Endocrine Flashcards
A CT head shows bleeding on the pituitary gland, what is this and what is the most common cause?
- Pituitary apoplexy is heamorrage of pituitary gland
- Often caused by tumour (macro adenoma)
What investigations should you do for pituitary apoplexy, IN THE ORDER OF MOST IMPORTANT?
What would you expect to see?
1) CT head-bright white in middle by pituitary gland
2) pituitary hormones
- cortisol>CHECK ASAP-if low give hydrocortisone
- thyroid
- sex hormones
- growth hormones
3) visual field problems (bilateral hemianopia a.k.a tunnel vision) caused by compression of the optic chiasma
If hypercalcemia is parathyroid dependant what would you expect to see?
- raised PTH
- high Calcium, low Phosphorus
treatment for thyroid storm?
Thyroid storm
1) Propylthiouracil
2) Hydrocortisol (prevent peripheral conversion of T3 and T4)
3) Symptom control
- Beta blocker
- IV fluids
**monitor heart for arrhythmias
Explain the negative feedback loop of the hypothalamus, anterior pituitary gland and the adrenal glands
Negative feedback loop
1. Hypothalamus produces cortico-trophic releasing hormone CRH
- This causes Anterior pituitary gland to release ACTH (adreno-cortico-trophic hormone)
- ACTH causes the adrenal cortex to release
a) mineralocorticoids(aldosterone)
b) glucocorticoids (cortisol)
c) androgens
What are the effects of the 3 hormones secreted by the adrenal gland?
Adrenal gland hormone
- Mineralocorticoids (aldosterone)
- Na+ and water retention>↑BP - Glucocorticoids (cortisol)
- immunosuppressant and anti inflammatory
- skin thinning
- metabolism (weight gain and insulin resistance
- bone effects (↑osteoclasts>osteopenia and osteoporosis) - Androgens
- more effect for females
Presentation of adrenal insufficiency?
ADRENAL INSUFFICIENCY PRESENTATION
- fatigue, depression, ↓self-esteem, psychosis
- tan/pigmentation (skin/buccal mucosa/palmar creases)
- anorexia and weight loss (can be mistaken for anorexia)
- signs of dehydration
- dizzyness/syncope
- nausea, vomiting (↓Na+)
- abdo pain, constipation or diarrhoea
- arthralgia/myalgia
- decreased libido
- low grade fever
- loss of hair
- can present ACUTELY with circulatory collapse
Investigations and findings of adrenal insufficiency? (bedside, bloods, imaging,special)
Bedside
- low BP and signs of dehydration
- ECG (tachy to compensate for low BP)
Bloods
- Us+Es (HYPONATREMIA, HYPERKALEMIA)
- 9am serum cortisol QUICKEST TEST (reduced)
- Glucose (hypoglyceamic-due to ↓cortisol)
- ABG (metabolic acidosis due to↓aldosterone> ↓HCO3- )
Imaging
-Could do if concerned primary malignancy, mets or infection (TB-CXR)
Special test
- SynACTHen test (diagnostic ∆ ) <420nmol/L cortisol suggests primary adrenal deff -however takes longer so would prob just treat before results
- Adrenal antibodies (21 hydroxylase Ab + ve 80% in Addisons). If negative consider TB
Long term management for Adrenal insufficiency?
ADRENAL INSUFFICIENCY MANAGMENT
- Mineralocorticoid replacement: fludrocortisone (only in primary because RASS has less effect)
- Glucocorticoid replacement: daily hydrocortisone (divided doses throughout day-mimic normal fluctuations)
- Androgen replacement: DHEA (Dehydroepiandrosterone is produced by adrenals whereas testes produce androgens)
What are the clinical effects of
↓Mineralocorticoids
↓ Glucocorticoids
↓Androgens
↓Mineralocorticoids (aldosterone)
- Hyperkaleamia ↑K+
- Hyponatreamia (↓Na+and ↓water retention)>↓BP> compensatory ↑HR
- Metabolic Acidosis (aldosterone reabsorbs bicarb(↓HCO3-)
↓Glucocorticoids
- weight loss
- fatigue
- ↓gluconeogenesis ↓blood glucose
↓Androgens (more effect on women)
- ↓libido
- ↓Pubic hair
-skin pigmentation our to compensatory hyper-pituitary activity → ↑melanocyte stimulating hormone
Causes of adrenal insufficiency
Causes of adrenal insufficiency
- ADDISONS DISEASE (autoantibodies against adrenal cortex +/- hydroxylase autoimmunity)
- infection
- malignancy or mets
- infiltration diseases (heamochromatosis or amyloidosis)
- adrenal heamorrage (warfarin) or infarction
- iatrogenic (Surgery)
- congenital adrenal hyperplasia
What are the cut-offs for cortisol test?
What does high ACTH mean? What does low/norm ACTH mean?
9am ↓Cortisol and ACTH
-allows differentiation of 1 vs 2
Cortisol < 100 (Addison’s likely admit to hospital )
100-500 (do Synacthen test);
> 500 (unlikely Addison’s)
↑ACTH = primary (pituitary trying to compensate);
↓ or norm ACTH = secondary (↓pituit. sec is the issue)
What things might interfere with cortisol test?
What would you do to overcome this?
- shift workers
- patients on long term steroids
- patients on oestrogen therapy
- do ACTH test instead
How does the ACTH stimulation test work?
-Synacthen® ACTH stimulation test is diagnostic ∆
- First, measure plasma cortisol
- Then, give IM Synacthen (tetracosactide), wait 30 min
- Then, measure plasma cortisol
- If 30 min cortisol < 500 nmol/L = Addison’s
- If 30 min cortisol > 550 nmol/L = not Addison’s
Refer to endocrinologist
What advice can you give to someone taking steroids for adrenal insufficiency?
STEROIDS ADVICE-ADRENAL INSUFFICIENCY
- Warn not to abruptly stop steroids (risk of crisis)
- DOUBLE hydrocortisone dose alone in febrile illness
- provide IM hydrocortisone if vomiting prevents oral intake
- give blue steroid card
Symptoms of addisonian crisis?
Addisonian crisis
- dehydration>hypotension>HYPOVOLEAMIC SHOCK>altered consciousness>death
- seizures
- stroke or cardiac arrest
What is the ACUTE management for Adrenal insufficiency?
ACUTE adrenal insufficiency
1) Sugar (dextrose)
2) Steroids (IM or IV)
2) Saline
3) Search for cause
What is Waterhouse-Friderichsen syndrome
- complication of sepsis (particularly meningococcal sepsis)
- hemorrhagic necrosis of the adrenal glands
- cause adrenal crisis
Explain how parathyroid hormone works?
- low levels of calcium detected in blood
- causes PTH gland to release PTH
- PTH causes:
a) ↑osteoclast activity and ↑calcium resorption from bone
b) Activates vitamine D so ↑Ca2+ absorption from gut
c) ↑Ca2+ reabsorption from kidneys
PTH also stimulates vitamin D production from kidneys
What is the most common cause of primary hyperparathyroidism
PRIMARY HYPERPARATHYROIDISM CAUSES
- Most common cause is Parathyroid adenoma (80%)
- Hyperplasia (20%)
- Parathyroid carcinoma (<0.5%)
What are risk factors for primary parathyroidism?
PRIMARY HYPERPARATHYROIDISM
- post menopausal women
- MEN1/2a
Symptoms of hyperparathyroidism? (nervous system, cardiac, GI, urinary, MSK)
PRIMARY HYPERPARATHYROIDISM (symptoms of high calcium- MOANS/BONES/ GROANS/ THRONES Nervous system -cognitive impairment -depression/fatigue -confusion>drowsy>siezures>coma
Cardiac
-Arrhythmias (do ECG)
GI system
- abdo pain
- N and V
- loss of appetite
- constipation
Urinary system
- kidney stones (most common)
- increased urination
- increased thirst
MSK
- bone pain
- muscle weakness
70-80% are asymptomatic and diagnosis is often incidental
What investigations would you do for hyperparathyroidism and what would they show? (bedside, bloods, imaging, special)
PRIMARY HYPERPARATHYROIDISM Bedside -Blood pressure (↑HTN)-PTH>aldosterone -ECG – may present with short QT interval -24hr Urinary Ca2+ (↑Ca2+)
Bloods (calcium should be corrected for albumin)
- U+Es (↑PTH / ↑Ca2+ / ↓PO4, check Mg (PPI causes low Mg and low Ca2+)
- LFTS - ↑ALP (bone resorption – osteopenia)
Imaging
-DEXA scan – determine level of osteoporosis/dystrophy (see complications)
Special- biopsy
-if ?carcinoma
What are the 2 options for hyperparathyroidism treatment?
PRIMARY HYPERPARATHYROIDISM
- Conservative if:
- kidneys working well with no stones
- only slightly elevated Ca2+
- bone density okay
- if surgery unsuccessful or unsuitable - Surgery
- high serum/urinary calcium
- osteoporosis
- ↓renal function/renal calculi
- age <50 years
What is the conservative management of primary hyperparathyroidism? (4)
Conservative treatment:
- ↑fluid intake and avoid thiazide diuretics
- Calcimimetics (Cinacalcet) -when surgery unsuitable/unsuccessful) ↑sensitivity of parathyroid cells to ca2+ levels → ↓PTH secretion
- Bisphosphonates if ↑fracture risk
- Replenish Vitamin.D (Cholecalciferol – non-active)
what is the surgical treatment for hyperparathyroidism?
What are the complications of surgical treatment?
SURGERY
-Parathyroidectomy
Complications
- hypothyroidism
- recurrent laryngeal nerve damage (hoarse voice)
- symptomatic ↓Ca2+ (check Ca2+ daily for ≥ 14 d post-op)
What type of lung cancer is associated with ↑PTH?
-Squamous cell carcinoma is associated with ↑PTH (also seen in breast and renal cancer)
What are two complications of primary Hyperparathyroidism (2)
Osteitis fibrosa cystica
- bones replaced by fibrous tissue
- salt and pepper skull
- brown tumours of long bones
- dissapearance of distal clavicle
Nephrocalcinosis-loads of calcium in kidneys
Define:
- primary Hyperparathyroidism
- secondary Hyperparathyroidism
- tertiary Hyperparathyroidism
Primary Hyperparathyroidism
-excess PTH independant of Ca2+ levels
Secondary Hyperparathyroidism
-excess PTH in response to chronic hypocalcaemia
Tertiary Hyperparathyroidism
- prolongued secondary hyperparathyroidism
- when secondary is treated, the PTH baseline is still increased → HYPERcalcaemia
What would the PTH/ calcium/vit D/phosphate/ALP be in primary/secondary/tertiary hyperparathyroisim?
osteomalacia?
Primary
↑PTH / ↑Ca2+ / ↑vitamine D / ↓phosphate/ ↑ALP
Secondary:
↑PTH /Ca2+↓ or normal /↓Vitamin D/ ↑phophate
Tertiary
↑↑PTH / ↑ Ca2+/ ↓Vitamin D/↓phosphate if CKD normal phosphate (if kidneys transplant)/ ↑ALP
Osteomalacia
↓Vit D ↓Ca ↓Ph ↑PTH ↑ALP
What is secondary hyperparathyroidism?
What is the most common causes?
SECONDARY HYPERPARATHYROIDISM
- excess PTH in response to chronic hypocalcaemia
- causes hyperplasia of PT gland to compensate for low calcium
Common causes:
- CKD (common)
- ↓Calcitrol (active vit.D)> ↓GI tract Ca2+ absorption> ↓free calcium ions
- Vitamine D defficiency (↓Calcitrol)
- lack of sunlight, poor vitamin D intake
-Bowel absorption problems/liver problems
What are the symptoms of secondary hyperparathyroidism?
SECONDARY HYPERPARATHYROIDISM
(symptoms of low calcium)
- Starts with confusion/tiredness
- Tetany – twitching, cramping, spasms
- Perioral paraesthesia
- Siezures
- Trousseau (BP cuff and cramp)
- Chvostek’s sign (tap parotid, causing facial twitch)
What is the treatment of secondary hyperparathyroidism?
SECONDARY HYPERPARATHYROIDISM
- Correct cause – treat CKD or Vitamin D def (Ergocalciferol-high dose. Colecalciferol for maintenance)
- Cinacalcet if PTH ≥ 85
What is tertiary hyperparathyroidism?
What is the treatment of tertiary hyperparathyroidism?
Tertiary hyperparathyroidism
-prolongued secondary >HYPERcalceamia
Treatment: surgery to remove hyperplasia glands and return PTH to baseline
What is the 2nd most common cause of hypercalceamia?
Cancer is 2nd most common cause of hyperparathyroidism (after primary HP)
What would the calcium/phosphate/PTH/phosphate/ALP be in hypercalcemia due to malignancy?
- ↑Ca2+ and ↓phosphate (↑Urine phosphate)
- normal or ↓ (compensation) PTH
- ↑Serum ALP
- low albumin
What would you see on ECG with HYPER calceamia?
ECG IN HYPERCALCEMIA Most common: Short Q/T interval -wide T-waves -BBB -prolonged PR interval -arrhythmia -J waves
Treatment of hypercalcemia of malignancy
HYPERCALCEMIA MALIGNANCY
Fluids → bisphosphonates
STEP 1: Fluids
- IV Fluids (rehydration)
- normal Saline 0.9% 3-4L/day (rate 250ml/hr) with adequate K+ (20 or 40mmols)
- administer with Furosemide if ↑risk of fluid overload (also promotes ↑Ca2+ excretion ☺)
STEP 2 IV BISPHOSPHONATES
- Zolindronic acid or Pamidronate (inhibit osteoclast bone resorption) if Ca2+ > 3
What are some causes of SECONDARY hyperlipidemia?
Secondary hyperlipidaemia
- Cushing’s synd
- Hypothyroidism
- Nephrotic syndrome
- Cholestasis (↓bile)
- Anorexia nervosa
- Alcohol
- Obesity
What are some signs of hyperlipidemia?
HYPERLIPIDEAMIA
- Premature corneal arcus – white grey opaque ring in corneal margin
- Tendon xanthomata – hard, non-tender nodular enlargement of tendons (knuckles and Achilles
- Xanthelasma – yellow plaques around eye
What bloods would you get in hyperlipideamia?
Hyperlipideamia (get full lipid profile)
- total cholesterol (refer to speilaist if >9)
- HDL-C
- non HDL-C
- Triglycerides
Phaeochromocytoma
Features?
Test?
Treatment?
Phaeochromocytoma (features are typically episodic)
- hypertension (around 90% of cases, may be sustained)
- headaches
- palpitations
- sweating
- anxiety
Tests
-24 hr urinary collection of METANEPHRINES
Treatment:
-Surgery is the definitive management.
-The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
What is the negetive feedback loop of thyroid hormones?
Hypothalamus produces thyotropin releasing hormone (TRH)
- Anterior pituitary gland produces TSH
- Thyroid gland produces T3 and T4 (thyroxine-converted to T3 in cells
What are the normal effects of T3 (more active hormone)
T3 normal functions ↑Basal metabolic rate ↑glucose ↓cholesterol ↑Cardiac output and contractility ↑vasodilation ↑gut motility ↑Bone resorption → thins bones ↑sympathetic nervous system -fetal and childhood growth
What are the autoimmune causes of primary HYPOthyroidism ?
Which one presents with a goitre?
Autoimmune primary HYPOthyroidism
- Hashimottos (most common cause of hypo in UK)
- hypertrophy + hyperplasia therefore causes goitre - Atrophic hypothyroidism (common in elderly)
What is the most common cause of HYPOthyroidism worldwide?
Iodine deficiency most common cause of HYPOthyroidism world-wide
what drugs cause HYPOthyroidism
HYPOthyroidism causing drugs
- antithyroid drugs
- amiodarone (can cause Hyper and hypo)
- iodine
- lithium
HYPOthyroidism symptoms
HYPOthyroidism symptoms
- Tiredness + lethargy
- Depression
- Cold
- Weight gain but decreased appetite
- Constipation
- Menorrhagia
- Poor cognition
- Hoarse voice
- Myalgia + Cramps
- ↓Libido
- ↓Memory + ↓Cognition → dementia like symptoms
What are the signs on examination of hypothyroidism (remember the mnemonic)?
BRADYCARDIC
Bradycardia ↓HR Reflexes relax slowly Ataxia (cerebella) Dry thin hair and skin (loss of lateral eyebrow) Yawning Cold Ascites, pericardial or pleural effusion Round puffy face Defeated demeanour Ileus Cystic fibrosis
Treatment of hypothyroidism?
Who should you start at lower doses? and why?
- Thyroxine replacement (levothyroxine) T4 is then converted to T3 in periferies (prescribed by GP)
- (if elderly/IHD start lower dose and titrate up because it can precipitate angina/MI and worsen osteoporsosis)
Thyroid function tests
- primary hypothyroidism
- secondary hypothyroidism look like?
- subclinical hypothyroidism (and your plan)
Thyroid function tests
1. Primary HYPOthyroidism
TSH = high (compensate)
T4/T3 = low
- Secondary HYPOthyroidism (pituitary tumour/hypothamous trauma)
TSH = normal or low if there is a lack from pituitary
T4/T3 = low - Subclinical hypothyroidism
TSH high
T3/T4 normal
RE-TEST in 2-4 months to see if TSH still high (would also want to look at TPO to see if you’ve caught HYPOthyroidism early)
What antibodies are found in hashimottos?
What antibodies are found in Graves?
Anti-TPO Ab=hashimottos (hypo)
TSH-receptor stimulating Ab (TRAB) GRAVES (hyper)
What is the most common cause of hyperthyroidism?
Explain what it is?
Grave’s disease
- Autoimmune disease caused IgG antibodies binding to TSH receptors
- Causing thyroid enlargement and increase in T3 and T4
- Also bind to antigens in extra ocular muscles (inflammation/proptosis/exopthalmous)
What is the name of ultimate hypothyroid state before death?
Management?
Myxodema coma (ITU and IV T3 or levothryoxine AND IV corticosteroids coexisting adrenal insufficiency has been excluded)
Causes of HYPERthyroidism?
- Graves disease
- Toxic multinodular goitre=multiple nodules that secrete thyroid hormones
- Toxic adenoma = solitary nodule producing T3 and T4
- Ectopic thyroid tissue - metastatic follicular thyroid cancer
What causes a painful goitre?
Treatment?
- Painful Goitre – subacute De-Quevain (following on from viral infection.
- Self limiting-treat with NSAIDS
How do you treat Graves disease
What is curative treatment?
Graves disease
-Carbimazole for 12-18 months!!! (relapse high)
(either on its own or part of a BLOCK AND REPLACE therapy with levothyroxine-less relapse)
-Aim is to try and make euthymic then just reassess
-Surgery diffinitive (more rarely done now)
What are some dangerous side effects of carbimazole?
Agranulocytosis-low neutrophils which can lead to sepsis
What are TFTs like in hyperthyroidism? (primary, secondary, subclinical)
PRIMARY HYPERTHYROIDISM
TSH = low (suppressed)
T4 + T3 = high
SECONDARY HYPERTHYROIDISM (TSH secreting pituitary adenoma) TSH= high T3/T4 high
SUBCLINICAL HYPERTHYROIDISM
TSH = low (suppressed)
T4 + T3 =normal
(recheck in 2 months)
What are graves specific signs? (4)
Graves specific signs
- Eye disease (exophthalmos, opthalmoplegia (paralysis of muscles within or surrounding eye → diplopia)
- Pretibial myxoedma – oedematous, discoloured swelling above lateral malleoli (also seen in hypothyroid)
- Thyroid Acropatchy – extreme manifestation with clubbing, painful finger + toe swelling
- Also Bruits (due to ↑vascularity in thyroid)
What is a hyperthyroid crisis called ?
What could precipitate it?
- Thyroid storm
- Precipitated by surgery/radioactive iodine (also infection, MI, trauma)
How does a thyroid storm present?
Severe hyperthyroidism: Fever AF Diarrhoea + vomiting Agitation>confusion>coma
Treatment of a thyroid storm?
- THYROID BLOCKING
- propylthiouracil - CORTICOSTEROIDS (stops the peripheral conversion of T3/T4). E.g. hydrocortisone
- SYMPTOM CONTROL
- IV propanolol or CCB
- IV fluids
- Paracetamol (anti-pyrexial)
1st line treatment for Toxic nodular goitre?
Toxic nodular goitre
1st line: radioactive iodine
(taken up preferably by autonomous nodule)
(toxic afterwards-stay clear of kids/pregnant ppl)
-surgery/drugs if radioactive iodine unsuitable (pregnancy/lactation) or if compressive symptoms
Thyroid function tests
1. ↑TSH and ↑T3/T4
- ↓TSH ↓T3/T4
- ↑TSH and ↑T3/T4
- Pituitary tumour (rare)
- Poor compliance with thyroxine, focus on TSH for monitoring (T3/T4 can be normal) - ↓TSH ↓T3/T4
- Sick euthyroid (sick hospital inpatient)
- Pituitary insufficiency
How does thyroiditis present?
What causes it?
Whats the treatment?
ACUTE THYROIDITIS
- Acute heat intolerance, tremor, neck discomfort
- Viral: de Quervians
- Drugs (amiodarone)
- Postpartum
Treatment: self limiting
Complications in hyperthyroidism?
Complications in hyperthyroidism
- AF
- High output HF
- Thyroid storm (precipitated by surgery, trauma or infection)
- Osteopenia/osteoporosis
- Upper airway obstruction (goitre)
- Visual effects/corneal ulcers
Cushings syndrome vs cushings disease?
Cushing’s syndrome
-the clinical state produced by chronic glucocorticoid excess (most common cause-exogenous steroids)
- Cushing’s disease
- excessive ACTH from the pituitary (due to a benign pituitary adenoma)
Aside from Cushing’s disease, what is another ACTH-dependent cause of Cushing’s syndrome?
Ectopic ACTH tumours e.g. small cell lung cancer
The classical symptoms of Cushing’s are absent in this one
What does a Cushing’s person look like?
Cushings Catabolic (inc androgens) -Skin thinning -Myopathy -Purple abdominal striae -Muscle/tendon wasting - recurrent Achilles tendon rupture -Osteoporosis -Acne -Hirsutism -Gonadal dysfunction - erectile dysfunction, irregular periods (↓GRH)
Glucocorticoid
- Diabetes/hyperglycaemia (↑Glucose)
- Infection prone + Poor healing wounds (↓inflam mediators)
- Truncal obesity/intrascapular fat pad
- Moon face
Mineralcorticoid
- HTN (↑BP)
- Hypo↓kalmia (opposite of addisons)
*Depression /Psychosis
What do you need to confirm a diagnosis of Cushing’s?
Confirm diagnosis with raised plasma cortisol
What is the first-line test (after establishing a raised plasma cortisol) for Cushing’s?
1st line Overnight dexamethasone suppression test
- give 1mg dexamethasone at midnight
- do serum cortisol at 8am
- normally, cortisol suppresses to <50nmol/L
Cushing’s = NO SUPPRESSION – cortisol remains high
False + ve in obesity, alcohol, phenytoin, rifampicin
What is an alternative to the overnight dexamethasone suppression test?
24 hour urinary free cortisol
- 3 collections
- also measures creatinine excretion
- diagnosed in 2+ collections measure cortisol excretion as >3 times the lab upper limit of normal
What is 2nd line test (if 1st line tests were abnormal) for Cushing’s?
48 hour dexamethasone suppression test
- give dexamethasone 0.5mg 4 times per day for 2 days
- measure cortisol at 0 and 48 hours
Cushing’s = NO SUPPRESSION
Apart from oral steroids, what are some other ACTH-independent causes of Cushing’s?
- Adrenal adenoma (do an adrenalectomy)
- Adrenal nodular hyperplasia
What test can you do to localise the cause of Cushing’s? (whether or not ACTH dependent)
Plasma ACTH
- LOW in cushings syndrome (adrenal tumour)
- HIGH in Cushings disease (ACTH-dependent cause)
How do you distinguish between a pituitary cause or ectopic ACTH producing cause of Cushing’s?
High dose dexamethasone suppression test
- pituitary adenoma >cortisol suppressed
- ectopic >no change
How does a growth hormone-producing tumour (pituitary adenoma) in children or adults?
Children = gigantism (most commonly prolactinoma) Adults = acromegaly
What visual defects do you get from a pituitary adenoma and why?
Bilateral temporal hemianopia due to compression of the optic chiasm
What other condition can be caused by pituitary adenoma?
- Diabetes insipidus (which is not related to diabetes mellitus).
- Characterised by polydypsia and polyuria (nocturia)
- It is due to reduced ADH secretion from the posterior pituitary
- Diagnostic test used is the water deprivation test.
When treating hypothyroidism secondary to hypopituitarism, what must you give before levothyroxine and why?
Steroids because thyroxine could precipitate and Addisonian crisis (=adrenal crisis)
What visual field problem would you see in pituitary adenoma?
PITUITRY ADENOMA-VISION
-bilateral temporal hemianopia a.k.a tunnel vision
What antibody is seen in Addisons adrenal insufficiancy?
ADDISONS: 21 hydroxylase Ab + ve
What is Conns syndrome?
What are the signs?
What is the 1st line investigation
Conns is a cause of primary hyperaldosteronism
HYPERTENSION and HYPOkalaemia (can be normal)
1st line investigation
- renin-aldosterone ratio will be high-renin high to compensate for low aldosterone (ideally, this should be taken whilst the patient is not taking any antihypertensives)
Treatment:
- surgery if adenoma,
- aldosterone antagonist e.g. spironolactone if hyperplasia
What is diabetes insipidous? (2 types)
Symptoms?
Diabetes insipidus
- issues with ADH action:
a) Cranial (HYPO ADH secretion)
b) Nephrogenic (Insensitivity of ADH) e.g. lithium
Symptoms of diabetes insidious?
Diabetes insipidus symptoms
- thirst
- polyuria (>3 litres per day)
- nocturia
What is the serum and urine osmolarity in diabetes insipidus?
Treatment?
Diabetes insipidus
↑Serum osmolarity (concentrated-hypernatremia)
↓Urine osmolarity (not very concentrated)
Tx: desmopressin (causes hyponatreamia)
What is the diagnostic test for diabetes insipidus?
Diagnostic test used is the water deprivation test. (deprived water, given ADH, reassessed)
(although if taking lithium-do Ca2+ first to rule out hypercalceamia)
What is the diagnostic test for acromegally?
Acromegally
-increased insulin like growth factors
After a water deprivation test what would you see for both nephrogenic and neurogenic diabetes insipidious?
After 8 hour water deprivation test
-both neurogenic and nephrogenic URINE OSMOLARITY would be LOW (normal responce would be to increase ADH to retain water but they cant)
After desmopressin test what would you see for both nephrogenic and neurogenic diabetes insidious?
After desmopressin test
- Neurogenic URINE OSMOLARITY would INCREASE (cos now they have ADH)
- Nephrogenic URINE OSMOLARITY would still be LOW (cos they dont know how to use ADH) e.g. lithium
What does HIGH osmolarity mean?
High osmolarity=high concentration
What are periods like in hyper/hypo thyroidism?
Hypo=irregular/heavy :(
Hyper=AMMENORREA no periods :)
How do we monitor responce to thyroxine?
Look at TSH (aim for 0.2-2)
- aim for a LOWER TSH than the general population
- If still high> bad compliance or not high enough
What tumours commonly metastasise to bone?
- Myeloma/melanoma
- Breast
- Lung (squamous most commonly) /lymphoma
- Thyroid
- Kidney
- Prostate
What is calcitonin?
Produced by the thyroid gland to LOWER CALCIUM by preventing osteoclasts
What is cholecalciferol?
Used for Vit D defficiency maintenance
What is Cinacalet?
When is it used?
REDUCES PTH!!!
- MOST COMMONLY used in primary hyperparathyroidism when parathyroidectomy is inappropriate!!!!!!
- Also used in secondary hyperparathyroidism (as well as treating cause)
What are some causes of hyPOparathyroidism?
Rarer than hyper
- Following thyroid surgery/radiotherapy
- Digeorge syndrome (parathyroid/cardiac/cleft palate)
- Infiltrative (Wilsons/haemachromatosis)
Treatment of addisonian crisis?
Addisonian crisis
1) STEROIDS
- 100mg hydrocortisone IV
2) SUGAR
- 200mg hydrocortisone IV in 5% glucose
3) SALINE
- 500ml 0.9% NaCl
- then rehydrate 3-4L over 24 hours
4) SEARCH FOR CAUSE
(suddenly stopped steroids/illness/surgery/trauma)
1st line treatment for micro- and macroprolatinomas?
Cabergoline (a dopamine agonist) is the first-line treatment for a micro- and macroprolatinomas.
What drug can be used to treat high cortisol in bushings disease
Metyrapone
If you cant find source of cusgings disease, what can you do?
Bilateral adrenalectomy
can also give adrnenolytic drug mitotane
What is a complication of Bilateral adrenalectomy
Nelsons syndrome (pituitary adenoma expands due to removal of adrenals-do MRI and monitor ATCH follow up after adrenalectomy)
- Dark
- Head
- bitemporal hemionopia
What is the treatment for prolactinomas (pituitary adenomas)
Carboligine (or bromocriptine)
Dopamine agonists
