endocrinology Flashcards

Question

Gliptin type MoA SE

Answer 1

type - DPP-4 inhibitors (DPP-4 destroys incretin) MoA - Raised incretin -> produce more insulin when needed SE - GI upset and flu-like symptoms

Answer 2

type - Oral hypoglycaemics MoA - Increase panc insulin secretion CI - Pregnancy SE - Hypo, weight gain

Answer 3

MoA Increases insulin sensitivity SE Weight gain, fluid retention and osteoporosis CI Heart failure and osteoporosis

Answer 4

precipitants Missed insulin, infection, intoxication, ischaemia, infarction ``` pres Abdominal pain + vomiting Polyuria, polydipsia, dehydration Kussmaul respiration (deep hyperventilation to correct acidosis) Acetone breath (pear drop) ``` patho decreased insulin -> 1. increased protein catabolism -> hyperglycaemia, glycosuria, osmotic diuresis, K+ depletion (acidosis buffer) -> dehydration acidosis coma + death 2. decreased cell glucose uptake -> hyperglycaemia etc 3. increased lipolysis -> Increased plasma FFA to liver. Ketogenesis: ketonuria and ketonaemia (beta hydroxybutyrate and aceto- acetate) -> dehydration, acidosis, coma, death ``` ix Plasma glucose: high >11 or known DM Plasma ketones: high >3mmol/l ABG: metabolic acidosis pH < 7.3 Urine dip: ketones (++) and glucose ``` mgmt ABCDE sats etc… + catheterise Volume depletion: IV NaCl (1L stat, over 1hr, 2h, 4h, 8h) *switch to 5% dex when glucose <12 Hyperglycaemia: IV insulin - will drop the potassium… *Fixed rate IV infusion: 0.1U/kg/hr add glucose when drops Hypokalaemia (as a result of fluids and insulin): K+in fluids >5.5 = nil 3.5-5.5 = 40mmol/L infusion solution <3.5 = senior review Acidaemia: IV bicarbonate if vomiting + decreased consciousness - gastric aspiration MONITOR - electrolytes + ABG, fluid balance, glucose ECG hourly

Answer 5

def FOUR IS THE FLOOR <4mmol/l neuroglycopaenia <3mmol/l ``` vital signs THIS PATIENT LOOKS UNWELL normal RR/BP peripheral vasoconstriction (alpha 1) pale cold clammy sympth overdrive tachycardia (B1) ``` neurological mani low GCS seizure - tonic/clonic -> todds paralysis (hemi parasis post seizure) brisk reflexes bilateral upgoing plantars -> ddx pontine haemorrhage

Answer 6

sensory except in acute segmental demyelination (GBS) where motor involvement is the main feature + hereditary sensory motor neuropathy eg charcot marie tooth disease

Answer 7

eg b12 affecting large myelinated sensory nerves neg symps - unsteady gait, walking on cotton wool as loss of discriminatory sensation posi symps - pins and needles, band-like feeling around calf

Answer 8

alcohol affecting small unmyelinated c fibres neg symps - loss of pain and temp sensation posi - painful dyasthesiae eg burning causalgia, hyperalgesia

Answer 9

diabetes | very variable - some have painful neuropathy others have no pain and profound loss of proprioception and unsteady gait

Answer 10

large - A alpha - proprioception medium - A beta - touch small - c fibre - pain/temp

Answer 11

screened using 10g monofilament over 3 toes, 3 points on ball of foot, 3 points near arch of heel instruction should be 'say yes when you feel it' 1-2 not felt = reduced sensation, 'at risk' foot all not felt = absent sensation

Answer 12

arthropathy is a progressive condition of the musculoskeletal system that is characterized by joint dislocations, pathologic fractures, and debilitating deformities patho 1. loss of protective sensation = repeated microtrauma -> degen change, joint destruction, rubbery feel when moving MetoTarsoPharngeal joints, ulceration 2. autonomic neuropathy = increased blood supply -> oedema, warmth, redness + increase in osteoclast activity = bone resorption mgmt vascular, infection control, pressure relief

Answer 13

who T2DM + elderly features extreme dehydration (but may not look it as all the water in the intravascular space) fatigue + n+v altered mental state, headache +/- seizures +/- delirium hyperviscosity = MI, stroke, peripheral arterial thrombosis comes on over many days in comp to DKA which is hours ``` precip infection MI dehydration inability to take normla meds thiazides + loop poor control ``` mech Hyperglycaemia -> osmotic diuresis = loss of na + k -> hyperosmolarity leading to fluid shift of water into intravascular compartment -> severe dehydration No ketosis as enough insulin to suppress ketogenesis criteria 1. Hypovolaemia 2. Marked hyperglycaemia (>30) without hyperketonaemia or acidosis 3. Osmolality > 320 mosmol/kg (concentration of blood) Calc osmolarity = 2(Na + K) + gluc + urea Plasma osmolality is a guide to intracellular osmolality -> if high will secrete ADH ``` ix Urinalysis: glycosuria +++. Ketonuria + Capillary glucose > 30 Serum osmolarity > 320mmol/L U+E -> AKI ABG -> normal Blood cultures -> rule out sepsis ``` mgmt GRADUAL Treat cause Safely normalise osmolality - replace fluid and electrolytes Normalise blood glucose ABCDE IV access, ECG, SaO2, BP Calculate osmolality frequently (2Na + gluc + urea) and plot on graph IV 0.9% NaCl -> aim for fall of Na by 10mmol/24 hours (if not switch to 0.45%), glucose 5mmol/hr Aim for 3-6 litres +ve by 12 hours IV insulin (0.05U/kg/hr) if glucose no longer falling + ketonuria + acidosis RAPID DECLINE IS HARMFUL Rising sodium is only a concern if the osmolality is NOT declining concurrently comp cerebral oedema central pontine myelinosis

Answer 14

Cluster of common abnormalities including insulin resistance, impaired glucose tol, reduced HDL, elevated triglycerides and HTN criteria 1. Truncal obesity: men ≥ 94cm, women ≥ 80cm or BMI > 30 2. BP: Systolic ≥130 diastolic ≥ 85 or prev Dx HTN 3. Reduced HDL: <1.03mmol/l (men), <1.29mmol/l (women) 4. High triglycerides: ≥ 1.7mmol/l 5. Fasting glucose ≥6.1mmol/l (prediabetes) increased risk of atherosclerosis - CVD, diabetes causes obesity ``` assoc NAFLD PCOS CVD T2DM ``` mgmt lifestyle - smoking, activity, diet HTN control lose weight comps hypercoag

Answer 15

catagory - 25-29.9 overweight 30-34.9 obese I 35-39.9 obese II ≥40 obese III - weight is imminent threat ``` causes MED Glitazone, sulfonylurea Anticonvulsants Antidepressants: tricyclics and mirtazapine Lithium Progesterone only contraception BB Corticosteroids CONDITIONS hypothyroid, PCOS, cushing, hypogonadism GENE - KRS2 - severe insulin resistance and reduced metabolic rate ``` ix hormone - sex + cortisol TFT mgmt tactics prev, correction, population, individual mgmt motivational interviewing Overweight: structured advice diet + ex, if comorbid consider drug post lifestyle Obese I: structured advice diet + ex, if comorbid consider drug post lifestyle Obese II: structured advice ± drug, consider referring for surgery Obese III: structured advice ± drug, consider referring for surgery DIET - NICE rec diet 600kcal deficit/low fat Low calorie 800-1600 may be considered Very low calorie < 800, for no more than 12 weeks EXERCISE - increases BMR, 30 mins mod x5/week MED - orlistat, 1 tablet 1 hour after each meal. lipase inhibitor, continue beyond 3M only if lose 5%, SE deficiency in DEAK, abdo discomfort, oily stool, CI cholestasis SURG - bariatric: 1. Restrictive: gastric banding 2. Malabsorptive: biliopancreatic diversion 3. Both: roux en y gastric bypass (RYGB) ``` comp HTN CaCo T2DM MI angina ovarian cancer sroke ```

Answer 16

``` def Enlargement of male breast tissue - disc of tissue under skin (true) ``` pathophys Oestrogens stimulate, androgens inhibit therefore ratio is important Conditions raising oestrogen Conditions dropping testosterone/androgen resistance Conditions causing increased conversion of androgens to oestrogen - aromatase (in increased adiposity causes 1. Physiological @ 14 (unilateral + tender) - assoc delayed testosterone, aging - low testosterone 2. Path (low test) - androgen resistance, Klinefelter’s, viral orchitis (mumps), renal disease 3. Path (high oes) - neoplasms secreting HCG (e.g. seminoma) or ectopic BCG lung, RCC, adrenal tumour (oestrogen), CAH, *liver disease - increased prod androstenedione and aromatisation to oestrogen), obesity, hyperThyroid 4. Path (high PRL) - prolactinoma 5. *Medication (25%) - DISCO BOOBS lol: Digoxin, isoniazid, spironolactone, cimetidine, oestrogen ix U/E, LFT, TFT homrones - Estradiol, testosterone, prolactin, bHCG, AFP, LH LH high + test low = testicular failure LH low + test low = increased oestrogens LH high + test high = androgen resistance or neoplasm imaging - USS, mammography if suspicious or unilateral + needle core biopsy ``` cancer risk BRCA1/2 klinfelters unilateral rapid fixed painful >5cm ```

Answer 17

``` hypothal TRH pit - ant TSH thyroid follicle circ t3/4: free or bound -> liver conjugation/excretion, peripheral conversion of T4 to active T3 target tissue THRa or THRb receptors renal excretion ```

Answer 18

TRH Thyrotropin releasing hormone TSH Thyroid stimulating hormone ``` T3 Tri-iodothyronine (active), 20% by thyroid T4 Thyroxine (inactive), 80% by thyroid T4->3 80% @ liver, 20% @ thyroid ``` diffuse goitre - physiological, graves, hasimotos nodular goitre - multinodular, adenoma, carcinoma painful goitre - de quervains constituents of t4 - tyrosine or iodine func thyroid hormones - control metabolic rate of tissues

Answer 19

assoc AI disease: T1DM, addisons, pernicious anaemia: 5x women causes Atrophic hypothyroidism (no goitre) Subacute: De Quervain’s painful goitre and raised ESR Riedel’s thyroiditis fibrous tissue replaces thyroid Postpartum thyroiditis (2.5%) often transient Iatrogenic: surgery or radioiodine treatment Drugs: lithium, amiodarone (*iodine rich may become hypo or hyper) Iodine deficiency most common in developing world may cause transient thyrotoxicosis in acute course subclinical types primary - as above secondary - isolated TSH disorders (Hypopituitary disorders: neoplasm, radiotherapy, infection Hypothalamic disorders: neoplasm and trauma) ``` pres - BRADYCARDIC Bradycardia Reflex relax slowly Ataxia Dry thin skin/hair Yawning/drowsiness Cold hands and cold intolerant Acites and non-pitting oedema Round puffy face Double chin/obese/deafeted demeanor Immobile and ileus CHF SYMPS - deep hoarse voice, mennorhagia, weight gain, constiaption, tired, lethargy, slow intellect (poor mem and diff conc), reduced libido, depression SIGNS - Dry coarse skin/hair Puffy face/hands/feet (myxoedema) Bradycardia Delayed tendon reflex Carpal tunnel Serous cavity effusions: pericarditis/pleural effusions ``` AI hypo + goitre + AAb + pres hashimotos (most common) or atrophic GOITRE 1. In Hashimoto’s = painless, diffuse, varying size, rubbery, irregular surface may be normal or abnormal TF 2. In atrophic patients are overtly hypothyroid and have no goitre AAb Anti-TPO (anti-thyroid peroxidase), anti-Tg (antithyroglobulin) in 90-95% pres - Viral infection -> local symptoms and tenderness with nodularity, starts thyrotoxic and then hypothyroid ix TFT: TSH, T3 and T4 -> (primary or secondary) Primary: high TSH, low T3/T4, secondary: low TSH, low T3/T4 Thyroid Ab: antiTPO and antiTg if untreated = high colesterol, trigylcerides, anaemia (normocytic/chromic) if asymmetrical = neoplasm - USS if ?secondary = pit imaging and visual field test, MRI ``` mgmt treat when symps or TSH >10 levothyroxine T4 for life 50-100mcg TFT every 3-4 weeks ``` risk of osteoporosis and arrhythmia

Answer 20

severe hypothyroidism Myxoedema: mucopolysaccharides accumulate under skin and tissue: thickening of facial features Ventilatory dysfunction and coma pres Expressionless face with peri-orbital fullness Pale cool skin with rough - doughy texture + purple tinge common places - face and hands 'tight rings' 'bunch of banana hands' Enlarged heart Megacolon Cerebellar ataxia Psychosis + encephalopathy -> worry in myxoedema coma (elderly) COMA - Hypo feats + seizures + hypothermia + decreased consciousness + hypoventilation precip infection mgmt IV levothyroxine + IV hydrocortisone (after blood cortisone) + resp support

Answer 21

low thyroid hormones in a clinical euthyroid patient mgmt treat underlying cause

Answer 22

causes Main = Grave’s disease (assoc thyroid eye disease) - 75% Toxic multinodular goitre - more common in >60 from high iodine (amiodarone or derbyshire) Toxic nodule/adenoma Subacute/De Quervain’s (transient) - toxicosis + fever + pain in neck + local tenderness: TFT - hyperthyroid + raised ESR - Rx: aspirin and pred - self resolve Drugs: amiodarone Exogenous thyroid hormone excess: treatment Ectopic thyroid tissue: metastatic follicular carcinoma or ovarian teratoma TSH secreting pituitary adenoma (secondary) RF fam hist high iodine smoking esp thyroid eye ``` symp Weight loss and increased appetite Irritable + weak Sweating, tremor Diarrhoea Mental illness: anxiety to psychosis Heat intolerant Loss of libido Oligomenorrhoea ``` ``` signs Sweaty/warm palms Fine tremor Tachycardia ± AF Hair thinning Goitre *Proximal myopathy (wasting and weakness) Gynaecomastia Brisk reflexes Urticaria/pruritus + thyroid acropachy + pretibial myxoedema ``` AI graves anti-TSH receptor abs react with orbital antigens path - AAb stimulate TSH receptor leading to excess secretion of thyroid hormones and hyperplasia of follicular cells -> diffuse goitre assoc - Thyroid eye disease: lid lag, lid retraction, ophthalmoplegia (upward gaze palsy), exophthalmos (aka proptosis best assessed from side), gritty eyes, diplopia, loss of colour vision, conjunctival oedema, papilloedema Worsened by radio-iodine + smoking IX TFT: TSH low, high T3/T4 Oligoclonal IgG AAb: anti-TSHR (99%) at Grave’s + anti thyroglobulin + anti TPO Imaging: USS ?cancer Radioisotope uptake scan hot = overactivity, no uptake @ DeQuervain’s ESR raised at DeQuervain’s If orbital involvement: visual fields, CT/MRI head mgmt BB - propanolol lubricating eye drops antithyroid drugs - carbimazole 10-20mg/day titrated based on monthly TFT - can do BLOCK and REPLACE tactic with carbimazole + thyroxine or dose titration Normally euthyroid at 4-8 weeks, then reduce carbimazole till lowest dose, remission at 18 months - stop drugs. 18 month F/U propylthiouracil - causes liver fail: reserve for preg and thyroid storm WARNING stop drugs if Sore throat: anti-thyroid drugs can cause myelosuppression - agranulocytosis + neutropenia sepsis OTHER MANAGEMENT PLANS 1. Radioactive iodine (CI at pregnancy/breast feeding) - Relapsed Grave’s or toxic nodular (worsens eye disease in Grave’s) 2. Surgery Only when euthyroid Subtotal thyroidectomy in 98% - comp = hypoparathyroidism + damage to recurrent laryngeal nerve

Answer 23

who graves or TMNG ``` pres Hyperpyrexia > 41 CVS: HR > 140, hypotension, AF, CHF GI: Nausea, jaundice, vomiting, diarrhoea, abdominal pain NEURO: Confusion, agitation, delirium ``` precip infection ``` ix sepsis screen TFT ECG CXR ABG U/E, LFT ``` mgmt treat infection resus o2, IV fluids, NG tube if vom antithyroid rx - oral carbimazole or propylthiouracil @4 hours - lugol's solution - aqueous iodine IV propanolol IV hydrocortisone keep cool with tepid sponging NOT PARACETAMOL

Answer 24

TYPES 70% papillary carcinoma - young females - excellent prognosis, lymphatic spread 20% follicular carcinoma - middle age, haematogenous spread anaplastic - 3% - elderly, v poor prog lymphoma - 1% medullary - 1% - rare, derived from parafollicular c cells, secretes calcitonin, assoc woth adrenal phaeochromocytoma + 1 HPT, mucosal neuromas PRES Thyroid nodules + CLNs IX radioiodine scan USS fine needle aspiration MGMT Total thyroidectomy Radioiodine to kill residual cells Yearly thyroglobulin to detect recurrence

Answer 25

in response to low calcium actions 1. BONE: increase osteoclastic activity - release Ca and PO4 2. KIDNEY: - 25-OH-D to 1,25-OH2-D (1-alpha hydroxylase) - increases Ca absorption gut - Increases reabs Ca, decreases reabs PO4 (increases PO4 in urine, decreases Ca) Net effect - increased Ca, decreased PO4

Answer 26

Produced by para-follicular (medullary) C cells of thyroid | inhibits osteoclast activity - reduces Ca and PO4

Answer 27

types 1. Primary - solitary adenoma at PTH glands (85%) postmenopausal women - high PTH, Ca, low phosphate - probs asymp 2. Secondary - as a result of low calcium - PT gland hyperplasia, *almost always associated with kidney, liver or bowel disease. High PTH, low Ca, high phosphate, low vitamin D (kidney) 3. Tertiary - ongoing hyperplasia of PT glands after correction of underlying renal disorder CKD . i.e. after prolonged secondary hyperplasia of all 4 glands - High PTH, high Ca, high phosphate, normal vitamin D, high alk phos (DDx primary) * Renal for 2 and 3 ddx benign familial hypocalciuric hypercalcaemia - AD

Answer 28

who postmenopausal women what 85% solitary adenoma 10% 4 gland hypertrophy assoc MEN 1/2 pres 80% asymp and diagnosed when hypercalc found Excess Ca absorption from bone: osteopenia and osteoporosis if extreme = osteitis fibrosa cystica (salt + pepper pot skull + subperiosteal resorption phalanges) Excessive renal Ca excretion: calculi Mild symptoms of hypercalcaemia: fatigue, weakness, muscle pain *Bones, stones, abdominal moans, thrones, psychic overtones ``` ix thiazide + lithium repeat plasma albumin adjusted calc - high check U/E measure PTH - high (which should trigger you to measure 25-OH-D, hydroxyvitamin D) phosphate levels - low DEXA - annual renal tract imaging USS XR - skull and hand ``` mgmt mild hypercalc + kid stones - surveillance - check creat + ca 6m vit D suppresses PTH avoid dehydration, thiazide diuretics MEDS = bisphos (alendronate), cinacalcet - reduces serum ca and PTH levels and raises PO4 (no affect on bone turnover) CURATIVE = surgery: Single adenoma = excision, 4 gland hypertrophy = 3.5 gland subtotal parathyroidectomy comps osteoporosis and peptic ulcers

Answer 29

acute early rare - bleeding, thryoid crisis (hyperthermia, fast AF, pulm oedema) damage to local structures - hypoparathyroidism -> hypocalc (chvostek's sign + trousseau's sign), damaged recurrent laryngeal nerve common - late hypothyroid, recurrent hyperthyroid hungry bone syndrome - Ca and PO4 rapidly deposited in bone

Answer 30

``` breast bronchus thyroid kidney prostate ```

Answer 31

Chvostek sign is contraction of facial muscles provoked by lightly tapping over the facial nerve anterior to the ear as it crosses the zygomatic arch

Answer 32

Trousseau's sign is carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes

Answer 33

midline goitre thyroglossal cyst ``` lateral lymph node solitary thyroid nodule vascular - aneurysm, carotid body tumour sebaceous cyst/lipoma cystic hygroma/branchial cyst salivary glands nerve: neurofibroma ```

Answer 34

goitre eye signs thyrotoxicosis

Answer 35

multinodular patients usually euthyroid - rarely go toxic indications for surg - patient choice, cosmetic, compression of local structures, (change of voice/ stridor) positive pemberton's test = retrosternal goitre, patient raises arms and holds them above head, pembertons sign is if the patient goes pink due to temp SVC obstruction + stridor

Answer 36

simple - physiological, colloid or non-toxic - typically small and smooth, common multinodular - usually euthyroid, gland large, firm, smooth, nodular - common graves - smooth soft +/- bruit hypo - NO GOITRE hashimotos - firm, small/med size

Answer 37

assoc CKD or vit D deficient patho Hyperplastic PT glands in response to to long term stimulation by chronic hypocalcaemia pres CKD pres with predominant bone pain If low vit D - osteomalacia and fracture ix High PTH, low Ca, PO4 high in renal disease, low in vitamin D deficiency mgmt Correct vitamin D deficiency In CKD: Ca supp, correct vit D, phosphate binders, calcimimetics (only at end-stage kidney disease)

Answer 38

assoc prolonged secondary, CKD patho glands become autonomous producing excess PTH even after cause of hypocalcaemia is corrected -> hypercalc hyperplasia of all 4 glands pres symps of high ca ``` ix high PTH high ca decreased phos alk phos elevated ``` mgmt cinacalet total or subtotal parathyroidectomy

Answer 39

Elevated serum Calcium > 1mg/dL above normal Hypercalciuria > 400mg/day Creatinine clearance < 30% compared with normal Episode of life threatening hypercalcaemia Nephrolithiasis Age < 50 years Neuromuscular symptoms Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)

Answer 40

main prob LOW CALC types PRIMARY - 1. congenital (digeorge, defect in PTH gene, defect in calc sensing) 2. acquired - neck surg, neck irradiation, alc, iron dep (haemochromatosis, copper (wilsons), mag def or excess SECONDARY - pseudohypoparathyroidism - defect in PTH action: Rare metabolic disorders with characteristic morphology and end-organ resistance to PTH morph = Low IQ, short stature, short 4th and 5th metacarpals ix = Low Ca, high PO4, high PTH (but fail action), urinary cAMP + phosphate following infusion of PTH -> in hypopara = increase in cAMP and phos, in pseudo = none are increased TERTIARY = Pseudopseudohypoparathyroidism Similar phenotype to above but normal biochemistry pres hypocalc features - tetany (muscle twitching, cramping and spasm), perioral paraesthesia, chronic - prolonged QT trousseau + chvostek sign ``` ix Low Ca, high PO4, low PTH, normal alk phos (@ pseudohypoparathyroidism = low Ca, high PO4, high PTH) Serum Mg - low U+E - to exclude CKD 25-hydroxyvitamin D3 to exclude vitamin D deficiency as cause of hypocalcaemia Low 24 hr urine calcium Echo in DiGeorge ECG - prolonged QT (hypocalcaemia) ``` mgmt if tetany = urgent IV calc diet rich in ca and vit d

Answer 41

Adenohypophysis GH: stimulates liver to produce IGF-1 and counteracts insulin Prolactin: promotes growth of mammary glands and reproductive organs FSH: stimulates release of sex steroids LH: stimulates release of sex steroids ACTH: adrenocorticotropic hormone: stimulates adrenal cortex to release glucocorticoids and androgens TSH

Answer 42

Neurohypophysis Supraoptic nucleus - vasopressin Paraventricular nucleus - oxytocin

Answer 43

affects - Excessive hormone, local effects, inadequate production by rest of gland assoc MEN-1 = parathyroid, endocrine gastric i.e. gastrinoma, insulinoma, and ant pit types benign adenoma = most common prolactinoma -> GH -> ACTH -> TSH -> LH/FSH hormonally active types 15% Eosinophilic/acidophile: GH/prolactin, prolactin normally small and intrasellar, GH may extend to suprasellar 15% Basophilic: ACTH - presents with Cushing’s, confined to sella turcica but may enlarge post adrenalectomy (Nelson’s syndrome) 70% Chromophobe: non-secretory i.e. incidentaloma (<1cm): often present with visual loss local affects cavernous sinus - CN3, 4, 5a, 5b, 6 optic chiasm headaches - retroorbital, bilateral worse on waking from stretching of dura visual field defect - bitemporal hemianopia ocular nerve palsies - squint hormonal deficiencies - Panhypopituitarism or varying degrees of loss of any problem Order of hypopituitarism - LH, GH, TSH, ACTH, FSH Pres = infertility/oligomenorrhoea, erectile dysfunction, loss of libido -> loss of muscle bulk and body hair gen ix Pituitary function tests - GH, prolactin, ACTH, FH, LSH, TFT Visual fields MRI with contrast ddx 1. Craniopharyngioma - from Rathke’s pouch, between pit and floor V3. Benign and cystic (grows down = lose bottom half vision) most common childhood IC neoplasm. Headache + visual field defects + hypopituitarism 2. pit hyperplasia 3. meningioma 4. brain metastases 5. lymphoma 6. hypophysitis 7. vascular malformation (e.g. aneurysm) mgmt Surgery: transsphenoidal transnasal hypophysectomy SE: pituitary dysfunction -> adrenal insufficiency, DI, SIADH Radiation: for recurrence Drugs: Prolactinoma - bromocriptine GH - somatostatin analogues Hormone replacement: *ensure steroids given before levothyroxine as thyroxine may precipitate adrenal crisis big worry pituitary apoplexy - rapid enlargement due to bleed into tumour -> mass effect, CV collapse and acute hypopituitarism

Answer 44

``` def Hyperprolactinaemia = raised prolactin in blood. Physiologically high in pregnancy, puerperium and stress (oestrogen promotes PRL + stress - hypothalamus) ``` effects of prolactin Women - inhibits GNRH -> reduced gonadotropin (FSH + LH) secretion -> menstrual dysfunction + galactorrhoea -> low oestrogen Men - direct reversible response on hypothalamus -> secondary hypogonadism -> decreased libido and ED causes Prolactinoma - benign adenoma - micro, macro, craniopharyngioma Hypothyroid -> raises TSH -> raises PRL Other endocrine = Cushing’s syndrome Antipsychotics -> block dopamine -> raise PRL Dopamine receptor antag: domperidone, metoclopramide, neuroleptics Dopamine depleting: methyldopa Antidepressants: e.g. TCA, MAOI, SRI Physiological - pregnancy, puerperium, stress, exercise Head injury assoc MEN1 - parathyroid tumours, prolactinoma, pancreatic islet tumour pres Women: oligomenorrhoea, amenorrhoea, galactorrhoea, infertility, hirsutism Men: slower pres, reduced libido, reduced beard growth, ED Children: growth failure and delayed puberty If macroprolactinoma Headache, vis disturb, bitemporal hemianopia or upper temporal quadrantanopia ``` ix PRL: normal < 400, if mild el = 400-1000 - repeat before referral > 5000 = true prolactinoma TFT Exclude pregnancy Assess other pituitary function MRI pituitary ``` mgmt Treat if effect of size, adverse effect hyperprolactinaemia Rx: dopamine agonist Cabergoline or bromocriptine -> reduce prolactin, allow oestrogen normalise SE: sleepiness, hypotension, cardiac/retroperitoneal/pulmonary fibrosis - monitor Use bromocriptine if fertility is goal (ergot deriv) If ineffective: trans-sphenoidal surgery long-term comp Of hyperprolactinaemia = hypogonadism - osteoporosis, reduced fertility, ED Sudden onset headache, visual symptoms = pituitary apoplexy (haemorrhage or infarction)

Answer 45

axis hypothalamus -> ant pit -> GH -> liver releases IGF1 and adipose tissue releases FFA which causes adrenal output main mediator IGF1 ``` Acromegaly = overgrowth of all organ systems bones, joints and soft tissues by IGF1 Giantism = excess GH or IGF1 before closure of epiphyseal plates ``` types macro + micro causes pituitary adenoma - 95% ectopic GHRH or GH production of tumour eg panc course slow growth - insidious onset ``` assoc MEN1 T2DM prolactinoma colon cancer ``` pres headaches bitemp hemianopia APPEARANCE -> large hands/feet, frontal bossing, thickened nose, coarsening facial features MOUTH -> macroglossia, OSA, snoring, wide spaced teeth, large jaw SKIN -> dark thick oily skin + sweating ARTICULAR -> arthralgia, osteoarthritis, jaw pain NERVE COMPRESSION -> bilateral carpal tunnel, acroparasthesia VISCERAL -> cardio/hepatomeg CARDIAC -> HTN, arrhythmia, LVH T2DM raised prolactin in 1/3 = galactorrhoea ``` ix GH - secretion is pulsatile and during peaks, this is inhibited by glucose - this is lost in acromeg serum IGF1 - raised OGTT - to confirm raised IGF1 (75g glucose load, Failure to suppress to < 0.4mcg/L) random GH >0.4mcg pit MRI prolactin blood glucose visual field test ``` mgmt FIRST LINE - transsphenoidal surgery SECOND LINE - SomatoStatin analogues - ocreotide (SE abdo cramps) THIRD - 1. GH receptor antagonist - pegvisomant - very effective (but doesnt reduce tumour size so still mass effect) 2. dopamine agonist - cabergoline (safe at preg), bromocriptine - chronic use of ergot derivatives = fibrosis, good for mixed acro + high prolactin comps CARDIAC - LVH, arrhythmia - monitor with ECG, echo HTN - serial BP monitoring sleep apnoea impaired glucose tolerance + diabetes carpal tunnel colon cancer increased risk - monitor every 3-5 yrs

Answer 46

cushings conns - hyperaldosteronism addisons - adrenal insufficency THE DEEPER YOU GET THE SWEETER YOU GET!!! zona glomerulosa - mineralcorticoids - ALDOSTERONE zona fasiculata - glucocorticoids - CORTISOL zona reticularis - androgens - DHEA

Answer 47

``` suppression of RIDGE reproduction immunity digestion growth energy (mobilisation of = elevated sugars - insulin ineffective) ``` diurnal variation - highest in morning, lowest at midnight CUSHINGS pit adenoma = bilateral adrenal hypertrophy

Answer 48

``` def Prolonged exposure to exogenous or endogenous glucocorticoids with clinical state of increased free cortisol and loss of negative feedback ``` types ACTH independent = Adrenal adenoma/adrenal carcinoma/excess glucocorticoids ACTH dependent = Excessive ACTH pit (Cushing's disease), ectopic ACTH producing tumours (due to lung cancer, small cell) most common Excess exogenous glucocorticoids ACTH dependent = next, Cushing’s disease = 80%, ectopic = 20% ACTH independent: 60% = adrenal adenoma, 40% = adrenal adenocarcinoma pres BODY Truncal obesity, buffalo hump, weight gain, prox muscle wasting FACE Facial fullness, moon face Diabetes or impaired GT: polyuria, polydipsia Hypertension Osteoporosis Infection prone and poor healing MOOD change: depression, lethargy, irritable, psychosis SKIN: atrophy, purple striae, easy bruising, hirsutism, acne, pigmentation, acne If ACTH adenoma: headaches, visual problems, galactorrhoea If hypopituitarism: amenorrhoea, loss of libido, ED ddx alcoholism poorly controlled diabetes ix serum glucose - elevated FIRST LINE - 1mg @ night DEXAMETHSONE SUPPRESSION TEST, measure 8am in morn- failure to suppress to <50mmol = +ve can confirm with late night salivary cortisol 24hr urinary free cortisol - should be high in 2/3 samples SECOND LINE - 48hr 2mg dex sup test - failure to suppress <50mmol if ABG then would see hypokalaemic met alkalosis - especially ectopic ACTH secretion localisation plasma ACTH: low = adrenal - CT high = distinguish pit from ectopic (give IV CRH - if rise = pit = MRI pit, if no rise = ectopic = IV contrast CT chest (SCLC), abdo (carcinoid) ectopic pres triad pig, hypokal, wt loss patho of pigment ACTH structurally similar to MSH (melanocyte stimulating hormone) -> increases melanin mgmt CUSHINGS = transsphenoidal pit adenomectomy surg fails? pit irradiation last resort = bilateral adrenalectomy - monitor @6/12 months with ACTH + MRI comp = nelsons syndrome = development of large ACTH secreting tumour: presents with pigmentation and VF defects. if anything else remove via surg ``` comp adrenal insuff post surg CV disease - main cause of death - HTN, DM, dyslipidaemia metabolic syndrome impaired immunity osteoporosis ```

Answer 49

one week course in self management of diabetes

Answer 50

1. glucojuice/tabs 2. glucogel 3. 10% glucose giving set 50ml syringe 4. glucagen

Answer 51

insulin never omitted in type 1 - though dose reduction may be needed need for prolonged 10% glucose infusion over 24-48hrs after gliclazide induced hypo coma. omit further doses until diabetes team seen them if <3, if 3-3.9 reduce dose by 50%

Answer 52

actrapid + humulin s have peak effect about 2 hours after injection lasts 6-8 hours carbohydrate snacks normally required between meals and at bedtime so inject 20 mins before

Answer 53

humalog novorapid peak = 1 hr after meal lasts 3-5 hours immediately before meal inject or upto 15 mins after snacks not usually necessary between meals

Answer 54

once or twice bedtime/morn dont need to be followed by food medium - human (humulin I + insulatard) long - genetically engineered (lantus + levemir) - usually once daily at night

Answer 55

provide basal + meal related insulin when They are usually given twice daily before breakfast and before tea, sometimes three times before meals. In elderly, they may occasionally be given once before breakfast. They are never given at bedtime types premixed - humulin M3 - 15-20 mins before a meal, NEVER at bedtime, bedtime snack necessary biphasic analogue mixtures - humalog mix25 and novomix 30, 15 mins after meal, NEVER at bedtime

Answer 56

multiple - basal bolus regime - long acting and quick for meals T1DM twice daily injections of insulin mixtures, often with metformin in type 2 diabetes once daily Of a medium or long-acting insulin at bedtime together with oral hypoglycaemic agents in type 2 diabetes Occasionally elderly patients are managed with a single injection of a long-acting insulin or an insulin mixture in the morning

Answer 57

AN INSULIN SYRINGE | - much smaller and if you use big syringe = fatal dose

Answer 58

the body can lack insulin within minutes if the infusion is interrupted or stopped diabetic ketoacidosis can develop within a few hours if intravenous insulin is interrupted in type 1 diabetes when discontinuing intravenous insulin the first dose of subcutaneous insulin should be given one hour before intravenous insulin is stopped (15 minutes before for Novorapid or Humalog) intravenous insulin and glucose are usually stopped once patient is eating and drinking

Answer 59

mimics cushings due to alc excess or sev depression will have a false posi dexmethasone suppression test or 24hr urinary free cortisol insulin stress test to differentiate

Answer 60

``` def Acute deficiency of glucocorticoid cortisol and mineralocorticoid ``` precip Major or minor infx, commonly vom/diarrhoea Injury, surgery, pregnancy causing acute exac of chronic insuff adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia) steroid withdrawal biggest RF long term steroid therapy ``` pres malaise fatigue n+v low grade fever muscle crmaps confusion which can progress to: hypotension and hypovolaemic shock ``` ix u+e - low sodium, high pot, creatinine raised, blood glucose - hypoglycaemia bloods for cortisol and ACTH mgmt IV/IM hydrocortisone (only as high dose = mineralcorticoid too) 100mg adult rehydration - fluids IL n. saline over 30-60 mins further hydrocortisone + glucose - 100mg in 5% over 24 hours continuous cardiac and electrolyte monitoring - ECG, reg U+E treatment of infection - IV abx

Answer 61

synonym primary causes of primary hyperaldosteronism aldosterone = Insertion of ENaC and ROMK to luminal membrane of DCT Leads to hypernatraemia, water retention and hypokalaemia ``` def excess production of aldosterone independent of RAAS system due to adrenal adenoma -> renin is suppressed ``` when to consider HTN, hypokalaemia, or alk in someone not on diuretics other causes adrenal adenoma bilateral adrenal hyperplasia secondary - due to high renin from decreased renal perfusion in renal art stenosis pres oedema HTN hpokalaemia - weakness, cramps, parasthesia met alk - secretion of H+ in exchange of K+ (more k+ in urine) in intercalated cells polyuria - from reduced ability of the kidney to concentrate urine ix U+E - hypernat, hypokal BP - high aldosterone:renin ratio >800 (imaging req) ECG for arrhythmia CT/MRI for confirmation of adrenal adenoma lyind and standing aldosterone: affected by posture ddx high ald, low renin = primary (conns, BAH, familial) high ald/renin = renal art stenosis, diuretics, bartters, gitelmans mgmt conns - medical mgmt prior to surg: - 4w spiro or eplerenone (aldosterone antag) - lapro adrenalectomy (only if unilat) surgery only considered if unilateral BAH - aldosterone ant (spiro - also blocks test so may cause gynaecomastia, ED, menstrual prob) eplerenone - doesnt cause gynaeco ENaC inhibitor: Amiloride, a potassium-sparing diuretic, may be used if aldosterone antagonists are not tolerated - worse option tho - weak HTNive comp HTN may persist

Answer 62

HYPERCHLORAEMIAC METABOLIC ACIDOSIS type 1 - distal inability to secrete H+ distally -> hypokalaemia, comp = renal stones type 2 = proximal inability to resorb HCO3 -> hypokalaemia, comp = osteomalacia type 3 - mixed - rare type 4 - reduced aldosterone -> reduced proximal tubule ammonium excretion, causes = hypoaldosteronism

Answer 63

``` def Catecholamine producing adrenal tumour @ adrenal medulla. Secrete autonomously from SNS ``` 10% rule are bilateral, malignant, extra-adrenal (organ of zuckerkandl), familial (MEN2) main worry life threat HTN + arrhythmias precip = anaesthesia, opiates, decongestants, drugs inhib reuptake catecholamines eg TCA, childbirth, xray contrast mgmt - Phentolamine or IV nitroprusside asoc MEN (bilateral) neurofibromatosis von-hippel lindau quartet Episodic headache + sweating + palpitations + tremor other pres sense of doom anxt course secrete constant or intermittent O/E Hypertension, postural hypotension, tremor, flushing, tachycardia ``` ix 24 hour urine catecholamines, metanephrines, Raised serum metanephrines Genetic testing Abdominal CT/MRI ``` mgmt surgery = definitive pre surg - alpha blocker - phenoxybenzamine for 7-10 days to allow expansion of blood volume pre surg BB - post alpha - use propanolol Monitor with 24 hour catecholamines + VMA 2 weeks after surgery

Answer 64

A1 - SM @ BV = reduces BP, SM contraction @ bladder neck = increased peeing A2 - Inhibit insulin release @ pancreas = more insulin B1 - Tachycardia + increased contractility -> decrease HR + CO Increased renin release -> decreased renin B2 - Bronchodilation -> bronchoconstriction

Answer 65

``` def tumour of enterochromaffin cell in liver ``` common pres flushing diarrhoea ``` other clin wheeze palps telangiectasia abdo pain hypotension ``` whats released = serotonin, other vasoactive peptides which tumours 30% of gut 5% bronchial assoc MEN1 ix serum chromogranin A/B urinary 5ht CT CAP - to find tumour, check liver mets mgmt localised disease - surgical resection - appear bright yellow + peri-opeative ocreotide infusion (to prevent carcinoid crisis - continue for 48 hours post)

Answer 66

stands for multiple endocrine neoplasia inheritance all AD type 1 cancers = parathyroid, pituitary, pancreas common pres = hypercalc type 2a RET oncogene cancers = parathyroid, phaechromocytoma, medullary thyroid type 2b RET oncogene cancers = Phaeochromocytoma + neuromas + marfanoid body in all proph thyroidectomy

Answer 67

types nephrogenic or cranial ``` def passage of large amounts of dilute urine due to hyposecretion or resistance to ADH/vasopressin (same thing) and inability to concentrate urine ``` amounts 3l of <300mOsm/kg ADH synth Synthesised at supraoptic nucleus of hypothalamus and transported in vesicles to posterior pituitary action Binds V2 receptor and inserts aquaporin 2 to luminal membrane of DCT and CD causes lithium - nephro CRANIAL damage to hypothalamus acquired = idiopathic, tumour (e.g. craniopharyngioma), intracranial surgery, head injury, granulomatous disease (sarcoid, TB, GPA), infection (men, enceph) inherited = AD vasopressin gene, DIDMOAD (association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness aka Wolfram's syndrome) NEPHROGENIC Acquired: hypokalaemia, CKD, lithium, RTA, hypercalcaemia Inherited: X linked mut V2 ADH receptor gene, AR AQuaPorin2 gene ``` pres Marked polyuria > 3 litres Polydipsia and chronic thirst Nocturia Symptoms of hypernatraemia -> lethargy, weakness, confusion Distended bladder ``` ix 24 hour urine collection >3l Urine osmolality <300mOsm/kg (2[Na+K] + urea + glucose) Serum osmolality: normal or high (normal/high sodium, calcium, potassium) Urine dip: -ve for glucose *Water deprivation test with *desmopressin response - tests ability of kidneys to concentrate urine: if cranial: dep <300, desmo >800 if nephrogenic: dep <300, desmo <300 psychogenic: dep >800, desmo >800 normal urine osmolality 500-800 MRI pituitary/hypothalamus mgmt cranial = desmopressin replacement, if overdose = hyponat nephrogenic = drink adequate fluid in response to thirst, stop causative drugs, treat underlying hypok, hyperca low sodium - either dietary or with thiazide + NSAID if hyernat - oral/IV fluids with hypotonic eg 5% dex or 0.45% saline - aim reduce 1mmol/hr thiazide - paradoxical effect: in this case they concentrate urine and decrease polyuria - slight hyponatraemia -> increased Na and water uptake

Answer 68

Acute hyponatraemia: low serum osmolality, low sodium or high water in blood: water moves into brain (higher conc Na/K/Cl) = cerebral oedema Chronic hyponatraemia: low serum osmolality - electrolytes (Na/K/Cl move out of brain as does water) to try and correct serum osmolality If rapid correction, = rapid increase in serum osmolality and rapid movement of water out of brain - osmotic demyelination

Answer 69

130- 135 Headaches 125-130 Weakness + lethargy <125 Agitation + coma

endocrinology Flashcards

(93 cards)