Endocrine Flashcards

Question

Outline the aetiology of carcinoid syndrome - Where are the carcinoid tumours in those with carcinoid syndrome often located? - Which tumours will produce symptoms, which will not? - What hormones and what is the tumour cell type

Answer 1

~80% of the tumours in people with carcinoid syndrome are located in the small intestine Carcinoid tumours are slow-growing neuroendocrine tumours mostly derived from serotonin-producing enterochromaffin cells. Common sites for carcinoid tumours that DO NOT result in carcinoid syndrome (because they are non-secretory) include appensix and rectum. Also other parts of large intestine, stomach, thymus, bronchus and other organs. The hormones that are released into the portal circulation are metabolised by the liver, so symptoms won't appear until there are hepatic metastases (resulting in secretion of tumour products into hepatic veins), OR release into systemic circulation from bronchial or extensive retroperitoneal tumours

Answer 2

Rare, annual UK incidence is one in 1 000 000. Asymptomatic carcinoid tumours are more common and may be an incidental finding after rectal biopsy or appendectomy. Ten percent of patients with multiple endocrine neoplasia (MEN) type 1 have carcinoid tumours.

Answer 3

1. Diarrhoea 2. SoB, wheezing, asthma due to seratonin leading to bronchoconstriction 3. Flushing (due to release of histamine and bradykinin, both vasodilators)- key! 4. Itching (due to histamine) ALCOHOL AND STRESS can worsen as they stimulate the neuroendocrine cells Confusion/inflamed skin due to pellagra (which is due to reduced niacin (=vit B3). Niacin is reduced because the increased seratonin production leads to reduced production of tryptophan, which is required for niacin)

Answer 4

Facial flushing, telangiectasia, wheeze Right side heart valve dysfunction and murmurs (seratonin leads to thickening and fibrosis of heart valve). Tricuspid regurg /stenosis and pulmonary stenosis Nodular hepatomagaly in metastatic disease Carcinoid crisis: profound flushing, bronchospasm, tachycarrdia and fluctatuating BP

Answer 5

Medical imaging (CT scan and octreoscan) Octreoscan: -Inject radiolabelled somatostatin analogue called octreotide. Because somatostatin receptor number is paradoxically increased in carcinoid, there will be increased uptake of the radiolabelled analogue in carcinoid areas 24 hr Urinalysis: - Gold standard- chromogranin A (CgA) - increased level of 5-hydroxyindoleacetic acid (5-HIAA) (breakdown product of seratonin). NOTE THIS MAY BE FALSELY +VE WITH HIGH INTAKE OF CERTAIN FRUITS/DRUGS e.g bananas and avacados, caffeine and paracetemol Blood tests - Niacin deficiency - Chromogranin A and B (non-specific released from neuroendocrine cells) Investigations for MEN-1

Answer 6

Mostly in the epithelial layer of the GI organs and the lungs They release hormones in response to stimulation by neurones but can also be inhibited by hormonal mechanism (e.g. somatostatin can bind receptors to stop release of seratonin) There are INCREASED somatostatin receptor expression on carcinoid tumour cells (perhaps unexpectedly!)

Answer 7

MEN type 1 (mutation in menin gene on chromosome 11): Parathyroid adenoma or hyperplasia, pancreatic endocrine tumours, pituitary adenomas. (3Ps) and carcinoid MEN type 2 (mutation in RET gene on chromosome 10): Medullary thyroid carcinoma, phaeochromocytoma and either parathyroid hyperplasia (MEN-2A) or mucosal neuromas on the lips or tongue (MEN-2B).

Answer 8

GnRH pulsatile secretion increases, which preferentially increases LH secretion. So LH is high and FSH is low. LH stimulates theca cells to produce androstenedione. But there is reduced conversion of androstenedione into oestrogen by granulosum cells in the ovary because granulosa cells respond to FSH, of which there is reduced secretion. But there is increased conversion of androstenedione into testosterone in the theca cells (because they are being stimulated by LH) rather than it being metabolised to oestrogen in granulosa cells Note that peripheral adipocytes produce more oestrogen than usual due to the increased production of adrostenedione. They do this using aromatase (note that both granulosa cells and adipose tissue contain aromatase, but granulosa cell aromatase responds to FSH stimulation)

Answer 9

Thyroid surgery Infection Myocardial infarction Diabetic ketoacidosis Radioactive iodine administration Hip replacement

Answer 10

Thyrotoxicosis, T1DM

Answer 11

They may have developed the rare neutropaenic side-effect of Carbimazole (agranulocytosis) A patient who develops neutropaenia on Carbimazole should NOT be treated with Propylthiouracil (PTU) either: PTU has a similar low risk of causing agranulocytosis (<0.5%) and cross-reactivity has been reported.

Answer 12

This is characteristic of erratic compliance: patients who don’t take the medication regularly, but remember to take it immediately before a blood test is due. This is enough to put their FT4 up, but not to suppress their TSH. A gentle chat about remembering to take the medication, and repeat TFTs in 6-8 weeks would be appropriate before adjusting the dose.

Answer 13

``` Renal artery stenosis Cushings syndrome Polycystic kidney disease Conns syndrome Phaeochromocytoma Acromegaly Aortic coarctation ```

Answer 14

Round face, centripetal obesity and thin legs

Answer 15

Sepsis and neurological disease (stroke) are some of the commoner causes. Also malignancy and lung abscess

Answer 16

pontine and extra-pontine myelinolysis

Answer 17

Fluid restriction (usually all that's needed in mild cases) Demeclocycline Hypertonic sodium chloride 1.8% IV (CAREFUL, in specialist care to avoid pontine and extra-pontine myelinolysis)

Answer 18

Background: - Blot haemorrhages - Microaneurysms (blot) - Hard exudates (leeked lipids from blood vessels) Pre-proliferative: -Above + soft exudates (regions of retinal ischaemia) Proliferative: new blood vessels begin to form in response to retinal ischaemia. ----- Maculopathy (a sub-type, not part of the above progression): In maculopathy, hard exudates are found near the macula. This can threaten direct vision.

Answer 19

Metabolic hyperglycaemic condition caused by absolute insufﬁciency of pancreatic insulin production.

Answer 20

Destruction of the beta cells in the centre of the islets of langerhans in the pancreas resulting in absolute insulin deficiency Type IV hypersensitivity response (genetic abnormality that causes loss of self tolerance of T cells that react to beta cell antigens) It's associated with HLA-DR3 and HLA-DR4 (but not everyone with these genes has DM, so it's environmental trigger too) Pancreatic beta cell autoantigens may also play a role in initiation or progression of T1DM, including GAD, insulin, insulinoma -associated protein 2 (IA-2) and ZnT8. Up to 90% of beta cells destroyed before symptoms

Answer 21

Usually appears in the young

Answer 22

Polyphagia- lipolysis and protein breakdown due to lack of insulin. Weight loss. Catabolic state leaves people feeling hungry. Glycosuria- renal threshold for reabsorption of sugar is reached. Polyuria- Water follows osmotically active glucose Polydipsia- dehydration and thirst Tiredness, weight loss.

Answer 23

Signs of complications: - DKA (see below) - Diabetic retinopathy on fundoscopy - Neuropathy on feet examination Signs of assicated conditions: - Vitiligo - Addison's - Autoimmune thyroid disease

Answer 24

``` Blood glucose (2 positive results needed before glucose): Fasting >7. Random >11. ``` HbA1C: estimated overall blood glucose levels in past 2-3 months FBC: MCV, reticulocytes (because reticulocyte turnover causes misleading HbA1c levels U&Es: monitor nephropathy OR hyperkalaemia due to ACEi *note you also get hyperkalaemia in DKA, look why below* Lipids Urine albumin creatinine ratio (to detect microalbulinaemia)

Answer 25

Glycaemia control. Conservative: advice and education Medical: -SC insulin: short acting insulin (lispro, aspart, glulisine) three times daily before each meal AND long acting insulin (isophane, glargine, detemir) once daily. ROTATE INJECTION SITES. Pumps can give better control, but are costly, and DKA can occur if it malfunctions. Patients can attend DAFNE (dose adjustment for normal eating) to learn how to calculate carb intake and adjust insulin accordingly Monitor: - Control of symptoms - Regular finger prick tests - Monitoring HbA1c (target <7%) ever 3-6 months Screening for complications of DM and of cardiovascular risk factors Treatment of DKA and hypoglycaemia below

Answer 26

Diabetic ketoacidosis (see below) Complications of insulin treatment: Weight gain, fat hypertrophy at insulin sites, hypoglycaemia (missing mealor overdosage of insulin- see signs of this below) Microvascular complications: retinopathy, neuropathy, nephropathy Macrovascular complictions: PVD, ischaemic heart disease, stroke/TIA. Increased susceptibility to infections (particuarly on feet)

Answer 27

Depends on early diagnosis, good glycaemic control and compliance with screening and treatment. Vascular disease and renal failure are major causes of increased morbidity and mortality.

Answer 28

Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin

Answer 29

Reduced insulin leads to lipolysis which generates fatty acids. The liver turns these into ketone bodies which increase the acidity of the blood. There is also increase of counter-regulatory hormones (e.g. epinephrine) leading to increased gluconeogenesis, but there is poor peripheral glucose utilisation. Renal reabsorption capacity of glucose is exceeded causing glycosuria, osmotic diuresis and dehydration. The ketones are useful because they be used by the cells for energy, but also causes acidosis. --------------------- Hyperkalaemia is associated. Because 1) There are K+/H+ exchangers on the cells. In the acidotic state, H+ is moved INTO the cells (in an attempt to reduce the acidity of the blood), in exchange for potassium which is moved out into the blood 2) Insulin activates the Na+/K ATPase, which moves potassium into cells. In insulin deficicient state, the potassium will remain outside cells. So note that even though the blood concentration of potassium is high, the total body store is low --------------------------------------- It can be the first presentation of T1DM. However, it can also be once somebody has been diagnosed with T1DM. E.g: In states of stress like infection, there is increased release of epinephrine which stimulataes the release of glucagon, which increase blood glucose and causes dehydration etc. And also, it causes a need for alternative energy, leading to generation of ketone bodies and acidosis ``` DKA may be caused by: Infection (30%) Errors in management (15%) Newly diagnosed diabetes (10%) Other medical disease (5%) No case identified (40%!) ```

Answer 30

``` Nausea Vomiting Abdominal pain Polyuria Polydipsia Drowsiness Confusion ```

Answer 31

Kussmaul respiration (deep, laboured breathing which is respiratory compensation to blow off CO2) Coma Fruity breath (ketone bodies are broken down further into acetone) Signs of dehydration (dry mucous membranes, reduced tissue turgor)

Answer 32

BLOOD: FBC: Increased WCC (even without infection). U&E: increase urea and creatinine from dehydration), hyperkalaemia LFT CRP glucose amylase (could increase) blood cultures ABG (metabolic acidosis with high anion gap) blood/urinary ketones URINE: Glycosura, increased ketones, MSU CXR: Exclude infection ECG: Rule out ischaemic changes

Answer 33

Consider HDU/ICU input, central line, arterial line and urinary catheter if severe acidosis, hypotensive or oliguric INSULIN: 50 U of soluble insulin in 50ml 0.9% saline, start at 0.1 U/kg/h (~6-7U/h) until,: -capillary ketones <0.3, venous pH >7.3 AND venous bicarbonate >18. Then, if patient can eat and drink, change to SC insulin. If not, change to IV sliding scale. Do not stop insulin infusion until 1-2hr after regular SC insulin is restarted. FLUIDS: 500ml 0.9% saline over 15-30 min until systolic BP >100mmHg. Then 1L 2-hourly X3, and 1L 3-hourly X3. IV dextrose is started in conjunction with 0.9 saline WHEN blood glucose reaches 11mmol/L: 1L 5% dextrose over 8h when blood glucose is 7-15mmol/L. Then 500ml 10% dextrose over 4h when blood glucose <7mmol/L POTASSIUM REPLACEMENT: -Start in the second bag of fluid, if passing urine. Adjust amoutn of ptassoim added to fluids according to plasma potassium (if >5.5: nil pottasium. If 2.5-5.5: 40mmol/L. If <2.5mmol/L, 60-80mmol/L) MONITOR BLOOD GLUCOSE, CAPILLARY KETONES, URINE OUTPUT HOURLY; U&Es 4HRLY and VBG at 0,2,4,6,8,12 h and before stopping fixed rate insulin regimen. Broad spectrum Abx if infection Thromboprophylaxis NBM for at least 6hr (gastroparesis common) NG tube (if GCS reduced, to prevent vomiting and aspiration) No strong evidence of IV bicarb If they have low potassium when they come in, don't give insulin until the potassium has come into the normal range

Answer 34

Mental state changes | Acute cerebral oedema

Answer 35

Adrenergic signs: pallor, sweating, tremor, tachycardia, palpitations, hunger Neuroglycopaenic signs: dizziness, personality change, fits, confusion, coma and focal neurology.

Answer 36

IF REDUCED CONSCIOUSNESS: 50ml of 50% glucose IV or 1mg glucagon IM. If conscious and cooperative: 50g oral glucose (e.g. lucosade, milk, sugar or 3 dextrose tablets), followed by a starchy snack. No drive for 45 minutes.

Answer 37

Autonomic neuropathy, b-blockers and brain adapting to recurrent episodes.

Answer 38

• One fasting blood glucose measurement > 7 mmol/L in a symptomatic patient • Two fasting blood glucose measurements > 7 mmol/L in an asymptomatic patient • One random blood glucose measurement > 11.1 mmol/L in a symptomatic patient • Two random blood glucose measurements > 11.1 mmol/L in an asymptomatic patient * Oral glucose tolerance test – 2 hr blood glucose > 11.1 mmol/L * HbA1c > 48 mmol/mol or > 6.5%

Answer 39

Candida, causing pruritus vulvae in females or penile inflammation (balantis) in males.

Answer 40

Urinary free cortisol level first (doesn't confirm diagnosis, but demonstrates pathalogical excess of cortisol) ...................... Then low dose dexamethasone test (0.5mg) and measure cortisol. This confirms Cushing's, but doesn't tell you whether it's at the pituitary gland (as this will continue to church out ACTH even with dexamethasone as -ve feedback is ineffective) or adrenal tumour (if the pituitary is working, dexamethasone will suppress the ACTH production, but the adrenal tumour no longer responds to ACTH and churns out cortisol even if ACTH is low) or an ectopic secreting ACTH (which, like the pituitary, won't suppress its ACTH production with dexamethasone administration). In the old days you would use high dose dexamethasone suppression, which slightly reduces cortisol production (because it ever so slightly suppresses ACTH from the pituitary). But now, we can just measure the ACTH (without dexamethasone, which is just used for the initial confirmatory test), which is HIGH in pituitary/ectopic secreting excess ACTH, and is LOW if there is an adrenal tumour/carcinoma. To then differentiate an ectopic from cushing disease (i.e. pituitrary), you give high dose dexamethasone, which will slightly reduce the ACTH from a pituitary adenoma (i.e. cushing's disease) BUT NOT suppress it from an ectopic. OR You can give meyrapone, which stops adrenal cortisol production, but not ectopic. IMAGING: MRI of pituitary, CT of adrenals, CT of chest, abdomen and pelvis

Answer 41

A simple goitre (B) is an idiopathic enlargement of the thyroid. Often the condition is associated with thyroid antibodies, but these do not cause any symptoms.

Answer 42

Riedel’s thyroiditis (C) is a rare inflammatory disease of the thyroid gland that is characterized by fibrosis of the thyroid gland and other structures in the neck. It is often stony or woody on palpation and patients are usually asymptomatic.

Answer 43

Addisons: Firstly, a short synacthen test confirms primary Addison’s disease, whereas ACTH deficiency or suppression by steroids can be confirmed by doing a long synacthen test. Cushings: Urinary free cortisol then the low-dose dexamethasone test

Answer 44

Catecholamine-producing tumours that usually arise from chromafﬁn cells of the adrenal medulla but are extra-adrenal in about 10% of cases 10% bilateral, 10% malignant. Extra-adrenal phaeochromocytoma's are known as "paragangliomas"

Answer 45

Sporadic. Unknown cause Familial (up to 30%). Familiacl cases seen in: 1) MEN2a 2) von Hippel Lindau syndrome 3) Neurofibromatosis type 1 (NF1) 4) Mutations in subunits of mitochondrial enzyme succinate dehydrogenase (SDHB, SDHD, SDHC)

Answer 46

Rare. <0.2% of hypertensive patients.

Answer 47

PAROXYSMAL epidoes of headache and sweating Cardio/resp: Palpitations, chest pain, dyspnoea GI: epigastric pain, nausea, constipation Neuo/psych: Weakness, tremor anxiety

Answer 48

HTN (50-70%): 2/3 sustained, 1/3 paroxysmal Postural HTN: secondary to reduced plasma volume. Pallor, tachycardia, fever, weight loss

Answer 49

24hr urine collection in ACID-CONTAINING bottle (vanillylmendelic acid (VMA)- catecholamine byproduct) for measurement of catecholamines, metanephrines Urinary creatinine should be measured to verify an adequate collection. (Note that come drugs can affect the measured catecholamines, see below) Blood glucose and calcium may be raised, potassium might be low. Plasma free metanephrines: in patients at high risk (sensitivity 99%) Tumour localisation with CT or MRI For large phaeo (>10cm) or paraganglioma, do I-MIBG scintigraphy

Answer 50

Certain drugs may increase the measured catecholamine (TCAs, levodopa)

Answer 51

Stress Physical exertion Certain foods containing tyramine: chocolate, cheese and wine

Answer 52

It is important to note that in a hypertensive, the triad of: headaches palpitations and diaphoresis (episodes of sweating) carries a high sensitivity (91%) and specificity (94%) for pheochromocytoma

Answer 53

Characterised by oligomenorrhoea/amenorrhoea and hyperadrogenism (clinical or biochemical). Associated with obesity, insulin resistance, TIIDM and dyslipidaemia

Answer 54

Environmental: related to diet and development of obesity Genetic variants: in genes regulating gonadotrophon, insulin etc. Hyperinsulinaemia results in increased ovarian androgen synthesis and reduced hepatic SHBG synthesis resulting in increased free androgens -------------------------------------- Oestrogen usually produced by 2 cell types: thecal and granulosa cells. Thecal cells respond to LH, and make androstenedione. Granulosa cells respond to FSH convert androstenedione into oestrogen using aromatase. In the early stages of the follicular phase, this oestrogen has negative feedback on the pituitary gland, but as the dominant follice grows (i.e. the one with most FSH and LH receptors), it produces more and more oestrogen, which eventually has a positive effect on pituitary and causes more FSH and LH release, which allows the follicle to rupture, the egg escapes and then travels down the fallopian tubes. IMPORTANT: In PCOS, the issue is that there is increased LH production. This means that the thecal cells produce loads and loads of androstenedione. It produces too much for the granulosa cells to be able to convert it all into oestrogen.

Answer 55

PCOS is the most common cause of infertility in women. Affects 6–8%of women.

Answer 56

Menstrual irregularities (oligomenorrhoea/amenorrhoea) Dysfunctional uterine bleeding Infertility Symtpoms of hyperadrogenism: Hirsutism Acne Male pattern hair loss

Answer 57

Hirsutism Acne Male pattern hair loss Acanthosis nigricans (signs of severe insulin resistance): velvety thickening and hyperpigmentation of the skin of axillae or neck

Answer 58

BLOOD: - Increased LH, increased LH:FSH ratio (>3) - Increase testosterone, androstenedione and DHEA-S - Reduced sex hormone binding globulin. - Exclude hyperprolactinaemia (serum prolactin), hypo/hyperthyroidism (TFTs), congeintal adrenal hyperplasia and cushing's syndrome - Fasting glucose HbA1c and fasting glucose (oral glucose test if either abnormal) - Fasting lipid profile TRANSVAGINAL USS: -Twelve or more follices in each ovary, measuring 2-9mm and/or increased ovarian volime >10mL

Answer 59

Hirsutism + oligomenorrhoea= diagnosis made Hirsutism + no olignomennoreah= measure 14 day progesterone to check for ovulation. If this revelas no ovulation, diagnose PCOS. If it shows ovulation, perform transvaginal USS. If polycistic ovarian morpholoy (see above), diagnose PCOS. No hirsutism= measure serum androgens (total/free testosterone and DHEAS). If any are elevated, diagnostic sequence is the same as when hirsuitsm is present (see above). If there is no hirsutism, all androgens are normal and there is a history of oligomenorrhoea, an ovarian ultrasound should be performed. Combined with such a history, polycystic ovarian morphology allows PCOS diagnosis

Answer 60

Probably TFTs and prolactin and 17-hydroxyprogesterone to exclude thyroid dysfunction, hyperprolactinaemia, and 21-hydroxylase deficient adrenal hyperplasia, respectively

Answer 61

In uncertain cases, elevated luteinising hormone/follicle-stimulating hormone ratio may support a diagnosis of PCOS. However, it is not diagnostic.

Answer 62

hyperandrogenism. Although the exact cause of PCOS is unknown, the disease has a very strong genetic component, which follows an autosomal dominant pattern with variable expressivity.

Answer 63

Elevation of one or more plasma lipid fractions

Answer 64

PRIMARY: -Familial hypercholesterolaemia: reduced hepatic LDL receptors. AD inheritence - Familial hypertriglyceridaemia: Unknown. Autosomal dominant. - Hypertriglyceridaemia: Lipoprotein lipase or apo-CII deﬁciency. Secondary: -HIGH CHOLSTEROL: Hypothyroidism, nephrotic syndrome, cholestatic liver disease, anorexia nervosa -HIGH TRIGLYCERIDES: DM, drugs (b blockers, thiazides, oestrogen), alcohol, chronic renal disease, hepatocellular disease

Answer 65

50 % of the UK population have a cholesterol level high enough to be a risk for CHD.

Answer 66

Asymptomatic Symptoms of CVS complications. Other CVS risk factors: DM, family Hx, smoking, HTN

Answer 67

Usually normal Signs of lipid deposits: - Xanthelasmas (eyes) - Corneal arcus - Tendon xanthomas (extensor tendons of hand etc) - Tuberous xanthomas (on knee and elbow) - Xanthomas in palmar creases --> REMNANT hyperlipidaemia SEVERE HYPERTRIGLYCERIDAEMIA: eruptive xanthomas and lipidaemia retinalis (pale retinal vessels)

Answer 68

Blood: Fasting lipid profile, exclude secondary causes (glucose, TFT, LFT U&E) CVS risk using framingham or Q risk

Answer 69

Conservative: exercise, lose weight, stop smoking, control DM, reduce alcohol Medical. Lipid lowering for primary prevention (when heart attack risk in 10 years >10%) and secondary prevention (coronary heart disease, aortic aneurysm, carotid artery disease). Target: total cholesterol <4mmol/L, LDL<2mmol/L. ---------------------------- High total cholesterol or LDL: -Statins (high dose! 40mg simvastatin) -Ezetimibe (inhibits cholesterol abzorption, if statin not tolerated) High triglycerides: -Fibrates (stimulates lipoprotein lipase activity via specific transcription factors)

Answer 70

Coronary artery disease, MI, PVD, strokes In hypertriglyceridaemia: PANCREATITIS AND RETINAL VEIN THROMBOSIS

Answer 71

Depends on early diagnosis, treatment of hyperlipidaemia and control of other CVS risk factors. There is some evidence that lipid-lowering agents prevent cerebrovascular accidents

Answer 72

1) Calcitonin 2) Thryoglobulin (used post-thyroidectomy to monitor completeness of removal- immediate follow up with radioiodine is indicated)

Answer 73

MEN type 1: menin gene chromosome 11 MEN type 2: RET gene on chromosome 10. Autosomal dominant

Answer 74

MEN 1: Primary hyperparathyroidism (90% of cases), pituitary adenomas, pancreatic endocrine tumours (e.g. gastrinoma, insulinoma) MEN2: Both present with thyroid medullary cancers (95-100%), and sometimes phaeochromocytomas. 2A: Also primary hyperparathyroidism 2B: Also marfanoid habitus and sometimes neurinomas. phaeochromocytoma

Answer 75

MEN1: Parathyroidectomy, excision of pancreatic tumor, transsphenoidal surgery for excision of pituitary tumour MEN2: Thyroidectomy (including cervical lymph nodes), rule out phaeos

Answer 76

On the lips or tongue

Answer 77

Insulin suppression test

Answer 78

Deficiency of one or more of the hromones released by the anterior pituitary gland.

Answer 79

Pituitary mass: Adenomas Parapituitary mass: Craniopharyndiomas, meningioma, mets, cysts etc. Inflammatory: TB, sarcoidosis, haemochromatosis, histiocytosis X Vascular: Pituitary apoplexy, Sheehan's syndrome Pituitary trauma: radiation, surgery, skull base fracture Hypothalamus (functional): Anorexia, starvation, over-exercise Infection: Meningitis, encephalitis, syphilis Genetics: Pit-1, Prop-1 genes Empty sella syndrome (see below)

Answer 80

1Pituitary apoplexy is the haemorrhage or infarction of a pituitary tumour. 2Sheehans syndrome is pituitary infarction, haemorrhage and necrosis following post-partum haemorrhage.

Answer 81

Hormone dependent: GH. Short stature in children. Low mood, fatigue, reduced exercise capacity/muscle strength TSH. Weight gain, cold intolerance, constipation. FSH/LH. Children=delayed puberty. Women= Loss of secondary sexual hair, breast atrophy, menstrual irregularities, dyspareunia Men=Loss of secondary sexual hair, impotence, loss of libido, small or soft testes Prolactin=Failure of breast milk production (in Sheehan's!) ACTH=orthostatic hypotension and tachycardia, weakness and lethargy,

Answer 82

Pituitary apoplexy Life-threatening hypopituitarism with headache, visual loss and cranial nerve palsies.

Answer 83

Pituitary function tests. Basal tests: 9am cortisol, LH, FSH, testosterone, oestradiol, IGF-1, prolactin, free T4 and TSH Dynamic tests: Insulin induced hypoglycaemia (CI in patients with epilepsy IHD, hypoadrenalism. Give 0.15U/kg IV insulin. In hypopituitarism, peak GH and cortisol response to insulin-induced hypoglycaemia are <20mU/L and <550nmol/L, respectively.

Answer 84

Hormone replacement. Hydrocortisone=20mg in morning, 10mg in evening (double dose for febrile illnesses, IM hydrocortisone during surgery) L-thyroxine= 100micrograms daily. TAKE AFTER hydrocortisone Sex hormones Growth hormones: SC 1.2 units/day in adults. Posterior pituitary deficiency (damage to pituitary stalk): desmopressin intranasally

Answer 85

Adrenal crisis, hypoglycaemia, myxoedema coma, infertility. Osteoporosis; dwarﬁsm (children). Complications of pituitary mass: Optic chiasm compression, hydrocephalus (third ventricular compression), temporal lobe epilepsy.

Answer 86

Pituitary gland shrinks due to atrophy, compression (sella turcica filled with CSF). Primary- associated with obese women Secondary- pituitary surgery, heard trauma, idiopathic intracranial hypertension

Answer 87

Partly true. Most pituitary tumours ARE hormone secreting (most common of which is prolactinoma) BUT it's not those tumours that cause hypopituitarism. The most common tumors that cause hypopituitarism are macroadenomas larger than 1 centimeter that don’t secrete any hormones.

Answer 88

For non-secreting macroadenomas, treatment is transsphenoidal resection, which is when the tumor is removed through the nose. If the surgery is successful, the pituitary function can recover completely. If not, hormonal replacement therapy might be needed.

Answer 89

Reduced ADH secretion, leading to cranial diabetes insipidus, with symtpoms like excessive thirst and frequent urination. Increased prolactin levels, causing galactorrhoea. This is because prolactin, unlike the other hormones, is under constant inhibition by dopamine secretion from the hypothalamus.

Answer 90

Craniopharyngioma

Answer 91

Pituitary apoplexy. Sudden haemoorahge of pituitary gland, usually in presence of pituitary adenoma Diplopia, or double vision, and ophthalmoplegia, which is the paralysis or weakness of the eye muscles, can also occur due to the blood buildup compressing cranial nerve III, which innervates the eye muscles.

Answer 92

T- mechsnism unclear

Answer 93

DO NOT WAIT FOR THYROID TEST RESULTS TO BE RETURNED. IV fluids and Abx is there is underlying infection that precipitated the crisus Oral propanalol and PTU and steroids. Cardiac monitoring and pulse oximetry

Answer 94

Thyroid function tests demonstrate marked elevation of free T4 Thyroid function tests demonstrate marked reduction of thyroid stimulating hormone (TSH)

Answer 95

F Radioiodine can precipitate/worsen thyroid crisis but can be useful for later management (possible focal hot nodule or diffuse uptake).

Answer 96

Amenorrhoea can be described as primary (menstruation has never occurred) or secondary (menstruation has stopped for at least 6 months in a patient who has previously menstruated).

Answer 97

Turner syndrome

Answer 98

Prolactinoma, pregnancy, haemochromatosis and polycystic ovarian syndrome can cease menstruation in women have menstruated before – thus causing secondary amenorrhoea.

Answer 99

It's a bit counterintuitive because an aldosterone-secreting adenoma leads to inappropriately elevated aldosterone levels. The excessive sodium reabsorption and potassium excretion caused by the high aldosterone leads to hypertension and hypokalaemia. So you would expect less urine. But Hypokalaemia induces nephrogenic diabetes insipidus, which, consequently, leads to polyuria and polydipsia. It can cause muscle weakness too SEE ECG FEATURES OF HYPOKALAEMIA

Answer 100

Pregnancy, medications that inhibit dopamine (e.g. | antipsychotics), hypothyroidism and benign pituitary tumours.

Answer 101

Characterized by impairment of ovarian function

Answer 102

Primary hypogonadism is when there is problem with the ovaries themselves (so there will be high gonadotrophins, due to low oestrogen) Secondary hypogonadism is when there is a problem with the signals to the ovaries, so the gonadotrophins are low. Primary and secondary amenorrhoea is different. In Primary amenorrhoea, the woman has never had a period before. In secondary, there is cessation of periods

Answer 103

Primary: - Premature ovarian failure - Gonadal dysgenesis: Turner's (note, this causes primary amenorrhoea) - Gonadal damage: Autoimmune (chemo, radiation, surgery) Secondary: - Functional: stress, low BMI, excessive exercise - Pituitary/hypothalamic tumours/infiltration: pituitary adenoma (compresses), craniopharyngioma, haemochromatosis - Hyperprolactinaemia: prolactinomas or tumours causing stalk comrpession - CONGENITAL GnRH deficiency (Kallman's syndrome). - Post pill amenorrhoea So you can see how Turner's and Kallman's are both causes of PRIMARY amenorrhea, but turner's is primary hypogonadism, whereas kallmans is secondary

Answer 104

Secondary hypogonadism is a more common cause of an ovulation and amenorrhoea than primary hypogonadism

Answer 105

1. PREGNANCY TEST! 2. LH, FSH, oestradiol 3. Day 21 progesterone 4. Prolactin, thyroid tests 5. Androgens 6. Chromosomal analysis (turners is XO) 7. USS ovaries/uterus

Answer 106

Turners syndrome: Short stature, low posterior hairline, high arched palate, widely spaced nipples, wide carrying angle, short fourth and ﬁfth metacarpals, congenital lymphoedema.

Answer 107

atients with autoimmune primary ovarian failure: Signs of other autoimmune diseases e.g. hyperpigmentation in Addisons disease or vitiligo.

Answer 108

``` Loss of libido Reduced muscle bulk Small testes Impotence Osteoporosis! ```

Answer 109

Primary hypogonadism: - Gonadal dysgenesis: Klinefelter's (XXY), undescended testes (cryptorchidism) - Gonadal damage (infection e.g. mumps, torsion, trauma, autoimmune, chemo, srugery, radiation) ``` Secondary: Pituitary/hypothalamic lesions again GnRH deficiency (Kallman's) Hyperprolactinaemia Systemic disease ``` Prader Weilli syndrome, laurence moon biedl syndrome

Answer 110

Myotonic dystrophy

Answer 111

Prader willi

Answer 112

Laurence-moon-biedle syndrome

Answer 113

LH, FSH, testosterone (if all low--> MRI pituitary) Prolactin Sperm count Chromosomal analysis

Answer 114

HLADR3, HLADR5

Answer 115

Characterizedbyautonomousaldosteroneoverproductionfromtheadrenal gland with subsequent suppression of plasma renin activity.

Answer 116

Adrenal adenoma (Conn's syndrome; 70%) or hyperplasia of the adrenal cortex (30%) Rarely, an aldosterone producing adrenal carcinoma

Answer 117

Excess aldosterone results in: raised Na and HTN, increased K renal loss and supression of renin

Answer 118

Aldosterone producing adenoma occurs more commonly in women and in younger patients (<50 years). Bilateral adrenal hyperplasia occurs more commonly in men and usually presents at an older age

Answer 119

IT'S NOT TALKING ABOUT CONGENITAL ADRENAL HYERPLASIA It's talking about bilateral hyerplasia of adrenal gland that happens more commonly in older people to result in hyperaldosteronism

Answer 120

Usually asymptomatic picked up on blood tests Hypokalaemia: Muscle weakness, polyuria and polydipsia (nephrogenic diabetes insipidus secondary to hypokalaemia), paraesthesia, tetany.

Answer 121

HTN and complications thereof

Answer 122

1) Plasma potassium (low in 20% of patients with PA, normal in 80%)- so normokalaemic hypertension constitutes the most common presentation of this disease. 2) Aldosterone/renin ratio. Stop antihypertensives (6wk for spironolactone , 2wk for most antihypertensives). Put on a blocker if anti-hypertensive needed). Correct hypokalaemia. Raised ratio.

Answer 123

F... serum Na usually normal (due to parallel increase in the water content of the blood).

Answer 124

After a raised aldosterone/renin ratio is found: 1) Saline supression test (according to Meeran) or Fludrocortisone suppression test is most reliable means to defintively confirm or exclude PA. Failure of upright (10 a.m.) plasma aldosterone on day 4 of fludrocortisone acetate administration, to suppress to <166 picomol/L (<6 nanogram/100 mL or <6 nanogram/dL) 2) Adrenal venous sampling

Answer 125

Allows distinction between Conns syndrome and bilateral adrenal hyperplasia by measuring adrenal vein aldosterone levels.

Answer 126

Idiopathic hyperaldosteronism (Conn's is second most common)

Answer 127

Metabolic alkalosis

Answer 128

Osteomalacia is a disorder of mineralization of bone matrix ("osteoid"). Rickets is a disorder of defective mineralization of cartilage in the epiphyseal growth plates of children.

Answer 129

Vitamin D deficiency: -Dietary deficiency/malabsorption (small bowel disease e.g. coeliac, IBD, bowel surgery, pancreatic insufficiency) - Reduced 25 hydroxylation of vit D (liver disease, anticonvulsants) - Reduced 1 hydroxylation (CKD, hypoparathyroidism, mutations in gene) - Vitamin D resistance

Answer 130

Osteomalacia: bone tenderness, proximal muscle weakness, WADDLING gait. Signs of hypocalcaemia Rickets: Bossing of frontal and parietal bones. Swelling of costochondral junctions (rickety rosary). Bow legs in early childhood, "knock knees" in later childhood. Short stature.

Answer 131

Vitamin D is low, PTH is high (secondary hyperparathyroidism). Due to this, Ca2+ can be low or normal (raised PTH can normalise Ca2+) Phosphate is low (due to raised PTH), and alk phos is high.

Answer 132

Phosphate. It can also be caused by renal phosphate wasting. e.g. Fanconi's syndrome (phosphaturia, glycosuria, amino aciduria), renal tubular acidosis type II.

Answer 133

Patients with renal tubular acidosis have normal anion gap hyperchloraemic metabolic acidosis.

Answer 134

If renal phosphate wasting or primary hyperparathyroidim are not the cause of hypophosphataemia, the fractional excretion of phosphate should be very low.

Answer 135

May appear normal or show osteopenia. Looser's zones or pseudofractures (radiolucent bands) in ribs, scapula, pubic rami or upper femur

Answer 136

Bone biopsy after double tetracycline labelling Tetracycline is deposited at the mineralization front as a band. After two courses of tetracycline (separated by a period of days), the distance between the bands of deposited tetracycline is reduced in osteomalacia. (not usually performed as osteomalavia can be diagnosed from lab and radiograph)

Answer 137

Vitamin D and calcium replacement. X-linked hypophsophataemia: oral phosphate and 1,25 vit D

Answer 138

Bone deformities, hypocalcaemia may cause epileptic seizures, cardiac arrhythmias, hypocalcaemia tetany, depression

Answer 139

a transient patchy inflammation of the thyroid gland that is associated either with granuloma formation (subacute granulomatous thyroiditis) or lymphocytic infiltration (subacute lymphocytic thyroiditis).

Answer 140

hile subacute granulomatous thyroiditis usually occurs after a viral upper respiratory tract infection, subacute lymphocytic thyroiditis occurs either during the postpartum period, in association with other autoimmune diseases, or as a side effect of certain drugs

Answer 141

Both forms of subacute thyroiditis are more common among women and are characterized by a triphasic clinical course that classically transitions from hyperthyroidism to hypothyroidism, before returning to a euthyroid phase. BUT The goiter is tender in subacte granulomatous thyroiditis (i.e. viral) but painless in lymphocytic (i.e. post partum)

Answer 142

Viral infections: mumps virus, coxsackie virus, influenza virus, echovirus, adenovirus Mycobacterial infections

Answer 143

α-interferon, lithium, amiodarone, interleukin-2, tyrosine kinase inhibitors

Answer 144

Most prevalent in women with type 1 diabetes mellitus.

Answer 145

1. Thyrotoxic stage. 2-8 weeks. Release of pre-formed colloid. 2. Hypothyroid phase. 2-8 weeks. Depletion of pre-formed colloid and impaired synthesis of new thyroid hormones 3. Euthyroid phase: Thyroid function recovers and pathological changes no longer present

Answer 146

T The disease is self-limiting in most cases but a few patients may experience relapses, and permanent hypothyroidism occurs in ∼ 15% of cases of subacute granulomatous thyroiditis!

Answer 147

Possible history of upper respiratory tract infections a few weeks prior to the onset of subacute thyroiditis Painful, diffuse, firm goiter, jaw pain Fever/malaise Features of hyperthyroidism followed by features of hypothyroidism

Answer 148

Painless, diffuse, firm goiter (thyroid size may be normal) Features of hyperthyroidism followed by features of hypothyroidism

Answer 149

Thyrotoxic phase: raised T3 and T4 , raised thyroglobulin, reduced TSH Hypothyroid phase: reduced T3 and T4, raised TSH

Answer 150

Raised ESR in subacute granulomatous thyroidits only (not post partum), which returns to normal after the hypothyroid stage Radioiodine uptake study shows reduced iodine uptake

Answer 151

Both types: Consider beta blockers to control symptoms of hyperthyroidism (palpitations and/or anxiety) NSAIDs for pain in acute granulomatous thyroiditis Corticosteroids in granulomatous thyroiditis if NSAIDs don't reduce pain/suppress inflammation. But corticosteroids not indicated in post partum thyroidits Hypothyroid stage: levothyroxine. The dose of levothyroxine should be as low as possible so that endogenous TSH levels are not suppressed, thus facilitating a TSH-mediated recovery to a euthyroid state. Patients who develop permanent hypothyroidism may require lifelong levothyroxine.

Answer 152

It's likely to be a non-functioning pituitary adenoma compressing the pituitary stalk (thus reducing dopaminergic inhibition of prolactin) A prolactinoma is likely to raise prolactin above 100ng/mL. Especially if it's big!

Answer 153

Raised PTH in the blood Primary= Raised secretion of PTH unrelated to plasma calcium concentration Secondary= Raised PTH secondary to hypocalcaemia Tertiary= Autonomous PTH secretion following chronic secondary hyperparathyroidism.

Answer 154

Primary= adenoma in the parathyroid gland or hyperplasia (80% single adenoma, 12% hyperplasia or multiple adenomas), rarely parathyroid carcinoma Secondary= vitamin D deficiency or CKD

Answer 155

Primary/tertiary. Mild hypercalacaemia is asymptomatic. May present with: Polyuria, polydipsia, renal calculi, bone pain, abdo pain, nausea, constipation, psychological depression and lethargy. Secondary: may present with symptoms and signs of hypocalcaemia and/or the underlying cause (chronic renal failure, vit D deficiency)

Answer 156

Primary/tertiary: -Raised Ca2+, low phosphate, raised alk phos, high/inappropriately normal PTH Secondary: -Ca2+ low or normal, phosphate high, raised alk phos,

Answer 157

Patients with parathyroid carcinomas are more likely to have a marked hypercalcaemia with very high serum PTH levels.

Answer 158

Hyperchloraemic acidosis (normal anion gap) caused by PTH inhibition of renal tubular reabsorption of bicarbonate.

Answer 159

Subperiostial erosions of phalanges, brown tumours (osteolucent bone defects), diffuse porotic mottling of skull caused by demineralization ("pepperpot" skull), sclerosis of superior and inferior vertebral margins with central demineralization ("rugger jersey" spine), renal calculi/nephrocalcinosis.

Answer 160

IV fluids. Manage conservatively if they don't meet surgical criteria. Avoid thiazide diuretics ------------------ Patients with hypercalcaemia secondary to malignancy are treated with rehydration and IV pamidronate (a bisphosphonate).

Answer 161

Subtotal parathyroidectomy, total parathyroidectomy (in MEN1). Indications: Symptomatic patients or asymptomatic patients with: Age <50 Bone density T score <2.5 Calculi Creatinine Difficult to follow up periodically Elevated serum calcium >0.25mMol above upper limit of normal

Answer 162

Treat the underlying renal failure. Calcium and vitamin D supplements.

Answer 163

Increased bone resorption, tubular calcium reabsorption and hydroxylation of Vit D leading to hypercalcaemia

Answer 164

Increased stimulation of osteoclasts and bone turnover leads to osteitis fibrosa cystica

Answer 165

Hypocalcaemia (need supplement) and recurrent laryngeal nerve palsy

Answer 166

Too much vasopressin is released from the posterior pituitary given the osmolality of the blood. This means that more water is reabsorbed, leading to lower blood osmolality

Answer 167

Osmoreceptors in the organum vasculosum sense the osmolality of the blood. These project to the hypothalamic PVN and SON to influence vasopressin release into the posterior pituitary. Increase in plasma osmolality --> osmoreceptor shrinks --> increased osmoreceptor firing --> VP release from hypothalamic PV and SON

Answer 168

There is increased vasopressin release Increased H2O reabsorption from the renal collecting ducts This leads to increased ECF volume INITIALLY Leading to hyponatraemia. So the sodium goes down because of the increased ECF. But then, ANP is released from the right atrium, which causes a natriuresis (i.e. excretion of sodium and therefore water too, leading to euvolaemia and also hyponatraemia)

Answer 169

Urine osmolality and [Na+] goes UP because there is.... Decreased urine volume (initially) Then this leads to reduced plasma Na+ mainly due to increased water reabsorption (and also natiuresis) These factors diagnose SIADH, in the absence of hypovolaemia/hypotension, oedema, renal failure, adrenal insufficiency and hypothyroidism. Investigate to identify underlying cause: CXR, CT CAP, MRI/CT head

Answer 170

Can be symptomless If Na+<120mM: fatigue, poor mental function and nausea If Na+<110mM: confusion, coma and death

Answer 171

CNS: subarachnoid haemorrhage, stroke, tumour TBI, GBS Pulmonary disease: pneumonia, bronchiectasis Malignancy: small cell lung cancer, lymphoma, leukaemia, pancreas etc. Drug related Idiopathic Metabolic: porphyria, alcohol withdrawal

Answer 172

Carbamazepine, SSRI, opiates

Answer 173

Treat for hyponatraemia: 1. Immediate: fluid restriction (0.5-1L/day) 2. Longer term: use drugs which prevent vasopressin action in the kidneys: demeclocyline (induced nephrogenic DI) or vaptans (non-competitive V2 receptor antagonists)- very expensive 3. In severe cases (seizures/reduced consciousness), slow IV hypertonic 3% saline and furesomide with close monitoring. Change in Na+ must not exceel 10mmol/L in first 24hr or 18 mmol/L in first 48hr, otherwise it could cause central pontine myelinolysis

Answer 174

Mild hyponatraemia: no signs Severe hyponatraemia: reduced reflexes, extensor plantar reflexes

Answer 175

Convulsions, coma, death. Central pontine myelinolysis (quadreparesis, respiratory arrest, ﬁts) occurs with rapid correction of hyponatraemia

Answer 176

Depends on the underlying cause. High morbidity and mortality with [Naþ] <110mmol/L. Up to 50% mortality with central pontine myelinolysis.

Answer 177

During the first trimester, the thioamide propylthiouracil may be used. Carbomazole is contraindicated in the first trimester of pregnancy, however after this time , it can be safely used.

Answer 178

excessive bone remodelling at one (monostotic) or more (polyostotic) sites resulting in bone that is structurally disorganized

Answer 179

Excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts) New bone formed = WOVEN bone structurally disorganised mechanically weaker than normal adult lamellar bone Mosaic pattern Marrow spaces filled by an excess of fibrous tissue

Answer 180

``` Often +ve family hx (genetic) Evidence of viral origin (measles) Men and women affected equally Disease usually not apparent under age 50y Most patients are asymptomatic ```

Answer 181

Characterised by abnormal, large osteoclasts – excessive in number

Answer 182

Skull, thoracolumbar spine, pelvis, femur and tibia most commonly affected Arthritis, fracture, pain, deformity INCREASED VASCULARITY--> WARMTH OVER AFFECTED BONE Deafness (cochlear involvement) Radiculopathy due to nerve compression

Answer 183

Bitemporal skull enlargement with frontal bossing Radiograph: osteoporosis circumscripta, enlargement of frontal and occipital areas, associated with a "cotton wool" appearance

Answer 184

Calcium is normal!!!!!!!! | Alk phos usually increased

Answer 185

Lytic lesions (early), thickened, enlarged, deformed bones (later)

Answer 186

Radionuclide bone scan

Answer 187

Loss of bony trabeculae, reduced bone mass, weaker bone predisposed to fracture after minimal trauma Defined as <2.5 deviations below peak bone mass achieved by HEALTHY ADULTS.

Answer 188

PRIMARY: Idiopathic, post menopausal SECONDARY: - Cushing's/steroid use, thyrotoxicosis, primary hyperparathyroidism, hypogonadism - Malignancy: myeloma, metastatic cancer - Drugs: CS, heparin - Rheum: RA ,ank spond - GI: malabsorption syndromes (coeliac disease, partial gastrectomy), liver disease (PBC), anorexia

Answer 189

Age, family history, low BMI, low calcium intake, smoking, lack of physical exercise, low exposure to sunlight, alcohol abuse, late menarche, early menopause, hypogonadism.

Answer 190

Femoral neck fractures (commonly after minimal trauma). Vertebral factures (loss of height or stooped posture or acute back pain after lifting). Colles fracture of the distal radius after fall onto outstretched hand

Answer 191

- tenderness on percussion (over vertebral fractures); . - thoracic kyphosis (if multiple vertebral fractures); - severe pain with leg shortened and externally rotated (in a femoral neck fracture).

Answer 192

Biochemistry absolutely normal unless there is a secondary cause.

Answer 193

Usually to diagnose fractures when symptomatic. Often normal (>30% loss in density before showing radiolucency, abnormal trabeculae or cortical thinning evident), biconcave vertebrae, crush fractures.

Answer 194

DEXA scan T-score: The number of standard deviations the bone mineral density measurement is above or below the young normal mean bone mineral density. T-score is used to deﬁne osteoporosis. . Z-score: The number of standard deviations the measurement is above or below the age-matched mean bone mineral density. Z-score may be helpful in identifying patients who may need a work-up for secondary causes of osteoporosis.

Answer 195

Dual Energy X-ray Absorptiometry (DEXA) - femoral neck and lumbar spine Mineral (calcium) content of bone measured, the more mineral, the greater the bone density (bone mass)

Answer 196

eg osteoblast senescence

Answer 197

Primary: - Hashimoto's thyroidits (AI destruction) - Iatrogenic (post surgery , radioiodine, medication for hyperthyroidism) - Severe iodine deficiency or iodine excess - Viral/post-partum thyroidits have a hypothyroid phase Secondary (<5%): Pituitary or hypothalamic disease (e.g. tumours) resulting in TSH or TRH and stimulation of thyroid hormone production

Answer 198

Insidious onset Cold intolerance, lethargy, weight gain, constipation, dry skin, hair loss, hoarse voice. Mental slowness, depression, dementia, cramps, ataxia, paraesthesia. Menstrual disturbances (irregular cycles, menorrhagia) in females. Hx surgery/radioiodine for hyperthyroidism Hx or family Hx of other AI conditions: Addison's, T1DM, pernicious, pre-mature ovaran failure

Answer 199

Hypothermia, hypoventilation, hyponatraemia, heart failure, confusion and coma.

Answer 200

Hands: bradycardia/cold Head/neck/skin: pale puffy face, goitre, oedema, hair loss, dry skin, vitiligo Chest: pericardial/pleural effusion Ascites Slow relaxation of reflexes, signs of carpal tunnel

Answer 201

Primary: reduced t3/t4, increased TSH Secondary: reduced t3/t4, reduced TSH (or inappropriately normal TSH) FBC: normocytic anaemia U&E: hyponatraemia

Answer 202

Elevated in over 90% of patients with autoimmune thyroiditis, the most common cause of primary hypothyroidism

Answer 203

Chronic: Levothyroxine (25-200micrograms per day) Rule out underlying adrenal insufficiency and treat prior to thyroid replacement to avoid Addisonian crisis. Adjust dosage according to TFT and clinical picture (monitor at 6 weeks). In patients with ischaemic heart disease, start at low dose (25mg/day) and gradually increase at 6 week intervals if ischaemic symptoms do not deteriorate.

Answer 204

Myxoedema coma - a VERY RARE complication of hypothyroidism Oxygen, rewarming, rehydration, INTRAVENOUS T4/T3 (for uncomplicated hypothyroidism you give oral!), IV hydrocortisone (in case hypothyroidism is secondary to hypopituitarism), treat the underlying disorder e.g. infection.

Answer 205

T4 (thyroxine sodium) This is not the active form. T3 is the active form (normally 80% in the circulation is from deiodination of T4 20% from direct thyroidal secretion)

Answer 206

TSH- in primary In secondary hypothyroidism, TSH will be low anyway due to anterior pituitary failure, so can't be used as a guide to dose. Here you aim for T4 in the middle of the reference range

Answer 207

Levothyroxine (T4) plasma half life of 6 days Liothyronine (T3) plasma half life 2.5 days

Answer 208

Approximately 99.97% of circulating T4 and 99.7% of circulating T3 are bound to plasma proteins, mainly thyroxine binding globulin (TBG) (NB do NOT confuse with thyroglobulin) Only the free (unbound) fraction of thyroid hormone is available to the tissues INCREASE PLASMA BINDING PROTEINS: - pregnancy - prolonged oestrogen/phenothiazine treatment FALLING PLASMA BINDING PROTEINS: - TBG falls with malnutrition, liver disease - Certain co-administered drugs (e.g. phenytoin, salicylates) compete for protein binding sites.

Answer 209

Excess secretion of GH from the anterior pituitary gland in ADULTS (Excess GH results in gigantism before puberty)

Answer 210

MOST CASES: GH-secreting pituitary adenoma. RARELY: Excess GRHR release from hypothalamic ganglioneuroma, bronchial carcinoid or pancreatic tumour causing somatotroph hyperplasia

Answer 211

Very gradual over many years Sweating, headaches, carpal tunnel Shoes getting tight Hypopituitarism (hypogonadism, hypothyroidism, hypoadrenalism) Visual disturbance (optic chiasm) Hyperprolactinaemia (irregular period, reduced libido, impotence)

Answer 212

Hands: Enlarged spade-like hands with thick greasy skin. Signs of carpal tunnel syndrome (see Carpal tunnel syndrome). Pre-mature osteoarthritis (arthritis also affects other large joints, temporomandibular joint). Prominent eyebrow ridge (frontal bossing) and cheeks, broad nose bridge, prominent nasolabial folds, thick lips, " gap between teeth, large tongue, prognathism, husky resonant voice (thickening vocal cords). Bitemporal superior quadrantanopia progressing to bitemporal hemianopia (caused by pituitary tumour compressing the optic chiasm). Multi-nodular goitre

Answer 213

Serum IGF-1 (screening test) Definitive test: Oral glucose tolerance test: Failure of suppression of GH after 75 g oral glucose load Imaging: MRI brain

Answer 214

Oral glucose tolerance test: Failure of suppression of GH after 75 g oral glucose load (falsepositive results are seen in anorexia nervosa, Wilson's disease, opiate addiction

Answer 215

XS GH production leads to increased endogenous glucode production and reduced muscle glucose uptake Insulin production goes up and leads to insulin resistance Impaired glucose tolerance and diabetes mellitus

Answer 216

1st line: -Transphenoidal surgery Medical treatment: - SC or monthly depot Somatostain analogue (octreotide) - Dopamine agonist (GH secreting pituitary tunours frequently express D2 receptors)- cabergoline Radiotherapy

Answer 217

Reduces GH secretion and tumour size Pre-treatment before surgery may make resection easier Use post-operatively if not cured or whilst waiting for radiotherapy to take effect (slow)

Answer 218

GI side effects common eg nausea, diarrhoea, gallstones can occur

Answer 219

Obstructive sleep apnoea HTN (direct effects of GH and IGF-1 as well as GH mediated renal sodium reabsorption) Cardiomyopathy (HTN, DM, toxic effects of excess GH on myocardium) Increased risk of cancer (colonic polyps)

Answer 220

Nasoseptal perforation, hypopituitarism, adenoma recurrence, CSF leak, infection (meninges, sphenoid sinus).

Answer 221

Vitiligo appears as hypopigmented patches, sometimes with hyperpigmented borders Alopecia areata is a condition that causes hair to fall out in small patches, Erythema ab igne (EAI), also known as hot water bottle rash, is a skin condition caused by long-term exposure to heat (infrared radiation). Prolonged thermal radiation exposure to the skin can lead to the development of reticulated erythema, `hyperpigmentation, scaling and telangiectasias in the affected area.

Answer 222

Hypo- menorrhagia | Hyper- oligo/amenorrhoea

Answer 223

Typically the goitre is firm, non-tender and moderate in size.

Answer 224

Anti-parietal cell

Answer 225

Patients with symptomatic hypothyroidism require thyroxine replacement. This is usually given as 25, 50 or 100 micrograms tablets. Typical doses of 100 to 150 micrograms are effective in most patients wever, caution should be exercised in the elderly and those with known heart disease, as thyroxine treatment may induce an acute coronary syndrome, myocardial infarction or even death due to tachycardia and increased cardiac work. It is therefore important to start replacement at a low dose then titrate up until the patient is euthyroid.

Answer 226

Insensitivity to insulin by peripheral tissues, impaired insulin secretion and increased HGO

Answer 227

Multifactorial. Genetic factor Obesity (adipokines contribute to peripheral insulin resistance)

Answer 228

Chronic pancreatitis Hereditary haemochromatosis Pancreatic cancer Endocrinopathies: Cushing's, acromegaly, phaeo, glucagonoma Drugs: corticosteroids

Answer 229

Plasma FFAs and adipokines contribute to peripheral insulin resistance Chronic hyperglycaemia can have toxic effect on beta cells (glucotoxicity) as can free fatty acid levels (lioptoxicity)

Answer 230

Can be incidental Polyuria, polydypsia, tiredness. Can present with hyperosmolar hyperglycaemic state Infection (infected foot ulcers, candidiasis, balanitis, pruritis vulvae)

Answer 231

Weight and height- calculate BMI BP

Answer 232

Ischaemic (reduced pulses, dry skin, ulceration, gangrene) Neuropathic (Charcot's foot, reduced sensation)

Answer 233

1. Well-demarcated plaques on the shins or arms with shiny atrophic surface and red–brown edges 2. Fesh-coloured papules coalescing in rings on the back of hands and ﬁngers 3. Diabetic dermopathy (depressed pigmented scars on shins)

Answer 234

Symptoms of diabetes + random plasma glucose >11.1 Fasting plasma glucose >7 (overnight fast 8hr) Two-hour plasma glucose >11.1 after 75g OGTT.

Answer 235

1. Conservative. Advice and information 2. Glycaemic control 3. BP control 4. Control of complications `

Answer 236

Information: Diabetic nurses, leaﬂets, websites, etc. explaining diabetes control, complications. Nutrition: Optimizing meal plans, diet (complex carbohydrates as opposed to simple sugars, reduced fat intake). Foot care: Regular inspection, appropriate footwear, role of chiropodist. Organizations: Local and national support groups. Recognition and treatment of hypoglycaemia. Monitoring capillary blood glucose and charting it. Monitoring for ketones during intercurrent illness. Pregnancy: Strict glycaemic control and planning of conception. Treatment: Action, duration and administration technique for insulin, change the site of injection (to avoid lipohypertrophy), explain the need to plan exercise

Answer 237

At diagnosis: Lifestyle advice + metformin If HbA1c >7% after 3 months 1st intensification: Lifestyle advice + metformin + gliptin (DPP4 inhibitor) /pioglitazone/sulphonylurea/SGLT-2i If HbA1c >7% after 3 months ``` 2nd intensification Triple therapy: Metformin + gliptin + sulphonylurea OR Starting insulin based treatment ``` If HbA1c >7% after 3 months 3rd intensification: Metformin, a sulfonylurea, and a glucagon-like peptide-1(GLP-1) mimetic

Answer 238

People at risk of lactic acidosis, which is people with: - DKA - eGFR<30mL/min (for standard release metformin) or <45 (for modified-release metformin) - Acute or chronic disease which may cause tissue hypoxia, such as cardiac or respiratory failure, recent myocardial infarction, or shock. - Hepatic insufficiency, acute alcohol intoxication, or alcohol addiction. - DISCONTINUE 48hrs BEFORE ELECTIVE SURGERY UNDER GENERAL, SPINAL OR PERIDURAL ANAESTHESIA and restart no earlier than 48hrs post-surgery

Answer 239

GI effects (nausea, vomiting, diarrhoea, abdo pain) Lactic acidos`is Vit b12 deficiency

Answer 240

A gliptin (dipeptidyl peptidase-4 inhibitor). Pioglitazone. A sulfonylurea. A Sodium-glucose cotransporter 2 inhibitors (SGLT-2i).

Answer 241

If an adult with type 2 diabetes is symptomatically hyperglycaemic, consider insulin therapy or a sulfonylurea. Review treatment when blood glucose control has been achieved.

Answer 242

Regular digital retinal photography, ophthalmology referral and laser photocoagulation if necessary.

Answer 243

Send first-pass early morning for ACR Measure creatinine for eGFR Manage with BP control, ACEi/ARBs

Answer 244

Diagnose CKD if the person's eGFR is persistently less than 60 mL/min/1.73 m2, and/or ACR is persistently greater than 3 mg/mmol.

Answer 245

Regular examination and inspection of the feet for ulcers, 10g monoﬁlament testing, joint vibration Treat with: foot hygiene, amitriptyline, duloxetine, gabapentin or capsaicin cream for painful neuropathy.

Answer 246

Clean and dress regularly, Swab for culture and sensitivity, IV antibiotics (e.g. ﬂucloxacillin, co-amoxiclav, cephalosporin and metronidazole). Look for osteomyelitis on X-ray. Surgical debridement or amputation if necessary.

Answer 247

Similar to DKA in that it commonly arises from infections and is characterised by hyperglycaemia and hyperosmolarity There is more insulin secretion with hyperosmolar hyperglycaemiac state though which is enough to suppress lipolysis and ketogenesis, but not enough to regulate hepatic glucose production/promote glucose utilisation

Answer 248

Osmotic diuresis leads to hypernatraemia Hypernatraemia and hyperglycaemia (potentially coupled with inadequate water intake) cause volume contraction The hypovlaemia leads to a decline in GFR The counter-regulatory hormones (in particular adrenaline) increase, which induce insulin resistance, decrease insulin production and increase lipolysis, ketogenesis and volume depletion, contributing to hyperglycaemic crises

Answer 249

Plasma glucose >33.3 Urinary ketones are negative or low (to distinguish DKA)

Answer 250

ALL PATIENTS: 1st line: IV fluids (0.9% Na solution, or 0.45% if serum Na+ >170mMol/L) + Vasopressor (IF hypotension persists after forced hydration. Start noradrenaline/dopamine). IF baseline K+ <3.3mmol/L, then give potassium chloride therapy until you reach 3.3mmol/L. At this point, start IV insulin therapy IF baseline K+ 3.3-5.3 mmol then give IV insulin therapy and potassium chloride therapy IF K+ >5.3 then given IV insulin therapy When HHS has resolved and patient can tolerate oral intake, switch to SUBCUTANEOUS INSULIN THERAPY

Answer 251

T An ACE Inhibitor is the first line antihypertensive in patients with diabetic nephropathy. Also patients should have all cardiovascular risk factors managed aggressively and maintain good glycaemic control.

Answer 252

Fluid resuscitation is extremely important and usually normal saline is used. Once glucose level falls below 15mmol/L (but not initially), 5% dextrose can be used.

Answer 253

DKA: Initially 4-8U of soluble insulin is given if glucose is >20mmol/L. An insulin sliding scale via and intravenous infusion should be prepared as soon as possible. HHS: 1-3U

Answer 254

Fludrocortisone may be helpful.

Answer 255

Uncommon peripheral diabetic neuropathic complaint. It presents with severe muscle weakness and pain with proximal thigh muscle atrophy. The weak knee flexion and quadriceps wasting is typical of diabetic amyotrophy

Answer 256

"Woody" swelling. Autoimmune condition, causes hypothyroidism in 25-50% of those affected Painless lump that can also cause local compressive symptoms like tracheal/oesophageal compression No lymph/cancer slymtpoms

Answer 257

sclerosing cholangitis and peculiarly responds to Tamoxifen, there can also be use for steroids.

Answer 258

peculiarly responds to Tamoxifen, there can also be use for steroids.

Answer 259

If they have grave's and can't get it settled with carbimazole, you can do surgery. KI is used pre-surgery to saturate the thyroid and reduce vascularity

Endocrine Flashcards

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