Endocrine Flashcards

Question

Causes of Cushing's syndrome?

Answer 1

1°: adenoma/ adenocarcinoma in zona fasciculata of adrenal secretes cortisol, hyperplastic adrenal gland/ nodular adrenal hyperplasia. 2°: iatrogenic (GCs) pit adenoma (Cushing’s disease), ectopic ACTH (benign bronchial carcinoid, malig oat cell Ca/ small cell lung ca. Carney complex: syndrome incl cardiac myxoma. Pseudo Cushing’s: mimics Cushing's, often due to alcohol excess or severe depression, cause false positive dexamethasone suppression test or 24hr urinary free cortisol, oestrogen contraceptives ↑ cortisol binding globulin ↑cortisol. ACTH dependent - Cushing's disease - pituitary tumour secreting ACTH producing adrenal hyperplasia - ectopic ACTH production - SCLC ACTH independent - iatrogenic - steroids - adrenal adenoma - adrenal carcinoma - Carney complex - micro nodular adrenal dysplasia (rare)

Answer 2

Metabolic syndrome DM Infection due to IS Fragility # due to osteoporosis Renal stones Venothrombolic event: hypercoag Necrosis of femoral head Glaucoma Poor libido, ED Amenorrhoea Hypokalaemia metabolic alkalosis ↓K common with ectopic ACTH

Answer 3

Overnight dexa suppression test: ↑ cortisol High dose dexa: ↓cortisol Cushing’s disease, ↑cortisol ↓ACTH adrenal cushing ↑cortisol ↑ACTH ectopic ACTH ↑24hr urinary free cortisol 9am + midnight ACTH if ACTH supressed then non-ACTH dependent cause likely: adrenal adenoma. If >4 ACTH dependend eg Cushing’s disease/ ectopic ACTH. CRH stimulation: if pit source, cortisol ↑, ectopic/adrenal, no change in cortisol. Psuedo: false pos dexamethasone suppression test or 24 urinary cortisol. Insulin test to differentiate

Answer 4

Wean steroid meds for iatrogenic Cushing;s Surgery: for adenoma or ectopic ACTH Pasierotide (somatostatin analogue), cabergoline (dopamine agonist), osilodrostat, ketoconazole, metyrapone, mitotane, etomidate (steroidogenesis inhibitor), mifepristone (glucocorticoid antagonist) Pituitary radiotherapy

Answer 5

hypoadrenalism reduced cortisol and aldosterone AI destruction of adrenal glands is commonest cause

Answer 6

hypoadrenalism reduced cortisol and aldosterone AI destruction of adrenal glands is commonest cause RF: F>M, adrenocortical IG, use of anticoags.

Answer 7

Primary causes - Addison's - tuberculosis - metastases (e.g. bronchial carcinoma) - meningococcal septicaemia (Waterhouse-Friderichsen syndrome) - HIV - antiphospholipid syndrome - Drugs that inhibit cortisol synthesis eg ketoconazole, suramin. Secondary causes - pituitary disorders (e.g. tumours, irradiation, infiltration) Exogenous glucocorticoid therapy

Answer 8

Lean, tanned, tired + tearful, weakness. lethargy, weakness, anorexia, nausea & vomiting, weight loss, 'salt-craving' hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia GI: abdo pain, anorexia, N/V, weight loss Vitiligo: AI destruction of melanocytes. hyponatraemia and hyperkalaemia may be seen crisis: collapse, shock, pyrexia * Primary Addison's is associated with hyperpigmentation whereas secondary adrenal insufficiency is not

Answer 9

ACTH stimulation test (short Synacthen test). Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM. insuff/ no cortisol produced. Addison’s excluded if 30 min cortisol >550nmol/L. Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated. 9am serum cortisol: > 500 nmol/l makes Addison's very unlikely < 100 nmol/l is definitely abnormal 100-500 nmol/l should prompt a ACTH stimulation test to be performed ``` Electrolyte abnormalities: hyperkalaemia hyponatraemia hypoglycaemia metabolic hyperchloraemic acidosis ``` ↑renin compensatory to ↓aldosterone Plasma dehydroepiandrosterone + DHEA sulphate suppressed. Abdo CT: enlarged adrenal glands with TB/malig, small if AI/ advanced TB. If infectious > calcifications

Answer 10

GC and MC replacement therapy > hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day > fludrocortisone Pt. education - emphasise the importance of not missing glucocorticoid doses - consider MedicAlert bracelets and steroid cards - patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis - discuss how to adjust the glucocorticoid dose during an intercurrent illness Management of intercurrent illness? - in simple terms the glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same

Answer 11

life-threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium, precipitated by physiological stress where sudden need for aldosterone + cortisol but body can't deliver Features = hypoglycaemia, circ collapse, shock fatal. Pain in back, abdo legs, severe N/V, pyrexia Causes - sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's, Hypopituitarism) - adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia) - steroid withdrawal Management - hydrocortisone 100 mg im or iv - 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic - continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action - oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

Answer 12

Severe, adrenal failure due to overwhelming infection, adrenal gland haem. Necrosis, adrenal crisis. Sx: Initial: fever, malaise, chills, headache, vomiting Shock: ↓BP ↑HR, tachypnoea Cyanosis Ix: CT: blood in adrenals Blood culture DIC: ↑fibrinogen degradation products, d dimer, prolonged PT, aPTT ↓plts, fibrinogen. Tx: IV GC Abx IV fluids, vasopressors

Answer 13

defined as a chronic condition characterised by abnormally raised levels of blood glucose

Answer 14

Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system This results in an absolute deficiency of insulin resulting in raised glucose levels Patients tend to develop T1DM in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis Genes (HLA-DR3/4, PTPN22, CD25) + environmental trigger (childhood enterovirus, bystander activation, molecular mimcry)

Answer 15

the most common cause of diabetes in the developed world. It is caused by a relative deficiency of insulin due to an excess of adipose tissue. In simple terms there isn't enough insulin to 'go around' all the excess fatty tissue, leading to blood glucose creeping up.

Answer 16

This term is used for patients who don't yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years. They, therefore, require closer monitoring and lifestyle interventions such as weight loss

Answer 17

Some pregnant develop raised glucose levels during pregnancy. This is important to detect as untreated it may lead to adverse outcomes for the mother and baby

Answer 18

A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

Answer 19

The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM

Answer 20

Any pathological process which damages the insulin-producing cells of the pancreas may cause diabetes to develop. Examples include chronic pancreatitis and haemochromatosis. Drugs may also cause raised glucose levels. A common example is glucocorticoids which commonly result in raised blood glucose levels

Answer 21

Polyuria, polydipsia, polyphagia. Glycosuria Dehydration Hypotension Blurred vision Gastroparesis Paraesthesia Unexplained weight loss ↓sensation, glove + stocking distribution Autonomic NS malfunction: sweating, passing gas

Answer 22

DKA: abdo pain, vomiting, ↓consciousness Infection Delayed wound healing Amputations Microvascular: retinopathy, nephropathy, ED Macrovascular: CV, cerebrovascular, peripheral vascular disease Hypoglycaemia Lipodystrophy

Answer 23

Random glucose/ 2hr GTT >11 Fasting: >7 HbA1c: >48. Not as useful in T1, as not accurately reflect rapid ↑ Urinalysis: albuminemia, glycosuria, ketones C peptide: byproduct of insulin production, if ↓ pancreas no longer producing enough insulin Autoantibodies against β cells: glutamic acid decarboxylase (GAD), insulinoma-associated-2 autoantibodies (IA-2A), islet cell autoantibodies, insulin autoantibodies (IAA), zinc transporter 8 (ZnT8Ab), tyrosine-phosphate like molecule – islet auto-antigen-2. Consider C-peptide and/or diabetes-specific autoantibodiesif T1DM suspected but clinical presentation includes atypical features (>50, BMI >25m slow evolution of hypoglycaemia or long prodrome)

Answer 24

Life long insulin Illness: maintain calorie intake, monitor glucose, ↑insulin if glucose rising. HbA1c: monitor 3-6 mnths, target 48 Self-monitoring - at least 4 times a day (before meals and bed), more frequent monitoring if frequent hypoglycaemic episodes, periods of illness, before, during and after sport, planning pregnancy and during, and while breastfeeding BG targets: 5-7 on waking, 4-7 before meals + other times. Metformin: BMI>25 Basal bolus: basal glargine + degludec, determir, bolus lispro (humalog), aspart (novorapid) Bipashic: Humalog mix 25: 25% quick acting, 75% intermediate acting. Insulin pumps

Answer 25

Lispro, aspart, glulisine 12-30 min onset Take prior to meal Peak 0.5-3 hours Duration 3-5 hours

Answer 26

Humulin S, Hypurin Porcine, Neutral Humulin S - 30mins Hypurin Porcine - 60 mins Taken 30 mins prior to eating a meal Humulin S - 2-3 hrs onset Hypurin Porcine - 2-5 hrs onset 6-8 hours duration

Answer 27

Insulin NPH 1.5-4 hour onset Taken twice daily in combination with rapid acting insulin Peak 4-12 hours Duration 14-24 hours

Answer 28

glargine/Lantus, detemir/Levemir 3-4 hour onset Used when rapid-acting insulin stops working Peak minimal, non-defined peak Duration >24 hours

Answer 29

FH physical inactivity poor diet obesity HTN hypertriglyceridemia >45 gestational DM prediabetes PCOS ↑BG level (GC, atypical antipsychotics, thiazide diuretics) LBW

Answer 30

Polyuria, polydipsia, polyphagia Glycosuria Weakness Blurred vision Acanthosis nigricans: hyperpigmented Candida infections Skin abscesses: cellulitis/ abscess UTIs Fatigue

Answer 31

↑risk CV, PAD. Hyperosmolar hyperglycaemic state. HTN: <80 clinic 140/90, HBPM 135/85. >80 150/90, HBPM 145/85 Neuropathy Diabetic food Retinopathy

Answer 32

↑insulin sensitivity, ↓hepatic gluconeogenesis, GI upsets, ↓B12 absorption, lactic acidosis (liver/ renal failure, MI, sepsis, dehydration), CI GFR <30 SE - Gastrointestinal side-effects Lactic acidosis

Answer 33

stimulate pancreatic β cells to secrete insulin, gliclazide, hypoglycaemia, hypersensitivity, ↓Na, weight gain. ↑appetite, weight gain, SiADH, liver dysfunction (cholestatic) SE - Hypoglycaemic episodes Increased appetite and weight gain Syndrome of inappropriate ADH secretion Liver dysfunction (cholestatic)

Answer 34

pioglitazone. Activate PPAR gamma receptor in adiopocytes, promote adipogenesis + fatty acid uptake. Weight gain, fluid retention, liver dysfunction, #. CI in HF. SE - Weight gain Fluid retention Liver dysfunction Fractures

Answer 35

gliptin, ↑incretin by ↓periph breakdown, inhibit glucagon secretion. Well tolerated, ↑ risk of pancreatitis. Don’t cause WL. SE - pancreatitis

Answer 36

gliflozins, inhib reabsorption of glucose in PCT. SE: UTIs. Gangrenous infection of peritoneum. DKA.

Answer 37

exenatide. Injection. Inhibits glucagon secretion. SE: N/V, pancreatitis

Answer 38

Non-fasting: >11.1, impaired gluc tol if >7.8 Fasting: prediabetes 6-7, DM >7 If asymptomatic above must be demonstrated on 2 occasions. HbA1c: >48. ↓than normal sickle cell, GP6D def, hereditary spherocytosis ↑than normal: vit B12/ folic acid def, Fe def anaemia, splenectomy.

Answer 39

abdominal pain polyuria, polydipsia, dehydration Kussmaul respiration (deep hyperventilation) acetone-smelling breath ('pear drops' smell)

Answer 40

T1 - typically <20, more acute (hours-days), recent weight loss typical, features of DKA how present, ketonuria is common T2 - typically >40, slower onset of weeks to months, obesity strong RF (WL rare), milder Sx (polydipsia/polyuria), ketonuria is rare

Answer 41

haemoglobinopathies haemolytic anaemia untreated iron deficiency anaemia suspected gestational diabetes children HIV chronic kidney disease people taking medication that may cause hyperglycaemia (for example corticosteroids)

Answer 42

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn't have diabetes but does have IGT.

Answer 43

defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

Answer 44

Lifestyle - high fibre, low glycemic index source of carbs, low-fat airy and oily fish, control sat fats and trans fatty acids, initial target weight loss in overweight person is 5-10% Metformin: titrated up slowly. If SE modified release Target HbA1c 48. If on gliclazide (or any drug causing hypoglycaemia, eg sulfonylurea) aim for 53. If HbA1c 58 add: sulfonylurea (gliclazide), gliptin (DDP-4), pioglitazone, SGLT-2 inhib (empagliflozin) If stays 58: metformin + gliptin + SU OR, metformin + SU + pioglitazone, OR metformin + SU + SGLT-2 inhib OR metformin, pioglitazone, SGLT-2. Insulin GLP-1 mimetic: exenatide, after triple therapy. Metformin + SU + GLP-1. RF modification - BP targets same as person without T2D

Answer 45

Increase frequency of blood glucose monitoring to four hourly or more frequently Encourage fluid intake aiming for at least 3 litres in 24hrs If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake It is useful to educate patients so that they have a box of 'sick day supplies' that they can access if they become unwell Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis If a patient is taking oral hypoglycaemic medication, they should be advised to continue taking their medication even if they are not eating much If a patient is on insulin, they must not stop it due to the risk of diabetic ketoacidosis. Hosp admission - underlying illness needing hospital, inability to keep fluids down, persistent diarrhoea, significant ketosis, BG persistently >20 despite additional insulin, unable to manage adjusts to DM management, lack of support

Answer 46

may be a complication of existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus may also develop DKA. stress, body releases epinephrine, glucagon release, ↑glucose, loss of glucose in urine, loss of water, dehydration, need alternative energy DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies, increases blood acidity most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction. anion gap metabolic acidosis

Answer 47

Key points glucose > 11 mmol/l or known diabetes mellitus pH < 7.3 bicarbonate < 15 mmol/l ketones > 3 mmol/l or urine ketones ++ on dipstick ECG: abnormal T/1 waves, K changes.

Answer 48

fluid replacement = isotonic saline is used initially, even if the patient is severely acidotic insulin = an intravenous infusion should be started at 0.1 unit/kg/hour once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started correction of electrolyte disturbance = following Tx with insulin high serum potassium falls to hypokalaemia, so potassium may be needed to be added to replacement fluids, if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required potassium level 3.5-5.5 = give 40mmol/L replacement in solution long-acting insulin should be continued, short-acting insulin should be stopped

Answer 49

pH >7.3 and blood ketones < 0.6 mmol/L and bicarbonate > 15.0mmol/L both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn't happened the patient requires senior review from an endocrinologist if the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin the patient should be reviewed by the diabetes specialist nurse prior to discharge

Answer 50

gastric stasis thromboembolism arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia acute respiratory distress syndrome acute kidney injury

Answer 51

medical emergency which is extremely difficult to manage and has a significant associated mortality SE of T2DM (typically elderly with T2DM) results in osmotic diuresis, severe dehydration, and electrolyte deficiencies Systemic cellular dehydration as water leaves cell into blood following glucose

Answer 52

Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood. Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.

Answer 53

General: fatigue, lethargy, nausea and vomiting, confusion Neurological: altered level of consciousness, headaches, papilloedema, weakness, LOC Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis) Cardiovascular: dehydration, dry mucous membranes, poor skin turgor, hypotension, tachycardia, warm skin w/o sweat Hallucinations Polyuria

Answer 54

1. Hypovolaemia 2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis (Ketones <3mmol/L, pH >7.3) 3. Significantly raised serum osmolarity (> 320 mosmol/kg) Low Na + K

Answer 55

1. Normalise the osmolality (gradually) > the serum osmolality is the key parameter to monitor > if not available it can be estimated by 2 * Na+ + glucose + urea 2. Replace fluid and electrolyte losses 3. Normalise blood glucose (gradually) Intravenous (IV) 0.9% sodium chloride solution is the first line fluid for restoring total body fluid. Replace 50% of estimated fluid loss within 1st 12 hrs, + remainder in following 12 hrs It is important to remember that isotonic 0.9% sodium chloride solution is already relatively hypotonic compared to the serum in someone with HHS. Therefore in most cases it is very effective at restoring normal serum osmolarity. If the serum osmolarity is not declining despite positive balance with 0.9% sodium chloride, then the fluid should be switched to 0.45% sodium chloride solution which is more hypotonic relative to the HHS serum osmolarity Keep BG 10-15 to avoid cerebral oedema A rapid decline in serum glucose is potentially harmful therefore insulin should NOT be used in the first instance unless there is significant ketonaemia or acidosis Measurement of ketones is essential for determining if insulin is required. If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture) Potassium should be replaced or omitted as required with KCl LWMH

Answer 56

infection inadequate insulin or oral antidiabetic therapy nursing home residents post op Cushing’s syndrome hyperthyroid acromegaly

Answer 57

High mortality Seizures Weakness down 1 side of body Occlusive events due to hyper viscosity of blood Central pontine myelinolysis

Answer 58

Damage to microvasculature, ↓of pericytes around cap endothelium (help sustain BBB), leaky, microaneurysm formation, new vessel formation from growth factors in response to retinal ischaemia, vascular permeability causes exudates, RF: poor diabetic control, co-existing HTN, smoking, pregnancy Non-proliferative: > mild - 1 or more microaneurysm > moderate - micro aneurysms, blot haemorrhages, hard exudates, cotton wool spots (soft exudates), venous bleeding/looping and intraretinal microvascular abnormalities (IRMA) > severe - blot haemorrhages and micro aneurysms in 4 quadrants, venous beading in at least 2 beading, IRMA in at least 1 quadrant > refer Proliferative: > retinal neovascularisation - may lead to vitrous haemorrhage > fibrous tissue forming anterior to retinal disc > more common in Type I DM, need urgent referral, 50% blind in 5 years Maculopathy > based on location rather than severity, anything is potentially serious > hard exudates and other 'background' changes on macula > check visual acuity > more common in Type II DM Management: > All patients optimise glycaemic control, blood pressure and hyperlipidemia > regular review by ophthalmology Maculopathy > if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors Non-proliferative retinopathy > regular observation > if severe/very severe consider panretinal laser photocoagulation Proliferative retinopathy > panretinal laser photocoagulation > intravitreal VEGF inhibitors > if severe or vitreous haemorrhage: vitreoretinal surgery Complications > retinal detachment > blindness Virectomy if severe vitreous haem or retinal damage.

Answer 59

a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes. ``` Features: HTN Hyperglycaemia Obesity Hyperlipidaemia Hypertriglyceridemia ``` ``` RF: poor diet sedentary life style age, genetics XS alcohol consumption stress ```

Answer 60

stress/infection poorly regulated glucose surgery MI pancreatitis chemo antipsychotics

Answer 61

``` Acute cerebral oedema: kids/ young adult particularly vulnerable. ↑K Aspiration pneumonia ↓K, Mg, P Thromboembolism Gastric stasis Arrhythmias ARDS AKI ```

Answer 62

may indicate pancreatic insulinoma hypoglycaemia Sx, low BG + resolution of Sx after ↑BG

Answer 63

Sweating, anxiety, hunger Tremor, palpitations Dizziness, nausea Generalised tingling Confusion, irritability Blurred vision Drowsiness Mutism Personality change Restlessness Incoherence: misdiagnosis of alcohol intoxication or psychosis Unexplained weight gain: insulinoma Unexplained WL: adrenal insuff

Answer 64

middle age, F, insulinoma, exogenous insulin, ethanol consumption, bariatric surgery, liver/renal failure intense exercise, fibromas, sarcomas, adrenal insuff (Addison’s disease), GH def, hypopituitarism, sepsis, glycogen storage disease, AN, malnutrition, ackee fruit ingestion, haloperidol, quine, fluroquinolone, SU, disopyramide, BB, salicylate, tramadol, PPI, alcohol (binge with no food), Addison’s.

Answer 65

Seizures | Comas

Answer 66

BG <3 Insulin >21 Serum peptide >200

Answer 67

Small high starch meals, if post-prandial slowly absorbed carbs (fibre). Conscious: 10-20g of quick acting carb snack, orange juice (repeat up to 3X) Conscious, uncooperative: glucose gel Unconscious: IV 20% glucose or SC/im glucagon Hypokit: IM/SC glucagon

Answer 68

insulinoma - increased ratio of proinsulin to insulin self-administration of insulin/sulphonylureas liver failure Addison's disease alcohol nesidioblastosis - beta cell hyperplasia

Answer 69

condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).

Answer 70

idiopathic post head injury pituitary surgery craniopharyngiomas infiltrative >histiocytosis X >sarcoidosis DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome) haemochromatosis

Answer 71

genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel electrolytes: hypercalcaemia, hypokalaemia lithium >lithium desensitizes the kidney's ability to respond to ADH in the collecting ducts demeclocycline tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

Answer 72

polyuria - even with restricted fluid intake polydipsia nocturne dehydration hypotension fatigue, nausea, poor concentration, confusion ↑Na: irritability, restlessness, lethargy, spasticity, hyperreflexia

Answer 73

high plasma osmolality, low urine osmolality > a urine osmolality of >700 mOsm/kg excludes diabetes insipidus water deprivation test - fluid deprivation 8 hrs. Urine osmolarity <300 despite no fluid, normally would rise >700. ADH analogue SC, ↑urine osmolality > central DI. If no change > nephrogenic. Cranial MRI ↓ ADH (neurogenic), urine osmolarity <300mmol/kg ↑ plasma osmolarity: >295mOsm/Kg for central, gestational + nephrogenic DI. If normal but still has polyuria + polydipsia could be dipsogenic.

Answer 74

nephrogenic diabetes insipidus: thiazides (increase urine excretion of Na, decrease blood osmolarity, and stops thirst, decrease polyuria), low salt/protein diet, NSAIDs/indomethacin (inhibit action of ADH), high dose desmopresin central diabetes insipidus can be treated with desmopressin, excision of tumour, chlorpropamide (enhance renal response to low ADH)

Answer 75

Gestational: placenta releases vasopressinase, breaks down ADH, gets worse until birth, can last 2 mnth after birth. Dipsogenic/psychogenic: drinking too much, schizophrenia, ↓blood osmolality, hypothalamus ↓ADH as normal physiological response

Answer 76

``` ↑Na Thrombosis Dehydration Bladder + renal dysfunction Iatrogenic ↓Na: desmopressin ``` Wolfram’s syndrome: cranial DI, optic atrophy, deafness

Answer 77

excess growth hormone in adulthood causes: > pituitary adenoma in over 95% of cases > ectopic GHRH or GH production by tumours e.g. pancreatic.

Answer 78

coarse facial appearance, spade-like hands, increase in shoe size large tongue, prognathism, interdental spaces excessive sweating and oily skin: caused by sweat gland hypertrophy features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia raised prolactin in 1/3 of cases → galactorrhoea 6% of patients have MEN-1

Answer 79

``` hypertension diabetes (>10%) cardiomyopathy colorectal cancer due to polyps CTS OSA arrhythmia ```

Answer 80

Growth hormone (GH) levels vary during the day and are therefore not diagnostic. Serum IGF-1 levels - first-line test, also used to monitor disease Then OGTT test (no suppression, normally suppressed to <2 mu/L) with serial GH measurement pituitary MRI of sella turcica with gadolinium CT scan chest/abdo: ectopic tumours ↑Ca, P Often: cortisol ↓, PRL↑

Answer 81

Trans-sphenoidal resection Somastostatin agonists: inhibit GH release, octreotide or lanreotide Dopamine agonists: bromocriptine, cabergoline. GHr antagonists: pegvisomant Radiation

Answer 82

GH hypersecretion in childhood. XS GH, GHRH, IGF-1 Pit gland Ca, pit adenoma, hypothalamic tumour, ectopic GH secretion, hereditary (McCune Albright syndrome, MEN1)

Answer 83

Linear growth of long bone Height sig above SD, XS fast growth in height Obesity: rapid weight gain due to XS IGF-1 Overgrowth of face/ extremities Headache/ compression of optic nerve Maxilla/ mandible protrusion Enlargement of skull bones Soft tissue swelling (hands + feet)

Answer 84

HTN Osteoarthritis Insulin resistance: DM CTS Organomegaly ↑PRL: ↓menstruation, breast enlargement in boys

Answer 85

MRI: pit tumours CT: tumours in other organs OGTT: hyperglycaemia, elevated IGF-1 Elevated GH + IGF-1

Answer 86

Normal variation in growth, temp delay, eventual adult height within normal range. RF: FH of delayed growth Transient GH or pit doesn’t start producing hormones on time ``` Sx: Normal size at birth Short preadolescent stature, growth rate falls, picks up again, matches to peers around age 4. (Height still lags behind) typically have growth spurt later + catches up Psychosocial stress Delayed pubertal development ``` Ix: XR: delayed bone development, hand XR for bone age, normally at least 1 yr less than actual age Management: Provide reassurance regarding eventual normal growth + development

Answer 87

Hypothalamic/ pit dysfunction, tumours, radiation, traumatic injury, AI disease, genetic (PROP1 mutation in GHRH receptor), Prader-Willi, Turner’s. idiopathic Sx: Newborn: hypoglycaemia, micropenis, XS jaundice Children: stunted growth/ short stature, delayed puberty, dwarfism, growth plates don’t fully fuse, delayed bone age, nystagmus, hypoglycaemia, retinal defects, cleft lip, delayed motor skills (↓ muscle development) Adults: ↓muscle mass, ↓bone mineral density, baldness ``` Complications: Psychosocial stress Delayed pubertal development Overweight # Cardiac conditions Psychological issues: memory problems, social issues, depression ``` Ix: > Serum GH levels <1ng/mL. Nonspecific affected by circadian rhythms, food, stress. > Serum IGF-1: more accurate, not affected by external factors. > Insulin tolerance test: regular insulin administered via IV > measure blood at 30 min intervals. Subnormal ↑ in serum GH Tx: Injection with recombinant GH, childhood > daily, adulthood 25% Tx for children

Answer 88

High prolactin Damage to hypothalamic-pit stalk (trauma, tumour, surgery, dopamine can’t reach lacotrophs to inhib) Prolactinoma/ lacotroph adenoma, Preg + BF, stress, exercise, sleep, PCOS Hypothalamus dys, Heavy metal poisoning, dopamine antagonists, oestrogen meds (stimulate more PRL), metoclopramide, haloperidol, methyldopa oestrogens, ecstasy, phenothiazines, SSRIs Renal failure 1° hyperthyroid (hypothalamus tries to ↑ thyroxine, release TRH)

Answer 89

Visual impairment (bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia), headaches, S+S of hypopituitarism Males: infertility, ED, impotence, ↓libido, gynecomastia, galactorrhoea Females: irregular menstrual cycles, infertility, dry vagina, galactorrhoea, painful breasts Osteoporosis

Answer 90

Head MRI/CT: tumours/ lesions in hypothalamic-pit area, if none + high serum levels, idiopathic hyperprolactinaemia High serum prolactin levels Lower bone density

Answer 91

Dopamine agonist: bromocriptine/ cabergoline - inhibit release of prolactin Surgical removal of tumour If hypothyroid > replacement thyroid hormones

Answer 92

escribes the inadequate production of one or more of the hormones secreted by the pituitary gland. Ant pit: GH, ACTH, PRL, TSH, LH, FSH Post: ADH, oxytocin

Answer 93

compression of the pituitary gland by non-secretory pituitary macroadenoma (most common) pituitary apoplexy Sheehan's syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage hypothalamic tumours e.g. craniopharyngioma trauma iatrogenic irradiation infiltrative e.g. hemochromatosis, sarcoidosis

Answer 94

Go Look For That Adenoma sequence of loss, GH, LH, FSH, TSH, ACTH. ``` low ACTH > tiredness > postural hypotension > weight loss > delayed puberty > low BG + Na > decreased skin pigmentation ``` low FSH/LH > amenorrhoea > infertility > loss of libido low TSH > feeling cold > constipation low GH > if occurs during childhood then short stature low prolactin > problems with lactation there may also be features suggestive of the underlying causes > pituitary macroadenoma → bitemporal hemianopia > pituitary apoplexy → sudden, severe headache

Answer 95

hormone profile testing Insulin stimulation: should ↓ blood sugar which stim GH + ACTH, if levels remain low = hypopit imaging - MRI scan, Sheehans pit ring sign (halo round empty sella) IGF ↓ Water deprivation + desmopressin response test

Answer 96

treatment of any underlying cause (e.g. surgical removal of pituitary macroadenoma) replacement of deficient hormones surgical excision of tumours Dopamine antagonist if PRL def + want to BF

Answer 97

Bitemporal adenoma ↓bone mass DI

Answer 98

is characterised by hyponatraemia secondary to the dilutional effects of excessive water retention ADH, water retention, dilutes plasma, ↓Na, extra fluid takes up more space in BV, inhibs aldosterone release, body dumps Na into urine, water follows Na, XS urine TA: erratic, independent of plasma osmolarity, ADH very high, lot of fluid retained, urine osmolality very high. TB: constant release of moderate ADH TC: baseline plasma Na set lower than normal, plasma Na stable, other types it falls. T4: ADH secretion normal but osmolality high.

Answer 99

CNS disorders enhance ADH production, trauma, stroke, haem, infection, SAH, subdural haemorrhage, mental illness through carbamazepine effects Ectopic ADH: lung malig (small cell), pancreas ca, prostate ca, TB, CF, pneumonia. Infection - TB, pneumonia Anticonvulsants, opioids, SU, SSRIs, TCAs, vincristine, cyclophosphamide Injury/ removal of pit Positive end expiratory pressure (PEEP) porphyria

Answer 100

correction must be done slowly to avoid precipitating central pontine myelinolysis fluid restriction - <800mL, if associated with subarach haem fluid restriction not recommended demeclocycline: Abx, reduces the responsiveness of the collecting tubule cells to ADH ADH (vasopressin) receptor antagonists (tolvaptan) have been developed IV saline for severe Furosemide High salt + protein diet

Answer 101

Body weakness Fatigue, lethargy Dizziness Confusion Nausea, anorexia, vomiting Headaches Muscle cramps, myoclonus, tremors

Answer 102

Cerebral oedema: confusion, mood swings, hallucinations, coma, death, seizures

Answer 103

Urinalysis: highly concentrated urine >100, high urine na >30 Serum: ↓Na, ↓osmolarity (<275mmol/kg), urea (<3.6mmol/L, due to mild volume expansion) Absence of hypo/hypervolaemia Fractional excretion of Na: >1%. Fractional excretion of urea: >55%

Answer 104

parathyroid secretes PTH independently of Ca. parathyroid adenoma, mutation, MEN. Parathyroid hyperplasia.

Answer 105

PTH stimulates osteoclasts, kidneys hold onto Ca + get rid of P Slower muscle contraction Stones, thrones, bones, groans, psychiatric overtones Poor sleep, fatigue, anxiety, memory loss, myalgias, paraesthesia, muscle cramps, constipation, abdo pain. 1°/3°: slower muscle contractions, less excitable neurons 2°: Sx CKD, ↓Ca Sx. Polyuria, polydipsia

Answer 106

``` 1°: brown tumours, large bone cysts (high osteoclast activity), osteitis fibrosa cystica, soft tissue calcifications Peptic ulceration Pancreatitis Bone pain/# HTN ```

Answer 107

1°: ↑Ca, ↓P, hypercalciuria, ↑PTH, vit D def, ↑ALP (high bone turn over) Pepper pot skull on XR

Answer 108

↓Ca ↑P ↓vit D, Ur+Cr ↑

Answer 109

↑PTH, ↑Ca, if person still has CKD ↑P, if had kidney transplant ↓K.

Answer 110

1/3°: calcimimetics (imitate Ca on PT cells), remove abnormal parathyroid glands. Vit supplements: ergocalciferol. Bisphosphonate. 2°: phosphate binders (sevelamer), vit D supplements, calcitriol (suppress PTH)

Answer 111

gland normal, XS PTH in response to chronic ↓Ca, impaired kidney function (↑P ↓calcitriol, ↓Ca intestine absorption) chronic lack of calcitriol (lack of sunlight, poor vit D intake.)

Answer 112

2° hyperparathyroid for many years develop 1° due to hyperplasia of PT glands.

Answer 113

genes F>M lithium

Answer 114

AI destruction Mg def, chronic alcoholism, malnutrition, malabsorption, diarrhoea Iatrogenic: parathyroid/ thyroid surgery/ radiation DiGeorge synd, AD hypoparathyroidism, Albright hereditary osteodystrophy (pseudo, kidneys/ bones resistant to PTH), haemochromatosis, tumours, Wilson’s

Answer 115

Muscle spasms/ cramps Tetany Chvosteks/trousseau Perioral numbness, paraesthesia Poor memory/ slowed thinking Chronic: BG calcifications dystonia, parkinsonism, athetosis, hemiballismus, oculogyric crisis, cataracts, dry coarse skin, brittle nails, patchy alopecia.

Answer 116

Seizures Resp paralysis Death

Answer 117

↓Ca, ↓PTH ECG: prolonged QT, ST, TdP, AF

Answer 118

IV calcium gluconate: if severe Oral Ca: carbonate/ citrate Vit D: calcitriol Synthetic PTH Mg sulphate Thiazide diuretic

Answer 119

Condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome. Gastrinoma, ↑acid secrtion + peptic ulcers. Usually malig Features - multiple gastroduodenal ulcers - diarrhoea, steatorrhoea - malabsorption - GORD - Abdo pain - N/V, bloating, belching - dysphagia, weight loss - GI bleed - oesophageal strictures - pancreatitis Diagnosis - fasting gastrin levels: the single best screen test - ^ gastrin - secretin stimulation test - ^ gastrin - endoscopy - ulcer, enlarged rugal folds, oesophagitis - endoscopic US - hypo echoic, homogenous mass Management - surgery - chemo - PPIs - Somatostatin analogue:↓gastrin levels.

Answer 120

a rare catecholamine secreting tumour. Cells darken. Arise from chromaffin cells in adrenal medulla. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome Rule of 10: 10% bilat, 10% kids, 10% metastasise, 10% calcify, 10% extra-adrenal. bilateral in 10% malignant in 10% extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

Answer 121

typically episodic Ps: perspiration, palpitation, pallor, ↑BP, pain (headache). Tachycardia hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety

Answer 122

24 hr urinary collection of metanephrines (sensitivity 97%*) this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%) CT/MRI

Answer 123

Surgery definitive management First stabilised with medical management: alpha-blocker (e.g. phenoxybenzamine), given before a beta-blocker (e.g. propranolol)

Answer 124

↑180/120 emergency: stroke, retinal haemorrhage, ischaemia, kidney failure, burst vessels Polycythaemia.

Answer 125

Multiple Endocrine Neoplasia 2P's and M: Medullary thyroid cancer (70%) Parathyroid (60%) Phaeochromocytoma Hirschsprungs, cutaneous lichen amyloidosis RET oncogene

Answer 126

Medullary thyroid cancer 1P and M: Phaeochromocytoma Marfanoid body habitus Neuromas RET oncogene

Answer 127

3 P's: Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia Pituitary (70%) Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration) Also: adrenal and thyroid AD, MEN1 gene Chr11, encodes menin > inactive > endocrine neoplasia Most common presentation = hypercalcaemia ↓BMD, nephrolithiasis Bitemporal hemianopia

Answer 128

``` CT/MRI: tumours Thyroid USS MTC: ↑CEA, calcitonin Parathyroid: ↑Ca, PTH Pheochromocytoma: ↑plasma fractionated metanephrines + 24hr urine metanephrine. ``` Tyrosine kinase inhibs Bisphosphonates CLA: intralesional steroids, antihistamines, UV light/ laser therapy Tumour resection

Answer 129

MRI/CT: tumour/mets Endoscopy: biopsy Endoscopic USS, somatostatin receptor scintigraphy: pancreatic neuroendocrine neoplasms. Parathyroid: ↑Ca, PTH PaNETs: ↑gastrin, insulin, VIP, ↓glucose MEN 1 gene mutation Treat tumour > see in other notes how to Surgical resection Radiation

Answer 130

Neuroendocrine tumours secrete: serotonin, histamine, bradykinin + prostaglandins. Appendix most common GIT site usually occurs when metastases are present in the liver and release serotonin into the systemic circulation may also occur with lung carcinoid as mediators are not 'cleared' by the liver

Answer 131

GIT tumour: hormone secretion inactivated by liver > no Sx. When liver mets > hormones released into circ > Sx flushing (often earliest symptom) diarrhoea bronchospasm hypotension Plt take up serotonin + use it to constrict BVs right heart valvular stenosis (left heart can be affected in bronchial carcinoid) other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing's syndrome pellagra (dermatitis, diarrhoea, mental Disturbance) can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

Answer 132

urinary 5-HIAA plasma chromogranin A y Sx worsened by alcohol or emotional stress CT: locate tumours Octreoscan: inject radiolabelled somatostatin analogue, octreotride which binds to increased somatostatin receptors on tumour cells Niacin deficiency

Answer 133

somatostatin analogues e.g. octreotide diarrhoea: cyproheptadine may help

Answer 134

1/3 metastasise 1/3 associated with secondary malig 1/3 multiple tumours Collagen fibre thickening, fibrosis, heart valve dysfunction > TR, PS

Answer 135

Transient central hypothyroid in severely sick. Thyroid gland functioning normal but thyroid hormone levels abnormal Less deiodinase in catabolic state, less T4> T3 conversion. everything (TSH, thyroxine and T3) is low. In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3). Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed. ``` Sx: Fatigue Cold intolerance Weight loss/ gain Constipation Muscle cramps Headache Hair loss/ brittleness Menstrual irregularities ``` Complication: Myxedema coma Investigations: Serum TSH: normal/ low Normal/low T4 Low T3 ``` Management: Levothyroxine Treat underlying cause when starts eating again/ recovers from illness thyroid hormones return to normal NO TX NEEDED ```

Answer 136

AI disease, TSH receptor antibodies, mimics TSH, can lead to thyroid hypertrophy + hyperplasia. RF: CTLA4, PTPN22, HLA-DR3, 20-40, F>M, tobacco RF for orbitopathy. Most common cause thyrotoxicosis

Answer 137

typical features of thyrotoxicosis goitre thyroid bruit eye signs (30% of patients) > exophthalmos > ophthalmoplegia pretibial myxoedema thyroid acropachy, a triad of: > digital clubbing > soft tissue swelling of the hands and feet > periosteal new bone formation

Answer 138

↓ TSH, ↑ T3, ↑ T4, ↑ TSI Autoantibodies > TSH receptor stimulating antibodies (90%) > anti-thyroid peroxidase antibodies (75%) Thyroid USS: diffuse enlargement, highly vascular Thyroid scintigraphy > diffuse, homogenous, increased uptake of radioactive iodine

Answer 139

BB: propranolol Refer to 2° care Carbimazole (complication, agranulocytosis) Radioiodine: CI in pregnancy (avoid 4-6 mnth after Tx) + <16 y/o, thyroid eye disease. Thyroidectomy Optic: steroids (pred),

Answer 140

AI: graves TSH disease: TSH secreting adenomas, TSH receptor stimulation with XS hCG (trophoblastic disease, hyperemesis gravidarum) Solitary autonomous adenoma XS iodine ingestion Toxic nodular goitre Job-Basedow syndrome: iodine induced Neonatal hyperthyroid: newborn mothers who have Graves. Amiodarone RF: F>M, smoking, genes

Answer 141

Thyroid: normal/ enlarged, goitre, palpable nodules. CV: bounding, rapid pulse, HTN, palpitations. GI: ↑appetite/ ↓weight, V/D, hyperdefecation Warm, flushed, moist skin, patchy hair loss, thyroid acropachy (clubbing), pretibial myxedema, XS sweating, red palms. Heat intolerance, fine tremor, agitation, insomnia Menstrual irregularities, ↓libido, infertility

Answer 142

Thyroid storm Congestive heart failure Osteoporosis Skeletal muscle atrophy AF

Answer 143

RAIU: ↑123I uptake confirms hyperthyroidism USS: benign/ malig nodules, microcalcifications, hypoechogenicity in malig nodules. 1°: ↓ TSH, ↑T4 + T3 ↑TSH, T3/4, TSH induced

Answer 144

Carbimazole, propylthiouracil Thyroidectomy Radioactive thyroid ablation BB: propranolol

Answer 145

rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm. More unbound thyroid hormones or tissue more sensitive to thyroid hormones or catecholamines Precipitating events: - thyroid or non-thyroidal surgery - trauma - infection - acute iodine load e.g. CT contrast media

Answer 146

``` fever > 38.5ºC tachycardia confusion and agitation nausea and vomiting hypertension heart failure abnormal liver function test - jaundice may be seen clinically ``` Can result in: MI, death

Answer 147

symptomatic treatment e.g. paracetamol treatment of underlying precipitating event beta-blockers: typically IV propranolol anti-thyroid drugs: e.g. methimazole or propylthiouracil Thioamides: block thyroid hormone production, iodine preparations, GC (dexamethasone), bile acid sequestrants, methimazole or propylthiouracil Plasmapheresis: blood plasma removed Intensive supportive care Lugol's iodine dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

Answer 148

describes a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism. Lack of iodine > ↓T3/4 > ant pit release TSH > thyroid hypertrophy/ hyperplasia. Some part of thyroid gland more responsive to TSH than others, uneven growth > multiple nodules > mutation in TSH receptor in 1 of follicles > cell active without TSH > ↑ thyroid hormone. Goitre Nuclear scintigraphy reveals patchy uptake. The treatment of choice is radioiodine therapy. Also surgery

Answer 149

1°: thyroid gland problem iodine def, AI (Hashimoto) congen (inborn errors, thyroid agenesis/ hypoplasia), iatrogenic (Tx of hyperthyroid/ neoplasm), 1° atrophic hypothyroid (diffuse lymphocytic infiltration leading to atrophy), post-partum thyroiditis, sarcoidosis, haemochromatosis. ↓T4 absorption (iron salts, cholestyramine), ↓T4>T3 (amiodarone), ↓clearance T4 (phenytoin, carbamazepine), lithium, IFNα, IL2, TK inhib, P-amino salicylic acid. 2/3°: not enough TSH/ TRH, pit/ hypothalamus disorder

Answer 150

Fatigue, cold intolerance Muscle weakness Headache ↑weight ↓appetite Brittle hair/ hair loss Menstrual irregularities, menorrhagia Goitre Difficulty concentrating, poor memory CTS, ↓reflexes, periph neuropathy. Myxoedema: periorbital oedema, tongue, enlargement, puffy face, lower leg (pretibial), ascites, pericardial/ pleural effusion Dry course skin Voice: hoarser/ deeper Ileus, constipation Congen: prolonged neonatal jaundice, delayed mental/ physical milestone short stature, puffy face, macroglossia, hypotonia.

Answer 151

Myxoedema coma: altered mental state, hypothermia, multi-organ failure, ↓BP, HR, Na, glucose, ventilation. Poorly managed hypothyroid, acute event eg trauma, infection, MI Dyslipoproteinaemia Dilated cardiomyopathy Anaemia Hyperprolactinaemia > galactorrhoea ↓clearance of drugs: antiepileptic, anticoag, ipiods, drug toxicity Congen: FTT, intellectual disability

Answer 152

1°: ↑TSH ↓T4/3 Central: ↓TSH, T4/3 Antibodies: anti-TPO/ TSH receptor, antithyroid peroxidase antibodies FBC: mild normocytic anaemia

Answer 153

Levothyroxine replacement, initial starting dose lower in elderly + ischaemic heart disease (25mcg), other pts (50-100mcg). TFTs 8-12 wks later. ↑dose in pregnancy. SE: hyperthyroid, ↓BMD worsening angina, AF. Fe/Ca carbonate ↓absorption Subclinical hypothyroid: ↑TSH normal T3/4. TSH 4-10 (<65 with Sx trial thyroxine, older watch + wait, repeat TFT in 6mnth), TSH >10 (Tx with thyroxine <70, older watch + wait). Poor compliance with thyroxine: ↑TSH, normal T3/T4 as pts take thyroxine in days before test. 2°: replacement steroid before thyroxine.

Answer 154

an autoimmune disorder of the thyroid gland. It is typically associated with hypothyroidism although there may be a transient thyrotoxicosis in the acute phase. It is 10 times more common in women Features: > features of hypothyroidism > goitre: firm, non-tender > anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies Associated with other AI conditions (coeliac, T1DM, vitiligo) and MALT lymphoma Stridor > tracheal compression Myxoedema: non pitting oedema, mucopolysaccharide deposition in upper skin layers, tibial area, may occur around eye + feet ↓T3 + T4 ↑TSH + TRH Tx: Levothyroxine Surgery

Answer 155

Three stages 1. Thyrotoxicosis - typically few mnths after delivery, last up to 8 wks 2. Hypothyroidism - can last up to 6 mnth 3. Normal thyroid function (but high recurrence rate in future pregnancies) RF: prev PP thyroiditis, pre-existing hypothyroid, T1DM, FH Thyroid peroxidase antibodies are found in 90% of patients Management the thyrotoxic phase is not usually treated with anti-thyroid drugs as the thyroid is not overactive. Propranolol is typically used for symptom control the hypothyroid phase is usually treated with thyroxine

Answer 156

rare cause of hypothyroidism characterised by dense fibrous tissue replacing the normal thyroid parenchyma associated with retroperitoneal fibrosis Hardened wood like, fixed painless + enlarged goitre Hypothyroidism SOB/dyspnoea > trachea fibrosis Voice hoarseness > recurrent laryngeal N Dysphagia > oesophageal fibrosis Parathyroid: ↓Ca ``` Anti-TPO ↓ T3 + T4 ↑ TSH + TRH Biopsy: predominant fibrous tissue, collagen + lymphocyte infiltration USS/CT/MRI: enlarged thyroid Middle aged women ``` ``` Management: CS Tamoxifen Levothyroxine Surgery ```

Answer 157

occur following viral infection and typically presents with hyperthyroidism. ``` There are typically 4 phases; phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR phase 2 (1-3 weeks): euthyroid phase 3 (weeks - months): hypothyroidism phase 4: thyroid structure and function goes back to normal ``` Investigations Initial ↑T3 + T4, ↓TSH low. ↑ESR + CRP thyroid scintigraphy: globally reduced uptake of iodine-131 Management usually self-limiting - most patients do not require treatment thyroid pain may respond to aspirin or other NSAIDs in more severe cases steroids are used, particularly if hypothyroidism develops

Answer 158

Bromocriptine

Answer 159

24 hr urinary collection of metanephrines

Answer 160

Low FSH/LH and low testosterone

Answer 161

EXPLAIN * Exogenous drugs (typically sulfonylureas or insulin) * Pituitary insufficiency * Liver failure * Addison's disease * Islet cell tumours (insulinomas) * Non-pancreatic neoplasms

Answer 162

an inhibitor of intestinal alpha glucosidases which delays the digestion of starch and sucrose. It does not appear in NICE guidance due to significant gastrointestinal side-effects this medication causes.

Answer 163

inhibits sodium-glucose co-transporter 2 in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion. It is contraindicated in active foot disease such as skin ulceration with a possible increased risk of toe amputation.

Answer 164

a thiazolidinedione that reduces peripheral insulin resistance and is contraindicated in patients with active or previous bladder cancer

Answer 165

works by inhibiting gastric and pancreatic lipase to reduce the digestion of fat

Answer 166

initial hyperthyroidism, painful goitre and globally reduced uptake of iodine-131

Answer 167

Cortical - not suppressed, ACTH - suppressed, = Cushing's syndrome (due to other causes adrenal adenomas) Cortisol - suppressed, ACTH - suppressed, = Cushing's disease (pituitary adenoma) Cortisol - not suppressed, ACTH - not suppressed, = ectopic ACTH syndrome

Answer 168

Papillary - 65%, generally young females. Metastasis to cervical lymph nodes. Thyroglobulin can be used as a tumour marker. Characteristic Orphan Annie eyes on light microscopy. Good prognosis Follicular - 20%, generally women >50 years old. Metastasis to lung and bones. Thyroglobulin can be used as a tumour marker. Moderate prognosis Medullary - 5%, sporadic or part of MEN2 syndrome. It originates from the parafollicular cells which produce calcitonin - can be used as a tumour marker. Anaplastic - very rare. Elderly patient. Very poor prognosis Lymphoma - 5%, might present with dysphagia or stridor

Answer 169

* urine osmolality after fluid deprivation: low | * urine osmolality after desmopressin: low

Answer 170

Primary hyperparathyroidism - occur with a high calcium and high (or abnormally high within reference rang) PTH without any other factors. Secondary - usually due to chronic renal failure so deranged U&Es, increase in PTH due to low calcium Tertiary - history of hypocalcaemia that has been corrected, long-standing renal failure,

Answer 171

is a life-threatening complication of type 2 diabetes and will usually present with marked hyperglycaemia without ketoacidosis. the diagnostic criteria for HHS include hypovolaemia, hyperglycaemia (blood sugar > 30mmol/L) and a serum osmolality > 320mosmol/kg.

Answer 172

commonly due to cytomegalovirus (CMV)-related necrotising adrenalitis.

Answer 173

Occurs due to rapid enlargement of a pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands (bilateral adrenalectomy) which is an operation used for Cushing's syndrome. Removal of both adrenal glands eliminates the production of cortisol, and the lack of cortisol's negative feedback can allow any pre-existing pituitary adenoma to grow unchecked. Continued growth can cause mass effects due to physical compression of brain tissue. Increased production of adrenocorticotrophic hormone (ACTH) can result in increased melanocyte stimulating hormone (MSH) which can result in hyperpigmentation. Nelson's syndrome is now rare because bilateral adrenalectomy is now only used in extreme circumstances. After bilateral adrenalectom follow-up should include awareness of Nelson's syndrome. Monitoring of ACTH level and pituitary MRI are recommended 3-6 months after surgery and regularly thereafter.

Endocrine Flashcards

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