PRIMARY CARE - psych, opthalmology, derm, paeds, GU, sexual health, misc Flashcards

1
Q

how is dementia investigated in primary care? (3)

A

1) initial assessment - hx (from px and family/friend) and examination (neuro signs, visual or auditory probs, cardio signs)
2) bloods to rule out organic causes - FBCs (anaemia), U&Es (metabolic), TFTs (hyper/hypo), serum B12 and folate (deficiency), calcium, HbA1c
3) assess cognition

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2
Q

examples of cognition screening tests that can be used when diagnosing dementia in primary care

A

10-point cognitive screener (10-CS), 6-item cognitive impairment test (6CIT), mini-cog

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3
Q

dementia management if the patient is severely disturbed/a health and safety risk OR if assessment in primary care isn’t appropriate?

A

arrange admission to secondary care

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4
Q

dementia management if urgent admission is not required?

A

refer to specialist dementia diagnostic service e.g. memory clinic

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5
Q

define fibromyalgia

A

chronic pain syndrome diagnosed by the presence of widespread body pain

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6
Q

epidemiology of fibromyalgia

A

more common in F

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7
Q

aetiology of fibromyalgia

A

unknown - associated with abnormalities in the stress response system and triggering events.

stressful event/s is a RF

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8
Q

signs and symptoms of fibromyalgia

A
  • diffuse tenderness on exam (commonly neck, shoulders, elbows, knees, buttocks)
  • chronic pain
  • fatigue unrelieved by rest
  • sleep & mood disturbance
  • stiffness
  • headaches
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9
Q

how is fibromyalgia diagnosed?

A

presence of >3 months of widespread pain and associated symptoms

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10
Q

non-pharm and pharm management of fibromyalgia

A

NON PHARM
- exercise
- relaxation therapy
- CBT

PHARM
- analgesia e.g. paracetamol, weak opioids
- antidepressants e.g. amitriptyline or duloxetine

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11
Q

what is acne vulgaris? what is it caused by?

A

a chronic inflammatory skin condition affecting mainly the face (99%), back and chest

blockage and inflammation of the pilosebaceous unit (hair follicle, shaft and sebaceous gland)

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12
Q

define mild, moderate and severe acne

A

mild - a few non inflamed lesions with or without sparse inflammatory lesions

moderate - more widespread, more inflammatory papules and pustules

severe - widespread inflammatory papules, pustules, nodules and cysts. may have scarring

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13
Q

what is the name for non-inflammatory lesions in acne? what are the subtypes?

A

= comedones

blackheads - open comedones
whiteheads - closed comedones

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14
Q

types of inflammatory lesions in acne

A
  1. papules and pustules - superficial raised lesions <5mm
  2. nodules/cysts - deeper, palpable, painful, >5mm
  3. sinuses - a cluster of severe nodules
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15
Q

how does acne vulgaris present? what MUST be present for diagnosis?

A
  • usually pubertal age
  • most present with a mix of inflammatory and noninflammatory (comedones) lesions
  • comedones must be present
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16
Q

investigations for acne vulgaris

A

normally clinical diagnosis

take detailed history
- duration, type and distribution of lesions
- prev tx
- psychosocial impact
- fam hx e.g. endocrine, PCOS, acne, skin conditions
- potential underlying causes e.g. drug hx, hyperandrogenism

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17
Q

management of mild to moderate acne

A

1st line = 12-week course of topical combination therapy:
- topical adapalene with topical benzoyl peroxide (AB)
- topical tretinoin with topical clindamycin (TC)
- topical benzoyl peroxide with topical clindamycin (BC)

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18
Q

management of moderate to severe acne

A

1st line = 12-week course of one of the following:
- topical adapalene with topical benzoyl peroxide
- topical tretinoin with topical clindamycin
- topical adapalene with topical benzoyl peroxide + either oral lymecycline or oral doxycycline
- topical azelaic acid + either lymecycline or doxycycline

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19
Q

what is a complication of long-term abx use in patients with acne?

A

gram-negative folliculitis

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20
Q

alternative tx to oral antibiotics in women with acne

A

COCP
should be used in combo with topical agents

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21
Q

when should patients with acne be referred to a dermatologist?

A
  1. if conglobate acne (rare, severe, nodules sinuses and cysts)
  2. if nodulo-cystic acne
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22
Q

what is
a) mean corpuscular volume (MCV)
b) mean corpuscular haemoglobin (MCH)
c) haematocrit

A

a) the average size of RBCs
macrocytic (>100fl), normocytic (80-100fl), microcytic (<80fl)

b) avg amount of haemoglobin in each RBC
hypochromic = less than normal

c) percentage expressed of the mass of RBCs compared to the plasma

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23
Q

normal haemoglobin in
a) men
b) women

A

a) 13-16 g/dl
b) 11-15 g/dl

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24
Q

what is iron deficiency anaemia?

what type of anaemia is it?

A

anaemia caused by lack of Fe > cannot support RBC production

microcytic anaemia

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25
Q

what is the most common cause of anaemia worldwide and in pregnancy?

A

iron deficiency

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26
Q

causes of Fe deficiency anaemia (4 categories)

A
  1. excessive blood loss
    - loss from GI (commonest in adult men and postmen women)
    - menorrhagia
  2. iron-poor diet
  3. failure of iron absorption
    - drugs e.g. tetracyclines and quinolones
    - antacids and PPIs (impairing absorption)
    - vit C deficiency
    - malabsorption conditions e.g. coeliac
    - gastrectomy
    - H.pylori infection
    - hookworm
  4. excessive iron requirements
    - rapid growth in kids
    - pregnancy
    - exfoliative skin disease
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27
Q

presentation of iron-deficiency anaemia

A

GENERAL
- pale skin + mucous mem
- tachycardia
- fatigue, lethargy
- dyspnoea
- palpitations
- headache

SPECIFIC
- brittle hair and nails
- atrophic glossitis
- koilonychia
- angular stomatitis

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28
Q

investigations for iron deficiency anaemia

A

FBC
- Hb low
- Fe low
- ferritin low
- reticulocytes low
- MCV low

Blood film - hypochromic microcytic

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29
Q

management of iron deficiency anaemia

A
  • address underlying cause e.g. treat menorrhagia, stop NSAIDs, eat more iron-rich food
  • 200mg oral ferrous sulphate/fumarate/gluconate daily
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30
Q

what is the most common cause of megaloblastic anaemia?

A

folate and B12 deficiency

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31
Q

which vitamin is low in folate deficiency?

A

vitamin B9

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32
Q

which vitamin is low in B12 deficiency? what is it needed for?

A

cobalamin

needed to form RBCs and DNA, needed in function and development of brain and nerve cells

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33
Q

causes of folate deficiency

A

MAIN = poor intake

dietary deficiency e.g. malabsorption (coeliacs etc), anorexia

excessive requirements e.g. pregnancy, infancy, malignancy, blood disorders

antifolate drugs

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34
Q

what is the most common cause of B12 deficiency? what is the pathophysiology?

A

PERNICIOUS ANAEMIA
- autoimmune destruction of intrinsic factor (IF)
- IF is produced by parietal cells in stomach
- B12 needs to bind with IF in distal ileum in order to be absorbed

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35
Q

other causes of B12 deficiency

A
  1. drugs - PPIs, colchicine, metformin, nitrous oxide
  2. gastric - atrophic gastritis, gastrectomy, H.pylori
  3. intestinal - crohn’s, malabsorption
  4. nutritional - malnutrition, veganism
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36
Q

presentation of B12/folate deficiency anaemia

A

symptoms
- cog changes
- dyspnoea
- headache
- indigestion
- loss of appetite
- palpitations
- tachypnoea
- weakness
- visual disturbance

signs
- anorexia
- angina
- angular cheilosis
- brown pigmentation in nail beds/skin creases
- diarrhoea
- glossitis
- mild jaundice
- mild pyrexia

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37
Q

what symptom is key for megaloblastic anaemia and a hallmark of folate deficiency?

A

loss of appetite/weight loss

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38
Q

which complications are strongly associated with B12 deficiency?

A

NEURO
- loss of mental/physical drive
- optic neuropathy
- muscle weakness
- psychiatric disturbance
- symmetrical neuropathy

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39
Q

investigations and results for B12/folate deficiency anaemia

A
  1. FBC
    - MCV high
    - haematocrit low
    - Hb low
    - reticulocytes low
    - WC/platelets may be low if severe
  2. blood film
    - macrocytic
    - may be megaloblasts
  3. either serum cobalamin or serum folate
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40
Q

management of folate deficiency anaemia

A

oral folic acid 5mg daily (check B12 levels before starting!!!)

diet - asparagus, broccoli, brown rice, brussel sprouts, chickpeas, peas

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41
Q

management of B12 deficiency anaemia
a) neuro involvement
b) no neuro involvement

A

a)
- urgent advice from neuro/haem
- consider starting B12 replacement while waiting

b)
- IM or oral B12 replacement e.g. hydroxocobalamin

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42
Q

what acne treatments are contraindicated in pregnant women?

A

topical and oral retinoid tx e.g. tretinoin

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43
Q

what is atopic dermatitis?

A

aka eczema - a chronic inflammatory skin condition affecting people of all ages

an episodic disease of flare-ups

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44
Q

when does atopic dermatitis most frequently present?

A

<5 years old (10-30% of all children)

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45
Q

risk factors for atopic dermatitis

A
  • atopy
  • family hx
  • environmental factors e.g. urban areas, smaller families, higher socioeconomic class
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46
Q

common triggers for atopic dermatitis

A
  • soap and detergents
  • animal dander
  • house-dust mites
  • extreme temps
  • rough clothing
  • pollen
  • foods
  • skin infections
  • stress
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47
Q

describe the typical rash that presents in atopic dermatitis. where does it tend to appear?

A
  1. dry
  2. red
  3. pruritic
  4. weeping/blistered/crusty/scaling/thickened
  5. in…
    adults - hands/limb flexures
    children - limb flexures
    infants - face
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48
Q

investigations for atopic dermatitis

A

clinical diagnosis

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49
Q

management for mild atopic dermatitis (2)

A
  1. emollients
  2. mild topical corticosteroid e.g. hydrocortisone 1%
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50
Q

management for moderate atopic dermatitis, including flare up and preventative tx (4)

A
  1. emollients
  2. moderately potent topical corticosteroid e.g. betamethasone valerate 0.025% (continue for 48h after flare has been controlled)
  3. antihistamine e.g. cetirizine if severe itch
  4. preventative tx = maintenance regime of topical corticosteroid
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51
Q

management for severe atopic dermatitis, including flare up and preventative tx (6)

A
  1. consider admission/referral
  2. emollients
  3. potent topical corticosteroid e.g. betamethasone valerate 0.1% for flares
  4. antihistamine for itch (if affecting sleep, consider sedating antihistamine e.g. chlorphenamine)
  5. if eczema causing psychological distress - oral prednisolone 30mg
  6. maintenance regime of topical corticosteroids
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52
Q

when are routine/urgent referrals to dermatology indicated for atopic dermatitis?

A

routine - current management not working

urgent - eczema is severe and not responding to tx within 1 week

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53
Q

what is otitis media?

A

infection of the middle ear (sits between tympanic membrane and inner ear)

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54
Q

what often precedes otitis media?

A

viral URT infection

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55
Q

what is the most common bacterial cause of otitis media in both children and adults?

A

Streptococcus pnuemoniae

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56
Q

other bacterial causes of otitis media (3)

A
  1. H.influenzae
  2. Moraxella catarrhalis
  3. S.aureus
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57
Q

RFs for otitis media in children? (5)

A
  1. young age (6-12m)
  2. male
  3. passive smoking
  4. bottlefeeding
  5. craniofacial abnormalities
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58
Q

general sx of otitis media

A
  1. EAR PAIN
  2. reduced hearing
  3. fever
  4. malaise
  5. coryzal sx
  6. maybe cough/sore throat (URT infection)
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59
Q

signs of ear pain in an infant with otitis media

A
  • tug at ear that hurts
  • irritable
  • disinterested in food
  • vomiting
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60
Q

investigations and results for otitis media

A
  1. otoscopy - erythematous and bulging TM, if perforated may see tear and discharge in ear canal
  2. may do bloods if systemically unwell
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61
Q

management of otitis media

A
  • normally self-revolving (3d-1w)
  • simple analgesics e.g. paracetemol
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62
Q

when would abx be indicated for otitis media? which would be used?

A
  • if pt has significant comorbidities/systemically unwell/immunocompromised
  • or if sx aren’t clearing up
  • or if it is bilateral
  • amoxicillin 5-7d
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63
Q

what is benign paroxysmal positional vertigo (BPPV)? what is it characterised by?

A

a disorder of the inner ear characterised by repeated episodes of POSITIONAL vertigo (sx occur with changes of head position)

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64
Q

what causes BPPV/what is it’s pathophys?

A

loose calcium carbonate debris (otoconia) in the semi-circular canals of the inner ear

head movement causes otoconia to move which moves inner ear fluid > vertigo

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65
Q

RFs for BPPV (9)

A
  • older age
  • head injury
  • prolonged recumbent position e.g. dentist/hairdresser
  • ear surgery
  • inner ear pathology
  • migraine
  • recent viral infection
  • female
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66
Q

how does BPPV present? what is NOT affected?

A
  1. vertigo sx brought on by specific movements/positions of head e.g. lying down, turning over, bending over
    - lasts less than 1 minute
    - asymptomatic between attacks
  2. may have associated N&V, light-headedness, imbalance
  3. may also have positional nystagmus

will NOT have affected hearing or tinnitus

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67
Q

investigations for BPPV

A

not normally required

  • neuro exam
  • Dix-Hallpike manoevre (provoke vertigo/nystagmus)
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68
Q

management of BPPV

A
  1. can watch and wait - sx should settle within 4 weeks
  2. if not settling - offer Epley manouvre and consider Brandt-Daroff exercises which pt can do at home
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69
Q

what is benign prostatic hyperplasia (BPH)?

A

a non-neoplastic condition involving enlargement of the prostate, obstructing bladder outlet and causing LUTS

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70
Q

at what age are almost all men affected by BPH?

A

70 and over

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71
Q

where in the prostate does BPH mainly effect? why do LUTS happen sooner than in prostate cancer?

A

hyperplasia of the transitional zone (v central) - so immediately causing problems for ureter which passes through

prostate cancer most commonly affects the peripheral zone - takes a while to get big enough to press on ureter

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72
Q

presentation of BPH

A

storage and voiding symptoms

storage:
- frequency
- urgency
- nocturia
- incontinence

voiding:
- hesitancy
- weak stream
- dribbling
- dysuria
- straining

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73
Q

examinations and investigations for BPH (4)

which scoring system can be used?

A
  1. DRE - smooth, enlarged
  2. abdo exam - palpable bladder
  3. urinalysis - normal (rule out cancer, UTI)
  4. consider PSA test

consider International Prostate Symptom Score assessment

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74
Q

management for BPH (symptoms not bothersome)

A

behavioural management!
- reducing fluids at night
- limiting caffeine/alcohol
- avoiding/modifying diuretic use

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75
Q

management for BPH (symptoms bothersome)
a) medical
b) surgical

A

a) 1st line = either…
- alpha-blockers e.g. terazosin, doxazosin
- 5-alpha-reductase inhibitors e.g. finasteride
- PDE-5 inhibitors e.g. tadalafil

b) TUIP (minimally invasive) or TURP (moderately invasive)

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76
Q

what is mastitis? who does it usually occur in and why?

A

a painful inflammatory condition of the breast
usually occurs in lactating women as is commonly caused by milk stasis

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77
Q

what is a breast abscess? who is it common in and what is it caused by?

A

a localised collection of pus within the breast (may or may not be associated with mastitis)

women aged 14-45

most often s.aureus

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78
Q

RFs for mastitis/breast abscess

A
  • poor breastfeeding technique
  • lactation
  • milk stasis
  • nipple injury/damage
  • hx of mastitis
  • nipple piercing
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79
Q

presentation of mastitis

A
  • painful, tender, red hot breast (pain esp on breastfeeding)
  • fever and general malaise may be present
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80
Q

signs that mastitis is infected

A
  1. nipple fissure
  2. purulent discharge
  3. flu and pyrexia lasting >24h
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81
Q

if untreated, what can mastitis develop into?

A

a breast abscess

82
Q

management for mastitis

what and when should abx be considered?

A

1st line = continue breastfeeding!
simple measures - analgesia and warm compresses

consider abx (oral flucloxacillin 10-14 days) IF
- systemically unwell
- nipple fissure present
- symptoms don’t improve after 12-24h of effective milk removal
- culture indicates infection

83
Q

how is a breast abscess generally treated?

A

referral to secondary care for incision and drainage

84
Q

bronchiolitis:
a) cause
b) presentation
c) diagnosis

A

a) RSV

b) child <1, increasing then peaking sx at 3-5 days - low grade fever, nasal congestion, rhinorrhoea, dry cough, feeding difficulties, inspiratory crackles and expiratory wheeze

c) clinical diagnosis if pt has coryzal syndrome lasting 1-3 days followed by…
- persistent cough AND
- either tachypnoea/chest recession AND
- wheeze or crackles

85
Q

when should a child with bronchiolitis be referred to hospital (999)?

A
  • apnoea
  • looks seriously unwell
  • severe resp distress e.g. grunting, marked chest recession, RR >70
  • central cyanosis
86
Q

when should a child with bronchiolitis be considered a referral to hospital?

A
  • RR >60
  • difficulty breastfeeding/inadequate intake
  • clinical dehydration
  • persistent O2 sats <92% on air
87
Q

how are most non-severe bronchiolitis cases treated in primary care?

A

advise parents to support at home with fluids, nutrition and temperature control
safety-netting - return if getting worse

88
Q

a) what is vulvovaginal candidiasis?
b) what is it most commonly caused by?
c) define acute/recurrent thrush

A

a) symptomatic inflammation of the vagina and/or vulva

b) caused by Candida yeast families (FUNGUS) - most common is candida albicans

c) acute = first/single isolated presentation
recurrent = four or more symptomatic episodes in one year

89
Q

presentation of vulvovaginal candidiasis (4)

A
  1. defining symptom = vulval/vaginal ITCHING
  2. non-offensive white discharge, ‘cheese-like’
  3. dyspareunia
  4. dysuria
90
Q

investigations for vulvovaginal candidiasis

A

often clinical, but can do…
1. self-collected LVS or HVS, STI screening
2. if recurrent, consider HVS for culture of secretions

91
Q

acute tx for vulvovaginal candidiasis
what if 1st line is contraindicated?
what can be used for vulval sx?

A

1st line = fluconazole 150mg oral capsule OD

if contraindicated - clotrimazole pessary

topical imidazole e.g. clotrimazole for vulval sx

92
Q

tx for recurrent vulvovaginal candidiasis

A

induction = three doses oral fluconazole 150mg
maintenance = oral fluconazole once weekly for 6m

93
Q

what is candida?

A

a yeast-like fungus part of the normal commensal flora of the GI tract

94
Q

RFs for oral thrush (pseudomembranous candidiasis) (8)

A
  1. extremes of age
  2. immunocompromised
  3. recent/concurrent drug use e.g. broad spec abx, inhaled corticosteroids
  4. DM
  5. endocrine disorders
  6. poor dental hygiene
  7. smoking
  8. poor diet/nutritional deficiency
95
Q

how does oral thrush present?

A

non-painful, curd-like, white/yellowish plaques on cheeks/gums/palate/tongue

96
Q

how is oral thrush treated?

A

first line = oral miconazole gel for 14 days

97
Q

what bacteria causes chlamydia?

A

Chlamydia trachomatis

98
Q

which parts of the body does Chlamydia trachomatis affect in…
a) adults
b) children

A

a) non-squamous epithelium e.g. urethra, endocervical canal, rectum, pharynx, conjunctiva
b) conjunctiva

99
Q

signs and symptoms of chlamydia

A

usually ASYMPTOMATIC!
- discharge
- friable cervix (easy bleeding) or abnormal bleeding
- penile discharge
- dysuria

100
Q

investigations for a) females and b) males for chlamydia

A

a) self-collected vulvovaginal swab
b) first void urine

NAAT - nucleic acid amplification test

101
Q

tx for chlamydia:
a) first-line
b) who is this contraindicated in?
c) alternative tx for contraindicated pts

A

a) doxycycline 100mg for 7 days

b) contraindicated in pregnant women

c) azithromycin, erythromycin, amoxicillin

102
Q

when should pts with chlamydia be advised to return to sexual activity?

A

only when 7 day tx is completed

103
Q

non-medical tx for chlamydia

A

partner notification and tx of partners

104
Q

define chronic fatigue syndrome

A
  • persistent fatigue for a minimum of 6 weeks
  • significantly impairs every day activities
  • cannot be explained by other illness
105
Q

diagnostic criteria for chronic fatigue syndrome (6)

A
  1. fatigue worsened by activity
  2. not caused by cognitive/physical/emotional/social exertion
  3. not relieved by rest
  4. post-exertional malaise (disproportionate to activity)
  5. sleep problems
  6. cognitive difficulties
106
Q

chronic fatigue syndrome is diagnosed by ruling out other conditions. suggest some investigations for this and what they would help rule out. (10)

A
  1. FBC, serum ferritin - anaemia, polycythaemia, malig
  2. ESR/CRP - infection, inflammation, autoimmunity, neoplasms
  3. LFTs - liver probs
  4. renal function - kidney disease/electrolytes
  5. TFTs - hypothyroidism
  6. HbA1c - diabetes
  7. IgA tissue transglutaminase - coeliac
  8. urinalysis - renal infection, inflammation, diabetes
  9. creatinine kinase - neuromusc cause
  10. bone chemistry and myeloma screen (if >60yrs)
107
Q

management options for chronic fatigue syndrome

A
  1. referral to secondary care specialist (if diagnostic criteria met)
  2. manage associated stress/depression
  3. advice on sleep hygiene
  4. referral to physio/OT
  5. pain management
  6. CBT
  7. review in primary care at least 1/year
108
Q

what is the conjunctiva? what is its job?

A

thin mucous membrane lining the eyelids and covering the sclera - keeps eye lubricated and protected from irritants

109
Q

what is conjunctivitis? what is it caused by? (5)

A

inflammation of conjunctiva due to…

  1. allergic/immunological reaction
  2. infection
  3. mechanical irritation
  4. neoplasia
  5. contact with toxic substances
110
Q

most common cause of conjunctivitis

A

infective - mainly viral, then bacterial

111
Q

presentation of conjunctivitis

A
  • acute onset conjunctival erythema
  • discomfort e.g. grittiness sensation, burning
  • watering and discharge
112
Q

indications of conjunctivitis being caused by a:
a) bacterial
b) viral
c) atopic/allergic

A

a) purulent discharge, crusting of lids sticking together
b) less discharge/more watery, may have URTI
c) may be recurrent due to seasonal or environmental factors

113
Q

investigations for conjunctivitis

A

clinical diagnosis

114
Q

red flags for conjunctivitis

A
  1. reduced visual acuity
  2. pain/headache
  3. red sticky eye in neonate
  4. hx of trauma/foreign body
  5. contact lens use
  6. copious rapidly progressive discharges (indicates gonococcal)
115
Q

conjunctivitis management:
a) viral
b) bacterial

A

a) self-limiting, self care e.g. bathing eyelids with saline soaked cotton wool, artificial tears

b) mostly self limiting but IF severe or sx don’t resolve in 3 days, consider topical abx - chloramphenicol 0.5%

116
Q

what is contact dermatitis? what are the two types? which is more common?

A

an inflammatory skin condition affecting the epidermis and dermis caused by exposure to irritant/allergen

  1. allergy CD - type IV (delayed) hypersensitivity reaction occurring after sensitisation and re-exposure
  2. irritant CD - non immunological reaction caused by direct physical/toxic effects of an irritant

irritant is more common

117
Q

acute vs chronic irritant contact dermatitis

A

acute - single overwhelming exposure
chronic - repeated exposure to weaker irritants e.g. detergents, soap, dust

118
Q

what is the most common irritant contact dermatitis in the first year of life?

A

nappy rash

119
Q

common allergens for allergen contact dermatitis

A
  1. products e.g. cosmetics, skincare, nail varnish, fragrances, sunscreen
  2. metals e.g. nickel and cobalt in jewellery
  3. topical meds e.g. corticosteroids
  4. plants
120
Q

common irritants for irritant contact dermatitis

A
  1. nappies
  2. sweat
  3. detergent. soap, cleaning agents
  4. solvents
  5. acid and alkalis
  6. reducing/oxygen agents e.g. sodium hypochlorite
  7. powders, dust, soil
121
Q

general features of contact dermatitis

A

acute - erythema, vesiculation, dry, scaling, bullae
chronic - dry, lichenification, fissuring

122
Q

indications of irritant vs allergy contact dermatitis

A
  1. varying sx e.g. stinging, burning, smarting, tightness, chapping
  2. protected areas e.g. under gloves remain clear
  3. anatomical distribution e.g. dermatitis in webs of fingers/under ring from repetitive exposure to water or detergents
  4. avoidance of causative = resolution within DAYS
123
Q

indications of allergy vs irritant contact dermatitis

A
  1. reaction 24-72hr following re exposure
  2. dominant sx = ITCHING
  3. blistering, weeping, oedema (severe)
  4. may affect areas not directly in contact e.g. transfer of nail varnish from finger to eye
  5. resolution = many days
124
Q

gold standard investigation for contact dermatitis

A

patch testing

125
Q

management of contact dermatitis

A

MAINSTAY = IDENTIFY AND AVOID CAUSATIVE AGENT
emollient
consider topical steroids

if can’t avoid - prevent/minimise e.g. rinse after, substitution of products, gloves, avoid accumulation of water/chemicals under jewellery

126
Q

define chronic fatigue syndrome (3 points)

A
  • persistent fatigue for a minimum of 6 weeks
  • significantly impairs ability to partake in usual daily activities
  • cannot be explained by another illness
127
Q

diagnostic criteria for chronic fatigue

A
  • 3 points from definition
  • debilitating fatigue worsened from activity and not relieved by rest
  • not caused by cognitive, physical, social or emotional exertion
  • post-exertional malaise: delayed in onset by hours/days, disproportionate to activity
  • sleep sx e.g. exhaustion/stiff/flu-like on waking, bad sleep, altered sleep pattern, hypersonic
  • cognitive difficulties
128
Q

how is chronic fatigue syndrome diagnosed? give some examples

A

rule out potential causes:
- FBC and serum ferritin
- ESR, CRP
- LFTs, TFTs
- HbA1c
- IgA tissue transgultaminase
- urinalysis
- creatinine kinase

129
Q

what investigation should be done when ruling out other diseases in a patient >60 with chronic fatigue? what is this ruling out?

A

bone biochemistry and myeloma screen - rule out myeloma

130
Q

management options for chronic fatigue syndrome (3)

A
  1. referral to specialist chronic fatigue service
  2. supportive - refer to physio/OT, pain management, CBT, dietary advice
  3. review in primary care once a year
131
Q

define cutaneous fungal infection - give 2 examples

A

superficial skin infection predominantly caused by dermatophytes
e.g. tinea corporis (body ringworm) , tinea cruris (groin and buttocks)

132
Q

RFs for cutaneous fungal infection (4)

A
  1. hot humid climate
  2. tight fitting clothing
  3. obesity
  4. immunocompromise
133
Q

presentation of cutaneous fungal infection - what are the typical body and groin lesions?

A

hx of itchy, scaly skin

BODY LESIONS
- single/multiple
- red/pink
- annular (ring-shaped) and asymmetrical
- varying sizes
- typically have central clearing (hence called ringworm)

GROIN LESIONS
- inguinal folds, proximal medial thigh
- penis and scrotum often spared
- red/red-brown
- uniform scale without central clearing

134
Q

how are cutaneous fungal infections spread?

A
  • direct contact with infected person/animal (think close contacts)
  • indirect contact with fomites e.g. clothing/towels/bed linen
135
Q

treatment of cutaneous fungal skin infection
a) mild
b) associated inflammation
c) severe

A

a) topical antifungal cream e.g. terbinafine or an imidazole (clotrimazole, miconazole)
b) consider topical corticosteroid in addition
c) oral antifungal e.g. terbinafine

136
Q

what are cutaneous warts? what are they caused by? where are they commonly found?

A

small rough growths caused by infection of keratinocytes with HPV
hands and feet

137
Q

when does the incidence of cutaneous warts peak?
how are they spread?

A
  • incidence increases in school years and peaks in adolescence
  • spread through direct contact/contamination e.g. shower floors, swimming pools
138
Q

presentation of cutaneous warts

A
  • firm, raised apples
  • rough surface
  • normally asymptomatic
139
Q

management of cutaneous warts

A

normally resolve spontaneously

140
Q

what are some treatment options for cutaneous warts? when are they indicated?

A
  • cryotherapy, topical salicylic acid
  • if wart painful, causing cosmetic probs or persistent
141
Q

who does the national chlamydia screening programme aim to screen? when? what for?

A
  • every sexually active woman under 25 annually OR when they change sexual partner
  • as a minimum, tested for chlamydia, gonorrhoea, syphilis, HIV
  • at GUM clinic
142
Q

what is folliculitis? what is it most commonly secondary to?

A

an inflammatory process involving any part of the hair follicle

normally secondary to infection e.g. with Staph aureus

143
Q

where does folliculitis commonly occur?

A

HAIRY AREAS e.g. head, neck, axillae, groin and buttocks

144
Q

RFs for folliculitis (5)

A
  1. immersion in hot tub/whirlpools/swimming pools/water slides
  2. drugs e.g. topical corticosteroids, abx, lithium, isoniazid, anticonvulsants
  3. shaving (skin cut = entry for microorganism)
  4. diabetes
  5. immunosuppression
  6. inflammatory skin diseases
145
Q

in which long-term inflammatory skin disease is folliculitis a complication of? why? which type of folliculitis would this be?

A

in acne patients - due to long-term oral abx therapy
would be gram-negative folliculitis

146
Q

which organism would normally be the cause of spa-pool folliculitis?

A

pseudomonas aeruginosa

147
Q

presentation of folliculitis

A

hx of RF e.g. shaving, hot tub, new medication

tender red papules with central umbilication OR pustules around hair follicles

148
Q

what investigations may be considered in suspected folliculitis?

A
  • bacterial/viral skin swab
  • skin scraping for mycology
  • tissue culture
149
Q

management of uncomplicated superficial folliculitis (e.g. staph aureus)

A
  • self-limiting
  • supportive e.g. use antibacterial soap, loose clothing, careful shaving techniques/stop shaving
150
Q

scoring system for psoriasis in primary care

A

DQLI

151
Q

what is otitis externa? what is it also known as?

A

inflammation of external ear canal

“swimmer’s ear”

152
Q

predisposing factors to otitis externa

A
  1. swimming
  2. trauma e.g. cotton buds, earplugs
153
Q

what organisms typically cause otitis externa?
a) bacterial
b) fungal

A

a) pseudomonas aeruginosa and s.aureas

b) asperillus, candida (think if pt has had lots of abx)

154
Q

what skin conditions can cause otitis externa (3)?

A
  1. eczema
  2. seborrheic dermatitis
  3. contact dermatitis
155
Q

presentation of otitis externa (4)

A
  1. ear pain
  2. discharge
  3. itchiness
  4. conductive hearing loss (if blocked)
156
Q

how is otitis externa diagnosed?

A

clinically with otoscopy

157
Q

what may otoscopy show in otitis externa?

A
  • erythema, swelling of ear canal
  • tenderness
  • pus/discharge
  • TM obstructed by wax/discharged
158
Q

management of otitis externa
a) mild
b) moderate
c) severe/systemic

A

a) acetic acid 2% - otc as EarCalm (can be used prophylactically e.g. before swimming)

b) topical abx and steroid e.g. otomize spray

  1. may need oral abx e.g. fluclox/clarithromycin, discuss with ENT
159
Q

what needs to be excluded before prescribing topical aminoglycosides e.g. gent/neomycin in otitis externa? why?

A

exclude perforated TM - potentially ototoxic

160
Q

complication of otitis externa

A

malignant otitis externa - spreads to bones surrounding ear canal and skull > osteomyelitis of temporal bone

161
Q

most common pathogen causing PID

what are some other causes?

A

chlamydia trachomatis

neisseria gonorrhoea, mycoplasma genitalium

162
Q

signs and symptoms of PID

A
  1. lower abdo pain
  2. fever
  3. deep dyspareunia
  4. dysuria
  5. menstrual irregularities
  6. discharge
163
Q

classic sign of PID on physical examination

A

cervical excitation

164
Q

investigations for PID (4)

A
  1. pregnancy test
  2. screen for chlamydia - NAAT and culture
  3. screen for gonorroea - HVS for women and MSU for men
  4. urinalysis
165
Q

ddx for PID

A

ectopic pregnancy

166
Q

management of PID

A

EITHER
- oral ofloxacin + oral metronidazole

  • IM ceftriaxone + oral doxycycline + oral metronidazole
167
Q

management of PID in someone with an IUD

A

abx and consider removal of IUD

168
Q

serious complication of PID and how it presents

A

Fitz-Hugh Curtis Syndrome - fever, PID, RUQ pain

169
Q

presentation of polymyalgia rheumatica

A

> 2 weeks of…
1. bilateral shoulder and/or pelvic girdle pain (shoulder may radiate to elbows)

  1. stiffness lasting >45 mins after waking
  2. other = systemic e.g. low grade fever, anorexia, weight loss, depression, peripheral MSK signs e.g. carpal tunnel, arthritis
170
Q

what is the diagnosis of PMR based on? (3)

A
  1. clinical pres
  2. response to steroids
  3. excluding differentials
171
Q

investigations for PMR

A
  1. bloods - raised ESR, CRP, full screen to rule out other causes
  2. trial of oral pred 15mg daily - should improve within a week
172
Q

management of PMR

A

initial = oral prednisolone 15mg daily

REDUCE slowly once sx fully controlled
- 12.5mg for 3 weeks
- 10mg for 4-6 weeks
- then reduce by 1mg every 4-6 weeks

173
Q

managing long-term steroid use (Dont STOP)

A

Don’t Stop - abruptly stopping = adrenal crisis

S - sick day rules (increase steroids when ill)
T - treatment card
O - osteoporosis with bisphosphonates, calcium and vit D
P - PPIs for gastroprotection

174
Q

features of the subtypes of psoriasis (which is most common?):

a) plaque
b) flexural
c) guttate
d) pustular
e) nail

A

a) most common!
demarcated red, scaly patches. extensor surfaces e.g. elbows and knees

b) skin smooth rather than scaly. groin, genitals, axilla, abdomen folds

c) frequently triggered by strep infection. more common in children. ‘tear-drop’ lesions on trunk and legs. acute onset.

d) pustules on palms and soles

e) features in psoriatic arthritis, pitting, onycholysis

175
Q

which genes are associated with psoriasis?

A

HLA-B13 and HLA-B17

176
Q

immunological pathophys of psoriasis

A
  1. t-cell mediated
  2. stimulate keratinocyte proliferation
  3. epidermal hyperproliferation
177
Q

environmental factors for psoriasis - what can improve or worsen it?

A

worsened by skin trauma, stress

improved by sunlight

can be triggered by strep infection (guttate)

178
Q

describe the skin lesions in psoriasis

A
  • well-defined (differentiates from eczema)
  • erythematous
  • scaly
  • papules/plaques
  • predominantly on extensor surfaces and scalp
179
Q

investigations for psoriasis

A

clinical diagnosis

180
Q

stepwise management of plaque psoriasis

A

general = regular emollients

1st line = topical potent corticosteroid (dermovate) plus vitamin D analogue (calcitriol/calcipotriol) - one in morning one in night

2nd line = stop corticosteroid, vitamin D analogue twice daily

3rd line = EITHER
- potent corticosteroid twice daily
- coal tar preparation once/twice daily
- short-acting dithranol cream

181
Q

secondary care management options for plaque psoriasis

A

1st line = narrowband ultraviolet B light

or photochemotherapy

182
Q

management of face/flexural/genital psoriasis

A

MILD/moderate potent corticosteroid (hydrocortisone) once/twice daily

183
Q

management of pustular psoriasis

A

medical emergency - arrange same-day specialist derm assessment

184
Q

management of guttate psoriasis

A

self-limiting - should resolve within 3-4 months

185
Q

which psoriasis tx is contraindicated in pregnancy?

A

vitamin D analogues

186
Q

most common type of prostate cancer

A

adenocarcinoma

187
Q

RFs for prostate cancer (5)

A
  1. older age
  2. family history/genetics
  3. black ethnicity
  4. high-fat diet
  5. high testosterone
188
Q

T staging of prostate cancer (4)

A
  1. non palpable
  2. palpable, confined to prostate
  3. palpable, through prostate capsule
  4. palpable and invading other structures
189
Q

what will be found on DRE in prostate cancer

A

abnormal, ‘craggy’ prostate

190
Q

presentation of prostate cancer

A

even advanced often asymptomatic!!

very general once established:
1. LUTs - nocturia, dysuria, hesitancy, terminal dribbling
2. other GU - ED, haematuria
3. general - fatigue, weight loss
4. mets - back pain, fractures, anaemia

191
Q

how does metastatic prostate cancer present?

A

bone pain

192
Q

investigations for prostate cancer - what is done first? when should PSA testing be offered?

A

1st = DRE

offer PSA testing if symptomatic

193
Q

when should a patient be referred for suspected cancer pathway for prostate cancer

A

if prostate feels malignant on DRE

194
Q

secondary care investigations for prostate cancer (3)

A
  1. transrectal USS + biopsy
  2. MRI/CT scan
  3. bone scan for mets
195
Q

normal upper limit for PSA

what might cause false positives when investigating prostate cancer?

A
  • 4ng/ml
  • prostatitis, UTI, BPH, vigorous DRE
196
Q

grading score system for prostate cancer

A

Gleason grading

197
Q

prostate cancer management: when is watch and wait used?

A
  • elderly
  • multiple co-morbidities
  • low gleason score
198
Q

prostate cancer management: what is active surveillance and which patients are managed this way?

A

= repeat PSA tests, if disease shows progression then treat

for LOW-RISK patients
- clinical stage T1c
- PSA density <0.15ng/ml/ml
- cancer in <50% of core biopsies
- <10mm of core involved

199
Q

surgical choice for localised prostate cancer. what is the most common SE post-surgery?

A

radical prostatectomy with removal of obturator nodes

common SE = erectile dysfunction

200
Q

hormonal therapy tx options for prostate cancer

A
  • bilateral orchidectomy (they release testosterone)
  • LNRH analogies, anti-androgens
201
Q

radiotherapy tx for prostate cancer - what is it used for? late complications?

A

can be potentially curative and also for palliative care

radiation proctitis and rectal malignancy = late problems

202
Q

before a PSA test, patients should NOT have…

A
  • an active UTI/one within last 6w
  • ejaculated in past 48h
  • exercised rigorously in past 48h
  • had urological intervention in last 6w