ENT Flashcards

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1
Q

What are drugs are ototoxic?

A
Aspirin (High dose)
Quinine
Aminoglycosides(Gentamicin.Neomycin)
Cytotoxic drugs containing platinum 
Diuretics-Furesemide
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2
Q

What Organisms can cause Otitis Externa?How can it be treated?

A

The most common cause of otitis externa is bacterial infection, caused by Pseudomonas aeruginosa or Staphylococcus aureus.

Treatment-Treating infection, usually with a topical preparation.
topical antibiotic with or without a topical corticosteroid

Topical acetic acid 2% spray is also a safe and effective treatment and can be used for mild cases.
Quinolone containing preparations (for example ciprofloxacin, or ofloxacin) only require twice daily dosing, and can be used in people with a perforated ear drum.
Otomycosis- antifungal eardrop – clotrimazole 1% ear drop.

Clean ear

Oral antibiotics are rarely indicated. Perscribe 7-day course of flucloxacillin, or clarithromycin (if allergic to penicillin). Only give if:
severe infection, or at high risk for severe infection

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3
Q

What is malignant otitis externa?

A

Malignant otitis externa is spread of otitis externa into the bone surrounding the ear canal (osteomyelitis) – mastoid, temporal and basal skull bones, and the infection will spread tocerebrospinal fluid causing meningitis.
Risk factors for malignant otitis include diabetes or radiotherapy to the head and neck.
Pseudomonas aeruginosa is the most common causative organism
Characterised by non-resolving AOE despite adequate topical treatment; deep severe pain causing insomnia; purulent otorrhoea; evidence of granulation and necrotic tissue within the ear canal
In severe cases, there may be evidence of conductive hearing loss and lower cranial neuropathies

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4
Q

What Investigations are done in BPH?

A

Renal function
PSA-do before PR

Ultrasound of kidney,bladder
Post voidal volume
Trans rectal USS of prostate

Uro flowmetry

Invasive-Cystoscopy ,trans rectal biopsy

IPSS -Scoring system

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5
Q

What can increase PSA?

A
Strenuous excercise 
Digital rectal exam
Recent ejaculation
BPH
Prostate Ca
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6
Q

How is BPH treated?

A

No to mild systems(0-7 score)-cut down caffeinated drinks,alcohol, regular check up,symptom monitoring,lifestyle management(bladder training,high fibre diet,less drinks at night,double voiding)

Medical treatment-moderate symptoms

alpha blocker(tamsulcosin,doxazocin)(relaxes the smooth muscles,improve urine flow)
S/E-Dizziness,fatigue,Erectile dysfunction 

5 alpha reductase(Finestride)-block production of DHT and reduce size of prostate.may take up to 3 months

Surgical-failure of medical management

Gold standard -TURP
Open prostatectomy-very large prostate( last prostate )

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7
Q

What are the side effects of TURP?

A
Bleeding,Infection,Death
TURP syndrome
Urinary retention -transient
Incontinence -usually transient 
Urethral stricture
Retrograde ejaculation 
Erectile dysfunction
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8
Q

Where does BPH arises from?

A

BPH normally arise from transitional zone(middle)different to prostate ca which arises from the pheriphery

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9
Q

What is TURP syndrome?

A

Transurethral resectionof prostate (TURP)syndromeis a complication characterised by symptoms changing from an asymptomatic hyponatremic state to convulsions, coma and death due to absorption of irrigation fluid duringTURP.

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10
Q

How does infectious mono present,how is it investigated and what are the complications?

A

Background

Aka glandular fever, mono.

Cause

Infection by Epstein-Barr virus (EBV, human herpesvirus 4), a double-stranded DNA virus.

A number of other pathogens can cause mononucleosis syndromes: CMV, syphilis, HIV seroconversion, toxoplasma, brucella.

Signs and symptoms

Generalised or cervical lymphadenopathy.

Systemic symptoms: low-grade fever, fatigue/malaise, anorexia.

Pharyngitis. Like Group A Strep, there may be tonsillar enlargement, exudate, and palatal petechiae, but unlike Group A Strep there is also rhinorrhea, congestion and cough.

Splenomegaly (50%). Hepatomegaly and jaundice, suggesting EBV hepatitis, is less common (10%).

Bilateral upper eyelid oedema.

If patients are mistakenly given a β-lactam antibiotic prescription, this may result in a diffuse maculopapular rash.

Investigations

Bloods:

FBC: ↑lymphocytes, ↓platelets.

↑ESR, differentiating from Group A Strep.

Mild ↑ALT/AST.

Diagnosis:

Heterophile antibody tests, either Monospot or Paul-Bunnell. Tests not for an EBV Ab, but the non-specific ‘heterophilic’ IgM released by EBV-stimulated B-cells. 70% sensitive initially, but reaches 90% by 3 weeks.

EBV antibodies if heterophile -ve. >95% sensitive. Viral capsid antigen (VCA) IgM and Ab to early antigen (EA) are +ve in the acute phase, while VCA-IgG and EBV nuclear antigen (EBNA) IgG become +ve within weeks.

EBV PCR is an alternative.

Others:

Blood film: atypical lymphocytes.

Throat swab: should be -ve for Group A Strep, though some are asymptomatic carriers.

Consider abdo US for splenomegaly and LP if there is meningism.

Management

Usually self-resolves.

Paracetamol for fever and pain.

Prednisolone PO can be used if there is airway obstruction or haemolytic anaemia.

To prevent splenic rupture, avoid contact sport for 8 weeks and avoid alcohol during illness, though evidence for the latter is weak.

Complications

Short-term:

Post-viral fatigue may persist for months.

Splenic rupture.

Autoimmune haemolytic anaemia or thrombocytopenia.

Myocarditis

Glomerulonephritis

CNS: meningoencephalitis, Guillain-Barré, optic neuritis, transverse myelitis.

Long-term:

2-fold multiple sclerosis risk in those who have had infectious mononucleosis (though the absolute risk is still <1%).

Epstein-Barr virus (EBV)

Aka human herpesvirus 4 (HHV-4).

Epidemiology and transmission

Spread through saliva or droplets. Kissing is a common transmission method.

90% of people are exposed at some point in their lives.

In developing countries, infection often occurs in early childhood and is asymptomatic.

In the developed world, around 50% are infected by age 12. Among those infected later, 50% develop some symptoms, with 30% developing infectious mononucleosis.

Pathophysiology and life cycle

Double-stranded, DNA virus.

In the oropharynx, infects epithelial cells and B cells in lymphoid tissue. Subsequently spreads through the lymphatic system.

4-6 weeks incubation time.

EBV mimics innate B cell activation signals, causing proliferation and differentiation to antibody-secreting plasma cells.

Provokes massive cytotoxic T cell response against viral antigens. The T and B cells produce the characteristic lymphadenopathy of infectious mononucleosis.

Some latent infected cells remain after the acute illness.

Long-term complications

Cancer: Burkitt’s lymphoma, Hodgkin’s lymphoma, nasopharyngeal carcinoma.

Hairy leukoplakia: non-malignant warty lesion on lateral tongue in the immunosuppressed. Can be scraped off.

MS. Near 100% EBV exposure in MS patients, vs. 90% in general population

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