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Haem Flashcards

1
Q

What is multiple myeloma?

A

MULTIPLE MYELOMA
Malignancy of plasma cells (mature B lymphocytes)

(second most common leukaemia)

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2
Q

What is the pathophysiology of multiple myeloma?

What is the precursor and how do you tell the difference

A

MULTIPLE MYELOMA

  • Proliferation of plasma cells from same pool (monoclonal)
  • These cells normally secrete antibodies (ab count increased)
  • Normally IgG

Precursor

  • MGUS (monoclonal gamopathy undetermined significance) is the precursor (5% of over 50s)
  • often IgG found on routine exam!
  • 1% of MGUS patients will get myeloma
  • Myleoma is defined when you have >10% plasma cells and END ORGAN DAMAGE
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3
Q

What are the main features myeloma? (5)

A

MULTIPLE MYELOMA features (CRAB symptoms)
1. Calcium (high) (increased osteoclasts)
• polyuria
• polydipsia
• constipation, N+V
• fatigue and confusion
2. Renal impairment (50%) (light chain AB get stuck)
3. Anemia (90%) (bone marrow infiltration)
4. Bone disease/pain (lytic lesions)
• backache
• pathological fractures
5. Signs of Bone marrow failure
-Low WCC>infection
-Low Hb>anaemia (SOB/pallor)
-Low platelets>bruising/bleeding

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4
Q

What are some other features of myeloma?

A

Myeloma

Neurological

  • parasthesia
  • spinal cord compression
  • hyperviscosity syndrome due to antibodies (can lead to stroke/siezure/coma)

Non -neuro

  • fever
  • splenomegally/hepatomegally
  • lymphadenopathy
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5
Q

How do you investigate for multiple myeloma? (bedside, bloods, imaging, special)

And what would you find?

A

Myeloma investigations (look for the antibodies)

Bedside
-Monoclonal detection
• protein/urine electrophoresis> Bence Jones proteins
• SFLC (serum free light chains)

Bloods 
 •Serum electrophoresis 
 • FBC (normocytic normochromic anaemia)
 • UsEs (↑Urea ↑Creat ↑Ca2+)
 • Bone profile 
 • LFTs (ALP high in healing fracture 
 • Blood film (Rouleux formation-stacking of RBC) ↑ESR
 • BETA 2 MICROGLOBIN (prognosis) 
Imaging 
-whole body MRI 
 •lytic lesions
 •pepper pot skull 
 •vertebral collapse/fractures

Special tests: bone marrow
-aspirate

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6
Q

What is the treatment of myeloma symptoms?

A

Treatment of myeloma
Chemotherapy followed by autologous transplant if young and not comorbid

MPT (Melphalan + Prednisolone + Thalidomide) or Lenalidomide + low-dose dexamethasone for those unsuitable for transplant

Hypercalceamia
-IV fluids, bisphosphonates

Bones

  • exclude SC compression (complication)
  • bisphosphonates to help ↓fractures ↓bone pain ↓Ca2+

Renal
-Fluids and follow AKI guidelines

Anemia
-RBC transfusion + EPO

Infections
-Abx (as appropriate) and regular IV Ig infusions if necessary

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7
Q

What is the treatment for myeloma itself? (3 stages)

A

Myeloma
INDUCTION
•3 drug chemo combo and steroids to induce remission

MAINTANANCE

  • on meds until relapse
  • autologous stem cell transplant good for longer remission (obliterate their own BM and save stem cells)

RELAPSE

  • almost all patients
  • continue or change treatment

**Monitor FBC, creat, Ca2+ serum/urine EP every 2-3 months

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8
Q

Complications of myeloma? (4)

What are the treatments?

A

Complications of myeloma
-hypercalceamia (IV fluids, bisphosphonates)
-SC compression (MRI and 16mg dex)
-hyperviscosity syndrome (plasmapheresis to remove light chains)
•reduced cognition/disturbed vision/bleeding
-AKI (give fluids, dialysis may be required)

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9
Q

Acute lymphoblastic leukaemia (ALL)

  • who normally gets it?
  • why do they get it?
A

Acute lymphoblastic leukaemia (ALL)
Who
-Always“Little people” (most common malignancy affecting children (peak 2-5 yo)
-If adults get it its an awful prognosis

Why
-both AML and ALL can progress from CML

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10
Q

Acute lymphoblastic leukaemia (ALL)

-What are 2 diagnostic investigations? (what would you see)

A

Acute lymphoblastic leukaemia (ALL)
BLOOD FILM
>20% lymphoBLAST cells on bone marrow (if less than 20% it is just mylodysplastic disorder)

TDT staining (positive)

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11
Q

What is the treatment for Acute lymphoblastic leukaemia)(ALL)

A

Acute lymphoblastic leukaemia (ALL)

-Imatinib (will relapse)

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12
Q

Who gets Acute myeloid leukaemia (AML)?

How do you get it?

A

AML=”Always Middle age”/Elderly
Who: incidence increases with age

Why: both AML and ALL can progress from CML

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13
Q

Acute myeloid leukaemia (AML)

-What is the diagnostic finding?

A

Acute myeloid leukaemia (AML)
-Auer rods, Auer rods, Auer rods!
(not always present but diagnostic)

*also see Myeloidblasts

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14
Q

What are the 2 types of AML and how do they present?

  • M3
  • M5
A

Acute myeloid leukaemia (AML)

  1. M3 (acute PROMYELOCITIC leukaemia)
    - medical emergency
    - presents with DIC and heamorrage
    - t15:17 translocation
  2. M5 (acute monocytic)
    - gum infiltration!!
    - lymphadenopathy and hepatosplenomegaly
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15
Q

What bloods would you expect from AML and ALL?

A

AML/ALL bloods present with bone marrow failure (↑lymphoid blasts infiltration)
↓Hb, ↓Plt ↓Neut,↑WBC (poor prognosis)

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16
Q

What is the presentation of AML and ALL?

A

AML/ALL present with rapid onset bone marrow failure:
ANEMIA
-sob/pallor/lethargy

THROMBOCYTOPENIA
-bleeding/bruising

NEUTROPENIA
-recurrent infections

Systemic

  • weight loss
  • fever
  • malaise
  • bone pain (BM failure)
  • splenomegally (spleen trying to eat all of extra cells)
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17
Q

ALL vs AML?

  • who?
  • diagnostic?
  • involvement?
A

ALL children, AML older age
ALL >20% lymphoidBLASTS, AML Auer rods
ALL brain involvement, AML gum involvement (mono M3)

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18
Q

Complication of ALL/AML?

How does it present?

A

Tumour lysis syndrome

  • can happen spontaneously or in response to treatment
  • can lead to AKI, can cause visual disturbances (contents pools in eyes)

Presentation: N+V, muscle cramps, confusion

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19
Q

What are the blood findings in tumour lysis syndrome?

A

Tumour lysis syndrome

  • HIGH uric acid
  • HIGH phosphate
  • HIGH potassium
  • LOW calcium
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20
Q

What is the treatment of Tumour lysis syndrome?

A

Treatment of tumour lysis syndrome:

  • hydrate
  • treat AKI
  • Rasburicase to lower uric acid levels
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21
Q

Translocation for AML?

Translocation for CML?

A

AML: t15:17
CML: t9:22 Philadelphia chromosome

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22
Q

Who gets chronic lymphocytic leukaemia? (CLL)?

How common is it?

A
  • CLL is a disease of the elderly (opposite of ALL)

- CLL is most common leukaemia

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23
Q

What cells are affected in CLL and what is a diagnostic finding?

A

chronic lymphocytic leukaemia? (CLL)

  • Almost always B Lymphocytes (99%)
  • SMUDGE/SMEAR cells are diagnostic (crushed little lymphocytes)
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24
Q

What would you see on bloods for CLL?

A

Chronic lymphocytic leukaemia? (CLL)

  • Bloods: ↑lymphocytes (normally Hb/platelets normal)
  • Normally an incidental finding, can cause ITP (mild bleeding and GP checkup)
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25
Q

What is the treatment fo chronic lymphocytic leukaemia? (CLL)?

A

Chronic lymphocytic leukaemia? (CLL)

  • watch and wait (because old and low grade malignancy)
  • if younger, could do a BM transplant
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26
Q

Complications of CLL?

A

Complications of CLL
-Autoimmune heamolysis
-Infections>death
-Richters transformation (transformation to aggressive lymphoma)
(basically like decompensated high grade CLL: B symptoms and swollen lymph nodes)

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27
Q

CLL vs CML on presentation?

A

CLL= more lymphadenopathy

CML=MASSIVE splenomegaly (abdo pain, can’t eat)

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28
Q

What cells are affected in Chronic myeloid leukaemia (CML)?

A

Chronic myeloid leukaemia (CML)

-Mature myeloid cells-granulocytes (basophils, eosinophils, neutrophils)

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29
Q

Who normally gets CML and what is the genetic translocation?

A

Chronic myeloid leukaemia (CML)
-Older pts. 40-60
-Philadelphia chromosome (95%) due to translocation T( 9:22)
(those without chromosome have worse prognosis (cant use TKI drugs)

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30
Q

What can be a complication of CML?

What is the prognosis of CML

A

Chronic myeloid leukaemia (CML) can cause AML (80%) and ALL (20%)

Poorer prognosis (than CLL) (5-6 years)

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31
Q

What is the treatment for CML?

A

Chronic myeloid leukaemia (CML)
TREATMENT IS IMATINIB (BCR-ABL tyrosine kinase inhibitor)

-Allogenic BM transplant if unsuccessful or for young patients as a curative therapy

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32
Q

What are the symptoms of CLL/CML?

A

CML/CLL symptoms

  • B symptoms (weight loss, night sweats)
  • Painless LN (only CLL)
  • Hepatosplenomegaly (MASSIVE in CML)
  • Neutropenia: recurrent infections
  • Anaemia: SOB/pallor/lethargy
  • Thrombocytopenia: bleeding/bruising
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33
Q

What is seen on a blood film of CML?

A 
Chronic myeloid leukaemia (CML) 
-Leucocytosis
-Basophilia 
-Eosinophilia 
-Blasts = indicate accelerated phase 
Thrombocytosis
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34
Q

What are 3 phases of CML?

A 
Chronic phase (few/no symptoms for months/years) 
Acclerated phase (increasing symptoms and spleen size)
Blast crisis +/- death (presents like acute leukaemia with blasts )
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35
Q

What is DIC?

A

Disseminated intravascular coagulation

  • systemic activation of clotting cascade
  • leading to consumption of clotting factors and platelets
  • micro clots and bleeding
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36
Q

What are some causes of DIC?

A

STOP Making Trouble

Sepsis / snakebites 
Trauma 
Obstetric complications 
Pancreatitis 
Malignancy 
Transfusion
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37
Q

What obstetric complications lead to DIC?

A

Obstetric complications-DIC

  • Amniotic fluid embolism
  • Pre-eclampsia
  • Placental abruption
  • Retained products of conception
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38
Q

What malignancies are associated with DIC?

A
  • Acute promyelocytic leukaemia (rare subtype of AML-M3)
  • Pancreatic, ovarian or gastric adenocarcinomas
  • NSCLC
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39
Q

How may DIC present?

A

Bleeding

  • Petechia, purpura, ecchymoses
  • Oozing from wounds
  • Haematuria
  • Blood in body cavities eg haemoperitoneum

Thrombosis

  • Acute renal failure (oliguria)
  • Hepatic dysfunciton (jaundice)
  • ARDs (dyspnoea, crackles)
  • PE (dyspnoea, chest pain, haemoptysis)
  • DVT
  • Neurodysfunction (altered mental status, stroke)
  • Purpura fulminans (extensive skin necrosis)
  • Waterhouse Friderichsen syndrome (adrenal heamorrage)
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40
Q

Describe the course of DIC depending on the cause

A

Acute eg following trauma / sepsis

Subacutely eg following malignancy

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41
Q

What findings on bloods suggest DIC?

What would you see on blood film?

A 
DIC 
Bloods
-Low platelets
-Low fibrinogen (all used up to make fibrin clot) 
-Low coagulation factors 
-High D-dimer 
-High PT and APTT

Blood film
-shistocytes (fibrin strands damage RBCs)

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42
Q

What are some ddx of DIC?

A

Severe hepatic dysfunction

Thrombotic thrombocytopenic purpura TTP

Heparin induced thrombocytopenia

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43
Q

How can severe hepatic dysfunction be differentiated from DIC?

A

FVIII assay

Would be low in DIC (all are low)

But NORMAL in chronic liver disease as not only made by hepatic cells (also sinusoidal endothelial cells)

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44
Q

How can thrombotic thrombocytopenic purpura be differentiated from DIC?

A

No consumption coaguloptahy - so normal PT and aPTT in thrombotic thrombocytopenic purpura

In DIC both are prolonged

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45
Q

What is the management of DIC?

A

DIC management

  • MED EMERGENCY, TREAT UNDERLYING CAUSE
  • Platelets, FFP (clotting factors), cryoprecipitate (fibrinogen), RBC

All transretinoic acid in promyelocytic leukaemia

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46
Q

What are the indications/purpose of transfusions in DIC?

A

Platelet concentrate:
- if platelets are <10,000 in an asymptomatic individual, or <50,000 with active bleeding or a surgery planned

FFP to replace clotting factors
- If PT or aPTT >1.5 normal value

Cryoprecipitate if fibrinogen <150mg/dL

Packed RBC

  • massive haemorrhage without response to fluids
  • or if Hb <70g /L
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47
Q

What are the two types of haematopoietic stem cell transplantation?

A

Autologous = removal and storage of patients own cells which are retransfused back after high dose chemo

Allogenous = transplant of stem cells from sibling or donor

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48
Q

What are the indications for autologous stem cell transplant?

A

Multiple myeloma and Lymphoma get AUTOlogous stem cell transplant

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49
Q

What are the advantages and disadvantages of autologous stem cell transplants?

A

Autologous stem cell transplants
Advantages
-Low risk of graft vs host disease
-Low risk late post transplant infection

Disadvantages

  • High risk of early post transplant infection (you’ve taken away their own bone marrow)
  • No graft vs tumour effect (when donated cells attack malignant cells)
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50
Q

What are some indications for allogenous stem cell transplantation?

A

To replace abnormal but non malignant cells in the lymphohamatopoietic system eg:

  • Immunodeficiency
  • Aplastic anaemia
  • Thalassaemia

**exception is leukaemia!

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51
Q

What are some advantages/disadvantages for allogenous stem cell transplantation?

A

Allogenous stem cell transplantation
Advantages
-Graft vs tumour effect
-Low risk early post transplant infection

Disadvantages

  • Risk of graft vs host disease
  • Late post transplant infection
  • Can cause chromosomal abnormalities in blood / bone marrow due to discrepancy between genotype and phenotype
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52
Q

Which drugs are associated with agranulocytosis?

A

Clozapine
Carbamazepine
Valproate
Carbimazole + other anti thyroids

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53
Q

What is the classic presentation of Hodjkins lymphoma?

Who gets it?

A

Hodgkins lymphoma

  • rubbery superficial cervical lymph node
  • painless and fluctuating
  • lymph node painful with alcohol
  • 1/3 have B symptoms (fever, weight loss, night sweats)
  • YOUNG ADULTS and ELDERLY
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54
Q

What infection is assosiated with Hodjkins?

A

EBV is associated with Hodjkins

also assosiated with non Hodjkins-Burkitts type

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55
Q

What lymphoma do you get Reed-Sternberg cells

A

HODJKINS lymphoma you get Reed-Sternberg cells (multi-nucleated giant cells)

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56
Q

What staging system is used for lymphomas?

A

Ann Arbor staging

  1. Single lymph node region
  2. Involvement of 2+ nodal areas on same side of diaphragm
  3. Involvement of nodes on both sides of diaphragm
  4. Spread beyond lymph nodes

Each stage has A (no systemic symptoms except pruritis) or B (systemic symptoms present)

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57
Q

What is 1st line investigation for Hodjkins?

What are the findings?

A

Hodjkins lymphoma

  • 1st line investigation is LN excision biopsy
  • can see Reed-Sternberg cells or lacunar cells
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58
Q

What blood test results indicate a worse prognosis in Hodgkin’s lymphoma?

A

Worse prognosis

  • High ESR
  • Low Hb
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59
Q

What is the treatment for Hodjkins lymphoma?

A

Radiotherapy and Chemotherapy (ABVD) – Adrimycin, Bleomycin, Vinblastine, Dacarbazine

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60
Q

What lymphomas does Non-Hodgkin’s lymphoma include?

A

All lymphomas without Reed-Sternberg cells

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61
Q

What is the most common type of non hodjkins lymphoma?

A

Diffuse large B-cell lymphoma is mot common type of non hodjkins lymphoma

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62
Q

What is the most common area for extranodal disease in Non-Hodgkin’s lymphoma?

A

GI tract

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63
Q

What are the 3 types of GI tract Non-Hodgkin’s lymphomas?

A
  1. Gastric MALT (h. pylori)
  2. Non-MALT gastric lymphoma
  3. Small bowel lymphomas
64
Q

What is Gastric MALT caused by?

A

H. Pylori causes gastric MALT

65
Q

In LFTs, what indicates a poorer prognosis in Non-Hodgkin’s lymphoma?

A

Raised LDH because it indicates increased cell turnover

66
Q

In terms of treatment/prognosis, what is the difference between low and high grade non-hodjkins lymphomas?

Give an example of each one

A

Non hodgkins lymphoma
-Low-grade - slow-moving but incurable and widely disseminated e.g. MALT

-High-grade - aggressive but often curable e.g. Burkitts (child with swollen jaw, assosiated with EBV, story sky appearance, treated with RCHOP)

67
Q

Presentation of non hodjkins lymphoma?

A

non hodjkins lymphoma
1. Lymphadopathy

  1. Symptoms of marrow involvement:
    - anaemia
    - infection
    - bleeding
  2. B symptoms (although less common than hodjkins and indicates disseminated disease)
68
Q

Non hodjkins lymphoma and skin rash, what is this?

A

Mycosis fungoides (cutaneous T-cell lymphoma/sezary syndrome

69
Q

What are the four groups of causes of iron deficiency anaemia?

A

IDA

  1. Excessive blood loss (periods, urinary, GI)
  2. Dietary inadequacy (malnutrition or breastfeeding)
  3. Iron malabsorption (coeliac)
  4. Excessive requirements (pregnancy)
70
Q

What condition can typically cause iron malabsorption?

A

Coeliac disease can typically cause IDA (affects the duodenum which is where iron is absorbed)

71
Q

What are some signs you see when examining an iron deficient patient?

A

Iron defficiency anemia signs

  • Angular stomatitis
  • Atrophic glossitis
  • Dysphagia = Plummer-Vinson syndrome (IDA, osophageal web, dysphagia)
  • Pallor
  • Pale palmar creases
  • Koilonychia (spooning of the nails)
  • Picca (cravings, e.g. ice/brick)
72
Q

What would a blood film look like in iron deficiency anaemia?

A

Iron deficiency anaemia
Hypochromic microcytic anaemia +/- anisocytosis and poikilocytosis + target cells

Hypochromia = low MCH (low mean corpuscular Hb)
Microcytosis = low MCV 
Anisocytosis = variation in size between RBCs 
Poikilocytosis = abnormally shaped RBCs
73
Q

What is the 1st line test for IDA?

A

Ferritin is 1st line.

although it correlates with total body iron stores, it can be raised in infection/inflammation

74
Q

What further investigations would you do in a patient with iron deficiency anaemia?

A

Iron deficiency anaemia investigations
Bloods
-FBC/blood film/B12 and folate/ heamolysis screen (coombs and bilirubin)/Coeliac screen/UsEs (CKD)/ TFT (hypothyroidism)/LFT (CLD)

Imaging
-If negative (and male or post-menopausal woman), refer for gastroscopy + colonoscopy to rule out GI bleed

Special
-Coeliac if concerned about that

75
Q

What is the treatment for iron deficiency anaemia and how long do you treat for?

A

Iron deficiency anaemia

  • Ferrous sulphate/fumerate 200-300mg 1-2 times a day
  • Once Hb levels are normal, continue treatment for a minimum of 3 months
76
Q

What are the main side effects of iron replacement therapy?

A

Iron replacement therapy

  • Constipation and black stools are main ones
  • Black stools
  • Nausea
  • Abdominal pain

(all reasons for iron not rising, despite therapy)

77
Q

What MCV is classified as microcytic?

What are the causes of microcytic anemia? (4)

A

Microcytic anemia (MCV<80)

  1. Iron deficiency anemia
  2. Thallasemias
  3. Anemia of chronic disease
  4. Sideroblastic (lead posining)
78
Q

What are the indications for blood transfusion?

A

Blood transfusion

  • if Hb <70g/L
  • if Hb <80g/L for cardiac comorbidity
79
Q

When would you give IV iron?

A

IV iron is indicated if oral hasn’t worked, or malabsorption or CKD

80
Q

Explain the pathophysiology of anemia of chronic disease?

A

Anemia of chronic disease

  • ‘functional’. They have the iron but don’t know how to use it
  • inflammation>↓erythropoisis ↑iron absorption (keeps it in the cells)
  • starts normocytic>then microcytic
81
Q

What would anemia of chronic disease look like on bloods? (ferritin, serum iron, transferrin, any others?)

A 
Anemia of chronic disease
↑Ferritin (but its all in cells) 
↓Serum iron 
↓Transferrin/TBIC (less iron in blood) 
↑Inflamitory markers
82
Q

Managment of Anemia of chronic disease

A

Anemia of chronic disease managment

  • treat underlying cause
  • iron supplements/EPO may help
83
Q

What is sideroblastic anaemia due to?

A

Sideroblastic anaemia

  • Impaired ability of bone marrow to produce normal RBC (ineffective erythropoiesis)
  • ↑iron absorption and ↑iron loading in marrow, heart, liver
84
Q

What will you see in blood test/blood film with sideroblastic anaemia

A

Sideroblastic anaemia

  • ↑Ferritin (just being dumped places)
  • SIDEROLASTS (circle of iron in middle)
85
Q

What are causes of sideroblastic anemia?

A

Sideroblastic anaemia

  • congenital X linked
  • TB medications
  • lead poisoning
  • myeloproliferative disorders
86
Q

What MCV is macrocytosis defined by?

A

MCV > 96 fL

87
Q

What is a megaloblast?

A
  • Megaloblasts are large immature RBC (due to defective DNA synthesis)
  • Found in megaloblastic microcytic anaemia
88
Q

What are the main causes of megaloblastic macrocytic anaemia and why?

A

Megaloblastic

  • Vitamin B12 and folate deficiency (they are required for normal DNA synthesis)
  • drug induced
89
Q

What drugs can cause folate deficiency?

A

Methotrexate
Anti-epileptics
Trimethoprim

90
Q

Where are folate and B12 absorbed?

What surgical procedure commonly causes vitamin B12 deficiency?

A

DUDE IS JUST FEELING ILL BRO (absorption)

  • duodenum: iron
  • Jejunum: folate
  • Ilium (terminal): B12

Gastrectomy (B12 requires IF from gastric parietal cells to aid absorption)

91
Q

What causes non-megaloblastic macrocytic anaemia?

A

non-megaloblastic macrocytic anaemia

  • Excess alcohol!!!!!!!!!!!!!
  • Hypothyroidism
  • Liver disease (LFTs and yGT)
  • Pregnancy
  • Reticulocytosis in haemolysis

*if you cant find the above causes, do BM biopsy for leukaemia

92
Q

What vitamin is folate?

A

Vitamin B9

93
Q

What can you see on blood film in B12 and folate deficiency?

A

B12 and folate defficiency

  • Megaloblastic RBC
  • Hypersegmented neutrophils
94
Q

Treatment of folate defficiency?

A

Folate defficiency

  • lifetyle: more leafy greens/nuts
  • Give 5mg folic acid every day
  • Always with hydroxocobalamin B12, (unless B12 is normal) otherwise may cause subacute combined degeneration of the cord
95
Q

Treatment of B12 defficiency?

A

B12 Deficiency

  • Give B12 injections 1mg IM for alternate days, 2 wks
  • Maintenance: 1mg IM every 3 months for life

If both B12 and folic acid deficient, start B12 injections first to avoid risk of SCDSC, then once B12 normalises, start Folic acid after

96
Q

What is pernicious anaemia?
How does it present?
Bloods?

A

Pernicious anaemia (tend to be > 40yo)

  • autoimmune condition
  • atrophic gastritis → lack of intrinsic factor from parietal cells → B12 can’t be absorbed in terminal ilium

Presentation: Lemon tinge due to pallor and mild jaundice

Bloods – Parietal cell Ab, IF auto-Ab

97
Q

Causes of normocytic anaemia?

A

Causes of normocytic anaemia include:

  • anaemia of chronic disease (starts normocytic>then microcytic)
  • aplastic anaemia (bone marrow disorder LOW RETICULOCYTES
  • haemolytic anaemia (HIGH RETICULOCYTES)
  • acute blood loss
  • chronic kidney disease
98
Q

What is a complication of B12 defficiency and how does it present?

A

Subacute combined degeneration of spinal cord!!!

  • complication of B12 defficiency
  • Classic triad: extensor plantar (UMN), absent ankle jerk (LMN) absent knee jerk (LMN)
  • Insidious onset symmetrical loss sensory, motor UMN and LMN
  • Proprioception and sense of vibration (1st to be lost)
  • Ataxia → stiffness and weakness

TO PREVENT: always replace B12 BEFORE folate

99
Q

Which blood types are universal donors and which are recipients?

A

O negative are universal dOnOrs (No antigens, A and B antibodies)

AB positive are universal recipients (A and B antigens, no A and B antibodies)

100
Q

List the types of immune related transfusion reactions that can occur (7)

A

TRANSFUSION REACTIONS
Early (<24 hours)
1) Acute haemolytic transfusion reaction
2) Acute non haemolytic febrile transfusion reaction
3) Minor allergic reactions
4) Anaphylaxis (IgA deficiency increases the risk)
5) TRALI

Delayed (after 24 hours)

6) Post transfusion purpura
7) Delayed haemolytic transfusion purpura

101
Q

What causes an acute haemolytic transfusion reaction?

A

ABO incompatibility (MISTAKE)> destruction of donor RBCs by recipient antibodies

102
Q

How may an acute haemolytic transfusion reaction present?

A

Acute haemolytic transfusion present in minutes

  • Fever↑Temp
  • Hypotension
  • Abdo pain or Chest pain
  • Flushing/nausea
  • Agitation/SOB
  • Oozing venepuncture sites/ pruritus
  • Burning at IV site
  • Can progress to DIC
103
Q

What are some complications of an acute haemolytic transfusion reaction?

A

Renal failure
DIC
Jaundice

104
Q

Managment of acute haemolytic transfusion reaction?

A

Acute haemolytic transfusion

  • STOP transfusion
  • Check identity/name on unit
  • IV fluids 0.9% saline
  • Coombs test - detects antiglobulins showing autoimmune haemolytic anaemia
  • Vasopressors to maintain perfusion - obstruction of vessels by haemolytic debris and hypotension can decrease perfusion
  • ECG - hyperkalaemia secondary to severe haemolysis can occur
  • If DIC develops - FFP and platelets
105
Q

What causes a nonhaemolytic febrile transfusion reaction to occur?

A

nonhaemolytic febrile transfusion
-Due to white blood cell HLA antibodies
-After periods of long storage of RBC
(cytokines may leak from donor RBCs and subsequently cause a mild immune reaction)

106
Q

How does a nonhaemolytic febrile transfusion reaction present?

A

Shiver and fever 1 hour after infusion

107
Q

Managment of nonhaemolytic febrile transfusion reaction?

A

SLOW/STOP transfusion

  • give paracetamol
  • if continues use a WBC filter
108
Q

How may anaphylaxis present following transfusion?

Management?

A

Anaphylaxis

  • Sudden onset
  • Shock
  • Hypotension

Manage

  • Stop transfusion
  • Secure airway (Call anaesthetist)
  • Adrenaline 0.5mg (1:1000) IM
  • Chlorphenamine 10mg
  • HDC 200mg
  • Salbutamol NEB upto 20mg
109
Q

What is a TRALI?

A

Transfusion related acute lung injury

  • Due to anti-leucocyte Abs
  • More common with FFP and platelets
110
Q

How does TRALI present?

A

TRALI

  • Cough
  • Breathlessness
  • Hypoxia ↓Sats %
  • Frothy sputum
  • Fever
  • Hypotension due to hypovolaemia
  • CHEST X RAY WHITE OUT
111
Q

Management of TRALI

A

TRALI managment

  • Stop transfusion
  • treat as ARDS (give oxygen>NIV>intubation +/- circulatory support)
112
Q

What is Graft-vs-host disease?

A

Graft-vs-host disease

  • Almost always fatal
  • Donated bone marrow or peripheral blood stem cells view recipients body as foregin and attack the body
  • Risk reduced by irradiation of blood products
113
Q

How does GvHD present?

A

Day 4-30 post transfusion

  • High fever
  • Diffuse erythematous skin rash
  • Diarrhoea and abnormal liver function
  • Pt deteriorates with bone marrow failure
  • Death from overwhelming infection
114
Q

What is TACO?

How does it present?

A 
Transfusion associated circulatory overload
Symptoms of hypervolaemia:
- SOB 
- S3 gallop 
- ↑JVP
- Basal creps
- HTN

-Pulmonary oedema (chest X ray)

115
Q

What is the treatment of TACO?

A

TACO

  • Diuretics (furosemide)
  • O2
  • Assisted ventilation if severe
116
Q

What electrolyte imbalances can occur following a transfusion?

A

Hyperkalaemia - esp rapid transfusions causing mechanical damage of RBC

Hypocalcaemia - formation of complexes with the added citrate (anticoagulant in the bag the blood is donated in)

117
Q

How do you treat post transfusion prupura?

A

Post transfusion prupura

  • IV Imunoglobilins
  • Platelet transfusions (because thrombocytopenia)
118
Q

What do lymphoid precursor cells produce?

A

B Lymphocytes
T lymphocytes
Natural killer cells

119
Q

What do myeloid precursor cells produce?

A

Erythrocytes (RBC)
Granulocytes (basophil, eosinophil, neutrophil)
Megakaryocytes (platelets)

120
Q

What is the most common cause of hypercoagulability in white populations?

A

Factor V Leiden is the most common cause of thrombophillia (autosomal dominant)

121
Q

Other than Factor V Leiden, name some inherited thromobophilias (hypercoagulablities)

A 
Protein C deficiency
Protein S deficiency 
Antithrombin III deficiency 
Hyper-homocysteinemia 
Plasminogen deficiency 
Sickle cell anaemia
122
Q

Antithrombin III deficiency is usually inherited (autosomal dominant). What can cause it to be acquired?

A

Liver failure
Renal failure
Nephrotic syndrome = urinary loss of antithrombin

123
Q

What can lead to acquired thrombophilia?

A 
Pregnancy
Inc age 
Smoking 
Obesity 
Surgery 
Immobilisation 
Trauma 
Malignancy (esp adenocarcinoma) 
Antiphospholipid syndrome 
Nephrotic syndrome 
OCP 
HRT 
SLE 
Heparin induced thrombocytopenia (Unfractionated more likely)
124
Q

What is the role of protein C?

A
  • Activated protein C inactivates factor V in the clotting cascade
  • This decreases the activation of thrombin (which would turn fibrinogen into fibrin creating a clot)
  • It is vitamin K dependant
125
Q

What is activated protein c resistance? What happens?

A

Factor V Leiden

Factor V does not get deactivated (protein C not working), so activates prothrombin to thrombin, fibrinogen gets turned to fibrin, thus there are an increase in thrombotic events

eg peripheral and cerebral vein thrombosis, recurrent pregnancy loss

126
Q

What is the role of antithrombin III?

What happens in a defficinency?

A

Normally binds to and inactivates thrombin (III) and Factor X = INHIBITING coagulation

Deficiency leads to decreased inhibition and elevated thrombin and factor X> increased clotting

127
Q

Mechanism of heparin?

A

Heparin

  • Indirectly inhibits the action of thrombin and factor Xa by increasing the activity of antithrombin III (an endogenous anticoagulant)
  • Basically BOOSTS antithrombin>reduces clotting

Acts on the intrinsic pathway

128
Q

Effect of heparin on bloods?

A

Heparin increases APPT (intrinsic pathway)

However in antithrombin III deficiency, there is no increase

129
Q

What complications may someone with antiphosppholipid syndrome have?

A

DVTs
Portal vein thrombosis
Strokes
Miscarriages - often experience clotting inside the placenta leading to spontaneous abortions

130
Q

What can cause impaired platelet PRODUCTION in bone marrow?

A 
Bone marrow failure
Bone marrow suppression (chemo / radiotherapy /drugs) 
Congenital thrombocytopenias 
Infection 
Malignancy 
Vit B12 deficiency 
Folate deficiency
131
Q

List some congenital thrombocytopenias

A

Wiskott-Aldrich syndrome
Alport syndrome
von Willebrand disease
Bernard-Soulier syndrome

132
Q

What are some causes of increased platelet turnover/reduced survival of platelets in periphery?

A

Immune thrombocytopenia
DIC
TTP and HUS
Drug induced immune thrombocytopenia e.g. HIT
Preeclampsia
HELLP
Prosthetic valves causing mechanical damage

133
Q

How is immune thrombocytopenic purpura (ITP) diagnosed?

A

Diagnosis of exclusion in isolated thrombocytopenia

134
Q

What is primary vs secondary ITP

A

Primary - idiopathic but may be triggered by infection

Secondary - lymphoma, leukaemia (esp CLL), SLE, HIV, Hep C, drug reactions

135
Q

ITP is common in which demographic and what onset is it usually?

A

Children - usually acute following infection (viral symptoms)

Women of childbearing age - insidious onset or incidental finding (>12 months)

136
Q

What is the management of children with ITP?

A

If no bleeding or only bruising / petechiae = observation regardless of platelet count

If severe bleeding = glucocorticoids +/- IV Ig

137
Q

What is the management of adults with ITP?

A

1st line - glucocortoids (to suppress AB production)
or Iv Ig

2nd line - splenectomy

138
Q

pathophysiology of ITP

A

IgG antibodies against glycoprotein on platelets

Platelet-antibody complex removed from circulation by spleen

Decreased platelet count

Bone marrow megakaryocytes and platelet production increases in response

139
Q

How do haemolytic anemias present?

A

Anaemia:
- Pallor, fatigue, exertional dyspnoea

Haemolysis:

  • Jaundice
  • Pigmented gallstones due to the build up of indirect bilirubin in bile
  • Splenomegaly
  • Back pain and dark urine in severe haemolysis with haemoglobinuria (nephrotoxic)

Sings of increased haemoposis (mostly in chronic eg thalassaemia)

140
Q

Heamolytic anemia investigations

  • findings of increased cell breakdown
  • findings of increased cell production
A 
Haemolytic anemia 
Findings of increased cell breakdown 
-Normal or Increased MCV
-↑UNconjugated bilirubin 
-↑ urinary urobilinogen (no conjugated) 
-↑ LDH

Findings of increased cell production
-↑Reticulocytes (cause ↑MCV because they are large)

141
Q

What test is used to differentiate between autoimmune and non-autoimmune haemolytic anaemias?

A

Coombs test

  • Direct Coombs positive = autoimmune
  • Direct Coombs negative = non-autoimmune

Direct Coombs test - detects antibodies on surface of RBCs

Indirect Coombs test - detects antibodies in serum (done in petri dish used to determine Rh status or transfusion matches)

142
Q

What is intravascular vs extravascular haemolysis?

A

Intravascular = RBC within vessel (JAUNDICE)

Extravascular = phagocytosis of RBC (AFFECTS SPLEEN)

143
Q

What can be measured to check for intravascular haemolysis? Is it low or high and why?

A

↓ HAPTOglobin =intravascular

  • protein that mops up free Hb
  • if it is low then there is free Hb (RBC have been destroyed)

*also get increased serum Hb

144
Q

What are the main IMMUNE causes of haemolytic anemia? (Direct coombs test +ve)

A

DIRECT COOMBS+ve =IMMUNE MEDIATED

  • Autoimmune haemolytic anemia (warm IgG, cold IgM)
  • Drug induced (penicillin, quinine)
  • Paroxysmal cold haemoglobinuria (infection with syphilis/viruses)
145
Q

What is Microangiopathic haemolytic anaemia (MAHA)?
When do you see it?
What do you see blood film?

A

Microangiopathic haemolytic anaemia (MAHA)

  • mechanical disruption of RBCs (HUS, DIC, pre-eclampsia)
  • blood film: Schistocytes
146
Q

What test should you do if you suspect malaria as the cause off haemolytic anemia?

A

Malaria

-Do a Thick + Thin blood film

147
Q

What is paroxysmal nocturnal haemoglobinuria?

A

PNH (cause of non immune haemolytic anemia)

-rare stem-cell disorder w/ bone marrow failure + thrombophilia

148
Q

What is the most common hereditary condition causing haemolytic anemia?

What does the blood film show?

A 
G6PD def
- X-linked 
-common in middle-east
-precipitated by drugs e.g. aspirin, sulfonureas, quinoline
HEINZ BODIES/BITE CELLS
149
Q

What are some causes of Coombs -ve autoimmune haemolytic anemia?

A

Direct Coombs -ve autoimmune haemolytic anemia:

  • autoimmune hepatitis B and C
  • post vaccine
150
Q

Tear dropped RBC?

A

Mylefibrosis
-proliferation> fibrosis of bone marrow>extramed haemopoisis MASSIVE SPLENOMEGALLY
> RBC squeezed through BM> TEAR SHAPED

151
Q

Classic features of polycythemia vera?
Mutation?
Treatment?

A

Polycythemia Vera

  • blurred vision/flushed/[almar erythema/ITCHING AFER BATH
  • JAK2 mutation
  • Venepuncture and aspirin
152
Q

What type of anaemia does thalassaemia cause?

A

Thalaseamias cause microcytic anaemia (if a suspicion IDA doesn’t respond to treatment think thalasseamia)

153
Q

How does hereditary spherocytosis present?

A

Hereditary spherocytosis

  • jaundice
  • gallstones
  • if poorly (can be splenic rupture)
154
Q 
What are the following in iron defficiency anemia?
Ferritin 
TBIC 
Serum iron 
Transferrin 
Transferrin saturation
A 
Iron deficiency anaemia
↓Ferritin 
↓Serum iron 
↓Transferrin saturation
↑TBIC (increasing its attractiveness to iron-because there is none, have to try harder to attract) 
↑Transferrin
155
Q

In sickle cell anemia, what is an aplastic crisis?

A

Aplastic crisis:

  • sudden drop of Hb
  • reduction in reticulocytes
  • often caused by parvovirus infection (rash)
156
Q

Pentad of symptoms in TTP?

A

TTP presents with a pentad of:

  • fever
  • neuro signs
  • thrombocytopenia
  • haemolytic anaemia
  • renal failure

5thyr (18 decks)

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