Respiratory Flashcards

(158 cards)

1
Q

Definition of chronic bronchitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give 3 risk factors for chronic bronchitis

A

Air pollutants
Dust and silica
Genetic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which ratio is particularly low in chronic bronchitis?

A

FEV1 to FVC ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

High due to air trapping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of cells line the airways?

A

Ciliated pseudostratified columnar epithelial cells- with goblet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give the two layers that make up the lamina propria

A

Basement membrane and loose connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give the two layers of the submucosa

A

Smooth muscle and connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is mucous made and secreted?

A

Made by goblet cells, secreted by bronchial mucinous glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Hypertrophy and hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the Reid Index and what value indicated chronic bronchitis

A

Thickness of glands/ thickness of wall

chronic bronchitis >40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give 5 Signs and Symptoms of chronic bronchitis

A
Wheeze
Crackles (rales)
Hypoxemia 
Hypercapnia 
Cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How would you treat chronic bronchitis?

A
Reduce risk factors
Manage associated illnesses
Supplemental oxygen
Medication:
Bronchodilators 
Inhaled steroids
Antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the characteristics of centriacinar emphysema

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Give a visible sign of emphysema
Air trapping and hyperinflation ('Barrel chest')
26
Give three signs you may see on a CXR in emphysema
Increased anterior-posterior diameter Flattened diaphragm Increased lung-field lucency
27
Give the three conditions in the atopic triad
Asthma Atopic dermatitis Allergic rhinitis
28
In allergic asthma, how is the allergen initially recognised by the body?
Allergen is picked up by dendritic cells and presented to T2 helper cells
29
Which cytokines are released by T2 helper cells in allergic asthma and what response do they induce?
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
30
At which point does allergic asthma become irreversible?
Signs of oedema, scarring, fibrosis
31
Describe the hygiene hypothesis
Reduced early exposure to bacteria/ viruses alters the proportion of immune cells
32
Give 4 symptoms of asthma
Dyspnoea Chest tightness Wheezing Coughing with sputum
33
How might asthma be classified?
Frequency of symptoms Measure amount of obstruction (FEV1 and PEFR) Frequency of medication use
34
Which medications may be used in the treatment of asthma?
Bronchodilators: SABAs, anticholinergics Severe- Daily corticosteroids, LABA, leukotriene antagonists Very severe- IV corticosteroids, magnesium sulfate, oxygen therapy
35
What percentage of lung cancer cases are small cell and non- small cell?
Small cell- 15% | Non-small cell- 85%
36
Describe the characteristics of small cell lung cancer
Tumour grows proximally close to the hylum Involved neuro-endocrine cells in the area Endocrine cells involved undergo mutation and produce hormones Paraneoplastic syndrome
37
Describe the characteristics of adenocarcinoma
Most common non-small cell lung cancer Tumour grows in peripheral lung tissue Involves glands within the lung
38
Describe the characteristics of squamous cell carcinoma
Tumour grows close to the main bronchus Obstruction of airway Cells lining airway mutate from columnar cuboidal to squamous
39
Describe the characteristics of large cell carcinoma
Can present in peripheral or proximal lung tissue | Fast growing
40
Give 5 signs and symptoms of lung cancer
``` Cough weight-loss Haemoptysis Dyspnoea Chest pain ```
41
Give 5 risk factors for lung cancer
``` Smoking Radon Air pollution Asbestos Nickel Arsenic Family/ genetic factors ```
42
Describe the affects of pancoast tumour involvement in lung cancer
Tumour growth on apical lung surface can block part of the brachial plexus: Shoulder/ arm pain Weakness of ipsilateral side Horner's syndrome
43
Give three examples of mediastinal involvement in lung cancer
Pleural effusion- chest pain and dyspnoea Pericardial effusion Obstruction of SVC- blocks flow
44
How does the stimulation of angiogenesis in lung cancer cause problems?
Leaky and tortuous vessels form and these may rupture causing haemoptysis
45
Give 4 examples of blood involvement in lung cancer
Anaemia Leukocytosis Thrombocytosis Hypercoaguable disorders
46
Give the common sites of metastases in lung cancer
Brian, liver, adrenal glands and bone
47
Define paraneoplastic syndrome and give which lung cancers it typically occurs with
``` Syndromes that occur not related to: Invasion Obstruction Metastasis of the primary tumour -Typically small cell lung cancer and squamous cell carcinoma ```
48
Describe ectopic Cushing's syndrome (Paraneoplastic)
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
49
Describe hypertrophic osteoarthropathy
Clubbing- fluid collecting in soft tissues at the end of fingers Periosteal proliferation of the tubular bone
50
Give 5 common clinical findings on a chest x ray in lung cancer
``` Hilal enlargement Pulmonary opacity Rib bone lesions Pleural effusion Lung collapse ```
51
How might lung cancer be managed?
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
52
Describe primary haemostasis
Platelets adhere and activate by collagen and tissue factor | Platelets recruit more and form a plug
53
Describe secondary haemostasis
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
54
How is fibrin broken down and what is the product?
Broken down by plasmin and produces D dimers
55
How might a clot in the heart progress if an atrial septal defect is present?
Goes from right to left atrium and bypasses the lungs, clot is pumped out often to the brain Embolic stroke
56
Give the three components of Virchow's Triad
Stasis: platelets and clotting factors contact the endothelium Hyper-coagulation: altered amounts of clotting factors Damage: Infections, chronic inflammation
57
How can a pulmonary embolism lead to R sided heart failure?
PE increases vascular resistance as the heart must exert more pressure to move blood past obstructed arteries
58
How would you diagnose a PE?
CT angiogram V/Q scan D-dimer blood test
59
How would you treat a pulmonary embolism?
``` Thrombolytic enzymes Pulmonary thrombectomy Long term: Anticoagulant medications: Warfarin, heparin Compression stockings Calf exercises ```
60
Give 3 features of TB that make it resistant
Can resist weak disinfectants Survives on dry surfaces Waxy cell wall- from mycelia acid
61
What does "acid fast" mean and how is it tested for?
Can hold on to dye despite alcohol exposure | Bright red when Ziehl-Neelsen stain is used
62
How does TB survive despite phagocytosis by a macrophage?
It produces a toxin which inhibits lysosome-phagosome fusion and proliferates
63
What is the difference between the following: Ghon focus, Ghon complex, Ranke complex
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
64
If there is reactivation of the Ghon complex in TB, where does the infection usually spread to and why?
Upper lobes of the lung as they are best oxygenated
65
When TB disseminates which systems can it affect and how?
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
How is TB tested for?
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
Give 5 signs and symptoms of TB
``` Fever Night sweats Weight loss Haemoptysis Fatigue ```
68
Give the treatment for latent TB
Isoniazid for 9 months
69
Give the treatment for active TB
Isoniazid and rifampicin for 6 months | Pyrazinamide and ethambutol for the first 2 months
70
Give 3 bacterial causes of typical pneumonia
Streptococcus pneumoniae Haemophilus Influenzae Staph Aureus
71
Give 3 bacterial causes of atypical pneumonia
Mycoplasma pneumonia Chlamydophilia pneumoniae Leigonella pneumoniae
72
Give an example of a fungal cause of pneumonia
Histoplasmosis | Blastomycosis
73
How is aspiration pneumonia acquired?
Gag reflex can be compromised by: Drug/ alcohol abuse Brain injury Swallowing issues
74
Define lobar pneumonia
Complete consolidation of whole lung lobe | Mostly caused by S. pneumoniae
75
Give the stages of lobar pneumonia
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
Give 4 symptoms of pneumonia
``` Dyspnoea Chest pain Productive cough Fatigue Fever ```
77
Describe a typical CXR for the following: Bronchopneumonia Lobar pneumonia Atypical pneumonia
- Patchy areas spread throughout - Fluid localised to a single lobe - Concentrated in perihilar region
78
Describe the difference between type I and type II pneumocytes
Type I- squamous cells, nearly continuous layer | Type II- cubes with microvilli, secreting surfactant which prevents alveolar collapse
79
Describe the process of pulmonary fibrosis after the alveolar lining is damaged
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
Give 3 risk factors for pulmonary fibrosis
Old age Being male Tobacco smoking
81
Give 3 ways in which interstitial lung disease affects lung function
Decrease in total lung capacity Decrease in forced vital capacity Decrease in forced expiratory volume
82
Give 4 signs and symptoms of pulmonary fibrosis
Coughing SOB Cyanosis Digital clubbing
83
Give two indicators of pulmonary fibrosis on a CT scan
"Honeycombing" and thickening of interstitial walls
84
Give 3 possible treatments for pulmonary fibrosis
Supplemental oxygen Antifibrotic medication Lung transplant
85
Define sarcoidosis
T-cell accumulation in organs, forming granulomas
86
Give 5 systemic symptoms of sarcoidosis
``` Fatigue Weakness Aching muscles Swollen lymph nodes Lack of appetite Weight loss ```
87
Give 4 respiratory symptoms of sarcoidosis
SOB Dry cough Wheezing Suffocation
88
Give 3 symptoms of sarcoidosis affecting the eyes
Blurred vision Tearing Photophobia
89
How would sarcoidosis be diagnosed?
CXR- looking for granulomas Blood test- looking for hyercalcaemia and raised ACE Biopsy- lung tissue/ skin/ lymph nodes
90
Define bronchiectasis
A disease in which there is permanent enlargement of parts of the airways
91
What type of genetic disorder is cystic fibrosis?
Autosomal recessive
92
Which gene in affected in cystic fibrosis
Cystic fibrosis transmembrane conductance regulator (CFTR gene)
93
What is the purpose of the CFTR protein?
It pumps chloride ions into secretions, drawing water with them to thin the secretions
94
How does the mutation affect the CFTR protein?
It is misfiled and so cannot migrate from the ER to the cell membrane
95
What is the risk in newborns with cystic fibrosis?
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
What happens if thick secretions block the pancreatic ducts in cystic fibrosis?
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
What happens if pancreatic enzymes back grade to cells lining pancreatic ducts in cystic fibrosis?
Self-digestion leading to acute/ chronic pancreatitis and the development of cysts and fibrosis This can cause insulin dependent diabetes
98
How does cystic fibrosis cause lung problems?
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
Give some possible consequences of chronic bacterial infection and inflammation in CF
Bronchiectasis- wall damage and permanent dilation of bronchi If inflammation erodes into a blood vessel this can cause haemoptysis
100
What is the risk of repeated CF exacerbations?
Respiratory failure
101
How is cystic fibrosis diagnosed?
Newborn screening detects pancreatic enzyme released into blood when pancreas is damaged (IRT-immunoreactive trypsinogen)
102
How is cystic fibrosis treated?
``` 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
Give 3 ways in which excess fluid builds up in the pleural space
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
Describe how a change in hydrostatic pressure can lead to pleural effusion
Heart failure leads to a back up of blood into the pulmonary vessels, increasing the pressure and forcing fluid into the pleural space
105
Describe how a change in oncotic pressure can lead to pleural effusion
Cirrhosis or nephrotic syndrome can lead to a drop in oncotic pressure
106
Give 4 causes of exudative pleural effusion
Malignancy Inflammatory conditions such as lupus Trauma Infection such as pneumonia
107
Give 2 causes of lymphatic effusion
Damage to the thoracic duct during surgery | Tumours
108
Give a characteristic of pleural effusion pain
Worse when lying down
109
How would pleural effusion be diagnosed?
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
After removal via thoracentesis how would different types of pleural effusion fluid appear?
Transudative fluid is clear Exudative fluid is cloudy- full of immune cells Lymphatic fluid is milky- full of fats
111
What is the light criteria to determine whether fluid is exudative?
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
How would you treat a small pleural effusion from heart failure?
Diuretics | Sodium restriction
113
How would you treat a large pleural effusion from lung cancer?
Draining with a tube
114
Describe a pneumothorax and presenting symptoms
``` Abnormal collection of air in the pleural space Symptoms: Chest pain SOB Tiredness ```
115
How does a tension pneumothorax occur?
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
How does the body compensate when a tension pneumothorax occurs?
Increases respiratory rate | Increases tidal volume
117
How would you treat a pneumothorax?
Conservative Needle aspiration Chest tube Pleurodesis
118
Give 3 ways in which pulmonary hypertension can occur
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
Give 3 congenital heart defects as causes of pulmonary HTN
Ventricular septal defect Atrial septal defect Patent ductus arteriosus
120
Give 4 examples of disorders which could lead to pulmonary HTN
Lupus Infections like HIV Thyroid disorders Inherited genetic mutations
121
How do connective tissue disorders such as Lupus/ thyroid disorders lead to pulmonary HTN?
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
Give 3 consequences of R sided heart failure when blood backs up into the venous system
Increased jugular venous pressure Fluid build up in the liver- hepatomegaly Fluid build up in the legs-oedema
123
How would pulmonary HTN be diagnosed?
Echocardiogram showing an increased pressure in pulmonary arteries and R ventricle Follow up tests to identify underlying cause
124
How would you treat pulmonary HTN?
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
Give 5 symptoms of a mesothelioma
``` Dyspnoea Swollen abdomen Chest wall pain Fatigue Weight loss ```
126
Give 3 risk factors for mesothelioma
Asbestos exposure Genetics Infection with simian virus 40
127
How would you diagnose a mesothelioma?
CXR and CT | Confirmed by examining fluid produced by cancer/ tissue biopsy
128
How would you treat a mesothelioma?
Surgery Radiation therapy Chemotherapy- cisplatin and pemetrexed Pleurodesis
129
Describe Goodpasture syndrome
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
Give 4 systemic symptoms of Goodpasture syndrome
Malaise Weight loss Fatigue Fever
131
Give 4 lung symptoms of Goodpasture syndrome
Haemoptysis Chest pain Cough Dyspnoea
132
Give 5 kidney symptoms of Goodpasture syndrome
``` Haematuria Proteinuria Oedema Increased urea in the blood HTN ```
133
How would you diagnose Goodpasture syndrome?
Biopsy to look for anti-GBM antibodies (anti-glomerular basement membrane)
134
How would you treat Goodpasture syndrome?
Plasmapheresis | Immunosuppressant drugs- Cyclophosphamide, prednisone and retuximab
135
Describe Wegner's syndrome
Systemic autoimmune disorder that involves granulomatosis and polyangitis
136
Give 5 signs and symptoms of Wegner's syndrome
``` Lungs- primary nodules, infiltrates, pulmonary haemorrhage: haemoptysis Kidney- glomerulonephritis Nose- pain, nosebleeds Ears- conductive hearing loss Eyes- scleritis ```
137
Which antibodies are responsible for the inflammation in Wegner's syndrome?
Anti-neutrophil cytoplasmic antibodies (ANCAs)
138
How would you treat Wegner's syndrome?
Immunosuppressants- Rituximab, cyclophosphamide and high dose corticosteroids Plasma exchange Kidney transplant
139
Give 5 symptoms of influenza
``` Fever Cough Nasal congestion Hoarseness Throat pain ```
140
Describe the differences between influenza A, B and C
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
Why should children and teenagers avoid taking aspirin during an influenza infection
It can lead to Reye's syndrome which is a rapidly progressive encephalopathy
142
Describe hypersensitivity pneumonitis
Inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dusts
143
Give 3 symptoms for each of acute, subacute and chronic hypersensitivity pneumonitis
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
What type of sensitivity is hypersensitivity pneumonitis
III and IV
145
Give 5 signs and symptoms of laryngitis
``` Dry/ painful throat Cough Increased saliva production Dysphagia Globus pharyngeus Swollen lymph nodes ```
146
Give examples of the 4 causes of laryngitis
Trauma- damage to vocal folds (iatrogenic) Fungal- histoplasma, blastomyces Bacterial-group A strep, strep pneumoniae Viral- rhinovirus, influenza, adenovirus
147
Give 3 causes of chronic laryngitis
Allergies Autoimmune Irritation of vocal folds due to reflux
148
How would you diagnose laryngitis?
``` Laryngoscopy: Erythema Oedema Dilated vessels (acute) Stiff vocal folds ```
149
How would you treat acute laryngitis?
Trauma- vocal hygiene Viral- analgesia, rest, mucolytics Bacterial- Abx Fungal- antifungals
150
How would you treat chronic laryngitis?
Granulomatous- systemic corticosteroids Reflux- antacids, PPI, behavioural changes Inflammatory- topical nasal steroids, immunotherapy, antihistamines Autoimmune- cyclophosphamide, prednisolone
151
Give 5 signs and symptoms of tonsillitis
``` Sore throat Red, swollen tonsils Pain on swallowing Fever Headache ```
152
Give 5 viral causes of tonsillitis
``` Adenovirus Rhinovirus Influenza Coronavirus Respiratory syncytial virus ```
153
Give the main bacterial cause of tonsillitis
Group A beta-haemolytic strep: strep throat
154
Give the treatment for tonsillitis
Analgesia | If bacterial: Abx- penicillin or amoxicillin
155
Give 3 symptoms of sinusitis
Headache/ facial pain Thick nasal discharge Localised headache/ toothache that is worsened by tilting the head forward and with valsalva manoeuvres
156
Give 5 possible complications of sinusitis
``` Orbital cellulitis Osteomyelitis of facial bones Middle ear problems Abscesses Meningitis ```
157
How can sinusitis be classified?
Acute <4 weeks Recurrent >4 episodes in a year Subacute <12 weeks Chronic >12 weeks ``` By location: Maxillary Frontal Ethmoidal Sphenoidal ```
158
Give potential causes of sinusitis
Dental origin Precipitated by an earlier upper resp tract infection: rhinoviruses, coronaviruses and influenza viruses Bacterial- strep. pneumoniae, haemophilus influenzae