GP - RENAL, DERM, MSK, ENDOCRINE & INFECTION Flashcards
OTITIS EXTERNA
What is otitis externa?
What is it associated with?
- Inflammation of external ear canal
- Swimmer’s ear as associated with frequent swimming
OTITIS EXTERNA
What is malignant otitis externa?
- Immunocompromised, DM or elderly where it can spread to the surrounding bones (mastoid + temporal)
OTITIS EXTERNA
What are some causes of otitis externa?
- Infection (staph. aureus, pseudomonas aeruginosa or fungal)
- Seborrhoeic dermatitis
- Contact dermatitis (allergic + irritant)
OTITIS EXTERNA
What is the clinical presentation of otitis externa?
- Ear pain (mild), itchy + discharge common, ?hearing loss
- Otoscopy = red, swollen or eczematous canal
OTITIS EXTERNA
What is the management of otitis externa?
- May need to clean ear canal first with syringing or irrigation
- Topical Abx or a combined topical Abx with steroid = 1st line
- PO flucloxacillin if infection spreading, swab before
T2DM
What is the pathophysiology of T2DM?
- Repeated exposure to glucose + insulin = resistance to effects of insulin so more required for a response
- Beta cells fatigued + damaged so produce less
- Low insulin + peripheral insulin resistance = impaired glucose tolerance
T2DM
What are some causes of T2DM?
How does it present?
- Genetics + environment (FHx, obesity, poor diet)
- Asian, men, older age
- No Sx but sometimes polyuria, polydipsia, lethargy, visual blurring
T2DM
What values are diagnostic for T2DM?
- HbA1c ≥48mmol/mol Dx
1 result if Sx, 2 separate if none: - Random glucose ≥11.1mmol/L
- Fasting glucose ≥7mmol/L
- OGTT 2h ≥11.1mmol/L
T2DM
What values suggest…
i) impaired fasting glucose?
ii) impaired glucose tolerance?
i) 6.1-6.9mmol/L
ii) 7.8-11.1mmol/L
T2DM
What is a main complication of uncontrolled T2DM?
- Hyperglycaemic hyperosmolar state
- Decrease insulin = increase serum glucose + serum osmolality + urination but no ketosis as still some endogenous insulin
T2DM
How does HHS present?
How is it diagnosed?
Management?
- Marked dehydration (polydipsia, polyuria, hypovolaemia) + impaired consciousness
- Plasma glucose >30mmol/L, plasma osmolality >320mOsm
- IV fluid replacement, infuse insulin, LMWH prophylaxis as hyperviscous blood
T2DM
What is the first line management of T2DM?
What are the HbA1c targets in T2DM?
- Lifestyle advice = exercise, less carbs/fat, smoking cessation
- <48mmol/mol for new pts or <53 if on ≥2 Tx
T2DM
List 6 medications that can be used in T2DM
- Metformin (biguanide, first line)
- Gliclazide (sulfonylurea)
- Sitagliptin (DPP4 inhibitor)
- Empagliflozin (SGLT)
- Glitazone (pioglitazone)
- GLP-1 mimetics
T2DM
What is the mechanism of action of…
i) metformin?
ii) gliclazide?
iii) sitagliptin?
i) Increased insulin sensitivity, reduced gluconeogenesis in liver + helps weight
ii) Stimulates beta cells to secrete insulin
iii) Increases incretin levels which inhibit glucagon production
T2DM
What is the mechanism of action of…
i) empagliflozin?
ii) glitazone?
iii) GLP-1 mimetics?
i) Blocks glucose reabsorption in PCT of kidneys + promotes excretion of excess glucose in urine
ii) Increases insulin sensitivity + decreases liver production of glucose
iii) Incretin (GLP-1) mimetic inhibits glucagon secretion (after triple therapy)
T2DM
What are some side effects of…
i) metformin?
ii) gliclazide?
iii) sitagliptin?
iv) empagliflozin?
v) glitazone?
vi) GLP-1 mimetics?
i) GI upset (D+V, abdo pain), lactic acidosis
ii) Hypoglycaemia + weight gain
iii) GI upset, pancreatitis
iv) Glucosuria, weight loss + UTI risk
v) Weight gain, fluid retention, heart failure
vi) Weight loss, N+V, pancreatitis
HYPERTHYROIDISM
What are the 3 mechanisms explaining the causes of hyperthyroidism?
- Overproduction of thyroid hormone
- Leakage of pre-formed hormone from thyroid
- Ingestion of excess thyroid hormone
HYPERTHYROIDISM
What is the most common cause of hyperthyroidism?
What is the pathophysiology?
- Graves’ disease
- Autoimmune induced excess production of thyroid hormone, esp T3
- TSH receptor stimulating antibody (TRAb, IgG), autoimmune link to T1DM, coeliac, Addison’s
HYPERTHYROIDISM
What are some other causes of hyperthyroidism?
- Toxic multinodular goitre = nodules secrete excess thyroid hormones (elderly women)
- Toxic adenoma = solitary nodule producing T3/4
- DeQuervain’s thyroiditis = acute inflammation
- Exogenous iodine (food, amiodarone)
HYPERTHYROIDISM
What are the general signs and symptoms of hyperthyroidism?
- Anxiety, irritability
- Sweating, palpitations (?AF), tremor, tachycardia
- Heat intolerance
- Weight loss, increased appetite, diarrhoea
- Oligomenorrhoea
- Thin hair, warm skin
HYPERTHYROIDISM
What are the Graves’ disease specific features?
- Diplopia, ophthalmoplegia, increased tears
- Exophthalmos, lid lag + retraction
- Thyroid acropachy (clubbing, painful digits)
- Pretibial myxoedema
HYPERTHYROIDISM
How would De Quervain’s thyroiditis present?
- PAIN in de QuerVAIN = tender goitre, fever, dysphagia (viral infection)
- Hyperthyroid phase > hypothyroid phase (TSH falls due to -ve feedback)
HYPERTHYROIDISM
What are some investigations for hyperthyroidism?
- TFTs (primary = low TSH, high T3/4, secondary = high TSH, high T3/4 hypothalamus or pituitary pathology)
- Thyroid autoantibodies
- Isotope scan
HYPERTHYROIDISM
What is a complication of hyperthyroidism?
Management?
- More severe presentation with pyrexia, tachycardia + delusion
- Admission, supportive (fluid resus), beta-blockers, ?anti-arrhythmic
HYPERTHYROIDISM
What is the management of hyperthyroidism?
- Beta-blockers for rapid sympathetic control (propranolol)
- Carbimazole 1st line, propylthiouracil 2nd
- Radioiodine therapy
- Surgical thyroidectomy
- NSAIDs + beta-blockers for self-limiting DeQuervain’s
HYPERTHYROIDISM
What are the 2 methods for administering anti-thyroid drugs?
What are side effects of them?
- Titration
- Block + replace (block all production + take levothyroxine)
- Carbimazole = agranulocytosis
- Propylthiouracil = severe hepatic reactions
HYPERTHYROIDISM
What are some risks with…
i) radioiodine therapy?
ii) surgical thyroidectomy?
i) C/I in pregnancy, breastfeeding + may leave patient hypothyroid
ii) Risk to recurrent laryngeal nerve (hoarse voice) + hypoparathyroidism
HYPOTHYROIDISM
What are some common causes of hypothyroidism?
- Primary autoimmune (atrophic thyroiditis, Hashimoto’s thyroiditis)
- Iodine deficiency (#1 worldwide)
- Secondary to carbimazole, radioactive iodine, thyroidectomy, lithium + amiodarone
- Central causes like hypopituitarism (Sheehan’s, tumours, radiation)
HYPOTHYROIDISM
What is…
i) atrophic thyroiditis?
ii) Hashimoto’s thyroiditis?
i) Diffuse lymphocytic infiltration of thyroid leading to atrophy + so no goitre
ii) Goitre due to lymphocytic + plasma cell infiltration, #1 cause in developed world
HYPOTHYROIDISM
What are some symptoms of hypothyroidism?
- Weight gain, decreased appetite + constipation
- Cold intolerance
- Lethargy, menorrhagia
HYPOTHYROIDISM
What are some signs of hypothyroidism?
BRADYCARDIC
- Bradycardia
- Reflexes relax slowly
- Ataxia
- Dry, thin hair/skin
- Yawning
- Cold hands
- Ascites
- Round puffy face
- Defeated demeanour
- Immobile
- CHF
HYPOTHYROIDISM
What are some investigations for hypothyroidism?
- TFTs = primary (high TSH, low T3/4), secondary (low TSH, low T3/4)
- Thyroid peroxidase antibody (TPO-Ab) + anti-thyroglobulin in Hashimoto’s
- Anti-TSH positive + TPO in atrophic thyroiditis
HYPOTHYROIDISM
What is the management of hypothyroidism?
Prescribing information?
- Lifelong levothyroxine to replace (titrate up)
- 30m before breakfast as iron decreases absorption of thyroxine
- Repeat TFTs monthly until stable
GALLSTONES
What is the clinical presentation of gallstones?
- Severe RUQ may radiate to tip of scapula
- N+V
- May be triggered by heavy, fatty meal
OSTEOARTHRITIS
What is osteoarthritis?
- Non-inflammatory wear + tear arthritis
- Destruction of articular cartilage makes exposed subchondral bone sclerotic > increases vascularity + subchondral cysts form where repair produces cartilaginous growth from chondrocytes which calify (osteophytes)
OSTEOARTHRITIS
What causes osteoarthritis?
Risk factors?
- Secondary OA can occur in joints due to congenital disease + damage
- Obesity, increasing age, trauma, female, FHx, occupation (manual labour)
OSTEOARTHRITIS
What are the main symptoms of osteoarthritis?
- Morning stiffness <30m
- Stiffness after rest (gelling)
- Bony swellings/joint deformities
- Reduced ROM, weak grip + reduced functioning
OSTEOARTHRITIS
What bony swellings may be seen in osteoarthritis?
- Distal IPJ = Heberden’s nodes
- Proximal IPJ = Bouchard’s nodes
- Squaring at base of thumb at carpometacarpal joint (saddle joint used in many activities so prone to wearing)
OSTEOARTHRITIS
What joints may be affected in osteoarthritis?
- Hips, knees, sacroiliac joints, MCP joint at base of thumb (squaring), wrist, cervical spine
OSTEOARTHRITIS
What would plain radiograph show in osteoarthritis?
LOSS –
- Loss of joint space
- Osteophytes
- Subarticular sclerosis (increased density of bone along joint line)
- Subchondral cysts (fluid filled holes in the bone)
OSTEOARTHRITIS
What is the conservative management of osteoarthritis?
- Education
- Lifestyle (weight loss)
- Physio to improve strength
- Orthotics to support activities + function (walking aids)
OSTEOARTHRITIS
What medical treatment may be given for osteoarthritis?
- Regular PO + topical NSAIDs
- PO NSAIDs (?+PPI) for intermittent use
- ?Opiates like codeine + morphine
- Intra-articular steroid injections to reduce inflammation
OSTEOARTHRITIS
What surgery may be offered in osteoarthritis?
- Arthroscopy for loose bodies (can cause locking e.g. knee)
- Osteotomy (changing bone length)
- Arthroplasty (joint replacement, risk of infection)
- Fusion (often ankle + foot)
GOUT
What is gout?
Pathophysiology?
- Inflammatory arthritis due to hyperuricaemia + intra-articular monosodium urate crystals
- Urate derived from breakdown of purines (adenine + guanine)
GOUT
What are some causes of gout?
Who is it most common in?
- Increased uric acid production = chemo, pyrazinamide
- Decreased uric acid excretion = diuretics, renal impairment, alcohol excess
- Older men
GOUT
What are some risk factors for gout?
What are some factors that may precipitate an attack?
- Alcohol, high purine diet (red meat + seafood), cell damage + Death (surgery, chemo)
- Dietary excess, diuretics, dehydration, sepsis
GOUT
How does gout present?
- Acute hot, swollen + painful joints (exclude septic)
- Wrists, base of thumb (carpometacarpal joint) + metatarsophalangeal joint of big toe
GOUT
What are some signs of gout?
- Chronic tophaceous gout = tophi (s/c deposits of urate crystals in skin + joints, often small joints of hands, elbows, ear)
- Chronic polyarticular gout = painful erythematous swelling
GOUT
What investigations would you do for gout?
- Serum urate elevated
- Joint fluid aspiration MC&S = no bacteria, Needle shaped crystals with Negative birefringent under polarised light
- XR = joint space maintained, lytic bone lesions, punched out erosions
GOUT
What is the management for gout for…
i) an acute flare?
ii) long-term prophylaxis?
i) NSAIDs like ibuprofen first line (unless C/I), colchicine second line (inhibits mitosis but SEs of diarrhoea), steroids last
ii) Allopurinol (xanthine oxidase inhibitor but start after acute attack settled in about 2w)
PSEUDOGOUT
What is pseudogout?
What is it associated with?
- Microcrystal synovitis due to deposits of calcium pyrophosphate crystals
- Hyperparathyroid, hypothyroid, haemochromatosis, hypophosphataemia
PSEUDOGOUT
How does pseudogout present?
- Acute hot, swollen + stiff joints
- Monoarthropathy affecting shoulders, wrists + knees
PSEUDOGOUT
What are the investigations for pseudogout?
- Joint fluid aspiration MC&S = no bacteria, Rhomboid shaped crystals with Positive birefringent under polarised light
- XR = may show soft tissue calcium deposition (chondrocalcinosis) = thin white line in middle of joint space
PSEUDOGOUT
What is the management of pseudogout?
- NSAIDs, colchicine
- Intra-articular steroids or PO
- Joint aspiration of arthrocentesis if severe
PMR
What is polymyalgia rheumatica (PMR)?
Associations?
- Inflammatory condition (vasculitis) causing pain + stiffness in shoulder, pelvic girdle + neck
- GCA
PMR
What is the clinical presentation of PMR
- Bilateral shoulder pain, may radiate to elbow
- Bilateral pelvic girdle pain
- Worse with movement + sleep interference
- Morning stiffness ≥45m
- Systemic Sx = weight loss, fatigue, low grade fever
PMR
What is the management of PMR?
- ESR/CRP raised, CK normal
- PO prednisolone shows dramatic response (diagnostic)
B12/PERNICIOUS ANAEMIA
What is the pathophysiology of B12 deficiency?
- Absorption of B12 in terminal ileum + intrinsic factor (via gastric parietal cells) dependent for transport across intestinal mucosa
B12/PERNICIOUS ANAEMIA
What are some causes of B12 deficiecny?
- Autoimmune (pernicious) = atrophic gastritis leading to destruction of parietal cells in stomach > less intrinsic factor + B12 deficiency (associated with other autoimmune)
- Malabsorption = Crohn’s, coelaic
- Dietary (vegans)
B12/PERNICIOUS ANAEMIA
What are the B12 specific features of the anaemia?
- Peripheral neuropathy with numbness or paraesthesia
- Loss of vibration sense or proprioception
- Visual, mood or cognitive changes
- Glossitis = beefy-red sore tongue
B12/PERNICIOUS ANAEMIA
Investigations for B12/pernicious anaemia?
- FBC (MCV>100fL, low Hb)
- Serum B12 decreased
- Blood film = hypersegmented neutrophil nuclei
- Intrinsic factor Ab for pernicious (gastric parietal cell Ab can be tested by less helpful)
B12/PERNICIOUS ANAEMIA
What is the management of B12/pernicious anaemia?
- PO B12 (cyanocobalamin) if dietary origin
- IM hydroxocobalamin if pernicious
- Do NOT give folate as can cause subacute combined degeneration of cord = distal sensory loss, ataxia + mixed UMN/LMN signs
AOCD
What are some mechanisms in anaemia of chronic disease (AOCD)?
- Decreased release of iron from bone marrow to developing erythroblasts
- Inadequate erythropoietin response to anaemia
- High levels of hepcidin expression (reduces iron transport from duodenal cells to plasma)
AOCD
What are some causes of AOCD?
- Chronic inflammatory diseases = Crohn’s, RA)
- Chronic infections (TB)
- Malignancy
- TB
AOCD
What is the management of AOCD?
- FBC (low Hb)
- Blood film = normochromic normocytic
- Low serum iron, transferrin saturation + TIBC
- High ferritin
- Treat underlying cause, sometimes recombinant erythropoietin
CLL
What is chronic lymphocytic leukaemia (CLL)?
- Monoclonal proliferation of well differentiated lymphocytes, 99% B cells
- # 1 leukaemia in adults
CLL
What are some complications of CLL?
- Warm autoimmune haemolysis > anaemia
- Infection (hypogammaglobulinaemia)
- Richter’s transformation = high-grade (large B cell) lymphoma
CLL
What is the clinical presentation of CLL
- Incidental finding on FBC
- Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
- Weight loss, sweats + anorexia
- Hepatosplenomegaly, rubbery non-tender lymphadenopathy
CLL
What are some investigations for CLL?
- FBC = pancytopenia
- Blood film = smudge or smear cells
- LDH may be raised
- Bone marrow biopsy is diagnostic
- CT CAP to stage
CLL
What is the management of CLL?
- No sx = watch + wait
- Chemo + radio to help lymphadenopathy + splenomegaly
- Bone marrow transplant
MYELODYSPLASTIC
What is myelodysplastic syndrome?
Risk?
- Immature blood cells in bone marrow do not mature properly + so do not become healthy blood cells
- Transform to AML
MYELODYSPLASTIC
How might myelodysplastic syndrome present?
- > 60y + previous chemo or radiotherapy
- ?Incidental finding
- Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
MYELODYSPLASTIC
Investigations for myelodysplastic syndrome?
- FBC = pancytopenia, reduced reticulocytes
- Blood film = blasts (ring sideroblasts)
- Bone marrow aspiration + biopsy = hypercellular bone marrow
MYELODYSPLASTIC
What is the management of myelodysplastic syndrome?
- Watch + wait with supportive Tx = blood transfusions, EPO, G-CSF
- Chemo or stem cell transplant
ARRHYTHMIAS
Give 3 effects hyperkalaemia on an ECG
GO - absent P wave
GO TALL - tall T wave
GO long - prolonged PR
GO wide - wide QRS
TYPE 1 DIABETES
what is T1DM?
Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.
TYPE 1 DIABETES
what is the pathophysiology of T1DM
- autoimmune destruction of beta cells in the Islets of Langerhans by autoantibodies cause insulin deficiency and continued breakdown of liver glycogen
this causes hyperglycaemia and glycosuria
TYPE 1 DIABETES
Is T1DM characterised by a problem with insulin secretion, insulin resistance or both?
Characterised by impaired insulin secretion - severe insulin deficiency
TYPE 1 DIABETES
what are the risk factors for developing T1DM?
- Northern European
- Family History:
- HLA DR3-DQ2 or
- HLA-DR4-DQ8 - Other autoimmune diseases:
- Autoimmune thyroid
- Coeliac disease
- Addison’s disease
- Pernicious anaemia
TYPE 1 DIABETES
what are the clinical features of T1DM?
Thirst (fluid and electrolyte losses)
Polyuria (due to osmotic diuresis)
Weight loss
- usually short history of severe symptoms
TYPE 1 DIABETES
Describe the epidemiology of T1DM
Onset younger (<30 years)
Usually lean
More Northern European ancestry
TYPE 1 DIABETES
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?
Fasting plasma glucose >7 mmol/L
TYPE 1 DIABETES
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?
Random plasma glucose >11 mmol/L
TYPE 1 DIABETES
What might someone’s HbA1c be if they have diabetes?
> 48 mmol/L
6.5%
TYPE 1 DIABETES
What happens to C-peptide in T1DM?
C-peptide reduces
TYPE 1 DIABETES
How do you treat T1DM?
Education
Glycaemic control through diet (low sugar, low fat, high starch)
Insulin SC
TYPE 1 DIABETES
Give 6 complications to Diabetes Mellitus
- Diabetic ketoacdiosis
- Diabetic nephropathy
- Diabetic retinopathy
- Diabetic neuropathy
- Hyperosmolar hyperglycaemic nonteotic coma
- Stroke, ischaemic heart disease, peripheral vascular disease
TYPE 1 DIABETES
Give 2 potential consequences of T1DM
- Hyperglycaemia
- Raised plasma ketones –> ketoacidosis
TYPE 1 DIABETES
How is insulin administered in someone with T1DM?
Subcutaneous injections
TYPE 1 DIABETES
Other than SC injections, how else can insulin be administered?
Insulin pump
TYPE 1 DIABETES
what are the different types of insulin used to treat T1DM?
- short acting - 4-6hrs
- short acting analogues -
- long acting - 12-24hrs
TYPE 1 DIABETES
Give 4 potential complications of insulin therapy
- Hyperglycaemia
- Lipohypertrophy at injection site
- Insulin resistance
- Weight gain
- Interference with life style
TYPE 2 DIABETES
Is T2DM characterised by problem with insulin secretion, insulin resistance or both?
Characterised by impaired insulin secretion and insulin resistance
TYPE 2 DIABETES
what is the aetiology of T2DM?
- Decreased insulin secretion and increased insulin resistance
- No immune disturbance
- No HLA disturbance but strong genetic link
- Polygenic
- Associated with obesity, lack of exercise, calorie and alcohol excess
TYPE 2 DIABETES
Describe the pathophysiology of T2DM
Insulin binds normally to its receptor – insulin resistance develops post-receptor
Circulating insulin levels are higher than in healthy patients but inadequate to restore glucose homeostasis
Increased glucose production in liver- inadequate suppression of gluconeogenesis and there’s reduced glucose uptake in peripheral tissues
Hyperglycaemia and lipid excess are toxic to beta cells - reduced beta cell mass
Don’t tend to develop ketoacidosis by do get glycosuria
TYPE 2 DIABETES
Why is insulin secretion impaired in T2DM
Due to lipid deposition in the pancreatic islets
TYPE 2 DIABETES
what are the risk factors for T2DM?
Increase w/ age
M > F
Ethnicity: African-Carribean, Black African and South Asian
Obesity
Hypertension
TYPE 2 DIABETES
What happens to insulin resistance, insulin secretion and glucose levels in T2DM?
Insulin resistance increase
Insulin secretion decreases
Fasting and post-prandial glucose increase
TYPE 2 DIABETES
Why do you rarely see diabetic ketoacidosis in T2DM?
Insulin secretion is impaired but there are still low levels of plasma insulin
Low levels of insulin prevent muscle catabolism and ketogenesis
TYPE 2 DIABETES
By how much has the beta cell mass reduced in T2DM when diagnosis usually occurs?
50% of normal beta cell mass
TYPE 2 DIABETES
Describe the epidemiology of T2DM
Onset older (>30)
Usually overweight
More common in African/Asian populations
Males > Females
TYPE 2 DIABETES
Describe the treatment pathway for T2DM
- Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
- Metformin
- Metformin and sulfonylurea (GLICLAZIDE)
- Metformin + sulfonylurea (GLICLAZIDE) + insulin
- metformin +sulonylurea (GLICLAZIDE) + insulin +PIOGLITAZONE
- Increase insulin dose as required
TYPE 2 DIABETES
How does metformin work in treating T2DM?
Increase insulin sensitivity and inhibits glucose production
TYPE 2 DIABETES
How does sulfonylurea work in treating T2DM?
Stimulates insulin release
TYPE 2 DIABETES
Give a potential consequence of taking Sulfonylurea for the treatment of T2DM
Hypoglycaemia
REACTIVE ARTHRITIS
What is reactive arthritis?
● A sterile synovitis which occurs following
o A GI infection with Shigella, Salmonella, Yersinia or Campylobacter
o Sexually acquired infection
● Typically affects lower limb
REACTIVE ARTHRITIS
What GI infections are associated with causing reactive arthritis?
Salmonella
Shigella
Yersinia enterocolitica
campylobacter
REACTIVE ARTHRITIS
What GU infections are associated with causing reactive arthritis?
Chlamydia
Ureaplasma urealyticum
REACTIVE ARTHRITIS
What is the classic triad of symptoms for reactive arthritis?
- Arthritis
- Conjunctivitis
- Urethritis
(can’t see, can’t pee, can’t climb a tree)
REACTIVE ARTHRITIS
What investigations might you do in someone you suspect to have reactive arthritis?
ESR + CRP - raised
ANA - negative
RF - negative
X-ray - sacroiliitis or enthesopathy
Joint aspirate - negative (exclude septic arthritis + gout)
REACTIVE ARTHRITIS
How is reactive arthritis treated?
NSAID
Corticosteroids
DMARD - chronic arthritis
FIBROMYALGIA
What is the diagnostic criteria for fibromyalgia?
Chronic widespread pain lasting for > 3 months with other causes excluded
Pain is at 11/18 tender point sites for 6 months
FIBROMYALGIA
Name 4 diseases that fibromyalgia is commonly associated with
- Depression
- Choric fatigue
- IBS
- Chronic headache
FIBROMYALGIA
Give 4 symptoms of fibromyalgia
- Neck and back pain
- Pain is aggravated by stress, cold and activity
- Generalised morning stiffness
- Paraesthesia of hands and feet
- Profound fatigue
- Unrefreshing sleep
- poor concentration, brain fog
FIBROMYALGIA
Give 3 disease that might be included in the differential diagnosis for fibromyalgia
- Hypothyroidism
- SLE
- Low vitamin D
FIBROMYALIGA
How is fibromyalgia diagnosed?
Everything seems normal
11/18 trigger points
Exclude other diagnoses
FIBROMYALGIA
Describe the management of fibromyalgia
- Educate the patient and family
- CBT and exercise programmes - reset pain thermostat
- Acupuncture
- Analgesics - tramadol, codeine
- Low dose antidepressants (amitriptyline) and anticonvulsants (pregabalin)
FIBROMYALGIA
what is the epidemiology of fibromyalgia?
women,
poor socioeconomic status,
20-50 year old
FIBROMYALGIA
what is the the pathophysiology of fibromyalgia?
Unknown, possibly pain perception/hyper excitability of pain fibres
FIBROMYALGIA
what are the complications of fibromyalgia?
- can really affect quality of life
- anxiety, depression, insomnia
- opiate addiction
FIBROMYALGIA
what is fibromyalgia?
Also known as chronic persistent pain
● Widespread msk pain after other diseases have been excluded
● Symptoms present at least 3 months and other causes have been excluded
● Characterised by central (non-nociceptive) pain
o Due to a central disturbance in pain processing
o Biopsychosocial factors important
● Not easily diagnosed as there is no specific pathology
GOUT
What is gout?
Crystal arthritis
Inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals
GOUT
Describe the epidemiology of gout?
● 5x more common in men
● Occurs rarely before young adulthood
● Rarely occurs in pre-menopausal females
● Often a family history
GOUT
What joint does gout most commonly affect?
Big toe metatarsophalangeal joint
GOUT
Describe the pathophysiology of gout
Purine –> (by xanthine oxidase) xanthine –> uric acid –> monosodium rate crystals OR excreted by kidneys
Urate blood/tissue imbalance –> rate crystal formation –> inflammatory response through phagocytic activation
Overproduction/under excretions of uric acid causes build up and precipitated out in joints
GOUT
Give 3 causes of gout
= Hyperuricaemia
- Impaired excretion - CKD, diuretics, hypertension
- Increased production - hyperlipidaemia
- Increased intake - high purine diet = red meat, seafood, fructose, alcohol
GOUT
Name 3 common precipitants of a gout attack
- Aggressive introduction of hypouricaemic therapy
- Alcohol or shellfish binges
- Sepsis, MI, acute severe illness
- Trauma
GOUT
Name 4 diseases that someone with gout might have an increased risk of developing
- Hypertension
- CV disease - e.g. stroke
- Renal disease
- Type 2 diabetes