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Medicine Phase 2A (OWN) > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Definition of chronic bronchitis

A

Inflammation of bronchial tubules, with a productive cough for 3/12 for at least 2 years

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2
Q

Give 3 risk factors for chronic bronchitis

A

Air pollutants
Dust and silica
Genetic factors

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3
Q

Which ratio is particularly low in chronic bronchitis?

A

FEV1 to FVC ratio

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4
Q

How is the total lung capacity usually affected in chronic bronchitis and why?

A

High due to air trapping

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5
Q

What type of cells line the airways?

A

Ciliated pseudostratified columnar epithelial cells- with goblet cells

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6
Q

Give the two layers that make up the lamina propria

A

Basement membrane and loose connective tissue

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7
Q

Give the two layers of the submucosa

A

Smooth muscle and connective tissue

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8
Q

How is mucous made and secreted?

A

Made by goblet cells, secreted by bronchial mucinous glands

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9
Q

How does exposure to irritants and chemicals affect the cilia?

A

They become shorter and less mobile which makes it more difficult for them to move mucous

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10
Q

How does exposure to irritants and chemicals affect the bronchial mucinous glands and goblet cells?

A

Hypertrophy and hyperplasia

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11
Q

What is the Reid Index and what value indicated chronic bronchitis

A

Thickness of glands/ thickness of wall

chronic bronchitis >40%

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12
Q

Give 5 Signs and Symptoms of chronic bronchitis

A 
Wheeze
Crackles (rales)
Hypoxemia 
Hypercapnia 
Cyanosis
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13
Q

How can pulmonary HTN occur as a result of COPD? What does this eventually lead to?

A

Blood vessels vasoconstrictor in areas with decreased gas exchange to shunt blood
In chronic bronchitis, this is a large proportion of the lung
Increases pulmonary vascular resistance
Increased work from R side of heart leads to right sided heart failure (Cor-Pulmonale)

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14
Q

How would you treat chronic bronchitis?

A 
Reduce risk factors
Manage associated illnesses
Supplemental oxygen
Medication:
Bronchodilators 
Inhaled steroids
Antibiotics
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15
Q

Give examples of the following which could be used for COPD:
Bronchodilators
Inhaled steroids

A

Salbutamol, salmeterol (Beta-2 agonists)
Ipratropium, tiotropium (anticholinergics)
Beclomethasone dipropionate

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16
Q

How does smoking lead to emphysema?

A

It causes an inflammatory reaction which leads to the release of immune cells and the release of proteases (elastase and collagenases) which break down structural proteins in the connective tissue layer of the alveoli

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17
Q

Use Bernoulli’s principle to explain why the airways collapse during exhalation in a patient with emphysema

A

Fluid moves at a higher velocity with a lower pressure
Low pressure pulls airways inwards
Since there is a loss of elastin, airways can no longer withstand this pressure during exhalation

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18
Q

How does a loss of elastin affect compliance in emphysema?

A

Increased compliance, therefore inhalation causes easy expansion and the lungs hold on to air rather than expelling it during exhalation

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19
Q

How does a loss of elastin affect area available for gas exchange in emphysema?

A

Reduced SA available for gas exchange since a loss of elastin leads to a breakdown of alveolar septa and therefore neighbouring alveoli form larger air spaces

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20
Q

Describe the characteristics of centriacinar emphysema

A

Most common
Seen with cigarette smoking
Damages proximal alveoli
Typically affects upper lobe of lungs

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21
Q

Describe the characteristics of panacinar emphysema

A

Associated with alpha-1 antitrypsin deficiency
Entire acinus affected equally
Typically affects lower lobes of the lungs

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22
Q

What is the usual purpose of alpha-1 antitrypsin and why can a deficiency lead to emphysema?

A

It is a protease inhibitor which protects against unintended damage
Deficiency means no inhibition and therefore damaged air sacs

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23
Q

Describe the characteristics of paraseptal emphysema

A

Affects distal alveoli
Affects peripheral lung tissue near interlobular septa
Ballooned alveoli can rupture and cause a pneumothorax

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24
Q

Give 5 symptoms of emphysema

A 
Dyspnoea 
Exhaling slowly through pursed lips (increases airway pressure and prevents collapse)
Weight loss
Hypoxaemia
Cough with some sputum
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25
Q

Give a visible sign of emphysema

A

Air trapping and hyperinflation (‘Barrel chest’)

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26
Q

Give three signs you may see on a CXR in emphysema

A

Increased anterior-posterior diameter
Flattened diaphragm
Increased lung-field lucency

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27
Q

Give the three conditions in the atopic triad

A

Asthma
Atopic dermatitis
Allergic rhinitis

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28
Q

In allergic asthma, how is the allergen initially recognised by the body?

A

Allergen is picked up by dendritic cells and presented to T2 helper cells

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29
Q

Which cytokines are released by T2 helper cells in allergic asthma and what response do they induce?

A

IL-4: Production of IgE antibodies which trigger mast cells, mast cells then go on to release histamine, leukotrienes and prostaglandins
IL-5: Production of eosinophils which release more cytokines and leukotrienes

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30
Q

At which point does allergic asthma become irreversible?

A

Signs of oedema, scarring, fibrosis

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31
Q

Describe the hygiene hypothesis

A

Reduced early exposure to bacteria/ viruses alters the proportion of immune cells

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32
Q

Give 4 symptoms of asthma

A

Dyspnoea
Chest tightness
Wheezing
Coughing with sputum

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33
Q

How might asthma be classified?

A

Frequency of symptoms
Measure amount of obstruction (FEV1 and PEFR)
Frequency of medication use

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34
Q

Which medications may be used in the treatment of asthma?

A

Bronchodilators: SABAs, anticholinergics
Severe- Daily corticosteroids, LABA, leukotriene antagonists
Very severe- IV corticosteroids, magnesium sulfate, oxygen therapy

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35
Q

What percentage of lung cancer cases are small cell and non- small cell?

A

Small cell- 15%

Non-small cell- 85%

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36
Q

Describe the characteristics of small cell lung cancer

A

Tumour grows proximally close to the hylum
Involved neuro-endocrine cells in the area
Endocrine cells involved undergo mutation and produce hormones
Paraneoplastic syndrome

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37
Q

Describe the characteristics of adenocarcinoma

A

Most common non-small cell lung cancer
Tumour grows in peripheral lung tissue
Involves glands within the lung

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38
Q

Describe the characteristics of squamous cell carcinoma

A

Tumour grows close to the main bronchus
Obstruction of airway
Cells lining airway mutate from columnar cuboidal to squamous

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39
Q

Describe the characteristics of large cell carcinoma

A

Can present in peripheral or proximal lung tissue

Fast growing

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40
Q

Give 5 signs and symptoms of lung cancer

A 
Cough
weight-loss
Haemoptysis
Dyspnoea
Chest pain
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41
Q

Give 5 risk factors for lung cancer

A 
Smoking
Radon
Air pollution
Asbestos
Nickel
Arsenic
Family/ genetic factors
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42
Q

Describe the affects of pancoast tumour involvement in lung cancer

A

Tumour growth on apical lung surface can block part of the brachial plexus:
Shoulder/ arm pain
Weakness of ipsilateral side
Horner’s syndrome

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43
Q

Give three examples of mediastinal involvement in lung cancer

A

Pleural effusion- chest pain and dyspnoea
Pericardial effusion
Obstruction of SVC- blocks flow

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44
Q

How does the stimulation of angiogenesis in lung cancer cause problems?

A

Leaky and tortuous vessels form and these may rupture causing haemoptysis

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45
Q

Give 4 examples of blood involvement in lung cancer

A

Anaemia
Leukocytosis
Thrombocytosis
Hypercoaguable disorders

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46
Q

Give the common sites of metastases in lung cancer

A

Brian, liver, adrenal glands and bone

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47
Q

Define paraneoplastic syndrome and give which lung cancers it typically occurs with

A 
Syndromes that occur not related to:
Invasion
Obstruction
Metastasis of the primary tumour
-Typically small cell lung cancer and squamous cell carcinoma
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48
Q

Describe ectopic Cushing’s syndrome (Paraneoplastic)

A

Hormone released by tumour stimulates the adrenal glands to release cortisol
Increase in ADH increases water retention
Increase in PTH, breaks down bone and releases calcium into plasma- hypercalcaemia

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49
Q

Describe hypertrophic osteoarthropathy

A

Clubbing- fluid collecting in soft tissues at the end of fingers
Periosteal proliferation of the tubular bone

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50
Q

Give 5 common clinical findings on a chest x ray in lung cancer

A 
Hilal enlargement
Pulmonary opacity
Rib bone lesions
Pleural effusion
Lung collapse
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51
Q

How might lung cancer be managed?

A

Surgery- removal of tumour for stage I and II
Radiotherapy
Chemotherapy- Radio/ Chemo combination for stage III
Laser therapy and stenting- to manage airway obstruction causing serious symptoms

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52
Q

Describe primary haemostasis

A

Platelets adhere and activate by collagen and tissue factor

Platelets recruit more and form a plug

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53
Q

Describe secondary haemostasis

A

Clotting factors made by the liver are cleaved and this activates fibrinogen to fibrin
Fibrin polymerises and deposits to form a mesh around the platelets forming a hard clot

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54
Q

How is fibrin broken down and what is the product?

A

Broken down by plasmin and produces D dimers

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55
Q

How might a clot in the heart progress if an atrial septal defect is present?

A

Goes from right to left atrium and bypasses the lungs, clot is pumped out often to the brain
Embolic stroke

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56
Q

Give the three components of Virchow’s Triad

A

Stasis: platelets and clotting factors contact the endothelium
Hyper-coagulation: altered amounts of clotting factors
Damage: Infections, chronic inflammation

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57
Q

How can a pulmonary embolism lead to R sided heart failure?

A

PE increases vascular resistance as the heart must exert more pressure to move blood past obstructed arteries

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58
Q

How would you diagnose a PE?

A

CT angiogram
V/Q scan
D-dimer blood test

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59
Q

How would you treat a pulmonary embolism?

A 
Thrombolytic enzymes 
Pulmonary thrombectomy 
Long term:
Anticoagulant medications: Warfarin, heparin
Compression stockings
Calf exercises
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60
Q

Give 3 features of TB that make it resistant

A

Can resist weak disinfectants
Survives on dry surfaces
Waxy cell wall- from mycelia acid

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61
Q

What does “acid fast” mean and how is it tested for?

A

Can hold on to dye despite alcohol exposure

Bright red when Ziehl-Neelsen stain is used

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62
Q

How does TB survive despite phagocytosis by a macrophage?

A

It produces a toxin which inhibits lysosome-phagosome fusion and proliferates

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63
Q

What is the difference between the following: Ghon focus, Ghon complex, Ranke complex

A

Ghon focus is a small area of granulomatous inflammation
Ghon complex is when adjacent lymph nodes are involves/ infected
Ranke complex is when there is calcification

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64
Q

If there is reactivation of the Ghon complex in TB, where does the infection usually spread to and why?

A

Upper lobes of the lung as they are best oxygenated

65
Q

When TB disseminates which systems can it affect and how?

A

Lungs- bronchopneumonia
Kidneys- sterile pyuria (WBC in urine)
Brain- meningitis
Lumbar vertebrae- Pott disease
Adrenal glands- Addison’s disease (adrenal insufficiency)
Liver- hepatitis
Cervical lymph nodes- lymphadenitis in the neck (scrofula)

66
Q

How is TB tested for?

A

Purified protein derivative (PPD)- Intradermal skin test (Mantoux skin prick)
Tuberculin- component of TB injected, if previously exposed there will be an immune reaction
Interferon gamma release assay- evidence in blood

67
Q

Give 5 signs and symptoms of TB

A 
Fever
Night sweats
Weight loss
Haemoptysis
Fatigue
68
Q

Give the treatment for latent TB

A

Isoniazid for 9 months

69
Q

Give the treatment for active TB

A

Isoniazid and rifampicin for 6 months

Pyrazinamide and ethambutol for the first 2 months

70
Q

Give 3 bacterial causes of typical pneumonia

A

Streptococcus pneumoniae
Haemophilus Influenzae
Staph Aureus

71
Q

Give 3 bacterial causes of atypical pneumonia

A

Mycoplasma pneumonia
Chlamydophilia pneumoniae
Leigonella pneumoniae

72
Q

Give an example of a fungal cause of pneumonia

A

Histoplasmosis

Blastomycosis

73
Q

How is aspiration pneumonia acquired?

A

Gag reflex can be compromised by:
Drug/ alcohol abuse
Brain injury
Swallowing issues

74
Q

Define lobar pneumonia

A

Complete consolidation of whole lung lobe

Mostly caused by S. pneumoniae

75
Q

Give the stages of lobar pneumonia

A

Congestion- blood vessels and alveoli fill with fluid
Red hepatization- exudate (neutrophils, RBCs and fibrin) fill airspaces
Grey hepatization- colour change, RBCs in exudate break down
Resolution- exudate digested by enzymes

76
Q

Give 4 symptoms of pneumonia

A 
Dyspnoea
Chest pain
Productive cough
Fatigue
Fever
77
Q

Describe a typical CXR for the following:
Bronchopneumonia
Lobar pneumonia
Atypical pneumonia

A
  • Patchy areas spread throughout
  • Fluid localised to a single lobe
  • Concentrated in perihilar region
78
Q

Describe the difference between type I and type II pneumocytes

A

Type I- squamous cells, nearly continuous layer

Type II- cubes with microvilli, secreting surfactant which prevents alveolar collapse

79
Q

Describe the process of pulmonary fibrosis after the alveolar lining is damaged

A

Type I pneumocytes release transforming growth factor beta-1
This causes the type II pneumocytes to stimulate fibroblasts to proliferate and develop into myofibroblasts
Therefore too much collagen is produced, thickening the interstitial layer

80
Q

Give 3 risk factors for pulmonary fibrosis

A

Old age
Being male
Tobacco smoking

81
Q

Give 3 ways in which interstitial lung disease affects lung function

A

Decrease in total lung capacity
Decrease in forced vital capacity
Decrease in forced expiratory volume

82
Q

Give 4 signs and symptoms of pulmonary fibrosis

A

Coughing
SOB
Cyanosis
Digital clubbing

83
Q

Give two indicators of pulmonary fibrosis on a CT scan

A

“Honeycombing” and thickening of interstitial walls

84
Q

Give 3 possible treatments for pulmonary fibrosis

A

Supplemental oxygen
Antifibrotic medication
Lung transplant

85
Q

Define sarcoidosis

A

T-cell accumulation in organs, forming granulomas

86
Q

Give 5 systemic symptoms of sarcoidosis

A 
Fatigue
Weakness
Aching muscles
Swollen lymph nodes
Lack of appetite
Weight loss
87
Q

Give 4 respiratory symptoms of sarcoidosis

A

SOB
Dry cough
Wheezing
Suffocation

88
Q

Give 3 symptoms of sarcoidosis affecting the eyes

A

Blurred vision
Tearing
Photophobia

89
Q

How would sarcoidosis be diagnosed?

A

CXR- looking for granulomas
Blood test- looking for hyercalcaemia and raised ACE
Biopsy- lung tissue/ skin/ lymph nodes

90
Q

Define bronchiectasis

A

A disease in which there is permanent enlargement of parts of the airways

91
Q

What type of genetic disorder is cystic fibrosis?

A

Autosomal recessive

92
Q

Which gene in affected in cystic fibrosis

A

Cystic fibrosis transmembrane conductance regulator (CFTR gene)

93
Q

What is the purpose of the CFTR protein?

A

It pumps chloride ions into secretions, drawing water with them to thin the secretions

94
Q

How does the mutation affect the CFTR protein?

A

It is misfiled and so cannot migrate from the ER to the cell membrane

95
Q

What is the risk in newborns with cystic fibrosis?

A

If the meconium is thick and sticky it can get stuck in the intestines, this is called a meconium ileus and is a surgical emergency

96
Q

What happens if thick secretions block the pancreatic ducts in cystic fibrosis?

A

Pancreatic enzymes don’t reach the small intestine
Proteins/ fat are therefore not absorbed which leads to:
Poor weight gain
Failure to thrive
Steatorrhea (fat containing stools)

97
Q

What happens if pancreatic enzymes back grade to cells lining pancreatic ducts in cystic fibrosis?

A

Self-digestion leading to acute/ chronic pancreatitis and the development of cysts and fibrosis
This can cause insulin dependent diabetes

98
Q

How does cystic fibrosis cause lung problems?

A

Thick mucous and defective mucociliary action leads to the colonisation of bacteria in the lung
Increased bacterial load can lead to a cough, fever and CXR changes

99
Q

Give some possible consequences of chronic bacterial infection and inflammation in CF

A

Bronchiectasis- wall damage and permanent dilation of bronchi
If inflammation erodes into a blood vessel this can cause haemoptysis

100
Q

What is the risk of repeated CF exacerbations?

A

Respiratory failure

101
Q

How is cystic fibrosis diagnosed?

A

Newborn screening detects pancreatic enzyme released into blood when pancreas is damaged (IRT-immunoreactive trypsinogen)

102
Q

How is cystic fibrosis treated?

A 
Fat-soluble vitamins
Extra calories
Replacement pancreatic enzymes
Chest physio
Inhalers
N-acetylcysteine- mucolytic
Lung transplant 
Lumacaftor- brings protein to cell membrane
Genetic treatment
103
Q

Give 3 ways in which excess fluid builds up in the pleural space

A

Transudative- too much leaves the capillaries due to an increase in hydrostatic or decrease in oncotic pressure
Exudative- Inflammation of pulmonary capillaries (so more leaky)
Too little fluid drained- lymphatic effusion

104
Q

Describe how a change in hydrostatic pressure can lead to pleural effusion

A

Heart failure leads to a back up of blood into the pulmonary vessels, increasing the pressure and forcing fluid into the pleural space

105
Q

Describe how a change in oncotic pressure can lead to pleural effusion

A

Cirrhosis or nephrotic syndrome can lead to a drop in oncotic pressure

106
Q

Give 4 causes of exudative pleural effusion

A

Malignancy
Inflammatory conditions such as lupus
Trauma
Infection such as pneumonia

107
Q

Give 2 causes of lymphatic effusion

A

Damage to the thoracic duct during surgery

Tumours

108
Q

Give a characteristic of pleural effusion pain

A

Worse when lying down

109
Q

How would pleural effusion be diagnosed?

A

Decrease in breath sounds
Dullness to percussion
Decrease in tactile fremitus
(If large effusion there may be decrease in aeration and trachial deviation)
In a standing X ray- fluid displaces air and there is a blurred costophrenic angle

110
Q

After removal via thoracentesis how would different types of pleural effusion fluid appear?

A

Transudative fluid is clear
Exudative fluid is cloudy- full of immune cells
Lymphatic fluid is milky- full of fats

111
Q

What is the light criteria to determine whether fluid is exudative?

A

Fluid protein: serum protein > 0.5
Fluid LDH: serum LDH > 0.6
Fluid LDH > 2/3 normal upper limit of serum LDH
If fluid cholesterol level is > 45mg/dL

112
Q

How would you treat a small pleural effusion from heart failure?

A

Diuretics

Sodium restriction

113
Q

How would you treat a large pleural effusion from lung cancer?

A

Draining with a tube

114
Q

Describe a pneumothorax and presenting symptoms

A 
Abnormal collection of air in the pleural space
Symptoms:
Chest pain
SOB
Tiredness
115
Q

How does a tension pneumothorax occur?

A

One way valve formed by an area of damaged tissue
More air enters but none can escape
There is an oxygen shortage and low blood pressure

116
Q

How does the body compensate when a tension pneumothorax occurs?

A

Increases respiratory rate

Increases tidal volume

117
Q

How would you treat a pneumothorax?

A

Conservative
Needle aspiration
Chest tube
Pleurodesis

118
Q

Give 3 ways in which pulmonary hypertension can occur

A

L sided heart failure or valvular dysfunction leading to a backup of blood in the pulmonary veins
Chronic lung disease leading to vasoconstriction in an attempt to shunt blood away from damaged areas
Chronic thromboembolic pulmonary HTN due to recurrent blood clots in pulmonary vessels increasing vascular resistance

119
Q

Give 3 congenital heart defects as causes of pulmonary HTN

A

Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus

120
Q

Give 4 examples of disorders which could lead to pulmonary HTN

A

Lupus
Infections like HIV
Thyroid disorders
Inherited genetic mutations

121
Q

How do connective tissue disorders such as Lupus/ thyroid disorders lead to pulmonary HTN?

A

They cause damage to endothelial cells lining pulmonary arteries, this releases chemicals such as endothelin-1, serotonin and thromboxane which cause pulmonary arteriole constriction and hypertrophy of the smooth muscle

122
Q

Give 3 consequences of R sided heart failure when blood backs up into the venous system

A

Increased jugular venous pressure
Fluid build up in the liver- hepatomegaly
Fluid build up in the legs-oedema

123
Q

How would pulmonary HTN be diagnosed?

A

Echocardiogram showing an increased pressure in pulmonary arteries and R ventricle
Follow up tests to identify underlying cause

124
Q

How would you treat pulmonary HTN?

A

Supplemental oxygen
Cause dependent:
If cariogenic- meds that boost heart performance and lower BP
If pulmonary arterial HTN- Endothelin receptor agonists and prostacyclins (dilate pulmonary arterioles and inhibit smooth muscle hypertrophy)

125
Q

Give 5 symptoms of a mesothelioma

A 
Dyspnoea
Swollen abdomen
Chest wall pain
Fatigue
Weight loss
126
Q

Give 3 risk factors for mesothelioma

A

Asbestos exposure
Genetics
Infection with simian virus 40

127
Q

How would you diagnose a mesothelioma?

A

CXR and CT

Confirmed by examining fluid produced by cancer/ tissue biopsy

128
Q

How would you treat a mesothelioma?

A

Surgery
Radiation therapy
Chemotherapy- cisplatin and pemetrexed
Pleurodesis

129
Q

Describe Goodpasture syndrome

A

An autoimmune disease i which antibodies attack the basement membrane (specifically alpha-3 subunit of type IV collagen) in the lungs and kidneys leading to failure

130
Q

Give 4 systemic symptoms of Goodpasture syndrome

A

Malaise
Weight loss
Fatigue
Fever

131
Q

Give 4 lung symptoms of Goodpasture syndrome

A

Haemoptysis
Chest pain
Cough
Dyspnoea

132
Q

Give 5 kidney symptoms of Goodpasture syndrome

A 
Haematuria
Proteinuria
Oedema
Increased urea in the blood
HTN
133
Q

How would you diagnose Goodpasture syndrome?

A

Biopsy to look for anti-GBM antibodies (anti-glomerular basement membrane)

134
Q

How would you treat Goodpasture syndrome?

A

Plasmapheresis

Immunosuppressant drugs- Cyclophosphamide, prednisone and retuximab

135
Q

Describe Wegner’s syndrome

A

Systemic autoimmune disorder that involves granulomatosis and polyangitis

136
Q

Give 5 signs and symptoms of Wegner’s syndrome

A 
Lungs- primary nodules, infiltrates, pulmonary haemorrhage: haemoptysis
Kidney- glomerulonephritis 
Nose- pain, nosebleeds
Ears- conductive hearing loss
Eyes- scleritis
137
Q

Which antibodies are responsible for the inflammation in Wegner’s syndrome?

A

Anti-neutrophil cytoplasmic antibodies (ANCAs)

138
Q

How would you treat Wegner’s syndrome?

A

Immunosuppressants- Rituximab, cyclophosphamide and high dose corticosteroids
Plasma exchange
Kidney transplant

139
Q

Give 5 symptoms of influenza

A 
Fever
Cough
Nasal congestion
Hoarseness
Throat pain
140
Q

Describe the differences between influenza A, B and C

A

A- natural hosts are wild aquatic birds, can cause pandemics in humans, most virulent human pathogens
B- Almost exclusively infects humans, degree of immunity acquired due to lack of genetic diversity
C- sometimes causes sever illness/ local epidemics, less common

141
Q

Why should children and teenagers avoid taking aspirin during an influenza infection

A

It can lead to Reye’s syndrome which is a rapidly progressive encephalopathy

142
Q

Describe hypersensitivity pneumonitis

A

Inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts

143
Q

Give 3 symptoms for each of acute, subacute and chronic hypersensitivity pneumonitis

A

Acute- fever, chills, malaise, cough, chest tightness, SOB
Subacute-SOB, fatigue, productive cough, weight loss, pleurisy
Chronic-cough, progressive SOB, fatigue, weight loss, clubbing, tachypnoea, respiratory distress, inspiratory crackles

144
Q

What type of sensitivity is hypersensitivity pneumonitis

A

III and IV

145
Q

Give 5 signs and symptoms of laryngitis

A 
Dry/ painful throat
Cough
Increased saliva production
Dysphagia
Globus pharyngeus 
Swollen lymph nodes
146
Q

Give examples of the 4 causes of laryngitis

A

Trauma- damage to vocal folds (iatrogenic)
Fungal- histoplasma, blastomyces
Bacterial-group A strep, strep pneumoniae
Viral- rhinovirus, influenza, adenovirus

147
Q

Give 3 causes of chronic laryngitis

A

Allergies
Autoimmune
Irritation of vocal folds due to reflux

148
Q

How would you diagnose laryngitis?

A 
Laryngoscopy:
Erythema 
Oedema
Dilated vessels (acute)
Stiff vocal folds
149
Q

How would you treat acute laryngitis?

A

Trauma- vocal hygiene
Viral- analgesia, rest, mucolytics
Bacterial- Abx
Fungal- antifungals

150
Q

How would you treat chronic laryngitis?

A

Granulomatous- systemic corticosteroids
Reflux- antacids, PPI, behavioural changes
Inflammatory- topical nasal steroids, immunotherapy, antihistamines
Autoimmune- cyclophosphamide, prednisolone

151
Q

Give 5 signs and symptoms of tonsillitis

A 
Sore throat
Red, swollen tonsils
Pain on swallowing
Fever
Headache
152
Q

Give 5 viral causes of tonsillitis

A 
Adenovirus
Rhinovirus
Influenza
Coronavirus
Respiratory syncytial virus
153
Q

Give the main bacterial cause of tonsillitis

A

Group A beta-haemolytic strep: strep throat

154
Q

Give the treatment for tonsillitis

A

Analgesia

If bacterial: Abx- penicillin or amoxicillin

155
Q

Give 3 symptoms of sinusitis

A

Headache/ facial pain
Thick nasal discharge
Localised headache/ toothache that is worsened by tilting the head forward and with valsalva manoeuvres

156
Q

Give 5 possible complications of sinusitis

A 
Orbital cellulitis
Osteomyelitis of facial bones
Middle ear problems
Abscesses 
Meningitis
157
Q

How can sinusitis be classified?

A

Acute <4 weeks
Recurrent >4 episodes in a year
Subacute <12 weeks
Chronic >12 weeks

By location:
Maxillary
Frontal
Ethmoidal
Sphenoidal
158
Q

Give potential causes of sinusitis

A

Dental origin
Precipitated by an earlier upper resp tract infection: rhinoviruses, coronaviruses and influenza viruses
Bacterial- strep. pneumoniae, haemophilus influenzae

Medicine Phase 2A (OWN) (10 decks)

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