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Medicine year 4 CDM > Case 6: extra > Flashcards

Case 6: extra Flashcards

1
Q

Types of pituitary tumours

A

1) Adenoma: slow growing benign tumour. 10% of people have one but are never found
2) Prolactinoma
3) Acromegaly

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2
Q

Pituitary adenoma

A
  • Microadenoma <1cm
  • Macroadenoma >1cm
  • Hormonal status: secretory or non-secretory
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3
Q

Secretory pituitary adenoma

A

Prolactinomas = the most common type
GH secreting
ACTH secreting

Most common = prolactinomas > non-secreting adenomas > GH secreting > ACTH secreting

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4
Q

How do pituitary adenomas cause symptoms

A
  • 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
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5
Q

Investigations into pituitary tumours

A

Pituitary blood profile
Formal visual field testing
MRI brain with contrast

Bloods: ACTH, FH, LSH, TFT’s, GH, Prolactin

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6
Q

Nelsons syndrome

A

Rapid enlargement of an ACTH producing adenoma

Occurs after the removal of both adrenal glands (adrenalectomy) - used for cushings disease

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7
Q

Multiple endocrine neoplasia

A

A group of disorders characterized by functioning tumors in more than one endocrine gland

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8
Q

MEN-1

A

3Ps:
- hypoparathyroidism
- pituitary disease
- pancreatic disease (e.g. insulinoma/gastrinoma leading to recurrent peptic ulceration)

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9
Q

MEN IIa

A

2 Ps:
- medullary thyroid cancer

Parathyroid
Phaeochromocytoma

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10
Q

MEN IIB

A

Medullary thyroid cancer

1P:
- phaeochromocytoma

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11
Q

Investigations and management of phaechromocytoma

A

24 hour urinary metanpehrines

Surgery is definitive
Must stabilise the patient first with an alpha blocker e.g. phenoxybenazime, before giving a beta blocker

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12
Q

when should be done when a patient with Addison’s has infection, trauma or is undergoing surgery

A

double glucocorticoid dose but not mineralocorticoid

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13
Q

Causes of Cushing’s

A
  • iatrogenic
  • basophilic pituitary adenoma
  • ectopic ACTH syndrome (ACTH secreting tumour): small cell lung cancer, pancreatic cancer, thyme carcinoid cancer
  • adrenal adenoma or adenocarcinoma
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14
Q

Autoantibodies: autoimmuneliver diseases

A

Autoimmune hepatitis: ANA + ASMA
PBC: AMA
PSC: p-ANCA

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15
Q

Random bloods liver

A

Alpha anti-trypsinogen: raised in young onset cirrhosis
IgG: raised in alcohol
IgA: raised in alcohol and non-alcohol
Serum caeruloplasmin: Wilsons

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16
Q

Tests after decompensated liver disease

A

Endoscopy- varices
DEXA- Osteoporosis
Paracentesis- Ascites: insert TIPS if persistent ascites
Ultrasounds + AFP- Liver cancer

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17
Q

Liver transplant indication

A

Indication: UKELD or MELD score, gives 3 month mortality. Measures INR, Creatinine, Bilirubin, Sodium

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18
Q

Diagnosing PSC, Gilberts and Haemochromatosis

A

PSC- MRCP
Gilberts- unconjugated bilirubin fraction
Haemochromatosis-HFE genotyping

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19
Q

Hepatitis A IgG and IgA

A
  • 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
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20
Q

Hepatitis B serology

A
  • 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
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21
Q

Granulomatosis with polyangitis (Wegeners granulomatosis)

A
  • Autoimmune vasculitis
  • Nosebleeds= saddle nose deformity
  • Conjunctivitis
  • Sensory neuropathy
  • Lungs: dyspnoea
  • Hearing loss
  • Kidney: rapidly progressive glomerulonephritis, haematuria with CKS
22
Q

Investigations: Granulomatosis with polyangitis

A

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)

23
Q

Management of GPA

A

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

24
Q

Indications for RRT

A

.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

25
Q

Possible complications of kidney transplant

A

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

26
Q

Hep C characteristics

A

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

27
Q

Management of secondary pneumothorax

A

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

28
Q

Bedside tests: neurology

A
  • 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
29
Q

Blood tests: neurology

A
  • Weakness: ESR (inflammation), CK, U&E’s
  • Confusion: LFT, ammonia
30
Q

ECG: neurology

A
  • 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
31
Q

CXR- neurology

A
  • 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
32
Q

CT head: neurology

A
  • 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
33
Q

MRI neurology

A

MRI indications: inflammation, MS (demyelination)

Most common: Axial

34
Q

MRI head: T1

A

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
35
Q

MRI head: T2

A
  • ‘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
36
Q

MRI head- Flair

A

‘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

37
Q

CSF analysis

A
  • 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
38
Q

Electroencephalogram (EEG)

A
  • 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
39
Q

NCS: nerve conduction study

A
  • 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
40
Q

EMG: Electromyogram (muscle study)

A
  • 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
41
Q

Causes of abnormal gait

A
  • 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
42
Q

Proximal weakness

A
  • 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
43
Q

Distal weakness

A
  • 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
44
Q

Hemiplegic weakness

A
  • 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)
45
Q

Growers sign

A

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.

46
Q

Trendelenburg gait

A

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.

47
Q

Foot drop and right hemiplegic gait

A

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.

48
Q

Numbness (sensory ataxia)

A
  • 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
49
Q

Causes of sensory ataxia

A
  • 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)
50
Q

Cerebellar ataxia: DANISH

A
  • 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

Medicine year 4 CDM (44 decks)

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