A Flashcards
define AAA
abdo aorta of >3cm
risk factors AAA
Male sex and increasing age.
Smoking.
Hypertension.
Positive family history.
Diabetes mellitus.
Chronic obstructive pulmonary disease.
AAA screening programme for whom
men over 65 years old, known AAA
categorise small, medium, large AAA and follow up Mx
no aneurysm at 65 years - nothing
small (3-4.4cm) - repeat at 12 months
medium (4.5-5.4cm) - repeat at 3 months
large (>5.5cm) - referral to vascular
typical achilles tendinopathy sx + screening questionnaire
heel aches, worse with pressure or activity, stiffness on inactivity
if 2-6cm proximal to insertion point suggests mid point tendinopathy, lower down is insertional
VISA-A questionnaire
risk factors achilles tendinopathy
diabetes mellitus, dyslipidaemia, and fluoroquinolone use
examining someone with sx of achilles tendinopathy (incl sx of rupture)
exclude tendon rupture (sudden pain, ‘snap’ can’t weight bear, +ve Simmonds test)
assess appearance, palpate, ROM, test function with hopping / heel raise
further inv for achilles tendinopathy
clinical dx
arrange lipid profile /hba1c if assoc issues / RFs
assessing achilles tendon rupture
a third don’t get any pain, otherwise pain + snap
calf aches, swelling, bruising, weakness, difficulty weight bearing (but some can)
Simmonds triad - (angle of declination, palpation, and the calf squeeze test)
feel for a gap in tendon
NB if chronic may just have wasted calf
mx of achilles tendinopathy or rupture
rupture - follow local protocol - same day ortho referral
otherwise:
- stop or modify any underlying causes
ice, simple analgesia , rest, weight bear as tolerated
refer physio if not improving after a week
no steroid injections for this!! bad.
if chronic or not responding can refer to ortho clinic ( they may do extracoroperal shockwave therapy, eccentric exercise programme or debridement if v chronic)
clinical features of acne vulgaris
must have comedones to be acne
may get papules / pustules / nodules too
scarring
pigementation
seborrhoea
mild vs mod vs severe acne classify
Mild acne — predominantly non-inflamed lesions (open and closed comedones) with few inflammatory lesions.
Moderate acne — more widespread with an increased number of inflammatory papules and pustules.
Severe acne — widespread inflammatory papules, pustules and nodules or cysts. Scarring may be present.
history for acne
duration / distribution
previous Mx and response
triggers - e.g. with cycle, OCP, cosmetics
any systemic features (acne fulminans - rare)
psychosocial impact
FH incl PCOS, endocrine
DH - steroids, ciclosporin, lithium , isoniazid, androgens
screen PCOS sx (hirsuitism, alopecia, irregular cycle)
ddx acne
rosacea
folliculitis
drug induced (steroids, antiseizure meds, B vitamins)
keratosis pilaris
acne - when to refer
urgently to derm if have very rare acne fulminans (young white males)
routinely if acne conglobata or nodulocystic acne
(must counsel about isotretinoin prior)
or if not responding to 2x treatments incl an abx or sig psychiosocial impact / scarring
primary care acne mx (mild/mod/severe)
basic lifestyle advice re cleaning / hygiene
mild/mod: 12 week course of:
adapalene with benzoyl peroxide OR topical tretinoin with 1% clinda OR topical benzoyl with clinda
mod-severe: as above + can try lymecycline/doxy OR azelaic acid
consider COCP for females
abx must always be used a part of dual therapy
important counselling considertation with acne treatments for women
can’t have retinoids or tetracyclines if pregnant / risk of pregnancy
assessment of acute childhood limp
DOPT
screen for trauma hx / maltreatment
any preceding viral illness?
pain?
muscle weakness?
birth / dev hx
FH of JIA, neuromusc / rheum
NB - localising reproducible pain usually # , OM or septic arth
pain during nappy change / back flexion may = discitis
examination of a child with acute limp incl screening exam name
screen septic cause with obs / child traffic light
assess for rash / bruising / LN raised
pGALS assessment screen (check for weight bearing, spina bifida, leg length discrepancy, calf muscle hypertrophy, skins signs, neurovasc status, gait)
look move feel
red flags in acute limp child
night pain waking
red/swollen/stiff joint
FLAWS sx
rash / brusing
morning stiffness
not wt bearing
severe pain / anxiety
palpable mass
ddx acute limp of child by age
<3, 3-10, teenager
or soft tissue inj
<3 years:
toddler #, subtle undisplaced # after twisting or fall
ligament sprain
child maltreatment
DDH
3-10 years
transient synovitis (dx of exclusion, postviral usually)
Perthes disease
10-19 years:
#, ST inj
SUFE
Perthes
Osgood Schlatter
Sever’s disease
osteochondritis dissecans
chondromalacia patellae
any age:
septic arth / OM
discitis
malignancy
sickle cell
haemophilia
rickets JIA
Lyme arthirits
neuromuscular
spina bifida o/e signs
hair at spine, scoliosis
muscular dystrophy quick sign
hypertrophic calves
DDH risk factors
DDH is a congenital conditon where the ball and socket hip joint fails to develop normally.
Risk factors include being a firstborn child, female sex, family history of DDH, breech presentation at birth, and oligohydramnios. A physical exam may reveal asymmetric skin folds, extremity shortening, and limited hip abduction.
Untreated, DDH may lead to hip pain and/or osteoarthritis in older children.
Perthes disease
An idiopathic avascular necrosis of the developing femoral head.
It is more common in boys than in girls.
Onset is usually over weeks, and the child will typically present with limitation of hip rotation and a subacute limp sometimes with referred pain to the groin, thigh, or knee. It is typically unilateral, though bilateral involvement is present in 10% of cases. The child is systemically well with no other joint involvement and no evidence of joint inflammation.
Most children with Perthes’ disease have good outcomes
SUFE
A displacement of the proximal femoral epiphysis from the metaphysis.
It is slightly more common in boys than girls and in children who are overweight.
It can present with an acute/insiduous onset of pain (hip, thigh, or knee), and the child may walk with an antalgic gait out-toeing, with shortening of the affected limb. It is sometimes associated with endocrine abnormalities, such as hypothyroidism, and in children being treated for growth hormone deficiency or with a history of radiotherapy treatment.
Prompt diagnosis is crucial to avoiding further displacement and the development of avascular necrosis
osgood schlatter
An overuse injury caused by multiple small avulsion fractures within the ossification centre (apophysis) of the tibial tuberosity at the inferior attachment of the patellar ligament.
It is a usually self-limiting disorder causing anterior knee pain during adolescence.
Sever’s disease
An overuse injury thought to be caused by repetitive microtrauma from the pull of the Achilles tendon on the unossified apophysis.
It is most common in boys aged 10–12 years who are active in sports, such as running and football, and produces heel pain as a result of inflammation of the calcaneal apophysis.
It often resolves within 2 weeks to 2 months, but a child may have recurrent symptoms until skeletal maturity.
osteochondritis dissecans
Occurs when a small piece of subchondral bone begins to separate from its surrounding area due to a disturbance of the local blood supply. This bone and the cartilage covering it may break loose, causing pain and possibly hindering joint motion.
It is the most common cause of a loose body in the joint space, typically affecting the knee between the ages of 10–19 years.
The aetiology is uncertain but trauma, vascular abnormalities, defects in ossification, and genetics have all been suggested as possible causes. Clinical findings are subtle and a small effusion or limited range of joint movement may be the only sign. Locking or instability suggest a loose body in the joint.
chondromalacia patellae
Describes anterior knee pain typically felt when walking up or down stairs.
Affects children between the ages of 10–19 years in a ratio of three girls to two boys.
referral /urgent or routine for acute limping child
Arrange urgent specialist assessment if the child:
Has a fever and/or red flags suggesting serious pathology, such as:
Pain waking the child at night — may indicate malignancy.
Redness, swelling, or stiffness of the joint or limb — may indicate infection or inflammatory joint disease.
Weight loss, anorexia, fever, night sweats, or fatigue — may indicate malignancy, infection, or inflammation.
Unexplained rash or bruising — may indicate haematological or inflammatory joint disease, or child maltreatment.
Limp and stiffness worse in the morning — may indicate inflammatory joint disease.
Unable to bear weight or painful limitation of range of motion — may indicate trauma or infection.
Severe pain, anxiety, and agitation after a traumatic injury — may indicate neurovascular compromise or impending compartment syndrome.
A palpable mass — may indicate malignancy or infection.
Is suspected of being maltreated. See the CKS topic on Child maltreatment - recognition and management for further information.
Is younger than 3 years of age — transient synovitis is rare in this age group; septic arthritis is more common.
Is older than 9 years of age with painful or restricted hip movements (in particular internal rotation) — to exclude slipped upper femoral epiphysis.
Arrange specialist assessment (the urgency depending on clinical judgement) if:
There is uncertainty about the cause of the limp — refer to paediatric orthopaedics or orthopaedics.
The cause of the limp cannot be managed in primary care — refer to an appropriate specialist.
A child presents with a limp on multiple different occasions — refer to paediatric orthopaedics or orthopaedics.
when can you manage acute limp in child in primary care
If the child is aged 3–9 years, well, afebrile, mobile but limping, and has had the symptoms for less than 72 hours (or more than 72 hours and improving):
usually transient synovitis but must have good safety net
when to suspect AKI
Nausea and vomiting, diarrhoea, or suspected dehydration.
Reduced urine output or changes to urine colour.
Confusion, fatigue, or drowsiness.
any acute illness or AKI risk factors
reasons for urgent review with bloods showing AKI
Respond to AKI warning stage test results within an appropriate timescale using clinical judgement, as suggested below. Consider arranging an urgent review and clinical assessment if there are:
Poor fluid intake or urine output.
Evidence of hyperkalaemia (especially if moderate with potassium 6–6.4 mmol/L or severe with potassium 6.5 mmol/L or more).
Previous AKI.
Known chronic kidney disease (CKD) stage 4 or 5 or history of renal transplant — urgent liaison with a nephrologist may be needed. See the CKS topic on Chronic kidney disease for more information.
A history of frailty and/or chronic disease such as diabetes, liver disease, or heart failure. See the CKS topics on Diabetes - type 1, Diabetes - type 2, and Heart failure - chronic for more information.
Suspected intrinsic kidney disease or urinary tract obstruction. See the CKS topics on LUTS in men and Chronic prostatitis for more information.
AKI stages 1-3
1 - 1.5x baseline or 26+ creat rise in 48 hrs
2- 2x baseline cr
3 - 3x baseline or > 350 creat
assessing someone with biochemical AKI
volume status assessment inl UO / oedema, bladder
monitor U+Es esp K+
screen LUTS, renal colic, any illness, fluid intake / UO, risk factors, rashes, arthralgia, uveitis, bleeding, drug hx, rhabdo risk factors
interpreting urine dip with known AKI primary care
negative dip - usually pre renal or drug cause
+ve blood protein - glomerular disease
wcc++ - interstitial nepthritis
AKI risk factors
old
prev AKI
known CKD
obstructive urological sx / hx
any chornic disease
neuro impairment
sepsis
dehydration
recent medication change
malignancy
category of AKI pre/renal/post
pre - most common, reduced renal perfusion
renal - structural kidney damage
post - least common - acute obstruction
pre renal AKI causes
hypovolaemia / dehydration
reduced cardiac output (heart/liver disease / sepsis / drugs)
antihypertensives or diuretics or analgesics(esp ACEx, ARB, NSAID)
renal AKI causes
nephrotoxics (abx, NSAIDs, PPI, allopurinol, iodine contrast, chemotherapy etc)
vascular - clots, vasculitis
glomerular - GN
tubular - rhabdo, ATN, myeloma
interstitial - AIN
post renal AKI causes
obstruction
stones, blocked catheter, enlarged prostate , recurrent UTI, neurogenic bladder
urgent hosp admission criteria for AKI
stage 3 aki
severe underlying cause suspected
no identifiable cause
sepsis
need fluids
complications
d/w renal if have stage 4 CKD or suspected intrarenal cause or raised potassium
managing stage 1 AKIs
review meds and amend as necessary
advice on fluid balance
manage underlying cause
regular monitoring
follow up after AKI
consider renal referral if known CKD or if eGFR <30ml/min
check U+Es 2 weeks after any medication restarts
complications AKI
electrolyte distrubance
fluid overload
uraemia
CKD
