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Phase 3a > GP > Flashcards

GP Flashcards

1
Q

Define acne vulgaris?

A

Acne vulgaris is a common skin disorder which usually occurs in adolescence.

Typically affects the face, neck and upper trunk and is characterised by the obstruction of the pilosebaceous follicles with keratin plugs which results in comedones, inflammation and pustules

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2
Q

What is mild acne vulgaris?

A

Open and closed comedones with or without sparse inflammatory lesions

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3
Q

What is moderate acne vulgaris?

A

Widespread non-inflammatory lesions and numerous papules and pustules

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4
Q

What is severe acne vulgaris?

A

Extensive inflammatory lesions, which may include nodules, pitting, and scarring

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5
Q

What bacteria usually colonises in acne vulgaris?

A

Propionibacterium acnes

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6
Q

What is the management of mild-to-moderate acne?

A

12-week course of topical combination therapy should be tried first-line:

Topical adapalene with topical benzoyl peroxide
Topical tretinoin with topical clindamycin
Topical benzoyl peroxide with topical clindamycin

Topical benzoyl peroxide may be used as a monotherapy

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7
Q

What is the management for moderate-to-severe acne?

A

12-week course of one of the following options:

Topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline
Topical tretinoin with topical clindamycin
Topical adapalene with topical benzoyl peroxide
A topical azelaic acid + either oral lymecycline or oral doxycycline

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8
Q

What should be avoided in pregnancy in terms of acne management? What would an alternative be?

A

Tetracyclines - therefore avoid giving doxycycline.

Erythromycin can be given as an alternative

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9
Q

What can be considered as an alternative to oral antibiotics in women?

A

COOP - should be used in combination with topical agents

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10
Q

When can oral oral isotretinoin be prescribed in pregnancy?

A

Only under specialist supervision (dermatologist)

Pregnancy is a contraindication to this.

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11
Q

What are the features of eczema younger children?

A

Itchy, erythematous rash on the extensor surfaces
The face and the trunk are most affected

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12
Q

What are the features of eczema in older children?

A

Itchy, erythematous rash on the flexor surfaces and the creases of the neck and face

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13
Q

When is the typical presentation of eczema and when does it usually clear?

A

It typically presents before 2 years old.

Clears in around 50% of children by 5 years of age.

Clears in around 75% of children by 10 years of age.

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14
Q

What is the general management for eczema?

A

Avoid irritants
Steroid creams and emollients - increased in stepwise manner from weakest to strongest
Wet wrapping

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15
Q

What is the mild topical steroid used in eczema?

A

Hydrocortisone 0.5-2.5%

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16
Q

What is the moderate topical steroid used in eczema?

A

Betamethasone valerate 0.025% (Betnovate RD)
Clobetasone butyrate 0.05% (Eumovate)

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17
Q

What is the potent topical steroid used in eczema?

A

Fluticasone propionate 0.05% (Cutivate)
Betamethasone valerate 0.1% (Betnovate)

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18
Q

What is the very potent tropical steroid used in eczema?

A

Clobetasol propionate 0.05% (Dermovate)

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19
Q

What is the mnemonic used for stepwise management of topical steroids in eczema?

A

Help Every Budding Dermatologist
Hydrocortisone (mild)
Eumovate (moderate)
Betnovate 0.1 (potent)
Dermovate (very potent)

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20
Q

What is the causative organism of bacterial vaginosis?

A

Gardnerella vaginalis

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21
Q

What disease can gardnerella vaginalis cause?

A

Bacterial vaginosis

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22
Q

Describe the pathophysiology behind bacterial vaginosis?

A

An overgrowth of predominately anaerobic organisms leading to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH.

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23
Q

What are the classical features of bacterial vaginosis?

A

Vaginal discharge: ‘fishy’, offensive
Asymptomatic in 50% of patients

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24
Q

What criteria is used for the diagnosis of bacterial vaginosis?

A

Amsel’s criteria (3/4):

Thin, white homogenous discharge
Clue cells on microscopy: stippled vaginal epithelial cells
Vaginal pH > 4.5
Positive whiff test (addition of potassium hydroxide results in fishy odour)

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25
Q

What is the management of bacterial vaginosis in an asymptomatic patient?

A

If the woman is asymptomatic, treatment is not usually required
Exceptions include if the patient is undergoing termination of pregnancy

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26
Q

What is the first line management of bacterial vaginosis in a symptomatic patient?

A

Oral metronidazole for 5-7 days
Single oral dose of 2g may be used if adherence is an issue

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27
Q

What are the alternative management options for bacterial vaginosis?

A

Topical metronidazole or topical clindamycin

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28
Q

Define tinea capitis?

A

Dermatophyte fungal infection of the scalp

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29
Q

What is the management for trichophyton tonsurans tinea capitis?

A

Oral antifungal - terbinafine

Topical ketoconazole shampoo for first two weeks to reduce transmission

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30
Q

What is the management for microsporum tinea capitis?

A

Oral antifungal - griseofulvin

Topical ketoconazole shampoo for first two weeks to reduce transmission

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31
Q

Define tinea pedis?

A

Dermatophyte fungal infection of the foot

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32
Q

Define tinea crurus?

A

Dermatophyte fungal infection of the groin

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33
Q

Define tinea corporis?

A

Dermatophyte fungal infection of the trunk, legs or arms

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34
Q

What is the management for tinea corporis?

A

Oral fluconazole

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35
Q

Define molluscum contagiosum?

A

Molluscum contagiosum is a common skin infection caused by molluscum contagiosum virus (MCV), a member of the Poxviridae family

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36
Q

How is molluscum contagiosum spread?

A

Transmission occurs directly by close personal contact, or indirectly via fomites (contaminated surfaces) such as shared towels and flannels

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37
Q

What are the classic features of molluscum contagiosum?

A

Pinkish or pearly white papules with a central umbilication
5mm in diameter
Children - typically trunk and flexures
Adults - Genitalia, pubis, thighs, and lower abdomen

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38
Q

What is the management for molluscum contagiosum?

A

Treatment is not usually recommended
Cryotherapy can be used or simple trauma

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39
Q

What HPV strains cause genital warts?

A

Types 6 and 11

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40
Q

What is the first line management for genital warts?

A

Topical podophyllum - when multiple and non-keratinised
Cryotherapy - when solitary and keratinised

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41
Q

What is the second line management for genital warts?

A

Imiquimod which is a topical cream

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42
Q

Define folliculitis?

A

An inflammatory process involving any part of the hair follicle; it is most commonly secondary to infection

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43
Q

What is the most common cause of folliculitis?

A

Staphylococcus aureus

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44
Q

What is the management for staph folliculitis?

A

Clindamycin or Flucloxacillin

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45
Q

What is the management for gram negative folliculitis?

A

Topical benzoyl peroxide

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46
Q

Define psoriasis?

A

A chronic skin disorder defined by red, scaly patches on the skin

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47
Q

Define plaque psoriasis?

A

The most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp

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48
Q

Define flexural psoriasis?

A

The same as plaque psoriasis but the skin is smooth

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49
Q

Define guttate psoriasis?

A

Transient psoriatic rash frequently triggered by a streptococcal infection.

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50
Q

Define pustular psoriasis?

A

Commonly occurs on the palms and soles

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51
Q

What may exacerbate psoriasis?

A

Trauma
Alcohol
Lithium
Drugs: beta blockers, antimalarials, NSAIDs, ACEi and infliximab
Withdrawal of systemic steroids

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52
Q

What is the first line management for chronic plaque psoriasis?

A

Potent topical corticosteroid OD + vitamin D analogue OD

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53
Q

What is the second line management for chronic plaque psoriasis?

A

Potent topical corticosteroid OD + vitamin D analogue BD

If no improvement after 8 weeks

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54
Q

What is the third line management for chronic plaque psoriasis?

A

Potent topical corticosteroid BD + vitamin D analogue BD

If no improvement after 8-12 weeks

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55
Q

What is the secondary care management for chronic plaque psoriasis?

A

Ultraviolet B light
Ultraviolet A light + psoralen

Oral methotrexate

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56
Q

What is the management for scalp psoriasis?

A

Potent topical corticosteroids used once daily for 4 weeks

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57
Q

What is the management for face, flexural, and genital psoriasis?

A

Mild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeks

Due to pronity of steroid atrophy of skin

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58
Q

What are some examples of vitamin D analogues?

A

Calcipotriol (Dovonex)
Calcitriol
Tacalcitol

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59
Q

How do vitamin D analogues work in psoriasis management?

A

Decrease cell division and differentiation, therefore there is decreased epidermal proliferation

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60
Q

How long between courses of topical corticosteroids in patients with psoriasis?

A

4 weeks

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61
Q

Define impetigo?

A

Impetigo is a superficial bacterial skin infection

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62
Q

What organisms can cause impetigo?

A

Staphylcoccus aureus
Streptococcus pyogenes

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63
Q

Where does impetigo tend to occur on the body?

A

Areas not covered by clothes:
Face
Flexures
Limbs

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64
Q

What is the incubation period for impetgo?

A

4 to 10 days

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65
Q

What are the features of impetigo?

A

Golden crust to the skin
Very contagious

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66
Q

What is the management for non-bullous impetigo?

A

First line - hydrogen peroxide 1% cream
Topical fusidic acid

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67
Q

What is the management for extensive impetigo?

A

Oral flucloxacillin
Oral erythromycin if allergy

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68
Q

What is the rule about schooling and impetigo?

A

Children should be excluded from school until the lesions are crusted and healed

OR

48 hours after commencing antibiotic treatment

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69
Q

What is urticaria?

A

Urticaria describes a local or generalised superficial swelling of the skin. Most common cause is allergy.

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70
Q

What are the features of urticaria?

A

Pale, pink raised skin.
Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
Pruritic

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71
Q

What is the management for urticaria?

A

Non-sedating antihistamines - continued for up to 6 weeks are first line
Sedating may be considered for night time use

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72
Q

What is the management for severe urticaria?

A

Prednisolone

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73
Q

Give some examples of sedating and non-sedating antihistamines?

A

Non-sedating antihistamines (e.g. loratadine or cetirizine)
Sedating antihistamines (e.g. chlorophenamine)

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74
Q

What drugs can commonly cause urticaria?

A

All People Need Oxygen:

Aspirin
Penicillins
NSAIDs
Opiates

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75
Q

What is the causative pathogen of chickenpox?

A

Primary infection with varicella zoster virus

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76
Q

What is the causative pathogen of shingles?

A

Reactivation of varicella zoster virus from dorsal root ganglion

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77
Q

Give an overview of chickenpox?

A

Spread via the respiratory route
Can be caught by someone with shingles
infective from 4 days before rash until 5 days after rash appeared

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78
Q

What is the incubation period for chickenpox?

A

10-21 days

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79
Q

What are the clinical features of chickenpox?

A

Prodromal phase - fever initially
Itchy, rash starting on head/trunk before spreading.
Systemic upset is usually mild

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80
Q

Describe the rash seen in chickenpox?

A

Initially macular then papular then vesicular

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81
Q

What is the management for chickenpox?

A

Keep cool
Trim nails
School exclusion until all lesions are dry and have crusted over

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82
Q

What demographic of patients should receive varicella zoster immunoglobulin (VZIG)?

A

Immunocompromised patients
Newborns with peripartum exposure

If chickenpox develops = IV aciclovir

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83
Q

What is a common complication of chickenpox? What may increase the risk of this?

A

Secondary bacterial infection particularly invasive group A streptococcal soft tissue infections may occur resulting in necrotising fasciitis

NSAIDs

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84
Q

Define acute bronchitis?

A

Acute bronchitis is a type of chest infection a result of inflammation of the trachea and major bronchi

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85
Q

What are the classical features of acute bronchitis?

A

Cough: may or may not be productive
Sore throat
Rhinorrhoea
Wheeze

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86
Q

What is the difference between acute bronchitis and pneumonia?

A

No other focal chest signs in acute bronchitis other than wheeze.
No systemic symptoms

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87
Q

What is the management of acute bronchitis?

A

Analgesia
Fluid intake

CRP 20-100 = delayed prescription antibiotics
CRP >100 = immediate antibiotics

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88
Q

What antibiotics are given in acute bronchitis when indicated?

A

Doxycycline if first-line
Amoxicillin if pregnant or child

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89
Q

What criteria used used to diagnose acute bronchitis?

A

MacFarlane Criteria:

An acute illness of <21 days
Cough as the predominant symptom
At least 1 other lower respiratory tract symptom, such as sputum production, wheezing, chest pain
No alternative explanation for the symptoms

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90
Q

What is the MacFarlane criteria used for?

A

A diagnosis of acute bronchitis

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91
Q

Define asthma? What type of sensitivity reaction is asthma?

A

A chronic inflammatory disorder of the airways secondary to type 1 hypersensitivity

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92
Q

Why is diagnosis of asthma in children difficult?

A

It is common for young children to wheeze when they develop a virus (‘viral-induced wheeze’)

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93
Q

Patient with asthma may also suffer from what conditions?

A

Other IgE-mediated atopic conditions such as:

Atopic dermatitis (eczema)
Allergic rhinitis (hay fever)

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94
Q

What are asthma patients most likely allergic to? What else will they have?

A

Aspirin
Will most likely have nasal polyps if this is the case

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95
Q

What are the features of asthma?

A

Cough - worse at night
Dyspnoea
Expiratory wheeze
Reduced peak expiratory flow rate

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96
Q

What is FEV1?

A

Forced expiratory volume - volume that has been exhaled at the end of the first second of forced expiration

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97
Q

What is FVC?

A

Forced vital capacity - volume that has been exhaled after a maximal expiration following a full inspiration

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98
Q

What are the typical spirometry results in asthma?

A

FEV1 - significantly reduced
FVC - normal
FEV1% (FEV1/FVC) < 70%

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99
Q

What are the first-line investigations for asthma?

A

Fractional exhaled Nitric Oxide OR
Eosinophil count

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100
Q

What is the second-line investigation for asthma?

A

Bronchodilator reversibility (BDR) with spirometry

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101
Q

What is the first line management for asthma?

A

Salbutamol

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102
Q

What is a side effect of salbutamol?

A

Tremor

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103
Q

What type of drug is salbutamol?

A

Short-acting-beta agonist (SABA)

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104
Q

What is the mechanism of action of salbutamol?

A

Relaxation of the smooth muscles of the airways

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105
Q

What is the additional second line management for asthma?

A

Inhaled corticosteroids

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106
Q

What are the side effects of inhaled corticosteroids?

A

Oral candidiasis
Stunted growth in children

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107
Q

Give some examples of inhaled corticosteroids in asthma?

A

Beclometasone dipropionate
Fluticasone propionate

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108
Q

What is the additional third line management for asthma?

A

Leukotriene receptor antagonist (LTRA) - Montelukast

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109
Q

What is the fourth-line management for asthma?

A

Salmetrol

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110
Q

What type of drug is salmetrol?

A

Long-acting beta-agonist

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111
Q

What is the mechanism of action of salmetrol?

A

They work by relaxing the smooth muscle of airways

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112
Q

What would the assessment of a moderate asthma attack show in children?

A

SpO2 > 92%
No clinical features of severe asthma

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113
Q

What would the assessment of a life-threatening asthma attack show in a child?

A

SpO2 <92%
PEF - PEF <33% best or predicted
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis

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114
Q

What would the assessment of a severe asthma attack show in children?

A

SpO2 < 92%
PEF - 33-50%
Too breathless to talk or feed
Use of accessory neck muscles

HR - >125 (>5 years), >140 (1-5 years)
RR - >30 (>5 years), >40 (1/5 years)

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115
Q

What is the management for mild-moderate acute asthma in children?

A

Beta-2-agonist via a spacer (>3 years use close fitting mask)
1 puff every 30-60 seconds. Max 10 puffs
If no symptom control refer to hospital

Steroid therapy for 3-5 days
2-5 years - 20mg prednisolone OD
>5 years - 30-40mg prednisolone OD

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116
Q

What would the assessment of a moderate asthma attack show in adults?

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

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117
Q

What would the assessment of a severe asthma attack show in adults?

A

PEFR 33 - 50% best or predicted
Can’t complete sentences
RR > 25/min
Pulse > 110 bpm

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118
Q

What would the assessment of a life-threatening asthma attack show in adults?

A

PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

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119
Q

What would the assessment of a
near-fatal asthma attack show in adults?

A

Raised pC02 and/or requiring mechanical ventilation with raised inflation pressures.

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120
Q

What is the management for a life-threatening acute asthma attack in adults?

A

Admission to hospital
15L oxygen in non-rebreathe mask if 02 sats low (until spO2 94-98)
Nebulised SABA (salbutamol)
40-50mg prednisolone PO - 5 days

Ipratropium bromide in all life-threatening or whom have not responded to SABA / Steroids

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121
Q

What is the criteria for discharge in patients who have had an acute asthma attack?

A

Stable on their discharge medication (i.e. no nebulisers or oxygen) for 12-24 hours
Inhaler technique checked and recorded
PEF >75% of best or predicted

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122
Q

Define bronchiolitis?

A

Bronchiolitis is a condition characterised by acute bronchiolar inflammation

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123
Q

What is the pathogen which causes bronchiolitis?

A

Respiratory syncytial virus (80%)
Rhinovirus (20%)

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124
Q

What is the investigation of choice for bronchiolitis?

A

Immunofluorescence of nasopharyngeal secretions may show RSV

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125
Q

What is the management for bronchiolitis?

A

If SpO2 persistently >92% - humidified oxygen

Accessory:
NG feeding
Suction of secretions

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126
Q

What would classify a patient as high-risk in bronchiolitis?

A

Bronchopulmonary dysplasia (e.g. Premature)
Congenital heart disease
Cystic fibrosis

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127
Q

Define COPD?

A

COPD is an umbrella term encompassing the older terms chronic bronchitis and emphysema

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128
Q

What are the features of COPD?

A

Cough: often productive
Dyspnoea
Wheeze
RSHF -> peripheral oedema

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129
Q

What would spirometry show for COPD?

A

Post-bronchodilator spirometry to demonstrate airflow obstruction: FEV1/FVC ratio less than 70%

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130
Q

What would a chest X-ray show for COPD?

A

Hyperinflation
Bullae: if large, may sometimes mimic a pneumothorax
Flat hemidiaphragm

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131
Q

What are the investigations for COPD?

A

Post-bronchodilator spirometry
Chest X-ray
FBC - exclude secondary polycythaemia
BMI calculation

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132
Q

What would mild COPD be using FEV1?

A

FEV1/FVC < 0.7
FEV1 of predicted >80%

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133
Q

What would moderate COPD be using FEV1?

A

FEV1/FVC < 0.7
FEV1 of predicted 50-79%

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134
Q

What would severe COPD be using FEV1?

A

FEV1/FVC < 0.7
FEV1 of predicted 30-49%

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135
Q

What would very severe COPD be using FEV1?

A

FEV1/FVC < 0.7
FEV1 of predicted <30%

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136
Q

What are the causes of COPD?

A

C4-GAS:

Cadmium
Coal
Cotton
Cement

Grain
Alpha-1 antitrypsin deficiency
Smoking - biggest risk factor

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137
Q

What is the general advice for COPD?

A

Smoking cessation
Annual influenza vaccination
One-off pneumococcal vaccination
Pulmonary rehabilitation

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138
Q

What is the first-line management for COPD in stable patients?

A

SABA - Salbutamol

OR

SAMA - Ipatropium bromide

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139
Q

What determines the second-line management in stable COPD patients?

A

Whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’

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140
Q

How do you determine whether a patient with COPD has asthmatic/steroid responsive features?

A

Previous diagnosis of asthma / atopy
Higher blood eosinophil count
Substantial FEV1 variation over time (>400ml)
Substantial diurnal variation in PEF (20%)

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141
Q

What is second-line management of COPD if a patient has NO asthma/steroid response features?

A

SABA - Salbutamol

LABA - Salmeterol
LAMA - Triotropium

If already taking a SAMA, discontinue and switch to a SABA

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142
Q

What is second-line management of COPD if a patient has asthma/steroid response features?

A

SABA - Salbutamol
OR
SAMA - Ipatropium bromide

Add the following:

LABA - Salmeterol and ICS

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143
Q

What is third-line management of COPD if a patient has asthma/steroid response features?

A

SABA - Salbutamol

Triple therapy:

LAMA - Triotropium
LABA - Salmetrol
ICS

If already taking a SAMA, discontinue and switch to a SABA

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144
Q

What pharmacological agent should be considered in patients with chronic productive cough in COPD?

A

Mucolytics

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145
Q

What pharmacological agent is given to patients with severe (+very severe) COPD to reduce the risk of exacerbations?

A

Phosphodiesterase-4 (PDE-4) inhibitors
E.g. roflumilast

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146
Q

When should LTOT not be offered to patients?

A

Those who continue to smoke despite being offered smoking cessation advice and treatment

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147
Q

What bacteria may cause a COPD exacerbation?

A

Haemophilus influenzae - most common cause overall
Streptococcus pneumoniae
Moraxella catarrhalis

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148
Q

What is the most common cause of viral COPD exacerbation?

A

Rhinovirus

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149
Q

What is the management for a COPD exacerbation?

A

Increase the frequency of bronchodilator use and consider giving via a nebuliser
30mg prednisolone for 5 days

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150
Q

When should antibiotics be given in a COPD exacerbation?

A

If sputum is purulent or there are clinical signs of pneumonia

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151
Q

What antibiotics are used in COPD exacerbation when indicated?

A

Amoxicillin or
Clarithromycin or
Doxycycline

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152
Q

What are the classical features of croup?

A

Cough which is barking and seal-like, with symptoms worse at night.

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153
Q

A cough which is barking and seal-like, with symptoms worse at night would indicate what?

A

Croup

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154
Q

What is the management for croup?

A

Single dose of oral dexamethasone regardless of severity.
Second line - Prednisolone

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155
Q

What is the emergency management for croup?

A

High-flow oxygen and nebulised adrenaline

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156
Q

Why would you never perform a throat examination on a child with suspected croup?

A

Never perform a throat examination on a patient with croup due to risk of airway obstruction

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157
Q

What sign would be seen on a posterior-anterior chest X-ray of a child with croup?

A

Subglottic narrowing, commonly called the ‘steeple sign’

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158
Q

What sign would be seen on a lateral chest X-ray of a child with croup?

A

Swelling of the epiglottis - the ‘thumb sign’

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159
Q

What is the main organism that causes croup?

A

Parainfluenza virus accounts for the majority of cases of croup

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160
Q

When is croup more common in the year?

A

Autumn

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161
Q

What type of influenza virus accounts for the majority of clinical disease?

A

A and B

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162
Q

What is the difference between the children and adult influenza vaccine?

A

Children - Live
Adult - Inactivated

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163
Q

Define rhino-sinusitis?

A

An inflammatory disorder of the paranasal sinuses and linings of the nasal passages that lasts 12 weeks or longer.

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164
Q

What are the features of rhino-sinusitis?

A

Facial pain - pressure when bending forward
Nasal discharge
Nasal obstruction - mouth breathing
Post-nasal drip

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165
Q

What is the management for rhino-sinusitis?

A

Avoid allergen
Intranasal corticosteroids
Nasal irrigation with saline solution

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166
Q

What are the red flag symptoms of rhino-sinusitis?

A

Unilateral symptoms
Persistent symptoms despite 3 months treatment
Epistaxis - nose bleed

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167
Q

What is pertussis? What is the causative pathogen?

A

Whooping cough (pertussis) is an infectious disease caused by the Gram-negative bacterium Bordetella pertussis

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168
Q

What are the features of pertussis in the catarrhal phase?

A

URTI symptoms

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169
Q

What are the features of pertussis in the paroxysmal phase?

A

Cough increases in severity
Worse at night or after feeding
Inspiratory whoop
Infants may have spells of apnoea

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170
Q

What are the features of the convalescent phase in pertussis infection?

A

Cough will subside over weeks to months

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171
Q

What is the diagnostic criteria for whooping cough?

A

Acute cough >14 days

AND one of following:

Paroxysmal cough
Inspiratory whoop
Post-tussive vomiting
undiagnosed apnoeic attacks in children

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172
Q

What is the management for pertussis?

A

An oral macrolide (e.g. clarithromycin, azithromycin or erythromycin)

Notify public health

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173
Q

What is atrial flutter?

A

Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves

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174
Q

What would ECG changes be for atrial flutter?

A

Sawtooth appearance (flutter waves / f wave)

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175
Q

What is the immediate management for atrial flutter?

A

Synchronised cardioversion with anticoagulant

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176
Q

Define AF?

A

Atrial fibrillation is the most common sustained cardiac arrhythmia in which there is an increased risk of stroke

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177
Q

What are the different types of AF?

A

First detected episode
Recurrent episodes
Permanent AF

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178
Q

What are the types of recurrent AF?

A

Paroxysmal AF - Terminates spontaneously
Persistent AF - Non-self terminating (>7 days)

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179
Q

What are the features of AF?

A

Palpitations
Dyspnoea
Chest pain
Irregularly irregular pulse

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180
Q

What are the two types of control used in the management of AF?

A

Rhythm control (preferred under certain criteria)
Rate control

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181
Q

What is the role of rhythm control in AF management?

A

Try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion.

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182
Q

What is the first-line criteria for rhythm control in haemodynamically unstable patients?

A

Haemodynamically unstable - electrical cardioversion

E.g. hypotension, heart failure

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183
Q

What is the criteria to use rhythm control first in AF management in haemodynamically stable patients?

A

Short duration of symptoms (less than 48 hours) OR
Be anticoagulated for a period of time prior to attempting cardioversion - 3 weeks.

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184
Q

What pharmacological agents are used for cardioversion in AF?

A

Amiodarone
Flecainide (if no structural heart disease)

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185
Q

What is the role of rate control on AF management?

A

Accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function

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186
Q

What pharmacological management is used for rate control in AF?

A

A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line

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187
Q

What happens if one drug does not control rate adequately in AF?

A

Combination therapy with any 2 of the following:
Betablocker
Diltiazem
Digoxin

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188
Q

What is a common contraindication for beta-blockers for rate control in patients with AF?

A

Asthma

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189
Q

When is there the highest risk of embolism leading to stroke in AF?

A

The moment a patient switches from AF to sinus rhythm

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190
Q

What is the CHA2DS2-VSAc score used for?

A

Calculates stroke risk for patients with atrial fibrillation

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191
Q

What score calculates stroke risk for patients with atrial fibrillation?

A

CHA2DS2-VSAc

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192
Q

What are the individual scores in the CHA2DS2-VaSc scoring system?

A

C - congestive heart failure - 1
H - hypertension - 1
A2 - Age - Age >= 75 - 2, Age 65-74 - 1
D - diabetes - 1
S2 - Prior Stroke, TIA or thromboembolism - 2
V - Vascular disease (IHD, PAD) - 1
S - sex (female) - 1

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193
Q

What is the anticoagulation strategy based on CHA2DS2-VSAc score?

A

0 - No treatment
1 - Male - consider coagulation, Female - no treatment
2 or more - Offer anticoagulation

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194
Q

What should be performed if CHA2DS2-VSAc score = 0 and why?

A

ECHO to exclude valvular heart disease

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195
Q

What pharmacological agents are used first-line for anticoagulation in AF?

A

DOACs:

Apixaban
Dabigatran
Edoxaban
Rivaroxaban

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196
Q

What pharmacological agent is used second-line for anticoagulation in AF?

A

Warfarin due to requiring regular blood tests to check the INR

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197
Q

What score is to assess the patient’s bleeding risk before anticoagulation is commenced?

A

ORBIT score

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198
Q

What is an ORBIT score used for?

A

To assess the patient’s bleeding risk before anticoagulation is commenced

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199
Q

List three types of supra-ventricular tachycardia?

A

Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular reentrant tachycardia (AVRT) e.g. Wolf-Parkinson White syndrome

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200
Q

What is the most common type of supra-ventricular tachycardia?

A

Atrioventricular nodal reentrant tachycardia (AVNRT)

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201
Q

What is the first line acute management for supra-ventricular tachycardia?

A

Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
Carotid sinus massage

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202
Q

What pharmacological management may be given for supra-ventricular tachycardias?

A

Intravenous adenosine:

Rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg

Verapamil if asthmatic

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203
Q

What is the definitive management for supra-ventricular tachycardias?

A

Radio-frequency ablation of the accessory pathway

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204
Q

Define Wolff-Parkinson White syndrome?

A

A congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)

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205
Q

What would an ECG show for right-sided accessory pathway Wolff-Parkinson-White syndrome?

A

Short PR interval
Wide QRS complex with slurred upstroke - Delta wave
Left axis deviation - majority of cases

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206
Q

What would an ECG show for left-sided accessory pathway Wolff-Parkinson-White syndrome?

A

Short PR interval
Wide QRS complex with slurred upstroke - Delta wave
Right axis deviation
Dominant R wave in V1

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207
Q

What is would ventricular fibrillation show on an ECG?

A

No QRS complex can be identified, ECG completely disorganised

Patient is likely to be unconscious

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208
Q

What is the management for ventricular fibrillation?

A

Immediate Dc cardioversion

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209
Q

What are the two types of ventricular tachycardia?

A

Monomorphic VT: most commonly caused by myocardial infarction

Polymorphic VT: A subtype of polymorphic VT is torsades de pointes

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210
Q

What is the management for ventricular tachycardia?

A

Immediate cardioversion
IV amioderone

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211
Q

Define ventricular ectopic?

A

Ventricular ectopics are premature ventricular beats

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212
Q

What is the management for ventricular ectopic?

A

Reassurance in otherwise healthy people
Beta blockers and Ca channel blockers for palpitations

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213
Q

What is the management for Torsades de Pointes?

A

IV magnesium sulphate

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214
Q

What is hypertension?

A

A clinic reading persistently above >= 140/90 mmHg, or:
A 24 hour blood pressure average reading >= 135/85 mmHg

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215
Q

What is primary hypertension?

A

This is where there is no single disease causing the rise in blood pressure but rather a series of complex physiological changes which occur as we get older

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216
Q

What is secondary hypertension?

A

Secondary hypertension may be caused by a wide variety of endocrine, renal and other causes

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217
Q

What are some renal causes of renal hypertension?

A

Glomerulonephritis
Chronic pyelonephritis
Adult polycystic kidney disease
Renal artery stenosis

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218
Q

What are some endocrine causes of hypertension?

A

Primary hyperaldosteronism
Phaeochromocytoma
Cushing’s syndrome
Liddle’s syndrome
Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
Acromegaly

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219
Q

What are some causes of hypertension outside of renal disease and endocrine disorders?

A

Glucocorticoids
NSAIDs
Pregnancy
Coarctation of the aorta
Combined oral contraceptive pill

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220
Q

What is the investigation for hypertension?

A

Blood pressure reading
24-hour blood pressure reading - more in recent years

U&Es - renal disease
HbA1c - co-existing diabetes mellitus
Lipids - hyperlipidaemia
ECG
Urine dipstick

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221
Q

What are the secondary investigations that should be organised if someone has hypertension?

A

Fundoscopy: to check for hypertensive retinopathy
Urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
ECG: to check for left ventricular hypertrophy or ischaemic heart disease

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222
Q

What is the first line management for hypertension in younger patients, <55 years old?

A

Angiotensin-converting enzyme (ACE) inhibitors

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223
Q

What is the mechanism of action of ACE inhibitors?

A

Inhibit the conversion angiotensin I to angiotensin II

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224
Q

Give some examples of ACE inhibitors?

A

Ramipril
End in ‘ipril’

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225
Q

What are the side effects of ACE inhibitors?

A

Cough
Angioedema
Hyperkalaemia

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226
Q

In what demographic would ACE inhibitors not be permitted for use?

A

Afro-Caribbean patients - less effective
Pregnant women - due to risk of worsening renal function

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227
Q

What is the first line management for hypertension in older patients, >55 years old?

A

Calcium channel blockers

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228
Q

Give some examples of CCB’s?

A

Amlodipine

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229
Q

What is the mechanism of action of calcium channel blockers?

A

Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction

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230
Q

What are the side effects of calcium channel blockers?

A

Flushing
Ankle swelling
Headache

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231
Q

What are thiazide type diuretics?

A

Inhibit sodium absorption at the beginning of the distal convoluted tubule

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232
Q

What are ARBs?

A

Angiotensin II receptor blockers (A2RB) - Block effects of angiotensin II at the AT1 receptor

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233
Q

Give an example of an ARB?

A

Candesartan

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234
Q

What is stage 1 hypertension?

A

Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

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235
Q

What is stage 2 hypertension?

A

Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

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236
Q

What is stage 3 hypertension?

A

Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

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237
Q

What are the lifestyle management strategies for hypertension?

A

A low salt diet <6g per day, ideally >3g/day
Reduced caffeine intake
Stop smoking
Less alcohol
Balanced diet rich in fruit and vegetables
More exercise

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238
Q

What is the management of stage 1 hypertension?

A

Treat if < 80 years of age AND any of the following apply; Target organ damage
Established cardiovascular disease
Renal disease
Diabetes
10-year cardiovascular risk equivalent to 10% or greater

OR

> 60 years old and QRICK under 10% can be considered for medication

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239
Q

What is the management for stage 2/3 hypertension?

A

Offer drug treatment regardless of age

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240
Q

What is step 1 management for hypertension in a patient who is under 55 years old or has T2DM?

A

ACE-i or ARB
ARB should be used when ACE-i is not tolerated

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241
Q

What is step 1 management for hypertension in a patient who is over 55 years old or African or African-Caribbean origin?

A

Calcium channel blocker

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242
Q

What is step 2 management for hypertension in a patient who is under 55 years old or has T2DM?

A

If already taking ACE-i or ARB then add CCB or thiazide-like diuretic

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243
Q

Give an example of thiazide-like diuretic?

A

Indapamide

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244
Q

What is step 2 management for hypertension in a patient who is over 55 years old or African or African-Caribbean origin?

A

If already taking CCB then add ACE-i or ARB or thiazide-like diuretic.

In African or African-Caribbean origin then ARB would be preferred

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245
Q

What is step 3 management for hypertension?

A

Add a third drug treatment:

ACE-i and CCB, then add thiazide-like diuretic
ACE-i and thiazide-like diuretic then add CCB

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246
Q

What should you do before commencing step 4 management for hypertension?

A

Confirm elevated clinic BP with ABPM or HBPM
Assess for postural hypotension.
Discuss adherence

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247
Q

What is step 4 management for hypertension?

A

If potassium < 4.5 mmol/l add low-dose spironolactone
If potassium > 4.5 mmol/l add an alpha- or beta-blocker

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248
Q

What are the blood pressure targets for those that are <80 years old?

A

Clinic BP - 140/90 mmHg
ABPM / HBPM - 135/85mmHg

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249
Q

What are the blood pressure targets for those that are >80 years old?

A

Clinic BP - 150/90 mmHg
ABPM / HBPM - 145/85 mmHg

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250
Q

Define peripheral vascular disease?

A

A major circulatory disorder characterised by arterial obstruction, leading to reduced blood supply and ischaemia in the lower limbs

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251
Q

What are the features of peripheral vascular disease?

A

1 or more of the 6 P’s
Pale
Pulseless
Painful
Paralysed
Paraesthetic
‘Perishing with cold’

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252
Q

What is the primary investigation for peripheral vascular disease?

A

Handheld arterial Doppler examination - if doppler signals are present then:

Ankle-brachial pressure index

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253
Q

What does an absent of pulse in the lower extremity indicate on doppler ultrasound?

A

Suspect acute limb ischaemia

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254
Q

What does an ABPI of >1.4 indicate?

A

Abnormally calcified vessels

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255
Q

What does an ABPI of 0.9-1.2 indicate?

A

Normal - does not exclude diagnosis if clinically indicated

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256
Q

What does an ABPI of 0.5-0.9 indicate?

A

Intermittent claudication - mild-to-moderate arterial disease

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257
Q

What does an ABPI of <0.5 indicate?

A

Critical limb ischaemia - rest pain, ulceration, gangrene

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258
Q

What is the first-line investigation for confirmed peripheral vascular disease?

A

Duplex ultrasound

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259
Q

What is the first line management for PVD?

A

Exercise + management of risk factors e.g. stop smoking

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260
Q

What is the first line pharmacological management for PVD?

A

Established cardiovascular disease - 80mg Atrovostatin

AND

Clopidogrel 75mg (used to be aspirin 75mg)

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261
Q

What is the management for severe PVD?

A

Surgery:
Endovascular revascularization
Surgical revascularization

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262
Q

Define varicose veins?

A

Dilated, tortuous, superficial veins that occur secondary to incompetent venous valves, allowing blood to flow back, away from the heart

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263
Q

Where do varicose veins usually occur?

A

Commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein

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264
Q

What are the risk factors for varicose veins?

A

Increasing age
Female
Pregnancy - uterus compression on pelvic vein
Obesity

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265
Q

What is the investigation of choice for varicose veins?

A

Venous duplex ultrasound: this will demonstrate retrograde venous flow

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266
Q

What are the conservative management options for varicose veins?

A

Leg elevation
Weight loss
Regular exercise
Graduated compression stockings

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267
Q

What are the reasons for varicose vein referral to secondary care?

A

Significant/troublesome lower limb symptoms e.g. pain, discomfort or swelling
Previous bleeding from varicose veins
Skin changes secondary to chronic venous insufficiency
Active or healed leg ulcer

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268
Q

What are the possible treatments for varicose veins?

A

Endothermal ablation
Foam sclerotherapy
Surgery - stripping or ligation

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269
Q

What is the management for venous ulcers?

A

Compression bandaging, four layer

Oral pentoxifylline, a peripheral vasodilator, improves healing rate

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270
Q

Where are venous ulcers typically seen?

A

Medial malleolus

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271
Q

Define acute stress reaction?

A

A stress reaction that occurs in the first 4 weeks after a person has been exposed to a traumatic event

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272
Q

What is the difference between acute stress reaction and PTSD?

A

Acute stress reaction - <4 weeks
PTSD - >4 weeks

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273
Q

What are the features of an acute stress reaction?

A

Intrusive thoughts e.g. flashbacks,
nightmares
Dissociation e.g. ‘being in a daze’, time slowing
Negative mood
Avoidance
Arousal e.g. hypervigilance, sleep disturbance

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274
Q

What is the management for an acute stress reaction?

A

First line - trauma-focused cognitive-behavioural therapy (CBT)
Benzodiazepines

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275
Q

What is OCD?

A

Obsessive-compulsive disorder (OCD) is characterised by the presence of either obsessions or compulsions, but commonly both.

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276
Q

Define obsession?

A

An obsession is defined as an unwanted intrusive thought, image or urge that repeatedly enters the person’s mind.

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277
Q

Define compulsion?

A

Compulsions are repetitive behaviours or mental acts that the person feels driven to perform.

A compulsion can either be overt and observable by others, such as checking that a door is locked, or a covert mental act that cannot be observed, such as repeating a certain phrase in one’s mind.

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278
Q

What would be defined as severe OCD?

A

Someone who spends > 3 hours a day on their obsessions/compulsions, has severe interference/distress and has very little control/resistance

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279
Q

What would the management be for an individual with mild functional impairment for OCD?

A

Low-intensity psychological treatments: cognitive behavioural therapy (CBT) including exposure and response prevention (ERP)

If this is insufficient or can’t engage in psychological therapy, then offer a choice of either a course of an SSRI or more intensive CBT (including ERP)

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280
Q

What would the management be for an individual with moderate functional impairment for OCD?

A

Offer a choice of either a course of an SSRI or more intensive CBT (including ERP)

Consider clomipramine (as an alternative first-line drug treatment to an SSRI)

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281
Q

In what case would you specifically given fluoxetine for a moderate functional impairement of OCD?

A

Fluoxetine is specifically given for body dysmorphic disorder

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282
Q

In what case would you give clomipramide for a moderate functional impairment of OCD?

A

Can be considered as an alternative first-line drug treatment to SSRIs if the person has had a previous good response to it.

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283
Q

What would the management be for an individual with severe functional impairment for OCD?

A

Refer to secondary care mental health team for assessment.

Whilst awaiting assessment - offer combined treatment with an SSRI and CBT (including ERP) or consider Clomipramine

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284
Q

What is exposure and response prevention (ERP)?

A

ERP is a psychological method which involves exposing a patient to an anxiety provoking situation (e.g. for someone with OCD, having dirty hands) and then stopping them engaging in their usual safety behaviour (e.g. washing their hands). This helps them confront their anxiety and the habituation leads to the eventual extinction of the response

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285
Q

What timeframe would you review a patient who is starting a sertraline and is under the age of 30?

A

1 week

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286
Q

Define anxiety?

A

Excessive worry about a number of different events associated with heightened tension.

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287
Q

List some medications that may trigger anxiety?

A

Salbutamol
Theophylline
Corticosteroids
Antidepression
Caffeine

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288
Q

What is step 1 of GAD management?

A

Education about GAD + active monitoring

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289
Q

What is step 2 of GAD management?

A

Low-intensity psychological interventions (individual non-facilitated self-help or individual guided self-help or psychoeducational groups)

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290
Q

What is step 3 of GAD management?

A

High-intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment.

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291
Q

What is step 4 of GAD management?

A

Highly specialist input e.g. Multi agency teams

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292
Q

What is the first line pharmacological management of GAD?

A

Sertraline is first-line

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293
Q

What would second-line pharmacological management for GAD?

A

If sertraline is ineffective, an alternative SSRI or SNRI can be used.

Duloxetine or Venlafaxine (SNRI examples)

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294
Q

What would the pharmacological management be for an individual with GAD who cannot tolerate SSRIs or SNRIs?

A

If the person cannot tolerate SSRIs or SNRIs, consider offering pregabalin

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295
Q

What must you warn patients of who are under the age of 30, before commencing SSRIs and SNRIs?

A

For patients under the age of 30 years NICE recommend you warn patients of the increased risk of suicidal thinking and self-harm.

Weekly follow-up is recommended for the first month

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296
Q

What is the first-line treatment of panic disorder in primary care?

A

Cognitive behavioural therapy or drug treatment

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297
Q

If there is no response to SSRIs for panic disorder in primary care, what can be offered?

A

If contraindicated or no response after 12 weeks then imipramine or clomipramine should be offered

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298
Q

What are some risk factors for developing GAD?

A

Aged 35- 54
Being divorced or separated
Living alone
Being a lone parent

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299
Q

What are some protective factors against GAD?

A

Aged 16 - 24
Being married or cohabiting

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300
Q

Define pseudodementia?

A

Severe depression can mimic dementia but gives a pattern of global memory loss rather than short-term memory loss - this is called pseudodementia

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301
Q

What is normal pressure hydrocephalus? What is it thought to be caused by?

A

Normal pressure hydrocephalus is a reversible cause of dementia seen in elderly patients. It is thought to be secondary to reduced CSF absorption at the arachnoid villi.

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302
Q

What is the classic triad of features seen in normal pressure hydrocephalus?

A

Urinary incontinence
Dementia and bradyphrenia
Gait abnormality (may be similar to Parkinson’s disease)

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303
Q

What would the triad of urinary incontinence, dementia and bradyphrenia, gait abnormality (may be similar to Parkinson’s disease) suggest?

A

Normal pressure hydrocephalus

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304
Q

What would normal pressure hydrocephalus present with on imaging?

A

Hydrocephalus with ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement

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305
Q

Ventriculomegaly without sulcal enlargement on imaging of the brain would indicate what?

A

Normal pressure hydrocephalus

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306
Q

What is the management of normal pressure hydrocephalus?

A

Ventriculoperitoneal shunting

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307
Q

What are the complications of ventriculoperitoneal shunting?

A

Around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages

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308
Q

What are some non-pharmacological managements of Alzheimer’s disease?

A

A range of activities to promote wellbeing that are tailored to the person’s preference
Group cognitive stimulation therapy for patients with mild and moderate dementia
Group reminiscence therapy and cognitive rehabilitation

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309
Q

What types of drugs are donepezil, galantamine and rivastigmine?

A

Acetylcholinesterase inhibitors

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310
Q

What pharmacological management can be given for mild to moderate Alzheimer’s disease?

A

Donepezil, Galantamine and Rivastigmine

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311
Q

What second line pharmacological management can be given for Alzheimer’s disease?

A

Memantine

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312
Q

What type of drug is memantine?

A

NMDA receptor antagonist

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313
Q

Under what conditions can the second line pharmacological management be used for Alzheimer’s disease?

A
  • For moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors.
  • As an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s.
  • Monotherapy in severe Alzheimer’s
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314
Q

What feature would contraindicate use of donepezil?

A

Bradycardia

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315
Q

What is an adverse effect of donepezil?

A

Insomnia

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316
Q

What is the characteristic pathological feature of lewy-body dementia?

A

Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

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317
Q

Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas would suggest what?

A

Lewy-body dementia

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318
Q

What are the features of lewy-body dementia?

A

Progressive cognitive impairment which typically occurs before parkinsonism, but usually both features occur within a year of each other.
Cognition may be fluctuating (different to other dementias)
Parkinsonism
Visual hallucinations + dementia = lewy -body dementia

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319
Q

Visual hallucinations + dementia would indicate what?

A

Lewy body dementia

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320
Q

What pharmacological management can be given for mild to moderate lewy body dementia?

A

Donepezil and Rivastigmine

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321
Q

What second line pharmacological management can be given for Lewy body dementia?

A

Memantine

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322
Q

What class of drugs should be avoided in lewy body dementia and why?

A

Neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism.

E.g, Risperidone and Haloperidol.

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323
Q

What is frontotemporal lobular degeneration?

A

Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.

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324
Q

What are the three recognised types of FTLD?

A

Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia

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325
Q

What are the common features of FTLD?

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

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326
Q

What are the most common features of Frontotemporal dementia (Pick’s disease)?

A

Characterised by personality change and impaired social conduct.

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327
Q

What axillary features ‘may’ be present in Frontotemporal dementia (Pick’s disease)?

A

Hyperorality
Disinhibition
Increased appetite
Perseveration behaviours

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328
Q

What would you see on imaging for frontotemporal dementia (Pick’s disease)?

A

Focal gyral atrophy with a knife-blade appearance.

Macroscopic - Atrophy of the frontal and temporal lobes

Microscopic: Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques

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329
Q

What is the most common feature of chronic progressive aphasia (CPA)?

A

Here the chief factor is non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.

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330
Q

What is the most common feature of semantic dementia?

A

A fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.

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331
Q

Define Alzheimer’s disease?

A

Alzheimer’s disease (AD) is a progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK

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332
Q

What are the risk factors for Alzheimer’s disease?

A

Increasing age
Family history
Inherited autosomal trait
Apoprotein E allele E4
Caucasian ethnicity
Down syndrome

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333
Q

What autosomal dominant traits are associated with an increased risk of Alzheimer’s disease?

A

Mutations in:
- The amyloid precursor protein (chromosome 21)
- Presenilin 1 (chromosome 14)
- Presenilin 2 (chromosome 1) genes

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334
Q

What genetic condition is associated with an increased risk of Alzheimer’s disease?

A

Down syndrome

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335
Q

What macroscopic pathological changes are seen in Alzheimer’s disease?

A

Widespread cerebral atrophy, particularly involving the cortex and hippocampus

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336
Q

What microscopic pathological changes are seen in Alzheimer’s disease?

A

Cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
Hyperphosphorylation of the tau protein has been linked to AD

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337
Q

What biochemical pathological changes are seen in Alzheimer’s disease?

A

There is a deficit of acetylcholine from damage to an ascending forebrain projection

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338
Q

What is the difference between Parkinson’s disease dementia and Lewy-body dementia?

A

Motor symptoms will be present before dementia symptoms for PDD.

PDD is diagnosed if a patient had a Parkinson’s disease diagnosis for at least 1 year.

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339
Q

What is Creutzfeldt-Jakob disease?

A

Creutzfeldt-Jakob disease (CJD) is rapidly progressive neurological condition caused by prion proteins.

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340
Q

What is the pathophysiology of Creutzfeldt-Jakob disease?

A

Prion proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.

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341
Q

What are the features of Creutzfeld-Jakob disease?

A

Dementia with rapid onset
Myoclonus

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342
Q

What would you see on imaging with an individual with Creutzfeldt-Jakob disease?

A

MRI - hyperintense signals in the basal ganglia and thalamus.

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343
Q

Hyperintense signals in the basal ganglia and thalamus of an MRI would indicate what?

A

Creutzfeldt-Jakob disease

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344
Q

What is vascular dementia?

A

It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.

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345
Q

What is the second most common form of dementia?

A

Vascular dementia

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346
Q

What are the subtypes of vascular dementia?

A

Stroke-related VD
Subcortical VD
Mixed dementia

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347
Q

What is stroke-related VD?

A

Vascular dementia caused by a multi-infarct or single-infarct dementia

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348
Q

What is subcortical VD?

A

Vascular dementia caused by small vessel disease.

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349
Q

What is mixed dementia?

A

The presence of both VD and Alzheimer’s disease

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350
Q

What are the risk factors for vascular dementia?

A

History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular

351
Q

In what disease would vascular dementia be inherited?

A

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopath)

352
Q

What is the typical presentation of vascular dementia?

A

Several months or several years of a history of a sudden or STEPWISE DETERIORATION of cognitive function.

353
Q

What may some features of vascualr dementia be?

A

Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance

354
Q

What criteria is used to diagnose vascular dementia?

A

NINDS-AIREN criteria

355
Q

The NINDS-AIREN criteria is used for what?

A

For a diagnosis of vascular dementia

356
Q

Outline the NINDS-AIREN criteria?

A

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event

Cerebrovascular disease defined by neurological signs and/or brain imaging

A relationship between the above two disorders inferred by:
- The onset of dementia within three months following a recognised stroke
- An abrupt deterioration in cognitive functions
fluctuating, stepwise
- Progression of cognitive deficits

357
Q

What is the management for for vascular dementia?

A

Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy

358
Q

What would be less severe depression according to the PHQ-9 score?

A

A PHQ-9 score of < 16

359
Q

What would be more severe depression according to the PHQ-9 score?

A

A PHQ-9 score of ≥ 16

360
Q

A PHQ-9 score of < 16 would indicate what?

A

Less severe depression

361
Q

A PHQ-9 score of ≥ 16 would indicate what?

A

More severe depression

362
Q

List the treatment options for less severe depression in order of preference by NICE?

A
  • Guided self-help
  • Group cognitive behavioural therapy (CBT)
  • Group behavioural activation (BA)
  • Individual CBT
  • Individual BA
  • Group exercise
  • Group mindfulness and meditation
  • Interpersonal psychotherapy (IPT)
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Counselling
  • Short-term psychodynamic psychotherapy (STPP)
363
Q

List the treatment options for less severe depression in order of preference by NICE?

A
  • A combination of individual cognitive behavioural therapy (CBT) and an antidepressant
  • Individual CBT
  • Individual behavioural activation (BA)
  • Antidepressant medication
    • Selective serotonin reuptake inhibitor (SSRI), or
    • Serotonin-norepinephrine reuptake inhibitor (SNRI), or
    • Another antidepressant if indicated based on previous clinical and treatment history
  • Individual problem-solving
  • Counselling
  • Short-term psychodynamic psychotherapy (STPP)
  • Interpersonal psychotherapy (IPT)
  • Guided self-help
  • Group exercise
364
Q

Define depression?

A

Five (or more) of the DSM-5 symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

365
Q

In which antidepressants is a direct switch possible?

A

Citalopram
Escitalopram
Sertraline
Paroxetine

(only when to another SSRI)

366
Q

What are the rules when switching from fluoxetine to another SSRI?

A

Withdraw then leave a gap of 4-7 days (as it has a long half-life) before starting a low dose of the alternative SSRI

367
Q

In which antidepressants is a direct switch to Venlafaxine possible?

A

Citalopram
Escitalopram
Sertraline
Paroxetine

368
Q

What are the rules when switching from an SSRI to a tricyclic antidepressant?

A

Cross-tapering is recommended (the current drug dose is reduced slowly, whilst the dose of the new drug is increased slowly)

369
Q

List some SSRIs?

A
  • Citalopram (Cipramil)
  • Dapoxetine (Priligy)
  • Escitalopram (Cipralex)
  • Fluoxetine (Prozac or Oxactin)
  • Fluvoxamine (Faverin)
  • Paroxetine (Seroxat)
  • Sertraline (Lustral)
  • Vortioxetine (Brintellix)
370
Q

List some SNRIs?

A
  • Desvenlafaxine (Pristiq, Khedezla)
  • Duloxetine (Cymbalta, Irenka)
  • Levomilnacipran (Fetzima)
  • Milnacipran (Savella)
  • Venlafaxine (Effexor XR)
371
Q

What is the mechanism of action of benzodiazepines?

A

They enhance the activity of the inhibitory neurotransmitter GABA in the CNS.

372
Q

What are the common benzodiazepines?

A

Diazepam (Valium) and Lorazepam, and Alprazolam (Xanax)

373
Q

What is the overdose management for benzodiazepines?

A

Flumazenil IV

374
Q

What is the mechanism of action of barbiturates?

A

Barbiturates act on GABA-A receptors by increasing the amount of time the chloride ion channel is opened, which increases the affinity of the receptor for GABA.

375
Q

What are the common barbiturates?

A

Pentobarbitone and Phenobarbitone

376
Q

What is the mechanism of action of opioids?

A

Opioids work via the endogenous opioid system by acting as a potent agonist to the μ receptor. This results in a complex cascade of intracellular signals resulting in dopamine release, blockade of pain signals, and a resulting sensation of euphoria.

377
Q

What is the triad of an opioid overdose?

A

Pinpoint pupils
Respiratory depression
Decreased level of consciousness

378
Q

What is the immediate management of an opioid overdose?

A

IV or IM Naloxone
Activated charcoal can be given in 3 hour window instead of 1 hour due to slowing of gastric motility by opiates

379
Q

What is the mechanism of action of naloxone?

A

Naloxone is a competitive opioid receptor antagonist

380
Q

What is the mechanism of action of amphetamines?

A

Amphetamines increase neurotransmission of dopamine (DA), serotonin (5-HT), and norepinephrine (NE) by entering neurons via the 5-HT and DA transporters and displacing storage vesicles.

381
Q

What is the overdose management for amphetamines?

A

Benzodiazepines for sedation and to control seizures
Activated charcoal if within 1 hour of amphetamine ingestion

382
Q

What is the overdose management for cocaine?

A

Benzodiazepines - These are CNS depressants and thus will counteract the effects of cocaine

383
Q

What is the overdose management of paracetamol?

A

N-acetylcysteine

384
Q

What is the overdose management for tri-cyclic antidepressants?

A

Sodium bicarbonate

385
Q

What is the overdose management for organophosphates?

A

Atropine

386
Q

What is the management for opioid detoxification?

A

Methadone or buprenorphine

387
Q

What is chronic fatigue syndrome (myalgic encephalomyelitis)?

A

Diagnosed after at least 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms

388
Q

What is the classical presentation of a tension headache?

A

Often described as a ‘tight band’ around the head or a pressure sensation.
Symptoms tend to be bilateral

389
Q

What is the management for tension type headaches?

A

Aspirin, paracetamol or an NSAID are first-line

390
Q

What type of hypersensitivity reaction is an allergy?

A

IgE mediated therefore type 1 hypersensitivity

391
Q

What are some common allergens?

A

House dust mite
Pollen
Mold
Foods
Drugs
Latex
Household chemicals

392
Q

What are the investigations for allergies?

A

Clinical diagnosis first line
Skin prick testing in children - wheal >2mm is positive result
RAST testing - measures total and allergen specific IgE in blood

393
Q

What is the management for allergies?

A

Avoid allergen
Oral antihistamines
Steroids e.g. prednisolone

394
Q

Define analphylaxis?

A

Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction

395
Q

What are some examples of causes of anaphylaxis?

A

Food (e.g. nuts) most common in children
Drugs
Insect venom (e.e. wasp sting)

396
Q

What are the features of anaphylaxis?

A

Airway and/or Breathing and/or Circulation problems

Airway - Swelling of throat and tongue
Breathing - Wheeze and dyspnoea
Circulation - Hypotension and tachycardia

397
Q

What is the immediate management of anaphylaxis for the specific age ranges?

A

<6 months - 100-150 μg adrenaline
6 months - 6 years - 150 μg adrenaline
6-12 years - 300 μg adrenaline
>12 years - 500μg adrenaline

Can be repeated every 5 minutes if necessary

398
Q

Where should adrenaline injection be given for anaphylaxis?

A

Anterolateral aspect of the middle third of the thigh

399
Q

What are the microcytic anaemias?

A

Iron deficiency anaemia
Thalassemia
Sideroblastic anaemia

400
Q

What are the haemolytic normocytic anaemias?

A

Sickle cell disease
Hereditary spherocytosis
G6PD deficiency
Autoimmune haemolytic
Malaria
Haemolytic disease of the newborn

401
Q

What are the megaloblastic macrocytic anaemias?

A

B12 deficiency
Folate deficiency

402
Q

Define alpha thalassaemia?

A

Alpha-thalassaemia is a autosomal recessive condition due to a deficiency of alpha chains in haemoglobin

403
Q

Where are the alpha-globulin genes located?

A

2 separate alpha-globulin genes are located on each chromosome 16

404
Q

Give an overview of alpha-thalassaemia where 1/2 alpha globulin alleles are affected?

A

If 1 or 2 alpha globulin alleles are affected then the blood picture would be hypochromic and microcytic, but the Hb level would be typically normal

405
Q

Give an overview of alpha-thalassaemia where 3 alpha globulin alleles are affected?

A

If are 3 alpha globulin alleles are affected results in a hypochromic microcytic anaemia with splenomegaly. This is known as Hb H disease

406
Q

Give an overview of alpha-thalassaemia where 4 alpha globulin alleles are affected?

A

If all 4 alpha globulin alleles are affected (i.e. homozygote) then death in utero (hydrops fetalis, Bart’s hydrops)

407
Q

What is the management for alpha-thalassaemia in severe cases?

A

Regular Blood Transfusions to maintain normal haemoglobin levels in severe cases.

Chronic transfusion therapy may lead to iron overload, hence iron chelation therapy with drugs like Deferasirox or Deferoxamine is necessary

408
Q

Define beta-thalassaemia?

A

Beta-thalassaemia trait is an autosomal recessive condition where there is deficiency in the production of the beta globulin chains of haemoglobin.

characterised by a mild hypochromic, microcytic anaemia..

409
Q

Where are the beta-globulin genes located?

A

Chromosome 11

410
Q

What is beta-thalassaemia trait?

A

Where there is a reduced beta chain due to either promotor region mutations or splice sites.

411
Q

What is beta-thalassaemia major?

A

Where there is absent beta chains due to either promotor region mutations or splice sites

412
Q

What are the features of beta-thalassaemia major?

A

Presents in the first year of life with failure to thrive and hepatosplenomegaly

413
Q

What is the management for beta-thalassaemia major?

A

Repeated blood transfusions
Iron chelation therapy due to potential of iron overload

414
Q

Define haemolytic disease of the newborn?

A

Also known as erythroblastosis fetalis, is a complex and potentially life-threatening condition arising from maternal-foetal blood group incompatibility.

415
Q

What are the investigations for beta-thalassaemia?

A

Hb electrophoresis:
HbA2 & HbF raised
HbA absent

FBC - Microcytic anaemia

416
Q

Define sickle cell anaemia

A

Sickle-cell anaemia is a genetic condition that results for synthesis of an abnormal haemoglobin chain termed HbS

417
Q

In what demographic is sick-cell anaemia more common and why?

A

It is more common in people of African descent as the heterozygous condition offers some protection against malaria

418
Q

When do features of sickle-cell anaemia develop and why?

A

Symptoms in homozygotes don’t tend to develop until 4-6 months when the abnormal HbSS molecules take over from fetal haemoglobin

419
Q

What is the pathophysiology behind sick-cell anaemia?

A

Polar amino acid glutamate is substituted by non-polar valine in each of the two beta chains (codon 6).
This decreases the water solubility of deoxy-Hb causing them to polymerase and ‘sickle’ where they haemolyse and block small vessels

420
Q

What is the inheritance pattern of sickle cell anaemia?

A

Autosomal recessive

421
Q

What is the investigation for sickle-cell anaemia?

A

Hb electrophoresis
FBC
Blood film

422
Q

Define sideroblastic anaemia?

A

Sideroblastic anaemia is a condition where red cells fail to completely form haem

423
Q

What is the congenital cause of sideroblastic anaemia?

A

Delta-aminolevulinate synthase-2 deficiency

424
Q

What are the investigations for sideroblastic anaemia?

A

FBC - hypochromic microcytic anaemia
Iron studies: ferratin, iron, transferrin saturation are all high

425
Q

What is the most common anaemia?

A

Iron deficiency anaemia

426
Q

What demographic has the highest incidence of iron deficiency anaemia?

A

Preschool-age children

427
Q

What are the features of iron deficiency anaemia?

A

Fatigue
SOB on exertion
Pallor
Palpitations
Koilonychia - spoon shaped nails
Angular stomtatitis

428
Q

What are the investigations for iron deficiency anaemia?

A

FBC - hypochromic microcytic anaemia:

Low serum Ferratin
Low serum Iron
Low Transferrin
Total iron binding capacity will be high

Anti-Transglutaminase Antibody (TTG) antibodies to rule out Coeliac disease

429
Q

What is the management for iron deficiency anaemia?

A

Treat underlying cause

Oral iron supplementation - ferrous sulphate or ferrous fumarate

IV iron (ferric carboxymaltose) if cannot give above

Blood transfusion in severe cases

430
Q

What is the pathogen which causes malaria?

A

Plasmodium protozoa:

Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae

431
Q

How is Malaria spread?

A

Female Anopheles mosquito

432
Q

Which species of plasmodium is responsible for severe malaria?

A

Plasmodium falciparum causes nearly all episodes of severe malaria. The other three types, of which Plasmodium vivax is the most common, cause ‘benign’ malaria.

433
Q

What are some protective diseases against malaria?

A

Sickle cell disease
G6PD deficiency
HLA-B53
Absence of Duffy antigen

434
Q

What is the classic triad of falciparum malaria infection?

A

Paroxysms of fever - cyclical (48 hours)
Chills
Sweating

435
Q

What is the first line management for falciparum malaria?

A

Artemisinin-based combination therapies (ACTs)

436
Q

What is the management for non-falciparum malaria?

A

Chloroquine, if ineffective then give ACTs.

Also give primaquine to destroy liver hypnozoites and prevent relapse.

437
Q

Define hereditary spherocytosis?

A

A type of anaemia characterised by a defect in the red blood cell cytoskeleton.

The normal biconcave shape of the red blood cell is replaced by a shpere-shaped blood cell. Red blood cell survival is reduced

438
Q

What is the most common form of anaemia in people of northern european descent?

A

Hereditary spherocytosis

439
Q

What are the features of hereditary spherocytosis?

A

Failure to thrive
Jaundice, gallstones
Splenomegaly
Aplastic crisis precipitated by parvovirus infection
Degree of haemolysis variable
MCHC elevated

440
Q

What is the acute management for hereditary spherocytosis?

A

Supportive treatment
Transfusion if necessary

441
Q

What is the long term management for hereditary spherocytosis?

A

Folate supplementation
Splenectomy

442
Q

What is the diagnostic test for hereditary spherocytosis?

A

EMA binding test

443
Q

What is the inheritance pattern of hereditary spherocytosis?

A

Autosomal dominant

444
Q

Define G6PD deficiency?

A

The commonest red blood cell enzyme defect

445
Q

What is the inheritance pattern of G6PD deficiency?

A

X-linked recessive

446
Q

In what demographic of patients is G6PD deficiency more likely?

A

It is more common in people from the Mediterranean and Africa

447
Q

What are the features of G6PD deficiency?

A

Neonatal jaundice is often seen
Intravascular haemolysis
Gallstones are common
Splenomegaly may be present

448
Q

What would you expect to see on a blood film of a patient with G6PD deficiency?

A

Heinz bodies on blood films.
Bite and blister cells may also be seen

449
Q

What is the investigation for G6PD deficiency?

A

G6PD enzyme assay - 3 months after an acute episode of haemolysis

450
Q

What drugs can trigger a haemolysis in those with G6PD deficiency?

A

Anti-malarials - Primaquine
Ciprofloxacin
Sulphonamides, Sulphasalazine, Sulfonylureas

451
Q

What are the two types of autoimmune haemolytic anaemia?

A

Autoimmune haemolytic anaemia (AIHA) may be divided in to ‘warm’ and ‘cold’ types, according to at what temperature the antibodies best cause haemolysis

452
Q

What are the features of AIHA?

A

Anaemia
Reticulocytosis
Low haptoglobin
Raised lactate dehydrogenase (LDH) and indirect bilirubin
Blood film: spherocytes and reticulocytes

453
Q

What is the investigation for AIHA?

A

Positive direct antiglobulin test (Coomb’s test)

454
Q

Define warm AIHA?

A

Most common type.
The antibody (usually IgG) causes haemolysis best at body temperature and haemolysis tends to occur in extravascular sites, for example the spleen.

455
Q

Define cold AIHA?

A

The antibody in cold AIHA is usually IgM and causes haemolysis best at 4 deg C.
Haemolysis is mediated by complement and is more commonly intravascular.
Features may include symptoms of Raynaud’s and acrocynaosis.

456
Q

What is the management for warm AIHA?

A

Steroids (+/- rituximab)

457
Q

What is the main role of vitamin B12 in the body?

A

Used in the body for red blood cell development and also maintenance of the nervous system.

458
Q

What are some causes of vitamin B12 deficiency?

A

Pernicious anaemia - most common
Post gastrectomy
Vegan / poor diet
Disorders of terminal ilium

459
Q

What is the management for vitamin B12 deficiency?

A

If no neurological involvement 1 mg of IM hydroxocobalamin 3 times each week for 2 weeks, then once every 3 months

If also folate deficient then treat B12 first.

460
Q

What is the management for folate deficiency?

A

Treat underlying cause e.g. stopping drugs or alcohol consumption
Folic acid supplements: always give alongside B12 - 5mg PO OD for 3 months

461
Q

What organism causes chlamydia?

A

Chlamydia trachomatis serovars D through K

462
Q

Chlamydia trachomatis serovars D through K causes which STI?

A

Chlamydia

463
Q

What is the incubation period of chlamydia?

A

The incubation period is around 7-21 days

464
Q

What percentage of men and women who have chlamydia are asymptomatic?

A

70% of women and 50% of men

465
Q

What are the features of chlamydia in women?

A

Cervicitis (discharge, bleeding)
Dysuria

466
Q

What are the features of chlamydia in men?

A

Urethral discharge
Dysuria

467
Q

What is the investigation of choice for chlamydia in men and women?

A

Nuclear acid amplification tests (NAATs) are now the investigation of choice.
Women: vulvovaginal swab is first-line
Men: urine test is first-line

468
Q

What type of organism is chlamydia?

A

Gram-negative, anaerobic bacterium

469
Q

What is the first line management for chlamydia?

A

Doxycycline (7 day course)

470
Q

What is the alternative management for chlamydia in patients who are pregnant?

A

Azithromycin, erythromycin or amoxicillin may be used
Azithromycin (1g od for one day, then 500mg od for two days)

471
Q

What organism most commonly causes septic arthritis in young adults?

A

Neisseria gonorrhoeae

472
Q

What is the causative organism of gonorrhoea?

A

Neisseria gonorrhoeae

473
Q

What is the incubation period of gonorrhoea?

A

2-5 days

474
Q

What type of bacterium is neisseria gonorrhoeae?

A

Gram-negative diplococcus

475
Q

What are the classical features of gonorrhoeae in males?

A

Urethral discharge and dysuria

476
Q

What are the classical features of gonorrhoea in females?

A

Cervicitis e.g. leading to vaginal discharge

477
Q

What is the first line management for gonorrhoea infection?

A

IM ceftriaxone 1g

478
Q

What is the first line management for gonorrhoea infection if there is a known resistance?

A

Oral ciprofloxacin 500mg

479
Q

What is the management for gonorrhoea if IM injection is refused?

A

Oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose)

480
Q

What are key features of disseminated gonococcal infection?

A

Tenosynovitis
Migratory polyarthritis
Dermatitis (lesions can be maculopapular or vesicular)

481
Q

Define pelvic inflammatory disease?

A

Pelvic inflammatory disease (PID) is a term used to describe infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surrounding peritoneum

482
Q

What are the features of pelvic inflammatory disease?

A

Lower abdominal pain
Fever
Deep dyspareunia
Dysuria and menstrual irregularities may occur
Vaginal or cervical discharge
Cervical excitation

483
Q

What are the causative organisms for PID?

A

Chlamydia trachomatis - most common
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis

484
Q

What are the investigations for pelvic inflammatory disease?

A

Pregnancy test - exclude ectopic pregnancy
High vaginal swab - often negative
Screen for Chlamydia and Gonorrhoea

485
Q

What is the first line management for PID?

A

Stat IM ceftriaxone +
14 days of oral doxycycline + oral metronidazole

486
Q

What is the second line management for PID?

A

Oral ofloxacin + oral metronidazole

487
Q

Is a UTI more common in boys or girls?

A

Urinary tract infections (UTI) are more common in boys until 3 months of age (due to more congenital abnormalities) after which the incidence is substantially higher in girls

488
Q

What are the complications of pelvic inflammatory disease?

A

Perihepatitis (Fitz-Hugh Curtis Syndrome) - 10%
Infertility
Ectopic pregnancy

489
Q

When should a child with UTI be referred?

A

Infants less than 3 months old should be referred immediately to a paediatrician.
Children aged more than 3 months old with an upper UTI should be considered for admission to hospital.

490
Q

What is the management for children with UTIs in the community?

A

Oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days

491
Q

What should be prompted if a child has a UTI?

A

Urinary tract infection (UTI) in childhood should prompt an investigation for possible underlying causes and damage to the kidneys

492
Q

What are the causative organisms for UTIs in children?

A

E. coli (responsible for around 80% of cases)
Proteus
Pseudomonas

493
Q

What are the risk factors for urinary incontinence?

A

Advancing age
Previous pregnancy and childbirth
High BMI
Hysterectomy
Family history

494
Q

What factors may predispose children to developing UTIs?

A

Incomplete bladder emptying
Vesicoureteric reflux
Poor hygiene

495
Q

What does vesicoureteric reflux predispose children to?

A

UTI - found in 30% of patients that present with UTI

496
Q

What are the different types of urinary incontinence?

A

Urge incontinence
Stress incontinence
Mixed incontinence
Overflow incontinence
Functional incontinence

497
Q

What is urge incontinence and what it is caused by?

A

The urge to urinate quickly followed by an uncontrollable leakage ranging from a few drops to complete emptying.

Due to detrusor muscle overactivity.

498
Q

What is stress incontinence and what is it caused by?

A

Leaking small amounts when coughing or laughing, due to a high abdominal pressure

499
Q

5The urge to urinate quickly followed by an uncontrollable leakage ranging from a few drops to complete emptying would be what type of incontinence?

A

Urge incontinence

500
Q

Urine leaking out when coughing or laughing, due to a high abdominal pressure would be what type of incontinence?

A

Stress incontinence

501
Q

What is mixed incontinence?

A

A mixture of both stress and urge incontinence

502
Q

What is overflow incontinence?

A

AKA neurogenic bladder - the bladder doesn’t empty completely which leads to an eventual leak e.g. prostate enlargement

503
Q

If the bladder doesn’t completely empty and causes an eventual leak, what type of incontinence is this?

A

Overflow incontinence - AKA neurogenic bladder

504
Q

What is the main cause of overflow incontinence?

A

Damage to the peripheral nerves or nerves of the brain and spinal cord

505
Q

What are the classic signs/symptoms of urge incontinence?

A

Frequent urination, especially at night

506
Q

Frequent urination, especially at night, would indicate what type of incontinence?

A

Urge incontinence

507
Q

What is functional incontinence?

A

Co-morbid physical conditions impair the patient’s ability to get to a bathroom in time

508
Q

What are some causes of functional incontinence?

A

Dementia
Sedating medication
Injury / illness resulting in decreased ambulation

509
Q

What are the classic signs/symptoms of overflow incontinence?

A

There is a weak or intermittent stream / hesitancy

510
Q

If there is a weak or intermittent stream / hesitancy when urinating, what type of incontinence is this?

A

Overflow incontinence

511
Q

What are the initial investigations for urinary incontinence?

A

Bladder diaries for a minimum of 3 days
Vaginal examination
Kegel exercises
Urine dipstick and culture
Urodynamic studies

512
Q

What is the first line intervention for urge incontinence?

A

Bladder retraining for 6 weeks minimum

513
Q

What is the first line pharmacological agent for urge incontinence?

A

Oxybutynin (immediate release)

514
Q

What class of drugs are used first line in urge incontinence?

A

Antimuscarinics (anticholinergics)

515
Q

What is a contraindication of using oxybutynin for urge incontinence?

A

Frail elderly women due to an increased risk of falls

516
Q

What is the second line pharmacological intervention for urge incontinence?

A

Tolterodine or Solifenacin

517
Q

What is a contraindication for Tolterodine or Solifenacin for urge incontinence?

A

Closed-angle glaucoma

518
Q

If a female patient is elderly with closed angle glaucoma, what is the pharmacological agent which can be given?

A

Mirabegron

519
Q

What class of drug is Mirabegron?

A

A beta-3-agonist

520
Q

What is the first line management for stress incontinence?

A

Pelvic floor retraining (Kegel exercises)

8 contractions performed 3 times per day for a minimum of 3 months

521
Q

What is the second line management for stress incontinence?

A

Surgical procedures: e.g. retropubic mid-urethral tape procedures

522
Q

What is the second line management for women for stress incontinence if they decline surgical procedures?

A

Duloxetine

523
Q

What class of drug is Duloxetine?

A

A combined noradrenaline and serotonin reuptake inhibitor

524
Q

What is the mechanism of action of Duloxetine?

A

Increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced contraction

525
Q

What is the management for overflow incontinence?

A

Re-establish a clear pathway for urine flow e.g. catheterisation or medications like alpha blockers, which relax smooth muscle e.g. Tamsulosin

526
Q

What are the risk factors for BPH?

A

Age:
50% of 50 year olds
80% of 80 year olds
Ethnicity - Black > White > Asian

527
Q

What are the categories of symptoms of BPH?

A

Voiding symptoms
Storage symptoms
Post-mictrition

528
Q

What are some examples of voiding symptoms in BPH?

A

Weak or intermittent urinary flow
Straining
Hesitancy
Terminal dribbling
Incomplete emptying

529
Q

What are some examples of storage symptoms in BPH?

A

Urgency
Frequency
Urgency incontinence
Nocturia

530
Q

What is involved in BPH assessment?

A

Urine dipstick
U&Es
PSA - if obstructive symptoms
Urinary frequency-volume chart - at least 3 days
IPSS

531
Q

What is the IPSS?

A

International Prostate Symptom Score (IPSS) - tool for classifying the severity of lower urinary tract symptoms (LUTS) and assessing the impact of LUTS on quality of life

532
Q

What are the scoring ranges for the IPSS?

A

Score 20-35: severely symptomatic
Score 8-19: moderately symptomatic
Score 0-7: mildly symptomatic

533
Q

What is the first-line management for moderate-to-severe BPH?

A

Tamsulosin, alfuzosin

534
Q

What type of drugs are Tamsulosin and alfuzosin?

A

Alpha-1 antagonists

535
Q

What are the side effects of alpha-1 antagonists in BPH?

A

Dizziness
Postural hypotension
Dry mouth
Depression

536
Q

What is the mechanism of action of alpha-1 antagonists for BPH?

A

Decrease smooth muscle tone of the prostate and bladder

537
Q

What management for BPH is indicated if a patient has a significantly enlarged prostate and is considered a high risk of progression?

A

Finasteride

538
Q

What class of drug is finasteride?

A

5 alpha-reductase inhibitor

539
Q

What is the mechanism of action of 5 alpha-reductase inhibitors?

A

Block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH

Causes a reduction in prostate volume and hence may slow disease progression. Can take up to 6 months.

540
Q

What are the side effects of 5 alpha-reductase inhibitors?

A

Erectile dysfunction
Reduced libido
Ejaculation problems
Gynaecomastia

541
Q

What is the management in BPH if a man has moderate-to-severe voiding symptoms and has a significantly enlarged prostate?

A

Combination therapy:

Alpha-1 antagonist
AND
5 alpha-reductase inhibitor

542
Q

What is the management for BPH if voiding and storage symptoms persist with a alpha-blocker alone?

A

Tolterodine
Darifenacin

543
Q

What type of drugs are tolterodine and darifenacin?

A

Antimuscarinic (anticholinergic)

544
Q

What is the most common form of prostate cancer and where does it lie in the prostate?

A

95% adenocarcinoma
Peripheral zone

545
Q

What scoring system is used for prostate cancer?

A

Gleason score

546
Q

What are the risk factors for prostate cancer?

A

Increasing age
Obesity
Afro-Caribbean heritage
Family history

547
Q

What are the features of prostate cancer?

A

Localised prostate cancer is often asymptomatic

Bladder outlet obstruction: hesitancy, urinary retention
Haematuria, haematospermia
Pain: back, perineal or testicular
DRE: asymmetrical, hard, nodular enlargement with loss of median sulcus

548
Q

What is PSA?

A

Prostate specific antigen.

A serine protease enzyme produced by normal and malignant prostate epithelial cells

549
Q

When should PSA testing be performed?

A

Considered in men with suspected prostate cancer
Offered to men older than 50 years of age who request a PSA test

550
Q

What are the PSA thresholds by age?

A

<40 - use clinical judgement
40-49 - >2.5ng/ml
50-59 - >3.5ng/ml
60-69 - >4.5ng/ml
70-79 - >5.5ng/ml
>79 - use clinical judgement

551
Q

What may also cause an increase in PSA?

A

BPH
Prostatitis and UTI
Ejaculation within 48 hours
Vigorous exercise within 48 hours
Urinary retention within 4 weeks

552
Q

What percentage of men with prostate cancer will have normal PSA?

A

15%

553
Q

What is the old first line investigation for prostate cancer? Why is it not anymore?

A

Transrectal ultrasound-guided (TRUS) biopsy

It can cause:
Sepsis
Pain lasting over 2 weeks
Fever
Haematuric and rectal bleeding

554
Q

What is now the first-line investigation for prostate cancer?

A

Multiparametric MRI then a biopsy if indicated

555
Q

What is the management for localised prostate cancer?

A

Conservative: active monitoring & watchful waiting - preferred

Radical prostatectomy
Radiotherapy: external beam and brachytherapy

556
Q

What is the management for advanced localised prostate cancer?

A

Hormonal therapy
Radical prostatectomy
Radiotherapy: external beam and brachytherapy

557
Q

What is a common complication of a radical prostatectomy?

A

Erectile dysfunction

558
Q

What may patients develop after radiotherapy for prostate cancer, what are they at increased risk of?

A

May develop proctitis

Increased risk of colon, bladder, and rectal cancer

559
Q

What is the management for metastatic prostate cancer?

A

Combination of:

Synthetic GnRH a(nta)gonist e.g. Goserelin
+ cyproterone acetate (anti-anrogen)
Bicalutamide
Bilateral orchidectomy

Chemotherapy with docetaxe

560
Q

What is the key aim of metatstaic prostate cancer hormonal therapy?

A

Reducing androgen levels

561
Q

What are some causes of chronic kidney disease?

A

Diabetic nephropathy
Chronic glomerulonephritis
Chronic pyelonephritis
Hypertension
Adult polycystic kidney disease

562
Q

How may chronic kidney disease be classified?

A

According to glomerular filtration rate

563
Q

What are the eGFR variables?

A

CAGE:

Creatinine
Age
Gender
Ethnicity

564
Q

What factors may effect GFR?

A

Pregnancy
Muscle mass (e.g. amputees, body-builders)
Eating red meat 12 hours prior to the sample being taken

565
Q

What is stage 1 chronic kidney disease?

A

Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests are normal, there is no CKD)
I.e. normal U&Es and no proteinuria

566
Q

What is stage 2 chronic kidney disease?

A

60-90 ml/min with some sign of kidney damage (if kidney tests are normal, there is no CKD)
I.e. normal U&Es and no proteinuria

567
Q

What is stage 3 chronic kidney disease?

A

Stage 3a - 45-59 ml/min, a moderate reduction in kidney function
Stage 3b - 30-44 ml/min, a moderate reduction in kidney function

568
Q

What is stage 4 chronic kidney disease?

A

15-29 ml/min, a severe reduction in kidney function

569
Q

What is stage 5 chronic kidney disease?

A

Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed

570
Q

What is the first-line management for chronic kidney disease if ACR >30 and there is co-existent hypertension?

A

ACE inhibitors (or angiotensin II receptor blockers)

All patients should be started on a statin

571
Q

What is the first-line management for chronic kidney disease if ACR >70?

A

ACE inhibitors (or angiotensin II receptor blockers) regardless of if hypertension is present or not

All patients should be started on a statin

572
Q

What is the management for chronic kidney disease with proteinuria?

A

SGLT-2 inhibitors

573
Q

What is the mechanism of action of SGLT-2 inhibitors in CKD?

A

Primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria

By blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalises tubuloglomerular feedback and thereby reduces intraglomerular pressure

574
Q

How may you differentiate between chronic kidney disease and acute kidney injury? What are some exceptions to this rule?

A

Renal ultrasound - most patients with CKD have bilateral small kidneys

Autosomal dominant polycystic kidney disease
Diabetic nephropathy (early stages)
Amyloidosis
HIV-associated nephropathy

Other features that suggest CKD - hypocalcaemia (due to lack of vitamin D)

575
Q

Describe how CKD causes mineral bone disease?

A

1-alpha hydroxylation occurs in the kidneys → CKD = low vitamin D
Kidneys normally secrete phosphorous → CKD leads to high phosphate

Increased phosphate drags calcium out of the bones.
Low calcium due to lack of vitamin D and high phosphorous

Low calcium, low vitamin D, high phosphorous = secondary hyperparathyroidism

576
Q

What is the management of secondary hyperparathyroidism due to CKD?

A

First-line - reduce phosphate intake
Vitamin D: alfacalcidol, calcitriol

Parathyroidectomy in severe cases

577
Q

Define constipation?

A

Defecation that is unsatisfactory because of infrequent stools (< 3 times weekly), difficult stool passage (with straining or discomfort), or seemingly incomplete defecation.

578
Q

What are first-line laxatives for constipation?

A

Ispaghula husk - a bulk forming laxative

579
Q

What are second-line laxatives for constipation?

A

Macrogol - an osmotic laxative

580
Q

Name some types of bulk forming laxatives?

A

Ispaghula husk
Methylcellulose

581
Q

Name some types of osmotic laxatives?

A

Lactulose
Macrogol

582
Q

Name some types of stimulant laxatives?

A

Senna
Bisacodyl

583
Q

Name a stool softener laxative?

A

Docusate sodium

584
Q

Name some laxative suppositories?

A

Glycerol
Bisacodyl

585
Q

Name some enema laxatives?

A

Phosphate
Sodium citrate
Docusate

586
Q

What is the mechanism of action of bulk forming laxatives?

A

They increase the bulk of the stool, usually take 2-3 days to work. It is important to drink plenty of water alongside bulk laxatives

587
Q

What is the mechanism of action of stimulant laxatives?

A

Stimulate the local nervous system within the gut wall which increase colonic contractility and secretions. They work in 6-12 hours. Better for those with difficulty emptying more so than infrequent motions

588
Q

What is the mechanism of action of osmotic laxatives?

A

These are poorly absorbable molecules that cause an osmotic effect drawing water into bowel lumen. Very commonly used and very effective in faecal impaction and infrequent bowel motions

589
Q

What is the mechanism of action of stool softening laxatives?

A

Lowers the surface tension, leading to water and fasts penetrating the stool.

590
Q

What is the mechanism of action of suppository laxatives?

A

Used to aid rectal emptying by stimulating the anal sphincter and initiating peristalsis.
Used when there is an inadequate response to oral, incomplete emptying, incontinence, or altered rectal sensitivity. Causes more rapid evacuation

591
Q

What is the mechanism of action of enema laxatives?

A

Include osmotic, softeners, and/or weak stimulants. A phosphate enema contains 128mL of liquid whereas other mini ones have 5mL. Act quickly to bring about a more rapid evacuation.

592
Q

Define diverticulosis?

A

Diverticulosis is an extremely common disorder characterised by multiple outpouchings of the bowel wall

593
Q

Where does diverticulosis most commonly occur?

A

Most commonly in the sigmoid colon.

594
Q

Define diverticulitis?

A

One of the diverticular become infected.

595
Q

What are the features of diverticulitis?

A

Left iliac fossa pain and tenderness
Anorexia, nausea and vomiting
Diarrhoea
Features of infection (pyrexia, raised WBC and CRP)

596
Q

What are the investigations for acute presentation of diverticulitis?

A

Plain abdominal films and an erect chest x-ray will identify perforation

A contrast enhanced CT will help identify inflammation and local complications.

597
Q

What are the investigations as part of a diverticular disease work-up in clinic?

A

Either a colonoscopy, CT cologram or barium enema

598
Q

What is the general management for diverticular disease?

A

Increase dietary fibre intake

599
Q

What is the management for diverticulitis?

A

Mild - oral antibiotics
Severe - hospital, nil by mouth, IV fluids, IV antibiotics

Peri colonic abscesses should be drained

600
Q

What antibiotics are typically given in diverticulitis?

A

Cephalosporin + metronidazole

601
Q

Define haemorrhoid?

A

Haemorrhoidal tissue is mucosal vascular cushions found in the left lateral, right posterior and right anterior portions of the anal canal (3 o’clock, 7’o’clock and 11 o’clock respectively).

Haemorrhoids are said to exist when they become enlarged, congested and symptomatic

602
Q

What are the features of haemorrhoids?

A

Painless rectal bleeding - most common
Pruritus
Pain: not significant unless thrombosed
Soiling may occur with third or forth degree piles

603
Q

What is the management for haemorrhoids?

A

Soften stools - increase fibre and fluid
Topical local anaesthetic and steroids
Rubber band ligation

Surgery is reserved for large symptomatic haemorrhoids which do not respond to above

604
Q

Define GORD?

A

Gastro-oesophageal reflux disease (GORD) may be defined as symptoms of oesophagitis secondary to refluxed gastric contents

605
Q

What is the investigation of choice for GORD, what are the indications?

A

Upper GI endoscopy

Age >55 years
Symptoms lasting more than 4 weeks
Dysphagia
Relapsing symptoms
Weight loss

606
Q

What is the gold standard investigation in GORD?

A

24-hr oesophageal pH monitoring

607
Q

What is the management for endoscopically proven oesophagitis?

A

Full dose PPI 1-2 months - if response then low dose PRN
No response double dose for one month

608
Q

What is the management for endoscopically negative oesophagitis?

A

Full dose PI for 1 month - if response then low dose PRN
If no response then H2RA or prokinetic for 1 month

609
Q

When should an IBS diagnosis be considered?

A

The following for 6 months:
(A)bdominal pain
(B)loating
(C)hange in bowel habit

610
Q

When should an IBS diagnosis definitely be made?

A

Patient has abdominal pain relieved by defecation or associated with altered bowel frequency stool form, in addition to 2 of the following 4 symptoms:
Altered stool passage
Abdominal bloating
Symptoms made worse by eating
Passage of mucus

611
Q

What are some red flag queries of IBS?

A

Rectal bleeding
Unexplained weight loss
Family history of bowel cancer
Onset after 60 years old

612
Q

What are the IBS investigations in primary care?

A

FBC
ESR / CRP
Coeliac disease screen (TTG)

613
Q

What are the first-line pharmacological agents used in IBS?

A

Pain: antispasmodic agents hyoscine butylbromide(Buscopan)
Constipation: laxatives but avoid lactulose
Diarrhoea: loperamide is first-line

614
Q

What is the general dietary advice for IBS?

A

Regular meal times
Avoid missing meals / long gaps
8 cups of fluid per day
Restrict tea and coffee
Restrict alcohol and fizzy drinks
Limiting high fibre foods
Limit fresh fruit
Increasing intake of oats and linseeds for wind and bloating

615
Q

What antispasmodic agent is used for IBS?

A

Hyoscine butylbromide(Buscopan)

616
Q

What laxative should be avoided in IBS?

A

Lactulose

617
Q

What pharmacological agent is used for constipation in IBS?

A

Loperamide

618
Q

What is the second line pharmacological agent used in IBS?

A

Tricyclic antidepressant - Amitriptyline 5-10mg at night

619
Q

What is the classic triad of infectious mononucleosis?

A

The classic triad of sore throat, pyrexia and lymphadenopathy (98%)

620
Q

What develops in 99% of patients while they take ampicillin/amoxicillin for infectious mononucleosis?

A

A maculopapular, pruritic rash

621
Q

What is the investigation of choice for infectious mononucleosis?

A

Heterophil antibody test (Monospot test) in the second week of illness

622
Q

What is the management for infectious mononucleosis?

A

Rest, fluid intake, avoid alcohol
Simple analgesia
Avoid contact sports for 4 week to reduce risk of splenic rupture

623
Q

What is the management for pharyngitis, tonsillitis, and laryngitis?

A

Paracetamol / Ibuprofen
Antibiotics not routinely offered

624
Q

What are the indications for antibiotics for pharyngitis, tonsillitis, and laryngitis?

A

Features of marked systemic upset secondary
Unilateral peritonsillitis
History of rheumatic fever
Increased risk of acute infection (children / HIV)
Centor criteria = 3 or more

625
Q

What is the Centor criteria used for? What scores are given?

A

Likelihood of strep pharyngitis, 1 for each of:

Presence of tonsillar exudate
Tender anterior cervical lymphadenopathy or lymphadenitis
History of fever
Absence of cough

626
Q

What antibiotics are given in pharyngitis, tonsillitis, and laryngitis if indicated?

A

Phenoxymethylpenicillin
Clarithromycin (if the patient is penicillin-allergic

627
Q

Define diabetes mellitus?

A

A chronic condition characterised by abnormally raised levels of blood glucose.

628
Q

What are the features of T1DM?

A

Abdominal pain
Polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)

629
Q

What are the investigations for T1DM?

A

Urine dip for ketones and glucose
Fasting glucose and random glucose
C-peptide levels (typically low)
Diabetes specific antibodies

630
Q

What test is not useful in T1DM and why?

A

HbA1c is not as useful for patients with a possible or suspected diagnosis of T1DM as it may not accurately reflect a recent rapid rise in serum glucose

631
Q

What antibodies may be seen in T1DM?

A

Anti-glutamic acid antibodies (anti-GAD)
Islet cell antibodies (ICA)
Insuline antibodies (IAA)
Insulinoma-associated-2 autoantibodies (IA-2A)

632
Q

What is the diagnostic criteria for diabetes?

A

Fasting glucose greater than or equal to 7.0 mmol/l OR
Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If asymptomatic then 2x positive tests on separate occasions

633
Q

How often should HbA1c be measured in T1DM? what is the target?

A

Every 3-6 months
Target of HbA1c level of 48 mmol/mol (6.5%) or lower

634
Q

How should patients measure glucose levels in T1DM?

A

Recommend testing at least 4 times a day, including before each meal and before bed
More frequently during sports, illness, planning pregnancy, during pregnancy, while breastfeeding

635
Q

What are the blood glucose targets for T1DM?

A

5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day

636
Q

What type of insulin is offered to patients with T1DM?

A

Multiple daily injection basal-bolus insulin regimens:
Twice-daily insulin detemir OR
Once-daily determir is alternative

Rapid-acting insulin analogues injected before meals

637
Q

What other medication can be given for those with T1DM if BMI is above 25?

A

NICE recommend considering adding metformin if the BMI >= 25 kg/m²

638
Q

What must a T1DM patient do on a sick day?

A

If a patient is on insulin, they must not stop it due to the risk of diabetic ketoacidosis
Check their blood glucose more regularly

639
Q

Aside from glucose level, what test can be used to diagnose T2DM specifically?

A

HbA1c of greater than or equal to 48 mmol/mol (6.5%)

If asymptomatic must be repeated to confirm diagnosis

640
Q

What is the first-line drug for T2DM?

A

Metforim - should be titrated up slowly to avoid GI upset
If standard release not tolerated, then use modified release

641
Q

What is the additional management for T2DM and when should it be added?

A

SGLT-2 inhibitors
The patient has a high risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
The patient has established CVD
The patient has chronic heart failure

642
Q

What would be the management of choice if a patient has a metformin contraindication?

A

If the patient has a risk of CVD, established CVD or chronic heart failure:
SGLT-2 monotherapy

If the patient does not have this risk:
DPP-4 inhibitor or pioglitazone or a sulfonylurea

643
Q

When would second line therapy for T2DM be indicated?

A

If the HbA1c has risen to 58 mmol/mol (7.5%) then further treatment is indicated

644
Q

What are the second line management options for T2DM?

A

Metformin + DPP-4 inhibitor
Metformin + pioglitazone
Metformin + sulfonylurea
Metformin + SGLT-2 inhibitor

645
Q

What are the third line management options for T2DM?

A

Metformin + DPP-4 inhibitor + sulfonylurea
Metformin + pioglitazone + sulfonylurea
Metformin + pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2
Insulin-based treatment

646
Q

What is the fourth line management for T2DM?

A

GLP-1 mimetic
Particularly in those that are BMI ≥ 35 kg/m²

647
Q

What are the HbA1c targets for different classes of patients with T2DM?

A

Lifestyle management = 48 mmol/mol (6.5%)
Lifestyle = Metformin = 48 mmol/mol (6.5%)
Drug which may cause hyperglycaemia = 53 mmol/mol (7.0%)

648
Q

Define T2DM?

A

A relative deficiency of insulin due to an excess of adipose tissue

The most common cause

649
Q

Define T1DM?

A

Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system

650
Q

What are the features of T2DM?

A

Polydipsia
Polyuria

Due to water being ‘dragged’ out of the body due to the osmotic effects of excess blood glucose being excreted in the urine (glycosuria).

651
Q

What is a contraindication of metformin?

A

Cannot be used in patients with an eGFR of < 30 ml/min

652
Q

What is the mechanism of action of metformin?

A

Increases insulin sensitivity
Decreases hepatic gluconeogenesis

653
Q

What is the mechanism of action of sulfonylureas?

A

Stimulate pancreatic beta cells to secrete insulin

Examples - gliclazide and glimepiride

654
Q

What is the mechanism of action of DPP-4 inhibitors?

A

Increases incretin levels which inhibit glucagon secretion

655
Q

What is the mechanism of action of SGLT-2 inhibitors?

A

Inhibits reabsorption of glucose in the kidney

656
Q

What should a patient with T2DM do on a sick day?

A

Advise the patient to temporarily stop some oral hypoglycaemic
Can be restarted when eating and drinking again

If on insulin therapy do not stop

657
Q

What are the macrovascular complications of T1DM?

A

Ischaemic heart disease
Heart failure
Peripheral vascular disease

Stroke

658
Q

What are the microvascular complications of T1DM?

A

Diabetic neuropathy
Diabetic nephropathy
Diabetic retinopathy

659
Q

What is primary hypothyroidism?

A

There is a problem with the thyroid gland itself, for example an autoimmune disorder affecting thyroid tissue

660
Q

What is secondary hypothyroidism?

A

Usually due to a disorder with the pituitary gland (e.g.pituitary apoplexy) or a lesion compressing the pituitary gland

661
Q

What are the general features of hypothyroidism?

A

Weight gain
Lethargy
Cold intolerance
Constipation

662
Q

What are the skin features of hypothyroidism?

A

Dry (anhydrosis), cold, yellowish skin
Non-pitting oedema
Dry, coarse scalp hair, loss of later aspect of eyebrows (Queen Anne’s sign)

663
Q

What is the gynaecological feature of hypothyroidism?

A

Menorrhagia

664
Q

What are the neurological features of hypothyroidism?

A

Decreased deep tendon reflexes
Carpal tunnel syndrome

665
Q

What are the features of congenital hypothyroidism?

A

Prolonged neonatal jaundice
Delayed mental/physical milestones
Short stature
Puffy face
Hypotonia

666
Q

What is the most common cause of hypothyroidism in children?

A

Hashimoto’s - autoimmune thyroiditis

Most common in developing world - iodine deficiency

667
Q

What would a TFT show for hypothyroidism?

A

High TSH
Low T3
Low T4

668
Q

What is the management for hypothyroidism?

A

Levothyroxine

669
Q

What are the side-effects of thyroxine therapy?

A

Hyperthyroidism: due to over treatment
Reduced bone mineral density
Worsening of angina
Atrial fibrillation

670
Q

What is the most common cause of hypothyroidism in adults?

A

Hashimoto thyroiditis - autoimmune

Associated with IDDM, Addison’s or pernicious anaemia
5-10x more common in women

671
Q

What is the formula for BMI?

A

BMI = weight (kg) / height (m) squared

672
Q

What would be considered underweight for BMI?

A

< 18.49

673
Q

What would be considered normal for BMI?

A

18.5 - 25

674
Q

What would be considered overweight for BMI?

A

25 - 30

675
Q

What would be considered obese for BMI?

A

30 - 35 - Obese class I
35 - 40 - Obese class II
> 40 - Obese class III

676
Q

What is the management for obesity?

A

Diet and exercise
Medical - orlistat and liraglutide
Bariatric surgery

677
Q

When can menopause be diagnosed?

A

Cessation of menses for at least 12 consecutive months

678
Q

When does menopause usually occur in women, what is the average age?

A

40-60 years old. Average age is 51 years.

679
Q

What is considered to be pre-menopausal?

A

Menopause before the age of 40 years.

680
Q

What are some contraindications of HRT?

A

Current or past breast cancer.
Any oestrogen sensitive cancer.
Undiagnosed vaginal bleeding.
Untreated endometrial hyperplasia.

681
Q

Unopposed oestrogen HRT can be given to women under what conditions?

A

If they do not have a uterus.

682
Q

Combined HRT should be given to women who have what?

A

A uterus

683
Q

What is a complication of oral HRT?

A

Increased risk of VTE, no increased risk with transdermal

684
Q

Which two cancers are associated with an increased risk due to HRT use?

A

Ovarian and breast

685
Q

What pharmacological agent can be given for women suffering from vasomotor symptoms (non-HRT)?

A

Fluoxetine

686
Q

What is oestrogen HRT called when it is given in oral form?

A

Estradiol

687
Q

What is progesterone HRT called when given in oral form?

A

Utrogestan (micronised progesterone)

688
Q

When is contraception needed until after menopause?

A

12 months after the last period in women > 50 years

24 months after the last period in women < 50 years

689
Q

Define bursitis?

A

Bursitis is an acute or chronic inflammatory condition of a bursa

690
Q

What is the management for bursitis?

A

Conservative management and analgesia

Second-line is corticosteroid injection - Methylprednisolone acetate

691
Q

Define fibromyalgia?

A

A syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites

692
Q

What are the risk factors for fibromyalgia?

A

Women are around 5 times more likely to be affected
Typically presents between 30-50 years old

693
Q

What are the features of fibromyalgia?

A

Chronic pain: at multiple site, sometimes ‘pain all over’
Lethargy
Cognitive impairment: ‘fibro fog’
Sleep disturbance, headaches, dizziness are common

694
Q

What are the non-phamacological management strategies for fibromyalgia?

A

Explanation
Aerobic exercise: has the strongest evidence base
Cognitive behavioural therapy
Relaxation techniques

695
Q

What are the pharmacological management strategies for fibromyalgia?

A

Pregabalin
Duloxetine
Amitriptyline

696
Q

What X-ray changes are seen with osteoarthritis?

A

LOSS mnemonic:
Loss of joint space
Osteophytes forming at joint margins
Subchondral sclerosis
Subchondral cysts

697
Q

What are the most common sites for osteoarthritis?

A

Knee - most common
Hip - second most common

698
Q

What are the risk factors for osteoarthritis?

A

Female
Increasing age
Obesity
Hypermobility
Developmental dysplasia of the hip

699
Q

What joints are affected in the hand with osteoarthritis?

A

Carpometacarpal joints (CMCs), distal interphalangeal joints (DIPJs) are affected more than the proximal interphalangeal joints (PIPJs)

700
Q

What are the features of osteoarthritis of the hand?

A

Inactivity stiffness
Heberden’s nodes at the DIP joints
Bouchard’s Nodes at the PIP joints
Squaring of the thumbs

701
Q

What is the investigation for osteoarthritis?

A

Usually diagnosed clinically
X-ray can be done

702
Q

What is the management for osteoarthritis?

A

Weight loss and advice with exercise
Topical NSAIDs are first line

Oral NSAIDs should be given with PPI

Intra-articular steroid injections if above is ineffective

703
Q

Define polymyalgia rheumatica?

A

Characterised by muscle stiffness and raised inflammatory markers

704
Q

What are the features of polymyalgia rheumatica?

A

Abrupt onset of bilateral early morning stiffness in over 60s

Weakness is not a symptom

705
Q

What are the investigations for polymyalgia rheumatica?

A

Raised inflammatory markers e.g. ESR > 40 mm/hr
Note creatine kinase and EMG normal

706
Q

What is the management for polymyalgia rheumatica?

A

Prednisolone e.g. 15mg/od

Patients should respond dramatically - failure should prompt consideration of alternate diagnosis

707
Q

Define gout?

A

A form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium.

It is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l)

708
Q

What factors may cause an decreased excretion of uric acid?

A

Drugs: diuretics + Aspirin
Chronic kidney disease
Lead toxicity

709
Q

What factors may cause an increased production of uric acid?

A

Myeloproliferative/lymphoproliferative disorder
Cytotoxic drugs
Severe psoriasis

710
Q

What are the features of acute gout?

A

Pain: this is often very significant
Swelling
Erythema

711
Q

What are the most common sites of gout?

A

1st metatarsophalangeal (MTP) joint - 70%
Ankle
Wrist
Knee

712
Q

What is the first line investigation for gout?

A

Measuring uric acid levels:
A uric acid level ≥ 360 umol/L supports diagnosis
Uric acid level < 360 umol/L during a flare - repeat 2 weeks after the flare has settled

713
Q

What would synovial fluid analysis show for gout?

A

Needle shaped negatively birefringent monosodium urate crystals under polarised light

714
Q

What is the acute pharmacological management of gout?

A

NSAIDs - also PPI

If peptic ulcer disease - colchicine

715
Q

What if long term management for gout?

A

Urate-lowering therapy:
Allopurinol (xanthine oxidase inhibitor)

Febuxostat (also a xanthine oxidase inhibitor) is second-line

716
Q

What is the general management for gout?

A

Reduce alcohol intake and avoid during an acute attack
Lose weight if obese
Avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products

717
Q

Define pseudogout?

A

A form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium.

718
Q

What are the risk factors for pseudogout?

A

Increasing age (>60 years)
Haemochromatosis
Hyperparathyroidism
Low magnesium, low phosphate
Acromegaly, Wilson’s disease

719
Q

What joints are most commonly affected in psuedogout?

A

Knee
Wrist
Shoulders

720
Q

What would synovial fluid analysis show for pseudogout?

A

Weakly-positively birefringent rhomboid-shaped crystals

721
Q

What would an x-ray of pseudogout show?

A

Chondrocalcinosis

722
Q

What is the management of pseudogout?

A

Aspiration of joint fluid, to exclude septic arthritis
NSAIDs or intra-articular, intra-muscular or oral steroids as for gout

723
Q

Define reactive arthritis?

A

A term which described a classic triad of urethritis, conjunctivitis and arthritis following an infection where the organism cannot be recovered from the joint

724
Q

What are the features of reactive arthritis?

A

Arthritis is typically an asymmetrical oligoarthritis of lower limbs
Dactylitis
Symptoms of urethritis
Conjunctivitis and/or anterior uveitis

725
Q

When does reactive arthritis typically develop?

A

Typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months

726
Q

What is the management of reactive arthritis?

A

Analgesia - NSAIDS, intra-articular steroids
Sulfasalazine and methotrexate are sometimes used for persistent disease

727
Q

What is osteoporosis?

A

Osteoporosis is a disorder affecting the skeletal system characterised by loss of bone mass.
WHO defines as presence of bone mineral density (BMD) of less than 2.5 standard deviations (SD) below the young adult mean density

728
Q

What are the risk factors for osteoporosis?

A

Corticosteroid use
Smoking
Alcohol
Low BMI
Family history

729
Q

What screening tool is used to measure a patients 10-year risk of developing a fragility fracture?

A

FRAX score

730
Q

A FRAX score is used to assess what?

A

Used to measure a patients 10-year risk of developing a fragility fracture

731
Q

What investigation is used to assess bone mineral density?

A

Dual-energy X-ray absorptiometry (DEXA)

732
Q

What bones does a DEXA scan look at?

A

Hip and lumbar spine.

733
Q

What is the first-line management for osteoporosis?

A

Alendronate OR
Risedronate OR
Etidronate

Vitamin D and calcium if deficient

734
Q

What class of drug is alendronate and Risedronate?

A

Oral bisphosphonates

735
Q

Explain the DEXA scan algorithm?

A

Step 1: Is a fragility fracture present?
- No = move on to step 2
- Yes = Make clinical diagnosis of osteoporosis if age ≥ 75 OR perform DEXA scan if age > 50

Step 2: Perform Fragility fracture risk assessment
- Low Risk = Repeat fragility fracture assessment in 5 years
- Intermediate-High Risk = perform DEXA scan

736
Q

What does intermediate-high risk on FRAX scoring indicate for investigation?

A

Perform DEXA scan

737
Q

What QFracture score would indicate a DEXA scan would be arranged?

A

> 10%

738
Q

What is the T score in a DEXA scan based off?

A

Based on bone mass of young reference population

739
Q

What does a T score of -1 indicate for a DEXA scan?

A

-1.0 means bone mass of one standard deviation below that of young reference population
Osteopenia

740
Q

What does a T score of -2.5 indicate for a DEXA scan?

A

-2.5 means bone mass of 2.5 standard deviations below that of young reference population
Osteoporosis

741
Q

What is a Z score in a DEXA scan?

A

Z score is adjusted for age, gender and ethnic factors

742
Q

What is the mechanism of action of bisphosphonates?

A

Bisphosphonates bind to hydroxyapatite in bone, inhibiting osteoclast-mediated bone resorption

743
Q

What advice should be given when prescribing oral bisphosphonates?

A

Oral bisphosphonates should be taken with a full glass of water, on an empty stomach, and the patient should remain upright for at least 30 minutes afterwards

744
Q

What is the second line management for osteoporosis?

A

Denosumab injection every 6 months

745
Q

What are the potential third-line managements for osteoporosis?

A

Strontium ranelate
Raloxifene
Teriparatide
Romosozumab

746
Q

What is the mechanism of action of denosumab?

A

Human monoclonal antibody that inhibits RANK ligand, which in turn inhibits the maturation of osteoclasts

747
Q

At what level of corticosteroids should osteoporosis management be commenced anticipatorily?

A

Equivalent of prednisolone 7.5mg a day for 3 or more months.

748
Q

List some causes of Parkinsonism?

A

Parkinson’s disease
Drug-induced e.g. antipsychotics, metoclopramide*
Progressive supranuclear palsy
Multiple system atrophy
Wilson’s disease
Post-encephalitis
Dementia pugilistica (secondary to chronic head trauma e.g. boxing)
Toxins: carbon monoxide, MPTP

749
Q

What is the cause of parkinsonism?

A

Parkinson’s disease is a progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra.

750
Q

What is the classic triad of parkinson’s disease?

A

The reduction in dopaminergic output results in a classical triad of features: bradykinesia, tremor and rigidity.

The symptoms of Parkinson’s disease are characteristically asymmetrical.

751
Q

Describe the bradykinesia seen in Parkinson’s disease?

A

Poverty of movement also seen, sometimes referred to as hypokinesia
Short, shuffling steps with reduced arm swinging
Difficulty in initiating movement

752
Q

Describe the tremor seen in Parkinson’s disease?

A

Most marked at rest, 3-5 Hz
Worse when stressed or tired, improves with voluntary movement
Typically ‘pill-rolling’, i.e. in the thumb and index finger

753
Q

What are some other ‘axillary’ characteristics seen in Parkinson’s disease?

A

Mast-like facies
Flexed posture
Micro-graphia
Drooling of saliva
Impaired olfaction
REM sleep disturbance
Fatigue
Postural hypertension

754
Q

What is the first line management for Parkinson’s disease if motor symptoms are affecting the quality of life?

A

Levodopa nearly always combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide)

755
Q

Why is levodopa combined with a decarboxylase inhibitor for Parkinson’s therapy?

A

This prevents the peripheral metabolism of levodopa to dopamine outside of the brain and hence can reduce side effects

756
Q

List some common side effects of levodopa?

A

Dry mouth
Anorexia
Palpitations
Postural hypotension
Psychosis

757
Q

What pharmacological agent can be given for excessive salivation in Parkinson’s disease?

A

Glycopyrronium bromide

758
Q

What pharmacological agent should be considered if a patient with Parkinson’s disease develops orthostatic hypotension? What is the mechanism of this drug?

A

Midodrine - acts on peripheral alpha-adrenergic receptors to increase arterial resistance

759
Q

What pharmacological agent should be considered if excessive daytime sleepiness occurs in a patient with Parkinson’s disease?

A

Modafinil

760
Q

What is the first line management for Parkinson’s disease if motor symptoms are NOT affecting the quality of life?

A

Dopamine agonist (non-ergot derived)
Levodopa
Monoamine oxidase B (MAO-B) inhibitor

761
Q

List some dopamine receptor agonists that are used in the treatment of Parkinson’s disease?

A

Bromocriptine
Ropinirole
Cabergoline
Apomorphine

762
Q

What investigations should be organised before prescribing ergot-derived dopamine receptor agonists?

A

Echocardiogram
ESR
Creatinine
Chest x-ray

Due to being associated with pulmonary, retroperitoneal and cardiac fibrosis

763
Q

What class of Parkinson’s drugs have potential for impulse control disorders?

A

Dopamine receptor agonists

764
Q

What is the mechanism of action of MAO-B inhibitors? Give an example of this class of drug?

A

Monoamine Oxidase-B inhibitors work by inhibiting the breakdown of dopamine secreted by the dopaminergic neurones.

Selegiline

765
Q

Give some examples of COMT inhibitors for Parkinson’s disease?

A

Entacapone
Tolcapone

766
Q

What is the mechanism of action of COMT inhibitors?

A

Catechol-O-Methyl Transferase inhibitors - an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy

767
Q

What is ‘end-of-dose’ wearing off phenomenon in Parkinson’s disease management?

A

Symptoms often worsen towards the end of dosage interval. This results in a decline of motor activity

768
Q

What is ‘on-off phenomenon’ in Parkinson’s disease management?

A

Large variations in motor performance, with normal function during the ‘on’ period, and weakness and restricted mobility during the ‘off’ period

769
Q

What side-effects may be seen at peak dose of levadopa?

A

Dystonia, chorea and athetosis (involuntary writhing movements)

770
Q

What are the classical features of a migraine?

A

A severe, unilateral, throbbing headache associated with nausea, photophobia and phonophobia
May be precipitated by aura

771
Q

What is the first line management for migraine?

A

Offer combination therapy with:
an oral triptan and an NSAID, OR
an oral triptan and paracetamol

772
Q

What formulation of triptan should be used in young people?

A

Nasal and not oral

773
Q

What are the prophylaxis management options for migraines?

A

Propranolol
Topiramate
Amitriptyline

774
Q

In what demographic of patient should topiramate be avoided for prophylactic management of migraines?

A

Should be avoided in women of childbearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives

775
Q

What are the rules surrounding migraines with aura and COC pill?

A

If patients have migraine with aura then the COC is absolutely contraindicated due to an increased risk of stroke

776
Q

Define trigeminal neuralgia?

A

Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain of the face

777
Q

What things may evoke pain in trigeminal neuralgia?

A

The pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously

778
Q

What is the management for trigeminal neuralgia?

A

Carbamazepine is first-line

779
Q

Define Bell’s palsy?

A

An acute, unilateral, idiopathic, facial nerve paralysis.

780
Q

What is the management of Bell’s palsy?

A

Oral prednisolone within 72 hours of onset of Bell’s palsy

781
Q

Define vasovagal syncope?

A

A type of syncope resulting from a failure in autoregulation of blood pressure, and ultimately, in cerebral perfusion pressure resulting in transient loss of consciousness.

782
Q

What are the investigations for syncope?

A

Cardiovascular examination
Postural BP and lying BP
ECG

783
Q

What is benign paroxysmal positional vertigo?

A

One of the most common causes of vertigo encountered.

It is characterised by the sudden onset of dizziness and vertigo triggered by changes in head position.

784
Q

What are the classical features of benign paroxysmal positional vertigo?

A

Vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
May be associated with nausea
Each episode lasts for approximately 10-20 seconds

785
Q

What investigation can be used to assess for benign paroxysmal positional vertigo?

A

Dix-Hallpike manoeuvre - rapidly lower the patient to the supine position with an extended neck. Positive test recreates symptoms. There is also rotary nystagmus

786
Q

What is the management for benign paroxysmal positional vertigo?

A

Epley manoeuvre

787
Q

Define blepharitis?

A

Inflammation of the eyelid margins

788
Q

What is blepharitis caused by?

A

Meibomian gland dysfunction (common, posterior blepharitis) OR
Seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)

789
Q

What are the features of blepharitis?

A

Bilateral symptoms
Grittiness and discomfort
Eyes may be sticky in the morning
Eyelid margins may be red
Swollen eyelid - staphylococcal blepharitis
Styes and chalazions are common

790
Q

What is the management for blepharitis?

A

Softening of the lid margin using hot compresses 2x/day
Lid hygiene - cooled boiled water and baby shampoo on cotton wool
Artificial tears for symptomatic relief

791
Q

Define styes (hordeola)?

A

Acute localised infection or inflammation of the eyelid margin

792
Q

What is the management for styes (hordeola)?

A

Cooled boiled water and baby shampoo on cotton wool

793
Q

Define chalazion (meibomian cyst)?

A

A chronic,non-infectious, inflammatory granulomacaused by blockage of meibomian gland duct(s)

794
Q

What is the management for a chalazion (meibomian cyst)?

A

Warm compress:apply a warm compress (for example, with a clean flannel rinsed with warm water) to the affected eye for 10–15 minutes, up to five times a day, to loosen meibomian gland content

795
Q

Define entropion?

A

Entropion isan inversion or inward turning of the eyelid margin

796
Q

Define ectropion?

A

Ectropion isan outward turning of the eyelid margin

797
Q

What is the most common form eye problem in primary care?

A

Infective conjunctivitis

798
Q

What are the features of bacterial conjunctivitis?

A

Sore, red eyes
Purulent discharge

799
Q

What are the features of viral conjunctivitis?

A

Sore, red eyes
Serous discharge
Recent URTI

800
Q

What is the management for infective conjunctivitis?

A

Usually self-limiting
Topical antibiotic - Chloramphenicol drops

Contact lenses should not be worn

801
Q

What are the causes for otitis externa?

A

Infection - bacterial (Staphylococcus aureus, Pseudomonas aeruginosa) or fungal
Seborrhoeic dermatitis
Contact dermatitis (allergic and irritant)
Recent swimming is a common trigger

802
Q

What are the features of otitis externa?

A

Ear pain, itch, discharge
Otoscopy: red, swollen, or eczematous canal

803
Q

What is the initial management for otitis externa?

A

Topical antibiotic or a combined topical antibiotic with a steroid
If tympanic membrane perforated = do not use amino-glycosides
If debris consider removal

804
Q

What are some second line management options for otitis externa?

A

Oral antibiotics (flucloxacillin) if the infection is spreading
Empirical use of antifungal agent - recurrent infection should warrant use of antifungal (Candida)

805
Q

Give an overview of measles?

A

RNA paramyxovirus
Spread via aerosol transmission
Infective from prodromal phase until 4 days after rash starts

806
Q

What is the incubation period of measles?

A

10-14 days

807
Q

What features does the prodromal phase of measles have?

A

Irritable
Conjunctivitis
Fever

808
Q

What are the classic features of measles?

A

Koplik spots before the rash develops (white spots)
Rash - behind ears then whole body
Diarrhoea

809
Q

Describe the rash seen in measles?

A

Discrete maculopapular rash becoming blotchy & confluent desquamation that typically spares the palms and soles may occur after a week

810
Q

What are the investigations for measles?

A

IgM antibodies detected within a few days of rash onset

811
Q

What is the management for measles?

A

Supportive mainly
Admission if immunocompromised or pregnant

Notifiable disease so inform public health

812
Q

What is the most common complication of measles?

A

Otitis media

813
Q

What is the most common form of death in measles?

A

Pneumonia

814
Q

What is the management for individuals who have come into contact with measles?

A

Offer MMR vaccine
Should be given within 72 hours

815
Q

Give an overview of mumps?

A

Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring
Spread by droplets

816
Q

What is the incubation period for mumps? When are people infective

A

14-21 days
Infective 7 days before and 9 days after parotid swelling starts

817
Q

What are the features of mumps?

A

Fever
Malaise, muscular pain
Parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%

818
Q

What is used for the prevention of mumps?

A

MMR vaccine (80%) efficacy

819
Q

What is the management for mumps?

A

Rest
Simple analgesia
A notifiable disease

820
Q

What organism causes syphilis?

A

The spirochaete Treponema pallidum

821
Q

The spirochaete Treponema pallidum causes which STI?

A

Syphilis

822
Q

What are the primary features of Syphilis?

A

Chancre - painless ulcer at the site of sexual contact
Local non-tender lymphadenopathy
Often not seen in women (the lesion may be on the cervix)

823
Q

How long is the incubation period of syphilis?

A

9-90 days

824
Q

How long after primary infection does it take for secondary features of syphilis to develop?

A

Occurs 6-10 weeks after primary infection

825
Q

What are the secondary features of syphilis?

A

Systemic symptoms: fevers, lymphadenopathy
Rash on trunk, palms and soles
Buccal ‘snail track’ ulcers (30%)
Condylomata lata (painless, warty lesions on the genitalia )

826
Q

What are the tertiary features of syphilis?

A

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

827
Q

What are some features of congenital syphilis?

A

Blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
Rhagades (linear scars at the angle of the mouth)
Keratitis
Saber shins
Saddle nose
Deafness

828
Q

What would a positive non-treponemal test + positive treponemal test indicate for potential syphilis infection?

A

Consistent with active syphilis infection

829
Q

What would a positive non-treponemal test + negative treponemal test indicate for potential syphilis infection?

A

Consistent with a false-positive syphilis result e.g. due to pregnancy or SLE

830
Q

What would a negative non-treponemal test + positive treponemal test indicate for potential syphilis infection

A

Consistent with successfully treated syphilis

831
Q

What is the first line management for syphilis?

A

Intramuscular benzathine penicillin is the first-line management

832
Q

What is the second-line management for syphilis?

A

Doxycycline

833
Q

What can sometimes be seen following treatment for syphilis? What is the management?

A

Jarisch-Herxheimer reaction
No treatment is needed other than antipyretics if required

834
Q

What are the classic features of genital herpes?

A

Painful genital ulceration
Tender inguinal lymphadenopathy
Urinary retention may occur

835
Q

What is the difference in features between primary and recurrent episodes of genital herpes?

A

The primary infection is often more severe than recurrent episodes - systemic features such as headache, fever and malaise are more common in primary episodes

836
Q

What is the investigation of choice for suspected genital herpes?

A

Nucleic acid amplification test

837
Q

What is the pharmacological management of genital herpes?

A

Oral aciclovir

838
Q

What is the general management for genital herpes?

A

Saline bathing
Analgesia
Topical anaesthetic agents e.g. lidocaine

839
Q

What is the advise surrounding genital herpes and pregnancy?

A

Elective caesarean section at term is advised if a primary attack of herpes occurs during pregnancy at greater than 28 weeks gestation
Women with recurrent herpes who are pregnant should be treated with suppressive therapy and be advised that the risk of transmission to their baby is low

840
Q

Which herpes virus normally causes oral herpes?

A

HSV-1 in 90%

841
Q

What is the management for oral herpes?

A

Analgesia - Paracetamol and Ibuprofen
Topical Acyclovir - can be purchased over counter
Oral acyclovir

842
Q

What are the two main types of contact dermatitis?

A

Irritant contact dermatitis: common - non-allergic reaction due to weak acids or alkalis

Allergic contact dermatitis: type IV hypersensitivity reaction

843
Q

What are the features of vaginal candidiasis?

A

‘Cottage cheese’, non-offensive discharge
Vulvitis: superficial dyspareunia, dysuria
Itch
Vulval erythema, fissuring, satellite lesions may be seen

844
Q

What factors make vaginal candidiasis more likely to develop?

A

Diabetes mellitus
Drugs; antibiotics and steroids
Pregnancy
Immunosuppression: HIV

845
Q

What are the investigations for vaginal candidiasis?

A

A high vaginal swab is not routinely indicated if the clinical features are consistent with candidiasis

846
Q

What is the first line management for vaginal candidiasis?

A

Oral fluconazole 150 mg as a single dose first-line

847
Q

What is the second line management for vaginal candidiasis? What would be an indication for this?

A

Clotrimazole 500 mg intravaginal pessary as a single dose
Oral treatments are contraindicated

848
Q

What would be considered recurrent vaginal candidiasis?

A

BASHH define recurrent vaginal candidiasis as 4 or more episodes per year

849
Q

What should be checked if a patient has recurrent vaginal candidiasis?

A

Compliance with previous treatment should be checked
High vaginal swab for microscopy and culture
Consider a blood glucose test to exclude diabetes

850
Q

What would an induction-maintenance regime be for recurrent vaginal candidiasis?

A

Induction: oral fluconazole every 3 days for 3 doses
Maintenance: oral fluconazole weekly for 6 months

851
Q

What is the causative organism of Lyme disease?

A

Spirochaete Borrelia burgdorferi and is spread by ticks

852
Q

What are the early features of Lyme disease?

A

Erythema migrans - 80% of patients
Headache
Lethargy
Fever
Arthralgia

853
Q

Describe erythema migrans?

A

Bulls-eye’ rash is typically at the site of the tick bite
typically develops 1-4 weeks after the initial bite
Usually painless, more than 5 cm in diameter and slowly increases in size

854
Q

What are the late features of Lyme disease?

A

Cardiovascular:
Heart block
Peri/myocarditis
Neurological:
Facial nerve palsy
Radicular pain
Meningitis

855
Q

What are the investigations for Lyme disease?

A

Lyme disease can be diagnosed clinically if erythema migrans is present

(ELISA) antibodies to Borrelia burgdorferi are the first-line test
If negative then another 4-6 weeks after is still suspicion

If still negative after 12 weeks then immunoblot

856
Q

What is the management for asymptomatic tick bites?

A

If tick still present - fine-tipped tweezers near to the skin then wash the skin

857
Q

What is the management for confirmed Lyme disease?

A

Doxycycline if early disease

Amoxicillin if pregnant or other contraindication

858
Q

What is the management for disseminated Lyme disease?

A

Ceftriaxone

859
Q

What can be seen following commencing antibiotics for Lyme disease?

A

Jarisch-Herxheimer

860
Q

Define anal fissure?

A

Longitudinal or elliptical tears of the squamous lining of the distal anal canal
Acute <6 weeks, Chronic >6 weeks

861
Q

What are the risk factors for anal fissures?

A

Constipation
Inflammatory bowel disease
STIs

862
Q

What are the features of an anal fissure?

A

Painful, bright red, rectal bleeding
Up to 90% occur in the posterior midline - if not then underlying causes should be considered e.g. Crohn’s disease

863
Q

What is the management for an acute anal fissure?

A

Bulk-forming laxatives - first line
Dietary advice - high-fibre, high-fluid
Lubricants before defecation
Topical anaethetics

864
Q

What is the management for a chronic anal fissure?

A

Topical glyceryl trinitrate (GTN) is first-line treatment as well as those in acute

Shincterotomy if after 8 weeks

865
Q

What is the most common cause of postmenopausal bleeding?

A

Vaginal atrophy

866
Q

Define hiatal hernia?

A

Protrusion of intra-abdominal contents into the thoracic cavity though an enlarged oesophageal hiatus of the diaphragm

867
Q

What is the classic symptom of hiatal hernia?

A

GORD in 50% of large hernias

868
Q

What are the investigations for hiatal hernia?

A

Upper GI endoscopy
Barium swallow to confirm diagnosis

869
Q

What is the management for a hiatal hernia?

A

Conservative management - weight loss
Medical management - PPI
Surgical management - only if symptomatic

870
Q

Define mastitis?

A

Painful inflammatory condition of the breast

871
Q

What is the first-line management for mastitis?

A

Continue breastfeeding

872
Q

What is the management for mastitis that does not improve after effective milk removal?

A

Oral flucloxacillin 10-14 days

Breastfeeding or expressing should continue through Abx treatment

873
Q

What is the most common causative organism for infective mastitis?

A

Staphylococcus aureus

874
Q

Define breast abscess?

A

A localised collection of pus within the breast.

Can be either lactational or non-lactational

Phase 3a (8 decks)

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