Monday LObs Flashcards
What is a thrombus composed of?
Leukocytes, Erythrocytes and Platelets within a Fibrin Mesh.
Discuss Verchow’s Triad, an explanation of its 3 sections, and its relevance in diagnosing DVT. Include a diagram
V’s Triad consists of 3 factors that are critically important in the development of venous thrombosis:
- Venous stasis
Venous stasis can occur as a result of anything that slows or obstructs the flow of venous blood. This results in an increase in viscosity and the formation of microthrombi, which are not washed away by fluid movement.
- Activation of blood coagulation
A hypercoagulable state can occur due to a biochemical imbalance between circulating factors. This may result from an increase in circulating tissue activation factor, combined with a decrease in circulating plasma antithrombin and fibrinolysins.
- Venous Damage
Endothelial (intimal) damage in the blood vessel may be intrinsic or secondary to external trauma. It may result from accidental injury or surgical insult.
Draw the 6 possible Fates of Thrombi
PIC 601
What is a Baker’s Cyst?
A Baker’s cyst, also known as a popliteal cyst, is a type of fluid collection behind the knee.
The synovial sac of the knee joint can, under certain circumstances, produce a posterior bulge, into the popliteal space, the space behind the knee.
It is now being increasingly recognised that a Baker’s (popliteal) cyst, ruptured or otherwise, may simulate deep vein thrombosis.
What is a Homer’s sign test?
Homan’s sign test is a physical examination procedure that is used to test for Deep Vein Thrombosis (DVT).
In performing this test the patient will need to actively extend his knee.
Once the knee is extended the examiner raises the patient’s straight leg to 10 degrees, then passively and abruptly dorsiflexes the foot and squeezes the calf with the other hand.
Deep calf pain and tenderness may indicate presence of DVT.
Draw the flow chart of Wells Score and diagnostic tests, “Could Pat Butcher Try Some Superb Cornish Pasties in an Alternative Past?”
DVT Infographic
In the context of testing, define the following:
Sensitivity
Specificity
PPV
NPV
Sensitivity is the ability of a test to correctly identify patients with a disease.
Specificity: the ability of a test to correctly identify people without the disease.
The positive and negative predictive values (PPV and NPV) are the proportions of positive and negative results in statistics and diagnostic tests that are true positive and true negative results.
What is the difference between Proximal and Distal DVT?
Proximal DVT: Located in the popliteal, femoral, or iliac veins.
Isolated Distal DVT is confined to the calf veins (peroneal, posterior, anterior tibial, and muscular veins)
What does a D-Dimer test do?
Measures the level of D-Dimer (a protein fragment hat’s made when a blood clot dissolves in your body) in your blood.
Has high sensitivity and low specificity = Many false positives.
Can therefore rule out DVT, but not confirm it.
How and why does Venous Thromboses frequently present in the lower extremity veins?
In the absence of rhythmic contraction of the leg muscles, as in walking or moving, blood flow in the veins slows and even stops in some areas, predisposing patients to thrombosis.
Studies have shown that low flow sites, such as the soleal sinuses, behind venous valve pockets, and at venous confluences, are at most risk for the development of venous thrombi. Most of these locations begin in the calf.
As many as 1/3 of untreated symptomatic calf vein DVT extend to the proximal veins. Although calf vein thrombi are rare sources of clinically significant pulmonary embolism (PE), the incidence of PE with untreated proximal thrombi is 29-50%.
Define Haemostasis, and outline its three stages.
Pic 603
Name three methods in which the endothelium of blood vessels inhibits haemostasis during healthy blood flow
- Nitrous Oxide and PGI2 (Prostacyclin)
Both are chemicals released by the endothelium to inactivate platelets, and thereby inhibit their binding to the endothelial lining.
- Heparin Sulfate
Glycosaminoglycan protein - bound to plasma membrane - that binds and activates A.T.III (Anti-Thrombin III), which degrades clotting factors II, IX and X.
- Thrombomodullin
Receptor for Thrombin - Thrombin activates Protein C - which degrades clotting factors V, and VIII
Describe the mechanism of Vascular Spasm
- When injured, endothelial cells in the blood vessels secrete Endothelin. This binds to Type 2 G protein ETB receptors in the smooth muscle to initiate contraction (like NE from Vasomotor centre)
- Myogenic mechanism of smooth muscle cells - in which they contract in response to mechanical trauma
- Nociceptors in blood vessels are stimulated by inflammatory mediators and mechanical trauma to stimulate pain and enact a contractile muscular response.
Give an outline of Platelet Plug formation
- vWF (von Wildebronn’s Factor) is secreted by injured endothelial cells
- Injury to endothelial cells inhibits secretion of NO and PGI2, and inhibits upkeep of Thrombomodullin/Heparin Sulfate, meaning platelets can freely bind to collagen with the help of vWF.
- Platelets bind to vWF using their Gp1b receptors, to release TxA2, ADP and Seratonin, which encourages platelet coagulation to vWF. Platelets bind to each other via fibrinogen and GpIIb/IIIa.
- The released chemicals stimulate further contraction of the smooth muscle, enhancing the vascular spasm effect and starting a +feedback loop of platelet aggregation.
Draw the overall Coagulation Cascade and Fibrolysis Map, as well as which factors require Ca+ or Vitamin K to function.
Factors requiring Ca+: II, VII-XI, XIII
Factors requiring Vit K:
II, VII, IX, X, Protein C, Protein S
(diSCo 1972)
Factor XIII is also activated by Factor II as a Fibrin Stabilising factor.
Explain Haemophilias a, b and c through factor deficiencies
PIC 604
Describe the effects of a PE in terms of pulmonary infarction and ischemia
PIC 605
Describe the effects of a PE in terms of v/q mismatch
PIC 606
Describe the effects of a PE upon the cardiovascular system
Pic 607
What would you see on the ABGs for a patient with PE?
ABG: Most commonly shows hypoxemia and hypocapnea (respiratory
alkalosis) due to hyperventilation:
• type 1 respiratory failure
• ↓PaO2 and ↓PaCO2
What would you find on an ECG for someone with PE?
ECG is often normal, often used to rule out Myocardial Infarction and Pericarditis
Common findings include:
1. Sinus Tachycardia
2. Inverted T waves
3. S1Q3S3 (see picture)
What would you expect to find on a CXR for someone with PE?
CXR is neither sensitive
nor specific for confirming PE, mainly useful to rule out other conditions in DDx e.g. pneumonia,
pneumothorax.
Chest radiographic signs include:
• Fleischner sign: enlarged pulmonary artery (20%)
• Hampton hump: peripheral wedge of airspace opacity and implies lung
infarction (20%)
• Westermark sign: regional oligaemia and highest positive predictive value
(10%)
What is Oligaemia?
Just another goddamn word for Hypovolemia
What is a pneumothorax?
A Collapsed Lung
Can a PE cause a pneumothorax?
Can a PE cause atelectasis?
The incidence of pneumothorax is not common.
The rare phenomenon of secondary spontaneous pneumothorax from pulmonary embolism is due to Pulmonary Infarction as a result of the PE.
However, PE may well cause edema and atelectasis because of depletion of surfactant as a result of decreased delivery of the components of surfactant production due to inhibited perfusion.
What is the difference between Transudative and Exudative fluid build up?
“Transudate” is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. Protein Poor.
“Exudate” is fluid buildup caused by tissue leakage due to inflammation or local cellular damage. Protein Rich.
In the context of Angela Robinson, how has her pleural effusion presented on the CXR?
Through loss of the costodiaphragmatic (costophrenic angle) in the left thoracic cavity.
In the context of Angela Robinson, how has her atelectasis presented on the CXR?
Through loss of visibility of the left hemidiaphragm on the X ray.
What rash did Angela develop in reaction to Rivaroxaban?
She developed acute spontaneous (idiopathic) urticaria as a hypersensitivity reaction to anti-coagulant medication. The pathophysiology is below:
Stimuli → mast cell degranulation → histamine and other proinflammatory mediators release → vasodilation and increased permeability of postcapillary venules to large plasma proteins, including albumin and immunoglobulins → transient skin or mucosal swellings due to plasma leakage
What is Malignancy?
The term “malignancy” refers to the presence of cancerous cells that have the ability to spread to other sites in the body (metastasize) or to invade nearby (locally) and destroy tissues.
What is cellulitis?
The term cellulitis is commonly used to indicate a non-necrotizing inflammation of the skin and subcutaneous tissues, usually from acute infection (see the image below). Cellulitis usually follows a breach in the skin, although a portal of entry may not be obvious; the breach may involve microscopic skin changes or invasive qualities of certain bacteria.
What is the journey from DVT to PE in flow chart form?
609
What is the lung parenchyma?
Lung parenchyma is the portion of the lung involved in gas transfer - the alveoli, alveolar ducts and respiratory bronchioles.
Why does a PE lead to Pulmonary Infarction and Haemoptysis?
Pulmonary infarction results from occlusion of the distal pulmonary arteries leading to ischemia, hemorrhage and ultimately necrosis of the lung parenchyma.
It is most commonly caused by acute pulmonary embolism (PE), with a reported incidence of around 30%.
Following an occlusion of the pulmonary artery, the bronchial arteries are recruited as primary source of perfusion of the pulmonary capillaries.
The relatively higher blood pressure in the bronchial circulation causes an increase in the capillary blood flow, leading to extravasation of erythrocytes (i.e. alveolar hemorrhage). If this hemorrhage cannot be resorbed, it results in tissue necrosis and infarction.
Why can a PE lead to a Pleural Effusion?
Increase in hydrostatic pressure with no decrease in oncotic pressure leads to increased filtration into the inter-pleural cavity.
What is a CT pulmonary angiogram (CTPA)
A medical diagnostic test that employs computed tomography (CT) angiography to obtain an image of the pulmonary arteries. Its main use is to diagnose pulmonary embolism (PE).
The patient receives an intravenous injection of an iodine-containing contrast agent at a high-rate using an injector pump.
A normal CTPA scan will show the contrast filling the pulmonary vessels, appearing as bright white. Any mass filling defects, such as an embolus, will appear dark.
What is Tricuspid regurgitation?
Tricuspid regurgitation is associated with a pansystolic murmur heard loudest over the tricuspid region during ventilation.
Tricuspid regurgitation occurs when there is backflow of blood from the right ventricle into the right atrium during ventricular systole. This causes an increase in right atrial pressure and elevated venous pressures (JVP)
Aetiology
Causes of tricuspid regurgitation include:
- Right ventricular dilatation (e.g. secondary to pulmonary stenosis or pulmonary hypertension)
- Rheumatic fever
- Infective endocarditis
- Carcinoid syndrome
- Congenital (e.g. atrial septal defect, AV canal, Ebstein anomaly)
Typical clinical features
Typical features of a tricuspid regurgitation murmur include:
- Pansystolic murmur
- Heard loudest over the tricuspid region
- Loudest during inspiration
What is tested on a Thrombophilia Screen?
A thrombophilia screen consists of:
- PT
- PTT
- Fibrinogen
- Antithrombin
- Protein C
- Protein S
- Lupus Anticoagulant
- Factor V Leiden
- Prothrombin G20210A mutations.
What is a V/Q Scan? (Otherwise known as Radionucleotide Imaging?)
Carried out in two parts.
- radioactive material is breathed in and pictures or images are taken to look at the airflow in the lungs.
- A different radioactive material is injected into a vein in the arm, and more images taken to see the blood flow in the lungs
What is the difference between Atelectasis and a Pneumothorax?
If it is a total lung collapse, it is called pneumothorax.
If only part of the lung is affected, it is called atelectasis.
What is the difference in time for activation of the Extrinsic and Intrinsic Pathways?
- Extrinsic pathway is fast (30secs)
- Intrinsic pathway is slow (5 mins)
Factors I, Ia, II, IIa, and III go by which alternative names?
I: Fibrinogen
Ia: Fibrin
II: Prothrombin
IIa: Trombin
III: Tissue Factor
Describe the differences between the APTT and PT tests.
What can APTT and PTT tests monitor in terms of prolonged time?
Give an overview of a TT test
Give an overview of a ‘Mixing Studies’ test.
If there is a prolonged PT or PTT.
Used to see if there is a deficiency in clotting factor or an inhibitor of factor activity.
50:50 plasma from patient and normal plasma.
If clotting normalises = factor deficiency (normal blood adds the missing factor).
If does not normalise, there may be a clotting inhibitor in the patients blood, i.e antiphospholipid antibodies
What does VTE stand for?
Venous Thrombo-Embolism
Outline the typical signs and symptoms of a PE
Draw the unbelievably cool table for the pathophysiology of Pulmonary Embolism
Draw the NICE guidelines chart for actions to take during a suspected PE
What is PAI-1 and why is it inhibited by Protein C?
PAI-1 is a serine protease inhibitor (serpin) that functions as the principal inhibitor of tissue plasminogen activator (tPA) and urokinase (uPA), the activators of plasminogen and hence fibrinolysis.
What are the 8 types of drugs that interact with Warfarin?
The 8 A’s:
- Antibiotics
- Antiplatelets
- Antifungals
- Anti-Inflammatory
- Anti-Depressants
- Acetaminophren
- Amiodarone
- Alternative Remedies
What is Emphysema?
In Emphysema, over time, the inner walls of the alveoli weaken and rupture — creating larger air spaces instead of many small ones.
What is an Echocardiogram and how is it utilised in managment/treatment of PE?
An echocardiography, echocardiogram, cardiac echo or simply an echo, is an ultrasound of the heart. It is a type of medical imaging of the heart, using standard ultrasound or Doppler ultrasound.[1]
It can provide assessment of:
Right/Left ventricular size/function
Regional wall motion
Valvular dysfunction
Intracardiac shunting
Thrombus visualization and
Hemodynamic assessment of right/left sided pressures.
Echocardiography is primarily used as a tool to guide therapy in patients with PE, and for reassessment of changes in right ventricular function and/or pulmonary artery pressures following thrombolysis and thrombectomy.
What is a Cardiac Shunt?
A cardiac shunt is a pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system.
It may be described as right-left, left-right or bidirectional, or as systemic-to-pulmonary or pulmonary-to-systemic.
The direction may be controlled by left and/or right heart pressure, a biological or artificial heart valve or both.
What is Lupus?
Lupus, technically known as systemic lupus erythematosus (SLE), is an autoimmune disease in which the body’s immune system mistakenly attacks healthy tissue in many parts of the body.[1]
Symptoms may be mild to severe.[1] Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face.[1]
Often there are periods of illness, called flares, and periods of remission during which there are few symptoms.[1]
What are the Lupus Anticoagulant and the Anticardiolipin antibody?
Antiphospholipid antibodies are antibodies directed against phospholipids, certain blood proteins they bind to, and the resulting complexes formed.
Their presence in an individual is heavily associated with a predisposition for blood clots.
What specifically activates platelets? And what chemicals are released as a result?
The binding with vWF causes conformational change to activated shape.
The chemicals released are:
More vWF
TxA2
ADP
Serotonin
PAI-1
Calcium
What is CPAP?
Continuous positive airway pressure (CPAP) is a form of positive airway pressure (PAP) ventilation in which a constant level of pressure greater than atmospheric pressure is continuously applied to the upper respiratory tract of a person.
What does NIV stand for?
Non-invasive ventilation (NIV) is the delivery of assisted mechanical ventilation to the lungs, without the use of an invasive endotracheal airway.
What is pneumonia?
Pneumonia is an infection that inflames the air sacs in one or both lungs. The air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia.
Draw the following:
The O2 Cascade
The Four types of Hypoxia
How the two relate together physiologically
How do you calculate the following:
Total Oxygen Capacity
Amount of Oxygen Delivery to Tissues
How do you calculate minute ventilation?
Tidal Volume x Breaths per Minute
What are the four main causes of Hypoxic Hypoxia?
Define Shunt and Deadspace Perfusion
What are the 4 main causes of Hypoxaemic Hypoxia?
What are the four main causes of Circulatory Hypoxia?
Name 3 of the main causes for Histotoxic Hypoxia
What are the main signs and symptoms of Respiratory distress and hypercapnia?
What are the three steps in treating respiratory distress?
What are the four main indications for intubation?
Give a 4-step plan to interpreting ABGs in someone with Hypoxia
- PaO2: Is it low? And on what % of Oxygen?
- PaCO2: Hypocapnic (e.g. hyperventilating) or Hypercapnic (e.g. exhaustion)?
- Is it acute? e.g. pH lowered as no HCO3 metabolic compensation. Is it chronic? e.g. pH normal as HCO3 metabolic compensation has had time to kick in
- What is the response to supplemental O2? Improves? High V/Q mismatch likely. No improvement? Low V/Q mismatch or shunt likely.
What are the normal percentages of the constituents of blood?
What are the timescales of the different facets of hemostasis?
Immediately:
Vascular Spasm
In Seconds:
Platelet Adhesion to vWF
Activation of pro-coagulation factors
In Minutes:
Platelet aggregation and plug
Fibrin Mesh formation
Plasminogen-Plasmin conversion
In Hours:
Fibrinolysis of clot.
Draw the different pro and anti coagulation mechanisms in both normal blood flow and in clot formation
NB: Note the negative charge presented on the exterior of undamaged endothelial cells
Give the same information as slide 76 but in table form:
Draw the platelet life cycle
Draw the best flow diagram yet of the coagulation cascade and the relationships between factors and inhibitory chemicals/drugs
Name some inherited and acquired bleeding disorders.
What are the four categories of test we can do to assess the hemostasis balance of a patient? What conditions will they look for?
How do the PTT/aPTT/TT tests work? Roughly.
- Plasma is isolated from blood sample through centrifusion
- The sample is citrated to negate any lasting Ca+
- The sample is then infused with -coagulation reagents (e.g. phospholipids or coag factors), Ca+ and of course a trigger/activator
- The time it takes for the clot to form is measured
What is Factor V Leiden?
Factor V Leiden is a genetic condition, arising from a point substitution in the genetic code of Factor V.
Consequently, protein C, is not able to bind normally to factor V and inhibit it’s activity, leading to a hypercoagulable state.
Homozygous increases your risk by 20%
