Haemoglobin and revision Flashcards
(42 cards)
1
Q
Thrombosis
A
blood clot that forms in a vessel not due to haemostasis. Can be arterial or venous
2
Q
Types of DVT
A
- Distal: popliteal and below
- Proximal: above popliteal- higher risk
- Line associated- low risk as clearly associated with risk factor
3
Q
Types of PE
A
- Central (pulmonary trunk or main pulmonary arteries)- higher risk
- Segmental
- Sub-segmental
4
Q
Consequences of thrombosis
A
- DVT: can cause scarring and narrowing of vessels leading to ongoing pain (post thrombotic syndrome)
- Pe: Pulmonary hypertension- narrowing or permanent occlusion in the pulmonary arteries causing right sided heart strain causing Chronic thrombotic pulmonary hypertension (CTEPH) which is fatal. Do echocardiogram if persistent breathing issues 3 months post PE
- Psychological: anxiety, stress, PTSD
5
Q
Provoking factors for VTE
A
- Cancer
- Pregnancy
- Surgery (requiring GA >30 minutes)
- Fracture
- Flight >4 hours
- Recent hospitalisation
- Hormonal therapy: COCP, HRT
- Immobility >3 days
6
Q
How long do we treat thrombosis
A
- Provoked: 3 months minimum, consider longer if ongoing risk factors or extensive
- Unprovoked dvt/pe: Long term treatment unless contraindicated
- Unprovoked Distal DVT: 6 months
- Warn patients after thrombosis that if they ever experience any long term immobility, surgery or long flight they should take prophylactic anticoagulants
7
Q
Types of medication in VT
A
- Rivaroxaban (DOAC): once daily taken with a meal, need ok renal function
- Dabigatran: twice daily, more GI side effects, need ok renal function
- Apixaban- twice daily, less side effects, hepatically excreted
- Warfarin: aim for INR 3-4. Done if severe renal impairment. Reversible but more likely to have an ICH
- Two reversible anticoagulants: warfarin, Dabigatran
8
Q
What do we check after VT
A
- Check for cancer: good history, check if up to date with screening
- Thrombophilia screen
- Antiphospholipid syndrome: check the three markers lupus anticoagulant, anti-beta2 glycoprotein IgG, anti-cardiolipin IgG. Might need higher intensity anticoagulant. Not inherited but acquired
9
Q
Post thrombotic syndrome
A
- Can be debilitating and affect work
- Symptoms: pain, cramps, heaviness, pruritus, paraesthesis
- Clinical signs: oedema, skin induration, hyperpigmentation, redness, pain during calf compression, venous ectasia
- Villalta score (5=PTS, >14=severe PTS)
- After 12 months consider vascular referral: stenting needed to proximal deep veins
- Don’t forget the stockings (Class 1 and 2)
10
Q
Chronic thromboembolic pulmonary hypertension (CTEPH)
A
o Affects 1-2% of PE patients
o Can be treated with ongoing anticoagulation, medication or surgery
o Persisting hypoxia, symptoms of SOB and chest pain
o Echo 3 months after PE to look for RV impairment and raised right heart pressures
o Refer on to pulmonary hypertension clinic
11
Q
Gynae and thrombosis
A
- All anticoagulants cause heavy periods: give mirena coil, progesterone implant, anti-fibrinolytics (tranexamic acid)
- Avoid oral oestrogen (COCP)
- If women on anticoagulants become pregnant: switch to LMWH when they have a positive pregnancy tests
- Might need thromboprophylaxis during pregnancy or post-partum if previous history of thrombosis
12
Q
AF and anticoagulants
A
- CHA₂DS₂-VASc scoring system- consider anticoagulants if not low risk. Low risk in males is a score of 0 and in females 1
- HAS-BLED: helps assess bleeding risk
- Prescribe warfarin or a DOAC
13
Q
Starting warfarin
A
give LMWH until INR is therapeutic in individuals with thrombotic tendency i.e. recent clot
14
Q
Warfarin
A
- Antagonises vitamin K- lowers vitamin K dependent clotting factors (factor 7, 9, 10 and prothrombin (2))
- Protein S, C and Z are also vitamin K dependent. These are natural anticoagulants. Means in the first few days of treatment they are more pro-thrombotic
- Normal INR is <1.5
- Therapeutic is 2-3
15
Q
Heparin and DOAC MoA
A
- Heparin increases the effects of anti-thrombin which inhibits thrombin. It’s the same mechanism for LMWH and unfractionated heparin.
- Dabigatran (DOAC) directly inhibits thrombin
- Other DOAC’S: XA inhibitors (apixaban, rivaroxaban) inhibit activated factor 10
16
Q
Choosing an anticoagulant
A
- Renal function - best is warfarin don’t use dabigratran
- Extremes of body weight – best is warfarin or LMWH
- Drug interactions: DOACs have fewest BUT there are some (antiepileptics, antifungal). Avoid warfarin
- Intensity of anticoagulation: Can only escalate intensity with warfarin and LMWH. Can reduce intensity with DOACs. If aiming for equivalent INR >3 can only use warfarin
17
Q
Stopping warfarin for surgery
A
- Top 5 days before procedure
- Consider bridging in patients who: have a high risk of VTE, have AF with a CHADs ≥ 4 or had a recent CVA/TIA, Have a metallic mitral valve (not aortic unless other risk factors)
- In bridging after you stop warfarin you give LMWH once there INR <2 up to a day before procedure
- When to give bridging (LMWH): Last dose 24 hrs pre surgery (give 50% before high risk if once daily dosing). Restart 48 hrs post high risk surgery
18
Q
DOAC lab tests
A
- Dabigatran: very prolonged TT (thrombin time), tends to prolong APTT
- Rivaroxaban: tends to prolong PT
- Apixaban: doesn’t effect clotting screen but can prolong PT
- Warfarin prolongs PT and the INR
19
Q
Stopping DOAC for surgery
A
- Low risk procedure and normal renal function: Stop 24 hrs before procedure
- High risk procedure and normal renal function: Stop 48 hrs before procedure. Do not reintroduce until at least 48 hrs post procedure. In patients with high thrombotic risk, consider thromboprophylaxis prior to reintroduction of DOAC
20
Q
Basics in preventing bleeding
A
- Do they need surgery/endoscopy
- Have they checked platelet count and Clauss fibrinogen
- Would tranexamic acid 1g IV be appropriate?
- Are they warm, with a normal calcium and a normal pH?
21
Q
Reversing warfarin
A
- Can take 2-5 days for the INR to return to normal after cessation
- Reversal: vitamin K IV 5mg will work in about 4-6 hours.
- If major bleed: Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP
22
Q
Heparin (both type) reversal
A
- UFH reversal: stop the infusion. Give Protamine (can cause reactions, bradycardia and drop in BP)
- LMWH: no reversal agent. Protamine might reverse 50%
23
Q
DOAC dabigatran reversal
A
- If last taken within 2hrs consider activated charcoal
- If reversal is needed then give 2 doses of Idarucizumab (praxabind) 2.5g 15mins apart IV
- Idarucizumab (praxabind) is a monoclonal antibody
- Dialysis only if Idarucizumab (praxabind) is not available
24
Q
DOAC: anti-XA inhibitor (rivaroxaban/apixaban/edoxaban) reversal
A
- If last taken within 2hrs consider activated charcoal
- There is no specific antidote currently available (on-going trials)
- If life or limb-threatening bleeding can consider Beriplex 30 U/kg
25
Inherited bleeding disorder
single gene mutation leading to defect in coagulation. Can be inherited or de novo
26
Presentation of bleeding disorders
* Perinatal: prolonged umbilical stump bleed, subdural haematoma
* Childhood: Non-accidental injury, easy bruising, prolonged APTT
* Adult: menorrhagia, bleeding tendency, prolonged APTT
* Sometimes diagnosis made by testing family members of known bleeding disorders
27
Coagulation factor disorder
* Lifelong bleeding tendency
* More common: Haemophilia A and B
* Rare: FVII and FXIII
* Bleeding with operations and trauma
* Joint hemarthroses and muscle haematomas (Haemophilia A and B)
28
ISTH BAT
* A bleeding assessment tool for inherited disorders
* Spontaneous bleeding: Intracranial bleeding, bruising, bleeding from minor wounds, muscle haematomas, Hemarthrosis, Epistaxis, oral cavity bleeding, GI bleeding, Menorrhagia, Haematuria
* Bleeding after haemostatic challenge: Tooth extraction, post partum haemorrhage (especially if no obvious cause), surgery
* Investigate when: >3 in children, >4 in adult males, >6 in adult females
29
Investigations and diagnosis for bleeding disorders
* Basic coagulation screen- PT, APTT, fibrinogen: Can be normal when bleeding disorder present e.g. factor XIII deficiency or mild deficiency. Can be abnormal when no bleeding disorder present e.g. factor XII deficiency is not associated with any bleeding problems
* Factor assays: Usually performed in groups e.g. VIII, IX, XI, XII. If prolonged PT test factor VII. If prolonged APTT then assess factor VIII, IX, XI
* VWF
* Tests for other bleeding disorders e.g. platelet function, other factors
30
Haemophilia A/B
* Genetic variant in factor 8 (Haemophilia A) or 9 (Haemophilia B) leading to low plasma levels
* Blood results: prolonged APTT (intrinsic pathway), normal PT, decreased factor VIII or IX
* X linked recessive predominates in males. All the sons of affected males are normal and all their daughters are carriers. 50% risk of carrier giving it to the child
* In pregnancy of known carriers manage delivery to reduce risk of ICH (intracranial haemorrhage).
* Can have de novo presentation where there is no family history
31
Clinical features Haemophilia A/B
* Male (X-linked recessive inheritance): rare females affected- carriers with X-inactivation or compound heterozygotes
* Joint bleeding: main presentation
* Prolonged wound and surgical bleeding
32
Severity of Haemophilia A and B (based on factor VIII levels)
* Severe <1%: early onset symptoms before 2 years of age. Presents with spontaneous bleeding into muscle or joints
* Moderate 1-5%: late onset. Bleeding with trauma or surgical procedure
* Mild 5-40%; May remain undetected until later in life. Few or no bleeding, mild bleeding with challenge. May be detected incidentally
33
Haemophilia treatment
* Replace or bypass what’s missing in order to: prevent joint damage, prevent surgical bleeding, treat traumatic/spontaneous bleeds
* Give prophylactic treatment to prevent bleeds
* Standard factor concentrates: plasma derived/recombinant
* Gene therapy: by establishing expression of factor 8 or 9. Transfer of functional gene
34
Rare clotting factor deficiencies
One of the other clotting factors i.e. factor I, II, V, V + VIII, VII, X, XI or XIII) is missing or not working. Individual variation in bleeding phenotype someone with 40% of the factor might have the same severity as someone with 1%.
35
Von Willebrand factor
* Complex glycoprotein with multiple binding sites
* VWF monomers are assembled in to large multimers prior to being released from endothelial cells
* VWF carries factor VIII to the injury site
* VWF binds to platelets in the injury site helping them mesh together and form a clot
* VWF is made in the endothelial cells and megakaryocytes
36
Von Willebrand disease
* Commonest inherited bleeding disorder ≈ 1/1000
* Effects males and females equally but as heavy periods is the main presentation females are more likely to be diagnosed
* Autosomal dominant inheritance
* Usually, mild bleeding disorder
* Mucosal bleeding: epistaxis, menorrhagia
* GI bleeding
* Post partum bleeding, post surgical bleeding
37
Von Willebrand disease treatment
* DDAVP
* pdVWF:FVIII
* rVWF
* Fibrinolytic inhibitors: g-aminocaproic acid, tranexamic acid, fibrin glue, topical thrombin
38
What to do with major Haemorrhage protocol
- Give Ca+2 alongside
- Major haemorrhage protocol: 1 pool of platelets, 4 packed red blood cells (PRBC), cryoprecipitate, 4 fresh frozen plasma
- Aim to do coag tests every 30 minutes
- If females of child bearing age give Group O Rh D-VE Kell-ve
39
Differentiating haemophilia A and B
Haemophilia B- presents later in life and more severe
40
Treatment for Haemophilia A and B
Minor bleeds: Desmopressin
Major bleeds: factors 8 and 9
Supportive and Tranexamic acid
41
Tests for iron deficient anaemia
Bedside: Urine dip, FIT test, PR exam
Bloods: FBC, ferritin, TIBC, transferrin saturation, B12/folate (rule out deficiency)
Investigations: upper and lower GI endoscopy
42
Causes of normocytic anaemia
3A's 2H's:
A - Acute blood loss
A- anaemia of chronic disease
A - aplastic anaemia
H - haemolytic anaemia
H - hypothyroidism
