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General Medicine Block > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

production of which protein by the liver is stimulated by GH in order to mediate growth and anabolism in the body?

A

IGF-1 (insulin-like growth factor 1)

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2
Q

define acromegaly

A

a clinical condition resulting from prolonged excessive GH and hence IGF-1 secretion in ADULTS, with loss of normal pulsatile secretion of GH.

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3
Q

most common cause of acromegaly?

A

pituitary adenoma

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4
Q

symptoms of acromegaly?

A 
enlargement of extremities- jaw enlargement=pronagthism, hands and feet- change in ring or shoe size?
bitemporal hemianopia
headaches
sweating increased
tiredness and lethargy
joint pains
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5
Q

signs of acromegaly?

A

facial appearance- coarse features, oily skin, frontal bossing, enlarged nose. deep nasolabial furrows, prognathism, increased interdental separation
deep voice-laryngeal thickeneing
macroglossia
CTS, soft tissue swelling
MSK changes- degeneration in joints leading to OA, generalised myopathy
goitre and other organomegaly

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6
Q

complications of acromegaly?

A

HTN
IHD, CVD, CCF, possible increased prevalence of regurgitant valvular heart disease
insulin resistance and impaired glucose tolerance/DM
OSA- soft tissue swelling in NP region
increase risk of colonic polyps and colonic Ca

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7
Q

dynamic function test for acromegaly?

A

oral glucose tolerance test

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8
Q

what dynamic function test is used in assessing pituitary insufficiency, and what are the contraindications to this test?

A

insulin stress test- insulin given to pt which will reduce glucose in blood, and so normally stimulate increased ACTH and GH levels.
CI in epilepsy as can cause a seizure, and in IHD as MI risk due to stress on heart with catecholamine release.

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9
Q

difference between hyperthyroidism and thyrotoxicosis?

A

thyrotoxicosis- clinical, physiological and biochemical findings in pt with excess thyroid hormones, for any reason e.g. secondary hyperthyroidism- TSH secreting pituitary tumour and in resistance to thyroid hormones.
hyperthyroidism- thyrotoxicosis (symptoms and signs of excess thyroid hormones) due to thyroid hyperfunction.

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10
Q

what ADR of carbimazole must pts with thyrotoxicosis be warned about looking out for symptoms of?

A

agranulocytosis- neutrophils significantly reduced, can lead to dangerous sepsis, also risk of with the antipsychotic clozapine, some NSAIDs and anti-epileptic drugs
warn about develop. of fever, sore throat or mouth ulcers

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11
Q

2 complications to be aware of in management of a hyponatraemic patient?

A

heart failure

central pontine myelinolysis

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12
Q

how is a dehydrated hyponatraemic pt assessed to determine cause?

A

we want to know where fluid being lost from. if urinary Na+ more than 20mmol/L, then Na+ and water are being lost via the kidneys e.g. Addison’s disease, renal failure, diuretic excess or osmolar diuresis e.g. high glucose in DM or urea.
if urinary Na+ 20 mmol/L or less, than Na+ and water are lost other than via kidneys e.g. vomiting, diarrhoea, fistulae, burns, SBO, CF, rectal villous adenoma.

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13
Q

1st consideration in determining cause of hyponatraemia?

A

is pt dehydrated or fluid overloaded

or euvolaemic

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14
Q

how is non-dehydrated hyponatraemic pt assessed?

A

want to know if fluid overloaded or not
if oedematous, pt may have nephrotic syndrome, CCF, liver cirrhosis or renal failure.
if not oedematous, want to know urine osmolality. If >500mmol/kg, then SIADH is the cause. If 500 or less, then causes may be water overload, severe hypothyroidism or glucocorticoid insufficency.

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15
Q

causes of SIADH?

A

malignancy- lung small cell carcinoma, pancreas,prostate, thymus or lymphome
CNS- abscess, stroke, SD or SA haemorrhage, SLE, vasculitis, head injury
Endocrine disease-hypothyroidism- reduced cardiac output triggers excess ADH release from carotid sinus baroreceptors
Drugs- opiates, SSRIs, psychotropics, cytotoxics
Other- trauma, symptomatic HIV

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16
Q

causes of hypoglycaemia?

A

Fasting hypoglycaemia:
most common= insulin or sulfonylurea tment in known diabetic e.g. with increased activity, missed meal, or OD.

if non-diabetic, EXPLAIN:
EXogenous- drugs e.g. insulin, oral hypoglycaemics, beta blockers, ACEIs
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours e.g. insulinoma, and immune hypoglycaemia e.g. in Hodgkin’s disease
Non-pancreatic neoplasms e.g. fibrosarcoma

post-prandial:
gastric/bariatric surgery
type 2 DM

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17
Q

investigation of fasting hypoglycaemia?

A

fingerprick glucose during attack, lab glucose if in hospital
drug history, exclude liver failure
72h fasting may be needed, take blood samples for glucose, insulin, c-peptide and plasma ketones if symptomatic

may be hypoglycaemic hyperinsulinaemia e.g. in insulinoma, sulfonylureas, insulin injection
if insulin low, and no excess ketones, think non-pancreatic neoplasm or anti-insulin receptor antibodies e.g. in Hodkin’s
if insulin reduced and ketones increased, thinck alcohol, pituitary insufficiency or addison’s disease

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18
Q

investigation of post-prandial hypoglycaemia?

A

prolonged OGTT

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19
Q

what is total T4 and T3 affected by in comparison to free T4 and T3?

A

thyroxine binding globulin (TBG)

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20
Q

when is thyronine binding globulin increased?

A

pregnancy
hepatitis
oestrogen therapy

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21
Q

when is TBG decreased?

A 
nephrotic syndrome
CLD
acromegaly
malnutrition
drugs e.g. corticosteroids, phenytoin, androgens
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22
Q

what is sick euthyroidism?

A

in any systemic illness, TFTs may become deranged
typical pattern is for everything to be LOW
should rpt test after recovery

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23
Q

causes of a normal TSH and abnormal T4?

A

changes in TBG
assay interference- due to Abs in serum
amiodarone-used in AF tment
pituitary TSH tumour

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24
Q

pts who should be screened for abnormalities in thyroid function?

A

AF
hyperlipidaemia
DM-on annual r/v
women with type 1 DM during 1st trimester and post delivery
those on amiodarone or lithium-e.g. for bipolar (6 mnthly)
those with down’s, or turner’s, or Addison’s disease (yrly)

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25
symptoms of thyrotoxicosis ( clinical effect of excess thyroid hormone)?
``` heat intolerance weight loss increased appetite diarrhoea sweats palpitations tremor irritability labile emotions oligomenorrhoea with or without infertility- oestrogen antagonised rarely psychosis, chorea, panic, itch, alopecia, urticaria ```
26
signs of throtoxicosis?
``` pulse fast or irregular-AF, SVT warm moist skin fine tremor palmar erythema thin hair lid lag and lid retraction goitre thyroid nodules bruit ```
27
signs of grave's disease?
exophthalmos-appearance of protruding eye, proptosis-eyes protrude beyond orbit, opthalmoplegia-espec. of upward gaze also corneal ulceration, loss of colour vision, papilloedema pt may complain of eye discomfort, grittiness, photophobia, diplopia, reduced acuity, increased tear production ,and optic nerve can become compressed due to afferent pupillary defect-may need decompression-and be wary more likely if eye cannot protrude! pretibial myxoedema- oedematous swellings above lateral malleoli seen over the shins due to excess glycosaminoglycan accumulation in dermis and subcutis of skin, immunological process e.g. anti-TSH receptor antibodies can bind to fibroblasts and stimulate them to increase GAG production thyroid acropachy- clubbing, painful finger and toe swelling, periosteal reaction in limb bones.
28
cause of grave's disease?
circulating IgG autoantibodies which bind to and activate thyrotropin receptors, causing smooth thyroid enlagement and increase hormone prod. espec. T3. react with orbital autoantigens triggered by stress, infection, childbirth
29
causes of thyrotoxicosis?
grace's disease toxic multinodular goitre- must follow symptomatic tment with radioiodine, surgery indicated for compressive symptoms e.g. dysphagia, dyspnoea toxic adenoma- solitary nodule secreting thyroid hormones, 'hot' on isotope scan, rest of gland suppressed, treat with radioiodine ectopic thyroid tissue e.g. metastatic follicular thyroid cancer, choriocarcinoma, struma ovarii-ovarian teratoma with thyroid tissue exogenous- iodine excess e.g. contrast media-thyroid storm, levothyroxine excess-causes increased T4, decreased T3 and thyroglobulin subacute de quervain's thyroiditis- post viral with painful goitre, low isotope uptake on scan, treat with NSAIDs drugs-amiodarone, lithium post partum TB
30
drug tment of thyrotoxicosis?
carbimazole- inhibitor of thyroid peroxidase required for iodination and thyroglobulin molecules. can be titrated e.g. 20-40mg/24hr PO for 4 wks, reduce according toTFTs every 1-2mnths, or block-replace- give with thyroxine. maintain on either in grave's for 12-18mnths, then withdraw beta blocker e.g. propranolol 40mg/6h for rapid symptom control
31
50% of pts likely to relapse after stopping carbimazole tment, what else can be done?
radioiodine surgery- thyroidectomy- but risk of recurrent laryngeal nerve damage-hoarse voice, and hypoparathyroidism, and pt can become hypo or hyperthroid
32
CIs to radioiodine tment in hyperthyroidism?
pregnancy lactation caution in active hyperthyroidism as risk of thyrotoxic storm- hyperthyroid crisis, also precipitated by recent thyroid surgery, infection, MI and trauma
33
signs and symptoms of thyrotoxic storm?
``` increased temperature confusion agitation coma tachycardia AF diarrhoea and vomiting goitre thyroid bruit acute abdomen HF CVS collapse ```
34
complications of thyrotoxicosis?
``` HF- thyrotoxic cardiomyopathy, increased in elderly angina AF OP ophthalmopathy gynaecomastia thyroid storm ```
35
main known RF for thyroid eye disease in Grave's?
smoking
36
action of PTH?
increase osteoclasr activity to relase Ca2+ and PO43- from bones increase Ca2+ and reduce PO43- reabsorption in kidney increase active production of calcitriol for Ca2+ absorption by the gut overall effect= increase Ca2+ and decrease PO43-
37
primary hyperparathyroidism causes?
solitary adeonoma hyperplasia of all glands parathyroid Ca
38
presentation of primary hyperparathyroidism?
often may seem asymptomatic signs relating to raised Ca2+: weak, tired, depressed, thirsty, dehydrated but polyuric, renal stones, abdo pain, pancreatitis, ulcers bone pain, fractures, osteopenia/OP raised BP- so check Ca2+ in everyone with HTN
39
results of investigations in primary hyperparathyroidism?
Ca2+ and PTH raised, or inappropriately normal- thiazides, lithium reduced phosphate, unless in renal failure ALP increased from bone activity 24hr urinary Ca2+ increased imaging: osteitis fibrosa cystica-RARE-subperiosteal erosions, cysts, DEXA-OP
40
management of mild primary hyperparathyroidism?
increase fluid intake to prevent renal stones avoid thiazides and high Ca2+ and Vit D intake see 6 mnthly
41
indications for surgery in primary hyperparathyroidism?
``` high serum or urinary Ca2+ bone disease OP renal calculi reduced renal function aged 50 or below ```
42
complications of surgery in primary hyperparathyroidism?
hypoparathyroidism RLN damage symptomatic decrease Ca2+, check daily for 2wks or more post-op removal confirmed by intra-op PTH sampling
43
example of drug used to increase sensitivity of parathyroid cells to Ca2+?
Cinacalcet must monitor Ca2+ within 1 wk of dose changes SE: myalgia, decrease testosterone
44
what is MEN?
multiple endocrine neoplasia: syndromes in which there are functioning hormone-producing tumours in mutilple organs inherited as autosomal dominants
45
components of MEN-1?
PPP Parathyroid hyperplasia/adenoma pancreas endocrine tumours pituitary prolactinoma or GH secreting tumour
46
characteristics of thyroiditis as a cause of thyrotoxicosis?
self-limiting, post-viral painful goitre- may make moving the neck uncomfortable, and dysphagia other symptoms over short time period of hyperthyroidism e.g. weight loss, palpitations then hypothyroidism after hyperthyroid phase
47
how often should TFTs be performed in pts on amiodarone e.g. for AF?
6 mnthly
48
why are TFTs performed 6mnthly in pts on amiodarone?
can cause both hyper and hypothyroidism iodine rich so can cause hypothyroidism by toxicity from iodine excess, inhibiting T4 release and hyper by causing a destructive thyroiditis causing hormone release
49
what can giving thyroxine to treat hypothyroidism precipitate?
angina, MI- especially in elderly and can cause OP
50
hypopituitarism affects the A.pituitary hormones in what order?
``` GH gonadotropins- FSH and LH prolactin TSH ACTH ```
51
causes of hypopituitarism?
hypothalamus: Kallman's syndrome, tumour, inflammation, infection-meningitis, TB, ischaemia. pituitary stalk: trauma, surgery, mass lesion-craniopharyngioma, meningioma, carotid artery aneurysm. pituitary: tumour, irradiation, inflammation, AI, infiltration-haemochromatosis, amyloid, metastases, ischaemia-Sheehan's syndrome-relation to PPH-more than 500ml blood loss significant*
52
features of hypopituitarism?
GH lack- central obesity, skin wrinkly and dry, atherosclerosis, reduced stregth, balacne and wellbeing, exercise ability reduced, CO reduced, OP, glucose reduced. gonadotropin lack-oligomenorrhoea or amenorrhea, fertility adn libido reduced, OP, breast atrophy, dyspareunia, men- erectile dysfunction, small testes, hair lack, reduced libido and muscle bulk. hypothyroidism features corticotropin lack- as for adrenal insufficiency e.g. fatigue, weight loss, anorexia, weakness, dehydration, abdo pain, dizziness, postural hypotension, faints, depression, myalgia, arthralgia NOT increased skin pigmentation prolactin lack-absent lactation
53
another name for congenital hypothyroidism?
cretinism
54
tests for hypopituitarism?
basal tests: LH, FSH- reduced or normal, testosterone or oestradiol- reduced, TSH- reduced or normal, T4 reduced, proclactin- maybe increased as lack dopamine inhibition, IGF-1- reduced. Us and Es- Na+ reduced from dilution, Hb reduced- normochromic normocytic anaemia. dynamic tests: short synacthen test insulin tolerance test arginine and GHRH test* glucagon stimulation test alternative to ITT when contraindicated cause can be investigated with MRI
55
contraindications to insulin tolerance test-dynamic function test used in suspected GH deficiency?
epilepsy heart disease adrenal failure
56
hypopituitarism tment?
hydrocortisone for secondary adrenal failure thyroxine, but TSH useless for monitoring testosterone enanthate oestrogen e.g. contraceptive pill, oestradiol transdermal patches gonadotropin therapy GH-somatotropin
57
why is atherosclerosis a risk in patients with hypopituitarism?
GH lack- central obesity- insulin resistance- dyslipidaemia
58
how can benign adenomas of pituitary be defined based on size?
microadenoma- less than 1cm across | macroadenoma- more than 1cm across
59
3 histological types of pituitary tumours?
chromophobe acidophil basophil
60
features of local pressure in pituitary tumours?
headache visual field defects- bitemporal hemianopia- optic chiasm compression cranial nerve palsies DI disturbance of hypothalamic centres controlling sleep, temperature, appetite CSF rhinorrhea through erosion through sella turcica
61
tests in pituitary tumours?
MRI visual field assessmrent screening tests:PRL, IGF-1, ACTH, cortisol, TFTs, LH/FSH, testosterone, short synacthen test, glucose tolerance test if acromegaly suspected, water deprivation test if DI suspected.
62
tment of pituitary tumours?
hormone replacement steroids before levothyroxine as thyroxine may precipitate an adrenal crisis surgery-trans sphenoidal, prolactinoma-dopamine agonist 1st line, with hydrocortisone 100mg IV/IM pre-op radiotherapy
63
define pituitary apoplexy
rapid pituitary enlargement from a bleed into a tumour, may cause mass effects, CVS collapse as acute hypopituitarism, and death.
64
when to suspect pituitary apoplexy?
acute onset of headache, meningism, reduce GCS, opthalmoplegia/visual field defect, may present like SAH. tment- urgent steroids and meticulous fluid balance +/-cabergoline if prolactinoma, and poss surgery- cause may be predisposition to thrombosis or antiphospholipid syndrome, must find.
65
what is a craniopharyngioma?
most common IC tumour in childhood originates from Rathke's pouch growth failure in c.hood amenorrhea, reduce libido, DI, sleep disturbance, or tumour mass effect in adults. CT/MRI tment- surgery, with or without post op radiation test pit function post op
66
why does hyperprolactinaemia cause OP?
high prolactin, inhibits GRH release from hypothalamus, so lower levels of LH and subsequently oestrogen which protects bone.
67
most common cause of oligomenorrhoea and amenorrhea?
PCOS
68
features of Turner's syndrome?
45, X: female with female genitalia, streak ovaries. ``` short stature webbed neck low set ears primary amenorrhea shield like chest high arched palate wide carrying angle of elbows ``` also increased incidence of AI disease, bicuspid aortic valves, aortic coarctation and dissection, CAD, HTN, type 2 DM, horseshoe kidneys, lymphoedema, reduced bone density, hearing problems and IBD.
69
what do the small ovarian cysts seen in PCOS represent?
arrested follicular development
70
hormone blood results characterising PCOS?
increase LH relative to FSH increased androgens-high free androgen index, testosterone may be normal or raised oestradiol normal, oestrone raised due to peripheral conversion but is rarely measured prolactin normal or raised sex hormone binding globulin (SHBG) often low due to high insulin levels, leading to high free androgens.
71
what is though to happen with GnRH in PCOS?
increased frequency of pulse generator, causing increased LH pulses and androgen secretion.
72
causes of hirsutism and virilization other than PCOS?
CAH Cushing's syndrome virilizing tumours of ovary and adrenal
73
associations of PCOS?
insulin resistance and hyperinsulinaemia, high prevalence of type 2 DM HTN, hyperlipidaemia and increased CVD risk
74
presentation of PCOS?
oligomenorrhoea/amenorrhea, hirsutism and acne, shortly after menarche. can present with just irregular periods, or even more frequent erratic bleeding. with hirsutism, often overweight or obese. insulin resistance may appear as acanthosis nigricans on neck and in axillae. if this appears in older individuals, often suggests an underlying malignancy.
75
features on ovarian USS of PCOS?
thickened capsule multiple 3-5mm cytsts hyperechogenic stroma
76
why do striae occur in cushing's syndrome?
due to thin skin skin is weakened so even normal stretching, or pressure of obesity, causes elastin to break, and on healing, depressed purple scars appear=striae.
77
Rotterdam criteria 2003 for PCOS diagnosis?
at least 2 of: clinical or biochemical evidence of hyperandrogenism e.g. hirsutism, acne evidence of oligo- or anovulation presence of polycystic ovaries on US
78
clomifene may be given to improve fertility in PCOS patients, what is the risk of this tment given for longer than recommended (6 cycles)?
ovarian Ca
79
3 key symptoms suggestive of addison's disease (primary adrenocortical insufficiency)?
pigmentation- palmar creases, buccal mucosa, new scars postural hypotension salt craving
80
how is dihydrotestosterone metabolised peripherally from testosterone?
by 5alpha-reductase
81
main control of mineralocorticoid secretion?
renin-angiotensin system
82
risk associated with acute illness in diabetes insipidus?*
severe dehydration with hypernatraemia | water unable to be retained through ADH action
83
how does addison's disease differ from hypothalamic-pituitary disease?
addison's- destruction of entire adrenal cortex, so mineralocorticoid, glucocorticoid and sex steroid production ALL reduced. HP disease- mineralocorticoid secretion relatively intact as predom stimulation=AngII, sex steroid prod. by adrenals also largely independent of pituitary action.
84
common autoantibody in addison's disease?
21-hydroxylase
85
causes of addison's disease?
``` AI TB surgical removal haemorrhage/infarction meningococcal septicaemia venography infiltration malignant destruction amyloid ```
86
symptoms of addison's disease?
``` relatively non-specific syncope from postural hypotension weight loss anorexia weakness malaise joint/back pain myalgia abdo pain N+V constipation diarrhoea confusion fever impotence/amenorrhea depression ```
87
signs of addison's disease?
``` increased pigmentation- palmar creases, buccal mucosa, new scars dehydration loss of weight postural hypotension general wasting body hair loss (vitiligo) ```
88
what does the short synacthen test do?
if cortisol is not raised to >550nmol/L, then confirms presence of hypoadrenalism, but doesn't differentiate addisn's from ACTH deficiency or iatrogenic suppression by steroid medication.
89
investigations in addison's disease, other than single cortisol measurements and short synacthen test?
a 09:00 hr plasma ACTH level- >80ng/L with low or low-normal cortisol confirms primary hypoadrenalism electrolytes and urea- low Na+, high K+, high urea blood glucose- may be low adrenal antibodies CXR, AXR-?TB amd/or calcified adrenals plasma renin activity- high as low serum aldosterone hypercalcaemia and anaemia after rehydration sometimes seen
90
management of an addisonian crisis (acute adrenal insufficency)?
1L 0.9% sodim chloride over 30-60min with 100mg bolus of IV hydrocortisone take blood for cortisol and ACTH if possible monitor blood glucose, infuse if hypoglycaemic blood, urine, sputum for culture, Abx e.g. cefuroxime 1.5g/8hr IV continue IV fluids, several L over 24hr guided by CVP line if necessary continue hydrocortisone, 100mg 6hrly IM/IV change to oral steroids after 72hr if pt's condition good treat underlying cause fludrocortisone not needed in emergency management as high cortisol provides sufficient mineralocorticoid activity, give later.
91
precipitating factors to addisonian crisis?
infection trauma surgery
92
what name is given to the emergency presentation of severe hypothyroidism?
myxoedema coma
93
signs and symptoms of myxoedema coma?
looks hypothyroid, goirtre often >65yrs hypothermia hyporeflexia hypoglycaemia hyponatraemia-renal dysfunction-reduced Na+ pump synthesis for Na+ reabsorption, also impaired renal perfusion with reduced CO and peripheral vasoconstriction to maintain core temp in longstanding poorly controlled hypothyroidism hypoventilation bradycardia seizures coma, although presenting mental state may be lethargy or stupor cardiac failure-reduced production of myocyte contractile proteins and enzymes e.g. Na+ pump pericardial effusions-decreased plasma volume and increased capillary permeability-this can cause ascites* cyanosis cardiogenic shock- low BP may have had radioiodine, thyroidectomy or pituitary surgery may have been psychotic (myxoedema madness) just before coma e.g. precipitated by infection, MI, stroke or trauma.
94
tment of myxoedema coma?
take venous blood for FBC, Us and Es e.g. Na+, T3, T4, TSH, cortisol, glucose, cultures arterial blood for PaO2 high flow O2 if cyanosed, correct any hypoglycaemia T3 5-20 micrograms over 12hr slowly, must be careful not to precipitate IHD hydrocortisone 100mg/8hr IV, espec. if pituitary cause e.g. no history of goitre, radioiodine or thyroid surgery IVI 0.9% sodium chloride cefuroxime 1.5g/8hr IVI if infection suspected treat HF as appropriate hypothermia tment with warm blankets in a warm room with warm drinks if possible. further tment: T3 5-20micrograms/4-12hr IV until sustained improvement, then levothyroxine 50micrograms/24hr PO. hydrocortisone and IV fluids as needed
95
management plan for thyrotoxic storm?
IVI 0.9% sodium chloride, 500ml/4hr, NGT if vomiting take blood for T3, T4, TSH, cultures (if infection suspected) sedate if necessarym monitor BP if no CI and CO is ok, give propranolol 40mg/8h PO, max IV dose 1mg over 1min, may need repeating e.g. 5 times at 2 or more min intervals. May need ultra short acting beta blocker if asthma and poor CO. high dose digoxin may be needed to slow heart e.g. 1mg over 2hr IVI carbimazole 15-25mg/6hr PO, after 4hr give Lugol's solution 0.3ml/8hr PO well-diluted in water for 1 wk to block thyroid hydrocortisone sodium succinate 100mg/6h IV or dexamethasone 4mg/6h PO treat suspected infection e.g. cefuroxime 1.5g/8h IVI adjust IV fluids as necessary, cool with tepid sponging and paracetamol after 5d, reduce carbimazole to 15mg/8h PO
96
tment of acute hypercalcaemia?
diagnose and treat underlying cause correct dehydration with IV 0.9% sodium chloride bisphosphonates- infusion may use furosemide- increases Ca2+ excretion BUT may worsen hypercalcaemia due to dehydrating the pt.
97
features of hypercalcaemia?
abdo pain, vomiting, constipation, polyuria, polydipsia, depression, anorexia, weight loss, tired, weak, HTN, confused, pyrexial, renal stones, renal failure, ectopic calcification, cardiac arrest.
98
most common causes of hypercalcaemia?
malignancy e.g. bone metastases, myeloma, PTHrP e.g. in squamous cell carcinoma of lung or primary hyperparathyroidism
99
features of hypocalcaemia
``` SPASMODIC spasms-carpopedal-trousseau's sign perioral paraesthesiae anxious, irritable, irrational seizures muscle tone increased in smooth muscle-colic, wheeze, dysphagia orientation impaired dermatitis impetigo chvostek's sign; choreoathetosis, cataract, cardiomyopathy- long QT interval on ECG ```
100
management of hypocalcaemia?
Ca2+ 5mmol/6h PO, daily plasma Ca2+ levels may require alfacalcidol- converted rapidly in liver to calcitriol, in CKD 10ml 10% calcium gluconate IV over 30min and rpt if nec in severe symptoms correct alkalosis if cause
101
management of acromegaly?
trans-sphenoidal surgery to remove the pituitary tumour is usually the tment of choice residual disease can then be treated with drugs, and this may be needed post surgery to reduce GH levels radiotherapy as adjuvant for large invasive tumours, for refractory disease and when surgery is CI drug tment=somatostatin analogues e.g. octreotide and lanreotide, GH secreting pituitary tumours can enalrge with tment so must monitor visual fields, can impair glucose tolerance (poss. as inhibit insulin release?) dopamine agonsits e.g. bromocriptine, more useful if tumour also secretes prolactin
102
problem with using radioiodine in grave's disease?
can worsen thyroid eye disease
103
investigations in suspected acromegaly?
``` GH increased IGF-1 increased MRI brain-pituitary adenoma visual fields and acuity-compression of optic chiasm by tumour-bitemporal hemianopia oral glucose tolerance test ``` other disease features and risk evaluation?-lipid profile, HbA1c, ECG

General Medicine Block (10 decks)

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