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Respiratory > Pulmonary vascular disease > Flashcards

Pulmonary vascular disease Flashcards

1
Q

Which arteries supply the lung?

A

Pulmonary arteries and Bronchial arteries

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2
Q

What is the pressure like in the pulmonary circulation?

A

Low pressure = 1/5th pressure in systemic circulation

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3
Q

Do the pulmonary arteries have a low or high incidence of atheromas?

A

Low incidence

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4
Q

What is pulmonary oedema and what spirometry pattern does it cause?

A

Accumulation of fluid in the lungs

Restrictive

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5
Q

What are the causes of pulmonary oedema?

A 
Haemodynamic (increase in hydrostatic pressure due to heart failure)
Cell injury (More localised oedema due to damage to alveoloar lining cells/capillary endothilium)
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6
Q

If oedema due to cell injury is generalised what can this lead to?

A

Adult respiratory distress syndrome

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7
Q

What is ARDS also known as and why?

A

Shock lung because it is associated with circulatory shock

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8
Q

What are the causes of ARDS?

A

Sepsis, diffuse infection (virus/mycoplamsa), severe trauma, reactive oxygen species

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9
Q

What is the pathogenisis of ARDS?

A

Bacterial endotoxin causing systemic infection
Infiltration of inflammatory cells which produce oxygen free radicals.
Release of cytokines which drive the immune response
ROS damage the cell membranes

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10
Q

What are the pathological findings in ARDS?

A

Fibrinous exudate lining alveolar walls (hyaline membranes)
Cellular regeneration
Inflammation

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11
Q

What are the potential outcomes for ARDS?

A

Death
Resolution
Fibrosis
Patients are often ventilated as there is a high chance of mortality but also resolution

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12
Q

What is an embolus?

A

Detached intravascular mass carried in the blood to a site in the body distant from its point of origin

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13
Q

What are the types of emboli?

A

Thrombi, Fat, Air, foreign bodies, tumour, amniotic fluid

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14
Q

What are the risk factors for PE and DVT (virchow’s triad)?

A

1) Endothilial damage
2) Hypercoaguable blood
3) Abnormal/turbulent flow

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15
Q

How does a PE present and what is the presentation dependent on?

A

Sudden death, Severe chest pain, dyspnoea, haemoptysis, pulmonary infarction, pulmonary hypertension
Dependent on: size of embolus, cardiac and respiratory function

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16
Q

Small pulmonary emboli are common. What is the most common sign?

A

Pulmonary hypertension

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17
Q

What is a pulmonary infarct and is a PE sufficient to cause a pulmonary infarct?

A

Ischaemic necrosis
PE is necessary but not sufficient as there are bronchial arteries. However bronchial artery can be compromised (eg cardiac failure)

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18
Q

What is the difference between primary and secondary pulmonary hypertension?

A

Primary- no known cause and occurs in young women

Secondary- due to another cause, more common

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19
Q

How does pulmonary hypertension develop?

A

1) Hypoxia => pulmonary vasoconstriction
2) Increased flow through pulmonary circulation (congenital heart disease)
3) Blockage (PE) or loss (emphysema) of pulmonary vascular bed
4) Back pressure from left ventricular failure

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20
Q

What morphalogical changes are seen in pulmonary hypertension?

A

Medial hypertrophy of arteries
Intimal thickening (fibrosis) of arteries
Atheroma
Right ventricular hypertrophy- detected on CXR/ECG
Plexogenic change/necrosis (extreme cases (congenital or primary pulmonary hypertension

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21
Q

What is cor pulmonale?

A

Heart disease secondary to lung disease
Lung disease leading to pulmonary hypertension => right ventricular hypertrophy => Right ventricular dialitaion => right heart failure

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22
Q

What are the cardiac causes of pulmonary venous hypertension?

A

Left ventricular failure
Mitral regurgitation or mitral stenosis
Cardiomyopathy

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23
Q

What is the normal MAP in the pulmonary vasculature and what is defined as pulmonary hypertension?

A

Normal = 12-20mmHg

Pulmonary hypertension >25mmHg

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24
Q

What are the causes of pulmonary arterial hypertension?

A

1) Hypoxia due to Lung Disease (COPD, OSA, alviolitis)
2) Multiple pulmonary emboli
3) Pulmonary vasculitis (SLE, Polyarteritis nodosa, systemic sclerosis)
4) Drugs (apitite supressors-fenfluramine)
5) HIV
6) Cardiac left to right shunt (ASD/VSD)
7) Primary pulmonary hypertension

25
Q

What are the clinical signs of pulmonary hypertension?

A 
Central cyanosis (if hypoxic)
Ankle oedema
Raised JVP
Right parasternal heave 
Tricuspid regurgitation 
Enlarged liver
26
Q

What are the largest risk factors for cor pulmonale?

A

Hypoxia and smoking

27
Q

What is CTEPH and how would you treat it?

A

Chronic thromboembolic pulmonary hypertension
Complication of PE
Treatment = Riociguat (pulmonary artery vasodilator)
Pulmonary Endartectomy- curative

28
Q

What investigations are needed for pulmonary hypertension?

A

ECG and CXR
SaO2 and ABGs
Pulmonary function testing
Echocardiogram to estimate RV systolic pressure or cardiac catherterisation to measure the mean pulmonary arterial pressure
D dimers and VQ scan if PE is suspected => CTPA
Cardiac MRI
Autoantibodies if vasculitis is suspected

29
Q

What is the prognosis of pulmonary hypertension?

A

3 years without treatment. 10 years with treatment

30
Q

What are the signs of primary pulmonary hypertension?

A

Progressive SOBOE and signs of right heart failure

Diagnosis of exclusion of all other causes

31
Q

What is the treatment for primary pulmonary hypertension?

A 
Prophylactic anticoagulant (Warfrin)
Oxygen if hypoxic
Pulmonary vasodilators (Ca++ channel blockers-nifedipine)
Other drugs 
Lung transplant
32
Q

What are the risk factors for DVT and PE?

A 
Thrombophilia 
Contraceptive pill/HRT
Pelvic obstruction (uterus/ovary/lymph nodes)- obesity
Pregnancy
Trauma 
Surgery on pelvis, hip or knee
Immobility- bed rest/ long haul flights
Malignancy
MI
Pulmonary hypertension/vasculitis
33
Q

Where are the common places for DVT to form?

A

Proximal- ileofemoral (most likely to embolise and lead to chronic venous insufficiency and leg ulcers)
Distal- Popliteal (least likely to embolise)

34
Q

Clinical presentation of DVT?

A

Whole leg/calf involved depending on site

Swollen, hot, red and tender

35
Q

What are the differential diagnosis for DVT?

A

Popliteal synovial rupture, superficial thrombophlebitis, calf cellulitis

36
Q

What investigations are needed if you suspect a DVT?

A

Ultrasound of the leg- non-invasive to exclude pelvic mass or cyst
CT scan of ileofemoral veins, IVC and pelvis

37
Q

What is the presentation of a small, medium and large PE?

A 
Small= recurrent progressive dyspnoea, pulmonary hypertension and right heart failure
Medium = Pleuritic pain, haemoptysis, breathless
Large = Cardiovascular shock, low BP central cyanosis and death
38
Q

With PE the predisposing PE is always obvious. True or false?

A

False- the DVT may be silent

39
Q

What is the PESI score?

A

Pulmonary embolism severity index

40
Q

What are the clinical signs of PE?

A

Tachycardia, tachypoea, cyanosis, fever, hypotention, crackles, rub, pleural effusion

41
Q

What would you expect to see in the ABGs of someone with a PE?

A

Low PaO2, Low SaO2, Normal or low PaCO2

Type 1 respiratory failure

42
Q

What would you expect to see in the CXR of someone with a PE?

A

Normal initially
Then infarction, basal atelectesis (collapse of lobe), consolidation and plural effusion
Wedged shaped infarct

43
Q

What would you expect to see in the ECG of someone with a PE?

A

Acute right heart strain pattern

44
Q

What would you expect to see in the D dimers of someone with a PE?

A

Usually raised although there are many reasons for D dimers to be raised
If its negative, it can be used to rule out a PE

45
Q

What would you expect to see in the V/Q scan of someone with a PE?

A

Perfusion defect before infarction

Ventilation and perfusion match defect after infarction

46
Q

What would you expect to see in the CTPA of someone with a PE?

A

Filling defect for larger clots in proximal vessels

47
Q

What would you expect to see in the Echocardiogram of someone with a PE?

A

Acute dilation of the right ventricle
D shaped left ventricle due to pressure on the sternum
Measure pulmonary artery pressure and RV size

48
Q

What would you expect to see in the TLCO of someone with a PE?

A

Low gas transfer due to perfusion defect

49
Q

How can a DVT be prevented?

A 
Early post op mobilisation
TED compression stockings 
Calf muscle exercises
SC low dose of LMWH 
Dabigatran- direct thrombin inhibator 
Rivaroxaban/Apixaban- direct factor Xa inhibator (given orally to prevent DVT post hip/knee surgery
50
Q

What happens if you anticoagulate and then get a haemorrage?

A

Stop anticoagulant and reverse effect
Reverse warfrin with vitamin K
Reverse heparin with Protamine
Give fresh frozen plasma for new oral drugs

51
Q

How is an acute DVT or PE treated?

A

Anticoagulants prevents fibrin clot propagation (SC heparin)

Therapeutic dose of SC LMWH- takes longer to act

52
Q

How is DVT and PE treated in the long term?

A

LMWH od SC and start warfrin at the same time (takes >3 days to work)
OR use dabigatran or rivaroxiban PO from the start

53
Q

How is DVT and PE treatment monitored?

A

Continue warfrin for 3-6 months.

Monitor to ensure INR = 2.5-3.5

54
Q

What interactions will increase anticoagulation?

A

Alcohol, antibiotics, asprin, NSAIDs, cimetidine, omeprazole and grapefruit

55
Q

How is a life threatening PE treated (severe hypoxia and low BP)?

A

1) Thrombolysis- streptokinase or tPA (intra catherter directed)
2) IVC filter to prevent embolism from large ileofemoral clot leading to recurrent PEs
3) Thrombo endartectomy- rarely indicated

56
Q

What is the INR used for?

A

International normalised ratio is used for monitoring warfrin

57
Q

What should the INR be for:

1) Normal people with no DVT/PE risk factors?
2) Following first PE/DVT?
3) Following >1 event?
4) Recurrent DVT/PEs?

A

1) Normal people with no DVT/PE risk factors = 1
2) Following first PE/DVT = 2-3
3) Following >1 event = 3
4) Recurrent DVT/PEs = 3.5

58
Q

How long should patients be on warfrin following:

1) Provoked PE/temporary risk factor?
2) Unprovoked low risk distal DVT/PE?
3) Unprovoked first PE?
4) High risk proximal DVT/PE?
5) Recurrent DVT/PE?

A

1) Provoked PE/temporary risk factor = 3 months
2) Unprovoked low risk distal DVT/PE = 3 months
3) Unprovoked first PE = 6 months
4) High risk proximal DVT/PE = 6 months
5) Recurrent DVT/PE = lifelong

Respiratory (26 decks)

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