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Medicine 2 > Respiratory medicine > Flashcards

Respiratory medicine Flashcards

1
Q

What is pleuritis
How is it commonly diagnosed
Main symptom

A

Inflammation of pleura
Pleural rub can be hears
Chest pain whenever you breath or cough

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2
Q

Role of central chemoreceptors

A

Detect changes in pCO2 via changes in [H+] from carbonic acid

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3
Q

Role of peripheral chemoreceptors ; where are they found?

A

In the aortic arch and carotid arteries
Involved mainly in detecting changes in pO2 ; cause hyperventilation when pO2 falls

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4
Q

The medulla comprise of two groups of nerves ; name them

A
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5
Q

Describe Cheyne-stokes breathing

A

Type of abnormal breathing

Characterised by crescendo-decrescendo pattern of tidal volume followed by a period of apnea

often seen in patients with congestive heart failure

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6
Q

Role of the DRG

A

Innervate the diaphragm and external ICM

Switches them on and off to cause a rhythmic breathing pattern

diaphragm contraction causes inspiration

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7
Q

Role of VRG

A

Involved in forced expiration
Innervate abdominal muscles and internal ICM

therefore involved during forced expiration

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8
Q

Describe the role of the pneumotaxic centre, state its location

A

Location is pons
Fine tunes breathing by sending inhibitory impulses to the DRG
Limits inspiration to prevent over inflation

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9
Q

Role of vagus nerve in respiration

A

Sends afferent information from there lungs to the DRG
Role is to prevent over inflation by switching off inspiration

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10
Q

Sputum colours and what they indicate

A

Grey/green indicates elevated WBC but not always

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11
Q

Causes of cough

A

Common cold
Tracheitis - painful cough due to viral infection
COPD
Pneumonia
Bronchitis
Bronchiectasis - enlarged air ways and excess mucus (can be due to CF)
TB
Congestive heart failure - plus breathlessness and oedema of ankles
Cancer
Anxiety (Nervous cough )

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12
Q

How do you differentiate between smokers cough and COPD cough ?

A

Smokers with persistent cough (>3 weeks)
History of smoking associated with haemoptysis (coughing up of blood)
Change in cough

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13
Q

Auscultation of lungs in COPD sufferer

Compare healthy and abnormal breathing

What is a polyphonic wheeze

A

Small pause between insipiration and expiration in healthy breathing

Patients with COPD have prolonged expiration (2-3 times as long than inspiration)

Polyphonic wheeze - varied freq common in COPD

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14
Q

What is a monophonic wheeze

A

Monophonic wheeze may indicate tumour in one lung

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15
Q

Use of spirometer in COPD

A

Confirm diagnosis - not used as first step
Tells us severity of airways obstruction
Identify those most at risk

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16
Q

How to diagnose between COPD or ephysema

A

COPD - chronic bronchitis and some emphysema

Emphysema - some chronic bronchitis

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17
Q

How to diagnose between COPD or ephysema

A

COPD - chronic bronchitis and some emphysema

Emphysema - some chronic bronchitis

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18
Q

Difference between obstructive and restrictive lung diseases

A

In obstructive low FEV1:FVC

In restrictive , both FEV1 and FVC are low so ratio unaffected

Low FEV1 in both

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19
Q

Why might Hb increase in COPD sufferers

A

Due to polycythaemia due to adaptation of body to prolonged hypoxia (bc impaired lung function )

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20
Q

Can beta blockers be prescribed to patients with COPD and hypertension

A

Yes as long as spirometer test rules out asthma

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21
Q

Location of central chemoreceptors

A

Medulla

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22
Q

explain respiratory acidosis

A

impaired lung function due to COPD/pneumonia/asthma/MG/muscle dystrophy can lead to CO2 accumulation and respiratory acidosis - kidneys respond by excreting [H+] and reabsorbing [HCO3-]

characterised by increased PaCO2 (arterial partial pressure of CO2)

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23
Q

pCO2, pO2 and pH are all ventilation stimuli

place them in order of importance

A

pCO2

pH

pO2

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24
Q

fucntion of neural regulation of ventilation

A

Sets the rhythm and pattern of ventilation

controls respiratory muscles

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25
Q

What is respiratory depression ?

how is it reversed ?

A

Occurs when the rate and/or depth of respiration is insufficient to maintain adequate gas exchange in the lungs

reverse by analeptics

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26
Q

Describe the role of the apneustic centre

A

Responsible for prolonged insipiratory gasps via prolonged DRG stimulation (apneusis) this is observed during severe brain injUrey

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27
Q

what is a sign an asthma attack is severe when you listen to the chest

A

Silent chest

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28
Q

How does pO2 and pCO2 change during an asthma attack

A

pO2 increase and pCO2 decreases at first due to hyperventilation

but as airways continue constricting, pCO2 increases and pO2 decreases as gas exchange does not work anymore

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29
Q

Should you give oxygen to a patient with long term chronic lung disease

A

No because their body has adapted to hypoxia

they will stop breathing if you give them oxygen

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30
Q

Healthy pO2 and pCO2

A

Healthy pCO2 4.5–6.0 kPa

healthy pO2 >10 kPa

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31
Q

Clinical presentation of COPD

A

Exercise tolerance reduced

hyper expanded chest

expiratory wheeze bilaterally

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32
Q

COPD spirometry

A

FEV1/FVC ratio reduced

little/no reversibility post inhaler

low FEV1

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33
Q

Type 1 and type 2 respiratory failure

A

type 1 - lungs unable to cope because of disease ; pCO2 goes down later

type 2 - chronically low pO2, dependent on hypoxic conditions,

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34
Q

Case 5: A 65 year old man presents with gradual onset breathlessness and dry cough which has worsened over 9 months. He previously smoked 10/day. On examination he is short of breath on mild exertion, clubbed and mildly cyanosed, with fine inspiratory crackles at both bases.

A)COPD

B)Left ventricular failure

C)Bronchiectasis

D)Pulmonary fibrosis

E)Lung cancer

A

D

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35
Q

what is pulmonary consolidation

A

presence of exudate in alveoli due to inflammation (seen as white on x-ray)

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36
Q

Most common pathogens causing CAP (COMMUNITY ACQUIRED PNEUMONIA)

A

S.pneumoniae

H.influenzae

both bacteria

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37
Q

what are the atypical bacteria causing CAP (COMMUNITY ACQUIRED PNEUMONIA)

A

M.pneumoniae (has no cell wall) ; extra-pulmonary features

L.pneumophila - accompanied by diarrhoea

both cause severe cases of CAP

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38
Q

Microbiological investigations for CAP

A

Sputum analysis / culture

immunofluorescence on sputum samples

blood cultures

urine sample - test for pneumococcal and legionella antigen

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39
Q

What factors indicate a high risk CAP patient

A

Confusion

Urea >7mmol/l

Respiratory rate >30 per min

Blood pressure : systolic BP >90mmHg

65 or older

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40
Q

S.pneumoniae typically infect 2 lobes

true or false

A

False ; typically infects 1 lobe only

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41
Q

what is bronchial breathing

A

it is abnormal if hear in the parts of the lung that are far from main airways

loud and tubular quality

high pitched

inspiration and expiration last the same amount of time (insipiration normally lasts longer)

definited gap between both phases; caused by asthma, bronchitis, bronchiectasis

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42
Q

What is asthma

A

Reversible increase in airway constriction
Bronchoconstriction and inflammation are the main features
Reversible decrease in FEV1:FVC

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43
Q

Describe COPD - symptoms , causes, clinical features

A

involves chronic bronchitis and emphysema (Destroyed alveoli )

can cause coughing up mucus, wheezing, shortness of breath, chest tightness

Clinical features : FEV1 reduced and little variation in PEF

caused by long-term exposure to lung irritants

44
Q

parasympathetic and sympathetic control of bronchial calibre

A

In parasympathetic control, ACh actors on muscarinic M3 receptors = bronchoconstriction and increased mucus

In sympathetic control, adrenaline acts of B2-adrenoreceptors = relaxation

45
Q

What provokes asthmatic attacks

A

Allergens
Cold air
Viral infections (colds)
Smoking
Exercise

46
Q

Characteristic features of asthma attacks

A

Wheezing
Breathlessness
Tight chest
Cough (worse at night in children/exercise)
Decreases in FEV1 that can be reversed by a β2-agonist

acute phase(caused by spasmogens) followed by late phase (caused by chemotaxins) ; late phase is more severe

Spasmogens and chemotaxins released by mast cells and mononuclear cells

47
Q

What are spasmogens

A

They cause bronchoconstriction - acute phase of asthma attack

derivants of arachidonic acid formed from membrane lipids

Main examples :

histamine, prostaglandin D2

leukotrienes (C4 & D4)

platelet activating factor (PAF)

48
Q

What are chemotaxins

A

Chemicals involved in late phase of asthma attack

Leukotriene B4, PAF(also a spasmogen)

attract leukocytes (eosinophils and mononuclear cells)

Cause inflammation and airway hyper-reactivity

49
Q

Describe the uses of short term and long-term β2-agonists and the problems with them

A

Short term: reverses asthma attack immediately by causing bronchodilation

long-acting beta agonists (LABA) given for long term prevention and overnight control

problems : receptor down-regulation (reduced expression of receptors and therefore less sensitivity to drug)

50
Q

What are xanthines

A

Bronchodilators but not as effective as beta2-adrenoceptors agonists

used in emergency

Have other effects :

adenosine receptor antagonist (increase HR/BP)

phosphodiesterase inhibitors

51
Q

Describe the use of muscarinic M-receptor antagonists *

A

Block parasympathetic bronchoconstriction

used to treat COPD , little value in asthma

52
Q

Anti-inflammatory agents used for asthma - describe their use and mode of action

A

Used as preventation , not reversal of an attack

corticosteroids

They work by activating intracellular receptors = altered gene transcription = decrease cytokine production = anti-inflammatory

53
Q

Describe action of corticosteroids

A

takes days for action

lipocortin/annexin A1 (secondary messenger) inhibits PLA2 enzyme = less leukotriene/prostaglandin

given with β2-agonists

54
Q

Describe action of leukotriene receptor antagonist *

A

Preventative and bronchodilator

antagonise action of leukotrienes (inflammatory mediators)

55
Q

Asthma treatment guidelines

A

If salbutamol used >2 times :

increase dose or check if technique is correct, give spacer device to help with delivery of drug, ensure bronchodilator is given before steroid

56
Q

How is COPD treated ?

A

stop smoking

vaccinations

β2agonists and long acting anti muscarinic

antibiotics for intercurrent infections

57
Q

NSAIDs and asthma

A

NSAIDs may provoke asthma in 15% of sufferers by increasing leukotriene production

58
Q

Describe the use of steroids as an asthma treatment

A

Given with beta2 agonists to reduce receptor down-regulation (long term effect of beta2 agonists)

side effects - throat infections and hoarsenses

59
Q

Type 1 hypersensitivity

What are the clinical effects

A

Characterised by damage to self material in response to recognition of foreign material
Mainly involves :
IgE mediated activation of mast cells - smooth muscle contraction and leaky capillaries

Clinical effects : hay fever, asthma, eczema, anaphylaxis

60
Q

Describe type II hypersensitivity
And give examples

A

IgG and IgM bind to antigen on body cells
Body cells directly attacked by antibodies via action of complement system , NK cells and macrophages

Examples :

Haemolytic disease of the newborne ( due to difference in blood type)
Allergic haemolytic anaemia

61
Q

Describe type III allergy /autoimmunity
Give 3 examples

A

Antigen form a complex with IgG which accumulate in joints, glomeruli and blood vessels
Results in activation of complement system
Tissue inflammation and destruction

Examples : rheumatoid arthritis, poststreptococcal glomerulonephritis

62
Q

Describe type IV allergy Give examples

A

Caused by cell mediated immunity

Involves TH1 cells

late response (takes days )

Examples : transplant rejection and contact dermatitis

63
Q

What is vital capacity

A

Max lung capacity (forced inhale/exhale)

64
Q

What is the functional residual capacity

A

Amount of air that remains in the lungs at the end of normal expiration

65
Q

Compare restrictive and obstructive deficits

A

Restrictive - reduced capacity of lungs ; lowered FVC but normal FEV1 ; increased/normal FEV1:FVC

examples : scoliosis and pulmonary fibrosis

obstructive - restriction in airways ; FVC Normal but reduced FEV1 ; low FEV1:FVC

examples : COPD

66
Q

What is FVC and FEV1?

A

Forced vital capacity (FVC) is the amount of air that can be forcibly exhaled from your lungs

The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath

67
Q

Predict the approximate effect (if any) that restrictive/obstructive deficits would have on:

  • Total lung capacity (TLC)
  • Functional residual capacity (FRC)
  • Residual volume (RV)
A

In restrictive ventilatory deficit (e.g. pulmonary fibrosis), TLC will decrease FRC will decrease and RV will remain unchanged.

In obstructive ventilatory deficit (e.g. severe asthma), TLC will remain unchanged FRC will decrease RV will decrease.

68
Q

List three factors that would decrease gas transfer

A

low Hb (anaemia)

Thickening of alveolar epithelium due to scarring of lung tissue

Decreased pulmonary capillary blood volume

69
Q

What is atelectasis

A

Collapse of lungs

70
Q

Name the examples vascular pulmonary disease

A
  • Pulmonary Hypertension
  • Pulmonary Embolism, Haemorrhage and Infarction
71
Q

Name examples of pleural disease

A

Pleurisy
Fluid/air in pleural cavity
Cancer

72
Q

Describe pneumonia

A

Inflammatory reaction of the alveoli and interstium (CT) of lung due to infectious pathogen
Symptoms : pus in alveolar space , inflammation of alveolar septa

73
Q

Explain the difference between bronchitis and pneumonia

A

Bronchitis is an invasive infection of the bronchi (chronic bronchitis due to prolonged exposure to irritants)

Pneumonia is due to an infection in the alveoli

74
Q

Causative organisms of pneumonia

A

Gram +ve and -ve bacteria
Virusus
Mycoplasma
Fungi
Inorganic agents (inhaled dust or gases)

75
Q

Causative organisms of pneumonia

A

Gram +ve and -ve bacteria
Virusus
Mycoplasma
Fungi
Inorganic agents (inhaled dust or gases)

76
Q

Describe the anatomical classification of pneumonia

A

Lobar pneumonia (organisms spread between alveoli)

Bronchopneumonia : spread from bronchi to alveoli ; starts off in one lobe and eventually spreads to whole lobe

77
Q

Describe the different types of pneumonia and their typical causative agent

A

Community acquired:
(Acute) Typical: S pneumoniae is most common cause.

Hospital acquired called Nosocomial

Immuno-compromised patient: S pneumoniae is responsible again

Aspiration pneumonia - occurs when gastric contents/saliva is breathed into the lungs

Chronic pneumonia - common in patients with COPD/lung cancer/immunocompromised/bronchiectasis

Necrotizing pneumonia and lung abscess - uncommon, severe complication of pneumonia ; occurs when infected lung commpresses alveolar capillaries - lung ischaemia

78
Q

Aspiration pneumonia

A

occurs when the gastric contents inter the trachea due to abnormal gag reflex e.g stroke/excessive drinking/brain injury/general anaesthesia

pneumonia follows due to irritation from acidic gastric contents and bacteria

symptoms : unconsciousness, repeated vomiting or underlying brain disease (typically MS), coughing up green/bloody phlegm

often necrotising/results in abcess formation

79
Q

Symptoms and treatment of acute bacterial pneumonia

A

Symptoms : fever, chill, dyspnoea (shortness of breath) , cough with pus-phlegm , crackles on ausculatiation, confirmation With x-ray

antibitoitic treatment

80
Q

Possible outcomes of pneumonia

A

Resolution (recovery)

organization (scarr tissue formation)

abscess formation

empyema (pockets of pus that have collected inside a body cavity)

81
Q

TB is a form of …

A

Chronic pneumonia

82
Q

Describe TB - symptoms and treatment

A

Localised lesion of granulomatous inflammation (called a Ghon focus)

symptoms : gradual decrease in appetite, weight loss, fever, night sweats, chest pain, prolonged cough with sputum production

slender robes under sputum analysis, identifiied by acid fast stain

83
Q

Describe the pathogenesis of TB

A

In first 3 weeks:

Inhaled mycobacteria engulfed by macrophages
Defective phagolysosome formation
Mycobacterial proliferation in macrophages
Mild flu symptoms/ asymptomatic

Cell mediated immune response

Macrophages drain to lymph nodes
Antigens presented to T cells
T cells converted to Th1 cells
Th1 cells activate macrophages (gamma IFN)
Monocytes recruited
Hypersensitivity of host

84
Q

What is miliary TB

A

Occurs upon rexposure of the mycobacterium tuberculosis

Cavitation - TB erodes into lung vasculature and then can spread to any organ via the pulmonary vein (most commonly liver,kidney and spleen)

85
Q

What is metastatic TB

A

Invasion of brain, kidneys, adrenal glands by mycobacterium tuberculosis

Often latent infection

86
Q

Describe the course of infection in primary and secondary TB

A

Primary TB :

  • Primary lesion is subpleural caseous granuloma: Ghon focus
  • When ghon focus spreads to lymph nodes on hilum and ghon focus begins being broken down via caseating necrosis: Ghon complex
  • Heals by fibrous encapsulation.
  • Latent TB in tubercle
  • Resistance of organism and hypersensitivity of host. Few symptoms

Secondary TB :

  • due to reactivation of old lesions/gradual progression of primary TB/reinfection
  • extensive tissue damage due to inflammatory response
  • caseation erodes into bronchial wall or vessel – live microbes in sputum
    • Tuberculous bronchopneumonia
  • Vessel: miliary or isolated organ
  • immunocompromised patients can go straight to secondary TB
87
Q

Compare restrictive and obstructive pulmonary diseases

A

Obstructive disease

Limitation of airflow due to obstruction

Airway narrowing (asthma), loss of elasticity (emphysema) or increased secretions (bronchitis/asthma)

Restrictive disease

Restrict normal lung movement during respiration

Reduced expansion of lung tissue due to fibrosis/chest wall disorders

damage to lungs impairs gaseous exchange leading to hypoxia

Decreased total lung capacity

88
Q

Describe chronic bronchitis

A

Hyper-secretion of mucus in large airways or small airways

defined clinically (persistent cough at least 3 consecutive months )

t cells macropahges and neutrophils present

remodelling of airway wall narrows lumen : increased mucus secreting glands/goblet cells/oedematous mucosa and bronchial wall fibrosis

89
Q

Describe the types of emphysema

A

Centriacinar (CA) or centrilobular

Dilated respiratory bronchioles

Most common

More common in upper lobes

Smoking related

Panacinar (PA) or panlobular

Dilated alveoli

More common in lower lobes

Hereditary

90
Q

Features of emphysema of a histological slide

A

Enlarged alveolar spaces

91
Q

Presentation and causes of emphysema

A

Caused by:

Smoking (99%)

Inherited emphysema - α1 anti-trypsin deficiency (protease inhibitor) (1%)

Presentation:

Shortness of breath and prolonged expiration

barrel chest due to use of accessory muscles

Prolonged onset >40 years

Congenital α1 anti-trypsin deficiency will present earlier

Often co-presents with chronic bronchitis - cough and excess mucus production

pursed lips breathing to maintain airway

92
Q

Mechanism of smoking related emphysema

A

Lung protected against protealytic enzymes (from inflammatoray cells) by anti-protease enzyme

anti-protease production affected by :

inherited deficiency

smoking stimulates realease of proteases = uncontrolled proteolysis of elastic tisssue

smoking also causes oxidative injury - tissue damage and inactivation of antiproteases

93
Q

Pneumoconioses

A

group of fibrosing diseases caused by silica and asbestos

develops over decades even after exposure is stopped

characterised by lesions of particulate laden macrophages and dense collagen (fibrosis)

silicosis and asbestosis associated with increased risk of cancer

94
Q

causes/symptoms of pleural efffusion

A

exudate (pus) from pneumonia and cancer

congestive heart failure, kidney disease (fluid overload)/liver disease

symptoms: dyspnea , sharp chest pain when breathing deeply, fever, cough

95
Q

Bronchiectasis - what is it, causes/symptoms

A

Permanent dilation of main bronchi and bronchioles from contraction of scar tissue = build up of excess fluid = lungs more vulnerable to infection (as music more likely to stagnate)

damage to epithelium causes bleeding (heamoptysis)

causes: recurrent infection, bronchial obstruction(due to CF/immunodeficiency/immotile cilia syndrome) or lung fibrosis

symptoms : persistent cough, dyspnoea, foul-smelling sputum, digital clubbing

96
Q

give examples of restrictive disorders if airway and gaseous exchange

A

Acute ARDS

pulmonary fibroses - scarring of airways due to pollutanuts, medicine or CT disease

pneumoconioses such as asbestosis and silicosis

granulomatous disease - genetic condition where phagocytes malfunction

97
Q

What is a tubercule ?

A

enlarged clump of macrophages and lymphocytes

fibroblasts on the outside

central region undergoes caseous necrosis to form a soft tubercule

may later calcify (shows up on x-ray)

98
Q

Describe emphysema

A

Irreversible obstructive disease

occurs in terminal bronchioles

dilation of bronchioles and alveoli / destruction of elastic tissue

decreased SA for gaseous exchange

99
Q

Describe lung fibrosis

A

Inflammation of alveolar walls - activation of macrophages stimulate fibroblasts

Damaged to pneumocytes = proliferation of type II pneumocytes

fibroblasts lay down collagen - decrease lung expansion

100
Q

pleural pathologies - describe characteristics and clinical signs

A

Infection - sharp pain on breathing deeply, dry coughing/sneezing sound

effusion - transudate(excess normal fluid) / exudate (pus)

tumour - pleural effusion can be due to local tumour/metastasis via lymphatics

101
Q

Infections of the kidneys result in progressive damage ti. The kidneys and impaired renal functions ; this results in

A

Metabolic acidosis

102
Q

Equation for alveolar ventilation rate (L/min)

A

Alveolar ventilation rate = (tidal volume - dead space) x respiratory rate

103
Q

What is consolidation caused by

A

fluid accumulation in the alveolar airspaces

pus, blood, malignant cells, lymphatic fluid

104
Q

Identify the conditions and suggest the possible causes

A

Right pleural effusion

infection , trauma, malignancy, CHF

105
Q

Identify the condition

A

left tension pneumothorax

left side of thorax is more visible compared to the right

lack of lung marking extending to the periphery

trachea and heart borders also shifted to the right

106
Q

Identify the condition

A

rounded area of increased density behind the heart = lung mass on the left side behind the heart

density of heart should be the same throughout but it is more dense on the left than right

107
Q

describe metabolic acidosis

A

due to decreased HCO3- (shift eqm to the right); characterised by low blood pH and hyperventilation ; causes - diabetes, lactic acid production during shock, renal impairment, severe diarrhoea, acid ingestion

Medicine 2 (14 decks)

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