Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Respiratory > Pulmonary vascular disease > Flashcards

Pulmonary vascular disease Flashcards

(58 cards)

Start Studying
1
Q

Which arteries supply the lung?

A

Pulmonary arteries and Bronchial arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the pressure like in the pulmonary circulation?

A

Low pressure = 1/5th pressure in systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Low incidence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Accumulation of fluid in the lungs

Restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Adult respiratory distress syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is ARDS also known as and why?

A

Shock lung because it is associated with circulatory shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of ARDS?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the pathological findings in ARDS?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the types of emboli?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

Pulmonary hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the cardiac causes of pulmonary venous hypertension?

A

Left ventricular failure
Mitral regurgitation or mitral stenosis
Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the causes of pulmonary arterial hypertension?

Study These Flashcards
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
What are the clinical signs of pulmonary hypertension?
``` Central cyanosis (if hypoxic) Ankle oedema Raised JVP Right parasternal heave Tricuspid regurgitation Enlarged liver ```
26
What are the largest risk factors for cor pulmonale?
Hypoxia and smoking
27
What is CTEPH and how would you treat it?
Chronic thromboembolic pulmonary hypertension Complication of PE Treatment = Riociguat (pulmonary artery vasodilator) Pulmonary Endartectomy- curative
28
What investigations are needed for pulmonary hypertension?
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
What is the prognosis of pulmonary hypertension?
3 years without treatment. 10 years with treatment
30
What are the signs of primary pulmonary hypertension?
Progressive SOBOE and signs of right heart failure | Diagnosis of exclusion of all other causes
31
What is the treatment for primary pulmonary hypertension?
``` Prophylactic anticoagulant (Warfrin) Oxygen if hypoxic Pulmonary vasodilators (Ca++ channel blockers-nifedipine) Other drugs Lung transplant ```
32
What are the risk factors for DVT and PE?
``` 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
Where are the common places for DVT to form?
Proximal- ileofemoral (most likely to embolise and lead to chronic venous insufficiency and leg ulcers) Distal- Popliteal (least likely to embolise)
34
Clinical presentation of DVT?
Whole leg/calf involved depending on site | Swollen, hot, red and tender
35
What are the differential diagnosis for DVT?
Popliteal synovial rupture, superficial thrombophlebitis, calf cellulitis
36
What investigations are needed if you suspect a DVT?
Ultrasound of the leg- non-invasive to exclude pelvic mass or cyst CT scan of ileofemoral veins, IVC and pelvis
37
What is the presentation of a small, medium and large PE?
``` 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
With PE the predisposing PE is always obvious. True or false?
False- the DVT may be silent
39
What is the PESI score?
Pulmonary embolism severity index
40
What are the clinical signs of PE?
Tachycardia, tachypoea, cyanosis, fever, hypotention, crackles, rub, pleural effusion
41
What would you expect to see in the ABGs of someone with a PE?
Low PaO2, Low SaO2, Normal or low PaCO2 | Type 1 respiratory failure
42
What would you expect to see in the CXR of someone with a PE?
Normal initially Then infarction, basal atelectesis (collapse of lobe), consolidation and plural effusion Wedged shaped infarct
43
What would you expect to see in the ECG of someone with a PE?
Acute right heart strain pattern
44
What would you expect to see in the D dimers of someone with a PE?
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
What would you expect to see in the V/Q scan of someone with a PE?
Perfusion defect before infarction | Ventilation and perfusion match defect after infarction
46
What would you expect to see in the CTPA of someone with a PE?
Filling defect for larger clots in proximal vessels
47
What would you expect to see in the Echocardiogram of someone with a PE?
Acute dilation of the right ventricle D shaped left ventricle due to pressure on the sternum Measure pulmonary artery pressure and RV size
48
What would you expect to see in the TLCO of someone with a PE?
Low gas transfer due to perfusion defect
49
How can a DVT be prevented?
``` 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
What happens if you anticoagulate and then get a haemorrage?
Stop anticoagulant and reverse effect Reverse warfrin with vitamin K Reverse heparin with Protamine Give fresh frozen plasma for new oral drugs
51
How is an acute DVT or PE treated?
Anticoagulants prevents fibrin clot propagation (SC heparin) | Therapeutic dose of SC LMWH- takes longer to act
52
How is DVT and PE treated in the long term?
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
How is DVT and PE treatment monitored?
Continue warfrin for 3-6 months. | Monitor to ensure INR = 2.5-3.5
54
What interactions will increase anticoagulation?
Alcohol, antibiotics, asprin, NSAIDs, cimetidine, omeprazole and grapefruit
55
How is a life threatening PE treated (severe hypoxia and low BP)?
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
What is the INR used for?
International normalised ratio is used for monitoring warfrin
57
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?
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
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?
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions