3) GI system 2 + endocrinology Flashcards

Question

EPIGASTRIC HERNIA - location? - what herniates through where? - risk factors? - management options? 2

Answer 1

pass through linea alba above the umbilicus normally fat herniates through abdo muscle (occasionally a bit of bowel if really large) risk factors are same as any other hernia (eg obesity, heavy lifting, chronic cough etc) watch and wait OR surgery

Answer 2

polyposis = numerous polyps in the bowel FAP (familial adenomatous polyposis) nb this is almost always asymptomatic!! and is only found if FHx of colon ca at early age or many polyps found on colonoscopy done for another reason! can also occur in crohns / ulcerative colitis and other rarer genetic conditions nb these include: (DON'T LEARN THESE!) - MUTYH-associated polyposis (MAP) - juvenile polyposis syndrome - Peutz-Jeghers syndrome - serrated polyposis syndrome.

Answer 3

autosomal dominant 40years norm age of cancer if not managed regular colonoscopies from teenage years have suspicous polyps removed during colonoscopies OR whole / part of large bowel resected prophylactically! (nb similar to prophylactic mastectomy for BRCA genes)

Answer 4

Often presents late with features of cirrhosis and decompensated chronic liver disease (DCLD) - RUQ pain (due to liver capsule stretch) - Hepatomegaly – ± mass and/or bruits - Splenomegaly - Fever, malaise - anorexia, ↓weight - Jaundice + Pruritis (Late = HCC; Early = CholangioCa)

Answer 5

↑AFP (80% of HCC) nb if +ve must check for testicular Ca Heb B and C serology! Liver biopsy – use with CAUTION, as it seeds tumour cells through resection plane surgical resection

Answer 6

- perianal warts - leukoplakia - lichen sclerosis - bowen's disease - crohn's disease

Answer 7

autosomal dominant 40years norm age of cancer if not managed regular colonoscopies from teenage years have suspicous polyps removed during colonoscopies OR whole / part of large bowel resected prophylactically! (nb similar to prophylactic mastectomy for BRCA genes)

Answer 8

leave to resolve spontaneously OR evacuated under local anaesthetic

Answer 9

- bleeding - pain - altered bowel habit - pruritis ani - masses - strictures

Answer 10

- perianal warts - leukoplakia - lichen sclerosis - bowen's disease - crohn's disease

Answer 11

nb always drain internal abscess if still present Fistulotomy + Excision for both types but slightly different methods HIGH fistula - ie involving continence musles of anus – requires 'seton suture' tightened over time to maintain continence LOW fistula - ie not involving muscles of continence – fistulotomy and laid open to heal by secondary intention

Answer 12

in starved state: body metabolises protein + fat (subsequent drop in circulating insulin) catabolic state also depletes intra-cellular phosphate (but serum levels norm) when start refeeding: insulin incrteases which increases cellular uptake of phosphate -> LOW SERUM levels of PHOSPHATE (hypophosphataemia) -> symptoms / features of syndrome - malignancy - post-GI surgery - anorexia nervosa - starvation - alcoholism

Answer 13

HYPO-PHOSPHAETEMIC state norm occurs within 4 hrs -> - rhabdomyolysis - red + white cell dysfunction - respiratory insufficiency - arrythmias - cardiogenic shock - seizures - sudden death

Answer 14

refeed SLOWLY oral or IV phosphate if complications do occur (or low serum levels) monitor bloods closely (glucose, lipids, Na, K, phosphate, Ca2+, Mg, zinc) involve nutritionist

Answer 15

dysphagia = difficulty swallowing odynophagia = painful swallowing globus = sensation of lump in the throat dyspepsia = indigestion (ie upper abdo fullness, heartburn, nausea, belching, or upper abdo pain)

Answer 16

in starved state: body metabolises protein + fat (subsequent drop in circulating insulin) catabolic state also depletes intra-cellular phosphate (but serum levels norm) when start refeeding: insulin incrteases which increases cellular uptake of phosphate -> LOW SERUM levels of PHOSPHATE (hypophosphataemia) -> symptoms / features of syndrome - malignancy - post-GI surgery - anorexia nervosa - starvation - alcoholism

Answer 17

SYSTEMIC ("AW FS FIN") - appetite - weight loss - fatigue - sleep changes - fever - itch / rashes (any skin changes / lesions) - night sweats PSYCH ("above head") - mood - stress - body image NEURO ("head") - headache - visual changes - sensory loss - muscle weakness DIET ("put in mouth") - change to diet - polydipsia (DM) - recreational drugs (eg cannabis, ritalin) HAEM ("lymph nodes") - lumps neck, under armpits, groin - bruising - repeated infections - pale (anaemia) RESP ("lungs") - cough - haemoptysis - SOB CARDIOVASCULAR ("heart") - palpitations - light-headedness / syncope - chest pain - leg swelling GI SYSTEM (mouth to anus) - mouth ulcers - dysphagia - dyspepsia / heart burn - vomiting - haematemesis - abdominal pain - bloating - jaundice - change in bowel habits (new IBS >50) - blood or pus per rectum URINARY SYSTEM (kidneys, bladder) - flank pain - pain on passing urine - incontinence - polyuria (DM) - haematuria (kidney/bladder Ca) GENITALS - breast lumps (or new lumps anywhere tbh) - testicular lumps - non-menstrual PV bleeding MSK / RHEUM ("knees") - joint pain / swelling or stiffness basically if someone presents just with weight kloss - do a full systems review until you find some positives then focus in on those (taking into account risk factors etc)

Answer 18

difficulty swallowing (either solids or fluids) MECHANICAL CAUSE = Oesophageal Ca (or gastric/pharyngeal) - oesophageal web or ring = peptic stricture (from repeated reflux) = lung Ca = mediastyinal lymph nodes - retrosternal goitre - aortic aneurysm - pharyngeal pouch ``` MOTILITY DISORDERS = achalasia = diffuse oesophageal spasm - systemic sclerosis (/CREST) - neurological bulbar palsy* ``` OTHER - oesophagitis (reflux or candida/HSV) - globus (techincally not true dysphagia) *nb bulbar palsy can be caused by many things incl parkinsons, chagas, myasthenia gravis

Answer 19

1) Was there (a) difficulty swallowing solids AND liquids from the start OR (b) was solids difficult first and now both? - both first = motility cause (achalasia, CNS) - solids first = stricture (benign or amlignant) 2) Is it difficult to make the swallowing movement? - yes = bulbar palsy (esp if pt coughs on 'swallowing') 3) is swallowing painful (odynophagia)? - yes = oesophageal ulcer (benign or malignant) = candida (immunocompromised or steroid INH) = Oesophageal spasm 4) is the dysphagia intermittent OR is it constant + getting worse? - intermittent = oesophageal spasm - constant + worsening = malignant stricture 5) does the neck bulge or gurgle on swallowing? - yes = suspect pharyngeal pouch

Answer 20

1) systemic sclerosis 2) CNS disease - eg parkinsons, myasthenia gravis etc

Answer 21

FBC (anaemia for Ca) U+E (dehydration) CXR (mediastinal enlargement, lung Ca) 1) Upper GI endoscopy + biopsy 2) barium swallow

Answer 22

EPIGASTRIC PAIN - related to hunger, specific foods or time of day +/- BLOATING FULLNESS after meals HEARTBURN (retrosternal pain + reflux) TENDER EPIGASTRIUM

Answer 23

- gastric malignancy - duodenal / peptic ulcer (PUD) - gastritis (h pylori, nsaids, alcohol) - functional (non-ulcer) dyspepsia - oesphagitis / GORD nb PUD norm occurs after prolonged gastritis IF EPIGATRIC PAIN, also remember: - CARDIAC causes (eg ACS) - RESP causes (eg PE, pneumonia) - OTHER GI causes (eg pancreatitis, gall bladder)

Answer 24

ALARMS symptoms ``` A = Anaemia L = Loss of weight A = Anorexia R = recent onset / progressive symptoms M = Meleana / haematemesis S = Swallowing difficulty (dysphagia) ```

Answer 25

urgent endoscopy 1) new onset >50 years 2) any ALARMS features INITIAL 1) STOP DRUGS causes dyspepsia (NSAIDs) 2) LIFESTYLE advice (reduce alcohol + smoking, big meals etc, weight loss) 3) OVER-THE-COUNTER ANTACIDS try for FOUR WEEKS IF NO IMPROVEMENT: - test for H Pylori if positive = triple therapy if negative = 4 wk PPI (then review) then if continued symptoms after eradication or 4wks of PPI then consider endoscopy

Answer 26

cause is often MULTIFACTORIAL!!! 1) SPHINCTER DYSFUNCTION = vaginal delivery (tears or pudendal nerve damage) - any surgical trauma to sphincter (following procedures for fistulas, haemorrhoids, fissures) ``` 2) IMPAIRED SENSATION = any spinal cord lesion = diabetes = MS = dementia ``` 3) FAECAL IMPACTION = overflow diarrhoea (v common in elderly) nb although there is often no clear cause found, esp in elderly women, is norm multifactorial

Answer 27

1) ABDO exam 2) NEURO exam incl DRE!!! - stool / contents of rectum - peri-anal sensation - rectal tone ACUTE faecal incontinence = always consider CAUDA EQUINA / cord compression - esp if neuro deficitis!

Answer 28

15% of rectal bleeding has upper GI source - diverticulitis - crohn's / UC - colorectal cancer - some infectious gasrtoenteritis (eg campylobacter, shigella, salmonella, e coli., amoebas) - ischaemic colitis - mesenteric ischaemia - haemorrhoids - other perianal disease (fistula, fissure)

Answer 29

UPPER GI bleed

Answer 30

MESENTERIC ISCHAEMIA - typically small bowel - due to embolism (AF is risk) - sudden onset, severe symptoms (abdo pain severe, out of keeping with exam findings) - lactic acidosis - urgent surgery - high mortality ISCHAEMIC COLITIS - large bowel - multifactorial - acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage - transient, less severe symptoms, bloody diarrhoea + abdo pain. - 'thumbprinting' on AXR - conservative management (surgery if peritonitis, perf or ongoing haemorrhage) nb can also get chronic mesenteric ishaemia - think of like intestinal angina - but this is rare

Answer 31

always do a DRE (looking for peri anal disease and also visualising blood) send off stool sample for MC+S - FBC - U+E - LFT - amylase - CRP - clotting - VBG - group + save (cross-match if still actively bleeding) to CONSIDER: - abdo X-ray - erect CXR (if peritonism or cardio/resp comorbidity) nb can consider colonoscopy but not while actively bleeding!! nb keep niol by mouth nb consider IV omeprazole (as may be an upper GI bleed) if signs of sepsis or perforation, give Abx

Answer 32

"the 5 Fs" - Fluid - Flatus - Faeces - Fat - Foetus

Answer 33

- ascites - bladder (retention) - large AAA SHIFTING DULLNESS

Answer 34

always ask a woman the date of the first day of her last period!! (ie to see if possibility of pregnancy) consider: - AXR - abdo USS ascitic tap if looks like ascites

Answer 35

1) PRE-HEPATIC - unconjugated 2) INTRA-HEPATIC - mainly conjugated (may be some unconjugated) 3) POST-HEPATIC - conjugated

Answer 36

over-production or increased breakdown of RBCs eg - DIC - malaria nb can also be due to impaired hepatic intake - eg some drugs (rifampicin, contrast agents) or right heart failure nb also can be dt impaired conjugation (eg Gilbert's syndrome)

Answer 37

basically anything that causes damage to hepatocytes (also often an element of cholestasis too) = alcohol = cirrhosis = liver cancer or mets = viral hepatitis (A, B, C etc) - CMV - EBV = certain medications - liver abscess - haemochromotosis - A1-anti-trypsin deficiency - wilson's - right heart failure

Answer 38

- primary billiary cirrhosis - primary sclerosing cholangitis = common bile duct stones / ascending cholangitis = pancreatic cancer - cholangiocarcinoma - external compression of bile duct (eg portahepatic lymph node enlargement) - choledochal cyst - biliary atresia consider MEDICATIONS (fluclox, co-amoxiclav, nitro, sulphonylureas, steroids, prochlorperazine etc) nb don't learn meds - just be aware to review meds in someone with jaundice, incl recent abx

Answer 39

LOCAL - vomiting (any blood) - abdo pain - abdo distension (ascites) - dark urine - pale stools (or blood) SYSTEMIC - appetite - weight loss - fatigue - sleep - fevers - itch!!!! - night sweats (also pitting oedema on legs)

Answer 40

MURPHY'S SIGN push up on liver edge as patient breathes out and then ask them to take a big breath in and if that causes them a lot of pain / to catch breath then murphy's positive murphy's is negative in biliary colic (may be positive or negative in cholangitis)

Answer 41

= gastroenteritis - gastric stasis / gastroparesis = peptic ulcer disease = intestinal obstruction - paralytic ileus = acute cholecystitis = acute pancreatitis (nb can also get haematemesis with things like variceal bleeds)

Answer 42

ALCOHOL / DRUGS = alcohol = antibiotics = opiates - cytotoxics - digoxin CNS CAUSES = meningitis / encephalitis = raised intracranial pressure - brainstem lesions = migraine - motion sickness - labarynthitis / meniere's METABOLIC / ENDOCRINE = uraemia = hypercalcaemia = hyponatraemia = pregnancy = diabetic ketoacidosis - addision's disease PSYCH = self-induced = psychogenic = bulimia nervosa OTHERS = myocardial infarction = sepsis (UTI, menigitis) = acute pain (eg ovarian torsion) - autonomic neuropathy

Answer 43

what vomit LOOKS like! - what ate? - billious? (green) - frank blood? - coffee ground? - feculent? (small bowel obstruction) ask about possibility of pregnancy!!!

Answer 44

MORNING - prganacy - raised ICP ONE HR POST FOOD - gastric stasis / gastroparesis (DM) PAIN RELIEVED BY VOMITING - peptic ulcer - biliary colic PRECEEDED BY LOUD GURGLING - obstruction (esp if also distended)

Answer 45

- abdo pain - abdo distension - when last opened bowels? - passed FLATUS? - passing urine? AW FS FIN for systemic assess for signs of DEHYDRATION hydration status

Answer 46

BLOODS: - FBC - U+Es - LFTs - amylase - glucose - VBG - calcium (/bone profile) (do trop + ECG if suspect MI) suspect obstruction = AXR suspect raised ICP = CT head urine PT on all young women w vomiting consider endoscopy if persistent vomiting

Answer 47

hypokalaemia if severe, can get a hypochloraemic alkalosis can see ketones on urine dip if segvere and really not keeping anything down (esp in pregnancy)

Answer 48

HISTAMINE (H1) = cyclizine - cinnarizine (safe in preg, vestibular causes) ``` DOPAMINE (D2) = metoclopramide = domperidone = prochlorperazine - haloperidol ``` SEROTONIN (5HT3) = ondansetron (chemical cuases, eg chemo, but 1st line for most things) OTHERS = dexamethasone (adjuvant, unknown action, also for raised ICP) = hyoscine hydrobromide (antimuscarinic) = midazolam (anti-emetic effect outlasts sedative effect)

Answer 49

avoid cyclizine in ELDERLY (and anyone else at risk of delirium) avoid metoclopramide in: - GI obstruction (as prokinetic) - parkinsons (as can induce EPSE's) nb generally avoid metoclopramide as can produce EPSEs in even young otherwise fit people

Answer 50

NEUROPATHY - loss of sensation - Warm, dry skin, foot pulses are palpable = 10g monofilament test PERIPHERAL ARTERY DISEASE - diabetes is big risk factor for this - Cool, pale foot with no palpable pulses = palpate for dorsalis pedis + posterial tibial artery pulse (+/- ABPI) need regular follow up at diabetic foot clinic: • deformity or • neuropathy or • non-critical limb ischaemia • previous ulceration or • previous amputation or • on renal replacement therapy or • neuropathy and non-critical limb ischaemia together or • neuropathy in combination with callus and/or deformity or • non-critical limb ischaemia in combination with callus and/or deformity BASICALLY ANYONE WITH ANYTHING MORE THAN A SIMPLE CALLUS! Nb although diabetic foot is often described as ischaemic or neuropathic - if often an element of both

Answer 51

Venous ulcers = shallow ulcers with a granulated base, often with other clinical features of venous insufficiency present Neuropathic ulcers = PAINLESS ulcers over areas of abnormal pressure (eg head of metatarsal bones or heal), often secondary to joint deformity in diabetics ALMOST ALWAYS on SOLE of feet! Arterial ulcers = found at distal sites, often with well-defined borders and other evidence of arterial insufficiency

Answer 52

aka CHARCOT'S FOOT The exact cause is unknown. Decreased pain and pressure perception, abnormal strain and weight distribution, as well as autonomic neuropathy that increases perfusion with a subsequent "washing out" of bone substance is suspected. - Tarsus and tarsometatarsal joints most commonly affected - Coexisting ulcers common - Acute: swelling, warmth, erythema - Chronic: painless bony deformities, midfoot collapse, osteolysis, risk of fractures - specialist review for consideration of off-loading abnormal weight - sometimes immobilisation of the affected joint in plaster

Answer 53

good glycaemic control prevents! - also regular screening and self-inspection of feet do x-ray to look for osteomyelitis / bone deformity - MRI if high clinical suspisiopn NEUROPATHIC ULCERS - regular chiropody - surgical debridement if appropriate - abx if become infected - may need offloading to allow to heal! - also dressing! - last line = amputation! if peripheral vascular disease - refer to vascular

Answer 54

66% of hyperthyroidism - toxic multinodular goitre - toxic adenoma - too much levothyroxine (nb can rarely get toxic thyroid tumours and also ovarian/testicular cancers which produce thyroid hormones) also thyroiditis - eg caused by drugs, radiation etc can rarely cause hyperthyroidism - but norm cause hypo! GRAVES - circulating IgG auto-Ab bind to and activate G-protein thyrotropin receptors → smooth thyroid hyperplasia → ↑T3 production = women aged 30-50 = a/w autoimmune conditions (eg vitiligo, type 1DM, Addison’s) common triggers: - infection - child birth - stress

Answer 55

subclinical = T3/4 are normal but TSH is abnormal! - Does NOT refer to presence or abscence of symptoms! subclinical hyperthyroidism: - norm T3/4 - low TSH subclinical hypothyroidism - norm T3/4 - high TSH may or may not be symptomatic! - if symptomatic treat the same as norm! (discuss w pt) - if asymptomatic: norm just observe and repeat in few months!

Answer 56

TSH receptor antibodies (TRAb) = GRAVES (90%) - may also be raised in hashimotos or multinodular goitre ``` Thyroid peroxidase antibodies (TPOAb or anti-TPO) = HASHIMOTOS (90%) = POSTPARTUM THYROIDITIS (>60%) - graves (70%) - can rarely be raised in thyroid cancer ``` ``` Thyroglobulin antibodies (TgAb) = HASHIMOTOS (80%) - thyroid cancer (25%) - other autoimmune diseases (40%) ^not great marker for diagnosis but important for thyroid cancer follow up / monitoring ```

Answer 57

Diffuse, smooth, non-tender goiter 1) THYROID EYE DISEASE (30%) - Exophthalmos - Opthalmoplegia (paralysis of muscles within or surrounding eye → diplopia) - lid lag - lid retraction - hjigh risk for corneal ulcers + abrasions 2) PRETIBIAL MYXOEDEMA - oedematous, discoloured swelling above lateral malleoli (see photos**) 3) THYROID ACROPACHY - extreme manifestation with clubbing, painful finger + toe swelling, - periosteal reaction in limb bones 4) THYROID BRUITS - due to ↑vascularity in thyroid gland nb not going to describe other symptoms / signs of hyperthyroidism as I've done them to death!! - but remember get OLIGOMENORRHOEA in HYPER (menorrhagia in hypo!) nb get hypertension with widened pulse pressure: - Systolic pressure is increased due to increased heart rate and cardiac output - Diastolic pressure is decreased due to decreased peripheral vascular resistance

Answer 58

see investigation algorithm 1st bloods: - TSH - free T3/4 do thyroid antibody bloods 2nd (after know that hyperthyroid) - TSH receptor antibodies (TRAb) - Thyroid peroxidase antibodies (TPOAb or anti-TPO) - Thyroglobulin antibodies (TgAb) if cause of hyperthyroid unclear after antibodies endocrinologist can do: - thyroid ultrasound with doppler - radioactive iodine uptake scan nb if TFTs show secondary hyperthyroidism - refer to endocrinologist for further tests nb TFTs often normal in thyroid cancer! nb don't do radioactive iodine scan if woman is pregnant!

Answer 59

control symptoms: BETABLOCKERS - propranolol (until can start Carbimazole - can only be started by an encrinologist!) nb if someone is unwell at diagnosis - admit them! 1ST line: CARBIMAZOLE ^Can give Carbimazole + Levothyroxine simultaneously (block and replace) – reduces risk of iatrogenic hypothyroidism nb carbimazole is norm given for 6 weeks until euthyroid then keep at level and gradually reduce - most people are of drugs after 2 years! if pregnant: PROPYLTHIOURACIL ``` IF RELAPSE - Radioactive iodine OR - thyroidectomy ^will need levothyroxine for life after both of these! ``` nb can't give radioactive iodine if: - breastfeeding - pregnant (or will becom ein next 6 months!)

Answer 60

- agranulocytosis - teratogen (make sure on contraception) - cholestatic jaundice (? is this one right? **)

Answer 61

nb only get thyroid eye disease in graves - not in any other cause of hyperthyroidism nb the patient may be eu-, hypo- or hyperthyroid at the time of presentation SMOKING = biggest risk factor! - Eye discomfort - ↑tears - photophobia - ophthalmoplegia + diplopia - ↓acuity - afferent pupillary defect (optic N compression) - Exophthalmos - proptosis - conjunctival oedema - corneal ulcers REFER ASAP!!! - artificial tears - high dose steroids (may need IV) - surgical decompression ^also stop smoking!

Answer 62

- typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature - Iatrogenic levothyroxine excess does not usually result in thyroid storm TRIGGERS - thyroid or non-thyroidal surgery - trauma - infection (or intercurrent illness) - acute iodine load e.g. CT contrast media - stopping anti-thyroid meds suddenly ^basically anything that causes a big stress/adrenaline response! - confusion + agitation - nausea + vomiting - heart failure - abnormal liver function test (jaundice may be seen clinically) - HTN (with wide pulse pressure) - tachycardia (norm w AF) - FEVER >38.5 deg ^also very sweaty!!

Answer 63

nb if lead to congestive heart failure, esmolol is the preferred beta blocker 1) PARACETAMOL - bring temp down 2) IV PROPANOLOL - reduce HR - can use calcium channel blocker if B blocker CI 3) PROPYLTHIOURACIL - anti-thyroid drug norm used in preg - better than carbimazole in acute setting 4) POTASSIUM IODINE - not sure how this works but they give it - aka Lugol's iodine 5) DEXAMETHASONE - blocks the conversion of T4 to T3 ALSO treat UNDERLYING TRIGGER! call ICU if need help!

Answer 64

METFORMIN - reduce glucose absorption (gut) - reduce glucose production (liver) - increase insulin secretion (pancreas) - increase peripheral glucose uptake (fat + muscle) weight LOSS CONTRAINDICATIONS - AKI - eGFR < 30 ADVERSE EFFECTS - GI symptoms - lactic acidosis

Answer 65

SULFONYLUREAS - eg gliclazIDE = stimulates Beta cells in pancreas - weight GAIN GLITAZONES - eg pioGLITAZONE = reduces peripheral insulin resistance - weight GAIN GLIPTINS - eg sitaGLIPTIN = stop breakdown of the molecules that stimulate insulin secretion post-food (so insulin stays around longer) - weight NEUTRAL ``` GLP-1 MIMICS - eg exenaTIDE = Increase insulin secretion, reduce glucagon secretion - weight LOSS = this is a SUB CUT injection! ``` SGLT-2 INHIBITORS - eg dapaGLIFLOZIN = Stop glucose being reabsorbed in kidneys (pee out sugar) - weight LOSS

Answer 66

SULFONYLUREAS - eg gliclazIDE CI: - Severe renal impair (accumulation can -> hypo) - Porphyria - G6PD deficiency ADVERSE EFFECTS - Weight gain - Hypos GLITAZONES - eg pioGLITAZONE CI: - Bladder Ca (or high risk) - Liver impairment - Heart failure - Severe renal impairment ADVERSE EFFECTS - Weight gain - Bladder cancer - Fluid retension GLIPTINS - eg sitaGLIPTIN CI: - Severe liver probs - Hx of pancreatitis - Lower dose in renal impairment - NOT CI! ADVERSE EFFECTS: - GI symptoms - headaches (BIG PROBS!) - Pancreatitis - Skin probs GLP-1 MIMICS - eg exenaTIDE (SC inject) CI: - eGFR < 30 - Hx of pancreatitis - Quite a few tbf ADVERSE EFFECTS - GI symp - Pancreatitis SGLT-2 INHIBITORS - eg dapaGLIFLOZIN CI: - eGFR <60 - Pts at risk of hypotension (eg frail elderly) - Stop during illness if dehydrated ADVERSE EFFECTS - euglycaemic DKA (+ hhs) - UTIs + thrush - polyuria - Skin rash

Answer 67

↓MINERALOCORTICOIDS (aldosterone) from z. glomerulosa → ↓stimulation of Na/K+ pump in kidney → ↑K+↓Na+; ↓water and ↓HCO3- (acidosis) reabsorption into blood ↓GLUCOCORTICOIDS (cortisol) from z. fasciculata →↓gluconeogenesis (formation of glucose from AA) → ↓blood glucose nb also slight: ↓Androgens → ↓testosterone (mild, most produced in testes)

Answer 68

Increases BP by retaining salt (and thus excreting K+)

Answer 69

ADDISONS - BP: LOW - Glucose: LOW - Na: LOW - K+: HIGH CUSHINGS - BP: HIGH - Glucose: HIGH - Na: HIGH - K+: LOW CONNS: - BP: HIGH - Glucose: norm - Na: HIGH - K+: LOW Cushings looks like conns because, at high levels, corticosteroids start acting on mineralocorticoid receptors!

Answer 70

``` ADDISON'S (80%) - autoimmune destruction of adrenal glands = 30-50y = females = PMHx autoimmune conditions ``` other primary - TB - mets (eg bronchial Ca) - meningococcal septicaemia (Waterhouse-Friderichsen syndrome) - HIV - antiphospholipid syndrome nb can also get through other causes of haemorrhage / infarction to adrenal glands (incl DIC) secondary causes: - pituitary disorders (e.g. tumours, irradiation, infiltration) - long-term steroid therapy

Answer 71

Lean + Tired: - Anorexia, Weight loss - Dizzy, Syncope, Postural hypoTN Tanned: - Bronze skin and pigmented palmar crease + buccal mucosa Tearful + Weak: - fatigue, depression, ↓self-esteem, psychosis GI: - Nausea, vomiting, abdo pain, diarrhoea or constipation (crave salty food!) in women can get ↓Androgen symptoms (rarely affects men due to testis) - ↓Sex drive - ↓Pubic hair (women) Primary Addison's is associated with HYPERPIGMENTATION whereas secondary adrenal insufficiency is not

Answer 72

1) 9am CORTISOL Also: - ACTH (high in addisons) - Adrenal Auto-Ab (+ ve 80% in Addisons) - U+Es (↑K+ ↓Na+ ↓HCO3-, mild ↑Ca2+) - glucose (low) DIAGNOSTIC TEST: Synacthen® ACTH stimulation test - repeated blood tests (do in hosp) AXR/CXR - exclude secondary causes - Identify past TB e.g. upper zone fibrosis or adrenal calcification - Check for lung neoplasms

Answer 73

nb usually managed by an endocrinologist ``` 1) GLUCOCORTICOID REPLACEMENT = norm hydrocortisone - give blue steroid card - tell not to stop abruptly - DOUBLE dose in acute illness (give IM hydrocortisone pack to use if vomiting prevents oral meds) ``` 2) HYDROCORTISONE REPLACEMENT = fludrocortisone (don't need to double in illness) nb can also give Androgen replacement: DHEA (Dehydroepiandrosterone)

Answer 74

norm cause: Stress (e.g., infection, trauma, surgery) in a patient with underlying adrenal insufficiency 1) Pain in back, abdomen or legs (can resemble peritonitis) 2) Diarrhoea + Vomiting → Dehydration 3) ↓BP → Hypovolaemic shock →↓Consciousness → Death (also often have fever) 3 Ss of Mx 1) SALT - 0.9% saline (a lot!) 2) SUGAR - 50% dextrose if hypo 3) STEROIDS - IV hydrosortisone high doses nb as well as someone with addisons getting this dt acute illness / surgery, can also get with: - adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia) - steroid withdrawal

Answer 75

HASHIMOTOS THYROIDITIS = most common in UK - may have initial hyper phase Sub-acute de Quervain's thyroiditis = thyroiditis following viral infection → hyperthyroidism (phase 1) → euthyroid → hypothyroid (phase 3) = painful goitre - self-limiting Riedel's thyroiditis = fibrous replacement of thyroid parenchyma → painless goitre Post-partum thyroiditis = initial hyper phase -> prolonged hypothyroid phase Iodine deficiency = most common cause worldwide drug-induced - LITHIUM - anti-thyroid drugs (eg carbimazole) - AMIODARONE (can cause hyperthyroid) post-hyperthyroid Mx - following radioiodine ablation or thyroidectomy Congenital - can be sporadic or inherited - very serious if not picked up! secondary hypothyroid is rare!! - norm from pituatory failure nb Non-painful Goitre – Hashimoto and Riedel Painful Goitre – De-Quevain

Answer 76

Female (5-10 times more common) - type 1 DM - addison's - perncious anaemia - Down's syndrome - Turner's syndrome - coeliac disease

Answer 77

- Weight gain despite loss of appetite - Fatigue, Lethargy ↑Sleeping,↓Mood - ↓Memory + ↓Cognition → dementia like symptoms - Constipation - MENORRHAGIA - Hoarse voice - Cold Sensitivity - Myalgia + Cramps - ↓Libido - Dry skin + Hair loss/thinning + Cold Hands (± loss of lateral eye brows) - ↓HR (bradycardia) ↑BMI - ↓Reflexes - Oedema (swelling in skin + soft tissue, typically lids, hands, face, tongue) - Peaches + cream complexion + Round puffy face may get Ascites, Pericardial or pleural effusion may also get cerebellar ataxia

Answer 78

- TSH (high in primary, low in secondary) - T3/4 (low in both) - autoantibodies (anti-TPO) - positive in hashimotos ?refer all to endocrinologist TSH used for monitoring primary! (if secandary need T3/4 too) LEVOTHYROXINE (T4) - review every 3-4wks until stable TSH - then r/v 4-6 months ^if elderly or IHD then start very low dose and slowly build up! SIDE EFFECTS: - hyperthyroidism (over treatment) - worsen angina - worsen AF - osteoporosis nb if high TSH and norm T3/4 then norm means non-compliance with levothyroxine nb Iron reduces absorption of levothyroxine – give at least 2hrs apart

Answer 79

poorly controlled hypothyroidism who undergo infection or surgery - low GCS (or confusion) - hypothermia Mx - IV thyroid replacement - IV fluid (incl IV electorylte correction) - IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded) - sometimes rewarming

Answer 80

aka non-thyroidal illness syndrome no thyroid symptoms - just abnormality in TFTs when someone is acutely unwell (esp in ICU) NORM LOW T3 - T4 nd TSH are normal or low Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed

Answer 81

PTH - pulls calcium from bone - decreased calcium loss in urine, loose more phosphate (and activate vit D) - increased absorption of calcium from gut ``` PRIMARY = Increased PTH secretion from PTH gland = norm dt single parathyroid ADENOMA - High PTH (or can be norm!), high Ca2+ - low phsophate, rasied ALP ``` ``` SECONDARY = Hypocalcaemia (norm dt CKD) -> reactive (and appropriate) increase in PTH - High PTH, low (or norm) Ca2+ - high phosphate - low Vit D ``` ``` TERTIARY = prolonged secondary → hypertrophy of PTH gland -> release PTH independent of Ca2+ levels - Very high PTH, high Ca2+ - low or norm vit D - low or norm phosphate - high ALP ``` nb phosphate norm does opposite to calcium so hypercalcaemic crisis may occur in primary or tertiary (but not secondary!

Answer 82

``` PRIMARY = PTH gland adenoma (85%) - hyperplasia / multiple adenomas (15%) - carcinomas (0.5%) - MEN (multiple endocrine neoplasia) type 1 or 2 ``` SECONDARY = CKD - malnutrition - vit D deficiency (low sun, nutritional deficiency, liver cirrhosis) - cholestasis (need bile to absorb fat-soluable vits like vit D) nb parathyroid adenoma most common in post-menopausal/elderly women!

Answer 83

the MAJORITY of pts with primary hyperparathyroidism are ASYMPTOMATIC! STONES - renal colic BONES - bone, muscle + joint pain - fragility fractures - pseudogout - Osteitis fibrosa cystica (cyst-like brown tumors) - Skull: granular decalcification (salt-and-pepper skull) ``` ABDO GROANS - anorexia - nausea (+ vomiting) - constipation = gastric or duodenal ulcers (get dyspepsia 1st) - pancreatitis ``` THRONES = polydipsia + polyuria + dehydration (nephrogenic diabetes insipidus) PSYCH OVERTONES - Depression - confusion - hallucinations - coma OTHER - hyporeflexia - muscle weakness - malaise short QT interval (rarely seen) can also get HYPERTENSION if severe can also get: Osteitis fibrosa cystica (severe) – pts. w/ sub-periosteal resorption of distal phalanges, tapering of distal clavicle, salt and pepper skull, brown tumours of long bones

Answer 84

BP will often be raised! - Calcium = high - PTH = high (or norm!!) - phosphate = low - ALP = high can also do a DEXA scan to determine levels of osteoporosis/dystrophy to lower Ca = LOTS of saline!!! (forces diuresis - may need to replace K and Mg as these will also lower, as well ac Calcium) AVOID THIAZIDE diuretics! (will raise calcium further!) (if really bad can have dialysis / haemofiltration) definitive = TOTAL PARATHYROIDECTOMY (surgery) if unfit for surgery: CINACALCET (calcimimetic) → ↑sensitivity of parathyroid cells to ca2+ levels → ↓PTH secretion - may also use bisphosphonates if have osteoporosis nb conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage AND asymptomatic!

Answer 85

Malignancy parathyroid related protein is produced by SCC lung cancer (breast and renal too) → mimics PTH → high calcium!

Answer 86

TREAT UNDERLYING CONDITION (ie norm CKD) - phosphate dietary restriction +/- phosphate binders - activated vit D (if deficienct)

Answer 87

Allow 12 months to elapse following kidney transplant as many cases will resolve with this The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit gland can be identified then it should be excised. Otherwise total parathyroidectomy and re-implantation of part of the gland may be required.

Answer 88

nb hyperklipidaemia and dyslipidaemia are used interchangably! predominantly high TRIGLYCAERIDES - obesity - alcohol - diabetes (type 1 + 2) - CKD - liver disease MEDS high TRIGLYCERIDES - thiazide diuretics - non-selective beta blockers - unopposed oestrogen predominantly high CHOLESTEROL - nephrotic syndrome - cholestasis - hypothyroidism can get various different hereditary hyperlipidaemia and hypercholesteraemias - often present at a young age and don't necessarily have obesity etc nb other drugs that cause dyslipidaemia are antipsychotics, corticosteroids or immunosuppressant drugs

Answer 89

most diagnosed on routine screening (ie asymptomatic!) nb Xanthoma = nodular lipid deposits in the skin and tendons TENDINOUS XANTHOMAS: firm nodules, located in tendons (typically extensor tendons of hands and the Achilles tendon) PALMAR XANTHOMAS: yellow plaques on the palms of the hands XANTHELASMAS: nodular lipid deposits around the eyelids - nb can be seen without lipid abnormalities! PREMATURE CORNEAL ARCUS: white grey opaque ring in corneal margin nb can also have eruptive xanthomas in familial causes on extensor surfaces (are red and yellow)

Answer 90

bloods = FULL LIPID PROFILE - Tchol, HDL-C, non-HDL-C, TG concentrations nb can do other bloods to rule out secondary causes: eg U+Es, TFTs, LFTs - BMI (norm BP too) - QRISK 2 - dietary advice - increase exercise - stop smoking statin if high QRISK 2 (see other flashcard)

Answer 91

anyone over the age of 40 (check this age with NICE CKS!!***) if >10% QRISK then start 20mg atorvastatin ON give 20mg atorvastatin (regardless of QRISK2) - CKD eGFR<60 - all adult type 1 diabetes - familial hyperlipidaemia (may be higher dose!) give 80mg atorvastatin for secondary prevention - any IHD - ischaemic stroke - peripheral artery disease

Answer 92

- decrease PTH norm secondary to thyroid surgery (nb this is still called primary though...) - autoimmune - di-george syndrome PSEUDOHYPOPARATHYROIDISM = abn G protein → failure of target cell response to PTH - Sx = short stature, low IQ, short 4th/5th metacarpals, round face - bloods: ↓Ca2+ ↑PO4- ↑PTH PSEUDOPSEUDOHYPOPARATHYROIDISM = morphological features of above but normal biochem

Answer 93

dt HYPOCALCAEMIA Tetany – muscle twitch, cramping, spasm Bone pain – turnover abnormally low → ↑mineral density Perioral paraesthesia TROUSSEAU'S SIGN - carpal spasm if brachial artery occluded by inflating BP cuff CHVOSTEK'S SIGN - tapping over parotid stimulates facial nerve → facial muscle to twitch (detects latent tetany)

Answer 94

low calcium = prolonged QT interval high calcium = shortened QT interval

Answer 95

PRIMARY hypoPTH - ↓Ca - ↑Phos - ↓PTH - normal ALP PSEUDO hypoPTH - ↓Ca - ↑Phos - ↑ or normal PTH can do U+Es to exclude CKD and Vit D to exclude deficiency ^can also cause low calcium (secondary hyperparathyroidism!) PSEUDO hypoPTH - Urinary cAMP - phos post-PTH infusion Mx = ALFACALCIDOL (active vit D - doesn't need kidneys to activate!) ? plus calcium supplements?

Answer 96

PAPILLARY (70%) - typically young pts - hist: papillary projections + pale empty nuclei = total thyroidectomy (+/- node excision +/- radioiodine) = yearly thyroglobulin levels to detect early recurrent disease FOLLICULAR (20%) - typically middle aged - hist: encapsulated with capsular invasion = total thyroidectomy (+/- node excision +/- radioiodine) = yearly thyroglobulin levels to detect early recurrent disease MEDULLARY (5%) - MEN syndrome (although 80% are sporadic!) - may produce calcitonin (opposite to PTH) = total thyroidectomy = phaecromocytoma screen ANAPLASTIC - elderly females - can comonly cause local pressure symptoms - poor prognosis: not responsive to Mx LYMPHOMA (rare) - females with hashimotos

Answer 97

tumours do NOT commonly secrete thyroid hormones so features of hyper/hypothyroidism are RARE 75% are asymptomatic!!! - firm painless thyroid nodules may be present! possible late features: - Dyspnoea - Dysphagia - Hoarseness (vocal cord paresis) - Horner syndrome - Possible SVC obstruction USS thyroid = 1st investigation!

Answer 98

nb with thyroid: toxic = functioning (ie changes TFTs) symptoms of HYPERthyroidism (+ nodular goitre) - do TFTs and see primary HYPERthyroid - is 2nd most common cause (25%) after graves RISK FACTORS - elderly - iodine deficient 10% of multinodular goitres (ie not-toxic) -> toxic multinodular goitres Nuclear scintigraphy shows PATCHY UPTAKE Mx - if just hyperthyroid -> radioiodine treatment - if also causes local symptoms (dysphagia/dyspnoea etc) -> surgery nb don't norm use carbimazole in toxic multi-nodular goitre! can use betablockers to control symptoms before referral!

Answer 99

symptoms of HYPERthyroidism (+/- palpable nodule) - do TFTs and see primary HYPERthyroid - is 3rd most common cause (5-10%) - female > male - 30-50 years Thyroid scintigraphy: = solitary, hot nodule (Shows radioiodine uptake by the hyperfunctioning nodules with suppression of rest of the gland) unsure on mx (but don't need to know as brief CC) nb is benign!

Answer 100

DIFFUSE (HYPER) - Graves - TSH-secreting pituitary adenoma (rare) ``` DIFFUSE (HYPO) - hashimoto's - sub-acute de quervain's (hyper first) (is PAINFUL) - riedel's ?postpartum too ``` DIFFUSE (EU) - iodine deficiency (can eventually lead to hypo OR hyperthyroid) NODULAR (HYPER) - toxic multi-nodular - toxic adenoma / nodule ``` NODULAR (EU) - thyroid cancer - non-toxic adenoma - cysts (also other causes of neck lumps) ``` do TFTs and USS thyroid

Answer 101

Compression of the TRACHEA → exertional dyspnea and, in severe cases, stridor or wheezing Compression of the OESOPHAGUS → dysphagia nb not sure if hoarse voice is due to hypothyroidism or due to compression from goitre!

Answer 102

May only have supression of some of these hormones!!! - ie not all! - if all = panhypopituitarism GROWTH HORMONE deficiency (see other flashcard) PROLACTIN deficiency → lactation failure following delivery (how Sheehan's often picked up!) FSH/LH deficiency → hypogonadotropic hypogonadism (secondary hypogonadism) TSH deficiency → secondary hypothyroidism ACTH deficiency → secondary adrenal insufficiency (do NOT get tanned skin, unlike in addisons) ^these are all ANTERIOR pituatory hormone if hypopit is extensive / caused by compressive aetiology then can get deficiency of POSTERIOR pituatory hormones: - ADH deficiency → central (neurogenic) diabetes insipidus - Oxytocin deficiency → no effect nb if hypopit is caused by a space occupying lesion then will also get neuro/ opthalmic symptoms (see later flashcards on pituatory adenomas)

Answer 103

IN CHILDREN - growth retardation (during childhood) - ↓ bone density - muscle atrophy - hypercholesterolemia IN ADULTS (is subtle!) - Central obesity - Dry, wrinkly skin - ↓Strength ↓Balance ↓Exercise ability - depression tbh basically the same but obvs doesn't affect growth in adults!

Answer 104

WOMEN - Oligomennorhoea or Amenorrhoea - ↓Fertility, ↓Libido, Dyspareunia - Breast atrophy MEN - Erectile dysfunction - ↓muscle bulk - Hypogonadism (↓hair, small testes, ↓ejaculate vol, ↓sperm)

Answer 105

sequence: 1) GH and prolactin 2) → FSH → LH 3) → TSH 4) → ACTH Because hypoprolactinemia is typically asymptomatic (except failure to lactate following delivery), GROWTH RETARDATION is the first presenting symptom among CHILDREN and HYPOGONADISM is the first clinical feature among ADULTS

Answer 106

``` COMPRESSIVE CAUSES = non-secretory pituatory macroadenoma (most common - 40% in adults!) - internal carotid aneurysms - meningiomas - craniopharyngioma - Rathke's cleft cyst ``` OTHER - pituatory apoplexy (infarction of gland - incl Sheehan's) - traumatic brain injury - iatrogenic (eg surgery to remove adenoma / pituatory irradiation) - infiltaration of pituatory +/or hypothalamus (haemochromatosis, meningitis, TB) nb pituatory apoplexy presents suddenly: severe headache, sudden hypotension, hypovolemic shock nb in sheehan's often have a postpartum haemorrhage but can occur without clinical evidence of haemorrhage see amboss if want to know full investigations and management etc of hypo pit! - but is basically measuring all the affected hormones and then replacing the ones that are deficient! (and surg/radio removal of anything compressing gland) - nb always replace corticosteroids before thyroid hormones (as levothyroxine can precipitate adrenal crisis if ACTH deficiency!)

Answer 107

``` MACRO = over 1cm MICRO = under 1cm ``` secretory or non-secretory! 1) PROLACTINOMA (40%) - Women: galactorrhea, amenorrhea, reduced bone density due to suppression of estrogen - Men: reduced libido and infertility 2) NON-SECRETORY (35-40%) - can cause hypopit by mass effect (copmmonest cause of hypopit - develops slowly!) 3) SOMATROPH (10-15%) (ie GH) - acromegaly or gigantism! 4) CORTICOTROPH (5%) (ie ACTH) - cushing's DISEASE - aka secondary hypercortisolism 5) THYROTROPH (1%) (ie TSH) - secondary hyperthyroidism 6) GONADOTROPH ADENOMA (rare) (ie LH, FSH) - rare! most non-functioning! nb Most secrete one pituitary hormone, with hyperplasia of only one type of endocrine cell. - The presence of multiple pituitary hormones should also raise the suspicion of atypical pituitary adenomas or pituitary carcinomas nb Mild hyperprolactinemia in a patient with a pituitary adenoma does not necessarily imply that the tumor is a prolactinoma; any sellar tumor can disrupt the inhibitory effect of the hypothalamus on the pituitary gland, which can result in hyperprolactinemia

Answer 108

1) HORMONE EFFECTS - hypo-pit if nonsecretory or effects of excess hormones if secretory 2) VISUAL FIELD DEFECTS - bitemporal hemianopia (dt compression of optic chiasm) - can less commonly also get squint and double vision dt CN 3, 4 +/or 6 palsy (not sure which most common) 3) HEADACHE - dt stretching of dura - worse on coughing, head down etc nb visual field defects are normlaly reversible with removal of adenoma (though not always)

Answer 109

INVESTIGATIONS 1) pitutatory blood profile (incl GH, prolactin, ACTH, FH, LSH and TFTs) 2) formal visual field testing 3) MRI brain with contrast MANAGEMENT - hormonal therapy (e.g. BROMOCRIPTINE is the first line treatment for prolactinomas) - surgery (e.g. transsphenoidal transnasal hypophysectomy) if large / increase in size - radiotherapy nb non-functioning microadenomas are very common (?10% of pop) but don't cause any symptoms or problems - BUT if you pick an adenoma up incidentally you need to do hormone panel to work out if functioning or not! nb Bromocriptine is a dopamine receptor agonist! - has inhibitory effect on prolactin production

Answer 110

ie too much GROWTH HORMONE - Coarse facial appearance, wide nose, puffy lips, eyelids - Excessive sweating, oily skin - ↑Growth of hands (spade-like), jaw, feet, tongue - Dark skin, acanthosis nigricans - Amenorrhoea, ↓Libido - Sleep apnoea - Proximal weakness and arthropathy nb if in kids (ie before growth plates fused) then get gigantism THIS IS NOT EVEN A CORE CONDITION - I just found interesting!

Answer 111

too much exogenous CORTICOSTEROID USE / stopping steroids too quickly - can also get following treatment of cushing's disease (ie removal of pituatory tumour) dt prolonged high corticosteroid levels having a negative feedback loop and suppressing hypothalamus and pituatory which then atrophy over time presents like addisons! - either slowly or suddenly in addisonian crisis! prevent by: - avoiding long-term steroid use - tapering steroids slowly is used for more than a week!

Answer 112

Rare catecholamine tumour arising from adrenal medulla -> ↑Adrenaline + ↑Dopamine 10% are familial - MEN type II - neurofibromatosis - von Hippel-Lindau syndrome rule of 10% - bilateral in 10% - extra-adrenal in 10% - malignant in 10% features are typically EPISODIC - headaches - anxiety - palpitations - sweating - tachycardia - HTN (90% - may be sustained) nb extra-adrenal norm at organ of Zuckerkandl adjacent to aorta bifurcation

Answer 113

24 hr urinary collection of metanephrines nb used to be 24 hr urinary collection of catecholamines but this is less sensitive stabilise with: 1) alpha-blocker (e.g. PHEnoxybenzamine) given before a 2) beta-blocker (e.g. propranolol) always give ALPHA blocker first (A before B) definitive mx = SURGERY!

Answer 114

``` ACTH INDEPENDENT = ie just lots of corticosteroids = EXOGENOUS STEROIDS - benign adrenal adenoma (5%) - adrenal nodular hyperplasia (rare) - Mc-Cune-Albright syndrome ``` ACTH DEPENDENT = ie somehting's producing too much ACTH - cushing's disease (benign pituatory adenoma) (80%) - ectopic ACTH (eg from SMALL CELL LUNG CANCER) (5-10%)

Answer 115

↑Weight (significant) → Obesity Muscle weakness + wasting → PROXIMAL MYOPATHY -ve mood change – depression, LETHARGY, irritability, psychosis GONADAL DYSFUNCTION (↓GRH) – irregular periods, hirstuism, erectile dysfunction ACNE Infection prone + Poor healing wounds (↓inflam mediators) - Risk of RECURRENT ACHILLES TENDON RUPTURE - osteoporosis plus all the other side effects of steroids...

Answer 116

- Central/truncal obesity, Moon face, Buffalo neck hump - Skin and muscle atrophy - HTN (↑BP) Hyperglycaemia (↑Glucose) - Bruises + Purple abdominal striae may see METABOLIC ALKALOSIS (with a low K+) ^ectopic ACTH especially give VERY low K+ levels

Answer 117

also obvs you check their meds first - if on steroids then that's the cause and no more investigations needed!!! 1st = overnight dexamthasone suppression test - or 24 hr urinary free cortisol if cushing's regardless of cause: cortisol will stay high (will be low if norm) 2nd = 9am and midnight plasma ACTH (and cortisol) levels - if ↓ACTH then ACTH-independent (eg adrenal adenoma) - if ↑ACTH then ACTH-dependent (either pituatory or ectopic ACTH) ^both have high cortisol! if ACTH-dependent then: 3rd) high dose dexamethasone suppression - if pituatory = cortisol suppressed - if ectopic = cortisol stays same! ^ie ectopic ACTH just doesn't respond to negative feedback etc nb can also do CRH stimulation test but ?not as good nb management: - Cushing’s syndrome – give Metyrapone - Iatrogenic = Stop medications i.e. steroids - Cushing’s disease – Removal of pituitary adenoma SE: ↑pigmentation - Adrenal adenoma – Adrenalectomy and adjuvant radiotherapy - Ectopic ACTH – resection of tumour or alternatively Metyrapone, Ketoconazole or Fluconazole → ↓cortisol secretion

Answer 118

Pseudo-Cushing's mimics Cushing's - get false positive dexamethasone suppression test or 24 hr urinary free cortisol ``` causes - alcohol excess - severe depression - obesity (also ? rifampicin and phenytoin) ``` insulin stress test may be used to differentiate

Answer 119

- bilateral adrenal hyperplasia (BAH) (70%) - unilateral adrenal adenoma (Conn's) (rarely can be adrenal carcinoma) norm no symptoms!!! (may occasionally get features of low K+) - HTN - low K+ - high Na - alkalosis nb in real life only 10-40% have low K+

Answer 120

DIAGNOSTIC = plasma Renin:Aldosterone ratio - ↑Aldosterone ↓Renin (if renin is high or normal, it excludes diagnosis of primary hyperAld – likely secondary) 2nd) HIGH-RESOLUTION CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess Mx - adrenal adenoma: surgery - bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

Answer 121

high aldosterone due to high renin from ↓renal perfusion - renal artery stenosis - accelerated HTN - diuretics - CHF (hypoperfusion) - hepatic failure Ix - ↓K+ ↑Na+, ↑Aldosterone ↑Renin ^ie same as primary but HIGH RENIN!

Answer 122

very rare to get isolated hypoaldosteronism - it's normally the first sign of Addison's / autoimmune primary adrenal insufficiency (ie before loose corticosteroids) DON'T get hypoaldosteronism if secondary (ie low ACTH) or tertiary (ie low CRH) adrenal insufficiency!

Answer 123

Hirsutism = androgen-dependent hair growth in women - e.g on the chin, above the upper lip, and around the umbilicus hypertrichosis = androgen-independent hair growth (eg in anorexia nervosa)

Answer 124

Polycystic ovarian syndrome = commonest Other causes include: - Cushing's syndrome - congenital adrenal hyperplasia - androgen therapy - obesity (dt insulin resistance) - adrenal tumour - androgen secreting ovarian tumour drugs: - phenytoin - corticosteroids

Answer 125

FERRIMAN-GALLWEY scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism - weight loss (if overweight) - cosmetic techniques (eg waxing/bleaching) - not available on the NHS - consider COCPs - facial hirsutism: topical EFLORNITHINE (CI: pregnancy + breast-feeding) ALSO TREAT UNDERLYING CAUSE!!!!

Answer 126

``` NEUROGENIC / CRANIAL = deficiency of ADH secretion - idiopathic (50%) - post head injury - pituitary surgery - craniopharyngiomas - histiocytosis X - DIDMOAD - haemochromatosis ``` ``` NEPHROGENIC = insensitivity to ADH - genetic causes - electrolytes:↓K+ ↑Calcium - drugs: demeclocycline, LITHIUM - tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis ``` both types: impaired water resorption in kidney → ↑excretion of large volumes (>3L/day) of dilute, low urine osmolality (<300 mOsmol/kg) and high serum osmolality > 300 - > SYMPTOMS: - polydipsia - polyuria incl nocturia (adults) or nocturnal enuresis (children) nb DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)

Answer 127

nb have HIGH SODIUM!! (effectively very dehydrated!) main DDx = diabetes mellitus! (do glucose!!) 1st) serum and urine osmolarity - serum = high - urine = low nb a urine osmolality of >700 mOsm/kg excludes diabetes insipidus 2nd) water deprivation test = tests ability of kidneys to concentrate urine for diabnosis of DI, and to localise cause - Deprive fluids 8hrs and test urine osmolality THEN repeat but with 2 mcg desmopressin (synthetic ADH) NEURO/CRANIAL = low urine osmolality < 300 before desmopressin, >800 after desmopressin - Mx: DESMOPRESSIN (also do hormone bloods and MRI pituatory to find cause) NEPHRO = low urine osmolality < 300 mosm before AND after desmopressin - Mx: --- treat cause --- thiazide diuretics (bendroflumethiazide) --- NSAIDs (lower urine vol and plasma Na+)

Answer 128

excessive secretion of ADH from the posterior pituitary or an ectopic source → ↑reabsorption of water at collecting duct → hypervolaemia and dilution of electrolytes (↓Na+) LOW SODIUM (in absence of hypovolaemia, oedema or diuretics) Urine and plasma osmolarity - urine = high - plasma = low ^ie opposite of diabetes insipidus!

Answer 129

MALIGNANCY = small cell lung cancer (- pancreas) (- prostate) NEURO - stroke - SAH - sub-dural haemorrhage - meningitis/encephalitis/abscess INFECTION - TB - pneumonia (esp atypical) MEDS - SSRIs - tricyclics - carbamazepine - vincristine - cyclophosphamides - sulfonylureas OTHER - positive end-expiratory pressure (PEEP) - porphyrias

Answer 130

Fluid restriction - must be slow due to risk of central pontine myelionlysis (if raise Na too quickly!) Demeclocycline - ↓responsiveness of collecting tubule to ADH nb see hyponatraemia flashcards for more indepth Mx

Answer 131

abnormal amount of breast tissue in males, usually caused by an increased oestrogen:androgen ratio important to differentiate the causes of galactorrhoea (due to the actions of prolactin on breast tissue) from those of gynaecomastia

Answer 132

normal in puberty (also for male infants!) - syndromes with androgen deficiency (kallman's, klinefelter's) - testicular failure (eg mumps) - liver disease (liver can't break down oestrogen) - testicular cancer (e.g. seminoma secreting hCG) - ectopic tumour secretion - hyperthyroidism - haemodialysis

Answer 133

commonest = SPIRONOLACTONE! - cimetidine (H2 antagonist) - digoxin - finasteride (blocks testosterone activation to shrink prostate) - cannabis - anabolic steroids - GnRH agonists e.g. goserelin, buserelin (puberty blockers) - oestrogens nb GnRH blockers have lots of uses (also in fibrids, part of IVF, CAH) ``` nb can also very rarely be caused by other drugs: tricyclics isoniazid calcium channel blockers heroin busulfan methyldopa ```

Answer 134

differentiate this from urinary frequency!! - eg caused by UTI / STI / pregnancy (norm have other symptoms like urgency =?-dysuria or abdo pain) this is weeing a large amount of VOLUME!! - Diabetes Mellitus (T1 or 2) - Diabetes Insipidous (cranial or nephro) - hypercalcaemia - chronic kidney disease - psychogenic (compulsive water drinking) - DIURETICS (also SGLT-2 inhibitors (eg dapaGLIFLOZIN)) remember LITHIUM is an important cause of NEPHROGENIC diabetes insipidous 1ST LINE = TEST FOR DIABETES MELLITUS (most common cause!)

Answer 135

1) SERUM OSMOLARITY ``` if HIGH (hypertonic hypernatraemia): - norm very high glucose (DKA of HHS) which is increasing osmolarity - so fix that then recheck Na! ``` if NORM (isotonic hyponatraemia): - TURP syndrome - pseudohyponatraemia (ie sodium is actually norm but measures as low dt high amounts of protein or lipids in plasma - eg hyperlipidaemia or multiple myeloma) ``` if LOW (hypotonic hyponatraemia): - TRUE hyponatraemia (then do the other investigations - see below, to find cause!) ``` ^this is all in the context of LOW SODIUM! IF PATIENT IS SYMPTOMATIC +/or SEVERE (eg seizures, coma, resp depression) then just TREAT with hypertonic asaline (+work out cause later!) 2) assess VOLUME STATUS - hypovolaemic - euvolaemic - hypervolaemic (see other flashcards for causes) 3) URINE OSMOLARITY (+/or sodium) - high - low (compare to serum osmolarity) (see other flashcards for causes)

Answer 136

``` HYPOvolaemia + HIGH urine Na = RENAL LOSSES (can't conc urine!) - diuretic excess (?norm thiazides) - primary adrenal insufficeincy (addison's) - cerebral salt wasting syndrome - renal tubular acidosis - salt-losing nephropathy ``` ``` HYPOvolaemia + LOW urine Na = EXTRARENAL LOSSES (kidney's working but just loosing a lot of fluid + salt) - vomiting - diarrhoea - burns - pancreatitis - trauma - third spacing (don't worry about) ``` nb see a better flow chart of all of this on my exam notes

Answer 137

EUvolaemia + HIGH urine Na - SIADH (very high urine Na!!) - severe hypothyroidism - secondary adrenal insufficiency - diuretics (ie before become hypovalemic) ``` EUvolaemia + LOW urine Na = appropriate body reaction! - primary/psychogenic polydipsia - beer potomania - exercise-induced - tea + toast diet ``` nb see a better flow chart of all of this on my exam notes

Answer 138

HYPERvolaemia + HIGH urine Na - renal failure (diuretic phase) (again can't concetrate urine!) HYPERvolaemia + LOW urine Na - congestive heart failure - liver cirrhosis - nephrotic syndrome remember these people are opverloaded with fluid!!! nb see a better flow chart of all of this on my exam notes

Answer 139

1) DURATION of hyponatremia: is it acute or chronic? 2) SEVERITY of hyponatremia: what is the sodium level? 3) SYMPTOMS: is the patient symptomatic? Acute hyponatremia: - Develops over < 48 hours - Usually from excessive fluid intake, either parenteral or oral - Common examples include post-operative parenteral fluids and athletes = Symptoms are usually severe Chronic hyponatremia: - If for >48hrs OR duration is unknown - Symptoms are usually less severe than acute - HIGHER CHANCE of causing Osmotic demyelination syndrome (aka central pontine myelinolysis) if correct too quickly!

Answer 140

``` MILD = 130-134 mmol/l - none or non-specific symp (headache, lethargy, nausea, vomiting, dizziness, confusion, muscle cramps) 1) fluid restriction 2) LOOP diuretics (if hypervolaemic) ``` ``` MODERATE = 120-129 mmol/l - (same as mild) 1) fluid restriciton 2) LOOP diuretics (if hypervolaemic) 3) 0.9% saline (be careful if already hypervolaemic) ``` SEVERE = Less than 120 mmol/l - Seizures, coma, and respiratory arrest 1) HYPERTONIC SALINE (1.8%) +/- loop diuretics 2) consider CONIVAPTAN (ADH receptor antagonist!) Can get symptoms at any level! - esp if acute drop! - if severe symptoms! - treat as SEVERE! (regardless of numbers) nb conivaptan is hepatoxic if have underlying liver disease!

Answer 141

ACUTE - max 1mmol/hr (24mmol/day) (check w senior first!) CHRONIC - max 10mmol/day ie do repeated U+Es to check!!