Endocrinology Flashcards
Causes of hyperthyroidism
Graves disease
Thyroid adenomas (solitary or multinodular)
Postpartum thyroiditis
Aminodarone induced hyperthyroidism
Ectopic thyroid tissue
Exogenous (levothyroxine, excessive iodine, contrast)
De Quervain’s thyroiditis
What is De Quervain’s thyroiditis? What are specific/prominent signs and symptoms? How is it treated differently? What should be watched for?
Transient hyperthyroidism post viral infection
Neck pain and fever at onset. Thyroid tenderness. Raised esr
Treat with aspirin and steroids.
Watch for following hypothyroidism
Generic symptoms of hyperthyroidism
Weight loss Increased appetite Palpitations Heat intolerance Irritability Anxiety Tremor Diarrheoa Goitre Oligomenorrhoea
Generic signs of hyperthyroidism
Tachycarida / AF Full pulse Warm Hyperkinesis Lid-lag (upper eyelid not following down as eye looks down revealing sclera above iris)
What is graves disease?
Autoimmune condition where antibodies stimulate tsh receptors
What signs differentiate graves disease from other forms of hyperthyroidism?
Eye signs - proptosis/exopthalmos, lid retraction, optic nerve atrophy, pain, grittiness, conjunctival swelling
Pre-tibial myxoedema
What is a bad prognostic indicator for eye signs in graves disease?
No protrusion - higher pressure!
What blood abnormalities are seen in graves disease other than the normal TFTs?
Raised tsh receptor antibodies
Raised antithyroid peroxidase (tpo)
What is the clinical course of graves disease?
Fluctuating
What examination findings and tests would suggests a nodule (single or multiple) is responsible for hyperthyroidism?
Can feel nodules!
Radioactive iodine shows hot nodules
Poor response to carbimazole and constant symptoms
General treatments for hyperthyroidism
Carbimazole Propulthiouracil (ptu) Beta blockers Radioactive iodine Thyroidectomy
How does carbimazole work?
What is its t1/2? What consequence is this? Serious adr?
Inhibits t3/t4 formation
Weeks - takes a while to work
Agranulocytosis
What should patients on carbimazole immediately report to a dr?
Mouth ulcers
Sore throats
What should be done prior to radioactive iodine therapy or thyroidectomy?
Render the patient euthyroid first
Compliactions of thyroidectomy
Laryngeal nerve palsy
Hypoparathyroidism
Transient hypocalcaemia
Hypothyroidism
Signs and symptoms of thyroid storm
Pyrexia Tachycardia Restlessness Hypertension Cardiac failure Liver dysfunction
What can trigger a thyroid storm?
Stress
Infection
Surgery
Radioactive iodine therapy
Treatment of thyroid storm
Propanolol
Potassium iodide
Carbimazole
Corticosteroids
Risks of hyperthyroidism during pregnancy?
Graves - mothers antibodies effect fetus - manage by treating mother
Use ptu in first trimester as carbimazole has rarely been teratogenic
Side effect of ptu?
Hepatotoxicity.
What regimes of antithyroid drugs can be used to treat hyperthyroidism?
Use carbimazole or ptu to lower thyroid hormones to normal levels
Block thyroid hormones completely and replace with thyroxine
Causes of hypothyroidism?
Hashimotos thyroditis Postpartum thyroiditis Primary atrophic hypothyroidism Iodine deficiency Drugs - carbimazole, ptu, amiodarone, lithium Hypopituitism
Presentation of hypothyroidism?
Dry hair Weight gain Cold intolerance Bradycardia Depression Goitre Constipation Myxoedema Tiredness Anaemia Amenorrhoea
What would hashimoto’s thyroiditis present with on bloods?
Raised tsh
Normal or decreased t3/4
TPO antibodies
Anaemia (of chronic disease)
What is a myxedema coma? How does it present?
Decompensated hypothyroidism often following acute insult (infection, stroke)
Confusion to coma
Hypothermia
Cardiac failure (bradycardia and low stroke volume)
Hypoglycaemia
Hyponatremia (decreased Na/katpase in kidneys)
Hypoventilation with T2 respiratory failure
Treatment for myxedema coma
ABCDEs inc ventilation IV T3 Steroids Glucose and sodium as required Passive rewarming
Why are steroids used in the treatment of myxoedema coma? What raises suspicion of need?
Incase it is secondary to hypopituitarism with associated adrenal insufficiency
No previous thyroid surgery, no previous goiter
Why is t3 used in myxoedema coma not t4. Risks?
T3 is active thus much faster action.
Higher risk of hyperthyroid issues like arrhythmia
General treatment for hypothyroidism
Thyroxine
What patients should get a lower starting dose of thyroxine?
Elderly
Long standing disease
IHD patients
How long after starting thyroxine would you expect symptom resolution?
6 months
What are four main diabetic eye changes?
Blurring due to high sugar
Cateracts
Diabetic retinopathy
Maculopathy
What are the subdivisions and features of diabetic retinopathy
Background - microaneurysms (small red dots), superficial haemorrhage (blots), hard exudates (small yellow/white blobs), cotton wool spots (oedema from infarcts)
Proliferative - blood vessels on retina surface, retinal fibrosis and detachment, surface haemorrhages, blood in vitreous humour
What is diabetic maculopathy?
Anurysms form and lead causing fluid, fat and protein deposition (oedema and exudate) with central loss of vision
Treatment option for diabetic retinopathy and maculopathy? Outcome?
Aggressive sugar control
Laser treatment - stops progression but doesn’t reverse
What is the mechanism behind diabetic kidney disease?
Glomerular damage with
- thickened basement membrane
- detached podocytes
- scarring
What is the physiological consequence of diabetic kidney disease?
Diabetic nephropathy
- proteinurea, hypoalbuminia, oedema
Is eGFR typically effected in early diabetic kidney disease?
No
What is an early sign of diabetic kidney disease? What treatments are important?
Microalbuminuria
Aggressive diabetes control
Ace inhibitors even in presence of normal BP
Mechanisms behind diabetic neuropathy?
1 - Uptake of glucose independent of insulin into neurones and schwann cells through glut3. Glucose - sorbitol catalysed by aldose reductase. High sorbitol interferes with neuronal conduction and mylination.
2 - Microvascular damage by non enzymatic glycosylation and vasoconstrictors reduces neuronal perfusion
3 - Oxidative stress from increased ROS production
Clinical pictures of diabetic neuropathy?
Symmetrical sensory neuropathy
Painful neuropathy
Mononeuropathy
Autonomic neuropathy
How are nerves physically effected in diabetic neuropathy?
demylination then axonal degridation
Senses lost in diabetic symmetrical sensory polyneuropathy
Vibration
Pain
Temperature
Proprioception
What complications result of a diabetic autonomic neuropathy?
Vagal neuropathy - tachycardia, gastroparesis
Sympathetics to blood vessels - postural hypotension
Nerves to bladder - incomplete emptying, stasis
Nerves to sexual organs - impotance
Causes of impotance in diabetes?
Neuropathy Anxiety/depression Vascular Medications Unrelated to diabetes at all!
Which sign of background diabetic retinopathy suggests proliferative retinopathy is imminent?
Cotton wool spots
What comorbidity should be aggressively treated in a patient with diabetic nephropathy
Htn
What are major complications of diabetic sensory neuropathy?
Lack of injury sense in foot leading to ulcerations, gangrene and amputation
Charcot arthropathy - microtrauma not detected resulting in chronic fractures and subluxation. Autonomic neuropathy causes hyperaemia and thus increases osteoclast activity causing bone destruction.
Differentials for charcots arthropathy?
DM Syphillis Leprosy Spinal cord injury Chronic alcoholism (b12 deficiency)
Features of charcots arthropathy
Deformity Swelling Pain Erythema Warmth (key! Check temp) Decreased sensation
Treatment of charcots arthropathy
Fitted boots
Diabetic control
Surgery to reduce ulceration risk if extremity in bad position
What sort of pain do patients with diabetic neuropathy often experience?
Electrical
What is the key pathological mechanism for diabetic macrovascular disease?
Injury to arterial wall
Chronic inflammation
Athrosclerosis
In addition to athroscleosis what other pathological mechanisms play a role in diabetic macrovascular disease?
Hypercoagubility
Impaired nitric oxide generation
Impaired fibrinolysis
Comorbidites - metabolic syndrome!!
Key macrovascular disease in diabetes?
CVD
Stroke
HTN
Gangrene
What leaves a diabetic at greater risk of a fatal MI as a direct result of the diabetes?
Athrosclerosis and hypercoagubility
Autonomic neuropathy causing tachycardia
Sensory neuropathy decreasing detection
CKD!
Treatment options for diabetic macrovascular prophylaxis?
Blood sugar control
Ace i and other htn control
Lipid control
When would you start statins in some one with t2dm? What about t1dm?
T2 - qrisk2 >10
T1 - over 40, diabetic for > 10 years, nephropathy or other risk factor
Causes of diabetes?
T1DM T2DM Gestational Metabolic Drugs Pancreatic disease Single gene disorders
Drugs that can cause diabetes?
Steroids
Antipsychotics
Thiazides
Metabolic causes of diabetes?
Acromegally
Cushings
Glucagonoma
Single gene disorders associated with diabetes
Prader willi
Maternally inherited diabetes and deafness
Insulin receptor mutations
Why are diabetics more at risk of infection?
Impaired chemotaxis and phagocytosis
Impaired superoxide generation
What hand sign may diabetics exhibit? Cause? Implication?
Prayer sign - unable to flatten fingers
Cherioarthropathy - thickened skin and limited joint mobility
Implication for anaesthetics
Commonest cause of hypoglycaemia in diabetics?
Treatment related
Insulin/sulphonylureas
What happens to long term diabetics with regards to hypoglycaemia?
Hypoglycaemia unawareness
Decreased glucagon and adrenaline response so no classic warning symptoms
Rarer causes of hypoglycaemia?
Insulinoma Paraneoplastic Postparandial hypoglycaemia Hepatic or renal failure reducing respective ability to release glucose Addisons / ACTH deficiency Drug induced Alcohol
What are the characteristic features of a insulinoma?
Whipples triad
- symptoms on fasting and exercise
- with confirmed hypoglycaemia
- relieved by glucose
What are causes of postparandial hypoglycaemia?
Excessive insulin for size of meal
Surgery removes food!
Alcohol with meal exaggerates insulin response
How dose alcohol cause hypoglycaemia?
Poor nourishment in alcoholics
Inhibits gluconeogenesis
Causes of type 1 diabetes?
Genetic susceptibility (HLA)
Diet
Hygiene hypothesis
Coxsackie virus
Presentation of type 1 diabetes?
Young Acute Weight loss Polyuria Polydipsia Ketoacidotic
Precipitants of diabetic ketoacidosis
First presentation
Omitting insulin
Incurrent illness
What occurs to potassium in diabetic ketoacidosis?
Potassium deficit due to urinary loss
Lack of insulin means less potassium shifted into cells so appears normal - high in spite of actual deficit
Causes of dehydration in DKA?
Osmotic diuresis
Vomiting
What contributes to potassium leaving cells into the ecf in dka?
Lack of insulin decreases nakatpase reducing potassium uptake
Acidosis increases ecf H so increased potassium release in exchange
Increased ecf tonicity pulls water out of cells increasing icf k concentration resulting in K release.
What effect does acidosis have on renal handling of k in dka? In what cells is potassium secreted renally?
Decreases k secretion maintaining k in body
Principal cells
Diagnosis of DKA?
Hyperglycaemia (>11)
Kentonaemia or heavy ketonuria
Acidosis
Management of DKA?
Fluids - 1L in 1, 2l in 4, 2 in 8, 2 in 12
Stat SC insulin 10 units
FRIVII (0.1unit/kg/hr)
Add glucose once BM
When should the FRIVII be switched off in DKA?
What should be done?
pH >7.3 OR bicarb >18 OR Ketones
Complications of DKA?
Hypovolaemic shock
Acidotic coma
DVT
Complications of DKA treatment?
Cerebra or pulmonary oedema
Hypoglycaemia
Hypokalaemia
Risk factors for T2DM
Genetic Ethnicity - asian, african Low birth weight Age Obesity Diet Sedentary lifestyle Hypertension High cholesterol
Presentation of T2DM
Old and fat Insidious Polyuria Polydipsia Weight loss Candidia infection Visual blurring Low energy Complications (retinopathy, neuropathy, large vessel disease)
Skin change associated with T2DM?
Other conditions seen in?
Acanthosis nigricans
PCOS, Cushings, acromegally, hypothyroid
Diagnostic criteria for DM?
Symptoms and one or asymptomatic and 2 of:
- fasting BM >7
- Glucose tolerance test >11
- HbA1c >6.5%
- Random BM >11
How is a Glucose tolerance test performed?
12 hr fast followed by 75g glucose. Measure 2 hours later
What is happening if someone is just under on a glucose tolerance test (e.g 9)
Impaired glucose tolerance - on the way to DM. Still at high risk of macrovascualr complications
What are the diagnostic values for maternal diabetes?
Fasting BM >5.6
GTT >7.8
Conservative management options for t2dm?
Diet - low sugar, high complex carbs, high fibre, low fat, low alcohol
Exercise - both informal and formal
Oral medical management of T2DM
Biguanides - metformin Sulfonylureas - gliclazide Glitazones - piogliazone Acarboze inhibitors Gliptins - saxogliptin SGLT2 inhibitors - dapagliflozin
Injectiable management of T2DM
GLP1 agonist - exenatide
Insulin
Non drug management of DM (not conservative)
Gastric banding
What is a typical management regime for T2DM with failure of 1st and 2nd line options. What would change 3rd line option?
Lifestyle mods
Metformin
Sulfonylurea - use pioglitazone if hypo risk high eg. Driver.
If lifestyle and 2 meds are not controlling t2dm what should be considered?
Triple oral therapy
Add insulin
Novel therapies
What is HONK?
Hyperosmolar hyperglycaemic state
Severe hyperglycaemia without ketosis
Presentation of honk?
Include notable absences
Severe dehydration with hyperosmolality
Hypernatraemia
Coma
No ketones or acidosis
Treatment of HONK
Isotonic fluids
Slowly increasing insulin
Predisposing factors for HoNK
Glucose rich food
Steroids
Illness
Thiazides
What is the mechanism behind PCOS?
Increased GNrH resulting in high LH and low FSH causing androgen secretion but not conversion into oestrogen.
There is also associated insulin resistance
Signs and symptoms of PCOS
Hirtuism Irregular or absent periods Infertility Acne Obesity Virilisation (baldness, clitoromegally)
Complication of PCOS?
Metabolic syndrome
What investigations should be done in suspected PCOS? What would you expect to see? Pitfalls?
Serum testosterone - high - must check for sex hormone binding globulin
LH - low - depends when taken as pulsetyle
USS - polycystic ovaries
Diagnostic criteria for PCOS
2 of
- clinical evidence of hyperandrogenism
- oligo or anovulation
- polycystic ovaries on USS
Treatment for PCOS?
Symptomatic - hair removal
Conservative - exercise, diet
Medical - OCP, spironolactone, metformin
What OCP to use in PCOS? What is the active ingredient? How does it work?
Dianette - cyproterone acetate
Progesterone - an antiandrogen
Why give PCOS spironolactone?
Antiandrogen properties hence side effect of gynacomastia
Why give PCOS metformin?
No only helps with insulin resistance but also with menstrual regularity and infertility
Differentials for PCOS for hirsutism?
Idiopathic hirsutism
Congenital adrenal hyperplasia
Cushings
Virilizing tumour of ovary or adrenal
What causes congenital adrenal hyperplasia?
Lack of enzyme in steroid metabolism that usually converts progesterone into aldosterone and cortisol. Causes a deficiency in aldosterone and cortisol with an excess in androgens as progesterone is pushed down this pathway.
Lack of cortisol causes high ACTH and thus adrenal hypertrophy
How does congenital adrenal hyperplasia present at birth if severe?
Ambiguous genitalia in females (cliteral hypertrophy, fused labia) Adrenal crisis (hypotension, hypoglycaemia) Mineralcorticoid deficiency (hypotension, hyponatraemia)
If not too severe, how would congenital adrenal hyperplasia present in adult life?
Precocious puberty
Hirsutism
Primary amenorrhoea
How can you test for congenital adrenal hyperplasia?
Administer ACTH and measure response
Treatment of congenital adrenal hyperplasia?
Replacement of glucocorticoids and mineralocorticoids
Genetic councilling
In diabetes glucose is found in the urine? Why? How is it normally dealt with by the kidney?
Freely filtered at the glomerulus so [high] in blood means the same in urine exceeding the transport maximum.
Usually glucose is reabsorbed in the PCT fully. On the luminal membrane using a glucose:Na cotransporter (SGLT2) and using Na/K ATPase with GLUT1/2
When are serum cortisol levels highest? Lowest? What can change the cycle?
High early morning
Low at midnight
Stress will cause a raise
What inhibitory trophic hormones are released by the hypothalamus into the portal circulation? What do they inhibit?
Dopamine - prolactin
Somatostatin - gh, tsh
Local effects of a pituitary tumour?
Compression of optic chiasm - bitemporal hemianopia
Compression of cavernous sinus - CN III, IV and VI dysfunction
Meningeal irritation - headache
Compression of hypothalamus - appetite, sleep, thirst disturbance, DI
Compression of ventricles - hydrocephalus
Sphenoid sinus invasion - csf rhinorrhoea
Effects of CN3,4 and 6 dysfunction in cavernous sinus compression?
3 - SR, IR, MR, IO, LPS, sphincter pupillae - ptosis, eye down and out, fixed dilated pupil
4 - SO - diplopia on looking down
6 - LR - cant abduct
All three together causes completely immobile eye
Causes of hypopituitarism?
Tumour Sheehans syndrome following post partum haemorrhage Infections Trauma Sarcoidosis Radiation/chemotherapy Anorexia nervosa / starvation
Zones of the adrenals with what they produce?
Zona glomerulosa - mineralocortiocoids
Zona fasicularis - corticosteroids
Zona reticularis - androgens
Major effects of glucocorticoids
Gluconeogenesis Protein catabolism Fat and glycogen deposition Sodium retention and potassium loss Immunosuppression
How does negative feedback work on the hpa axis?
Cortisol inhibits CRH and ACTH formation
When should basal cortisol and acth levels be taken? What consideration?
At peak between 0800 and 0900
Stress should be minimised
What main tests are used in patients with high levels of cortisol to determine cause? How do they work?
Dexamethasone suppression tests
Low dose - patients with Cushing’s syndrome will not significantly suppress cortisol on administration of dexamethasone
High dose - patients with Cushing’s disease will significantly suppress cortisol indicating cause is likely ectopic or adrenal if failed to suppress
If cortisol levels are low what main tests can be used to identify the cause? Differentiate them.
Synacthen
Short - if no response to ACTH confirms hypoadrenalism but could be primary, secondary or iatrogenic
Long - if no response suggests primary adrenal failure
Why does secondary hypoadrenalism result in a positive short synacthen test? Why does this change with a long one?
Adrenal atrophy
On a long test the adrenals are kicked into life unless there is a primary pathology
What CLINICALLY would differentiate addisons from secondary hypoadrenalism?
Pigmentation from high ACTH
Low mineralocorticoids producing hypotension and electrolyte imbalance
What tests can be used in suspected addisons disease (generally)
Random cortisol Synacthen tests U+Es BM Adrenal antibodies Abdo xray Serum aldosterone
What might be seen in an abdominal xray of an addisons patient?
Calcified adrenals
Evidence of tb
Causes of addisons disease?
Autoimmune TB Surgical removal Haemorrhage/infarction Malignant destruction
Causes of secondary hypoadrenalism
Exogenous steroids
Pituitary disease
Emergency management of addisons crisis?
NaCl
Hydrocortisone
Glucose
Long term treatment of hypoadrenalism?
Gluticorticoids - e.g. Hydrocortisone
Mineralocorticoids - e.g. Fludrocortisone
What is the most common cause of cushings syndrome?
Exogenous steroids
What are causes of cushings syndrome?
Iatrogenic
Disease - increased ACTH from pituitary
Atopic ACTH from a tumour
Endogenous cortisol secretion from adrenals
A patient with a history of cushing type symptoms has a positive low dose dexamethasone suppression test. What tests will help diagnose the source?
Adrenal ct Pituitary mri K levels High dose dexamethasone test Plasma acth Cheat xray
A patient with a history of cushing type symptoms has a positive low dose dexamethasone suppression test. A high dose dexamethasone suppression test is negative, his potassium is normal and there are no signs on the chest xray. A ct of adrenals is negative and there is nothing on a pituitary mri. Where is the likely lesion? Why?
Pituitary. Most acth secreting tumours are too small to see on mri. Normal potassium suggests not ectopic and a response to the high dose tests suggests a pituitary source.
What causes death in untreated cushings?
Htn with mi and heart failure
Infection
How is cushings treated?
Ketoconazole to reduce plasma cortisol
Removal of source if possible
If not bilateral adralectomy with replacement
What is the risk with bilateral adrenelectomy for cushings?
Nelsons syndrome
No feedback so massive enlargement of pituitary
Hazards to discuss on starting steroids for any condition
Infection Suppress own steroids Hypertension Pancreatitis Weight gain Diabetes Depression Osteoporosis Thin skin and bruising Cataracts
What is diabetes insipidus?
Deficiency ir insensitivity to adh resulting in polyurea, nocturea and compensatory polydipsia
What is the biochemical profile of diabetes insipidus?
High plasma osmolality
Low urine osmolality
High plasma sodium
High urine volumes
You suspect diabetes insipidus. How do you test for it?
Water deprivation test for up to eight hours
Plasma osmolality should stay the same whilst urine osmolality should increase in a normal person.
If this does not occur sufficiently give synthetic ADH (desmopressing) and monitor change to differentiate cranial from renal.
When should a water deprevation test be stopped?
If >3% body weight reduction
Causes of cranial diabetes insipidus?
Hypothalmic-pituitary surgery Trauma Infection Tumour Necrosis - sheehans Famililal Idiopathic
Causes of nephrogenic diabetes insipidus
Familial Idiopathic Renal disease Lithium Hypokalaemia Hypercalcaemia Sickle cell disease
Treatment of cranial diabetes insipidus
Desmopressin
Treatment of nephrogenic diabetes insipidus
Reverse cause if possible
Other causes of polyuria and polydipsia not diabetes insipidus
Diabetes mellitus
Hypokalaemia
Hypercalcaemia
Primary polydipsia - psychiatric, too much water, low plasma osmolarity
How does SIADH present?
Dilutional hyponatraemia with low plama osmolality
Euvolemic with no hypotension
Normal potassium
No response to 1-2 L of 0.9% sodium chloride
Treatment of SIADH
Fluid restriction
Demeclocycline to inhibit adh
Cautious use of hypertonic saline in severe illness
Causes of siadh
Tumours Pneumonia Head injury Alcohol withdrawal Drugs carbamazepine
Causes of hyponatraemia with hypovolaemia?
Vomiting, diarrheoa, burns, haemorrhage, osmotic diuresis, diuretics, addisons,
Causes of hyponatraemia with euvolaemia?
SIADH Overenthusiastic 5% glucose use Exertion with only water replacement psychogenic polydipsia Desmopressin Addisons Mannitol Sickle cell syndrome
Causes of hyponatraemia with hypervolaemia
Heart failure, liver failure, hypoalbuminaemia
What is the mechanism behind hyponatraemia with hypovolaemia with respect to adh.
Loss of salts out of proportion to loss of water causing low osmolarity
Due to volume depletion adh still released to maintain volume lowering osmolarity further still
What are signs and symptoms of very low sodium concentrations? What sort of values do they occur at? Why do they occur?
Caused by water moving into neurones - hyponatraemic encephalopathy
Who are most at risk of hyponatraemic encephalopathy?
Children,
Premenopausal women
Hypoxaemic patients
What should be done in a patient with hyponatraemia with euvolaemia to further diagnose?
Plasma and urine electolytes and osmalarities
Screen for addisons and siadh
Treatment of hyponatraemia with euvolaemia
Fluid restriction
Slow 0.9% nacl
Severe neurological signs - hypertonic saline
Causes of hypernatraemia?
Water deficite (impaired thirst, unable to drink, diabetes insipitus, osmotic diuresis) Excessive sodium administration (NaCl overuse, drugs with high na content)
Symptoms of hypernatraemia?
Nausea Vomiting Fever Confusion Polydipsia
Investigations of hypernatraemia
Urine and plasma osmolality and sodium
Symptoms and signs of acromegally
Bone - pronounced brow, wide nose, large jaw, macroglossia, wide spaced teeth, large hands and feet
Skin - acanthosis nigracans, darker skin, curly hair
Physiological - snoring, OSA, DM, HTN, headaches, decreased libido, carpal tunnel
Tests in suspected acromegally
Glucose tolerance test - +ve with failed suppression of growth hormone
MRI pituitary
Treatment of acromegaly
Lesion removal
Somatostatin analogues
GH antagonist
Causes of hyperprolactinaemia
Pituitary adenoma secreting prolactin
Compression of pituitary stalk
Medications - antipsycotics, metaclopramide, ecstacy
Physiological - pregnancy, breastfeeding
Presentation of hyperprolactinaemia
Female - amenorrhoea, oligomenorrhoes infertility, galactorrhoea
Male - galactorrhoea, impotence, hypogonadism,
Both - osteoporosis,
Test in suspected hyperprolactinaemia
Prolactin levels between 8 and 160
Pregnancy test
Differentiate cause of hyperprolactinaemia from prolactin levels
> 5000 from prolactinoma
>10000 from macroprolactinoma
Treatment of microprolactinoma
Dopamine agonist eg bromocryptine
Treatment of macroprolactinoma
Bromocriptine
If no response and visual symptoms etc then surgery
Causes of diabetes insipidus
Cranial - idiopathic, trauma, congenital, tumour, haemorrhage
Renal - inherited, lithium, ckd, hypokalaemia
Tests to run in suspected diabetes insipidus?
DM screen
U+E
Serum and urine osmolarities
What changes in osmolarity would you see in urine and plasma (and ratio!) in diabetes insipidus?
Raised plasma
Lowered urine
U:P ratio
Diagnostic test for diabetes insipidus
Water deprivation test - urine should normally concentrate
If it fails to give desmopressin and urine should then concentrate if cranial and not if nephrogenic
Differentials of diabetes insipidus
DM
Lithium
Diuretic use
Primary polydipsia
Treatment of diabetes insipidus
Cranial - desmopressin, treat cause
Renal - treat cause, nsaids, bendroflumethiazide
Commonest hormones secreted by pituitary tumours
Prolactin
ACTH
GH
A patient with a know pituitary tumour presents with sudden headache, meningism and visual field defect. What should be considered?
Pituitary apoplexy - bleed into tumour
Features of growth hormone deficiency
Loss of muscle, difficulty exercising, decreased cardiac output, low glucose, osteoporosis
Treatment of gh deficiency
Somatotrophin
Causes of primary hyperaldosteronism
Adenoma - conns
Bilateral adrenocortical hyperplasia
If someone has hyperaldosteronism but their k is nor,al what other blood test will be deranged?
Alkalosis
What should be tested in suspected hyperaldosteronism
U+e
Renin and aldosterone levels
What tests to run on a patient with proven primary hyperaldosteronism?
Mri
If adrenal mass seen take adrenal vein sampling bilat to see if it the source
Treatment of primary hyperaldosteronism?
Conns - remove adenoma
Spironolactone
Causes of secondary hyperaldosteroneism
High renin due to low renal perfusion
Renal artery stenosis
Diuretics
Ccf
What is the 10% rule in phaeochromocytomas
10% malignant, extra adrenal, bilateral, familial
Where are most extraadrenal phaeochromocytomas
Aortic bifurcation
Who should be screened for thyroid problems?
AF Hyperlipidaemia Lithium DM Amiodarone Downs
What independantly influences prognosis and risk of thyroid eye disease
Smoking
What causes a goitre in hashimotos?
Wbc infiltration
