OSCE specific Flashcards
Warfarin ATHLETICS
A: Thins blood to prevent blood clots, does this by blocking vitamin K which is usually used by the body to make proteins that cause the blood to clot
T: Take once a day in the morning
H: Oral tablet
L: Usually 3 months for a DVT, 6 months for PE, lifelong for DVT
E: Effects take 48-72hrs
T: INR on days 3, 4, 5 until INR 2-3. then regularly after that, can extend to up to 3 months
I:
C: Pregnancy, significant risk major bleeding, active bleeding
S: Bleeding - gums, easy bruising, epistaxis, blue toes
Intervention for rapid AF
Statin ATHLETICS
● Action/how it works - inhibits the production of
cholesterol and increases the uptake of cholesterol by
the liver
● Timing - once daily
● How to use it - tablet
● Length of time - long term until lipid and cholesterol
levels are under control
● Effects - muscle aches, mild transient gastrointestinal
symptoms, headache, aminotransferase elevation
● Tests required - baseline aminotransferase and
creatinine kinase
● Important side effects – rhabdomyolysis (seek
medical attention if any dark urine or any muscle
pain, tenderness or weakness, especially in the first
4-6 weeks after starting/increasing dose)
● Contraindications – treatment with systemic sodium
fusidate, pregnancy (less relevant for Bill)
ACE-I ATHLETIC
● Action/how it works: reduces narrowing of the blood
vessels, amount of salt + water retained and
sympathetic activity
● Timing: once daily
● How to use it: tablet
● Length of time: until no longer clinically indicated
● Effects: dry cough, dizziness, anaemia
● Tests required: UEC (esp potassium), eGFR
● Important SFEs: angioedema, hyperkalaemia, AKI
● Contraindications: renal artery stenosis, pregnancy,
PMHx hereditary/idiopathic angioedema, severe
renal impairment (d/w specialist), hyperkalaemia,
hypotension
Metformin ATHLETICS
Action: Increases your response to insulin so your cells take up more glucose from your blood, and increases amount of glucose produced by the liver
Timing: If you miss a dose, take it asap, unless it is too close to the next dose
How: Oral tablet that you take once daily (initially) with food, asap after your meal at a fixed date and time
500mg BD (then review after 1-2 weeks)
Length: Lifelong required, with close monitoring of complications
Effects:
Tests: Before starting long term therapy, take urea and electrolyte levels; HbA1C every 3-6 months until stable, then 6 monthly
Important Side effects: Nausea, diarrhoea abdominal pain, weight loss, lactic acidosis - can’t be taken on day of or two days after anaesthetic or after having general anaesthetic
C: Renal impairment, ketoacidosis, low BMI
Reversible causes of cardiac arrest
4H’s 4Ts:
- Hypoxia
- Hypovolemia
- Hyperkalemia/hypokalemia
- Hypothermia
- Tension pneumothorax
- Tamponade
- Toxins
- Thrombosis
SGLT2i ATHLETICS
GLP1 ATHLETICS
Anti-psychotic ATHLETICS
Clozapine ATHLETICS
Beta Blocker ATHLETICS
Dementia counselling
Parkinsons counselling
Acute asthma exacerbation - mgmt
Croup management
DOAC ATHLETICS
Risk factors for osteoporosis - SHATTERED
SHATTERED
● Steroid use, e.g. prednisolone
● Hyperthyroidism or hyperparathyroidism
● Alcohol/tobacco use (see social history)
● Thin (BMI <17)
● Testosterone – low
● oEstrogen – low
● Renal/liver disease
● Erosive (i.e. multiple myeloma) or inflammatory (i.e.
rheumatoid arthritis) bone disease
● Diabetes mellitus (type 1) or low dietary calcium
intake (see social history)
o Calcium rich foods include dairy (e.g. milk,
yoghurt), seafood (e.g. snapper, prawns,
salmon) and green vegetables (e.g. cucumber,
kale, bok choy)
Bisphosponate ATHLETICS
First line: bisphosphonates, i.e. alendronate, zoledronic acid
“ATHLETICS” mnemonic for medication counselling
● Action: Slows down the breakdown of bone
● Timing: Depends on agent – can be taken once daily,
weekly or monthly as a tablet, or yearly as an
intravenous infusion
● How to use it:
○ Tablet: Take first thing in the morning on an
empty stomach with water and stay upright
for 30 minutes to avoid GI side effects
○ Intravenous infusion: Administered over at
least 15 minutes
● Length of time: 5 years, then assess ongoing need for
treatment, consider drug holiday due to risk of
atypical fracture
● Effects: GI (e.g. oesophagitis, oesophageal ulcers,
gastric irritation)
● Tests required:
○ Serum ionised calcium
○ Vitamin D level (25-hydroxy vitamin D)
○ UEC
● Important side effects: Osteonecrosis of the jaw,
atypical fractures
● Contraindications
○ Hypocalcaemia
○ Oral: oesophagitis, achalasia, oesophageal
varices, oesophageal stricture, Barrett’s
oesophagus
○ Intravenous: reduced renal function (eGFR
≤35 mL/min
Breaking bad news mnemonic - SPIKES
Setting - appropriate setting
Perception - understanding, patient ICE
Invitation - pt wanting to hear results?
Knowledge - Chunk and check, simple language
Empathy -
Summary and strategy - make plan for next steps, arrange follow up, provide information, clarify understanding
CAGE screen
Cutting down
Annoyed
Guilt
Eye opener
5A’s for cessation
Ask
Assess
Advise
Assist
Arrange follow up
4D’s for smoking cessation
Delay
Deep breathe
Drink water
Do something else
Benefits of quitting smoking - short term and long term
Short/medium-term health benefits
○ Heart rate and blood pressure drop within 20
minutes
○ Carbon monoxide level in the blood drops to
normal within 12 hours
○ Lung function improves within 2-12 weeks
○ Coughing, shortness of breath, and wheezing
decreases within 1-9 months
Long-term benefits
○ Risk of coronary heart disease is half that of a
smoker within 1 year
○ Stroke risk is the same as that of a non-smoker
within 5 years
○ Risk of lung cancer decreases to half of that of a
smoker
○ Other – reduced risk of dementia, other cancers
(i.e. mouth, throat, oesophagus, bladder, cervix,
pancreas), fertility issues, vision loss,
osteoporosis, dental and gum disease, infections
Assessing and addressing barriers to cessation
Motivation to quit
Likes of (smoking)
Dislikes of (smoking)
Barriers of quitting
Risk factors for breast cancer?
Non-modifiable:
● Genetic mutations (BRCA1/2, RAS, PTEN, Li-Fraumeni
syndrome)
● Family history (first degree relatives)
● Age
● Early menarche, late menopause
● Nulliparity
Modifiable:
● HRT
● Physical inactivity
● Obesity
● Ionising radiation
● Alcohol
Treatment for HER-2 positive breast cancer and side effects?
Trastuzumab (Herceptin)
○ Humanised monoclonal antibody against
HER2 tyrosine kinase receptor
○ Typically every 3 weeks for 12 months
○ NOTE: would combine with chemotherapy as
doesn’t work well alone
● Main side effect
○ Cardiotoxicity (dilated cardiomyopathy) -
investigate with stress echo
ARB ATHLETIC
Angiotensin receptor blocker (ARB), e.g. candesartan
● Action/how it works: reduces narrowing of the blood
vessels, amount of salt + water retained and
sympathetic activity
● Timing: once daily
● How to use it: tablet
● Length of time: until no longer clinically indicated
● Effects: dizziness, headache
● Tests required: UEC (esp potassium), eGFR
● Important side effects: hyperkalaemia, AKI, sprue-like
enteropathy (severe chronic diarrhoea + weight loss,
months to years after initiation of drug)
● Contraindications: renal artery stenosis, pregnancy,
severe hepatic impairment, severe renal impairment
(d/w specialist), hyperkalaemia, hypotension
CC blocker ATHLETIC
Action/how it works: causes blood vessels to
expand/dilate → lowering resistance that blood has
to flow against
● Timing: once daily
● How to use it: tablet
● Length of time: until no longer clinically indicated
● Effects: peripheral oedema, facial flushing, headache,
tachycardia
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● Tests required: BP, HR
● Important side effects: gingival hyperplasia (rare)
● Contraindications: cardiogenic shock, aortic stenosis,
heart failure w/ reduced ejection fraction,
hypotension
What to do is missed dose of ACE-I/ARB?
If you forget to take one or more doses: take your next dose at the
normal time and in the normal amount, do not take any more than has
been prescribed
○ If you miss one dose, skip it and continue with your normal schedule
Treatment for alcohol use disorder
Psychosocial
○ Individual or group counselling
○ Link to social and welfare services
○ Self-help - Alcoholics Anonymous
○ Monitoring and support from health practitioner(s)
Pharmacotherapy
○ Naltrexone: opioid antagonist, reduces craving and effects reward circuitry of
alcohol
○ Acamprosate: reduces cravings, residual anxiety
○ Disulfiram: alcohol dehydrogenase inhibitor, causes adverse effects to alcohol
Symptoms of alcohol withdrawal
Mild (6-24 hours post-cessation):
○ Anxiety, tremors, N/V, insomnia
Severe (10-72 hours):
○ Hallucinations (esp visual), paranoia, diaphoresis, HTN
- Seizures (24-48 hours)
- Delirium tremens (5%, 3-10 days): global confusion + sympathetic overdrive
Psoriasis topical therapies + other options
● Topical steroids
○ Particularly helpful with flares
○ Short term (e.g. up to 6 weeks with
intermittent use)
○ Pulse treatment (e.g. steroid for 2
days/week, different drugs on other days)
■ Intermittent or pulse treatment will
help minimise adverse effects and
loss of efficacy (tachyphylaxis)
● Topical calcipotriol (vitamin D analogue)
○ May take up to 6 weeks for best results
○ Often used in combination with steroids for
greater efficacy
● Topical tars/salicylic acid
○ Safe and effective treatment however for
some patients, the colour/odour/
consistency of prepar
If topical therapy is not adequate, there are other
therapies available often coordinated with a
dermatologist (phototherapy, acitretin,
methotrexate, ciclosporin, biologics)
Non-pharmacological management of psoriasis
Keep skin moisturised
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● SNAP-W: Smoking, Nutrition, Alcohol, Physical
Activity, Weight Loss
○ Prevention for CVD and T2DM
○ Smoking cessation will also specifically
reduce risk of aggravation of psoriasis
Describe psoriasis - what, where, diagnosis. treatment considerations
Psoriasis is a chronic inflammatory skin condition, which usually presents with red, silverywhite scaly plaques which are well circumscribed and often symmetrically distributed.
Plaque psoriasis is the most common type primarily affecting the knees, elbows, and lower
back. Other types include guttate psoriasis, flexural psoriasis, nail psoriasis, palmoplantar
psoriasis, and erythrodermic psoriasis.
Diagnosis is primarily clinical, and biopsy is rarely required. However, tools such as the PASI
score (Psoriasis Area and Severity Index) can be used to assess the extent and severity of the
psoriasis
It is worth noting that treatment can be difficult and response to therapy can be variable.
Assessment of the psychosocial impact of the disease is important as is involvement of a
dermatologist for some patients.
Investigations for suspicion of SLE
Bloods: FBE (anaemia/ thrombocytopenia), UEC
(renal), ESR, CRP (inflammatory markers), ANA
(Anti-dsDNA, Anti-Sm if ANAs positive), Low
complement, Direct Coombs test, Antiphospholipid
antibodies
● Urinalysis/ urine dipstick (renal function)
● Imaging: depends on organ involvement
o X-ray joints
o X-ray/CT chest
o Echocardiogram
Etiology of SLE - who gets it, RF’s, type of sensitivity reaction?
Etiology
● Autoimmune disorder
● More common in women of childbearing age
● Genetic predisposition: HLA-DR2, HLA-DR3
● Risk factors: increased oestrogen, cigarette smoking, silica exposure, UV exposure,
infections, drugs (drug-induced lupus erythematosus)
● Type III hypersensitivity: immune complex formation in small vessels → complement
activation → organ damage in skin, kidneys, joints, vessels
Common SLE symptoms
○ malar rash
○ discoid rash
○ generalised photosensitivity
○ arthritis
○ Raynaud phenomenon
○ oral ulcers
○ nonscarring alopecia
○ constitutional symptoms (fever, fatigue, weight loss)
Complications of SLE
○ Cardiovascular disease: Libman-Sacks endocarditis, AMI
○ Infections
○ Renal failure
Treatment for SLE - non-pharmacological
● Avoid sun exposure
● Smoking cessation
● Immunisations
Treatment for SLE - pharmacological
● Hydroxychloroquine (all patients with lupus should use HCQ unless contraindicated)
● NSAIDS, low dose corticosteroids for mild to moderate symptom relief
● High doses of corticosteroids and immunosuppressants (azathioprine, methotrexate,
mycophenolate) for severe disease
Clinical presentation of Graves disease
Signs of hyperthyroidism
○ General: weight loss, increased appetite, heat intolerance, diarrhoea, fatigue,
pretibial myxedema
○ Cardiovascular: palpitations, hypertension
○ MSK: tremor
○ Endocrine: oligomenorrhea/ amenorrhea, gynaecomastia, decreased libido,
infertility
○ Neurological: anxiety, depression, restlessness, insomnia
Signs specific to Grave’s disease
○ Diffuse goitre
■ Smooth, uniformly enlarged
■ Bruit may be heard
○ Grave’s ophthalmopathy
■ Exophthalmos, lid lag, proptosis
Investigations to diagnose Graves disease
Diagnosis
● Most useful: Thyroid function test
○ Elevated T3/T4, decreased TSH
● Detect thyroid antibodies
○ Elevated TRAbs
○ May have elevated anti-Tg and anti-TPO antibodies (not specific to Grave’s
disease)
● Radioactive iodine scanning
○ Diffuse uptake of radioactive iodine
● Thyroid ultrasound
○ Enlarged, hyperactive thyroid gland
Management of graves disease
● Symptomatic treatment: beta blockers
● Anti-thyroid medications (e.g propylthiouracil (PTU), carbimazole, methimazole)
● Radioactive iodine ablation
● Surgical total thyroidectomy
Investigations for Chlamydia/Gonorrhea
Bedside Investigations
● Urinalysis to check for haematuria, nitrites,
leukocytes to rule out UTI/renal stones
Pathology
● First void urine sample for nucleic acid amplification
test (NAAT) for presence of Chlamydia trachomatis
and Neisseria gonorrhoeae
● Urine MCS. Rule out UTI
● Urethral swab for gram stain, culture and
susceptibility testing for Neisseria gonorrhoeae
● FBE, CRP, UEC
Imaging
● Ultrasound to rule out testicular torsion (as indicated)
Aspects of sexual history
● Sexually activity
● Sexual partners
● Type of intercourse
● Protected/unprotected sex, contraception use
● STI history
● Dyspareunia
● Discharge (urethral, vaginal, anal)
● Genital lesions/rashes/blisters
● IVDU, tattoos, piercings
Imaging for renal calculi
CTKUB
Investigations for glandular fever
FBE + Blood film (lymphocytosis + atypical
lymphocytes)
* LFTs: can be deranged (transaminitis)
* ESR/CRP- elevated
* ASOT (check for GA Strep throat DDx)
* EBV Monospot test (agglutination test for
heterophile antibodies)
* EBV/CMV serology
Symptoms for T2DM diagnosis
● Lethargy, polyuria or polydipsia
● Frequent fungal or bacterial infections
● Blurred vision
● Loss of sensation (i.e. touch, vibration, cold)
● Poor wound healing
● Weight loss
Eczema explanation
Also called atopic dermatitis.
* Common skin condition affecting children
triggered by overactive immune system that
causes chronic inflammation of the skin +
reduced barrier function of skin.
* Lesions of dry, red bumpy, very itchy skin
* Appears in areas such flexural areas (forearm
and behind knees), neck and scalp in younger
children
Eczema triggers
Heat, low humidity, allergens (pollen, dust,
fomites), wool, stress
Eczema prognosis
Can self-resolve as children get older but some
people have it lifelong.
Eczema pharmacological mgmt
Between flares
* Moisturisers–regular, daily. Apply top to toes,
after shower and swimming.
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Flare Management
* Apply moisturiser 4x a day
* Topical Steroids
* Only for flares/active eczema –withdraw if
in remission
* Use appropriate strength for age & part of
skin being treated
* Use with wet compress/ dressings e.g.
hydrocolloid: 1-4 times daily for at least 3
days. Parents education with nursing
* If crusting/ pus in wounds consider
Antimicrobials
o Impetigo→ mupirocin, bleach bath,
o Eczema herpeticum→ antiviral IV
Symptom management – itchiness
* Antihistamines eg Zyrtec
* Cold compress
Eczema non-pharmacological mgmt
Avoid triggers e.g. wool, synthetic fabrics, hot
showers
● Avoid soaps, shampoos, can irritate the skin
SSRI ATHLETIC
Action: Sertraline belongs to a group of
antidepressants called SSRIs, which increase the
serotonin levels in your brain, resulting in positive effects on mood.
○ They are relatively safe, tolerable and
effective.
○ Approximately 60% of people with major
depression respond to treatment with an
initial antidepressant.
- not associated with adverse pregnancy outcomes, which would be appropriate medication for her to commence.
● Timing: Once daily, best with food in the morning
● How to use: Start on a 50mg oral tablet (can go lower
if elderly/sensitive to SEs). Start low, go slow.
○ If missed dose: Take as soon as you remember,
but not if close to the next dose (i.e. don’t
double up).
-
● Length of time: We will monitor your symptoms and
may gradually stop the medication in 6-12 months if
they improve.
● Effects: Takes at least 2 weeks to work, and you might
not see any benefit until 4-6 weeks.
○ It is important to keep taking them even if
they don’t seem to be working at first.
■ Do not stop them suddenly as you
may experience withdrawal
symptoms, such as nausea, sweating,
electric shock-like sensations, anxiety,
tremor and even seizures. (“FINISH” -
see notes section)
- Tests: TFTs, FBE, EUC, LFTs
- Important side effects:
Discusses common side effects of SSRI’s effecting multiple systems including GIT (nausea, reduced appetite, diarrhoea), neurological (insomnia, sweating) and sexual dysfunction (lowered libido, anorgasmia). Critical
Discusses adverse effects of initiating antidepressants known as “activation syndrome” which can include symptoms of restlessness, lability, agitation and anxiety during the initial weeks. Critical
Discusses risk of serotonin syndrome associated with SSRIs and advises to avoid medications (and over-the-counter medications such as St John’s Wort’s) which may increase serotonin activity. Symptoms include shivers, increased sweating, diarrhoea, altered mental status, autonomic hyperactivity and neuromuscular symptoms (clonus, hyperreflexia, tremors, seizures). Critical
Discusses the risk of sudden withdrawal from SSRI including flu-like symptoms, insomnia, nystagmus, ataxia, sensory disturbances (i.e. hallucinations) and hyperarousal. Critical
Explains that SSRI initiation can result in increased suicidal thoughts. Critical
Discusses that antidepressants carry the risk of mania.
- Contraindications:
Discusses precautions to commencing sertraline such as patients with a history of bipolar affective disorder, patients at high risk of bleeding or undergoing surgery.
Follow up in 2 weeks and 4 weeks to review progress and side effects
SSRI discontinuation sydrome mnemonic ‘FINISH’
- Flu-like symptoms
- Insomnia
- Nausea
- Imbalance
- Sensory disturbance
- Hyperarousal
Risk factors for GDM
High Risk Factors
● Previous GDM
● Previously elevated blood glucose level
● Maternal age ≥40 years
● Family history DM (1st degree relative with diabetes
or a sister with GDM)
● BMI > 35 kg/m2
● Previous macrosomia (baby with birth weight >
4500 g or > 90th centile)
● Polycystic ovarian syndrome
● Medications: corticosteroids, antipsychotics
Moderate Risk Factors
● Ethnicity: Asian, Indian subcontinent, Aboriginal,
Torres Strait Islander, Pacific Islander, Maori,
Middle Eastern, non‐white African
● BMI 25 – 35 kg/m2
GDM diagnostic criteria
2hr OGTT 75g >8.5
When to test OGTT during pregnancy?
In early pregnancy and 24-28 weeks if normal results
Risk factors for cervical cancer
- Early onset of sexual activity - Risk X2 for those <18 yrs compared to 21 yrs
- Immunosuppression
▪ HIV infection
▪ Diabetes
▪ Corticosteroids
▪ Renal transplant - Hx of vulvar or vaginal squamous cancer
- Hx of STI
- Multiple sexual partners - X2 with 2 partners
- Long term COCP (at least 5years and more)
- Smoking —– Tobacco damages cervical cells, making cancer more likely in those who
also have HPV
Interprestation of LSIL (CIN1)
low grade - usually disappear without treatment
Interpretation of HSIL (CIN2/3)
Pre cancerous - have potential to develop into cervical cancer
in 10-15 yrs if untreated
HSIL (CIN2/3) treatment and impact on future pregnancy
Further treatment would involve cutting out the affected cells from the cervix
- Large loop excision of the transformation Zone (usually done for HSIL) – LA is used
usually
o Cut tissue with a loop that’s heated by electricity
- Cold knife cone biopsy: usually done under GA with surgical knife in day surgery
- Laser conization
Cone biopsy or LLETZ causes a slightly higher risk of preterm labour and
miscarriage as the procedure can weaken the cervix
- The cone biopsy has a greater risk compared to LLETZ
- Serious problems can be prevented with a suture and the stitch is cut before you
go into labour usually at 37 weeks
CST follow up following HSIL findings
Test of cure needed for those with treated high grade intraepithelial lesion (HSIL)
- Perform co test (HPV + cytology done in the same test) at 12 and 24 months post
treatment
- If negative for both tests twice consecutively, return to normal 5 yearly screening
interval
COCP ATHLETIC
What is it: I would like to recommend the combined oral contraceptive pill (COCP) (Levlen) that contains both oestrogen and progesterone. It is 95-98% effective if used correctly. Since you didn’t find that you liked the mini pill and prefer not to get Injections (depo provera), we might try the COCP first. The other options are a little more long acting and might be more suitable
for someone who wanted longer term contraceptives, but we can consider them if the oral contraceptive pills aren’t working the best.
How does it work: It works by thickening the cervical mucus so sperms cannot swim through, thins the wall of the uterus so embryo cannot implant, and inhibit release of a new egg
(ovulation)
How to take: Take on the first day of menstrual period, or sometime between Day 1-5, if you decide to take it at any pointthen it would be advisable to take use other contraceptive
options for the next 7 days.
Side effects: Mood changes, bloating, breakthrough bleeding, nausea, breast tenderness, headaches
Things to take note: Can increase the risk of breast cancer and of forming blood clots in your leg (DVT)
Benefits Easy to achieve fertility by stopping the pill should you intend to fall pregnant next time
Disadvantages Requires you to remember to take your pills at a certain time every day
Reiteration of STI protection
While these methods of contraceptive do reduce the chances of incidentally falling pregnant, they unfortunately do not prevent the transmission of sexually transmitted infection, so it would be
important to use barrier contraception (condoms for males) and get regular STI checks to reduce the rate of transmission
Contraindications to COCP
■ Smoking (+ age >35)
■ Hx/FHx of
● Venous thromboembolism
● Breast/cervical cancer
● Migraine with aura
liver disease
What to do if 1 COCP missed
If you miss just one pill for > 24h,
then take the missed pill the next day, along with the pill meant
for the next day. (so 2 in a day) and resume as per normal.
What to do if 2 or more COCP missed
Take the last missed
pill and the one meant for today, don’t take any of the other missed pills. Then, tomorrow, resume the rest of the pack as normal. To prevent ovulation, use protection (condom, refrain from intercourse etc.) for the next 7 days.
What does being Rh- mean?
When you are Rh-, that means you have no antigens, so we will give you a man-made temporary Rh Ab that will prevent your body from creating its own Ab.
This is important because in the event that the child you give birth to has Rh- blood group, and there is mixing of your blood with your
baby’s blood, your body will recognize your babies’ antibodies as foreign, and will start to create its own Rh+ antibodies, to protect
you, but these will attack your babies’ red blood cells.
Usually, the first child is not affected but blood group Rh+ children in subsequent pregnancies might be.
What happens to neonate in a hemolytic reaction to Rh-?
Red blood cells are oxygen
carrying cells that are essential for their survival and as a result they can end up falling very sick with haemolytic jaundice- where their
cells are destroyed and it the process, this releases a yellow pigment which gives rise to the jaundiced appearance.
When are Anti-D injections given and why?
They are given at 28 weeks and 34 weeks to ensure enough coverage.
625IU of Rhesus D immunoglobulin, Intramuscularly, either via the
deltoid or anterolateral thigh. Avoid the buttocks.
Indications for Anti-D injections
- Miscarriage
- Antepartum haemorrhage
- Termination of pregnancy
- External cephalic version for breech babies
- Invasive prenatal testing: Chorion villus sampling, amniocentesis, cardocentesis
- IUFD
- Ectopic pregnancy
- Abdominal trauma
- Rhesus + platelet transfusion
- Manual delivery of placenta
What does the Kleihauer Test test and when is it done?
Performed for abdominal trauma/vaginal bleeding in pregnancy
To determine fetomaternal haemorrhage volume, and ensure a
significant Rhesus D immunoglobulin dose - means that there is fetal Hb in maternal
blood, indicating concealed antenatal bleeding
Indications for IOL
When we do inductions we carefully balance the risks of the baby staying inside vs delivery.
There are a lot of reasons why inductions are performed and these are when evidence has shown that the benefits outweigh the risks.
Some common ones include:
● Pre-eclampsia
● Gestational diabetes on insulin
● Abnormal CTG findings
● Post-term pregnancy - 41 weeks +
● Advanced maternal age ( > 40)
● Fetal Macrosomia
● High maternal BMI
● Premature prelabour rupture of membranes/prelabour rupture of membranes
The reason you are having an induction of labour is because you have pre-eclampsia, which puts you at a greater risk of having eclampsia and seizures the longer
you remain pregnant.
We will schedule your induction for
37 weeks to ensure that baby has grown to term.
The timing of induction varies depending on the indication
What is an IOL?
An induction of labour is when we stimulate your body to start and undergo the labour process, the process can vary a bit depending on how ready your body is but can involve
some physical/mechanical as well as medical stimulation
Contraindications to IOL
● Fetal Malpresentation
● previous classical C-section
● Placenta praevia or vasa praevia
Risks of IOL
There are risks associated with any medical procedure including spontaneous labour itself. Some risks specific to an induction are
● Uterine hyperstimulation
● Failure of induction -> conversion to emergency Csection
● Uterine rupture
Process of IOL
There are a few different ways that labour is induced, the method of induction will depend on how ready your cervix is.
If your cervix is not ready, you may need priming either with a Balloon Catheter OR Prostaglandins.
- Catheter: You will come in the day before your
actual labour and we will put in a little balloon to
put pressure on your cervix and prepare it for
labour. You can then go home and come in the
next day where we will take out the balloon and
rupture your membranes/break your water with a little hook. - Pg: gel or tablet inserted into the vagina to soften the cervix. You will need to stay at the hospital after the gel has been applied so that we can monitor you.
After your membranes have ruptured, we will start you on a medication called syntocinin which is the natural hormone your body makes to stimulate the uterus to contract.
Indications for instrumental delivery
Maternal factors: Prolonged 2nd stage of labour, maternal fatigue, maternal medical condition resulting in excessive cardiac strain, eclampsia
Fetal factors: Fetal distress reflected on CTG , Fetal malposition preventing progress in 2nd stage of labour, Breech babies, Cord prolapse
Both vacuum/ventouse and forceps methods are fairly successful, effective and safe, but they have their differences. Our choice will be influenced predominantly by the position the baby is in at time of delivery, maternal contractions, and wellbeing of baby which we
will monitor throughout
What to expect after assisted vaginal delivery
Heavier bleeding can be expected in assisted deliveries, especially in the day immediately after the delivery, this will settle down and
some light bleeding can be expected in subsequent days.
There is a chance that an episiotomy/cut has to be made so the instrument can fit nicely, there are also higher risks of vaginal tears
but these will be stitched immediately with dissolvable stitches.
More severe 3rd or 4th degree tears involving muscle and the wall of the anus or rectum respectively, can affect 4 in 100 people after
forceps birth and between 8-12 in 100 after forceps birth
Contraindications of vacuum/ventouse
Babies in OP (breech) position, Babies with IUGR, pre term
or at risk of haemophilia
Advantages and disadvantages of ventouse
Advantages: Less painful for mother, less maternal trauma, often fairly painless - can be done without pain relief. An episiotomy will
be made if it has to be
Disadvantages: Requires fair amount of maternal effort, if mother cannot push it can be very unsafe and result in a dangerous
subgaleal haematoma - a head injury that has severe repercussions
Disadvantages of forceps delivery
- Can be very painful for mother
Risk of damage to vagina and surrounding area - Usually requires an additional small cut to be made (episiotomy) to reduce the risk of damage to muscles that help to control urination
- Baby might have a forceps mark but that usually disappears in a day
- Baby has an extremely low risk of forceps laceration and very rarely, damage to nerves supplying the face and eye damage
Advantages of forceps delivery
Can be done regardless of gestational age, even for the pre term babies. Can be done on babies in breech (feet down) position. Does not require as much maternal effort in terms of pushing, compared to ventouse.
What are the requirements for assisted vaginal delivery
Fully dilated cervix (~10cm), known fetal vertex position, vertex station of at least 0, adequate analgesia, empty bladder, adequate contractions
Information giving in OSCES - BUCES with detail
B - Brief history
Take a brief history of the presenting complaint. This should be concise, especially in an
OSCE setting.
U - Understanding
Assess the patient’s baseline understanding. For example: “What’s your understanding of
what anaphylaxis is?’
C - Concerns
Ask the patient about their concerns. This can help tailor your approach to providing
information about their diagnosis.
E - Explanation
Provide an explanation of what the disease is. A good approach to this is:
● Explain normal anatomy/physiology
● Explain the disease and what causes/triggers it
● Explain common symptoms
● Explain complications
○ Don’t forget to safety net, and highlight any red flags that should prompt the
patient to seek medical attention
● Explain management options - non-pharmacological (e.g. anaphylaxis management
plan) and pharmacological
S - Summarise
Ensure the patient understands by summarising what you have told them, and
supplementing this with additional resources for reference (e.g. pamphlets). Make sure all
their questions have been answered!
4C’s of measles
○ Cough
○ Coryza
○ Conjunctivitis
○ C(K)oplik Spots (begins with a K but to make mnemonic work)
■ Pathognomonic of Measles; small white spots on inner buccal mucosa
MMR vaccine timing
12 and 18 months
Explain appendectomy
Appendicitis is inflammation or swelling of the
appendix, which is a little tube at the end of your intestines, it has a bit of bacteria in it and normally does no harm. But when the tube gets blocked, the bacteria multiply and lead to the swelling or inflammation.
● Appendectomy is the removal of the appendix when it becomes inflamed/swollen or it ruptures
○ It will most likely be done laparoscopically or
through keyhole, which means we’ll make three
small holes in your abdomen using a camera and tools to look inside your abdomen and take out the appendix.
○ If we cannot find the appendix or there are some issues, we may have to turn it into an open surgery, where we make a cut into the abdomen to see a bit better.
Benefits of appendectomy
Stop the appendix from rupturing and turning into an abscess or peritonitis.
● Laparoscopic operations have been seen to lead to shorter hospital stays and quicker recovery time.
Risks of appendectomy
● Bleeding
● Infection
● Perforation/damage to nearby organs
● May not get all the appendix, could potentially have
another episode
● Allergy to anaesthetics
● May need to convert to open surgery
Alternative treatment for appendicitis
Antibiotics - can be good in uncomplicated cases
o Leave the appendix in and put you on some
antibiotics instead. They can work in about 20-
30% of cases but only if they are uncomplicated
o Means that there is a risk that it can happen
again.
Preparation for appendectomy
On the day
o Need to fast from tonight, won’t be able to drink or eat
o Will need to stay in hospital post-op for at least 1-2 days to make sure there were no issues after the surgery, then you can go home.
● Are you happy to have this procedure?
What are the long term complications of abdominal surgery?
● Bowel obstruction
● Hernia
● Regional pain syndrome
Consent station mnemonic (NBARCO)
Nature - discussing what the patient has and what the surgery is and what it involves.
● Benefits - why using this method to manage them (e.g. surgery vs conservative management)
● Alternatives - what other options do they have (e.g. Antibiotics)
● Risks - what are the risks of the treatment
● Consequences - what will happen if the condition is not managed.
● On the day/opt out/other:
○ discuss what the patient may need to do on the day if coming into hospital or
discussing what will happen to the patient prior to the surgery if the patient is inpatient.
○ Letting them know they have the option to opt out if they wish to do so.
○ Anything that may be specific to the treatment.
What is a UGIB?
● Defined as bleeding from above the Ligament of Treitz (duodeno-jejunal flexure)
● Up to 50-150 pts per 100,000 population per year
● Mortality of 11-33%
S&S of UGIB to look for in Hx and exam
Hints on Hx/Ex
● Hx: Melena, haematemesis, iron deficiency anaemia, Hx liver disease/cirrhosis,
certain Mx (NSAIDs, anticoagulants), EtOH, H. Pylori/PUD
● Ex: Pallor, hypovolaemia and haemodynamic compromise, signs of chronic liver
disease (e.g. variceal bleeding)
Important DDx of UGIB
Important DDx
● Peptic ulcer disease
● Oesophagitis/gastritis/duodenitis
(severe)
● Oesophagogastric varices
● Portal hypertensive gastropathy
● Angiodysplasia
● Mallory-Weiss and Boerhaave
Risk stratification tool for UGIB
the Blatchford-Glasgow score
● If low risk (no risk factors) then can manage very conservatively
● If high risk, requires admission and prompt management
What to do with haemodynamically unstable UGIB
● This dictates the priority of management. Unstable bleeds MUST be stabilised
with resuscitative measures +/- massive transfusion protocols before any
formal investigation/management (oesophagogastroduodenoscopy/variceal
banding etc.)
Risks of blood tranfusions
Risks which you must inform patients of for consent
o Common/expected: Fever, mild rash/itching, feeling unwell
o SOB (due to over-transfusion)
o Haemolysis
o Transfusion reactions (mild to life threatening)
o Viral infection/other blood-borne disease from donor (very rare)
o Severe harm and death
Management of haemodynamically stable UGIB
Regular obs + reassessment; keep NBM + ?catheterise
● Recognise need for transfusion
o Bonus if able to quote criteria (Hb <70g/L
(90 if high risk), serious clinical
deterioration, 2L crystalloids w/ no
response)
● Consider IV PPI
o No octreotide, IV ABx, or terlipressin given
no sign of variceal bleed as the cause
● Erect AXR/CXR to determine if pneumoperitoneum
● Refer to gastro/gen surg for likely
diagnostic/therapeutic
oesophagogastroduodenoscopy
Contraindications to colonoscopy
A perforation is known or suspected
● Patient unable to tolerate sedationrespiratory/cardiac reasons
● pregnant
● Acute diverticulitis
● Fulminant colitis
Alternatives to colonoscopy
Barium enema, sigmoidoscopy, CT, pill cam
Risks of colonoscopy
Common risks: bleeding, infection, anaesthesia,
risks to damaging surrounding structures
● Specific risks:
- Abdominal discomfort
- Discomfort during bowel motion for a while
after procedure
- Perforation (rare)
- Allergic reaction to bowel preparation
● Risks of NOT undergoing procedure:
- Disease can be undetected and untreated -
disease progression
Details of colonoscopy procedure (before, during, after)
Before:
- Cease certain medications e.g. anticoagulants and oral iron 5-7 days prior to procedure
- Clear fluids and low fibre diet at least 1 day prior
- Bowel prep 1 day prior- will need to go toilet often (ensure have access)
- Need to be fasted 4-8 hours before the procedure
During:
- Day procedure- the colonoscopy itself takes 20-30 minutes
- Will be under sedation (asleep) throughout the
procedure
- What are we looking for:
● Signs of inflammation, ulcers, polyps,
lumps, any active bleeding
- Tissue samples can be taken for further laboratory investigations or ‘ abnormal lumps’ can be removed
After:
- Able to go home few hours after as sedative effects wear off
- Driving is not recommended (for 24 hrs)- have
someone to pick up
Differential diagnoses of oesophageal dysphagia
Oesophageal dysphagia is associated with a sensation of food arresting after swallowing. It
is important to distinguish if this is associated with solids only, or both liquids and solids.
● If affecting both, this can indicate a motility disorder, e.g. achalasia, connective tissue
disorder
● If only affecting solids, this suggests an anatomical obstruction, e.g. strictures,
malignancy
What is oropharyngeal dysphagia and what causes it?
Oropharyngeal dysphagia occurs at the oral and pharyngeal phase. It is associated with
difficulty initiating a swallow, affects both liquids and solids and is accompanied by choking,
coughing and regurgitation. Causes include:
● Neuromuscular disorders (e.g. stroke, CNS tumours, Parkinson’s, Alzheimer’s,
Myasthenia Gravis)
● Anatomical causes (e.g. compression from tumour or thyroid mass, Zenker
diverticulum)
Hepatic/cholestatic/RUQ investigations and reasonings
Bedside Investigations
* Urine dipstick – expect elevated urinary bilirubin due to jaundice. Will be able to decrease likelihood of UTI/renal causes of the abdominal pain if the dipstick results are negative for presence of protein, nitrites and blood.
* ECG – to rule out cardiac causes due to CV RFs and sudden onset. May have tachycardia given febrile and unwell
Bloods:
* FBE – may have elevated WBC count due to
infection, low platelets.
* LFT – if patient has a gallbladder-related pathologycausing their RUQ, ALP and GGT may be elevated. For hepatitis, expect AST and ALT to be significantly elevated (in the 1000s) with ALP being mildly elevated and GGT being normal. Bilirubin levels are also expected to be elevated in a patient with jaundice. The patient may have low albumin due to impaired synthetic function of the liver, however this would be associated with fulminant hepatitis (acute liver failure) or chronic liver disease, which is not consistent with this presentation.
* Coagulation profile – may see prolonged INR due to impaired clotting factor production, however this would be associated with fulminant hepatitis (acute liver failure) or chronic liver disease, which is
not consistent with this presentation.
* CRP – may be elevated if there is an infection
causing the abdominal pain.
* Hepatitis serology (see question below for details)
* Lipase – lipase less than 3x upper limit of normal help rule out acute pancreatitis as a cause of the abdominal pain.
* Ca, Phosphate, Magnesium – if have elevated
calcium and phosphate levels this may suggest
presence of kidney stones or renal pathologies.
Imaging for ?liver/gallbladder/RUQ presentation
Abdominal ultrasound – observe for hepatomegaly and dilation of hepatic vessels. In hepatitis, it is expected to see coarsened hepatic echogenicity and hepatomegaly.
* Hepatic doppler ultrasound – used to assess
patency of the hepatic vasculature and blood flow through the portal system.
* Biliary tract ultrasound – observe for any stones, masses, thickening of the gallbladder wall or dilation of the bile ducts which may indicate the presence of gallstones as the cause of the RUQ pain.
* Chest x ray – may show consolidation due to
pneumonia which may be causing RUQ pain if the pneumonia is affecting the lower lobe of the right lung. Will demonstrate if there is air under diaphragm which may suggest a perforated viscus, but this is unlikely to cause localised RUQ pain. In hepatitis, the chest x ray findings are expected to be normal.
* CT abdomen – expect to see fatty strands and
oedema around the liver, hepatomegaly,
lymphadenopathy.
4 stages of acute viral hepatitis
- Incubation period: The virus multiplies and spreads without causing symptoms (see
table).
● Prodromal (pre-icteric) phase: Nonspecific symptoms occur; they include profound
anorexia, malaise, nausea and vomiting, a newly developed distaste for cigarettes (in
smokers), and often fever or right upper quadrant abdominal pain. Urticaria and
arthralgias occasionally occur, especially in HBV infection.
● Icteric phase: After 3 to 10 days, the urine darkens, followed by jaundice. Systemic
symptoms often regress, and patients feel better despite worsening jaundice. The
liver is usually enlarged and tender, but the edge of the liver remains soft and
smooth. Mild splenomegaly occurs in 15 to 20% of patients. Jaundice usually peaks
within 1 to 2 weeks.
● Recovery phase: During this 2- to 4-week period, jaundice fades.
‘SPIDER’ acronym for DKA mgmt
‘SPIDER’ acronym:
1. Saline IV (rehydrate!)
a. initial bolus (N/Saline 10mL/kg) →
maintenance (N/Saline + potassium)
b. do this before insulin, as insulin causes
glucose to re-enter cells → brings water (i.e.
will dehydrate further)
2. Potassium infusion once <5 until normal lab values
are reached and glucose <10
a. insulin stimulates Na/K ATPase (K+ into
cells) → risk hypokalaemia, even if patient
is ‘hyperkalemic’
3. Insulin (SA) → when BSL <15, add 5% dextrose
a. slow insulin infusion until acidosis resolved,
if too quick you risk cerebral oedema from
high CSF/low plasma glucose
4. Eat nothing (NBM)
5. Reason (find the underlying cause)
a. in this case most likely due to
noncompliance; in the long-term, discussion
with Sasha should be arranged re: risks of
insulin non-compliance, current concerns
with body image/friend groups, EtOH as
precipitate for DKA etc.
HEEADSSS screenting tool - best completed with adolescent pt alone
Home
Education and employment
Eating and exercise
Activities
Drugs and alcohol
Sexuality and gender
Suicide, depression and self harm
Safety
Approach to vomiting in a child
It’s a UTI until proven otherwise - always do a dipstick!
● Severity is often best assessed by asking for symptoms of dehydration (e.g. number
of wet nappies)
● Progressive non-bilious projectile vomits in an infant (especially 4-6 weeks old) are a
sign of hypertrophic pyloric stenosis (HPS), which requires surgery
● DKA is the first presentation of T1DM in only 10-20% of cases
● Diarrhoea is practically part of the definition of gastroenteritis – it’s highly unlikely to
be this if the child is only vomiting (unless it’s early on in the disease course)
Metabolic acidosis causes - high (more common - LTKR) and normal anion gap
i. high gap (HAGMA) is more common: ‘Left Total Knee Replacement’
(Lactate, Toxins, Ketones, Renal)
ii. normal gap (NAGMA) e.g. diarrhoea, renal tubular acidosis, N/Saline
Risk factors for haemorrhoids
● Age
● Diet
● History of chronic constipation
● Obesity
● Pregnancy
● Portal hypertension – for internal haemorrhoids
Investigations for elderly pt with acute confusion
Bedside tests:
● ECG (arrhythmia, MI)
● Capillary BGL (hypoglycaemia)
● Urine dipstick & MCS
Biochemistry:
● Complete blood examination
○ WCC (infection)
○ Hb (IDA)
● Electrolyte, urea, creatinine
○ Electrolyte disturbances → hyponatraemia as a
particularly common cause of delirium
○ Urea elevated in isolation → bleed
● Liver function tests
● Thyroid Function Tests, Thiamine, Vitamin B12, Folate
● Urine MC&S and urinalysis (UTI)
● Bladder scan if urinary retention present
● Others: Blood cultures and urine toxicology & drug
screen and blood alcohol level (BAL)
Imaging
● CXR (pneumonia)
● CT Brain
○ Rule out intracranial pathology
○ Have to include for dementia screening for
diagnosis, delirium +/- consult consultant
Other non routine investigations for consideration
● Lumbar puncture (only if suspecting meningitis)
● EEG (only if seizure suspected)
Acute management of delirium - non-pharmacological
- Behavioral charts - to record antecedents, behavioural aspects, consequences
- All about me tool - to understand tools that bring patients a sense of comfort + assist with behavioural deescalation
- Alcohol withdrawal scale - for people with a strong history of binge drinking
- Charts - fluid balance, bowel, bladder
- Pain scores
- Environmental sensitization - give patient visual and hearing aids, re-orientation with calendars and clocks, provide 1 to 1 nursing, ensure patient is in a well lit and
well ventilated quiet environment - Frequent communication + reassurance of patients; provide electronics for patients to video call family
Manage precipitating factors
Ensure good hydration, adequate pain relief, bowels open and patient not in a state of faecal retention or urinary retention (bladder scan if necessary)
Pharmacological management of acute delirium
Haloperidol or lorazepam (patients with no sedation)
Risperidone (patients already on sedative)
Psychosis in the context of delirium (antipsychotics +/- benzodiazepines)
Important medications to think of in acute delirium
○ Anti-hypertensives
○ Anti-psychotics
○ Antidepressants
○ Medications with high anticholinergic burden- even if not directly anticholinergics
Aspects of falls history taking
Mechanism of injury
- Positioning
- Timing of injury, duration
- Witnesses of fall
- Presence of headstrike, loss of consciousness
- Loss of function and motion, ability to weight bear
- Previous functional level
- Past history of fractures
- Stiffness, swelling, pain level, tenderness
Risk factors for hip fracture
Osteoporosis/osteopenia
o Low hip BMD weakens proximal femur and increases hip fracture risk
- Older age
- Malignancy
o Pathological fractures caused by metastatic cancer to the bone, primary
bone tumour
- Female sex
- Falls
o Balance issues, muscle weakness, visual impairment, cognitive impairment,
depression, functional decline
- High energy trauma in younger patients
- Medications
o Drugs increasing fracture risk
§ Levothyroxine: Decrease bone density
§ Loop diuretics: Impairs renal calcium absorption
§ PPI: Reduce calcium absorption
§ Corticosteroids: Long term use can cause osteoporosis
§ Long term bisphosphonates: Can cause atypical hip fractures
o Drugs increasing falls risk
§ Antidepressants, sedatives: Increase falls risk due to sedation
§ Antihypertensives: Increase falls risk due to postural hypotension
and dizziness
§ Opioid analgesics: increase falls risk due to sedation
- Alcohol consumption
Blood supply to femoral head
External iliac artery → common femoral artery → profunda femoris artery →
medial + lateral circumflex femoral artery → retinacular arteries
o Medial circumflex femoral artery provides major blood supply for the
femoral neck
- Retrograde blood supply similar to the scaphoid
- Intracapsular NOF fracture disrupts blood supply of retinacular arteries and can
lead to AVN
Explanation, benefits and risk of CT + contrast
Explains that it is a form of imaging that uses ionising radiation, just like simple X-rays, but in greater doses, the risk of which is minimal as described
Explains the indication of a CT scan for the patient’s case, that it would help in confirming their diagnosis, ruling out other possible differentials, identifying the aetiology, and assessing the complications
Describes both benefits and risks of CT scan, and that the benefits outweigh the risks. Benefits include added confirmation, a clue to aetiology, and ruling out of complications or further masked conditions. Risk is minimal in the form of radiation exposure that is not a concern outside pregnancy or prior radiation-induced problems.
Explains that contrast-enhanced CT scan uses a dye similar to any other medication and will be injected both intravenously and consumed orally prior to the scan
Touches on some contraindications for dye administration such as prior allergic reactions or current medication use
Describes the need for necessary laboratory investigations prior to the scan, especially for evaluation of renal function
Investigations for neonatal jaundice <24hrs
FBE, reticulocyte count, blood film, neonatal blood group, bilirubin, coombs test and G6PD screening
‘A thorough examination is essential to assess the baby’s general wellbeing and detect birth trauma or ongoing haemorrhage. Investigations include FBE, film and reticulocytes, neonatal blood group, direct antiglobulin test (Coombs), and possibly G6PD screening. Septic workup is appropriate if neonatal sepsis is suspected.’
Causes of pathological neonatal jaundice
Early onset jaundice (<24 hours) is pathological, with causes such as sepsis or haemolysis, including isoimmunisation (ABO or Rhesus D alloantibodies), RBC enzyme defects (G6PD, hereditary spherocytosis, alpha thalassemia), haemorrhage (cerebral, intra-abdominal), and blood extravasation (bruising/birth trauma).
Causes of physiological neonatal jaundice
Physiological jaundice results from excessive bilirubin formation, with the neonatal liver unable to clear bilirubin rapidly. In normal term babies, unconjugated hyperbilirubinaemia usually appears between 24-72 hours, peaks on the 4th-5th day, and disappears after 14 days. No further investigations are needed unless red flags suggest other causes.
What does a rise in conjugated bilirubin indicate?
Conjugated bilirubin at any age point raises suspicion of neonatal hepatitis, extrahepatic obstruction (e.g., biliary atresia, choledochal cyst), and metabolic diseases.
Management of neonatal jaundice
Phototherapy is initiated when total serum bilirubin (TSB) reaches the phototherapy threshold, with lower thresholds for preterm and low birth weight babies.
Regular monitoring for vital signs, including temperature, hydration status, and urine output, is crucial.
Phototherapy is ceased when serum bilirubin is below the conventional phototherapy level.
Exchange transfusion is considered when TSB reaches the exchange transfusion threshold.
Menoupause/perimenopause symptoms
Vasomotor/General physical symptoms - recognises hot flushes, headaches, muscles/joints pain, formication, sleep disturbances as common symptoms in menopause Critical
Urogenital symptoms - assesses dyspareunia and vaginal dryness, postcoital bleed and urinary frequency as part of the genitourinary syndrome of menopause (GSM) Critical
Psychological symptoms - asks about depressive/anxiety symptoms, sleep disturbances, decreased concentration and memory
Differential diagnoses of menopause
Hyperthyroidism - recognises that irregular menses, heat intolerance, and mood changes are potential clinical manifestations of hyperthyroidism. Differentiating features can include increased bowel movements, tremors, appetite and weight changes. Critical
Hypothyroidism - recognises that irregular menses and mood changes are potential clinical manifestations of hypothyroidism. Differentiating features can include decreased bowel movements, heat intolerance, appetite and weight changes. Critical
Hyperprolactinemia - differentiating features can include increased lactation.
Endometrial carcinoma - recognises irregular/heavy/ prolonged bleeding is a common finding in endometrial carcinoma, although most endometrial cancers occur in patients >55 years of age. May be accompanied by constitutional symptoms of malignancy. Critical
Sexually-transmitted infections/Pelvic inflammatory disease - recognises abnormal uterine bleeding and dyspareunia as possible manifestations in STI/PID. Differentiating features can include pelvic pain and abnormal vaginal discharge. Critical
Pregnancy - Amenorrhoea with breast tenderness, fatigue, nausea, and an enlarging abdomen may indicate pregnancy.
Contraindications to HRT
Cardiovascular, liver or thromboembolic disease may represent a relative or absolute contraindications to MHT
Patients with hysterectomy can be put on menopausal hormonal therapy (MHT) with oestrogen therapy alone whereas patients with an intact uterus require oestrogen/progesterone therapy.
Explanation of menopause and perimenopause
Menopause usually happens between age 45 and 55 years, when the ovaries stop producing eggs (ovulating) and menstrual periods end. A woman is said to have completed menopause once she has gone a full year without having a period.
Perimenopause is the time when your periods start to change (usually becoming less frequent). This phase lasts an average of four years and ends when you have your final period.
The average age for a woman to stop having periods is 51 years. After menopause, a woman can no longer get pregnant.
Menopause occurs because the ovaries run out of eggs. During this time, many women also start to have menopausal symptoms. These result from declining levels of oestrogen in the body and can include hot flashes, night sweats, mood changes, sleep problems, and vaginal dryness.
Common screening tests for menopause
Consider the following test to exclude common causes of fatigue, mood change, hotness: TSH (thyroid disease), FBC and iron stores (iron deficiency)
Pharmacological treatment options for menopause
Consider menopausal hormonal therapy (MHT) for the relief of troublesome vasomotor symptoms (VMS). In this case, she requires a combination of oestrogen and progesterone replacement since she still has an intact uterus. Cyclical MHT should be used. Critical
In addition to relieving hot flashes, MHT may help with other symptoms of menopause as well, including vaginal dryness, depression, and other mood problems.
If patient does not prefer hormonal options, alternatives include SSRI and SNRI
To manage localised urogenital symptoms, the patient can consider vaginal oestrogen therapy (ring/cream) or moisturisers/lubricants
Investigations for RA
Bloods:
A Full Blood Examination (FBE): is a standard investigation for most conditions. In rheumatoid arthritis, it may show anemia of chronic disease.
ESR and CRP: non-specific markers of inflammation that are commonly elevated in RA patients. Therefore, they are useful in monitoring disease activity and response to treatment.
Rheumatoid Factor: is an antibody that is present in the serum of approximately 70-80% of RA patients. It is not specific to RA and may also be elevated in other autoimmune diseases and infections, but it is used in the criteria for diagnosing rheumatoid arthritis.
Anti-CCP antibodies: are more specific to RA than RF and can be detected in up to 60-80% of RA patients. Therefore, they are a more reliable marker for the diagnosis of RA.
What is HLA-B27 and what is it associated with
HLA-B27 is a genetic marker that is associated with the seronegative spondyloarthropathies: ankylosing spondylitis, psoriatic arthritis, reactive arthritis and enteropathic arthritis. It is not associated with RA.
Characteristic findings of RA on Xray
Joint space narrowing
periarticular erosions
bony deformities
First line agent for RA mgmt and how does it work
Methotrexate is considered the gold standard Disease-Modifying Anti-Rheumatic Drug (DMARD) for RA and is typically the first-line agent used in most patients.
It has been shown to effectively reduce inflammation and joint damage in RA and is usually well-tolerated.
Folic acid is routinely co-prescribed with methotrexate to reduce the risk of side effects.
What tests should be ordered before starting methotrexate?
FBE, EUC, LFT, Hep B and C serology, HIV serology, CXR
Methotrexate can be hepatotoxic and is an immunosuppressive agent. It is therefore important to ascertain any baseline liver derangements and chronic infections.
An FBE assesses for any cytopaenias before initiation to ensure that the patient has no underlying hematological disorders that may be exacerbated by methotrexate.
Methotrexate is renally cleared and may be contraindicated, require dose adjustment or additional monitoring in patients with renal impairment.
Metrotrexate can cause hepatotoxicity, thus it is necessary to measure liver function before starting the treatment, as well as after treatment is initiated.
Methotrexate is an immunosuppressive agent; consequently, it is important to be aware of any chronic underlying infections. If escalation of immunosuppression is considered in future, treatment of latent infection or prophylaxis may be required. It is thus necessary to perform serology for both hepatitis B and C, and HIV prior to commencement, as well as chest X-ray to assess for latent tuberculosis.
Common side effect of methotrexate and what to do if it occurs
The most common side effect of methotrexate is nausea. One option to address this is to switch to injectable methotrexate which is typically associated with fewer gastrointestinal side effects
Time before methotrexate reaches its full efficacy?
Methotrexate does not work immediately and it can be 3 months before it reaches full efficacy
What to do if methotrexate not providing adequate response for RA?
Can increase dose
Try another DMARD
Commence another DMAR (leflunomide) with methotrexate
Typical presentation pneumonia
Pneumonia is associated with dyspnoea that progresses over days rather than years. It may also be associated with a productive cough, fever and focal lung findings on examination. The dyspnoea returns to baseline with resolution of the infection.
Typical presentation pulmonary fibrosis
Pulmonary fibrosis can present in a very similar way to COPD but may not be associated with a significant smoking history and may include exposure to environmental toxins such as asbestos or beryllium (historically used in fluorescent light manufacture and aerospace production).
Typical presentation COPD
Clinically, it is characterised by progressive dyspnoea and loss of exercise tolerance. It is often associated with a cough, which may be productive, and intermittent respiratory tract infections that can trigger acute exacerbations. A significant smoking history is vitally important in making the diagnosis.
Typical presentation Bronchiectasis and chronic bronchitis
Bronchiectasis and chronic bronchitis are both associated with chronic infections and may be difficult to differentiate from COPD initially. Again, the key point is a significant smoking history. However, be aware there is significant overlap, with 50% of people with chronic bronchitis having COPD.
Reversibility definition for asthma vs COPD
Administering a short acting bronchodilator, such as salbutamol, waiting 15 minutes and then repeating the test.
Asthmatic patients should demonstrate an increase above pre-bronchodilator baseline in FEV1 and/or FVC of at least 12% and 200mL.
If reversibility is less than this, COPD is suggested.
Non-pharmacological Rx of COPD - improving prognosis
Smoking cessation
Pulmonary rehabilitation programs - usually 6-8 week programs - manage breathlessness and improve wellbeing
Influenza, pneumococcal, COVID and RSV vaccinations
Physical activity - aerobic and resistance
Pharmacological treatment of stable COPD
COPD patients can be classed into GOLD A,B,C and D according to number of exacerbations/hospitalisations in the past year as well as severity of symptoms according to the modified Medical Research Council (mMRC) scale.
GOLD A - short acting bronchodilators - The two main types are short-acting beta-2 agonists (salbutamol) and short acting anti-cholinergics (ipratropium bromide). These can be inhaled and are ‘reliever’ therapies.
GOLD B - long-acting bronchodilators can be used. These include long acting beta-2 agonists (LABA) such as eformeterol and salmeterol. They also include long acting anti-cholinergics such as tiotropium bromide. Again, these therapies are inhaled and have been shown to improve quality of life in comparison to short-acting bronchodilators. This is the key area of difference with asthma, where long acting bronchodilators are introduced AFTER inhaled corticosteroids and LABA therapy is NEVER indicated without the use of inhaled corticosteroids.
GOLD C - LAMA monotherapy is initiated.
GOLD D - dual therapy with LAMA/LABA is the mainstay of treatment. Inhaled corticosteroids can be added. They are indicated in patients with an eosinophil count of >300cells/μL and those suffering 2 or more exacerbations requiring systemic corticosteroids and antibiotics in a 12 month period. They aim to reduce the number of exacerbations and improve quality of life by controlling dyspnoeic symptoms. Combinations of long acting bronchodilators and inhaled corticosteroids are available to help improve compliance.
Other pharmacological treatment for COPD
Systemic corticosteroids and antibiotics are indicated in the treatment of acute exacerbations of COPD.
Theophylline is an end-stage therapy in patients who can’t tolerate inhaled therapies or have otherwise uncontrollable symptoms. It’s rarely used today.
Mucolytic therapy may be used to improve symptoms and reduce the frequency of exacerbations in patients with a chronic productive cough.
Home oxygen is used as a last-line treatment for symptom control.
Explanation of COPD
COPD causes non-reversible airway destruction and is predominantly caused by long term tobacco use.
Hallmark symptoms include progressive dyspnoea and reduced exercise tolerance.
COPD can be diagnosed based on a clinical history of progressive dyspnoea in the context of long term tobacco smoking and demonstrated on chest X-ray and with the use of pulmonary function tests.
The primary intervention is smoking cessation, no pharmacological treatment can alter the disease course as much as this can.
Explanation of post-streptococcal glomerulonephritis
Acute Post-streptococcal Glomerulonephritis (APSGN) is a classic example of acute nephritic syndrome marked by sudden onset of gross haematuria, oedema, hypertension, and renal insufficiency.
It ranks among the most common causes of gross haematuria in children due to Group A Streptococcal infections, typically resolving completely in over 95% of cases with rare recurrences.
Mortality in the acute phase can be prevented by effectively managing acute renal failure, cardiac failure, and hypertension.
Investigations for suspected nepritic syndrome
Urinalysis
Complement levels (C3 and 4)
Anti streptolysin O Titre (ASOT)
EUC
Urinalysis: In APSGN, there will be the presence of RBCs, RBC casts, proteinuria, and some polymorphonuclear leukocytes.
C3 & C4 levels: Serum C3 level is significantly reduced in over 90% of patients during the acute phase and returns to normal within 6-8 weeks. The C4 level will be normal. If both levels are low, an alternate diagnosis needs to be considered.
Anti Streptolysin O Titre (ASOT): A raised titre establishes recent exposure to streptococcus, which helps to confirm the diagnosis. It is important to note that ASOT is rarely raised after streptococcal skin infections. A positive throat culture report might support the diagnosis or might simply represent the carrier state.
Renal function tests: In acute glomerulonephritis, acute renal failure is a recognised complication. Hence, it is necessary to perform a renal function test to assess a child with decreased urine output.
Not indicated: renal US (may show slight kidney enlargement)
Differential between nephotic and nephritic syndrome in child
Nephrotic syndrome (NS): In uncomplicated idiopathic NS, it is rare for a child to present with haematuria or hypertension.
Common cause of respiratory distress/ increased RR in PSGN
Acute Pulmonary Oedema:
This is a common cause of respiratory distress in APSGN patients. Due to hypertension and hypervolaemia, cardiac failure can develop, leading to pulmonary oedema. The patient may also show signs like orthopnoea and cough. Pulmonary oedema results in tachypnoea as the body attempts to compensate for reduced oxygenation and increased fluid in the lungs.
Metabolic Acidosis:
APSGN can cause acute renal failure, which may lead to metabolic acidosis due to impaired excretion of hydrogen ions. The respiratory system compensates by increasing the respiratory rate to expel CO2 and maintain acid-base homeostasis. This mechanism results in tachypnoea as a compensatory response.
Presentation of influenza
Influenza is suggested by myalgia, lethargy and tiredness, with a bad cough, fever and nasal congestion. It has a faster onset and more severe course. The common cold has nasal stuffiness and a cough commonly, and in children may also have fevers. It has a slightly slower onset and is less severe in nature.
Complications of URTI
acute rhinosinusitis, bronchitis, pneumonia, asthma exacerbation, and acute otitis media.
Management of common cold
Analgesics (paracetamol/NSAIDs), nasal decongestant + anti-histamine and zinc lozenges all at least have some partial evidence for effectiveness. Cough suppressants, antibiotics, anti-virals and vitamin C all have little to no evidence for the standard cold/flu that is non-severe and non-complicated.
Spread of common cold
Mostly hand contact
Presentation of intussusception
The classic triad of symptoms includes colicky abdominal pain, vomiting, and “currant jelly” stool, which is indicative of gastrointestinal bleeding.
However, not all patients present with this triad, and symptoms may be nonspecific, such as irritability, lethargy, or inconsolable crying.
In some cases, intussusception may lead to bowel obstruction, causing abdominal distension, palpable mass, and signs of peritonitis if perforation occurs.
Age ranges for intussusception
Intussusception primarily affects infants and young children, typically between the ages of 3 months and 3 years.
Risk factors for intussusception
While often idiopathic, several predisposing factors have been identified.
These include viral infections, such as adenovirus or rotavirus, which can lead to lymphoid hyperplasia in the intestine, serving as a lead point for intussusception.
Additionally, structural abnormalities in the intestine, such as Meckel’s diverticulum or polyps, may predispose individuals to intussusception.
Certain medical conditions, such as cystic fibrosis or Henoch-Schönlein purpura, have also been associated with an increased risk of intussusception.
Imaging for suspected intussusception
Abdominal ultrasound is the preferred initial diagnostic modality due to its high sensitivity and specificity in detecting intussusception. Ultrasonographic findings may include the classic “target sign” or “doughnut sign,” indicating the presence of the telescoped bowel segments.
Treatment for intussusception
In cases where ultrasound findings are inconclusive or unavailable, contrast enema can be performed both diagnostically and therapeutically.
Contrast enema not only confirms the diagnosis but also allows for non-operative reduction of the intussuscepted bowel under fluoroscopic guidance. Currently either air enema or saline enema is commonly used for nonoperative reduction.
In enema reduction, air or liquid contrast material is injected into the rectum under controlled pressure and reduction of the telescoped bowel segment is observed by imaging. Success rates for non-operative reduction range from 70% to 90%.
Minimally invasive surgical techniques, such as laparoscopic or laparoscopic-assisted procedures, have become increasingly utilized, offering advantages such as shorter hospital stay and faster recovery time.
Iron tablets ATHLETIC
A: Replace your body’s store of iron, a mineral required to make RBCs
T: 1-3 times daily tablet or syrup or infusion once
H: Infusion, oral tablet
L: Takes 3-4 weeks for Hb to normalise, then further 3 months to normalise iron stores (oral)
E:
T: Hb in 1 month to assess response
I: GI irritation, abdominal pain, black/green stools, metallic tast
C: None
Investigation for suspected aortic dissection
A CT angiogram (CTA) is the gold standard diagnostic investigation for aortic dissection. It provides high yield information, is reliable, widely available and is relatively efficient.
A chest X-ray is a reasonable investigation to consider. It is commonly done during initial work up to assist with differentiating causes of chest pain. The most common finding suggestive of aortic dissection is widening of the aortic silhouette (Image). However a chest X-ray is insufficient in providing definitive diagnosis of aortic dissection and provides little to no information regarding further management planning.
An echocardiogram is a reasonable investigation to consider. A transoesophageal echocardiogram (TOE) can be used for confirming the diagnosis of aortic dissection. However, a CTA is considered the superior investigation and is more readily accessible. A transthoracic echocardiogram (TTE) can be considered but is less reliable.
Type of shock following aortic dissection - tachycardic, hypotensive and SpO2 94%RA, distended neck veins, muffled heart sounds, bibasal crepitations
This is the picture of obstructive shock (cardiac tamponade). Although Mr Lim is likely bleeding (given the clinical picture and haemoglobin drop) and there may be some hypovolaemic element to his presentation, this clinical picture could not be explained by hypovolaemic shock alone, and the examination findings do not support it.
The presentation of Beck’s triad: hypotension, muffled heart sounds and distended neck veins is highly suggestive of acute cardiac tamponade. In addition, Mr Lim’s telemetry via arterial line shows pulsus paradoxus, which is commonly associated with cardiac tamponade, especially in the post-operative setting.
What is pulsus paradoxus?
Pulsus paradoxus is a phenomenon where a patient’s blood pressure falls by at least 10mmHg during normal inspiration.
What is the management of cardiac tamponade?
Surgical intervention (surgical drainage) is preferred in severe haemodynamic compromise, the history of recent aortic dissection and surgical repair and the need for direct visualisation of the pericardium and aorta to stop further bleeding and to insert new drains
Although pericardiocentesis is an effective option for managing tamponade, it is not preferred in this scenario due to reasons outlined above.
Management of pleural effusion
Chest drain
Breast cancer typical presentation
Breast cancer typically presents as a painless lump in the breast of a post-menopausal woman.
Most commonly lump in Upper outer quadrant
May also see dimpling of skin, nipple retraction
Initial investigation of suspected breast cancer
U/S of axilla: The axilla is clinically negative (no palpable lymphadenopathy), however radiological assessment of the lymph nodes is also required. If any appear suspicious, this should be FNA’d (only confirmation of malignant cells in abnormal lymph node is required)
U/S affected breast: Ultrasound imaging of the affected breast can give more information regarding the offending lump, as well as assess the rest of the breast for other, non-symptomatic lesion
Bilateral Mammography – Imaging of both breasts is paramount; mammogram to assess the breast with the lesion but also to assess the non-affected side in case of any suspicious, asmptomatic findings there.
Core biopsy: Core biopsy is the main pathological investigation for a suspected breast cancer. It can confirm the presence of non-invasive or invasive malignancy, as well as give additional information regarding type/subtype, grade, hormone and HER2 receptor status and proliferative index.
If not suspiscous for malignancy:
Fine needle aspiration – Fine needle aspiration can be used to investigate breast lumps, however is not the best for a solid lump. It is often used for cystic lesions. If a breast cancer is FNA’d, it will still need core biopsy for further diagnostic imaging and therefore core would be the preferred initial biopsy methody.
Prognosis for small-moderate sized localised breast cancer, hormone positive
Greater than 80%
Septic screen
“Septic screen” often consists of chest x-ray, cultures of blood, urine, and other specimens as directed by history and physical examination.
Which pathogens for pneumonia should be considered in immunocompromised patients?
In addition to common pathogens, opportunistic infections, such as Cryptococcus spp, Pneumocystis jirovecii should be considered in immunocompromised patients with pneumonia.
Treatment for cryptococcal infections
Amphotericin B, in combination with flucytosine, is the recommended induction treatment for cryptococcal pneumonia in immunocompromised patients
Amphotericin B is associated with adverse effects including electrolyte disturbances, infusion reactions, and nephrotoxicity.
When are fine inspiratory crackles heard typically?
Fine inspiratory crackles is typically heard in pulmonary fibrosis. In contrast, coarse inspiratory crackles are heard in congestive cardiac failure or pneumonia.
Typical bacteria causing CAP? SHEPS KM
Streptococcus pneumoniae
Haemophilus influenzae
Escherichia coli
Pseudomonas aeruginosa
Staphylococcus aureus
Klebsiella pneumoniae
Moraxella catarrhalis
Atypical bacteria causing CAP? MLC
Mycoplasma pneumoniae
Legionella pneumophila
Chlamydia pneumoniae
Viral causes of CAP? IRP
Influenza
Respiratory syncytial virus
Parainfluenza
Does Interferon-gamma release assay test for latent or active TB?
Interferon-gamma release assays (e.g., Quantiferon-tuberculosis) are used to diagnosed latent rather than active tuberculosis (TB) infection.
Timelines for PCI and thrombolysis for MI
In cases where a PCI facility is not available or if the hospital with a PCI facility is more than 120 minutes, thrombolytic therapy should be started immediately. If PCI is available, it should be the immediate management option (performed within 90 minutes). If the patient’s symptoms do not resolve after thrombolytic therapy, the patient should be referred to a hospital with PCI capability.
Long term therapy after MI
Long-term management of a myocardial infarction includes dual anti-platelet therapy, cardiac rehabilitation, statin, and consideration of prescribing a beta-blocker and/or ACE inhibitor, and MRA (spironolactone)
As per existing guidelines, dual-antiplatelet therapy in the form of aspirin and clopidogrel should be prescribed as part of long-term management post-MI unless it cannot be tolerated.
All patients are recommended to undergo cardiac rehabilitation after a MI to help to prevent secondary complications.
Statins (that is HMG-CoA reductase inhibitors) are indicated for patients as well, unless contraindicated.
Patients with evidence of heart failure, diabetes, existing hypertension, anterior infarct, or left ventricular systolic dysfunction are recommended ACE inhibitors such as perindorpil, or ARBs.
Beta-blockers such as metroprolol are also recommended for all patients who have signs of reduced left ventricular systolic function, measured by a LVEF of less than 40%.
Spironolactone should be added as the patient has severely reduced LV function. This is mineralocorcpid receptor antagonist and will help with cardiac remodelling and provide. survival benefit
When to refer for PCI after thrombolysis for MI
Referring the patient for percutaneous intervention (rescue PCI) is the next step when a patient fails thrombolysis. This occurs when the patient’s symptoms are persisting or there is evidence of < 50% ST-segment resolution (ST segments remain elevated).
Non-pharmacological management for GORD
Losing weight (if overweight)
Avoiding chocolate, citrus drinks, tomato-based foodstuffs, coffee
Having small frequent meals
Avoiding food within three hours of bedtime
Elevating the head of the bed
Use of an acid-suppressing medication.
Pharmacologic management of GORD
A proton pump inhibitor (eg, pantoprazole, esomeprazole) could be considered, only following life style advice.
An H2-receptor antagonist (such as ranitidine) would also be considered, along with PRN usage of an antacid.
Red flag symptoms indicating need for upper GI endoscopy (e.g. in a presentation of suspected GORD)
Unintentional weight loss
Vomiting blood
Dysphagia
Symptoms of anaemia
Age over 45 with long-standing reflux symptoms
Recent onset of reflux symptoms in an elderly patient
Obesity with weekly reflux symptoms
Wheezing or a cough.
CHA2DS2 Vas score - details, indication and interpretation
Calculates stroke risk for patients with atrial fibrillation
CHF history (+1)
HTN (+1)
Age (65-74 +1, 75+ +2)
Diabetes (+1)
Sex (female +1)
Stroke/TIA/Thromboembolism history (+2)
Vascular disease Hx (prior MI, PAD, aortic plaque) (+1)
Interpretation:
0 for men or 1 for women = low risk, may not require anticoagulation
1 for men, 2 for women = low-moderate risk, consider anticoagulation
2 or more for men, 3 or more for women = moderate-high risk, anticoagulation candidate
HAS-BLED score - details, indication and interpretation
Estimates risk of major bleeding for patients on anticoagulation to assess risk-benefit in atrial fibrillation care.
HTN (+1)
Age (>65 +1)
Stroke hx (+1)
Bleeding - major or predisposed (+1)
Labile INR (+1)
Ethanol use (>8 drinks/wk +1)
Disease: Liver (+1), renal (+1)
Medications (aspirin, clopidogrel, NSAIDs +1)
0: anticoagulation should be considered
1: Anticoagulation should be considered: Patient has a relatively low risk for major bleeding (~1/100 patient-years).
2: Anticoagulation can be considered, however patient does have moderate risk for major bleeding (~2/100 patient-years).
3+: Alternatives to anticoagulation should be considered: Patient is at high risk for major bleeding.
Typical causes of exudative effusion
Amyloidosis
Chylothorax
Constrictive pericarditis
Malignancy
Pulmonary embolism
Sarcoidosis
Trapped lung
Sensitivity and specificity defn
Sensitivity refers to a test’s ability to designate an individual with disease as positive. A highly sensitive test means that there are few false negative results, and thus fewer cases of disease are missed.
The specificity of a test is its ability to designate an individual who does not have a disease as negative.
Explain atrial fibrillation and its complications
For example: Your heart is made up of four chambers, the top two chambers are called the atrium and the lower two chambers are the ventricles. Electrical impulses help your atrium to contract so that blood is pushed into the ventricles before it circulates the body. With atrial fibrillation, the abnormal electrical rhythm causes your atrium to contract at different times, meaning there is poor blood flow out of your heart. This abnormal electrical can cause palpitations and other symptoms such as chest pain and shortness of breath.
Explains the complications of atrial fibrillation (i.e. risk of clotting leading to stroke, ischaemic bowel, ischaemic limb) and poor cardiac output (i.e. risk of acute myocardial infarction).
Pharmacological mgmt of AF
DOAC
Beta blocker - Discuss that rate control with a beta-blocker i.e. metropolol, is important to prevent haemodynamic deterioration by controlling ventricular rate. (Critical)
Discuss that this is indicated in patients who are symptomatic, or have a high ventricular rate.
ACD counselling points
Clear explanation of what is involved in an ACD including: Critical
- Appointing substitute decision makers
- Main goals for care
- Any treatment that the patient decline.
Explain that an ACD will only take effect if the patient cannot make their own decisions, either temporarily or permanently. Critical
Explain that the patient can change their ACD at any time, provided they have capacity to make decisions at that time.
Explain that an ACD does not replace a will, and cannot be used to make any financial decisions.
Ask the patient if they have considered their wishes for end-of-life care.
Explore the patient’s values and goals regarding care.
Arrange follow-up in an appropriate timeframe to further discuss any questions that they may have or help them complete the ACD.
Advanced care planning is an important process in which patients can document what medical and personal care they would want if they are not able to communicate their wishes or make decisions about their care. The process of discussion and advanced care plan allows patients to take time to consider their values and what type of care they want, before they are unwell or unable to make these decisions. Advanced care discussions should be had with any patients that are elderly, have terminal illnesses or conditions that may affect their cognitive function.
An Advanced Care Directive is a legal document that allows patients to appoint one or more substitute decision-maker(s) as well as state their wishes and goals for care. It may also include refusal of any specific care (for example CPR or blood transfusions). For an ACD to be valid it must be voluntarily made and made whilst the patient has decision-making capacity. If there is doubt about a patient’s capacity, a formal capacity assessment should be performed.
It is important to discuss the patient’s own expectations, values and goals for care rather than that of family, and encourage them to be as specific as possible when preparing an ACD. ACDs should include a patient’s wishes for both medical care as well as their preferences for accommodation, personal care and religious or spiritual care.
Once an ACD has been prepared, it can be updated and changed at any time providing the patient continues to have capacity. If there is an active ACD and the patient expresses wishes that differ to those documented in the ACD, these should still be taken into account providing the patient has capacity to make these decisions. A substitute decision maker should make decisions that are in line with the patient’s values, their wishes and what is in their best interest.
An ACD does not replace a will as it documents medical and personal care wishes whilst the patient is alive, and does not dictate the management of their estate following their death.
Osteoporosis screening tests and reasoning
Laboratory investigations: FBE, CMP, EUC, LFTs, TFTs.
Laboratory investigation justifications: FBE to determine if there is an elevated white cell count which can indicate infection or anaemia which may occur in multiple myeloma. CMP and EUC to determine if there is evidence of electrolyte abnormalities (hypocalcaemia etc.) or renal failure which is associated with osteoporosis. LFTs as these can be elevated in bone disease. TFTs as hyperthyroidism can contribute to osteoporosis risk.
Imaging for suspected crush fracture
Imaging/other: Spine X-ray, Spinal CT, bone density test (DEXA scan - if not already completed).
Imaging/other investigation justifications: The X-ray can be used to assess for a potential vertebral crush fracture, with a CT to assess for other possible causes such as a disc compression. A DEXA scan can further provide insights regarding the extent of the osteoporosis.
Different diagnoses for crush #/osteoporosis
malignancy, metabolic bone disease, ankylosing spondylitis, hyperparathyroidism, hyperthyroidism, osteomalacia, and infection.
Side effects of lithium? LITHIUM-R
Leucocytosis
Insipidus
Tremor / teratogenic
Hypothyroidism, hyperparathyroidism, hypercalcaemia
Increased weight
Upset stomach (nausea, vomiting, diarrhoea)
Misc: muscle weakness, memory impairment, metallic taste, ECG
Renal failure
Lithium ATHLETIC
A: Lithium is the drug of choice for preventing manic or depressive episodes, as well as treatment of acute mania, and has been associated with reduced risk of suicide. The mode of action of lithium remains unknown, however, it is hypothesised to inhibit dopamine while enhancing serotonin release.
T: Daily, maximum benefits of lithium can be delayed, occurring within one to three weeks of commencing lithium.
H: Oral, initially 750-1000mg and can be up-titrated by 250-500mg daily if necessary
L: Life long
E:
T: Initial investigations such as an ECG and FBE, UEC, TFT, calcium, magnesium and phosphate levels are required before starting lithium.
Explains measurement of lithium concentration will be monitored within a week after starting treatment and after each dose change until stabilised.
Further ongoing tests with FBE, UEC, TFT, calcium, magnesium and phosphate levels, as well as serum lithium levels, are required every three months.
Hydration status is an important factor that can influence the concentration of lithium.
The therapeutic range for an adult patient with mania is 0.5–1.2 mmol/L. Lithium concentration >1.5 mmol/L (or >1.2 mmol/L in the elderly) may result in lithium toxicity which may present with neurological and gastrointestinal symptoms as well as seizure, coma and death.
Increased monitoring may be required in unwell patients (i.e. gastroenteritis), in individuals who are actively having manic or depressive phases, with changes in weight or diet, pregnancy and commencement of new medications such as diuretics.
I: LITHIUM-R
Leucocytosis
Insipidus
Tremor / teratogenic
Hypothyroidism, hyperparathyroidism, hypercalcaemia
Increased weight
Upset stomach (nausea, vomiting, diarrhoea)
Misc: muscle weakness, memory impairment, metallic taste, ECG
Renal failure
C: Discusses that lithium needs to be used cautiously in patients with renal insufficiency, thyroid disease and adrenocortical deficiency, none of which apply to this patient..
Outlines that lithium is teratogenic and that strict adherence to the oral contraception pill is advised.
Discusses with the patient to be aware of signs and symptoms of lithium toxicity (i.e. extreme thirst and frequent urination, nausea and vomiting), especially during illness, excessive sweating or low fluid intake. Critical
Explains that if these occur, stop taking the tablets and seek medical attention or present to the emergency department immediately due to the risk of coma and death.
Follow up: 1 week in clinic and sooner in community setting if acute episode of mania.
Explain bipolar disorder
Bipolar one disorder is defined as having persistently elevated mood lasting over a week (or if hospitalisation is required) with periods of mood disturbances (≥3 of inflated self-esteem, decreased need for sleep, talkatively, flight of ideas, distractibility, increased goal activity or psychomotor agitation, excessive high-risk behaviour). These symptoms must result in social and occupational functioning and are not attributable to substance use or another medication condition.
Pharmacological management of bipolar
Mood stabilisers such as lithium, sodium valproate and lamotrigine are the preferred pharmacological agents for Bipolar Disorder. They can be used as monotherapy or in combination with second-generation antipsychotics such as quetiapine and aripiprazole. In patients with severe bipolar disorder, electroconvulsive therapy and transcranial magnetic stimulation can be considered.
Definition of CKD
Chronic kidney disease (CKD) is defined as the presence of kidney damage or an estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73m2, persisting for three months or more. The most common causes of CKD are poorly controlled diabetes mellitus and hypertension.
Clinical presentation of CKD
Patients with CKD may show symptoms like oedema or hypertension due to reduced kidney function. Often, CKD is detected incidentally during routine tests when elevated serum creatinine, reduced eGFR, or abnormal urinalysis are found. Imaging tests may reveal kidney damage or abnormalities, such as small and echogenic kidneys on ultrasound.
Symptoms of prolonged kidney failure, such as weakness, fatigue, anorexia, vomiting, and itching, may also occur, especially in advanced stages of CKD. Decreased urine output (oliguria or anuria) is rare with CKD alone but may suggest AKI when present.
Labratory findings of CKD
Laboratory tests often show:
- increased serum creatinine, BUN, and proteinuria, with possible abnormalities in red or white blood cells in urine.
Anaemia
hyperphosphataemia, hyperkalaemia, acidosis, hypocalcaemia, and elevated parathyroid hormone levels are common laboratory findings in CKD, varying in severity depending on the stage of the disease.
General management principles of CKD
- Treatment of reversible causes of kidney failure
- Preventing or slowing the progression of kidney disease
- Treatment of complications of kidney failure
- Adjusting drug doses based on eGFR
- Identification and adequate preparation for renal replacement therapy
Treatment of reversible causes of kidney failure: May include managing conditions such as hypertension, diabetes, or urinary tract obstruction, as well as addressing lifestyle factors like smoking and obesity.
Preventing or slowing the progression of kidney disease: Involves controlling blood pressure and blood glucose levels within target ranges, reducing proteinuria through medications such as ACE inhibitors or ARBs, and implementing lifestyle modifications such as adopting a healthy diet low in salt and saturated fats, maintaining a healthy weight, and regular exercise. SGLT2 inhibitors should also be considered for slowing the progression of kidney disease. Fluid status should be monitored routinely.
Treatment of complications of kidney failure: Management of these complications may involve medications such as statins for dyslipidaemia, erythropoiesis-stimulating agents for anaemia, phosphate binders for hyperphosphatemia, and vitamin D supplements for bone health.
Adjusting drug doses based on eGFR: May involve dose reductions, extended dosing intervals, or switching to alternative medications with lower renal clearance. Nephrotoxic medications should be avoided.
Identification and adequate preparation for renal replacement therapy: Timely identification and preparation for kidney replacement therapy (such as dialysis or kidney transplantation) are essential. Involves educating patients about their treatment options, addressing psychosocial concerns, and facilitating access to specialised care from nephrology and transplant teams.
Immediate management of acute asthma exacerbation
Immediate management entails the following:
- Involvement of specialists and senior staff.
- Performing an ABCDE assessment and ensure that patient is stable.
- Provide humidified oxygen if SpO2 is below 90%.
- 12 puffs salbutamol Metered dose inhaler (MDI) via a spacer and mask. 3 doses to be given every 20 minutes.
- 8 puffs of ipratropium bromide MDI via spacer and mask; 3 doses to be given every 20 minutes.
- Establishing IV access.
- Oral or IV steroids (Methylprednisolone / Hydrocortisone / Dexamethasone).
- Ongoing monitoring of work of breathing, mental state, oxygen saturations and activity levels.
- Continue to provide salbutamol and ipratropium bromide if there are not signs of improvement.
- Second line IV treatment options include Magnesium sulphate and/or aminophylline.
Signs of severe asthma
Involves the occurrence of agitation, notable increased work of breathing with accessory muscle usage, tachycardia, major difficulty in being able to talk, and may also include signs of anaphylaxis.
What is immune thrombocytopenia (ITP)
Immune Thrombocytopenia (ITP) is an autoimmune disorder characterised by the production of antibodies against platelets, leading to their premature destruction.
This condition is classified into primary ITP, which occurs without an identifiable cause, and secondary ITP, which is associated with other conditions such as autoimmune diseases, infections, or medications.
Who does ITP affect?
It predominantly affects children under five years, where it usually presents as a self-limiting condition, and adults over 55 years, in whom it often progresses chronically. It is more commonly diagnosed in females.
The aetiology of primary ITP is typically idiopathic, while secondary ITP may be triggered by autoimmune diseases (such as SLE), infections (such as HIV or hepatitis C), malignancies (including lymphoma and leukaemia), or adverse reactions to medications like quinine and heparin.
Diagnosis of ITP
ITP is primarily a diagnosis of exclusion, confirmed by a low platelet count with normal morphology and the absence of other systemic causes as assessed by coagulation parameters.
Investigations for ITP
Key investigations include CBC, peripheral blood smear, and specific screenings for underlying causes such as HIV or hepatitis C. A bone marrow biopsy may be necessary in atypical or unresponsive cases to exclude other haematological abnormalities.
Management of ITP
Management strategies in ITP aim to address the underlying autoimmune activity and prevent bleeding complications. This includes:
In children, the majority of cases are self-limiting, and many paediatric patients can be managed conservatively with minimal complications.
Emergency treatment for severe cases includes haemostatic control measures, corticosteroids, IVIG, and platelet transfusions.
What age and gender does slipped upper femoral epiphysis occur in?
It is most common in secondary-school aged male students, particularly those who are overweight.
Presentiation of slipped upper femoral epiphysis
Displacement of the femoral neck.
It may be unilateral or bilateral, and acute, chronic or acute-on-chronic.
Symptoms can vary but often include vague hip (or knee) pain with instability of the joint.
Examination findings may include antalgic gait with out-toeing and shortening of the affected limb, reduced hip internal rotation and abduction.
Drehmann’s sign is a characteristic feature of SUFE, and is characterised by thigh external rotation and abduction with hip flexion.
Treatment of SUFE
Treatment for SUFE is primarily operative, involving internal fixation with a cannulated screw. The patient should be made non-weight bearing while awaiting surgery to prevent further damage.
Complications of SUFE
Complications include osteonecrosis in around half of patients, even in those who have had surgical correction. Other complications can include chondrolysis, osteoarthritis and femoral acetabular impingement.
What is perthes disease?
Perthes disease is a deformity of the femoral head caused by avascular necrosis.
Who gets perthes disease?
It is more common in younger children, typically between 4 and 8 years old, and is usually managed conservatively
What is transient synovitis and who gets it?
Transient synovitis is the most common cause of limping in children and is an important differential. It typically occurs in primary-school-aged children (3-10 years old) and is often preceded by a viral upper respiratory tract infection. The condition presents with the acute onset of hip pain and limping without systemic illness. It is a clinical diagnosis made after more serious conditions are excluded through history, normal imaging, and blood tests. Management involves simple analgesia, and the condition typically self-resolves.
Definition of growth faltering
Not a diagnosis - need to find underlying cause
Growth faltering (GF; previously known as failure to thrive), refers to a condition where a child’s weight-for-age falls below the 3rd or 5th percentile for their age and sex. Additionally, it can be defined by similar percentiles for weight-for-length and BMI-for-age or a drop over two percentiles within a span of three months.
Causes of growth failure
GF is categorised into organic, inorganic (psychosocial), and mixed causes, with most cases under three years attributed to organic factors, predominantly malnourishment.
These include a wide spectrum of conditions that either affect caloric intake (undernutrition), caloric losses (malabsorption syndromes), or caloric consumption (systemic diseases e.g. cystic fibrosis, infections). Often, a psychosocial component in the form of emotional abuse, neglect, or poor psychosocial dynamic (possibly lower socioeconomic status in this family) contributes to these organic causes, leading to mixed cases of GF.
Symptoms of hyperglycemia/DKA
Polyuria, polydipsia, abdominal pain, weakness, fruity breath, SOB, confusion and fatigue
When does nausea and vomiting in pregnancy typically present and end?
Symptoms of NVP typically start at five to six weeks of gestation, peak at approximately nine weeks, and usually subside by 16 to 20 weeks. However, symptoms may persist until the third trimester in 15 to 20 % of patients and until delivery in 5 %.
Although commonly referred to as “morning sickness,” symptoms may occur at any time of day, may only manifest in the evening, and often persist throughout the day.
Complications of hyperemesis gravidarum
Short term:
- Dehydration and electrolyte imbalances may result in acute kidney injury, cardiac arrhythmias, and neuromuscular symptoms.
- Protein-calorie malnutrition and vitamin deficiencies, including vitamin K, B1, B6, and B12 deficiencies, can lead to various complications, such as coagulopathy, neuropathy, and Wernicke encephalopathy.
Longer term/fetal:
Severe NVP or HG has been associated with placental dysfunction, foetal growth restriction, preterm birth, pre-eclampsia, and placental abruption. Foetal surveillance is recommended in the third trimester.
Scoring system for severity of nausea and vomiting in pregnancy and the cut off score for consideration of inpatient management and investigation?
The severity of NVP can be graded using the Motherisk Pregnancy-Unique Quantification of Emesis and Nausea (PUQE-24) scoring system. No additional investigations are required for women with a PUQE score ≤12.
Women with severe NVP/HG (PUQE-24 scores ≥13) may require inpatient management and should undergo the following investigations - next card
Investigation for nausea and vomiting in pregnancy with PUQE-24 score over 12
- Urinalysis - ketones (as a general rule, 3/4+ requires admission), specific gravity.
- Comprehensive metabolic panel - for hyponatraemia, hypochlorameia, hypokalaemia and hypomagnesaemia.
- Complete blood examination - for increased haematocrit.
- Live function tests - for raised ALT, AST and bilirubin.
- Obstetric ultrasound - to rule out multi-foetal gestation or gestational trophoblastic disease.
- Tests to exclude alternative diagnoses where indicated (e.g. urine microscopy, culture and sensitivity to rule out urinary tract infection; TSH levels where thyroid dysfunction is likely).
Management of NVP/hyperemesis gravidarum
Management involves implementing dietary and lifestyle adjustments, alongside complementary therapies like ginger, acupressure, and acupuncture, all of which are deemed safe during pregnancy and may offer relief to certain individuals. Notably, oral ginger and/or pyridoxine (vitamin B6) are recommended for managing mild to moderate NVP. If symptoms persist, oral anti-emetics (such as doxylamine, promethazine, metoclopramide, or ondansetron) are the next available options. Women experiencing mild to moderate NVP are ideally managed within the community setting.
IV therapy when dehydrated or oral anti-emetics not effectively managing symptoms
Corticosteroids if IV anti-emetics ineffective
Pattern of inheritance of vWD
Autosomal dominant
Specific tests for vWD
Specific tests for vWD include measurement of factor VIII, vWF antigen and function (e.g., ristocetin cofactor, collagen binding)
full blood count and full coagulation profile: thrombocytopenia and prolonged activated partial thromboplastin time may be present
Common symptoms of vWD
patients may present with bleeding manifestations ranging from mucocutaneous bleeds, epistaxis, to more severe forms such as gastrointestinal bleeding and menorrhagia.
Bleeding assessment tool for evaluating bleeding symptoms with inherited bleeding disorders
ISTH-SCC
What is cholelithiasis
Stones being lodged in the gall-bladder
What is Type 2 respiratory failure?
Type 2 respiratory failure means that the patient is in a state of respiratory acidosis, with hypercapnia and hypoxia
Triggers for GORD
Alcohol
Caffeine
Complications of GORD
If left unaddressed for a long period of time, GORD can can increase the risk for development of complications that can cause dysphagia (Oesophageal strictures/Schatzki ring), become pre-malignant (Barrett’s oesophagus) and malignancy (oesophageal adenocarcinoma).
5W’s of post op fever
Wind (day 1-2): Atelectasis
Water (day 3-5): UTI
Walk (day 4-6): DVT/PE
Wound (day 5-7): wound infection
Wonder about drugs (day 7+)
Approach to post surgical history taking (AMPLE)
Allergies
Medications
Past medical history
Last meal or intake
Events leading to this presentation
What is Uthoff’s phenomenom?
A feature of MS that is noteworthy is that some patients may develop worsening of symptoms with showering, or exertion - this is referred to as Uthoff’s Phenomenon (this was occurring in this patient)
Presentation of MS
Patients with MS tend to typically present with unilateral eye problems, such as a change to vision (with loss of colour vision), and pain in the eye - this is referred to as unilateral optic neuritis. However, patients can also present with a number of other symptoms including bilateral/unilateral lower limb weakness, issues with eye adduction, nystagmus, paraesthesia and changes to mood.
As the disease progresses, patients may also develop other symptoms such as those due to cerebellar abnormalities (such as tremor and abnormal gait), problems with memory, and bowel/urinary problems.
Risk factors for MS
Female under 40
low levels of vitamin D
past EBV infection
Smoking
Some differential diagnoses for MS
Guillain-Barré syndrome/AIDP, ALS, CVA, diabetes, peripheral neuropathy, Vitamin B12 deficiency, depression, brain malignancy, Myasthenia Gravis, Graves disease, chronic fatigue syndrome, fibromyalgia, dermatomyositis, polymyositis.
Discuss elements of cranial nerve examination for all 12 cranial nerves
I: Olfactory
- Sense of smell
II: Optic
- Pupillary light reflex
- Relative afferent pupillary deficit
- Accommodation reflex
- Visual field assessment
- Visual acuity
- Colour vision and opthalmoscope - view optic nerve
III: Oculomotor
IV: Trochlear
VI: Abducens
- H test for eye movements - ask pt to report any double vision or blurriness
V: Trigeminal
- Sensation - forehead, cheek, jaw
- Motor - clench teeth, palpate masseter
VII: Facial
- Observe for facial droop, particularly forehead
- Motor - raise eyebrows, close eyes, keep eyes closed. Puff cheeks out, smile with teeth, close lips together
VIII: Vestibulocochlear nerve
- Hearing whisper test
- Weber test - check on chest first, then on middle of forehead
- Rinne test: Place fork on mastoid process, tell them to let you know when it stops, then place next to ear canal and ask if they can hear it.
A positive test is when air conduction > bone, and negative is when bone > air
IX: Glossopharyngeal
X: Vagus
- Ask about changes to taste
- Assess uvula
- Ask to cough
- Refer to testing gag reflex
XI: Spinal accessory nerve
- Shrug shoulders and resist
- Turn head to left and right and resist
XII: Hypoglossal nerve
- stick tongue out
- Move tongue from side to side to assess srength
Imaging for stroke
CT brain stroke series (non-contrast CT, CT angiogram, CT perfusion) This is the gold-standard workup, with the non-contrast CT being conducted first. If there is a hemorrhagic stroke - then stop with the non-contrast CT.
MRI gold standard but
Bloods for suspected stroke
Bloods, including VBG, FBE, Group and hold, coagulation profile. These would be useful in helping to determine if the patient needs urgent management that may be life-threatening.
Simplified Cranial nerve exam
Speaking with patient, confirmation, and consent.
Inspection of patient and room
CN I: assessing smell
CN II: assessing vision, with the usage of a Snellen chart, and assessing vision across the quadrants of vision. Also assessing pupillary construction responses.
CN III, IV, VI: assessing capability to move the eye muscles.
CN V: assessing sensation across the face.
CN VII: assessing movement of muscles across the face, as well as checking for any facial drooping.
CN VIII: assessing balance and hearing. This also entails determining if the hearing issue may be sensorineural or conductive
CN VIII, IX: assessing palate, and functioning of tongue and gag reflex
CN XI: assessing capability to move specific neck muscles
CN XII: assessing muscles of tongue, and movements of tongue.
Unilateral forehead sparing facial droop indicates
stroke
Triple test for worrying breast lump
History and breast examination.
Imaging (mammography or ultrasound).
Biopsy (fine needle aspiration or core biopsy).
Explanation of procedures ‘PICBRAND’
Procedure: Explain what the procedure is and what will happen.
Indication: Explain why the procedure is required.
Contraindications: Explain/explore factors that may make the patient ineligible for the procedure.
Benefits: Explain the benefits of going through with the procedure.
Risks: Explain overall risks of the procedure.
Alternatives / Nothing: Explain other possible options, including doing nothing.
Do you consent: Explicitly getting informed consent.
Extra management for women diagnosed with cancer under 50
As this patient is under the age of 50, it is recommended that her other female members undergo some kind of genetic testing, for mutations such as BRCA1 and BRCA2, by their doctors in order to guide monitoring protocols for these family members.
Age range for kawasaki disease
Typically under 5yo, rare under 6mo
Five principle features of kawasaki disease + fever length
Need to have had a fever for at least 5 days plus 4/5 of:
bilateral conjunctival injection
changes in the lips and oral cavity
cervical lymphadenopathy
extremity changes
polymorphous rash
For incomplete KD (don’t meet diagnostic criteria but suspicious), what should you test for?
Consider incomplete KD in:
Child with fever ≥5 days + 2-3 clinical features
Infant with fever ≥7 days ± irritability, aseptic meningitis
Child/infant with prolonged fever + shock, cervical adenitis not responsive to oral antibiotics.
For children meeting one of the above criteria, check for elevated acute-phase reactants (CRP ≥30 mg/L or ESR ≥40 mm/hour). If present, children with three of the following criteria should be treated as incomplete KD and have treatment initiated:
WBC count ≥15× 109 /L
Anaemia
Platelet cell count ≥450× 109 /L after 7th days of illness
Non-neutrophilic (sterile) pyuria (≥10 WBCs/high-power field)
Serum ALT >50 units/L
Serum albumin ≤30 g/L
Aside from kawasaki disease, what else do you need to rule out for a child with prolonged fever and how would you do it?
In children with prolonged fever, it is crucial to rule out infections of unknown sources or sepsis. This involves conducting tests such as urine MC&S, CXR, blood culture & sterile site PCR, and considering a lumbar puncture if meningitis is suspected. It is reasonable to initiate empirical antibiotics and discontinue them if test results indicate no infection.
Treatment for kawasaki disease
Intravenous immunoglobulin (IVIG) is administered at a dosage of 2 g/kg as a single IV infusion upon diagnosis of KD. It is ideally administered within the first 10 days of illness.
Live vaccines should be deferred or re-vaccination considered as appropriate.
Aspirin is prescribed at a low dose of 3-5 mg/kg orally daily until a normal echocardiogram is observed on follow-up, typically for a minimum of six weeks. There is minimal risk of Reye syndrome associated with low-dose aspirin therapy.
Symptoms of Kawasaki Disease ‘CREAM’
Conjunctivitis
Rash
Extremity oedema
Adenopathy
Mucosal involvement
Complications of Kawasaki Disease
Coronary artery aneurysm
Wells criteria for PE and score interpretation
Clinical signs and symptoms of DVT (+3)
PE is #1 diagnosis or equally likely (+3)
HR >100 (+1.5)
Immobilisation 3 days or past surgery in past 4 weeks (+1.5)
Previous DVT or PE (1.5)
Haemoptysis (+1)
Malignancy w treatment within 6mo or palliative (+1)
<2 low risk
2-6 moderate risk (16.2% chance in ED popn)
>6 high risk (40.6% chance in ED popn)
PERC criteria for ruling out PE
If one or more present cannot rule out PE
Age >50
HR >100
O2 sat on room air <95%
Unilateral leg swelling
Haemoptysis
Recent surgery or trauma
Prior PE or DVT
Hormone use (OCP, HRT, estrogenic)
Investigations for suspected DVT
Skip D-dimer if highly likely, straight to duplex US
Mgmt of DVT
Generally, patients with proximal DVT and PE should receive anticoagulant therapy (DOAC unless renal impairment) for at least three months, with some requiring extended therapy up to six months. However, there remains uncertainty regarding the optimal duration of anticoagulation for distal DVT.
Investigation for all cases of overt UGIB
An endoscopy is warranted in all cases of overt UGIB.
How do gallstones form?
Gallstones (cholelithiasis) are most commonly formed by supersaturation of cholesterol in bile.
Risk factors for gallstones
The common risk factors of cholesterol stones are all related to cholesterol supersaturation in bile. These include conditions that increase oestrogen (since oestrogen increases cholesterol production) such as pregnancy, OCP use, and female gender, and which increase progesterone (increases biliary stasis) such as pregnancy. Dyslipidaemia and family are other important risk factors that are related to cholesterol overproduction.
Four F’s of cholelithiasis
‘F’emale,
F’ertile
‘F’at,
over ‘F’orty years of age.
Complications of cholelithiasis
Cholelithiasis is mostly asymptomatic, but those within the gallbladder could be associated with:
inflammation - acute cholecystitis
obstruction - biliary colic
Stones travelling down the biliary tree could be complicated by:
obstructive jaundice
acute pancreatitis
What is choledocholithiasis? Clinical features, inital Ix and diagnostic Ix, Rx
Choledocholithiasis refers to the presence of gallstones in the common bile duct (CBD).
Characteristic clinical features include right upper quadrant pain and signs of extrahepatic cholestasis.
Initial diagnostic evaluation includes an ultrasound and routine laboratory studies, and based on the diagnostic likelihood, confirmatory imaging may involve an endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance cholangiopancreatography (MRCP), or endoscopic ultrasound (EUS).
Treatment consists of stone removal (endoscopically or surgically) and preventing recurrence (e.g., via laparoscopic cholecystectomy).
What is bilirubin
Catabolite of heme, produced in breakdown of RBCs, conjugated with glucoronic acid in the liver
Causes of rise in unconjugated bilirubin
Overproduction - hemolysis, ineffective EPO (e.g. in folate or iron deficiency)
Impaired uptake (prehepatic) - CHF, portosystemic shunts, drugs (rifampin)
Impaired conjugation (intrahelpatic) - Neonates, chronic hepatitis, advanced cirrhosis, hyperthyroidism, crigler-najjar syndrome
Causes of rise in conjugated bilirubin
Cholestasis - greater in obstructive, including:
- Choledocholithiasis, tumors (pancreatic, cholangiocarcinoma), primary sclerosing cholangitis, pancreatitis, strictures after procedrues
Non-obstructive causes:
Hepatitis (viral, alcohol-associated, NASH)
Primary biliary cholangitis
Drugs (e.g., alkylated steroids, chlorpromazine)
Sepsis
Infiltrative diseases (e.g., amyloidosis, sarcoidosis, tuberculosis)
Pregnancy
Dubin Johnson syndrome
Rotor syndrome
Non-pharmacological treatment of BPH
Encouraging smoking cessation, reduced alcohol consumption, a balanced diet and
regular exercise are important lifestyle interventions
Pharmacological treatment of BPH
Alpha blockers (e.g. prazosin, tamsulosin): These help to relax the prostate smooth
muscle
○ 5-alpha reductase inhibitor (e.g. finasteride): Helps to reduce the growth of the prostate
by preventing the conversion of testosterone to DHT
Surgical interventions for BPH
○ Trans-perineal biopsy - this can help to formally diagnose prostate cancer
○ TURP (trans-urethral prostate resection) - A procedure in which excess prostate tissue
surrounding the urethra is resected to try and increase the lumen diameter for urine to
flow through
○ Prostatectomy - this is when the entire prostate is removed
Causes of atrial fibrillation (ATRIALFIB)
● Alcohol abuse
● Thyroid disease
● Rheumatic heart disease
○ Other valvular heart disease
● Ischaemic heart disease
● Atrial myxoma
● Lung
○ Pulmonary Embolism
○ Chronic Obstructive Pulmonary
Disease
● (F) Phaeochromocytoma
● Idiopathic
● Blood pressure
Other causes of Atrial fibrillation
● Pericarditis or Myocarditis
● Congestive Heart Failure
● Structural heart defects (Cardiomyopathy)
● Cardiac surgery
● Obstructive Sleep Apnoea
● Sepsis
● Obesity
● Medication that causes sympathetic activation
Risk factors for AF
● Hypertension
● Diabetes Mellitus
● Alcohol excess
● Cardiovascular conditions
○ Coronary artery disease
○ Heart failure
○ Valvular disease
○ Sinus node disease
Pharmacological cardioversion for AF
Effectively restores sinus rhythm in ~50% of
patients if recent onset
● Flecainide
○ Indication: Atrial Fibrillation with normal
left ventricular function and no coronary
disease
○ Dose: 1.5-2mg/kg (up to 150mg) over 10
minutes
● Amiodarone
○ Indication: Atrial Fibrillation with left
ventricular dysfunction or coronary disease
○ Dose: 300mg infusion over 1-2 hours,
followed by 900mg infusion over 24 hours
When to use rhythm control for AF patients
Reasonable for:
● Patients who are highly symptomatic
● Those with left ventricular dysfunction
● Long term rhythm control needs to be
balanced against the potential adverse
effects of antiarrhythmic drugs, the patient’s
symptoms and preferences
When to use rate contol for AF patients
Reasonable for:
● Asymptomatic patients
● Those with normal left ventricular function
● Patients who do not respond to rhythm control
Rate control options for AF
B-blocker:
- Metoprolol or atenolol
- If HfRef present, use carvedilol or bisoprolol
Non-dihydropyridine ca channel blocker (alternative if B blocker not tolerate or CI’d)
- Diltiazem or verapamil
- Should not be used in pts with LV dysfunction due to negative inotropic effect
Amiodarone (if above B-blocker or Ca channel blocker not tolerated, CI’d or LV dysfunction)
Digoxin (additional if failure to control rate with above medications)
AF complications
CVA
MI
CHF
Causes of cardiogenic shock
- Reduction in CO
- Cardiomyopathic (incl MI)
- Arrhythmia (including sustained VT, complete heart block)
- Mechanical (valvular insufficiency - mitral: rupture of papillary muscle or chordae tendinae, aortic dissection into aortic ring, wall rupture) - Compensation (BP = CO x SVR)
- Reduced CO due to peripheral vasoconstriction, increasing afterload and overburdens myocardium - Impaired perfusion and cellular hypoxia
- End organ damage - prolonged loss of perfusion causes lasting damage to vital organs
○ Heart: congestive heart failure signs
○ Brain: altered mental status
○ Kidney: reduced urine output
○ All cells: increased lactate
Types of distributive shock
Neurogenic
Septic
Anaphylactic
Treatment for septic shock
● O2 support
● CVS support: IV fluids initially, if resistant then
vasopressors
● Hydrocortisone IV if further resistance to fluid
resuscitation
● Empirical antibiotics depending on the
suspected source
○ Start with broad (e.g. pip/taz or
meropenem) and add additional agents
depending on RFs or comorbidities
○ Narrow spectrum once source is
confirmed
Investigations for septic shock
Bloods: FBC, U/Es, creatinine, liver enzymes,
lactate, INR, PTT, blood cultures x 2 (prior to Abx)
○ Other cultures dependent on suspected
source
○ e.g. nasopharyngeal swab, sputum culture,
throat swab, etc.
● ABG
● CXR or other imaging depending on suspected
source of infection
Three main goals for hypovolemic shock in ED
● Fluid resuscitation
● Maximise oxygen delivery
● Prevent further blood loss
Investigation findings in hypovolemic shock
● Increased blood urea nitrogen (BUN) and
serum creatinine (due to prerenal kidney
failure)
● Hyper/hyponatremia
● Hyper/hypokalemia
● Lactic acidosis (due to anaerobic metabolism,
however large GI losses can lead to alkalosis)
● Decreased haematocrit/Hb (in haemorrhagic
causes)
Blood transfusion ratios for haemorrhagic cause of hypovolemia
For haemorrhagic causes of hypovolemic shock, fluid
resuscitation is often given in the form of blood
transfusions using a 1:1:1 or 1:1:2 ratio of plasma to
platelets to red cells.
RIsk factors for colorectal cancer
Family history
● Obesity
● Physical inactivity
● Dietary factors: Diet high in red meat, animal
fat and low in fibre, fruits and vegetables:
○ Fibre alters colonic bacterial flora, and
absorbs luminal toxins, therefore
reducing the carcinogenicity of the
luminal contents
● Tobacco smoking
● Alcohol consumption
Specific symptoms for right sided colorectal cancer
Insidious onset of iron deficiency anaemia (due to occult faecal blood loss)
● Lethargy
● Palpable right iliac fossa mass (especially if
Caecal cancer)
Late presentations:
● Distal ileal obstruction
● Acute appendicitis (due to caecal cancer occluding the opening of the appendix)
Specific symptoms for right sided colorectal cancer
Alteration of bowel habit - constipation
alternating with diarrhoea
● Abdominal distension
● Tenesmus (feeling of incomplete bowel evacuation)
● Passage of mucus and blood in stools
● Palpable mass in the left-side of the abdomen
Normal urine output
0.5-1ml/kg/hr
~35-80ml/hr
What is the sepsis six? ‘OF A TBL’
Take urine
Blood culture
Lactate
Give fluids
Give antibiotics
Give oxygen
Blood tests in post op fever
Bedside:
VBG, urine dipstick
Bloods:
Cultures
FBC, CRP, EUC, LFT, coagulation studies, group and hold
Imaging:
CXR, other as indicated (operative site CT or US)
Other:
Urine, wound, sputum swab, stool
QSOFA score
2/3 of
RR >22
Altered mental status
BP <100
Seven causes of post op fever (7C’s)
- Chest infection
- Cut (wound infection)
- Collections (abdomen, pelvic)
- Calves (DVT)
- Cannula (infection)
- Central line (infection)
Side effects of NSAIDs (I-GRAB)
- Interactions with other medications (such as Warfarin)
- Gastric ulceration (consider adding a PPI when prescribing NSAIDs long-term)
- Renal impairment (use NSAIDs sparingly in those with poor renal function)
- Asthma sensitivity (triggers 10% of individuals with asthma)
- Bleeding risk (due to their effect on platelet function)
Weak opiates
Codeine
Strong opiates
Morphine
Oxycodone
Fentanyl
Side effects of opiates
- constipation and nausea. Thus, laxatives and anti-emetics should be prescribed concurrently.
- sedation or confusion, respiratory depression, pruritus, and tolerance and dependence (both of the latter are relatively rare).
Preferred opiates for pt with renal impairment
Oxycodone or fentanyl
Avoid morphine
Non-pharmacological treatment of neuropathic pain
Cognitive behaviour therapy
Transcutaneous electric nerve stimulation (TENS)
Capsaicin cream (typically for localised pain)
Factors detrimental to wound healing
- Obesity
- Nutritional deficiency vit C
- CVD or DM
- Increasing age
- Local blood supply, infection, foreign material
Systematic assessment of a wound (TIMES)
- Tissue involved (, such as viable or non-viable)
- Infection or inflammation
- Moisture levels
- Edge of the wound
- Surrounding skin
Wound healing steps in secondary intention
- Haemostasis – a large fibrin mesh forms, which fills the wound
- Inflammation – an inflammatory response acts to remove any cell debris and pathogens present
- Proliferation – granulation tissue forms at the bottom of the wound
- Remodelling – the inflammatory response begins to resolve, and wound contraction can occur
Risk factors for venous ulcers
Increasing age
pre-existing venous incompetence
history of venous thromboembolism including varicose veins
Pregnancy
Obesity or physical inactivity
Severe leg injury or trauma
Appearance and symptoms of venous ulcers
Appear shallow with irregular borders and a granulating base, characteristically located over the medial malleolus
Can be painful (particularly worse at the end of the day)
Associated symptoms of chronic venous disease, such as aching, itching, or a bursting sensation, will be present often before venous leg ulcers appear.
Prone to infection and can present with associated cellulitis
Management of venous ulcers
- leg elevation and increased exercise
- weight reduction and improved nutrition
- Antibiotics should only be prescribed with clinical evidence of a wound infection (most wounds are colonized, therefore swab results should only be acted upon if evidence of infection).
- The mainstay of management is via multicomponent compression bandaging, changed once or twice every week; 30-75% of venous leg ulcers will heal after six months of compression therapy.
- Importantly, the ABPI must be measured as at least greater than 0.6 before any bandaging is applied. Appropriate dressings and emollients are crucial in maintaining surrounding skin health.
- If there is concurrent varicose veins, these should be treated with endovenous techniques or open surgery*, as improving venous return will allow for the healing of the venous ulcers.
Risk factors of arterial ulcers
Same as peripheral arterial disease, smoking, diabetes mellitus, hypertension, hyperlipidaemia, increasing age, positive family history, and obesity and physical inactivity
Appearance and symptoms of arterial ulcers
- small deep lesions with well-defined borders and a necrotic base. They most commonly occur distally at sites of trauma and in pressure areas (e.g the heel).
- preceding history of intermittent claudication or critical limb ischaemia (pain at night).
- cold limbs, thickened nails, necrotic toes and hair loss.
- the limbs will be cold and have reduced or absent pulses. In pure arterial ulcers, sensation is maintained (unlike neuropathic ulcers).
Investigations for arterial ulcer
- Ankle Brachial Pressure Index (ABPI) measurement, (>0.9 = normal; 0.9-0.8 = mild; 0.8-0.5 = moderate; <0.5 = severe).
- duplex ultrasound, CT Angiography, and / or Magnetic Resonance Angiogram (MRA).
Management of arterial ulcers
- Referred for a vascular review
- smoking cessation, weight loss, and increased exercise
- statin therapy, an antiplatelet agent (aspirin or clopidogrel), and optimisation of blood pressure and glucose.
- Surgical – Angioplasty (with or without stenting) or bypass grafting (usually for more extensive disease).
- Any non-healing ulcers despite a good blood supply may also be offered skin reconstruction with grafts.
Risk factors for neuropathic ulcers
- Neuropathic ulcers can develop with any condition with peripheral neuropathy, the most common being diabetes mellitus and B12 deficiency.
- foot deformity or concurrent peripheral vascular disease.
Appearance and symptoms of neuropathic ulcers
- “punched out appearance”
- They occur most commonly on sites of pressure on feet (e.g. metatarsal heads or heels).
- Additionally, there may be a peripheral neuropathy (classically in a ‘glove and stocking’ distribution) with warm feet and good pulses (unless element of concurrent arterial disease).
burning/tingling in legs (painful neuropathy) - single nerve involvement (mononeuritis multiplex, such as CN III or median nerve), or amotrophic neuropathy (painful wasting of proximal quadriceps).
Investigations for neuropathic ulcers
- Blood glucose levels
- serum B12 levels.
- Concurrent arterial disease should be assessed with an ABPI +/- duplex.
- Signs of infection require a microbiology swab
- any evidence of deep infection (e.g. visible bone or ulcers extending into joints), may warrant an X-ray to assess for osteomyelitis.
- 10g monofilament test, along with testing vibration sensation with a 128Hz tuning fork.
Management of neuropathic/diabetic foot ulcers
- specialised diabetic foot clinics for patients with neuropathic ulcers, where they are managed via a full multidisciplinary (MDT) team.
- Diabetic control should be optimised, targeting HbA1c <7%.
- Improved diet and increased exercise
- any cardiovascular risk factors present managed accordingly.
- maintain good foot hygiene and appropriate footwear provided (e.g. non-weight bearing shoes).
- Any signs of infection will warrant swabs taken and antibiotics (e.g. flucloxacillin) started.
- Ischaemic or necrotic tissue may require surgical debridement. In severe cases, necrotic or infected digits may need amputation.
Describe the process of abscess drainage
Procedure
The aim of the procedure is to drain the abscess, remove unhealthy tissues and ensure the cavity does not close to prevent abscess reformation. The wound is left open to heal (known as healing by secondary intention).
Take a sample of pus with the syringe MC+S
Wash out cavity with the sterile saline in the syringe.
Pack cavity loosely with the alginate ribbon dressing
If the patient is diabetic, then the abscess should ideally be drained on the same day of admission,
Be aware of any developing necrotising fasciitis (more common in patients with a background of immunosuppression), which can present with sepsis, a rapidly spreading infection, and / or palpable surgical emphysema.
Presentation of perforation/rupture in abdomen
Sudden onset of diffuse, excruciating pain. Patients will lie still to minimize pain. Peritoneal signs are prominent.
DDx of perforation/rupture in abdomen
Oesophageal perforation (Boerhaave syndrome):
- recurrent vomiting/hematemesis (not always)
- commonly presents with retrosternal and epigastric pain.
Other GI perforation: Associated with
- PUD
- Cancer
- Diverticulitis
- IBD
Ruptured abdominal aortic aneurysm (AAA):
- Most common in male smokers >65 years of age.
- Periumbilical pain that radiates to the back.
- Abdominal exam may reveal pulsatile mass.
Ruptured ectopic pregnancy/ovarian cyst:
- Presents with first-trimester bleeding, abdominal pain, and hypovolemic shock.
- Abdominal pain is usually localized to the pelvis
- bHcg is vital sign
Presentation of obstruction in abdomen
Sudden onset of severe, colicky, intermittent pain. Patients cannot sit still. Peritoneal signs are usually absent.
DDx of obstruction in abdomen
SBO
- from adhesions post surgery, incarcerated hernia, IBD, cancer
- constipation
- high pitched bowel sounds
Volvulus
- insidious onset, continuous, intermittent exacerbations associated with peristalsis
- nausea, distension, obstipation
- if peritonitis or caecal volvulus -> immediate surgery, otherwise endoscopic detorsion
Ureteric/biliary obstruction
- Nephrolithiasis causing colicky pain that usually radiates to the groin and may cause hematuria/pyuria.
- costovertebral angle tenderness (CVAT).
- Biliary colic is most common in multiparous, overweight women (female, forty, fertile, and fat).
- Fatty meals exacerbate pain. There are no signs of peritoneal irritation.
Presentation of inflammation in abdomen
Gradual onset, constant, poorly localised, patient lie still to minimise pain, peritoneal signs prominent
DDx of inflammation in abdomen
Appendicitis
- McBurney’s point tenderness, rosvings sign
Cholecystitis
- Murphy’s sign
Diverticulitis
- LLQ pain
- Change in bowel habits
- Nausea and vomiting
- Palpation or rectal exam may reveal mass
PID
- STI hx/young female with unsafe sexual practices
- Cervical motion tenderness and adnexal tenderness
DDx and corresponding presentation of ischemic bowel
Acute mesenteric ischemia
- Pain and hematochezia
- Hx Afib or recent AAA repair
Ischemic colitis
- Post prandial ab pain
- Hematochezia/melena
Strangulated hernia
- Irreducible bulge in abdominal area
Ovarian torsion
- Sudden onset pain
- Nausea vomiting
- Palpation reveal mass
Tests to rule out extra-abdominal mimics in acute abdominal pain
- Troponins and ECG for MI
- d-dimer/CT angiogram for pulmonary embolism
- CXR for pneumonia
Tests to rule out non-surgical abdomen causes, if appropriate
- Amylase/lipase in patient consistent with pancreatitis (nausea/vomiting, epigastric pain, hunched over),
- CT abdomen without contrast in patient consistent with kidney stones/pyelonephritis (hematuria, flank pain, radiation to groin),
- paracentesis for patient consistent with systolic blood pressure (ascites, fever)
Test to rule in SBO, volvulus, perforation
- X-ray of the abdomen: Perforation: SBO, volvulus
Tests for diverticulitis, IBD, abscess, cancer, AAA
CT angiogram
Blood tests and actions for unstable pts with suspected haemorrhage
- Blood typing, cross-matching and transfusion as needed.
Management of stable acute abdomen pts
- Expectant management, possibly including NPO status, NG tube placement (for decompression of bowel in the setting of obstruction or acute pancreatitis)
- IV fluids, placement of a Foley catheter (to monitor urine output and fluid status), and vital sign monitoring with serial abdominal exams and serial labs.
Newborn examination
- Birth + pregnancy history from mom (urine, meconium, feeding, concerns)
- Weight
- General observations (pallor, jaundice, cyanosis)
- Assess tone
- Head circumference
- Head shape
- Palpate anterior fontanelle
- Observe face (epicanthic folds, scars, asymmetry)
- Eyes for discharge, redness, symmetry
- Red reflex on fundoscopy
- Nose for patency
- Mouth for clefts and tongue tie
- Ears for accessory auricle, skin tags, pits
- Skin for lacerations, jaundice, pallor, cyanosis
- Neck for webbed neck, cysts, clavicle fractures
- Chest symmetry, number of fingers, palmar crease, brachial pulse
- Pulse oximetry, RR, WOB
- Auscultate heart and lungs
- Abdomen for distension, hernia, palpate for organomegaly
- Check genitals for fused labia, urethral meatus, testicles present
- Check anus for patency
- Check lower limb for number of limbs, scars, oedema
- Check range of movement of knees and tone, femoral pulses
- Perform Barlow and Ortolani test
- Check back for scoliosis, hair tufts, sacral pits
- Reflexes, palmar grasp, rooting reflex, Moro
General questions of sick child paediatric history taking
- Irritability
- Fever
- Lethargy or increased sleepiness
- Poor feeding (volume taken in previous 24 hours <50% of normal)
- Vomiting
- Apnoea
- Decreased tone
- Past history of brief resolved unexplained event (BRUE) or seizures
Red flags for admission in unwell child
Pale
Blue (cyanotic)
Does not wake or stay awake
High pitched continuous cry
Grunting
Reduced skin turgor
Non blanching rash
Bulging fontanelle
Neck stiffness
Seizures
Neurological signs
General management unwell child
- early administration of empiric antibiotics (IV/IM/IO)
- prompt management of sepsis
- consider aciclovir
- adequate analgesia and sedation
- Careful fluid management:
- fluid resuscitation as required
- maintenance fluids (account for oral intake)
- Consider a nasogastric tube on free drainage if bowel obstruction is suspected
- Early referral to the paediatric, surgical and/or sub-specialist teams as indicated
- In neonates with suspected duct dependent congenital cardiac condition, consider IV prostaglandin.
Causes of birth asphyxia
- maternal hypoventilation or hypotension
- placental insufficiency
- knotting of the umbilical cord.
Symptoms of birth asphyxia
- irritability and poor feeding to lethargy, hypotonia, apnea, seizures, and death.
Complications of birth asphyxia
- developmental delays and cerebral palsy.
Treatment of birth asphyxia
- Therapeutic hypothermia over 72h to minimise brain damage
Key developmental milestones
Referral points
- doesn’t smile at 10 weeks
- cannot sit unsupported at 12 months
- cannot walk at 18 months
6 weeks – smile
3 months - good head control, reaches for objects, turns towards sound, laughs
6 months - Pulls self to sitting, rolls front to back, holds objects, ‘adah’
7-8 months – sits without support
9 months – crawls, points, mama dada
12 months – walks with support, good pincer grip, waves bye bye, knows name
15 months – walks unsupported, knows some words/commands, drinks from cup
18 months – squats to pick up toy
2 years – runs, combine 2 words, uses spoon
3 years – climbs stairs, short sentences, counting
4 years – hops, asks how, when, why, plays with other kids
Signs that may be concerning for autism
- Some signs that may be concerning for autism spectrum disorder include failure to achieve certain language milestones (eg, babbling/gesturing by 12 months of age, use of two-word phases by 24 months of age), impaired social interaction, restricted interest in objects/activities, and insistence on routine.
Most common presenting symptom of cerebral palsy
The most common presenting symptom of cerebral palsy is delayed motor development.
- Toe walking/scissor gait
- May be associated with hearing, visual, GI, behavioural disorders, seizure disorders, speech deficits
Presentation of cystic fibrosis
- Most patients diagnosed on newborn screening
- Neonates: Meconium ileus (obstruction of the distal ileum caused by abnormally thick meconium; 15% of presenting cases).
- Patients <1 year of age: Cough, wheezing, or recurrent respiratory infections. Patients may also have steatorrhea and/or FTT.
- Most patients >1 year of age: FTT (caused by pancreatic insufficiency) or chronic sinopulmonary disease/sputum production.
Causes of growth failure
- Poor oral intake- incorrect preparation of formula feed, cleft palate, child neglect, GORD
- Increased requirement- malignancy, congenital heart defects
- Inadequate absorption- CF, pyloric stenosis, IBD, celiac, cows milk protein allergy
Presentation and symptoms of growth failure
- vomiting
- diarrhoea
- recurrent infections
- developmental delay
- pallor, dry skin, weak hair
- heart murmur in congenital cardiac disease
- atopic dermatitis in food allergy
- dysmorphic features in genetic abnormalities
- suspicious fractures or contusions in child abuse
Investigations for growth failure
- BINDS PDF
- Number and frequency of feeds
- Food refusal
- Observation of feed
- inquire about preparation of formula and feeding practices
- CBC for anaemia, immunodeficiency, malignancy
- CMP for renal causes
- TFT for hypothyroidism
- Urinalysis for renal pathology or infection
- Stool culture for infection or malabsorption
- Lead, iron, coeliac tests
- Diagnostic testing: Targeted to suspected etiologies when indicated and no improvement occurs after ensuring adequate nutrition. Imaging modalities include echocardiogram for congenital heart defects and upper gas- trointestinal (GI) series for GI causes.
Age of presentation GORD in infant
Typically before 8 weeks
Age of presentation cows milk allergy in infant
Typically in first 3 months
Presentation of GORD in infant
Milky vomits after feed
Reposition during feeds 30deg head up
Treatment of GORD in infant
Trial of thickened formula
Presentation of cows milk protein allergy in infant
Regurg, vomiting, wheezing, cough, urticaria
Usually grow out of it
Clinical diagnosis but cando skin prick
Treatment of cows milk protein allergy in infant
Continue breastfeeding and eliminate cows milk from maternal diet or use extensive hydrolysed formula milk
Presentation of physiological neonatal jaundice
- abdominal distention
- delayed passage of meconium
- light-colored stools
- dark urine
- infection, or birth trauma (cephalohematomas, bruising, pallor, petechiae).
Causes of neonatal hemolytic jaundice
- ↑ unconjugated bilirubin
- Hemolysis (ABO or Rh incompatibility)
- Erythrocyte enzyme deficiency (glucose-6-phosphate dehydrogenase [G6PD] and pyruvate kinase deficiency)
- Erythrocyte structural defects (sickle cell anemia, hereditary spherocytosis)
- Ineffective erythropoiesis (thalassemias)
- Sepsis with disseminated intravascular coagulation (DIC)
Investigations for neonatal jaundice
For indirect hyperbilirubinemia
* complete blood cell count (CBC) with peripheral blood smear (abnormal RBCs and signs of hemolysis)
* blood typing of mother and infant (ABO or Rh incompatibility);
* Coombs test and bilirubin levels
For direct hyperbilirubinemia
- liver function tests (LFTs), bile acids, assess liver anatomy and biliary tract via ultrasound and/or hydroxy iminodiacetic acid (HIDA) scan can confirm suspected cholestatic disease
A jaundiced neonate who is febrile, hypotensive, and/or tachypneic needs a full sepsis workup and intensive care unit (ICU) monitoring
Other causes of physiological neonatal jaundice
Breast milk jaundice
- unconjugated
- peaks in second week of life
- self-resolving
Breastfeeding jaundice
- Unconjugated bilirubin
- Due to inadequate milk
- Occurs in first week of life
- Treatment is hydration
Impaired conjugation of bilirubin
Gilbert syndrome
What is duchenne muscular dystrophy?
- An X-linked recessive disorder resulting from a deficiency of dystrophin, a cytoskeletal protein.
- Onset is usually at 3 to 5 years of age.
- Affects axial and proximal muscles more than distal muscles
- May present with progressive clumsiness, fatigability, difficulty standing or walking, increased toe walking, Gowers maneuver (using the hands to push off the thighs when rising from the floor), and waddling gait
- Pseudohypertrophy (fibrofatty replacement of muscle) of the gastrocnemius muscles also seen
- Intellectual disabilities commonly present
Diagnosis of duchenne muscular dystrophy
- Creatine kinase (CK) levels >10 to 20 times normal suggest DMD.
- Confirmation is made with genetic testing.
- Muscle biopsy shows replacement of muscle by fat and fibrotic tissue.
- Electromyography (EMG)
- Screening with ECG and echocardiogram can detect dilated cardiomyopathy or conduction abnormalities.
What causes developmental hip dysplasia?
Excessive hip flexion in utero (eg, breech presentation) leads to excessive stretching of the posterior hip capsule
- Most commonly found in firstborn girls born in the breech position.
- ↑ risk occurs with family history.
Describe the barlow manouevre
Posterior pressure is placed on the flexed hip, and then the hip is adducted, leading to an audible “clunk” as the femoral head dislocates posteriorly.
Describe the ortolani manouevre
Thighs are gently abducted from the midline with anterior pressure on the greater trochanter. A soft click signifies a reduction of the femoral head into the acetabulum.
Complications of DDH
If not treated in infancy, older children present with hip pain and leg length discrepancy, causing a waddling or Trendelenburg gait.
AVN of femoral head
Treatment of DDH
Treatment should begin early even though the condition may resolve on its own before 2 weeks of age.
<6 months: Rigid brace, splint with a Pavlik harness (maintains the hip as flexed and abducted); to prevent AVN, the hips should not be flexed >60 degrees
6 to 18 months: Spica cast
>18 months: Open reduction followed by spica cast
What is perthes disease an who gets it?
- Idiopathic AVN and osteonecrosis of the femoral head
- Most common in boys 4 to 10 years of age.
Presentation of perthes disease
- a painless limp, antalgic gait, and thigh muscle atrophy.
- Pain sometimes present. If it is present, it can be in the groin or anterior thigh, or it may be referred to the knee.
- Limited abduction and internal rotation; atrophy of the affected leg.
- Usually unilateral (85%–90%).
Treatment of perthes disease
- Observation is sufficient if limited femoral head involvement or if full range of motion (ROM) is present.
- If extensive necrosis or ↓ ROM, the physician can consider bracing, hip abduction with a Petrie cast, or an osteotomy.
Imaging Ix of SCFE
- X-rays of both hips in anteroposterior and frog-leg lateral views reveal posterior and inferior displacement of the femoral head
- In patients under the 10th percentile of height, the physician can rule out hypothyroidism with thyroid-stimulating hormone (TSH).
Presentation of SCFE
- Insidious onset of dull hip pain, or referred knee pain, and a painful limp
- Restricted ROM and inability to bear weight (differentiates unstable from stable SCFE)
- Bilateral in 40% to 50% of cases
- Limited internal rotation and abduction of the hip; patients hold hip in passive external rotation
Treatment of SCFE
- The disease is progressive, so treatment should begin promptly.
- Immediate surgical screw fixation can reduce the risk for AVN.
- No weight-bearing should be allowed until the defect is surgically stabilized.
Causes of meningitis
Bacterial:
S pneumoniae, N meningitidis, and Escherichia coli
Viral:
Enteroviruses most common
Describe kernig sign
- Kernig sign (reluctance of knee extension when the hip is flexed)
Describe brudinzki sign
- Brudzinski sign (hips are flexed in response to forced flexion of the neck)
CSF findings in bacterial meningitis
findings include high WBC, low glucose, high protein, ⊕ Gram stain, and ⊕ culture.
CSF findings in viral meningitis
- In viral meningitis, the patient may just have a high WBC level with normal to high protein.
Treatment of meningitis
For adults and children 2 months or older
ceftriaxone 2 g IV OR cefotaxim PLUS dexamethasone
Dexamethasone is not indicated in neonates (up to 1 month of age)
What causes fifth disease (erythema infectiosum)
Parvovirus B19
Presentation of fifth disease
- Prodrome: None; fever often absent or low grade
- Rash: “Slapped-cheek,” pruritic, maculopapular, erythematous rash
- Rash starts on the arms and spreads to the trunk and legs; rash worsens with fever and sun exposure
What causes measles
Paramyxovirus
Presentation of rubella
- Prodrome: Asymptomatic or tender, generalized lymphadenopathy (clue: posterior auricular lymphadenopathy)
- Rash: An erythematous, tender maculopapular rash that also spreads from head to toe
- In contrast to measles, children with rubella often have only a low-grade fever and do not appear as ill
- Polyarthritis may be seen in adolescents
Presentation of roseola
- Prodrome: Acute onset of high fever (>40°C [>104°F]); no other symptoms for 3–4 days
- Rash: A maculopapular rash that appears as fever breaks (begins on the trunk and quickly spreads to the face and extremities) and often lasts <24 hours
- Febrile seizures that may result from rapid fever onset
Presentation of chickenpox (varicella)
- Prodrome: Mild fever, anorexia, and malaise that precede the rash by 24 hours
- Rash: Generalized, pruritic, “teardrop” vesicles on red base; lesions are often at different stages of healing
- rash usually appears on the face and spreads to the rest of the body, sparing the palms and soles
- Infectious from 24 hours before eruption until lesions crust over
Hand foot and mouth virus and presentation
- Coxsackie A
- Prodrome: Fever, anorexia, oral and throat pain Rash: Oral ulcers; maculopapular vesicular rash on the hands and feet and sometimes on the buttocks
Treatment for bronchiolitis
- primarily supportive with hydration, suctioning, and supplemental O2.
- For patients with a history or strong family history of asthma, treatment with bronchodilators may be considered
- Hospitalization of patient is necessary if infant’s hypoxia and/or tachypnea interfere with feeding or if signs of severe illness are present.
- Ribavirin is an antiviral drug sometimes used in high-risk infants with underlying heart, lung, or immune disease.
- RSV prophylaxis with injectable monoclonal antibodies (palivizumab) is recommended in the fall/winter for high-risk patients ≤2 years of age (eg, those with a history of prematurity, chronic lung disease, or CHD)
Important DDx to consider for bronchiolitis
Foreign body aspiration: sudden- onset wheezing or respiratory distress
Objects that cause airway compromise or that cause mucosal damage (batteries) should be removed immediately with bronchoscopy.
Definition of croup
An acute viral inflammatory disease of the larynx, caused by parainfluenza virus, primarily within the sub- glottic space usually 3 months-3 years
Presentation of croup
- Prodromal URI symptoms are typically followed by low-grade fever and mild dyspnea
- inspiratory stridor that worsens with agitation
- hoarse voice
- characteristic barking cough that worsens at night.
Treatment of croup
- Mild cases: Outpatient management with cool-mist therapy and fluids
- Moderate cases: May require supplemental O2, oral or intramuscular (IM) corticosteroids, and nebulized racemic epinephrine
- Severe cases (eg, respiratory distress at rest, inspiratory stridor, accessory neck muscle use): Hospitalization and nebulized racemic epinephrine. The physician should consider intubation if there is danger of airway compromise.
Findings of croup on XR
Steeple sign
Presentation of epiglottitis and initial management
- inspiratory stridor, muffled voice, drooling, tripoding
- Clinical diagnosis but definitive diagnosis is made via direct fibreoptic visualization of cherry- red, swollen epiglottis and arytenoids.
- Thumbprint sign on lateral x ray
- The airway must be secured before a definitive diagnosis can be made.
- In light of potential laryngospasm and airway compromise, an examination of the throat should only be done in the presence of an anaesthesiologist
- Secure the airway first with endotracheal intubation or tracheostomy and then give IV antibiotics (ceftriaxone or cefuroxime).
History taking for anemia in childhood
- Medication history: past and current, particularly those that may cause haemolysis in the instance of G6PD deficiency
- Dietary history: iron intake (with particular attention to iron-rich foods, breast feeding and cow’s milk intake), vitamin B12 intake, recent fava/broad bean ingestion (may precipitate haemolysis in the case of G6PD deficiency)
- Family history: anaemia, jaundice, gallstones or splenomegaly
Signs/symptoms of anemia in childhood
Pallor
Pale conjunctivae
Tachycardia
Cardiac murmur
Lethargy
Poor growth
Poor concentration
Weakness
Shortness of breath
Signs of cardiac failure
Signs of haemolysis include jaundice, scleral icterus, splenomegaly and dark urine
Investigations for suspected anemia in childhood
- Full blood film (FBC), ferritin and reticulocyte count.
- Iron studies or serum iron should not be requested to diagnose iron deficiency. Serum iron reflects recent iron intake and does not provide a measure of the iron stores.
Microcytic anemia with normal ferritin is caused by
Thalasseamia minor
Normocytic anemia with increased reticulocyte count is caused by
Haemolysis or blood loss
Normocytic anemia with no increased reticulocyte count or abnormalities in other parameters raises suspicion for?
Leukemia
Marrow hypoplasia
Infiltration
Test for normocytic, normal ferritin differentiation
HPLC/Hb electrophoresis
Elevated HbA2 >3.5% and/or elevated HbF - beta thalassemia minor
Normal - alpha thalassemia minor
Red flags (for admission) in anemia in childhood
- Hb <60 g/L (including iron deficiency)
- Tachycardia, cardiac murmur or signs of cardiac failure
- Features of haemolysis (dark urine, jaundice, scleral icterus)
- Associated reticulocytopenia
- Presence of nucleated red blood cells on blood film
- Associated thrombocytopenia or neutropenia may indicate malignancy or an infiltrative disorder
- Severe vitamin B12 or folate deficiency
- Need for red cell transfusion: Where possible defer transfusion until a definitive diagnosis is made.
Age range febrile seizures
6mo - 6yo
Features of complex febrile seizures
o have a focal onset
o last longer than 15 minutes
o recur within 24 hours.
Features of simple febrile seizures
o most common type
o usually generalized
o last under 15 minutes
o and do not recur within 24 hours.
Investigations for febrile seizures
- No workup necessary for first-time simple febrile seizures, and no laboratory studies needed if consistent with febrile seizures.
- Infants <6 months of age need a sepsis workup (CBC; urinalysis [UA]; and blood, urine, and CSF culture).
- If complex febrile seizures exclude herpes encephalitis, and include lumbar puncture, CT scan, and/or EEG.
Febrile seizure counselling points
Fever with generalised tonic-clonic seizure, duration <15 minutes, complete recovery within 1-hour, single episode in febrile illness, developmentally normal child
- Occur in 3% of healthy children
- Benign
- Occur between 6 months and 6 years of age
- This does not mean the child will have epilepsy (1% risk – similar to population risk)
- Explain that the child has a 1/3 risk of another febrile convulsion with further febrile illnesses
- Explain that if another convulsion occurs within this febrile illness, this makes it a “complex” febrile convulsion, and would need to be re-evaluated in hospital
- Arrange follow up with GP
- Safety netting about what to do if patient has another seizure
Red flag symptoms/features in febrile seizure
- Developmental delay
- Seizure >15 minutes
- Focal features at onset or during the seizure
- Incomplete recovery within 1 hour
- Recurrence within the same febrile illness
Who gets pyloric stenosis?
- Nonbilious emesis typically begins around 3 to 6 weeks of age and progresses to projectile nonbilious emesis after most or all feedings.
- More common in first-born infant boy
Presentation of pyloric stenosis
- Nonbilious emesis typically begins around 3 to 6 weeks of age and progresses to projectile nonbilious emesis after most or all feedings.
- Infants are hungry after episodes of vomiting; they initially feed well but eventually suffer from dehydration and malnutrition.
- PE may reveal a palpable, olive-shaped, mobile, nontender epigastric mass and visible gastric peristaltic waves.
Investigations for pyloric stenosis and findings
- Abdominal ultrasound will reveal a thickened, elongated pylorus
Treatment for pyloric stenosis
- Keeping the patient NPO (nothing by mouth), establishing IV access, and correcting dehydration and acid-base/electro- lyte abnormalities
- Definitive treatment: Surgical correction with pyloromyotomy
Where does intussusception usually occur?
- A condition in which a portion of the bowel invaginates, or “telescopes,” into an adjacent segment, usually proximal to the ileocecal valve
Epidemiology for intussusception
- The most common cause of bowel obstruction in children between 6 months and 3 years of age (boys > girls)
Presentation of intussusception and examination findings
abrupt-onset, episodic abdominal pain in apparently healthy children, often accompanied by flexed knees and vomiting.
- The classic triad involves severe abdominal pain, vomiting (initially non- bilious and then bilious as obstruction develops), and bloody mucus in stool (“currant jelly stool,” a late finding).
- During examination, the physician should look for abdominal tenderness, a ⊕ stool guaiac test, a palpable “sausage-shaped” right upper quadrant (RUQ) abdominal mass, and “empty” right lower quadrant (RLQ) on palpation (Dance sign).
Diagnosis of intussusception
- Ultrasonography is the initial test of choice and may show a “target sign”
- An ultrasound must be conducted during a painful episode to diagnose intussusception.
Treatment of intussusception
- The physician should correct any volume or electrolyte abnormalities, check CBC for leukocytosis, and consider placement of a nasogastric (NG) tube for decompression.
- High clinical suspicion calls for an air insufflation enema without delay, as it is diagnostic and curative in the vast majority of patients.
- Surgical resection is indicated if the child has peritoneal signs, air insufflation enema reduction is unsuccessful, or a pathologic lead point is identified.
What is malrotation with volvulus
Congenital malrotation of the midgut results in abnormal positioning of the small intestine (cecum in the right hypochondrium) and formation of fibrous bands known as Ladd bands which predispose to obstruction and volvulus with constriction of blood flow.
Presentation of malrotation with volvulus
Often presents in the first month of life with bilious emesis, crampy abdominal pain, distention, and passage of blood or mucus in the stool.
Postsurgical adhesions can lead to obstruction and volvulus at any point in
life.
Diagnosis of malrotation with volvulus
Barium contrast enema may reveal the characteristic narrowed “bird-beak” appearance and air-fluid levels, but may also appear normal.
Upper GI series is the study of choice if the patient is stable and shows an abnormal location of the ligament of Treitz.
Ultrasound may be used, but sensitivity depends on the user’s experience.
Treatment of malrotation with volvulus
NG tube insertion to decompress the intestine; IV fluid hydration
Emergent surgical correction is needed when there is ischemic bowel/GI
tract; definitive management is surgical (Ladd’s procedure)
What is a meckel diverticulum and who gets it?
- true diverticulum containing all three layers of the small intestine.
- This is the most common congenital abnormality of the small intestine, affecting up to 2% of children (boys > girls).
Presentation and complications of meckel diverticulum
Typically asymptomatic and often discovered incidentally. Patients most commonly symptomatic <2 years of age.
- Classically presents with painless rectal bleeding
Complications: Intestinal perforation or obstruction, diverticulitis (which
can mimic acute appendicitis), and intussusception
Diagnosis of meckel diverticulum
A Meckel scintigraphy scan (technetium-99m pertechnetate; detects ecto- pic gastric tissue) is diagnostic.
Indications for and treatment of meckel diverticulum
Definitive treatment: Surgical excision of the diverticulum together with the adjacent ileal segment, which may be ulcerated
Indications for urgent/emergent surgery include hemorrhage, diverticuli- tis, intestinal perforation, and obstruction/intussusception
Cause of hirschsprung disease
- Characterized by congenital lack of ganglion cells in the distal colon. This leads to decreased motility and uncoordinated peristalsis
Hischsprung disease associations
- Associated with male sex, Down syndrome, Waardenburg syn- drome, and multiple endocrine neoplasia type 2 (RET gene mutation).
Presentation of hirschsprung disease
- Neonates present with failure to pass meconium within 48 hours of birth, accompanied by bilious vomiting and FTT
- children with less severe lesions may present later in life with chronic constipation.
- PE may reveal abdominal distention and explosive discharge of stool after a rectal examination; lack of stool in the rectum; and/or abnormal sphincter tone.
Investigations for suspected hirschsprung disease
- Best initial test: X-rays reveal distended bowel loops with a paucity of air in the rectum.
- Barium enema is the imaging study of choice and reveals a narrowed distal colon with proximal dilation (rectosigmoid transition zone). This test differentiates Hirschsprung disease from meconium ileus (seen in CF patients), which would show a microcolon on barium enema testing.
- Most accurate test: Rectal suction biopsy confirms the diagnosis and reveals absence of the myenteric (Auerbach) plexus and submucosal (Meissner) plexus along with hypertrophied nerve trunks enhanced with acetylcholinesterase stain.
History taking for rheumatological conditions (PRISM)
Pain
Rashes, raynauds
Immune conditions in family, eyes, uveitis
Stiffness
Malignancy - paraneoplastic syndromes
Alternative consent for surgical procedure (PR BRA)
Procedure
Rationale
Benefits
Risk
Alternatives
‘My sleepy thoughts cant affect me’ - fatigue causes
- Malignancy
- Sleep
- Thyroid
- CKD, CHF
- Anemia
- Menstruation
Treatment for hirschsprung disease
Traditionally a two-stage surgical correction is used, involving the creation of a diverting colostomy at the time of diagnosis, followed several weeks later by a definitive “pull-through” procedure connecting the remaining colon to the rectum.
What is a greenstick fracture and how is it managed?
Incomplete fracture involving the cortex of only one side (tension/trauma side) of the bone
Reduction with casting X-rays at 10–14 days
What is a nursemaids elbow?
Radial head subluxation secondary to being pulled or lifted by the hand
Pain, pronation, and refusal to bend the elbow; no sensory deficits or wrist drop
Manual reduction
No immobilization
Most common paediatric elbow fracture?
Supracondylar humerus fracture
Complications of supracondylar humerus fracture
Injury to median nerve or brachial artery
Compartment syndrome possible as pain increases despite analgesics
Proximity to the brachial artery increases the risk of Volkmann contracture; the physician should beware of brachial artery entrapment (check radial pulse)
Pre-conception counselling
Before conception
- optimise general health
- assess emotional and social wellbeing: DV
- vaccinations
- Routine supplements and lifestyle
1. Weight: Maternal failure to gain appropriate weight is associated with fetal growth restriction (FGR), whereas excess weight gain is associated with diabetes
An additional 100–300 kcal/day; additional 500 kcal/day during breastfeeding
2. Folate to avoid neural tube defects from 3 months prior to pregnancy - 12 weeks
high dose folate for BMI> 30, diabetic, fhx of NTD
3. Iodine for thyroid support for mum and fetus
4. Iron, calcium, vitamin D and B12 for vegans
- Thirty minutes of moderate exercise daily, while avoiding contact sports
- Avoid fish with high mercury levels
- Moderate caffeine intake
- Avoid uncooked meat, fish, eggs
- Avoid unpasteurized dairy
- Smoking cessation support, discuss alcohol and drugs
- Review medications: ACE, carbamazepine, lead, lithium, methotrexate, phenytoin, valproic acid, vitamin A, warfarin
- Medical co-morbidities: consider referral for pre-conception counselling in context of pre-existing medical conditions, particularly cardiac, diabetes, renal
- reproductive carrier screening
- 3 gene test for CF, fragile X and SMA (spinal muscular atrophy)
Investigations for bHCG positive
- FBE: Anaemia, MCV → thalassemia, ferritin
- blood group and antibody screen
- syphilis serology: at booking, 28 weeks, 36 weeks, delivery, post-partum
give penicillin - midstream urine: pyelo
- STI screen: clamydia, gono, trich, HIV, Hep B, Hep C
- CST
- GTT if risk factors: previous GDM, advanced maternal age, ethnicity, family history,
BMI >30, previous macrosomnia, PCOS, medications eg antipsychotics, corticosteroids - dating U/S
- pre-eclampsia
aspirin reduces the risk of pre-eclampsia for those at risk by about 25% 100mg nocte from 12-36 weeks
diabetes, previous pre-eclampsia, autoimmune diseases
Screening for trisomy 13, 18, 21
Cell-free DNA screening most sensitive and specific screening tool available for trisomies 13, 18, and 21
It is accepted as a primary screening option
28 and 36 week antepartum investigations
28 Week Investigations
- GTT
- FBE Rh (D antigena) immune globulin for Rh⊖ women (after antibody screen)
- STI screen: Syphillis
36 Week Investigations
- GBS screening
- FBE
- STI screen Syphillis
Indications for intrapartum GBS prophylaxis
- GBS-positive rectovaginal swab at 36 to 38 weeks
- GBS bacteriuria/urinary tract infection (UTI) any time during pregnancy
- Prior infant with early-onset GBS sepsis
labor at <37 weeks, intra-partum fever, rupture of membranes >18 hours - Intrapartum prophylaxis: Intravenous (IV) penicillin
Postpartum investigations
Postpartum
- FBE
- UEC
- LFT
- GTT at 6 weeks
- CST
- discuss contraception
progesterone only → minipill or IUD
Screening options for genetic abnormalities
Nuchal Translucency
- Recommended at weeks 9 to 14
- can detect ∼91% of cases of Down syndrome and ∼95% of cases of trisomy 18
- The progress of your pregnancy. The fluid underneath the skin along the back of the fetus’s neck, called the nuchal translucency, or nuchal fold. In some pregnancies, when the fetus has Down syndrome, trisomy 13 or trisomy 18, there is extra fluid behind the neck.
Advantages:
Available earlier than chorionic villus sampling (CVS) and less invasive than CVS
Chorionic Villus Sampling
- 10-12 weeks
- Transcervical or transabdominal aspiration of placental tissue
- Genetically diagnostic
Available at an earlier GA than amniocentesis
- Risk for foetal loss relatively high (1%) Cannot detect open neural tube defects Limb defects associated with CVS at <9 weeks
Cell free foetal DNA
- 10 weeks
- Isolation of foetal DNA from blood sample obtained from pregnant patient
- Non-invasive
- May be limited because of low concentration of foetal DNA in maternal circulation
Amniocentesis
- 15–20 weeks
- Transabdominal aspiration of amniotic fluid, using an ultrasound-guided needle
- Genetically diagnostic
- Premature rupture of membranes (PROM), chorioamnionitis, fetal- maternal hemorrhage
Inevitable miscarriage presentation and treatment
- heavy bleeding with clots and pain
- open cervical os and absent fetal cardiac activity
- misoprostol or methotrexate to medically evacuate retained products of conception
- if haemodynamically unstable→ dilation and curettage
Threatened miscarriage presentation and treatment
- painless vaginal bleeding occurring before 24 weeks, but typically occurs at 6 - 9 weeks
- the bleeding is often less than menstruation
- cervical os is closed
Incomplete miscarriage presentation and treatment
- not all products of conception have been expelled
- pain and vaginal bleeding
- cervical os is open
- misoprostol or methotrexate to medically evacuate retained products of conception
missed/delayed miscarriage presentation and treatment
- a gestational sac which contains a dead fetus before 20 weeks without the symptoms of expulsion
- mother may have light vaginal bleeding / discharge and the symptoms of pregnancy which disappear. Pain is not usually a feature
- cervical os is closed
Management of suspected ectopic pregnancy
if >6 weeks → transvaginal ultrasound scan
If < 6 weeks gestation and women have bleeding, but NO pain or risk factors for ectopic pregnancy → advised:
to return if bleeding continues or pain develops
to repeat a urine pregnancy test after 7–10 days and to return if it is positive
a negative pregnancy test means that the pregnancy has miscarried
Urine/serum hCG: to confirm pregnancy. Critical
Transvaginal ultrasound: determine location of the pregnancy (ectopic vs intrauterine), investigate for differentials (miscarriage, ovarian cyst accident). Critical
Speculum examination: to assess possible volume and origin of bleeding, and assess if cervix is open (threatened miscarriage). Critical
FBE: determine impact of blood loss.
UEC, LFT, coagulation profile.
Urinalysis and urine MCS if indicated: investigate for UTI.
Rh blood type: determine need of administration of anti-D injection.
Group and hold: if patient unstable and in need of immediate resuscitation
Presentation and examination findings ectopic pregnancy
- light bleeding in early pregnancy
- lower abdo pain
- history of amenorrhoea
- shoulder tip pain and pain on defecation / urination
- sometimes hypovolemic shock from concealed intraabdominal haemorrhage
Examination:
- abdominal tenderness
- cervical excitation (also known as cervical motion tenderness)
- adnexal mass
Treatment of ectopic pregnancy
- observation → self limiting if unruptured, asymptomatic, no fetal heart beat
- medical → methotrexate, if unruptured, no sig pain, no fetal HB
- surgical (if pain, visible HB, rupture)→ salpingectomy or salpingotomy if contralateral tube damage
- if haemodynamically stable→laparoscopic salpingectomy
- open salpingectomy is reserved for emergency cases where there is rupture of the Fallopian tube and with haemodynamic instability.
Risk factors for placental abruption
- fall, domestic violence, acute trauma such as car crash
- cocaine and meth
- 35YO
- previous abruption strongest RF
After how many weeks gestation is a placental abruption more likely?
> 20
Management of placental abruption
IV fluids and blood product
Fetus alive and < 36 weeks
- fetal distress: immediate caesarean
- no fetal distress: observe closely, steroids, no tocolysis, threshold to deliver depends on gestation
Fetus alive and > 36 weeks
- fetal distress: immediate caesarean
- no fetal distress: deliver vaginally
Fetus dead
- induce vaginal delivery
Complications of placental abruption
- DIC
- Haemorrhagic shock
- Renal failure
- Intrauterine hypoxia
Causes of PID
- Chlamydia trachomatis most commonly, followed by Neisseria gonorrhoeae and Mycoplasma genitalium.
- In most cases of pelvic inflammatory disease, no pathogen is identified.
Presentation of PID
- Lower abdominal pain (generally bilateral), which may progress to acute abdomen
- Nausea, vomiting
- Fever
- Dysuria, urinary urgency
- Menorrhagia, metrorrhagia
- Dyspareunia
- Abnormal vaginal discharge (yellow/green color)
Investigations for PID
- nucleic acid amplification testing (NAAT) for C. trachomatis, N. gonorrhoeae, and M. genitalium
- Gram stain and culture of N. gonorrhoeae for susceptibility testing.
- If speculum examination is not possible, a first-void urine sample or patient-collected vaginal swab can be used.
- Collect blood samples for culture and susceptibility testing for patients in hospital.
Treatment for PID
Ceftriaxone IM + Metronidazole + Azithromycin
Past medical conditions to ask about before starting corticosteroids
Diabetes
HTN
Epilepsy
Liver disease
Heart disease
Kidney disease
Stomach ulcers
Corticosteroid ATHLETIC
A: Corticosteroids, or steroids, are medications used to reduce inflammation and suppress the immune system in various conditions.
They are involved in many physiological processes, including stress and immune response, inflammation, and electrolyte levels.
T: Steroids should be taken at the same time(s) each day, usually in the morning. This is because steroids can cause insomnia.
“If you forget to take your steroid at the prescribed time, take it as soon as you remember. However, if it’s almost time for your next dose, skip the missed dose and resume your regular dosing schedule. Do not take an extra dose to make up for a missed dose
H:
L: The duration of steroid treatment and the dose prescribed will depend on how well your body responds to the treatment, as well as the nature and severity of the condition being treated. Although steroids are very effective, we try to use them for the shortest possible time and at the lowest dose. This reduces the risk of any side effects
E:
T: “Before starting steroids, you will need some baseline tests like your blood pressure, weight and an eye examination. You will also need a blood test to check your blood sugar and electrolyte levels.”
“When you are taking steroids, we will review you regularly. It is important to monitor your blood pressure, blood sugar and weight
I: Some common short-term side effects include trouble sleeping, increased appetite causing weight gain, indigestion, and mood changes making you feel irritable or short-tempered
“If you take steroids for a long time, you may be at risk of more serious side effects like muscle and bone weakness, stomach ulcers, mental health problems, and increased risk of infections.”
“Corticosteroids can also increase your risk of developing diabetes, hypertension, and cataracts. If you have any concerns or notice new symptoms while taking steroids, it’s important to seek advice.
It’s important to talk to your doctor before stopping steroids. Never stop them suddenly. If you have been taking steroids for a long time, stopping them abruptly can cause a life-threatening condition called an adrenal crisis. This occurs because your body’s natural production of steroids has been switched off.”
“An adrenal crisis can cause symptoms such as tummy pain, feeling sick, dizziness, fever, headache, weight loss or feeling extremely tired and weak. If you experience any of these symptoms, especially if they occur suddenly or severely, seek urgent medical help.”
“When stopping steroids, your doctor will very gradually reduce your dose, allowing your body to start making its own steroids again.”
A steroid emergency card is a small card you should always carry if you take regular steroids. This card is important if you become acutely unwell, the healthcare team need to know that you take steroids as stopping or missing a dose could be life-threatening. Always keep it with you at all times and show it to any healthcare professional you see
When you get sick, your body naturally produces more steroids to help you cope with the stress of the illness. However, if you have been taking steroids for a long time, your body’s natural production of steroids may have been switched off, which can lead to a life-threatening adrenal crisis.”
“To avoid this, it is important to follow sick day rules. If you become suddenly unwell, we may need to increase your steroid dose. Please contact us if you become unwell whilst taking steroids
Blood transfusion PR BRA
P: Before the transfusion, a small sample of your blood needs to be obtained to check your blood group. This will be sent to a lab for testing. A small needle called a cannula will be put into a vein in your arm or hand. You will be asked to give your name and date of birth and this will be checked against your ID band and the details on the bag of donor blood selected for you.”
“The blood will flow slowly from the bag via a plastic tube into your vein. It usually takes 2 to 4 hours for each bag of blood to be transfused. Your temperature, blood pressure and pulse will be checked before, during and after the transfusion.”
The patient’s arm or hand (depending on where the cannula was inserted) may ache and/or have a bruise for a few days after.
Remind the patient that they should contact their GP if they feel unwell, particularly within 24 hours of having a blood transfusion, but any time in the 2 weeks following the transfusion. This is especially important if they have pain in their chest or back, any breathing difficulties, or notice a change in the colour of their skin or urine.
R:
B:
Receiving a blood transfusion can relieve symptoms caused by anaemia
It can prevent damage caused to organs associated with anaemia
It can allow earlier mobilisation and quicker recovery after an operation, acute illness or injury
R:
“Blood transfusion is very safe, but as is the case with any medical procedure, there are some risks.”
“Donated blood is carefully tested and processed, so the risk of infection due to bacteria or viruses like hepatitis or HIV is tiny – less than 1 in a million. We have to check carefully that we match the right blood for you, so you need to wear an ID band and you will be asked to state your name and date of birth before starting. Occasionally, people develop a reaction during the transfusion, such as a temperature or a rash. Rarely, these can be serious. There is a small risk that fluid could build up in your circulation, making you feel short of breath.”
“Events such as these are unlikely and we will check you regularly during the transfusion. It is very important to tell a member of staff if you feel unwell at any point, so we can deal with any problems quickly. Sometimes, after one transfusion your immune system can make antibodies against the donor blood cells. These won’t affect you, but they can make it harder for us to find blood that is a match for you if you needed another transfusion.”
A:
Potential alternatives to blood transfusion may include:
Iron replacement therapy: by tablet or intravenous infusion
Cell salvage: also known as autologous blood transfusion. This can be performed in surgery and is a process in which the blood lost during or just after the operation is collected, filtered and given back to the patient.5
Erythropoietin injections: the hormone that stimulates the body to make its own red blood cells
Doing nothing
Tranexamic acid: can be used to reduce blood loss during surgery
Iron supplementation: can correct anaemia in patients with iron deficiency
Vaccination PR BRA
P:“When you come into the clinic, the nurse will ask a few questions about how your baby is, including whether they have been unwell recently, whether they have any medical conditions and if they have any allergies. This is to make sure it is suitable to give the vaccination.”
“The vaccination will be given as an injection, usually in the thigh.”
R:
B:
“The vaccination programme is very safe, and almost all babies will have them. The reason for vaccination is both to protect your child from harm and to protect the community as a whole.”
“Giving a child a vaccination against a disease dramatically lowers the risk of them catching the illness which could be extremely harmful to them both in the short and long-term. By stopping the disease developing in your child, we also stop your child being able to spread the disease, so it can be considered a public health benefit too. The aim is to immunize enough people so that we can stop the disease completely – this happened with smallpox in some countries.”
R:
“It is normal for your baby to be a bit upset by the injection and cry at the time. You may find they are a little more irritable for 48 hours afterwards and may have a bit of a temperature. If this occurs there are a few things you can do to help including giving some Calpol for the temperature and making sure they are still drinking regularly. In about 1 in 10 children, the place of injection can be a bit red and sore for a day or so – this again should be relieved by Calpol, some reassurance and a cold compress may also help.
“If there is a large swelling at the site of injection, or you notice any rashes or swelling elsewhere (especially around the lips and mouth) it is important to contact the doctor urgently. Very occasionally, a child may have an adverse reaction to the vaccine and may have a temperature that does not respond to Calpol. Children sometimes can experience seizures when they have a raised temperature and if this happens you should seek medical review.”
“Complications of vaccines are very rare (less than 1 in 1000, with the chance of anaphylaxis being less than 1 in 500,000). Complications of the diseases which we are vaccinating against are more common and often more serious, and that is why we feel it is for the best to immunize children.”
A:
Explaining chronic conditions ‘Normally we can probably manage’
Normal anatomy
What the disease is
Cause
Problems/complications
Management
CKD NWCPM
Normal anatomy/physiology
“Think of your kidneys as a coffee filter. When you make coffee, the filter keeps the coffee grains inside, but allows water to pass through. Your kidneys do something similar. They keep the things you need inside your body, but filter out things you don’t need.
The normal function of the kidney is to remove water, control BP and electrolytes, activate vitamin D and RBC production, and remove toxins.”
What the disease is
abnormal kidney function or structure present for greater than three months. CKD has 5 stages. It can be diagnosed and staged based on GFR (which is a measure of your kidney function) or protein in urine. Damaged kidneys are not able to keep you healthy. They cannot filter your blood well enough, and they cannot do their other jobs as well as they should. Kidney disease does not happen overnight. It happens slowly, and in stages. Most people in the early stages do not have any symptoms. They may not know that anything is wrong. But if it is found and treated, kidney disease can often be slowed or stopped.
Cause
most commonly due to diabetes and high BP
Problems/complications
If kidney disease gets worse, wastes can build to high levels in your blood and make you feel sick such as uraemic encephalopathy: Due to the build-up of toxins in the blood which can affect brain function
You may get other problems like high blood pressure, a low red blood cell count (anemia), weak bones, poor nutrition, and nerve damage.
You will also have a higher chance of getting heart and blood vessel disease.
Pulmonary oedema: Due to fluid overload, which builds up in the lungs
If it keeps getting worse, it can lead to kidney failure. This means your kidneys no longer work well enough to keep you alive, and you need a treatment like dialysis or a kidney transplant.
Management
Nonpharmacological:
Exercise
Healthy weight loss
Smoking cessation
Good glycaemic control
Control of blood pressure
Immunisations: influenza and Pneumococcus
Avoidance of nephrotoxic medication
Diet: adequate protein intake, restricted sodium and phosphate intake
Pharmacological
Patients should be assessed for cardiovascular risk factors (lipid profile, BMI, exercise, and alcohol and smoking consumption) and offered a statin and antiplatelet drug for the prevention of cardiovascular disease.
Good blood pressure control is vital in slowing the progression of CKD. In patients with diabetic renal disease or significant proteinuria, an ACE inhibitor or an angiotensin receptor blocker are the first agents of choice, but conversely, they need to be used with care in patients with renovascular disease or those who are at risk of volume depletion or impaired renal perfusion
An SGLT-2 inhibitor may be offered if the patient is taking the highest dose of ACE inhibitor or angiotensin receptor blocker that they can tolerate.
Phosphate binders (e.g. calcium acetate, sevelamer, lanthanum) to control hyperphosphataemia
Generally, patients begin dialysis when their GFR reaches approximately 5-10 mL
There are two treatments for kidney failure – dialysis and kidney transplantation.
*Dialysis is a treatment that removes wastes and extra water from your blood. Two types of dialysis are available: haemodialysis or peritoneal dialysis.
Haemodialysis involves pumping blood from the body through a dialyser (artificial kidney). Blood is removed from body, and into dialyser and clean blood is returned to the body. This can be performed in a hospital or at home. Hospital-based regimens are typically for 4 hours three times a week.
Peritoneal dialysis is a treatment for kidney failure that uses the lining of your abdomen to filter your blood inside your body. The dialysate is delivered to your abdomen where it clears your blood and waste is removed from your body into drainage bag. Peritoneal dialysis is daily. Not appropriate for obese people/multiple abdominal surgeries.
*A kidney transplant is an operation that places a new kidney inside your body. The new kidney will take over the work of your failed kidneys. The new kidney may come from a living donor (usually a relative or friend) or someone who died and wanted to be an organ donor.
provides the best long-term outcome.
Summarise
“Is there anything I have explained that you’d like me to go over again?”
“Do you have any other questions before we finish?”
Follow-up appointment
Leaflets
COPD NWCPM
Normal anatomy/physiology
What the disease is
Airway becomes obstructed so air is trapped in lungs.
Diagnosed based on clinical symptoms chronic productive cough for 3 months for 2 years
Cause
Smoking, air pollution like sulphur/nitrogen dioxide, dust, silica, family history
Irritants causes increased cells and mucus in airways so narrows them down causing air trapping.
Problems/complications
Lung infections are more common as mucus is plugged in airways.
There will be more CO2 and less oxygen in blood vessels in the lungs constrict as they are not getting much oxygen from the lungs and so this increases the pressure in the lungs which can lead to right side heart failure.
Management
Avoid exposure to irritants such as smoke and air pollution.
pneumococcal and annual flu vaccination
physical activity and nutrition
manage co morbidities
pulmonary rehab if symptomatic
pharmacotherapy is stepwise approach
1. SABA (salbutamol) as needed
2. Regular LAMA or LABA
3. LAMA and LABA
4. Add ICS (prednisolone) triple therapy
Supplemental oxygen
Summarise
“Is there anything I have explained that you’d like me to go over again?”
“Do you have any other questions before we finish?”
Follow-up appointment
Leaflets
Depression NWCPM
What the disease is
episodic mood disorder primarily characterized by depressed mood and anhedonia (reduced ability to experience pleasure) lasting for at least two weeks.
Cause
Reduced levels of neurotransmitters serotonin, noradrenaline and dopamine
Biological: family history
Psychological: traumatic and stressful experiences
Comorbidities
Management
Lifestyle modification can include improving sleep hygiene, undertaking adequate physical activity, consuming a healthy diet (Mediterranean diet: vegetables, fruits, nuts, cereals, legumes and fish, diets with high levels of processed foods have been found to contribute to depressive symptoms) minimising alcohol consumption, reducing stress, and reviewing daily routines and social support.
In mild major depression, psychological therapies are preferred; antidepressants are not routinely recommended but can be used if psychological therapies are not available or based on patient preference.
In moderate major depression, either psychological therapies or antidepressants can be used; base initial treatment choice on patient preference. For some patients, concurrent use of psychological therapy and an antidepressant is the most effective management.
In severe major depression, start treatment with an antidepressant. If the patient is willing and able, start concurrent psychological therapy. Electroconvulsive therapy (ECT) may be considered for some forms of severe depression (eg melancholic depression).
In psychotic depression, refer the patient for urgent treatment by a psychiatrist, specialist centre or mental health team.
Once an acceptable response has been achieved, continue treatment for the recommended duration (6 months at least) after a single episode of major depression because there is a high risk of relapse.
more frequently at the start of treatment because activation and suicidal thoughts are more common during the first 7 to 10 days.
Assess response to antidepressant treatment after 2 to 4 weeks. Response to treatment usually becomes apparent after at least 1 to 2 weeks; full benefit may take 4 to 6 weeks or longer. Approximately 60% of people with major depression respond to treatment with an initial antidepressant but only 40% will achieve full resolution of symptoms.
Diabetes NWCPM
“After we eat a meal, the food is broken down into sugar, which is released into our blood. This sugar is the fuel for all the cells that make up our body, and needs to get from the blood into the cells for them to function properly.”
Explain to the patient that they should think of sugar like a car, insulin like a key and the cells in their body as a garage.
“When you drive home, you use your key, the garage opens and you can park your car. This is what normally happens in our body too. If we imagine sugar is the car, the cells are the garage, and a hormone called insulin is the key, sugar can only enter the cells when insulin is working properly.”
What the disease is
Sugar cannot get into the cells and therefore builds up in the tubes of the body which supply the cell with blood. This build-up of sugar in the blood can cause damage to the cells if it remains too high for too long – whether that be the cells of the heart, eyes, liver, kidneys etc.”
Cause
a combination of genetic and environmental factors (e.g. diet, obesity and overall lifestyle). People with type 2 diabetes have a combination of inadequate insulin production and increased insulin resistance (the cells ignore the insulin and don’t allow the sugar in).
Problems/complications
high levels of sugar in the blood can damage the blood vessels of:
* the kidneys causing kidney failure
* the heart which can increase the risk of heart attacks
* the brain which can increase the risk of stroke
* the eyes causing loss of vision
* the nerves of the lower limbs causing peripheral neuropathy
Also, outline how diabetes can cause slow healing of wounds and explain the risk of diabetic ulcers (including what these look like).
Management
Although we cannot cure it, we can manage it so that we stop these complications from happening and you can live your day-to-day life
* Lifestyle change: healthy diet (avoiding foods high in sugar), losing weight, regular exercise.
* Stop smoking (if relevant)
* 3 monthly cardiovascular assessment + HbA1c
* Yearly lipids, renal function, podiatry
* 2 yearly ophthalmology
* Counselling on starting metformin (this helps the garage recognise the key i.e. increases insulin sensitivity) or other oral hypoglycaemics
* How: Oral tablet that you take once daily with food, asap after your meal at a fixed date and time
Doses: 500mg BD (then review after 1-2 weeks)
Duration: Lifelong required, with close monitoring of complications
* Side effects: Nausea, diarrhoea abdominal pain, lose energy
* If you miss a dose, take it asap, unless it is too close to the next dose
* Managing any complications as they arise
Eczema NWCPM
Normal anatomy/physiology
“The normal function of the skin is to act as a barrier. We can imagine the skin to be layers of bricks stacked on top of each other. In normal skin, the mortar between the bricks prevents irritants from getting in and prevents water from getting out which stops the skin from drying out.”
What the disease is
“In eczema, the ‘bricks’ become dry and cracked, and the mortar between the bricks can be lost, compromising the waterproofing. This means that the moisture from the skin can escape, causing it to become dry and itchy, and increasing the exposure to irritants which causes it to become red, inflamed and itchy. These patches of skin are most commonly located in skin creases, such as the front of the elbows and wrists, backs of the knees and around the neck.”
It is a relapsing and remitting condition that presents with areas of red, itchy, dry skin on the body, face and/or scalp.
Cause
“Eczema is a condition that mostly affects children, who may grow out of it, however sometimes it can affect adults. We typically see eczema come and go in what we call flares, in which affected skin becomes more sore, dry, and red than usual, after which it may settle down.”
“We don’t know exactly what causes eczema, but we do know that it can run in families. Family members can have eczema, hay fever or asthma or a combination of these conditions. People who suffer from eczema are more likely to get allergic reactions to food, clothing, dyes etc. but eczema is not an allergy itself. It is caused by a complex immune reaction in the skin.”
“Eczema is normally diagnosed by inspecting the affected skin for signs of the disease. We don’t usually need to do any additional tests for eczema. It is not caused by an allergy, so allergy tests do not help us make the diagnosis.”
Problems/complications
One of the serious complications of eczema is an infection of the skin. The signs to look out for are if your skin starts to ooze, crust, you see clusters of blisters or if you have any of these symptoms with a fever.
Management
- avoid any exacerbating factors/triggers such as soaps with perfumes, detergents, wool, pets etc.
The management of eczema follows a stepwise approach
- Topical emollients (ointments, creams) are the first step
- followed by topical steroids
During a flare, we suggest that you use a topical steroid cream. Steroids work by reducing inflammation, and we know that the best way to do this in eczema is to rub it directly onto the inflamed skin. We recommend that you continue to use this for 48 hours after your skin improves, to help prevent it flaring up again, but we don’t suggest continuing to use it after that. Steroids should not be used on the face as they can cause thinning of the skin and other serious side effects. You should always wash your hands after applying steroid creams.”
“In most people, the treatments we have discussed will control your eczema extremely well. However, we do have other options for treatment if these are not successful and we can discuss those if it becomes appropriate.”
These include immunomodulators, then phototherapy, and finally systemic treatments. Antihistamines are only used to reduce itching when this causes problems with sleeping.
Emergency contraception BUCES NWCPM
Brief history
* Details of the unprotected sexual intercourse (UPSI) including dates and times
* Whether there has been other UPSI this menstrual cycle
* Details of the patient’s menstrual cycle, including the first day of their last period. You will need to calculate where they are in their cycle, and when you might expect them to ovulate (14 days before menstruation).
* Details of any current contraception being taken
* Offer STI screen
* Ask if UPSI was consensual
Understanding
* “Have you heard of emergency contraception?”
* “What do you already know about emergency contraception?”
Concerns
* “Do you have any particular worries about emergency contraception?”
Explain
“Emergency contraception helps to reduce the risk of you becoming pregnant after having unprotected sex. It will not stop an existing pregnancy, and it is not the same thing as a termination.”
“There are three types of emergency contraception available. Two of these are types of ‘morning-after pill’, which both work in similar ways. These pills are called Levonelle® and ellaOne®. There is also the option of inserting a copper IUD, which is more effective than the morning after pill but involves a procedure.”
“We will talk through these options together and see which one works best for you.”
Levonelle (levonestrogel)
A: Inhibits ovulation if taken before LH surge
T: 72hr window for use
H: Oral tablet, can be used alongside other hormonal contracpetion
L:
E: Less effective than other forms of emergency contraception
T: weight
I: Vomiting, change to menses
C: Double dose for BMI >26 / Weight >70kg
Ella one (ulipristal acetate tablet)
A: Delays ovulation; effective before or at the start of the LH surge
T: 5 day window for use
H:
E: Not effective when progestogens have been taken in the 7 days preceding or 5 days following use (stop progesterone for the next 5 days)
T:
I: Vomiting, change to menses
C: Not suitable for patients with severe asthma
Copper IUD:
A: An inhibitory effect on both fertilisation and implantation due to copper toxicity
T: 5-day window for use; and can be inserted up to 5 days after the earliest expected date of ovulation
H: Requires insertion
L:
E: 99% effective, ongoing contraception for 5-10 years
T:
I: Infection, expulsion, perforation, ectopic pregnancy
Summary
Perform pregnancy test 3 weeks after UPSI, to ensure that they have not become pregnant. This should be done even if they have bleeding as this may not represent a normal period.
Epilepsy NWCPM
Normal
Basically, when a certain area of the brain is needed, it activates and sends signals out to our body to do its job
What the disease is
“A seizure is an event that occurs when there is a chaotic burst of signalling that interferes with the brain’s normal function
Epilepsy is a condition that affects the brain and causes a person to have an increased tendency to have something called seizures
Most seizures only last a few seconds to one minute. Some people have warning signs before they experience a seizure. This pre-warning is called an aura and can be anything from a sound you hear, a warm feeling in your stomach, a smell or any other type of sensation.”
When someone has a seizure, they may lose consciousness, or they may stay awake during it. The symptoms of a seizure depend on the area of the brain affected by the chaotic signals. For example, if a seizure occurs in the part of the brain that only controls your left leg, you may remain awake but notice that your left leg begins shaking and moving uncontrollably. If the seizure then spreads to affect your whole brain, you would lose consciousness and your whole body would begin shaking. After a seizure, you might be very tired, confused and need sleep to recover. Full recovery typically happens within several hours.”
Cause
“Epilepsy does not have one specific cause. Some people are born with epilepsy, and some develop it later on in life. It may be caused by events that happen before you are even born or during the process of birth. Epilepsy can develop later in life as a result of head injury, infection, brain tumour or a stroke. In many cases, however, the cause of epilepsy remains unknown.”
“There are certain circumstances and substances that increase the risk of people with epilepsy having a seizure and we call these triggers. Some examples of triggers include heavy alcohol use, dehydration, lack of sleep, use of certain medications, recreational drugs, fevers, flashing lights and missing doses of epilepsy medication.”
Problems
“Because a seizure can happen at any time, you should consider avoiding activities that put you at an increased risk of injury if a seizure were to occur, such as taking baths or swimming alone, or activities like mountain climbing or skiing. If your seizures are not controlled, you will also have to avoid driving by law until one year passes without a seizure. You may fall and injure your head during a seizure; young children or individuals with frequent seizures may be encouraged to wear a helmet to protect against this.”
“If prolonged seizure activity occurs without recovery, this is known as ‘status epilepticus’. Status epilepticus is a medical emergency that can result in permanent brain damage if not recognised and treated promptly. You should inform family and friends if you are carrying an emergency medicine that they can give you, usually in your mouth, if status epilepticus occurs, and they should be aware of the need to seek immediate medical attention.”
“In rare instances, people with epilepsy may die suddenly for reasons that are unexplained, often during sleep or when no one else is around. This may occur during or after a seizure. This only happens to about 1 in every 1000 people with epilepsy per year, however, it is important to be aware of this as you can decrease your risk by taking your medications as prescribed and checking in with your doctor if your seizures are not under control.”
“You may experience some side effects of the medication you are taking to control your seizures. These will vary based on the medication that has been chosen for you, but may include fatigue, depression, nausea, vomiting, dizziness, and sleep disturbance
Management
“The primary goal of treating your epilepsy is to reduce the number of seizures you experience. It may take some time to find out what works for you, and we will work together to optimize your treatment to allow you to live your life as normally as possible.”
“It is extremely important to take your epilepsy medication as prescribed. You may also be given an emergency medication in the form of a small packet of gel, that someone can squish out into your cheek if you are having a very long seizure.”
“In addition to the medication, you can choose to make some lifestyle changes that could reduce your risk of having seizures. These include making sure you get enough sleep, avoiding alcohol and recreational drugs, and managing your stress. You may notice something in your life that may trigger you to have seizures, and if you do, it is important to avoid this wherever possible. In addition, you might notice you get a warning sign, known as an aura, before you have a seizure. This can be helpful as you can sit or lie down if possible and alert someone nearby.
You may find it helpful to educate some of the people that you spend a lot of time with on what to do if you have a seizure. This includes supporting your head and turning you onto your side if you fall to the ground, timing the seizure, and calling emergency services if the seizure lasts more than 5 minutes or if you injure yourself during a seizure. If you carry emergency medication, you can instruct them on where you keep it and how to give it to you. You can also tell them what they can expect after you have a seizure, such as being groggy or confused
HIV NWCPM
Normal anatomy/physiology
“Normally body has cells called T cells that fight infections.”
What the disease is
“In HIV, the virus attacks these T cells, and the immune system fails. Overtime, T cell numbers decrease, and the virus increases. When the T cells drop low enough, you might have swollen lymph nodes, white patches on tongue, yeast infection in mouth. We detect the virus by looking at antibody in your blood.”
Cause
most commonly due to sexual transmission. Needle sharing, during childbirth from mother to child.
Problems/complications
When T cells drop extremely low, we call it AIDS. You might experience persistent fever, weight loss, fatigue, diarrhoea, recurrent bacterial pneumonia, fungal infections, cancers.
Management
Currently no cure but treatment can reduce risk of transmission and help people live longer and healthier lives.
ART (antiretroviral therapy) which is a combination of medicine called HIV regime help immune system recover, slows down replication of virus.
HIV-positive patients should be monitored every 3-6 months in early disease and 2-3 months in late disease, to assess for opportunistic infection, changes in viral load and CD4+ count.
Life-expectancy is lower for HIV-positive individuals but is significantly improved with early initiation and strict adherence to antiretroviral therapy.
Questions to ask about previous anaesthetics
- Has the patient had any previous anaesthetics? If so, was that under general anaesthetic or another method? – e.g. peripheral nerve blocks, spinal, epidural and/or sedation
- Did they have any problems with previous anaesthetics?
Example: malignant hyperthermia, anaphylaxis, difficult airway - How long did they take to wake up? Was it a few hours or a few days?
- Did they require intensive treatment unit (ITU) admission post-op due to problems waking up?
- Is there any family history of problems with anaesthetics?
- Have they or their family members had any specific testing? – i.e. genetic, allergy or other testing relating to anaesthetic agents (MH or suxamethonium apnoea)
- Did they experience postoperative nausea and vomiting previously?
Which medications to ask about specifically in anaesthetic pre-op assessment
Peniciilin - allergy to this
NSAIDs - allergies to these
Anticoagulants
Antiplatelet agents
Antihypertensives
- for all above, when they last took them.
OTC and herbal medications
Structure of anaesthetic pre-op assessment
Previous Anaesthetics
Previous medical history
Medications
Allergies
PC
Fasting period
Airway assessment
Additional investigations as indicated
Airway assessment in pre-op anaesthetic assessment
- Weight
- Head and neck movement
- Jaw movement
- Receding mandible
- Teeth (loose/dentition)
Fasting periods before anaesthetic
Fasting period
- Water – up to 2 hours before induction of anaesthetic
- Food/milk – up to 6 hours before induction of anaesthetic
- Chewing gum up to 2 hours before induction
Anaesthetic pre-op PMHx questions
- Resp and cardio conditions, GORD, diabetes, renal/liver disease, bleeding, loose teeth, pregnancy
- Who manages their chronic condition?
- Recent GP visits and hospital admissions relating to a chronic condition
- Recent changes in treatment
- Associated complications of condition and body systems affected
Tip: with chronic conditions its useful to ask more questions to gauge their severity. - Smoking stop 1-3 days
- Pregnant?
- LMP
When to stop medication before anaesthetics
Stop warfarin (6d), heparin (4h), dabigatran/apixban (48h), antiplatelets (7d), diabetic meds omitted day of, steroids (may need supplementary steroids), COCP, Monoamine oxidase inhibitors (MAOi) (antidepressant), St John Wort (2 weeks)
Explain the bowel cancer screening program
Explaining the program
“The bowel cancer screening test is for people aged 50-74. It is done every two years. You will be posted a free kit you use at home. It involves collecting a single sample of poo into a small plastic sample bottle and then posting this back to a laboratory for testing. This sample is used to check for tiny amounts of blood in your poo. It does not diagnose bowel cancer, but it’s a simple way to find out if you need further tests.”
Method of collection
“Use a container or layers of toilet paper to catch the poo sample and don’t let the poo touch the toilet water. Collect a sample by scraping the stick along the poo until all grooves are covered. Only a small amount of poo is required for the test. Push the stick back into the sample bottle and click the cap to close it. Do not reopen the bottle after use.”
Explaining result
“Your result should be posted to you within 2 weeks of sending off your kit. A normal result means that no blood was found in your poo sample and therefore you do not need to do anything else. You’ll be invited to do another screening test in 2 years. An abnormal result means that blood was found in your poo sample, but this does not necessarily mean you have bowel cancer, as the blood may be due to other conditions such as gastroenteritis, haemorrhoids, anal fissures. You’ll be offered another test called a colonoscopy to check for signs of bowel cancer. A colonoscopy involves the insertion of a thin tube with a camera at the end into your bottom.”
Consenting for a CST
Explaining the procedure
“Today I need to perform a cervical screening test. This looks for the presence of a virus called HPV. If HPV is found, the lab will perform another test on the sample (cytology) to look for any abnormal cells caused by the virus. If abnormal cells are seen, you may need further investigations. The procedure will involve me inserting a small plastic device called a speculum into the vagina. This will allow me to visualise the neck of the womb (your cervix). I will then place a very small brush into the vagina and take a sample of cells from the neck of the womb. It shouldn’t be painful, but it will feel a little uncomfortable. You can ask me to stop at any point. You may experience some light vaginal bleeding after the procedure.”
Chaperone
“One of the female ward staff members will be present throughout the examination, acting as a chaperone, would that be ok?”
Consent
“Do you understand everything I’ve said? Do you have any questions? Are you happy for me to carry out the procedure?”
Ask the patient if they have any pain or if they think they may be pregnant before proceeding with the clinical examination. Establish their last menstrual period (cervical screening is not recommended during menstruation). Provide the patient with the opportunity to pass urine before the examination. Explain to the patient that they’ll need to remove their underwear and lie on the clinical examination couch, covering themselves with the sheet provided. Provide the patient with privacy to undress and check it is ok to re-enter the room before doing so.
Presentation of acute fatty liver of pregnancy
- typically manifest third trimesters
- rare, life-threatening obstetric emergency
- presents with Sudden onset of jaundice, RUQ pain, nausea, and vomiting, coagulopathy
- bright white liver on US
- immediate delivery regardless of gestational age
Pharmacological treatment for smoking cessation
- combination nicotine replacement therapy (NRT) (use of a slow-acting NRT [nicotine patch] with a medium-acting form [eg gum, lozenge or inhalator] and/or a fast-acting form [nicotine mist spray])
- varenicline: The most effective drug therapy is the nicotine agonist varenicline, closely followed by NRT.
- bupropion: when combination NRT and varenicline are not suitable.
Medium- or fast-acting NRT can be safely added to varenicline or bupropion if required to control cue-driven cravings. - If one first-line drug therapy is not suitable or effective after an adequate trial, consider another first-line drug before considering nortriptyline or nicotine vaping products.
Smoking cessation history taking questions
- How long has the patient been smoking?
- How much does the patient smoke? (pack-years = [number of years smoked] x [average number of packs smoked per day]; one pack is equal to 20 cigarettes)
- What type of tobacco/nicotine does the patient use?
- In what situations does the patient smoke?
- How does smoking make the patient feel?
- How does smoking affect the patient’s life and interpersonal relationships?
- How does the patient finance their smoking habit?
- How much would the patient save if they quit smoking?
- Has the patient previously tried to quit? If so, what resulted in the patient relapsing?
- Does the patient experience any withdrawal symptoms? (e.g. craving, irritability, dizziness, low mood, fatigue, insomnia)
STAR approach to assist smoking cessation
- Set a quit date based on the patient’s willingness, motivation and agreement. This should usually be within 2-4 weeks (abrupt quitting is usually more effective than gradual quitting).
- Tell family and friends. Advise the patient to make family and friends aware that they are quitting to provide further accountability and support.
- Anticipate challenges that a patient will face and make plans on how to overcome them.
- Remove all tobacco products as well as recommending counselling programs and pharmacological therapies as indicated
Specific questions for rash in a child under 12mo
For Measles: “You’ve noted a cough and runny nose along with the rash. These symptoms, combined with the presence of Koplik’s spots and recent exposure, point towards measles. Could you confirm if these spots appeared before the rash spread?” Critical
For Roseola: “Roseola often begins with a sudden high fever that drops as a rash emerges. Did the fever precede the rash, and how quickly did the rash follow the fever?”
For Fifth Disease: “Fifth disease typically presents with a ‘slapped cheek’ appearance before spreading. Did the rash start on his cheeks and spread from there?”
For Scarlet Fever: “Does Lucas show any signs of a sore throat or a ‘strawberry’ tongue along with his rash? These are indicators of scarlet fever.”
Management for unstable angina
● Admit to Short Stay Unit
● 300mg aspirin stat
● Antiplatelet therapy (e.g. ticagrelor)
● Pain relief e.g., morphine or IV nitrates
● Antiemetics if required
● Fluids if required
● Arrange cardiology consult
● Repeat troponins and ECG at 6-8 hrs
● Cardiac stress test before discharge
● Investigation of worsening angina
● Modification of lifestyle factors and anti-anginal Mx
e.g., adding a beta blocker or long acting nitrates
Team roles in ALS
Team roles
● Team leader: communicating, directing and checking in with team, ordering
investigations, establishing diagnosis, coordinating management
● Airway: ensuring patency, ventilating patient
● Circulation: early IV access (2 large bore cannulas, intraosseous if unable), obtain
bloods
● Defibrillation: applying defib pads, following COACHED approach, ensuring safety
● Scribe: documenting time of events, administering medications, rhythm during
evaluation
● Medications: preparing and administering medications
CDE of ABCDE
○ Circulation: ?haemorrhage, signs of shock (pulse, CRT, skin colour, BP),
12-lead ECG, IV access
○ Disability
■ GCS: Eyes 4 points, Verbal 5 points, Motor 6 points
● Alternatively, the FOUR score (EMBR: eye response, motor
response, brainstem reflexes, respiration)
● Or AVPU: awake, verbal stimulus, pain stimulus, unresponsive
■ Pupils: size, symmetry, reflex
■ BSL - DEFG = Don’t ever forget glucose!
■ Quick neuro Ex: squeeze fingers, move toes, poke out tongue
○ Environment/exposure: allergens, adequate exposure to identify injuries,
maintaining temperature
What is beurgers test?
Test for arterial insufficiency
Elevate leg 45deg - assess for pallor
Drop leg over bed 90deg (seated) - assess for cyanosis
LL pulses for palpation
● Femoral
● Popliteal
● Posterior tibial
● Dorsalis pedis
● Abdominal aorta
Neurovascular examination general inspection findings
o Amputation
o Ulcers
o Colour
▪ Erythema
▪ Pallor
o Necrosis
o Venous staining
o Varicosities
o Atrophy (muscle wasting)
o Scars
o Loss of hair
o Nail changes
o Charcot’s joints
Symptoms of aortic stenosis
Exertional syncope, exertional chest pain
Pathophysiology of asthma
- Bronchoconstriction
● Airway edema and inflammation
● Airway hyperreactivity
● Airway remodeling
Common RFs for heart failure exacerbation
Common triggers for exacerbation/decompensation include:
- AMI, Arrhythmia, hypoxia, infection, anaemia, AKI
- Medications can exacerbate heart failure including: NSAIDs, corticosteroids, calcium
channel blockers, tricyclic antidepressants.
Mgmt of acute HF exacerbation
The first line therapy for acute heart failure and relief of congestion are diuretics
- In patients with severe HF, the use of IV loop diuretics in hospital are recommended
- In mild HF, increasing oral diuretics can provide symptomatic relief.
Mgmt of CHF
Management of chronic heart failure:
- Using a combination of ACE inhibitors/ARBs, MRA and beta blockers
- Repeat echocardiograms
- Use of multi-disciplinary teams to manage heart failure (cardiologists, nurses, GP,
physiotherapists)
- Regular weigh-in, at home or in the clinic to monitor.
Non-cardiac causes of APO
Other non-cardiac causes of APO include liver
failure, nephrotic syndrome, sepsis, pulmonary
infections etc.
Difference between APO and pleural effusion
While pulmonary oedema occurs within the lung
parenchyma, pleural effusion occurs within the
pleural space. The two can occur simultaneously.
On examination, pulmonary oedema
accompanies reduced breath sounds +/- crackles on auscultation, while pleural effusion
often accompanies dullness on percussion.
Signs of biventricular HF
Biventricular heart failure. Dyspnoea, orthopnea
and PND are signs of pulmonary congestion due to blood backing up in lungs in left heart failure.
Peripheral oedema is a sign of right heart failure as blood backs up in the systemic veins.
Causes of chronic cough in adult
Chronic cough:
- Adults:
- Upper airway cough syndrome (aka postnasal drip)
- Asthma
- GERD
- Chronic bronchitis
- ACEi
- Emphysema
- Bronchiectasis
- Chronic hypersensitivity pneumonitis
- Lung cancer/metastasis
- TB
- ILD (sarcoidosis, silicosis)
- CF
Causes of chronic cough in child
- Children
- foreign body
- Asthma
- URTI
- GERD
- Pertussis
- Viral bronchitis
- CF
- immune deficiency
RF’s for OSA
- Older males, postmenopausal women
● Obesity (BMI >30)
● Craniofacial and upper airway abnormalities
● Smoking
● Family history of snoring or OSA
● Comorbidities e.g. CHF, atrial fibrillation, pulmonary hypertension, hypertension,
ESKD, COPD etc
Diagnostic test for OSA and interpretation
Ultimately, the gold-standard diagnostic test for OSA is polysomnography which looks at
apneoa:hypopneoa index (AHI), arousal events on EEG, O2 saturations, pulse pressure etc.
Classification of severity can be according to AHI, but this is not entirely predictive of the
presence and severity of symptoms and complications.
● Mild: AHI 5-14
● Moderate: AHI 15-30
● Severe: AHI >30
Presentation, RFs and Rx for sponatneous bacterial peritonitis
Spontaneous bacterial peritonitis (SBP) is defined as infection of ascitic fluid in the absence
of an identifiable intra-abdominal treatable source. It is seen almost exclusively in cirrhotic
patients with ascites. The presentation of SBP is subtle compared to secondary bacterial
peritonitis (i.e. from a ruptured appendix) and classically includes a triad of fever, diffuse
abdominal pain* & worsening ascites. Untreated SBP can result in shock and multisystem
organ failure.
*Abdominal pain due to SBP is milder due to the presence of ascites and some patients may
even be asymptomatic. For this reason, empirical antibiotic therapy is initiated immediately
following paracentesis for MC&S when there is a high clinical suspicion (ceftriaxone or
cefotaxime) or prophylactically for cirrhotic patients with a previous episode of SBP
(trimethoprim sulfamethoxazole).
Investigations for suspected IBS
- FBE (UEC, LFT)
● B12, folic acid
● Faecal Calprotectin, Faecal Lactoferrin
● IgA TTG, IgA EMA, IgG DGP
● Stool MCS+ PCR
Consider:
● Endoscopy: c-scope, g-scope, s-scope +/- biopsy
● Abdo X-ray/CT
Investigations for celiac disease
tTG IgA - IgA tissue transglutaminase antibody
Total igA - IgA deficiency
Additional:
Deamidated gliadin peptide
HLA-DQ2 and DQ8 99% association
Cluster headache diagnostic criteria
Requires ALL of the following:
1. At least five attacks
2. Attacks characterised by severe or very severe unilateral orbital,
supraorbital and/or temporal pain lasting 15 to 180 minutes when
untreated; during part (but less than half) of the time-course of cluster
headache, attacks may be less severe and/or of shorter or longer
duration
3. Either or both of the following:
● At least one of the following symptoms or signs ipsilateral to the
headache:
○ Conjunctival injection and/or lacrimation
○ Nasal congestion and/or rhinorrhoea
○ Eyelid oedema
○ Forehead and facial sweating
○ Miosis and/or ptosis
● A sense of restlessness or agitation
4. Attacks have a frequency between one every other day and eight per
day; during part (but less than half) of the active time-course of cluster
headache, attacks may be less frequent
5. Not better accounted for by another ICHD-3 diagnosis
Subdural hematoma explanation and findings on CTB
Subdural haemorrhage (SDH) is a collection of venous blood between the dura and
arachnoid mater. It is most frequently associated with trauma or falls
- Epidural haematoma appears as a lentiform (lemon-shaped) on CT
● Subdural haematoma is typically crescentic (banana-shaped) on CT
Presentation of ACA stroke
ACA strokes present with:
- Dysarthria
- Aphasia
- Unilateral contralateral motor weakness (with leg/shoulder involvement more
common than upper limb/face involvement)
- Limb apraxia
- Urinary incontinence
Presentation of horners syndrome and causes
Horner syndrome (HS) is a neurological disorder characterized by a symptom triad of miosis (an abnormally small pupil), partial ptosis (drooping of the upper eyelid), and facial anhidrosis (absence of sweating).
This condition results from lesions that interrupt the ipsilateral sympathetic nervous supply to the head, eye, and neck. Most cases of HS are idiopathic, but conditions such as brainstem stroke, carotid dissection, and neoplasm are occasionally identified as the cause of HS.
Causes of chorioamnioitis
Most commonly due to ascending cervicovaginal bacteria
Common bacteria: Ureaplasma urealyticum (up to 50% of cases), Mycoplasma hominis (up to 30% of cases), Gardnerella vaginalis, bacteroides, group B Streptococcus, E. coli
Risk factors
Prolonged labor or premature rupture of membranes (PROM)
Pathological bacterial colonization of vaginal tract (e.g., STDs, frequent UTIs)
Iatrogenic: multiple digital vaginal exams, invasive procedures (e.g., amniocentesis)
Clinical features
Management of chorioamnionitis
Most commonly due to ascending cervicovaginal bacteria
Common bacteria: Ureaplasma urealyticum (up to 50% of cases), Mycoplasma hominis (up to 30% of cases), Gardnerella vaginalis, bacteroides, group B Streptococcus, E. coli
Risk factors
Prolonged labor or premature rupture of membranes (PROM)
Pathological bacterial colonization of vaginal tract (e.g., STDs, frequent UTIs)
Iatrogenic: multiple digital vaginal exams, invasive procedures (e.g., amniocentesis)
Clinical features
Tendon reflexes and corresponding nerve roots
○ Biceps jerk - C5, C6
○ Brachioradialis jerk - C5, C6
○ Triceps jerk - C7, C8
○ Finger jerk - C8
- Knee Jerk: L3, L4
● Ankle Jerk: S1, S2
● Plantar Reflex: L5, S1, S2
LL myotomes
Hip flexion: L2, L3
● Hip extension: L5, S2
● Hip abduction: L4, L5, S1
● Hip adduction: L2, L3, L4
● Knee flexion: L5, S1
● Knee extension: L3, L4
● Dorsiflexion: L4, L5
● Plantarflexion: S1, S2
● Foot inversion: L5, S1
● Foot eversion: L5, S1
Delirium causes ‘PINCH ME’
Pain
Infection
Nutrition
Constipation
Hydration
Medication
Environment
Dementia types and specific questions for each
Alzheimers - Short term memory impairment, gradual onset, apathy, irritability, poorly oriented (to time, people and place)
Vascular dementia - Major cardiac RFs (FHx, smoking, diabetes, cholesterol, obesity, physical inactivity, gradual decline with stepwise progression
Frontotemporal dementia: language difficulties, personality change, impulsive or inappropriate behaviours, apathy, loss of empathy, difficulty with comprehension
Lewy body dementia: Delusions or hallucinations, Parkinsonism, issues with attention/visuospatial function
Other causes of dementia aside from major subtypes
HIV history (IVDU, blood
transfusion, risk sexual behaviour, positive test), risk of prion disease (UK in the 80s)
Parkinson’s Dx (screen symptoms:
bradykinesia, mask like facies, tremor, rigidity, mental slowness, postural instability)
FHx of Huntington’s Disease
TBI - LOC, contact sports, ETOH consumption
Depression
Delirium - med changes, lack of sleep and other causes
Stroke
Other symptoms to consider screening for in dementia/memory loss
Mania, psychosis, depression, anxiety
Non-pharmacological treatment - dementia
At home supports with ADLs - OT
Psychology referral for low mood/irritability
Falls and balance classes and risk assessment - physio, EP
Webster packs for medication mgmt
Muti-d involvement of social worker, pharmacist
Nutritional needs - dietician
ACD planning -geriatrician, social work
Language difficulties - speech pathologist
Carer and spouse support
Resources
Pharmacological treatment - alzheimers
Donezepil - cholinesterase inhibitor
*Cholinesterase inhibitors affect the sinoatrial and atrioventricular nodes and increase the risk of bradycardia, syncope, and heart block.
Memantine - NMDA receptor antagonist
Risk factors for alzheimers
Genetic
HTN
DM
Dyslipidemia
Alcohol use
TBI
Sleep deprivation
Lack of physical activity
Age
Family Hx (strongest)
Routine blood tests for memory loss/dementia
Full blood count (FBC)
Erythrocyte sedimentation rate (ESR)
Liver function test (LFT)
Calcium
Thyroid function
B12, folate
CT scan of brain without contrast
Lipids
What is glutamate
The main excitatory neurotransmitter in the brain, released by almost half of brain synapses. Clinically important for its role in neurotoxicity secondary to neural injury
What is GABA
An inhibitory neurotransmitter that reduces neuronal excitability and muscle tone
Benzodiazepine MOA
GABA receptor agonists
Effects of benzodiazepines
Anxiolysis
Sedation
Hypnotic action
Muscle relaxation
Anticonvulsant action
Amnesia
DDx questions for nephrotic syndrome
Foamy urine
Minimal change disease: Most common in children, often idiopathic, can be infection, nsaids. Rx with prednisolone. Effacement of foot processes
Focal segmental glomerulosclerosis: Most common in adults, HIV, heroin, sickle cell, obesity, interferon treatment. Rx with prednisolone
Diabetic nephropathy: associated retinopathy, neuropathy. Rx with ACE-I/ARB, glycemic control
Lupus nephritis: rashes, mouth ulcers, arthralgias
Henoch-schonlein purpura - Petechial/purpuric rash, arthralgia, abdo pain
Management of nephrotic syndrome in children
- Admit to paeds for first presentation
● Educate parents
● Manage oedema - fluid and salt restriction, daily
weighs, daily urine dipstick for 1-2 years + document
● High dose pred (60mg/m2/day for 4 weeks and wean
slowly) + defer live vaccines while on high dose
Additional:
- Albumin: 20% IV albumin 5 mL/kg (1g/kg) over 4
hours + IV furosemide: 1 mg/kg (max 40 mg) over 20
minutes for intravascular depletion,
severe/symptomatic oedema
● ABx prophylaxis: Pen V 125mg/dose 12hrly if <5yrs,
250mg/dose 12hrly if >5yrs
● Renal Bx if non-responsive to steroids
● Acid-suppressing therapy if GI Sx from steroids
Complications of nephrotic syndrome
● Infections: immune cells (proteins lost in urine)
o Spontaneous bacterial peritonitis due to
ascites
o Cellulitis of oedematous skin
● Intravascular hypovolemia
o Decreased sodium, increased haematocrit
● Thromboembolism - arterial and venous
o Increased haematocrit and hyperlipidaemia
o Urinary loss of antithrombin III (anticoagulant)
Nephrotic symptoms (NAPHROTIC) or (PALE)
● Na+ decrease (hyponatraemia)
● Albumin decrease (hypoalbuminemia) <25g/L
● Proteinuria (HEAVY) >3.5g/day
● Hyperlipidaemia (liver goes into overdrive to compensate for low albumin)
● Renal vein thrombosis
● Orbital oedema
● Thromboembolism
● Infection (loss of immunoglobulins in urine)
● Coagulability (also loss of antithrombin 3 in urine)
Proteinuria (heavy)
HypoAlbuminemia
HyperLipidemia
Edema
Clinical presentation of candidiasis (thrush)
Thick, white ‘cottage cheese’ discharge
Vulval irritation or penile ash
Superficial dyspareunia
External dysuria
Risk factors: immunocompromised, recent antibiotic use, high oestrogen state
(COCP, HRT, pregnancy)
Clinical presentation Bacterial vaginosis
Thin grey-white discharge, ‘fishy’ odour
Clinical presentation chlamydia
90% of cases are asymptomatic
Minimal or milky discharge
Dysuria
Deep dyspareunia
Post-coital or intermenstrual bleeding
Anorectal symptoms
Clinical presentation gonorrhea
Thick, green-yellow discharge
Dysuria
Deep dyspareunia
Post-coital or intermenstrual bleeding
Anorectal symptoms
Associated conjunctivitis
Clinical presentation of PID
Pelvic pain, fever, N/V
Deep dyspareunia
Abnormal vaginal discharge or vaginal bleeding
History of STIs or risk of STIs
Cervical mucopurulent discharge on speculum exam
Cervical motion tenderness +/- adnexal tenderness on bimanual exam
Clinical presentation trichomonas vaginalis
Offensive green-yellow frothy discharge
Vulvar irritation
Dysuria
Superficial dyspareunia
‘Strawberry cervix’ on speculum exam
Investigations for STI/abnormal vaginal discharge
Examinations
● Gynaecological: speculum or bimanual vaginal exam
Investigations
● High vaginal/ endocervical swab for:
○ Microscopy and Gram stain
○ pH test
○ NAAT
● Consider other swabs: anorectal and pharyngeal
● Consider urinalysis
Precaution for any abnormal vaginal discharge
Consider contact tracing
