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Endocrinology Flashcards

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1
Q

DIABETES MELLITUS

What are the three main types of diabetes mellitus and their respective pathophysiologies?

A
  • T1DM = autoimmune destruction of insulin-producing beta cells of the islets of Langerhans in the pancreas leading to absolute insulin deficiency + high glucose
  • T2DM = insulin resistance + relative insulin deficiency due to excess adipose tissue
  • Pre-diabetes = misses criteria for T2DM but likely to develop over next few years
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2
Q

DIABETES MELLITUS

What are some risk factors for T2DM?

A
  • Obesity + inactivity
  • Asian
  • FHx
  • Gestational diabetes
  • PCOS
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3
Q

DIABETES MELLITUS
What is the clinical presentation of…

i) T1DM?
ii) T2DM?
iii) diabetes in general?

A

i) Polyuria, polydipsia, weight loss, ?DKA in young
ii) Often ASx + incidental, may have polyuria/polydipsia
iii) Visual blurring, candida infections, acanthosis nigricans

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4
Q

DIABETES MELLITUS

How do you diagnose diabetes mellitus?

A

Asymptomatic and 2x results or symptomatic with 1 result:

  • Fasting glucose ≥7.0mmol/L
  • Random glucose or OGTT after 2h ≥11.1mmol/L
  • HbA1c ≥48mmol/mol (6.5%)
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5
Q

DIABETES MELLITUS

What additional investigations would you consider in T1DM?

A
  • C-peptide (low) + useful if atypical features
  • Diabetes-specific Ab (anti-GAD + ICA)
  • Monitor for other autoimmune conditions e.g., Addison’s, coeliac, thyroid
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6
Q

DIABETES MELLITUS
When investigating diabetes mellitus, how would you diagnose someone with…

i) impaired fasting glucose?
ii) impaired glucose tolerance?

A

i) 6.1 ≤ fasting glucose < 7.0mmol/L

ii) Normal fasting glucose but 7.8 ≤ OGTT 2-h value < 11.1mmol/L

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7
Q

DIABETES MELLITUS
What are the HbA1c targets in diabetes mellitus?
How can falsely elevate/reduce HbA1c levels?

A
  • T1DM/T2DM on lifestyle ± metformin = 48mmol/mol
  • T2DM on drug which can cause hypoglycaemia = 53mmol/mol
  • Lower = reduced RBC life (sickle cell, G6PD, HS)
  • Higher = increased RBC life (splenectomy, low vitamin B12 + folate)
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8
Q

DIABETES MELLITUS
What dietary advice is given in diabetes mellitus?
How do you manage pre-diabetes?

A
  • High fibre, low glycaemic index sources of carbs, low salt/fat
  • Structured exercise, diet change + weight loss, regular HbA1c testing
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9
Q

DIABETES MELLITUS
What is the management of T1DM?
What are some side effects of this?

A
  • S/c insulin
  • Basal bolus preferred (bedtime long-acting + short-acting before each meal) or BD biphasic (mixed rapid + long-acting before breakfast/tea)
  • Hypoglycaemia, weight gain, lipodystrophy (rotate sites)
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10
Q

DIABETES MELLITUS
What are the BM targets in T1DM?
What are the sick day rules?

A
  • 5-7mmol/L on waking, 4-7mmol/L before meals, measure QDS

- Continue insulin, check BMs frequently, monitor ketones

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11
Q

DIABETES MELLITUS

What is the first-line management of T2DM?

A
  • Metformin
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12
Q

DIABETES MELLITUS
A woman with a diagnosis of T2DM comes for a review. She currently takes metformin and her HbA1c is 53mmol/mol. What should you do and why?

A
  • Increase metformin dose (if possible) as only add second PO hypoglycaemic agent if HbA1c is ≥58mmol/mol
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13
Q

DIABETES MELLITUS
A woman with a diagnosis of T2DM comes for a review. She currently takes 2 oral hypoglycaemic agents and her HbA1c is 60mmol/mol. What should you do and why?

A
  • Either triple therapy or consider insulin therapy as HbA1c is ≥58mmol/mol
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14
Q

DIABETES MELLITUS
If triple therapy is not effective, tolerated or contraindicated, what would you consider?
What is the criteria?

A
  • Metformin + sulfonylurea + GLP-1 mimetic
  • BMI ≥35 + physical or psychological issues associated with obesity
  • BMI <35 where insulin has occupational implications or weight loss would benefit other obesity-related comorbidities
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15
Q

DIABETES MELLITUS

What is the criteria for continuing on a GLP-1 mimetic?

A
  • Reduction of at least 11mmol/mol in HbA1c AND weight loss of at least 3% initial body weight in 6m
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16
Q

DIABETES MELLITUS
What are the 6 types of oral hypoglycaemic agents?
Give an example for each.

A
  • Biguanides e.g., metformin
  • Sulfonylureas e.g., gliclazide
  • DPP4 inhibitors e.g., sitagliptin
  • Thiazolidinediones e.g., pioglitazone
  • SGLT-2 inhibitors e.g., empagliflozin
  • GLP-1 mimetic e.g., s/c exenatide
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17
Q

DIABETES MELLITUS
Biguanides:
i) mechanism of action?
ii) side effects?

A

i) Increased insulin sensitivity AND decreased hepatic gluconeogenesis
ii) GI upset (D+V), lactic acidosis

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18
Q

DIABETES MELLITUS
Sulfonylureas:
i) mechanism of action?
ii) side effects?

A

i) Stimulate pancreatic beta cells to secrete insulin

ii) Hypoglycaemia, weight gain, hyponatraemia

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19
Q

DIABETES MELLITUS
DPP4 inhibitors:
i) mechanism of action?
ii) side effects?

A

i) Increases incretin levels which inhibit glucagon secretion
ii) Increased pancreatitis risk

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20
Q

DIABETES MELLITUS
Thiazolidinediones:
i) mechanism of action?
ii) side effects?

A

i) Activate PPAR-gamma receptor in adipocytes to promote adipogenesis + fatty acid uptake to reduce insulin resistance
ii) Fluid retention, weight gain, increased risk of bladder ca

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21
Q

DIABETES MELLITUS
SGLT-2 inhibitors:
i) mechanism of action?
ii) side effects?

A

i) Reversibly inhibits Sodium-GLucose co-Transporter 2 (SGLT-2) in PCT to reduce glucose reabsorption + increase urinary glucose excretion
ii) Increased UTI risk, Fournier’s gangrene, weight loss, (euglycaemic) DKA

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22
Q

DIABETES MELLITUS
Glucagon like peptide-1 mimetics:
i) mechanism of action?
ii) side effects?

A

i) Incretin mimetic which inhibits glucagon secretion

ii) N+V, pancreatitis + weight loss

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23
Q

DKA

What is the pathophysiology of diabetic ketoacidosis (DKA)?

A
  • Absence of insulin leads to uncontrollable lipolysis = increased production of FFA which are oxidised in the liver to ketone bodies leading to ketoacidosis
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24
Q

DKA

What is the clinical presentation of DKA?

A
  • Acetone breath (pear drops)
  • Vomiting, dehydration + abdo pain
  • Hyperventilation due to acidosis = Kussmaul’s breathing
  • Drowsiness, coma + hypovolaemic shock
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25
DKA | What are the diagnostic features of DKA?
- Glucose >11mmol/L or known DM - pH <7.3 - Bicarb <15mmol/L - Blood ketones >3.0mmol/L or urine ketones ++ on dipstick
26
DKA | What other investigations would you consider in DKA?
- FBC, U&E, blood cultures + CXR for ?cause (infection) | - ECG = signs of hypokalaemia
27
DKA | What are some potential complications of DKA?
- Cerebral oedema (especially in paeds) - VTE - Hypokalaemia > arrhythmias - AKI - Gastric stasis
28
DKA | What is the most important step in managing DKA?
- Aggressive IV fluid resuscitation
29
DKA | How do you initially manage IV fluid resuscitation for DKA in paeds?
- Shocked = 1st bolus 0.9% NaCl 20ml/kg, subsequent 10ml/kg over 15m - Not shocked = 0.9% NaCl 10ml/kg over 1h
30
DKA How do you calculate the fluid requirement for DKA in paeds? What do you give?
- Deficit + maintenance ( – not shocked fluids) over 48h | - 0.9% NaCl with 20mmol KCl in 500ml
31
DKA How do you calculate the fluids required to make up the deficit? How do you quantify the deficit?
- Fluids (ml) = % deficit x 10 x kg - 5% = pH 7.2–7.29 or bicarb <15 (mild) - 7% = pH 7.1–7.19 or bicarb <10 (moderate) - 10% = pH <7.1 or bicarb <5 (severe)
32
DKA How quickly do you give the IV fluids required for DKA in paeds? Why and what would you do if this happened?
- Rehydrate slowly over 48h | - Risk of cerebral oedema (headache, altered GCS) > CT head, IV mannitol + hypertonic saline
33
DKA | How do you manage IV fluid resuscitation for DKA in adults?
- 1L 0.9% NaCl over 1h initially - Consider adding K+ after first bag (>5.5 = nil, 3.5–5.5 = 40mmol, <3.5 = seek ICU help) - 1L over 2h/2h/4h/4h/8h
34
DKA After you've sorted IV fluid resuscitation, what is the next step in managing DKA? What are you aiming for? What would you do if you don't achieve this?
- Insulin infusion of Actrapid 50 units in 50ml saline at 0.1unit/kg/h - Continue long-acting insulin as usual, stop short-acting - Ketones fall 0.5mmol/h, bicarb rise 3mmol/L/h, glucose fall 3mmol/L/h - Increase infusion 1 unit/h until reached
35
DKA After you've sorted IV fluid resuscitation and the insulin infusion, what else would you need to consider when managing DKA? How does this differ for paeds/adults?
- Prevent hypoglycaemia - Adult glucose <14mmol/L = 125ml/h 10% glucose alongside saline - Paeds glucose <14mmol/L = add 5% dex so give 0.9% NaCl + 20mmol KCl + 5% dex in 500ml
36
DKA | What parameters should be monitored during DKA?
- Capillary glucose + ketones, obs + GCS hourly | - VBG at 2/4/8/12/24h
37
DKA When is DKA considered resolved? What do you do then? What if it hasn't resolved?
- pH >7.3 AND blood ketones <0.6mmol/L AND bicarb >15mmol/L - Stop fixed-rate insulin - Ketonaemia + acidosis not resolved within 24h = senior endo review
38
HHS | What is the pathophysiology of hyperosmolar hyperglycaemic state (HHS)?
- Hyperglycaemia results in osmotic diuresis with renal losses of water more than Na + K leading to severe volume depletion > significantly raised serum osmolarity so hyperviscosity of blood
39
HHS | What are some causes of HHS?
- New T2DM - Infection - High dose steroids - Surgery - Impaired renal function
40
HHS | What is the clinical presentation of HHS?
- Confusion/altered GCS - N+V - Dehydration - Fatigue - Shock
41
HHS What is the diagnostic criteria for HHS? What is the key parameter to monitor?
- Severe hyperglycaemia ≥30mmol/L (but no significant ketonaemia or acidosis), hypotension, hyperosmolality >320mosmol/kg - Serum osmolarity = 2Na + glucose + urea
42
HHS | What are some potential complications of HHS?
- Vascular = MI, stroke + peripheral arterial thrombosis - Central pontine myelinolysis if serum osmolarity declines too quickly - Fluid overload, cerebral oedema
43
HHS | What is the most important part of HHS management?
- IV 0.9% NaCl initially as very fluid deplete - Aim for +ve balance of 3–6L by 12h + remaining within next 12h - If serum osmolarity not declining, then switch to 0.45% NaCl - 40mmol KCl added if K 3.5-5.5
44
HHS | What other aspects should be considered in HHS management?
- Insulin at 0.05units/kg/h only if ketones >1mmol/L or glucose fails to fall - VTE prophylaxis in most patients
45
HYPOGLYCAEMIA What is hypoglycaemia? What are some causes?
- Blood glucose <4.0mmol/L | - Drugs (insulin, sulfonylureas), sepsis, insulinoma, adrenal insufficiency
46
HYPOGLYCAEMIA | What is the clinical presentation of hypoglycaemia?
- Sweating/shaking - Hunger - Nausea - Confusion, convulsions, coma
47
HYPOGLYCAEMIA What investigations might you consider to work out whether this could be endogenous production or exogenous administration?
- Measure serum insulin, C-peptide + proinsulin - All high = endogenous production - High insulin but low C-peptide + proinsulin = exogenous administration
48
HYPOGLYCAEMIA | What is the management of hypoglycaemia in a patient who is conscious and able to swallow?
- PO glucose 15–20g liquid, gel or tablet or quick-acting carb like fruit juice - Repeat after 15m until BM above 4mmol/L - Follow-up with slow acting carb afterwards e.g., toast, two biscuits
49
HYPOGLYCAEMIA | What is the management of hypoglycaemia in a patient who is unconscious or unable to swallow?
- 200ml 10% dextrose IV | - 1mg glucagon IM if no IV access
50
DIABETIC COMPLICATIONS | What are the potential complications of diabetes?
- Neuropathy = peripheral, gastroparesis, autonomic - Microvascular = nephropathy, retinopathy - Macrovascular = MI, stroke, PVD - Diabetic foot disease
51
DIABETIC COMPLICATIONS | What is the presentation of peripheral neuropathy?
- Sensory not motor loss in a glove + stocking distribution with the lower legs being affected first due to the length of the sensory neurones - Vibration sensation lost first
52
DIABETIC COMPLICATIONS | What is the management of peripheral neuropathy?
- First-line = amitriptyline, duloxetine, gabapentin or pregabalin - Pain management clinics may be useful if resistant problems
53
DIABETIC COMPLICATIONS What causes gastroparesis? How does it present?
- (Vagus) nerve damage to autonomic nervous system | - Delayed gastric emptying, bloating, offensive gas + vomiting
54
DIABETIC COMPLICATIONS | What is the management of gastroparesis?
- Prokinetics like metoclopramide, domperidone | - Abx like erythromycin to tackle bacterial overgrowth
55
DIABETIC COMPLICATIONS What is the presentation of autonomic neuropathy? What is the conservative management? What is the medical management?
- Postural hypotension with a fall in BP >20/10mmHg within 3 mins of standing - Increase dietary salt, raise head of bed, elasticated stockings to overcome venous pooling - Fludrocortisone or midodrine
56
DIABETIC COMPLICATIONS What is diabetic nephropathy? How is it identified?
- Development of proteinuria + progressive decline in renal function - ALL patients screened annually using urinary albumin:creatinine ratio (ACR) from early morning specimen where ACR >2.5 = microalbuminuria
57
DIABETIC COMPLICATIONS What is the conservative management of diabetic nephropathy? What is the medical management of diabetic nephropathy?
- Dietary protein restriction, tight glycaemic control, BP <130/80mmHg - ACEi/ARB if urinary ACR ≥3mg/mmol
58
DIABETIC COMPLICATIONS | What is the pathophysiology of diabetic retinopathy?
- Poor glycaemic control can lead to vascular occlusion + leakage of the capillaries supplying the retina > retinal ischaemia, new vessel formation + if not managed, loss of sight
59
DIABETIC COMPLICATIONS | What are the three main types of diabetic retinopathy?
- Non-proliferative diabetic retinopathy (NPDR) - Proliferative diabetic retinopathy (PDR) - Diabetic maculopathy
60
DIABETIC COMPLICATIONS | How is NPDR sub-categorised?
- Mild = ≥1 microaneurysm - Moderate = microaneurysms, blot haemorrhages, hard exudates + cotton wool spots (soft exudates = retinal infarction) - Severe = blot haemorrhages + microaneurysms in all 4 quadrants, venous beading in ≥2 quadrants, intraretinal microvascular abnormalities (haemorrhage) in ≥1 quadrant
61
DIABETIC COMPLICATIONS | What is proliferative diabetic retinopathy?
- Retinal neovascularisation (on retina or optic disc) ± vitreous/pre-retinal haemorrhage
62
DIABETIC COMPLICATIONS | What is diabetic maculopathy?
- Macular oedema (+ hard exudates) caused by leakage of vessels close to macula which can significantly threaten vision + needs urgent treatment
63
DIABETIC COMPLICATIONS What is the management of... i) NPDR? ii) PDR? iii) maculopathy?
i) Regular eye tests, ?laser photocoagulation ii) Laser photocoagulation, intravitreal VEGF inhibitors e.g., ranibizumab, vitreoretinal surgery in severe disease iii) Change in visual acuity > VEGFi (ranibizumab)
64
HYPERTHYROIDISM | What are the causes of hyperthyroidism?
- Most common = Graves' disease (autoimmune) - Toxic multinodular goitre or toxic adenoma secreting excess hormones - Subacute (De Quervain's thyroiditis) - Exogenous iodine excess (food, drugs like amiodarone, thyroxine)
65
HYPERTHYROIDISM | What generic symptoms would you expect in hyperthyroidism?
- General = weight loss, increased appetite, diarrhoea, heat intolerance - Psych = anxious, irritable, ?psychotic - Sympathetic = sweating, palpitations, tremor - Gynae = oligomenorrhoea, usually seen in women aged 30–50
66
HYPERTHYROIDISM | What are some generic signs in hyperthyroidism?
- Nodules on thyroid gland - Irregular pulse (AF) - Thin hair - Warm skin
67
HYPERTHYROIDISM | What are some Graves' disease specific signs?
- Thyroid eye disease (exophthalmos, ophthalmoplegia, lid lag + retraction) - Diffuse goitre without nodules - Thyroid acropachy - Pretibial myxoedema
68
HYPERTHYROIDISM What is... i) thyroid acropachy? ii) pretibial myxoedema?
i) Triad of: digital clubbing, soft tissue swelling of hands + feet & periosteal new bone formation ii) Mucin deposits under pretibial skin giving discoloured appearance due to reaction to TRAb
69
HYPERTHYROIDISM | What is the clinical presentation of De Quervain's thyroiditis?
- Post-viral infection where initially hyperthyroid with painful goitre + raised ESR - Euthyroid > hypothyroid (longer phase than hyper) - Eventually thyroid structure + function normalises
70
HYPERTHYROIDISM | What are some important investigations in suspected hyperthyroidism?
- Thyroid function tests - Thyroid autoantibodies (TSH receptor stimulating antibody TRAb IgG + anti thyroid peroxidase in Graves') - Thyroid scintigraphy (isotope scan) - ?Investigate for other autoimmune conditions such as Addison's, coeliac, T1DM
71
HYPERTHYROIDISM | What patterns of hyperthyroidism might you see on TFTs?
- Primary = low TSH, high T3/4 - Secondary = high TSH, high T3/4 (hypothalamus or pituitary pathology) - Subclinical = low TSH, normal T3/4
72
HYPERTHYROIDISM | What patterns of hyperthyroidism might you see on thyroid scintigraphy?
- Patchy uptake = toxic multinodular goitre - Globally reduce uptake = De Quervain's - Homogenous uptake = Grave's disease
73
HYPERTHYROIDISM What is an important complication in hyperthyroidism and what can cause it? How does it present?
- Thyroid storm/thyrotoxicosis - Thyroid/non-thyroidal surgery, trauma, infection or acute iodine load (e.g., CT contrast) - Fever, tachycardia, HTN, confusion, heart failure, N+V
74
HYPERTHYROIDISM | What is the management of thyrotoxicosis?
- IV propranolol (digoxin if fails or C/I e.g., asthma) - Propylthiouracil NG followed by Lugol's iodine 6h later - High dose corticosteroids
75
HYPERTHYROIDISM | What are the main management options for hyperthyroidism?
- Symptomatic relief with non-selective beta-blocker propranolol - Anti-thyroid drugs by either titration or block & replace - Radioiodine (131) therapy to radiate + destroy thyroid cells - Surgical thyroidectomy either total or removal of nodules
76
HYPERTHYROIDISM What is the first-line anti thyroid drug? What are some side effects? What other anti thyroid drug is there and why is it not first line?
- Carbimazole – agranulocytosis + not used in first trimester - Propylthiouracil – small risk of severe hepatic reactions
77
HYPERTHYROIDISM What are the indications for radioiodine therapy? What are some side effects? What are some contraindications?
- Toxic multinodular goitre + adenomas treatment of choice - Hypothyroidism (needs levothyroxine) - Pregnancy, breast feeding, <16y + thyroid eye disease (may worsen)
78
HYPERTHYROIDISM What are the indications for thyroidectomy? What are some side effects of this procedure?
- Recurrence, obstructing goitres + ?cancers | - Risk to recurrent laryngeal nerve (hoarse voice), hypothyroidism (needs levothyroxine) + hypoparathyroidism
79
HYPERTHYROIDISM | What is the management of thyroid eye disease?
- Smoking #1 modifiable risk factor for development - Topical lubricants to prevent corneal inflammation due to exposure - ?Steroids, ?radiotherapy, ?surgery - Any changes to vision > eye casualty
80
HYPERTHYROIDISM | What is the management of De Quervain's thyroiditis?
- Self-limiting with NSAIDs for pain | - Beta-blockers for Sx
81
DIABETIC COMPLICATIONS | Why does diabetic foot disease occur?
- Neuropathy = loss of protective sensation, Charcot's arthropathy - Peripheral arterial disease = macro + microvascular ischaemia
82
DIABETIC COMPLICATIONS | What are some complications of diabetic foot disease?
- Calluses - Cellulitis, osteomyelitis + gangrene - Charcot's joint/arthropathy
83
DIABETIC COMPLICATIONS | How does Charcots' arthropathy present?
- 6Ds = Destruction, Deformity, Degeneration, Dislocation, Dense bones + Debris - Classically tarsometatarsal joints - Joint may be swollen, red + warm - Loss of mid-foot arch
84
DIABETIC COMPLICATIONS | What is the management of diabetic foot disease?
- Annual diabetic foot review with ischaemic (dorsalis pedis + posterior tibial artery pulses) + neuropathy (10g monofilament) screening
85
HYPOTHYROIDISM | What are the causes of hypothyroidism?
- Hashimoto's = #1 developed world (goitre + TPO) - Autoimmune atrophic thyroiditis = no goitre, TPO + anti-TSH - Iodine deficiency = #1 worldwide - De Quervain's thyroiditis - Iatrogenic/drugs - Central (secondary hypothyroidism)
86
HYPOTHYROIDISM What are some iatrogenic/drug causes of hypothyroidism? What are some central causes of hypothyroidism?
- Carbimazole, amiodarone, lithium, thyroidectomy | - Pituitary tumours, infection, radiation + Sheehan's syndrome
87
HYPOTHYROIDISM | What are some symptoms of hypothyroidism?
- General = weight gain, decreased appetite, constipation + cold intolerance - Gynae = menorrhagia
88
HYPOTHYROIDISM | What are some signs of hypothyroidism?
BRADYCARDIC – - Bradycardia - Reflexes relax slowly - Ataxia - Dry thin hair/skin - Yawning - Cold hands - Ascites - Round puffy face - Defeated demeanour - Immobile - CCF
89
HYPOTHYROIDISM | What are some investigations for hypothyroidism?
- TFTs | - Thyroid antibodies = thyroid peroxidase Ab (TPO), anti-thyroglobulin (Hashimoto's) + anti-TSH receptor
90
HYPOTHYROIDISM | What are some patterns of hypothyroidism seen on TFTs?
- Primary = TSH high, T3/4 low - Secondary = TSH low, T3/4 low - Sick euthyroid syndrome = TSH normal, T3/4 low (TSH may be low) - Subclinical = TSH raised, T3/4 normal
91
HYPOTHYROIDISM What is a complication of hypothyroidism? How does it present? How is it managed?
- Myxoedema coma - Confusion + hypothermia - IV thyroid replacement, IV corticosteroids (avoid precipitating Addisonian crisis) + IV fluids
92
HYPOTHYROIDISM What is the management of hypothyroidism? What are the key patient information points for it? What are the side effects?
- Lifelong levothyroxine 50–100mcg OD (start 25mcg if >50y or cardiac Hx) - Dose titrated until TSH normal, repeat TFTs every 3m until stable - Take 30m before breakfast + 4h apart from iron + calcium carbonate tablets as decrease absorption of thyroxine - SE = osteoporosis + cardiac arrhythmias
93
HYPOTHYROIDISM | What is the management of subclinical hypothyroidism?
- TSH 4–10mU/L, <65 + Sx = trial levothyroxine, stop if no improvement - TSH 4–10mU/L + asymptomatic = TFTs in 6m - TSH >10mUL + <70y = levothyroxine even if asymptomatic - >80 no matter TSH = watch + wait
94
ADRENAL INSUFFICIENCY | What are the three types of adrenal insufficiency and their respective pathophysiology?
- Primary (Addison's disease) = reduced cortisol (glucocorticoid) + aldosterone (mineralocorticoid) due to adrenal damage - Secondary = inadequate ACTH release which leads to low cortisol due to lack of stimulation of adrenals - Tertiary = inadequate CRH release by hypothalamus
95
ADRENAL INSUFFICIENCY | What are the causes of primary adrenal insufficiency (Addison's disease)?
- #1 UK = autoimmune destruction of adrenal glands - #1 developing world = TB - Adrenal metastases (e.g., bronchial carcinoma) - Meningococcal septicaemia leading to adrenal haemorrhage (Waterhouse-Friderichsen syndrome) - HIV - Antiphospholipid syndrome
96
ADRENAL INSUFFICIENCY What are the causes of... i) secondary adrenal insufficiency? ii) tertiary adrenal insufficiency?
i) Pituitary damage e.g., surgery, infection, radiation, Sheehan's syndrome ii) Long term PO steroids (>3w) causing hypothalamus suppression when stopped (must be weaned off)
97
ADRENAL INSUFFICIENCY | What is the clinical presentation of adrenal insufficiency?
- "Thin, tanned, tired + tearful" - Weight loss, N+V, fatigue + weakness - Postural hypotension - Skin hyperpigmentation (primary only as ACTH stimulates melanocytes > melanin)
98
ADRENAL INSUFFICIENCY What investigations would you do in suspected adrenal insufficiency? What investigation is diagnostic?
- Bloods (U&Es, glucose, VBG, ACTH, renin, aldosterone) - Early morning cortisol (9am) - Adrenal autoantibodies (anti-21-hydroxylase Ab) - CT adrenals ?tumour ?haemorrhage - Short synacthen test = diagnostic
99
ADRENAL INSUFFICIENCY What would you expect to see in adrenal insufficiency on... i) U&Es? ii) glucose? iii) VBG? iv) ACTH and cortisol? v) renin? vi) aldosterone?
i) Low Na and high K ii) Hypoglycaemia iii) Metabolic acidosis iv) Primary = ACTH high cortisol low, secondary = both low v) high vi) low
100
ADRENAL INSUFFICIENCY | How would you manage the early morning cortisol results?
- >500nmol/L = unlikely Addison's - 100–500nmol/L = short synacthen test - <100nmol/L = abnormal
101
ADRENAL INSUFFICIENCY What is a key complication of adrenal insufficiency? How does it present? What causes it?
- Addisonian crisis - Reduced GCS, pyrexia + shock - Sepsis, surgery, adrenal haemorrhage, steroid withdrawal
102
ADRENAL INSUFFICIENCY | How do you manage an Addisonian crisis?
- Hydrocortisone 100mg IM/IV, no fludrocortisone needed - Aggressive fluid resus - May need glucose if hypoglycaemic
103
ADRENAL INSUFFICIENCY | What is the medical management of adrenal insufficiency?
- Hydrocortisone (glucocorticoid) with majority given in the first half of the day - Fludrocortisone (mineralocorticoid)
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ADRENAL INSUFFICIENCY | What is the general management of adrenal insufficiency?
- MedicAlert bracelets + steroid cards - Emphasise importance of hydrocortisone doses - Acute illness = double hydrocortisone dose or use IM kit, fludrocortisone dose stays the same
105
CUSHING'S SYNDROME What is Cushing's syndrome? How are the aetiologies categorised?
- Disorder of glucocorticoid (cortisol) excess - ACTH-dependent causes - ACTH-independent causes - Pseudo-Cushing's
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CUSHING'S SYNDROME | What are some ACTH dependent causes of Cushing's?
- Cushing's disease #1 = pituitary adenoma secreting ACTH > adrenal hyperplasia - Ectopic ACTH usually paraneoplastic SCLC
107
CUSHING'S SYNDROME | What are some ACTH independent causes of Cushing's?
- Exogenous steroids | - Adrenal adenoma or carcinoma
108
CUSHING'S SYNDROME What causes pseudo-Cushing's? How is it diagnosed?
- Alcohol excess or severe depression | - False positive dexamethasone suppression test or 24h urinary free cortisol so insulin stress test
109
CUSHING'S SYNDROME | What is the clinical presentation of Cushing's?
- Physical = "moon" face, central obesity, purple abdominal striae, buffalo hump, acne + hirsutism, proximal limb wasting - High cortisol = HTN, cardiac hypertrophy, T2DM, depression + insomnia - Osteoporosis, easy bruising + poor skin healing
110
CUSHING'S SYNDROME | How would you investigate Cushing's initially?
- Diagnostic = overnight dexamethasone suppression test (low cortisol = normal, high/normal cortisol = cushing's) - 24h urinary free cortisol
111
CUSHING'S SYNDROME | After the initial investigations for Cushing's, how would you localise the cause?
- 9am/midnight ACTH + cortisol with high-dose dexamethasone suppression test - Cushing's disease = cortisol + ACTH suppressed - Cushing's syndrome = cortisol not suppressed, ACTH suppressed - Ectopic ACTH syndrome = cortisol + ACTH not suppressed
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CUSHING'S SYNDROME | What other investigations would you consider in Cushing's?
- Petrous sinus sampling of ACTH to differentiate between pituitary + Ectopic ACTH secretion - CT chest/abdo + MRI pituitary if ?tumour
113
CUSHING'S SYNDROME | What is the management of Cushing's syndrome?
- Cushing's disease = transsphenoidal removal of pituitary adenoma - Adrenal tumour or ectopic ACTH tumour = surgical removal - If surgery inappropriate, ?bilateral adrenalectomy with lifelong steroids
114
ACROMEGALY What is the pathophysiology of acromegaly? What are some causes?
- Excessive GH leads to increased insulin-like growth factor 1 + so insidious bone + soft tissue growth after epiphyseal fusion - 95% pituitary adenoma, ectopic GHRH/GH release from cancer (lung, pancreas)
115
ACROMEGALY | What is the clinical presentation of acromegaly?
- SOL = headache, hypopituitary, bitemporal hemianopia - Tissue overgrowth = coarse facies (prominent forehead), spade-like hands, increase shoe size, large tongue, prognathism + interdental spaces - Excessive sweating + oily skin due to GH causing sweat gland hypertrophy
116
ACROMEGALY What is the first-line investigation of acromegaly? What is the diagnostic investigation of acromegaly? What are some other investigations to consider?
- Insulin-like growth factor 1 levels (raised) - OGTT if IGF-1 raised (normally glucose suppresses GH levels, may show impaired glucose tolerance) - MRI head to visualise tumour - Ophthalmology referral for formal visual testing
117
ACROMEGALY | What are some potential complications of acromegaly?
- HTN, T2DM, cardiomyopathy, colorectal cancer (increased polyps) - OSA, osteoarthritis, carpal tunnel syndrome + MEN-1
118
ACROMEGALY What is the first-line management of acromegaly? What are some other options?
- Trans-spehnoidal surgery - Dopamine agonist (cabergoline) in mild disease, somatostatin analogue (octreotide) directly inhibits GH or GH receptor antagonist pegvisomant - Radiotherapy if surgery + medical therapy fails
119
SIADH | What is the pathophysiology of syndrome of inappropriate ADH (SIADH)?
- Euvolaemic hyponatraemia due to inappropriate ADH release causing water reabsorption from the kidneys + so low plasma osmolality but high urine osmolality with a high urinary sodium (conc urine)
120
SIADH | What are some causes of SIADH?
- Malignancy = paraneoplastic SCLC, pancreas, prostate - Neuro = CVA, SAH, SDH, meningitis, encephalitis, abscess - Infections = pneumonia, TB - Drugs = sulfonylureas, SSRIs, TCAs, carbamazepine
121
SIADH | What is the clinical presentation of SIADH?
- Headache, fatigue, muscle aches + cramps | - Severe hyponatraemia can cause seizures + reduced GCS
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SIADH | How is SIADH diagnosed?
- Hyponatraemia (U&E) - Concentrated urine (high urinary sodium >20mM + urine osmolality) - Low plasma osmolality in euvolaemic patient with no oedema or diuretics - Look for cause (CXR, CT CAP, CT/MRI head)
123
SIADH What is a key complication of SIADH? How does it occur? How does it present?
- Central pontine myelinolysis/osmotic demyelination syndrome - Complication of rapidly correcting severe hyponatraemia >10mmol/24h caused by water rapidly shifting out of brain cells to blood - Dysarthria, dysphagia, confusion, seizures, quadriparesis + locked-in syndrome
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SIADH | What is the management of SIADH?
- Treat underlying cause + fluid restrict 500–1000ml (slow correction) - ADH receptor antagonists like tolvaptan, demeclocycline
125
HYPERALDOSTERONISM | What are the two types of hyperaldosteronism?
- Primary = increased mineralocorticoid (aldosterone) secretion from adrenal cortex (zona glomerulosa) = Na+ retention, K+ loss - Secondary = excess renin due to reduced renal perfusion
126
HYPERALDOSTERONISM | What are the causes of primary and secondary hyperaldosteronism?
- Primary = #1 = bilateral adrenocortical hyperplasia, adrenal adenoma (Conn's syndrome) - Secondary = renal artery stenosis, heart failure
127
HYPERALDOSTERONISM What is the clinical presentation of hyperaldosteronism? What are some features you may see on routine investigations?
- HTN - Hypokalaemia = muscle weakness, hypotonia - U&E = high Na, low k - VBG = metabolic alkalosis - ECG = low K (flat T waves, U waves, prolonged PR + QT)
128
HYPERALDOSTERONISM | What is the first-line investigation in hyperaldosteronism?
- Plasma aldosterone/renin ratio - High aldosterone, low renin (ratio>20) = primary - Both high (ratio<20) = secondary
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HYPERALDOSTERONISM | If high aldosterone levels are found, how would you investigate for a cause in hyperaldosteronism?
- High-resolution CT abdomen and adrenal venous sampling (AVS = gold standard) - If CT ok = AVS can distinguish if unilateral adenoma or bilateral hyperplasia
130
HYPERALDOSTERONISM | What is the management of hyperaldosteronism?
- Conn's = laparoscopic adrenalectomy - Bilateral adrenocortical hyperplasia = aldosterone antagonist spironolactone - Renal artery stenosis = percutaneous renal artery angioplasty via femoral artery
131
DIABETES INSIPIDUS | What is the pathophysiology of diabetes insipidus?
- Either lack of ADH (cranial) or lack of response to ADH (nephrogenic) preventing the kidneys concentrating the urine so passage of excess dilute urine
132
DIABETES INSIPIDUS | What are the causes of cranial diabetes insipidus?
- Idiopathic - Post head-trauma - Pituitary tumours - Genetic (Wolfram's syndrome/DIDMOAD, haemochromatosis)
133
DIABETES INSIPIDUS | What are the causes of nephrogenic diabetes insipidus?
- Lithium (desensitises kidney's response to ADH), demeclocycline - CKD - Metabolic = high Ca2+, low K+ - Genetic (most affect ADH receptor, some affect aquaporin 2 channel)
134
DIABETES INSIPIDUS | What is the clinical presentation of diabetes insipidus?
- Polyuria (>3L of dilute urine in 24h), polydipsia + dehydration - Hypernatraemia = confusion, coma
135
DIABETES INSIPIDUS What investigations would you do in diabetes insipidus? What investigation is diagnostic?
- U&Es (high Na+), Ca2+, glucose, urine (low) and plasma (high) osmolality - Water deprivation test = diagnostic
136
DIABETES INSIPIDUS | What happens during water deprivation test?
- Restrict fluids for 8h then measure urine osmolality, give desmopressin + measure urine osmolality 8h later - Cranial = low after deprivation, high after ADH - Nephrogenic = low after both
137
DIABETES INSIPIDUS | What is the management of diabetes insipidus?
- Cranial = desmopressin (synthetic ADH analogue) - Nephrogenic = restrict salt/protein, thiazide (bendroflumethiazide) diuretics, NSAIDs as inhibits prostaglandins which inhibits ADH action
138
HYPERPARATHYROIDISM | What is the physiology of the parathyroid gland?
- Chief cells produce parathyroid hormone in response to hypocalcaemia - Increases Ca2+ via increased osteoclast activity, intestinal absorption, kidney reabsorption + vitamin D activity - Also causes decreased phosphate
139
HYPERPARATHYROIDISM What is the pathophysiology of primary hyperparathyroidism? What causes it? What is it associated with?
- Uncontrolled PTH production > hypercalcaemia - 80% solitary adenoma, 20% hyperplasia - HTN + MEN-I + MEN-IIa
140
HYPERPARATHYROIDISM What is the pathophysiology of secondary hyperparathyroidism? What causes it?
- Previous low Ca2+ leads to compensatory parathyroid gland hyperplasia as they respond to increased need for PTH - CKD (unable to activate vitamin D) or low vitamin D levels
141
HYPERPARATHYROIDISM What is the pathophysiology of tertiary hyperparathyroidism? What causes it?
- Prolonged secondary hyperparathyroidism leads to ongoing hyperplasia + so autonomous PTH secretion - Long standing renal disease
142
HYPERPARATHYROIDISM | What is the clinical presentation of hyperparathyroidism?
- Bones = bony pain - Stones = renal stones - Groans = abdo pain, N+V - Thrones = constipation or urinary frequency, increased thirst - Psychiatric moans = depression, confusion
143
HYPERPARATHYROIDISM | What investigations would you do in hyperparathyroidism and what would they show in primary, secondary and tertiary?
- PTH, Ca2+ + phosphate - Primary = high/normal PTH, high Ca2+, low phos (inappropriate response) - Secondary = high PTH, low/normal Ca2+, high phos (appropriate response) - Tertiary = high PTH/Ca2+, low/normal phos (inappropriate response) - Pepperpot skull may be seen on XR - DEXA scan for ?osteoporosis
144
HYPERPARATHYROIDISM What is the management of... i) primary? ii) secondary? iii) tertiary?
i) Parathyroidectomy, calcimimetics (cinacalcet) mimics action of Ca2+ on tissues if no surgery ii) Correct vitamin D deficiency (calcitriol, alfacalcidol) iii) Partial/total parathyroidectomy
145
HYPOPARATHYROIDISM | What are the three main types of hypoparathyroidism?
- Primary = decreased PTH secretion (thyroidectomy, DiGeorge syndrome with congenital abnormal PT gland development) - Pseudo = genetic failure of target organs to respond to normal levels of PTH - Pseudopseudo = features of pseudo but NORMAL biochemistry
146
HYPOPARATHYROIDISM | What is the clinical presentation of hypoparathyroidism?
Secondary to low Ca2+ (SPASMODIC-QT) – - Spasms - Perioral paraesthesia - Anxious - Seizures - Muscle tone increased - Orientation impaired - Dermatitis - Impetigo herpetiformis - Chvostek's sign (tap facial nerve = facial muscle spasm) - QT prolongation - Trousseau's (finger spasm if BP cuff inflated above systolic)
147
HYPOPARATHYROIDISM | What investigations would you do in hypoparathyroidism and what would they show in primary, pseudo and pseudopseudo?
- PTH, Ca2+, phosphate, Mg2+ (required for PTH secretion) - Primary = PTH/Ca2+ low, phos high (inappropriate response) - Pseudo = PTH high, Ca2+ low, phos high (appropriate response) - Pseudopseudo = all normal - XR hand as pseudo can lead to short 4th/5th metacarpals
148
HYPOPARATHYROIDISM | What is the management of hypoparathyroidism?
- Calcium + vitamin D (alfacalcidol) supplementation
149
HYPERPROLACTINAEMIA | What are the causes of hyperprolactinaemia?
- Ps = Physiological, Pregnancy, Prolactinoma, PCOS, Primary hypothyroidism - Dopamine antagonists e.g., metoclopramide, antipsychotics
150
HYPERPROLACTINAEMIA | What is the clinical presentation of hyperprolactinaemia?
- Women = amenorrhoea, infertility, galactorrhoea, osteoporosis - Men = impotence, loss of libido, galactorrhoea - Mass effects (macroadenoma) = headache, superior bitemporal hemianopia
151
HYPERPROLACTINAEMIA | What are some investigations for hyperprolactinaemia?
- Prolactin - TFTs - Pregnancy test - Visual fields examination - MRI head
152
HYPERPROLACTINAEMIA | What is the management of hyperprolactinaemia?
- First-line = dopamine agonists like bromocriptine, cabergoline - Second-line = trans-sphenoidal surgery
153
PITUITARY DISEASE | What are some causes of hypopituitarism?
- Kallmann's syndrome = GnRH deficiency + anosmia - Sheehan's syndrome = pituitary infarction after PPH - Pituitary apoplexy = enlarged pituitary due to infarction + haemorrhage - Infection (meningitis/TB) - Surgery or trauma
154
PITUITARY DISEASE | What is the management of hypopituitarism?
- Basal hormone tests ± dynamic pituitary function tests - MRI head - Hormone replacement
155
PITUITARY DISEASE | What are some causes of pituitary tumours?
- Pituitary adenoma #1 (microadenoma <10mm, macroadenoma >10mm) - Craniopharyngioma in children arising from Rathke's pouch
156
PITUITARY DISEASE | How might pituitary tumours present?
- Mass effects = superior bitemporal hemianopia (inferior chiasmal compression), CN3/4/5/6 palsy due to cavernous sinus pressure, headache - Endocrine = hyperprolactinaemia, acromegaly, Cushing's - Craniopharyngioma = growth failure, amenorrhoea, decreased libido, inferior bitemporal hemianopia (superior chiasmal compression)
157
PITUITARY DISEASE What are some investigations for pituitary tumours? What is the management?
- Visual fields, hormone levels/suppression tests, MRI head | - Trans-sphenoidal surgery
158
THYROID CANCER | What are the 5 main types of thyroid cancer?
- Papillary carcinoma #1 - Follicular adenoma - Follicular carcinoma - Medullary carcinoma - Anaplastic carcinoma
159
THYROID CANCER | What are some key features of papillary carcinoma?
- Young females with excellent prognosis - Follicular cells + Orphan Annie eyes on microscopy - Lymph node metastasis predominates
160
THYROID CANCER | What are some key features of follicular adenoma and carcinoma?
- Adenoma = solitary thyroid nodule | - Carcinoma = macroscopically encapsulated, microscopically capsular invasion, mostly vascular invasion
161
THYROID CANCER | What is the management of papillary and follicular carcinomas?
- Total thyroidectomy - Followed by radioiodine I-131 to kill residual cells - Yearly thyroglobulin levels to detect early recurrent disease
162
THYROID CANCER | What are some key features of medullary carcinoma?
- Arises from parafollicular C cells derived from neural crest + so serum calcitonin levels may be raised + this is used for detecting recurrence - Associated with lymphatic + haematogenous metastasis
163
THYROID CANCER | What are some key features of anaplastic carcinoma?
- Rare, aggressive + rapidly invasive | - Seen in elderly with poor prognosis
164
PHAEOCHROMOCYTOMA What is a phaeochromocytoma? What are some key characteristics
- Rare catecholamine secreting tumour - Rule of 10s: 10% bilateral, 10% malignant, 10% extra-adrenal, 10% familial and can be associated with MEN type II, neurofibromatosis + von Hippel-Lindau syndrome
165
PHAEOCHROMOCYTOMA | What is the clinical presentation of phaeochromocytoma?
- HTN, headaches + sweating = classic | - May have palpitations + anxiety
166
PHAEOCHROMOCYTOMA | What are the investigations for phaeochromocytoma?
- 24h urinary collection of metanephrines + plasma (replaced catecholamines) - CT chest, abdomen + pelvis
167
PHAEOCHROMOCYTOMA | What is the management of phaeochromocytoma?
- Initial medical stabilisation with alpha blocker (phenoxybenzamine) given BEFORE a beta-blocker (propranolol) then definitive surgical management
168
MULTIPLE ENDOCRINE NEOPLASIA What are the multiple endocrine neoplasia (MEN) conditions? What types are there?
- Autosomal dominant group of hormone producing tumours in endocrine organs - MEN type I (MEN1 gene), MEN type IIa and MEN type IIb (both RET oncogene)
169
MULTIPLE ENDOCRINE NEOPLASIA | What is the presentation of MEN type I?
3Ps – - Parathyroid = hyperparathyroidism due to hyperplasia - Pituitary - Pancreas = insulinoma, gastrinoma (recurrent peptic ulceration)
170
MULTIPLE ENDOCRINE NEOPLASIA | What is the presentation of MEN type IIa?
2Ps – - Parathyroid - Phaeochromocytoma - Medullary thyroid cancer majority
171
MULTIPLE ENDOCRINE NEOPLASIA | What is the presentation of MEN type IIb?
1P – - Phaeochromocytoma - Medullary thyroid cancer
172
``` MULTIPLE ENDOCRINE NEOPLASIA How does an insulinoma present? What are some expected findings on investigations? How is it diagnosed? How is it managed? ```
- Hypoglycaemia (early morning/pre-meal), rapid weight gain - High insulin, raised proinsulin:insulin ratio, high C-peptide - Supervised prolonged fasting (72h) + CT pancreas - Surgery or diazoxide + somatostatin if no surgery
173
HYPONATRAEMIA | How is the aetiology of hyponatraemia split?
Hypovolaemic – - Urinary Na >20mM = renal cause (diuretics, Addison's) - Urinary Na <20mM = extra-renal (D+V, burns, sweating) Euvolaemic – - Urinary Na >20mM = SIADH, hypothyroidism Hypervolaemic – - Urinary Na <20mM = oedema (cardiac/liver/renal failure, nephrotic syndrome, psychogenic polydipsia)
174
HYPONATRAEMIA What is the progressive clinical presentation of hyponatraemia? What are some complications?
- N+V, anorexia > headaches + confusion > seizures + coma - Untreated = cerebral oedema - Treated too quickly = central pontine myelinolysis
175
HYPONATRAEMIA | What investigations would you do in hyponatraemia
- U&E = Na 130–134 = mild, 120–129 = moderate, <120 = severe | - Urine/serum osmolality (2Na + urea + glucose), urinary sodium, TFTs
176
HYPONATRAEMIA | What is the management of hyponatraemia based on the cause?
- Hypovolaemic = rehydration with 0.9% NaCl slowly - Euvolaemic = fluid restrict 500–1000ml + trial ADH receptor antagonists - Hypervolaemic = fluid restrict 500–1000ml, ?loop diuretics, ?vaptans - Acute, severe or Sx = hypertonic saline (3% NaCl)
177
HYPERNATRAEMIA | What are the causes of hypernatraemia?
- Excess water loss = diabetes insipidus, DKA/HHS, D+V, sweating - Decreased thirst = old age + acute illness - Excessive hypertonic fluid = IVI, TPN + enteral feeds
178
HYPERNATRAEMIA | What is the clinical presentation and features of hypernatraemia?
- Lethargy, weakness, confusion, seizures + coma | - High urine osmolality = osmotic diuresis, low = diabetes insipidus
179
HYPERNATRAEMIA | What is the management of hypernatraemia?
- IV 5% dextrose slowly aim for ≤0.5mmol/h as rapid correction > cerebral oedema
180
HYPERCALCAEMIA | What are the two main causes of hypercalcaemia?
- Primary hyperparathyroidism (non-hospitalised) | - Malignancy (hospitalised) = bony mets, myeloma, PTHrP from squamous cell lung cancer
181
HYPERCALCAEMIA | What are some other causes of hypercalcaemia?
- Sarcoidosis - Vitamin D intoxication - Acromegaly - Thyrotoxicosis - Thiazides + dehydration - Addison's disease
182
HYPERCALCAEMIA | What is the clinical presentation of hypercalcaemia?
- Bones = bony pain - Stones = renal stones - Groans = abdo pain, N+V - Thrones = constipation or urinary frequency, increased thirst - Psychiatric moans = depression, confusion
183
HYPERCALCAEMIA | What investigations would you do in hypercalcaemia?
- U&Es, bone profile (Ca2+, phosphate, ALP), LFTs, PTH | - ECG = short QT interval
184
HYPERCALCAEMIA | What is the management of hypercalcaemia?
- Underlying cause management - IV 0.9% NaCl + then IV bisphosphonates to inhibit osteoclasts or calcitonin (faster) - Furosemide may be trialled but caution to not worsen + volume deplete
185
HYPOCALCAEMIA | What are some causes of hypocalcaemia?
- Vitamin D deficiency = malnutrition/malabsorption, CKD - Hypoparathyroidism - Hyperphosphataemia = tumour lysis, rhabdo - Hypomagnesaemia (magnesium needed for PTH release) - Acute pancreatitis
186
HYPOCALCAEMIA | What is the clinical presentation of hypocalcaemia?
SPASMODIC-QT – - Spasms - Perioral paraesthesia - Anxious - Seizures - Muscle tone increased - Orientation impaired - Dermatitis - Impetigo herpetiformis - Chvostek's sign (tap facial nerve = facial muscle spasm) - QT prolongation - Trousseau's (finger spasm if BP cuff inflated above systolic)
187
HYPOCALCAEMIA | What are some investigations for hypocalcaemia?
- ECG = prolonged QT | - Bloods = U&E, bone profile (calcium, phosphate, ALP), PTH, magnesium, vitamin D
188
HYPOCALCAEMIA | What is the management of hypocalcaemia?
- CKD = alfacalcidol, Mg2+ supplements if low - Mild = PO calcium supplements - Severe = 10ml 10% calcium gluconate IV with ECG monitoring
189
HYPOKALAEMIA | How can the causes of hypokalaemia be split?
With alkalosis – - Vomiting, thiazide/loop diuretics, Cushing's + Conn's With acidosis – - Diarrhoea, renal tubular acidosis, acetazolamide, partially treated DKA
190
HYPOKALAEMIA | What is the clinical presentation of hypokalaemia?
- Muscular function = weakness, hypotonia, hyporeflexia + cramps - Cardiac arrhythmias
191
HYPOKALAEMIA | What are some investigations for hypokalaemia?
- U&E = K 3.1–3.5 mild, 2.5–3 mod, <2.5 severe - Mg2+ - ECG = U have no pot + no T but a long PR + a depressed ST – U waves, small/absent T waves, prolonged PR, ST depression
192
HYPOKALAEMIA | What is the management of hypokalaemia?
- Mild = PO slow release KCl + regular U&Es - Severe/symptomatic/ECG changes – Continuous cardiac monitoring – Check + correct Mg2+ as causes renal K+ wasting – IV 1L 0.9% NaCl with 40mmol KCl with max rate 20mmol/h KCl (unless central line)
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