Phase 2a things Flashcards
End Stage Renal Failure Levels:
Stage 1: > 90 mL/min/ 1.73m2
Stage 2: 60-89
Stage 3A: 45-59
Stage 3B: 30-44
Stage 4: 15-29
Stage 5/ESRF: <15
Gastric Ulcer vs Duodenal Ulcer
Gastric: pain immediately after eating
Duodenal: relived by eating, pain comes a while after eating
H. Pylori: 1 PPI + 2 antibiotics
AKI stages and causes
Stages of AKI:
1:
Creatinine is 1.5-1.9 times higher than baseline
urine output < 0.5ml/kg for > 6 consecutive hours
2:
Creatinine is 2-2.9 times higher than baseline
urine output < 0.5ml/kg for > 12 consecutive hours
3:
Creatinine is >3 times higher than baseline
Urine output < 0.5ml/kg for > 24 consecutive hours
Anuria for > 12 hours
NSAIDS, ACEi, ARBs, CCBs, a-blockers, b-blockers, opioids, diuretics, acyclovir, trimethoprim, lithium and more can cause AKIs
Renal Colic investigations
1st: USS
Diagnostic: CTKUB (CT scan of Kidneys, Ureter, Bladder)
Conns Syndrome
Causing primary hyperaldosteronism
Aldosterone acts on the kidneys to increase sodium absorption and as a result causes potassium excretion leading to Hypernatremia and hypokalaemia
The management is a potassium-sparing diuretic like spironolactone.
Varicose Veins: RF
- old
- female
- pregnancy: the uterus causes compression of the pelvic veins
- obesity
Varicose Veins: Pathophysiology
- dilated, tortuous, superficial veins that occur secondary to incompetent venous valves, allowing blood to flow back, away from the heart
- most commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein
- extremely common, but most patients do not require intervention
Varicose Veins: S+S
- aching, throbbing
- itching
Varicose Veins: Complications
- varicose eczema (aka venous stasis)
- haemosiderin deposition → hyperpigmentation
- lipodermatosclerosis → hard/tight skin
- atrophie blanche → hypopigmentation
- bleeding
- superficial thrombophlebitis
- venous ulceration
- DVT
Varicose Veins: Investigations
- venous duplex ultrasound: shows retrograde venous flow
Varicose Veins: Management
Conservative:
- leg elevation
- weight loss
- regular exercise
- graduated compression stockings
Referral to secondary care:
- pain, discomfort, swelling
- previous bleeding from varicose veins
- skin changes secondary to chronic venous insufficiency (e.g. pigmentation and eczema)
- superficial thrombophlebitis
- venous leg ulcer
Treatments:
- endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
- foam sclerotherapy: irritant foam → inflammatory response → closure of the vein
- surgery: either ligation or stripping
Venous Ulceration
- typically above medial malleolus
Investigations:
- ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing
- ‘normal’ ABPI: 0.9 - 1.2
- < 0.9 indicate arterial disease (or >1.3 as could be false-negative results from arterial calcification in diabetics)
Management
- compression bandaging, four layer [best]
- oral pentoxifylline: peripheral vasodilator
- little evidence for: flavinoids, hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression
Peripheral Arterial Disease: 3 main patterns of presentation
intermittent claudication
critical limb ischaemia
acute limb-threatening ischaemia
Peripheral Arterial Disease: Intermittent Claudication
S+S:
- intermittent claudication: aching or burning in the leg muscles following walking
- can walk a predictable distance before symptoms start
- relieved within minutes of stopping, not present at rest
Investigations:
- 1st: duplex ultrasound
- femoral, popliteal, posterior tibialis and dorsalis pedis pulses
- ankle brachial pressure index (ABPI): 1 = normal, <0.6= claudication
- magnetic resonance angiography (MRA) should be performed prior to any intervention
Peripheral Arterial Disease: Critical Limb Ischaemia
Features should include 1 or more of:
- rest pain in foot for more than 2 weeks
- ulceration
- gangrene
- hanging legs out of bed can ease pain
ABPI < 0.5 = critical limb ischaemia
Peripheral Arterial Disease: Acute Limb-threatening Ischaemia
Features - 1 or more of the 6 P’s
- pale
- pulseless
- painful
- paralysed
- paraesthetic
- ‘perishing with cold’
Investigations
- Doppler arterial
- ABPI
- Determine whether ischaemia is due to thrombus (rupture of atherosclerotic plaque) or embolus (e.g. secondary to atrial fibrillation)
Peripheral Artery Disease: Management
Lifestyle
- quit smoking
- comorbidities: HTN, DM, obesity
- exercise training
- clopidogrel + atorvastatin
Medical
- naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
Surgical
- endovascular revascularization/angioplasty with stent (<10cm stenosis)
- surgical revascularization/bypass/endarterectomy (>10cm stenosis)
- amputation
Polymyalgia Rheumatica
- Relatively common condition seen in older people
- Characterised by muscle stiffness and raised inflammatory markers
- Related to temporal arteritis + vasculitis
S+S:
- typically > 60 years old
- rapid onset (e.g. < 1 month)
- aching, morning stiffness in proximal limb muscles
- weakness is not considered a symptom of PMR
- mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
Investigations
- ESR > 40 mm/hr
- Creatine kinase and EMG normal
Treatment
- prednisolone (should be very effective, if not consider DD)
Osteoarthritis: RF
F>M 3:1
Rare before 55yrs
Previous trauma
Obesity
Hypermobility
Occupation
Osteoporosis reduces the risk of OA
Osteoarthritis: Pathophysiology
“Wear and Tear”
- localised loss of cartilage
- remodelling of adjacent bone
- associated inflammation
Affects:
Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints
Osteoarthritis: S+S
- Asymmetric/Unilateral
- Episodic joint pain: intermittent ache provoked by movement and relieved by resting
- Transient morning stiffness <30 min (vs in RA)
- Painless bony swellings: (osteophyte formation)
- Heberden’s nodes at DIPD
- Bouchard’s nodes at PIPD
Osteoarthritis: Investigations
X-Ray: (LOSS)
- Loss of joint space
- Osteophytes
- Subarticular sclerosis
- Subchondral cysts
Osteoarthritis: Management
- Lifestyle: weight loss, exercise, walking aids
- 1st: topical NSAIDs
- 2nd: oral NDAIDs +ppi
- intra-articular steroid injections
- arthroplasty (joint replacement)
Rheumatoid Arthritis: RF
- HLA DR4 and HLA DR1
- can present anytime: any age (OA=old)
- smoking
Rheumatoid Arthritis: Pathophysiology
- chronic systemic autoimmune disorder causing symmetrical deforming autoimmune polyarthritis
- primarily synovial disease
Affects:
- MCP, PIP joints
Rheumatoid Arthritis: S+S
- Symmetrical, bilateral
- Swollen, painful joints in hands and feet, improves on movement
- Morning Stiffness
- Develops over months
- Positive ‘squeeze test’ - discomfort on squeezing across the metacarpal or metatarsal joints
- Hand deformities
- Ulnar deviation
- Swan neck/z thumb (P extension, D flexion)
- Boutonnier deformity (P flexion, D extension
Ocular manifestations
- keratoconjunctivitis sicca (most common)
Rheumatoid Arthritis: Investigations
Bloods
- Rheumatoid factor (also +ve in Felty, Sjogrens, IE, SLE)
- Anti-cyclic citrullinated peptide antibody (higher specificity)
- DAS28 monitor RA
X ray
- loss of joint space
- juxta-articular osteoporosis
- soft-tissue swelling
- periarticular erosions
- subluxation
Rheumatoid Arthritis: Management
DMARD monotherapy +/- a short-course of bridging prednisolone
- Methotrexate: monitor FBC & LFT: risk of myelosuppression, liver cirrhosis, pneumonitis
- Sulfasalazine
- Leflunomide
- Hydroxychloroquine
TNF inhibitors: if 2 DMARDs fail
- etanercept
- infliximab
- adalimumab
- rituximab
Rheumatoid Arthritis: Complications
Extra-articular complications:
- respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy
- ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy
- osteoporosis
- ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
- increased risk of infections
- depression
Less common
- Felty’s syndrome (RA + splenomegaly + low white cell count)
- amyloidosis
Rheumatoid Arthritis: pregnancy
- patients with early or poorly controlled RA should be advised to defer conception until disease is more stable
- RA symptoms tend to improve in pregnancy but only resolve in a small minority. Patients tend to have a flare following delivery
- methotrexate is not safe in pregnancy and needs to be stopped at least 6 months before conception
- leflunomide is not safe in pregnancy
- sulfasalazine and hydroxychloroquine are considered safe in pregnancy
- low-dose corticosteroids may be used in pregnancy to control symptoms
- NSAIDs may be used until 32 weeks but after this time should be withdrawn due to the risk of early close of the ductus arteriosus
- patients should be referred to an obstetric anaesthetist due to the risk of atlanto-axial subluxation
Gout: RF
- males
- purine-rich food: alcohol, red meat, liver, seafood, high fructose (sweets, fruit), saturated fats
- drugs (aspirin, thiazide, loop diuretics)
- FH
- renal CKD (reduce uric acid excretion)
- increased production from lymphoma, leukaemia, haemolysis, rhabdomyolysis
Gout: Pathophysiology
- inflammatory arthritis associated with hyperuricaemia and intra-articular monosodium urate crystals
- purines need to be excreted as uric acid (hypoxanthine → xanthine → uric acid with enzyme xanthine oxidase)
Lesch-Nyhan syndrome
- hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
- x-linked recessive therefore only seen in boys
- features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
Gout: S+S
Episodes lasting several days when their gout flares and are often symptom-free between episodes
- pain: significant
- swelling
- erythema
- tophaceous gout: persistently high uric acid can become chronic if monosodium urate form tophi on skin or joints, also release proteolytic enzymes leading to bone erosion
Gout: Investigations
Joint fluid aspiration + Microscopy: (diagnostic)
- needle shaped negatively birefringent monosodium urate crystals under polarised light
- increased leucocytes
- >360 serum uric acid in acute settings
X ray
- joint effusion is an early sign
- well-defined ‘punched-out’ erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
- relative preservation of joint space until late disease
- eccentric erosions
- no periarticular osteopenia (in contrast to rheumatoid arthritis)
- soft tissue tophi may be seen
Gout: Management
1st: weight loss + lifestyle + vit Cm avoid some foods
Acute Gout:
- NSAIDs + ppi + Colchicine
- Colchicine: inhibits microtubule polymerization by binding to tubulin, interfering with mitosis + inhibits neutrophil motility and activity, avoid if eGFR < 10 ml/min BNF
- Intra-articular steroid injection
Chronic Gout:
- allopurinol: inhibits xanthine oxidase
- febuxostat as alternative
Pseudogout “acute calcium pyrophosphate crystal deposition disease”
microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium
Mostly >60, if <60, mostly likely has:
- haemochromatosis
- hyperparathyroidism
- low magnesium, low phosphate
- acromegaly, Wilson’s disease
Investigations:
- knee, wrist and shoulders most commonly affected
- joint aspiration: weakly-positively birefringent rhomboid-shaped crystals, radio-opaque (gout= radiolucent)
- x-ray: chondrocalcinosis (in the knee this can be seen as linear calcifications of the meniscus and articular cartilage)
Management
- aspiration of joint fluid, to exclude septic arthritis
- NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
Trochanteric Bursitis
Greater trochanteric pain syndrome is also referred to as trochanteric bursitis.
It is due to repeated movement of the fibroelastic iliotibial band and is most common in women aged 50-70 years.
Features
pain over the lateral side of hip/thigh
tenderness on palpation of the greater trochanter
Fibromyalgia
Syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites. Unknown cause
RF: women 5x, 30-50yrs
S+S:
- chronic pain: at multiple site, sometimes ‘pain all over’
- lethargy
- cognitive impairment: ‘fibro fog’
- sleep disturbance, headaches, dizziness are common
Investigations:
- tender in at least 11 of these 18 points stated
Management:
- explanation
- aerobic exercise: has the strongest evidence base
- cognitive behavioural therapy
- medication: pregabalin, duloxetine, amitriptyline
Muscular Dystrophy
- Duchenne MD – one of the most common and severe forms, it usually affects boys in early childhood; people with the condition will usually only live into their 20s or 30s
- Becker MD – closely related to Duchenne MD, but it develops later in childhood and is less severe; life expectancy isn’t usually affected as much
- myotonic dystrophy – a type of MD that can develop at any age; life expectancy isn’t always affected, but people with a severe form of myotonic dystrophy may have shortened lives
- facioscapulohumeral MD – a type of MD that can develop in childhood or adulthood; it progresses slowly and isn’t usually life-threatening
- limb-girdle MD – a group of conditions that usually develop in late childhood or early adulthood; some variants can progress quickly and be life-threatening, whereas others develop slowly
- oculopharyngeal MD – a type of MD that doesn’t usually develop until a person is between 50 and 60 years old, and doesn’t tend to affect life expectancy
- Emery-Dreifuss MD – a type of MD that develops in childhood or early adulthood; most people with this condition will live until at least middle age
Reactive Arthritis/Reiter’s syndrome
Reiter’s Triad: urethritis, conjunctivitis and arthritis (can’t pee, see, climb trees)
Caused by distant infection, usually STI/GI
- Shigella
- Salmonella
- Yersinia enterocolitica
- Campylobacter
- Chlamydia trochomatis
Management
- symptomatic: analgesia, NSAIDS, intra-articular steroids
- sulfasalazine and methotrexate are sometimes used for persistent disease
- symptoms rarely last more than 12 months
Discoid Meniscus: Pathophysiology, S+S
- A congenital anomaly of the knee in which the meniscus, instead of having the usual crescent (C-shape), is abnormally thickened and disc-shaped
- More common in children and adolescents and typically affects the lateral meniscus of the knee.
Anatomical Variation:
- A discoid meniscus covers a larger portion of the tibial plateau compared to the normal meniscus
- It is less flexible and more prone to injury
S+S:
Clicking or snapping sensation in the knee.
Pain: Especially after activity.
Swelling or stiffness of the knee.
Mechanical symptoms: Locking or giving way of the knee
Discoid Meniscus: Investigations + Management
Types (Watanabe Classification):
Type I (Complete): Fully disc-shaped and more prone to tearing.
Type II (Incomplete): Partially disc-shaped.
Type III (Wrisberg): Normal-shaped meniscus but lacks posterior attachments, leading to hypermobility.
Investigations:
- MRI: Preferred method to visualize the discoid shape and identify any associated tears.
- X-ray: May show widened joint space if the discoid meniscus is thickened
Management:
- Conservative for asymptomatic or mildly symptomatic cases
- Physical therapy to improve knee strength and stability.
- Surgical Treatment if symptomatic + tear present: Meniscectomy or Meniscoplasty
Infectious mononucleosis (glandular fever)
Causes:
- Epstein-Barr virus (EBV, aka human herpesvirus 4, HHV-4): 90% causes
- Others: cytomegalovirus and HHV-6
- most common in adolescents and young adults
S+S: resolves 2-4 weeks
Triad:
1. sore throat,
2. pyrexia,
3. lymphadenopathy (posterior triangles of the neck, vs tonsillitis only in upper anterior cervical chain)
- malaise, anorexia, headache
- palatal petechiae
- splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
- hepatitis, transient rise in ALT
- lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
- haemolytic anaemia secondary to cold agglutins (IgM)
- a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
Diagnosis
- heterophil antibody test (Monospot test)
- FBC
- do both in 2nd week of the illness to confirm a diagnosis
Management
Supportive treatment: rest during the early stages, drink plenty of fluid, avoid alcohol, simple analgesia for any aches or pains
- Avoid contact sports for 4 weeks to reduce risk of splenic rupture
Complications
- Splenic rupture
- Hepatitis/pericarditis/myocarditis
- HUS
Lyme Disease: S+S, Investigations
Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks.
Early features (within 30 days)
- erythema migrans:
- ‘bulls-eye’ rash at the site of the tick bite
- 1-4 weeks after the initial bite
- painless, > 5 cm diameter, slowly increases size
- systemic features: headache, lethargy, fever, arthralgia
Later features (after 30 days)
- cardiovascular
- heart block
- peri/myocarditis
- neurological
- facial nerve palsy
- radicular pain
Investigations
- Can be diagnosed clinically if erythema migrans
- 1st: ELISA antibodies to Borrelia burgdorferi, repeat after 4-6 weeks if negative but still suspected
- if positive/12 weeks of sx, do immunoblot test
Lyme Disease: Management
Management of asymptomatic tick bites
- if the tick is still present, remove with fine-tipped tweezers + wash
- NICE guidance does not recommend routine antibiotic treatment to patients who’ve suffered a tick bite
Management of suspected/confirmed Lyme disease
- doxycycline (amoxicillin if CI)
- Erythema migrans → commenced on antibiotic asap
ceftriaxone if disseminated disease
- Jarisch-Herxheimer reaction (fever, rash, tachycardia after first dose of antibiotic) can be seen
Contact dermatitis
There are two main types of contact dermatitis
1. irritant contact dermatitis: common - non-allergic reaction due to weak acids or alkalis (e.g. detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare
2. allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicated
Cement is a frequent cause of contact dermatitis. The alkaline nature of cement may cause an irritant contact dermatitis whilst the dichromates in cement also can cause an allergic contact dermatitis
Squamous Cell Carcinoma
Squamous cell carcinoma is a common variant of skin cancer. Metastases are rare but may occur in 2-5% of patients.
RF:
- sunlight / psoralen UVA exposure
- actinic keratoses and Bowen’s disease
- immunosuppression e.g. renal transplant, HIV
- smoking
- long-standing leg ulcers (Marjolin’s ulcer)
- genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism
S+S
- sun-exposed sites such as head, neck, dorsum hands and arms
- rapidly expanding painless, ulcerate nodules
- possible cauliflower-like appearance
- possible bleeding
Invsetigations:
- Surgical excision (4mm or 6mm margins if >20mm diameter)
- Mohs micrographic surgery: high-risk patients/cosmetic
Poor prognosis:
- poorly differentiated, >20mm diameter, >4mm deep, immunosupression
Ulcerative Colitis
Peak incidence: 15-25 yrs, 55-65 yrs
RF: stress, NSAIDs, antibiotics, NOT smoking
S+S
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features: APIESAC (Ankylosing spondolitis, Pyoderma gangrenosum, Iritis, Erythema nodosum, Sclerosing cholangitis, Aphthous ulcers/Amyloidosis, Clubbing)
Ulcerative Colitis: Investigations
Colonoscopy + biopsy:
- red, raw mucosa, bleeds easily
- no inflammation beyond submucosa (only colonic mucosa + submucosa affected)
- widespread ulceration with pseudopolyps
- inflammatory infiltrate
- crypt abscesses (neutrophils)
- goblet cell depletion
- avoided in severe colitis colonoscopy: risk of perforation - a flexible sigmoidoscopy preferred
Barium enema:
- loss of haustrations
- superficial ulceration, ‘pseudopolyps’
- long-standing disease: colon is narrow and short -‘drainpipe colon’
Bloods
- pANCA (anti-neutrophilic cytoplasmic antibody) +ve (-ve in Crohn’s)
- high ESR, CRP, WCC, platelets
- low albumin
- fecal calprotectin increased (normal in IBS)
Ulcerative Colitis: Management
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
Inducing remission: mild + moderate
- topical aminosalicylate: rectal mesalazine
- + oral aminosalicylate
- + topical or oral corticosteroid
- if severe: hospital tx, IV steroids/IV ciclosporin, surgery (proctocolectomy with ileostomy)
Maintaining remission
- aminosalicylate
- oral azathioprine/mercaptopurine
(immunosupressant)
Crohn’s Disease: RF, Pathophysiology
RF: Genetic (NOD2, CARD15, HLA-B27), smoking, NSAIDs, stress, late adolescence/early adulthood
- Commonly terminal ileum and colon but can be anywhere from mouth to anus
- inflammation occurs in all layers, down to the serosa: prone to strictures, fistulas, adhesions
Distribution:
80%: small bowel, usually ileum
50%: ileocolitis
20%: colitis exclusively
30%: perianal
