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Phase 3a Finals > General Practise/Primary Care > Flashcards

General Practise/Primary Care Flashcards

1
Q

What is Acne Vulgaris?

characterised by?

most common bacterium

common areas affected

A

Chronic Inflammatory Dermatosis

increased sebum production
follicle hyperkeratinisation
inflammation

triggered by Propionibacterium acnes

face neck upper trunk

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2
Q

Aetiology of Acne Vulgaris

A

Age : adolescents

Environment: diet, stress, pollutants

Genetics: FHX

Hormones: Androgens: testosterone, dehydroepiandrosterone sulfate - stimulated sebaceous gland activity.

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3
Q

Pathophysiology of Acne Vulgaris

A

Increased sebum production by increased androgens

lipid rich environment of sebaceous glands favouring skin micro-organism proliferation and therefore follicular occlusion.

keratinocyte proliferation further follicular occlusion. differentiation within pilosebaceous unit.

overgrowth of P.acnes

inflammation - release of IL-1/8, tnf-a cause papules,pustules,nodules,cysts

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4
Q

List of different lesions in Acne Vulgaris

A

Macules - flat skin marks
Papules - small skin lumps
Pustules - small skin lump with yellow pus
Comedomes - skin coloured papules blocked pilosebaceous unit
Blackheads - open comedomes
Ice pick scars - small indents in skin after acne lesion heal
Hypertrophic scars - small skin lump after acne lesion heal
Rolling Scars - irregular wave like skin after acne lesion heal

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5
Q

tell me a little about comedomes - acne

A

due to dilated sebacous follicle

closed - white - obstructed completely
open - black - partially obstructed

non inflammatory lesion.

hyperkeratinisation caused increased sebum production.

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6
Q

Tell me about papules and pustules - acne

A

when the follicle bursts releasing irritants

inflammation around blocked follicle- papules

papule - papule with pus because of neutrophil infiltration.

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7
Q

tell me a little about nodules and cysts - acne

A

severe inflammatory response.
macrophages,lymphocytes, plasma cells and tissue destruction causing fibrosis.

nodules - firm lumps under skin
cysts - fluctuant due to liquified necrotic material in fibrous tissue.

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8
Q

what would you see in drug induced acne

A

monomorphic

pustules in steroid use

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9
Q

what acne fulminans

A

severe acne with systemic upset like a fever

hospital admission required

oral steroids - tx

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10
Q

How would you treat Acne Vulgaris

A

mild - open/closed comedomes with/without sparse inflammatory lesions
moderate - widespread non-inflammatory and papules/pustules
severe: extensive inflammatory lesions

mild-moderate: 12 week course of topical combo therapy 1st line
1. fixed combo - topical adapalene + topic benzoyl peroxide
2. fixed combo - topical tretinoin + topical clindamycin
3. fixed combo - topical benzoyl peroxide + topical clindamycin

could use benzoyl peroxide as monotherapy if contraindicated

moderate- severe: 12 week course of:
1. fixed combo topical adapalene + topical benzoyl peroxide
2. fixed combo - topical tretinoin + topical clindamycin
3. fixed combo - topical adapalene + topical benzoyl peroxide+ either oral lymecycline/doxycycline
4. topical azelaic acid+ either oral lymecycline/doxycycline

oral isotretinoin: not pregnancy - specialist supervision

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11
Q

who would you avoid tetracycline in and why?

A

pregnancy
breastfeeding women
children under 12.

use erythromycin instead in pregnancy.

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12
Q

side effect of minocycline - acne tx

A

possible irreversible pigmentation

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13
Q

why should you give topical retinoid with oral abx

A

reduce the risk of abx resistance developing.

dont combine topical and oral abx

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14
Q

complication of long term abx use

how would you treat

A

gram negative folliculitis

tx: high dose oral trimethoprim

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15
Q

name an alternative to oral abx in women for acne tx?

side effects

A

combined oral contraceptive
combine with topical agents

dianette (co-cyprindiol) - anti-androgen properties.

increased risk of vte - use 2nd line - only for 3 months.

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16
Q

rules for administering abx - acne

A

don’t combine topical and oral abx
monotherapy with oral abx
mono with topical abx

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17
Q

what is acne conglobate?

A

rare and severe of acne found mostly in men that presents with extensive inflammatory papules, suppurative nodules and cysts on the trunk.

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18
Q

side effect of tetracycline

A

teeth discoloration if used in children under 8 years or pregnant.

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19
Q

side effect of isotretinoin

A

its potent oral retinoid used for severe acne

teratogenicity
hyperlipidaemia
hepatotoxicity

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20
Q

side effects of isotretinoin

A

dry skin and lips
photosensitivity of skin to sunlight
depression, anxiety, aggression and suicidal ideation.

rarely Steven-Johnson syndrome and toxic epidermal necrolysis

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21
Q

tell me a little bit about isotretinoin

A

retinoid
reducing inflammation and reducing bacterial growth.

teratogenic.

stop it at least a month before becoming pregnant.

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22
Q

What is Acute Bronchitis?

leading cause
resolve time

A

chest infection
self-limiting

inflammation of trachea and major bronchi

associated with oedematous large airways and sputum production.

resolves in 3 weeks.

viral infection - leading cause

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23
Q

Clinical Features of Acute Bronchitis

A

cough - could be productive
sore throat
rhinorrhoea
wheeze

most have normal chest exam some have:
low grade fever
wheeze

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24
Q

how would you investigate acute bronchitis

A

clinical diagnosis
crp testing to guide whether to give abx.

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25
Q

differentials for acute bronchitis

A

pneumonia if:

sputum wheeze breathlessness - at least 1

focal chest signs - dullness to percussion, crepitations and bronchial breathing

systemic features - malaise myalgia and fever

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26
Q

how would you manage acute bronchitis

A

analgesia
fluids

abx if:
systemically unwell , pre-existing comorbidities
crp of 20-100 - delayed prescription
crp over 100 mg/L - abx immediate.

DOXYCYCLINE - 1ST LINE . - not in kids or pregnant. - amoxicillin alternative

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27
Q

What is Acute Stress Reaction?

A

psychological shock following exposure to severe stress/traumatic event.

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28
Q

pathophysiology of acute stress reaction

A

acute disruption in homeostasis due to stress

hyperarousal of sympathetic nervous system.

releases adrenaline and cortisol

physical and psychological symptoms.

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29
Q

Aetiology of Acute Stress Reaction

A

Genetic Predisposition : serotonin transporter gene and dopamine receptor D2 gene.

Prior Psych Hx.

Neurobiological faqctors: dysregulation of HPA axis and altered amygdala function

traumatic incident.
sudden life change
socioeconomic status
coping mechanisms
social support lack of

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30
Q

differentials for acute stress reaction

A

panic disorder - intense fear, sweating, shaking but difference is trigger. panic attacks are recurrent unexpected but ASR is acute single episode.

PTSD - both traumatic event. PTSD must be following 1 month after trauma. ASR resolves within 4 weeks.

adjustment disorder - anxiety and depressed mood both. develops gradually over time to life stresses rather than acute traumatic event.

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31
Q

Clinical Features of Acute Stress Reaction

A

pt with traumatic event, cognitive behavioural and physiological responses. immediately after, can be few hours or days post trauma.

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

behavioural:
-avoidance
-hypervigilance

physiological sx :
- tachycardia and htn
- sweating and trembling

non-specific:
- insomnia
-irritability
-fatigue
-GI disturbances

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32
Q

how would you manage acute stress reaction?

A

immediate:
- psychological 1st aid: calm supportive environment, basic needs met, active listening
-if severe: possible short term benzodiazepines or antipsychotics.

ongoing mx:
- CBT
-mindfullness
-if sx persist: ptsd assess

follow-up:
- monitor
- refer to mental health

cultural consideration:
- be sensitive

educational resources:
- pt education on ASR reduces fear and uncertainty.
- give info on common reactions to trauma, coping strategies.

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33
Q

What is an allergy?

A

hypersensitivity of immune system to allergens which are proteins that the immune system see as foreign.

these proteins are antigens

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34
Q

what is the skin sensitisation theory of allergy?

A

break in infants skin - allows allergens to cross the skin and react with immune system.

child doesnt have contact with allergen from gi tract - absence of gi exposure to allergen.

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35
Q

name some conditions as a result of hypersensitivity reactions

A

asthma
atopic eczema
allergic rhinitis
hayfever
food allergies
animal allergies

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36
Q

tell me about the coombs and gell classification

A

underlying pathology of different hypersensitivity reactions

TYPE 1 - IGE antibodies to specific allergen trigger mast cells and basophils , release histamines and other cytokines.

TYPE 2 - IGG AND IGM antibodies. react to allergen activate complement system, direct damage to local cells. eg: transfusion reactions, haemolytic disease of newborn.

Type 3 - immune complexes accumulate, damage to local tissues. SLE, RA , henoch-schonlein purpura

type 4 - cell mediated hypersensitivity caused by t lymphocytes. t cells inappropriately activated = inflammation= damage to lcoal tissue. eg: organ transplant rejection, contact dermatitis

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37
Q

investigations in allergy

A

skin prick testing

RAST - bloods for total and specific immunoglobulin E (IgE)

food challenge testing. - gold standard. takes time.

skin prick and RAST assess sensitisation not allergy.

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38
Q

how does skin prick testing work?

A

drop of each allergen at marked points.

with water control
histamine control

fresh needle makes tiny break in skin at site of allergen.

after 15 mins size of wheals to each allergen checked.

compare to controls

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39
Q

what is patch testing?

A

most helpful in allergic contact dermatitis.

not for food allergy.

latex perfume cosmetics plants.

patch on pt skin.

2-3 days , skin reaction to patch checked.

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40
Q

what is RAST testing

A

measures total and allergen specific IgE quantities in blood.

in eczema and asthma, itll come back positive for everything u test.

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41
Q

how would you manage allergy?

A

establish allergen and avoid

hoover and change sheets

stay indoors when high pollen

prophylactic antihistamines

give adrenaline auto-injector for at risk pt of anaphylaxis

potentially immunotherapy? - exposure over months to allergen

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42
Q

following exposure how would you manage allergy?

A

antihistamine - cetrizine

steroids - predinisolone , topical hydrocortisone or iv hydrocortisone

intramuscular adrenaline - anaphylaxis

antihistamine and steroid - dampen immune response.

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43
Q

What is an Anal Fissure?

what is anoderm?

A

longitudinal tear in anoderm commonly caused by increased anal resting pressure, trauma and constipation

anoderm is specialised squamous epithelium lining distal anal canal

peak incidence: 30-40

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44
Q

Aetiology of Anal Fissure

A

young adults and middle aged.

primary idiopathic - no clear cause.
could be :
increased anal resting pressure: elevated internal anal sphincter pressure. reduced blood flow to anorderm = ischemic injury.

trauma - hard stools
constipation/straining: increased pressure in anal canal.

secondary anal fissure - underlying condition
IBD - chrons and uc - inflammaiton in rectum and anus.
infectious: STI eg syphilis, hsv, hiv
malignancy: presenting sx of anal/rectal malignancy.
other causes: iatrogenic during surgery, radiation proctitis.

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45
Q

what is a chronic anal fissure?

A

fibrosis and hypertrophy of anal papilla and sentinel pile formation.

can get granulation tissue which further impairs healing process

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46
Q

classifying anal fissure

where most anal fissures occur?

A

acute - less than 6 weeks
chronic - more than 6 weeks

90% - posterior midline

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47
Q

Clinical Features of Anal Fissures

A

Pain - sharp severe localised to anus. during and after bowel movement most intense. mins to hours. can lead to avoidance of bowel movement and constipation.

Bleeding - bright red on toilet paper or bowel. minimal, self-limiting.

Pruritis ani : itching around anus - particularly in chronic

constipation : avoid of bowel movements

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48
Q

key findings on physical examination of anal fissure patient

Visual Inspection
Gental Palpation
DRE

A

Visual Inspection: erythema,oedema,discharge. linear tear in anoderm could have sentinel pile (hypertrophied skin tag) at distal end.

Gental Palpation: localised tenderness or induration. sentinel pile could be small firm nodule

DRE: with caution, extreme pain. assess tone of anal sphincter. check for mass, strictures or abnormalities.

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49
Q

How would you manage anal fissure?

A

if less than 6 weeks:
- diet - high fibre high fluid
- bulk forming laxative 1st line - if not lactulose
- lubricant before shitting
-topical anaesthetics
-analgesia
- NO TOPICAL STEROIDS

over 6 weeks:
- above techniques
-topical gtn -1st line for chronic
- if gtn not effective after 8 weeks then secondary care - surgery or botulinum toxin

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50
Q

What is Anaphylaxis?

A

life threatening systemic hypersensitivity reaction.

type 1 hypersensitivity reaction IgE mediated.

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51
Q

how does anaphylaxis happen?

A

IgE stimulated mast cells to rapidly release histamine and other pro-inflammatory chemicals. = mast cell degranulation.

u get rapid onset of sx.
airway breathing circulation compromise.

52
Q

triggers of anaphylaxis

A

variety of allergens

foods - peanuts, tree nuts, fish milk eggs
insect venom - bees wasps fire ants
meds - penicillin , nsaids
latex: natural rubber latex.
idiopathic: unknown

53
Q

clinical features of anaphylaxis

airway
breathing
circulation

issues

A

airway : swelling of throat and tongue - hoarse voice and stridor

breathing: respiratory wheeze, dyspnoea

circulation problems: hypotension, tachycardia

80-90% pts have skin and mucosal changes:
generalised pruritus
widespread erythematous or urticarial rash.

54
Q

presentation of anaphylaxis

A

pt with hx of allergy - can be idiopathic tho

rapid onset:
- urticaria
-itching
-angio-edema - swelling around lips and eyes
- abdo pain

-sob
-wheeze
-swelling of larynx causing stridor
-tachy
-lightheaded
-collapse

55
Q

how would you manage anaphylaxis?#

a
b
c
d
e

A

intramuscular adrenaline

under 6 months : 100-150 micrograms- 0.1-0.15 ml 1 in 1000
6months-6yrs - 150 micro - 0.15ml
6-12 yrs - 300 micro 0.3ml
12+ - 500 micro 0.5 ml 1 in 1000

repeat every 5 mins if necessary.

im - anterolateral aspect of middle third of thigh

a - secure airway
b - give ox if needed. salbutamol with wheeze
c - iv fluids
d - lie flat improve cerebral perfusion
e - check for angiodema urticaria flushing

56
Q

what is refractory anaphylaxis?

A

respiratory/cardio problems despite 2 doses of im adrenaline
iv fluids for shock

57
Q

once youve stabilised an anaphylaxis pt then what to do?

A

non sedating oral antihistamine- if urticaria - chlorphenamine/cetrizine

can give steroid: iv hydrocortisone

check serum tryptase levels - stay high 12 hrs following anaphylaxis - check if it actually was this

adrenaline injector - give interim measure. - 2 of them - teach how to use

58
Q

discharging after anaphylaxis

A

2 hrs after sx stopped if:
- single dose

6 hrs :
2 doses or previous biphasic reaction

12 hrs:
severe reaction over 2 doses. severe asthma. late night presentation.

59
Q

how to use an adrenaline autoinjector?

A

remove safety cap on non needle end. - blue cap on epipen and yellow on jext

grip device in a fist with needle pointing down. - orange in epi black on jext. - dont put thumb over end.

adminster firmly jabbing into outer portion of mid thigh until device clicks. - can do thru clothing.
epi hold for 3 seconds
jext 10 seconds

remove
massage area 10 seconds

phone ambulance.
second dose after 5 mins if needed.

60
Q

What is generalised anxiety disorder?

A

excessive worry about number of different events.
sx persistent ocurring most days for at least 6 months and not caused by substance use or another condition.

more females than men

61
Q

clinical features of generalised anxiety disorder

A

excessive and persistent worry about events at least 6 months

difficulty controlling worry
restlessness , on edge
fatigue
irritable
muscle tension
sleep disturbance
significant distress or impairement
difficulty concentrating or mind going blank

62
Q

what medications could trigger anxiety?

alternative causes of anxiety?

A

salbutamol
theophylline
corticosteroids
antidepressants
caffeine
cocaine

hyperthyroidism
cardiac disease
phaeochromocytoma
cushings
substance withdrawal - alcohol, benzodiazepine

63
Q

how would you manage generalised anxiety disorder?

A

monitor
low intensity psychological intervention - self-help or group education
high intensity psycological intervention - CBT/drug tx (1st line SSRI sertraline)
- high specialist input - multi agency team

64
Q

what is panic disorder?

A

recurring panic attacks.

unexpected. worry about further attacks.

maladaptive behaviour changes related to attacks - avoiding activities.

65
Q

how would you manage panic disorder?

A
  1. diagnosis
  2. tx in primary care - cbt or ssri 1st line. if ci’d or no response after 12 weeks give imipramine or clomipramine.
  3. review
  4. refer to mental health
  5. care in specialist mental health
66
Q

presentation of panic attacks

A

sudden intense physical and emotion sx of anxiety.
last short time like 10 mins max.

physical sX:
tension
palpitations
tremors
sweating
dry mouth
chest pain
sob
diziines
nausea

emotional sx: panic, fear,danger,depersonalisation, loss of control

67
Q

phobia examples

closed space
heights
spider
public speaking
needles

A

extreme fear of situations -

claustrophobia - closed space
acrophobia- heights
arachnophobia- spider
glossophobia - public speaking
trypanophobia - needles

68
Q

what is the questionaire to assess severity of anxiety?

A

GAD-7

seven questions.

5-9 : mild anxierty
10-14 : moderate
15-21 = severe

69
Q

why might propanolol be given in anxiety tx?

A

doesnt treat anxiety.

nonselective beta blocker

treats physical sx of anxiety. reduces SNS overactivity.
stops palpitations tremors and sweating

contraindication: ASTHMA - causes bronchoconstriction.

70
Q

how do benzodiazepines work for anxiety?

NOT RECOMMENDED TO USE

A

STIMULATE GABA RECEPTOR
RELAXING EFFECT OF BRAIN.

71
Q

What is obsessive compulsive disorder?

A

obsession: unwanted intrusive thought,image or urge.

compulsion: repetitive behaviour or mental act that person driven to do. can be overt or seen by others.

72
Q

Aetiology of ocd

A

genetic
psychological trauma
paediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS)

associations:
depression
schizophrenia
sydenams chorea
tourettes syndrome
anorexia nervosa

73
Q

Clinical Features of ocd

A

obsessive:
- contamination fears
- harm related obsession
-unwanted sexual thoughts
-religious/moral obligations
-perfectionisms/symmetry

compulsions:
- cleaning/washing
-checking rituals
- counting/repeating rituals
-ordering/arranging behaviour
-mental neutralizing strategies

74
Q

how would you diagnose ocd?

Tx

A

yale brown obsessive compulsive scale - Y-BOCS : severity of obsessions and compulsions

DSM-5
ICD-11

obsessive-compulsive inventory-revised: OCI-R : self report questionaire asesses severity.

DBT

75
Q

how would you manage ocd?

A

if functional impairement mild:
- CBT and response prevention (ERP)
- if not then SSRI or more intensive CBT

if moderate functional impairement:
- SSRI any but if body dysmorphic disorder then fluoxetine. or more intensive CBT including ERP

if severe:
- combined ssri and cbt

ssri continue at least 12 months - prevent relapse
if ssri ineffective try another

can give clomipramine - TCA

76
Q

WHAT IS ERP? - ocd?

A

psychological method
expose pt to anxiety provoking situation
stopping them engaging in their usual safety behaviour.

77
Q

cycle of ocd

A

obsession
anxiety
compulsion
temporary relief

78
Q

how to measure bmi?

A

weight (kg) / heigh (m) squared

underweight - under18.49
normal 18.5-25
overweight 25-30
obese class 1 30-35
2 - 35-40
3 - over 40

79
Q

how would you manage obesity

A

diet and exercise

med: orlistat (pancreatic lipase inhibitor) , liraglutide

surgical

80
Q

when can orlistat be prescribed?

side effects

A

faecal urgency/incontinence
flatulence

bmi of 28 or more with associated risk factors

or bmi of 30 or more

continued weight loss eg 5% at 3mnths

use for lss than1 yr.

81
Q

what is liraglutide?

when to use?

A

as adjunct for weight loss in class 2 obese

glucagon like peptide 1 mimetic - use in t2dm

once daily sub cut

bmi at least 35

prediabetic hyperglycaemia

82
Q

types of bariatric surgery

primarily restrictive
primarily malabsorptive
mixed

A

primarily restrictive operations:
laparoscopic-adjustable gastric banding - LAGB
- 1st line for bmi 30-39
- less weight loss than malabsorption or mixed but fewer comps.

  • sleeve gastrectomy - stomach reduced to 15% of original size
    -intragastric baloon - baloon left in stomach for 6 months max

primarily malabsorptive options:
- biliopancreatic diversion with duodenal switch - only for very obese - bmi over 60

mixed:
roux-en-y gastric bypass surgery - restrictive and malabsorptive

83
Q

obesity in pregnancy is defined as:

A

bmi over or equal to 30 at first antenatal visit

84
Q

Maternal Risks of obesity for pregnancy

A

miscarriage
vte
gestational diabetes
pre-eclampsia
dysfunctional labour, induced labour

postpartum haemorrhage
wound infections

higher risk of C section

85
Q

fetal risks of obesity - pregnancy

A

congenital anomaly
prematurity
macrosomia
stillbirth
increased risk of developing obesity and metabolic disorders in childhood
neonatal death

86
Q

Management of obesity in pregnancy

A

tell them not to diet.

5mg of folic acid rather than 400mcg

screen for gestational diabetes with ogtt at 24-28 weeks

if bmi 35 or more consultant led birth.
if bmi 40 or more antenatal consultation with obs anaesthetist and make plan

87
Q

What is the whooping cough? (pertussis)

A

gram negative bacterium bordetella pertussis causing infectious disease.

children.

cough of 100 days.

88
Q

immunisation against whooping cough (pertussis)

A

routinely immunised at 2,3,4 months and 3-5 years.

vaccination for pregnant women.

neither infection nor immunisation = lifelong protection.

16-32 weeks pregnant give vaccine

89
Q

features of whooping cough (pertussis)

A

catarrhal phase: sx similar viral urti. lasts 1-2 weeks. mild coryzal sx. - poss mild dry cough.

paroxysmal phase: cough increases in severity.
- worse at night, after feeding, ended by vomiting, associated central cyanosis.
- inspiratory whoop: not always present - caused by forced inspiration against closed glottis.
- infants: poss spells of apnoea.
- persistent coughing may cause subconjunctival haemorrhages or even anoxia leading to syncope and seizures.
- lasts between 2-8 weeks

convalescent phase:
- cough subsides over weeks to months

90
Q

diagnostic criteria for whooping cough - pertussis

A

suspect if person has acute cough lasted for 14 days or more without another apparent cause and 1 of:

  • paroxysmal cough
    -inspiratory whoop
    -post-tussive vomiting
    -undiagnosed apnoeic attacks in young infants
91
Q

how to diagnose whooping cough

A

per nasal/nasopharyngeal swab culture for bordetella pertussis - may take several days or weeks to come back

PCR and serology are now increasingly used as their availability becomes more widespread

per nasal with pcr - within 2-3 weeks.

if cough present more than 2 weeks test for anti-pertussis toxin immunoglobulin G. - test in oral fluid of kids 5-16 and in blood over 17.

92
Q

how would you manage whooping cough?

is it a notifiable disease?

A

infants under 6 months with suspected pertussis - admit

notifiable disease

oral macrolide - (clarithromycin, azithromycin or erythromycin) - if onset of cough is within previous 21 days to eradicate the organism

give household contacts abx prophylaxis

abx : doesnt alter course of illness

school exclude: 48 hrs after commencing abx ( or 21 days from onset if no abx)

93
Q

complications of whooping cough

A

subconjunctival haemorrhage

pneumonia

bronchiectasis

seizures

if cough really hard can pneumothorax vomit faint.

94
Q

What is roseola infantum?

A

infancy
caused by human herpes virus 6

incubation 5-15 days.

affects children aged 6 months to 2 yrs.

no need school exclusion

95
Q

features of roseola infantum

A

high fever - lasting a few days followed later by:

  • maculopapular rash
  • nagayama spots: papular enanthem on uvula and soft palate
    -febrile convulsion in 10-15%
  • diarrhoea and cough commonly seen
96
Q

possible consquences of hhv6 other than roseola infantum?

main complication of it

A

aseptic meningitis

hepatitis

febrile convulsions due to high temperature. immunocompromised at risk of :
- myocarditis
-thrombocytopenia
-Gullain barre syndrome

97
Q

what is an exanthem?

A

eruptive widespread rash.

6 viral exanthemas : first,2,3,4,5,6

first: measles
second: scarlet fever
third: rubella (german measles)
fourth: dukes disease
5th: parvovirus b19
6th: roseola infantum

98
Q

tell me about measles
caused by

contagious?
spread?
sx start
sx

when does it resolve?

isolated?

notifiable?

A

measles virus.
RNA paramyxovirus
spread by aerosol tranmission
infective from prodome until 4 days after rash starts.
incubation: 10-14 days

highly contagious via resp droplets.

sx start 10-12 days after exposure with fever coryzal sx and conjunctivitis.

koplik spots: greyish white spots on buccal mucosa. - 2 days after fever. pathognomic for measles.

rash starts on face: behind ears, 3-5 days after fever. spread to rest of body. erythematous macular rash with flat lesions.

self resolving: 7-10 days of sx.

isolate kid until 4 days after sx resolve.

notifiable disease - report to public health.

99
Q

complications of measles

A

pneumonia
diarhoea
dehydration
encephalitis
meningitis
hearing loss
vision loss
death

100
Q

what is scarlet fever?

associated with ?

whats it caused by?

A

group a haemolytic streptococcus infection, usually tonsillitis. not virus.

children 2-6 yrs old. peak at 4

respiratory route spread by inhaling or ingesting resp droplets or by direct contact with nose and throat discharges.

caused by a exotoxin produced by streptococcus pyogenes (group a strep) bacteria.

101
Q

presentation of scarlet fever

features

A

red-pink blotchy macular rash with rough “sandpaper” skin that tarts on the trunk and spreads outwards.
red flushed cheeks.
- desquamination in later course of illness , esp around fingers and toes
- fine punctuate erythema (pinhead) which generally appears 1st on the torso and spares the palms and soles.
- children flushed with circumoral pallor. rash obvious in flexures.

fever
lethargy
flushed face
sore throat
strawberry tongue
cervical lymphadenopathy

102
Q

treatment of scarlet fever

A

abx for underlying strep infection.

phenoxymethylpenicillin (pen v ) for 10 days.

notifiable disease. - report to public health.

children no school until 24 hrs after starting abx.

103
Q

other than scarlet fever what 2 other conditions can you have associated with group a strep infection?

A

post-streptococcal glomerulonephritis

acute rheumatic fever

104
Q

tell me about rubella
its cause?
contagious?
spread/
sx start?

incubation?

presentation?

A

rubella virus - togavirus. after mmr its very rare.

incubation: 14-21 days

highly contagious
respiratory droplets

2 weeks after exposure
infectious from 7 days before sx appear to 4 days after onset of rash

milder erythematous macular rash compared to measles.

rash start on face and spread to rest of body.

last 3 days.

mild fever
joint pain
sore throat

enlarged lymph nodes (lymphadenopathy) behind ears and back of neck.

105
Q

mx of rubella

A

supportive. self limiting.

notifiable disease

no school 5 days after rash comes.

avoid pregnant women

non immune mothers: give MMR vaccination in post-natal period.

dont give MMR vaccine to women known to be pregnant or attempting to become it!

106
Q

comps of rubella

A

thrombocytopenia

encephalitis

dangerous in pregnancy: congenital rubella syndrome : triad of deafness blindeness and congenital heart disease

107
Q

what is dukes disease?

A

no identifable organism viral or bacterial cause.

4th disease.

non specific viral rashes.

108
Q

parvovirus b19
tell me about it

other names of it
caused by

presentation

A

5th disease
slapped cheek syndrome
erythema infectiosum

caused by parvovirus b19

mild fever
coryza
non specific viral sx: muscle aches and lethargy.

after 2-5 days, rash appears quite rapidly: diffuse bright red rash on both cheeks

few days later reticular mildly erythematous rash affecting trunk and limbs appear can be raised and itchy. (Reticular means net-like)

109
Q

management of parvovirus b19

do you need to stay off school?

A

self-limiting illness
rash and sx fade over 1-2 weeks.

manage supportively with plenty of fluids and simple analgesia.

its infectious before rash forming once its formed its not so you dont need to stay off school.

110
Q

what patients are at risk of complications

complications of parvovirus b19

A

immunocompromised
pregnant women
sickle cell anaemia,thalassaemia,hereditary spherocytosis, haemolytic anaemia.

so you do serology testing for parvovirus to confirm - check fbc and reticulocyte count for aplastic anaemia.

aplastic anaemia
encephalitis or meningitis
pregnancy comps: fetal death
rarely hepatitis, myocarditis or nephritis

111
Q

women exposed early in pregnancy (before 20 weeks) what to do ?

parvovirus

A

check maternal IgM and IgG

112
Q

other presentations of parvovirus

A

asymptomatic

pancytopenia in immunosuppressed patients

aplastic crises eg sickle cell disease
- parvovirus b19 suppresses erythropoiesis for about a week so aplastic anaemia is rare unless there is chronic haemolytic anaemia

  • hydrops fetalis
  • parvovirus b19 in pregnant women can cross placenta in pregnant women.
  • causes severe anaemia due to viral suppression of fetal erythropoiesis = hf secondary to severe anaemia = accumulation of fluid in fetal serous cavities (ascites, pleural and pericardial effusions)
  • tx : intrauterine blood transfusions
113
Q

how would you diagnose scarlet fever?

A

throat swab - abx commence immediately
dont wait for results

114
Q

scarlet fever is usually a mild illness but may be complicated by what and why?

A

otitis media : mc comp

rheumatic fever: typically 20 days after infection

acute glomerulonephritis: 10 days after infection

invasive comps (bacteraemia, meningitis, necrotizing fasciitis) rare but might present acutely wit life-threatening illness

115
Q

features of measles

A

prodromal phase:
- irritable
-conjunctivitis
-fever

koplik spots:
- typically develop before rash
- white spots (grain of salt) on the buccal mucosa

rash:
- starts behind ears then to the whole body
- discrete maculopapular rash becoming blotchy and confluent
- desquamation that spares palms and soles might happen after a week

diarhoea - 10% pts

116
Q

how would you investigate measles

A

IgM antibodies - within few days of rash onset

117
Q

how would you manage measles

A

mainly supportive

admission considered in immunosuppressed or pregnant patients

notifiable

118
Q

complications of measles

A

otitis media: mc comp

pneumonia: mc cause of death

encephalitis: typically occurs 1-2 weeks following onset of illness

subacute sclerosing panencephalitis: very rare, might present 5-10 yrs following an illness

febrile convulsions
keratoconjunctivitis, corneal ulceration
diarhoea
increased incidence of appendicitis
myocarditis

119
Q

how would you manage contacts of measles?

A

give within 72 hours

if child not immunised against measles comes into contact with measles then MMR should be given.

vaccine induced measles antibody develops more rapid that natural infection post.

120
Q

complications of rubella

A

arthritis
thrombocytopenia
encephalitis
myocarditis

121
Q

features of rubella

A

prodome: low grade fever

rash: maculopapular, initially on the face before spreading to whole body, usually fades by 3-5 day

lymphadenopathy: suboccipital and postauricular

122
Q

features of congenital rubella syndrome?

A

sensorineural deafness

congenital cataracts
congenital heart disease (pda)
growth retardation
hepatosplenomegaly
purpuric skin lesions
salt and pepper chorioretinitis

microphthalmia
cerebral palsy

123
Q

how would you diagnose rubella?

A

discuss with HPU

IgM antibodies raised in women recently exposed to virus

very difficult to distinguish rubella from parvovirus b19 clinically. important to check parvovirus b19 serology 30% risk of transplacental infection, with a 5-10% risk of fetal loss

124
Q

venous ulceration, typically seen where?

A

medial malleolus

125
Q

ix of venous ulceration

how could you get a false negative result?

A

ankle-brachial pressure index (abpi) - important in non-healing ulcers to assess for poor arterial flow which could impair healing.

“normal” abpi might be regarded as between 0.9-1.2.
below 0.9: arterial disease.
above 1.3: artieral disease.

false negative result: secondary to arterial calcification (in diabetic)

126
Q

how would you manage venous ulceration?

A

compression bandaging - 4 layer - only tx that acc helps

oral pentoxifylline - peripheral vasodilator, improves healing rate.

small evidence base supporting use of flavinoids

hydrocolloid dressing,topical growth factors, uss therapy and intermittent pneumatic compression - doesnt help

127
Q
A

Phase 3a Finals (25 decks)

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