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3A > GP > Flashcards

GP Flashcards

1
Q

Most common cause of painful rectal bleeding on a background of constipation

A

Anal fissure

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2
Q

What should be done if someone vomits within 3 hours of taking their combined oral contraceptive pill

A

An additional pill should be taken as soon as possible

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3
Q

Describe the tricycling method of taking the combined oral contraceptive pill

A

Take the pill everyday for 9 weeks and then take a 4-7 day free interval

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4
Q

What is the most effective form of emergency contraception?

A

the intrauterine device (IUD)

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5
Q

What is suggested if someones total cholesterol is greater tha 5mmol/L

A

20mg atrovastatin

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6
Q

What non-invasive emergency contraception can be used for up to 5 days after unprotected sex?

A

ellaOne (ulipristal acetate)

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7
Q

How do you work out units of alcohol?

A

(concentration (percent) x volume )/ 1000

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8
Q

What contraceptive is migraine with aura a contraindication for?

A

The combined oral contraceptive pill

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9
Q

First line treatment for severe depression

A

SSRI (citalopram)

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10
Q

What happens if the progesterone only pill is missed for more than 3 hours

A

Take the missed pill and wear condoms for 48 hours

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11
Q

How long after remission should an antidepressant be continued for?

A

6 months

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12
Q

Treatment of cellulitis

A

oral flucloxacillin

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13
Q

Why may creatinine be high after treatment with trimethoprim

A

competitive inhibition of creatinine secretion from the renal tubules

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14
Q

What percent of FEV1 reversibility should be achieved by bronchodilator therapy in asthma?

A

At least 12%

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15
Q

What form of contraception can be used in women with breast cancer?

A

non-hormonal methods such as the copper IUD

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16
Q

First line investigation for angina

A

CT coronary angiogram

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17
Q

Treatment of urge incontinence which is often used in frail elderly patients

A

Mirabegron

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18
Q

What medications are a risk factor for gout?

A

low dose aspirin, thiazide like diuretics and immunosuppressive medications

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19
Q

What test is used to confirm iron deficiency anaemia?

A

ferritin (below 30mcg/l)

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20
Q

What is the best contraptive method at preventing pregnancy?

A

The contraceptive implant

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20
Q

Most appropriate antibiotic for bacterial tonsilitis?

A

Oral penicillin V (phenoxymethylpenicillin)

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20
Q

Can an IUD be used in someone with active chlamydia?

A

no

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20
Q

What antibiotic is recommended to treat UTIs in elderly patients with CKD?

A

trimethoprim

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21
Q

What can topical corticosteroids cause in patients with darker skin types

A

depigmentation

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21
Q

FEV1 of stage 2 COPD

A

50-80%

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22
Q

FEV1 of stage 3 COPD

A

30-50%

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23
Q

FEV1 of stage 4 COPD

A

<30%

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24
Q
A
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25
Q

Causes or secondary anal fissures

A

Constipation, IBD colorectal cancer,dermatological conditions such as psoriasis. Bacchanal, viral and fungal infections, anal trauma, pregnancy and child birth

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26
Q

Where do 90% or anal fissures present?

A

The posterior midline - If elsewhere other conditions such as crohns should be considered

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27
Q

Treatment of anal fissures lasting more than a week

A

Topical GTN applied twice a day for 6 to 8 weeks is first line
If GTN not effective consider surgery or Botox

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28
Q

Acute treatment of anal fissures

A

Soften stool- high fibre, high fluid intake, bulk forming laxatives
Lubricants such as petroleum jelly before defecation
Topical anaesthetics
Sitting in a warm bath

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29
Q

What type of reaction is anaphylaxis

A

Type 1 hypersensitivity reaction

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30
Q

Common causes of anaphylaxis

A

Food such as nuts - most common cause in children
Drugs
Venom

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31
Q

Resuscitation council uk definition of anaphylaxis

A

Sudden onset of:
Airway problems: swelling of the throat leading to hoarse voice and stridor
Breathing problems - wheeze, dyspnoea
Circulation problems - hypotension, tachycardia

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32
Q

Presentation of anaphylaxis

A

Sudden onset of:
Dyspnoea
Wheeze
Tachycardia
Urticaria
Angiooedema
Collapse

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33
Q

Dose of adrenaline in less than 6months

A

100 to 150 micrograms

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34
Q

Dose of adrenaline in 6months to 6years

A

150 micrograms

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35
Q

Dose of adrenaline in 6 to 12 years

A

300 micrograms

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36
Q

Dose of adrenaline in over 12 years

A

500 micrograms

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37
Q

What test can be done to confirm anaphylaxis after the event

A

Mast cell tryptase - collected 1-2 hours after onset but no later than 4

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38
Q

Common causes of bacterial vaginosis

A

Gardnerella vaginalis
Prevotells species
Bacteriodes species
Peptostreptococcus species

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39
Q

How does bacterial vaginosis present

A

Offensive fishy smelling discharge
No soreness or irritation

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40
Q

Amstel criteria for bacterial vaginosis

A

Vaginal pH > 4.5
Typical discharge - thin, off-white, homogenous
Positive whiff-amine test
Clue cells on microscopy

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41
Q

Explain the whiff-amine rest

A

Fishy odour on adding 10% potassium hydroxide to the vaginal fluid

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42
Q

Treatment of bacterial vaginosis in non-pregnant women

A

Oral metronidazole 400mg BD for 5 to 7 days
OR
Single dose high dose 2g metronidazole
OR
400mg intravaginal metronidazole gel OD for 5 day

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43
Q

Treatment of bacterial vaginosis in pregnant women

A

400mg oral metronidazole BD for 5 to 7 days
Or
400mg metronidazole intravaginal gel OD for 5 day

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44
Q

Complications of bacterial vaginosis

A

Can increase the risk of transmission of STIs
Can cause pregnancy complications- late miscarriage, low birthweight, premature rupture of membranes

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45
Q

Pathophysiology of BPH

A

Hyperplasia of the stromal and epithelial cells of the prostate
Usually occurs in the transitional zone of the prostate

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46
Q

Presentation of BPH

A

Voiding symptoms - weak intermittent urinary flow, straining, hesitancy, terminal dribbling, incomplete emptying
Storage symptoms - urgency , frequency, urinary incontinence , nocturia

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47
Q

How can BPH be diagnosed

A

DRE - smooth symmetrical enlarged prostate with maintenance of the central sulcus
May use PSA to screen for prostate cancer
Urine dipstick to assesss for haematuria and proteinuria

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48
Q

Treatment of BPH

A
  1. Alpha blockers such as tamsulosin
  2. 5 alpha reductase inhibitors such as finasteride
  3. TURP - transurethral resection of the prostate
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49
Q

What is Bell’s palsy

A

An acute unilateral idiopathic facial nerve paralysis

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50
Q

What happens to the forehead in Bell’s palsy

A

It will be included in paralysis as it is a lower motor neurone lesion - upper lesion would have forehead sparing due to bilateral inner action of the forehead

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51
Q

What additional symptoms may be present in Bell’s palsy

A

Post auricular pain
Altered taste
Dry eyes
Hyperacusis

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52
Q

What is Benign Paroxysmal Positional Vertigo

A

A common cause of recurrent vertigo triggered by head movement

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53
Q

Pathophysiology of Benign Paroxysmal Positional Vertigo

A

Caused by otoconia - loose debris of calcium carbonate
These are within the semicircular canals (most commonly the posterior canal)
Attacks are triggered by head movements causing movement of the otoconia, abnormal motion of the endolymph and feelings of vertigo

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54
Q

Presentation of Benign Paroxysmal Positional Vertigo

A

Short episodes of vertigo, usually lasting less than a minute
Episode will be triggered by head movements such as rolling over in bed
Vertigo may cause nausea and vomiting

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55
Q

How is Benign Paroxysmal Positional Vertigo diagnosed

A

Dix- hallpike manoeuvre
The manoeuvre will trigger rotational nystagmus and symptoms of vertigo in positive patients

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56
Q

How is Benign Paroxysmal Positional Vertigo treated

A

Epley manoeuvre
Patient can do Brandt- daroff exercises at home

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57
Q

Most common causes of bronciolitis

A

Respiratory syncytial virus
Other - rhinovirus, adenovirus

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58
Q

Most common side effect of allopurinol

A

Rash

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59
Q

What medication does clarithromycin interact with ?

A

Atrovastatin

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60
Q

What antibiotic should be used if treating a UTI in someone on methotrexate

A

Pivmacillinam

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61
Q

Emergency contraception in women with bmi greater than 26

A

Double dose of levonelle

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62
Q

What is an absolute contraindication to the combined pill?

A

A DVT

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63
Q

In what trimester should nitrofuratoin be avoided

A

Third

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64
Q

Where does impetigo rash typically start

A

On the face of it

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65
Q

First line prophylaxis of migraines

A

Propranolol, tropiramate or amitriptyline

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66
Q

Who should topiramate be avoided in?

A

Pregnant women

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67
Q

Who should topiramate be avoided in?

A

Pregnant women

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68
Q

What hormone do ovulation test strips monitor for?

A

LH- there is an lh surge before ovulation

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69
Q

How is diagnosis of a salivary gland stone made?

A

Sialogram

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70
Q

What criteria can be used to diagnose rheumatic fever

A

The jones criteria - evidence of recent strep infection with 2 major of 1 major plus 2 minor criteria

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71
Q

What is a contraindication to the ellaOne emergency contraception?

A

Severe asthma

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72
Q

What cancers are at increased risk with oral contraceptive pill

A

Increased risk of breast and cervical cancer
Decreased risk of ovarian and endometrial cancer

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73
Q

What antibiotic is given second line in tonsilitis in the event of penicillin allergy

A

Clarithromycin

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74
Q

What is seen on the blood film in coeliacs

A

Howell jolly bodied

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75
Q

What finding on microscopy is indicative of bacterial vaginosis

A

clue cells

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76
Q

How does tamsulosin work?

A

it is a alpha 1 antagonist- it decreases smooth muscle tone of the prostate and bladder

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77
Q

What is the first line treatment of BPH in those with moderate to severe voiding symptoms

A

tamulosin

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78
Q

Side effects of tamulosin

A

dizziness, postural hypotension, dry mouth, depression

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79
Q

What is the action of finasteride

A

blocks the conversion of testosterone to dihydrotestosterone
which is known to induce BPH

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80
Q

What is an indication for using finasteride in BPH

A

it is indicated in those with an enlarged prostate that is considered to be at high risk of progression

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81
Q

How long does it take for finasteride to work?

A

6 months

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82
Q

side effects of finasteride

A

erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

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83
Q

What is mastitis

A

inflammation of the breast tissue typically associated with breast feeding

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84
Q

How does mastitis present?

A

painful tender red hot breast
may have fever and general malaise

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85
Q

RF for mastitis

A

smoking, poor breast feeding technique, nipple damage, maternal stress, previous mastitis

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86
Q

What is mastitis called when it is associated iwth breast feeding

A

puerperal mastitis

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87
Q

Pathophysiology of mastitis

A

usually occurs due to milk stasis- from inadequate milk removal or infrequent feeding
Cracked sore nipples- provide entry point for bacteria

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88
Q

most common organism associated with mastitis

A

Staphylococcus aureus

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89
Q

What can mastitis develop into if left untreated?

A

breast abscess

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90
Q

first line management of mastitis

A

continue breast feeding

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91
Q

First line pharmacological treatment of mastitis

A

oral flucloxacillin (10-14 days)

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92
Q

Overview of the treatment of mastitis

A

continue breastfeeding
analgesia
warm compress
oral flucloxacillin (continue breastfeeding)

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93
Q

When should someone be treated for mastitis

A

if systemically unwell, if a nipple fissure is present, if symptoms do not improve after 12-24 hours of effective milk removal or if culture indicates infection

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94
Q

What is a breast abscess?

A

a collection of pus within an area of the breast usually caused by a bacterial infection

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95
Q

what are the two types of breast abscesses?

A

lactation and non lactational breast abscess

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96
Q

What is the most common causative agents of breast abscesses

A

staphylococcus aureus

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97
Q

Presentation of a breast abscess

A

a swollen, fluctuant lump within the breast
(fluctuant means the fluid can be moved around within the lump using pressure on palpation)
If active infection the abscess may be hardened
May also have features of mastitis- tender, swollen red breast

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98
Q

How are breast abscesses confirmed

A

USS

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99
Q

1st line treatment of a breast abscess

A

surgical intervention - needle aspiration or surgical incision and drainage
plus antibiotics

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100
Q

What are causes of parkinsonisms (not just parkinsons)

A

parkinsons disease
drug induced (antipsychotics, metoclopramide)
progressive supranuclear palsy
multiple system atrophy
wilsons disease
post encephalitis
dementia with lewy bodies

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101
Q

Are the symptoms of parkinsons symmetrical or asymmetrical

A

they are characteristically asymmetrical

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102
Q

Who is most commonly affected by parkinsons

A

men aged 65

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103
Q

Triad of parkinsons

A

bradykinesia
resting tremor
cogwheel rigidity

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104
Q

How many bradykinesia present in parkinsons

A

poverty of movement
short shuffling gait with reduced arm swing
small handwriting
reduced facial movements

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105
Q

Describe the tremor associated with parkinsons

A

resting tremor
usually 3-5 Hz
worse when tired or stressed
improves with voluntary movement
described as ‘pill-rolling’

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106
Q

Features of parkinsons (apart from the classic triad)

A

mask like face
flexed posture
soft voice
drooling saliva
Depression (affects about 40%)
postural instability
loss of sense of smell
sleep disorder

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107
Q

How does drug induced parkinsons differ from parkinsons disease in its presentation

A

drug induced is mroe likely to have a rapid onset and bilateral symptoms
it is less likely to have rigidity and resting tremour

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108
Q

How is parkinsons diagnosed

A

clinical
may use SPECT or CT/MRI scan

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109
Q

First line treatment of parkinsons if affecting quality of life?

A

levodopa

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110
Q

first line treatment of parkinsons if not affecting someones life

A

dopamine agonist (cabergoline), monamine oxidase B inhibitor or levodopa

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111
Q

If a patient with Parkinson’s is on the optimal dose of levodopa but still has symptoms what medication may be added?

A

MAO-B or COMT inhibitor

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112
Q

pathophysiology of parkinsons disease

A

loss of dopaminergic neurones in the substantia nigra of the basal ganglia

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113
Q

Side effects of levodopa

A

dry mouth
anorexia
palpitations
postural hypotension
psychosis

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114
Q

How does levodopa work?

A

it breaks down into dopamine once it crosses the blood brain barrier

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115
Q

What may be combined with levodopa to prevent peripheral breakdown and release of dopamine outside of the brain

A

decarboxylase inhibitor (carbidopa or benserazide)

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116
Q

What is the end-of-dose wearing off phenomenon that occurs with levodopa

A

symptoms worsen towards the end of the levodopa interval

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117
Q

What is the on-off phenomenon associated with levodopa

A

there are large variations in motor performance with normal function during an on period and weakness and restricted mobility during a off

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118
Q

what may parkinsons patients experience when on the peak dose of levodopa

A

dyskinesias - chorea, dystonia and athetosis (involuntary writhing movements)

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119
Q

What may parkinsons patients experience if they stop levodopa suddently

A

acute dystonia

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120
Q

Which parkisnons medication is known to cause problems with impulse control

A

dopamine agonists (cabergoline)

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121
Q

What complications is associated with dopamine agonists that requires monitoring investigations before beginning?

A

pulmonary and cardiac fibrosis
Patients should have an ECHO, ESR, creatinine and chest ray before starting

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122
Q

how do monamine oxidase B inhibitors work?

A

inhibit the breakdown of dopamine secreted by dopaminergic neurones

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123
Q

what is an example of a MAO-B inhibitor

A

selegiline

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124
Q

How do COMT inhibitors work

A

inhibits the breakdown of dopamine- used as an adjunct to levodopa

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125
Q

Give some examples of COMT inhibitors

A

entacarpone, tolcapone

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126
Q

What disease is parkinsons disease commonly related to?

A

lewy body dementia

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127
Q

how does lewy body dementia present?

A

progressive cognitive impairment - typically before parkinsonisms
parkinsonsism
visual hallucinations

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128
Q

How can you differentiate between parkinsons disease and lewy body dementia

A

in parkinsons motor symptoms are usually present for a year before cognitive impairment whereas in lewy body dementia cognitive impairment usually comes first

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129
Q

How is lew body dementia diagnosed?

A

usually clincial however SPECT scans are increasing used

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130
Q

How is lewy body dementia treated?

A

Acetylcholinesterase inhibitors (rivastigmine, donepezil) and memantine can be used

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131
Q

what type of drug should be avoided in lewy body dementia and why

A

neuroleptics - associated with irreversible parkonsonisms

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132
Q

What complications can occur with both antipsychotics and parkinsons drugs (levodopa)

A

neuroleptic malignant syndrome

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133
Q

how does neuroleptic malignant syndrome present?

A

pyrexia, muscle rigidity, autonomic lability (hypertension, tachycardia and tacypnoea) , agitated delirium

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134
Q

What might bloods show in someone with neuroleptic malignant syndrome

A

raised creatinine kinase is present in most
may have AKI and leukocytosis in severe

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135
Q

What is the most prevalent STI in the UK

A

chlamydia

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136
Q

what bacteria causes chlamydia

A

chlamydia trachomatis

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137
Q

How common is chlamydia

A

affects approx 1 in 10 young women

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138
Q

what type of pathogen is chlamydia

A

an intracellular bacterium
gram negative bacilli

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139
Q

Incubation period of chlamydia

A

7 to 21 days

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140
Q

what % of patients with chlamydia are asymptomatic

A

70% of women, 50% of men

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141
Q

How does chlamydia present in women

A

cervicitis- discharge, bleeding
dysuria

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142
Q

how does chlamydia present in men

A

urethral discharge
dysuria

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143
Q

how is chlamydia diagnosed

A

NAAT- from vulvovaginal swab in women and first void urine in men

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144
Q

treatment of chlamydia

A

7 days doxycycline

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145
Q

complications of chlamydia

A

pelvic inflammatory disease
epididymitis
reactive arthritis
conjunctivits and pneumonia in neonates if infected mother
perihepatitis (Fitz-Hugh-Curtis syndrome)
infertility
increased ectopics

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146
Q

if doxycycline is contraindicated in chlamydia what may be used?

A

azithromycin (1g OD and then 500mg OD for 2 days)

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147
Q

what is used to treat chlamydia in pregnancy

A

azithromycin, erythromycin or amoxicillin

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148
Q

How long after exposure should chlamydia testing be done?

A

2 weeks

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149
Q

What bacteria causes gonorrhoea

A

gram negative diplococci neisseria gonorrhoeae

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150
Q

incubation period of gonorrhoea

A

2 to 5 days

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151
Q

what percentage of patients with gonorrhoea are aysmptomatic

A

90% of men and 50% of women

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152
Q

how does gonorrhoea present

A

men- urethral discharge
dysuria

women - vaginal discharge (yellow green thick)
abdominal pain
dyspareunia

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153
Q

how is gonorrhoea diagnosed?

A

NAAT taken from vaginal swab in women and first pass urine in men

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154
Q

treatment of gonorrhoea

A

IM ceftriaxone 1g

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155
Q

RF of gonorrhoea

A

young age
new sexual contact
inconsistent condom use
MSM
current or prior STI
incareration

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156
Q

complications of gonorrhoea

A

pelvic inflammatory disease, pregnancy complications, development of stricture
epididymitis, orchitis, prostatitis, infertility

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157
Q

What causes infectious mononucleosis

A

Epstein-Barr virus (EBV- also known as herpesvius 4)

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158
Q

What is a less common cause of infectious mononucleosis

A

cytomegalovirus and HH6

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159
Q

Triad of infectious mononucleosis

A

sore throat (with whitewash exudate)
pyrexia
lymphadenopathy (commonly in the anterior and posterior triangles of the neck )

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160
Q

how does lymphadenopathy differ in EBV and tonsilitis

A

EBV more likely to be in the anterior and posterior triangles of the neck
Tonsilitis more likely to be in the upper anterior cervical chain

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161
Q

presentation of EBV

A

triad: lymphadenopathy, pyrexia, sore throat
- malaise
- palatal petechiae
- splenomegaly
- hepatitis
- lymphocytosis
- haemolytic anaemia

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162
Q

How long does it usually take for EBV to resolve?

A

2-4 weeks

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163
Q

How is EBV diagnosed?

A

heterophil antibody test (monospot test)
FBC- may show haemolytic anaemia and lymphocytosis
LFTs may be elevated

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164
Q

Why can you get haemolytic anaemia in EBV

A

due to cold agglutins (IgM)

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165
Q

Differentials for EBV

A

strep throat, lymphoma and leukaemia, viral illnesses (e.g mumps)

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166
Q

Treatment of EBV

A

rest and analgesia
Avoid playing contact sport - splenic rupture

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167
Q

what type of virus causes mumps

A

an RNA paramyxovirus

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168
Q

how is mumps spread

A

respiratory droplets

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169
Q

incubation period of mumps

A

14-21 days

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170
Q

when are patients with mumps infective

A

7 days before and 9 days after parotid swelling starts

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171
Q

pathophysiology of mumps

A

spread via respiratory droplets
replicates in the upper respiratory mucosa
spreads to the parotid gland

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172
Q

How does mumps present?

A

fever
malaise
parotitis (usually presents as ear ache or pain on eating)

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173
Q

how does parotitis present in mumps?

A

ear pain or pain on eating
usually begins unilateral and then spreads to be bilateral

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174
Q

How is mumps diagnosed?

A

usually clinical - can be confirmed with saliva sample to detect IgM

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175
Q

differentials for mumps

A

viral infections- EBV
acute supparative parotitis
parotid duct obstruction

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176
Q

Treatment of mumps

A

no specific treatment- fluids, rest, analgesia
notifiable disease

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177
Q

complications of mumps

A

parotitis
orchitis- occurs in post-pubertal men and can lead to impairments in fertility. May present as pain and swelling of the testicals
hearing loss- usually transient
meningoencephalitis
pancreatitis

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178
Q

what type of pathogen is trichomonas vaginalis

A

a highly motile flagellated protozoan parasite

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179
Q

Presentation of trichomonas vaginalis

A

vaginal discharge- offensive, yellow/green frothy discharge
vulval itching
dysuria

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180
Q

Examination findings of trichomonas vaginalis

A

strawberry cervix
pH greater than 4.5
yellow-green frothy discharge with a fishy odour
inflammation of the vulva and vagina

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181
Q

How can the diagnosis of trichomonas vaginalis be confirmed

A

microscopy of a wet mount shows motile trophocytes

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182
Q

how does trichomonas vaginals present in men

A

usually asymptomatic- can have urethritis

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183
Q

How is trichomonas vaginalis treated?

A

oral metronidazole for 5-7 days

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184
Q

Complications of trichomonas vaginalis

A
  • perinatal sepsis
  • PID
  • increased risk of cervical cancer
  • fascilitated HIV
  • infertility
  • increased risk of prostate cancer
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185
Q

What is conjunctivitis

A

inflammation of the conjunctiva
if corneal involvement - keratoconjunctivitis

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186
Q

Causes of conjunctivits

A

bacterial
viral
allergic

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187
Q

how does bacterial conjunctivitis present

A

red eye
purulent discharge
eye may be stuck together in the morning

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188
Q

how does viral conjunctivitis present?

A

red eye
serous discharge (clear)
recent URTI
pre-auricular lymph nodes

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189
Q

How does allergic conjunctivitis present?

A

red eye
bilateral
swollen eyelids
itching is common symptom

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190
Q

treatment of infective conjunctivitis

A

topical antibiotic treatment- chloramphenicol or fusidic acid drops
avoid wearing contact lenses
avoid sharing towels
clean eyes

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191
Q

Treatment of allergic conjunctivitis

A

1st line topical or systemic antihistamines
2nd line: topical mast-cell stabilisers

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192
Q

differentials of conunctivitis that are typically associated with increased pain

A

foreign body
acute closed angle glaucoma
anterior uveitits
corneal abrasions
scleritis

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193
Q

What are the two strains of the herpes simplex virus?

A

HSV-1 and HSV -2

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194
Q

What does HSV-1 cause

A

oral lesions- cold sores

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195
Q

what does HSV-2 cause

A

genital herpes

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196
Q

pathophysiology of HSV-1

A

it is commonly contracted in childhood and remains dormant until at times of stress it can reactivate in the trigeminal nerve and cause cold sores

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197
Q

how is HSV-2 predominately spread

A

it is mainly an STI

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198
Q

where does HSV-1 lay dormant

A

trigeminal nerve ganglai

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199
Q

where does HSV-2 lay dormant

A

sacral nerve ganglia

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200
Q

symptoms of genital herpes

A

painful genital ulceration
dysuria
pruritis
may have systemic illness (particularly in the primary infection) - headache, fever, malaise
Tender inguinal lymphadenopathy
urinary retention
neuropathic like pain

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201
Q

How does oral herpes (cold sores) present?

A

prodromal pain, burning and tingling for 6-48 hours
crops of vesicles that rupture and lead to superficial ulcers before crusting over and healing

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202
Q

How are genital herpes diagnosed?

A

NAAT

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203
Q

treatment of genital herpes

A

saline bathing, analgesia, topical anaesthetic (lidocaine)
oral aciclovir

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204
Q

If a pregnant women has a gential herpes infection during pregnancy how is it treated?

A

she should have an elective caesarean if primary attack occurs during a pregnancy at greater than 28 weeks

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205
Q

what is gingivostomatitis

A

a common presentation of herpes in young children where they present with vesicles and ulcers on the tongue, lips, gums and buccal mucosa

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206
Q

what is a severe complication of herpes?

A

herpes encephalitis

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207
Q

How is gingivostomatitis treated

A

oral aciclovir and chorhexidine mouthwash

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208
Q

how are cold sores treate

A

topical aciclovir

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209
Q

what is polymyalgia rheumatica?

A

a chronic inflammatory condition characterised by pain and stiffness in the shoulders, pelvic girdle and neck

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210
Q

who is most commonly affected by PMR

A

patients over the age of 60
more common in women

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211
Q

What does NICE describe as the core features of PMR

A

symptoms present for at least 2 weeks:
- bilateral shoulder pain that radiates to the elbow
- bilateral pelvic girdle pain
- worse on movement
- interferes with sleep
- stiffness for at least 45 minutes in the morning

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212
Q

what systemic features may be present in PMR

A

weight loss, lethargy, low grade fever, night sweats, low mood

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213
Q

How is PMR diagnosed?

A

usually based on its clinical presentation and response to treatment
- ESR - raised (usually >40)
- creatinine kinase and EMG are normal

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214
Q

treatment of PMR

A

initially 15mg of prednisolone a day
assess after 3-4 weeks (should have 70% improvement in symptoms and inflammatory markers should be normal)
Steroid reducing regime:
- 15mg until fully controlled
- 12.5mg for 3 weeks
- 10mg for 4-6 weeks
- reduce by 1mg every 4,8 weeks

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215
Q

what additional medication may be given to patients treated with steroids for PMR

A

osteoporosis prophylaxis- bisphosphonates, calcium and vitamin D
PPI for gastric protection

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216
Q

what disease is associated with PMR

A

giant cell arteritis

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217
Q

What is the most common type of prostate cancer?

A

95% are adenocarcinomas (usually in the peripheral zone of the prostate)

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218
Q

RF of prostate cancer

A

increasing age
family history
black african or caribbean origin
anabolic steroid use
tall stature

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219
Q

are prostate cancers androgen dependent

A

yes

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220
Q

How does prostate cancer present?

A

LUTS (hesitance, frequency, weak flow, terminal dribbling, nocturia)
haematuria
erectile dysfunction
symptoms of metastases (bone pain most common)

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221
Q

How can prostate cancer be screened for

A

PSA
DRE

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222
Q

how does prostate cancer present on DRE

A

hard, irregular, craggy

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223
Q

first line investigation for prostate cancer

A

mulitparametric MRI

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224
Q

gold standard investigation for prostate cancer

A

USS and biopsy- transrectal

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225
Q

How is prostate cancer graded?

A

gleason score (higher the score the worse)

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226
Q

What nodes does prostate cancer first spread to

A

obturator nodes

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227
Q

Treatment options for prostate cancer

A

external beam radiotherapy
brachytherapy- radioactive seed implanted into the prostate
radical prostatectomy
hormonal therapy- androgen receptor blocker, GnRH agonist, orchidectomy (stop testosterone production)

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228
Q

complication of radiotherapy for prostate cancer

A

radiation proctitis and rectal malignancy

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229
Q

complication of TURP (transurethral resection of the prostate)

A

erectile dysfunction

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230
Q

complicationsof TRUS biopsy

A

sepsis
pain
fever
haematuria and rectal bleeding

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231
Q

Why do GnRH agonists lead to lower LH levels?

A

they cause overstimulation which results in disruption to the endogenous hormonal feedback

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232
Q

what is a side effect of GnRH agonists in treatment of prostate cancer

A

an initial tumour flare as there may be an initial rise in testosterone
often given with an anti-androggen

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233
Q
A
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234
Q

What is the centor criteria

A

used to determine if tonsillitis is bacterial or viral

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235
Q

what features of the centor criteria suggest that tonsilitis is bacterial

A

tonsillar exudate
tender anterior cervical lymphadenopathy
fever >38
Absence of a cough

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236
Q

complications of tonsillitis

A

quinsy (peri-tonsillar abscess)
otitis media
rheumatic fever and glomerulonephritis

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237
Q

aetiology of tonsilitis

A

most frequently viral infection
can be bacterial- group A betal haemolytic strep (strep pyogenes)

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238
Q

what two criteria can be used to determine if tonsilitis is bacterial or viral

A

the centor score or the feverPAIN score

239
Q

what are the components of the feverPAIN score

A

fever
purulence
attend rapidly (within 3 days)
Inflammed tonsils
No cough or coryza

240
Q

What investigation may be done to exclude a differential of tonsilitis

A

monospot test to exclude EBV

241
Q

treatment of bacterial tonsilitis

A

phenoxymethypenicillin (penV) for 5-10 days (clarithromycin or erythromycin if allergic)

242
Q

who is offered tonsilectomy

A

those who have had:
- 7 or more episodes in the past year
- 5 per year or more in the past 2 years
- 3 or more in the preceding three years
or if there has been one epsiode of quincy or airway obstruction

Other: febrile convulsions, obstructive sleep apnoeaco

243
Q

complications of tonsilectomy

A

haemorrhage and pain

244
Q

What is urticaria

A

superficial swelling of the skin that is intensely red, raised and itchy

245
Q

what defines acute urticaria

A

symptoms have been present for less than 6 weeks

246
Q

What defines chronic urticaria

A

symptoms have been present for at least 6 weeks

247
Q

pathophysiology of urticaria

A

there is a release of histamine and other inflammatory mediators from mast cells which leads to increased vascular permeability and the production of wheals

248
Q

two main causes of acute urticaria

A

acute viral infection
allergen- food, insect bites, latex, drugs (penicillin, aspirin etc)

249
Q

What are the two types of chronic urticaria

A

chronic spontaneous urticaria
chronic inducible urticaria

250
Q

describe chronic spontaneous uritcaria

A

where urticaria has occured with no known identifiable cause, however symptoms may be aggravated by heat, stress, drugs.
Autoimmune urticaria is part of this group

251
Q

what is chronic spontaneous urticaria

A

urticaria that occurs in response to a physical stimulus

252
Q

give some examples of chronic inducible urticaria

A

aquagenic
cholinergic (occurs after active or passive warming)
cold
delayed pressure
solar

253
Q

What feature may accompany urticaria that presents as swelling of facial features

A

angioedema

254
Q

How is urticaria diagnosed?

A

mainly a clinical diagnosis
May do:
- allergy tests
- inflammatory markers
- skin biopsies
- urinalysis

255
Q

1st line treatment of urticaria after removing triggers

A

non-sedating antihistamines - e.g cetrizine

consider a sedating antihistamine at night

256
Q

2nd line treatment of urticaria

A

alternative/ high dose antihistamines or leukotriene receptor antagonist

257
Q

what can be used for a short period in severe episodes of urticaria

A

prednisolone

258
Q

what is vasovagal syncope

A

a form of reflex syncope characterised by a transient loss of consciousness in response to certain triggers

259
Q

What can trigger vasovagal syncope

A

emotional events
pain
prolonged standing
heat exposure
physical exertion

260
Q

pathophysiology of vasovagal syncope

A

there is a brief loss of cerebral perfusion due to an abrupt fall in blood pressure

This occurs due to changes in the activation of the autonomic nervous system:
- cardoinhibitory response: there is increased parasympathetic activity causing bradycardia
- vasodepressor response: there is decreased sympathetic activity leading to systemic vasodilation and hypotension

261
Q

what are the physiological mechanisms which cause the fall in BP associated with vasovagal syncope

A

cardioinhibitory response causing bradycardia
vasodepressor response causing vasodilation

262
Q

how does vasovagal syncope present ?

A

a prodrome of nausea, pallor, sweating, light-headedness, palpitations, visual alterations and reduced hearing

loss of consciousness (usually brief lasting 8-12 seconds)

may have some residual fatigue after

263
Q

Management of vasovagal syncope

A

lifestyle changes: trigger avoidance, increased fluid and salt intake, compression stockings

medical therapy to improve BP:
- fludrocortisone
- midodrine

264
Q

What is the gold standard investigation for vasovagal syncope?

A

tilt table test - will induce cardioinhibitory and vasodepressor response and lead ot hypotension

265
Q

RF for haemorrhoids

A

pregnancy
obesity
increased age
increased intraabdominal pressure (e.g. weight lifting, chronic coughing), constipation

266
Q

how do haemorrhoids present?

A

painless bright red bleeing
pruritis
anal mass
perianal pain ( if thrombosed)

267
Q

how are haemorrhoids classified

A

internal and external
internal is above the dentate line while external is below

268
Q

what are the 4 grades of internal haemorrhoids

A

1- no protrusion into the anal canal
2- protrusion on straining
3- protrusion that is manually reducible
4- permanent protrusion

269
Q

which type of haemorrhoid can cause pain?

A

external (as below the dentate line so sensate skin)

270
Q

1st line treatment of haemorrhoids

A

conservative management (soften stools) and topical anaesthetic or corticosteroids

271
Q

surgical mangament options for haemorrhoids

A

rubber band ligation
injection sclerotherapy
surgical removal

272
Q

what is peripheral arterial disease?

A

a range of arterial syndromes characterised by reduced blood flow to the extremities - most commonly the aortic-ileac and infra-inguinal arteries

273
Q

What are the three conditions included in peripheral arterial disease

A

intermittent claudication
acute limb ischaemia
critical limb ischaemia

274
Q

What are RF for peripheral arterial disease?

A

smoking, diabetes, atherosclerosis, hypertension, physical inactivity, obesity

275
Q

what is the most common cause of peripheral arterial disease

A

atherosclerosis

276
Q

aside from atherosclerosis what else can cause peripheral arterial disease

A

coarctation of the aorta
arterial dissection
arterial embolism
arterial thrombus
vasospasm
tumour

277
Q

how does intermittent claudication present?

A

crampy pain after physical activity
stopping causes the pain to go away
common in the calf muscles

278
Q

how does acute limb ischaemia present

A

rapid onset of limb ischaemia occuring due to a blockage of the arterial supply
presents with:
- pain
- pallor
- pulselessness
- perishingly cold
- paraesthesia

279
Q

How will acute limb ischaemia caused by a thrombus and an embolus differ

A

if caused by a thrombus there will be pre-existing claudication with sudden deterioration
if caused by an embolus there will be no pre-existing claudication with sudden onset of painful leg

280
Q

What is critical limb ischaemia

A

end stage peripheral arterial disease
there will be pain at rest, ulcers and gangrene
typical presentation is burning pain that is worse at night as the leg is raised

281
Q

What is Leriche syndrome

A

occlusion of the distal aorta or proximal iliac artery leading to a triad of
- thigh/buttock claudication
- absent femoral pulses
- male impotence

282
Q

how do arterial ulcers present

A

small, deep, well defined borders, punched out appearance and pain

283
Q

What is Buerger’s test

A

a test to identify peripheral arterial disease
- patient lays down and lifts legs to 45 degrees for 1-2 mins
- pallor suggest there is insufficient arterial supply to overcome gravity
- then get patient to sit up and hang legs over the edge of the bed
- in healthy legs they will go pink however in peripheral arterial disease they will go blue first and then dark red

284
Q

How can peripheral arterial disease be diagnosed

A

ankle-brachial pressure index

285
Q

what value of ABPI suggests critical limb ischaemia

A

less than 0.3

286
Q

what value on ABPI suggests mild arterial disease

A

0.6 to 0.9

287
Q

what value of APBI suggests moderate to severe peripheral arterial disease

A

0.6 to 0.3

288
Q

what does an APBI above 1.3 suggest

A

calcification of the arteries making them difficult to compress

289
Q

first line treatment of peripheral arterial disease

A

atrovastatin and clopidogrel

290
Q

what lifestyle changes should be recommended for patients with peripheral arterial disease?

A

stop smoking
optimise medical treatment of comorbidities
exercise training

291
Q

what surgical options can treat peripheral arterial disease?

A

endarterectomy
surgical bypass with autologous or prosthetic material
amputation

292
Q

endovascular techniques for peripheral arterial disease

A

percutaneous transluminal angioplasty +/- stent placement

293
Q

which patients should be treated with endovascular techniques for PAD

A

short segment stenosis (<10cm) , aortic iliac disease and high risk patients

294
Q

which patients should be treated with surgical techniques for PAD

A

those with long segment stenosis (>10cm), multifocal lesions, lesions of the common femoral and purely popliteal disease

295
Q

what dilatory drug may be used in severe PAD which is associated with poor QoL

A

naftridofuryl oxalate

296
Q

How does trichomonas vaginalis present on light microscopy-

A

motile trophozoites

297
Q

What is reactive arthritis

A

arthritis occurring after an infection - most commonly urogenital (chlamydia, gonorrhoea) and GI infections (salmonella, shigella)

298
Q

What group of diseases is reactive arthritis part of?

A

spondyloarthropathies- associated with HLA B27

299
Q

How does reactive arthritis present?

A

asymmetrical oligoarthritis, usually of the lower limb (painful red swollen knee)
inflammatory back pain
dactylitis
enthesitis
extra-articular manifestations ( keratoderma blenorrhagica, circinate balnitis, uveitis)

300
Q

what are the extra articular manifestations of reactive arthritis

A

cant see cant wee cant climb a tree
- uveitis, conjunctivitis
- circinate balanitis
- enthesitis

301
Q

What is enthesitis

A

inflammation of the insertion of soft tissue to bone- tendons, fascia
Commonly on ankle causing archilles tendonitis and planta fascia

302
Q

What is keratoderma blenorrhagica

A

Skin lesions similar to psoriasis on the palms and the soles

303
Q

what is circinate balanitis

A

dermatitis on the glans penis

304
Q

first line treatment for reactive arthritis

A

symptomatic control - NSAIDS

305
Q

Treatment of reactive arthritis

A

NSAIDS
intra-articular steroids
If unresponsive DMARDS- methotrexate
if chronic biologics - anti-TNF agents (e.g. infliximab)

306
Q

Usual time course of reactive arthritis

A

typically arises around 4 weeks after the initial infection
symptoms usually last 4-6 months

307
Q

What types of lesions make up acne

A

non-inflammatory comedones (whiteheads and blackheads)
inflammatory papules, pustules, nodules and cysts

308
Q

Pathophysiology of acne

A
  1. sebaceous gland hyperplasia and excess sebum production
  2. abnormal follicular differentiation - keratinocytes usually shed however in acne they are retained due to inreased cohesiveness
  3. cutibacterium acne colonisation
  4. inflammation and immune response
309
Q

What bacteria is mainly present in acne

A

c. acnes

310
Q

What is acne fulminans

A

a severe form of acne accompanied by systemic features that require hospitalisation and corticosteroids

311
Q

First line treatment of mild - moderate acne

A

12 week course of topical combination therapy (one of the below combinations)

topical adapalene + topical benzy peroxide

Topical tretinoin and topical clindamycin

Topical benzy peroxide and topical clindamycin

312
Q

Treatment of acne if 12 week combination therapy does not work?

A

add in oral lymecycline or doxycycline , or add in topical azelaic acid

313
Q

if a pregnant women experiences acne what should definitely not be involved in the treatment

A

tetracycines- lymecycline
(erythromycin can be used instead)

314
Q

what could be considered in the treatment of acne in women

A

the combined oral contraceptive pill

315
Q

what COCP has antiandrogen properties and why is it not used first line in acne treatment

A

dianette (co-cyprindiol)
has a higher risk of DVT

316
Q

Which patients with acne should be referred to dermatology

A

acne that hasnt responded to treatment
acne with scarring
acne with persistent pigmentary changes
patients with nodulo-cystic acne
acne causing severe psychological distress
patients with conglobate acne

317
Q

what is an anal fissure

A

a longitudinal or eliptical tear of the squamous lining of the distal anal canal

318
Q

what are secondary causes of anal fissures

A

constipation
IBD
STIs
colorectal cancer
anal trauma
adverse drug reactions
pregnancy and childbirth

319
Q

What is an acute anal fissue

A

one that has been present for less than 6 weeks

320
Q

what is a chronic anal fissure

A

one that has been present for more than 6 weeks

321
Q

how do anal fissures present

A

painful bright red rectal bleeding

322
Q

what is the treatment of acute anal fissures

A

soften stool- high fibre diet, high fluid intake, bulk forming laxatives
lubricants before passing stool - petroleum jelly
topical anaesthetics
analgesia

323
Q

first line treatment of anal fissures that are present for > 1 week

A

topical glyceryl trinitrate (GTN) twice daily for 6-8 weeks

324
Q

If topical GTN is not effective after 8 weeks in treating anal fissures what may be considered

A

sphincterotomy or botulism toxin

325
Q

what type of reaction is anaphylaxis

A

a type I hypersensitivty reaction

326
Q

pathophysiology of anaphylaxis

A

SENSITISATION:
- an allergen enters the body and is taken up by an antigen presenting cell
- this interacts with a T helper 2 cell
- this stimulates B cells to produce specific IgE to the allergen
- the IgE binds to mast cells and basophils

RE-EXPOSURE:
- when the allergen enters the body again mast cells with the specific IgE will bind to it
- this leads to activation and degranulation causing the release of pro-inflammatory mediators (histamine, tryptase, cytokines)
- the mediators cause local inflammation, vessel dilation, loss of vascular integrity and fluid extravasation causing oedema
- the oedema and vasodilation causes airway obstruction, bronchoconstriction and reduced cardiac output

327
Q

Presentation of anaphylaxis

A

sudden onset of :
- airway problems: swelling of the throat and tongue
- breathing problems: resp wheeze, SOB
- circulation problems: hypotension, tachycardia

And skin symptoms: urticaria, itching, angiooedma

328
Q

dose of adrenaline in under 6 months

A

100-150 micogram

329
Q

dose of adrenaline in 6 months - 6 years

A

150 micrograms

330
Q

dose of adrenaline in 6-12 years

A

300 micrograms

331
Q

does of adrenaline in >12 years

A

500 micrograms

332
Q

what blood test can confirm anaphylaxis (after treatment)

A

mast cell tryptase

333
Q

when should mast cell tryptase tests be done in anaphylaxis

A
  • immediately after treatment
  • 1-2 hours after
  • 24 hours after (gives baseline level)
334
Q

what is refractory anaphylaxis

A

respiratory and/or cardiovascular problems that persist despite 2 doses of IM adrenaline

335
Q

Management of refractory anaphylaxis

A

IV fluids for shock
IV adrenaline infusion

336
Q

management of anaphylaxis after stabilisation

A

non-sedating oral antihistamines (e.g. chlorphenamine) if remaining skin reaction

referral to a specialist allergy clinic if first time

2 adrenaline autoinjectors

337
Q

What is folliculitis?

A

inflammation of the hair follicles

338
Q

what pathogen is most commonly involved in folliculitis

A

staphylococcus aureus

339
Q

what is the most common cause of septic arthritis in young adults

A

gonorrhoea

340
Q

what is the first line investigation of genital herpes?

A

NAAT (not viral culture)

341
Q

what might an area of rapidly worsening eczema be a sign of

A

eczema herperticum

342
Q

how does primary syphilis present

A

painless ulceration and lymphadenopathy

343
Q

give examples of non-sedating antihistamiens

A

loratadine
cetirizine
fexofenadine

344
Q

what malignancies is EBV associated with

A

burkitt’s lymphoma
non-hodgkins lymphoma
naso-pharyngeal carcinoma

345
Q

How does eczema herpeticum present?

A

monomorphic punched out erosions usually 1-3 mm in diameter

346
Q

how long might it take for finasteride to start working on BPH

A

6 months

347
Q

if treatment of a upper respiratory tract infection with amoxicillin leads to a widespread maculopapular itchy rash what is the likely cause

A

EBV

348
Q

what is presbycusis

A

age related sensorinerual hearing loss

349
Q

If an anal fissure is lateral what investigation should be done

A

faecal calprotectin (normal anal fissures are usually in the posterior midline)

350
Q

what are common x ray findings of psoriatic arthritis

A

plantar spur and pencil in cup deformitites

351
Q

What is urge incontinence?

A

incontinence caused by overactivitiy of the detrusor muscle of the bladder.

352
Q

How does urge incontinence present?

A

sudden urges to pass urine, having to rush to the bathroom and then not arriving before urination occurs.
People may avoid activities where a toilet isnt easily accessible

353
Q

What is stress incontinence?

A

incontinence due to weakness of the pelvic floor and sphincter muscles

354
Q

How does stress incontinence present?

A

urinary leakage while coughing, laughing or when suprised

355
Q

What is overflow incontinence

A

incontinence that occurs when there is chronic urinary retention due to an obstruction in the outflow tract.

356
Q

How does overflow incontinence present?

A

overflow of urine causing incontinence without the urge to pass urine

357
Q

What can cause overflow incontinence

A

anticholinergic drugs, fibroids, neuro conditions (MS, diabetes, spinal cord injury), prostate enlargement

358
Q

What is functional incontinence

A

when a comorbid physical condition impairs someones ability to get to the bathroom in time - may be caused by dementia, sedating medication, injury

359
Q

investigations of urinary incontinence

A

1st - bladder diary for minimum of 3 days
urine dipstick
vaginal examination
urodynamic studies

360
Q

what are examples of urodynamic studies

A

cystometry
uroflowmetry
leak point pressure
post-void residual bladder volume

361
Q

lifestyle changes for urinary incontinence

A

avoid caffeine, alcohol, diuretics
restrict fluid intake
weight loss

362
Q

1st line treatment of stress incontinence

A

pelvic floor exercises - at least 8 contractions performed at least 3 times a day for a minimum of 3 months

363
Q

1st line drug treatment of stress incontinence

A

duloxetine

364
Q

surgical procedures for stress incontinence

A

tension-free vaginal tape, autologous sling procedure, coposupsension, intramural urethral bulking

365
Q

1st line treatment of urge incontinence

A

bladder retraining for 6 weeks

366
Q

1st line drug treatment for urge incontinence in young

A

anticholinergic medications- oxybutynin, tolterodine

367
Q

1st line drug treatment of urge incontinence in elderly

A

mirabegron

368
Q

SE of mirabegron

A

raised BP- hypertensive crisis
increases TIA and stroke risk

369
Q

invasive treatments of urge incontinence

A

botulinum toxin
sacral nerve stimulation,

370
Q

what is the most common cause of leg ulcer?

A

venous ulcer

371
Q

Where do most venous ulcers occur?

A

the gaiter area (between the top of the foot and the bottom of the calf muscle

371
Q

RF for venous ulcers

A

increasing age
obesity
immobility
limited ankle motion
previous ulcer
family or personal history of varicose veins
history of DVT
female sex
multiple pregnancies
history of leg trauma

372
Q

pathophysiology of venous ulcers

A

occurs due to sustained venous hypertension leading to chronic venous insufficiency due to venous valve incompetence or impaired calf muscles

373
Q

how do venous ulcers present?

A
  • gaiter area
  • large, superficial ulcers
  • gently sloping edges
  • symptoms worse at end of the day and relieved by raising leg
  • chronic venous skin changes (hyperpigmentation, venous eczema, lipdermatosclerosis)
374
Q

Investigation of venous ulcers

A

ABPI to assess for any arterial disease (normal is 0.9 to 1.2)
FBC
ESR and CRP

375
Q

1st line treatment of venous ulcers

A

compression bandages (need to exclude arterial disease)

376
Q

drug treatment of venous ulcers

A

oral pentoxyfylline- peripheral vasodilator that improves healing rate

377
Q

What are varicose veins?

A

dilated superficial veins commonly found on the lower limbs

378
Q

RF for varicose veins

A

age
pregnancy
female
woman
previous DVT

379
Q

Pathophysiology of varicose veins

A

increased pressure in the small superficial veins due to venous insufficiency caused by valvular incompetence

380
Q

how do varicose veins present?

A

can be asymptomatic
May have:
- pain/tenderness
- pruritis
- restless legs
- cramps
- bleeding
- dilated superficial veins
- venous eczema

381
Q

Diagnosis of varicose veins

A

venous duplex USS - demostrates retrograde venous flow

382
Q

conservative treatment of varicose veins

A

weight loss
avoid prolonged standing
elevate legs when possible
compression stockings
regular exercise

383
Q

What indications are there to refer someone with varicose veins to vascular surgery

A

symptomatic primary or recurrent varicose veins
skin changes
superficial vein thrombosis and suspected venous incompetence
active venous ulcer
healed venous ulcer

384
Q

What are potential invasive treatments for varicose veins

A

sclerotherapy - irritant foam is injected into a vessel and causes closure of the vein
Endothermal ablation
phlebectomy
high ligation and vein stripping

385
Q
A
386
Q

Which of episcleritis and scleritis is painful

A

Scleritis

387
Q

What two causes of vaginal discharge create a pH greater than 4.5

A

Trichomonas vaginalis and bacterial vaginosis

388
Q

What is the most common form of prostate cancer

A

Adenocarcinoma

389
Q

What bacteria is associated with bacterial keratitis in contact lens wearers

A

Pseudomonas aeuginosa

390
Q

What type of bacteria cause lyme’s disease?

A

Spirochetes

391
Q

Most common bacteria associated with lymes disease

A

Borrelia burgdoferi

392
Q

How is lymes disease spread?

A

The bacteria is transmitted to humans via ticks
Ticks attach onto humans to have a ‘blood meal’
The longer they are attached the increased likelihood of transmission

393
Q

After how long of attachment is lymes disease usually spread from ticks

A

After being attached for 36-48 hours

394
Q

If not treated, what three phases will lymes disease go through

A
  1. Early localised disease - expanding target like rash of erythema migrans 1-36 days after tick bite
  2. Early disseminated disease- weeks to months after bite, patients have multiple secondary erythema migrans, arthritis, carditis, cranial nerve palsy
  3. Late disseminated disease - presents months to years after the initial infection, oligoarthritis, skin manifestations and involvement of the peripheral nervous system
395
Q

What is post treatment Lyme disease syndrome

A

Persisting symptoms of lymes disease such as fatigue, pain or joint and muscle aches

396
Q

Describe the rash associated with erythema migrans

A

Erythema migrans
Target like rash - bulls eye
Develops 1-4 weeks after bite

397
Q

How is lymes disease diagnosed

A

If erythema migrans is present it can be diagnosed clinically
If not then ELISA test for antibodies to Borrelia burgdorferi is 1st line test

398
Q

If the ELISA test is negative for Lymes disease what should be done

A

If tested within 4 weeks of symptom onset it should be repeated after another 4-6 weeks
If still negative after 12 weeks the immunoblot test should be done

399
Q

How are asymptomatic tick bites treated

A

Remove the tick if still present- fine tipped tweezers, grasp as close to skin as possible and then wash skin

400
Q

Management of confirmed/suspected Lyme disease

A

Doxycycline if early disease
Ceftriaxone if disseminated disease

401
Q

What reaction might occur after starting antibiotics for Lymes disease

A

Jarisch- Herxheimer reaction

402
Q

What bacteria causes syphilis

A

Treponema pallidum

403
Q

RF for syphilis

A

Unprotected sex, multiple sexual partners, transactional sex, substance misuse, social vulnerability

404
Q

Incubation period of syphilis

A

21 days

405
Q

How does primary syphilis present?

A

A painless ulcer (chancre) and local lymphadenopathy

406
Q

How long after infection does secondary syphilis present?

A

6-10 weeks post infection

407
Q

How does secondary syphilis present?

A

Systemic involvement including skin and hair changes, maculopapular rash on trunk palms and soles, condylomata lata (moist wart like lesion on the genitalia), patchy alopecia, oral lesions (snail tract lesions), generalised lymphadenopathy and low grade fever

408
Q

What is early latent syphilis

A

Confirmed infection without any current features

409
Q

What classifies late syphilis

A

More than 2 years after infection

410
Q

What two phases of latent syphilis are there?

A

Late latent syphilis where there is confirmed disease but no current features
Tertiary syphilis- granulomatous lesions on the skin and bone (Gummas), cardiac disease (aortic aneurysms), and/or neurological disease (general paralysis of the insane, tabes dorsalis, Argyll - Robertson pupil_

411
Q

Features of tertiary syphilis

A

Gummas (granulomatous lesions of the skin and bone)
Ascending aortic aneurysms
General paralysis of the insane
Tabes dorsalis
Argyll Robertson pupil

412
Q

What two types of serological tests can be used to test for syphilis

A

Non-treponemal tests - not specific to syphilis but looks at the reactivity of serum to cardiolipin-cholesterol-lecithin antigen

413
Q

side effect of doxycylcine

A

photosensitivity

414
Q

what is the treatment of severe urticaria where antihistamines dont work

A

a short course of oral steroids

415
Q

how often can adrenaline be given

A

every 5 mintues

416
Q

How can you differentiate spinal stenosis and peripheral arterial disease

A

Spinal stenosis is more likely to have:
- pain the improves with sitting down or crouching
- weakness in the leg
- lack of smoking history
- lack of cardiovascular history

417
Q

what is the most common cause of anaphylaxis in children

A

food

418
Q
A
419
Q

How should utis be treated in patients on methotrexate

A

Nitrofurantoin- trimethoprim caused bone marrow suppression

420
Q

Blood film findings of coeliac disease

A

Howell jolly bodies and targets cells

421
Q

what is the most sensitive test for pernicious anaemia

A

anti-parietal cell antibodies-
anti - intrinsic factor antibodies are highly specific but not very sensitive

422
Q

how does normal pressure hydrocephalus present on neuroimaging?

A

ventricular enlargement with relative perservation of cortical sulci

423
Q

How would you manage arterial stenosis in PAD of less than 10cm

A

endovascular revascularisation (angioplasty)

424
Q

Causes of atrial fibrillation and how to remember?

A

mrs SMITH
Sepsis
Mitral valve pathology (stenosis or regurgitation)
Ischaemic heart disease
Thyrotoxicosis
Hypertension

425
Q

Overall features of the pathology of AF (4)

A
  • irregularly irregular ventricular contractions
  • tachycardia
  • heart failure due to poor filling of the ventricles during diastole
  • increased stroke risk due to pooling of the blood in the heart
426
Q

What are the 4 classifications of AF

A

paroxysmal
acute
persistent
permanent

427
Q

what defines paroxysmal AF

A

AF that spontaneously stops within 7 days

428
Q

What defines acute AF

A

AF that started within 48 hours

429
Q

What defines persistent aF

A

AF that lasts for more than 7 days and is not self-terminating

430
Q

How might AF present ?

A

palpitations
dyspnoea
dizziness
syncope
chest pain
irregularly irregular pulse

431
Q

What 3 findings are there on ECG in AF

A
  • absent P waves
  • narrow QRS complex tachycardia
  • irregularly irregular ventricular rhythmn
432
Q

When would you do rhythm control in AF

A
  • patient has heart failure due to AF
  • patient has new onset AF within the past 48 hours
  • patient has a reversible cause of their AF
433
Q

What is the first line rate control for AF?

A

beta blocker (bisoprolol) or CCB (not in HF)

434
Q

what is second line rate control in AF

A

combine 2 of bisoprolol, CCB or digoxin

435
Q

what two types of rhythmn control are there in AF

A

pharmacological - IV amiodarone
electrical

436
Q

when would you do immediate and when would you do delayed cardioversion

A

immediate if AF onset was within 48 hours or if the patient is haemodynamically unstable

delayed if over 48 hours since onset and patient is table

437
Q

describe delayed cardioversion

A

patient takes anticoagulants for >3 weeks and then has cardioversion

438
Q

What invasive treatment may be used for AF if drug treatment is inadequate of not tolerated?

A

catheter ablation

439
Q

What is the first line anticoagulant in AF?

A

DOAC - apixaban

440
Q

what is the second line anticoagulant in AF?

A

warfarin

441
Q

What scoring system can be used to determine if someone with AF needs anticoagulation?

A

CHA2DS2VASc score

442
Q

What makes up the CHA2DS2VASC ?

A

Congestive HF = 1
Hypertension= 1
Age >75 =2
Diabetes
Stroke or TIA history =2
Vascular disease= 1
Age 65-74= 1
Sex- female= 1

443
Q

What score on the CHA2DS2VASc indicates anticoagulation?

A

2 (1 in males)

444
Q

What are causes of COPD

A

smoking causes 90% of cases
alpha 1 antitrypsin deficiency
occupational exposures

445
Q

how does alpha-1-antitrypsin cause COPD?

A

alpha-1-antirypsin is a protease inhibitor that opposes the action of elastase in the lungs
If decreased elastase can break down elastin in the wall of the alveoli

446
Q

two types of patients with COPD

A

pink puffers (emphysema) and blue bloaters (chronic bronchitis)

447
Q

describe chronic bronchitis

A

chronic cough lasting 3 months or more, occurs due to chronic inflammation of the bronchi

448
Q

microscopic features of chronic bronchitis

A

goblet cell hyperplasia
mucus hypersecretion
chronic inflammation and narrowing of the small airways

449
Q

describe emphysema

A

damage and dilation of the alveoli decreasing the surface area for gas exchange to occur in the lungs

Occurs as inflammatory cells produce proteases that break down elastin in the walls of the alveoli

450
Q

How does COPD present?

A

chronic productive couhg
breathlessness
frequent infections
wheeze
pursed lip breathing
signs of right heart failure

451
Q

How is COPD diagnosed?

A

spirometry shows FEV1/FVC < 70% with no/little reversibility

Chest X ray

FBC - may show secondary polycythaemia in response to chronic hypoxia

452
Q

what can be seen on chest X ray of COPD (3)

A

hyperinflation of the lungs
flattened hemidiaphragm
bullae

453
Q

What general management is used in COPD

A

stop smoking
annual flu vaccine
pneumonoccal vaccine

454
Q

Management of COPD

A
  1. SABA or SAMA
  2. Determine if steroid response or not
    - if responsive add LABA and ICS
    - if not responsive add LABA and LAMA
  3. SABA as needed then triple therapy : LABA, LAMA and ICS
455
Q

What medications may be able to reduce risk of COPD exacerbations

A

prophylactic azithromycin
mucolytics
phosphdiesterase inhibitors (roflumilast)

456
Q

What is the most common pathogen associated with COPD exacerbations

A

haemophilus influenzae

457
Q

What features suggest that COPD is steroid responsive (4) ?

A

atopy or asthma diagnosis
variation in FEV1 of more than 400ml
raised blood eosinophils
diurinal variability in PEF

458
Q

criteria for having long term oxygen therapy in COPD

A

NO SMOKING

A pO2 < 7.3kPa or 7.3-8 if one of the following features is present:
- secondary polycythaemia
- peripheral oedema
- pulmonary hypertension

459
Q

why does cor pulmonale occur in COPD

A

chronic hypoxia causes vasoconstriction of the pulmonary vessels
This increases pulmonary pressure and causes right heart failure

460
Q

Explain heart failure with a reduced ejection fraction, including some specific causes

A

heart failure with an ejection fraction less than 50%
Usually due to systolic dysfunction
Causes include:
- IHD
- arrhythmias
- dilated cardiomyopathy
- myocarditis

461
Q

Explain heart failure with a preserved ejection fraction and give some causes

A

heart failure with an ejection fraction more than 50% , usually due to diastolic dysfunction during filling
causes include:
- hypertrophic obstructive cardiomyopathy
- restricted cardiomyopathy
- cardiac tamponade

462
Q

Presentation of heart failure (7)

A

breathlessness
peripheral oedema
cough- pink, white frothy
orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema
fatigue

463
Q

signs of heart failure (8)

A

tachycardia
tachypnoea
hypertension
murmurs
3rd heart sound
bibasal crackles
raised JVP
peripheral oedema

464
Q

first line investigation for heart failure

A

NT-proBNP

465
Q

investigation of heart failure after BNP (and how quickly should it be done)

A

if BNP is between 400-2000 then echo within 6 weeks
if BNP is over 2000 then echo in 2 weeks

466
Q

what can cause falsely raised BNP (9)

A

LV hypertrophy
ischaemia
tachycardia
eGFR <60
sepsis
COPD
diabetes
>70
liver cirrhosis

467
Q

What can cause a falsely low BNP (6)

A

obesity
diuretics
ACEi
beta blockers
ARB
aldosterone agonists

468
Q

what may be seen on chest x ray of someone with heart failure

A

Alveolar oedema
Kerly B lines
Cardiomegaly
Dilated upper lobe veins
pleural Effusion

469
Q

what classification system is used in heart failure

A

the NYHA classification
1- no symptoms
2- mild symptoms on activity
3- moderate symptoms on any activity
4- symptoms at rest.

470
Q

1st line management of heart failure

A

ACEi and beta blocker

471
Q

What may be added to ACEi and beta blocker if heart failure is not controlled

A

aldosterone antagonist (spironolactone)

472
Q

what specialist drugs may be used to manage heart failure (5)

A

ivabradine
SGLT-2 inhibitor
ivabradine
hydrazalizine with a nitrate
digoxin

473
Q

X ray findings of osteoarthritis

A

LOSS
Loss of joint space
Osteophyte formation
Subchondral sclerosis
subchondral cysts

474
Q

what type of bony deformities might be seen in osteoarthritis

A

Herbeden’s nodes - swelling of DIP

Bouchard’s nodes - swelling of PIP

475
Q

1st line management of osteoarthritis

A

oral paracetamol and topical NSAIDs

476
Q

2nd line management of osteoarthritis

A

oral NSAIDs +PPI cover

477
Q

RF for osteoporosis

A

SHATTERED
steroid use
hyperthyroidism/hyperparathyroidism
Alcohol and tobacco
thin (BMI <22)
testosterone reduced
Early menopause
Renal/liver disease
Erosive/inflammatory disease
Decreased dietary calcium and diabetes

478
Q

What are fragility fractures?

A

a fracture from a fall from standing height or less
most commonly of the wrist spine and hip

479
Q

What scan is used to measure bone density in osteoporosis?

A

DEXA scan

480
Q

What defines osteoporosis on a DEXA scan

A

a bone mineral density 2.5 standard deviations away from peak mass (of an average young person)- shown by a T score of -2.5 or less

481
Q

what result of a DEXA suggests osteopenia

A

-2.5 to -1.0

482
Q

what risk score can be used to assess for osteoporosis?

A

FRAX - measures the risk of a patient having an osteoporotic fracture in the next 10 years.
If > 10% should DEXA

483
Q

Who should be offered a DEXA scan?

A
  • Those over 50 with a history of a fragility fracture
  • those less than 40 if they have a major risk factor
484
Q

1st line management of osteoporosis

A

Bisphosphonates- taken weekly on an empty stomach (e.g. alendronate)

485
Q

2nd line management of osteoporosis

A

denosumab (monoclonal antibody that targets osteoclasts)

486
Q

pathophysiology of type 1 diabetes

A

autoimmune destruction of the insulin secreting beta cells in the islets of langerhans of the prancreas

487
Q

pathophysiology of type 2 diabetes

A

repeated insulin and glucose exposure causes cells to become resistant to insulin
This means that more insulin is needed to have the desired effect
Overtime the pancreas becomes tired and starts to reduce insulin production

488
Q

what fasting glucose level is indicative of diabetes?

A

7 mmol/l

489
Q

what result on the oral glucose tolerance test/ random plasma glucose test is indicative of diabetes?

A

11.1 mmol/l

490
Q

what level HbA1c is indicative of diabetes?

A

> 48 mmol/mol (>6.5%)

491
Q

what level HbA1c is indicative of pre-diabetes?

A

42-27mmol/mol (6-6.4%)

492
Q

how often should HbA1c be measured in diabetes?

A

every 3 - 6 months

493
Q

what should be the aimed HbA1c in newly diagnosed diabetics?

A

48 mmol/mol

494
Q

what should be the aimed HbA1c in diabetes treated on more than one diabetes medication?

A

53mmol/mol

495
Q

give an example of a short acting insulin

A

actrapid

496
Q

give and example of a long acting insulin

A

lantus

497
Q

1st line treatment of type 2 diabetes?

A

metformin +/- SGLT-2 inhibitor

498
Q

who is given an SGLT-2 inhibitor in diabetes?

A

those with an increased cardiovascular risk (QRisk > 10%) , established cardiovascular disease or heart failure

499
Q

what should be given first line if metformin is contraindicated ?

A

if CVD risk - SGLT-2 inihibitor
If no CVD risk - piolglitazone, sulfonylurea or DPP-4 inhibitor

500
Q

what should be given first line if metformin isnt tolerated due to GI side effects?

A

modified release metformin

501
Q

what is given second line if diabetes is not controlled with metformin

A

One of the following:
- DDP-4 inhibitor
- pioglitazone
- sulfonylurea
- SGLT-2 inhibitor

502
Q

What is given 3rd line for the treatment of T2DM

A

triple therapy or insulin

503
Q

what can be given if T2DM is not controlled on triple therapy, or if insulin isn’t suitable

A

one of the medications can be swaped to a GLP-1 mimetic

504
Q

action of metformin

A

increase insulin sensitivity and decrease hepatic glucogenesis

505
Q

SE of metformin

A

GI upset
lactic acidosis due to AKI

506
Q

what eGFR is requried for metformin ?

A

> 30

507
Q

action of SGLT-2 inhibitors ?

A

inhibit reabsorption of glucose in the kidneys by blocking the SGLT-2 channel

508
Q

examples of SGLT-2 inhibitors (2)

A

empaglflozin
dapagliflozin

509
Q

SE of SGLT-2 inhibitors

A

UTI and thrush due to glycosuria
weight loss
hypoglycaemia- DKA

510
Q

what type of drug is pioglitazone

A

a thiazolidinedione

511
Q

action of pioglitazone

A

activates the PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

512
Q

SE of pioglitazone

A

weight gain
fluid retention
increase bone fractures
bladder cancer

513
Q

action of sulfonylurea

A

stimulates insulin release from the pancreas

514
Q

example of a sulfonylurea

A

gliclazide

515
Q

SE of sulfonylureas

A

weight gain
hypoglycaemai

516
Q

examples of DPP-4 inhibitors

A

sitagliptin
alogliptin

517
Q

action of DPP-4 inhibitors

A

increase incretin levels which is a hormone that inhibits glucagon secretion

518
Q

SE of DPP-4 inhibitors

A

usually well tolerated by can cause headaches, acute pancreatitis

519
Q

action of GLP-1 mimetic

A

mimic incretin and inhibit glucagon release

520
Q

SE of GLP-1 mimetic

A

nausea and vomiting
pancreatitis
weight loss

521
Q

what is acute bronchitis?

A

a self limiting lower respiratory tract infection caused by infection of the bronchial airways, not lung parenchyma

522
Q

Most common cause of acute bronchitis

A

usually viral infections - coronavirus, rhinovirus, RSV, adenovirus

523
Q

presentation of acute bronchitis

A

cough
rhinorrhoea
sore throat
wheeze
low grade fever

524
Q

How can acute bronchitis be differentiated from pneumonia on examination?

A

there will be an absence of focal chest signs- consolidation, crackles

525
Q

What test may be done in acute bronchitis if considering antibiotics?

A

CRP

526
Q

What CRP cut off is used to determine if immediate antibiotics should be given in acute bronchitis?

A

> 100

527
Q

Management of acute bronchitis (4)

A

analgesia
fluid intake
antibiotics may be considered- if CRP 20-100 consider delayed Abx, if > 100 give immediately
May consider giving a SABA

528
Q

What is an acute stress reaction?

A

also known as psychological shock - a psychiatric condition that manifests after exposure to severe stress or traumatic events

529
Q

How might an acute stress reaction present?

A

cognitive symptoms:
- confusion
- disorientation
- intrusive thoughts
- derealisation and depersonalisation

Behavioural symptoms:
- avoidance behaviour
- hypervigilance

Physiological symptoms:
- tachycardia and hypertension
-sweating and trembling

530
Q

how is acute stress reaction be differentiated from panic disorder and PTSD?

A

ASR is more situational than panic disorder
PTSD is when ASR has occurs from over 4 weeks

531
Q

Management of acute stress reaction

A

1st line - trauma focused CBT

benzodiazepines may have benefit in short term

532
Q

If an antibioitic is prescribed in acute bronchitis what is usually recommended?

A

doxycyline

533
Q

what yeast infection is the most common cause of thrush?

A

candida albicans

534
Q

RF for thrush

A
  • increased oestrogen (higher in pregnancy, lower post menopause and pre-puberty)
  • poorly controlled diabetes
  • immunosuppression
  • broad spectrum antibiotic use
  • local irritants
  • sexual activity
  • HRT
535
Q

How can thrush be differentiated from BV on swab?

A

in thrush the vaginal pH is < 4.5 whereas in BV it is likely > 4.5

536
Q

1st line treatment of thrush ?

A

oral fluconazole 150mg tablet

537
Q

what is another name for chronic fatigue syndrome?

A

myalgic encephalomyelitis

538
Q

what is chronic fatigue syndrome ?

A

a sudden or gradual onset of persistent disabling fatigue, post-exertional malaise, unrefreshing sleep, cognitive and autonomic dysfunction and pain

539
Q

For how long should chronic fatigue be present for a diagnosis?

A

NICE recommends after 3 months

540
Q

What investigations may be used to rule out other diagnosis in chronic fatigue syndrome?

A

FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening and also urinalysis

541
Q

What should be involved in the management of chronic fatigue syndrome?

A
  • CBT
  • energy management
  • sleep hygiene
542
Q

What are the four key symptoms that build the NICE criteria for chronic fatigue syndrme

A

disabling fatigue without a cause and not relieved by rest
post-exertional malaise
unrefreshing sleep
cognitive difficulties (brain fog)

543
Q

How can chronic kidney disease be differentiated from AKI?

A

renal USS- CKD usually has bilateral small kidneys

544
Q

How can CKD present?

A

may be asymptomatic
- fatigue
- pallor
- foamy urine
- muscle cramps
- itching (uraemia)
- loss of appetite
- oedema
- hypertension

545
Q

Common causes of chronic kidney disease

A

diabetes
hypertension
medications such as lithium and NSAIDS
glomerulonephritis
polycystic kidney disease

546
Q

what investigations may be involved in the diagnosis of CKD?

A

GFR
albumin creatinine urine ratio
haematuria on urine dipstick
USS
biopsy

547
Q

How can CKD be staged with GFR (give the values for each stage)

A

G1- >90
G2- 60 to 89
G3a - 45-59
G3b - 30-44
G4- 15-29
G5- < 15

548
Q

What are 4 main complications that can occur in CKD?

A

anaemia
renal bone disease
cardiovascular disease
peripheral neuropathy

549
Q

why does anaemia occur in CKD and how is it treated?

A

kidney cells produce EPO which stimulates the production of RBC

Can be treated with erythropoeisis stimulating agents such as erythropoietin and darbepoetin.

550
Q

What HLA are associated with coeliac disease?

A

HLA DQ2 and HLA DQ8

551
Q

what is the gold standard investigation for coeliac disease and what findings are there?

A

endoscopy and biopsy- shows crypt hyperplasia, villous atrophy and lymphocyte infiltration

552
Q

what vaccine is offered to those with coeliac disease?

A

5 yearly pneumococcal vaccine

553
Q

What malignancy can be associated with coeliac diseasE?

A

enteropathy-associated T-cell lymphoma of small intestine

554
Q

what three types of primary constipation are there?

A

normal transit (most common)
slow transit
dyssynergic defecation (can’t relax the pelvic floor muscles)

555
Q

list some causes of secondary constipation

A

Neuro- parkinsons, spinal cord injury, hirschprungs
Metabolic- hypercalcaemia
Endocrine - hypothyroidism
Medications- iron supplements, antispasmodics, calcium channel blockers, opiates
GI - IBD, strictures

556
Q

What criteria is used in the diagnosis of constipation

A

the rome IV criteria

557
Q

3 key features of constipation

A

infrequent stools (< 3 weekly)
difficulty passing stool
a sensation of incomplete emptying

558
Q

First line medication for constipation in adults

A

bulk forming laxatives- ispaghula husk

559
Q

second line medication for constipation in adults

A

osmotic laxative (e.g. macrogol, lactulose)

560
Q

How should faecal impaction be treated?

A

high dose macrogol with suppositories and enemas

561
Q

how do stimulant laxatives work and give and example

A

stimulate the local nervous system in the gut wall to increase contractility and secretions

example is senna

562
Q

Give some examples of newer therapies that may be given to those with ongoing constipation

A

prokinetics
secretagogues
opioid antagonists (naloxegol) - blocks opioid receptor in bowel to reduce constipation in those one opioids

563
Q

Complications of constipation

A

overflow diarrhoea
acute urinary retention
haemorrhoids

564
Q

first line laxative in children

A

movicol

565
Q

what two types of contact dermatitis are there?

A

irritant and allergic contact dermatitis

566
Q

what is contact dermatitis

A

an inflammatory skin condition that effects the epidermis and dermis and occurs as a result of exposure to an external irritant or allergen

567
Q

pathophysiology of allergic contact dermatitis and give an example

A

a delayed type IV hypersensitivity reaction

Commonly cosmetics, skincare, latex, plants, nickel

568
Q

difference in the presentation of irritant and allergic contact dermatitis

A

irritant can be quicker onset but is often less severe with localised area of erythema

allergic can develop over 24-72 hours and presents as acute weeping, blistering eczema

569
Q

gold standard diagnosis of contact dermatitis

A

patch testing

570
Q

what causes cutaneous warts?

A

infection of keratinocytes with HPV

571
Q

What types of warts are there?

A
  • common warts: firm raised papules resembling a cauliflower
  • plane warts- round, flat-topped wards
  • palmar and plantar warts (veruccae)
  • mosaic warts
  • filiform warts
572
Q

treatment of cutaneous warts

A

usually do not treat but may be done if painful, unsightly or on patients request.

  • topical salicylic acid
  • cryotherapy with liquid nitrogen
573
Q

secondary care treatment options for resistant warts

A

physical ablation
anitmitotic treatments
immunomodulatory therapy

574
Q

How does diverticulitis present?

A

abdominal pain
change in bowel habit
rectal bleeding
fever

575
Q

What is diverticulitis

A

symptomatic inflammation and infection of diverticular in the bowel (sac like protrusions of the colonic mucosa through the muscular wall)

576
Q

Complications of diverticulitis

A

perforation
abscess formation
fistulae to adjacent organs
haemorrhage

577
Q

Gold standard investigation for diverticulitis

A

contrast CT of abdo pelvis

578
Q

factors that contribute to the development of gout

A

purine overproduction- increased cell turnover or lysis (e.g. myeloproliferative disorders, psoriasis, chemotherapy )

increased purine intake- seafood, red meat

decreased uric acid excretion - diuretics, AKI, CKD

579
Q

Which joint is most commonly affected in gout

A

the first metatarsophalangeal joint

580
Q

gold standard investigation of gout

A

joint aspiration and microscopy- shows negatively bifringent needle shaped crystals

581
Q

why shouldn’t uric acid levels me measured in an acute attack of gout?

A

as levels often fall during an acute attack - instead should be measured 4-6 weeks after an attack

582
Q

what may be seen on x ray of gout

A

subcortical cysts or bone erosions

583
Q

what crystal causes gout

A

monosodium urate crystals

584
Q

first line management of acute gout

A

NSAIDs or colchicine

585
Q

second line management of acute gout

A

intra-articular or oral steroids

586
Q

1st line treatment in chronic gout

A

allopurinol

587
Q

how does allopurinol work?

A

xanthine oxidase inhibitor

588
Q

what can be used if allopurinol does not work/isnt tolerated in gout prevention

A

febuxostat

589
Q

what is the most common cause of tonsilitis?

A

group A beta haemolytic strep such as strep. pyogenes

590
Q

What are the two broad types of lung cancer?

A

small cell lung cancer and non-small cell lung cancer

591
Q

What is the most common category of lung cancer?

A

non-small cell lung cancer

592
Q

list some types of non-small cell lung cancer, which is most common?

A

adenocarcinoma (most common)
squamous cell (most associated with smoking)
large cell
alveolar cell
bronchial adenoma

593
Q

What is a mesothelioma and what is it associated with?

A

malignancy of the mesothelial cells of the pleura
Linked with asbestos exposure

594
Q

What extrapulmonary manifestions of lung cancer might be present?

A
  • hoarse voice- occurs due to compression of recurrent laryngeal nerve, most common in pancoast tumours
  • phrenic nerve palsy (leads to diaphragm weakness)
  • superior vena cava syndrome
  • horners syndrome
  • syndrome of inappropriate ADH
  • cushings (ectopic ACTH from small cell)
  • ectopic PTH -> hypercalcaemia
  • hypercal
595
Q

How does superior vena cava syndrome present?

A

facial swelling
difficulty breathing
distended veins in the neck and upper chest

596
Q

How is lung cancer diagnosed?

A

chest x ray
CT
bronchoscopy and biopsy
PET scan

597
Q

how might lung cancer present on x ray

A

hilar enlargement
peripheral opacity
pleural effusion
collapse

598
Q

How does lung cancer present?

A

shortness of breath
cough
haemoptysis
finger clubbing
recurrent pneumonia
weight loss
supraclavicular lymphadenopathy
metastases - bone pain

599
Q
A

3A (42 decks)

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