EENT Flashcards
(152 cards)
1
Q
A
2
Q
What neurotransmitter controls the ciliary muscles for accommodation?
A
Acetylcholine via parasympathetic muscarinic receptors.
3
Q
What causes pupil dilation (mydriasis)?
A
Sympathetic stimulation of radial muscle via α1-adrenoceptors.
4
Q
How is aqueous humor drained from the eye?
A
Via trabecular meshwork to Schlemm’s canal and uveoscleral route.
5
Q
What increases aqueous humor production?
A
β2-adrenoceptor stimulation in the ciliary body.
6
Q
What drugs reduce aqueous humor production?
A
α2-adrenoceptor agonists (e.g. brimonidine), β-blockers, carbonic anhydrase inhibitors.
7
Q
What is the primary pathology in glaucoma?
A
Progressive optic neuropathy due to raised intraocular pressure (IOP).
8
Q
What are early symptoms of glaucoma?
A
Often symptomless; later shows peripheral vision loss, halos around lights.
9
Q
What distinguishes open-angle from angle-closure glaucoma?
A
Open-angle: blocked meshwork; Angle-closure: iris blocks outflow angle.
10
Q
What is the first-line treatment for open-angle glaucoma?
A
Prostaglandin analogues (e.g. latanoprost).
11
Q
How do prostaglandin analogues work in glaucoma?
A
Increase uveoscleral outflow of aqueous humor.
12
Q
What is selective laser trabeculoplasty (SLT)?
A
Laser treatment to improve drainage via trabecular meshwork.
13
Q
What are emergency treatments for acute angle-closure glaucoma?
A
IV acetazolamide, pilocarpine, beta-blockers, steroids, then surgery (e.g. iridotomy).
14
Q
What is the function of VEGF in the eye?
A
Promotes new blood vessel growth and increases permeability.
15
Q
What causes wet AMD?
A
Choroidal neovascularisation due to VEGF overexpression.
16
Q
What is the treatment for wet AMD?
A
Intravitreal injection of anti-VEGF agents (e.g. ranibizumab, aflibercept).
17
Q
What is the difference between dry and wet AMD?
A
Dry: drusen and minor loss; Wet: blood vessel growth and rapid vision loss.
18
Q
How is pupil constriction (miosis) achieved?
A
Parasympathetic stimulation of circular iris muscle via muscarinic receptors.
19
Q
What are cycloplegic drugs?
A
Drugs that paralyse the ciliary muscle and prevent accommodation (e.g. tropicamide).
20
Q
Why must glaucoma patients be adherent to treatment?
A
To prevent irreversible vision loss by controlling IOP.
21
Q
What non-drug action improves topical eye drug delivery?
A
Closing the eye and pressing nasolacrimal duct after instillation.
22
Q
What is acute otitis media (AOM)?
A
Inflammation of the middle ear with effusion and rapid onset of infection symptoms.
23
Q
Which pathogens commonly cause AOM?
A
Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Streptococcus pyogenes.
24
Q
Why are children more prone to AOM?
A
Shorter, more horizontal Eustachian tubes and higher viral infection rates.
25
List three risk factors for AOM.
Passive smoking, formula feeding, day care attendance.
26
What are classic symptoms of AOM?
Earache, fever, irritability, difficulty sleeping, red or bulging tympanic membrane.
27
What physical sign is used to confirm AOM diagnosis?
Bulging or non-mobile tympanic membrane on otoscopy.
28
What is otitis media with effusion (glue ear)?
Fluid in the middle ear without signs or symptoms of infection.
29
What is the first-line antibiotic for AOM?
Amoxicillin.
30
Which antibiotic is used if the patient is penicillin-allergic?
Clarithromycin or erythromycin (if pregnant).
31
When should antibiotics be given immediately for AOM?
If patient has high fever, immunodeficiency, severe symptoms, or complications.
32
What pain relief options are recommended for AOM?
Paracetamol or ibuprofen, possibly ear drops with anaesthetic (e.g. Otigo®).
33
How long does AOM usually take to resolve without antibiotics?
Most resolve in 3 days, though may take up to a week.
34
What are potential complications of AOM?
Hearing loss, perforation, mastoiditis, meningitis, abscess, facial nerve paralysis.
35
What is the role of shared decision-making in AOM management?
Improves antibiotic stewardship, patient satisfaction, and adherence.
36
What does CHESTSSS stand for in consultations?
Concerns, History, Expectations, Symptoms explanation, Timeline, Shortcomings of antibiotics, Self-care, Safety-netting.
37
Name two non-drug ways to prevent AOM.
Vaccination (pneumococcal), avoid second-hand smoke, reduce dummy use after 6 months.
38
How do α1 adrenergic agonists relieve nasal congestion?
They cause vasoconstriction by stimulating α1 receptors in nasal blood vessels.
39
What is the main action of phenylephrine?
Selective α1 agonist with reduced β activity; acts as a nasal decongestant.
40
Why is phenylephrine not metabolised by COMT?
It lacks the catechol structure, extending its duration of action.
41
What is a side effect of oral decongestants like phenylephrine?
Hypertension, CNS stimulation (especially in hypertensive patients).
42
What type of drugs are xylometazoline and oxymetazoline?
2-Arylimidazoline α1 agonists used topically in nose and eyes.
43
What is the structural requirement for α1 activity in imidazoline agonists?
Lipophilic ortho groups and correct spatial distance from nitrogen.
44
What is the mechanism of pseudoephedrine?
Indirect sympathomimetic; increases norepinephrine release.
45
Which enantiomer of ephedrine has direct α and β activity?
(-)-Ephedrine (R,S).
46
What is the main advantage of pseudoephedrine over ephedrine?
Fewer CNS side effects.
47
What are the four drug classes for treating inflammation in EENT conditions?
Antihistamines, intranasal steroids, leukotriene receptor antagonists, mast cell stabilisers.
48
What is the mechanism of ketotifen?
H1 inverse agonist + mast cell stabiliser.
49
Why does ketotifen cause fewer CNS effects?
Second-generation antihistamine; poor BBB penetration.
50
What is the mechanism of chloramphenicol?
Inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit.
51
Why is chloramphenicol used topically?
To avoid serious systemic toxicity (e.g. aplastic anaemia).
52
What is the purpose of chloramphenicol C-3 palmitate prodrug?
Masks bitter taste for paediatric oral use.
53
What is the purpose of chloramphenicol C-3 hemisuccinate prodrug?
Improves water solubility for IV administration.
54
What modification causes chloramphenicol resistance?
Acetylation by chloramphenicol acyltransferase.
55
Which group in chloramphenicol is linked to toxicity?
The para-nitro group, reduced to aromatic amine.
56
How is chloramphenicol synthesised chemically?
Using nucleophilic acyl substitution (addition-elimination) reactions.
57
What are the roles of H1 receptor inverse agonists?
Suppress basal histamine receptor activity and reduce allergy symptoms.
58
What is hypersensitivity?
An overreaction of the immune system causing tissue damage.
59
Which immune system is involved in hypersensitivity?
The adaptive immune system.
60
Name the 4 types of hypersensitivity.
Type I (Immediate), Type II (Cytotoxic), Type III (Immune complex), Type IV (Delayed).
61
What antibody is involved in Type I reactions?
IgE.
62
Which cells are activated in Type I hypersensitivity?
Mast cells.
63
What happens during sensitisation in Type I?
Allergen activates Th2 → B cells make IgE → binds mast cells.
64
What triggers Type I allergic reactions?
Re-exposure to allergen → IgE cross-linking → mast cell degranulation.
65
What are early mediators in Type I reactions?
Histamine, cytokines.
66
What is the late phase of Type I?
Eosinophils and more inflammation hours later.
67
Give 3 examples of Type I hypersensitivity.
Hay fever, asthma, anaphylaxis.
68
What is atopy?
A genetic tendency to develop allergic diseases.
69
Name 3 drug types for allergies.
Antihistamines, steroids, leukotriene blockers.
70
What antibodies are involved in Type II?
IgG or IgM.
71
What are 2 mechanisms of Type II?
Complement damage (CMC) and cell killing (ADCC).
72
Give 2 examples of Type II hypersensitivity.
Myasthenia gravis, blood transfusion reactions.
73
What happens in Type III hypersensitivity?
Antibody-antigen complexes deposit in tissues.
74
Where can Type III reactions cause damage?
Kidneys, lungs, joints (e.g., glomerulonephritis).
75
What cells are involved in Type IV?
T cells and macrophages.
76
How long does a Type IV reaction take?
24–48 hours (delayed).
77
Give an example of a Type IV reaction.
Mantoux test (TB skin test).
78
What is hypersensitivity?
An exaggerated immune response causing tissue damage, seen after re-exposure to an antigen.
79
Which immune system mediates hypersensitivity?
The adaptive immune system.
80
List the four types of hypersensitivity with key mediators.
Type I – IgE, Type II – IgG/IgM, Type III – Immune complexes, Type IV – T cells.
81
What triggers Type I hypersensitivity?
Allergen cross-links IgE on mast cells → histamine and cytokine release.
82
What are examples of Type I hypersensitivity?
Hay fever, asthma, eczema, urticaria, anaphylaxis.
83
What is atopy?
A tendency to develop IgE-mediated allergies (runs in families).
84
What happens during the sensitisation phase?
Th2 cells activate B cells to produce allergen-specific IgE, which binds to mast cells.
85
What happens during the early phase of Type I?
Histamine release → itching, redness, swelling.
86
What happens during the late phase of Type I?
Recruitment of eosinophils and more inflammation (hours later).
87
What drugs treat Type I reactions?
Antihistamines, corticosteroids, mast cell stabilisers, leukotriene blockers.
88
What happens in Type II hypersensitivity?
IgG/IgM antibodies attack cells → complement or NK cell killing.
89
What are examples of Type II reactions?
Myasthenia gravis, blood transfusion reactions.
90
How does complement-mediated cytolysis (CMC) work?
Antibodies activate complement, leading to membrane damage and cell death.
91
What is ADCC?
Antibodies mark cells → NK cells or phagocytes destroy them.
92
What happens in Type III hypersensitivity?
Immune complexes deposit in tissues → inflammation and damage.
93
What is an example of a Type III reaction?
Glomerulonephritis.
94
What happens in Type IV hypersensitivity?
T cells and macrophages cause delayed inflammation (24–48 hours).
95
What is an example of Type IV hypersensitivity?
Mantoux test for TB (delayed skin reaction).
96
What is the difference between early and late Type I phases?
Early = histamine; Late = eosinophils and other immune cells.
97
What site-specific effects are seen in Type I allergies?
Red eyes, runny nose (rhinitis), wheezing (asthma), rashes (urticaria).
98
What is acute otitis externa (AOE)?
Diffuse inflammation of the external ear canal, often caused by bacterial infection.
99
What are the main pathogens in AOE?
Pseudomonas aeruginosa and Staphylococcus aureus.
100
What is chronic otitis externa usually caused by?
Fungal infections such as Aspergillus or Candida albicans.
101
What is malignant otitis externa?
A severe, life-threatening infection involving the temporal bone, usually in immunocompromised patients.
102
Name three risk factors for AOE.
Swimming, trauma from cleaning, use of hearing aids.
103
What are key symptoms of AOE?
Itchy ear, pain, discharge, tenderness of tragus or pinna.
104
What signs indicate AOE on examination?
Red, swollen ear canal, debris, discharge, tenderness, possible lymphadenitis.
105
What non-drug advice is given for AOE?
Keep ear dry, avoid swimming, avoid cotton buds, use acetic acid ear drops.
106
What antibiotics are used topically in AOE?
Aminoglycosides or fluoroquinolones, sometimes with corticosteroids.
107
When are oral antibiotics used for AOE?
If infection is severe, spreading, or patient is immunocompromised.
108
When are aminoglycoside drops contraindicated?
If there's a perforated tympanic membrane due to ototoxicity risk.
109
When should AOE be followed up?
If no improvement in 48–72 hours or unresolved after 2 weeks.
110
What is earwax composed of?
Dead skin cells, cerumen, sebum, and external particles.
111
What are symptoms of earwax impaction?
Hearing loss, earache, itchiness, fullness, tinnitus, or cough.
112
When should earwax be removed?
If it causes symptoms or obscures the tympanic membrane.
113
What drops can soften earwax?
Sodium bicarbonate 5%, olive oil, almond oil, or saline.
114
When should drops not be used for wax?
If there's a perforated eardrum, active infection, or allergy to components.
115
What is the next step if drops fail to clear wax?
Irrigation by a trained professional.
116
What advice should patients get about ear hygiene?
Don’t insert objects like cotton buds; avoid ear candles.
117
Name 2 serious complications of untreated earwax impaction.
Infections, hearing aid interference, social isolation due to hearing loss.
118
What are common symptoms of a sore throat?
Painful swallowing, dry/scratchy throat, redness, bad breath, cough, swollen neck glands, fever in children.
119
What is acute pharyngitis?
Rapid-onset sore throat with inflammation of the pharynx, possibly with exudate.
120
What suggests bacterial pharyngitis?
Sore throat >3 days, absence of cough/nasal symptoms, swollen tonsils with exudate, fever.
121
What causes acute pharyngitis?
Usually viral (e.g., rhinovirus), sometimes bacterial (GAS), or fungal (Candida).
122
What is the first-line antibiotic for streptococcal sore throat?
Phenoxymethylpenicillin.
123
What scoring tools are used to assess sore throat?
FeverPAIN and Centor criteria.
124
What is a high FeverPAIN or Centor score associated with?
Higher likelihood of Group A Strep infection.
125
Name 3 red flag symptoms in sore throat.
Difficulty breathing/swallowing, dehydration, blood in saliva.
126
What is the recommended management for most sore throats?
Self-care, analgesia (paracetamol/ibuprofen), medicated lozenges, mouthwash, review if no improvement.
127
What is pseudomembranous candidiasis?
Oral thrush; white/yellow plaques with mild burning or dysphagia.
128
What are risk factors for oral candidiasis?
Immunosuppression, ICS use, diabetes, dentures, poor hygiene, broad antibiotics.
129
What is the first-line treatment for mild adult oral candidiasis?
Miconazole oral gel for 14 days.
130
What is the treatment for extensive or severe oral thrush?
Oral fluconazole systemically for 14 days.
131
What antifungal is used for children <4 months?
Nystatin suspension (if miconazole unsuitable).
132
What are key non-drug measures for oral thrush?
Good dental hygiene, clean dentures, stop smoking, rinse mouth after ICS.
133
What are common symptoms of nasal congestion?
Blocked/stuffy nose, runny nose, postnasal drip, facial pain, sneezing, itching, loss of smell.
134
List 3 causes of nasal congestion.
Infection (e.g. sinusitis), allergy (e.g. hay fever), nasal deformity.
135
Name 3 treatments for nasal congestion.
Steam inhalation, saline sprays, corticosteroid nasal sprays.
136
What is rhinitis?
Inflammation/irritation of nasal mucosa; can be allergic or non-allergic.
137
What is allergic rhinitis?
IgE-mediated inflammation due to allergen exposure.
138
What are key symptoms of allergic rhinitis?
Sneezing, blocked/runny nose, itchy nose, postnasal drip, itchy eyes.
139
Differentiate intermittent and persistent allergic rhinitis.
Intermittent: <4 days/week or <4 weeks; Persistent: >4 days/week and >4 weeks.
140
Name 2 intranasal antihistamines and a key side effect.
Azelastine (bitter taste, irritation); Olopatadine.
141
Name 2 oral antihistamines and a caution.
Cetirizine, Loratadine; reduce dose in renal/hepatic impairment.
142
What is a common intranasal cromone and its use?
Sodium cromoglicate; for allergy prevention.
143
What are side effects of xylometazoline?
Rebound congestion, nasal irritation, sleep disturbance.
144
What is the caution with long-term use of intranasal decongestants?
Rebound congestion and mucosal damage if used >5–7 days.
145
How does ipratropium bromide work?
Anticholinergic that reduces nasal secretions.
146
What is a leukotriene receptor antagonist used in rhinitis?
Montelukast.
147
What are causes of non-allergic rhinitis?
Infections, irritants, medications, hormonal changes, cold air.
148
What is sinusitis?
Inflammation of nasal cavity and sinuses (rhinosinusitis).
149
Differentiate acute and chronic sinusitis.
Acute: <12 weeks; Chronic: >12 weeks with symptoms like congestion, facial pain.
150
Name 3 causes of sinusitis.
Viral URTI, allergic rhinitis, nasal polyps or trauma.
151
What is the first-line treatment for sinusitis pain?
Paracetamol or NSAIDs.
152
When should antibiotics be used in acute sinusitis?
If symptoms persist >10 days or worsen; consider back-up antibiotics.
