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106 Cards in this Set

  • Front
  • Back

Normal lung function

Gas exchange
Acid base balance
Barrier to external infection - mucociliary escalator, BALT, alveolar macrophages

Copd features

Bronchiectasis
Chronic bronchitis
Emphysema chronic asthma
Bronchiolitis

Causes of copd

Main cause is smoking
Amospheric pollution or occupational
Respiratory infection
Inherited diseases eg cystic fibrosis alpha 1 antitrypsin deficiency

Acute asthma features

Charcot Leyden crystals
Creola bodies
Smooth muscle hyperlplasia
Thickened BM
Epithelial sloughing
Mucus plugging

Histology of acute asthma

Bronchiectasis

Permanent dilation of bronchioles and bronchi because of chronic and necrotising infections
Tissue destruction
Inflammation

Bronchiectasis

Clinical symptoms of bronchiectasis

Cough
Foul smelling sputum
Fever

Causes of bronchiectasis

Congenital eg CF primary ciliary dyskinesia
Airway obstruction due to foreign body, tumour, mucous impaction
Necrotising pneumonia eg tb staph strep flu aspergillus
Traction - pulmonary fibrosis

Chronic bronchitis definition
Cough productive of sputum for at least 3/12 of the year for the past 2/1

Features of chronic bronchitis

Hypersecretion of mucous
Associated with smoking and infections
Reversible airway obstruction
Bronchiolitis
Acute inflam destruction of the smaller bronchioles
Virus, babies young children usually
GVH disease
Path changes in chronic bronchitis

Goblet cell hyperlplasia causing increased mucous
Hyperlplasia of mucous glands in bronchial sub mucosa
Hypertrophy of bronchial smooth muscle
Inflam and oedema in bronchial muscles
Peri bronchiolar fibrosis

Emphysema definition

Abnormal permanent dilation of the airspace distal to the terminal bronchiole with destruction of their walls but not fibrosis

Emphysema effects

Enlargement of the acinus
Over inflation and distension

Classifications of emphysema

Pan acinar
Centrilobular / centriacinar
Para septal

Alpha 1 antitrypsin deficiency

Normally synthesised in the liver


AD
Means destruction of alveolar walls and connective tissue framework leading to emphysema

What causes chronic pulmonary fibrosis (honeycomb lung)

Idiopathic


Allergic alveolitis


Pneumoconiosis (CWP Asbestosis Silicosis)


Radiation


Drugs (bleomycin)


Connective tissue disorders (RA Sclerodema SLE)


Diffuse malignancy


Wegners Grannulomatosis


Berylliosis


Sarcoid

Restrictive lung disease
Reduced movement
Chronic cough
Shortness of breath
Progresses to respiratory failure

Pathogenesis of restrictive lung disease

Acute and chronic interstitial diseases
Cwp
Asbestosis
Silicosis
Other causes of lung fibrosis
Bone muscle and nerve problems

Fibrosing (intetstitial) lung diseases

Diffuse involvement of connective tissue and bronchiole / alveolar element
Stiffness and decreased compliance

Usual intetstitial pneumonia (idiopathic pulmonary fibrosis)

Ie cryptogenic fibrosing alveolitis
Worse prognosis than lung cancer
Subplural fibrosis

Acute intetstitial pneumonia

ARDS is clinical syndrome
Drug / toxin reactions
Radiation
Diffuse alveolar damage wih development of hyaline membrane disease

Coal miners pneumoconiosis

Nodular fibrosis aggregates of dust laden macrophages and surrounding collagen
Progressive massive fibrosis widespread coalescent fibrous nodules causing scarring with contraction of the lung
?emphasema

Silicosis

Fibrogenic chronic interstitial
Fibrotic nodules with refractile silica around respiratory bronchioles

Diseases caused by asbestosis

Recurrent pleural effusions
Benign pleural plaque formation
Interstitial fibrosis (asbestosis)
Mesothelioma
Carcinoma of the lung

Patholophysiology of asbestosis

Fibres inhaled macrophages can't phagocytose macrophage death follows


Macrophage cytokines and death cause fibrosis


haemosiderin remains

Cor pulmonale

Pul arteriolar vasoconstriction and medial hypertrophy
Raises pul arterial pressure
RV dilation / hypertrophy
RHS failure

Resp failure

Normal drive to breathe is hypercapnia and hypoxia
Late stages there is hypoxaemia which causes pulmonary artery vasoconstriction
Leads to pulmonary hypertension
Structural changes in vessels
RV strain, RV failure, cor pulmonale

Blue bloater

Mismatched vq
Hypoxia cyanosed polycthaemic so blue
Chronically hypercapnic and primary respiratory drive is hypoxia if taken away with O2 treatment this reduces drive and causes respiratory arrest

Pink puffer

High vq
Can maintain O2
Dead space
Working hard due to all muscles working from loss of elasticity
Patients have normal oxygen until tire and decompensate with respiratory failure

Sarcoidosis -


Almost confluent non-caseating granulomas in a lymph node. But TB must be considered

Types of lower resp tract infection
Lobar pneumonia
Bronchopneumonia
Bronchiectasis
Lung abcess
Emphysema
Tb lon
Lobar pneumonia
Classically strep pneumoniae
Congestion to red hepatisation to grey hepatisation to resolution or death
Complications of lobar pneumonia three
Abscess emphysema sepsis
Bronchopneumonia
Patchy inflam in lung around airways
Worse at bases because of gravity
Common in immobile patients who can't cough well with other diseases
Organisms that can cause bronchopneumonia
Staph strep haemophilus pseudomonas
Complications of bronchopneumonia
Abscess emphysema sepsis
Bronchiectasis
Focal destruction of bronchi and bronchioles because of infection leading to dilation
Mechanism of bronchiectasis
Obstruction to mucous flow due to Timor or foreign body
Viscid mucoid preventing drainage eg cf
Ciliary abnormalities eg kartageners syndrome
Commonly pseudomonas
Bronchiectasis outcome
Cannot resolve
Chronic reinfect ion
Scarring
If focal may need to be excised
Complications of bronchiectasis

Abcess
Sepsis
Worsening
Clubbing
Secondary amyloidosis– raised inflammatory markers can cause deposits

Lung abscess
Focal destructive infection of lung are chums surrounded by fibrous capsule
Mechanisms of lung abscess
Apiration of infected material
Following pneumonia etc
Septic emboli
Direct trauma
Lung abscess effects
Scarring, may need drainage
Lung abcess complications
Sepsis
Clubbing
Secondary amyloidosis
Empyema
Focal pyogenic infection of pleural space
Becomes compartmentalised
Tb behaviour

Behaves like a cancer
Destructive mass lesions
Spreads by lymphatic to local lymph nodes
Disseminates in the bloodstream
Can reappear years after treatment in the same or distant sites

Reactivated tb

Often affects lung apices
Causes caseating necrosis and cavitation
Bleeding may cause haemoptysis
Cough with haemoptysis described as consumption

Miliary tb
Spread through bloodstream
Kidneys meninges bone and any other site
In inmunocompromised pattern can be unusual with early dissemination
Primary tb
Bronchopneumonia
Spreads to Hilar lymph nodes leaving scar and enlarged scarred node (gohn complex)
Infection usually controlled
Asthma prevalence
0.5–3% of UK population
More common in children but more severe in adults
Clinical presentation of asthma
Rapid onset of difficulty in expiration with wheezing
Reduced peak flow
Asthma improved by
Steroids
Beta two agonists
Anticholinergics
Others
Types of asthma

Defined by trigger
Extrinsic eg environmental occupational

Intrinsic
We don't know trigger
More common in adults

Cause of rapid asthma onset
Type one sensitivity
Sudden release of histamine from mast cells and other mediators
Both can be activated by non specific factors eg cold
Pathology of asthma
Smooth muscle contraction
Oedema and inflam exudate
Excess mucus secretion
Long term consequences of asthma
Overdistension of lung
Focal lung collapse
Bronchiectasis
Infection aspergillus etc
Causes of pulmonary embolism
Usually thrombus
Fat – bone marrow from fracture
Amniotic fluid during parturition
Injected material eg drugs
Risk factors include immobility, surgery, hypercoagulability, contracteptive pill, underlying malignancy, pelvic mass with obstruction of venous return
Causes of dvt
Trauma, inflam
Innate or acquired increased clotting
Reduced flow
Commonest cause due to immobility of muscle pump
Genetic predisposition to clotting usually also
Predisposing conditions to dvt
Surgery
Obesity
Pro coagulant States eg
Oestrogenic drugs
Hyperviscosity
Malignancy
Auto antibodies
Inherited
Presentation of DVT
Acute painful swelling of calf or whole leg
Superficial veins may be distended
Skin red and warm as blood gets round obstruction
Pitting oedema
Swollen painful leg could be
Dvt
Cellulitis
Ruptured bakers cyst synovial due to arthritis of the knee

Obese elderly can be predisposed to all three
Pelvic thrombus caused by
Tumours
Inflam
Surgery

Effects of pulmonary thromboembolism depend on

Size
Large saddle embolus causes death
Multiple small causes pulmonary hypertension
Medium sized embolus causes wedge shaped infarct

Clinical presentation of thromboembolis

Large – collapse breathlessness death
Intermediate – pleuritic chest pain tachypnea cyanosis haemoptysis
Small – may be a symptomatic may be pleuritic pain
Paradoxical embolus
Misses lungs and enters systemic circulation via shunt eg septal defect
May cause stroke limb or bowel ischaemia etc

Amniotic fluid embolus

Fluid contains everything that falls off foetus
Lodges in small vessels
Causes diffuse intravascular coagulation, shock, death
Fat embolus
Follows major trauma
Lodges in small vessels
90% of major trauma
No allergic response
Causes symptoms only when massive

Pulmonary oedema effects

Causes dyspnoea
May be severe enough to teach upper airways– frothing
Haemodynamic causes of pulmonary oedema
Lhs failure
Mitral stenosis
Volume overload
Pulmonary vein obstruction
Lymphatic obstruction
Decreased oncotic pressure eg low albumin nephrotic syndrome liver disease protein losing enteropathies
Micro vascular injury causes of pulmonary oedema

Inhaling noxious gases
Smoke, oxygen 100%
Infections especially viruses and mycoplasma
Aspiration
Near drowning – water pops cells
Drugs
Radiation
Shock – not enough oxygen

Shock lung – ARDS
Diffuse damage to alveolar wall capillaries and epithelium
Membrane of inflam exudate, dead cells
Lungs become firm and lose elasticity
Severe impairment of gas transfer, refractory to oxygen therapy
Causes of ARDS
Same as cause PE but more severe
Hypoxic patient on ventilator
May follow shock
Often associated with damage to other organs eg renal failure by same cause
Primary hypertension

Idiopathic
Children or young women
Progressive rhs failure
Death if not treated
May need heart or lung transplant
Intimal thickening (?) as result of high pressure in lungs

Secondary hypertension

Chronic
Loss of capillaries
Hypoxia causes vasoconstriction
Recurrent pulmonary embolism – ends with multiple lumens
Lhs failure increased filling pressure

Lung transplant consideration
Hypertensive heart due to hard lung may be too much for new lung, so may need lung and heart transfer

What usually worsens asthma? what usually worsens COPD?

Allergen
Infection
Cause of blackened lymph nodes in the lung
Uptake of anthracotic pigment by macrophages (carbon from polluted air)
Seen in older people and smokers

Yellowish lung lobe

Consolidation due to infection eg secondary to tumour

Why small cell carcinoma of the lung so dangerous

Metastasises early (as do many lung cancers), often widely disseminated before the primary lung tumour is diagnosed.
Squamous cell carcinoma metastasises quite late.

Definition of pneumonia
Acute or chronic inflammation of the alveoli
Non infection causes of pneumonia (6)
Neoplasia
Sarcoid
Amyloid
Vascullitis
Drugs
radiotherapy
Chronic pneumonia and six causes
Pneumonic illness >1/52
Associated cxr changes
Causes
Tb
Mycobacterium
Nocardia
Fungi
Protozoa
Worms
Aspiration pneumonia
Elderly or altered consciousness at risk
Much of damage immediate and due to acid
Infection may follow a few days later
Atypical pneumonia
Fails to respond to usual antibiotics
Bacteriology fails to provide diagnosis
Mycoplasma pneumoniae
Chlamydiaophila
Ventilator associated pneumonia
Ventilated patient >48h/ intubation
Epidemiology of cap
50+
1/100 /1
Mid winter or spring
60–90% have underlying disease
20% require hospital
5–10% mortality
Rfs for death are age severe inter current illness recent anaesthetic smoker heart failure hiv copd
Causes of cap
Viral bacterial fungi
Strep pneumoniae is most common cause, is a commensal
Certain organisms peak in epidemic years
Some from environment eg legionella or animals eg chlamydiophilla psittaci
How can bacteria get into lungs
From upper airways, exogenous or already colonising
Less commonly via haematogenous spread
Commensal s pneumoniae
Can invade if we acquire new epithelial serotypes
Flu can cause activation, strep will bind more to receptors
Signs of pneumonia
Fever
Low bp
Increased resporatory rate
Tachycardia
Cobsolidation / effusion

Severe
Exhaustion
Cyanosis
Use of accessory muscles
Effusion vs consolidation
Effusion compresses lung
Consolidation is an infiltration of the lung
Parapneumonic effusion
Exudative phase – pleural inflam generates fluid
Fibropurulent stage – fibrin deposition, organisms invade
Pleural glucose and ph fall
Look up final stage

Investigations for pneumonia

FBC
u&e
Crp
Lft
Abg if unwell
Cxr
Ct in recurrent, those unresponsive to treatment or sometimes in Inmunocompromised early
Microbiological investigations
Blood cultures, not often positive but very useful
Serology useful in outbreak situation
Antigen testing
Pleural fluid sampling
Sputum
Bal
Sputum samples
Not a good means of diagnosing pneumonia because bugs come through mouth
Only six percent produce sputum
Half of cultures are negative
Useful when non–commensal bacteria are being considered
Cold agglutinins
Lung biopsy rare useful for immunocompromised patients
In all severe pneumonia patients check
Pneumococcal antigen blood sputum urine
Legionella antigen .. Others
Management of pneumonia
Early antibiotics
Switch to oral at 48h if doing well
Longer for legionella gram negative or staph aureus
Guide to drugs in notes
3–5/365 for mild generally oral route
1–2/52 in severe or longer for invasive staph
If fail to respond to antibiotics
Older may take longer as may multilobe involvement or pre exiting lung disease
Consider resistant organisms
Complications
Empayema
Sepsis
Abcess
Ards
Metastatic infection
Rarely neurological sequelae
Bronchiectasis (less common in antibiotic era)
Hospital acquired pneumonia
>48h after admission
Risk factors age immobility coexisting illness sepsis dysphasia reduced consciousness instrumentation etc
Bugs of HAP
Staph aureus
Chlamydia trachomatis
Pneumocystis jerovecii (commonest opportunistic infection in hiv patients)
History of atypical
Cxr worse than signs suggest
Usually lower loves
Mild urti followed by pneumonia
Legionella colonises what

Water piping systems

Pott's disease

Collapse of the spine due to TB infection