Consultation Flashcards
What features in history would be inkeeping with pericarditis?
- Pleuritic chest pain
- Positional - relieved by sitting forwards, worse lying back
- Prodromal viral illness - cough, sore throat, fatigue, low-grade fever
- Associated symptoms: palpitations, SOB, dizziness, syncope
- Causes: viral, HIV/TB, uraemia, cancer, autoimmune disease e.g. RA, Lupus, previous trauma/cardiac surgery/MI (Dressler’s)
What are the DDx of pericarditis?
- Pneumonia
- PE
- MI
What findings on examination would be in-keeping with pericarditis?
- Pericardial rub - sounds ‘squeaky’ like walking in fresh snow
- If tamponade: Beck’s triad of hypotension, elevated JVP and muffled heart sounds. Tachycardia to maintain CO is also an early sign
- Pulsus paradoxus: SBP drops >10mmHg on inspiration
- Kussmaul’s sign - elevated JVP on inspiration
- Signs of an underlying cause e.g. rheumatoid hands
What are some underlying causes of acute monoarticular pain and swelling?
- Trauma
- Infective arthritis
- Inflammation (e.g. crystal arthritis like gout and pseudogout, reactive arthritis and acute sarcoidosis)
- Haemarthrosis (bleeding into the joint cavity secondary to trauma or bleeding disorders)
- Degenerative (flare of osteoarthritis)
How do you differentiate between articular and peri-articular problem with the joints?
Articular Problem:
- Global restriction of joint movements (e.g. global restriction of shoulder movements in gleno-humeral joint disease)
- Active and passive movements are equally restricted
- Swelling of the entire joint (e.g. filling of the parapatellar gutters and suprapatellar pouch with knee effusion)
Peri-articular Problem:
- Restriction of movements in only a certain plane (e.g. restriction of abduction alone in supraspinatus tendinitis)
- Greater restriction in active range of movements
- Localised swelling (e.g. anterior swelling over the lower half of the patella in pre-patellar bursitis)
What investigations should be requested in a patient with acute monoarthritis?
- Bloods including FBC, U&Es, LFTs, CRP, Uric acid
- Blood cultures in those with suspected septic arthritis
- Synovial fluid analysis and culture
- No need to request a plain radiograph unless there is preceding trauma or suspicion of pseudogout
- USS of the knee may be useful for USS guided aspiration in difficult cases.
Outline the pathology of Osteoarthritis
Characterised by degeneration of articular cartilage and bone remodelling. The primary event in OA is breakdown of articular cartilage, which usually occurs at the central load-bearing portion of the joint. It is NOT due to preceding synovitis (unlike in RA, because of synovial hypertrophy and release of cytokines). The breakdown of cartilage can be visualised on plain radiographs as loss of joint space.
Bone remodelling leads to thickening of subchondral bone (seen as sub-chondral sclerosis on XR), formation of bone cysts and growth of osteophytes at articular margins. The clinical effects of osteophytes depend on the site of formation. Osteophytes that form in the hands usually don’t cause symptoms, while those in the acromioclavicular joint could press on the rotator cuff and present with shoulder impingement, and those that form around the vertebrae could cause nerve root compression or spinal stenosis.
The breakdown products of cartilage may cause synovitis (as a secondary event) and expansion of the joint may stretch the surrounding ligaments, tendons or bursae, causing pain.
What views of radiograph would you get for a patient with suspected knee OA?
- Anteroposterior
- Lateral
- Sky-line view
What symptoms must be enquired about if a patient has a history in-keeping with PMR?
Symptoms related to GCA:
- Headache
- Visual symptoms
- Jaw claudication
- Scalp tenderness i.e. when combs hair
What rare complications can arise as a result of GCA?
- Stroke (due to involvement of cerebral blood vessels)
- Aortic aneurysm or dissection (due to involvement of the aorta)
What would be the key points of examination in a patient presenting with ?GCA
- Vital signs
- Palpate temporal arteries, checking for thickening, tenderness and reduced pulsation
- Record visual acuity in both eyes separately, especially if there are visual complaints
- Examine hips and shoulders to check range of movements (PMR)
How should a patient with suspected GCA be investigated?
- Bloods including FBC, U&Es, LFTs, CRP, ESR, Glucose, HbA1c and vitamin D
- Temporal artery USS - characteristic finding is a ‘non-compressible halo’ caused by oedema around the vessel wall
- Temporal artery biopsy
Outline some specific underlying causes of low back pain.
- Infection
- Malignancy
- Axial spondyloarthropathy
- Vertebral compression fracture
- Prolapse of the intervertebral disc
- Cauda equina syndrome
- Spinal Stenosis
What are the features of Cauda Equina syndrome?
- Retention of urine (most consistent feature)
- Inability to feel urine passing down the urethra
- Loss of anal tone
- Perianal anaesthesia (‘numb bum’)
- Bilateral leg pain
What are the red flag symptoms in patients with back pain?
- Age >50 years
- Hx of malignancy
- Unexplained weight loss
- Unremitting or progressively worsening pain
- Poor response to conservative measures
What are the important risk factors to consider for osteoporosis in men?
- Alcohol
- Steroid use
- Hypogonadism
What diagnosis should be considered in a patient with back pain, previous history of fragility fractures and recurrent infections?
- Multiple Myeloma
What should you look for on examination of a patient presenting with back pain with red flag features?
- Examination of spine
- Look for signs that may suggest cancer - e.g. finger clubbing, lymphnode enlargement, hard liver, splenomegaly and abdominal mass
- Neurological examination of the legs is only indicated in those with radicular or neurological symptoms and could be abbreviated or omitted if pain is confined to the back.
What investigations should be requested in a patient with thoracic back pain with red flag symptoms?
- Plain XRays of thoracic spine
- CXR
- Bloods including FBC, U&Es, LFTs, CRP, Bone Profile, PSA, ESR, Myeloma screen
- Depending on above tests - MRI thoracic spine or CT CAP should be considered
Give an overview of Multiple Myeloma
Plasma cells produce immunoglobulins. There are 5 classes of immunoglobulin: IgG, IgM, IgD, IgA and IgE. Each immunoglobulin molecule consists of two heavy and two light chains. There are 5 types of heavy chain (gamma, miu, delta, alpha and elipson) and two types of light chain (kappa and lambda), Each individual plasma cell produces only one type of immunoglobulin, with any one of 5 heavy chains and one of two light chains.
In multiple myeloma, there is monoclonal proliferation of plasma cells, which results in excess production of one type of immunoglobulin, usually IgG, IgD or IgA. This is different from polyclonal proliferation of plasma cells that occurs in infection or inflammation, where multiple clones of plasma cells produce different types of immunoglobulins.
Screening tests for myeloma (serum protein electrophoresis and serum-free light chains) essentially look for evidence of monoclonal proliferation of plasma cells.
What results can be found in Multiple Myeloma
- High ESR - due to elevated immunoglobulin
- Bone osteolysis because of osteoclast stimulation by myeloma cells
- Hypercalcaemia due to stimulation of osteoclasts, which leads to release of calcium from bones into blood
- Renal impairment - secondary to direct toxic effect of light chains on renal tubules, hypercalcaemia or hyperviscosity
- Pancytopenia - because myeloma cells take up the bone marrow space and reduce the production of normal blood cells.
- Immune paresis - production of one type of immunoglobulin by myeloma cells suppresses the production of other types of immunoglobulin, thus increasing the risk of infection (e.g.suppression of IgA and IgM in patients with IgG myeloma
CRAB - High serum calcium, renal impairment, Anaemia, Bone osteolysis
How is Myeloma diagnosed?
- ‘M’ band on serum protein electrophoresis and/or abnormal kappa/lambda ratio
- Evidence of CRAB
- Immune paresis
- Bone Marrow biopsy
- Serum B2 microglobulin level is useful for prognostication - higher levels = poorer outcome
Name some organic causes of widespread pain.
- Inflammatory arthritis (e.g. Rheumatoid arthritis, seronegative spondyloarthropathy)
- OA
- Autoimmune connective tissue disease (e.g. systemic lupus erythematous, Sjogren’s)
- Osteomalacia
- Thyroid dysfunction
- Statin therapy
- Malignancy
Name some features of fibromyalgia
- Chronic widespread pain, fatigue and non-restorative sleep
- Other functional somatic symptoms, such as chronic headache, functional bowel disturbance and dysmenorrhoea
- Psychological distress, and unhelpful thoughts, emotions and behaviours
- Absence of clear evidence of an organic problem
What features in the history should raise the suspicion of an autoimmune connective tissue disease?
- Joint Pain
- Tightening of the skin (difficulty in making a fist or opening the mouth
- Skin rashes (e.g. photosensitivity, telangiectasias)
- Dysphagia or symptoms of GORD
- Breathlessness (due to interstitial lung disease)
- Proximal muscle weakness
- Sicca symptoms (dry eyes and dry mouth)
What should you look for in examination of a patient with scleroderma?
- Examine the hands - look for evidence of sclerodactyly, telangiectasia and calcinosis
- Check for signs of systemic sclerosis in the face, trunk and legs
- Check peripheral pulses
- Ask for BP - high BP suggestive of impending renal crisis
- Listen to lung bases for crackles and heart sounds for loud pulmonary component of the second heart sound (Pulm HTN)
How would you investigate a patient with suspected scleroderma?
- Blood tests including FBC, LFTs and serum creatinine - autoimmune conditions may cause anaemia, leucopenia and thrombocytopenia. In those with isolated Raynaud’s phenomenon a FBC may help to detect haematological conditions that cause hyperviscosity and sluggishness of the circulation (e.g. essential thrombocytosis, polycythaemia rubra vera)
- Urinalysis - to screen for renal involvement
- ANA and anti-ENA - positive ANA increases likelihood of future development of scleroderma, while a negative result reduces the likelihood.
- Anti-centromere antibody is associated with Limited scleroderma
- Anti-Scl-70 antibody is associated with diffuse scleroderma
- PFTs (with gas transfer) - reduction in gas transfer may be secondary to ILD or Pulm HTN
- Echo
What medication would you prescribe for Raynaud’s phenomenon?
Nifedipine
What key questions should be asked in patients with suspected vascular claudication?
- What is the level of the lesion
- What is the severity of the disease
- Are there manifestations of atherosclerosis elsewhere (e.g. coronary, cerebral, renal, mesenteric)?
- What (modifiable) risk factors for vascular disease are present?
What is a key DDx in patients presenting with chronic limb ischaemia?
Thromboangiitis obliterans (TAO) also known as Buerger’s disease. It causes segmental inflammation and thrombosis of small- and medium sized arteries and veins, superficial thrombophlebitis and Raynaud’s phenomenon usually in the distal extremities of the limbs. It is strongly associated with use of tobacco products. Patients are typically young men (<45 years), without risk factors for atherosclerosis.
What should you look for on examination in a patient with suspected peripheral arterial disease?
- Carefully inspect front and back of legs (including soles and web spaces between toes)
- Look for ischaemic changes, like pallor (especially when the limb is elevated), loss of hair, nail dystrophy, reduced cap refill, coldness, ulcers and gangrene. You should note if it is dry (well demarcated and black) or wet (moist, swollen and blistering). Wet gangrene should be referred to vascular surgeon urgently.
- Palpate peripheral pulses, including femoral, popliteal, dorsalis pedis, posterior tibial, radial, brachial and carotids
- Check for irregular pulse
- Auscultate over femoral and popliteal arteries for bruits
- Ask for BP
- Listen to heart for murmurs
- Test sensation and power in distal legs
What investigations should you request in a patient with suspected PAD?
- Bloods including FBC, renal function, glucose and HbA1c
- ABPI - compare systolic pressure at the ankle (posterior tibial or dorsalis pedis artery) and the higher of the two systolic pressures in the arms (brachial artery). ABPI </= 0.9 is suggestive of PAD. Over 1.4 is also suggestive of arterial wall stiffening due to calcification.
- Duplex arterial scan
- CT Angio
What are the risk factors for DVT?
- Recent prolonged immobilisation (e.g. major surgery, hospitalisation or confinement to bed for >3 days, long distance travel)
- High oestrogen state (e.g. pregnancy, combined oral contraceptive pill, hormone replacement therapy)
- Active malignancy, congestive heart failure and IBD
- Obesity (BMI >30)
- Smoking
When should thrombophilia be suspected?
- If thrombosis is unprovoked (i.e. occurs in absence of risk factors)
- It is recurrent
- It occurs in an unusual site
- There is a positive FHx (unprovoked thrombosis in a first-degree relative <50 years of age)
How would you investigate a patient with a suspected DVT?
- Bloods including FBC, LFTs, U&Es, Coag
- Urine pregnancy test
- D-dimer
- USS Doppler of lower limb
What can causes thrombophilia?
Inherited causes:
- Deficiency of anti-thrombin
- Deficiency of protein C
- Deficiency of protein S
- Factor V Leiden mutation
- Prothrombin gene mutation
Acquired causes:
- Anti-phospholipid syndrome
- Malignancy
- High oestrogen states
- IBD
- Myeloproliferative diseases
What bloods should be checked if you are suspecting anti-phospholipid syndrome
- Anti-cardiolipid antibody
- Lupus anticoagulant
- Beta2 glycoprotein 1 antibody IgM and IgG
What happens to Iron levels in anaemia of chronic disease?
Increased production of Hepcidin prevents the release of Iron from storage sites to developing red cells. The total body iron isn’t reduced
What is sideroblastic anaemia
It is anaemia whereby there is a biochemical block that prevents iron from combining with protoporphyrin (i.e. pyridoxine deficiency)
What are the causes of Iron Deficiency Anaemia?
Increased Loss - most commonly due to GI blood loss in men or post-menopausal women. Can also occur in menorrhagia in pre-menopausal women. Other sources of blood loss include haematuria (e.g. RCC), chronic epistaxis (e.g. hereditary haemorrhagic telangiectasia) and regular blood donation.
Reduced dietary intake (e.g. red meat, green leafy vegetables)
Reduced absorption (e.g. coeliac disease, Crohn’s disease)
Name some GI sources of blood loss
- Ingestion of aspirin or NSAIDs
- Oesophagitis or oesophageal carcinoma
- Peptic ulcer disease
- Gastric cancer
- Coeliac disease
- Colon cancer
- Haemorrhoids
- Angiodysplasia
What should you look for in examination in IDA?
- Look for telangiectasias in the nose and mouth (HHT), oral ulcers (Crohn’s), buccal pigmentation (Peutz-Jeugers syndrome) and dermatitis herpetiformis over the extensor aspects of the elbows (coeliac disease)
- Examine the abdomen - check for tenderness (PUD), mass (stomach or colon ca) and organomegaly (palpable liver due to mets)
- Examine CV system - signs of severe anaemia include tachycardia, ankle oedema and flow murmurs
How should you investigate patients with IDA?
- Iron studies including serum iron, total iron binding capacity, ferritin and transferrin saturations, Serum B12 and Folate
- Screening for coeliac disease - anti-TTG or anti-endomysial antibody. Also check serum IgA
- Urine dip - check for haematuria
- Refer to Gastro for consideration of Upper and Lower Scopes
Name some causes of macrocytic anaemia
- Vitamin B12 and Folate deficiency
- Haemolytic anaemia
- Aplastic anaemia or myelodysplasia
- EtOH
- Hypothyroidism
Name some causes of haemolytic anaemia
Immune:
- Primary
- Secondary - drugs (e.g. cephalosporins, piperacillin, methyldopa), infections (e.g. mycoplasma or infectious mono), cancers (CLL, lymphoma), autoimmune disease (SLE)
Non-Immune:
- Congenital - haemoglobinopathy (e.g. sickle cell anaemia, thalassaemia), Red cell membrane problem (e.g. hereditary spherocytosis), Enzyme problem (e.g. G6PD or pyruvate kinase deficiency)
- Acquired - mechanical (e.g. prosthetic heart valves, thrombotic microangiopathy), infections (e.g. malaria
How should you examine a patient with suspected macrocytic anaemia?
- Look for icterus
- Lymphadenopathy
- Hepatomegaly
- Splenomegaly
- Signs of autoimmune disease (e.g. synovitis, skin rashes)
How to investigate a patient with haemolytic anaemia
- Tests to look for evidence of haemolysis - reticulocyte count (high), bilirubin, LDH (high) and haptoglobins (low)
- Peripheral blood film - spherocytes are seen in autoimmune haemolytic anaemia
- Direct anti-globulin test
- ANA (screen for SLE)
- Group and save (in anticipation for the need for blood transfusion)
- CT Neck/Thorax/Abdo/Pelvis - to check for haematological malignancy (e.g. cervical, intra-thoracic or intra-abdominal lymphadenopathy, splenomegaly and hepatomegaly)
What would you ask a patient about in the history if they presented with low platelets?
- Ensure vitals are satisfactory and no obvious bleeding
- Epistaxis
- Bleeding from gums
- Haemoptysis
- Haematemesis
- Rectal bleeding
- Haematuria
- Screen for neurological and intra-abdominal symptoms
- Check for clues that may suggest an infection - fevers, history of recent travel or residence in endemic areas, infectious contacts, high-risk sexual behaviour)
- Drug history - several cause thrombocytopenia including co-trim, antibiotics, heparin, quinine, statins, rifampicin, ACEis)
- Ask about alcohol
- Ask about features of CTD (e.g. joint pain, skin rashes, muscle weakness, dry eyes and mouth, Raynaud’s phenomenon, previous thrombosis or pregnancy loss)
What are the causes of thrombocytopenia?
- Thrombotic microangiopathy
- Infections - including malaria, dengue, HIV, Hep C, Infectious Mono, CMV, Leptospirosis
- Bone marrow failure
- Immune-mediated thrombocytopenia
- Drugs
What is thrombotic microangiopathy?
TMA is characterised by widespread formation of microthrombi in the circulation. It is the diagnosis not to miss if a patient presents with thrombocytopenia. The endothelium produces von Willebrand factor (vWF), which helps to clump platelets during the formation of a primary haemostatic plug. A small amount of vWF is continuously secreted in the basal state (i.e. even when there is no need to form a haemostatic plug) in the form of ultra-large multimers, but inappropriate platelet aggregation is prevented because the protease enzyme ADAMTS-13 keeps breaking these multimers into smaller units.
TMA features include:
- Thrombocytopenia - as platelets are used up for formation of microthrombi
- Microangiopathic haemolytic anaemia (MAHA) - as red cells get severed as they try to get past microthrombi
- Fragmented or severed red calls (schistocytes) in blood film
- Elevated LDH (due to haemolysis and tissue ischaemia)
What is the pentad of TTP?
- Thrombocytopenia
- MAHA
- Fever
- CNS dysfunction
- AKI
Name some causes of thrombotic microangiopathy
- DIC
- Thrombotic thrombocytopenic purpura
- HUS
- Malignant HTN
- Pre-eclampsia
What should you look for on examination in a patient with thrombocytopenia
- Signs of autoimmune connective tissue disease (e.g. synovitis, skin rashes)
- Purpura or petechiae
- Examine abdomen and look for splenomegaly
What investigations would you request in a patient with thrombocytopenia?
- Coag
- ANA - if positive check anti-dsDNA, complement levels and urinalysis to check for renal involvement
- CXR, blood glucose and screening tests for Hep B and C prior to starting steroid therapy
- LDH, DIC screen (TT, fibrinogen, D-Dimer), stool cultures or serology for E. Coli 0157:H7 and ADAMTS-13 activity (in suspected TMA)
- Screening for malaria, dengue, EBV, CMV, HIV and Hep C (if suspected infection-related thrombocytopenia)
- Bone marrow biopsy, Vit B12 and folate (in patients with suspected bone marrow failure)
What are the causes of generalised lymphadenopathy?
- Infections i.e. infectious mononucleosis, cytomegalovirus, TB, HIV, infection, Hep B and C, secondary syphilis, toxoplasmosis
- Malignancy e.g. Hodgkins disease, NHL, Leukaemia
- Inflammatory conditions e.g. SLE, sarcoid
- Drugs e.g. serum sickness
How would you investigate a patient who presented with lymphadenopathy?
- Vitals
- Check for lymphadenopathy
- Abdominal examination - check for enlarged liver and spleen
- Drainage areas to look for evidence of cancer or infection e.g. breasts in patients with axillary nodes, ENT exam in those with cervical lymphadenopathy
How would you investigate a patient with lymphadenopathy?
- FBC, LFTs, U&Es, CRP
- Peripheral blood film to look for evidence of leukaemia
- ESR
- LDH - may be elevated in lymphoma but is non-specific. Other causes for elevation include conditions that cause cell death e.g. MI, liver disease, haemolysis
- CXR - to look for mediastinal lymphadenopathy
- Tests to look for supportive evidence of infection like EBV IgM, CMV IgM, hepatitis screen, HIV test, toxoplasma IgM and syphilis screen
- Excision biopsy of cervical node
Name some causes of Splenomegaly
- Portal hypertension
- Haemolytic anaemia - hereditary spherocytosis, thalassaemia
- Blood borne infections - malaria, leishmaniasis, typhoid, infective endocarditis
- Haematological malignancy - leukaemia, lymphoma
- Rare causes: Felty’s syndrome, amyloidosis, sarcoidosis, glycogen or lipid storage disorders
Why does splenomegaly occur?
- There is a larger volume of blood being held in the venous sinuses (portal hypertension)
- There is proliferation of splenic macrophages to phagocytose the red cells that are pre-maturely destroyed
- Extra-medullary haemopoiesis (haemolytic anaemia)
- Reactive proliferation of white cells (infection)
- Clonal proliferation of white cells (leukaemia or lymphoma)
How would you investigated a patient with splenomegaly?
- Bloods including FBC, peripheral blood film, LFTs, U&Es
- AUSS
If concerns re CML then may carry out Fluorescence in situ hybridisation (FISH) or PCR to check for evidence of BCR-Abl fusion gene. May also carry out cytogenetic studies to look for the Philadelphia chromosome. Bone marrow studies will provide the information needed for staging.
What medication is used if patient has BCR-Abl gene mutation?
Imatinib
Name some complications of acromegaly
- HTN
- Diabetes
- Proximal myopathy
- Carpal tunnel syndrome
- Congestive cardiac failure
- OSA
- Osteoarthritis
- Colon Cancer - excess GH facilitates the growth of colonic polyps, which could potentially turn cancerous
What important questions should be asked in patients that could have acromegaly?
- Ask if hat/glove/ring/shoe size has increased
- Ask if they have any old photographs
- Ask about visual symptoms
- Check for complications
- Ask if they sweat a lot (excessive sweating is a feature of active acromegaly)
- Ask about sexual dysfunction - ask about issues with erection and in women ask about amenorrhoea and galactorrhoea
What should you look for on examination if you are concerned about acromegaly?
- Look for features of acromegaly - inspect face from front and sides, look at hands and feet, ask to see teeth (gingival hypertrophy and increased space between teeth), look at tongue for evidence of macroglossia, check for thick greasy skin
- Ask for BP
- Examine visual fields to check for bitemporal hemianopia
- Check for proximal myopathy
- Check for signs of carpal tunnel syndrome
- Look around the axillae for skin tags and acanthosis nigricans
- Palpate the abdomen for a mass (because of increased risk of colon cancer)
How would you investigate a patient with suspected acromegaly?
- Start with IGF-1 blood test
- If level is equivocal do an oral glucose tolerance test (OGTT). Glucose normally suppresses production of GH.
- MRI scan of pituitary
- Fasting blood glucose, serum calcium (ask for PTH if calcium is high) and serum prolactin (as 30% with acromegaly co-secrete prolactin
- Think of MEN if hyperparathyroidism present and pituitary tumour
- Pituitary function should be fully assessed as large tumours may compress the normal pituitary gland and reduce the secretion of other pituitary hormones - TSH, TFTs, ACTH, cortisol, prolactin, FSH/LH, testosterone or oestradiol)
- Need to be referred for a colonoscopy
What medications are used in the treatment of acromegaly?
- Octreotide (somatostatin receptor agonist)
- Cabergoline or Bromocriptine (dopamine agonists)
- Pegvisomant (GH receptor antagonist
What questions would you ask to assess thyroid status?
- Weight and appetite
- Bowel habits
- Preference of heat or cold
- Menstruation
- Sleep
- Tremors
- Palpitations - if reports palpitations ask about frequency, rate, rhythm (regular or irregular) and associated symptoms like breathlessness, dizziness or syncope
- Ask about proximal myopathy
- Ask about eye symptoms - pain/swelling/redness. Is she able to close eyes fully? able to see normally? double vision?
- Ask if she has noticed any swelling at the front of her neck (goitre) - if any swelling ask about pressure symptoms like dysphagia, stridor and change in voice
- Ask what med problems - esp asthma as will want to start Beta-blockers in hyper
- Ask about meds
- Ask if pregnant, planning pregnancy or just delivered
- Ask about smoking - thyroid eye disease worse in smokers
What should you look for in examination of a patient with suspected Graves?
- Check for tremor
- Check for sweaty palms and palmar erythema
- Check pulse for AF
- Check for proximal muscle weakness
- Examine eyes - go behind patient and look at eyes from above and sides to check for proptosis. Check for lid retraction. Test for lid lag. Ask patient to close eyes fully. Check visual acuity. Check eye movements for ophthalmoplegia
- Examine swelling in the neck. Ask to drink water and see if swelling moves up. Feel swelling
- Inspect for enlarged nodes
- Listen for thyroid bruits
- Percuss for size of goitre
- Inspect shins for pretibial myoxedema
How would you investigate a patient with suspected Graves disease?
- FBC, LFTs, U&Es
- TFTs
- Check T3 if T4 is normal and TSH is low
- Thyroid antibodies - TSH receptor antibiotics (TRAbs) and thyroid peroxidase antibodies (TPO)
- Thyroid USS
- Thyroid scintigraphy scan - diffuse is graves, single area of focal uptake in focal nodular goitre and multiple areas of increased uptake in multi-nodular goitre
- CT or MRI orbits
Lists some features of Cushing’s syndrome
- HTN
- Diabetes Mellitus
- Proximal myopathy
- Osteopenia or osteoporosis, leading to an increased risk of low-trauma fractures
- Avascular necrosis of the bone
- Redistribution of fat to the upper half of the body and face (“moon facies”) and accumulation of fat in the supraclavicular and dorsocervical regions (“buffalo hump”)
- Thinning of the skin (e.g. abdominal striae, easy bruising, poor wound healing)
- Acne and hirsutism
- Cataract and glaucoma
- Insomnia, Depression or mood swings
- Menstrual irregularities
Name some underlying causes of glucocorticoid excess
- Glucocorticoid therapy (by far, the most common cause)
- Increased cortisol production by an adrenal tumour
- Increased ACTH production by a pituitary tumour (the commonest cause of endogenous hypercortisolism)
- Ectopic ACTH production (usually due to small cell lung cancer)
What should you look for on examination of a patient with suspected Cushing’s
- Should have noticed truncal obesity and moon facies
- Test power in limbs - confirm proximal weakness
- Ask for BP
- Look at abdominal wall for striae
- Examine her joints to quickly check for synovitis or joint deformities
- Visual fields only need to be examined if hx of headache or visual disturbance and no other obvious cause of Cushing’s
What investigations would you request if you suspected Cushing’s?
- Fasting blood gluocse and HbA1c to screen for diabetes
- Lipid profile
- Serum vitamin D level
- Bone density scan for osteopenia/osteoporosis
What screening tests are there for Cushings?
- Low Dose Dexamethasone test
- Late night salivary cortisol
- 24 hour urinary free cortisol
What investigations would you request in a patient with suspected Addison’s disease?
- Short synacthen test
- Thyroid Function Tests
- 21-hydroxylase adrenal antibodies (normally requested by Endocrinologist)
- CXR - to look for evidence of TB or Lung Ca
- Adrenal CT if adrenal antibodies are negative
Name some symptoms of adrenal insufficiency
- Light-headedness due to orthostatic hypotension
- Abdominal pain, nausea, vomiting and diarrhoea
- Weight loss
- Tiredness, exhaustion, weakness and low mood
- Pigmentation or tanning (only occurs in primary adrenal insufficiency)
Name some medical conditions that may cause osteoporosis
- Endocrine conditions such as hyperthyroidism, hyperparathyroidism, hypogonadism, Cushing’s syndrome, T1DM
- Inflammatory rheumatic conditions - rheumatoid arthritis, ankylosing spondylitis
- GI diseases - coeliac’s disease, IBD
- Chronic liver or kidney disease
- Haematological malignancies - multiple myeloma
- Anorexia nervosa
What should you look for on examination of a patient with suspected osteoporosis?
- Ask for height and weight measurements
- Look for evidence of medial conditions that cause osteoporosis (hyperthyroidism and Cushing’s)
What investigations should be requested in a patient with suspected osteoporosis?
- DEXA scan
- Blood tests including FBC, ESR, LFTs, U&Es, TFTs, Calcium and 25(OH) vitamin D level
- Further investigations such as PTH, serum testosterone, myeloma screen and coeliac screen may be indicated in some patients depending on results of initial investigation
- Plan XR of thoracolumbar spine should be requested in those with suspected vertebral compression fracture
How does PTH increase serum calcium?
- Mobilises calcium from the bone
- Activates vitamin D in the kidney (which helps to increase calcium absorption from the intestines
- Increases calcium reabsorption from renal tubules
What are the different types of hyperparathyroidism?
- Primary (usually due to parathyroid adenoma, and rarely, hyperplasia or carcinoma
- Secondary (due to CKD, as deficiency of activated Vitamin D reduces calcium absorption, which leads to increased PTH via negative feedback)
- Tertiary (autonomous secretion of PTH in chronic kidney disease after long standing secondary hyperparathyroidism
How does hypercalcaemia occur in thiazide use?
Calcium is reabsorbed in the renal tubule
How does hypercalcaemia occur in lithium use?
Lithium promotes increased PTH secretion
How does hypercalcaemia occur in hyperthyroidism?
There is increased bone resorption
How does hypercalcaemia occur in sarcoidosis?
Granulomatous tissues secrete 1,25(OH)2 cholecalciferol
List some causes of hypercalcaemia
- Calcium supplementation
- Hyperparathyroidism, Hyperthyroidism
- Iatrogenic, Immobilisation
- Multiple Myeloma, Milk-alkali syndrome, Medications (e.g. thiazides, lithium)
- Parathyroid hyperplasia or adenoma
- Alcohol
- Neoplasm (e.g. breast cancer, lung cancer)
- Zollinger-Ellison syndrome
- Excessive Vitamin D
- Excessive Vitamin A
- Sarcoidosis
What symptoms are associated with hypercalcaemia?
- Loss of appetite
- Abdo pain
- Constipation
- Polyuria (due to nephrogenic DI)
- Lethargy
- Cognitive decline
What questions should you ask a patient with suspected hypercalcaemia?
- Ask about other symptoms of hypercalcaemia - loss of appetite, nausea, abdo pain, constipation, polyuria, lethargy and problems with memory or concentration
- Ask if he has ever fractured a bone
- Ask if he smokes and check for symptoms of cancer like cough, haemoptysis and loss of weight
- Ask about symptoms that may suggest sarcoidosis like joint pain, skin rashes, swollen lymph glands and breathlessness
- Ask about symptoms of hyperthyroidism - palpitations, tremor, diarrhoea, weight loss, neck swelling
What should you look for in an examination in a patient with hypercalcaemia?
- Check for signs of intravascular volume depletion (dryness of mucus membranes and reduced skin turgor)
- Perform a general examination to look for possible clues that may suggest an underlying cause of hypercalcaemia (e.g. finger clubbing, supraclavicular lymphadenopathy, skin rashes of sarcoidosis)
- Listen to lungs and palpate abdomen for hepatomegaly or mass
- Check thyroid status
What blood tests should be requested in a patient with hypercalcaemia?
- Bloods including PTH, Bone profile, Vitamin D and TFTs
- CXR - may reveal Lung cancer or hilar lymphadenopathy of sarcoidosis
- 12 lead ECG may show short QT interval
Some patients may also warrant the following:
- Serum ACE and 1,25(OH)2 Vitamin D (in suspected sarcoidosis)
- Myeloma screen and CT CAP (for cancer screening)
- 24-hour urine calcium (in suspected familial hypocalciuric hypercalcaemia)
- BMD scan in patients with hyperparathyroidism - forearm BMD is preferred as hyperparathyroidism tends to affect cortical bone, which is predominant in the radius
- Plain XRays of the hands may show sub-periosteal bone resorption, and Xrays of long bones, skull or pelvis may show osteitis fibrosa cystica (“brown tumour”) in hyperparathyroidism
What can cause amenorrhoea?
- Ovarian insufficiency
- Hypothalamus or pituitary disorder
- Excess prolactin
- Excess androgens - PCOS, late-onset congenital adrenal hyperplasia and adrenal and ovarian tumours that produce androgens
- Thyroid disease (hypo or hyperthyroidism)
Prolactin and androgens cause amenorrhoea by reducing the release of GnRH via negative feedback inhibition
Hypothyroidism - occurs because of elevated prolactin
Hyperthyroidism - increased sex hormone binding globulin enables more oestrogen to be bound thus reducing the level of free oestrogen
What things would you ask a patient presenting with amenorrhoea?
- Eating and exercise habits
- Change in body weight
- Stressors
- Any headache or visual disturbance (?pituitary tumour)
- Any milk discharge from the nipple (to suggest high prolactin)
- Any abnormal hair growth or acne (would suggest excess androgens)
- Any symptoms of thyroid disease
- Any menopausal symptoms - hot flushes, vaginal dryness, headache, low mood
- What medications she takes (e.g. ovarian failure secondary to chemo agents, increased prolactin due to dopamine antagonists)
- Are there risk factors for osteoporosis - low oestrogen of any cause increases risk
Name some causes of elevated prolactin
- Prolactin secreting tumour
- Dopamine antagonists (chlorpromazine, domperidone, metoclopramide)
- Tumours that compress the pituitary stalk (the part that connects the hypothalamus and pituitary gland)
- Hypothyroidism
What should you look for on examination of a patient with amenorrhoea?
- Thyroid status
- Look for hirsutism and acne
- Check for bitemporal hemianopia - especially in patients with headache or visual disturbance
How would you investigate a patient with amenorrhoea?
- Serum prolactin
- Serum LH and FSH
- TFTs
- Pituitary MRI (if prolactin high)
- Serum testosterone, dehydroepiandrosterone and 17-OH progesterone (in patients with features of virilisation or androgen excess)
Name some causes of polyuria
- Diabetes Mellitus
- Medications (e.g. diuretics)
- Alcohol
- Chronic Kidney Disease
- Hypercalcaemia - can cause nephrogenic DI
- Hypokalaemia - can cause nephrogenic DI
- Diabetes Insipidus
- Psychogenic polydipsia
What questions should you ask in a patient with polyuria?
- Headache and visual symptoms (pituitary tumour)
- Difficulty in raising arms or rising from a seated position (proximal weakness due to hypokalaemia)
- Loss of appetite, nausea, constipation and abdominal or back pain (hypercalcaemia)
- Past medical problems - renal or neurological disease, surgery or trauma to the head, psychiatric problems and tuberculosis
- Medications taken and alcohol intake
What would you look for on examination of a patient with polyuria?
- Check for signs of intravascular volume depletion (e.g. reduced skin turgor, dryness of mucus membranes)
- Examine the visual fields for evidence of bitemporal hemianopia
What investigations would you request in a patient with polyuria?
- U&Es, Bone profile
- Plasma and urine osmolality
- MRI of pituitary if suspected central DI
How would a hypertensive emergency manifest?
- Hypertensive encephalopathy or stroke
- Retinopathy
- Left heart failure
- ACS
- Aortic dissection
- Acute Kidney Injury
- Thrombotic microangiography
In whom should you suspect a secondary cause of hypertension?
- Patients <35 years old
- Those who develop HTN after the age of 55
- Those who are resistant to three or more anti-hypertensive medications
What are the secondary causes of hypertension?
- Renal causes (acute or chronic glomerulonephritis, PKD, renal artery stenosis)
- Endocrine causes (Cushing’s syndrome, primary aldosteronism, phaeochromocytoma, hyperparathyroidism, hyperthyroidism)
- Drugs (e.g. corticosteroids, NSAIDs, Ciclosporin, illicit drugs like cocaine and amphetamine)
- Pregnancy-related HTN (pre-eclampsia and eclampsia)
- Coarctation of the aorta
- Obstructive sleep apnoea
What questions should be asked in a patient with HTN?
- Headaches
- Focal neurological symptoms
- Seizures
- Visual symptoms
- Breathlessness
- Chest pain
- Reduced urine output
- Features that suggest renal disease (e.g. change in colour of urine or frothing of urine, ankle swelling, previous diagnosis of kidney disease, history of recurrent UTI, FHx of kidney disease)
- Features that may suggest endocrine disease (e.g. change in weight, easy bruising, proximal limb weakness, tremors, palpitations, diarrhoea, heat intolerance, ‘panic attacks’
- Snoring and daytime sleepiness (OSA)
- Leg claudication or cold feet (coarctation of aorta)
- Medication take (including over the counter and illicit drugs)
- Last menstrual period
How would you examine a hypertensive patient?
- Check peripheral pulses and ask for BP in both arms
- Check for radio-femoral delay
- Examine heart and check for murmurs/signs of HF
- Examine abdomen for palpable kidneys and audible renal bruit
- Look for signs that may suggest an endocrine cause
What tests should you request in a patient who has presented with HTN?
- Bloods including FBC, U&Es, Fasting glucose
- Urinalysis - looking for microscopic haematuria
- ACR
- Pregnancy test
- 12 lead ECG - L ventricular hypertrophy or strain - would suggest long-standing HTN
- CXR - might reveal signs of HF or notching of the ribs in patients with coarctation
- Duplex USS of the kidneys
- Aldosterone-Renin ratio (aldosterone raised and renin suppressed in primary aldosteronism, while both are elevated in secondary aldosteronism (e.g. renal artery stenosis))
In selected patients:
- Screening for Cushing’s syndrome (Dexamethasone suppression test, 24 hour urinary cortisol, late-night salivary cortisol) and 24 hour urinary catecholamines and metanephrines (for phaeochromocytoma)
- Serum calcium and TSH
- ESR (in suspected Takayasu’s arteritis)
- CT or MR angio of aorta in patients with suspected coarctation of aorta or Takayasu’s arteritis
- Sleep studies in patients with suspected OSA
Name some causes of acute glomerulonephritis.
- Post-infective causes (post-streptococcal GN, IgA nephropathy)
- SLE
- Systemic vasculitis (e.g. ANCA associated vasculitis, Henoch-Schonlein purpura)
- Goodpasture’s syndrome
- Idiopathic rapidly progressive GN
Outline some general screening questions for autoimmune connective tissue disease
- MSK - joint pain
- Mucocutaneous - skin rashes, photosensitivity, hair loss, mouth ulcers, dry eyes and mouth
- Constitutional - fever, weight loss, fatigue
- Vascular - Raynaud’s, previous thrombosis (due to anti-phospholipid syndrome)
- Ocular - red eyes (iritis or scleritis)
- ENT - sinusitis, nasal crusts, epistaxis, hearing loss - due to ANCA-associated vasculitis)
- Neurological - headache, altered mental state, focal neurological symptoms like weakness or numbness (e.g. proximal muscle weakness, mononeuritis mulitplex)
- Cardiorespiratory - cough, breathlessness (e.g. ILD), haemoptysis (e.g. diffuse alveolar haemorrhage), pleuritic chest pain (due to pleurisy or pericarditis)
- Abdominal - abdo pain, rectal bleeding (due to mesenteric vasculitis)
- Obstetric - previous pregnancy morbidity (recurrent miscarriages or still births due to anti-phospholipid syndrome)
What should you look for on examination of a patient with oliguria?
- Check for signs of fluid overload
- Perform a thorough general exam to pick clues of SLE/vasculitis
- Ask for a urine dipstick
How would you investigate a patient with suspected GN?
- Urine dip
- Urine ACR
- FBC, U&Es, LFTs, blood glucose, lipid panel, coag (in anticipation of need for renal biopsy) and vitamin D
- Autoantibodies - including ANA, anti-double stranded DNA antibody, anti-ENA (this includes anti-Ro, anti-La, Sm and RNP), ANCA and anti-GBM antibody
- ESR and complement levels - low complement levels would suggest an immune complex mediated GN as immune complexes consume complement
- Anti-streptolysin O titre - +ve would suggest post-strep GN
- Screen for Hep B and Hep C
- Urine pregnanct test
- CXR - to look for fluid overload or pulmonary shadows suggestive of vasculitis or Goodpasture’s syndrome
- USS Kidneys - to exclude structural abnormalities
- Renal biopsy may be required depending on results
Name some causes of Proteinuria
- Diabetic nephropathy
- Hypertensive nephropathy
- Autoimmune disease e.g. SLE
- Infections (e.g. Hep B or Hep C, HIV)
- Drugs (e.g. NSAIDs, gold, penicillamine)
- Pregnancy
What should you look for on examination of a patient with peripheral oedema?
- Check extent of oedema, and look for signs of fluid overload (elevated JVP, lung creps)
- Look for signs that may suggest an underlying cause (e.g. skin rashes or synovitis due to autoimmune connective tissue disease)
- Palpate the abdomen to check for enlarged kidneys
- Ask for a urine dipstick examinations
What investigations should be requested in a patient with bilateral pitting oedema?
- Urine ACR
- Urinalysis - looking for red cells and casts
- Bloods including FBC, LFTs, U&Es, fasting glucose, HbA1c, lipid profile, Hep B, Hep C, HIV and vitamin D
- ANA (screening for SLE)
- CXR - may reveal signs of fluid overload or pleural effusion
- Renal ultrasound scan - useful before planning a renal biopsy and to look for evidence of PKD.
Name some causes of nephrotic syndrome
Primary causes:
- Membranous GN
- Focal segmental glomerulosclerosis
- Minimal change disease
Secondary causes:
- Diabetes
- SLE
- Drugs (e.g. NSAIDs, Gold, Penicillamine)
- Infections (e.g. Hep B, Hep C, HIV)
- Obesity-related glomerulopathy
- Amyloidosis
- Malignancy
How are patients with nephrotic syndrome managed?
- Refer to nephrologist
- Commence diuretic (Furosemide), Lisinopril and Statin
- Advise to restrict intake of fluid and salt
- Get pneumococcal vaccine due to increased risk of infection (due to loss of complements and immunoglobulins in the urine)
- Anticoagulation (due to loss of anti-thrombin III in the urine)
What questions should you ask in a patient who has presented with haematuria?
- Any recent trauma (e.g. urological procedures, catheterisation or prostate biopsy)
- Any frothing of the urine and leg swelling (due to proteinuria), recent throat infection (e.g. IgA nephropathy or post-streptococcal nephritis), joint pains, skin rashes, breathlessness, haemoptysis, ENT symptoms or ocular inflammation (GN due to vasculitis or SLE)
- Any pain in the abdomen or back?
- Any dysuria, urgency or frequency of micturition?
- Sexual history if appropriate
- Any family history of renal disease
- In men - poor stream, hesitancy, poor stream and terminal dribbling
What should be looked for on examination of a patient with haematuria?
- Ask for vitals
- Examine abdomen and check for renal angle tenderness, mass and enlarged kidneys
- Perform a general examination
- Look for clues which may suggest an underlying medical condition, like autoimmune connective tissue disease
What conditions can cause renal cysts?
- Tuberous sclerosis
- von Hippel Lindau disease
- PKD
What are the associations with ADPKD?
- Hepatic, splenic and pancreatic cysts
- Valvular heart disease (aortic or mitral incompetence)
- Diverticular Disease
- Berry aneuryms
What investigations should be carried out in a patient with suspected PKD?
- AUSS or CT
- FBC, U&Es, LFTs, CRP
- Urinalysis including microscopic examination and ACR
- MRA of brain if diagnosis of ADPKD confirmed on imaging
- Echo should also be requested, especially in heart murmurs
What investigations would you want if a patient had a suspected glomerular cause of haematuria?
- ANA, anti-dsDNA, C3 and C4
- ANCA
- Anti-GBM antibody
- ASO titre
- Screening for Hep B and C
What investigations would you want if a patient had a suspected non-glomerular cause of haematuria?
- Urine culture (patient with fever and other symptoms of UTI, white cells in urine or +ve nitrite)
- Renal USS
- CT scan (non-contrast) - for patients with suspected renal calculi
- Cystoscopy (refer to urology if no evidence of infection or calculi or if there are risk factors of malignancy)
How would the children of patients with ADPKD be monitored?
- AUSS in late teens - if normal then repeat when aged 30. Can be virtually excluded if no cysts by age 30.
- Genetic testing is problematic because a large number of mutations are associated with ADPKD.
- Children should get BP, renal function and proteinuria checked on an annual basis
- Cousins should also be screened
- Should be referred to a geneticist
Name some risk factors for male UTI?
- Structural problems of the urinary tract (e.g. calculus, tumour, prostate hypertrophy, urethral stricture, ADPKD, horseshoe kidney)
- Functional problems (e.g. neurogenic bladder, vesicuoureteric reflux)
- Catheterisation (long term use of indwelling catheter or intermittent self-catheterisation) or recent instrumentation (e.g. cystoscopy, nephrostomy)
- Diabetes mellitus
- Immunosuppression
- SGLT2 inhibitors
What questions should you ask a male patient with UTI?
- Ask about other symptoms of UTI - fever, chills, rigors, nausea and vomiting, back pain, cloudy or foul-smelling urine, and blood in the urine
- Ask if they have had UTIs in the past
- Look for features that may suggest an underlying problem such as renal colic, passage of stones in the urine, urinary hesitancy and poor stream, urinary catheterisation and recent instrumentation of the urinary tract
- Ask if he is diabetic or has any osmotic symptoms like polyuria or polydipsia
- Ask about PMHx and regular medications
- Check for diabetes, neurological conditions that affect the bladder and immunosuppression
- Obtain a family history - is there anyone with kidney problems
- Obtain a sexual history
What would you look for on examination in a patient who had presented with a probable UTI?
- Ask for vitals
- Check hydration status
- Palpate the renal angle for tenderness
- Examine the abdomen to check for suprapubic tenderness and enlarged kidneys
- Offer to do a PR exam to check for enlarged prostate
What investigations would you request in a male presenting with probable UTI?
- Bloods including FBC, LFTs, U&Es and glucose
- In patients with suspected renal calculus you should also ask for Bone Profile and uric acid
- Urinalysis and microscopic examination - looking for nitrites, pyuria and red cells
- Ask for urine culture
- If systemically unwell then get blood cultures
- Imaging - USS of renal tract or CT AP - indicated in patients with suspected renal stone or obstructive lesion, all men with UTI, patients who do not respond well to initial antibiotic therapy and those with recurrent UTIs
What are the key questions to ask when faced with a patient with AKI?
- Are there any life-threatening complications (e.g. acute pulmonary oedema due to volume overload, severe hyperkalaemia or metabolic acidosis)?
- Is there an indication for urgent dialysis?
- What is the underlying cause of the kidney injury (pre-renal, intrinsic or post-renal)?
What are the indications for dialysis in patients with an acute kidney injury?
- Acidosis (severe metabolic acidosis pH<7.2)
- Electrolyte imbalance (refractory hyperkalaemia0
- Intoxication
- Oedema (refractory pulmonary oedema)
- Uraemia (symptomatic uraemia - encephalopathy or pericarditis)
What are the causes of AKI?
Pre-renal:
- Intravascular volume depletion (e.g. diarrhoea, vomiting, blood loss)
- Hypotension due to cardiogenic shock or sepsis
- Drugs (e.g. NSAIDs, ACEi)
Post-renal:
- BPH
- Stones
- Tumours
- Strictures
Intrinsic renal (pathology in glomeruli, tubules, interstitium or vasculature):
- Glomerulonephritis
- Acute tubular necrosis - due to prolonged renal hypoperfusion, toxins like aminoglycosides and radiographic contrast media, immunoglobulin light chains or myoglobulin
- Interstitial nephritis - usually caused by an allergic reaction to NSAIDs, PPIs or antibiotics
- Vascular (e.g. SLE, malignant HTN, thrombotic thrombocytopenic purpura, HUS
NSAIDs cause AKI by blocking action of prostaglandins which help keep the renal blood vessels open
What symptoms should you ask about in a patient who presents with AKI?
- Ask about urine output
- Symptoms that may suggest a pre-renal cause (e.g. diarrhoea, vomiting, recent blood loss, fever or other symptoms of infection
- Obstructive symptoms like urinary hesitancy, poor stream and terminal dribbling
- Symptoms of GN like ankle swelling or facial puffiness, frothy urine and ‘coke coloured’ urine
- Features that may suggest an underlying cause of GN - recent pharyngitis, joint pain, skin rashes, haemoptysis, mononeuritis multiplex, ENT symptoms
- Recent contrast procedures (e.g. CT, coronary angiogram)
- Background medical problems (e.g. HTN, diabetes, SLE, Hep B, Hep C, HIV)
- Meds taken including over the counter
- FHx of renal disease
What should you look for on examination of a patient with AKI?
- Assess hydration status - HR, BP (including postural drop, skin turgor, dryness of mucous membranes, JVP and lung creps
- Examine the abdomen - percuss over suprapubic area to check for bladder enlargement
- Look for clues that may suggest an underlying cause (e.g. vasculitis)
- Examine the muscle power in all groups and check for muscle tenderness
How would you investigate a patient with suspected Rhabdomyolysis
- Serum CK, LFTs, Bone Profile - in rhabdo PO4- is released from muscle and is therefore high and binds to calcium causing hypocalcaemia
- Urinalysis to check for proteinuria, haematuria and casts
- CXR
- Renal USS - to assess size of kidneys (small would suggest CKD) and exclude urinary outflow obstruction
- Urine ACR
- Screening for underlying GN (ANA, anti-dsDNA, ANCA, anti-GBM, C3/C4, Hep B, Hep C and HIV
- Myeloma screen (in patients >40 years of age with an unexplained AKI)
- Peripheral blood film (in patients with suspected thrombotic microangiopathy)
How would you distinguish between AKI and CKD?
- Previous lab test results
- The size of the kidneys on AUSS - bilateral contracted kidneys on USS would suggest CKD. There are exceptions because CKD due to certain aetiologies (e.g. diabetic nephropathy, amyloidosis or PKD) may not lead to a reduction in kidney size
- Anaemia, hypocalcaemia, hyperphosphataemia - a normal Hb or serum PO4- would be unusual in CKD
What questions would you ask a patient presenting with probable CKD for the first time?
- Blood tests done in the past to check kidney function
- Med hx - esp diabetes, HTN, PVD, previous CVA or heart attack, autoimmune connective tissue disease
- Symptoms that would suggest overload (e.g. breathlessness, orthopnoea, ankle swelling), volume depletion (e.g. recent diarrhoea, vomiting or blood loss) or anaemia (tiredness)
- Symptoms of urinary outflow obstruction (e.g. hesitancy, poor stream, terminal dribbling)
- Meds taken including over the counter
- FHx of kidney disease (ADPKD, Alport syndrome)
- Smoking habit, EtOH intake, personal background and occupation
Name some underlying causes of CKD
- Diabetic nephropathy
- Hypertensive nephropathy
- Chronic glomerulonephritis
- Chronic or recurrent UTI
- Adult-onset PKD
- Renovascular disease
- Urinary tract obstruction
What should you look for on examination of a patient with CKD?
- Ask for BP and check peripheral pulses
- Check volume status
- Look for signs that may suggest an underlying cause (e.g. synovitis or skin rashes of autoimmune connective tissue disease)
- Palpate abdomen for enlarged kidneys and listen for renal artery bruit
Name some causes of dysphagia?
Oropharyngeal dysphagia:
- Stroke
- Parkinson’s Disease
- Polymyositis or Dermatomyositis (muscle)
- Myasthenia Gravis (neuromuscular junction)
- GBS (nerve roots and peripheral nerves)
- MND (cranial nerve nuclei)
Oesophageal dysphagia:
- Benign stricture due to GORD
- Malignant stricture due to cancer in the oesophagus or gastric fundus
- Achalasia
Rare causes:
- Extrinsic compression (e.g. goitre, bronchogenic carcinoma, mediastinal lymphnode, aortic aneurysm, enlarged Left atrium)
- Systemic sclerosis
- Diffuse oesophageal spasm
- Oesophageal web
- Schatzki ring (narrowing of lower oesophagus caused by a ring of mucosal tissue
What should be looked for on examination of a patient with dysphagia?
- Check nutritional status
- Look for signs that may point to an underlying cause of her dysphagia (e.g. goitre, right supra-clavicular lymphnode enlargement)
- Palpate the abdomen to particularly check for hepatomegaly (metastases) and epigastric mass
- Listen to base of lungs for creps
- In patients with oropharyngeal dysphagia, the nervous system should be examined to check for signs of stroke, PD and lower cranial palsies
How would you investigate a patient with dysphagia?
- Should be referred for upper GI endoscopy
- Bloods including FBC, U&Es, LFTs
- CXR - may show an air fluid level in patients with achalasia or reveal conditions that compress the oesophagus (e.g. lung cancer, pericardial effusion, aortic aneurysm, enlarged L atrium, retrosternal goitre)
Name some causes of long-standing epigastric pain
Oesophagus:
- Reflux oesophagitis
Cardiovascular:
- Myocardial ischaemia
Pancreas:
- Chronic pancreatitis
- Pancreatic cancer
Hepatobiliary:
- Gallstones
Stomach and Duodenum:
- Peptic ulcer
- Gastric ulcer
- Functional dyspepsia
Intestine:
- Mesenteric ischaemia
What would you ask a patient with dyspepsia?
- Ask about associated symptoms - loss of appetite, dysphagia, nausea and vomiting, haematemesis and malena, weight loss, change in bowel habits and jaundice
- Ask if they get heart burn - sour taste in the mouth or cough
- Ask if discomfort is worse with specific foods (e.g. milk in lactose intolerance, wheat in coeliac, fat in gallstones)
- Ask about diet and eating habits - what kind of food do they eat, what is portion size
- What meds does he take - esp NSAIDs/aspirin
- Ask about PMHx, FHx (e.g. stomach cancer), smoking, alcohol, occupation and lifestyle
- Ask if this problem has been investigated before
What alarm features would there be in a patient with dyspepsia?
- Dysphagia
- Persistent vomiting
- GI bleeding or IDA
- Unintentional weight loss
- Mass in epigastrium
What should you look for on examination of a patient with dyspepsia?
- Ask for BMI and BP
- Check for pallor
- Examine abdo for epigastric tenderness, mass and organomegaly
How would you investigate a patient with dyspepsia?
- Bloods including FBC, LFTs and U&Es
- Non-invasive test for H. Pylori - urea breath test (test of choice in adult patients because of its excellent sensitivity and specificity (the stool antigen test is preferred in children)
Name some underlying causes of UGIB
- PUD
- Mallory-Weiss tear
- Oesophageal or gastric varices
- Oesophagitis
- Oesophageal or gastric malignancy
What should you look for on examination in a patient with haematemesis?
- Look for signs of chronic liver disease - ascites, splenomegaly, spider naevi (>5), gynaecomastia, loss of axillary hair, palmar erythema, dupuytren’s contracture, finger clubbing
- Palpate for epigastric tenderness
- Check for features of EtOH withdrawal e.g. delirium, tremor, sweating), especially if you think they are still drinking
- Offer to do a PR exam
How would you investigate a patient with haematemesis?
- Group and cross match - 4-6 units if actively bleeding
- Infection screen (e.g blood and urine cultures, CXR)
- UGI endoscopy
- AUSS once stable - to look for cirrhosis (splenomegaly, ascites and shrunken liver) and identify obvious cause of HCC
What questions should be asked in a patient presenting with jaundice?
- Any change in colour of urine/stools
- Any itching
- Any abdo pain
- Any recent travel - if +ve travel history ask where they stayed, what they did there and who accompanied them. Ask if had any vaccines prior to trip or take any precautions against malaria
- Ask about risks of Hep B/Hep C - high risk sexual behaviour, receipt of blood products and sharing of needles for IV drug use, tattoos or body piercings
- Obtain a detailed drug history and ask about alcohol intake
- Ask if any previous diagnosis of liver disease, FHx of liver disease, occupation, date of last menstrual period and obstetric history
What is Charcot’s triad?
- RUQ pain, cholestatic jaundice and fever/rigors
What should be looked for on examination of a patient with jaundice?
- Look for icterus in sclera and skin
- Check for signs of encephalopathy - altered mentation, fetor hepaticus and hepatic flap
- Look for signs of chronic liver disease
- Examine the abdomen
- Check for hepatomegaly, splenomegaly and ascites. Feel for tenderness esp in RUQ and R costal margin
Name some common causes of Hepatitis?
- Infections - viral hepatitis, EBV, CMV, malaria, yellow fever, leptospirosis and herpes simplex
- Toxic causes - prescription drugs, alcohol, ‘over the counter’ preparations, recreational drugs, paracetamol overdose and mushroom poisoning
What are the most likely causes of elevated ALT?
- MASLD
- Medication or alcohol induced liver disease
- Chronic viral hepatitis
- Autoimmune hepatitis
What should you look for on examination in a patient with deranged LFTs
- Ask for BMI
- Check for markers of chronic liver disease
- Examine the abdomen
What investigations would you carry out in a patient with suspected MASLD?
- Fasting blood glucose, HbA1c and lipid panel
- Screen tests for Hep B and C (Hep B surface antigen and anti-hepatitis B surface antibody, anti-hepatitis B core IgG and hepatitis C antibody
- AUSS to assess liver
What should you look for on examination in Paracetamol OD?
-Vitals
- Check conscious and alert
- Ask for capillary blood glucose
- Check her pupils
- Examine abdomen for tenderness and check for hepatic flap and markers of chronic liver disease
- Ask for body weight (to calculate paracetamol taken in mg/kg) and see if looks malnourished
How would you investigate a patient after a paracetamol OD?
- Bloods including FBC, LFTs, U&Es, Venous blood glucose, lactate and salicyclate levels
- Prothrombin time or INR
- Serum paracetamol level - only check this if paracetamol taken all at once. Shouldn’t be checked before 4 hours from the time of overdose (as absorption may not be complete) or after 24 hours.
- Result then plotted on normogram to see if requires treatment or not
- ABG - indicated in patients with high anion gap and those with fulminant liver failure to decide need for transplantation
- Urine pregnancy test
What criteria are used for consideration of liver transplant in paracetamol OD?
Kings Criteria
Patient should be transferred to transplant centre if:
- pH <7.3 - absolute indication for transplant
- INR >6.5 (PT>100secs)
- Creat >300micromol/L
- Grade III or IV hepatic encephalopathy
INR, Creat and encephalopathy criteria must all be met for consideration.
Name some common causes of chronic diarrhoea
- IBD
- IBS
- Coeliac disease
- Infections (e.g. Giardiasis, TB, Salmonella, Cryptosporidium)
- Medications (e.g. antibiotics, laxatives, PPIs)
- Hyperthyroidism
- Malabsorption (e.g. chronic pancreatitis, lactose intolerance)
What questions should be asked when a patient presents with chronic diarrhoea?
- Have they noticed blood in stool
- Do they wake up at night to move their bowels - more suggestive of an organic pathology like IBD
- Ask about tenesmus. Do they feel that they haven’t emptied their bowels completely even after going to the toilet due to a sensation of fullness in the rectum? - feature of IBD, rectal cancer
- Any steatorrhea? - fat malabsorption - small bowel disease, bile salt deficiency or pancreatic insufficiency
- Any abdo pain?
- Weight loss?
- Symptoms of hyperthyroidism - palpitations, tremors, heat intolerance lump over neck
- Travel history
- Prior antibiotic use
- Ask about joint pain, back pain, skin rashes (pyoderma gangrenosum and erythema nodosum in Crohn’s or dermatitis herpetiformis in coeliac), previous episodes of red eyes (ocular inflammation due to uveitis) and mouth ulcers (Crohn’s disease)
What should you look for on examination of patients with chronic diarrhoea?
- Hydration status
- General examination - cachexia, malnourished, pallor or cutaneous signs of IBD or coeliac’s disease, oral ulcers in Crohn’s or signs of hyperthyroidism
- Examine abdomen - check for tenderness, rigidity, guarding, and rebound tenderness
How would you investigate a patient with chronic diarrhoea?
- Bloods including FBC, U&Es, LFTs, CRP
- Faecal calprotectin - protein released by neutrophils in bowel wall
- Coeliac screen - anti-EMA and anti-tTg and serum IgA
- TFTs
- ASCA (more specific for Crohn’s) and p-ANCA (more specific for UC)
- Colonoscopy and biopsy
- Stool examination
Name some GI manifestations of scleroderma
- Dry mouth due to associated Sjogren’s syndrome
- Dysphagia due to oesophageal involvement
- GORD
- Vomiting due to gastroparesis
- Haematemesis or IDA due to gastric antral vascular ectasia
- Malabsorption due to small bowel involvement
- Faecal incontinence due to rectal or anal involvement
- Small intestinal bacterial overgrowth (SIBO)
Due to malabsorption may develop oedema or muscle wasting (protein), osteoporosis or osteomalacia (calcium) and peripheral neuropathy (Vitamin B12)
What investigations should be carried out in scleroderma patients presenting with GI symptoms?
- Bloods including FBC, LFTs, U&Es, CRP, Bone Profile, Iron, Vit B12, Folate and Vitamin D
- Other tests that may be requested include serum zinc, magnesium and selenium
- Faecal elastase - for suspected exocrine pancreatic insufficiency
- Hydrogen breath test to diagnose SIBO (usually requested by gastroenterologist)
List some red flags in patients with constipation
- Recent onset of constipation in an elderly patient
- Weight loss
- GI bleeding (overt or occult)
- Vomiting, abdo pain and distention
- FHx of bowel cancer
- Abdominal mass
- Unexplained IDA
How would you investigate a patient with new constipation?
- Refer for colonoscopy
- Bloods including FBC, U&Es, LFTs, CRP, Bone Profile, TFTs and Mg2+
- Request a CEA to screen asymptomatic patients for colorectal cancer
What causes elevation of CEA?
- Bowel Cancer
- Breast cancer
- Ovarian cancer
- Thyroid cancer
- Non-malignant conditions such as chronic liver disease and IBD
Name some causes of angina in a young person
- Premature atherosclerosis (e.g. familial hyperlipidaemia)
- Valvular heart disease (e.g. AS or AR) and HOCM - this occurs due to increased oxygen demand and compression of coronary branches by the hypertrophied L ventricle. In AR the back flow of blood from the aorta to the LV reduces coronary perfusion
- Coronary vasculitis due to Takayasu’s arteritis
- Coronary vasospasm due to cocaine
What features in an angina history may point towards Takayasu’s arteritis?
- Constitutional symptoms (fever, weight loss or joint pain)
- Arm claudication (pain in arms when elevated above head)
What should you look for on examination of a patient who presents with angina on a background of FHx of heart attack
- Ask for BMI and waist-hip circumference
- Look for pallor
- Check for tendon xanthomas (look at extensor tendons), xanthelasma and corneal arcus
- Ask for BP in both arms (difference of >10mmHg between sides may suggest Takayasu’s)
- Examine CV system
- Palpate peripheral pulses, listen to carotid and femoral arteries for bruit and auscultate for heart murmurs
What signs on examination are suggestive of Familial Hypercholesterolaemia?
- Tendon xanthomas at age <45 years
- Corneal arcus at age <45 years
- Elevated LDL-cholesterol
- Premature CAD
- FHx of elevated LDL-cholesterol or premature CAD
FH is an autosomal dominant condition. It can be homozygous (2x faulty genes) or heterozygous (one faulty gene). In those with homozygous FH, cardiovascular events usually occur as early as the first or second decade of life.
Outline the classification of AF
- pAF - lasts <7 days
- Persistent AF - lasts >7 days
- Long-standing persistent AF (lasts >1 year)
- Permanent AF (if the decision is made to not restore sinus rhythm)
Name some underlying causes of AF
- IHD
- Hypertensive heart disease
- Structural heart disease characterised by atrial enlargement (e.g. mitral valve disease, ASD, cardiomyopathy)
- Thyrotoxicosis
- Hypoxia (e.g. pneumonia, pulmonary embolism, OSA)
- Electrolyte abnormalities (e.g. hypokalaemia, hypomagnesaemia)
- Toxins (e.g. alcohol, anti-depressants, sympathomimetics)
- Sepsis
What you should look for on examination of a patient with AF?
- Pulse rate and rhythm
- Check for signs of cardiac failure
- Listen to heart for murmurs
- Check for signs of hyperthyroidism
What investigations should you do in a patient who has presented with AF?
- Bloods including FBC, U&Es, LFTs, CRP, TFTs, Bone profile, Mg2+
- CXR
- Echo - to look for structural heart disease and to assess cardiac function
Name some pointers in the history that suggest cardiogenic syncope
- Exertional syncope
- Syncope that occurs without warning (malignant syncope)
- Syncope in a supine position
- Cardiac symptoms like chest pain or dyspnoea, murmur or clinical signs of heart failure
- FHx of sudden cardiac death
Name some causes of chronic shortness of breath
- Cardiac failure
- Respiratory causes (e.g. COPD, ILD, chronic pulmonary thromboembolism, pleural effusion, neuromuscular disease affecting the respiratory muscles, thoracic cage problem)
- Other causes (e.g. anaemia, CKD, thyroid disease, gross obesity, anxiety)
Outline some underlying causes of diffuse parenchymal lung disease
- Autoimmune disease (e.g. RA, Systemic sclerosis, SLE, anti-Jo1 antibody syndrome, sarcoidosis)
- Drugs (e.g. MTX, Amiodarone)
- Occupational or environmental exposure to inorganic or organic dust (e.g. asbestosis, coal workers’ pneumoconiosis, silicosis, farmer’s lung, extrinsic allergic alveolitis)
- Radiotherapy
- Cancer (e.g. lymphangitis carcinomatosis)
Name some causes of breathlessness in a patient with Rheumatoid arthritis
- ILD related to rheumatoid arthritis
- Drug-induced pneumonitis (e.g. methotrexate)
- Opportunistic infection due to immunosuppressive therapy (e.g. TB, PCP)
- Pleural effusion
- Bronchiectasis or bronchiolitis obliterans with organising pneumonia
- Lung cancer
- Pulmonary HTN
- Congestive cardiac failure (secondary to HTN or IHD)
- Anaemia of chronic disease
What is the classification of reversible spirometry
- Improvement in FEV1 or FVC by >12% and >200ml following administration of bronchodilators
Outline the MRC grading system of Dyspnoea in COPD
- Grade 0 - Gets breathless with strenuous exercise
- Grade 1 - Gets breathless while hurrying on level ground or walking uphill
- Grade 2 - Walks slower than people of same age due to breathlessness
- Grade 3 - Gets breathless after 100m or a few minutes of walking on level ground
- Grade 4 - too breathless to leave the house or gets breathless even while dressing or undressing
What risks are associated with OSA?
- HTN
- Insulin resistance
- IHD
- Stroke
- Arrhythmias (e.g. AF)
- Pulmonary HTN
- Congestive heart failure
What are the risk factors for OSA?
- Male Sex
- Older age (>50 years)
- Obesity
- Large neck circumference (>17 inches in men and >16 inches in women)
- Orofacial abnormalities (e.g. acromegaly, retrognathia, large tongue, enlarged tonsils or adenoids, low-lying soft palate)
What questions should you ask someone who has presented with OSA?
- Ask if their sleeping partner has ever commented that they stop breathing in the middle of the night
- Ask about occupation and daytime sleepiness affecting performance at work
- Ask how sleepiness affects day to day life
- Ask if he drives and if he has ever dozed off behind the wheel
- Ask about weight gain - if recent, screen for thyroid and adrenal issues
What should you look for on examination in a patient with suspected OSA?
- Ask for BMI and measure neck circumference
- Ask for BP
- Examine neck and orofacial region (e.g. acromegaly, goitre, retrognathia, large tongue, enlarged tonsils, low-lying soft palate)
- Listen to lungs - OSA often co-exists with COPD) and pulmonary area of the heart for a loud P2 sound
- Check for leg oedema (cor pulmonale)
How would you manage a patient with suspected OSA?
- Refer to a sleep clinic - measures apnoeic-hyponoea index (AHI) which is the total number of episodes of apnoea (complete cessation of breathing for >/= 10 seconds or hypopnoea (reduction in ventilation by >50% for >/= 10 seconds) per hour. AHI of <5 is normal, 5-14 mild sleep apnoea, 15-29 moderate sleep apnoea, >/=30 severe sleep apnoea
What features would suggest a Marfinoid body habitus?
- Tall stature
- Long limbs
- Arachnodactyly
- Joint hypermobility
- Kyphoscoliosis
- Pectus carinatum or excavatum
- Hind foot deformity
- High-arched palate
What conditions present with a Marfinoid body habitus?
- Marfan syndrome
- Ehlers Danlos syndrome
- Loeys-dietz syndrome
- Homocystinuria
Outline Marfan’s syndrome?
- Caused by a mutation of FBN1 gene on chromosome 15, which codes for fibrillin 1, an extra-cellular matrix protein that provides elasticity to connective tissues (3Fs: FBN1, Fibrillin, Fifteen)
- Autosomal dominant
- Phenotype is characterised by skeletal, ocular and cardiovascular manifestations
What are the clinical manifestations of Marfan’s syndrome?
- Hypermobility of joints, kyphoscoliosis, pectus excavatum or carinatum, hindfoot deformity (pes planus +/- valgus), arachynodactyly, increased arm spain (arm spain to height >1.05), reduced upper to lower segment ratio (<0.85)
- Ectopia lentis (subluxation of lens) - upwards and outwards in Marfan’s. Myopia
- Aortic root dilatation, aortic dissection, mitral valve prolapse and regurgitation, aortic valve regurgitation
- Spontaneous PTX, apical blebs and bullae
- Dolichocephaly (longer head), enophthalmos, malar hypoplasia, high-arched palate
Describe Ehlers Danlos Syndrome
- An umbrella term used for 13 clinically and genetically hetergeneous conditions
- Due to defective synthesis and processing of collagen
- All subtypes are characterised by abnormalities of skin (e.g. skin hyper-extensibility, easy bruising, atrophic scarring, poor wound healing)
- Joint hypermobility
- Tissue fragility
What questions would you ask a patient with suspected Marfan’s syndrome?
- Family history
- Any previous PTX
- Any cardiac symptoms - SOB, palpitations, dizziness on standing up or syncope
- Any joint pain
- Is he double jointed or do joints become easily dislocated
- Does skin stretch easily
- Do they bruise easily or do the wounds heal poorly
- Ask if short sighted
What should you look for on examination in patients with suspected Marfan’s syndrome?
- Marfanoid features - ask for arm span and height (>1.05) and upper to lower segment ratio (<0.85)
- Examine hands for thumb sign and wrist sign which would suggest arachnodactyly
- Look at the sternum for pectus carinatum/excavatum
- Check spine for kyphoscoliosis
- Check legs for hind foot valgus deformity
- Look for facial features including dolichocephaly
- Look for iridodonesis (tremulous iris during eye movement due to subluxation of lens)
- Look for high arched palate, cleft palate and bifid uvula
- Examine skin for hyperextensibility, atrophic scars and striae
- Asucultate heart
What scoring system is used to assess joint hypermobility?
Beighton score
- Passive hyperextension of 5th metacarpalphalangeal joint beyond 90 degrees
- Passive apposition of the thumb to the flexor aspect of the forearm
- Passive hyperextension of the elbow beyond 10 degrees
- Passive hyperextension of the knee beyond 10 degrees
- Ability to flex the spine with the knees fully extended so that the palms fo the hands rest flat on the ground
How would you diagnose Marfan’s syndrome?
If +ve FH, must have any of the following:
- Aortic root dilatation (Z score >/=2)
- Ectopia lentis
- Systemic score >/= 7 (calculated based on skeletal manifestations, PTX, myopia, skin striae and facial features
In absence of FHx, they require:
- Aortic root dilatation plus ectopia lentis
- Aortic root dilatation plus systemic score >/= 7
- Aortic root dilatation plus FBN1 mutation
- Ectopia lentis plus FBN1 mutation with previous aortic involvement
What investigations are required in a patient if Marfan’s syndrome is suspected?
- Echo - to check for aortic root dilatation
- Slit lamp exam - to check for ectopia lentis
- XRay pelvis to look for protrusio acetabuli
- MRI pelvis to check for dural ectasia
What is used to slow aortic root enlargement in Marfan’s syndrome?
- ACEi and Beta blockers
Name some causes of transient neurological dysfunction
- TIA
- Post-ictal paralysis after generalised tonic-clonic seizure
- Hemiplegic migraine
- Hypoglycaemia
- Hypertensive encephalopathy
- MS
- Chronic subdural haematoma
- Functional neurological disorder
What should you examine in patients presenting with probable TIA?
- Neuro exam
- Focussed CV exam looking for AF, Carotid bruits and heart murmurs
How would you investigate a patient presenting with TIA?
- Non-contrast CT Head or MRI (ideally within 24 hours of symptom onset)
- Bloods including FBC, LFTs, U&Es, Fasting blood glucose and lipid panel
- ECG
- Telemetry as inpatient or Holter monitor in OP setting to detect AF
- Echo - to look for cardiac source of embolism e.g. patent foramen ovale, valvular heart disease or thrombus in heart
- Imaging of carotids and cerebral circulation (e.g. CT angio)
- Carotid Doppler
- CT perfusion
What scoring system is used in TIA?
ABCD2 score
Age:
- >60 years - 1
- <60 years - 0
BP:
- Systolic >/=140 or diastolic >/=90 - 1
- Normotension - 0
Clinical syndrome:
- Unilateral weakness - 2
- Speech disturbance - 1
- Neither - 0
Duration of symptoms:
- >/= 60 minutes - 2
- 10-59 mins - 1
- <10mins - 0
Diabetes
- Yes - 1
- No - 0
List some provoking factors for seizures
- Toxic (e.g. alcohol or drug withdrawal, use of illicit drugs and pro-convulsant medications, such as theophylline, tramadol, quinolones and clozapine)
- Metabolic (e.g. hypoglycaemia, hyperosmolar hyperglycaemia, hyponatraemia, hypocalcaemia)
- Infection or Inflammation (e.g. meningoencephalitis)
- Structural brain lesion (e.g. tumour, abscess, tuberculoma, cerebral infarct or haemorrhage)
What important questions should you ask if a patient presents with seizure?
- Ask about occupation and hobbies
- Ask if they are pregnant or planning to get pregnant or if they take the oral contraceptive pill - some anti-epileptics are teratogenic (sodium valproate, phenytoin, carbamazepine) or may interfere with efficiency of contraceptive pill (e.g. lamotrigine)
- Ask if they drive
What should you look for in a patient who has presented with seizures?
- Perform a general exam
- Check for any injuries that they may have sustained when they fell.
- Inspect the tongue
- Check for signs of meningism
- Do a quick screen for focal neurological deficits
- Examine fundus for papilloedema
How would you investigate a patient who has presented with seizures for the first time?
- Bloods including FBC, U&Es, LFTs, CRP, Glucose, Bone Profile, Mg2+
- ECG - as cardiac syncope can cause hypoxic seizures
- EEG within 24 hours
- Brain imaging - preferably MRI or CT if MRI not available
- LP if suspected meningoencephalitis or SAH but only if CT Head normal
- Toxicology screen (if drug toxicity is suspected)
Name some underlying causes of secondary headache
Intracranial:
- Head trauma (resulting in intracranial haemorrhage)
- Meningeal inflammation (e.g. bacterial or TB meningitis, SAH)
- Raised ICP (e.g. tumour, abscess, haematoma, obstructive hydrocephalus, cerebral venous sinus thrombosis, IIH)
Extra-cranial:
- Giant cell arteritis (in patients >50 years)
- Acute narrow angle glaucoma
- Sinusitis
- Dental problem
- Cervical spondylosis
- Medications that cause vasodilatation (e.g. calcium channel blockers, nitrates)
What should you look for on examination of a patient with a headache?
- Examine fundus to check for papilloedema
- Check eye movements for evidence of 3rd or 6th nerve palsy
- Check visual fields for homonymous hemianopia
- Perform a quick neurological examination to detect focal neurological deficits
- Ask for BP
- Offer to perform a thorough general examination to detect evidence of malignancy (e.g. breast mass, malignancy, lymphadenopathy)
How should a patient with a headache be investigated?
- MRI with MRV
- If MRI not available then CT Head
- If MRI or CT Head clear then LP to measure opening pressure and to analyse the CSF
What are the treatment options in IIH?
- Weight loss
- Discontinuation of offending drugs (e.g. minocycline)
- Acetazolamide
- Repeated LPs to reduce CSF pressure
- Optic nerve sheath fenestrations (to reduce the pressure of CSF around the optic nerve)
- Ventriculoperitoneal or Lumboperitoneal shunt (to divert CSF into the peritoneal cavity
Name some features of Migraine
- Commonly affects young or middle aged women
- Usually triggered by certain foods, sleep deprivation, menstruation, irregular meals or dehydration
- May or may not be preceded by aura
- Unilateral headache but may be bilateral
- Throbbing or pulsating in nature
- Associated with nausea, vomiting, photophobia and phonophobia
- Usually lasts 4 hours to 3 days
What is involved in the HINTS examination?
- Head impulse test
- Nystagmus
- Test of skew
How would you investigate a patient presenting with vertigo
- MRI
- CT Head +/- CT Angio
- Bloods including FBC, LFTs, U&Es, CRP, blood glucose and lipid profile
- Cardiac investigations to identify a source of embolism including ECG, Echo and cardiac rhythm monitoring with telemetry or Holter
What questions would you ask a patient with a suspected 7th cranial nerve palsy
- How rapidly symptoms began and at what time he was last well
- Screen for other neurological symptoms - limb weakness/numbness, visual loss, double vision, facial numbness, hearing loss, tinnitus, vertigo, speech disturbance and dysphagia
- Ask if there is pain in or around the ear
- Ask if any change to taste
- Ask if sounds are louder on the affected sides
- Ask if they have noticed any lumps in the neck or face (parotid enlargement)
- Any cough, breathlessness, joint pain, skin rashes (sarcoidosis)
- Ask about recent travel or tick bites (Lyme’s)
Name some causes of LMN lesions of the facial nerve
- Bell’s palsy (most common cause)
- Brain stem stroke, tumour or demyelination
- Cerebellopontine angle tumour (e.g. acoustic neuroma)
- Ramsey-Hunt syndrome (herpes zoster of the geniculate ganglion)
- Middle ear infection of cholesteatoma
- Lyme disease
- Sarcoidosis
- GBS
- Parotid tumour or parotidectomy
What should you look for on examination in a patient with unilateral facial weakness?
- Examination of CN VII (muscles of facial expression, taste of anterior 2/3rds of tongue, corneal reflex)
- Examine other cranial nerves, particularly eye movements (for CN VI involvement - lesion in pons) and CN V and VIII (cerebellopontine angle tumours)
- Briefly examine the limbs to test strength - cross paralysis from brain stem stroke
- Check for parotid enlargement
- Ask for BP (incase you wish to start patient on corticosteroid)
- Patients with ear pain should be referred to ENT for examination to check for vesicles of herpes zoster
What investigations should be sent in a patient with suspected Bell’s palsy
- Blood glucose - diabetes increases risk of Bell’s palsy and will start steroids
- MRI of brain or internal acoustic meatus is only need in patients with other focal neurological deficits that may suggest a tumour
- EMG and NCS - mainly used to provide prognostic information and predict the outcome in patients with severe Bell’s palsy
- Other investigations t request in selected patients may include Lyme’s serology, tests for sarcoidosis (e.g. CXR, ACE, Bone profile, biopsy of lymphnode) and audiometry in patients with hearing loss
How would you manage a patient with Bell’s palsy?
- Artificial tears
- Ointment at night
- Wear sunglasses during the day and an eye patch at night to protect the eye
- 10/7 of oral steroids within 72 hours of onset
- If severe paralysis some warrant an antiviral medication as well
- In severe cases can consider surgical decompression
What questions would you ask a patient who presents with Tremor?
- Which parts of the body are affected?
- Is the tremor present at rest or only when they try to do something?
- Does it get worse when you are distracted?
- Check for Parkinsonism features - do they feel stiff? Have they become slower? Do they take a longer time to finish a meal or cover a certain distance while walking? Have they fallen due to loss of balance?
- Ask about symptoms of thyroid disease (e.g. diarrhoea, palpitations, weight loss, heat intolerance, neck swelling)
- Obtain a detailed medical history
- Obtain a FHx (ET has autosomal dominant inheritance)
- Ask about medical problems, occupation, smoking habit and alcohol consumption
- Ask about effect of alcohol on tremor - tremor of ET may be suppressed by alcohol
What medications can cause tremor?
- Beta agonists
- Amphetamines
- Ciclosporin
- Valproate
- Lithium
- Theophylline
- Tacrolimus
How would you examine a patient who presents with Tremor?
- Observe at rest
- Note if there is a voice tremor
- Ask patient to count back from 20 to distract them (will make PD tremor more obvious)
- Ask to stretch out hands and check for postural tremor
- Ask them to drink from a glass of water and check handwriting - tremor from ET worsens during voluntary activity (hence they spill water), while PD improves (they can drink without spilling). Handwriting of patients with PD is smaller while ET is large and tremulous
- Check for cerebellar signs (finger nose test and past pointing, dysdiadochokinesis, nystagmus, dysarthria, ataxic gait, heel-shin incoordination)
- In patients with rest tremor check for signs of PD (rigidity, bradykinesia, paucity of facial expression, lack of arm swing while walking, shuffling gait)
- Look for signs of thyroid disease
How should a patient with tremor be investigated?
- ET is a clinical diagnosis
- Functional imaging - DAT scan - PD is characterised by depletion of dopamine
- TFTs
- In patients under 40 years, Wilson’s disease should be excluded
How is essential tremor managed?
- Propranolol or Primidone
- 2nd line agents include gabapentin, alprazolam or topiramate
Name some causes of bilateral diplopia
- Brain stem lesions (stroke, demyelination, tumour)
- CN III, IV and VI involvement (e.g. cavernous sinus thrombosis, Miller Fisher syndrome, Wernicke’s encephalopathy, 3rd nerve palsy due to diabetes or posterior communicating artery aneurysm(
- Neuromuscular junction (e.g. myasthenia)
- Ocular muscles (e.g. Graves’ disease, giant cell arteritis)
Why is important to ask if images are separated horizontally or vertically when patients have diplopia?
- A lesion in CN VI causes horizontal diplopia because of lateral rectus weakness, while a lesion in CN IV causes vertical diplopia because of superior oblique weakness.
- A lesion in CN III, myasthenia gravis and thyroid eye disease will cause both horizontal and vertical diplopia
What questions should be asked if suspecting a diagnosis of myasthenia gravis?
- Ask about drooping of eyelids, problems with eyesight and pain in their eyes or headache
- Ask about features that may suggest generalised MG (e.g. breathlessness, problems with swallowing or choking while eating, problems with speech or voice, difficulty in raising the arms or rising from a seated position, performing repetitive movements or walking long distances
- Screen for thyroid disease (e.g. diarrhoea, weight loss, palpitations, heat intolerance, neck swelling)
- Ask if they drives
How should you examine a patient with suspected MG?
- Examine eye movements
- Examine visual acuity and pupils - check for CN III palsy - pupil size helps differentiate between medical or surgical causes of CNIII palsy
- Check for fatiguability - ask to look up for a sustained period (may bring on ptosis), ask patient to count up to 50 to check for voice fatiguability, test shoulder abduction before and after repetitive arms movement (move the arm up and down around 20 times)
How should patients with suspected MG be investigated?
- ACh-R antibodies
- Anti-MUSK antibodies
- TFTs
- Neurophysiological tests in patients with negative ACh-R antibodies and anti-MUSK antibodies - repetitive nerve stimulation causes decremental response
- Edrophonium testing - short acting acetylcholinesterase like edrophonium is administered. An improvement in muscle strength would suggest MG. Seldom used due to risk of life-threatening bradycardia
- CT scan of thorax - should be requested in all patients with MG as 10% have thymoma
- Forced vital capacity - to check for respiratory muscle weakness
How would you manage a patient with MG?
- Acetylcholinesterase inhibitors e.g. pyridostigmine
- Corticosteroids
- Steroid sparing immunosuppression (e.g. azathioprine, mycophenolate, ciclosporin, rituximab
- If thymoma present then refer for thymectomy. Even in absence of thymoma, thymectomy is recommended for younger patients (<65 years) with generalised MG and +ve ACh receptor antibodies, as it increases the chance of remission.
- Some patients may develop life-threatening respiratory muscle weakness (myasthenic crisis). May be difficult to distinguish this from cholinergic crisis which occurs because of excess acetylcholine in patients on anti-cholinesterase treatment. Edrophonium testing is useful in this case. Patients with myasthenic crisis are managed aggresively with mechanical ventilation, high dose steroids, plasmapheresis, IVIG
Name some underlying causes of proximal myopathy
- Toxic (statins, fibrates, corticosteroids, alcohol)
- Metabolic (e.g. thyroid, parathyroid, adrenal and pituitary disease, osteomalacia, glycogen and lipid storage disorders)
- Inflammatory causes (polymyositis, dermatomyositis, and inclusion body myositis)
- Infection (e.g. HIV, Hep B and C, cysticercosis, trichimosis)
- Malignancy
- Hereditary muscular dystrophies
- Miscellaneous (e.g. sarcoidosis)
What inherited muscle diseases can present in adulthood?
- Girdle muscular dystrophy
- Fascioscapulohumeral dystrophy
- Becker dystrophy
How would you investigate a patient with proximal muscle weakness?
- Perform a focussed neurological examination - check power in all 4 limbs to confirm presence of neurological weakness
- Look for skin signs suggestive of dermatomyositis
- Listen to base of lungs for creps (ILD)
- Offer to perform a detailed examination to check for signs of malignancy (e.g. lymphadenopathy, hepatomegaly, breast mass)
What are the skin manifestations of Dermatomyositis?
- Heliotrope (meaning purplish rash) over the upper eyelids
- Erythematous rash over the malar area of the face and nasolabial folds
- Erythematous rash over the anterior chest and shoulders
- Erythematous, scaly papules over the dorsum of the metacarpophalangeal and interphalangeal joints of hands, extensor aspect of knees and elbows (Gottron’s papules)
How would you investigate a patient with proximal myopathy?
- Bloods including FBC, LFTs, U&Es, CKD, TSH and vitamin D
- Urine examination - in patients with CK >10 times the upper limit of normal
- Specialist investigations may include a myositis autoantibody panel (anti-Jo1 - associated with ILD, anti-SRP associated with cardiac involvement, higher risk of cancer with anti-TIFF-gamma and anti-NXP2
- EMG - used to identify inflammation and guide a suitable site for biopsy
- Muscle biopsy - definitive diagnostic procedure
- Screen for malignancy if confirmed - PETCT or if not available CT CAP. ENT opinion should be sought as there is an association between nasopharyngeal carcinoma and DM, particularly in Southeast Asian patients
What conditions can present with dysarthria, dysphagia and dyspnoea?
- Polymyositis (muscle)
- Myasthenia Gravis (NMJ)
- GBS (polyradiculoneuropathy)
- MND (anterior horn cell)
What questions would you ask a patient with leg weakness?
- Are they able to raise arms to comb or wash hair, put on shirt or reach for objects above head?
- Are they able to turn a door handle or key without difficulty?
- Do they struggle to rise from a seated position?
- Do they slap their feet when they walk?
- Any double vision or drooping of eyelids?
- Any problems with speech, swallowing (‘Do you choke when you eat?’) or breathing?
- Any numbness?
- Any fluctuation in strength or fatiguability?
- Any thinning of muscles or rippling sensation in the muscles?
- Any pain in the neck, back or limbs?
- Any problems with bladder or bowel?
- Any change in higher mental functions (memory, mood, behaviour or personality)?
Name the underlying causes of neurological illnesses?
- Congenital or hereditary (e.g. muscular dystrophies, hereditary sensory-motor neuropathies)
- Trauma (e.g. SDH, spinal cord trauma)
- Infection or Inflammation (e.g. HIV, syphilis, TB, SLE)
- Neoplasm (e.g. brain or spinal cord tumour)
- Vascular (e.g. stroke, SAH, vasculitis)
- Degeneration (e.g. MND, Parkinson’s disease)
- Demyelination (e.g. MS, GBS)
- Deficiency (e.g. subacute combined degeneration of the cord due to Vit B12 deficiency or nitrous oxide
- Toxic (e.g. peripheral neuropathy due to alcohol, statin-induced myopathy)
- Metabolic (e.g. hypothyroidism, hepatic encephalopathy)
How should a patient with suspected MND be investigated?
- MRI of brain and spinal cord - helps to rule out lesions that compress the cord or nerve roots (an important DDx for MND is spondylotic cervical myelopathy and peripheral neuropathy)
- Neurophysiological studies - EMG and NCS
- Bloods including TFTs, Vit B12/Folate, CK, ANA, HIV and syphilis
- Neurologist may ask for muscle biopsy and LP in some patients
What can cause an elevated CK in the non-acute setting?
- Strenuous exercise
- Toxins
- Hypothyroidism
- Idiopathic inflammatory myopathy
- Familial muscle diseases
- Presence of macro-CK
Acute setting: MI, Stroke, Seizures, muscle injuries and prolonged immobilisation after a fall
What factors increase the risk of statin-induced myopathy?
- Preparation - lipophilic statins like simvastatin, atorvastatin and lovastatin are more likely to cause muscle toxicity (as they are more permeable to muscle cells) than hydrophilic statins like pravastatin, fluvastatin or rosuvastatin.
- Dose of statin
- Genetic factors
- Older age
- Renal or liver dysfunction
- Hypothyroidism
- Alcoholism
- Heavy exercise
- Medications that inhibit cytochrome P450, which helps to metabolise statins (e.g. fibrates, colchicine, macrolide antibiotics, ciclosporin, protease inhibitors)
What should you check on examination in a patient with elevated CK?
- Muscle power and check for muscle tenderness
- Check for dermatomyositis rash
- Check thyroid status
How should you investigate a patient with elevated CK and muscle weakness
- TFTs
- Vitamin D
- FBC, U&Es, LFTs, CRP
- EMG, muscle biopsy or HMG-CoA reductase antibody are only indicated if CK continues to rise or the patient develops muscle weakness
What can happen if malignant hypertension is corrected too quickly?
- Can lead to ‘watershed’ cerebral and retinal infarction
What features in the history would suggest Eisenmenger’s syndrome?
- Worsening dyspnoea, peripheral oedema, syncope, palpitations, haemoptysis
- PMHx: congenital heart disease
- Explore family planning - pregnancy contraindicated in severe PAH
- Dentition - risk of endocarditis
What are the complications associated with Eisenmenger’s syndrome?
- Chronic hypoxaemia causes polycythaemia/viscosity symptoms - dizziness, headache, visual problems, ischaemic skin ulceration, angina, MI, HF and stroke
- IDA due to polycythaemia
- Gallstones (pigmented bilirubin), gout and renal stones (urate) due to high RBC turnover
- Paradoxical emboli - stroke
What are the DDx of Eisenmenger’s syndrome?
Other causes of Pulm HTN e.g. rheumatological, autoimmune (mixed connective tissue disease, SLE, systemic sclerosis), infectious (Hep B, C, HIV)
What would you find on examination in a patient with Eisenmenger’s syndrome?
- Central cyanosis
- Digital clubbing (toes > fingers in PDA distal to L subclavian artery)
- Precordium scars
- R parasternal heave
- Loud P2
- Murmur (shunt murmur may be absent as R and L chamber pressures similar but TR common)
- R heart failure - high JVP, ascites, hepatomegaly, SOA
What is the pathophysiology of Eisenmenger’s syndrome?
- Large, often congenital LTR shunts e.g. ASD, VSD, ASVD, PDA, unrepaired tetralogy
- Permanent pulmonary vascular changes (vascular smooth muscle proliferation, in situ thrombosis and lumen obliteration), PAH and elevated peripheral vascular resistance
- Reverses the shunt direction from R to L causes cyanosis
How would you investigate a patient with Eisenmenger’s syndrome?
- CXR (pulmonary vascular pruning, large PA, cardiomegaly)
- ECG (R heart strain pattern)
- FBC (polycythaemia)
- Iron studies
- BNP
- Lung function tests
- CTPA
- Echo
- R heart catheterisation
How would you treat a patient with confirmed Eisenmenger’s?
- Pulmonary vasodilator therapy e.g. Endothelin receptor antagonist, PDE5 inhibitor, epoprostenol
- Anticoagulation
- Symptomatic: iron supplementation, allopurinol, diuretic, anti-arrhythmic, oxygen (if hypoxaemia responsive)
- Supportive: contraception (pregnancy contraindicated), avoidance of extreme heat/dehydration (hypotension) and isometric exercise, immunisations, avoidance of relative anaemia
Surgical:
- Correction of shunt is generally contraindicated as RTL shunt prevents worsening peripheral vascular resistance and maintains systemic blood flow/O2 delivery despite hypoxaemia
- Heart-lung transplantation
What is the prognosis in Eisenmenger’s syndrome?
- 50% mortality at 1 year
What findings would be seen in CSF in bacterial infection?
- Low glucose
- High protein
- Neutrophils
- Gram +ve cocci
What findings would be seen in CSF in bacterial infection?
- Normal glucose and protein
- Mononuclear cells
Name some causes of thunderclap headache
- SAH
- Meningitis
- ICH
- Cerebral venous sinus thrombosis
- Malignant hypertension
What are the precipitating factors for DKA?
- Infection
- Insulin Forgotten
- Infarction
- Injury
What complications can arise from DKA?
- Retina: diabetic changes, papilloedema
- Pulse and BP: haemodynamic compromise
- Auscultate chest: aspiration pneumonia
- Gastroparesis due to diabetic autonomic neuropathy
What investigations would you request in a patient presenting with DKA?
- Finger prick glucometer
- Urine dip and finger prick for ketones
- ABG: metabolic acidosis with resp compensation. Also to monitor response to treatment with venous HCO3-
- FBC, U&Es, LFTs, Glucose, CRP
- ECG (to check for silent MI)
- Blood and urine cultures (to check for sepsis)
- CXR (to check for pneumonia or aspiration)
What are the criteria for safe discharge in asthma
- Clinical signs suitable for home management
- PEFR >75%
- Inhaler technique has been checked and ability to record PEFR
- Written asthma management plan
- F/U arranged by GP/asthma nurse within 2 working days
- Hospital F/U in 1 month (resp physician or asthma nurse specialist)
