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Phase 2 Med > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Chronic obstructive pulmonary disorder (COPD) definition

A

A disease state characterised by airflow limitation that is not fully reversible.
Encompasses emphysema and chronic bronchitis.
Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Associated with type 2 respiratory failure (decreased PaO2, increased PaCO2)

Chronic bronchitis

  • airways inflammation and narrowing
  • increased mucus production
  • bronchitis is often temporary but need to be chronic to cause COPD

Emphysema

  • destruction and dilation of air spaces
  • can’t recoil and expel air
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2
Q

COPD aetiology

A

Smoking is the cause in over 90% of cases
Other causes: cystic fibrosis, industrial exposure to irritants eg mining, heavy industry etc alpha-1-antitrypsin deficiency (ver rare, about 2% of emphysema)

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3
Q

COPD pathophysiology

A

Chronic bronchitis: airways become inflamed due to irritants, narrowing them and leading to increased mucus producing. Smoking causes mucus glands to increase in number and the irritants damage the cilia meaning that the mucus can’t effectively be removed from the airway, causing a chronic cough and mucus/phlegm production

Emphysema: alveoli become large and lose their elasticity - they therefore cannot recon and expel all of the air out. Smoking causes this damage as it causes release of inflammatory factors (to fight off irritants) which break down collagen and elastin in the airways. When breathing the alveoli become more full than they should, causing a barrel chest.

Alpha-1-antitrypsin (A1AT) deficiency: A1AT regulates elastase activity. No A1AT leads to uncontrolled elastase activity. Elastase builds up in the liver causing cirrhosis. Elastase destroys alveoli leading to emphysema. In A1AT deficiency, the lower acinar (alveoli) are more affected whereas those at the top are more affected in normal COPD (irritants get less far down the lungs)

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4
Q

COPD clinical manifestations

A

Signs: dyspnoea, tachypnoea, barrel chest, ankle swelling (caused by resulting heart failure), cyanosis may be present

Symptoms: SOB, chronic cough, recurring chest infections

Chronic bronchitis (blue boater):

  • clinical diagnosis
  • daily productive cough for three or more, in at least two consecutive years
  • chronic respiratory infections
  • overweight and cyanotic
  • elevated haemoglobin
  • peripheral oedema
  • hypoxemia and hypercapnia - may lead to cyanosis
  • crackles *due to airways opening when large amounts of mucus is present)
  • rhonchi (coarse respiratory sounds due to secretions I the bronchial airways) and wheezing
  • hypoxic vasoconstriction of the pulmonary arterioles leads to increased pulmonary vascular resistance and therefore pulmonary hypertension - putting strain on the right side of the heart which leads to right heart enlargement - leading to right sided here failure (COR PULMONE)

Emphysema (pink puffer):

  • pathological diagnosis
  • permanent enlargement and destruction of airspace’s distal to the terminal bronchiole
  • older and thin
  • severe dyspnea - may exhale slowly through pursed lips to increase pressure I airways and keep them from collapsing (puffer)
  • weight loss can result from increased breathing effort
  • can lead to hypoxemia
  • cough with some sputum (less then chronic bronchitis) may be present
  • air trapping and hyperinflation can lead to barrel chest
  • quiet chest
  • CXR - hyperinflation with flattened diaphragms
  • hypoxic vasoconstriction of the pulmonary arterioles leads

A1AT deficiency: always consider in young COPD patients with deranged LFTs or other liver signs eg ascites, jaundice

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5
Q

COPD 1st line investigations

A

CXR

  • emphysema: hyperinflation of the lungs, a flattened diaphragm and a barrel shaped chest
  • do to exclude cancer
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6
Q

COPD gold standard investigations

A

Spirometry: obstructive picture, FEV1/FVC < 70%, does not respond to reversibility testing with SABA

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7
Q

COPD other investigations

A

FBC: chronic hypoxia may cause polycythemia
BMI: weight loss - lung cancer
Serum A1AT
DLCO: shows how well CO2 is diffusing in and out of the blood, reduced in COPD patients as the exchange pathway is impaired.

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8
Q

COPD management

A

Acute:

  • oxygen
  • nebuliser SABA - salbutamol
  • inhaled steroids
  • treat any current infection
Chronic 
Fundamentals of COPD care 
- smoking cessation 
- offer pneumococcal and influenza vaccines 
- pulmonary rehabilitation if indicated

Start inhaled therapy if: previous advice given, clinical need for inhaled therapies
Step 1:
- SABA (ie salbutamol or terbutaline) or SAMA (ipratropium bromide)
Step 2:
- if no asthmatic/steroid response: LABA (ie salmeterol) + LAMA (ie tiotropium)
- if asthmatic/steroid response: LABA (ie salmeterol) and ICS (ie budesonide); can be given in combined Symbicort inhaler (Formoterol (LABA) + budesonide (ICS))
Step 3:
- add long term oxygen therapy

Exacerbations:
Steroids (hydrocortisone/prednisolone) + nebuliser bronchodilators (salbutamol/ipretropium bromide) + Abx

If severe: IV aminophylline (bronchodilator), may need ventilation (usually BiPAP as tends to cause type II respiratory failure)

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9
Q

COPD monitoring

A

MRC Dyspnea Scale

  • Grade 1: not troubled by breathlessness except on strenuous exercise
  • Grade 2: SOB when hurrying on a level or when walking up a slight hill
  • Grade 3: walks slower than most people on the level, stops after a mile or so or stops after 15 mins walking at own pace
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10
Q

COPD complications

A 
Infective exacerbations (IE COPD) 
Emphysema: increased pneumothorax risk due to bullae
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11
Q

Asthma definition

A

Reversible chronic obstructive disease. Asthma is sometimes called bronchial hyperrespnsiveness (twitchy airways). Characterised by bronchocontricton and excessive secretion production.

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12
Q

Asthma aetiology

A

In most cases is an allergic disease (atopic asthma) often associated with atopy and allergy. Allergic inflammation is characterised by the recruitment of eosinophils. Atopy is the tendency to develop IgE mediated reactions to common aeroallergens.
Atopic triad: asthma, eczema, allergic rhinitis (hay fever)

Can divide asthma into eosinophils and non-eosinophilic. Asthma is often linked to COPD especially in smokers. Eosinophilic asthma can be further divided into atopic and non-atopic. Non-eopsinophilic asthma is often smoking or obesity related.

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13
Q

Asthma exacerbates

A

Infection, menstrual cycle, allergens, pollution, smoking, mould, stress, some medications (ACEi, beta blockers (cause bronchoconstriction), NSAIDs and aspirin), cold weather, obesity, laughter, emotions

Occupational: animals, fumes, dusts

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14
Q

Asthma pathophysiology

A

Airflow limitation
- caused by bronchial muscle contraction, mucosal inflammation and increased mucus production
Characterised by muscular hypertrophy and inflammation

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15
Q

Asthma clinical manifestatins

A

Auscultation: episodic wheeze - widespread (localised suggests foreign body), polyphonic, generally no crackles

Diurnal variation (typically worse in morning and night)
Can have mucus (usually clear)
Cough, breathless ness
Characteristically comes and goes and depends on triggers

Classic progression is childhood onset, better in teenage years and recurrence

Brittle asthma: recurrent, severe attacks. Can be type 1 - chronic severe variability of PEFR or type 2 - sudden unpredictable drops in PEFR

COPD is more of a relentless progressive disease and there is less diurnal variation

Associated problems: eczema, hay fever, nasal disease, food and drug allergies, reflux disease (reflex at night can exacerbate asthma)

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16
Q

Asthma classification

A 
Classifying attacks: 
Uncontrolled/moderate
- PEFR > 50% 
- RR < 25
- pulse < 110 
- Normal speech, no severe markers

Severe: ano ONE of:

  • PEFR 33-50% predicted
  • RR >/= 25
  • HR >/= 110
  • inability to complete sentences

Life-threatening: any ONE of:

  • PEFR < 33%
  • SaO2 <92% or PaO2 < 8kPa
  • normal PaCO2
  • altered consciousness, exhaustion, arrhythmia, hypotension, silent chest, poor effort cyanosis

Near fatal:
- raised PaCP2 and/or requiring ventilation

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17
Q

Asthma 1st line investigations

A

Spirometry with reversibility testing (patients >5yrs)

  • obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7
  • peak flow (PEFR)
  • use bronchodilator to test reversibility
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18
Q

Asthma other investigations

A

Blood count: eosinophils, raised
Tests for atopy and allergy: SPTs (skin prick tests) and IgE
CXR often useful
O2 stats
Specific tests of airway inflammation
- becoming more common
- exhaled nitric oxide (PeNO), a marker of eosinophilic inflammation - not specific as elevated in smokers, viral infections an rhinitis

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19
Q

Asthma management

A

Drug classes:

  • bronchodilators: beta agonists, leukotrine receptor antagonists, theophylline, LABAs, anticholinergics
  • anti–inflammatory drugs: steroids - important as these actually reduce inflammation unlike bronchodilators which only relieve symptoms. Inhaled steroids given due to less side effects
  • new biologics: omalizumab, mepolizumab

Treatment pathway:

  1. SABA (eg sabutamol)
  2. Inhaled corticosteroid (ICS eg budesonide)
  3. Leukotriene receptor antagonist (LRTA eg Montelukast)
  4. LABA (eg salmetrol)
  5. Increase ICS dose

Emergency management of severe or life-threatening asthma:

  • oxygen (40-60%)
  • salbutamol nebulizer 5mg (+ipratropium neb 0.5mg if life threatening)
  • prednisolone 30-60mg (+/- hydrocortisone 200mg IV)
  • consider magnesium or aminophylline IV
  • ABGs
  • CXR

Very important to monitor PEFR regularly as well as K= and glucose, aim for SATs >92

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20
Q

Asthma complications

A

Emergency: pneumothorax, arrhythmias, hypokalaemia

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21
Q

Lung cancers classification

A

Bronchial carcinoma
- non small cell (80-85%)
Squamous - most strongly associated with cigarette smoking
Adenocarcinoma (MOST COMMON TYPE and most common in non-smokers)
- small cell (10-15%) - strongly associated with cigarette smoking
- metastatic: prostate, kidney, breast, bone, thyroid, ovary, colon

Cancer of the Pleura
- mesothelioma

22
Q

Lung cancers risk factors

A

Lung cancers: smoking, metal dusts (chromium), asbestos, radon exposure, pulmonary, HIV, genetics

Mesothelioma: asbestos exposure

23
Q

Lung cancers clinical manifestations

A

Lung cancers
- symptoms: persistent cough, SOB, chest pain, haemoptysis (coughing)
- signs: anaemia, weight loss, finger clubbing, supreclavicular or axillary node enlargement
Basic form of staging seen here. TNM (tumour, node, metastasis) staging used for pre-surgical staging

Metastatic symptoms

  • bone pain
  • headaches, seizures, neuro deficit
  • abdominal pain

Preneoplastic changes (rare but important)

  • raised PTH - hyperparathyroidism
  • raised ADH - SiADH
  • raised ACTH - Cushing’s disease

Mesothelioma:

  • classic cancer symptoms: weight loss, fever, SOB, fatigue
  • persistent cough
  • clubbing
  • pain near affected site
24
Q

Lung cancers management

A

Stage I/II: surgical intervention and radiotherapy
Stage III/IV: palliative chemo, radiotherapy and palliative care

Mesothelioma: almost always palliative as usually presents much later and progresses quickly

25
Q

Lung cancers complications

A
  • Pancoast’s Tumour (tumour in the apex of the lung) causing Horner’s syndrome - tumour in the lung invades sympathetic plexus in the neck causing compression of the plexus causing Horner’s (ptosis, mitosis (constricted pupil)), anhidrosis (decreased sweating))
  • recurrent laryngeal nerve palsy - can lead to a hoearse voice
  • metastasis (to outside the lung): liver, bone, adrenal glands, brain
  • phrenic nerve palsy
  • SVC obstruction
  • Lambert eat syndrome (SCLC)
  • neuroendocrine tumours:
  • raised PTH - hyperparathyroidism
  • raised ADH - SiADH
  • raised ACTH - Cushing’s disease
26
Q

Pulmonary embolism definition

A

A consequence of thrombus formation with a deep vein of the body. Thrombus formation occurs due to Virchow’s triad: venous states, trauma and hyper coagulability

27
Q

Pulmonary embolism risk factors

A

Recent immobility, previous DVT/PE, pregnancy, thrombophilic syndromes eg antiphospholipid, malignant, hormone therapy eg HRT or COCP, smoking

28
Q

Pulmonary embolism key presentation

A

Sudden onset SOB and pleuritic chest pain and Hx of painful calves (DVT) and recent long haul flight/immobilisation = think PE

29
Q

Pulmonary embolism signs and symptoms

A

Signs: hyperaemia, pyrexia, cyanosis, tachycardia, tachypnoea, hypertension, raised JVP, red swollen leg, haemoptysis, syncope, hyperaemia, crepitations

30
Q

Pulmonary embolism investigations

A

Well’s Score w/pints:

  • clinical signs of PE/DVT: 3
  • PE most likely diagnosis: 3
  • tachycardia >100: 1.5
  • immobility (>3/7, surgery in last 4/52): 1.5
  • previous PE/DVT: 1.5
  • haemoptysis: 1
  • malignancy +/- treated in last 6 months: 1

Well’s score = 4 moderate possibility, do a D-dimer
Well’s score >4, PE likely do immediate CTPA, offer interim anticoagulation if CTPA delay

D-dimer - negative excludes PE but positive does not prove it. If positive, do imaging
GOLD STANDARD: CTPA

31
Q

Pulmonary embolism management

A

Oxygen
Analgesia

Anticoagulation - apixaban or rivaroxaban or LMWH
- 3 months if provoked PE, >3 months if unprovoked PE

If haemodynamically unstable

  • presents with hypotension, raised JVP - patient is acutely unwell
  • continuous unfractionated heparin + thrombolysis (alteplase)

Otheroptions: surgical embolectomy, vena cava filter

32
Q

Infections - TB definition

A

Pulmonary Tuberculosis is caused by mycobacterium tuberculosis. TB most commonly involves the lungs and is communicable in this form but can affect many organs: lymph nodes, CNS, liver, bones, GU tract and GI tract. Associated with restrictive disease

33
Q

Infections - TB epidemiology

A

Majority of cases from Africa and Asia (India and China). About 2 billion people are infected with mycobacterium tuberculosis

34
Q

Infections - TB aetiology

A

Mycobacterium tuberculosis

  • aerobic, non-motile, non-sporing, slightly curved-bacilli with a thick waxy capsule
  • acid-fast bacilli - turns red/pink with Ziehl-neelsen stain
  • slow growing
  • resistant to phagolysosomal killing and able to remain dormant

Spread is via airborne droplets

35
Q

Infections - TB risk factors

A

Recent foreign travel or exposure to a person who has travelled eg India
Risk factors for developing active TB:
- recent tuberculin skin test conversion (test goes from negative to positive within 24hrs)
- homeless, IV drug users
- smokers
- immunocompromised (diabetes, corticosteroid therapy, renal disease, malnutrition, HIV, haematological malignancy

36
Q

Infections - TB pathophysiology

A

Development of TB requires infection by Mycobacterium tuberculosis and inadequate containment by the immune system. Latent TB describes Mycobacterium tuberculosis infection without clinical, bacteriological or radiographic evidence of active TB

Active TB may occur from re-activation of previously latent infection or from progression of primary infection

  1. Alveolar macrophages insect bacteria and rods proliferate inside them. At this point the patient has primary tuberculosis (signs of infection after exposure), most people are asymptomatic or have a mild flu like illness
  2. About 3 weeks later, cell-mediated immunity kicks in forming a granuloma with a necrotic core (caveating granuloma). This granulomatous area is known as a Gohn focus
  3. TB can spread to the hilarity lymph nodes (via lymphatic spread or infiltration from John focus), caseating necrosis can also occur here. These hilarious lymph nodes and gohn focus make up a Gohn Complex (usually in lower lobes)
  4. These can become fibrosed and calcified and are then called a Ranke Complex
  5. In some cases the TB is killed off but it can remain viable (although dormant), reactivation of the Gohn complex may occur due to immunocomprimisation (AIDS, ageing etc), infection can spread and it usually occurs in the upper lobes (greatest oxygenation, TB is highly aerobic)
  6. Memory T cells release cytokines causing further caseous necrosis although this time it tends to lead to cavity formation
  7. This can allow the TB to disseminate (spread) via airways or lymphatics, causing bronchopneumonia, it can also spread through the vascular system and can affect other parts of the body - systemic miliary TB
  8. Systemic miliary TB can lead to the following complications

Kidneys: sterile pyuria (WBCs in urine)
Meninges: meningitis
Lumbar vertebrae: Pott disease (osteomyelitis and arthritis in the vertebrae)
Adrenal glands: Addison’s disease
Liver: hepatitis
Cervical lymph nodes: lymphadenitis (chronic inflammation), also known as scrofula

This is an example of delayed hypersensitivity reaction. Successful containment of TB is particularly dependent on T-helper cells as they, along with macrophages, form a granuloma with a necrotic caseous centre.

Approximately 10% of people with latent infection will progress to active disease in their lifetime (highest risk is within 2yrs)

37
Q

Infections - TB clinical manifestations

A

Systemic symptoms: weight loss, low grade fever, anorexia, drenching night sweats, malaise

Pulmonary symptoms: productive cough, haemoptysis, cough > 3 weeks (dry or productive), breathlessness, sometimes chest pain

Signs: signs of bronchial breathing, dullness to percuss, decreased breathing, fever, crackles

38
Q

Infections - TB 1st line investigations

A

1st line:

  • CXR - typically shows fibronodular opacities in upper lobes with or without cavitation (abnormal thick-walled gas-filled spaces within the lung), may see Gohn focus - small calcified nodule often in upper lower lobes or lower upper lobes, these occur where bacteria settle
  • sputum test (3x) w/ acid-fast bacilli smear - Ziehl-Neelsen stain (used for acid-fast organisms). Follow up with nucleic acid amplification for confirmation

Sputum culture: most sensitive and specific test but can take weeks for results, grow on Lowenstein Jansen agar

Diagnosing latent TB:
Tuberculin skin test ‘Mantoux’: negative does not rule out active TB
- immune reaction occurs if there has been previous exposure
- reaction can take 2-3 days, induration (hardening) >5mm is generally considered positive regardless of BCG vaccination history
- shows that there has been some sort of exposure

Interferon gamma release assay - detects WBCs response to TB antigens

39
Q

Infections - TB management

A

Ntoifiable disease - report to public health England immediately

1st Line for ACTIVE TB: RIPE abx regimen
- Rifampicin (6 months - bactericidal - blocks protein synthesis) Side effects: red urine, hepatitis

  • Isoniazid (6 months - bactericidal - blocks cell wall synthesis) Side effects: hepatitis, neuropathy
  • Pyrazinamide (2 months - bactericidal initially, less effective later) Side effects: gout, arthralgia, rash, hepatitis
  • Ethambutamol (2 months - bacteriostatic, blocks cell wall synthesis) Side effects: optic neuritis

Treatment for LATENT TB:
Usually 9 months of isoniazid

40
Q

Infections - pneumonia (CAP & HAP) definition

A

Pneumonia is inflammation of the lungs with consolidation (a region of lung is filled with liquid instead of air) or interstitial lung infiltrates, most often categorised according to the causative organism. Causes 30% of ICU deaths

41
Q

Infections - pneumonia aetiology

A

Community-acquired pneumonia (CAP) - pneumonia acquired outside hospital or healthcare facilities

  • streptococcus pneumoniae is the most common - characterised by rusty sputum
  • haemophiliac influenzae
  • mycoplasma pneumoniae
  • other: staphylococcus aureus (inc MRSA), group A streptococci and Moraxella catarrhalis

Hospital-acquired pneumonia (HAP) - acute lower respiratory tract infection that is acquired after at least 48hrs of admission to hospital and is not incubating at the time of admission. Mostly caused by aerobic gram-negative bacilli:

  • Pseudomonas aeruginosa
  • Escherichia coli
  • Klebsiella pneumoniae
  • HAP after 5 days admission is more likely to be Pseudomonas aeruginosa or MRSA. Within 4 days after admission the causative organism is most likely the same as in CAP ie S.pneumoniae/S.aureus

Atypical pneumonia - bacterial pneumonia caused by atypical organisms not detectable on Gram stain and cannot be cultures using standard methods

  • mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Legionella pneumophila - consider if travel Hx (eg Spain)

Pneumonia in immunocompromised patients
- eg pneumocystis jiroveci (fungal) - occurs in severely immunocompromised patients eg HIV

42
Q

Infections - pneumonia risk factors

A
  • infants and elderly
  • COPD, other lung disease
  • immunocompromised eg HIV
  • nursing home residents
  • impaired swallowing
  • diabetes
  • cardiovascular disease and congestive heart failure
  • alcoholics and IV drug users
43
Q

Infections - pneumonia clinical manifestations

A

Clinical features: fever, productive cough, dyspnoea/tacypnoea, tachycardia, low BP, confusion (esp elderly), rights, malaise, pleuritic chest pain

Signs: dull to percussion, decreased air entry, bronchial breath sounds

44
Q

Infections - pneumonia investigations

A 
FBC - elevated WBC 
Determine causative organism 
- sputum sample and blood cultures 
- urinary antigen test - Legionellas 
- Thoracentesis (pleural tap)

Gold standard: CXR showing consolidation

  • Multilobar: Streptococcus pneumoniae, Staphylococcus aureus
  • Multiple abscesses: S.aureus
45
Q

Infections - pneumonia assess severity

A 
CURB-65 (each score 1 point) 
C - confusion 
U - blood urea nitrogen (BUN) >7mmol/L 
R - respiratory rate >/= 30 
B - blood pressure = 90 systolic OR diastolic = 60 
- >/= 65 yrs old 
Max score is 5

Score 1: treat as an outpatient
Score 2: consider short stay in hospital/monitor closely as outpatient
Score 3+: hospitalisation, consideration for ITU

Can use CRB-65 in a community setting

46
Q

Infections - pneumonia management

A

ABCDE approach: IV fluids, CPAP etc
Analgesia for chest pain eg paracetamol
Abx - start empirically then guided after cultures
Thromboprophylaxis - risk of venous thromboembolism

Abx for community acquired pneumonia (CAP) (done by CURB-65 score)
Mild (0-1): oral amoxicillin at home
Moderate (2): oral amoxicillin and macrolide (eg clarithromycin), consider hospitalisation
Severe (3+): IV co-amoxiclav and macrolide (eg clarithromycin), consider ITU

Abx for Legionellas
- ciprofloxacin and clarithromycin

47
Q

Interstitial Lung Disease definition

A

Interstitial lung disease (ILD) is an umbrella term used for a group of diseases that cause scarring (fibrosis) of the lungs. Most interstitial lung disease fall into the category of restrictive disease

48
Q

Interstitial Lung Disease aetiology

A

Can be divided into acute or chronic
Acute ILDs
- trauma, infection, drugs (therapeutic and recreational), radiation, aspiration, gas inhalation, paraquat (herbicide) poisoning
- leading to ARDS - adult respiratory distress syndrome

Chronic ILDs

  • idiopathic
  • idiopathic pulmonary fibrosis (IPF)
  • scarring of the lungs -> pulmonary fibrosis -> respiratory failure -> cor pulmonale
  • shows classic ‘honeycombed’ CXR due to fibrosis with inflammatory infiltrate
  • IPF has a median survival of 2-5 yrs from diagnosis
  • previously thought to be inflammatory, now known that drugs targeting inflammation do more harm than good
  • generally presents >60yrs, more common in men
  • autoimmune
  • rheumatoid arthritis ILD, Sjorgens, SLE, polymyositis, dermatomyositis, systemic sclerosis
  • pneumoconiosis - inhalation of something causing lung damage
  • coal worker pneumoconiosis - inhales coal gets taken up by macrophages and congregate in the lungs
  • silicosis - inhaled stone.sand from mining
  • asbestosis - inhaled asbestos irritates lungs
  • extrinsic allergic alveolitis/hypersensitivity pneumonitis (covered in separate table)
  • inflammation driven process
  • Type III hypersensitivity (IgG) and immune complex from causing inflammation in the lungs -> chronic exposure leads to pulmonary fibrosis
  • may also have fever, weight loss etc
  • eg Farmer’s lung, pigeon fanciers lung etc
  • secondary to other disease: TB, pneumonia, sarcoidosis
  • sarcoidosis
  • chronic granulomatous disorder of unknown aetiology affecting the lungs, skin and eyes
  • lungs and mediastinal lymph nodes are most affected
  • bimodal age distribution with 2 peaks in 3rd and 5th decades
  • non-caveating granulomas form due to CD-4 interactions - type 4
  • check serum ACE levels- secreted from nodules

Some ILDs will go on to become progressive fibrosis ILD “Pulmonary Fibrosis” such as idiopathic pulmonary fibrosis but others will not necessarily

49
Q

Interstitial Lung Disease pathophysiology

A

Idiopathic pulmonary fibrosis
- fibroblasts repair damaged tissue
- fibroblasts migrate to the lungs and become myofibroblasts
- myofibroblasts deposit collagen in the extracellular matrix
- IPF these fibroblasts proliferate and form fibroblastic foci
- the thickened tissue leads to lower gas exchange efficiency in the lungs
Histology shows spatial heterogeneity (normal lung tissue next to abnormal tissue)

50
Q

Interstitial Lung Disease clinical manifestations

A

Idiopathic pulmonary fibrosis

  • dyspnoea, cough, crackles
  • weight loss, fatigue, malaise

Sarcoidosis

  • cough, dyspnoea, wheezing, rhonchi
  • lymphadenopathy
  • photophobia, red painful eye, blurred vision
  • arthralgia, chronic fatigue
51
Q

Interstitial Lung Disease investigations

A

Idiopathic pulmonary fibrosis
CXR - generally lungs look smaller
Spirometry - restrictive
TLCO or DLCO - reduced (reduced gas exchange due to thickening of alveolar layer)
HRCT (best imaging) - honeycombing is characteristic, typically affects periphery and base of the lungs, thickened dilated bronchus are seen, often has a ground glass appearance
Exercise testing

Sarcoidosis
CXR - hisar or mediastinal nodal enlargement is most common at presentation, although may present with parenchymal disease only or end stage disease (pulmonary fibrosis)
Serum ACE: often elevated
Calcium: often raised

52
Q

Interstitial Lung Disease complications

A

GORD, pulmonary infections, pulmonary hypertension

Phase 2 Med (9 decks)

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