2. Bleeding Flashcards

1
Q

History taking bleeding

A
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2
Q

Examination bleeding

A
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3
Q

buffer

A
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4
Q

buffer

A
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5
Q

Broad categories of why someone may have prolonged bleeding/symptoms of bleeding?

A

Clotting cascade deficiencies
- congenital eg haemophilia
- acquired eg lymphoma, SLE, amyloidosis

Platelet dysfunction
- VWF disease
- thrombocytopenia (destruction) eg ITP, TTP, HIT, HUS, medications, alcohol
- thrombocytopenia (decreased production) eg leukemia, myelodysplastic, myeloma

Widespread coagulopathy
- DIC
- low vitamin K (newborn, warfarin)
- major haemorrhage
- liver failure

Other
- vasculidities
- scurvy

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6
Q

symptoms that indicate a platelet disorder

A

Bleeding immediately after trauma
Bleeding of mucus membranes- epistaxis, bleeding gums
Cutaneous and subcutaneous bleeding- petechiae, purpura, easy bruising
Menorrhagia

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7
Q

symptoms that indicate a coagulation disorder

A

Delayed bleeding after trauma
Deep tissue bleeding- hemarthrosis , hematomas
Large, palpable ecchymoses

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8
Q

Presentation haemophilia

A
  • bleed excessively in response to minor trauma
  • spontaenous haemorrhage eg bleeding into joints (haemoathrosis) and muscles are a classic feature of severe haemophilia

intracranial haemorrhage, haematomas and cord bleeding in neonates.

Abnormal bleeding can occur in other areas:
Gums
Gastrointestinal tract
Urinary tract causing haematuria
Retroperitoneal space
Intracranial
Following procedures

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9
Q

investigations haemophilia

A

Diagnosis is based on bleeding scores, coagulation factor assays and genetic testing.
Prolonged APTT
Low factor VIII/IX coagulant level with normal levels of vWF
Others are normal
Family history

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10
Q

management haemophilia

A

The affected clotting factors (VIII or IX) can be replaced by intravenous infusions. This can be either prophylactically or in response to bleeding.

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11
Q

management of acute bleeding/ preventing bleeding during surgical procedures haemophilia

A

Infusions of the affected factor (VIII or IX)

Desmopressin to stimulate the release of von Willebrand Factor

Antifibrinolytics such as tranexamic acid

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12
Q

haemophilia A vs B are which clotting factor deficiencies

A

Haemophilia A is caused by a deficiency in factor VIII (8).

Haemophilia B (also known as Christmas disease) is caused by a deficiency in factor IX. (9)

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13
Q

which is the most common hemophilia

A

A

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14
Q

inheritance hemophilia

A

X linked recessive

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15
Q

risk with what is a complication of hemophilia treatment?

A

IV clotting factors (VIII or IX)

A complication of this treatment is formation of antibodies against the clotting factor resulting in the treatment becoming ineffective.

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16
Q

acquired coagulation disorders? what can cuase? pathophysiology?

A

Lymphoma and SLE can lead to acquired clotting factor deficiencies by the creation of antibodies against clotting factors

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17
Q

presentation von willebrand disease

A

Often asymptomatic
Bleeding from mucosa (epistaxis, menorrhagia, gums)
Easy bruising
Postoperatively
Family history of bleeding

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18
Q

invetsiations von willebrand

A

Prolonged bleeding time with normal platelet count
APTT may be prolonged or normal
Decreased plasma vWF
Decreased factor VIII activity

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19
Q

management VWF disease

A

Care when using NSAIDs, antiplatelets (e.g. aspirin, clopidogrel): can cause increased bleeding

Desmopressin-induces vWF release from endothelial cells

Factor VIII concentrates containing vWF-during surgery

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20
Q

what should you not / be cautious when prescribing vwf

A

NSAIDs, antiplatelets (e.g. aspirin, clopidogrel): can cause increased bleeding

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21
Q

what symptoms are associated with thrombocytopenia below 50x 1089/L

A

Nosebleeds
Bleeding gums
Heavy periods
Easy bruising
Haematuria (blood in the urine)
Rectal bleeding

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22
Q

what are platelet counts below 10x1089/L at risk of?

A

high risk for spontaneous bleeding. Particularly concerning are:
Intracranial haemorrhage
Gastrointestinal bleeding

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23
Q
A
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24
Q

What blood product have the highest risk of bacterial contamination

A

Platelet transfusions have the highest risk of bacterial contamination compared to other types of blood products

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25
Q

At what platelet level should you give platelets in active bleeding

A

Offer platelet transfusions to patients with a platelet count of <30 x 10 9 with clinically significant bleeding (World Health organisation bleeding grade 2- e.g. haematemesis, melaena, prolonged epistaxis)

Platelet thresholds for transfusion are higher (maximum < 100 x 10 9) for patients with severe bleeding (World Health organisation bleeding grades 3&4), or bleeding at critical sites, such as the CNS.

It should be noted that platelet transfusions have the highest risk of bacterial contamination compared to other types of blood product.

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26
Q

At what platelet level should you give patients platelets pre-invasive procedure

A

Platelet transfusion for thrombocytopenia before surgery/ an invasive procedure.

Aim for plt levels of:
> 50×109/L for most patients
50-75×109/L if high risk of bleeding
>100×109/L if surgery at critical site

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27
Q

At what platelet level should you give patients platelets if no active bleeding and no planned invasive procedure

A

A threshold of 10 x 109 except where platelet transfusion is contradindicated or there are alternative treatments for their condition

For example, do not perform platelet transfusion for any of the following conditions:
Chronic bone marrow failure
Autoimmune thrombocytopenia
Heparin-induced thrombocytopenia, or
Thrombotic thrombocytopenic purpura.

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28
Q

what is ITP

A

Immune (or idiopathic) thrombocytopenic purpura (ITP) is an immune-mediated reduction in the platelet count. Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex. It is an example of a type II hypersensitivity reaction.

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29
Q

what type of hypersensitivity reaction is ITP

A

type 2

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30
Q

Presentation ITP

A

usually children

bruising
petechial or purpuric rash
bleeding is less common and typically presents as epistaxis or gingival bleeding

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31
Q

Investigations ITP

A

full blood count should demonstrate an isolated thrombocytopenia

blood film

bone marrow examinations is only required if there are atypical features e.g.
lymph node enlargement/splenomegaly, high/low white cells
failure to resolve/respond to treatment

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32
Q

management ITP

A

usually, no treatment is required
ITP resolves in around 80% of children with 6 months, with or without treatment
advice to avoid activities that may result in trauma (e.g. team sports)

other options may be indicated if the platelet count is very low (e.g. < 10 * 109/L) or there is significant bleeding.
Options include:
- oral/IV corticosteroid
- IV immunoglobulins
- platelet transfusions can be used in an emergency (e.g. active bleeding) but are only a temporary measure as they are soon destroyed by the circulating antibodies

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33
Q

education and advice ITP

A

Avoid contact sports
Avoid intramuscular injections and procedures such as lumbar punctures
Avoid NSAIDs, aspirin and blood thinning medications
Advice on managing nosebleeds
Seek help after any injury that may cause internal bleeding, for example car accidents or head injuries

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34
Q

complications ITP

A

Chronic ITP
Anaemia
Intracranial and subarachnoid haemorrhage
Gastrointestinal bleeding

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35
Q

what is TTP

A

Thrombotic thrombocytopenic purpura (TTP) is a condition where tiny thrombi develop throughout the small vessels, using up platelets. As the problem is in the small vessels, it is described as a microangiopathy. microangiopathic haemolytic anaemia

TTP is caused by a deficiency in ADAMTS13, a metalloprotease that cleaves von Willebrand factor multimers. This leads to the accumulation of ultra-large von Willebrand factor multimers, which promote platelet aggregation and thrombus formation.

This may be inherited or acquired (Autoimmune disease, where antibodies are created against the protein (acquired)

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36
Q

Pentad TTP

A

Microangiopathic haemolytic anaemia
Fever
Disturbed neurological function (Tissue ischaemia and end-organ damage)
Renal failure (Tissue ischaemia and end-organ damage)
Thrombocytopenia

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37
Q

treatment of choice TTP

A

Plasma exchange

Treatment is guided by a haematologist and may involve plasma exchange, steroids and rituximab.

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38
Q

what does ADAMTS13 usually do?

A

This protein normally:
Inactivates von Willebrand factor
Reduces platelet adhesion to vessel walls
Reduces clot formation

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39
Q

what is heparin-induced thrombocytopenia?

A

Heparin-induced thrombocytopenia (HIT) involves the development of antibodies against platelets in response to heparin (usually unfractionated heparin, but it can occur with low-molecular-weight heparin). Heparin-induced antibodies target a protein on platelets called platelet factor 4 (PF4).

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40
Q

presentation and pathophysiology HIT?

A

The condition typically presents around 5-10 days after starting treatment with heparin. HIT antibodies bind to platelets and activate the clotting system, causing a hypercoagulable state and thrombosis (e.g., deep vein thrombosis). They also break down platelets and cause thrombocytopenia. Therefore, there is a counterintuitive situation where a patient is on heparin, has a low platelet count, and develops abnormal blood clots.

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41
Q

diagnosis HIT

A

testing for HIT antibodies on a blood sample.

42
Q

management HIT

A
  1. Stop heparin
    + using an alternative anticoagulant guided by a specialist (e.g., fondaparinux or argatroban).
43
Q

What is HUS? triad?

A

triggered by a bacterial toxin called shiga toxin –>
thrombosis within small blood vessels throughout the body (THROMBOCYTOPENIA)

blood clots (thrombi) partially obstructing the small blood vessels –> destruction of red blood cells as they travel through the circulation
through the circulation (HAEMOLYTIC ANAEMIA)

red blood cells block the kidneys –> (ACUTE KIDNEY INJURY)

44
Q

what increases the risk of developing HUS?

A

The use of antibiotics and anti-motility medications such as loperamide to treat gastroenteritis caused by these pathogens increases the risk of developing HUS.

45
Q

Presentation HUS?

A

brief gastroenteritis, often with bloody diarrhoea
The symptoms of haemolytic uraemia syndrome typically start around 5 days after the onset of the diarrhoea.

Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Oedema
Hypertension
Bruising

46
Q

management HUS

A

Urgent referral to the paediatric renal unit for renal dialysis if required
Antihypertensives if required
Careful maintenance of fluid balance
Blood transfusions if required
70 to 80% of patients make a full recovery.

47
Q

what drugs are well-known for causing thrombocytopenia?

A

Sodium valproate

Methotrexate

48
Q

how does alcohol affect platelet levels

A

Drinking alcoholic beverages regularly and in higher than recommended quantity has been shown to cause bone marrow suppression, defective platelet formation, a decrease the lifespan of a platelet leading to premature removal from the body, and impaired platelet function.

49
Q
A
50
Q

what leukemia is the most common in children

A

acute lymphoblastic leukemia

51
Q

which leukemia is associated with downs

A

acute lymphoblastic leukemia

52
Q

which leukemia is associated with richers transformation and smudge cells

A

CLL

53
Q

which leukemia is associated with philedelphia chromosome

A

CML

54
Q

which leukenia is assocated with transformation from a myeloproliferative disorder and is associated with auer rods

A

AML

55
Q

how does leukemia cuase pancytopenia

A

Leukaemia is a form of cancer of the cells in the bone marrow. A genetic mutation in one of the precursor cells in the bone marrow leads to excessive production of a single type of abnormal white blood cell.

The excessive production of a single type of cell can lead to suppression of the other cell lines, causing underproduction of other cell types. This results in a pancytopenia, which is a combination of low:
Red blood cells (anaemia),
White blood cells (leukopenia)
Platelets (thrombocytopenia)

56
Q

what is required urgently when leukemia is a ddx for a presentation

A

An urgent full blood count

57
Q

features of leukemia?

A

anaemia: lethargy/fatigue and pallor
neutropaenia: frequent or severe infections
thrombocytopenia: easy bruising, petechiae

Hepatosplenomegaly: due to leukemic infiltration
Fever: A persistent, recurrent or refractory fever that is most likely a constitutional symptom and may present alongside a history of night sweats, weight loss.
Lymphadenopathy: a build-up of large numbers of cancerous cells which have travelled from the bone marrow
Failure to thrive (children)

58
Q

why does leukemia cause hepatosplenomegaly

A

due to leukemic infiltration

59
Q

why does leukemia cause lymphadenopathy

A

a build-up of large numbers of cancerous cells which have travelled from the bone marrow

60
Q

when should ?leukemia be sent for immediate specialist assessment

A

They recommend children or young people with petechiae or hepatosplenomegaly are sent for immediate specialist assessment.

61
Q

initial investigation leukemia

A

FBC

62
Q

investigation leukemia

A
  • FBC
  • lactate
  • bone marrow biopsy
  • CT and PET scans
  • lymph node biopsy
  • genetic tests
63
Q

what are the two cell lines coming from multipotential hematopoeitic cells

A
  • myeloid –> (megakaryocyte (–> thrombocytes), erythrocyte, mast cells, myeloblast ) then myeloblast –> basophil, neutrophil, eosinophil, monocyte (–> macrophage)
  • lymphoid –> natural killer cell and small lymphocyte. small lymphocyte –> T lymphocyte, B lymphocyte (–> plasma cell)
64
Q

presentation CLL

A

slow proliferation of a single type of well-differentiated lymphocyte, usually B-lymphocytes. It usually affects adults over 60 years of age. It is often asymptomatic but can present with infections, anaemia, bleeding and weight loss. It may cause warm autoimmune haemolytic anaemia.

65
Q

smudge cellsa ssociated with?

A

CLL

66
Q

what is richters transformation

A

Richter’s transformation refers to the rare transformation of CLL into high-grade B-cell lymphoma.

67
Q

phases of CML

A

chronic - years of high WCC

accelerated - blast cells push out other types - anaemia, thrombocytopenia, immunodeficiency

blast phase - over 20% blasts in blood - severe symptoms and is often fatal

68
Q

CML genetic associtaed

A

philedelphia chromosome

This refers to an abnormal chromosome 22 caused by a reciprocal translocation (swap) of genetic material between a section of chromosome 9 and chromosome 22.

69
Q

AML age

A

from middle age onwards

70
Q

what may cause AML

A

myeloprolifertaive disorder such as polycythaemia vera or myelofibrosis

71
Q

blood film AML

A

A blood film and bone marrow biopsy will show a high proportion of blast cells. Auer rods in the cytoplasm of blast cells are a characteristic finding in AML.

72
Q

management leukemia

A

Leukaemia is mainly treated with chemotherapy and targeted therapies, depending on the type and individual features.
Examples of targleted therapies include (mainly used in CLL):
Tyrosine kinase inhibitors (e.g., ibrutinib)
Monoclonal antibodies (e.g., rituximab, which targets B-cells)

Other treatments options include:
Radiotherapy
Bone marrow transplant
Surgery

73
Q

complications of chemo

A

Failure to treat cancer
Stunted growth and development in children
Infections due to immunosuppression
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity (heart damage)
Tumour lysis syndrome

74
Q

what is tumor lysis syndrome

A

Tumour lysis syndrome results from chemicals released when cells are destroyed by chemotherapy, resulting in:
High uric acid
High potassium (hyperkalaemia)
High phosphate
Low calcium (as a result of high phosphate)

Uric acid can form crystals in the interstitial space and tubules of the kidneys, causing acute kidney injury. Hyperkalaemia can cause cardiac arrhythmias. The release of cytokines can cause systemic inflammation.
Very good hydration and urine output before chemotherapy is required in patients at risk of tumour lysis syndrome. Allopurinol or rasburicase may be used to suppress the uric acid levels.

75
Q

what is myelodysplastic syndorme

A

Precancerous disease of myeloid cells in bone marrow whereby the dysplastic cells may cause abnormal or inadequate blood cell rpoduction
Badly fucntioning → anaemia, thrombocytopenia, leukopenia etc.
Tries to compensate by increasing haematopoeisis
Dysplasia has risk of progressing to acute myeloid leukemia

76
Q

FBC myelodysplastic syndrome

A

Myelodysplastic syndrome causes low levels of blood components that originate from the myeloid cell line:

Anaemia (low haemoglobin)
Neutropenia (low neutrophil count)
Thrombocytopenia (low platelets)

77
Q

risk factors myelodysplasia

A

older age and previous chemotherapy or radiotherapy.

78
Q

presentation myelodysplasia

A

Patients may be asymptomatic. It may be diagnosed after incidental findings on a full blood count.
They may present with symptoms of:
Anaemia (fatigue, pallor or shortness of breath)
Neutropenia (frequent or severe infections)
Thrombocytopenia (bleeding and purpura)

79
Q

blood film myelodysplasia

A

Full blood count will be abnormal. There may be blasts on the blood film.
Bone marrow biopsy is required to confirm the diagnosis.

80
Q

management myelodyspalsia

A

Watchful waiting
Supportive treatment (e.g., blood or platelet transfusions)
Erythropoietin (stimulates red blood cell production)
Granulocyte colony-stimulating factor (stimulates neutrophil production)
Chemotherapy and targeted therapies (e.g., lenalidomide)
Allogenic stem cell transplantation (risky but potentially curative)

81
Q

what is myeloma

A

Myeloma is a cancer of the plasma cells (type of B lymphocytes that produce antibodies). Cancer in a specific type of plasma cell results in large quantities of a single antibody being produced.

82
Q

what is Monoclonal gammopathy of undetermined significance (MGUS)

A

is where there is an excess of a single type of antibody or antibody components without other features of myeloma or cancer.

83
Q

pathophysiology myeloma

A

B cells in bone marrow producing antibodies → genetic mutation causing one antibody to be produced uncontrollably (50% of the time this is IgG)

Bone marrow infiltration → anaemia, neutropaenia, thrombocytopaenia
Plasma cells releasing cytokines → increased osteoclast activity → myeloma bone disease → skull, spine, long bones affected → bone pain / pathological fractures → releasing lots of calcium from bones → hypercalcaemia

Kidney failure is common in patients with a monoclonal gammopathy, most frequently due to hypercalcemia or myeloma cast nephropathy. Immunoglobulin crystallization is an uncommon phenomenon that also results in kidney injury
hypercalcaemia can ppt kidney stones,

84
Q

presentation myeloma

A

PC: anaemia
PC: neutropenia
PC: thrombocytopenia
PC: pathological fractures
PC: bone pain, particularly back pain
PC: myeloma renal disease
PC: hyperviscosity
PC: kidney stones

85
Q

Initial tests myeloma

A

FBC: anaemia
Calcium and bone profile: hypercalcaemia
U&Es : renal failure
ESR
Plasma viscosity

If suggetsive –>

then very urgent (within 48hrs)
- protein electrophoresis
- bence-jones urine test

if +ve 2ww
bone marrow biopsy and look at all results

86
Q

diagnostic criteria multiple myeloma

A

The diagnostic criteria for multiple myeloma requires one major and one minor criteria or three minor criteria in an individual who has signs or symptoms of multiple myeloma.

Major criteria
Plasmacytoma (as demonstrated on evaluation of biopsy specimen)
30% plasma cells in a bone marrow sample
Elevated levels of M protein in the blood or urine

Minor criteria
10% to 30% plasma cells in a bone marrow sample.
Minor elevations in the level of M protein in the blood or urine.
Osteolytic lesions (as demonstrated on imaging studies).
Low levels of antibodies (not produced by the cancer cells) in the blood.

87
Q

what is a Autologous hematopoietic cell transplantation

A

involves the removal of a patient’s own stem cells prior to chemotherapy, which are then replaced after chemotherapy

88
Q

what is allogenic haematopoeitic stem cell transplant

A

Allogenic hematopoietic cell transplantation

is not commonly used in myeloma due to high rates of overall mortality and symptoms of graft-ve

89
Q

stages of myeloma treatment

A

A combination of drugs is used to treat myeloma - ‘induction therapy
targeted drugs (such as thalidomide, lenalidomide, bortezomib, daratumumab)
chemotherapy (such as cyclophosphamide or melphalan)
steroids (such as prednisolone or dexamethasone)

The particular combination depends on whether a patient may be suitable for autologous hematopoietic cell transplantation or not.

Autologous hematopoietic cell transplantation
involves the removal of a patient’s own stem cells prior to chemotherapy, which are then replaced after chemotherapy
prolong both event-free and overall survival when compared with non-transplant strategies
typically it is younger, healthier patients who are suitable for stem cell transplantation and rigorous chemotherapy regimes.

90
Q

symptom management and complication avoidance myeloma

A

pain: treat with analgesia (using the WHO analgesic ladder)

pathological fracture: zoledronic acid is given to prevent and manage osteoporosis and fragility fractures as these are a large cause of morbidity and mortality, particularly in the elderly.

infection
patients receive annual influenza vaccinations
they may also receive Immunoglobulin replacement therapy.

venous thromboembolism prophylaxis

fatigue
treat all possible underlying causes
if symptoms persist consider an erythropoietin analogue.

91
Q
A
92
Q

mechanism of DIC

A

Sepsis and trauma lead to a release of pro-inflammatory cytokines in a so-called systemic inflammatory response. In other conditions, the expression of certain pro-coagulant factors, such as tissue factor, is upregulated.

→ activate clotting cascade → micro clots → multi-organ failure due to tissue ischaemia. plus clotting factors used up –> bleeding eg petechiae

93
Q

how does the cause of DIC relate to presentation and blood results

A

Infection and septic shock tend to cause a more prothrombotic form of DIC, which predominantly causes excess clot formation. Alternatively, DIC due to obstetric catastrophes or leukemia tends to cause depletion of fibrinogen leading to hemorrhage.

Low fibrinogen is more common in predominantly fibrinolytic types of DIC (e.g., patients with acute promyelocytic leukemia or obstetric-related DIC).
Sepsis increases fibrinogen levels, so sepsis-induced DIC may have elevated or normal levels of fibrinogen. Falling fibrinogen may suggest ongoing DIC with consumption of fibrinogen.

94
Q

Management of DIC

A

Stopping bleeding
- Platelet transfusions should be considered if the patient is bleeding. The platelet count should be maintained >50 x 109/L in the presence of bleeding.
- In bleeding patients with a prolonged PT and/or APTT, fresh frozen plasma can be considered.
- If there is severely low fibrinogen then transfusions of cryoprecipitate or fibrinogen concentrate should be considered.

Stopping clotting
- If thrombosis is a prominent feature, then therapeutic doses of heparin should be considered. If there is co-existing high risk of bleeding, then unfractionated heparin can be used since this has a significantly shorter half-life and is more readily reversible than low molecular weight heparin.
- In other patients who are non-bleeding, prophylactic doses of heparin are recommended to protect against VTE.

95
Q

How does liver fialure affect coagualiton

A

Liver failure impacts all three stages of hemostasis: primary hemostasis, coagulation, and fibrinolysis

Thrombocytopenia
- platelet sequestration due to congetsive splenomegaly as a result of portal HTN
- bone marrow suppression by alcohol/foalte def
- imapired hepatic synthesis of TPO

Coagulation
- reduced synthesis of clotting factors
- also reduction in anticoagualtion factors : Natural anticoagulant protein levels fall progressively with increasing severity of liver disease.6 Antithrombin, protein C and protein S levels

OVerall
“rebalanced hemostasis” According to this model, the hemostatic alterations that occur result in a new balance within and between procoagulant, anticoagulant and fibrinolytic systems (Figure 2).7 Because of the relative deficiency of procoagulant and anticoagulant factors, the hemostatic balance is more precarious and may tip toward bleeding or thrombosis depending on provoking circumstantial risk factors.

96
Q

which babies are at higher risk of Haemorrhagic disease of the newborn

A

Breast-fed babies are particularly at risk as breast milk is a poor source of vitamin K. Maternal use of antiepileptics also increases the risk

97
Q

pathophysiology and presentation scurvy

A

The condition is caused by a lack of vitamin C in the diet, which is essential for the production of collagen and other important functions in the body. Symptoms of scurvy can include fatigue, weakness, joint pain, and bleeding gums. In severe cases, patients may experience anaemia and skin lesions.

98
Q

warfarin Major bleeding (e.g. variceal haemorrhage, intracranial haemorrhage)

A

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*

99
Q

warfarin INR > 8.0
Minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

100
Q

INR > 8.0
No bleeding

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

101
Q

warfarin INR 5.0-8.0
Minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0

102
Q

warfarin INR 5.0-8.0
No bleeding

A

Withhold 1 or 2 doses of warfarin (2 days)
Reduce subsequent maintenance dose