Endocrinology Flashcards
How do you tell the difference between an ischaemic and neuropathic foot ulcer?
Plantar location or sites of pressure makes neuropathic more likely
Cold, pulseless, hairless makes ischaemic more likely
Charcot joint is caused by neuropathy
HOw would you investigate a diabetic foot?
Swab ulcer
FBC, U&E, CRP, fasting lipids, TFT, HBA1c, urine ACR
Doppler to assess vascular supply
PLain foot XR for osteomyelitis
MRI is often needed to exclude osteomyelitis
COnsider bone biopsy if ongoing infection
How would you treat a diabetic foot?
Orthotics- pressure relieving
Appropriate treatment for PVD eg revascularisation
Broad spectrum antibiotics covering staphs, streps and anaerobes if any suggestion of infection and adjust according to microbiology
Surgical review
Optimise glycaemic control
What are the symptoms of diabetes?
Thirst, polyuria, polydipsia
Weight loss
Blurred vision
Recurrent infections
What conditions are assoc with neuropathic ulcers?
Diabetes Leprosy Tabes dorsalis Amyloidosis Alcoholic neuropathy Hereditary neuropathies (charcot-marie-tooth) Drugs Deficiencies eg B12, thiamine
How would you manage an obese patient with T2DM
MDT support- dietician, exercise advice
Drugs: metformin, orlistat, exenatide/liraglutide- incretin (GLP1) mimetics which stimulate insulin secretion, slow emptying of stomach and inhibit production of glucose by liver, also suppress appetite and aid weight loss
Surgery: gastric band or bypass
What are the causes of secondary diabetes?
Steroid use PCOS Hyperthyroidism Chronic pancreatitis Cystic fibrosis Haemochromatosis Acromegaly Phaeochromocytoma Cushings syndrome Glucagonoma
What are the symptoms of autonomic neuropathy?
Dysregulated sweating including gustatory Constipation with bacterial overgrowth Diarrhoea Postural hypotension Bladder and erectile dysfunction Cardiac dysarythmias
What different types of neuropathy are seen in diabetes?
Progressive sensory Mononeuritis eg CN Pressure palsies Amyotrophic Autonomic
What are the steps of intensification in managing diabetes?
- Metformin alone (if GI side effects then try modified release) (SGLT-2 i if metformin not tolerated)
- Metformin + DPP-4 inhibitor or
Metformin + pioglitazone (C/I in heart failure, hepatic impairment, bladder cancer) or
Metformin + sulfonylurea - Metformin + DPP-4 inhibitor + Sulphonylurea or
Metformin + pioglitazone + sulphonylurea or
Insulin therapy - Insulin therapy
Other options
GLP-1 mimetic if:
1. have a BMI of 35 kg/m2 or higher (adjust accordingly for people from black, Asian and other minority ethnic groups) and specific psychological or other medical problems associated with obesity or
2. have a BMI lower than 35 kg/m2 and
for whom insulin therapy would have significant occupational implications or
weight loss would benefit other significant obesity-related comorbidities
What is a DPP4-i and give some examples?
Block dipeptidyl peptidase 4 (DPP4) which would normally inactivate GLP-1 so increasing amount GLP-1 Promote insulin release Inhibit glucagon release Sitagliptin Vildagliptin
How would you diagnose T2DM?
random ≥11.1 mmol/L or fasting ≥7 mmol/L WITH symptoms
In asymptomatic people with an abnormal random plasma glucose, two fasting venous plasma glucose samples in the abnormal range (≥7 mmol/L)
HBA1c= 48mmol/L (6.5%)
What are the differential diagnosis of hyperthyroidism and what in the history may you need to enquire about?
Most common Graves disease (ask about autoimmune history and eye sight) and Toxic multinodular goitre
Other:
Thyroiditis -ask about neck pain and recent childbirth
Drug induced- ask about iodine/contrast, amiodarone, lithium, interferon therapy
Gestational thyrotoxicosis
How would you treat hyperthyroidism?
Correcting hyperthyroidism
- Carbimazole and propylthiouracil
- Titration: initial dose of carbimazole of 30-40mg tapered down over 4-8weeks to maintenence of 5-10mg
- Block and replace: 40mg carbimazole used initially then add 100mcg levothyroxine when free T4 is in normal range (after 4 weeks usually)
Treatment course around 18months
Warn about rash and risk of agranylocytosis
Radio-iodine- likely to result in long term hypothyroidism, may exacerbate eye disease
Surgery- may result in long term hypothyroidism, hypoparathyroidism, hoarse voice
Treat symptoms: beta blocker
How is proptosis quantified?
Hertel’s exophthalmometer, readings >20mm = proptosis
How would you manage a patient with Graves opthalmopathy?
- stop smoking
- lubricating eye drops and raising head of bed
- essential to keep euthyroid (raised TSH or thyroid hormone are assoc with worse clinical outcomes)
- Active eye disease (indicated by soft tissue signs- scleral injection, chemosis, periorbital oedema) may require immunosuppresion (steroids)
- Diplopia or significant proptosis need opthalmological assessment- diplopia may need prisms, worsening may require IV steroids, orbital decompression/irradiation
- Any change in visual acuity or colour vision needs immediate opthalmological input and high dose iV steroids, immunosuppresion, irradiation or decompression of orbit
What do you knwo about the use of radio-iodine in patients with graves eye disease?
Radio-iodine may exacerbate thyroid eye disease and is contraindicated in patients with active or severe opthalmopathy. It can be used in patients with mild eye disease with steroid cover.
It can occasionally precipitate thyroid eye disease
Which types of thryoid disease have high uptake on thyroid uptake scans and which have low uptake?
High uptake:
- Graves disease- diffuse
- Toxic multinodular goitre- focal uptake
- Toxic adenoma (focal uptake)
Low uptake:
- thyroiditis
- iodine/amiodarone induced hyperthyroidism
- factitious: people taking thyroxine
Non-functioning nodules are more likely to be malignant
How would you manage a patient with toxic multinodular goitre?
Radioactive iodine: may cause transient enlargment of goitre before reduction
Surgery: particularly compressive symptoms
Anti-thyroid drugs are not a long term option for toxic multinodular goitre as thyrotoxicosis recurs when treatment stops.
If TSH is normal and patient is unsuitable for radioiodine or surgery then small doses of levothyroxine can be given to suppress TSH levels and reduce chance of goitre enlarging- not very effective
What are the indications for treatment in non-toxic multinodular goitre?
Compression and obstruction- trachea, oesophagus, venous outflow
Cosmetic
Marked intra-thoracic extension
Explain the difference between hot and cold nodules
Cold nodule: diminished uptake when compared to surrounding thyroid tissue (5-10% malignant)
Hot nodule: increased uptake with suppressed uptake in thyroid tissue (hot nodules are never malignant)
What is the differential diagnosis of a solitary thyroid nodule?
Thyroid cyst Thyroid adenoma Thyroid carcinoma Metastatic cancer Lymphoma Sarcoma Parathyroid cyst
What are symptoms of hypothyroidism?
Dry skin and hair loss Cold intolerance Constipation Peripheral oedema Tingling and paraesthesia in hands (carpal tunnel) Neck swelling Menstrual disturbance Snoring and early morning headache (assoc OSA) Skin pigment changes Depression
What are the signs of hypothryoidism?
Bradycardia Coarse, brittle hair Coarse facial features Periorbital oedema Jaundice Macroglossia Goitre Loss of lateral eyebrows Hyporeflexia Oedema- non pitting (myxoedema) or pitting
How should you finish your examination of thyroid>
Ask patient to stand up with their arms folded in front of them (proximal myopathy)
Then kneel on chair to examine ankle jerks
Remember to look for tremor at start of examination
What are the causes of hypothyroidism?
Hashimotos thyroiditis (most common TPO Ab)
After thyroid ablation, surgery or radioiodine
Thyroiditis: post transient hyperthyroid stage
Drugs: amiodarone, lithium, interferon, anti-thyroid drugs
Tell me about hypothyroidism and pregnancy?
Hypothyroidism particularly in the 1st 12 weeks of pregnancy has been shown to have detrimental effects on foetal neurodevelopment.
Thyroid hormone requirements rise substantially in pregnancy with dose range increments 25-50%. Should have TFTs checked every trimester and aim for TSH 0.5-2.0. After delivery can return to normal dose.
Tell me how you would initiate levothyroxine replacement therapy in an elderly patient with hypothyroidism
They can often have been hypothyroid for some time before diagnosis as symptoms can be attributed to aging. They may have co-existing IHD and is therefore prudent to start with low initial dose of 12.5-25mcg levothyroxine and titrate up cautiously but 25mcg every 2-4weeks
What is myxoedema coma?
Severe form of hypothyroidism resulting in altered mental status, hypothermia, bradycardia and hyponatraemia. Cardiomegaly, pericardial effusion and ascites may be present.
May be consequence of long term hypothyroidism or precipitated by an insult eg infection.
What are the symptoms of acromegaly/what would you ask in a history?
Sweating
SYmptoms of hyperglycaemia- polyuria/polydipsia
Hypertension
Daytime somnolence, early morning headaches (OSA)
Change in bowel habit/rectal bleeding
Trouble with peripheral vision/bumping into obejects
Weakness- proximal
Joint pains- hips and knees
What are the signs of acromegaly
Large, doughy spade like hands Sweaty (implies active disease Oedema Absence of rings Carpal tunnel syndrome BM testing marks Goitre Kyphosis (due to osteoporotic #) Proximal muscle weakness Oedematous eyelids Bi-temporal hemianopia Prominent supra-orbital ridges Marked enlargement of nose and ears Proganthism Macroglossia Widened interdenticular spaces Surgical scars- transphenoidal/transcranial Gynaecomastia Displaced apex beat (cardiomegaly) Acanthosis nigricans Skin tags
What are signs of active acromegaly?
Sweating, skin tags, hypertension, peripheral oedema
What investigations would you do in somebody with suspected aWcromegaly?
OGTT- failure to suppress GH to <2nmol/L (random GH measurements are not diagnostic due to episodic secretion and short half life of GH)
IGF-1: used to monitor disease progression
MRI pituitary
Formal goldman or Humphrey visual fields
Check T4 (TSH unhelpful in pit disease)
LH, FSH, testosterone/oestradiol
Short synacthen test, ACTH, cortisol
What is the treatment for acromegaly?
Surgery: treatment of choice, trans-sphenoidal
Radiotherapy: can be used as a adjunct to surgery
Drug therapy: often used pre-operatively
- Somatostatin analogues (eg octreotide) reduce GH secretion but do not significantly reduce tumour size
- Dopamine agonists (eg bromocriptine) only effective in <20% cases
- Pegvisomont, a competitive GH antagonist, normalises IGF1 levels
What are the complications of acromegaly?
Diabetes Hypertension Cardiomyopathy OSA Colonic polyps/bowel cancer OA Hypercalciuria
What may be the significance of a raised calcium?
May indicate a MEN syndrome.
MEN1 (Werners syndrome; 2 or more of pituitary tumour, islet cell tumour, parathyroid tumour, adrenal tumour)
MEN2a: medullary thyroid cancer (90%), phaeochromocytoma (50%), parathyroid adenoma (20-30%)
MEN2b: medullary thyroid cancer (90%), phaeochromocytoma, marfanoid habitus
What role is there for GH in medical treatments?
GH is used in childhood cases of short stature secondary to Turners syndrome and GH def, but has no role in constitutional short stature.
GH therapy in hypopituitarism improves well-being, lipid profile and bone mineral density and possibly reduces cardiovascular mortality
What are the causes of macroglossia?
Acromegaly
Amyloidosis
Hypothyroidism
Down’s syndrome
What are the complications of pituitary surgery?
Diabetes insipidus SIAD Hypopituitarism CSF leak Intracranial bleed
What is the pathophysiology of Addisons disease?
Primary adrenal insuffiency due to an autoimmune destruction of adrenal gland causing hypocortalism. Antibodies against steroid 21-hydroxylase can be found in about 85% of patients. Clinical and biochemical insufficiency only occurs once >90% of the gland is destroyed.
What are the symptoms/things to ask about in an Addisons history?
New skin pigmentation (esp if disproportionate to sun exposure)
Change in pigment of existing scars
Exhaustion
Weight loss
Symptoms of postural hypotension
Loss of appetite, abdo pain, nausea/vomiting
Muscle and joint pains
Amenorrhoea
PH/FH of autoimmune disease eg thyroid/diabetes
Travel abroad and TB
Previous surgery: adrenalectomy
What are the signs of Addisons disease?
Hyperpigmentation diffuse and more marked in:
- palmar creasess
- lips and buccal membranes
- exposed and pressure areas (feet, elbows, belt lines)
- non-sunexposed areas
- scars
Sparse body hair (loss of androgens in complete failure)
Vitiligo
Abdo scars- bilateral adrenalectomy- rooftop scar
Visual field defect- if anterior pit funciton compromised
Ask to measure L/S BP
What investigations of Addisons disease?
Short synacthen test: a normal response is basal cortisol to rise >170nmol/L above basal result and/or peak >530nmol/L
ACTH: raised in primary hypoadrenalism
Other blood tests: adrenal autoantibodies, K+, Na, Blood glucose
CXR: ?TB
CT/MRI adrenals
How do you treat Addisons syndrome?
Glucocorticoid replacement: hydrocortisone divided dosease, 20mg am, 10mg pm
Mineralocorticoid replacment: fludrocortisone
Androgen replacement
What are the causes of hypoadrenalism?
Primary:
- Autoimmune adrenalitis
- Granulomatous: TB, histoplasmosis, sarcoidosis
- Amyloidosis
- Haemochromatosis
- Mets infiltration
- Thrombotic disease
- Congenital adrenal hyperplasia
- Adrenoleukodystrophy (rare, X-liked inherited disorder)
- Iatrogenic (bilateral adrenalectomy)
Secondary:
- Anterior pit failure
How may a patient with an acute Addisonian crisis present?
Nausea, vomiting, hypotension
Hypoglycamia and confusion may or may not be present
May present with shock and central cyanosis
What disease are assoc with Addisons disease?
Listed in order of frequency
- Vitiligo
- Autoimmune thyroid disease (Hashimotos and Graves)
- Diabetes mellitus
- Pernicious anaemia
- coeliac disease
- premature ovarian failure
- Hypoparathyroidism
What are the polyglandular autoimmune syndromes?
Type 1:
- Mild immune def
- Chronic mucocutaneous candidiasis, hypoparathyroidism and Addisons disease
Type 2 (Schmidt's syndrome): - Addisons disease, T1DM and thyroid disease
What are the mechanisms of hyperpigmentation in adrenal failure and can you name some causes of hyperpigmentation?
Pituitary gland produces a pre-hormone pro-opiomelanocortin which is cleaved to ACTH and melanocyte stimulating hormone.
In adrenal failure there is lack of negative feedback so this pre-cursor is made in excess leading to higher than normal levels of MSH which stimulates melanocytes causing pigmentation.
Other causes of pigmentation:
- racial
- sun exposure
- uraemia
- Haemochromatosis
- Primary biliary cirrhosis
- porphyria cutanea tarda
What is Nelsons syndrome?
Rapid enlargement of a pituitary adenoma with very high ACTH levels and hyperpigmentation.
Tumour may compress optic chiasm causing visual field defects. Can occur after bilateral adrenalectomy for Cushings disease (lack of negative feedback loop)
What is the difference between Cushing’s syndrome and Cushing’s disease?
Cushings syndrome results from excess endogenous or exogenous steroid hormones.
Cushings disease is Cushings syndrome that specifically results from excess ACTH secretion from an adenoma of pit gland with consequent overstimulation of adrenal glands.
What questions would you ask somebody with weight gain, leg weakness, difficulty climbing stairs and recently diagnosed diabetes?
Diabetes Weight gain and distribution Easy bruising Skin thinnning New stretch marks Proximal muscle weakness Low mood Taking steroids? COPD? Hypertesion
What are signs of Cushings?
Increased adipose tissue in face, upper back (at base of neck- inter-scapular fat pad, NOT Buffalo hump) Facial plethora Skin bruising Thin skin Violaceous striae Adrenal masses- rare Proximal weakness Measure BP and anal tone- cord compression
What investigations would you do in suspected Cushings syndrome?
COnfirmation of hypercortalism
- overnight dexamethasone suppression test (1mg dex at midnight and check 9am cortisol, abnormal if cortisol >50nmol/L)
- 3 x 24hr urine free cortisol
Ideally do both tests
Identification of causes of Cushings syndrome
- Plasma ACTH level: undetectable if adrenal cause, normal/elevated if pit or ectopic
- High dose dexaemethasone suppression test (2mg dex 6hrly for 48hrs and measure baseline and 48hr cortisol. Cortisol levels should fall by >50% in pit Cushings but not in adrenal or ectopic)
- Corticotrophin releasing hormone test- will cause a rise if pit cushings but not ectopic/adrenal
Radiological localisation (after biochemical confirmation as pit and adrenal incidentalomas are common)
- Adrenal CT: incidentalomas can cause problems
- MRI Pit: will identify 50-80% of ACTH secreting microadenomas
If uncertainty whether it is pit or ectopic ACTH- inferior petrosal sinus sampling
Consider HRCT chest to look for ectopic source
What are the treatments for Cushings?
Pituitary Cushing’s:
- Transphenoidal resection
- Pit radiotherapy
- Bilateral adrenalectomy (rarely done)
Adrenal Cushing’s
- Adrenalectomy
Other options include:
- Ketoconazole
- Mitocane (if Cushings caused by adrenal carcinoma)
What are the causes of hypercortalism?
Exogenous steroids Pit adenoma (Cushing's disease) Adrenal adenoma/hyperplasia Adrenal carcinoma Ectopic ACTH (eg Small cell lung)
What is pseudo-Cushings?
Usually due to alcoholism or depression.
Can display signs and symptoms and abnormal hormone levels seen in Cushings syndrome but there is no intrinsic problem with hypothalamic-pit-adrenal axis. Symptoms normalise rapidly of cessation of underlying cause.
How can pseudo-Cushing’s be distinguished from Cushings syndrome?
Can be very difficult
CRH test after a low dose dex suppression test is reported to be of some value. Test utilised the premise that suppression of ACTH by dex is greater in normal subjects and depressed patietns than in patients with cushings disease. Therefore following suppression with dex, serum cortisol is not increased after CRH stimulation in depressed patients but is increased in individuals with Cushing’s.
What are the symptoms of Klinefelters syndrome?
Infertility
Gynaecomastia
SYmptoms of hypoandrogenism: fatigue, weakness, erectile dysfunction, low shaving frequency
Academic difficulties and behavioural issues
Remember to ask about symptoms related to differentials:
- Smell: Kallmans syndorme
- Joint pain, change in skin colour, diabetes: haemochromatosis
What are signs of Klinefelters syndrome?
Usually tall and slim (but would not have arm span >height like Marfans)
Examine for gynaecomastic and breast tenderness
Paucity of facial and axillary hair
Mitral valve prolapse
Small soft testes
What are you differentials for Klinefelters syndrome?
Kallmans syndrome Testicular disease Pit disease Haemochromatosis Fragile X syndrome (more severe learning disabilities)
What investigations would you perform for Klinefelters syndrome?
Confirm gonadal failure (high LH/FSH, low testosterone)
Karoytyping
ECHO for MVP
Bone density
What is treatment of Klinefelters?
Testosterone replacment (important to reduce risk of CV disease, high cholesterol, osteoporosis) Fertility assessment and assistance (Majority infertile except those with significant mosaicism) Surgery for gyanecomastia
Reassure that sexual functioning and orientation are normal.
What is commonest karyotype in Klienfelters syndrome?
47 XXY in >80% cases
XXXY and XYY variants exist
What is Kallmans syndrome?
Hypogonadotrophic hypogonadism accompanied with anosmia or hyposmia.
Caused by reduced migration of gonadotrophin releasing hormone secreting neurons from forebrain to hypothalamus
How can testosterone be given?
IM injection (every 2-3 weeks or longer acting 3monthly injections)
Gel
PAtches
What questions would you ask a patient presenting with erectile dysfunction?
Assess libido ( low libido suggests hypogonadism rather than penile/neurovascular issue)- could ask is the mind willing but body isnt or are both not particularly willing!
Gradual onset suggests organic cause wherease sudden suggests psychological causes
Ask about erection timing and quality, presence of morning erections suggests psychogenic cause
Tell me what you know about PCOS- diagnosis, features and treatment
Commonest cause of infertility in women
Diagnosis (Rotterdam criteria): requires 2 out of 3:
- Hyperandrogenism
- polycystic ovaries on US
- Oligo/amenorrheoa
Clinical features:
- Acne
- Hirsutism
- male pattern baldness
- obesity and acanthosis nigricans
High LH:FSH ratio
Normal/mildly raised testosterone
Metformin improves both insulin resistance and period regularity
What are the differentials in a women with hyperandrogenism?
PCOS
Congenital adrenal hyperplasia (elevated 17-hydroxyprogesterone)
Androgen secreting tumour (very elevated tesosterone/DHEA-S)
What are the features of Turner’s syndrome (45XO)?
Lack of secondary sexual characteristics
short stature
Widely spaced nipples
Webbed neck with low posterior hairline
Endocrine: diabetes, hypothyroidism
Cardiovascular: congenital lymphoedema, aortic dissection, biscupid aortic valve, coarctation of aorta
GI: coeliac disease, angiodysplasia
Renal: horseshoe kidneys, aberrant vascular supply
MSK: short 4th and 5th metacarpal, nail hypoplasia, high arched palate
Skin: multiple pigmented naevi
Noonans is similar but can occur in men and does not cause infertility
What are the important questions to ask about regarding infertility?
- pubertal development
- duration of infertilty
- previous fertility
For men:
- COnditions which could lead to erectile dysfunction: diabetes, neurological disorders
- Childhood illnesses: testicular torsion, mumps, developmental delay
- Galactorrhoea or visual disturbances (pit tumour)
For women:
- periods
- symptoms of hypothyroidism
- previous STI
- galactorrhoea
What are the causes of hyperprolactinaemia?
Physiological:
Pregnancy.
Puerperium.
Breast stimulation (including suckling a child).
Stress - physical (including excessive exercise) or psychological - including venepuncture.
Non-fasting sample.
Macroprolactinaemia: complexes with immunoglobulins, no bioactivity, consider cause if asymp
Intracranial: Pit tumour Head injury Brain sugery Post ictal
Endocrine: Hypothyroidism (due to increased synthesis of TRH). Cushing's syndrome. Chronic renal failure. Severe liver disease. Polycystic ovarian syndrome. Coeliac disease (possibly).
Drugs: Dopamine receptor antagonists, eg domperidone, metoclopramide, neuroleptics. Dopamine-depleting agents, eg methyldopa. Antidepressants, e.g tricyclic antidepressants, monoamine-oxidase inhibitors, serotonin reuptake inhibitors. Verapamil. Opiates. Protease inhibitors. Bezafibrate. Omeprazole. H2-receptor antagonists. Oestrogens, anti-androgens. Cyproheptadine. Cocaine.
What does pigmentation in Cushings disease tell you?
ACTH high so must be a pituitary cause or ectopic ACTH secreting tumour
How do you manage pre-existing diabetes in pregnancy?
weight loss for women with BMI of > 27 kg/m^2
stop oral hypoglycaemic agents, apart from metformin, and commence insulin
folic acid 5 mg/day from pre-conception to 12 weeks gestation
detailed anomaly scan at 20 weeks including four-chamber view of the heart and outflow tracts
tight glycaemic control reduces complication rates
treat retinopathy as can worsen during pregnancy
How do you manage gestational diabetes?
newly diagnosed women should be seen in a joint diabetes and antenatal clinic within a week
women should be taught about selfmonitoring of blood glucose
advice about diet (including eating foods with a low glycaemic index) and exercise should be given
if the fasting plasma glucose level is < 7 mmol//l a trial of diet and exercise should be offered
if glucose targets are not met within 1-2 weeks of altering diet/exercise metformin should be started
if glucose targets are still not met insulin should be added to diet/exercise/metformin
if at the time of diagnosis the fasting glucose level is >= 7 mmol/l insulin should be started
if the plasma glucose level is between 6-6.9 mmol/l, and there is evidence of complications such as macrosomia or hydramnios, insulin should be offered
What are the glucose targets in pregnancy?
Fasting 5.3
1hr post meal 7.8
2hr post meal 6.4
What are the causes of hypoglycaemia in a patient without diabetes?
Exogenous drugs (e.g insulin, oral hypoglycemics, ethanol intoxication, quinine, chloroquine, beta-blocker overdose, valproate overdose, salicylate overdose, pentamidine)
Pituitary insufficiency
Post-prandial hypoglycemia (e.g. ’late dumping’ after gastric surgery)
Liver disease (e.g hepatocellular cancer, hepatitis and rare genetic defects)
Addison’s disease
Islet cell tumours (e.g. insulinomas)
Immune hypoglycemia (e.g. anti-insulin receptor antibodies in Hodgkin’s disease or anti-insulin antibodies that release insulin when insulin levels are relatively low)
Infection (e.g. severe sepsis, malaria)
Non-pancreatic neoplasms (e.g fibromas, sarcomas, mesotheliomas, and small cell carcinomas that produce IGF-2; extensive metastases that overwhelm the body’s ability to produce glucose)
Starvation and malnutrition
Hypothyroidism (myxoedema coma)
What is wernickes and korsakoffs syndrome?
Wernickes
Neuropsychiatric disorder caused by low thiamine
- nystagmus (the most common ocular sign)
- ophthalmoplegia
- ataxia
- confusion, altered GCS
- peripheral sensory neuropathy
Can progress to Korsakoffs which is antero/retrograde amnesia + confabulation
