Endocrinology

Question 1

HYPERTHYROID PRESENTATION

i) what would be seen in relation to weight and appetite?
ii) what may the patient be intolerant to?
iii) how may periods be affected? what type of mood may be seen?
iv) how may bowel habits be affected?
v) name two important things to ask about in the history

Answer 1

i) weight loss with increased appetite
ii) heat intolerant
iii) oligomenorrhoea (sparse/infrequent) with anxiety/panic
iv) diarrhoea or increased frequency
v) ask about pregnancy and family hx of thyroid disease

Question 2

HYPERTHYROID - EXAMINATION

i) name two things that may be seen in the hands
ii) two things that may be felt in the pulse
iii) name two things seen in the neck? do you expect to see enlarged LNs?
iv) name four things that may be observed in the eyes? what is the one part for the eye that may not be inflammed?

Answer 2

i) see fine tremor / sweaty hands
ii) feel sinus tachy or AF in pulse
iii) neck - goitre that moves on swallow, bruit (graves), dont expect to see large LNs
iv) eyes - lid retraction, proptosis, diplopia, inflamm of everywhere apart from eye itself

Question 3

THYROID FUNCTION TESTS - HYPERTHYROID

i) what TSH and FT4/3 levels would be expected in hyperthyroid?
ii) which antibodies should be tested for?
iii) what does the patient have if they have thyroid eye disease?

Answer 3

i) see low TSH and high FT4/3
ii) test for thyroid auto antibods (TRAB) > indicates graves thyrotoxicosis
iii) TED - graves thyrotoxicosis

Question 4

HYPERTHYROID TREATMENT

i) give three broad options for treatment
ii) give two complications that may arise if not treated?

Answer 4

i) medical, radioactive iodine, surgery
ii) complications - dysrhythmias, osteoporosis

Question 5

TOXIC MULTINODULAR GOITRE

i) will the patient be hypo or hyper thryoid?
ii) what treatment would be reccomended?
iii) what type of scan would be useful to diagnose?

Answer 5

i) hyperthyroid - nodules produce thyroid hormone
ii) radioiodine treatment
iii) thyroid uptake (isotope) scan

Question 6

POST PARTUM THYROIDITIS

i) what is it? hat three phases are seen?
ii) is it usually self limiting?
iii) does it respond to anti thyroid drug therapy?
iv) is it suitable for radio iodine therapy

Answer 6

i) transient thyrotoxic phase then hypothyroid phase, then euthyroid
ii) usually self limiting
iii) does not respond to anti thyroid drug therapy
iv) not suitable for RI therapy

Question 7

HYPOTHYROID - HISTORY AND EXAMINATION

i) what weight change may be seen?
ii) what may they be intolerant to?
iii) give three other symptoms
iv) what heart rate may be seen if prolonged/severe?
v) how may reflexes be affected?

Answer 7

i) weight gain
ii) cold intolerance
iii) tiredness, constipation, menorrhagia
iv) bradycardia
v) slow relaxing reflexes - upstroke of reflex normal but long to relax

Question 8

HYPOTHYROID - INVESTIGATIONS AND TX

i) what antibody may be investigated for?
ii) what is the treatment? in which two groups of patients would you start on a lower dose?
iii) how long should be waited before repeating thyroid function tests if the patients symptoms are not improving?

Answer 8

i) look for thyroid auto antibody (TPO)

ii) treat with thyroxine (T4) - start on 100ug
- if very elderly/ischaemic heart disease - use lower dose (25ug)

iii) wait 6 months before repeating TFTs, even if the patient doesnt feel better (there can be a lag phase before patients feel better)

Question 9

HYPERCALCAEMIA

i) what symptoms are usually seen in mild/mod disease? how is it usually detected?
ii) what symptoms may be seen in severe disease? (stones, bones, abdo gorans, psychic moans)
iii) how may the PT gland be acting in hypercalc?

Answer 9

i) mild/mod = usually no symptoms
- detected on routine blood testing

ii) severe - stones (kidney stones), bones (bone pain), abdo groans (GI symptoms), psychic moans (lethargy, depression, confusion)
iii) primary hyper parathyroidism (autonomous function of PT gland)

Question 10

HYPERCALCAEMIA - FURTHER INVESTIGATIONS

i) what may you screen for with US? what condition can be screened for with a DEXA scan?
ii) what group of people is surgery reserved for?
iii) what is 1st, 2nd and 3rd line methods for pre op localisation of a parathyroid adenoma?
iv) would a mild/mod case with no symptoms or end organ damage be treated?
v) what calcium levels would indicate treatment is needed?

Answer 10

i) screen for end organ damage eg renal stones and osteoporosis
ii) surgery for young people (under 50)
iii) pre op loc - 1st line neck US, 2nd line isotope (sestamibi) scan, 3rd line 4D neck CT
iv) no treatment if mild/mod with no symptoms
v) calcium concentration >2.85

Question 11

HYPERCALCAEMIA TREATMENT

i) what is the only curative option?
ii) what two things should be monitored in surveillance?
iii) what can be used to monitor bone mineral density?
iv) what should be recommended for - fluid intake? calcium intake? vitamin D intake?

Answer 11

i) surgery is only curative option
ii) monitor calcium and renal function every 12 months and do a DEXA scan 2 yrly
iii) use DEXA to monitor bone mineral density
iv) good fluid intake to reduce risk of kidney stones, normal dietary calcium intake (dont restrict), vit D supplements to protect the bones

Question 12

HYPERCALCAEMIA AND MALIGNANCY

i) what type of patients is this usually seen in?
ii) what type of malignancy is it seen in?
iii) what is it usually due to?
iv) what PTH levels will be seen?

Answer 12

i) usually seen in very unwell patients
ii) metastatic malignancy
iii) usually due to PTHrP (PTH related protein - paraneoplastic peptide)
iv) see supressed levels of PTH

Question 13

OTHER CAUSES OF HYPERCALC

i) give three others causes of hypercalcaemia
ii) what levels of PTH may be seen? (2)

Answer 13

i) granuloamtous disease/lymphoma/multiple myeloma/familial hypocalcuria (mut in calcium sensing receptor)
ii) PTH may be low or inappropriately normal

Question 14

OSTEOMALACIA

i) what calcium levels will be seen?
ii) what is lacking in OM? how can this be tested?
iii) what could be a DD?
iv) how is it treated?

Answer 14

i) low calcium levels
ii) lack of vitamin D (from skin/dietary) - can they get up from a chair without using arms? eg is there proximal myopathy
iii) DD - malabsorptive eg coeliac
iv) treat with calcium and vitamin D replacement

Question 15

HYPONATREMIA

i) what medication should be checked for in patients presenting with hyponat?
ii) what is the main thing you look for on examination? what would be seen in each case?
iii) name four further tests you would order

Answer 15

i) look to see if patient is on diuretics

ii) O/E - is the patient hypo/eu/hypervolaemic
- hypovol = tachycardia, orthostatic HTN
- hypervol - oedema, ascites, raised JVP

iii) further tests - plasma osmolality, urine osmolality, urine Na+, TFTs, 9am cortisol

Question 16

T1DM

i) what is it? what is the genetic concordance in twins? when does it usually present?
ii) name three presenting features? what blood glucose is seen? how may it present acutely? how is it dx? does C peptide and auto ABs confirm dx? when should the patient not be screened?
iii) what may be seen on bloods? name three other RF? what should be done if the patient is symptomatic (weight loss)? (3) name three auto antibodies that may be positive?
iv) what treatment should be offered first? what is first line insulin treatment? what is second line? how often should glycaemic control be checked?

Answer 16

i) autoimmune/idiopathic destruction of panc beta islet cells, low genetic concordance in twins
- Usually presents in childhood/puberty

ii) polydipsia, polyuria, weight loss, ketosis,
* Raised venous glucose (>7mmol/L fasting or >11.1mmol/litre random),
* May present acutely with DKA
- Dx on clinical grounds - what is the pt presenting with?
* C peptide & diabetes auto Abs (doesn’t confirm dx)

iii) Hyperglycaemia, ketosis, rapid WL, age <50yrs, BMI <25, family history of AI disease
* May be positive for auto Abs (ICA, IAA, GAD, IA-2A)
* Microalbuminuria, decreased renal function
* Random venous >11mmol/l
* Fasting plasma glucose >7mmol/L
* 2 hour post OGTT >11.1mmol
* HbA1c >48mmol/mol
* dont screen during asymptomatic phase
IF PT IS SYMPTOMATIC (weight loss)
* Random plasma glucose, Fasting plasma glucose, 2 hour plas glucose (2hrs post OGTT) and HbA1c

iv) 1) Offer lifestyle advice - diet/exercise
2) Treat with insulin - basal bolus (first line) or mixed regimen (second)
3) Review glycaemic control annually (HbA1c <48mmol is ideal)
4) Follow up for eye/foot/nerve complications

Question 17

COMPLICATIONS OF DIABETES MELLITUS

i) name three acute complications? which type does gastropariesis present with? how is it treated? (2)
ii) which CV conditions are pts more predisposed to? (3) what other dysfunction may they get?
iii) what three things can it predispose to in the kidney? what levels should be monitored annually? (2) what medication should be offered to any pts with nephropathy?
iv) what type of eye disease is seen? name two components of this? what three types of retinopathy can occur? what is maculopathy? name another eye pathology it can pre dispose to
v) what can neuropathy lead to? how does it result in toxic metabolite build up? what distribution does peripheral neuropathy have? name two other manifestations

Answer 17

i) Acute > DKA, HHS/HONK, Hypoglycaemia
- Gastroparesis > T2DM with erratic gluc control/unexplained gastric bloating or vomiting
- Tx with metoclopramide or domperidone

ii) CV > More predisposed to ACS, angina, periph artery disease, 4x likely MI, 2x likely to have stroke
- also get Erectile dysfunction

iii) Nephropathy > Can predis to pap necrosis, renal fail & UTI
- Monitor annually for microalbuminuria (small inc inc in albumin excretion by kidneys, indep risk factor for complicats) - use early am albumin:creatinine ratio (ACR)
- monitor annually for proteinuria (ACR >30mcg)
- Optimise risk factors and offer ACEi therapy to any pts with nephropathy, prot/microalbuminuria, T1DM

iv) Eye disease - microvascular retinal disease > retinal ischaemia & new vessel formation (VEGF)
- Can cause retinopathy - non prolif (mild, microaneursym), moderate (microan, blot haemm, venous bleed), severe (widespread haemm, severe intraretinal abnorm)
- Maculopathy - decrease in vis acuity, macular oedema, retinal thickening, hard exudates
- Cataracts/rubeous iridis (neovasc over iris = red)/glaucoma

v) Neuropathy > major cause of foot ulcers
- Microvasc damage & ischaemmia to vasa vasorum > tox metab bup
- periph sensorimotor neuropathy (glove stocking)
- painful neuritis, amyotrophy (prox lower limb musc weak and wasting), autonomic, mononeuropathy

Question 18

T2DM

i) what is it? what is the twin concordance? what is the precursor?
ii) which group of patients does it commonly present in? (4) is it usually symptomatic? name three symptoms? what is random and fasting glucose levels? HbA1c?
iii) what is first line tx? what is second line? what is given in HbA1c is 58? what if it is >58?

Answer 18

i) Decreased insulin secretion with or without Insulin resistance, high concordance in twin studies
- Progresses from impaired glucose tolerance/impaired fasting glucose tolerance

ii) Usually presents in older patients, obese, poor diet, sedentary lifestyle
- Usually asymptomatic but can present with complications eg MI
- can px with Polydipsia, polyuria, High BP and lipid levels
- random >11mol/l, fasting >7mmol/l, HbA1c >48mmol

iii) Individualised care plan
1) Lifestyle mod (diet, weight control, exercise, BP control)
2) Monotherapy (metformin - GI SEs)
3) HbA1c = 58 = dual therapy (Met + DDP4/pioglitazone/SU/SGLT-2i)
* HbA1c >58mmol = triple therapy or insulin

Question 19

HYPOGLYCAEMIA

i) what is it defined as? what is the most common cause? name the causes in non diabetics? (EXPLAIN)
ii) name four autonomic symptoms that may be seen? name three neuroglycopaenic symptoms? what are the three criteria for dx? (whipples triad)
iii) what should be thought about if insulin levels are high? (2) what cause could be responsible if low insulin/no excess ketones? (2) low insulin and high ketones? (2)
iv) what can be given if episodes are often? what needs to be reviewed? name two ways glucose can be given if concious? how is it given if unconcious? (2)

Answer 19

i) Plasma glucose <3mmol/L
Emergency
* Fasting hypo - most common cause is insulin/sulphonyurea tx
* Non diabetics - EXPLAIN
Exogenous drugs, Pit insuffic, Liver fail, Addisons, Islet cell tumours, Non panc neoplasms

ii) Autonomic - sweating, anxiety, hunger, tremor, palp, dizzy
Neuroglycopenic - confusion, drowsy, visual change, seizure, coma
Three criteria for dx (whipples triad) -
1) hypoglycaemia
2) Symptoms indicative of hypo
3) Resolution of symptoms post treatment

iii) If hyperinsulinaemia - think insulinoma, SUs, insulin injection (no inc in C peptide, only secreted with endog ins)
* If low insulin/no excess ketones - non panc neoplasm or anti insulin receptor antibodies
* low insulin & high ketones - alcohol, pit insuff, addisons

iv) If episodes are often - small high starch meals
* rationalise insulin therapy in DM
* oral/liquid glucose or buccal glucogel if concious
* if unconcious - 125ml 20% dextorse or 250ml of 10% dextrose or 1mg glucacgon by IM injection

Question 20

DKA

i) what is it? what is it provoked by? (3) what is ketoacidosis? what does DKA occur in relation to excess glucose?
ii) what are the three main signs? name four other symptoms a patient may present with?
iii) what four bloods should be done? name two bedside tests? what imaging?
iv) what two things need to be replaced? what should be given if systolic BP <90? what should be added into fluids? when should K+ replacement start? what type of insulin is given? how often should cap glucose and ketones be checked?
v) name four complications? what type of insulin can patient be put on once eating and drinking?

Answer 20

i) Medical emergency 2nd to abso insulin defic/resistance
* Provoked by poor tx adherence, infection, trauma, illness
* Ketoacidosis = alt metab pway used in starvation states > prod acetone
* DKA = excess glucose but no ins so cant be taken into cells > body in starvation state

ii) 1) Acidaemia (blood pH <7.3/HCO3 <15)
2) Hyperglycaemia (blood gluc >11)
3) Ketoneaemia (>3mmol)/ketoneuria ++
* gradual drowsy, vomiting, dehy (T1), vom, abdo pain, polydip/uria, ketotic breath, coma

iii) Urine: ketones and glucose, MCS, Cap glucose and ketones, VBG: acidosis + ↑K, Bloods: U+E, FBC, glucose, cultures, CXR: evidence of infection

iv) Replace volume and correct metabolic defects
* Give K+ replacement (K+ shuttled for H+)
* Large bore cannula - fluid (1L 0.9% saline if systolic BP <90) more until SBP >90
- Then: 1L over next 2h, 1L/2h, 1L/4h, 1L/4h, 1L/6h
- Add 10% dextrose 1L/8h when glucose <14mM
- Start Potassium Replacement in 2nd Bag of Fluids
* Add fixed rate insulin infusion (actrapid)
* Check cap glucose & ketones hourly

v) Cerebral oedema
* aspiration pneumonia
* hypokalemia
* hypomagnesia
* hypophosphatemia
* thromboemolism
- patient can be transferred to sub cut insulin once eating and drinking

Question 21

HYPEROSMOLAR HYPERGLYCAEMIC STATE

i) how is it characterised? (3) what type of DM does it typically occur with? name three things that ppt it? what is pH/ketones/insulin levels? why are they profoundly dehydrated? which group of patients does it commonly present in?
ii) name two key symptoms? what will the patients volume status be? name four other symptoms?
iii) what will blood glucose be? what will be seen in the urine? (2) what will serum osmolality be?
iv) what is the main aim of treatment? how is this done? what is given to prevent clots? how is insulin given? when should K+ replacement be given?
v) what levels of glucose/plasma osmolal are seen once resolved? what else is improved? what insulin is given to pt before weaning off IV insulin?

Answer 21

i) characterised by profound hyperglycaemia (glucose >30 mmol/L hyperosmolality , and volume depletion in the absence of significant ketoacidosis (pH >7.3 and bicarbonate >15 mmol/L)
- Typically occurs as complication of T2DM - ppt by disease state/illness
* can be first presentation of DM
* pH remains above 7,3 and ketones are absent low (no acidosis/ketosis)
* there is some insulin but not enough
* hypergly > wee out glucose > pull water with it = profound dehy
* Patients are often elderly

ii) Dehydration & profound hyperglycaemia (>33)
* Hyperosmolality (due to hypergly)
* Hypovolaemia in absence of ketoacidosis
- also get Muscle cramps and confusion, profound weakness, weight loss, polydip/uria

iii) Very high blood glucose
* Urine - glucose with low/absent ketones
* serum osmolality = high (usually very tight control)

iv) Main aim of tx is to correct profound dehydration (IV 0.9% NaCl/dextrose when gluc less 15)
* Give LMW heparin ro prev clots
* IV Actrapid insulin - fixed rate
* K+ replacement if <5.5

v) Resolved : Gluc <16.7, plasma osmolal <315, improved mental status
* Give subcut insulin before eweaning patient off IV insulin

Question 22

SIADH

i) what is it? name four causes? what two things does it result in? why is there no oedema?
ii) what sodium status is seen? what is the osmolality of urine? what is plasma osmolarity?
iii) what will serum sodium levels be? name two other causes for this?
iv) what ultimately needs to be treated? what should be done in relation to fluid intake? what drug should be considered if there is no improvement? what other drug may be given?

Answer 22

i) Pathological processes causing inapprop ADH secretion
* Due to malignancy (ectopic ADH prod from neoplastic cells), SCLC, meningitis, surgery
* results in h2o retention + hyponatremia (no oedema due to urinary excretion of Na+)

ii) Hyponatremia (dilutional due to excess water retention) - mild is usually asymp and severe is confusion/drowsy
*Hyperosmolar urine
* Plasma hypo-osmolarity / urine hyper osmolarity

iii) Serum sodium levels will be low - (<135, often incidental finding)
* Other hyponat causes - thyroid/adrenal insuff
* urine osmolality (elevated), urinary Na (>40)

iv) Treat any underlying causes
* Fluid restrict - will help correct hyponat by inc serum sodium
* If no improvement - consider demeclocycline (abx but reduces efficacy of ADH at CD as a SE)
* Consider V2 receptor antagonists in CD (prev ADH working eg conivaptan)

Question 23

CUSHING SYNDROME

i) what is overproduced? name three conditions associated with a higher incidence? what is a common cause? what are 80% caused by? what type of cancer may it be associated with?
ii) name five characteristic signs? how may the skin be affected? (3) how may psych be affected? (2) what BP may be seen? what is there increased risk of? how may periods be affected?
iii) which test is done? when is cortisol tested? what other cortisol test can be done? what do low or high ACTH levels indicate?
iv) what is done if the cause is a pituitary adenoma? what is done if adrenal adencoma? what if given if surgery cant be done?

Answer 23

i) Pathological over production of cortisol
* higher incidence if diabetes, HTN, osteoporosis
* Steroid therapy is a common cause
* 80% caused by pit adenoma secreting excess ACTH
* 10% caused by a cortisol secreting adrenal adenoma
* ACTH secreting tumours can be assoic, assoc with SCLC

ii) Suprascapular fat pads, abdo striae, depression, truncal obesity, easy bruising
* Moon face, buffalo hump
* Skin - thin, fragile, acne, hirsutism
* Psych - depress, anx, irritable, decreased lib
* Vasc - new or worse high BP
* increased risk of fractures
* Reprod - irreg/absent periods, erectile dysf

iii) 1g overnight Dex supress test - test cortisol at 8am and if not supressed then CS
* 24hr free urine coirtsol - three collections but can be difficult
* Low ACTH levels = adrenal pathology
* High ACTH levels = do high dose (8g) dex test if >50% supress with high dex = CS pit source, if <50% supress = ACTh secreting tumour

iv) If pit adenoma (80%) - trans-sphenoidal sx resection + GC support
* if ectopic tumour (adrenal adenoma) - adrenalectomy w GC support
* If cant do sx - use steroidgenesis inhibitor (mifepristone) less effective than sx

Question 24

ADDISONS DISEASE

i) what is it? what is it usually caused by? what is most common cause worldwide? how may it present acutely? explain
ii) name three symptoms? what is it often associated with? (3) what electrolyte levels are seen - sodium, glucose, calcium, potassium? how is skin pigmentation affected?
iii) what may be seen on U&Es? (3) what hormone test should be done early in the morning? what is a short synacten test? what will it show in AD? what plasma ACTH levels are seen?
iv) name two things that need to be replaced? how is this done? what needs to be given in minor illness/surgery to avoid crises?

Answer 24

i) Primary adrenal insufficiency (usually due to AI destruction of the gland)
* TB is most common cause worldwide
* Can present acutely w addisonian crisis - ppt event eg illness > inc demand for MC/GC = shock and hypogly

ii) Fatigue, weight loss, depression
* Assoc with other AI conditions eg vitiligo, pernicious anaemia, hashimotos
* Electrolyte imbalance - hypnonat, hypogly, hypocalc but hyperkal (in primary insuff)
*Hyperpigmentation - espec in buccal mucosa & palmar creases

iii) U&E - hyponat/calc/gly but hyperkal
* Early am serum cortisol - <100-500ml = further investigation (if >500 probs not adrenal insuff)
* Short synacthen test (analog of ACTH) - ig adrenal insuff then cortisol levels don’t rise
* Plasma ACTH - ACTH levels are high but cortisol is low

iv) Replace GC/MCs - give hydrocortisone/fludrocortisone
* Hydrocortisone doses inc 2-3x IM/IV in minor illness/surgery to avoid crises

Question 25

CONNS SYNDROME

i) what is it? what is the primary cause? what is a secondary cause? how does it present in relation to sodium, potassium and blood pressure?
ii) by which mechanism does this occur? what two things may present if CS is severe and prolonged?
iii) name three symptoms? what will be shown on U&E? (3) what will the aldosterone:renin ratio be? is this always the case? which drug should be stopped before testing the ratio?
iv) what is first line therapy for primary disease? when is medical therapy first line? name three drugs that may be used

Answer 25

i) Overproduction of aldosterone
* Primary - due to adrenal adenoma/70% due to bilat adrenal hyperplasia
* Secondary due to overproduction of renin
- Classical presentation of hypernatremia, hypertension, hypokalemia (K+ may be normal)

ii) excess aldo prod > excessive sodium reabsorption via ENaC sodium channels within the distal nephron, leading to hypertension and suppression of renin-angiotensin II. Urinary loss of potassium and hydrogen ions, exchanged for sodium at the distal nephron, may result in hypokalaemia and metabolic alkalosis if severe and prolonged

iii) Headaches, lethargy, muscle cramps
- U&Es - hypernat, hypokal, alkalosis
* Aldo:renin = low renin and high aldo (normal in 2 disease) aldo neg fback to renin
* stop spironolactone before testing

iv) primary hyperaldo (conn) - adrenalectomy is first line
* if caused by bilat adrenal hyperplas then medical therapy is first line - use aldo antag eg spironolactone, eplerenone, amiloride (aka K+ sparing diuretics)

Question 26

HYPERPARATHYROIDISM

i) what is it? how is it confirmed biochemically? name four symptoms? name two things there may be a history of? what may be found in the neck?
ii) what is the cause in 80% of cases? name four risk factors?
iii) what may serum calcium be? what PTH levels will be seen? urinary calcium levels?
iv) what surgical procedure is first line? which drug class may also be given? what can be given if the patient has osteoporosis?

Answer 26

i) Primary hyperparathyroidism (PHPT) is an endocrine disorder in which autonomous overproduction of parathyroid hormone (PTH) results in derangement of calcium metabolism
- dx is confirmed biochemically with synchronous elevation of serum calcium and inappropriate elevation of parathyroid hormone (PTH).
- Depression, cognitive changes, change in sleep pattern, fatigue, and myalgia or muscle weakness
- There may be a history of nephrolithiasis or low bone mineral density.
- Physical examination is usually normal, but examination of the neck is essential to look for a hard, dense mass, suggestive of parathyroid carcinoma

ii) over-production of PTH is due to a single parathyroid adenoma and, less commonly, multi-gland involvement may occur
- RFs - female sex. age ≥50-60 years, family history of PHPT, multiple endocrine neoplasia (MEN)

iii) elevated serum calcium,
- inappropriately unsuppressed serum intact PTH levels
- normal or raised urinary calcium in the presence of normal renal function

iv) parathyroidectomy
- may also give vitamin D if deficient
- osteoporosis > give bisphosphonates
- may just monitor if no indication for surgery

Question 27

HYPOPARATHYROIDISM

i) what causes it? how does this affect corrected serum calcium and phosphate? when do most patients present?
ii) name three risk factors? name four symptoms? what is chvosteks sign - is this a common or uncommon finding? what is trousseau sign?
iii) what serum calcium may be seen? what may be seen on ECG? what may PTH be?
iv) what treatment is given for severe hypocalc (corrected <1.8)? what magnesium levels may also be seen and how is this treated? what is given if asymptomatic
v) what can be given in chronic hypocalcaemia? (2)

Answer 27

caused by relative or absolute deficiency of plasma parathyroid hormone (PTH) synthesis and secretion

• This leads to low albumin-corrected serum total calcium and elevated serum phosphate
• most pts present post-surgery for benign and malignant thyroid disorders, hyperparathyroidism, and laryngeal or other head and neck cancers

ii) RFs thyroid surgery, parathyroid surgery, hypomagnesaemia, moderate and chronic maternal hypercalcaemia
symptoms - chronic alcoholism, malnutrition, malabsorption, diarrhoea. muscle twitches, spasms, cramps
- Chvostek - Ipsilateral contraction of facial muscles when facial nerve is tapped in front of the ear (uncommon finding)
- Trousseau - Painful clasping response of fingers and hands when blood pressure cuff is inflated above systolic blood pressure (uncommon)

iii) low serum calcium, prolonged QT on ECG, low or normal PTH

iv) give IV calcium and parenteral magnesium
- if asymp give oral calcium

v) oral calcium and calcitriol + human recombinant PTH

Question 28

THYROTOXICOSIS

i) what is it? name five symptoms? name hand, neck, face sign? name two things that may be seen if graves disease?
ii) what TSH, T3 and T4 levels will be seen? what causes 60% of thyrotox? name three other causes? name two drugs that can cause it
iii) what two drugs may be given? what can be done if medical tx doesnt work?
iv) name three signs of thyroid storm? name two things that can ppt it? how is it treated?

Answer 28

i) The clinical effect of ↑T4, usually from gland hyperfunction (too much circulating thyroid hormone)
- Diarrhoea, increased appetite but ↓ wt. Sweats, heat intolerance. Palpitations, Tremor, Irritability, Oligomenorrhoea ± infertility
- if graves > exopthalmos and pre tibial myxoedema

ii) low TSH, ↑T4/↑T3
- 60% caused by Graves
- also caused by toxic multinodular goitre, toxic adenoma, hashimoto thyroiditis
- thyroxine and amiodarone can also cause

iii) if symptomatic: β-B (e.g. propranolol 40mg/6h) or Anti-thyroid: carbimazole (inhibits TPO)
- ~50% relapse → surgery or radioiodine (SE: agranulocytosis)

iv) ↑temp, Agitation, confusion, coma, Tachycardia, AF, Acute abdomen, Heart failure
- ppt by Recent thyroid surgery or radio-iodine Infection, trauma
- tx w Fluid resuscitation + NGT, Bloods: TFTs + cultures if infection suspected, give Propranolol PO/IV. Digoxin may be needed
- Carbimazole then Lugol’s Iodine 4h later to inhibit thyroid

Question 29

DIABETES INCIPIDUS

i) what is it? what are the two types? name three causes for each? which type can lithium treatment cause?
ii) name the two main clinical features? what do both forms result in? how does this affect sodium levels? what will urine osmolality be?
iii) which test can be done to aid diagnosis? how does it work? how can central and nephrogenic be differentiated?
iv) how is central DI treated?
v) how is nephrogenic DI treated? why may thiazides be given?

Answer 29

i) direct or relative ADH deficiency (opposide to SIADH)
- nephrogenic (kidney cant respond to ADH) - caused by lithium use, congenital (V2 AQP mutation)
- cranial (ADH isnt produced by post pit) - insults to pit or CNS lesions (surgery, meningitis, head trauam)

ii) polyuria and polydipsia (can also get nocturia)
- both forms result in excretion of dilute urine > hypernatremia (causing excessive thirst)
- low urine osmolality

iii) water deprivation test > deprive pt of water for 8 hours (without DI there will be reduced urine vol and more conc) with DI have high urine volume and low osmol (less conc)
- to differentiate give desmopressin injection after water deprivation (if osmol increases > central DI, if it doesnt > nephrogenic)

iv) central > replace ADH with desmopressin (IV acutely or intranasal for long term use) - measure sodium regularly

v) nephrogenic > harder to treat (cant just replace ADH)
- identify underlying cause (lithium use may be irreversible)
- advise drinking lots of fluid and low sodium diet
- consider thiazides (help increase fluid resorption in PT > help fluid and electrolyte balance and net benefit)