Endocrinology / Metabolic Flashcards
1
Q
Hyponatremia - Sx? Ix & Approach? What happens if you correct Na too fast?
A
Sx: confusion, altered GCS, headaches, seizures, encephalopathic
Ix: fluid status, U&E, paired osmolalities (urine, serum), urine Na
Fluid status:
- HYPOvolaemic (dehydrated) - WASTING (diarrhoea/vomiting, diuretics) –> IV fluids
- EUvolaemic (normal) - ENDOCRINE (SIADH, hypothyroidism, Addison’s) –> fluid restrict + Tx underlying cause
- HYPERvolaemic (fluid overload) - FAILURE (liver, renal, heart) –> fluid restrict + Tx underlying cause
Urine Na: >20 mmol/L –> SIADH (BUT if on diuretics, urine Na can’t be interpreted) –> fluid restrict
Na corrected too fast (>10) = osmotic demyelination syndrome (central pontine myelinolysis) –> pseudo-bulbar palsy, paraparesis, locked-in syndrome
2
Q
Potassium homeostasis - areas involved? Hypo/hyper? Appearance on ECG? Hyper Tx?
A
Areas involved:
- Dietary intake
- Absorption in GI tract
- Adrenals & kidneys - regulate serum K concentration
HYPOkalaemia:
- Poor dietary intake, vomiting/diarrhoea
- Diuretics - loop/thiazide (block channels causing K reabsorption)
- Hyperadrenalism (Conn’s, bilateral adrenal hyperplasia, Cushing’s)
- Conn’s/BAH - excess aldosterone - NOTE: Aldosterone promotes reabsorption Na, excretion K
- Cushing’s = excess cortisol –> off-target effect on mineralocorticoid receptors –> mimics aldosterone
HYPERkalaemia:
- false = HAEMOLYSIS –> repeat sample
- Kidney failure e.g. on dialysis (kidneys = main route to remove K)
- Anti-HTN/diuretics
- ACEi/ARB - reduce kidney hyperfiltration, mainly a risk if CKD
- K+-sparing diuretics e.g. spironolactone/amiloride
- Addison’s disease (failure - can’t produce enough cortisol/aldosterone)
- NOTE: appearance on ECG = tented T-waves, broad QRS, prolonged PR interval
Hyperkalaemia Tx:
- Protect heart - IV 10-30ml 10% Ca Gluconate (repeat /15m, x5 MAX)
-
Reduce K+:
- 1st line - 10U Actrapid (insulin > drive K into cells) AND 100mL 20% glucose (to prevent hypo)
- 2nd line - 5mg Salbutamol NEB (b-agonist)
- Ix cause: drug chart, U&E (kidney funct), short SynACTHen test (Addison’s)
3
Q
Calcium homeostasis?
Hyper Sx? Ix & causes? Mx?
Hypo Causes? Sx? Ix? Mx?
A
Hormone production:
-
Parathyroid gland - PTH –> INCREASE Ca:
- Bone resorption
- GI absorption
- Kidney - decreased excretion, increases 1alpha-hydroxylation (vitD activation)
- Vit D3 aka cholecalciferol (UV)/ergocalciferol (diet)
- In Liver –> 25-OH(D) aka calcidiol
- In Kidney + 1alpha-hydroxylase –> 1,25-OH2(D) aka Calcitriol (activated vitD) –> INCREASE Ca
- GI absorption
- Kidney - decreased excretion
HYPERcalcemia
-
Sx:
- Stones - urinary tract calculi
- Bones - fractures
- (Abdo) moans - dyspepsia
- Thrones - polyuria, constipation
- (Psych) overtones - depression, psychosis
- Ix - check PTH:
- Low - hypercalcemia of malignancy (PTH axis is functioning normally) - bone mets, PTHrP (released by lung SCC), myeloma (CRAB)
- Normal/high - primary hyperparathyroidism (as if serum Ca high, PTH should be low) - adenoma, hyperplasia, MEN 1&2
- Other:
- Fluid status, ECG (short QT), protein electrophoresis, 24hr urinary Ca (familial hypocalciuric hypercalcemia)
- Bloods - bone profile (Ca, PO4), U&E
- Imaging: CXR
- Mx:
- IMMEDIATE = aggressive IV 0.9% fluid resus (4-6L over 24krs), repeat Ca
- Tx underlying cause:
- Parathyroid adenoma - minimally invasive surgery (subtotal/total parathyroidectomy)
- Malig - Zalendronate/Pamidronate (inhibit osteoclast activity), slow infusion
- Other:
- If bone mets –> bisphosphonates
- If renal failure –> Cinacalcet (reduce PTH)
- Recheck serum Ca @day 2 –> 4
HYPOcalcaemia
- Causes:
- Hypoparathyroidism (PO4 high, PTH low)
- Pseudohypoparathyroidism (PO4 high, PTH high) = PTH resistance
- CKD (high PO4, PTH high, ALP high)
- Vit D def (rickets/osteomalacia, low/normal PO4, high PTH, high ALP)
- Hypomagnesaemia (low/normal PO4, low/normal PTH, normal ALP)
- Presentation:
- Peri-oral numbness, digital paraesthesia, dermatitis
- +ve Trousseau’s (BP cuff 20 over SBP for 3mins –> salt bae hand), Chovstek signs (tap over the masseter muscle in the inferior pre-auricular area)
- Laryngospasm (wheeze, dysphagia, muscle cramps)
- Confusion, seizures, prolonged QT
- Ix: serum Ca, PO4, Mg, PTH, U&E, Vit D
- Mx: PO/IV replacement of Ca
4
Q
Hyperparathyroidism sub-categories?
A
- Primary - PTH secretion from primary parathyroid tumour/ectopic secretion from another tumour (high Ca, high PTH)
- Secondary - PT hyperplasia to maintain control of hypocalcemia, normally from CKD (low Ca, high PTH, normal -ve feedback)
- CKD –> bone profile, parathyroid hormone lvl every 3-6 months
- Tertiary - prolonged secondary, becomes irrepressible by serum Ca lvls. Mostly kidney transplant patients (high Ca, very high PTH)
5
Q
Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?
A
Presentation: polyuria, polydipsia, dehydration
- Ketosis - malaise, vomiting
- FHx, other endo disorders
- If known DM:
- Previous DM control (hyp/hyper)
- Micro/macrovascular complications
- Diabetic eye disease (Dx & Tx)
RFs: overweight, FHx (DM), PMHx (GDM), PCOS, HTN, dyslipidemia, CVD
Criteria for Dx (repeat test needed for Dx):
- Fasting plasma glucose of ≥7.0 (normal ≤6)
- OGTT (BM 2hours after 75g glucose-load)/ Sx + random plasma glucose of ≥11.1mmol/l (normal <7.8)
- HbA1c ≥48mmol/mol (≥6.5%) - not for young/T1DM, acutely ill, haem disease, preg, iatrogenic
T1DM Mx: exogenous insulin to avoid DKA & long-term complications
- Diet - lower fat, higher carbs = counting carbs (adjust insulin around diet rather than limiting eating)
- Diabetic specialist nurse - EDUCATE
- Insulin regimens:
- 1st line - Basal-bolus regimen
- Basal (background) - BD insulin detemir (or Levemir/Lantus/Tresiba) as basal insulin
- Bolus (before meals) - analogue rapid-acting insulin e.g. insulin Lispro (Humalog)/Aspart (Novorapid)/Neutral (Actrapid)
- Other:
- BD biphasic (premixed insulin, hypos common) e.g. Novomix, Humulin M3, Humalog Mix
- OD before bed long-acting (for T2DM)
- NOTE: intermediate-acting insulin e.g. Humulin I, Insulatard
- 1st line - Basal-bolus regimen
T2DM Mx:
- 1st line - Lifestyle changes -
- HbA1c targets:
- No hypoglycaemics - 48mmol/mol
- Hypoglycaemics - 53mmol/mol
- Escalate Tx - 58mmol/mol
- HbA1c targets:
- Medication:
- 2nd - Metformin (SEs: diarrhoea, LA - avoid if eGFR <30)
- 3rd - ADD Sulphonylurea e.g. Gliclazide (SEs: hypoglycaemia, weight gain)
- 4th - ADD other DM med:
-
Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
- C/I in HF, bladder cancer
-
SGLT-2 inhibitor e.g. Empagliflozin (SEs: Hypoglycaemia, weight loss, UTI)
- Not recommended in impaired renal funct
- DPP-4 inhibitor e.g. Linagliptin (APPROVED FOR USE IN CKD, weight neutral)
-
GLP-1 analogues e.g. Exenatide/Liraglutide (SE: weight loss - useful if BMI >35; vomiting)
- Not recommended in impaired renal funct
-
Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
- 5th - If on triple therapy & not providing control –> commence insulin
- CVD risk Mx - anti-HTN, anti-lipid, QRISK-3 score
- Diabetic nephropathy Mx:
- Monitor albumin-creatinine ratio (ACR)
- Consider ACEi/ARB early
- Diabetic neuropathy Mx:
- Annual Sx review (erectile dysfunction, autonomic neuropathy - orthostatic hypotension, gastroparesis, bladder emptying difficulties)
- Annual foot screen + specialist foot Mx, monitor for diabetic foot/ulcers ± amputation
- Diabetic retinopathy: retinal screen annually (age ≥12yrs)
- Background: need to tighten control
- Venodilation, microaneurysms (dots), hard exudates (lipid deposits)
- Tx: tighten glycaemic control, refer if near macula
- Pre-proliferative (mild) - soft exudates (cotton wool spots e.g. infarcts)
- Proliferative - neovascularization (+ floaters, reduced acuity)
- Tx: pan-retinal photocoagulation
- Diabetic maculopathy - hard exudates, oedema (+ blurred vision, reduced acuity)
- Tx: intravitreal triamcinolone acetonide decreases macula oedema
- NOTE: Pre-diabetic –> refer to diabetes prevention programme (DPP)
- Background: need to tighten control
Diabetes complications:
- Microvascular:
- Eye - diabetic retinopathy (± cataracts, glaucoma)
- Kidney - diabetic nephropathy
- Neuropathy - damage to PNS –> diabetic neuropathy (peripheral neuropathy - glove & stockings distribution) –> diabetic ulcers/gangrene
- Macrovascular:
- Brain - stroke/TIA/cog impairment
- Heart - coronary heart disease
- Extremities - PVD, diabetic ulcers/gangrene
6
Q
Acromegaly cause? presentation? Ix? Mx? Complications?
A
Cause: macroadenoma in anterior pituitary
Presentation: coarse facial features
- Skin (acanthosis nigricans - thick & dark in creases), sweating, carpal tunnel syndrome (bilateral)
- Arthropathy, sleep apnoea, reduced sexual functioning, visual field defects (bitemporal hemianopia)
- Assoc: DM, HTN, MEN type 1 (15%)
Ix:
- Bedside: CN VI palsy, urine dip (glucose), ECG (cardiomyopathy)
- Bloods: elevated IGF-1, GH lvl during OGTT (not suppressed in acromegaly)
- Imaging: MRI brain (macroadenoma), sleep studies, colonoscopy (screening), visual field testing (driving)
Mx:
- Transsphenoidal hypophysectomy (curative)
- Medical: somatostatin analogue (octreotide)
- External pituitary radiotherapy (long-term 5-10yrs)
Complications:
- General: HTN, DM, carpal tunnel syndrome, sleep apnoea, colorectal cancer, LVH/cardiomyopathy/IHD
- Anterior pituitary hypofunction: hypogonadism
- Local compressive: bitemporal hemianopia
8
Q
Hyperosmolar Hyperglycaemic State
- What does insulin do? Pathophysiology of HHS?
- HHS criteria? HHS Mx? HHS Mx Targets?
A
Insulin:
- High level of insulin –> reduces serum BM (pushes into surrounding tissues & hepatic glucose store)
- Low level of insulin –> switches off ketone production
Pathophysiology:
- HHS = complication of T2DM
- In HHS have enough insulin to switch of ketone production but not enough to reduce BM lvls
- High glucose - osmotically active –> polyuria –> dehydration
HHS criteria:
- Hypovolaemia
- Glucose >30mmol/L
- NO ketonaemia
- Serum osmolality >320mOsmol/kg
Mx: REHYDRATE = IV 0.9% NaCl (3-6L by 12hrs, deficit 110-220mL/kg)
- Targets:
- Reduce Na by less than 10mmol/L/day (otherwise risk osmotic demyelination syndrome)
- Reduce BM by over 5mmol/L/hr
- NOTE: if targets not met by 0.9% saline –> 0.45% instead
- If fluid alone are not enough –> 0.05 units/kg/hr fixed-rate insulin infusion
9
Q
SIADH - pathophysiology? criteria? causes?
A
Criteria:
- True hyponatraemia (<125)
- High urine osmolality (>500/kg)
- Excessive Urine Na excretion (>20)
- Decreased serum osmolality (<260)
- Clinically euvolemic
- Dx of exclusion (9am cortisol + TFTs must be normal)
Causes:
- Malig (small cell lung cancer, breast cancer) - ectopic ACTH production
- CNS disorders (encephalitis, abscess)
- Chest disease (pneumonia, TB)
- Drugs (opiates, SSRIs, carbamazepine)
10
Q
Diabetes insipidus - Sx? Types? Ix? Tx?
A
Sx: hypernatremia (lethargy, thirst, irritable, confusion, coma, fits), polyuria, urine plasma osmolality <2 (very dilute)
Types:
- Central (lack of ADH prod in hypothalamus) – pituitary surgery, irradiation, trauma, infarction
- Nephrogenic (resistance to ADH effects) – hypercalcaemia, hypokalaemia, meds (lithium)
Ix: rule out DDx (BM, review drugs, K/Ca lvls)
- U&E, Ca, BM, serum & urine osmolarities
- Dx: 2-step fluid deprivation test = give desmopressin (DDAVP):
- Normal/primary polydipsia –> urine concentrates on fluid deprivation (>600)
- Cranial DI - giving desmopressin allows ADH prod –> urine conc
- Nephrogenic DI: urine never concentrates
- NOTE: DI excluded if urine to plasma (U: P) osmolarity ratio >2:1
- Cranial MRI - if suspect cranial DI
NOTE: Fluid deprivation test process:
- Baseline urine osmolality
- Fluid deprivation for 8hrs, take urine osmolality
- Give desmopressin, wait 8hrs, take urine osmolality
Tx:
- Nephrogenic DI –> fluids (+ monitor UO) + thiazide diuretics (hydrochlorothiazide - weird/does not make sense)
- Central DI –> fluids + desmopressin
11
Q
Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?
A
Hypothyroidism:
- Causes:
-
Primary:
-
Hashimoto’s thyroiditis - most common hypothyroidism (chronic AI/lymphocytic thyroiditis)
- Goitre, AI disease (vitiligo, pernicious anaemia, T1DM, Addison’s)
- Elderly females
- May be initial ‘Hashitoxicosis’
- +++ Autoantibody titres
- Antithyroid peroxidase (TPO) & antithyroglobulin (TG)
-
Atrophic AI thyroiditis
- No goitre, anti-TPO/TSH
- Iodine def, meds (carbimazole, lithium), thyroid surgery
-
Hashimoto’s thyroiditis - most common hypothyroidism (chronic AI/lymphocytic thyroiditis)
-
Secondary: pituitary gland fails to produce TSH
- Tumour, vascular (Sheehan syndrome), radiation, inf
-
Primary:
- Ix:
- Bedside: ECG (pericardial effusion, ischaemia)
- Bloods: FBC, U&E, TFTs, Lipids, Prolactin, Anti-TPO/TG
- Imaging: CXR (effusions, HF)
- Mx: thyroid replacement therapy (levothyroxine)
- Monitor with serum TSH, careful with dose in elderly (prone to IHD)
- Myxoedema coma - A-E & active warming, T3 slow IV, hydrocortisone IV
- Associated complications:
- Cardiac - HF
- Serous effusions (pleural, peritoneal, pericardial, joint)
- Neuro - carpal tunnel, proximal myopathy, cerebellar dysfunction, myxedema coma
- Systemic - dyslipidemia, anaemia
Hyperthyroidism:
- Presentation:
- Weight loss, increased appetite
- Heat intolerance, tremor, sweating, palpitations
- Mood (anxious, irritable)
- Bowel habit (diarrhoea), menses (oligomenorrhoea)
- Goitre
- Eye Sx (watering, gritty, red)
- Other AI disease (vitiligo)
- Signs:
- Lid lag (eyes)
- Palmar erythema
- Brisk reflexes
- Sinus tachy/AF
- Ix: TSH low, T3/4 high, TPO (may be raised), anti-TSHr ab (in Graves), technetium 99m uptake scan (diffuse/reduced)
- Causes:
- High-uptake:
-
Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
- Eye signs: proptosis –> exophthalmos, diplopia, visual loss
- Peripheral signs: pretibial myxoedema, thyroid acropatchy, onycholysis, bruit over thyroid
- Toxic multinodular goitre aka Plummer’s disease: hot nodules, painless (
- Toxic adenoma: 5%, single ‘hot nodule’ on isotope scan (1 area of uptake)
-
Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
- Low-uptake:
-
Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
- Tx: NSAIDs
- Postpartum thyroiditis (like De Quervain’s but postpartum)
-
Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
- High-uptake:
- Mx:
- Conservative: lifestyle changes, corneal lubricants
-
Medical:
- Sx relief – B-blockers
- Antithyroid meds - Carbimazole (or propylthiouracil)
- SEs: rashes, agranulocytosis - monitor
-
Radioiodine:
- acts slowly, effective, best Tx for toxic multinodular goitre
- Risk of permanent hypothyroidism (10%)
- CI in preg/lactating women
- Surgical: subtotal thyroidectomy (in large goitre/relapse)
- Monitoring with TFTs annually
-
Thyroid storm: acute state of shock, pyrexia, confusion, vomiting
- HDU/ITU support
- Propylthiouracil 600mg –> 200mg QDS
- Stable iodine (Lugol’s iodine) ≥1hr later
- Propranolol, dexamethasone & IV fluids
12
Q
Adrenal disease breakdown? Causes? Presentations? Ix? Mx?
A
Cushing’s #HighCortisol
- Causes:
- ACTH-dependent:
- Pituitary tumour (85%) = “Cushing’s disease”
- Ectopic ACTH-prod tumour (5%) - SCLC/carcinoid tumour
- ACTH-independent:
- Adrenal tumour (10%)
- Iatrogenic steroid use
- ACTH-dependent:
- Presentation:
- Thin skin, easy bruising, proximal myopathy, obesity (moon face, buffalo hump), other (hirsutism, acne)
- Exam: vertical abdo striae
- HTN, DM, osteoporosis (back/bone pain)
- Ix:
- Exclude pseudo-Cushing’s - depression, alcohol excess, chr inf (no muscle weakness)
- Confirm Dx: low-dose dex suppression test - fail to suppress cortisol in all
- Overnight dexamethasone suppression test (1g @11pm) OR
- 48hr low-dose 0.5mg/6h PO dexamethasone supression test OR
- 24-hr urinary free cortisol (test x3 as low sensitivity)
-
Plasma ACTH measured:
- High - CRH test identifies if pituitary or ectopic
- Could also do bilateral inferior petrosal sinus sampling –> if no mass –> CT contrast CAP for ectopic
- Low - adrenal tumour –> CT/MRI adrenal glands –> if nothing –> adrenal vein sampling
- High - CRH test identifies if pituitary or ectopic
- Mx: treat underlying disease e.g. withhold steroids or surgical removal of the lesion
- Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
- 2nd - pituitary radiotherapy (also used if still high cortisol post-surgery) –> progressive anterior pituitary failure
- Metyrapone & ketoconazole - sometimes before/after surgery
- 3rd - laparoscopic bilateral adrenalectomy in refractory (but require lifelong glucocorticoid/mineralocorticoid replacement + risk of Nelson’s syndrome (increased skin pigment from high ACTH
- Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
Hypoadrenalism
- Causes:
- AI: Addison’s disease (>70%)
- Malig: mets (lung, breast. kidney)
- Inf: TB (>10%), HIV (CMV adrenalitis), Fungal
- Infiltration: granulomatous disease, hemochromatosis, amyloidosis
- Iatrogenic: ketoconazole, rifampicin, phenytoin, bilateral adrenalectomy
- Congenital: congenital adrenal hyperplasia (late-onset) - commonly 21-hydroxylase def
- Presentation:
- Anorexia/weight loss, fatigue/weakness, postural dizziness, reduced libido, sweating
- N&V, diarrhoea, salt craving
- Signs: hyperpigmentation in skin creases/lip/mouth, vitiligo, sparse axillary/pubic hair
- Ix:
- Bedside - postural hypotension, IGRA (TB inf)
- Bloods - FBC, U&E (↑ K+, ↓ Na+), low glucose, serum Ca, AI/auto-ab screen, plasma renin & aldosterone, short snACTHen 250mcg IM test (not Addison’s if 30min cortisol rises >550nmol/L
- Imaging: CXR (past TB), adrenal CT (for TB/mets)
- Mx:
- Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
- Ppt factors: inf, trauma, surgery, missed steroid doses
- Ix: Cortisol, ACTH, U&E
- Mx: IV hydrocortisone + IV fluids ± fludrocortisone (if primary adrenal lesion)
- Monitor BM ± IV dextrose
- Bloods, urine, sputum culture ± abx
- Chronic: hydrocortisone + fludrocortisone (Na homeostasis), education (compliance, increase steroid dose if ppt factors, follow-up
- Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
Hyperaldosteronism (incl. Conn’s)
- Primary (HTN, ↑ Na+ ↓ K+):
- Conn’s - aldosterone-secreting adrenal adenoma
- Bilateral adrenal hyperplasia
- Secondary - decreased renal perfusion (high renin –> Na reabsorption –> HTN) - RAS, HF, liver failure
- Ix: aldosterone-renin ratio (ARR), CT/MRI adrenals, adrenal vein sampling
- Conn’s is very high (high aldosterone, low renin) VS BAH has both high (high aldosterone, high renin)
- Mx: spironolactone, unilateral adrenalectomy (for Conn’s)
PHaeochromocytoma #HighCatecholamines
- Cause: adrenal medulla tumour –>↑ catecholamines (adrenaline/NA)
- Presentation: episodic headache, sweating, tachycardia, hypertension, arrhythmias, death if untreated
- 10% exta-adrenal, 10% bilateral, 10% malignant
- Ix: ECG (LVF, increased ST seg, VT), 24hr urinary metanephrines, abdo CT/MRI
- Mx: specialist endo centre - alpha blockade = PHenoxybenzamine then beta-blockade –> then surgery when BP controlled (after 4-6wks)
13
Q
Hyperprolactinaemia - causes? presentation? Ix? Mx
A
Causes:
- Prolactinoma (macroprolactinoma >6000)
- Adenoma (non-funct pituitary adenoma 1000-5000, from compression & DA lvls)
- DA antagonist (metoclopramide, anti-psychotics, methyldopa)
- Hypothyroidism (increased TRH stimulates prolactin prod)
- Physiological (pregnancy, breastfeeding)
Presentation: irreg periods, decreased libido, galactorrhoea
- Bilateral hemianopia
Ix:
- Bedside - pregnancy test, visual fields assessment
- Bloods - serum prolactin, TFTs, U&E
- Imaging - pituitary MRI
Mx:
- Asymptomatic pre-menopausal/post-menopausal with microadenoma - observation
- Symptomatic pre-menopausal/macroadenoma post-menopausal/male:
- Dopamine agonist (Cabergoline/Bromocriptine), 2nd line - COCP (not if want pregnancy)
- Trans-sphenoidal surgery (if visual Sx/pressure effects refractory to medical Tx)
- Follow-up: monitor prolactin, check visual fields
14
Q
DDx for tiredness & lethargy? Ix?
A
DDx:
- Anaemia - PUD, altered bowel habit? occult blood loss?
- Thyroid disease - thyroiditis?
- DM - polyuria, polydipsia, weight loss
- Adrenal insufficiency
- Primary hyperparathyroidism - constipation, urinary stones, abdo pain, depression
- Hypopituitarism (Note: Sheehan’s syndrome - post-partum hypopituitarism)
- Anxiety & depression - sleep disturbances, poor appetite, recent stress
Ix:
- FBC, U&E, LFTs, CRP, bone profile, HbA1c, TFTs, haematinics
- CXR
15
Q
DDx for weight loss?
A
DDx:
- Thyrotoxicosis - heat intolerance, palpitations, SoB, mood (irritable/anxious), bowel habit, menses, goitre, exophthalmos, recent pregnancy
- GI-related conditions (IBD, upper GI pathology, coeliac disease, chr pancreatitis) - dysphagia, vomiting, regurgitation, abdo pain, altered bowel habit
- Eating disorders (Anorexia nervosa) - reduced eating, compulsive exercise
- Systemic conditions (malignancy) - FLAWS
Ix:
- FBC, U&E, CRP, LFTs, fasting BM, bone profile, TFTs, anti-TTG, IgA levels, haematinics
- CXR
16
Q
What are the causes of goitre?
A
Diffuse: Graves’ disease, Hashimoto’s thyroiditis, De Quervain’s thyroiditis
Nodular: Multinodular goitre, adenoma, carcinoma
17
Q
Diabetic Ketoacidosis (DKA)
- Normal glucose transport & during starvation?
- The problem in insulin deficiency (diabetes)? How does this relate to Sx of DKA?
- Ix? Dx criteria? Mx? Monitoring Tx & hourly targets?
A
Normal glucose transport: diet –> blood –insulin–> hepatic glucose store –GH, Cortisol, Adrenaline, Glucagon–> blood
- During starvating - GH, Cortisol, Adrenaline, Glucagon make sure there is enough glucose in the blood BUT liver also produces ketones
- Ketones can cross BBB providing an alternative source of fuel for the brain when low glucose
- Pancreatic beta cells –> insulin prod –> reduces glucose (high glucose has–> feedback on pancreatic beta cells –> produce more insulin)
- High insulin (associated with high glucose) –> -ve feedback on ketone prod
In insulin deficiency - high glucose but unable to produce insulin + no -ve feedback on ketone prod –> high glucose, high ketones
- High glucose - osmotically active (moves along concentration gradient into urine –> pulling more water with it) –> POLYURIA –> DEHYDRATION
- High ketones - acidic (metabolic acidosis) –> enzyme dysfunction –> COMA & DEATH
DKA Ix:
- Bedside - urine dip, ECG, continuous cardiac monitoring
- Bloods - VBG, FBC, U&E, BC, BM
- Imaging - possibly CXR
DKA Dx:
- BM: ≥11mmol/L
- Ketones: ≥3mmol/L (serum) OR ≥2+ (urine)
- Acidaemia: pH <7.3 OR Bicarb <15mmol (ketoacidosis)
DKA Mx: A-E assessment
-
IV FLUIDS (rehydrate)
- Bolus –> 1L over 1hr –> 2hr –> 3hr –> 4hr
- Add 40mmol KCL to fluids after bolus
-
0.1 U/kg/hr fixed-rate INSULIN infusion (reduce ketones)
- If BM <14 –> start 125ml/hr 10% dextrose
- Insulin infusion continues until ketones normalise (not BM)
- NOTE: follow local trust guidelines for DKA Tx as varies slightly between trusts
Monitor - BM, ketones, VBG (K conc)
- Hourly targets:
- Fall in BM ≥3
- Fall in ketones ≥0.5
- Rise in HCO3 ≥3
- Continue until: blood ketones <0.6, pH >7.3, HCO3 >18
23
Q
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