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Y4 Cancer Care > 18 - Haematology Principles > Flashcards

18 - Haematology Principles Flashcards

1
Q

What will tests show if there is haemolytic anaemia?

A
  • Low Hb
  • High bilirubin
  • Reticulocytosis
  • Raised LDH
  • Raised urinary urobilinogen
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2
Q

What are the different classifications of haemolytic anaemia and give some examples of each?

A
  • *• Hereditary** v Acquired
  • *• Immune** (Coombs +ve) v Non-immune (Coombs -ve)
  • *• Extravascular** v Intravascular
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3
Q

What can inherited haemolytic anaemias be classified by?

A
  • Erythrocyte membrane
  • Haemoglobin molecule e.g sickle cell, thalassemia
  • Metabolic disturbance e.g G6PD deficiency
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4
Q

What can acquired haemolytic anaemias be classified by?

A

Immune Mediated

  • Haemolytic transfusion reactions
  • Haemolytic disease of the newborn
  • Cold and Warm AIHA

Non-immune mediated

  • Mechanical trauma - due to heart/large blood vessel pathology
  • Microangiopathic haemolytic anaemia (e.g. HUS, TTP, DIC)
  • Burns
  • Infections
  • Drugs & chemicals
  • Hypersplenism

RBCs may become mechanically damaged from the impact on abnormal surfaces such as metallic heart valves or as they pass through abnormal, intravascular fibrin strands that may be seen in microangiopathic haemolytic anaemias

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5
Q

What are some signs and symptoms of haemolytic anaemia?

A

Symptoms

  • Fatigue
  • Weakness
  • Paraesthesia
  • Dyspnoea
  • Gastrointestinal symptoms (e.g. nausea, dyspepsia)
  • Weight loss

Signs

  • Atrophic glossitis
  • Pallor
  • Fever
  • Splenomegaly
  • Evidence of underlying disease

Haemolysis

  • Jaundice
  • Abdominal pain (e.g. gallstones)
  • Dark urine (e.g. haemoglobinuria secondary to intravascular haemolysis)

Underlying aetiology

  • Neurological signs (e.g. TTP)
  • Splenomegaly
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6
Q

What tests do you need to do for a haemolysis screen and what will they show if there is hameolysis?

A
  • FBC inc Reticulocyte count
  • Blood film: spherocytes which is prominent feature in AIHA
  • Direct Coombs Test
  • Bilirubin
  • LDH
  • Haptoglobin
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7
Q

What is the MCV in haemolytic anaemia?

A

Normocytic

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8
Q

What might you see on blood film with haemolytic anaemia?

A
  • Spherocytes (e.g. hereditary spherocytosis)
  • Schistocytes (e.g. microangiopathic haemolytic anaemia)
  • Sickle cells (e.g. sickle cell disease)
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9
Q

What is the pathophysiology of immune mediated haemolytic anaemia?

A

Binding of antibodies (allo or auto) to erythrocyte membrane, which can lead to fixing of complement and phagocytosis by macrophages

  • Alloantibodies: antibodies produced by one individual that will react with antigens of another individual of the same species e.g haemolytic transfusion reaction
  • Autoantibodies: generated against components of the individuals own tissue, may be seen in AIHA
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10
Q

What is the difference between cold and warm AIHA?

A

Warm AIHA:

Antibody reaction against erythrocytes at higher temperatures (e.g. > 37°), which then leads to agglutination

May be idiopathic, or associated with immune dysfunction secondary to infection, chronic inflammation or malignancy. (HIV, EBV, SLE, CLL, NHL)

Cold AIHA

Reaction against erythrocytes at lower temperatures (e.g. < 32°), which then leads to agglutination.

May be idiopathic or associated with systemic diseases such as lymphoma, Mycoplasma pneumoniae infection and infectious mononucleosis.

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11
Q

Why can it be difficult to cross match patients with AIHA?

A

Autoantibody can react with several or all of the red cell antigens resulting in agglutination reactions with the entire panel of red cells

Can make it very difficult, if not, impossible to provide compatible blood. It may be impossible to tell if a patient has an alloantibody as all the tests are positive due to the presence of the pan-reacting autoantibody

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12
Q

How are patients with AIHA crossmatched?

A

To exclude the presence of alloantibodies (in addition to the known autoantibodies) the autoantibody must be removed from the serum

Done in National Blood Service laboratories so acquiring compatible blood can take a long time

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13
Q

How is AIHA managed?

A
  • Blood transfusions
  • Prednisolone (steroids)
  • Rituximab (a monoclonal antibody against B cells)
  • Splenectomy
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14
Q

How are hereditary spherocytosis and elliptocytosis managed?

A
  • Folate supplementation
  • Splenectomy
  • Cholecystecomy if gallstones are an issue
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15
Q

What can trigger haemolytic anaemia in the X-Linked recessive disease G6PD deficiency?

A
  • Infections
  • Medications: primaquine (antimalarial), ciprofloxacin, sulfonylureas, sulfasalazine
  • Broad beans

Usually Heinz bodies on blood film. Diagnosis can be made by doing a G6PD enzyme assay

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16
Q

What are some causes of Microangiopathic Haemolytic Anaemia (MAHA)?

A

Small blood vessels have structural abnormalities that cause haemolysis of the blood cells travelling through them

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17
Q

What is paroxysmal nocturnal haemoglobinuria?

A

Mutation of haemopoietic stem cells leading to loss of the proteins on the surface of red blood cells that inhibit the complement cascade. Results in activation of clotting cascade against RBC

Red urine in the morning containing haemoglobin and haemosiderin. They are also predisposed to thrombosis (e.g. DVT, PE and hepatic vein thrombosis) and smooth muscle dystonia (e.g. oesophageal spasm and erectile dysfunction)

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18
Q

What is the significance of a raised reticulocyte count in anaemia?

A

Bone marrow is responsive to EPO

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19
Q

What are the different pathways in the coagulation cascade?

A
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20
Q

What tests are done on a clotting screen?

A

PT/INR (12-13 seconds/0.8-1.2)

Time taken for blood to clot via the extrinsic pathway

Measure of overall clotting factor synthesis or consumption.

This test can be affected by liver disease, DIC, vit K deficiency and warfarin

APTT (35-45 seconds)

Time time taken for blood to clot via the intrinsic pathway

APTT, however, can indicate issues with factors VIII (vWF), IX, and XI

Bleeding time (1-6 minutes for finger prick)

Patelet specific disorders will increase the overall bleeding time

Thrombin time (10-15 seconds)

This is a test of how fast fibrinogen is converted to fibrin by thrombin.

Similar to prolonged PT, this can be due to DIC, liver failure, malnutrition, abnormal fibrinolysis and many other conditions.

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21
Q

What are the main conditions leading to an abnormal APTT result?

A
  • Haemophilia A (VIII – X-linked recessive)
  • Haemophilia B (IX – X-linked recessive)
  • Haemophilia C (XI – autosomal recessive)
  • von Willebrands disease (as vWF pairs up with factor VIII)

Note: anti-phospholipid syndrome can cause a high APTT despite being a disorder that causes clots, due to it inactivating the phospholipid used in APTT.

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22
Q

What are the main conditions that increase the bleeding time?

A
  • von Willebrand’s disease (vWF deficiency – autosomal dominant)
  • TTP/ITP/HUS/DIC
  • Thrombocytopaenia
  • Bernard Soulier syndrome
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23
Q

What are some additional tests that can help you to interpret abnormalities on a clotting screen?

A
  • FBC for platelet levels
  • LFTs for general liver function
  • Albumin
  • D-Dimer
  • Levels of specific factors
  • Antibodies
  • Thrombophillia screens
  • ADAMTS13 (for TTP)
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24
Q

How can you tell the difference between DIC and ITP/TTP/HUS on a coagulation screen?

A
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25
What should you never give to patients with ITP/TTP/HUS?
Platelets
26
What do anticoagulants and antiplatelets do to a clotting screen?
* **Anticoagulants**: increase PT/INR and APTT * **Antiplatelets:** increase bleeding time but normal PT/INR and APTT
27
What do the following conditions do to a clotting screen?
28
What are some cause of a high INR?
29
How do you manage a high INR?
If concern regarding head injury and intracranial haemorrhage, consider CT head **_Major bleeding_** * Stop anticoagulants * Administer IV vitamin K * Administer FFP or prothrombin complex **_Minor bleeding_** * Stop anticoagulants * Administer IV vitamin K * Repeat INR after 24 hours, may need further vitamin K **_No bleeding with INR \> 8_** * Stop anticoagulants * Administer IV or oral vitamin K * Repeat INR after 24 hours **_No bleeding with INR \> 5_** * Withhold 1-2 doses of anticoagulant * Review maintenance dose of anticoagulant
30
What questions should you ask a patient with a high INR and what should you look for on examination/basic investigations?
**History** * Dosing history of anticoagulant/compliance * Concurrent illness * Change in medications * Change in diet/lifestyle (including alcohol and tobacco use) * History of any falls/injuries * History of blood loss * Haemoptysis * Haematemesis * Melaena * Bleeding from the gums **Bloods** * FBC to check for concurrent anaemia, signs of infection * Clotting screen to check for other clotting abnormalities **Examination** * Evidence of bleeding * Overt blood loss * Bruising
31
What are the inherited and acquired risk factors for VTE?
Hormone therapy with oestrogen
32
What are some thrombophillias that predispose to VTE?
33
What is the Well's score for DVT and how do you manage it depending on the score?
34
How are VTEs treated and how long for?
Treatment dose ***apixaban*** or ***rivaroxaban*** * ***DOACs:*** suitable for most patients, including patients with cancer * ***Warfarin:*** vitamin K antagonist, first-line in patients with antiphospholipid syndrome (who also require initial concurrent treatment with LMWH) * ***Low molecular weight heparin*** (***LMWH***): first-line in pregnancy
35
In patients with an unprovoked DVT, what differentials should you be considering?
* **Thrombophilia testing**: Offered if coming off anticoagulation * **Cancer**: especially breast and testicular
36
What is the mechanism of action of the following DOACs?
37
What is the mechanism of action of LMWH and unfractionated heparin and when would you use one over the other?
38
What is Heparin-induced thrombocytopaenia (HIT)?
* Antibodies form against complexes of platelet factor 4 (PF4) and heparin * Develops 5-10 days of treatment * Low platelets but prothrombotic condition * 50% reduction in platelets, thrombosis and skin allergy
39
How do you reverse heparin overdose?
Protamine Sulphate Only partially works in LMWH, fully works in UFH
40
What monitoring is done for * DOACs * Warfarin * UFH * LMWH
**DOACs:** Annually do FBC, U+Es, serum creatinine **Warfarin:** INR **UFH**: APTT **LMWH:** Anti-Factor Xa not not needed routinely
41
What is the most common complication of a DVT?
**Post-thrombotic syndrome** Chronic swelling, pain and skin changes from venous stasis secondary to chronic venous hypertension Can lead to ulcers and gangrene
42
What is Von Willebrand Disease and how does it present?
* Most common ***inherited*** haemophilia * Autosomal dominant **_Presentation_** Unusually easy, prolonged or heavy bleeding: * Bleeding gums with brushing * Nose bleeds * Heavy menstrual bleeding * Heavy bleeding during surgical operations * Family history
43
How is Von Willebrand disease diagnosed and managed?
**Diagnosis** History of abnormal bleeding, family history, bleeding assessment tools and laboratory investigations **Management** Only need to manage if bleeding or prophylaxis before surgery * ***Desmopressin*** can be used to stimulates the release of VWF * ***VWF*** can be infused * ***Factor VIII*** is often infused along with plasma-derived VWF
44
Haemophilia A (Factor 8 deficiency) and Haemophillia B (Factor 9 deficiency) are both X-Linked recessive. How do they tend to present?
Spontaneous haemorrhage without trauma or excessive bleeding in response to minor trauma * Intracranial haemorraghe * Haematomas * Cord bleeding * Haemarthrosis * Gum bleeding * Gastrointestinal tract bleeding * Urinary tract causing haematuria * Retroperitoneal space
45
How is Haemophillia diagnosed and managed?
**Diagnosis** * Bleeding scores * Coagulation factor assays * Genetic testing **Management** * ***Infusions*** of the affected factor (VIII or IX) * ***Desmopressin*** to stimulate the release of ***von Willebrand Factor*** * ***Antifibrinolytics*** such as ***tranexamic acid***
46
What are some causes of thrombocytopenia?
Either ***problem with production*** or an ***over destruction*** **Severe** * ITP * DIC * TTP * Haematological malignancy **Moderate** * Heparin induced thrombocytopenia (HIT) * Drug-induced (e.g. quinine, diuretics, sulphonamides, aspirin, thiazides) * Alcohol * Liver disease * Hypersplenism * Viral infection (EBV, HIV, hepatitis) * Pregnancy * SLE/antiphospholipid syndrome * Vitamin B12 deficiency
47
How may thrombocytopenia present?
* Asymptomatic and found incidentally * Platelet counts \<50 x 109/L will result in easy or spontaneous bruising and prolonged bleeding times. They may present with nosebleeds, bleeding gums, heavy periods, easy bruising or blood in the urine or stools. * Platelet counts \< 10 x 109/L are high risk for spontaneous bleeding e.g intracranial haemorraghe or GI bleeding
48
What is ITP, what is it cause by and how will it present?
* May be detected incidentally following routine bloods * Petichae, purpura * Bleeding (e.g. epistaxis)
49
What is the difference between ITP in children and adults?
**Children**: transient following viral infection **Adults:** chronic relapsing remitting disease
50
What investigations should you do to diagnose ITP?
* **FBC** * **Blood film** * **Bone marro**w only required if atypical * Further tests to exclude other differential diagnoses (e.g. aplastic anaemia, leukaemia, thrombocytic thrombocytopenic purpura)
51
How is ITP managed?
* **Oral prednisolone** first line * **IVIG** is quicker way of raising platelets than steroids so use if actively bleeding * **Rituximab** (a monoclonal antibody against B cells) * **Splenectomy** rarely
52
What is some supportive care for ITP patients?
* Inform when to seek help e.g malena, persistent headache * Suppress menstruation * Control blood pressure
53
What is **Thrombotic Thrombocytopenic Purpura** and the pathophysiology of this**?**
Abnormally large and sticky multimers of von Willebrand's factor cause platelets to clump within vessels so **blood clots** throughout small vessels cause **thrombocytopenia** and **bleeding under the skin** Blood clots break down and cause a **haemolytic anaemia** **Deficiency of ADAMTS13** (a metalloprotease enzyme) which breakdowns large multimers of von Willebrand's factor Overlaps with haemolytic uraemic syndrome (HUS)
54
What are some causes of TTP?
* **Post-infection** e.g. urinary, gastrointestinal * **Pregnancy** * **Drugs:** ciclosporin, oral contraceptive pill, penicillin, clopidogrel, aciclovir * **Tumours** * **SLE** * **HIV**
55
How does TTP present and why does it need to be treated urgently?
Fatal if not managed as causes blockage of small vessels to heart, brain, kidneys etc * Fever * Fluctuating neuro signs (microemboli) * Microangiopathic haemolytic anaemia * Thrombocytopenia * Renal failure
56
How is TTP managed?
***Plasma exchange***, ***steroids*** and ***rituximab***
57
What are the functions of the spleen?
* Immunity against encapsulated bacteria * Controls level of WBC, RBC, Platelets * Filters blood and removes any old or damaged red blood cells
58
What are some causes of hyposplenism?
* Sickle cell * Coeliacs * Lymphoma * Bone marrow transplant
59
What will blood results show in hypersplenism?
* Increased platelet count * Lymphocytosis * Monocytosis * Howell Jolly Bodies on peripheral blood smear
60
How is hyposplenism managed?
* **Pneumococcal, Meningitis and Flu vaccine** * **Malaria prophylaxis** when travelling * **Prophylactic Penicillin V** in first few years and then if high risk after that * **Splenectomy card**
61
What are some indications for a splenectomy?
* **Trauma** * **Spontaneous rupture:** e.g in EBV * **Hypersplenism** * **Neoplasia:** lymphoma or leukaemic infiltration. * **With other viscera:** total gastrectomy, distal pancreatectomy. * **Other indications:** splenic cysts, hydatid cysts, splenic abscesses
62
What are some complications with splenectomy?
* OPSI * Thrombocytosis (7-10 days post op)
63
What is some post splenectomy prophylaxis given?
64
What are some causes of splenomegaly?
* Malaria * Leukaemia/Lymphoma * EBV * RA * Cirrhosis * Haemolytic anaemia
65
What is benign polyclonal hypergammaglobulinaemia? (image is important)
* Usually asymptomatic * It is an immune response to infections or autoimmune disease or cancers * Cannot be myeloma as it is not monoclonal
66
What are some causes of benign polyclonal hypergammaglobulinaemia?
No M spike like in multiple myeloma
67
What is amyloidosis and the pathophysiology of this?
* Group of conditions caused by the **deposition of extracellular insoluble fibrins** in organs and blood vessels. * **Primary:** deposition of monoclonal light chains in tissues. Happens spontaneously or in association with Multiple Myeloma or Waldenstrom's macroglobulinaemia * **Secondary:** underlying disorders
68
What is an amyloid fibril?
Insoluble protein fibres that are resistant to degradation Beta pleated sheets
69
AL amyloidosis is seen in multiple myeloma. What are some of the clinical features of this?
* **Heart failure**: shortness of breath, orthopnoea, oedema * **Arrhythmias**: palpitations * **Pleural effusions** * **Asymptomatic proteinuria:** frothy urine * **Nephrotic syndrome** * **CKD** * **Hepatomegaly** * **Dysmotility of gut** * **Peripheral neuropathy** * **Autonomic neuropathy** * **Abnormal clotting**
70
How is amyloidosis diagnosed?
**Tissue biopsy from abdominal fat pad or rectum** ***Congo red staining***, which leads to ***apple-green birefringence*** under polarised light
71
What is a paraproteinaemia?
Build-up of monoclonal protein (either the full antibody or antibody fragments) in the serum or urine Classified into pre-malignant (MGUS) and malignant types (MM, WM)
72
What are some risk factors for DIC?
* Major trauma or burns * Multiple-organ failure * Severe sepsis or infection. * Severe obstetric complications * Solid tumours or haematological malignancies
73
What do you find on blood tests with DIC?
* Thrombocytopenia * Increased prothrombin time * Increased fibrin degradation products (such as D-dimer) * Decreased fibrinogen
74
What are some side effects of Methotrexate? (Methotrexate Monday, Folate Friday)
* **Cytopenia** - Monitor FBC and advise patients to report suspected infections and bruising * **Hepatotoxicity -** Monitor LFTs, discontinue if they rise to more than 3x * **Renal impairment** - Monitor renal function. * **Pulmonary fibrosis -** Take baseline CXR. Advise patients to report respiratory symptoms eg. dyspnoea/dry cough. * **Teratogenicity -** Advise patients to use contraception while taking and for 3 months after use.
75
What are side effects of corticosteroids?
* **Adrenal suppression of cortisol** * **Immunosupression** so live vaccines CI * **Reactivation of latent infections (**TB / Hepatitis B/C / Herpes viruses) * **Cushingoid appearance** with central obesity, buffalo hump, moon face * **Acne** * **Thinned skin with striae** * **Hyperglycaemia.** * **Cushing's disease** - *Hypo*kalaemic *hyper*tension * **Growth retardation in children** * **Muscle wasting** * **Mood swings** * **Steroid psychosis** * **Dyspepsia** * **Glaucoma** * **Cataracts** * **Raised white cell count**
76
How is adrenal suppression with long term steroids avoided?
* If they are taken for less than 3 weeks steroids can be safely stopped abruptly. * If taken for longer than this, the steroids must be tapered down slowly. * 'Sick day rules' - if acutely unwell double the usual dose of prednisolone or supplement IV hydrocortisone (usually 100mg 6-hourly) if unable to tolerate oral medication. * If nil-by-mouth (or vomiting prednisolone before it can be absorbed), convert the increased daily dose of prednisolone to the equivalent IV hydrocortisone.
77
In MHP what is an important investigation to do to check platelets?
Thromboelastography (TEG)
78
When does Graft Vs Host disease present?
**1-2 weeks after transfusion** May present with fever, skin rash, GI issues, pancytopenia Uncommon now as blood is leucodepleted, only issue in immunosuppressed patients Can be seen in first degree relative blood transfusions if blood not irradiated
79
How can you tell the difference between TACO and TRALI?
**TACO:** raised BP, No temp **TRALI**: low BP, temp LOOK AT CXR

Y4 Cancer Care (19 decks)

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