A

Question 1

define AAA

Answer 1

abdo aorta of >3cm

Question 2

risk factors AAA

Answer 2

Male sex and increasing age.
Smoking.
Hypertension.
Positive family history.
Diabetes mellitus.
Chronic obstructive pulmonary disease.

Question 3

AAA screening programme for whom

Answer 3

men over 65 years old, known AAA

Question 4

categorise small, medium, large AAA and follow up Mx

Answer 4

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

Question 5

typical achilles tendinopathy sx + screening questionnaire

Answer 5

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

Question 6

risk factors achilles tendinopathy

Answer 6

diabetes mellitus, dyslipidaemia, and fluoroquinolone use

Question 7

examining someone with sx of achilles tendinopathy (incl sx of rupture)

Answer 7

exclude tendon rupture (sudden pain, ‘snap’ can’t weight bear, +ve Simmonds test)

assess appearance, palpate, ROM, test function with hopping / heel raise

Question 8

further inv for achilles tendinopathy

Answer 8

clinical dx
arrange lipid profile /hba1c if assoc issues / RFs

Question 9

assessing achilles tendon rupture

Answer 9

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

Question 10

mx of achilles tendinopathy or rupture

Answer 10

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)

Question 11

clinical features of acne vulgaris

Answer 11

must have comedones to be acne

may get papules / pustules / nodules too

scarring
pigementation
seborrhoea

Question 12

mild vs mod vs severe acne classify

Answer 12

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.

Question 13

history for acne

Answer 13

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)

Question 14

ddx acne

Answer 14

rosacea
folliculitis
drug induced (steroids, antiseizure meds, B vitamins)
keratosis pilaris

Question 15

acne - when to refer

Answer 15

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

Question 16

primary care acne mx (mild/mod/severe)

Answer 16

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

Question 17

important counselling considertation with acne treatments for women

Answer 17

can’t have retinoids or tetracyclines if pregnant / risk of pregnancy

Question 18

assessment of acute childhood limp

Answer 18

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

Question 19

examination of a child with acute limp incl screening exam name

Answer 19

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

Question 20

red flags in acute limp child

Answer 20

night pain waking
red/swollen/stiff joint
FLAWS sx
rash / brusing
morning stiffness
not wt bearing
severe pain / anxiety
palpable mass

Question 21

ddx acute limp of child by age
<3, 3-10, teenager

Answer 21

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

Question 22

spina bifida o/e signs

Answer 22

hair at spine, scoliosis

Question 23

muscular dystrophy quick sign

Answer 23

hypertrophic calves

Question 24

DDH risk factors

Answer 24

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.

Question 25

Perthes disease

Answer 25

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

Question 26

SUFE

Answer 26

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

Question 27

osgood schlatter

Answer 27

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.

Question 28

Sever’s disease

Answer 28

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.

Question 29

osteochondritis dissecans

Answer 29

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.

Question 30

chondromalacia patellae

Answer 30

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.

Question 31

referral /urgent or routine for acute limping child

Answer 31

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.

Question 32

when can you manage acute limp in child in primary care

Answer 32

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

Question 33

when to suspect AKI

Answer 33

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

Question 34

reasons for urgent review with bloods showing AKI

Answer 34

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.

Question 35

AKI stages 1-3

Answer 35

1 - 1.5x baseline or 26+ creat rise in 48 hrs

2- 2x baseline cr

3 - 3x baseline or > 350 creat

Question 36

assessing someone with biochemical AKI

Answer 36

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

Question 37

interpreting urine dip with known AKI primary care

Answer 37

negative dip - usually pre renal or drug cause

+ve blood protein - glomerular disease

wcc++ - interstitial nepthritis

Question 38

AKI risk factors

Answer 38

old
prev AKI
known CKD
obstructive urological sx / hx
any chornic disease
neuro impairment
sepsis
dehydration
recent medication change
malignancy

Question 39

category of AKI pre/renal/post

Answer 39

pre - most common, reduced renal perfusion

renal - structural kidney damage

post - least common - acute obstruction

Question 40

pre renal AKI causes

Answer 40

hypovolaemia / dehydration
reduced cardiac output (heart/liver disease / sepsis / drugs)

antihypertensives or diuretics or analgesics(esp ACEx, ARB, NSAID)

Question 41

renal AKI causes

Answer 41

nephrotoxics (abx, NSAIDs, PPI, allopurinol, iodine contrast, chemotherapy etc)

vascular - clots, vasculitis

glomerular - GN

tubular - rhabdo, ATN, myeloma

interstitial - AIN

Question 42

post renal AKI causes

Answer 42

obstruction

stones, blocked catheter, enlarged prostate , recurrent UTI, neurogenic bladder

Question 43

urgent hosp admission criteria for AKI

Answer 43

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

Question 44

managing stage 1 AKIs

Answer 44

review meds and amend as necessary

advice on fluid balance

manage underlying cause

regular monitoring

Question 45

follow up after AKI

Answer 45

consider renal referral if known CKD or if eGFR <30ml/min

check U+Es 2 weeks after any medication restarts

Question 46

complications AKI

Answer 46

electrolyte distrubance

fluid overload

uraemia

CKD