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phase 2a mine > haem middle tier > Flashcards

haem middle tier Flashcards

1
Q

polycythaemia =

types

A

too many rbc, HB high and high packed cell volume (cell part of blood)

opposite of anaemia

primary - polycythaemia rubra vera
secondary- rbc rise in order to compensate (Reactive)

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2
Q

polycythaemia rubra vera =

  • cause
  • effect
A

primary polycythaemia

  • Overactive bone marrow
  • no external cause. genetic mutation in JAK2 gene
  • Myeloproliferative disorder.
  • oversesntivie to EPO –> increased RBC production

Increase in rbc, also in wbc and platelets

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3
Q

secondary causes of polycythaemia

A
  • Increase in rbc to compensate/ reactive : …
  • High altitude
  • resp issue inc smoking, lung disease
  • heart issue
  • Anabolic steroid
  • EPO (erythropoeitin) taken
  • chronic hypoxia
  • abnormal rbc structure
  • stimulates bone marrow to make rbc
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4
Q

signs of polycythaemia

A

hepato/splenomegaly
abnormal FBC
hypertension

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5
Q

symptoms of polycythaemia

A
  • Plethoric = rosy cheeks, also hands and feet
  • Itching after hot bath
  • Effects of thrombus
  • easing brusing/bleeding
  • fatigue
  • hyperviscosity –> headaches, dizzy, vision impaired
  • tinnitus
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6
Q

polycythaemia investigations

A
  • FBC (PCV, Hb, RBC) , blood film
  • bone marrow biopsy
  • genetic testing JAK2 gene (polycythaemia vera)
  • if this is negative, look for secondary cause
  • serum EPO = low(insitgates rbc production)
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7
Q

polycythaemia management

A
  • Aspirin
  • Venesection (take blood)
  • Hydroxycarbamide (chemo)- suppresses bone marrow
  • allopurinol to reduce gout
  • radioactive phosphorus if over 70 but increases risk of leukaemia
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8
Q

polycythaemia complications

A

Acute myeloid leukaemia

Thrombotic events -clots etc

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9
Q

relative polycythaemia

A

Apparent polycytaemia

  • Chronic
  • Associated with obesity, hypertension, high intake of alcohol/ tobacco

Dehydration

  • Acute
  • Cause = dehydration eg alcohol , diuretics
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10
Q

primary causes of polycythaemia

A
  • Mutations in EPO receptor
  • High oxygen affinity haemoglobins
  • polycythaemia vera
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11
Q

disseminated intravascular coagulation causes inc cause pathophysiology

A

Secondary – NEVER occurs in isolation

  • Extensive damage to vascular endothelium so tissue factor is exposed
  • Tissue factor expression is enhanced by monocytes, in response to cytokines
Malignancy
Major trauma and tissue destructin
Infections, sepsis
Hemolytic transfusion reactions
Liver disease
Obstetric complications
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12
Q

disseminated intravascualr coagulation phtophysiology

A
  • Thrombin (coagulation system) activated inappropriately
  • Clotting occurs inappropriately, widespread, until clotting factors are exhausted inc widespread fibrin generation and deposition.
  • This can cause microvascular thrombosis and so can lead to multiorgan failure (Esp kidneys and brain)….
  • At this point uncontrolled bleeding occurs due to the consumption of platelets
    Aka Thrombosis followed by bleeding
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13
Q

disseminated intravascular coagultion symptoms

A 
Acute, 
Bleeding - shock
Nose 
Mouth
Venipuncture sites
Skin
- Purpura
- Petechiae
- Localised infarction
- Bruising 
Confusion
Fever
Organ effects due to thrombosis --- brain and kidneys especially
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14
Q

dissemintated intravascular coagulation investigations

A
  • Long prothrombin time and other similar sounding times
  • Platelets v low
  • Fibrinogen low
  • High D dimer (fibrin degradation product)
  • Blood film = fragmented RBCs
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15
Q

disseminated intravascular coagulation management

A

Treat underlying cause
Platelet transfusion
‘Fresh frozen plasma’ to replace the coagulation factors
Cryoprecipitate to replace fibrinogen and some coagulation factors
Red cell transfusion if patient is bleeding
Activated protein c

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16
Q

over anti-coagulation bleeding risk factors/ causes

A

iatrogenic – excess use of anticoagulation therapy

  • inappropriate presecription of warfarin/ heparin
  • Cardiac bypass surgery - lots of heparin use
  • Unfractionated heparin treatment
  • bad compliance
  • polypharmacy
17
Q

over anti-coagulation bleeding - heparin action and effects

A
  • Heparin binds to platelet factor 4 (a protein) to form a complex (PF4/Hepain)
  • IgG binds to this complex to form a new complex (IgG/PF4/Heparin)
  • This complex (IgG/PF4/Heparin) binds and activates platelets
  • So platelets are consumed, resulting in thrombocytopenia
  • Also - thrombosis and skin necrosis occurs
18
Q

over anti-coagulation bleeding general pathophysiology

A

Excess use of anticoagulation therapy

Anticoagulation causes blood to inappropriately avoid clotting → bleeding

19
Q

over anti-coagulation bleeding symptoms

A

Bleeding

  • Bruising
  • Melena (black poo - upper GI bleed)
  • Epistaxis (nose bleeds)
  • Haematemesis
  • Haemoptysis
20
Q

over anti-coagulation bleeding investigations (heparin)

A

Sharp fall in platelets 5-10 days after starting heparin treatment

21
Q

over anti-coagulation bleeding management

A
  • Vitamin k (phytomenadione) for warfarin
  • Protamine sulphate for heparin
  • Do not re-expose patient to heparin ever again
22
Q

warfarin effect

A

Warfarin poo poos on clotting factors 2, 7, 9, 10

23
Q

which is more common immune thromboyctopenic purpua (ITP) or thrombotic thrombocytopenic purpura (TTP)

A

ITP

24
Q

immune thromboyctopenic purpua (ITP) causes

A

Reduced platelet production in bone marrow

Excess destruction of platelet cells

  • Enlarged spleen
  • – Spleen is where autoantibodies are made
  • – Spleen is where platelets are phagocytosed
25
Q

immune thromboyctopenic purpua (ITP) pathophysiology

A

Antibodies form against platelets → Autoimmune platelet destruction → Thrombocytopenia

Muco-cutaneous bleeding

26
Q

immune thromboyctopenic purpua (ITP) types

  • age
  • chronic/ acute
  • assocaited disorders
  • gender
A

Primary

  • in children (2-6y)
  • acute

Secondary

  • in adults
  • Women
  • Associated with other autoimmune disorders, CLL, viral infections and tumours
  • chronic
27
Q

immune thromboyctopenic purpua (ITP) presentation

A 
Purpura
-- Rapid onset 
Easy bruising
Epistaxis (nose bleed)
Menorrhagia
Major haemorrhage rare
May have history of viral infection /immunisation
28
Q

immune thromboyctopenic purpua (ITP) investigations

A

FBC = isolated thrombocytopenia
Platelet autoantibodies
Bone marrow biopsy

29
Q

immune thromboyctopenic purpua (ITP) management

A
  • First line = corticosteroids (prednisolone)
  • Immunoglobulin given - to raise platelet count
  • Second line = splenectomy
  • If this fails, immunosuppression
30
Q

thrombotic thrombocytopenic purpura (TTP) causes

A

Defiecincy of ADAMTS 13 (ADAMTS 13 is a protease that degrades vWF)

  • Congenital (absence of ADAMTS 13)
  • Autoantibody mediated (against ADAMTS 13)
  • Cancer
  • Drug associated
  • Pregnancy
  • Idiopathic
31
Q

thrombotic thrombocytopenic purpura (TTP) pathophysiology

A

Deficiency of ADAMTS 13 (due to genetic abscence or autoantibodies). ADAMTS 13 is a protease that degrades vWF

→ widespread adhesion and aggregation of platelets → microvascular thrombosis → profound thrombocytopenia

32
Q

thrombotic thrombocytopenic purpura (TTP) presentation

A 
Florid purpura
Fever
Fluctuating cerebral dysfunction
Hemolytic anaemia
Renal failure
33
Q

thrombotic thrombocytopenic purpura (TTP) investigations

A
  • FBC - low platelets
  • Raised lactact dehydriogenase (from ischaemic/necrotic cells - as a result of haemolysis)
  • Coagulation screen normal
34
Q

thrombotic thrombocytopenic purpura (TTP) management

A
  • Plasma exchange - remove autoantibodies to ADAMTS13
  • Corticosteroids (methylprednisolone)
  • Rituximab (monoclonal antibody)
  • Last resort = splenectomy
35
Q

what could cause reduced platelet function (but normal numbers

A
  • Congenital abnormality
  • Medication eg Aspirin
  • Von willebrand disease – reduced vwF so platelets are unable to bind to damaged blood vessels resulting in platelet dysfunction (muco-cutaneous bleeding results)
  • Uraemia
36
Q

hypersplenism effect on platelets

A

thrombocytopenia

portal HTN can cause - increased blood flow

37
Q

liver damage effect on platelets

A

thrombocytopenia

as liver produces TPO which stimulates platelet production and less TPO is produced in liver damage

also: liver damage –> cirrhosis –> portal HTN –> splenomegaly –> thrombocytopenia

38
Q

what could decrease production of platelets

A

Congenital thrombocytopenia
- due to reduced/ malfunctioning megakaryocytes

Infiltration of bone marrow
- leukaemia, metastatic malignancy, lymphoma, myeloma

Reduced platelet production

  • Low B12/ folate
  • Reduced TPO eg liver disease
  • Medication eg chemotherapy
  • Toxins eg alcohol
  • Infection eg HIV, TB
  • Aplastic anaemia = autoimmune
39
Q

what could increase destruction of platelets

A

Autoimmune
- ITP

Hypersplenism
- portal hypertension and splenomegaly

Drug related immune destruction
- eg heparin

Consumption of platelets

  • DIC
  • TTP
  • in these cases their is activation of coagulation (via thrombin with DIC and lack of ADAMTS 13 with TTP) causing coagulation and platelet consumption so there are then fewer platelets (two steps!)

phase 2a mine (38 decks)

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