Polymyalgia rheumatica
Polymyalgia rheumatica (PMR) is a relatively common condition seen in older people
characterised by muscle stiffness and raised inflammatory markers. Whilst it
appears to be closely related to temporal arteritis the underlying cause is not fully
understood and it does not appear to be a vasculitic process.
Features
● typically patient > 60 years old
● usually rapid onset (e.g. < 1 month)
● aching, morning stiffness in proximal limb muscles
○ weakness is not considered a symptom of polymyalgia rheumatica
● also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night
sweats
Investigations
● raised inflammatory markers e.g. ESR > 40 mm/hr
● note creatine kinase and EMG normal
Treatment
● prednisolone e.g. 15mg/od
○ patients typically respond dramatically to steroids, failure to do so
should prompt consideration of an alternative diagnosis
Lithium toxicity
Lithium is a mood stabilising drug used most commonly prophylactically in bipolar
disorder but also as an adjunct in refractory depression. It has a very narrow
therapeutic range (0.4-1.0 mmol/L) and a long plasma half-life being excreted
primarily by the kidneys. Lithium toxicity generally occurs following concentrations >
1.5 mmol/L.
Toxicity may be precipitated by:
● dehydration
● renal failure
, ● drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor
blockers, NSAIDs and metronidazole.
Features of toxicity
● coarse tremor (a fine tremor is seen in therapeutic levels)
● hyperreflexia
● acute confusion
● polyuria
● seizure
● coma
Management
● mild-moderate toxicity may respond to volume resuscitation with normal
saline
○ IV fluids with isotonic saline, until euvolemic, then typically twice
maintenance rate
○ monitor serum sodium closely (every 4 hours with serial lithium
concentrations) if there is a concern about lithium-induced
nephrogenic diabetes insipidus
● haemodialysis may be needed in severe toxicity
● sodium bicarbonate is sometimes used but there is limited evidence to
support this
○ by increasing the alkalinity of the urine it promotes lithium excretion
Mycophenolate mofetil
Mycophenolate mofetil is an immunosuppressant commonly used to prevent
rejection of organ transplants.
Mode of action
● inhibits inosine monophosphate dehydrogenase, which is needed for purine
synthesis
● as T and B cells are particularly dependent on this pathway it can reduce the
proliferation of immune cells
,Opioid misuse
Opioids are substances which bind to opioid receptors. This includes both naturally
occurring opiates such as morphine and synthetic opioids such as buprenorphine
and methadone.
Features of opioid misuse
● rhinorrhoea
● needle track marks
● pinpoint pupils
● drowsiness
● watering eyes
● yawning
Complications of opioid misuse
● viral infection secondary to sharing needles: HIV, hepatitis B & C
● bacterial infection secondary to injection: infective endocarditis, septic
arthritis, septicaemia, necrotising fasciitis
● venous thromboembolism
● overdose may lead to respiratory depression and death
● psychological problems: craving
● social problems: crime, prostitution, homelessness
Emergency management of opioid overdose
● IV or IM naloxone: has a rapid onset and relatively short duration of action
Harm reduction interventions may include
● needle exchange
● offering testing for HIV, hepatitis B & C
Management of opioid dependence
● patients are usually managed by specialist drug dependence clinics although
some GPs with a specialist interest offer similar services
● patients may be offered maintenance therapy or detoxification
● NICE recommend methadone or buprenorphine as the first-line treatment in
opioid detoxification
, ○ methadone is a full agonist of the mu-opioid receptor - binds to these
receptors in the brain and fully activates them. This action can relieve
withdrawal symptoms and cravings. Has a long half-life
○ buprenorphine is a partial agonist of the mu-opioid receptor and an
antagonist of the kappa-opioid. It binds to the mu-opioid receptors in
the brain but only partially activates them. This partial activation is
enough to alleviate cravings and withdrawal symptoms in individuals
with opioid dependence. Furthermore, the binding of buprenorphine to
the mu-opioid receptor is very strong, or 'high affinity,' meaning it can
displace other opioids from these receptors and prevent them from
exerting their effects. As a kappa-opioid receptor antagonist,
buprenorphine may contribute to its ability to reduce symptoms of
opioid withdrawal and potentially reduce depressive and dysphoric
states.
● compliance is monitored using urinalysis
● detoxification should normally last up to 4 weeks in an inpatient/residential
setting and up to 12 weeks in the community
Avascular necrosis of the hip
Avascular necrosis (AVN) may be defined as death of bone tissue secondary to loss
of the blood supply. This leads to bone destruction and loss of joint function. It most
commonly affects the epiphysis of long bones such as the femur.
Causes
● long-term steroid use
● chemotherapy
● alcohol excess
● trauma
● haematological / vascular
○ sickle cell disease
○ inherited thrombophilia: e.g. Factor V Leiden
○ acquire thrombophilia: e.g. antiphospholipid syndrome
Features
● initially asymptomatic
● deep, aching pain
○ most commonly hip or groin pain
Polymyalgia rheumatica (PMR) is a relatively common condition seen in older people
characterised by muscle stiffness and raised inflammatory markers. Whilst it
appears to be closely related to temporal arteritis the underlying cause is not fully
understood and it does not appear to be a vasculitic process.
Features
● typically patient > 60 years old
● usually rapid onset (e.g. < 1 month)
● aching, morning stiffness in proximal limb muscles
○ weakness is not considered a symptom of polymyalgia rheumatica
● also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night
sweats
Investigations
● raised inflammatory markers e.g. ESR > 40 mm/hr
● note creatine kinase and EMG normal
Treatment
● prednisolone e.g. 15mg/od
○ patients typically respond dramatically to steroids, failure to do so
should prompt consideration of an alternative diagnosis
Lithium toxicity
Lithium is a mood stabilising drug used most commonly prophylactically in bipolar
disorder but also as an adjunct in refractory depression. It has a very narrow
therapeutic range (0.4-1.0 mmol/L) and a long plasma half-life being excreted
primarily by the kidneys. Lithium toxicity generally occurs following concentrations >
1.5 mmol/L.
Toxicity may be precipitated by:
● dehydration
● renal failure
, ● drugs: diuretics (especially thiazides), ACE inhibitors/angiotensin II receptor
blockers, NSAIDs and metronidazole.
Features of toxicity
● coarse tremor (a fine tremor is seen in therapeutic levels)
● hyperreflexia
● acute confusion
● polyuria
● seizure
● coma
Management
● mild-moderate toxicity may respond to volume resuscitation with normal
saline
○ IV fluids with isotonic saline, until euvolemic, then typically twice
maintenance rate
○ monitor serum sodium closely (every 4 hours with serial lithium
concentrations) if there is a concern about lithium-induced
nephrogenic diabetes insipidus
● haemodialysis may be needed in severe toxicity
● sodium bicarbonate is sometimes used but there is limited evidence to
support this
○ by increasing the alkalinity of the urine it promotes lithium excretion
Mycophenolate mofetil
Mycophenolate mofetil is an immunosuppressant commonly used to prevent
rejection of organ transplants.
Mode of action
● inhibits inosine monophosphate dehydrogenase, which is needed for purine
synthesis
● as T and B cells are particularly dependent on this pathway it can reduce the
proliferation of immune cells
,Opioid misuse
Opioids are substances which bind to opioid receptors. This includes both naturally
occurring opiates such as morphine and synthetic opioids such as buprenorphine
and methadone.
Features of opioid misuse
● rhinorrhoea
● needle track marks
● pinpoint pupils
● drowsiness
● watering eyes
● yawning
Complications of opioid misuse
● viral infection secondary to sharing needles: HIV, hepatitis B & C
● bacterial infection secondary to injection: infective endocarditis, septic
arthritis, septicaemia, necrotising fasciitis
● venous thromboembolism
● overdose may lead to respiratory depression and death
● psychological problems: craving
● social problems: crime, prostitution, homelessness
Emergency management of opioid overdose
● IV or IM naloxone: has a rapid onset and relatively short duration of action
Harm reduction interventions may include
● needle exchange
● offering testing for HIV, hepatitis B & C
Management of opioid dependence
● patients are usually managed by specialist drug dependence clinics although
some GPs with a specialist interest offer similar services
● patients may be offered maintenance therapy or detoxification
● NICE recommend methadone or buprenorphine as the first-line treatment in
opioid detoxification
, ○ methadone is a full agonist of the mu-opioid receptor - binds to these
receptors in the brain and fully activates them. This action can relieve
withdrawal symptoms and cravings. Has a long half-life
○ buprenorphine is a partial agonist of the mu-opioid receptor and an
antagonist of the kappa-opioid. It binds to the mu-opioid receptors in
the brain but only partially activates them. This partial activation is
enough to alleviate cravings and withdrawal symptoms in individuals
with opioid dependence. Furthermore, the binding of buprenorphine to
the mu-opioid receptor is very strong, or 'high affinity,' meaning it can
displace other opioids from these receptors and prevent them from
exerting their effects. As a kappa-opioid receptor antagonist,
buprenorphine may contribute to its ability to reduce symptoms of
opioid withdrawal and potentially reduce depressive and dysphoric
states.
● compliance is monitored using urinalysis
● detoxification should normally last up to 4 weeks in an inpatient/residential
setting and up to 12 weeks in the community
Avascular necrosis of the hip
Avascular necrosis (AVN) may be defined as death of bone tissue secondary to loss
of the blood supply. This leads to bone destruction and loss of joint function. It most
commonly affects the epiphysis of long bones such as the femur.
Causes
● long-term steroid use
● chemotherapy
● alcohol excess
● trauma
● haematological / vascular
○ sickle cell disease
○ inherited thrombophilia: e.g. Factor V Leiden
○ acquire thrombophilia: e.g. antiphospholipid syndrome
Features
● initially asymptomatic
● deep, aching pain
○ most commonly hip or groin pain
