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141 Cards in this Set
- Front
- Back
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how do you tell the difference in terms of sodium between DI and SIADH?
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SIADH - hyponatramemia
DI - hypernatraemia |
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What is the main cause of hypercalcaemia?
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primary hyperparathyroidism
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What is the main cause of primary hyperparathyroidism?
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solitary adenoma (81%)
then hyperplasia (15) carcinoma Men I and IIa |
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What is pseudohypercalcaemia?
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increased protein binding leading to an elevation in serum caclium without a rise in the ionised free form e.g., hyperalbuminaemia from severe dehydration
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What is the management of severe hypercalcaemia?
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Rehydration (hypercal can result in severe deydration and electorlyte abnormalities)
IV bisphosphonates In acute life threatening situations give IV or IM calcitonin (decreases bone resorption, increases renal excretion) Can give steroids for refractory hypercal (Often due to malignancy, vit D intoxication, sarcoidosis) Do not use frusemide except if fluid overloaded can cause increased dehydration |
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What is the syndrome caused by a genetic mutation that results in hypercalcaemia?
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familial hypocalciuric hypercalcaemia (FHH)
Mutation in calcium receptor sensing gene --> inappropriate PTH secretion and tubal calcium reabsorption |
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MOA of bisphosphonates?
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Inhibit osteoclasts
Promote renal excretion of calcium |
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Which bisphosphonate is commonly used to treat maligancny related hypercalcaemia
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palimdronate
zoledronic acid clodronate |
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Clinical features of acute hypocalcaemia?
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tetany
paraesthesias: perioral, hands and feet delirium hyperreflexia psychiatric Sx |
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What are the 2 signs that you can look for in hypocalcaemia?
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Chvostek's sign - percussion of the facial nerve just anterior to the external auditory meatus elicits unilateral spasm of the orbicularis oculi or orbucularis oris mm
Trousseau's sign - inflation of a BP cuff above systolic pressure for 3 minutes elicts carpal spasm and paraesthesia |
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What can cause tetany?
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hypocalcaemia
metabolic alkalosis hypokalaemia hypomagnesemia |
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How do you manage hypocalcaemia?
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Severe: IV calcium gluconate
Mild: oral calcium |
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What are some causes of hypocalcaemia?
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Iatrogenic hypoparathyroidism
Primary hypoparathyroidism: idiopathic/autoimmune, infiltrative diseases, HIV Chronic low magnesium impairs PTH secretion cf. acute Mg will stimulate PTH secretion Haemachromatosis |
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How do you calculate the corrected calcium?
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measured ca + 0.25 (40-albumin)/10
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Clinical features of hypermagneseamie?
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drowsiness, hyporeflexia, respiratory depression ,depressed deep tendon reflexes
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What is paget's disease?
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Metabolic disease characterised by excessive bone desturction and repair resulting in disorganised bone formation and weaker bone that is larger, less compact and more vascular
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What is the aetiology of paget's disease?
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Thought to be related to a slow progressing viral infection of osteoclasts
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What are the clinical features of paget's disease?
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Usually asymptomatic
Bone pain Hot bones (increased vascularity) Skeletal deformities Involvement of skull --> HA, increased hat size, deafness |
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What does paget's disease look like on imaging?
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Initial lesion - destructive and radiolucent
Involved bones are expanded with cortical thickening and denser than normal multiple fissure fractures in long bones |
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What is a complication with paget's disease?
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Osteosarcoma/sarcomatous change
Found in 1-3% Indicated by marked bone pain, new lytic lesions and sudden increase in ALP |
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Management of paget's disease?
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Symptomatc therapy
Treat if ALP > 3x N Bisphosphonates Calcitonin Adeuquate Ca and Vit D |
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What are the consequences of hyperprolactinaemia?
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galactorrhea (lactation without breastfeeding)
hypogonadism oligomenorrhea or amenorrhea |
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Which drugs can contribute to hyperprolactinaemia?
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Dopamine antagonists (antipsychotics, antidepressants, antiemetics)
Dopamine depleting drugs (methyldopa) Oestrogens - OCP |
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What are the main physiological causes of hyperprolactinaemia?
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pregnancy
nipple stimulation stress |
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What are some pathologic causes of hyperprolactinaemaia?
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prolactinoma (benign tumour of the lactotroph cell)
Decreased dopaminergic inhibition of prolactin secretion (damage to dopaminergic neurons of hypothalamus, pituitary stalk section or drugs that block dopamine receptors) |
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What features on ECG do you see with hypoercalcaemia?
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short QT
Arrhythmias |
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How might someone with acute hypercalcaemia present?
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Renal stones
Pancreatitis and other abdo groans Reduced LOC, psychosis Short QT and arrhythmias Hypertensive crisi Hypovolaemia Hypotonia, hyporeflexia |
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What local complications might someone with a pituiary tumour present with?
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Headache
bitemporal hemianopia Dipoplia Disconnection hyperprolactinaemia (ie disconnection between hypothalamus and pituitary leads to lack of dopamine inhibition?) acute infarction/expansion (pituiary apoplexy) |
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What is the definition of a pituiary microadenoma and a macroadenoma? Why is this important?
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Micro < 10mm
Macro > 10mm Macro more likely to present wiht mass effect rather than hormone excess Research suggests that if micro are very slow growing |
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Which hormones are stimulated by hypoglycaemia?
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ACTH - cortisol
GH - IGF Glucagon Prolactin |
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Will surgical removal of a pituitary tumour return the pituiary hormone production back to normal?
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If patien thas panhypopituitarism before surgery pituitary function is unlikely to recover
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How do you manage pituitary hypofunction?
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Hydrocortisone oral 3 times daily
L-thyroxine Testosterone IM every 3 weeks - boys Oestrogen - transdermal oestradiol patches, implants or oral therapy - girls GH replacement - can give more during puberty |
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What is empty sella syndrome
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Occurs when subarachnoid space extends into sella turcica partially filling it with CSF resulting in remodelling and enlargement of sella turcica and flattening of the pituiary gland
Usually eupituitary no treatment necessary |
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How do you investigation panhypopituiatirsm?
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Triple bolus test
Insulin (should stimulate ACTH, GH), GnRH, TRH (should stimulate TH and Prolactin) |
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What is the pathophysiology of diabetes insipidius?
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Deficient ADH --> passage of large volumes of dilute urine
Central: insufficient ADH due to post-pituiary surgery, tumours, stalk lesion etc Nephrogenic: collecting tubules in kidneys resistant to ADH (drugs - lithium, hypercalcaemia, hypokalaemia, chronic renal disease) Can be hereditary |
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What produces ADH?
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posterior pituitary
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How do you differentiate between central DI and nephrogenic DI?
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response to exogenous ADH (desmopressin)
If response - central problem If no response - nephrogenic problem |
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What is desmopressin (DDAVP)
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synthetic replacement for vasopressin
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How do you manage nephrogenic DI?
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If lithium toxicity has already damaged tubules - it is irreversible
Treating hypercalcaemia will reverse DI Aim of treatment is to reduce urine output solute restriction thiazide diuretics |
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How do you manage central DI?
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desmopressin (nasal spray) or vasopressin
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What are the 2 most common causes of nephrogenic diabetes inspidius?
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lithium
hypercalacemia |
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What causes SIADH?
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Malignancy (lung, pancreas, lymphoma)
CNS disease Respiratory disease (TB, pneumonia, empyema) Drugs Stress (post-surgical) |
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How do you treat SIADH?
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treat underlying cause
fluid restriction Can give demeclocylcline (antibiotic with anti-ADH properties) |
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Why is oedema not a feature of SIADH?
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Because water is evenly distributed across all comparments
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What is somatotropin?
What is somatoliberin? |
somatotropin = growth hormone
somatoliberin = GHRH |
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What are the symptoms of acromegaly?
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Arthralgia/arthritis - esp of spine - kyphosis
BP raised Carpal tunnel syndrome and cardiomegaly Diabetes Enlarged organs Field defect (visual) Generalised mm weakness Coarsening of facial features Proganthism (jaw protrudes forward) |
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What is the best investigation to perform if acromegaly is suspected
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OGTT - failure to suppress GH in response to glucose
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What do people with acromegaly usually die from?
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heart failure and cancer
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What type of colonic disease is associated with acromegaly?
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Colonic neoplasia
? trophic effect of IGF-1 on the proliferation of epithelial cells |
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What is macrognathia?
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enlarged jaw
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Why do patients with acromegaly get arthropathy?
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Synovial tissue and cartilage enlarge causing hypertrophic arthropathy
Back pain (kyphosis is common) |
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Which visceral organs are enlarged in acromegaly?
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thyroid
heart liver lungs kidneys |
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Management of acromegaly?
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1. Transsphenoidal surgery if pituitary adenoma
2. If continuing GH excess after surgyer or if unsuitable for surgery - 1st line: Somatostatin analogue (GH inhibitory hormone) e.g., octreotide SE: cholelithiasis, abdo pain, diarrhoea 2nd line Dopamine agonists - cabergoline, bromocriptine |
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Why is it better to test for IGF-1 than GH?
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IGF-1 doesn't vary from hour to hour according to food intake, exercise or sleep but reflects integrated GH secretion during the preceding day or longer
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Which thyroid hormone is more biologically active (i.e. more potent) Which has a longer half life?
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T3 = more biologically active
T4 = longer half life |
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MOA metformin
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sensitises peripheral tissues to insulin which increases glucose uptake
decreases hepatic glucose production |
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CI for metformin
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renal dysfunction GFR < 30 (excreted entirely by the kidney)
Moderate to severe liver dysfunction Cardiac dyfunction Avoid in elderly |
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SE of metformin
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abdo discomfort, bloating, diarrhoea
lactic acidosis anorexia |
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MOA sulfonyreas
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stimulates insulin release from beta cells by causing K channel closure --> depolarisation --> calcium mediated insulin release
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SE sulfonyreas
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weight gain
hypoglycaemia |
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CI sulfonyureas
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moderate to severe liver dysfunction
Adjust dose if severe kidney dysfunction DO NOT combine with meglitidnides (stimulate same receptor but at different site) |
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What is acarbose?
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alpha glucosidase inhibitor
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What conditions are acarbose (alpha glucosidase inhibitors) CI in ?
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IBD
Severe liver dysfunction |
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MOA glitazones (actos)
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reduce insulin resistance (sensitise peripheral tissues to insulin)
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Which drug should you never combine glitazones (actos) with?
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Insulin
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SE of glitazones (actos)
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Fractures
Peripheral and pulmonary oedema CHF Anaemia Weight gain |
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SE of alpha glucosidase inhibitor (Acarbose)
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diarrhoea, flatulence, abdominal cramps
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Why are thiazides no longer first line as BP control in patients with diabetes?
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Can precipitate diabetes and increased lipids
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What drugs are first line and second line management of type 2 diabetes?
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1st: metformin
2nd: sulfonylreas |
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What's the main problem with thiazolidnendiones
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Can precipitate cardiac failure in anyone with a heart problem
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MOA DDP-IV inhibitors (sitagliptin - januvia)?
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inhibits degradation of endogenous antihyperflycaemia incretin hormones which stimulate insulin secretion and inhjibit glucagon release
Incretins increase GLP-1 and GIP which inhibit counter regulatory hormones |
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SE of DDP-IV inhibitors?
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headache
URTI Nasopharyngitis NOT hypoglycaemia |
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Which medications for Type 2 DM have hypoglycaemia as their side effect/
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Sulfonylreas and non-sulfonylrease (e.g., repalinide, and nateglinide)
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MOA of alpha glucosidase inhibitor?
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decrease carbohydrate GI abospriton by inhibiting brush border alpha glucosidase
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Why is a somatostatin analogue used in acromegaly?
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Suppressor of GH - hypothalamic that stops release but not synthesis of GH in pituitary
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SE of somatostatin anaglogues?
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biliary calculi, biliary colic
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What is teriparatide?
What is it used for? |
Synthetic PTH
Osteoporosis Duration - 18 months |
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what is the most common drug cause of gynaecomastia?
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spironolactone
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What SE can you get with dopamine agonists?
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orthostatic hypotension
nasal congestion peripheral oedema psychiatric disorders |
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Cranial diabetes inspidus values for water deprivation test
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serum osm: high
final urine osm: <300 urine osm post DDAVP: >600 |
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Nephrogenic diabetes inspidus values for water deprivation test
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serum osm: high
final urine osm: <300 urine osm post DDAVP: <300 |
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Psychogenic polydipsia values for water deprivation test
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serum osm: low
final urine osm: >400 urine osm post DDAVP: >400 |
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Features of MODY
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dev of type 2 DM <25 yrs old
inherited autosomal dominant ketosis not a feature |
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Features of acromegaly
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facial hair
spadelike hands large tongue excessive sweating features of pituitary tumor: hypopituitarism, headaches, bitemporal hemianopia raised prolactin in 1/3 of cases --> galactorrhea 6% have MEN1 complications: HTN, diabetes, cardiomyopathy, colorectal cancer |
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Features of subacute thyroiditis
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hyperthyroidism
painful goitre raised ESR reduced uptake on iodine 131 scan occurs following viral infection |
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Treatment of subacute thyroiditis
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self-limiting
NSAIDs for pain |
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Most important risk factor in thyroid eye disease (Grave's)
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smoking
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Presenting features of hemachromatosis
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erectile dysfunction
arthralgia bronze pigmentation diabetes liver problems cardiac failure hypogonadism |
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When do you give exenatide?
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only when insulin would otherwise be started and obesity is a problem (BMI >35)
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SEs of pioglitazone
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CHF, pulmonary edema, peripheral edema, fractures, anemia, weight gain
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Pharm treatment of infertility PCOS
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clomifene (anti-estrogen), then metformin
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Treatment of diabetic neuropathy
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one of these, depending on SEs: amitriptyline, carbamazepine, gabapentin, pregabalin, capsaicin
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Symptoms of thyroid storm
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fever >38.5, tachycardia, confusion/agitation, N & V, HTN, HF, abnormal LFTs
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Treatment of thyroid storm
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symptomatic (paracetamol), treat underlying, anti-thyroid drugs (propylthiouracil), lugol's iodine, dexamethasone, propanolol
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T/F ketones are present in HONKC
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true, trace amounts!
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What gives you hypercholesterolemia rather than hypertriglyceridemia?
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nephrotic syndrome
cholestasis hypothyroidism |
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Dx test in acromegaly
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oral glucose tolerance test with growth hormone test
normal: GH is suppressed with hyperglycemia acromegaly: no suppression of GH |
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What period of time do you need to recheck HbA1c?
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2-3 months
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MOA of rosiglitazone
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PPAR-gamma receptor agonist
but has been withdrawn due to CV SEs |
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Best investigation for insulinoma
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supervised fasting (up to 72 hours)
CT pancreas |
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Features of insulinoma
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hypoglycemia (typically early morning or just before meal)
rapid weight gain high insulin:proinsulin ratio high C-peptide |
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What is an insulinoma?
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neuroendocrine tumor from pancreatic islets of Langerhans cells
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Treatment of insulinoma
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surgery
if not, diazoxide and somatostatin |
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What treatment may worsen thyroid eye disease in Grave's?
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radio-iodine
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Diagnostic combination in Hashimoto's thyroiditis
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hypothyroidism + goitre + anti-TPO
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Treatment of gestational diabetes
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insulin
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Difference between insulin and sulfonylurea abuse
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insulin abuse: raised insulin, low C-peptide
sulfonylurea abuse: raised insulin, raised C-peptide |
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What can trigger Graves disease
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Pregnancy
Iodine excess LIthium Viral or bacterial infections Steroid withdrawal |
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What is lid lag
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Sclera can be seen above the iris as the patient looks downward
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What is acropachy and which condition is it seen in?
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clubbing and thickening of distal phalanges
Graves disease |
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Goal for HDL cholesterol in diabetes
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men: >1
women: >1.2 |
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Goal for triglycerides in diabetes
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< 1.7
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Goal for blood glucose in diabetes
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< 7.2
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Goal for LDL cholesterol in diabetes
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<2.6 (<1.8 if macrovascular disease)
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Goal for BP in diabetes
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<130/80 (<125/75 if 1g+ of proteinuria)
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Goal for total cholesterol in diabetes
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< 4
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What are the values in impaired glucose tolerance?
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fasting: <6.1
post-prandial: < 7.8-11 Remember IGT has normal fasting values, but abnormal post-prandial! |
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When is drug therapy indicated in diabetes instead of lifestyle
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end-organ complications
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Greatest risk factor for diabetic foot disease
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previous amputation and ulceration
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Rx of Addison's disease
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hydrocortisone + fludricortisone (gluco + mineralo cover)
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What is exenatide? When do you use it?
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GLP-1 like, incretin
obese patients |
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At what HbA1c do you start insulin?
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at 7.5
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Symptoms of hypercalcemia
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'bones, stones, abdominal groans and psychic moans'
Plus: * polydipsia, polyuria * peptic ulceration/constipation/pancreatitis * bone pain/fracture * renal stones * depression * hypertension |
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Is weight loss or weight gain a feature of GLP-1 mimetics?
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weight loss
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What are the 2 big risks in using exenatide?
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severe pancreatitis
severe renal dysfunction |
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What is sick euthyroid syndrome?
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Changes in circulating thyroid hormones in patients with serious illness, trauma or stress
You get Initially decreased T3, then decreased TSH, then decreased T4 DOn't give TH - it will worsen the outcome |
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Which bacteria is associated with HUS?
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E Coli
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Symptoms of niacin deficiency
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4 Ds: diarrhea, dermatitis, dementia, death
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What does not go into the definition of metabolic syndrome
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LDL cholesterol
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Pharm Rx of obesity? MOA?
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orlistat, pancreatic lipase inhibitor
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How do you change management in Addison's disease when pt is ill?
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2x hydrocortisone, leave fludrocortisone the same
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What size do adrenal massess need to be before you take them out?
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5cm
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What metabolic abnormalities do you get with hypothyroidism?
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hyponatraemia
Hyperlipidaemia increased serum creatinine increased homocysteine |
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How does hyperthyroidism affect bone?
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stimulates bone resorption
increase in serum calcium |
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If a diabetic patient is at risk of hypos, what hypoglycemic agent should be used?
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DPP-4 inhibitor or thiazolidinedione
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Increase or decrease?
What does growth hormone do in response to glucose? |
normal: should decrease
acromegaly: increase |
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Increase or decrease?
What does cortisol do in response to insulin? |
increase
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What LFT is elevated in pregnancy?
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ALP
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What is ALP a measure of?
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bone formation
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When is maternal AFP decreased? increased?
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decreased: downs, gestational diabetes, trisomy 18
increased: neural tube defects, Abdominal wall defects (omphalocele and gastroschisis) Multiple pregnancy |
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Which drugs cause hyperthyroidism?
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amiodarone
lithium thyroxin |
