GENERAL PRACTICE 2 - Sexual Health, Contraception, Infect Dis, Derm, MSK Flashcards
What are some causes of erectile dysfunction?
Organic causes (80%)
* Cardiovascular CHD
* Diabetes Mellitus >35% of diabetic men have erectile dysfunction, May be the presenting feature of DM.
- Neurological, e.g. pelvic surgery, spinal injury, multiple sclerosis
Androgen deficiency – hypoth/pit/testes - Pituitary issue – adenoma. Prolactinoma stops the productions of gonadotrophins
- Side effects of prescription drugs
- Smoking (incidence i x2), alcohol, or drug abuse
Psychogenic causes
* Performance anxiety
* Depression or stress
* Relationship failure
* Fear of intimacy
* you ain’t slick
What are some drugs that can cause erectile dysfunction?
thiazide diuretics and beta blockers
Finasteride - used to treat pattern hair loss and benign prostatic hyperplasia
Antidepressants (e.g. SSRIs)
antiandrogens
What examinations/causes/investigations should you be conisdering in Erectile dysfunction?
How can you determine physcogenic vs organic causes for erectile dysfunction
CVD and DM—check BP, peripheral pulses, and blood for fasting lipid
profile and glucose
* Psychological distress—consider depression/anxiety screening
* Testosterone insufficiency—genitals (small/absent), breasts i, d beard
(d frequency of shaving). If suspected, check serum testosterone,
blood tests - Testosterone (1), HbA1C (1), Lipid panel (1). Also accept PROLACTIN, FBC
Organic – normal libido/sex drive.
Psychogenic – reduced libido.
What is the management for erectile dysfunction?
dentifying and treating any curable causes of ED
hormonal
androgen deficiency – treat with testosterone
Stop any drugs that are causing ED
initiating lifestyle change and risk factor modification - stop smoking, drink less
providing psychosexual/ relationship therapy, counselling to patients and their partners, CBT
first line medical treatment
Phosphodiesterase 5 inhibitors (e.g. sildenafil, tadalafil, vardenafil) are mainstays
vacuum erection devices:
What are some medical conditions that would contribute to premmature ejaculation
THYROID HYPER/HYPO, DM, LOW SEROTONIN e.g. DEPRESSION+ANXIETY, PROSTATITIS/UTI, PEYRONIE DISEASE
What are some treatment options for premmature ejaculation?
se of daily selective serotonin reuptake inhibitor (SSRI)
Sertraline, Paroxetine and fluoxetine are recommended
application of topical anesthetic to reduce penile sensitivity, eg. lidocaine-prilocaine cream (5%) applied 20-30 minutes before sexual activity
behavioural techniques - . ‘Stop-start’ techniques, thicker condoms
taking breaks during sex
Couples therapy advice
What are some causes of Dyspareunia in females?
infection - especially, trichomonas, vaginal candidiasis
vaginal atrophy - postmenopausal shrinkage; infrequent intercourse
psychological - vaginismus, fear, ignorance, previous painful intercourse
poor sexual stimulation
pelvic inflammatory disease
endometriosis
What are some investigations for dyspareunia in females?
In majority of cases, investigations are not necessary.
vaginal and endocervical swabs if indicated
a urinalysis to reveal any UTI
a pelvic ultrasound – to check for hydrosalpinx and fibroids
laparoscopy if deep dyspareunia and cause is not apparent on examination
What is the treatment for dyspareunia in females?
Management typically focuses on treating underlying causes where appropriate
A penetration desensitisation programme is useful in dyspareunia and vaginismus
Fenton’s procedure - increase the dimensions of the introitus
intramuscular injection of botulinum toxin
Psychological therapy may be useful in some patients.
sensitive assessment and exploration of the woman’s fears and thoughts is important
issues connected with the birth of the child may be discussed with a counsellor
encourage the patient to talk to her partner and resolve any relationship difficulties they might have or refer them to a couples counsellor
if psychosexual problems persist refer her to a psychosexual therapist
What is the treatment for a simple UTI
First line treatment for a UTI as per BNF is nitrofurantoin or trimethoprim, 3 days
What is reterograde ejacualtion? what can cause it?
Retrograde ejaculation Semen passes into the bladder rather than the urethra—complication of TURP or bladder neck incision.
May also occur as a result of spinal injury or DM. The patient can usually achieve an orgasm but there is no ejaculate or the volume of the ejaculate is decreased. Urine may be cloudy after having sex.
Also Tamulosin medication, used in BPH and male pattern hair loss
What is vaginismus, and what are some common causes of it?
Vaginismus Usually apparent at vaginal examination—severe spasm of the vaginal muscles and adduction of thighs.
Common causes:
* Fear of the unknown
* local pain
* Past history of rape, abuse, or severe emotional trauma
* Defence mechanism against growing up
What is the management of vaginismus?
progressive relaxation
used manage anxiety, and consists of alternately tensing and relaxing groups of muscles in a prescribed sequence e.g - beginning from the feet and moving upwards
desensitisation - vaginal trainers, and encouraging the woman to examine herself
physiotherapy
hypnotherapy
topical lidocaine applied within the vagina
antidepressants
What causes menopause?
- It is caused by a lack of ovarian follicular function, resulting in changes in the sex hormones associated with the menstrual cycle
- Oestrogen and progesterone levels are low
- LH and FSH levels are high in response to an absence of negative feedback from oestrogen
How does the menopause begin?
- The menopause begins with a decline in the development of ovarian follicles
- Without the growth and development of the follicles there is reduced production of oestrogen
- This results in increasing levels of LH and FSH as oestrogen has a negative feedback on these hormones in the pituitary gland
How can menopause be diagnosed?
- Symptoms without blood test
- Use FSH blood test in women under 40 or aged 40-45 with menopausal symptoms
What is the management of perimenopausal symptoms?
Hormone replacement therapy (HRT)
Tibolone, a synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)
Clonidine, which act as agonists of alpha-adrenergic and imidazoline receptors
Testosterone can be used to treat reduced libido (usually as a gel or cream)
Vaginal oestrogen cream or tablets, to help with vaginal dryness and atrophy (can be used alongside systemic HRT)
Vaginal moisturisers, such as Sylk, Replens and YES
What can be used to help with the vasomotor symptoms of the menopause? The hot flushses and night sweats
Clonidine which is a alpha-2 agonist
What are the indications of HRT?
Replacing hormones in premature ovarian insufficiency, even without symptoms
Reducing vasomotor symptoms such as hot flushes and night sweats
Improving symptoms such as low mood, decreased libido, poor sleep and joint pain
Reducing risk of osteoporosis in women under 60 years
What are the contraindications of HRT?
Undiagnosed vaginal bleeding
Pregnancy
Breastfeeding
Oestrogen receptor-positive breast cancer
Acute liver disease
Uncontrolled hypertension
History of breast cancer or venous thromboembolism (VTE)
Recent stroke, myocardial infarction or angina
How does the COCP prevent pregnacy?
Preventing ovulation (this is the primary mechanism of action)
Progesterone thickens the cervical mucus
Progesterone inhibits proliferation of the endometrium, reducing the chance of successful implantation
the COCP contains both oestrogen and progesterone -what do these do in the body to act as contraception?
Oestrogen and progesterone have a negative feedback effect on the hypothalamus and anterior pituitary, suppressing the release of GnRH, LH and FSH.
No LH and FSH - ovulation cannot occur
With the COCP the lining of the endometrium is maintained in a stable state, will then have a withdrawal bleed when the pill is stopped
(actually protective against ovarian and endometrial cancer)
What are the two types of COCP and which are the main ones used?
Monophasic pills contain the same amount of hormone in each pill
Multiphasic pills contain varying amounts of hormone to match the normal cyclical hormonal changes more closely
The NICE Clinical Knowledge Summaries (2020) recommend using a pill with levonorgestrel or norethisterone first line (e.g. Microgynon or Leostrin). These choices have a lower risk of venous thromboembolism.
Microgeon or Loestrin
What are the side effects of COCP?
One way to remember the COCPs effect on various cancers is that it increases the risk of the cancers we screen for (breast, cervical) and is protective against those we don’t (endometrial, ovarian)
Unscheduled bleeding is common in the first three months and should then settle with time
Breast pain and tenderness
Mood changes and depression
Headaches
Hypertension
Venous thromboembolism (the risk is much lower for the pill than pregnancy)
Small increased risk of breast and cervical cancer, returning to normal ten years after stopping
(actually protective against ovarian and endometrial cancer)
Small increased risk of myocardial infarction and stroke
as contains oestrogen, will suppress breast milk production if they want to breast feed (not that they should be on it anyway if theyve just given birth, as they’ll already be in a prothrombotic state)
What are the contraindications of the COCP?
Uncontrolled hypertension
Migraine with aura
History of VTE
Aged 35 and smoking 15 cigarettes a day
Surgery
Vascular disease
IHD
Liver cirrhosis
SLE
Having just given birth as they will already in a prothrombotic state
How long after taking the COCP pill are you protected
If started on day 1-5 of menstrual cycle then protection is immediate
If started after this then it takes 7 days to have protection
What COCPs can be used in the treatment of acne and hirsutism?
Dianette and other COCPs containing cyproterone acetate (i.e. co-cyprindiol) can be considered in the treatment of acne and hirsutism. Cyproterone acetate has anti-androgen effects, helping to improve acne and hirsutism.
Greater risk of VTE though
What is theoretial rules of protection when it comes to taking the pill?
What should you do if you miss one pill, but less than 72 hours since the last one was taken?
theoretically women will be protected if they perfectly take the pill in a cycle of 7 days on, 7 days off. This will prevent ovulation.
Missing one pill is when the pill is more than 24 hours late (48 hours since the last pill was taken).
Missing one pill (less than 72 hours since the last pill was taken):
Take the missed pill as soon as possible (even if this means taking two pills on the same day)
No extra protection is required provided other pills before and after are taken correctly
What should you do if you have missed more than one pill? (more than 72 hours since the last pill was taken)
Take the most recent missed pill as soon as possible (even if this means taking two pills on the same day)
Additional contraception (i.e. condoms) is needed until they have taken the pill regularly for 7 days straight
What should you do if you have missed more than one pill? (more than 72 hours since the last pill was taken), on days 1-7, 8-14, and 15-21?
If day 1 – 7 of the packet they need emergency contraception if they have had unprotected sex
If day 8 – 14 of the pack (and day 1 – 7 was fully compliant) then no emergency contraception is required
If day 15 – 21 of the pack (and day 1 – 14 was fully compliant) then no emergency contraception is needed. They should go back-to-back with their next pack of pills and skip the pill-free period.
Theoretically, additional contraception is not required if more than one pill is missed between day 8 – 21 (week 2 or 3) of the pill packet and they otherwise take the pills correctly, although it is recommended for extra precaution.
7 days on, 7 days off xx
What are the two types of Progesterone only pill, and how long can you delay taking them for them still to be effective?
The traditional progestogen-only pill ( Norgeston or Noriday ) cannot be delayed by more than 3 hours. Taking the pill more than 3 hours late is considered a “missed pill”.
The desogestrel-only pill (Cerazette) can be taken up to 12 hours late and still be effective. Taking the pill more than 12 hours late is considered a “missed pill”.
Postpartum women (breastfeeding and non-breastfeeding) can start the progestogen-only pill at any time postpartum
Contraception is not required before day 21 postpartum
What is the MOA of the tradiational progesterone only pill? ( Norgeston or Noriday )
Taking more than how many hours late constitutes a missed pill?
Postpartum women (breastfeeding and non-breastfeeding) can start the progestogen-only pill at any time postpartum
Traditional progestogen-only pills work mainly by:
Thickening the cervical mucus
Altering the endometrium and making it less accepting of implantation
Reducing ciliary action in the fallopian tubes
taken 3 hours or later = missed pill
What is the MOA of the Desogesterol-only pill? (Cerazette)
Postpartum women (breastfeeding and non-breastfeeding) can start the progestogen-only pill at any time postpartum
Takinf the pill how many hours late constitutes a missed pill?
Desogestrel works mainly by:
Inhibiting ovulation
Thickening the cervical mucus
Altering the endometrium
Reducing ciliary action in the fallopian tubes
12 hours late = missed pill
What is the only main thing that taking the POP is contraindicated in?
Active Breast Cancer
regarding the POP and COCP, if you want to be protected immediately, when in the menstraul cycle do you need to be taking it?
Both can be started within the first 5 days of the menstrual cycle and work immediately, as it is very unlikely a woman will ovulate this early in the cycle.
Postpartum women (breastfeeding and non-breastfeeding) can start the progestogen-only pill at any time postpartum
Contraception is not required before day 21 postpartum
if you start taking the POP after day five of the menstrual cycle long would additional contraception be required for? Why?
What would you need to do if you ‘missed’ a day on the POP?
It can be started at other times of the cycle provided pregnancy can be excluded. Additional contraception is required for 48 hours. It takes 48 hours for the cervical mucus to thicken enough to prevent sperm entering the uterus.
The POP can be started even if there is a risk of pregnancy, as it is not known to be harmful in pregnancy. However, the woman should do a pregnancy test 3 weeks after the last unprotected intercourse.
POPs are only effective on the day taken - missing even one day reduces effectiveness. Patient should be advised to use condoms for the next two days
What are some side effects of the POP?
Changes to the bleeding schedule is one of the primary adverse effects of the progestogen-only pill. Unscheduled bleeding is common in the first three months and often settles after that.
Approximately:
20% have no bleeding (amenorrhoea)
40% have regular bleeding
40% have irregular, prolonged or troublesome bleeding
Other side effects include:
Breast tenderness
Headaches
Acne
Increased risk of depression
What does the Progesterone only injection contain?
How long does it last for, as a method of contraception?
depot medroxyprogesterone acetate (a type of progestin). DMPA
Women need to have injections every 12 – 13 weeks. Delaying past 13 weeks creates a risk of pregnancy. The FSRH guidelines say it can be given as early as 10 weeks and as late as 14 weeks after the last injection where necessary, but this is unlicensed.
What is the MOA of the progesterone only injection?
The main action of the depot injection is to inhibit ovulation. It does this by inhibiting FSH secretion by the pituitary gland, preventing the development of follicles in the ovaries.
Additionally, the depot injection works by:
Thickening cervical mucus
Altering the endometrium and making it less accepting of implantation
What are the main side effects/risks for the Depot progesterone only injection
Changes to the bleeding schedule is one of the primary considerations with progestogen-only contraception.
Reduced bone mineral density (osteoporosis) = Oestrogen helps maintain bone mineral density in women, produced by the follicles in the ovaries.
Weight gain is also a key side
effect
Only form of contraception that causes weight gain and osteoporosis - so wouldnt be first choice in a young woman, long term
What is the progesterone only implant? How does it work and how long does it work
What is it CI in
The progestogen-only implant is a small (4cm) flexible plastic rod that is placed in the upper arm, beneath the skin and above the subcutaneous fat.
It slowly releases progestogen into the systemic circulation. It lasts for three years and then needs replacing.
The primary mode of action of the contraceptive implant is inhibition of ovulation
The only UKMEC 4 criteria for the implant is active breast cancer.
What is the bleeding pattern seen in the progesterone only implant? What is the maagement of problematic bleeding with it?
What is its primary mode of contraception?
1/3 have infrequent bleeding
1/4 have frequent or prolonged bleeding
1/5 have no bleeding
The remainder have normal regular bleeds
Problematic bleeding is managed similarly to the progestogen-only implant. The FSRH guidelines suggest the combined oral contraceptive pill (COCP) in addition to the implant for three months when problematic bleeding occurs, to help settle the bleeding (provided there are no contraindications).
(med school mock said POP)
The primary mode of action of the contraceptive implant is inhibition of ovulation
What are the two kinds of contraceptive intrauterine device?
There are two types of intrauterine device (IUD):
Copper coil (Cu-IUD): contains copper and creates a hostile environment for pregnancy
Levonorgestrel intrauterine system (LNG-IUS): contains progestogen that is slowly released into the uterus
What things must be considered/down before a coil is inserted?
Screen for Chlamydia and Gonorrhoea before insertion of the coil in women at risk of STD (ie under 25 years old)
Perform Bimaniaul (pelvic) exam beforehand, to check postion and size of uterus
Record BP and heart rate before and after
If the threads of the coil cannot be seen on palpated, what 3 things need to be excluded?
When the coil threads cannot be seen or palpated, three things need to be excluded:
Expulsion
Pregnancy
Uterine perforation
Before the coil is removed, women need to abstain from sex or use condoms for 7 days, or there is a risk of pregnancy.
What are some drawbacks to having a coil fitted?
It can cause heavy or intermenstrual bleeding (this often settles)
Some women experience pelvic pain
It does not protect against sexually transmitted infections
Increased risk of ectopic pregnancies
Can fall out
Related to the IUS
There can be systemic absorption causing side effects of acne, headaches, or breast tenderness
What is the main type of IUS, and how long can it stay in for?
There are four types of IUS you may come across, all containing levonorgestrel:
Mirena: effective for 5 years for contraception, and also licensed for menorrhagia and HRT
The IUS to remember is the Mirena coil. It is commonly used for contraception, menorrhagia and endometrial protection for women on HRT. It is licensed for 5 years for contraception, but only 4 years for HRT.
How does the IUS (containing Levonorgesterel) work?
The LNG-IUS works by releasing levonorgestrel (progestogen) into the local area:
Thickening cervical mucus
Altering the endometrium and making it less accepting of implantation
Inhibiting ovulation in a small number of women
Give some benefits of coils
Copper:
Reliable contraception
It can be inserted at any time in the menstrual cycle and is effective immediately
It contains no hormones, so it is safe for women at risk of VTE or with a history of hormone-related cancers
It may reduce the risk of endometrial and cervical cancer
IUD:
Can make periods lighter
No effect on bone mineral density (unlike the depo injection)
No increase in thrombosis risk (unlike the COCP)
No restrictions for use in obese patients (unlike the COCP)
The Mirena has additional uses (i.e. HRT and menorrhagia)
What are the treatment options for UPSI? (unprotected sexual intercourse)
What are the rules around using the Copper Coil In UPSI?
IUD - Copper coil is most effective and should be offered first, but in practise most women tend to go for one of the 2 oral hormonal methods.
Cant have copper coil if receiving treatment for a STI!
Coil can be used within 120 hours of UPSI, OR up to 5 days after the likely ovulation date
2 types of hormone contraceptives = levonorgestrel and ulipristal,
What are the two types of hormonal contraceptives for UPSI?
How long after UPSI can these two contracpetives be effective?
What else to remember with ulipristal
both levonorgestrel and ulipristal (sold as EllaOne) are progesterone receptor modulators.
Ulipristal may reduce the effectiveness of hormonal contraception. Contraception with the pill, patch or ring should be started, or restarted, 5 days after having ulipristal. Barrier methods should be used during this period
caution should be exercised in patients with severe asthma
There are no such restrictions on the use of levonorgestrel
Levonorgestrel should only be given up to 3 days after UPSI. After this, it is not as effective
Give some contraindications of perscribing ulipristal acetate
Diseases of malabsorption (eg. Crohns), Allergy, Severe hepatic dysfunction, patient taking rifampicin, Breast feeding, Asthma, drugs increasing gastric pH (omeprazole, ranitidine)
What are the doses of levongesterel and ulipristal?
single dose of levonorgestrel 1.5mg (a progesterone)
the dose should be doubled for those with a BMI >26 or weight over 70kg
ulipristal - 30mg oral dose taken as soon as possible, no later than 120 hours after intercourse
How long will it take before different methods of contraception can be relied on, if not taken in first days of cycle?
Contraceptives - time until effective (if not first day period):
instant: IUD
2 days: POP
7 days: COC, injection, implant, IUS
outline some clinical symptoms regarding pain seen in fibromyalgia
Widespread muscle pain of >3 months
Pain
Pain worse with stress, cold weather activity
Morning stiffness <1 hour
Non-restorative sleep
Headache/diffuse abdominal pain
outline some clinical symptoms regarding neurocognition seen in fibromyalgia
Neurocognitive features
Poor sleep
Fatigue
Mood disorder
Poor concentration
Memory
Outline some of the pathophysiology that is thought to cause fibromyalgia.
Problems with pain signals
Low serotonin – inhibits pain signals
Raised substance P and nerve growth factor – increased pain signals
How would you diagnose fibromyalgia?
Diagnosis of fibromyalgiais based on clinical features:
- Chronic pain that has been present for at least 3 months
- Widespread pain - involved left and right sides, above and below waist, and the axial skeleton.
- Palpate tender point sites - severe pain in 3 to 6 different areas of your body, or you have milder pain in 7 or more different areas
- No other reason for symptoms has been found
What investigations would you do in suspected fibromyalgia to rule out other conditions can could cause the symptoms seen?
TFTs – rule out hypothyroidism
ANAs and dsDNA – to exclude SLE
ESR and CRP – to exclude Polymyalgia rheumatica (PMR)
Calcium and electrolytes – to exclude high calcium
Vitamin D – to rule out low vitamin D
Examine patient and CRP – to rule out inflammatory arthritis
What are some non pharmalogical measures for fibromyalgia?
MDT approach advise there is not one specific treatment that will defo work
Regular exercise for CV fitness eg fast walking, biking, swimming, or water aerobics can help by reducing pain and fatigue.
- Relaxation techniques and good sleep hygiene can also help.
- Physiotherapy and rehabilitation
- CBT
What are some pharmacological measures to help manage fibromyalgia
- Amitriptyline - tricyclic antidepressant
- Serotonin-norepinephrinereuptake inhibitors (SNRIs) e.g. duloxetine
Anticonvulsants like pregabalin and gabapentinwhich slow nerve impulses
Steroids or NSAIDS are not recommended because
there is no inflammation (if it does respond, reconsider your diagnosis!)
What is otitis externa?
Otitis externa is a condition that causes inflammation (redness and swelling) of the external ear canal, which is the tube between the outer ear and eardrum.
What is the presentation of Otitis externa
Ear pain
Discharge
Itchiness
Conductive hearing loss (if the ear becomes blocked)
Examination can show:
Erythema and swelling in the ear canal
Tenderness of the ear canal
Pus or discharge in the ear canal
What is the treatment of otitis externa?
advise analgesia, e.g. paracetamol 9 ibuprofen
* prescribe ear drops—options are: aluminium acetate drops (as effective as antibiotics); and antibiotic and/or steroid drops
Avoid going in water/inserting things into your ear
Skin of the pinna adjacent to the ear canal is often affected by eczema.
Treat with topical corticosteroid cream/ointment—avoid prolonged use
What is malignant/necrotising otitis externa and what are the risk factors?
The infection spreads to the bones surrounding the ear canal and skull. It progresses to osteomyelitis of the temporal bone of the skull.
Diabetes
Immunosuppressant medications (e.g., chemotherapy)
HIV
What is otitis media?
- Infection of the middle ear which is the space that sits between the tympanic membrane and the inner ear
- This is where the nerves are found
What causes otitis media?
What often precedes it?
- Bacteria enter from the back of the thorat through the eustachian tube - Strep pneumoniae is most common
- A Viral URTI often precedes otitis media
What is the presentation of otitis media?
- Ear pain
- Reduced hearing
- Feeling unwell
- Signs of URTI
Examination otitis media?
- Otoscope tympanic membrane will look bulging red and perforation will show discharge and hole in tympanic membrane
Management otitis media?
Most otitis media cases will resolve without antibiotics within around three days, sometimes up to a week. Antibiotics make little difference to symptoms or complications.
Amoxicillin for 5-7 days first-line
Clarithromycin (in pencillin allergy)
Erythromycin (in pregnant women allergic to penicillin)
What is otitis media with effusion? When should you think about it?
Its inflammation and accumulation of fluid in the middle ear, without any symptoms of acute inflammation
Earache/hearing loss may not be present
Behavioural problems should alert the GP to assess a child for OM with effusion
What is fungal infections of the skin called, and what are the specific names
Ringworm is a fungal infection of the skin and also known as tinea Fungal infections have specific names depending on the area they affect:
Tinea capitis refers to ringworm affecting the scalp (caput meaning head)
Tinea pedis refers to ringworm affecting the feet, also known as athletes foot (pedis meaning foot)
Tinea corporis refers to ringworm on the body (corporis meaning body)
Onychomycosis refers to a fungal nail infection
How does Ringworm present with, specifically
Tinea Capitis,
Tinea Pedis, and
Onychomycosis?
Ringworm presents as an itchy rash that is erythematous, scaly and well demarcated.
Tinea capitis can present with well demarcated hair loss. There will also be itching, dryness and erythema of the scalp. This is more common in children than adults.
Tinea pedis (athletes foot) presents with white or red, flaky, cracked, itchy patches between the toes. The skin may split and bleed.
Onychomycosis (fungal nail infections) presents with thickened, discoloured and deformed nails.
TOM TIP: Check the toenails in someone presenting with ringworm, you may find they have a fungal nail infection that has spread to the skin.
What is the management for ringworm?
Treatment of ringworm is with anti-fungal medications:
Anti-fungal creams such as clotrimazole and miconazole
Anti-fungal shampoo such as ketoconazole for tinea capitis
Oral anti-fungal medications such as fluconazole, griseofulvin and itraconazole
What causes scabies? How long can it take for symptoms to appear with it after the initial infestation?
Scabies are tiny mites called Sarcoptes scabiei that burrow under the skin causing infection and intense itching. They lay eggs in the skin, leading to further infection and symptoms.
It can take up to 8 weeks for any symptoms or rash to appear after the initial infestation.
What is the presentation of scabies
Scabies presents with incredibly itchy small red spots, (papular rash) possibly with track marks where the mites have burrowed.
The classic location of the rash is between the finger webs, but it can spread to the whole body.
Itching tends to be worse at night.
What is the treatment of scabies
Treatment is with permethrin cream. This needs to be applied to the whole body, completely covering skin. It is best to do this when the skin is cool (i.e. not after a bath or shower)
The cream should be left on for 8 – 12 hours and then washed off. This should be repeated a week later to kill all the eggs that survived the first treatment and have now hatched.
When one person is diagnosed, all household and close contacts should also be treated in exactly the same way, even if asymptomatic. This is because they may be infected and not yet have symptoms.
What are warts, and what is the main cause of them?
Warts are non-cancerous viral growths usually occurring on the hands and feet but can also affect other locations, such as the genitals or face.
Warts are caused by the human papillomavirus (HPV). There are about 130 known types of human papillomaviruses.
HPV infects the squamous epithelium, usually of the skin or genitals
What is the treatment for warts?
Salicylic acid (wart paints), or cryotherapy
What is mumps? what percentage of protection does the mump vaccine offer?
Mumps is a viral infection spread by respiratory droplets.
Taking a vaccination history is essential when considering a diagnosis of mumps. The MMR vaccine offers around 80% protection against mumps.
How long do symptoms take for show in mumps, and what is the clinical presentation
Patients experience an initial period of flu-like symptoms known as the prodrome. These occur a few days before the parotid swelling:
Fever
Muscle aches
Lethargy
Reduced appetite
Headache
Dry mouth
Parotid gland swelling, either unilateral or bilateral, with associated pain is the key feature that should make you consider mumps.
What is the management of mumps?
The diagnosis can be confirmed using PCR testing on a saliva swab. The blood or saliva can also be tested for antibodies to the mumps virus.
Mumps is a notifiable disease, meaning you need to notify public health of any suspected and confirmed cases.
Management is supportive, with rest, fluids and analgesia. Mumps is a self limiting condition. Management of complications is also mostly supportive.
What are some of complications of mumps?
It can also present with symptoms of the complications, such as:
Abdominal pain (pancreatitis)
Testicular pain and swelling (orchitis)
Confusion, neck stiffness and headache (meningitis or encephalitis)
What bacteria causes Lyme disease?
B burgdorferi
What are the symptoms of Lyme disease?
- Tick bite with rash called erythema migrans - (resembles a bulls eye)
- Fever
- Headache
- Myalgias
- Stiff neck
- Facial palsy
What is the treatment for Lyme disease?
Doxycycline, unless there is just a rash that can’t be distinguished from cellulitis then use amoxicillin
What causes infectious mononucleosis - and how can it be spread
nfection with the Epstein Barr virus (EBV). It is commonly known as the “kissing disease”, “glandular fever” or “mono”
This virus is found in the saliva of infected individuals. Infection may be spread by kissing or by sharing cups, toothbrushes and other equipment that transmits saliva.
What are some symptoms of infectious mononucleosis
Features
Fever
Sore throat
Fatigue
Lymphadenopathy (swollen lymph nodes)
Tonsillar enlargement
Splenomegaly and in rare cases splenic rupture
Virus targets circulating B lymphocytes (lifelong latent infection) and squamous epithelial cells of oropharynx
Antibody tests for infectious mononucleosis - what is the heterophile antibodies? Outline its sensitivity and specificity
In infectious mononucleosis, the body produces something called heterophile antibodies, which are antibodies that are more multipurpose and not specific to the EBV antigens (takes 6 weeks for them to be produced)
We can test for these heterophile antibodies using two tests:
Monospot test: this introduces the patient’s blood to red blood cells from horses. Heterophile antibodies (if present) will react to the horse red blood cells and give a positive result.
Paul-Bunnell test: this is similar to the monospot test but uses red blood cells from sheep.
These tests are almost 100% specific for infectious mononucleosis, however not everyone who has IM produces heterophile antibodies, and it can take up to six weeks for the antibodies to be produced. Therefore they are only 70 – 80% sensitive.
What is the management for infectious mononucleosis?
- Is usually self-limiting and lasts 2-3 weeks but can cause fatigue for several months
What can cause a rash in infectious mononucleosis?
Mononucleosis causes an intensely itchy maculopapular rash in response to amoxicillin or cefalosporins.
Look out for the exam question that describes an adolescent with a sore throat, who develops an itchy rash after taking amoxicillin
What is the advice given to patients with infectious mononucleosis?
- Avoid alcohol as EBV impacts the livers ability to process it
- Avoid contact sports due to risk of splenic rupture
What are the complications of infectious mononucleosis?
Splenic rupture
Glomerulonephritis
Haemolytic anaemia
Thrombocytopenia
Chronic fatigue
EBV infection is associated with certain cancers, notable Burkitt’s lymphoma.
What groups of people are offered a yearly flu vaccine, free on the NHS?
Aged 65 and over
Young children
Pregnant women
Chronic health conditions, such as asthma, COPD, heart failure and diabetes
Healthcare workers and carers
What are some presenting features of being infected with the influenza virus?
Delay between exposure/Sx typically ~2d
Fever
Lethargy and fatigue
Anorexia (loss of appetite)
Muscle and joint aches
Headache
Dry cough
Sore throat
Coryzal symptoms
Give some differences between a presentation of flu, and a presentation of the common cold
Flu tends to have an abrupt onset, whereas a common cold has a more gradual onset. Fever is a typical feature of the flu but is rare with a common cold. Finally, people with the flu are “wiped out” with muscle aches and lethargy, whereas people with a cold can usually continue many activities.
What are some investigations for those with the influenza virus?
Point-of-care tests using swabs are available, giving a rapid result. They detect viral antigens
Viral nasal or throat swabs can be sent to the local virology lab for polymerase chain reaction (PCR) analysis
What is some treatment for:
Those at risk of complications of influnza virus
Those who need post exposure prophylaxis - aka chronic diseasee/immunosuppression
For complications
* Oral oseltamivir (BD for 5d)
Inhaled zanamivir (BD for 5d)
PEP
* Oral oseltamivir 75mg OD for 1od
Inhaled zanamivir 10mg OD for 10d
What are some complications of influenza virus ?
Otitis media, sinusitis, bronchitis
Viral pneumonia
2y bacterial pneumonia
Worsening chronic health conditions - COPD, HF
Febrile convulsions (young children)
Encephalitis
What would someone with primary syphilis present with?
A painless genital ulcer (chancre). This tends to resolve over 3 – 8 weeks.
Local lymphadenopathy
What would someone with secondary syphilis present with?
ypically starts after the chancre has healed, with symptoms of:
Maculopapular rash
Condylomata lata (grey wart-like lesions around the genitals and anus)
Low-grade fever
Lymphadenopathy
Alopecia (localised hair loss)
Oral lesions
How can you test for syphilis?
Antibody testing for antibodies to the T. pallidum bacteria can be used as a screening test
or
Samples from sites of infection can be tested to confirm the presence of T. pallidum with:
Dark field microscopy
Polymerase chain reaction (PCR)
What is the management for syphilis
. As with all sexually transmitted infections, patients need:
Full screening for other STIs
Advice about avoiding sexual activity until treated
Contact tracing
Prevention of future infections
A single deep intramuscular dose of benzathine benzylpenicillin (penicillin) is the standard treatment for syphilis.
What are the most common causes of tonsillitis?
MC cause is a viral infection
Rhinovirus
Coronavirus
Adenovirus
In tonsillitis associated with infectious mononucleosis, MC is EBV
What are the most common bacterial causes of tonsillitis?
bacterial tonsillitis = group A streptococcus pyogenes
2nd MC cause bacterial = streptococcus pneumoniae
Other bacterial causes:
H.influenzae
M.catarrhalis
S.aureus
What are the most commonly affected tonsilis in tonsilitis?
Waldeyer’s tonsillar ring
- In pharynx at back of throat = ring of lymphoid tissue
- 6 areas of lymphoid tissue in Waldeyer’s ring (adenoids, tubal tonsils, palatine tonsils + lingual tonsil)
- Palatine tonsils typically infected & enlarged in tonsillitis = tonsils at either side at back of throat
What are some signs and symptoms of tonsillitis?
O/E - throat red, inflamed, enlarged tonsils ± exudates (small white patches of pus on tonsils)
Tonsillar erythema + enlargement
Also may be anterior cervical lymphadenopathy (swollen, tender lymph nodes in anterior triangle of neck) ==> Tonsillar lymph nodes just behind angle of mandible
Sore throat (sudden onset)
Fever (above 38º)
Pain on swallowing
Headache
Abdo pain
What is the centor criteria?
- Used to estimate the probability that the tonsillitis is due to a bacterial infection
Fever over 38
Exudate on tonsils
Absence of cough
Tender cervical lymph nodes
FEAT
A score of 3 or more indicates a 40-60% likelihood it is bacterial
What is the fever PAIN score?
A score of 2 – 3 gives a 34 – 40% probability, and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis:
Fever during previous 24 hours
P – Purulence (pus on tonsils)
A – Attended within 3 days of the onset of symptoms
I – Inflamed tonsils (severely inflamed)
N – No cough or coryza
What is the management for tonsillits? (non antibiotic)
Mostly self limiting and resolve spontaneously
Analgesia, fluids
Admission if:
* Immunocompromised
* Systemically unwell
* Dehydrated
* Has stridor
* Respiratory distress
Evidence of peritonsillar abscess or cellulitis
What are some investigations for Tonsillitis?
Throat culture
Rapid streptococcal antigen test (+ve for GABHS)
Other serological testing
WBC count - raised neutrophil ± lymphocyte count
HIV viral load assay to rule out
What is the antibiotic that you’d prescribe for tonsillits?
What about in a penicillin allergy, and what medication is CI w this antiobitoic?
Consider ABX prescription if CENTOR score 3+ or feverPAIN 4+
Penicillin V (phenoxymethylpenicillin) 10 day course = 1st line (relatively narrow spectrum + effective against S.pyogenes)
Clarithromycin 1st line in penicillin allergy
Clarithromycin interacts with atorvastatin and increases the risk of rhabdomyolysis, so it is advised to stop atorvastatin during courses of clarithromycin.
For recurrent episodes of tonsillitis -> tonsillectomy
What is rhinosinusitis?
Sinusitis refers to inflammation of the paranasal sinuses in the face. This is usually accompanied by inflammation of the nasal cavity and can be referred to as rhinosinusitis.
What is the basic anatomy of the paranasal sinuses, and what causes sinusitis?
The paranasal sinuses are hollow spaces within the bones of the face, arranged symmetrically around the nasal cavity. They produce mucous and drain into the nasal cavities via holes called ostia. Blockage of the ostia prevents drainage of the sinuses, resulting in sinusitis.
What is classed as acute sinusitis and what is classsed as chronic sinusutis.? What are some causes of it?
Acute (less than 12 weeks)
Chronic (more than 12 weeks)
Inflammation of the sinuses can be caused by:
Infection, particularly following viral upper respiratory tract infections
Allergies, such as hayfever (with allergic rhinitis)
Obstruction of drainage, for example, due to a foreign body, trauma or polyps
Smoking
Patients with asthma are more likely to suffer from sinusitis.
What are some of the presenting features of sinusitis?
What would examination reveal
The typical presentation of acute sinusitis is someone with a recent viral upper respiratory tract infection presenting with:
Nasal congestion
Nasal discharge
Facial pain or headache
Facial swelling over the affected areas
Loss of smell
Fever
Tenderness to palpation of the affected areas
How may chronic sinusitis present with?
Chronic sinusitis involves a similar presentation but with a duration of more than 12 weeks. Chronic sinusitis may be associated with nasal polyps, which are growths of the nasal mucosa.
What are the investigations for sinusitis?
In most cases, investigations are not necessary. In patients with persistent symptoms despite treatment, investigations include:
Nasal endoscopy
CT scan
Functional endoscopic sinus surgery (FESS) involves using a small endoscope inserted through the nostrils and sinuses. Instruments are used to remove or correct any obstructions to the sinuses. Obstruction may be caused by swollen mucosa, bone, polyps or a deviated septum (surgery to correct a deviated septum is call septoplasty).
What is the management for sinusitis?
Systemic infection/sepsis -> hospital
Most viral cases self resolve
Supportive therapy, analgesics, antipyretics
Sx for 10+ days: high dose steroid nasal spray for 14d e.g. mometasone
Delayed ABX prescription if worsening/not improving within 7d (phenoxymethylpenicillin 1st line)
Derm - Define what is meant by macular, or what a macular rash would look like
Flat, nonpalpable lesion with color change (hyper- or hypopigmented, erythematous) less than
5-10mm
Derm - Define what is meant by papule, or what a papular rash would look like
Raised lesion less than 5-10 mm (wart, actinic keratosis)
Derm - Define what is meant by a vesicle, or what a vesicular rash would look like
Name some conditions where you may see some
Well circumscribed fluid-filled lesion up to 5-10mm - seen in herpes, Varicella
Derm - Define what is meant by a petechiae ,or what a petechiae rash would look like. What are some illness where you see petechiae?
small (< 5mm) hemorrhagic (red-purple) non-blanchable discolorations
meningococcemia, DIC, viral exanthem
Derm - when the following skin lesions are greater than 10mm, what are they known as?
Macules
Papules
Vesicles
Petechiae (when >5mm)
Changes with size
Macules => patches
Papules => plaques (or nodules)
Vesicles => bullae
Petechiae => Purpura
What is the definition of a macular papular rash?
Give some diseases where you may see it
A maculopapular rash is a mix of macules (flat discolored areas of skin) and papules (small raised bumps) that usually cover a large area of skin.
scarlet fever, measles, secondary syphilis, rubella, HIV,
What is the presentation of measles?
Known as first disesase (of the 6 original viral exanthemas)
fever, (high, whereas rubella tends to be a lower fever)
Resp Symptoms - 3Cs (only mild or absent in rubella)
conjunctivitis,
coryza,
cough
diarrhea,
Koplik spots (white spots on the red buccal mucosa, like small grains of sand)
Then generalized, maculopapular rash, classically face/neck->trunk->limbs - (lasts 5-7 days, Rubella rash tends to last about 3)
What is the treatment for measles?
Supportive. Isolate children in hospital. In immunocompromised patients, antiviral drug ribavirin can be used.
Vitamin A, which may modulate the immune
response should be given in low-income countries.
Prevention by immunization is the most successful
strategy for reducing the morbidity and mortality of
measles.
What causes scarlet fever? What ages does it most commonly affect?
Known as second disesase (of the 6 original viral exanthemas)
Scarlet fever infectious disease caused by Streptococcus pyogenes, a Group A streptococcus
The infection is a type of Group A streptococcal infection (Group A strep). It most commonly affects children between five and 15 years of age
What are some signs and symptoms of scarlet fever
Erythematous ‘pinhead’ Sandpaper rash, spares the face, desquamates around the fingers and toes + ‘Strawberry tongue’
Fever, Malaise, headache, nausea.
Scarlet fever usually follows from a group A streptococcal infection
What is the treatment for scarlett fever?
Swab throat
Prescribe a 10-day course of phenoxymethylpenicillin (penicillin V) first-line.
Azithromycin if allergic
What is Rubella? How is it spread and when is it common?
Known as third disease (of the 6 original viral exanthemas) - aka German Measles
It is a mild disease in childhood caused by the rubella virus. More common in winter and spring, it is spread by the respiratory route, frequently from a known contact.
The prodrome is usually mild with a low-grade fever or none at all.
What are the signs of a Rubella infection? How is it treated?
The maculopapular rash is often the first sign of infection, appearing initially on the face and then spreading centrifugally to cover the whole body. It fades in 3 days to 5 days.
Lymphadenopathy, particularly the suboccipital and
postauricular nodes, is prominent.
May have low grade fever
There is no effective antiviral treatment, so immunisation is key
What are some complications of rubella? What is seen in congenital rubella syndrome?
Complications are rare but include thrombocytopenia and encephalitis. Rubella is dangerous in pregnancy and can lead to congenital rubella syndrome, which is a triad of deafness, blindness and congenital heart disease.
What is slapped cheek syndrome, and what causes it?
Known as fifth disesase (of the 6 original viral exanthemas)
(fourth disease, or Dukes disease, isn’t really a thing anymore btw)
one of several possible manifestations of infection by parvovirus B19.
It typically presents as a rash and is more common in children
Also known as Erythma Infectiosum, or fifth disease
What are some symptoms of slapped cheek syndrdome, and how does it affect the body?
HPV-B19 infects the erythroblastoid red cell precursors
in the bone marrow.
asymptomatic infection – common; about 5% to
10% of preschool children and 65% of adults have
antibodies
* erythema infectiosum – the most common illness,
with a viraemic phase of fever, malaise, headache,
and myalgia followed by a characteristic rash on
the face (slapped-cheek) a week later, progressing
to a maculopapular, ‘lace’-like rash on the trunk
and limbs;
arthralgia or arthritis can be common in adults
When can infection with Human Parvovirus B19/slapped cheek syndrome be particularly dangerous?
In Pregnant women, as can be transfered to foetus
Miscarriage or fetal death
Severe fetal anaemia
Hydrops fetalis (fetal heart failure)
Maternal pre-eclampsia-like syndrome
In those with sickle cell anaemia or Thalassaemia - Can send them into a aplastic crisis
Treatment is supportive
What is Roseola Infantum? What causes it
Known as sixth disesase (of the 6 original viral exanthemas)
Roseola infantum is also known as just roseola or sixth disease. This is caused by human herpesvirus 6 (HHV-6) and less frequently by human herpesvirus 7 (HHV-7).
What is the pattern of illness seen in roseola?
It presents 1 – 2 weeks after infection with a high fever (up to 40ºC) that comes on suddenly, lasts for 3 – 5 days and then disappears suddenly.
There may be coryzal symptoms, sore throat and swollen lymph nodes during the illness.
When the fever settles, the rash appears for 1 – 2 days. The rash consists of a mild erythematous macular rash across the arms, legs, trunk and face and is not itchy.
The main complication to be aware of is febrile convulsions, due to high temperature
What is psoriasis?
Psoriasis is a chronic autoimmune condition that causes recurrent symptoms of psoriatic skin lesions.
What are the 4 main types of psoarisis?
Plaque psoriasis
Guttate psoriasis
Pustular psoriasis
Erythrodermic psoriasis
Outline what is seen in Plaque psoriasis
Thickened erythematous plaques (1-10cm diameter)
Silver scales
Commonly seen extensor surfaces and scalp
MC form in adults
Skin changes caused by rapid generation of new skin cells
Results in abnormal build up/thickening of skin
Outline what is seen in guttate psoriasis - what is it often triggered by?
2nd MC form, commonly occurring in children
Many small raised papules (mildly erythematous, scaly)
Across trunk and limbs
Over time papules -> plaques
Often triggered by streptococcal throat infection/stress/meds
Often spontaneously resolves 3-4mths
Outline what is seen in Pustular and Erythrodermic psoriasis
Both rare, and medical emergency
Pustular - Pustules form under skin, pts can be systemically unwell
erythrodermic -Extensive erythematous inflamed areas, covering a large SA of skin - skin comes away in large patches
What are some features of a presentation of psoriasis? Where is it often seen, and what can it be associated with?
Typically erythematous, circumscribed scaly papules and plaques on elbows, knees, extensor surfaces of limbs, scalp, and, less commonly, nails, ears, and umbilical region.
Pruritus
Also associated with:
Nail psoriasis (pitting, thickening, discolouration, ridging & onycholysis)
Psoriatic arthritis
Psychosocial implications - depression, anxiety
Plaques, erythematous, painful regions
Bottom right - Gauatte psoriasis, and rest - plaque psoriasis
What are some specific signs you may see in a pt with psoriasis?
Auspitz sign refers to small points of bleeding when plaques are scraped off
Koebner phenomenon refers to the development of psoriatic lesions to areas of skin affected by trauma (psoriasis on scars)
Residual pigmentation of the skin after the lesions resolve
What are some of the mangaement options for mild plaque psoriasis?
What is a complication of one of the treatments ?
topical corticosteroids **(eg hydrocortisone topical) and a topical vitamin D analogue (eg calcipotriol topical) for 4 weeks
Topical corticosteroids may cause depigmentation in patients who have darker skin types.
Dithranol - non steroidal, slows growth of plaques
review every 4 weeks
Should use topcial steroids for more than 8 weeks in a row
acitretin - a retinoid (vit a derritiavte)
What are some of the mangaement options for moderate plaque psoriasis?
For moderate
Phototherapy
Methotrexate, as a folic acid antagonist that works as an antiproliferative and anti-inflammatory agent
cyclosporine - an immunosuppressant, or infliximab
What are the treatment options for guttate psoarisis?
Phototherapy
Ciclospoin
Methotrexate
acitretin
What is Folliculitis?
Folliculitis is the infection and inflammation of one or more hair follicles.
Manifests clinically as erythematous papules or pustules around hair follicles
What are some causes of folliculitis?
Bacterial, fungal, viral and parasitic micro-organisms
MC cause superficial folliculitis = S.aureus
Trauma, including shaving and extraction
Tight clothes causing friction
Profuse sweating (hyperhidrosis)
Recent Hx immersion in spa water: hot tub, whirlpool, swimming pool, water slides etc
What is the management of follicultitis?
Other interventions: can resolve spontaneously, warm compress w/ antiseptic use, loose fitting clothing, avoid shaving
Topical antibiotics:clindamycin
Oral antibiotics: tetracycline, cephalosporin (used in extensive involvement)
Fungal: fluconazole, itraconazole
What is Urticaria?
What is the pathophysiology behind it?
Urticaria are also known as hives. They are small itchy lumps that appear on the skin. They may be associated with a patchy erythematous rash.
Urticaria are caused the release of histamine and other pro-inflammatory chemicals by mast cells in the skin.
This may be part of an allergic reaction in acute urticaria or an autoimmune reaction in chronic idiopathic urticaria.
What are some causes of acute Urticaria
Acute urticaria is typically triggered by something that stimulates the mast cells to release histamine. This may be:
Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)
What are some causes of chronic Urticaria
Chronic urticaria is an autoimmune condition,
Can be idiopathic
Chronic inducible urticaria describes episodes of chronic urticaria that can be induced by certain triggers, such as:
Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)
What is the management for urticaria?
Antihistamines are the main treatment for urticaria. Fexofenadine is usually the antihistamine of choice for chronic urticaria. Oral steroids may be considered as a short course for severe flares.
In very problematic cases referral to a specialist may be required to consider treatment with:
Anti-leukotrienes such as montelukast
Omalizumab, which targets IgE
Cyclosporin
Define Osteoarthritis
A non-inflammatory degenerative joint disorder characterised by joint pain and functional limitation.
It commonly affects the synovial joints
Disease of bone and joint cartilage
“wear and tear of the joints”
What is the pathophysiology of OA?
It appears inflammatory cytokines interrupt normal repair of cartilage damage.
(IL-1) (TNF-alpha) stimulate metalloproteinase production which degrade the collagen and proteoglycans, and inhibits collagen production
As cartilage is lost, the joint space narrows. Bone on bone interaction may occur, leads to stress and over time subchondral sclerosis (via a process called eburnation) seen on x-ray.
Essentially, cartilage is lost and chondroblasts are unable to replace and repair the lost cartilage, this leads to abnormal bone repair.
What are the symptoms of OA?
Joint pain - exacerbated by movement and relieved by rest
Worse as the day goes on
Joint Stiffness
Swelling
OFTEN ASSYMETIRCAL
Joint Locking - inability to straighten joints
What are the clinical signs of OA?
Hands:
Bouchard’s Nodes
Heberden’s Nodes
Thenar Muscle wasting
First CMC Joint affected most
Weak grip
Knees:
Crepitus
Hips:
Antalgic gait
Restricted internal rotation
All affected Joints:
Joint tenderness
What is Heberden’s and Bouchard’s Nodes?
Bouchard’s - Bony swelling at PIP - (tom has this on his deformed finger)
Heberden’s Bony swelling at the DIP
Remember B before H and proximal before distal
What joints are the most commonly affected in OA?
Knees
Hips
Sacro-ileac joints
Cervical spine
Wrist
base of thumb (carpometacarpal)
finger joints (interphalangeal)
What are the primary investigations to diagnose OA?
Joint X rays show OA hallmarks: LOSS:
Loss of Joint space
Osteophytes
Subarticular Sclerosis
Subchondral Cysts
What other investigations may be done in OA? (ruling out other diseases)
Bloods - normal in OA
ESR/CRP - inflammatory markers to distinguish between RA or Gout
Negative anti-nuclear antibodies
What is the non pharmological management of OA?
Weight loss if overweight to reduce the load on the joint
Physiotherapy to improve strength and function
Occupational therapy to support activities and function
improved diet
anti-inflammatory foods (basically less processed foods: fewer ingredients = less
processed),
Orthotics to support activities and function (e.g., knee braces)
What medical treatments can be used in OA?
Analgesics to control pain and Sx:
1st. Oral paracetamol / topical NSAIDs
2nd. Add oral NSAIDs
3rd . Consider Opiates - Codeine
If these fail:
Inter-articular steroid injections
Joint replacement
How can a diagnosis of osteoarthritis be made?
If someone is over 45 and has typical activity related pain with no morning stiffness or stiffness lasting less than 30 minuets
Define what rheumatoid arthritis is
Chronic systemic inflammatory disease due to deposition of immune complexes in synovial joints which causes symmetrical, deforming polyarthritis
Can progress to involve larger joint and other organs such as the skin and lungs
What are some risk factors for rheumatoid arthritis?
- Female gender
- Smoking
- Family history
- Infections
- Hormones: increased risk post-menopause, potentially due to a reduction in oestrogen levels
Outline the pathophysiology behind RA - what do the autoantibodies produced by plasma cell as and T cells go on to do? 2
enter the circulation and reach the joints.
Here, T cells secrete cytokines (e.g. Interferon-gamma and IL-17) = recruits macrophages. Macrophages also produce cytokines (TNF, IL-1 and IL-6)
These makes the Synovial cells proliferate, making a Pannus.
What are two autoantibodies that are found in rheumatoid arthritis?
What can chronic inflammation lead to?
- Rheumatoid factor - IgM antibody that targets altered IgG
- Anti-CCP anti-cyclic citrullinated peptide - targets citrullinated proteins. = forms an immune complexes, that activate complement system,
Chronic inflammation can also cause angiogenesis, allowing more inflammatory cells to arrive.
What other parts of the body can RA affect?
Inflammatory cytokines can also escape the joint space and affect multiple organ systems
Brain
Lungs
Heart
Eyes
Liver
Blood vessels
What are some issues that RA can cause when it spreads to other areas of the body? (Brain, lungs, eyes, liver, blood vessels)
fever in brain, Peripheral neuropathy
Lungs - Plural Effusions/ pulmonary fibrosis
Heart - Increased IHD risk, Pericarditis, MI
Eyes -Episcleritis
Liver - Increase in Hepcidin, which leads to less iron absorption in the blood - Anaemia
Blood - Atherosclerotic Plaque deposition, Vasculitis
Renal - Glomerulonephritis
Oral - Sjogrens Syndrome
Rheumatoid skin nodules
What are some signs of Rheumatoid arthritis?
-
Symmetrical polyarthritis: (on both sides of body)
- Swollen, warm and tender small joints of the hands and feet (MCP, PIP, MTP)
- Progresses to larger joints (shoulder, elbow, knee, ankle)
- Boutonniere deformity:
- Swan-neck deformity:
- Z-thumb deformity:
- Ulnar deviation of the fingers
- Popliteal cyst: synovial sac bulges posteriorly to the knee
- Rheumatoid nodules -
Signs of Rheumatoid arthritis - what is
- Boutonniere deformity:
- Swan-neck deformity:
- Z-thumb deformity: ??
- Boutonniere deformity: PIP flexion and DIP hyperextension
- Swan-neck deformity: PIP hyperextension and DIP flexion
B before S, so in Boutonniere - F before H, and Swan Neck - H before F
- Z-thumb deformity: hyperextension of the thumb IP joint with flexion of the MCP joint.
What are some symptoms of Rheumatoid arthritis?
- Morning stiffness: > 30 mins and improves throughout the day
- Malaise
- Myalgia
- Low-grade fever
What investigations would you do for Rheumatoid arthritis?
Serology -
Rheumatoid factor (RF)
anti-cyclic citrullinated peptide (anti-CCP) antibody
ESP and CRP will be elevated
May show anaemia of chronic disease - Low Hb Count
Joint x-rays -
Do baseline Kidney and liver functions, as will need to monitor these if on DMARDs
What would you see on an x ray for rheumatoid arthritis?
can see
X-ray – LESS
Loss of joint space
Erosions (peri-articular)
Soft tissue swelling
Soft bones (osteopenia)
What is some first line primary care for Rheumatoid arthritis?
- NSAID: low dose NSAID (e.g. ibuprofen) to cover the period between symptom onset and rheumatology referral
- Refer to specialist care
- Physiotherapy and occupational therapy
What is the first-lie monotherapy for rheumatoid arthritis?
What is the mildest anti rheumatic drug?
Disease-Modifying Anti-Rheumatic Drugs (DMARDs)
Any one of methotrexate, leflunomide or sulfasalazine.
Hydroxychloroquine can be considered in mild disease, mildest anti rheumatic drug
METHOTREXATE - TAKE ONCE A WEEK, SUPPLEMENTING FOLIC ACID AS WELL
What are some side effects of
Methotrexate
Sulphasalazine
Gout can be precipitated by methotrexate use
Methotrexate can also cause liver damage
Haemolytic anaemia is a side effect of sulphasalazine,
after Disease-Modifying Anti-Rheumatic Drugs (DMARDs), what else can you give in rheumatoid arthritis?
Biologics:
Abatacept - Suppress T Cells
Rituximab - Suppress B Cells
T cell drug ends in T, B cell drug ends in B
Infliximab, or etanercept - Suppress TNF a
Anakinra - Suppress IL-1
What is methotrexate contraindicated in?
Methotrexate
Must give folate supplements as methotrexate inhibits folic acid synthesis
Contraindicated in pregnancy
S/E – can lead to malignancy, most commonly skin
Both men and women should stop taking methotrexate for at least 6 months before they want to start conceiving
How do you monitor RA?
measure ESR and CRP levels
What are some things you need to monitor when looking at methotrexate?
Monitor FBC every 3 months, looking at white cell count as can cause abrupt bone marrow suppression
Can be toxic to liver, so need to monitor LFTs
Can be GI toxic, so need to ask about any diarrhoea or stomatitis, and stop it if a patient gets any symptoms w it
Can also cause pulmonary toxicity
need to be vigilant for any sore throat/tonsilitis/illness - so do urgent same day bloods for anyone ill on a DMARD!
Oultline some differences between RA and Osteoarthritis
osteoarthritis
Morning stiffness <30mins
Affects older people more
Cartilage loss
Degenerative disease
Asymmetrical
Can affects DIP joint
Rheumatoid Arthritis
Morning stiffness >60 mins
Joints hot and red
affects younger people
Symmetrical
Inflamed Synovium
Autoimmune disease
rarely effects DIP joint
What factors can increase uric acid production?
Malignancy - increased cell turnover
Cytotoxic drugs
Purine rich diet - seafood and alcohol, red meat
Obesity
Psoriasis
Increased production of purines - seen in high fructose corn syrup drink like tango, fanta
What are the decreased secretion of uric acid causes of gout?
CKD
Diuretics e.g., thiazide and loop
Dehydration,
Alcohol intake
Lead toxicity
High fructose intake
Low dose asprin
Describe the pathophysiology of gout?
Uric acid is formed as a breakdown product if purines
Uric acid has a limited solubility in the blood
If too much urate accumulates, it’ll turn into urate ion and bind to sodium, forming monosodium urate crystals
This forms urate crystals which deposit in areas with slow blood flow the joints and kidney tubules
What are some non pharmalogical ways to prevent gout
Lifestyle – calorie-restriction, modify diet, weight loss, reduce alcohol, hydration
Foods =Dairy – protective, Also, cherries and vitamin C
What are the symptoms of gout?
Rapid onset severe joint pain
Joint stiffness
Commonly swollen red big toe which is painful you cannot put weight on i
What the signs of Gout and where is affected?
What are deposits of uric acid called?
Gout tophi are deposits of uric acid
Ears
Most common site in gout is 1st MTP joint
Base of big toe Podagra - gout of the foot
Wrists
Base of thumb
How would you diagnose gout?
Can be made on just clinical presentation but excluding septic arthritis is key
Joint aspiration and analysis of Synovial fluid will show:
no bacterial growth,
Needle shaped crystals, displaying Negative bifringement under polarised light
undergoing polarised microscopy
Monosodium urate crystals
Measure serum urate levels 4-6 weeks after attack as they can be low at time of attack
What is the first line and second line + 3rd line treatment for gout?
1st line - NSAIDs – naproxen, ibuprofen
2nd line - Colchicine (if NSAIDs contraindicated i.e. peptic ulcer, diabetes, renal disease) - Inhibits WBC migration
3rd line - Steroids
remember that colchicine was also seen in treatment for pericarditis?
What is given to prevent gout?
Lifestyle management and a Xanthine oxidase inhibitor
First-line Allopurinol, w NSAID or colchicine cover
NICE recommend 4 weeks of NSAID or colchicine cover with allopurinol
Diarrhoea will likely precede pain relief is a key side effect of colchicine
2nd line prevention of gout - Second line prevention of gout after Allopurinol is Febuxostat, a non-purine selective
xanthine oxidase inhibitor that reduces the production of uric acid
What is pseudo gout?
Known as Calcium Pyrophosphate Arthropathy,
it’s the Deposition of Calcium Pyrophosphate crystals in the synovium
Calcium pyrophosphate crystals are deposited in the joint causing joint problems.
Can lead to calcium around the hyaline cartilage - chondrocalcinosis
What are some risk factors for getting psuedo gout
- Increasing age: the greatest known risk factor for pseudogout
- Previous joint trauma
- Hyperparathyroidism
- Haemochromatosis
- Acromegaly
- Wilson’s disease
- Diabetes
-
Hypomagnesaemia
-Hypophosphataemia
Describe the pathophysiology of pseudogout?
What is produced as a result?
Deposition of calcium pyrophosphate triggers synovitis with the knee, shoulder and wrist most commonly being affected
Produces the radiological appearance of chondrocalcinosis (linear calcification parallel to the articular surfaces)
Can be acute or chronic
What are some some signs and symptoms of psuedogout?
Very similar to gout and usually indistinguishable until joint aspiration is performed.
- Signs
- Joint inflammation: pain, erythema and swelling
- Signs can be monoarticular (1 joint) or polyarticular (several joints)
- Symptoms
- Rapid onset severe joint pain: knee, shoulder and wrist are most commonly affected
- Joint stiffness
What investigations should you do for suspected pseudo gout? What is a key one to do in order to rule out a another condition that would be a medical emergency?
Joint aspiration:weakly-positively birefringent rhomboid-shaped crystals under polarised microscopy confirm the diagnosis.
If any bacterial growth, then patient is likely to have septic arthritis - MEDICAL EMERGENCY
Joint X-ray:chondrocalcinosis (calcification of articular cartilage) is seen in 40% of casesand is highly suggestive of pseudogout but is not diagnostic; theabsenceof chondrocalcinosis doesnotexclude pseudogout
FBC – raised WBCs
Pseudogout - positive birefringent crystals
What is the management of acute pseudogout?
Acute
- Anti-inflammatory:NSAIDs or colchicine, particularly in polyarticular disease
- Corticosteroid:intra-articularsteroids can be used in monoarticular disease orsystemicsteroids in polyarticular disease
- Cool packs and rest
- Aspiration of the joints - relieves pain
What is the management of chronic pseudogout?
- DMARDs: e.g. methotrexate and hydroxychloroquine may be considered in chronic pseudogout
- Joint replacement: only indicated in chronic, recurrent cases with severe joint degeneration
What is osteoporosis
a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture.
Bones become more porous due to increased breakdown
What is osteopenia? What is it defined by
Osteopenia refers to a less severe reduction in bone density than osteoporosis.
Defined as bone mineral density 1-2.5 standard deviations below young adult mean value
What are the primary causes of Osteopenia?
What are some secondary causes of osteopenia?
Primary – menopause and age, as Oestrogen protects bones
Secondary – to disease or drugs
rememeber as SHATTERED
S – steroid use (prednisolone)
H – hyperthyroidism/hyperparathyroidism
A – alcohol/smoking
T – thin (low BMI)
T – testosterone low
E – early menopause
R– renal or liver failure
E – erosive/inflammatory bone disease e.g. RA, myeloma
D – dietary calcium low
Name some diseases that can increase the risk of getting oesteoporosis.
Joint disease e.g. RA, SLE
Hyperthyroidism and hyperparathyroidism – increased bone turnover
High cortisol – Cushing’s (increases bone resorption and induces osteoblast apoptosis)
Low oestrogen/testosterone e.g. hypogonadism, anorexia, menopause
Renal disease – decreased vitamin D
Previous fracture
Anorexia
Pathophysiology of OP - How can old age and oestrogen affect bone turnover?
As we age, the activity of osteoclasts increases and is not matched by osteoblasts.As such bone mass decreases.
Oestrogen is key to the activity of bone cells with receptors found on osteoblasts, osteocytes, and osteoclasts. The mechanisms are still being understood, but it appears osteoclasts survive longer in the absence of oestrogen, and there is arrest of osteoblastic synthetic architecture.
What screening tool can you use in osteoporosis?
FRAX = fracture risk assessment tool
Predicts the risk of a fragility fracture over the next 10 years. Usually the first step of assessment and is done on patients at risk of osteoporosis
BMI, co-morbidities, smoking, alcohol and family history +/- bone mineral density
- It gives results as a percentage 10 year probability of a:
- Major osteoporotic fracture
- Hip fracture
What is the gold standard investigation you would do for suspected osteoporosis?
DEXA Scan (dual-energy xray absorptiometry)
Measures bone mineral density by measuring how much radiation is absorbed by the bones
Scanning Hip is best
Gives T score (main one) - number of standard deviations below the mean for a healthy young adult their bone density is.
and Z score - represent the number of standard deviations the patients bone density falls below the mean for their age.
What T scoring on a DEXA scan would be indicative of
Better than reference
No evidence of oesteoporosis
Osteopenia (offer lifestyle advice)
Osteoporosis
T-score
>0 BMD = is better than the reference.
0 to -1 = BMD is in the top 84%: no evidence of osteoporosis.
-1 to -2.5 = Osteopenia. Risk of later osteoporotic fracture. Offer lifestyle advice.
-2.5 or worse = Osteoporosis. Offer lifestyle advice and treatment Repeat DEXA in 2yrs.
What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?
Activty and exercise
Weight control
Reduce alcohol/stop smoking
NICE recommend calcium supplementation with vitamin D - eg Calcihew-D3
vitamin D supplementation.
What is the treatment for someone at high risk of a fracture? (specific drug name)
Bisphosphonates- they interfere with osteoclast activity reducing their activity.
Alendronate 70mg once weekly
What are the side effects of bisphosphonates?
Oesophagitis/Reflux and oesophageal erosions.
GI distress
Renal Toxicity
Hypocalcaemia
Oesophageal ulcers
Osteonecrosis (death of bone tissue) of the jaw and external auditory canal
What are some other treatment options for osteoporosis?
Hormone replacement therapy should be considered in women that go through menopause early.
Raloxifene - Selective oestrogen receptor
Teriparatide - recombinant PTH, increases bone formation
How can you differentiate between gout and pseudo gout ?
Joint aspiration, microscopy
Gout - Negatively birefringent crystals
Pseudogout - positive birefringent crystals
note - most commonly affected joint in gout is 1st MTP of the big toe, most commonly affected joint in pseudogout is the knee joint
How should you take bisphosphonates?
Take once a week in the morning and at least 30 minutes before any food
the patient should remain upright for at least half an hour after taking
What are the symptoms of GCA?
Main symptom is headache that us unilateral and around forehead and temple.
Irreversible painless complete sight loss
Jaw claudication
Scalp tenderness may be noticed when brushing hair
What are the primary investigations of GCA?
1st line:
INCREASED ESR - ELEVATED IN 83% OF CASES
ANCA Negative
Temporal Artery biopsy - diagnostic
Fundoscopy
Picture - diagnostic criteria
What is the management for giant cell arthritis?
What may happen if a patient with GCA was to stop taking these medication immediately?
1st Line:
Corticosteroids - Oral Prednisolone
If you stop steroid doses abruptly, could cause an Adrenal crisis
What are some complications of GCA?
How should it be dealt with?
Amaurosis Fugax: Sudden painless vision loss of one eye (optic neuropathy)
Must be dealt with ASAP via high dose IV METHYL PREDNISOLONE
What is Polymyalgia Rheumatica?
What condition is it associated with
Chronic inflammatory rheumatic condition causing chronic pain in the shoulders, pelvic girdle and neck.
This condition affects both muscles and joints
Often associated with and occurs alongside Giant cell arteritis
What will you see in Polymyalgia Rheumatica?
Large cell vasculitis presenitng as chronic pain syndrome (similar to fibromyalgia) Patients are ALWAYS OVER 50.
Wil have Raised ESR and CRP, temporal artery biopsy may show giant cell arteritis
What is ankylosing spondylitis?
A chronic progressive inflammatory arthropathy. It mainly affects the spine and cause progressive stiffness and pain.
Ankylosis= abnormal stiffening and immobility of a joint due to the fusion of a bone
Outline the pathophysiological process behind Ankylosing Spondylitis.
Inflammation destroys the intervertebral joints, facet joints and sacroiliac joints
Fibroblasts replace the destroyed joints with fibrin 🡪 formation of tough fibrin band around joints which limits range of motion
Ossification occurs (fibrous tissue turns to bone) and makes spine immobile
Syndesmophytes – new bone formation and vertical growth from anterior vertebral corners
What are some symptoms of ankylosing spondylitis?
Weight loss
Fever
Fatigue
- Pain and stiffness of joints
- Lower back pain
- Sacroiliac pain (buttock region)
Pain worst with rest and improves with movement
Neck or back pain/stiffness – cervical/thoracic region - Can lead to SOB
Acute, anterior uveitis
think - kind of similar to Rheumatoid arthritis for the spine?
What investigations would you do for someone with ankylosing spondylitis?
- CRP and ESR - elevated
- Genetic testing - HLA-B27?
- Early stages - MRI of spine if x-ray is normal - can show early changes which show up as bone marrow oedema (red arrows) as well as erosions, sclerosis and ankylosis
Give the order of management for Ankylosing spondyltis.
Physio and hydrotherapy
Long term high dose NSAIDs e.g. ibuprofen or naproxen
DMARDs e.g. methotrexate – treat peripheral arthritis but not the disease
Biologics– Anti-TNF e.g. etanercept or monoclonal antibodies against TNF e.g. infliximab,
Monoclonal antibodies targeting IL-7 - e.g. secukinumab
What is reactive arthritis?
An arthritis that is triggered following an infection (probs by molecular mimicry)
Also known as Reiter syndrome
Its a type of Seronegative spondyloarthropathy - RF is absent
What are the typical infections/bacteria that are known to precede/trigger reactive arthritis?
-
Gastroenteritis
- Salmonella
- Shigella
- Camplobacter
-
Sexually transmitted infections
- Chlamydia trachomatis.
- Gonorrhea (may also cause gonococcal septic arthritis, so this must be considered)
Outline the pathophysiology that is thought to be behind reactive arthritis
Thought that the lipopolysaccharide (Endotoxin) on the gram negative bacteria produces a particularly strong response from immune system.
This response also results in antibodies or inflammation that also affect the joints.
In reactive arthritis, there are no actual joint infections (as seen in septic arthritis). The infection is at another site!
What is the key presentation of reactive arthritis?
Acute, asymmetrical monoarthritis typically in lower leg (knee).
Can also present with triad of: Urethritis, arthritis and conjunctivitis
Can’t see, pee or climb a tree THIS TRIAD IS KNOWN AS REITER’S SYNDDROME
What are the investigations for reactive arthritis?
- ESR and CRP - elevated
- Infectious serology ask about history of infection
- Genetic testing for HLA-B27
- If diarrhoea - culture stool
Aspirate joints to rule out septic arthritis/Gout - should be sterile in RA
Sexual health review
What is the management of Reactive arthritis?
Management
Treat cause of infection – antibiotics
NSAIDs ± steroid joint injections
Consider use of methotrexate and sulfasalazine as steroid sparing agents if >6 months
- Recurrent/ persistent reactive arthritis
- DMARDs e.g. methotrexate or sulfasalazine
- Anti-TNF
What is septic arthritis? What are the two ways in which it can occur?
Septic arthritis is defined as the infection of 1 or more joints caused by pathogenic inoculation of microbes.
It occurs either by direct inoculation or via haematogenous spread.
It is a medical emergency!- CAN AFFECT ANY JOINT, MOST COMMONLY KNEE
What are the common bacteria that are mostly likely behind septic arthritis?
Gonococcal Arthritis-
- Neisseria gonorrhoeae - young, sexually-active adults
Non Gonococcal Arthritis - (more common)
- Staphylococcus aureus - the most common cause in all age groups
- Staphylococcus epidermidis - prosthetic joints
- Streptococcus pyogenes - children under 5 years old
- Escherichia coli - immunosuppressed, eldery and IV drug abuse
Due to vaccine against haemophilus influenzae, it is now a rare cause of septic arthritis
What are the signs and symptoms of septic arthritis?
Normally only one joint is affected. Most commonly the knee.
Hot tender and swollen joint
Limited range of movement
Difficulty weight bearing
Fever
What investigations would you do for septic arthirits? What is gold standard?
- FBC: leukocytosis
- CRP and ESR: elevated due to inflammation and used for monitoring response to treatment
- Blood cultures: should be performed onallpatients before commencing antibiotics
Joint aspiration (arthrocentesis): definitive investigation ideally prior to commencing antibiotics; synovial fluid should be sent to the lab for microscopy and culture having a prosethitci joint is a CI for aspiration
What is the management for Septic arthritis?
- IV antibiotics
- Empirical therapy: flucloxacillin is first-line
- Penicillin allergy: clindamycin
- Suspected or confirmed MRSA: vancomycin
- Gonococcal arthritis or gram-negative infection: cefotaxime or ceftriaxone
-
Joint drainage
- Aspiration
- Arthroscopic drainage
- Open drainage
What is osteomyelitis?
Inflammation of the bone marrow (infection localised to bone) caused by an infecting organism, most commonly Staphylococcus aureus.
What bacteria can cause osteomyelitis?
- Staphylococcus aureus:A gram-positive cocci. Includes MRSA - MOST COMMON
- Pseudomonas aeruginosa:A gram-negative rod. More commonly seen in IV drug users.
- Salmonellaspp.:Gram-negative rods. Most commonly seen in patients with sickle cell anaemia.
What are some risk factors for getting osteomyelitis?
Diabetes mellitus - vascular compromise due to high blood sugar
Trauma – bone exposed to outside environment (open fractures)
Surgery
Peripheral vascular disease
Malnutrition
Inflammatory arthritis
Debilitating disease
Immunosuppression – HIV or immunosuppressive drugs
Sickle cell disease
Prosthetic material
RISK FACTORS FOR OSTEOMYELITIS ARE THE SAME AS THOSE FOR SEPTIC ARTHRITIS
What are some symptoms of osteomyelitis?
Onset – several days
Dull pain at site of OM
Fever
Weakness
Redness/Swelling
May be aggravated by movement
What are some signs of osteomyelitis? (systemic and local)
Systemic - Fever, Rigors, Sweats, Malaise
Local
Acute OM
Tenderness, warmth, erythema and swelling
Chronic OM
Tenderness, warmth, erythema and swelling
Draining sinus tract
Deep/large ulcers that fail to heal despite several weeks’ treatment
What investigations would you do for suspected osteomyelitis?
Bloods
- FBC - elevated WCC
- CRP and ESR - elevated
Microbiology
- Urine MSU
- Blood cultures
- Wound swabs
Imaging
-
X-ray of suspected area
- Local osteopenia
- Areas of bone lysis
- Cortical loss
- Periosteal reaction
- Sequestrum and involucrum may be seen in advanced disease
GOLD STANDARD - MRI
- MRI
- Good visualisation of bone and surrounding soft tissue
- Bone marrow oedema can be seen early on
What is the management for osteomyelitis? What can surgery do for osteomyelitis?
6 weeks for acute OM
3 months for chronic OM
Abx:
IV Flucloxacillin/Or Vancomycin for MRSA cover
Immobilise
Surgery can remove any abscess, or necrotic bone/sequestrum
What would you see on x-ray of Ankylosing spondylitis, at later stages of the disease?
Bamboo spine
calcification of all the ligaments of the spine
squaring of the vertebral bodies
subchondral sclerosis
Syndesmophytes - bony outgrowths from the spinal ligaments as they attach to adjacent vertebral bodies
fusion of joints (facet / sacroiliac / costovertebral)
what is a shared care protocol
SCP are clinically focused and provide the info required to support safe and effective shared care for specified medicines,
have standardised lists and protocols - So GP can prescribed on the behalf of the specialist, and prompts you when to seek advice
eg Methotrexate, Sulfasalazine
Amiodarone, Ciclosporins
What is the treatment for Acute pyelonephritis? What 2 main antibiotics are given?
- Broad spectrum antibiotics (e.g. co-amoxiclav) , and Cefalexin for 7 to 10 days
until culture and sensitivities are avaliable
- Hydration
- Other/ adjuncts
- Admission if systemically unwell or complicated
- IV rehydration
- Analgesia
- Antipyretics
What are the first and second line treatment for non-pregnant women with cystitis/Lower UTI (drug and duration)
and give duration of treatment too
First line: Antibiotic course for 3 days - nitrofurantoin or trimethoprim
Second line: Antibiotic course for 3 days - nitrofurantoin or pivmacillinam or fosfomycin single-dose sachet
What are the first and second line treatment for pregnant women with cystitis/Lower UTI (drug and duration)
First line: Antibiotic course for 7 days - nitrofurantoin
but avoid nitrofuratnoin in third trimester, give a penicllin instead
Second line: Antibiotic course for 7 days - amoxicillin or cefalexin (1st Gen Cephalosporin)
What are the first and second line treatment for men with cystitis/Lower UTI?
What duration as well?
First line: Trimethoprim 200 mg twice a day for 7 days
Second line - Nitrofurantoin:
If not resolving, consider an alternative diagnosis !
What are some things that trimethorpin should be avoided in ?
what atnbx would you give for UTI if the above is both trimethoprim and nitrofurantoin was contraindicated in?
Trimethoprim carries a teratogenic risk in the first trimester as it inhibits folate synthesis. - avoid throughtou all pregancy
Methotrexate is listed as a severe interaction with trimethoprim in the BNF, due to the increased risk of haematological side effects that can be fatal.
Trimethorprin - can cause transient raise in creatine, so can lead to an eGFR based on creatine levels to look falsely low.
Pivmecillinam 400mg initial dose, if both CI
What are some things that nitrofuratnoin is CI in?
What do you give if neither Nitrofurantoin or trimethoprin is suitable?
Although Nitrofurantoin is first line in pregnant women with lower urinary tract infections, it
should be avoided in third trimester as it may cause neonatal haemolysis
also Nitrofurantoin is contraindicated in patients with an **eGFR of less than 45
G6PD deficiency is listed as a contra-indication to nitrofurantoin in the BNF.
Pivmecillinam 400mg initial dose, if both CI
what antibiotics do you need to give for EBSL?
confer resistance to both penicillin and cephalosporin-based antibiotics
Give nitrofurantoin or fosfomycin if systemically well
or Carbapenems like meropenem IV if systemically unwell
What are some signs in a history of poor asthma contorl?
reduced effectiveness of bronchodilator
reduce exercise tolerance
asthma attack within the last two years
history of waking up at night with wheeze/cough/chest pain or daytime asthma symptoms (three times a week or more)
What are some medications used to help with smoking addiction,
(stop smoking, reduce cravings, reduce pleasure)
NRT (stop smoking cigarettes), Champix/Varenicline (reduce cravings),
Bupropion/Zyban (reduce pleasure
Bupropion can lower the seizure threshold, so CI in epilepsy
what is the only pharamlogical anti smoking therapy that is safe to take in pregnancy?
Nicotine replacement therapy is the only pharmacological therapy which is safe to prescribe during pregnancy
How can you gauge the severity of pneumonia in
a) the hospital
b) the community
Give the values that lead to scoring
CRB-65 out of hospital and CURB-65 in hospital. The only difference is that out of hospital you do not count urea.
C – Confusion (new disorientation in person, place or time)
U – Urea > 7
R – Respiratory rate ≥ 30
B – Blood pressure < 90 systolic or ≤ 60 diastolic.
65 – Age ≥ 65
outline How does the scoring for CURB-65 dictate treatment and mortality, for dealing with pneumonia
Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment
0 = Low risk (<1% mortality)
1-2 = Intermediate risk (1-10% mortality)
3-4 = High Risk (>10% mortality)
requires in-patient admission and IV antibiotics. Normally a CAP is treated with Co-Amox and Clarithromycin (to cover for atypicals). HAPs are treated with Tazocin, however this may change depending on trust guidelines.
What are the most common causes of
HAP
CAP
HAP - strep pneumoniae, H. Influenzae, someitmes mycoplasma, legionella
CAP - Pseudomonas argeunoisa, staph aureus, klebsiella pneumonia
