General Practise/Primary Care Flashcards
What is Acne Vulgaris?
characterised by?
most common bacterium
common areas affected
Chronic Inflammatory Dermatosis
increased sebum production
follicle hyperkeratinisation
inflammation
triggered by Propionibacterium acnes
face neck upper trunk
Aetiology of Acne Vulgaris
Age : adolescents
Environment: diet, stress, pollutants
Genetics: FHX
Hormones: Androgens: testosterone, dehydroepiandrosterone sulfate - stimulated sebaceous gland activity.
Pathophysiology of Acne Vulgaris
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
List of different lesions in Acne Vulgaris
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
tell me a little about comedomes - acne
due to dilated sebacous follicle
closed - white - obstructed completely
open - black - partially obstructed
non inflammatory lesion.
hyperkeratinisation caused increased sebum production.
Tell me about papules and pustules - acne
when the follicle bursts releasing irritants
inflammation around blocked follicle- papules
papule - papule with pus because of neutrophil infiltration.
tell me a little about nodules and cysts - acne
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.
what would you see in drug induced acne
monomorphic
pustules in steroid use
what acne fulminans
severe acne with systemic upset like a fever
hospital admission required
oral steroids - tx
How would you treat Acne Vulgaris
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
who would you avoid tetracycline in and why?
pregnancy
breastfeeding women
children under 12.
use erythromycin instead in pregnancy.
side effect of minocycline - acne tx
possible irreversible pigmentation
why should you give topical retinoid with oral abx
reduce the risk of abx resistance developing.
dont combine topical and oral abx
complication of long term abx use
how would you treat
gram negative folliculitis
tx: high dose oral trimethoprim
name an alternative to oral abx in women for acne tx?
side effects
combined oral contraceptive
combine with topical agents
dianette (co-cyprindiol) - anti-androgen properties.
increased risk of vte - use 2nd line - only for 3 months.
rules for administering abx - acne
don’t combine topical and oral abx
monotherapy with oral abx
mono with topical abx
what is acne conglobate?
rare and severe of acne found mostly in men that presents with extensive inflammatory papules, suppurative nodules and cysts on the trunk.
side effect of tetracycline
teeth discoloration if used in children under 8 years or pregnant.
side effect of isotretinoin
its potent oral retinoid used for severe acne
teratogenicity
hyperlipidaemia
hepatotoxicity
side effects of isotretinoin
dry skin and lips
photosensitivity of skin to sunlight
depression, anxiety, aggression and suicidal ideation.
rarely Steven-Johnson syndrome and toxic epidermal necrolysis
tell me a little bit about isotretinoin
retinoid
reducing inflammation and reducing bacterial growth.
teratogenic.
stop it at least a month before becoming pregnant.
What is Acute Bronchitis?
leading cause
resolve time
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
Clinical Features of Acute Bronchitis
cough - could be productive
sore throat
rhinorrhoea
wheeze
most have normal chest exam some have:
low grade fever
wheeze
how would you investigate acute bronchitis
clinical diagnosis
crp testing to guide whether to give abx.
differentials for acute bronchitis
pneumonia if:
sputum wheeze breathlessness - at least 1
focal chest signs - dullness to percussion, crepitations and bronchial breathing
systemic features - malaise myalgia and fever
how would you manage acute bronchitis
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
What is Acute Stress Reaction?
psychological shock following exposure to severe stress/traumatic event.
pathophysiology of acute stress reaction
acute disruption in homeostasis due to stress
hyperarousal of sympathetic nervous system.
releases adrenaline and cortisol
physical and psychological symptoms.
Aetiology of Acute Stress Reaction
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
differentials for acute stress reaction
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.
Clinical Features of Acute Stress Reaction
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
how would you manage acute stress reaction?
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.
What is an allergy?
hypersensitivity of immune system to allergens which are proteins that the immune system see as foreign.
these proteins are antigens
what is the skin sensitisation theory of allergy?
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.
name some conditions as a result of hypersensitivity reactions
asthma
atopic eczema
allergic rhinitis
hayfever
food allergies
animal allergies
tell me about the coombs and gell classification
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
investigations in allergy
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.
how does skin prick testing work?
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
what is patch testing?
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.
what is RAST testing
measures total and allergen specific IgE quantities in blood.
in eczema and asthma, itll come back positive for everything u test.
how would you manage allergy?
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
following exposure how would you manage allergy?
antihistamine - cetrizine
steroids - predinisolone , topical hydrocortisone or iv hydrocortisone
intramuscular adrenaline - anaphylaxis
antihistamine and steroid - dampen immune response.
What is an Anal Fissure?
what is anoderm?
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
Aetiology of Anal Fissure
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.
what is a chronic anal fissure?
fibrosis and hypertrophy of anal papilla and sentinel pile formation.
can get granulation tissue which further impairs healing process
classifying anal fissure
where most anal fissures occur?
acute - less than 6 weeks
chronic - more than 6 weeks
90% - posterior midline
Clinical Features of Anal Fissures
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
key findings on physical examination of anal fissure patient
Visual Inspection
Gental Palpation
DRE
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.
How would you manage anal fissure?
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
What is Anaphylaxis?
life threatening systemic hypersensitivity reaction.
type 1 hypersensitivity reaction IgE mediated.
how does anaphylaxis happen?
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.
triggers of anaphylaxis
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
clinical features of anaphylaxis
airway
breathing
circulation
issues
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.
presentation of anaphylaxis
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
how would you manage anaphylaxis?#
a
b
c
d
e
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
what is refractory anaphylaxis?
respiratory/cardio problems despite 2 doses of im adrenaline
iv fluids for shock
once youve stabilised an anaphylaxis pt then what to do?
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
discharging after anaphylaxis
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.
how to use an adrenaline autoinjector?
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.
What is generalised anxiety disorder?
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
clinical features of generalised anxiety disorder
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
what medications could trigger anxiety?
alternative causes of anxiety?
salbutamol
theophylline
corticosteroids
antidepressants
caffeine
cocaine
hyperthyroidism
cardiac disease
phaeochromocytoma
cushings
substance withdrawal - alcohol, benzodiazepine
how would you manage generalised anxiety disorder?
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
what is panic disorder?
recurring panic attacks.
unexpected. worry about further attacks.
maladaptive behaviour changes related to attacks - avoiding activities.
how would you manage panic disorder?
- diagnosis
- tx in primary care - cbt or ssri 1st line. if ci’d or no response after 12 weeks give imipramine or clomipramine.
- review
- refer to mental health
- care in specialist mental health
presentation of panic attacks
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
phobia examples
closed space
heights
spider
public speaking
needles
extreme fear of situations -
claustrophobia - closed space
acrophobia- heights
arachnophobia- spider
glossophobia - public speaking
trypanophobia - needles
what is the questionaire to assess severity of anxiety?
GAD-7
seven questions.
5-9 : mild anxierty
10-14 : moderate
15-21 = severe
why might propanolol be given in anxiety tx?
doesnt treat anxiety.
nonselective beta blocker
treats physical sx of anxiety. reduces SNS overactivity.
stops palpitations tremors and sweating
contraindication: ASTHMA - causes bronchoconstriction.
how do benzodiazepines work for anxiety?
NOT RECOMMENDED TO USE
STIMULATE GABA RECEPTOR
RELAXING EFFECT OF BRAIN.
What is obsessive compulsive disorder?
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.
Aetiology of ocd
genetic
psychological trauma
paediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS)
associations:
depression
schizophrenia
sydenams chorea
tourettes syndrome
anorexia nervosa
Clinical Features of ocd
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
how would you diagnose ocd?
Tx
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
how would you manage ocd?
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
WHAT IS ERP? - ocd?
psychological method
expose pt to anxiety provoking situation
stopping them engaging in their usual safety behaviour.
cycle of ocd
obsession
anxiety
compulsion
temporary relief
how to measure bmi?
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
how would you manage obesity
diet and exercise
med: orlistat (pancreatic lipase inhibitor) , liraglutide
surgical
when can orlistat be prescribed?
side effects
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.
what is liraglutide?
when to use?
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
types of bariatric surgery
primarily restrictive
primarily malabsorptive
mixed
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
obesity in pregnancy is defined as:
bmi over or equal to 30 at first antenatal visit
Maternal Risks of obesity for pregnancy
miscarriage
vte
gestational diabetes
pre-eclampsia
dysfunctional labour, induced labour
postpartum haemorrhage
wound infections
higher risk of C section
fetal risks of obesity - pregnancy
congenital anomaly
prematurity
macrosomia
stillbirth
increased risk of developing obesity and metabolic disorders in childhood
neonatal death
Management of obesity in pregnancy
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
What is the whooping cough? (pertussis)
gram negative bacterium bordetella pertussis causing infectious disease.
children.
cough of 100 days.
immunisation against whooping cough (pertussis)
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
features of whooping cough (pertussis)
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
diagnostic criteria for whooping cough - pertussis
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
how to diagnose whooping cough
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.
how would you manage whooping cough?
is it a notifiable disease?
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)
complications of whooping cough
subconjunctival haemorrhage
pneumonia
bronchiectasis
seizures
if cough really hard can pneumothorax vomit faint.
What is roseola infantum?
infancy
caused by human herpes virus 6
incubation 5-15 days.
affects children aged 6 months to 2 yrs.
no need school exclusion
features of roseola infantum
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
possible consquences of hhv6 other than roseola infantum?
main complication of it
aseptic meningitis
hepatitis
febrile convulsions due to high temperature. immunocompromised at risk of :
- myocarditis
-thrombocytopenia
-Gullain barre syndrome
what is an exanthem?
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
tell me about measles
caused by
contagious?
spread?
sx start
sx
when does it resolve?
isolated?
notifiable?
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.
complications of measles
pneumonia
diarhoea
dehydration
encephalitis
meningitis
hearing loss
vision loss
death
what is scarlet fever?
associated with ?
whats it caused by?
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.
presentation of scarlet fever
features
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
treatment of scarlet fever
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.
other than scarlet fever what 2 other conditions can you have associated with group a strep infection?
post-streptococcal glomerulonephritis
acute rheumatic fever
tell me about rubella
its cause?
contagious?
spread/
sx start?
incubation?
presentation?
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.
mx of rubella
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!
comps of rubella
thrombocytopenia
encephalitis
dangerous in pregnancy: congenital rubella syndrome : triad of deafness blindeness and congenital heart disease
what is dukes disease?
no identifable organism viral or bacterial cause.
4th disease.
non specific viral rashes.
parvovirus b19
tell me about it
other names of it
caused by
presentation
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)
management of parvovirus b19
do you need to stay off school?
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.
what patients are at risk of complications
complications of parvovirus b19
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
women exposed early in pregnancy (before 20 weeks) what to do ?
parvovirus
check maternal IgM and IgG
other presentations of parvovirus
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
how would you diagnose scarlet fever?
throat swab - abx commence immediately
dont wait for results
scarlet fever is usually a mild illness but may be complicated by what and why?
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
features of measles
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
how would you investigate measles
IgM antibodies - within few days of rash onset
how would you manage measles
mainly supportive
admission considered in immunosuppressed or pregnant patients
notifiable
complications of measles
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
how would you manage contacts of measles?
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.
complications of rubella
arthritis
thrombocytopenia
encephalitis
myocarditis
features of rubella
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
features of congenital rubella syndrome?
sensorineural deafness
congenital cataracts
congenital heart disease (pda)
growth retardation
hepatosplenomegaly
purpuric skin lesions
salt and pepper chorioretinitis
microphthalmia
cerebral palsy
how would you diagnose rubella?
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
venous ulceration, typically seen where?
medial malleolus
ix of venous ulceration
how could you get a false negative result?
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)
how would you manage venous ulceration?
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
What is bursitis?
Inflammation of a bursa, small fluid filled sac that cushions and reduces friction between bones, tendons and muscles around the joints.
common locations of bursitis?
Shoulder (subcromial) - Overhead activities, repetitive arm movement
Elbow (olecranon) - Leaning on elbows “student’s elbow”
Hip (trochanteric) - Runners or prolonged standing
Knee (prepatellar or anserine). Common in people who kneel often
Heel (retrocalcaneal)
how does bursitis occur and present?
Causes:
- Friction from repetitive movements
- Trauma
- Inflammatory arthritis
- Infection (Septic bursitis)
Presentation:
- Swollen, warm, tender, fluid filled
- If infection: Hot, more tender, redness to surrounding skin, fever, features of sepsis.
Consider septic arthritis if reduced ROM
what do the various joint aspirations result suggest for bursitis?
Pus - Infection
Straw coloured fluid - Less likely to be infeced
Blood stained - Trauma, infection, inflammatory cause
Milky - Gout/Pseudogout
Fluid should be sent for MCS
mx of bursitis?
Reduce activity of affected joint
Ice
Compression
Elevation
Analgesia
Steroid injections and aspiration may help
Functions of kidney
AWETBED
Acid-base homeostasis
Water balance
Electrolyte balance
Toxin/waste product removal
Blood pressure control
Ertyhropoietin
D (vitamin D activation)
bp targets in ckd
140/90 or 130/80 if coexisting diabetes
ACEi used (reduce filtration pressure, less proteinuria)
define aki
A sudden decline in kidney function leading to a rise in serum creatinine and fall in urine output.
Dysregulation of
- Fluid balance
- Acid-base homeostasis
- Electrolyte imbalance
drugs to stop in AKI
DAAMN
D - Diuretics
A - ACEi/ARB
A - Aminoglycosides
M - Metformin
N - NSAIDs
ACEi/ARB protective in Chronic
6 pre renal causes of AKI
Hypoperfusion
Hypovolaemia (bleeding, reduced cardiac output (CHF), cardiogenic shock)
Liver failure (hypoalbuminaemia)
Renal artery blockage/stenosis
ACEi & NSAID
Sepsis causing systemic vasodilation
Dehydration
4 intrarenal causes of aki
Intrinsic disease of kidney
Acute tubular necrosis
Acute interstitial nephritis (these 2 can be drug induced)
Glomerulonephritis
Small vessel vasculitis
4 post renal causes of aki
Obstruction to urinary outflow, causing back pressure into kidney. (Obstructive uropathy)
- BPH
- Urolithiasis
- Cervical and prostate cancer
- Bladder neck stricture
electrolyte consequence of AKI
Hyperkalaemia and azotaemia (increased blood creatinine and urea)
Metabolic acidosis
Symptoms of pre renal AKI
Hypotension
Reduced capillary refill
Dry mucus membranes
Reduced skin turgor
Cool extremities
intrarenal aki symptoms
Infection/ signs of underlying disease (vasculitis, glomerulonephritis etc)
post renal aki symptoms
Loin to groin pain
Haematuria
Palpable bladder/prostate
Prostatic urinary issues (dysuria, terminal dribbling, hesitancy)
causes of acute tubular necrosis
Ischaemia - Pre renal disease
Nephrotoxicity - (aminoglycosides, chemotherapy), contrast in CT, myoglobin, multiple myeloma
define ckd
Progressive deterioration in renal function over at least 3 months characterised by eGFR of <60ml/min/1.73m²
what 2 tests are considered in CKD classification?
eGFR and albumin:creatinine ratio
how is eGFR used to stage ckd?
Stage 1 - >90 (normal)
Stage 2 - 60-89 (mild reduction, only CKD if symptoms)
Stage 3a - 45-59 (mild-moderate reduction)
Stage 3b - 30-44 (moderate-severe reduction)
Stage 4 - 15-29 (severe reduction)
Stage 5 <15 (End stage kidney failure)
how is albumin:creatinine ratio used to stage CKD?
Checks proteinuria to give A score
A1 - <3mg/mmol
A2 - 3-30mg/mmol
A3 - >30mg/mmol
what can be used as evidence of renal damage?
Albuminuria (ACR>3)
Electrolyte abnormalities
Histological abnormalities
Structural abnormalities on imaging
Kidney transplant history
Urine sediment abnormalities
at what egfr is metformin contraindicated?
<30ml/min/1.73² (stage 3b)
causes of ckd
Most common: Diabetes and HTN
Nephrotoxic drugs
Glomerulonephritis
Systemic disease e.g. rheumatoid arthritis/SLE
how does ckd lead to its complications?
low eGFR = azotaemia (which can cause encephalopathy and pericarditis)
Urea affects platelet function (bleeding)
Uremic frost (urea crystals in skin)
Kidneys normally activate vit D. No activation = hypocalcaemia = PTH secretion = bone resorption (renal osteodystrophy)
Low fluid to kidney = RAAS activation = HTN
HTN causing increased intraglomerular pressure - causing shearing and loss of selective permeability (protein/haematuria)
Kidneys produce less EPO = Anaemia
signs/symptoms of ckd
Asymptomatic at first
Uraemic frost (tiny yellow white urea crystals on skin)
Uraemia swallow (pale/brown colour on skin)
Pallor
Fatigue
Lethargy
Frothy urine
Swollen ankles/oedema
Increased bleeding
what does anaemia, with low calcium and low phosphate imply?
ckd
ix in ckd
Urine dipstick
- Haematuria, glycosuria
eGFR and urine albumin:creatinine ratio
U&E
FBC
- Normocytic normochromic anaemia
Bone profile/PTH
- Ca2+ low, phosphate high, PTH high, ALP high
Renal ultrasound
Bilateral kidney atrophy (small kidneys)
comps of ckd
Anaemia (EPO reduced)
Osteodystrophy (decreased vit D activation)
Neuropathy/encephalopathy
Pericarditis
mx of ckd
No cure except transplant, can only treat symptoms
Anaemia - EPO + Iron
Osteodystrophy - Vit D supplementation
CVD - ACEi + statins
Oedema - Diuretics
(ACEi help in CKD but harm in AKI)
what is RRT and what are its indications?
Renal replacement therapy - Persistent severe complications (electrolyte, oedema, uraemia) or Stage 5 CKD
AEIOU
Acidosis > 7.2 - Acidosis not helped by sodium bicarbonate
Electrolytes K+>7mmol/L
Intoxication - Stage 5 CKD
Oedema
Uraemic pathology - Encephalopathy, pericarditis etc
what are the types of RRT?
Haemodialysis (most common)
- Blood taken from artery, filtered and returned into vein at AV fistula.
- 3x4 hours a week
- Complications: hypotension, nausea, chest pain, infected catheter (sepsis)
Peritoneal dialysis
- Peritoneal catheterisation, exchange of solutes across peritoneal membrane
- Done at home
- Complications: Peritonitis, abdominal wall hernia
causes of ckd mineral bone disease
Reduced 1-alpha hydroxylase activity (reduced vit D activation)
Reduced renal excretion of phosphate (phosphate stimulates bone resorption)
tx of ckd mineral bone disease
Reduced dietary phosphate (fish, meat, poultry)
Vit D replacement (calcitriol is already 1-alpha-hydroxylated)
Phosphate binders
Bisphosphonates
copd risk factors
Age (>40)
Smoking (biggest)
Air pollution
Occupational exposure (coal, cement, dust, smelting)
Frequent respiratory infections
Gender (men)
Alpha 1 anti-trypsin deficiency- (young patients presenting with COPD!!)
O2 saturation targets for a normal person and for someone with an acute COPD exacerbation. And at what O2 sats is someone considered hypoxic
Normal: 95-100%
COPD exacerbation: 88-92% (normal COPD maintained above 92%)
Normal <94%
COPD exacerbation <88%
What 2 organisms usually cause infective exacerbations of COPD
H. influenza
S. pneumoniae
define chronic bronchitis
Inflammation of the bronchial tubes. Considered chronic when it causes a productive cough for at least 3 months a year for 2 years.
Pathophysiology of chronic bronchitis
Overall
- Hypersecretion
- Ciliary dysfunction
- Narrowed lumen
Explanations:
Irritation of epithelium of bronchi causes inflammation. This leads to hypertrophy and hyperplasia of the bronchial mucous glands in bronchi, and goblet cells in bronchioles.
Epithelial layer becomes ulcerated, eventually replacing the columnar epithelium with squamous (metaplasia), and smoking makes cilia shorter and less mobile
Chronic inflammation causes infiltration of epithelium, narrowing lumen.
Shortened immobile cilia and narrow, easily blocked lumen predispose to infection
explain the lung spirometry tests (4)
1) FVC (Forced vital capacity) - Max air volume in 1 breath (<80%)
2) FEV1 (Forced Expiratory Volume in 1 second) - Max air 1 second (<80%)
3) FEV1:FVC Ratio (<0.7 obstructive)
4) TLC (total lung capacity) (increased in COPD due to air trapping)
signs/symptoms of chronic bronchitis
Blue Bloater
- Chronic productive cough
- Cyanosis
- Dyspnoea on exertion
- Usually overweight
- Purulent sputum
- Crackles, wheezes when breathing
Hypoxia/aemia (insufficient oxygen in tissues/blood) and hypercapnia (high CO2)
symptoms of co2 retention
drowsiness
asterixis
confusion
cyanosis
complications of chronic bronchitis
2ndary polycythaemia vera
Pulmonary HTN due to reactive vasoconstriction to hypoxaemia
Cor pulmonale due to chronic pulmonary HTN
define emphysema
Damage to/destruction of the alveolar air sacs. This causes the alveoli to permanently enlarge and lose elasticity. This means the lungs are unable to recoil, so patients have trouble exhaling
Pathophysiology of emphysema
Irritants trigger inflammation in lungs, releasing proteases (collagenases, elastases), which break down elastin. Normally, elastin prevents low pressure environment from collapsing. In emphysema, elastin is lost and airways collapse.
This causes:
- Air trapping distal to point of collapse
- Airways stretch during inhalation but cant breath out fully.
- Elastin loss also causes breakdown of thin alveolar walls (Septa), causing neighbouring alveoli to coalesce. This reduces the area for gas exchange.
types of emphysema
Centriacinar - most common. Damages central/proximal alveoli in each acinus, in the upper lobes of lungs. Seen in smokers.
Pan-acinar - Whole acinus affected. Seen in A1AT, affecting lower lobes.
Para-septal - Distal alveoli, can cause a pneumothorax when alveoli rupture
Irregular - Irregular acinar involvement. Scarring/fibrosis
signs/symptoms of emphysema
Pink puffer
- Pursed lip breathing
- Barrel shaped chest
- Hyperresonance on percussion
- Downward displacement of liver
- Dyspnoea, cough, weight loss
imaging signs of emphysema
Increased anterior-posterior diameter
Flattened diaphragm
Increased lung field lucency
signs of copd (6)
Barrel chest
Hyperresonance on percussion
Cyanosis
Pursed lip breathing
Wheezing/crackling
Productive cough with purulent sputum
what scale is used to assess breathlessness?
MRC dyspnoea scale.
Breathlessness:
1 - on exercise
2 - on hurrying/slight hill
3 - walks slower than others/ has to stop to catch breath
4 - Stops to catch breath after 100m
5 - breathless on minimal activity (getting changed)
ix in copd
Clinical diagnosis - Over 35, smoking history, signs/symptoms of COPD.
Spirometry
- FEV1<80% expected
- FEV1/FVC <0.7, with no bronchodilator reversibility
Chest X ray -
- Flattened diaphragm
- Hyperinflation
- Bullae
CHECK FBC - COPD causes chronic hypoxia -> polycythaemia vera.
how is copd classified?
GOLD classification
Goes down based on FEV1
e.g. FEV1>80% = 1 (mild),
FEV1 50-79 = 2 (moderate) etc
FEV1 49-30 = 3 (Severe)
FEV1 <30 = 4 (very severe)
name all 5 drugs used in copd tx
Bronchodilators:
- Short acting Beta 2 agonist (salbutamol)
- Long acting Beta 2 agonist (salmeterol)
-
- Short acting muscarinic antagonists (Ipratropium bromide)
- Long acting muscarinic antagonists (Tiotropium)
Inhaled corticosteroid (Beclometasone)
tx algorithm of copd (inhalers)
1) SABA or SAMA
2) LABA and LAMA regularly (ICS if asthma features)
3) LABA + LAMA + ICS
+ SABA at any stage (can still be taken as required)
other tx of copd
Long term Oxygen if sats below 92 at rest
Oral Theophylline (bronchodilator)
Oral mucolytic
Prophylactic azithromycin!
How does pulmonary hypertension cause cor pulmonale, and what are its clinical manifestations
Pulmonary vasoconstriction and HTN means right heart must pump against high pressures, eventually failing.
Causes peripheral oedema, raised JVP, hepatomegaly
comps of copd (4)
Cor pulmonale (RH failure secondary to pulmonary HTN)
Pneumothorax
Type 1/2 resp failure and respiratory acidosis
Infections
define copd exacerbation with abg finding
Acute worsening of symptoms, usually due to infective cause (H influenza, S pneumoniae).
Shows respiratory acidosis (low pH and high CO2). Increased bicarbonate (HCO3-) shows compensation by kidney
Treated with amox
what are the criteria for bronchodilator reversibility?
> 12% increase in FEV1
AND volume increase >200ml post bronchodilator
Define infective conjunctivitis?
Sore, red eyes associated with sticky discharge. Can be bacterial or viral
Bacterial
- Purulent discharge, eyes may be stuck together
Viral
- Serous discharge
- Recent URTI
- Preauricular lymph nodes
how is conjunctivitis mx?
Self limiting but can be treated with Abx
- Chloramphenicol drops or ointment
- Drops every 2-3 hours, ointment QDS
- Topical fusidic acid in pregnancy women BD!!
how is conjunctivitis mx in contact lens users?
Topical fluoresceins to identify corneal staining
Contact lens should NOT be worn
No school exclusion
What are the types of dermatitis and whats a common cause?
Irritant: Common, non allergic. Related to weak acid or alkali exposure. Often seen on hands. Erythema, crusting, vescicles rare
Allergic: T4 Hypersensitivity. Less common. Often seen on head following hair dyes. Acute weeping eczema, predominantly affecting the margins of the hairline, rather than scalp. Potent topical steroid!!!!!!
Cement is a common cause, due to alkaline nature. Dichromates in cement can cause allergic dermatitis too.
Patch testing to differentiate
What is gout with risk factors?
Monosodium urate crystal deposition in joints. MTP most common.
Elderly
Male
Purine rich foods
Obesity
HTN
Impaired kidney function
T2DM
Family history
causes of gout
Increased uric acid production
- Increased cell turnover (leukaemia, haemolytic anaemia)
- Purine rich diet (shellfish, red meat, organ meat)
- Obesity/metabolic syndrome
Decreased excretion
- CKD
- Diuretics/aspirin/pyrazinamide
- Lead toxicity
what foods predispose to gout, what diet is protective?
High Purine diet can raise uric acid levels
- Red meat
- Seafood
- Sugary beverages
- Beer
recommended diet with gout
high diary diet protective
signs/symptoms of gout
Generally monoarticular (can be up to 4) joint swelling, tenderness, erythema.
- Usually 1st MTP but can affect ankle, wrist, knee, small hand joints.
Gouty tophi (nodular masses of urate crystals - massive lump under skin) can appear
Flares last between 7-10 days, first 12 hours worst
ix in gout
Joint x ray:
- Joint effusion, preserved joint space.
- Lytic lesions
- Punched out erosions with sclerotic margins and overhanging edges
- Loss of joint space is a very late sign
Joint aspiration w/ polarised microscopy:
- Needle shaped crystals with negative birefringence
mx of gout
general life advice
acute flares
prevention
General life advice:
- Low purine, lose weight, avoid alcohol (especially beer)
Acute flares:
- NSAID+PPI OR colchicine OR steroid injection 2nd line
Prevention:
- Allopurinol (xanthine oxidase inhibitor)
comps of gout caused by hyperuricaemia
Urate nephrolithiasis: Hyperuricaemia can cause urate renal stones
define pseudogout
Pseudogout is an inflammatory arthritis caused by deposition of calcium pyrophosphatase crystals in synovium
rf of pseudogout
Increasing age
Female
Previous joint trauma
Hyperparathyroidism
Hypomagnesaemia
Hypophosphataemia
Haemochromatosis
Acromegaly
pathophys of pseudogout
Also known as chondrocalcinosis.
Calcium pyrophosphatase crystals trigger synovitis, most commonly in the knee, shoulder and wrist.
Acute - mainly larger joints in elderly
Chronic - Inflammatory RA-like symmetrical arthritis
signs/symptoms of pseduogout
Usually indistinguishable from gout, except that knee, wrist, ankle are most affected
- Inflammation: warm, swelling, erythema, pain and joint stiffness
ix in pseudogout
X ray: Chondrocalcinosis (suggestive but not diagnostic, absence doesn’t exclude)
Joint aspiration w/ polarisation: Weakly positively birefringent rhomboid shaped crystals
Also check: Bone profile/PTH, Iron studies, serum magnesium to check cause
mx of pseudogout
Acute
- NSAID or colchicine or corticosteroid injection
- Cool packs + rest
Chronic
- DMARD (methotrexate) or joint replacement
main differential of crystal athropathies
septic arthritis
gout vs pseduogout joint aspiration
Gout - Negative birefringent needle shaped crystals
Pseudogout - Positively birefringent rhomboid shaped crystals
define osteoarthritis
Non inflammatory, progressive synovial joint damage caused by wear and tear of most commonly used joints.
joints commonly affected in osteoarthritis?
Knees
Hips
Sarco-ileac joints
Wrist
Carpometacarpal
Interphalangeal
risk factors for osteoarthritis
Age
Female sex
Raised BMI/obesity
Joint injury/trauma
Joint malalignment (congenital or not)
pathophys of osteoarthritis
Usually, cartilage breakdown and production by chondrocytes is under balance.
In OA, chondrocytes secrete more metalloproteinases (degrading enzymes) leading to loss of Type 2 cartilage. (Type 1 has less elasticity)
IL-1 and TNF-a also stimulate metalloproteinase production and inhibit collagen production.
Causes decreased joint space, which causes damage to bones on movement. Bone attempts to repair itself with type 1 collagen but causes bony overgrowths
signs/symptoms of osteoarthritis?
Asymmetrical non inflamed joint pain, which gets worse as the day goes on
Herbeden’s nodes (DIP Swelling)
Bouchard’s nodes (PIP swelling)
Fixed flexion deformity of carpometacarpal
Joint pain worse with activity
Mechanical locking
Joint stiffess, tenderness, crepitus (crunching sensation when moving)
NO EXTRA ARTICULAR MANIFESTATIONS
typical presentation of osteoarthritis
> 45 years old
Typical activity related pain
No morning stiffness (<30 mins)
ix in osteoarthritis
1st - X ray (LOSS)
L - Loss of joint space
O - Osteophytes (bony overgrowths)
S - Subchondral sclerosis
S - Subchondral cysts
non pharmacological treatments of osteoarthritis
Weight loss
Low impact exercise
Physiotherapy
Occupational therapy
Heat/cold packs at site of pain
Orthotics (helps with foot issues)
pharmacological tx of osteoarthritis
1st - Oral paracetamol, topical capsaicin, topical NSAID
Topical NSAID first for knee
Others:
- Intra articular steroid injection
- Joint replacement
define prostate cancer with 4 risk factors
Adenocarcinoma of the prostate gland (usually peripheral zone).
Associated with BRCA1 and BRCA2
Age
Afro Caribbean
Family history
signs/symptoms of prostate cancer
LUTS- Voiding: Hesitancy, weak stream, straining, dysuria, incomplete emptying, terminal dribbling.
Storage: Urgency, frequency, nocturia, incontinence
Bone pain (if metastasised to bone)
Wight loss, fatigue, night sweats
ix of prostate cancer
DRE: Hard, asymmetrical, nodule, irregular prostate with loss of median sulcus
PSA
Transrectal ultrasound
Prostate Biopsy - GOLD. Used with Gleason score.
Bone scan to check for bone metastasis (Lesions)
what scoring system is used in prostate cancer?
Gleason scoring - Uses biopsy to grade prostate cancer
1-5
1 - Well differentiated cancer
5 - Anaplastic (Extremely poorly differentiated)
1st and 2nd most prevalent histological patterns graded and added together to give score out of 10.
mx of prostate cancer?
Local - prostatectomy
Active surveillance if >70 or not severe
If metastatic
- Radiotherapy
- Hormone therapy (GnRH e.g. Goserelin) or bilateral orchidectomy (remove testicles) - reduce testosterone
- Androgen receptor blocker
other causes of raised psa
bph
prostatitis
uti
vigorous exercise
recent ejaculation
what is infectious mononucleosis, what its cause and association
AKA Glandular fever
Caused by EBV and associated with Hodgkin’s, Burkitt’s and nasopharyngeal carcinoma
presentation of glandular fever
Classic triad
Fever, pharyngitis, lymphadenopathy
Usually presents in adults and young children
Shows atypical lymphocytes on blood film
Investigated with monospot test/agglutination test
how does glandular fever spread and what are its complications?
Spread through saliva (kissing, sexual activity)
Lifelong latent infection, can cause chronic fatigue
what is lyme disease?
Caused by spirochaete Borrelia burgdorferi and spread by ticks.
<30 days
- Bulleye rash (erythema migrans), usually 1-4 post bite. Painless, >5cm and slowly grows.
- Headache, lethargy, fever, arthralgia
> 30 days
- Heart block, peri/myocarditis, meningitis
ix and mx of lyme disease?
Can be diagnosed if erythema migrans (bullseye rash) seen
ELISA Antibodies to Borrelia burgdorferi
Managed with tick removal (tweezer) and washing.
If Lyme disease, doxycyline, with amox as alternative
Jarisch-Herxheimer reaction (fever, rash, tachycardia, after first dose) possible
define reactive arthritis?
Reactive arthritis (Reiter’s syndrome) refers to synovitis following a infection in other part of body.
Most commonly gastroenteritis or STIs. Affects men 30-50x more than women
causes of reactive arthritis
STI
- Chlamydia
- Gonorrhoea
Gastroenteritis
- Salmonella
- Shigella
- Campylobacter
- Yersinia enterocolitica
signs and symptoms of reactive arthritis
“Cant see, pee, climb a tree” Urethritis, arthritis (of lower leg), conjunctivitis
Acute, asymmetrical monoarthritis, typically of lower leg.
- Warm swollen join
- Keratoderma blennorhagica
- Mouth ulcers
ix of reactive arthritis
“Hot joint” policy - assume warm swollen joint is septic
- Joint aspiration - Culture and gram stain. Should show no organism, excludes differential (Septic arthritis).
- ESR/CRP raised
- RF/ANA negative
Sexual health review/stool test will be diagnostic of underlying cause
X ray:
- Enthesitis
- Sacroiliitis with periosteal reaction
mx of reactive arthritis
Give antibiotics and aspirate joint
NSAID, Steroids
Methotrexate
describe oral candidiasis
Creamy white/yellow spotty plaque adhered to oral mucosa. May be bleeding and redness under this. Most commonly found on buccal mucosa, tongue and palate.
Can also present atrophic with a burning pain or under dentures (denture stomatosis - negative test on mucosa but positive on dentures)
mx of oral candidiasis
topical antifungals: 1st line for mild to moderate:
- nystatin suspension
-miconazole gel
systemic antifungals: severe or refractory case:
- oral fluconazole
What are diverticula?
A diverticulum is an outpouching of colonic mucosa and underlying connective tissue of colon wall. Usually 0.5-1cm. Usually caused by weakness in circular muscle that become larger gaps over time, causing mucosal herniation through the gap.
Where are diverticula most likely to occur?
Sigmoid (MC) also right colon (ascending/transverse)
Through colonic weak points such as where blood vessels pass through muscle, or gaps in taeniae coli muscle
Give the type of diverticular disease
Diverticulosis - Presence of diverticula, asymptomatic patient
Diverticular disease - Diverticula cause milder symptoms, e.g. intermittent abdominal pain without inflammation or infection
Diverticulitis - Diverticula become inflamed and infected, causing more severe symptoms
what is a false diverticulum?
Not all layers involved in the outpouching (in true diverticula, ALL Layers involved)
False are most common.
causes/risk factors of diverticular disease
Low fibre diet
Old age
NSAID
Connective tissue disorders (Ehlers-Danlos/Marfans)
Obesity
Smoking
what are 2 possible consequences of diverticula?
Blood vessels supplying colon can rupture, allowing blood into lumen, causing haematoschezia
Diverticula themselves can rupture, causing fistula formation, usually with bladder (colovesicular fistula), causing gas in bladder or stool in urine
signs/symptoms of diverticulitis?
Asymptomatic - Detected incidentally on colonoscopy
Diverticulosis:
- LLQ abdominal pain
- Rectal bleeding possible
Diverticulitis:
- LLQ/LIF pain and guarding (If Sigmoid. Right sided if right colon affected)
- LIF tender mass (if abscess)
- Constipation
- Fresh rectal bleeding
- Diarrhoea
ix in diverticulitis
CT abdomen/pelvis with contrast
- Identify divertcula/diverticulitis and complications
differentials for diverticulitis
Colorectal cancer
Appendicitis
UTI
Pyelonephritis
mx of diverticulitis
Diverticulosis - No treatment
Diverticular disease - Increase fibre, hydration, cut out smoking. Analgesia such as paracetamol and anti-spasmodic such as mebeverine may be used
Diverticulitis:
- Analgesia/anti-spasmodic. Fluid or low residue diet, to rest bowel.
- Co- amoxiclav
- Surgery if complications
comps of diverticulitis
Colovesical fistula - Faecaluria, pneumaturia (stools and gas in urine)
Abscess
Perforation/ rupture onto peritoneum -> Bacterial peritonitis
Bowel obstruction
Define haemorrhoids/piles
Haemorrhoids are normally spongy vascular structures in anal canal that act as cushions for stool as it passes through.
Haemorrhoidal disease (haemorrhoids) is when they get swollen and inflamed
classifications of haemorrhoids
Internal - above dentate line
External - below dentate line
Internals graded
1 - No protrusion out of anal canal
2 - Protrusion during stool passage but retract
3 - Protrude, dont retract but can be pushed in
4 - Prolapsed haemorrhoids that cannot be pushed in
causes of haemorrhoids
Recurrent increased abdominal pressures
- Straining during bowel movements
- Chronic diarrhoea, constipation
- Congestion from pelvic tumour
signs/symptoms of haemorrhoids and investigations
Internal: Usually asymptomatic, can be slightly uncomfortable, and have fresh red blood
External: Very painful, patients cant sit. Have discharge, swelling and itching.
Rectal exam and proctoscopy for internal
mx of haemorrhoids
1 - Increase fibre/fluids
- Stool softeners
- Topical analgesia or steroids
2/3/4 - Rubber band litigation, sclerotherapy or surgical treatment
Define Polymyalgia Rheumatics
older people
muscle stiffness and raised inflammatory markers.
features of polymyalgia rheumatics
over 60
rapid onset - under a month
aching, morning stiffness in proximal limb muscles - WEAKNESS NOT A SX OF IT.
- mild polyarthralgia, lethargy, depression, low grade fever, anorexia, night sweats
ix for polymyalgia rheumatics
raised inflammatory makrers - eg - esr over 40mm/hr
creatinine kinase and EMG normal
tx of polymyalgia rheumatica
prednisolone - 15mg/od
they respond dramatically to steroids. if they dont respond: alternative diagnosis
What is chronic rhinosinusitis
inflammatory disorder of paranasal sinuses and linings of nasal passages that last over 12.
predisposing factors to chronic rhinosinusitis
atopy: hay fever, asthma
nasal obstruction e.g. Septal deviation or nasal polyps
recent local infection e.g. Rhinitis or dental extraction
swimming/diving
smoking
features of chronic rhinosinusitis
facial pain: frontal pressure pain worse on bend forward
nasal discharge: clear if allergic/vasomotor.
thicker, purulent if secondary infection
nasal obstruction: mouth breathing
post nasal drip: could produce chronic cough
how would you manage chronic rhinosinusitis
avoid allergen
intranasal corticosteroids
nasal irrigation with saline solution
name 3 red flag symptoms associated with chronic rhinosinusitis
unilateral sx
persistent sx: despite compliance with 3 months of tx
epistaxis
do acute sinusitis
