Case 6: extra Flashcards
Types of pituitary tumours
1) Adenoma: slow growing benign tumour. 10% of people have one but are never found
2) Prolactinoma
3) Acromegaly
Pituitary adenoma
- Microadenoma <1cm
- Macroadenoma >1cm
- Hormonal status: secretory or non-secretory
Secretory pituitary adenoma
Prolactinomas = the most common type
GH secreting
ACTH secreting
Most common = prolactinomas > non-secreting adenomas > GH secreting > ACTH secreting
How do pituitary adenomas cause symptoms
- excess of hormone secretion if it is secretory
- depletion of a hormone due to compression of the pituitary
- stretching of the dura within/around the pituitary fossa (headaches)
- compression of the optic chiasm
Investigations into pituitary tumours
Pituitary blood profile
Formal visual field testing
MRI brain with contrast
Bloods: ACTH, FH, LSH, TFT’s, GH, Prolactin
Nelsons syndrome
Rapid enlargement of an ACTH producing adenoma
Occurs after the removal of both adrenal glands (adrenalectomy) - used for cushings disease
Multiple endocrine neoplasia
A group of disorders characterized by functioning tumors in more than one endocrine gland
MEN-1
3Ps:
- hypoparathyroidism
- pituitary disease
- pancreatic disease (e.g. insulinoma/gastrinoma leading to recurrent peptic ulceration)
MEN IIa
2 Ps:
- medullary thyroid cancer
Parathyroid
Phaeochromocytoma
MEN IIB
Medullary thyroid cancer
1P:
- phaeochromocytoma
Investigations and management of phaechromocytoma
24 hour urinary metanpehrines
Surgery is definitive
Must stabilise the patient first with an alpha blocker e.g. phenoxybenazime, before giving a beta blocker
when should be done when a patient with Addison’s has infection, trauma or is undergoing surgery
double glucocorticoid dose but not mineralocorticoid
Causes of Cushing’s
- iatrogenic
- basophilic pituitary adenoma
- ectopic ACTH syndrome (ACTH secreting tumour): small cell lung cancer, pancreatic cancer, thyme carcinoid cancer
- adrenal adenoma or adenocarcinoma
Autoantibodies: autoimmuneliver diseases
Autoimmune hepatitis: ANA + ASMA
PBC: AMA
PSC: p-ANCA
Random bloods liver
Alpha anti-trypsinogen: raised in young onset cirrhosis
IgG: raised in alcohol
IgA: raised in alcohol and non-alcohol
Serum caeruloplasmin: Wilsons
Tests after decompensated liver disease
Endoscopy- varices
DEXA- Osteoporosis
Paracentesis- Ascites: insert TIPS if persistent ascites
Ultrasounds + AFP- Liver cancer
Liver transplant indication
Indication: UKELD or MELD score, gives 3 month mortality. Measures INR, Creatinine, Bilirubin, Sodium
Diagnosing PSC, Gilberts and Haemochromatosis
PSC- MRCP
Gilberts- unconjugated bilirubin fraction
Haemochromatosis-HFE genotyping
Hepatitis A IgG and IgA
- Positive HAV-IgM and positive HAV-IgG suggests acute hepatitis A infection.
- Negative HAV-IgM and positive HAV-IgG suggests past hepatitis A infection or immunity.
- HAV- RNA shows acute infection
Hepatitis B serology
- Hepatitis B surface antigen (HBsAg): will only be positive in current infection
- Hepatitis B surface antibody (Anti-HBs): positive for live after an infection or vaccination
- Hepatitis B core antibody (Anti-HBc): only positive in previous or current infection, never vaccination
Granulomatosis with polyangitis (Wegeners granulomatosis)
- Autoimmune vasculitis
- Nosebleeds= saddle nose deformity
- Conjunctivitis
- Sensory neuropathy
- Lungs: dyspnoea
- Hearing loss
- Kidney: rapidly progressive glomerulonephritis, haematuria with CKS
Investigations: Granulomatosis with polyangitis
Bedside: Obs, BP etc.
Bloods: cANCA (positive in 80-90% of patients), Anti-GBM, urea and electrolytes
Imaging: Renal biopsy – epithelial crescents in Bowmans capsule, CT/X-RAY might show opacities / caveating lesions, cystoscopy (for frank haematuria in anyone over 55)
Management of GPA
Induction of remission:
Methylprednisolone IV for 3-5 days followed by oral
prednisolone and cyclophosphamide for 3-6 months until
remission achieved
Consider plasmapheresis
Maintenance of remission:
Prednisolone + methotrexate with folic acid OR
Prednisolone + azathioprine
Indications for RRT
.For Haemodialysis/Peritoneal Dialysis; symptoms/uraemia causing large impact on QoL, electrolyte disturbance, fluid overload, eGFR 5-7
For Transplant; predicted to be a lived in 5 years, on dialysis/starting within 6 months of being listed (provided not an emergency case), treatment team agree it is suitable, chronic + irreversible kidney disease
Possible complications of kidney transplant
Longterm immunosuppression
Short-term; infection, bleeding, DVT/PE, anastomosis issues, SEs of immunosuppression, rejection (hyperacute/acute), urine leakage, UTI
Long-term; graft artery/ureter stenosis, opportunistic infection, malignancy (SCC, BCC, EBV driven non-Hodgkin’s, Kaposi), disease recurrence, rejection (chronic
Hep C characteristics
1) Acute infection: often asymptomatic. Less spontaneous clearance then HBV- more progress to chronic infection
2) Chronic infection- slow development to cirrhosis
3) No reactivation- cure is possible
4) Multiple genotype- reinfection possible
5) No vaccine
Management of secondary pneumothorax
If patient >50 and air >2cm or symptoms insert chest drain
If between 1-2cm attempt aspiration- If fails use chest drain
If <1cm give oxygen and admit for 24hrs monitoring
Bedside tests: neurology
- Peripheral nervous system/NMJ patients (GBS and MG)- Spirometry (to see if respiratory function is preserved)
- Paneoplastic syndrome: breast exam
- Painful myelopathy: spinal exam
- Parkinson’s patients/falling patients-lying and standing blood pressures
- Stumbling, pain in feet- Glucose
Blood tests: neurology
- Weakness: ESR (inflammation), CK, U&E’s
- Confusion: LFT, ammonia
ECG: neurology
- Always do in LoC or collapse in case of arrhythmia
- Done if systematic muscle disease suspected: MND. May need pacemaker if heart involvement
- Anticonvulsants and antipsychotics can prolong the QT
CXR- neurology
- Apical tumour in Horner’s syndrome: small pupil, ptosis
- Lung lesion in paraneoplastic syndrome or cord compression: i.e. lung cancer mets
- Cord compression: back pain, leg weakness, brisk reflexes
- Lung changes in sarcoidosis or TB: peripheral neuropathy, inflammatory brain lesions, weakness
CT head: neurology
- Useful for showing bleeding (trauma, subarachnoid haemorrhage), fracture and large masses (tumour)
- Stroke: excludes bleed
- Bone and skull: white
- Shows if safe to do LP: drowsy
- Water, CSF: grey
- Air: black
- Quick, easy: can be done safely in emergencies i.e. car crash
- CT angiogram; to show thrombus in stroke, not done as often
MRI neurology
MRI indications: inflammation, MS (demyelination)
Most common: Axial
MRI head: T1
Used for more detailed imaging when you have time and the patient is stable
- Default
- White matter is white and grey matter is grey’
- Good for showing structure; abnormalities usually dark (harder to describe)
- CSF black, white matter light, grey matter dark grey
MRI head: T2
- ‘grey matter is white and white matter is grey’, reversed image
- Good for showing pathology; infection, inflammation, demyelination etc usually bright. Shows infarction i.e. acute stroke
- CSF white, White matter grey, Grey matter light
MRI head- Flair
‘grey matter is white and grey matter is white’, reversed image but with dark CSF. Same as T2 but with CSF digitally made dark. Differentiating possible pathology near CSF is easier. Useful for MS for example where demyelination often occurs near the CSF-containing ventricles
CSF analysis
- Taken via LP
- Shows inflammation, infection, deranged biochemistry, cytology and immunological findings. Show raised protein which is in autoimmune nerve disorder i.e. GBS or degenerative disk disease. In autoimmune can have high WCC
- Bacterial: increased protein, decreased glucose, positive gram stain, neutrophils, turbid appearance
- Viral: clear, normal to decreased protein, normal glucose, negative gram stain, predominantly lymphocytes
- SAH: can be bloody or clear, Xanthochromic, increased protein, normal glucose, negative gram stain
Electroencephalogram (EEG)
- Detection of electrical (voltage) differences between surface points on the scalp
- Does not diagnose epilepsy but can pick up sub-clinical seizures or classify seizure types
- More useful in children between events
- Can detect encephalopathy in adults
- Can wear ambulatory EEG if unclear if epilepsy in order to catch them
NCS: nerve conduction study
- Demyelinating neuropathy causes slowing of the action potentials: more reversible. More caused by autoimmune
- Axonal neuropathy causes a reduced or smaller action potential: caused by toxic or metabolic
EMG: Electromyogram (muscle study)
- Small brief discharges with fibrillation suggest inflammation
- Increased amplitude and bigger motor unit potential suggest loss of motor nerves innervating motor units such as MND
Causes of abnormal gait
- Weakness-global or focal (hip, foot)
- Loss of sensory input to allow proprioception (sensory ataxia)
- Loss of coordination (cerebellar ataxia)
- Movement paucity or excess (extrapyramidal)
- Normal gait requires: strength (proximal or distal), co-ordination, proprioception, refining of movement
Proximal weakness
- Difficulty standing from a chair, climbing stairs, rising from the floors (Gower’s)
- Waddling, swaying gait as unable to stabilise pelvis
- Many causes-subacute inflammatory (PMR) or autoimmune, chronic-steroids/drugs, inherited myopathy (DMD), endocrine cause (thyroid, hypoparathyroid, vitamin D deficiency)
- Weakness on top of the arms and thighs
Distal weakness
- Most obvious manifestation is foot drop-many causes including focal compression, MND, MS, vasculitic multifocal neuropathy
- When there is common peroneal nerve compression
- Wrist drop less common except for radial nerve compression and in vasculitic multifocal neuropathy
Hemiplegic weakness
- The commonly described pyramidal weakness seen after stroke or cerebral injury. Seen in haemorrhage and tumour
- Anti-gravity distribution: leg extension and arm flexion with increased tone and reflexes (spasticity)
Growers sign
Shows proximal myopathy. Difficult standing up from sitting. When you climb up your legs using your hands when rising from the floor. Seen in Duchenne’s Muscular dystrophy.
Trendelenburg gait
Seen in proximal muscle weakness. Its an abnormal gait seen in people with weak Hip abductor muscles which are supplied by the superior gluteal nerve. When the hip falls when walking. Tend to waddle.
Foot drop and right hemiplegic gait
Foot drop: high steppage gait, foot cant clear the floor unless they bring their knee high
Right hemiplegic gait with cortical fist: extended leg and in-toeing, the arm on the same side is flexed and made into a fist.
Numbness (sensory ataxia)
- Sensory ataxia is the loss of balance due to lack of proprioceptive input from the feet “I don’t know where my feet are”
- Cant feel their feet
- More marked in low light (showering, at night) or when patients look away from their legs
- Often confused with cerebellar ataxia as broad-based gait adopted to increase stability
- Problems in dorsal column
- Examination: loss of joint position sense, Rombergism, lack of cerebellar feature
Causes of sensory ataxia
- Toxic (chemotherapy, alcohol, anticonvulsants, nitrofurantoin)
- Metabolic (diabetes mellitus, B12 deficiency)
- Autoimmune (Sjogren’s syndrome)
- Infective (HIV myelopathy, syphilis)
- Structural lesion in dorsal column: can cause isolated sensory ataxia of the hands (rare)
Cerebellar ataxia: DANISH
- Dysdiadokinesia
- Ataxia (Rombergs- shouldn’t make a different whether there eyes are open or closed, finger to nose)
- Nystagmus (draw H)
- Intention tremor (touch nose and pen)
- Slurred, Stacatto speech
- Hypotonia: Heel-shin test
