Week 7: Respiratory Flashcards

1
Q

Restrictive Lung disease

A

-Reduction in lung volume due to a pathology in the lungs, pleura, or surrounding strcutures

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2
Q

Causes of Restrictive Lung disease

A

** PAINT**
P Pleural Pathologies
A Alveolar Pathologies
I Interstitial Pathologies
N Neuromuscular Patholgies
T Thoracic cage abnormalities

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3
Q

Intrinsic vs extrinsic causes of Restricitve lung disease

A

Intrinsic: Intersitial, alveolar, diffuse cellular infiltrates
Extrinsic: Low Resp muscle tone, chest wall defomities, space occupying

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4
Q

Symptoms of Restrictive Lung disease

A

Dyspnoea: reduced lung compliance = increased work of breathing
Cough: Increased interstitial lung tissues stiffness triggers reflex
Malaise: Chronic hypoxia
Muscle weakness: Prolonged hypoxia and Resp muscle overuse

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5
Q

Sings of RLD

A

Reduced chest expansion
Tachypnoea
Decreased breath sounds upon auscultation
Inspiratory crackles (due to fibrosis)
Cyanosis

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6
Q

RLD Ventilation and perfusion

A

Impaired Ventilation: Stiff, less compliant lung tissue restricts lung expansion, decreasing total lung capacity and tidal volume.
Gas Exchange Issues: Thickened alveolar-capillary membrane slows oxygen diffusion, causing hypoxemia, especially during physical exertion.
Perfusion: Lung perfusion may remain normal or increase, but uneven ventilation worsens hypoxemia.
Dyspnea: Patients experience increased shortness of breath, particularly during activities that raise oxygen demands.

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7
Q

RLD: V/Q mismatch

A

Mismatch Impact: Areas of the lung receive inadequate oxygen, leading to hypoxemia.
Hypoxic Vasoconstriction: Alveolar hypoxia causes pulmonary arteriolar constriction, diverting blood flow from poorly ventilated areas.
Long-term Effects: Chronic hypoxemia can lead to pulmonary hypertension and right heart strain.
RLD Feature: V/Q mismatch is a hallmark of restrictive lung diseases, affecting gas exchange and oxygen delivery.

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8
Q

hypoxaemia

A

Low oxygen in blood

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9
Q

Interstitial Lung disease (ILD)

A
  • Effects the tissues between the capilary endothelium and alveolar endothelium
  • can progress to pulmonary fibrosis
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10
Q

Classifications of ILD

A
  • Inorganic exposure: non organic substances eg asbestos or silica dust
  • Organic exposure:
  • Smoking
  • Rare forms of ILD: eg LAM or vasculitis
  • Idiopathic: unknown cause
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11
Q

How does asbestos cause ILD

A

inhalation of asbestos fibres, resulting in lung scarring and impaired respiratory function.

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12
Q

Mesothelioma

A

A rare and aggressive cancer that primarily affects the lining of the lungs, abdomen, or heart, and is strongly associated with asbestos exposure.

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13
Q

Diagnosing RLD

A

Chest X-Ray: reduced lung volume, flattened diaphragm, other abnormailites
Spirometry: decreased TLC, VC, FVC
aterial blood gas: reduced PaO2, normal or low PaCO2

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14
Q

Management of RLD

A
  • Minimise exposure
  • Steroids: to reduce inflammation
  • Lung transplantation
  • Pulmonary rehab, eduction + Resp muscle conditioning
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15
Q

Management of RLD

A
  • Minimise exposure
  • Steroids: to reduce inflammation
  • Lung transplantation
  • Pulmonary rehab, eduction + Resp muscle conditioning
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16
Q

Management of RLD

A
  • Minimise exposure
  • Steroids: to reduce inflammation
  • Lung transplantation
  • Pulmonary rehab, eduction + Resp muscle conditioning
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17
Q

Mucous Layer as a Immune Defence

A

Traps pathogens and/or foreign particles; expels them via the muco-ciliary escalator

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18
Q

Epithelium as a resp immune defence

A

Contains goblet cells that secrete mucous; creates a physical barrier

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19
Q

Lamina Propria as resp immune defence

A

Contains immune cells (e.g., macrophages, dendritic cells)

20
Q

Type I Pneumocytes role in immune defence

A

Physical barrier between the lung and the airway

21
Q

Type II Pneumocytes role in immune defence

A

Secrete surfactant to protect the lung against collapse and/or infection

22
Q

Compromised resp immunity causes

A

Defective mucous Inability for the lung to trap/remove pathogens (e.g., in cystic fibrosis)
Dysfunctional cilia E.g., dysfunction caused by smoking or drug use
Immune cell defects

23
Q

Process of Acute Pulmonary Inflamation

A

Recognition, Innate Immunity, Adaptive Immunity, Repair phase

24
Q

Process of Acute Pulmonary Inflamation - Recognition

A

Innate immune cells detect threats using pattern recognition receptors, such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), which identify pathogen- associated molecular patterns (PAMPs) from pathogens and damage-associated molecular patterns (DAMPs) from damaged or dying cells.

25
Q

Process of Acute Pulmonary Inflamation - Innate Immunity

A

Activated macrophages, ILCs, and dendritic cells release cytokines that induce vasodilation and recruit additional immune cells to the site of inflammation.

26
Q

Process of Acute Pulmonary Inflamation - Adaptive

A

Antigen-presenting cells activate T cells, with CD8+ T cells executing targeted cell killing and CD4+ T cells assisting B cells in producing specific antibodies for
enhanced pathogen clearance.

27
Q

Process of Acute Pulmonary Inflamation - Repair Phase

A

Damaged tissue is cleaned by macrophages and fluid is resorbed by lymphatics, while TGF-beta-induced fibrosis and type II pneumocyte proliferation restore the
alveolar lining and repair tissue integrity.

28
Q

Chronic Pulmonary inflamation steps

A
  1. Recognition Cells persistantly dectect and respond to stimuli, leading to continous activation
  2. Resolution release of anti inflmatory mediators and removal of inflamatory cells to counteract Inflmation
  3. Remodelling Persistant inflmation leads to tissuse remodelling, chronic famage results in structural chnages and fibrosis as the tissuse atempts to repair and adpat
29
Q

Granuloma

A

an organised collection of macrophages that have transformed into epithelioid cells, forming a compact cluster
Typically found in chronic inflamatory conditions such as Tb, serve as a structual attmept to contain and isolate persistant pathogens or irritants

30
Q

Alveoli Inflmation changes

A

Inflammation impairs gas exchange, causing symptoms like shortness of breath and hypoxemia.

31
Q

Bronchi Inflamation changes

A

Inflammation leads to swelling and mucus production, resulting in cough, wheezing, and difficulty breathing.

32
Q

Interstitium inflamation changes

A

Inflammation reduces lung compliance and gas exchange, causing chronic dry cough and progressive dyspnoea.

33
Q

Parenchyma

A

Inflammation affects overall lung function, leading to decreased lung volumes and symptoms such as fatigue and exercise intolerance.

34
Q

Cold (URTI) Management

A

Antivirals - used in high risk patients
Antibiotics - only indicated in cases of secondary bacterial infection (0.5-2.0% of cases)

35
Q

Complications of Pharyngitis

A
  1. Peritonsillar abscess - pus near tonsils cuasing pains and difficulty swallowing
  2. Deep Neck space infection - afffects breathing and swallowing
  3. Rheumatic fever - caused by strepcoc A
  4. Glomerulonephritis - Caused by Streptoccocal, blood in urine and high BP
    5.** Scarlett fever** - also strep
36
Q

Management of Pharyngitis

A
  1. Assess for life threatening features - Check for airway obstruction, deep neck space infection, sepsis
  2. Antibiotics - used if bacterial cuases suspected, hugh risk Rheumatic fever, severe symptoms, not improving after 7 days, or immunosupressed
  3. Tonsillectomy Consider for recurrent significant pharyngitis; refer if ≥7 episodes/year, ≥5 episodes/year for 2 years, or ≥3 episodes/year for 3 years.
37
Q

Laryngitis

A

Symptoms: Voice Hoarsness and other
almost always caused by virus, but alsp vocal strain or excessive coughing

38
Q

Epiglottitis

signs, symptoms

A

Signs and Symptoms:
1. Fever
2. Resp Distress
3. Stridor
4. Neck Hyperextension
5. Tripod position
NB: it is a life threatening airway obstrcution

39
Q

Epiglottitis Management

A
  1. Secure airway - Prioritise airway management; only do with specialist involvement
  2. Limit Intervention - Avoid procedures that could worsen the condition before expert help is available.
  3. Antibitoic therpay - Give IV antibiotics (3rd generation cephalosporin), with steroids if necessary.
40
Q

Acute Otitis Media (AOM)

A

What is it:
presence of fluid in the middle ear along with acute inflammation, often associated with dysfunction of the Eustachian tube (pharyngotympanic tube).
Symptoms:
typically include ear pain, hearing loss, fever, and lethargy, and ear discharge may occur if the tympanic membrane ruptures.

41
Q

Acute Otitis Media (AOM) Complications

A
  1. Otitis Media with Effusion (OME) - Persistant fluid in middle ear, can lead to hearing loss
  2. Chronic Suppurative Otitis Media (CSOM). - Long term ear infection
  3. Mastoiditis - spread of infection to mastoid air cells, cuases erythema, swelling and pain
42
Q

Signs and Symptoms of Lung Cancer

A

Lung Cancer Specific
* New or changed cough
* Chest/shoulder pain
* Hoarse voice
* Loss of weight or appetite
* Recurrent/persistent chest infection
* Lymphadenopathy
* Haemoptysis
General Cancer
* Fatigue, weight loss, night sweats

43
Q

Investigations to do for lung cancer

A

Blood tests
* CBE
* Electrolytes
* Calcium
* Liver function tests
* Albumin
* Lactate dehydrogenase
Imaging
* Chest X-ray
* CT chest
* PET scan

44
Q

Purpose of Imaging in cancer

A
  • To identify the primary tumour
  • To identify spread to regional lymph nodes
  • To identify spread to distant organs (metastasis)
45
Q

PET Imaging

A

Positron emission tomography
* Injection of a tracer that is then imaged
* Functional imaging based on the glucose activity of tissue
* metabolic activity of tumour/Lymph nodes/metastasis