deficit, Liver disease, DIC or prophylactically in patients undergoing surgery w/ bleeding risk. (i.e. clinically significant w/o major haemorrh.)
▪ Cryoprecipitate – used to replace fibrinogen (usually if <1.5g/L)
▪ Whole Bloods – very rarely used, exchange transfusions

18
Q

Non-Hodgkin Lymphoma (90%)

A

all lymphomas w/o Reed-Sternberg cells, typically derived from B-cell lines

SYX: systemic syx LESS severe then hodgkins.

IVX: marrow biopsy, staging via CXR

MANAGEMENT: High grade lymphoma

  • Burkitts (childhood disease characterised by jaw lymphadenopaty
  • Treat: R-chop REGIME
  • high risk tumour lysis sydrome for all blood cancers –> AKI
19
Q

Acute Myeloid leukaemia

A

Always Mature people (older)

  • -> Systemic Sx
  • brusing, bleeding, breathless, fatigue
  • -> Bone pain + splenomegaly
  • -> Marrow failure

Can progress from CML

20
Q
Hodgkin vs Non Hodgkin 
Age
Prognosis
Associated pathology:
Staging

B syx

A

age: Hodgkin= 30s, NH = 70s
Prognosis: H =higher survivial NH = lower
H : Reed Sternberg NH: MALT and Burkitts

Staging: Arbor for both

B symptoms refer to systemic symptoms of fever, night sweats, and weight loss

21
Q

Prognosis in Hodgkin’s lymphoma is influenced by?

A

Age, stage, presence of B symtpoms and elevated ESR.

22
Q

1st line treatment for patients with chronic myeloid leukaemia?
CML chromasome?

A

tyrosine kinase inhibitors such as imatinib!!
IMATINIB!
Philadelphia chromosome