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Cardiorespiratory 2 PBL > PBL 4 > Flashcards

PBL 4 Flashcards

1
Q

Define wells score

A

this is the criteria that gives the chance that the patient has a VTE or PE, the person has to have a score of 2 in order to have a chance of having a VTE which requires further investigation

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2
Q

define pulmonary embolus

A

Clot in pulmonary arteries

Due to dislodgement of all or part of DVT

Clot moves up the venous system, through R heart and into pulmonary arteries.

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3
Q

define pitting oedema

A

pitting oedema is when there is swelling of body tissues due to fluid accumulation that can be demonstrated by applying pressure to the swollen area, this causes the area to pit and not bounce back immediately

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4
Q

define lung crackles

A

this is often associated with inflammation and infection of the small bronchi and bronchioles, crackles that do not clear after a cough can indicate pulmonary oedema, pulmonary fibrosis, fluid in the alveoli or it is due to heart failure

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5
Q

How does a DVT form

A
  • Activated by 12 spontaneous factors in contact with a charged surface that triggers the intrinsic system
  • Stagnant blood triggers the intrinsic system
  • Upstream of the valve you can get little pools of blood
  • When there is no or very little flow through a vein blood can form a stagnant pool in the recesses just above the venous valves;
  • (the same thing can happen in the auricles of the atria in patients with atrial fibrillation).
  • The stagnant blood then forms a thrombus due to activation of the intrinsic system. The thrombus can then get dislodged and form an embolus
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6
Q

why does DVT occur in the deep veins and not really the superficial veins

A
  • Activated by 12 spontaneous factors in contact with a charged surface that triggers the intrinsic system
  • Stagnant blood triggers the intrinsic system
  • Upstream of the valve you can get little pools of blood
  • When there is no or very little flow through a vein blood can form a stagnant pool in the recesses just above the venous valves;
  • (the same thing can happen in the auricles of the atria in patients with atrial fibrillation).
  • The stagnant blood then forms a thrombus due to activation of the intrinsic system. The thrombus can then get dislodged and form an embolus
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7
Q

describe why DVT occurs more in pregnant women

A
  • It is 5-10 times more likely to develop than non pregnant women
  • The level of blood clotting proteins increases during pregnancy while anticlotting proteins level decrease
  • The uterus also enlarges during pregnancy and puts the lower veins in the body under more pressure
  • More common in women over 35 and overweight
  • Or a close family member who has had a blood clot before
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8
Q

what are the three causes of DVT (virchows triad)

A
  1. Reduced blood flow
  2. Vessel wall pathology
  3. Hypercoagubility of the blood
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9
Q

describe how reduced blood flow can lead to DVT

A
  • Long-haul flights especially >8hours (prolonged sitting ) means muscle pump inactive: blood stasis in veins
  • Immobilisation in bed due to other conditions eg hip/pelvis fracture
  • Obesity causing reduced exercise
  • Sickle cell disease: red cell precipitation can occlude vessels
  • Surgery there is a significant increased risk in the months following any form of surgery (partly due to immobilization)
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10
Q

describe how the endothelium prevents DVT

A

PG12
- Prostacyclin (also called prostaglandin PGI2) inhibits platelet activation.
- PG12 binds to and stimulates a platelet prostacyclin receptor.
- This makes the platelet produce cAMP.
- cAMP inhibits platelet activation by von Willebrand factor and fibrinogen and also inhibits entry of calcium into platelets and vascular smooth muscle.
Nitric oxide
- constantly released from healthy endothelium.
- It inhibits platelet activation by stimulating production of cAMP in the platelets
- also acts as a powerful vasodilator to keep blood moving.
Heparan sulphate
- (different to low-molecular weight heparin) is expressed on the surface of healthy endothelial cells.
- It is attached to the surface of the cells by a transmembrane protein backbone.
- Various lengths of heparin sulphate polysaccharides form feathery projections into the lumen of the blood vessel. - These projections create a “non-stick” surface on the endothelial cells that prevents platelet adhesion

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11
Q

describe how damage to the vessel wall can cause DVT

A

Endothelium

  • However endothelial cells can release endothelin in response to hypoxia, oxidized LDL, pro-inflammatory cytokines, and bacterial toxins.
  • Plasma endothelin concentrations are high in conditions associated with endothelial-cell injury, as well as in essential hypertension and congestive heart failure
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12
Q

describe how blood hypercoagulability can cause a VTE

A
  • Genetic factors include overactive coagulation factors such abnormal factor V (Factor V Leiden)
  • Blood group O individuals are at a reduced risk relative to groups A, B, &AB due to reduced levels of von Willebrand factor & factor VIII
  • Cancer of any sort, but especially when there are metastases. Cancerous cells may secrete procoagulants. Also, chemotherapy can damage endothelial walls, bone marrow etc.
  • Pregnancy is associated with an increased risk of thrombosis (Estrogen, when used in the combined oral contraceptive pill and in perimenopausal hormone replacement therapy, is associated with a significant increased risk of venous thrombosis).
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13
Q

describe the other factors that can cause a VTE

A
  • cancer – cancer treatments such as chemotherapy and radiotherapy can increase this risk further
  • heart disease and lung disease
  • infectious conditions, such as hepatitis
  • inflammatory conditions, such as rheumatoid arthritis
  • thrombophilia – a genetic condition where your blood has an increased tendency to clot
  • antiphospholipid syndrome – an immune system disorder that causes an increased risk of blood clots
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14
Q

describe the risk factors while pregnant that can cause a VTE

A
  • Being over 35
  • Being obese
  • Expecting 2 or more babies
  • Having a C section recently
  • Being immobile for long periods of time
  • Smoking
  • Having severe varicose veins
  • Dehydration
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15
Q

describe the risk factors that can lead to VTE

A

Major – hip/pelvis fracture, hip/knee replacement surgery, major general surgery esp for malignancy, major trauma, spinal cord injury, hospitalisation

Moderate – previous VTE, malignancy/chemotherapy, pregnancy/post-partum, OC pill/hormonal therapy, thrombophilia, other medical conditions eg IBD

Weak – obesity, long haul flight, age, varicose veins, smoking
Can also be idiopathic ie no risk factors identified

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16
Q

List some drugs for the treatment of DVT

A
  • LMWH
  • Heparin
  • Warfarin
  • DOACs
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17
Q

describe LMWH

A
  • Subcutaneous (SQ) administration
  • Half life - about 4 hours
  • Predominantly anti factor Xa effect
  • Fixed, weight-adjusted dose once or twice daily
  • No monitoring (unless renal failure, pregnant, obese
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18
Q

Describe what heparin does

A
  • Heparin prevents conversion of fibrinogen to fibrin thus preventing the formation of clots
  • does not break down clots that have already formed but stimulates the body natural clot lysis to break down existing clots
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19
Q

describe what warfarin does

A
  • Warfarin is a small molecule that acts as a Vitamin K antagonist
  • Reduces level of factors II, VII, IX, X in plasma
    • Can be administered orally
    • Long half-life - 36 hours
    • Delayed onset of action (so start treatment with heparin)
    • Primarily affects INR, & dose must be adjusted to maintain INR in range 2.0-3.0
    • Has multiple drug interactions
    • Risks to fetus – teratogenicity, therefore cant be used in pregnancy maternal bleeding – so never given during pregnancy or suspected pregnancy
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20
Q

what factors does warfarin reduce

A
  • Reduces level of factors II, VII, IX, X in plasma
21
Q

describe how rivaroxban works

A
  • Rivaroxaban is an orally active factor Xa inhibitor that inhibits platelet activation by blocking the active site of factor Xa
    • it is indicated for treatment of DVT or PE
    • It is also indicated for prophylaxis of DVT in patients undergoing knee or hip replacement surgery.
    • It is also used to prevent blood clots in atrial fibrillation.
  • Not in liver disease or end stage kidney disease people
22
Q

describe how Apixaban works

A
  • Another factor Xa inhibitor
23
Q

describe how Dabigatran works

A
  • Orally active direct thrombin inhibitor
  • It has a delayed onset of action so is indicated for the treatment of DVT and PE in patients who have been treated with a parenteral anticoagulant for 5-10 days.
  • It is also used to prevent blood clots following hip or knee replacement and in those with a history of prior clots.
  • It is used as an alternative to warfarin and does not require monitoring by blood tests.
  • have to start with heparin and then switch over after a week
24
Q

what drugs would you and wouldn’t you use while pregnant

A
  • Warfarin and DOACs cross placenta
  • Warfarin teratogenic 6-12/40 and bleeding risk
  • DOACs effects unclear – presumed bleeding
  • Use LMWH throughout pregnancy
25
Q

what are the tests and diagnosis done to confirm DVT

A

D dimer
- blood test measuring fibrin fragments after fibrinolysis. A non-specific marker of fibrin formation (usually raised in VTE but also in cancer, infection, inflammation, post-op, pregnancy)

Ultrasound test to confirm DVT

  • Usually compression ultrasound*, as non-invasive
  • Sometimes venography (gold standard) e.g. if looking for calf DVT for which ultrasound is insensitive
  • Other techniques – CT scan, MR venography
26
Q

name some of the wells score factors used

A

Active cancer within last 6 months 1
Paralysis, paresis, recent plaster immobilisation 1
Recently bedridden ≥ 3 days, major surgery <12 weeks 1
Localised tenderness along distribution of deep veins 1
Entire leg swollen 1
Calf swelling ≥ 3 cm (10 cm below tibial tuberosity) 1
Pitting oedema confined to symptomatic leg 1
Collateral superficial veins (non-varicose) 1
Previous documented DVT 1
Alternative diagnosis at least as likely as DVT -2

27
Q

what wells score total do you need

A

If the total score is greater than or equal to 2 then DVT is likely, if it is less than or equal to 1 then it is unlikely

28
Q

how does pregnancy effect circulation system

A
  • pregnancy stress the heart
  • blood volume increases from 30 to 50 percent to nourish the growing baby
  • heart rate increases
  • increases in CO
  • increases in compliance
  • increase in ECF
  • decreases in BP
  • increase in total peripheral resistance
  • BP gradually falls during pregnancy
29
Q

how does pregnancy effect clotting

A
  • Pregnancy increases clotting factors
  • Such as thrombin fibrinogen
  • Protein S decreases
  • Protein C and antithrombin III remain constant
  • Fibrinolysis is impaired by an increase in plasminogen activator inhibitor -1
  • Prolonged bed rest can cause hypercoagulability
30
Q

explain her signs and symptoms on her second visit to A&E

A
  • Breathing problems - PE
  • Wheezing when she goes up the stairs - PE
  • Breathing is painful – due to pulmonary artery blockage
  • Sweating a lot
  • Cough
  • Coughed up blood – due to blood present in lungs
  • Tachypnoea
  • Tachycardia
  • Lung crackles – due to some oedema
  • Slightly accentuated second heart sound – due to PE
  • These are common in patients with PE
31
Q

what diagnostic test would they use to confirm she has a PE

A
  1. CT Pulmonary Angiogram (CTPA)
  2. Isotope lung scan (V/Q scan – looks at the ventilation perfusion ratio in different parts of the lung ),
  3. Echocardiogram - diagnostic at bedside in massive PE
  4. Pulmonary angiogram - gold standard, invasive
  5. Leg ultrasound especially if symptomatic
  6. D-dimer – use in conjunction with low Wells score
32
Q

what is the treatment for PE

A
  • Given an injection of anticoagulant medication
  • Prevents new clots
  • Continue with anticoagulant injections for at least 5 days
  • Also need to take anticoagulant tablets for at least 3 months
  • Expected to make a full recovery from a pulmonary embolism if its spotted and treated early
  • Apixaban, edoxaban, and rivaroxaban inhibit factor Xa, whereas dabigatran is a direct thrombin inhibitor. Rivaroxaban (Xarelto) is an oral factor Xa inhibitor approved by the FDA in November 2012 for the treatment of DVT or PE, and to reduce risk of recurrent DVT and PE following initial treatment.
  • Fibrinolytic therpay also called clot busters
  • Vena cava filter – a small metal device placed in the vena cava
  • Percutaneous thrombectomy – long thin hollow tube can be threaded through the blood vessles
33
Q

what are some complications of PE

A

Signs of bleeding in the digestive system:

  • Bright red vomit or vomit that looks like coffee grounds
  • Bright red blood in your stool or black, tarry stools
  • Abdominal pain

Signs of bleeding in the brain:

  • Severe headache
  • Sudden vision changes
  • Sudden loss of movement or feeling in your legs or arms
  • Memory loss or confusion
34
Q

describe the vneous anaotmy of deep veins

A

Ant and post tibial + peroneal veins

Popliteal

Superficial femoral vein (!!)

Superficial + deep femoral to form common femoral vein

External iliac – after passing through inguinal ligament

External + internal iliac to form common iliac

R and L common iliac form IVC

35
Q

describe the superifical veins

A

Lesser saphenous – lateral foot draining into popliteal vein

Greater saphenous – medial foot drain into common femoral vein

Perforating veins – joining deep and superficial veins. Presence of valves to ensure one way blood flow.

36
Q

what is the definition of a thormbus

A

blood clot in arterial or venous system

much more common in venous system due to sluggish blood flow

37
Q

the more proximal a clot the more ..

A

complciations

38
Q

describe a DVT

A

partially or completely blocked deep vein.

Originates from deep venous sinuses in calf muscle

May remain localised and fibrinolysed spontaneously or can extend proximally up the leg

More proximal = more complications

39
Q

what from family history can increase the risk of a DVT

A

Factor V Leiden

Prothrombin variant G20210A

Deficiencies of anti-thrombin, protein C, protein S

Negative test for thrombophilia doesn’t mean pt doesn’t have one, there might not be a test for it yet!

40
Q

what is factor V leiden

A

Factor V is usually a co-factor to allow Xa to activate prothrombin.

Protein C (anti-coagulant) that normally inhibits Factor V to limit the extent of clotting.

Mutation results in a Factor V variant that cannot easily be degraded by Factor V leading to increased risk of clotting.

41
Q

what does prothormbin varient G20210A resutl in

A

higher than normal levels of prothrombin in the blood

42
Q

what are the investgations of DVT

A

D-dimer test – circulating fibrin degradation product

USS – diagnosis must be confirmed from imaging!

Thrombophilia tests

Urine dip – malignancy

CXR/CT CAP if >40 years - malignancy

43
Q

what are the regular blood tests for DVT

A

FBC – platelet count, looking for underlying malignancy (anaemia, leucopenia)

Clotting – INR/APTT

U&E – LMWH is renally excreted

LFT – affects clotting factor synthesis and warfarin metabolism

Calcium - malignancy

44
Q

describe the flow chart for diagnosing DVT

A

If low risk: do d-dimer first. If positive, confirm using USS. If negative, DVT excluded

If high risk: do both d-dimer and USS. Both positive or only USS positive, treat for DVT.

If USS negative but d-dimer positive, re-scan in 1 week

45
Q

what is important to avoid in pregnancy and why

A

Avoid warfarin!!
- Teratogenic, can cause placental abruption and foetal/neonatal haemorrhage

Safe for breast feeding

46
Q

what are the complciations of DVT

A

Embolise to form fatal/non-fatal PE

Post-thrombotic syndrome

  • Long term persistent/intermittent discomfort and swelling in legs
  • Can be minor or severely chronic with leg ulcers
  • Can be prevented by wearing knee-length graduated compression stockings during the day for minimum 2 years after diagnosis.
47
Q

what does a wells score have to be greater than in PE

A

> 4 immediate CTPA

<4 D-dimer. If positive, immediate CTPA

48
Q

what is the differntiational diagnosis for PE

A 
Pericarditis
Aortic stenosis
ARDS
Angina
Anxiety disorders
AF
Cardiogenic shock
Cor Pulmonale
Dilated cardiomyopathy
Pneumonia
49
Q

how do you manage a PE in pregnancy

A

= Risk of DVT/PE raised in all 3 trimesters and 6-12 weeks after delivery.
- If low suspicion – do d-dimer, if negative then diagnosis excluded.

If high suspicion – bilateral leg doppler

  • If positive, start treatment
  • If negative, CTPA. To exclude contrast-induced hypothyroidism, all neonates exposed to iodinated contrast in utero need to have TSH levels checked in the first week

Heparin and fibrinolysis are safe in pregnancy
- LMWH used throughout pregnancy until delivery, continuing anti-coagulation for 4-6 weeks post-partum for a total of minimum 6 months

Pregnant women who have a hypercoagulable state or previous VTE should receive prophylactic anticoagulation during pregnancy.

Cardiorespiratory 2 PBL (10 decks)

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