Endocrinology station Flashcards

Question 1

Q

what is a DKA

Answer

A

BM > 11.1
Ketones > 3
pH < 7.3

rapid onset

Question 2

Q

DKA causes

Answer

A

infection, surgery, insulin missed, alcohol

Question 3

Q

DKA treatment

Answer

A

Fluids 500ml bolus over 15m
Insulin 0.1U/kg/hour FRII + normal insulin regime
Potassium – 4-mmol KCL even if potassium is normal
1-% dextrose when BM <14
VTE prophylaxis

Question 4

Q

what is HHS

Answer

A

BM >33.3
Hyperosmolar >330mmol/kg
Volume depleted

Slow onset

Question 5

Q

HHS treatment

Answer

A

LMWHP (VTE proph)
Slow rehydration over 48 hours
3-6L over 12 hours
insulin

Question 6

Q

hypothyroidism symptoms

Answer

A

Fatigue and low energy
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin and hair loss

Question 7

Q

autoimmune thyroiditis

Answer

A

Hashimoto’s thyroiditis. autoimmune inflammation of the thyroid gland and under activity .
antithyroid peroxidase (anti-TPO) antibodies and antithyroglobulin antibodies.

Question 8

Q

Hyponatremia - Sx? Ix & Approach? What happens if you correct Na too fast?

Answer

A

Sx: confusion, altered GCS, headaches, seizures, encephalopathic

Ix: fluid status, U&E, paired osmolalities (urine, serum)

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 –> hypovolaemia (increased Na reabsorption in kidneys –> increasing H20 retention –> reducing 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

Question 9

Q

Potassium homeostasis - areas involved? Hypo/hyper? Appearance on ECG? Hyper Tx?

Answer

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)

Question 10

Q

Calcium homeostasis?

Hyper Sx? Ix & causes? Mx?

Hypo Causes? Sx? Ix? Mx?

Answer

A

Hormone production:

Parathyroid gland - PTH –> INCREASE Ca:
- Bone resorption
- GI absorption
- Kidney - decreased excretion, increases 1alpha-hydroxylation (vitD activation)
Vit D₃aka 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

Question 11

Q

Hyperparathyroidism sub-categories?

Answer

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)

Question 12

Q

Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?

Answer

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:
- Self-adjust dose - DAFNE course for T1DM (D for DM)
- Fingerprick glucose
- Calorie intake & carb counting
- Phone support
Don’t stop insulin during acute illness, maintain calorie intake
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

T2DM Mx:

1st line - Lifestyle changes - DESMOND course for T2DM (D for DM), dietician input, self-BM monitoring (individual HbA1c target <6.5)
- HbA1c targets:
  - No hypoglycaemics - 48mmol/mol
  - Hypoglycaemics - 53mmol/mol
  - Escalate Tx - 58mmol/mol
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
- 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)

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

Question 13

Q

Acromegaly cause? presentation? Ix? Mx? Complications?

Answer

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

Question 14

Q

Hyperosmolar Hyperglycaemic State

What does insulin do? Pathophysiology of HHS?
HHS criteria? HHS Mx? HHS Mx Targets?

Answer

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

Question 15

Q

SIADH - pathophysiology? criteria? causes?

Answer

A

Criteria:

True hyponatraemia
High urine osmolality
Clinically euvolemic
Dx of exclusion (9am cortisol + TFTs must be normal)

Causes:

Malig (small cell lung cancer, breast cancer)
CNS disorders (encephalitis, abscess)
Chest disease (pneumonia, TB)
Drugs (opiates, SSRIs, carbamazepine)

Question 16

Q

Diabetes insipidus - Sx? Types? Ix? Tx?

Answer

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

Question 17

Q

Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?

Answer

A

Hypothyroidism:

Causes:
- Primary:
  - Hashimoto’s thyroiditis - most common hypothyroidism
    - 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
- Secondary: pituitary gland fails to produce TSH
  - Tumour, vascular (Sheehan syndrome), radiation, inf
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)
- 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)
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

Question 18

Q

Adrenal disease breakdown? Causes? Presentations? Ix? Mx?

Answer

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
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
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

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)
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

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)

Question 19

Q

Mx of obesity?

Answer

A

Conservative measures
Medical (none proven to provide sustainable weight loss)
- Orlistat (gut lipase inhibitor, SEs: profound flatus, diarrhoea)
Surgical – bariatric surgery (BMI >40 OR >35 w/ comorbidity assoc w/ obesity)
- Needs extensive screening + commitment to long-term follow-up

Question 20

Q

Hyperprolactinaemia - causes? presentation? Ix? Mx

Answer

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

Question 21

Q

DDx for tiredness & lethargy? Ix?

Answer

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
Anxiety & depression - sleep disturbances, poor appetite, recent stress

Ix:

FBC, U&E, LFTs, CRP, bone profile, HbA1c, TFTs, haematinics
CXR

Question 22

Q

DDx for weight loss?

Answer

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

Question 23

Q

What are the causes of goitre?

Answer

A

Diffuse: Graves’ disease, Hashimoto’s thyroiditis, De Quervain’s thyroiditis

Nodular: Multinodular goitre, adenoma, carcinoma

Question 24

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?

Answer

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

Question 25

Q

What are the hand signs of Acromegaly on examination?

Question 26

Q

What are the arm signs of Acromegaly on examination?

Question 27

Q

What are the face signs of Acromegaly on examination?

Question 28

Q

What are the extra (not hand, arms, face) signs of Acromegaly, on examination?

Question 29

Q

What is needed to complete an Acromegaly examination?

Question 30

Q

What are the differentials of Macroglossia?

Question 31

Q

What are the differentials for Acanthosis Nigricans?

Question 32

Q

What are the key symptom questions in an Acromegaly history?

Question 33

Q

What are the key association questions in an Acromegaly history?

Question 34

Q

What are the bedside investigations for Acromegaly?

Question 35

Q

What are the blood investigations for Acromegaly?

Question 36

Q

What are the imaging investigations for Acromegaly?

Question 37

Q

What are the other (not bedside, blood or imaging) investigations for Acromegaly?

Question 38

Q

What are the complications of Acromegaly?

Question 39

Q

What is the General Management of Acromegaly?

Question 40

Q

What is the 1st line Management of Acromegaly?

Question 41

Q

What is the 2nd line Management of Acromegaly?

Question 42

Q

What is the 3rd line Management of Acromegaly?

Question 43

Q

What is the Follow up Management of Acromegaly?

Question 44

Q

What are the hand signs of Cushing’s Syndrome?

Question 45

Q

What are the arm signs of Cushing’s Syndrome?

Question 46

Q

What are the face signs of Cushing’s Syndrome?

Question 47

Q

What are the abdomen signs of Cushing’s Syndrome?

Question 48

Q

What are the extra (not, hand, face, arms) signs of Cushing’s Syndrome?

Question 49

Q

What is needed to complete a Cushing’s Syndrome examination?

Question 50

Q

What are the significant negatives in Cushing’s Syndrome?

Question 51

Q

What are the differentials for Cushing’s Syndrome?

Question 52

Q

What are the questions in a Cushing’s Syndrome history?

Question 53

Q

What are the causes of Cushing’s Syndrome?

Question 54

Q

What are the bedside investigations for Cushing’s Syndrome?

Question 55

Q

What is the investigation to confirm raised Cortisol in Cushing’s Syndrome?

Question 56

Q

How is the cause investigated in Cushing’s Syndrome?

Question 57

Q

What are the complications of Cushing’s Syndrome

Question 58

Q

What is the general management of Cushing’s Syndrome?

Question 59

Q

What is the management of the various causes of Cushing’s Syndrome?

Question 60

Q

What are the main signs of Addison’s Disease on examination?

Question 61

Q

What are the Extras signs (not main signs) of Addison’s Disease on examination?

Question 62

Q

What are the key questions in an Addison’s Disease examination?

Question 63

Q

What are the blood investigations for Addison’s Disease?

Question 64

Q

What are the investigations needed to confirm the Addison’s Disease diagnosis?

Answer 25

A

Other differentials:

Smooth Goitre
Nodular Goitre
Solitary Nodule

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Endocrinology station Flashcards

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