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Endocrinology Flashcards

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
Q

DKA

What are the diagnostic features of DKA?

A
  • Glucose >11mmol/L or known DM
  • pH <7.3
  • Bicarb <15mmol/L
  • Blood ketones >3.0mmol/L or urine ketones ++ on dipstick
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26
Q

DKA

What other investigations would you consider in DKA?

A
  • FBC, U&E, blood cultures + CXR for ?cause (infection)

- ECG = signs of hypokalaemia

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27
Q

DKA

What are some potential complications of DKA?

A
  • Cerebral oedema (especially in paeds)
  • VTE
  • Hypokalaemia > arrhythmias
  • AKI
  • Gastric stasis
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28
Q

DKA

What is the most important step in managing DKA?

A
  • Aggressive IV fluid resuscitation
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29
Q

DKA

How do you initially manage IV fluid resuscitation for DKA in paeds?

A
  • Shocked = 1st bolus 0.9% NaCl 20ml/kg, subsequent 10ml/kg over 15m
  • Not shocked = 0.9% NaCl 10ml/kg over 1h
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30
Q

DKA
How do you calculate the fluid requirement for DKA in paeds?
What do you give?

A
  • Deficit + maintenance ( – not shocked fluids) over 48h

- 0.9% NaCl with 20mmol KCl in 500ml

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31
Q

DKA
How do you calculate the fluids required to make up the deficit?
How do you quantify the deficit?

A
  • 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)
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32
Q

DKA
How quickly do you give the IV fluids required for DKA in paeds?
Why and what would you do if this happened?

A
  • Rehydrate slowly over 48h

- Risk of cerebral oedema (headache, altered GCS) > CT head, IV mannitol + hypertonic saline

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33
Q

DKA

How do you manage IV fluid resuscitation for DKA in adults?

A
  • 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
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34
Q

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?

A
  • 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
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35
Q

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?

A
  • 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
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36
Q

DKA

What parameters should be monitored during DKA?

A
  • Capillary glucose + ketones, obs + GCS hourly

- VBG at 2/4/8/12/24h

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37
Q

DKA
When is DKA considered resolved?
What do you do then?
What if it hasn’t resolved?

A
  • 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
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38
Q

HHS

What is the pathophysiology of hyperosmolar hyperglycaemic state (HHS)?

A
  • 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
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39
Q

HHS

What are some causes of HHS?

A
  • New T2DM
  • Infection
  • High dose steroids
  • Surgery
  • Impaired renal function
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40
Q

HHS

What is the clinical presentation of HHS?

A
  • Confusion/altered GCS
  • N+V
  • Dehydration
  • Fatigue
  • Shock
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41
Q

HHS
What is the diagnostic criteria for HHS?
What is the key parameter to monitor?

A
  • Severe hyperglycaemia ≥30mmol/L (but no significant ketonaemia or acidosis), hypotension, hyperosmolality >320mosmol/kg
  • Serum osmolarity = 2Na + glucose + urea
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42
Q

HHS

What are some potential complications of HHS?

A
  • Vascular = MI, stroke + peripheral arterial thrombosis
  • Central pontine myelinolysis if serum osmolarity declines too quickly
  • Fluid overload, cerebral oedema
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43
Q

HHS

What is the most important part of HHS management?

A
  • 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
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44
Q

HHS

What other aspects should be considered in HHS management?

A
  • Insulin at 0.05units/kg/h only if ketones >1mmol/L or glucose fails to fall
  • VTE prophylaxis in most patients
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45
Q

HYPOGLYCAEMIA
What is hypoglycaemia?
What are some causes?

A
  • Blood glucose <4.0mmol/L

- Drugs (insulin, sulfonylureas), sepsis, insulinoma, adrenal insufficiency

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46
Q

HYPOGLYCAEMIA

What is the clinical presentation of hypoglycaemia?

A
  • Sweating/shaking
  • Hunger
  • Nausea
  • Confusion, convulsions, coma
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47
Q

HYPOGLYCAEMIA
What investigations might you consider to work out whether this could be endogenous production or exogenous administration?

A
  • Measure serum insulin, C-peptide + proinsulin
  • All high = endogenous production
  • High insulin but low C-peptide + proinsulin = exogenous administration
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48
Q

HYPOGLYCAEMIA

What is the management of hypoglycaemia in a patient who is conscious and able to swallow?

A
  • 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
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49
Q

HYPOGLYCAEMIA

What is the management of hypoglycaemia in a patient who is unconscious or unable to swallow?

A
  • 200ml 10% dextrose IV

- 1mg glucagon IM if no IV access

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50
Q

DIABETIC COMPLICATIONS

What are the potential complications of diabetes?

A
  • Neuropathy = peripheral, gastroparesis, autonomic
  • Microvascular = nephropathy, retinopathy
  • Macrovascular = MI, stroke, PVD
  • Diabetic foot disease
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51
Q

DIABETIC COMPLICATIONS

What is the presentation of peripheral neuropathy?

A
  • 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
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52
Q

DIABETIC COMPLICATIONS

What is the management of peripheral neuropathy?

A
  • First-line = amitriptyline, duloxetine, gabapentin or pregabalin
  • Pain management clinics may be useful if resistant problems
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53
Q

DIABETIC COMPLICATIONS
What causes gastroparesis?
How does it present?

A
  • (Vagus) nerve damage to autonomic nervous system

- Delayed gastric emptying, bloating, offensive gas + vomiting

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54
Q

DIABETIC COMPLICATIONS

What is the management of gastroparesis?

A
  • Prokinetics like metoclopramide, domperidone

- Abx like erythromycin to tackle bacterial overgrowth

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55
Q

DIABETIC COMPLICATIONS
What is the presentation of autonomic neuropathy?
What is the conservative management?
What is the medical management?

A
  • 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
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56
Q

DIABETIC COMPLICATIONS
What is diabetic nephropathy?
How is it identified?

A
  • 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
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57
Q

DIABETIC COMPLICATIONS
What is the conservative management of diabetic nephropathy?
What is the medical management of diabetic nephropathy?

A
  • Dietary protein restriction, tight glycaemic control, BP <130/80mmHg
  • ACEi/ARB if urinary ACR ≥3mg/mmol
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58
Q

DIABETIC COMPLICATIONS

What is the pathophysiology of diabetic retinopathy?

A
  • 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
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59
Q

DIABETIC COMPLICATIONS

What are the three main types of diabetic retinopathy?

A
  • Non-proliferative diabetic retinopathy (NPDR)
  • Proliferative diabetic retinopathy (PDR)
  • Diabetic maculopathy
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60
Q

DIABETIC COMPLICATIONS

How is NPDR sub-categorised?

A
  • 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
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61
Q

DIABETIC COMPLICATIONS

What is proliferative diabetic retinopathy?

A
  • Retinal neovascularisation (on retina or optic disc) ± vitreous/pre-retinal haemorrhage
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62
Q

DIABETIC COMPLICATIONS

What is diabetic maculopathy?

A
  • Macular oedema (+ hard exudates) caused by leakage of vessels close to macula which can significantly threaten vision + needs urgent treatment
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63
Q

DIABETIC COMPLICATIONS
What is the management of…

i) NPDR?
ii) PDR?
iii) maculopathy?

A

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)

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64
Q

HYPERTHYROIDISM

What are the causes of hyperthyroidism?

A
  • 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)
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65
Q

HYPERTHYROIDISM

What generic symptoms would you expect in hyperthyroidism?

A
  • 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
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66
Q

HYPERTHYROIDISM

What are some generic signs in hyperthyroidism?

A
  • Nodules on thyroid gland
  • Irregular pulse (AF)
  • Thin hair
  • Warm skin
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67
Q

HYPERTHYROIDISM

What are some Graves’ disease specific signs?

A
  • Thyroid eye disease (exophthalmos, ophthalmoplegia, lid lag + retraction)
  • Diffuse goitre without nodules
  • Thyroid acropachy
  • Pretibial myxoedema
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68
Q

HYPERTHYROIDISM
What is…

i) thyroid acropachy?
ii) pretibial myxoedema?

A

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

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69
Q

HYPERTHYROIDISM

What is the clinical presentation of De Quervain’s thyroiditis?

A
  • Post-viral infection where initially hyperthyroid with painful goitre + raised ESR
  • Euthyroid > hypothyroid (longer phase than hyper)
  • Eventually thyroid structure + function normalises
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70
Q

HYPERTHYROIDISM

What are some important investigations in suspected hyperthyroidism?

A
  • 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
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71
Q

HYPERTHYROIDISM

What patterns of hyperthyroidism might you see on TFTs?

A
  • Primary = low TSH, high T3/4
  • Secondary = high TSH, high T3/4 (hypothalamus or pituitary pathology)
  • Subclinical = low TSH, normal T3/4
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72
Q

HYPERTHYROIDISM

What patterns of hyperthyroidism might you see on thyroid scintigraphy?

A
  • Patchy uptake = toxic multinodular goitre
  • Globally reduce uptake = De Quervain’s
  • Homogenous uptake = Grave’s disease
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73
Q

HYPERTHYROIDISM
What is an important complication in hyperthyroidism and what can cause it?
How does it present?

A
  • 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
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74
Q

HYPERTHYROIDISM

What is the management of thyrotoxicosis?

A
  • IV propranolol (digoxin if fails or C/I e.g., asthma)
  • Propylthiouracil NG followed by Lugol’s iodine 6h later
  • High dose corticosteroids
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75
Q

HYPERTHYROIDISM

What are the main management options for hyperthyroidism?

A
  • 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
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76
Q

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?

A
  • Carbimazole – agranulocytosis + not used in first trimester
  • Propylthiouracil – small risk of severe hepatic reactions
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77
Q

HYPERTHYROIDISM
What are the indications for radioiodine therapy?
What are some side effects?
What are some contraindications?

A
  • Toxic multinodular goitre + adenomas treatment of choice
  • Hypothyroidism (needs levothyroxine)
  • Pregnancy, breast feeding, <16y + thyroid eye disease (may worsen)
78
Q

HYPERTHYROIDISM
What are the indications for thyroidectomy?
What are some side effects of this procedure?

A
  • Recurrence, obstructing goitres + ?cancers

- Risk to recurrent laryngeal nerve (hoarse voice), hypothyroidism (needs levothyroxine) + hypoparathyroidism

79
Q

HYPERTHYROIDISM

What is the management of thyroid eye disease?

A
  • 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
Q

HYPERTHYROIDISM

What is the management of De Quervain’s thyroiditis?

A
  • Self-limiting with NSAIDs for pain

- Beta-blockers for Sx

81
Q

DIABETIC COMPLICATIONS

Why does diabetic foot disease occur?

A
  • Neuropathy = loss of protective sensation, Charcot’s arthropathy
  • Peripheral arterial disease = macro + microvascular ischaemia
82
Q

DIABETIC COMPLICATIONS

What are some complications of diabetic foot disease?

A
  • Calluses
  • Cellulitis, osteomyelitis + gangrene
  • Charcot’s joint/arthropathy
83
Q

DIABETIC COMPLICATIONS

How does Charcots’ arthropathy present?

A
  • 6Ds = Destruction, Deformity, Degeneration, Dislocation, Dense bones + Debris
  • Classically tarsometatarsal joints
  • Joint may be swollen, red + warm
  • Loss of mid-foot arch
84
Q

DIABETIC COMPLICATIONS

What is the management of diabetic foot disease?

A
  • Annual diabetic foot review with ischaemic (dorsalis pedis + posterior tibial artery pulses) + neuropathy (10g monofilament) screening
85
Q

HYPOTHYROIDISM

What are the causes of hypothyroidism?

A
  • 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
Q

HYPOTHYROIDISM
What are some iatrogenic/drug causes of hypothyroidism?
What are some central causes of hypothyroidism?

A
  • Carbimazole, amiodarone, lithium, thyroidectomy

- Pituitary tumours, infection, radiation + Sheehan’s syndrome

87
Q

HYPOTHYROIDISM

What are some symptoms of hypothyroidism?

A
  • General = weight gain, decreased appetite, constipation + cold intolerance
  • Gynae = menorrhagia
88
Q

HYPOTHYROIDISM

What are some signs of hypothyroidism?

A

BRADYCARDIC –

  • Bradycardia
  • Reflexes relax slowly
  • Ataxia
  • Dry thin hair/skin
  • Yawning
  • Cold hands
  • Ascites
  • Round puffy face
  • Defeated demeanour
  • Immobile
  • CCF
89
Q

HYPOTHYROIDISM

What are some investigations for hypothyroidism?

A
  • TFTs

- Thyroid antibodies = thyroid peroxidase Ab (TPO), anti-thyroglobulin (Hashimoto’s) + anti-TSH receptor

90
Q

HYPOTHYROIDISM

What are some patterns of hypothyroidism seen on TFTs?

A
  • 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
Q

HYPOTHYROIDISM
What is a complication of hypothyroidism?
How does it present?
How is it managed?

A
  • Myxoedema coma
  • Confusion + hypothermia
  • IV thyroid replacement, IV corticosteroids (avoid precipitating Addisonian crisis) + IV fluids
92
Q

HYPOTHYROIDISM
What is the management of hypothyroidism?
What are the key patient information points for it?
What are the side effects?

A
  • 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
Q

HYPOTHYROIDISM

What is the management of subclinical hypothyroidism?

A
  • 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
Q

ADRENAL INSUFFICIENCY

What are the three types of adrenal insufficiency and their respective pathophysiology?

A
  • 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
Q

ADRENAL INSUFFICIENCY

What are the causes of primary adrenal insufficiency (Addison’s disease)?

A
  • # 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
Q

ADRENAL INSUFFICIENCY
What are the causes of…

i) secondary adrenal insufficiency?
ii) tertiary adrenal insufficiency?

A

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
Q

ADRENAL INSUFFICIENCY

What is the clinical presentation of adrenal insufficiency?

A
  • “Thin, tanned, tired + tearful”
  • Weight loss, N+V, fatigue + weakness
  • Postural hypotension
  • Skin hyperpigmentation (primary only as ACTH stimulates melanocytes > melanin)
98
Q

ADRENAL INSUFFICIENCY
What investigations would you do in suspected adrenal insufficiency?
What investigation is diagnostic?

A
  • 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
Q

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?

A

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
Q

ADRENAL INSUFFICIENCY

How would you manage the early morning cortisol results?

A
  • > 500nmol/L = unlikely Addison’s
  • 100–500nmol/L = short synacthen test
  • <100nmol/L = abnormal
101
Q

ADRENAL INSUFFICIENCY
What is a key complication of adrenal insufficiency?
How does it present?
What causes it?

A
  • Addisonian crisis
  • Reduced GCS, pyrexia + shock
  • Sepsis, surgery, adrenal haemorrhage, steroid withdrawal
102
Q

ADRENAL INSUFFICIENCY

How do you manage an Addisonian crisis?

A
  • Hydrocortisone 100mg IM/IV, no fludrocortisone needed
  • Aggressive fluid resus
  • May need glucose if hypoglycaemic
103
Q

ADRENAL INSUFFICIENCY

What is the medical management of adrenal insufficiency?

A
  • Hydrocortisone (glucocorticoid) with majority given in the first half of the day
  • Fludrocortisone (mineralocorticoid)
104
Q

ADRENAL INSUFFICIENCY

What is the general management of adrenal insufficiency?

A
  • MedicAlert bracelets + steroid cards
  • Emphasise importance of hydrocortisone doses
  • Acute illness = double hydrocortisone dose or use IM kit, fludrocortisone dose stays the same
105
Q

CUSHING’S SYNDROME
What is Cushing’s syndrome?
How are the aetiologies categorised?

A
  • Disorder of glucocorticoid (cortisol) excess
  • ACTH-dependent causes
  • ACTH-independent causes
  • Pseudo-Cushing’s
106
Q

CUSHING’S SYNDROME

What are some ACTH dependent causes of Cushing’s?

A
  • Cushing’s disease #1 = pituitary adenoma secreting ACTH > adrenal hyperplasia
  • Ectopic ACTH usually paraneoplastic SCLC
107
Q

CUSHING’S SYNDROME

What are some ACTH independent causes of Cushing’s?

A
  • Exogenous steroids

- Adrenal adenoma or carcinoma

108
Q

CUSHING’S SYNDROME
What causes pseudo-Cushing’s?
How is it diagnosed?

A
  • Alcohol excess or severe depression

- False positive dexamethasone suppression test or 24h urinary free cortisol so insulin stress test

109
Q

CUSHING’S SYNDROME

What is the clinical presentation of Cushing’s?

A
  • 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
Q

CUSHING’S SYNDROME

How would you investigate Cushing’s initially?

A
  • Diagnostic = overnight dexamethasone suppression test (low cortisol = normal, high/normal cortisol = cushing’s)
  • 24h urinary free cortisol
111
Q

CUSHING’S SYNDROME

After the initial investigations for Cushing’s, how would you localise the cause?

A
  • 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
112
Q

CUSHING’S SYNDROME

What other investigations would you consider in Cushing’s?

A
  • Petrous sinus sampling of ACTH to differentiate between pituitary + Ectopic ACTH secretion
  • CT chest/abdo + MRI pituitary if ?tumour
113
Q

CUSHING’S SYNDROME

What is the management of Cushing’s syndrome?

A
  • 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
Q

ACROMEGALY
What is the pathophysiology of acromegaly?
What are some causes?

A
  • 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
Q

ACROMEGALY

What is the clinical presentation of acromegaly?

A
  • 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
Q

ACROMEGALY
What is the first-line investigation of acromegaly?
What is the diagnostic investigation of acromegaly?
What are some other investigations to consider?

A
  • 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
Q

ACROMEGALY

What are some potential complications of acromegaly?

A
  • HTN, T2DM, cardiomyopathy, colorectal cancer (increased polyps)
  • OSA, osteoarthritis, carpal tunnel syndrome + MEN-1
118
Q

ACROMEGALY
What is the first-line management of acromegaly?
What are some other options?

A
  • 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
Q

SIADH

What is the pathophysiology of syndrome of inappropriate ADH (SIADH)?

A
  • 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
Q

SIADH

What are some causes of SIADH?

A
  • Malignancy = paraneoplastic SCLC, pancreas, prostate
  • Neuro = CVA, SAH, SDH, meningitis, encephalitis, abscess
  • Infections = pneumonia, TB
  • Drugs = sulfonylureas, SSRIs, TCAs, carbamazepine
121
Q

SIADH

What is the clinical presentation of SIADH?

A
  • Headache, fatigue, muscle aches + cramps

- Severe hyponatraemia can cause seizures + reduced GCS

122
Q

SIADH

How is SIADH diagnosed?

A
  • 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
Q

SIADH
What is a key complication of SIADH?
How does it occur?
How does it present?

A
  • 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
124
Q

SIADH

What is the management of SIADH?

A
  • Treat underlying cause + fluid restrict 500–1000ml (slow correction)
  • ADH receptor antagonists like tolvaptan, demeclocycline
125
Q

HYPERALDOSTERONISM

What are the two types of hyperaldosteronism?

A
  • Primary = increased mineralocorticoid (aldosterone) secretion from adrenal cortex (zona glomerulosa) = Na+ retention, K+ loss
  • Secondary = excess renin due to reduced renal perfusion
126
Q

HYPERALDOSTERONISM

What are the causes of primary and secondary hyperaldosteronism?

A
  • Primary = #1 = bilateral adrenocortical hyperplasia, adrenal adenoma (Conn’s syndrome)
  • Secondary = renal artery stenosis, heart failure
127
Q

HYPERALDOSTERONISM
What is the clinical presentation of hyperaldosteronism?
What are some features you may see on routine investigations?

A
  • 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
Q

HYPERALDOSTERONISM

What is the first-line investigation in hyperaldosteronism?

A
  • Plasma aldosterone/renin ratio
  • High aldosterone, low renin (ratio>20) = primary
  • Both high (ratio<20) = secondary
129
Q

HYPERALDOSTERONISM

If high aldosterone levels are found, how would you investigate for a cause in hyperaldosteronism?

A
  • High-resolution CT abdomen and adrenal venous sampling (AVS = gold standard)
  • If CT ok = AVS can distinguish if unilateral adenoma or bilateral hyperplasia
130
Q

HYPERALDOSTERONISM

What is the management of hyperaldosteronism?

A
  • Conn’s = laparoscopic adrenalectomy
  • Bilateral adrenocortical hyperplasia = aldosterone antagonist spironolactone
  • Renal artery stenosis = percutaneous renal artery angioplasty via femoral artery
131
Q

DIABETES INSIPIDUS

What is the pathophysiology of diabetes insipidus?

A
  • 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
Q

DIABETES INSIPIDUS

What are the causes of cranial diabetes insipidus?

A
  • Idiopathic
  • Post head-trauma
  • Pituitary tumours
  • Genetic (Wolfram’s syndrome/DIDMOAD, haemochromatosis)
133
Q

DIABETES INSIPIDUS

What are the causes of nephrogenic diabetes insipidus?

A
  • 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
Q

DIABETES INSIPIDUS

What is the clinical presentation of diabetes insipidus?

A
  • Polyuria (>3L of dilute urine in 24h), polydipsia + dehydration
  • Hypernatraemia = confusion, coma
135
Q

DIABETES INSIPIDUS
What investigations would you do in diabetes insipidus?
What investigation is diagnostic?

A
  • U&Es (high Na+), Ca2+, glucose, urine (low) and plasma (high) osmolality
  • Water deprivation test = diagnostic
136
Q

DIABETES INSIPIDUS

What happens during water deprivation test?

A
  • 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
Q

DIABETES INSIPIDUS

What is the management of diabetes insipidus?

A
  • Cranial = desmopressin (synthetic ADH analogue)
  • Nephrogenic = restrict salt/protein, thiazide (bendroflumethiazide) diuretics, NSAIDs as inhibits prostaglandins which inhibits ADH action
138
Q

HYPERPARATHYROIDISM

What is the physiology of the parathyroid gland?

A
  • 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
Q

HYPERPARATHYROIDISM
What is the pathophysiology of primary hyperparathyroidism?
What causes it?
What is it associated with?

A
  • Uncontrolled PTH production > hypercalcaemia
  • 80% solitary adenoma, 20% hyperplasia
  • HTN + MEN-I + MEN-IIa
140
Q

HYPERPARATHYROIDISM
What is the pathophysiology of secondary hyperparathyroidism?
What causes it?

A
  • 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
Q

HYPERPARATHYROIDISM
What is the pathophysiology of tertiary hyperparathyroidism?
What causes it?

A
  • Prolonged secondary hyperparathyroidism leads to ongoing hyperplasia + so autonomous PTH secretion
  • Long standing renal disease
142
Q

HYPERPARATHYROIDISM

What is the clinical presentation of hyperparathyroidism?

A
  • Bones = bony pain
  • Stones = renal stones
  • Groans = abdo pain, N+V
  • Thrones = constipation or urinary frequency, increased thirst
  • Psychiatric moans = depression, confusion
143
Q

HYPERPARATHYROIDISM

What investigations would you do in hyperparathyroidism and what would they show in primary, secondary and tertiary?

A
  • 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
Q

HYPERPARATHYROIDISM
What is the management of…

i) primary?
ii) secondary?
iii) tertiary?

A

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
Q

HYPOPARATHYROIDISM

What are the three main types of hypoparathyroidism?

A
  • 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
Q

HYPOPARATHYROIDISM

What is the clinical presentation of hypoparathyroidism?

A

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
Q

HYPOPARATHYROIDISM

What investigations would you do in hypoparathyroidism and what would they show in primary, pseudo and pseudopseudo?

A
  • 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
Q

HYPOPARATHYROIDISM

What is the management of hypoparathyroidism?

A
  • Calcium + vitamin D (alfacalcidol) supplementation
149
Q

HYPERPROLACTINAEMIA

What are the causes of hyperprolactinaemia?

A
  • Ps = Physiological, Pregnancy, Prolactinoma, PCOS, Primary hypothyroidism
  • Dopamine antagonists e.g., metoclopramide, antipsychotics
150
Q

HYPERPROLACTINAEMIA

What is the clinical presentation of hyperprolactinaemia?

A
  • Women = amenorrhoea, infertility, galactorrhoea, osteoporosis
  • Men = impotence, loss of libido, galactorrhoea
  • Mass effects (macroadenoma) = headache, superior bitemporal hemianopia
151
Q

HYPERPROLACTINAEMIA

What are some investigations for hyperprolactinaemia?

A
  • Prolactin
  • TFTs
  • Pregnancy test
  • Visual fields examination
  • MRI head
152
Q

HYPERPROLACTINAEMIA

What is the management of hyperprolactinaemia?

A
  • First-line = dopamine agonists like bromocriptine, cabergoline
  • Second-line = trans-sphenoidal surgery
153
Q

PITUITARY DISEASE

What are some causes of hypopituitarism?

A
  • 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
Q

PITUITARY DISEASE

What is the management of hypopituitarism?

A
  • Basal hormone tests ± dynamic pituitary function tests
  • MRI head
  • Hormone replacement
155
Q

PITUITARY DISEASE

What are some causes of pituitary tumours?

A
  • Pituitary adenoma #1 (microadenoma <10mm, macroadenoma >10mm)
  • Craniopharyngioma in children arising from Rathke’s pouch
156
Q

PITUITARY DISEASE

How might pituitary tumours present?

A
  • 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
Q

PITUITARY DISEASE
What are some investigations for pituitary tumours?
What is the management?

A
  • Visual fields, hormone levels/suppression tests, MRI head

- Trans-sphenoidal surgery

158
Q

THYROID CANCER

What are the 5 main types of thyroid cancer?

A
  • Papillary carcinoma #1
  • Follicular adenoma
  • Follicular carcinoma
  • Medullary carcinoma
  • Anaplastic carcinoma
159
Q

THYROID CANCER

What are some key features of papillary carcinoma?

A
  • Young females with excellent prognosis
  • Follicular cells + Orphan Annie eyes on microscopy
  • Lymph node metastasis predominates
160
Q

THYROID CANCER

What are some key features of follicular adenoma and carcinoma?

A
  • Adenoma = solitary thyroid nodule

- Carcinoma = macroscopically encapsulated, microscopically capsular invasion, mostly vascular invasion

161
Q

THYROID CANCER

What is the management of papillary and follicular carcinomas?

A
  • Total thyroidectomy
  • Followed by radioiodine I-131 to kill residual cells
  • Yearly thyroglobulin levels to detect early recurrent disease
162
Q

THYROID CANCER

What are some key features of medullary carcinoma?

A
  • 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
Q

THYROID CANCER

What are some key features of anaplastic carcinoma?

A
  • Rare, aggressive + rapidly invasive

- Seen in elderly with poor prognosis

164
Q

PHAEOCHROMOCYTOMA
What is a phaeochromocytoma?
What are some key characteristics

A
  • 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
Q

PHAEOCHROMOCYTOMA

What is the clinical presentation of phaeochromocytoma?

A
  • HTN, headaches + sweating = classic

- May have palpitations + anxiety

166
Q

PHAEOCHROMOCYTOMA

What are the investigations for phaeochromocytoma?

A
  • 24h urinary collection of metanephrines + plasma (replaced catecholamines)
  • CT chest, abdomen + pelvis
167
Q

PHAEOCHROMOCYTOMA

What is the management of phaeochromocytoma?

A
  • Initial medical stabilisation with alpha blocker (phenoxybenzamine) given BEFORE a beta-blocker (propranolol) then definitive surgical management
168
Q

MULTIPLE ENDOCRINE NEOPLASIA
What are the multiple endocrine neoplasia (MEN) conditions?
What types are there?

A
  • 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
Q

MULTIPLE ENDOCRINE NEOPLASIA

What is the presentation of MEN type I?

A

3Ps –

  • Parathyroid = hyperparathyroidism due to hyperplasia
  • Pituitary
  • Pancreas = insulinoma, gastrinoma (recurrent peptic ulceration)
170
Q

MULTIPLE ENDOCRINE NEOPLASIA

What is the presentation of MEN type IIa?

A

2Ps –

  • Parathyroid
  • Phaeochromocytoma
  • Medullary thyroid cancer majority
171
Q

MULTIPLE ENDOCRINE NEOPLASIA

What is the presentation of MEN type IIb?

A

1P –

  • Phaeochromocytoma
  • Medullary thyroid cancer
172
Q 
MULTIPLE ENDOCRINE NEOPLASIA
How does an insulinoma present?
What are some expected findings on investigations?
How is it diagnosed?
How is it managed?
A
  • 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
Q

HYPONATRAEMIA

How is the aetiology of hyponatraemia split?

A

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
Q

HYPONATRAEMIA
What is the progressive clinical presentation of hyponatraemia?
What are some complications?

A
  • N+V, anorexia > headaches + confusion > seizures + coma
  • Untreated = cerebral oedema
  • Treated too quickly = central pontine myelinolysis
175
Q

HYPONATRAEMIA

What investigations would you do in hyponatraemia

A
  • U&E = Na 130–134 = mild, 120–129 = moderate, <120 = severe

- Urine/serum osmolality (2Na + urea + glucose), urinary sodium, TFTs

176
Q

HYPONATRAEMIA

What is the management of hyponatraemia based on the cause?

A
  • 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
Q

HYPERNATRAEMIA

What are the causes of hypernatraemia?

A
  • Excess water loss = diabetes insipidus, DKA/HHS, D+V, sweating
  • Decreased thirst = old age + acute illness
  • Excessive hypertonic fluid = IVI, TPN + enteral feeds
178
Q

HYPERNATRAEMIA

What is the clinical presentation and features of hypernatraemia?

A
  • Lethargy, weakness, confusion, seizures + coma

- High urine osmolality = osmotic diuresis, low = diabetes insipidus

179
Q

HYPERNATRAEMIA

What is the management of hypernatraemia?

A
  • IV 5% dextrose slowly aim for ≤0.5mmol/h as rapid correction > cerebral oedema
180
Q

HYPERCALCAEMIA

What are the two main causes of hypercalcaemia?

A
  • Primary hyperparathyroidism (non-hospitalised)

- Malignancy (hospitalised) = bony mets, myeloma, PTHrP from squamous cell lung cancer

181
Q

HYPERCALCAEMIA

What are some other causes of hypercalcaemia?

A
  • Sarcoidosis
  • Vitamin D intoxication
  • Acromegaly
  • Thyrotoxicosis
  • Thiazides + dehydration
  • Addison’s disease
182
Q

HYPERCALCAEMIA

What is the clinical presentation of hypercalcaemia?

A
  • Bones = bony pain
  • Stones = renal stones
  • Groans = abdo pain, N+V
  • Thrones = constipation or urinary frequency, increased thirst
  • Psychiatric moans = depression, confusion
183
Q

HYPERCALCAEMIA

What investigations would you do in hypercalcaemia?

A
  • U&Es, bone profile (Ca2+, phosphate, ALP), LFTs, PTH

- ECG = short QT interval

184
Q

HYPERCALCAEMIA

What is the management of hypercalcaemia?

A
  • 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
Q

HYPOCALCAEMIA

What are some causes of hypocalcaemia?

A
  • Vitamin D deficiency = malnutrition/malabsorption, CKD
  • Hypoparathyroidism
  • Hyperphosphataemia = tumour lysis, rhabdo
  • Hypomagnesaemia (magnesium needed for PTH release)
  • Acute pancreatitis
186
Q

HYPOCALCAEMIA

What is the clinical presentation of hypocalcaemia?

A

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
Q

HYPOCALCAEMIA

What are some investigations for hypocalcaemia?

A
  • ECG = prolonged QT

- Bloods = U&E, bone profile (calcium, phosphate, ALP), PTH, magnesium, vitamin D

188
Q

HYPOCALCAEMIA

What is the management of hypocalcaemia?

A
  • CKD = alfacalcidol, Mg2+ supplements if low
  • Mild = PO calcium supplements
  • Severe = 10ml 10% calcium gluconate IV with ECG monitoring
189
Q

HYPOKALAEMIA

How can the causes of hypokalaemia be split?

A

With alkalosis –
- Vomiting, thiazide/loop diuretics, Cushing’s + Conn’s
With acidosis –
- Diarrhoea, renal tubular acidosis, acetazolamide, partially treated DKA

190
Q

HYPOKALAEMIA

What is the clinical presentation of hypokalaemia?

A
  • Muscular function = weakness, hypotonia, hyporeflexia + cramps
  • Cardiac arrhythmias
191
Q

HYPOKALAEMIA

What are some investigations for hypokalaemia?

A
  • 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
Q

HYPOKALAEMIA

What is the management of hypokalaemia?

A
  • 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)

FINALS (20 decks)

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