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Medicine GEP Year 1 (BCS paper 1) > GEP (Life Support) Week 3 > Flashcards

GEP (Life Support) Week 3 Flashcards

1
Q

What is serous fluid

A

Pleural cavity contain serous fluid.
-Lubricates the surfaces of pleurae allows them to slide over each other
-Creates surface tension → pulls the parietal and visceral pleurae together → ensures that both the thorax and lungs expand during inspiration (i.e., not thorax alone!) → allows lungs to fill with air

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2
Q

Describe brief overview of the 3 stages of haemostasis

A

Stage 1
-Vasoconstriction (Immediate)
-Platelet adhesion (seconds)
-platelet aggregation and contraction (minutes)
Unstable platelet plug is formed from the 1st stage. The second stage is required to stabalise it

Stage 2 (clotting cascade)
-The clotting cascade → fibrin stabilises the platelet plug

Stage 3 (Fibrinolysis)
-This is the enzymatic breakdown of fibrin

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3
Q

What are the stages of platelet plug formation

A

-It all starts with vasoconstriction first.
-Platelet adhesion -> Platelet activation -> Platelet aggregation

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4
Q

Describe the secondary stage of haemostatis

A

There are 3 different pathway
-Extrinsic (damage to endothelium, starts with tissue factor (III)
-Intrinsic (starts with factor XII)
-Common (This starts with the extrinsic and intrinsic path meeting at factor X)

-The coagulation cascade requires calcium
-Factors 10, 9, 7 and 2 require vitamin K (DiSCo 1972)
-Factors 1, 3, 5 and 8 are thrombin dependent

Intrinsic pathway (factors 12, 11, 9, 8)
Extrinsic pathway (factors 3 and 7)
Common pathway (factors 1, 2, 5, 8 and 10) begins with factor X
Thrombin (factor 2a) is activated
Thrombin activates fibrin (1a)
Stabilisation of platelet plug

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5
Q

Describe the bodys natural way of controlling the coagulation cascade

A

-Proteins C + S - these are natural anti-coagulants that inhibit factors Va and VIIIa

-Anti-thrombin - i.e., anti-factor IIa

-Tissue Factor Pathway Inhibitor - regulates tissue factor (factor III) induced coagulation

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6
Q

Describe the Tertiary stage of haemostatis

A

-Fibrin is broken down enzymatically
-tPa is released by the damaged endothelium
-tPa activates plasminogen to be converted to plasmin
-Plasmin causes fibrin clot degradation

= Fibrin Degradation Products (FDPs) e.g. D-DIMER

tPa is essential to dissolve clots -> relevant later when discussing thrombolytic drugs e.g., alteplase

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7
Q

What are the different clotting tests

A

-Prothrombin Time (PT) - Tests the EXTRINSIC pathway
-Activated Partial Thromboplastin Time (APTT) - Tests the INTRINSIC pathway
-Thrombin Time (TT) - Tests the COMMON pathway
-INR = International normalised ratio; calculation based on PT results (required for warfarin monitoring)
PT test/PT normal = INR

Playing Table Tennis (indoors) (PTT mnomonic for Intrinsic pathway)
Playing Tennis (outdoors) (PT mnomonic for extrinsic pathway)

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8
Q

These flashcard is the summary of the high yield notes to take

A
  • -Primary haemostasis – platelet adhesion, activation and aggregation form a temporary platelet plug
  • Secondary haemostasis – coagulation cascade creates a fibrin mesh that reinforces platelet plug
  • Factor 7 is essential for coagulation, factor 12 is not as important i.e., extrinsic pathway is key
  • Factor 3 = tissue factor, released from damaged endothelium
  • Extrinsic pathway is fast – 30s
  • Intrinsic pathway is slow – 5mins
  • Damaged endothelium releases tissue factor (factor 3)
  • Extrinsic pathway – factor 3 + factor 7 = 10
  • Calcium is required for clotting cascade
  • Vitamin K dependent factors – S, C, 10, 9, 7, 2 (DiSCo 1972)
  • aPTT – intrinsic (table tennis – indoors)
  • PT – extrinsic (playing tennis – outdoors)
  • TT – common
  • Most clotting factors are produced in the liver
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9
Q

What are the difference between a Thrombus and Embolus

A
  • Blood clot = a product of haemostasis, formed of RBC, platelets and fibrin
  • Thrombus = a clot that forms in veins / arteries
  • Thrombosis = when a blood clot blocks an artery or vein e.g., DVT
  • Embolus = a thrombus which has detached and can travel elsewhere via the blood stream
  • Embolism = when an embolus becomes stuck and occludes a vessel e.g., PE
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10
Q

What are the different pathway after a thrombosis has occured

A
  • Resolution = clot is broken down by fibrinolysis
  • Organisation = ingrowth of endothelial cells, smooth muscle cells and fibroblasts – leads to fibrosis
  • Recanalisation = some degree of blood flow is re-established by capillary channels
  • Embolisation = thrombus detaches to becomes a emboli and travels to occlude vessels
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11
Q

What are the different types of Emboli

A
  • Fat – usually after a long bone injury -> fat surrounding bone and muscle gets into broken blood vessels
  • Amniotic fluid – in pregnancy, opening of amniotic fluid leaks into bloodstream (immunogenic proteins in fluid can lead to clots -> associated with premature pregnancy)
  • Thrombus
  • Bacteria – IV drug abuse -> infection (staphylococcus species) from skin into blood
  • bacteria go to tricuspid valve
  • vegetations formed
  • go to RV
  • lodged into pulmonary artery
  • Air – deep sea diving (decompression sickness) – when a diver surfaces too rapidly
  • as they descent body along with gas they are breathing (O2, N2) are under increasing pressure
  • nitrogen bubbles can form in tissues and bloodstream
  • Tumour
  • tumour within blood vessels

Best way to remember is FATBAT

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12
Q

What is virchow’s Triad

A

1) Haemostasis: Long-haul flights, Immobility, Varicose veins
2) Endothelial Damage: Trauma (e.g., surgery) , Smoking, Hypertension
3) Hypercoagulability: Pregnancy, Malignancy, Infection,
Oestrogen therapy (HRT & COCP)

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13
Q

What is Thrombophilia and the different types

A

-Thrombophilia is an abnormal tendency to develop blood clots

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14
Q

What is DVT and its clinical presentation

A

DVT (deep vein thrombosis) is the formation of a thrombus in a deep vein causing an occlusion.

Clinical presentation (almost always unilateral):
* 1. Erythematous, swollen leg (usually calf)
* 1. Dilated superficial veins
* 1. Redness
* 1. Tenderness
* 1. Oedema

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15
Q

What are the risk factors of VTE (venous thromboembolism)

A

**Continuing risk factors **
History of DVT
Malignancy
Age (>60)
Heart failure
Obesity
Thrombophilia
Varicose veins
Smoking
Polycythaemia
SLE

**Temporary risk factors **
Immobility
Pregnancy
Hormone therapy with oestrogen
Long-haul flights
Trauma (incl. to a vein)
Recent surgery or hospitalisation

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16
Q

What is an pulmonary embolsim (PE)

A

-A blood clot in the pulmonary arteries.
-Most often caused by DVT.
-Blood flow to the lung tissue is blocked.
-Strain to the right side of the heart.

17
Q

What are the clinical presentation of PE

A

~Pleuritic chest pain (worse on inspiration)
~Sudden dyspnoea (SOB)
~Tachypnoea (↑RR)
~Cough
~Haemoptysis (coughing up blood)
~Signs & symptoms of DVT
~Tachycardia (↑ HR)
~Haemodynamic instability causing hypotension
~Low grade fever

18
Q

What is the respiratory pathology of PE

A

**V/Q Mismatch **
High V/Q
High ventilation, but low perfusion - due to embolus blocking capillaries
= hypoxia and breathlessness

**Dead space ventilation **
Volume of inhaled air that does not partake in gas exchange, because it either remains in the airways or reaches alveoli that are poorly perfused

**PE Obstruction **
Reduced blood supply to the lungs and pleura – infarction and inflammation
Cytokine release -> bronchoconstriction -> decreased O2 on inspiration
Haemoptysis and pleuritic chest pain

19
Q

What is the cardiovascular pathology of PE

A

Right heart strain
1. PE
2. Increased pulmonary artery pressure
3. Back pressure of pulmonary artery into RV causes increased RV pressure at end diastole
4. RV hypertrophy (cor pulmonale) = ineffective contraction (and bowing of the septum)
5. Tricuspid valve between RA and RV becomes non-compliant over time due to increased pressure
6. Increased RA pressure due to incompetent tricuspid valve
7. Elevated JVP due to back pressure from RA

Left heart strain
1. Ineffective contraction of RV & interventricular septal deviation
2. Decreased CO from left ventricle detected by baroreceptors
3. Stimulates sympathetic nervous system
4. Tachycardia + vasoconstriction

Whatever happens to one side, it affects the other side.

20
Q

How can a DVT cause a stroke

A

Clot can break off and travel to IVC back to RA. In a patent foramen ovale, it can then enter the LA, then LV, and be directed to the brain via the aorta

21
Q

Describe the wells score and what it is used for

A

The wells score is to identify how much at risk the patient is for a PE.
>4 well score= PE likely –> Immediate CTPA (or anticoagulation while waiting)
< or equal to 4 wells score= PE unlikely –> D-DIMER within 4 hours
(or anticoagulation while waiting for result)

22
Q

What are the investigations for PE

A

ECG (not diagnostic)
Sinus tachycardia most common
Deep S wave in I, Q wave in III and T wave inversion in III = SI QIII TIII (less common)
Occurs due to right sided heart strain

ABG findings
Type 1 respiratory failure
pO2 <8kPa
pCO2 <6.5kPa
Respiratory alkalosis

23
Q

PE occasional signs on a CXR

A

Occasional Signs:

Atelectasis - collapse of small area of lung tissue

Fleischner sign – enlarged pulmonary artery

Hampton’s hump – peripheral wedge of airspace opacity, implies lung infarction

Westermark sign – clarified area of lung distal to a large vessel that is occluded by a PE

24
Q

PE and CTPA (CT pulmonary angiogram)

A

Chest CT with IV contrast allowing visualisation of pulmonary arteries
FIRST LINE!
*Pregnancy, contrast allergy, renal failure → do VQ scan instead of CTPA *
Ventilation-perfusion scan
Radioactive isotopes are inhaled – image taken to show ventilation
Isotopes are injected – image is taken to show perfusion
Images are compared
In PE → good ventilation but poor perfusion

Saddle pulmonary embolismcommonly refers to a largepulmonary embolismthat straddles the bifurcation of thepulmonary trunk, extending into theleftandright pulmonary arteries.

25
Q

What is the management of PE (short term)

A

Supportive management – O2 as required, analgesia if required, monitor for any deterioration

If Haemodynamically Stable
DOACs – apiXaban or rivaroXaban (1ST LINE)
LMWH if pregnant, breastfeeding or active cancer
Warfarin for patients with antiphospholipid syndrome

Not Haemodynamically stable ((massive PE – BP<90 systolic or drop >40mmHg in 15 minutes))

Continuous UFH infusion
Thrombolysis – streptokinase or alteplase
Surgical thrombectomy in those with failed fibrinolysis, or patients with a free-floating thrombus in the RA or RV

UFH is a parenteral anticoagulant that works by inactivating thrombin (IIa) and factor Xa via antithrombin.

26
Q

What is the management of PE (Long term)

A

Continue anticoagulation for:
-3 months if PE was provoked
->3 months if PE was unprovoked, recurrent VTE or irreversible underlying cause (e.g., thrombophilia)
-3-6 months in active cancer, then review

27
Q

What are the antithrombotic drugs

A

**Anti-platelets **
Inhibit platelets from binding together, preventing thrombus formation
**Anti-coagulants **
Interfere with coagulation factors to prevent thrombus formation
Do not dissolve clots that have already formed by act prophylactically to prevent new clots from forming
**Thrombolytics **
Break down clots
After thrombolytic therapy, antiplatelets / anticoagulants are used to prevent formation of new clots

28
Q

What is the Arachidonic Acid Pathway and how does it have an anti-thrombotic effect.

A

-NSAIDs inhibit the activity of cyclooxygenase enzymes (COX1 and/or COX2) –> reduced platelet aggregation
i.e., NSAIDs are antiplatelets

Examples of NSAIDs:
Aspirin
Ibuprofen
Naproxen
Indomethacin

29
Q

What are the anti-platelet drugs, what are their MICRAs.

A
30
Q

What are direct oral anticoagulants (DOACs), what are their MICRAs.

A
31
Q

Micra Warafin

A
32
Q

What is warafin induced clotting

A

Warfarin inhibits vitamin K recycling and proteins C & S which are anti-coagulants

Half-life of protein C is shorter than the clotting factors that it inhibits so protein C levels decrease quicker than clotting factors – for the first 48 hours, the patient can be pro-coagulant

This temporary pro-coagulant state is normally managed with simultaneous heparin administration initially

Patients who are not on anticoagulation – INR usually ≤ 1.1
Patients who are on anticoagulation – INR usually 2-3 (i.e., blood takes longer to clot than usual)

33
Q

MICRA Heparin

A
34
Q

MICRA thrombolytics

A

Medicine GEP Year 1 (BCS paper 1) (19 decks)

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