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Imperial Medicine Year 3 > Endocrinology AS > Flashcards

Endocrinology AS Flashcards

1
Q

Diabetes Mellitus definition

A

Multisystem disorder due to an absolute or relative lack of endogenous insulin –> Metabolic and vascular complications

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2
Q

Type 1 DM

A

T1DM

  • Pathology: autoimmune destruction of B-cells –> absolute insulin deficiency
  • Age: usually starts before puberty
  • Presentation: Polyuria, polydipsia, decreased weight, DKA.
  • Genetics: concordance only 30% in MZ
  • Association: HLA-D3 and D4, other AI disease
  • Abs: Anti-islet, anti-GAD
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3
Q

T2DM?

A

Pathology: Insulin resistance and B-cell dysfunction –> relative insulin deficiency
Age: Usually older patients
Presentation: polyuria, polydipsia, complications
Genetics: concordance 80% in MZs
Associated: Obesity, decreased exercise, calorie and ETOH excess

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4
Q

Diagnosis of symptomatic diabetes?

A

Symptomatic - Polyuria, polydipsia, decreased weight, lethargy.
Need 1 test
- Increased plasma venous glucose detected once!
- Fasting >7mm
- Random >11.1
- 2 hr Plasma glucose >11.1 2hr after ingestion of glucose during OGTT (need to check with blood)
- HbA1c >48 mmol/ >6.5

Beware that sickle cell anaemia and other haemoglobinopathies can give falsely low HbA1c readings due to decreased lifespan of RBCs.

Sickle cell, G6PD, hereditary is low.

Vit B12, folic acid and iron deficiency anaemia, splenectomy give higher readings due to higher red blood cell lifespan.

Consider measuring C-peptide after initial presentation if there is difficuly distinguishing type 1 from others. C-peptide is low in T1DM. Normal or high in Type 2

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5
Q

Diagnosis of Asymptomatic diabetes?

A

in an asymptomatic person, the diagnosis of diabetes should never be based on a single abnormal HbA1c or fasting plasma glucose level; at least one additional abnormal HbA1c or plasma glucose level is essential. If the second test results are normal, it is prudent to arrange regular review of the person.

  • Increased venous glucose on 2 separate occasions.
  • Or 2h OGTT >11.1 mM
  • 2 Separate HbA1c readings.
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6
Q

What is a OGTT?

A
  • Only needed if borderline fasting or random glucose measurements
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7
Q

What is normal fasting glucose?

A

<6.1 (<41)

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8
Q

What is impaired fasting glucose defined as?

A
  1. 1-6.9 fasting (42-47)

- These patients should be recommended diet and exercise.

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9
Q

What is diabetes defined as on fasting glucose?

A

> 7 (>48)

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10
Q

What is normal in a 75g OGTT?

A

<7.8

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11
Q

What is impaired glucose tolerance

A

7.8-11

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12
Q

What is diabetes on OGTT?

A

> 11.1

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13
Q

What are secondary drug causes of DM?

A

Drugs: Steroids, anti-HIV, atypical neuroleptics, thiazides

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14
Q

what are secondary pancreatic causes of DM?

A

CF, chronic pancreatitis, HH, pancreatic Ca

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15
Q

What are secondary endo causes of DM?

A

Phaeo, Cushings (increases blood sugar), Acromegaly, hyperthyroidism

Other: glycogen storage

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16
Q

What is metabolic syndrome?

A
  • Central obesity (increased weight circumference >102 in men, 88 women
  • Triglycerides 150mg/dl
  • HDL-cholesterol <40mg/dL in men and <50 mg/dl in women
  • HTN: BP 130/85
  • DM, IGT, IFG
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17
Q

Conservative management of diabetes?

A
  • MDT

GP, endorinologist, surgeons, specialist nurses, dieticians, chiropodists, fellow patients (education groups)

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18
Q

The 4Cs of diabetes monitoring?

A 
Control - glycaemic 
- Record of coplications: DKA, HONK, Hypos 
- Capillary blood glucose 
Fasting: 4.5-6.5mM
2h post prandial: 4.5-9mM
  • HbA1C
    Reflects exposure over last 6-8 weeks
    Aim <45-50mM (7.5-8%)

BP, lipids

Complications 
- Macro 
Pulses, BP, cardiac auscultation 
- Micro
Fundoscopy, ACR+U&Es, Sensory testing plus foot inspection

Competency

  • With insulin injections
  • Checking injection sites
  • BM monitoring

Coping

  • Psychosocial e.g depression
  • Occupation
  • Domestic
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19
Q

Lifestyle modifications for Diabetes Mellitus?

A 
DELAYS 
- Diet 
Same as that considered healthy for everyone 
Decreased total calorie intake
decreased refined CHO, increased complex CHO
Increased soluble fibre
decreased fat (especially saturated) 
decreased salt 
Avoid binge drinking
  • Exercise
  • Lipids
    Risk of hyperlipidaemia
    Primary prevention with statins if over >40 yrs
  • ABP
    decreased Na intake and ETOH
    Keep BP <130/80
    ACEi best (B-B: mask hypos, thiazides: increased glucose)
  • Aspirin
    Primary prevention if >50yrs or <50 with other CVD RFs.

Yearly/ 6-monthly check:

Smoking cessation

HTN - HbA1c checked every 3-6 months until stable, then 6 monthly. Target on lifestyle or with metformin = 48. Inclusion of a sulphonylurea = 53.

BP and Diabetes - No end organ damage: <140/80
End organ damage: <130/80

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20
Q

Management of diabetes - Oral hypoglycaemics - first line after lifestyle modification?

A

Aim HbA1c <6.5% / 48mmol

  1. Lifestyle Modification: delays
  2. Start Metformin (if HBA1c >target after lifestyle changes to reduce micro and macrovascular complications)
    SE: Nausea, diarrhoea, abdo pain, lactic acidosis
    CI: GFR<30, tissue hypoxia (sepsis, MI), morning before GA, iodinated contrast media, CKD (increase risk of lactic acidosis)
    500mg after evening meal, increasing to 2g max.

Advise is to stop if patient is ill due to renal impairment.

If Metformin is contraindicated offer a DPP4 (gliptins), pioglitazone, sulfonylurea, SGLT-2 inhibitor)

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21
Q

Management of diabetes - Oral hypoglycaemics - after metformin?

A

If HbA1c >58 mmols (7.5%)

For non-obese patients

Metformin + Sulphonylureas (if HBA1c >target) such as gliclazide. Major hypoglycaemia concern with unpredictable eating/exercise habits).
OR
Metformin + SGLT2 inhibitor (empagliflozin) 10mg OD. (reduce CVS risk and renal benefits).
OR
Metformin + pioglitazone (contraindicated in patients with heart failure due to fluid retention).
OR
Metformin + DPP4 (gliptin) - sitagliptin (do not offer cardiovascular benefits, but few identified side effects). No weight gain, oral preparation. Therefore for obese patients.

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22
Q

What dual therapy do you use if metformin is not suitable?

A
  • Gliptin plus pioglitazone (contraindicated if bladder cancer)
  • Gliptin (DPP4 inhibitor) plus sulphonylurea (gliclizide)
  • Pioglitazone + sulphonylurea

Gliptins = DPP4 = Inactivating GLP1 therefore block this to increase action of GLP1

Pioglitazone = PPAR - modifies transcription of insulin. Class is the Thiazolidinedione

Gliclazide = Sulphonylureas.

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23
Q

What is 3rd line treatment for diabetes mellitus

A

HBA1c >58

Triple therapy

  • Metformin, gliptin and a sulphonylurea
  • Metformin, pioglitazone (thiazolidinedione), sulphonylurea
  • Metformin, pioglitazone or sulphonylurea and an SGLT-2 (pee out glucose)

Sensitise your body to insulin (metformin)

Starting insulin treatment - safe starting dose 0.1-0.3 U/kg

  • Neutral Protamine Hagedorn (1-2 daily) + short-acting insulin
  • Insulin determir or glargine alternative to NPH.
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24
Q

What if third-line is ineffective for DM?

A
  • Consider Metformin, sulphonylurea and GLP-1 (exenatide) for those with BMI >35 or those with BMI <35 who would have occupational problems with insulin.

Exenatide leads to increased insulin secretion + inhibits glucagon secretions. Leads to weight loss. Within 60 mins before the morning and evening meals.

Consider adding exenatide to metformin and a sulfonylurea if:
BMI >= 35 kg/m² in people of European descent and there are problems associated with high weight, or
BMI < 35 kg/m² and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities.

  • Consider acarbose if unable to use other glucose-lowering drugs.
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25
Q

What are the principles of insulin?

A

Ensure pt education about

  • Self-adjustment with exercise and calories
  • Titrate dose
  • Family member can abort hypo with sugary drink or GlucoGel
  • Fasting BM before meals informs re long-acting insulin dose.

Type 1: 5-7 mmol on waking and 4-7 before meals at other times of the day.

  • Finger-prick BM after meals informs re shorting-acting insulin dose (for that last meal)
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26
Q

What are the common insulin regimes?

A

HbA1c - monitored every 3-6 months.
Adults should have a target of HbA1c level of 48.
Monitor 4 times a day.

1 ml = 100 units.
10ml = 1000 units.

1) Basal-bolus insulin regimen
- Bedtime long-acting (glargine) + short acting before each meal (lispro)
Adjust dose according to meal size
~50% of insulin given as long-acting
Allows flexible lifestyle for T1DM
Best outcome

2) 1,2 or 3 insulin injections per day (biphasic)
- Usually short-acting insulin or rapid-acting mixed with intermediate-acting insulin (Biphasic regimen)
- 30 mins before breakfast and dinner
Rapid: actrapid
Intermediate/long-acting: insulatard
- Associated with fasting hyperglycaemia
- Suitable for children, older patients (regular lifestyle).

3) Continuous subcutaneous insulin infusion (insulin pump) - this is a programmable pump that offers regular insulin in the form of rapid acting) by subcut/cannula.

Rapid insulin = 5 mins - peak 1 hr (Novorapid)

Short acting = 30 mins onset, 3 horus peak, last 6-8hrs (Actrapid)

Intermediate-acting insulin = 2hr peak 5-8hrs, duration 12-18hrs. (isophane insulin)

Long-acting insulin analogues = 1-2 hrs, flat profile uper to 24hrs. (Insulin Determir, insulin glargine).

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27
Q

Management of insulin during illness?

A
  • Insulin requirements usually increased (even if food intake decreases)
  • Maintain calories (e.g with milk)
  • Check BMs >4hrly and test for ketonuria.
  • Increased insulin dose if glucose rising
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28
Q

Side effects of insulin?

A

Hypoglycaemia

  • At risk: ETOH binge, B-B (mask symptoms), elderly
  • Need to admit sulphonylurea-induced hypo

Lipohypertrophy
- rotate injection sites: abdomen, thighs

Weight gain in T2DM
- increased weight gain if insulin given with metformin

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29
Q

What are the complications of diabetes?

A 
Hyperglycaemia: DKA, HONK
Hypoglycaemia
Infection
Macrovascular: MI, CVA
Microvascular
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30
Q

Macrovascular complications of diabetes?

A

MI: may be silent due to autonomic neuropathy
PVD: Claudication, foot ulcers
CVA: Strokes

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31
Q

Management of Macrovascular complications?

A

CV risk factors

  • BP (aim <130/80) if end-organ damage otherwise 140/80. ACEi have renoprotective effect in diabetes give as 1st line. Otherwise for African/Caribbean give ACEi + thiazide/CCB.
  • Smoking
  • Lipids
  • HBA1c

Prevention

  • Good glycaemic control prevents both macro- and micro-vascular complications
  • Regular screening: fundoscopy, ACR, foot checks.
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32
Q

Diabetic Foot

A 
Due to 
Ischaemia 
- Critical toes
- Absent pulses (do ABPI) 
- Ulcers: painful, punched-out, foot margins, pressure points

Neuropathy

  • Loss of protective sensations
  • Deformity: Charcot’s joints (weakening of foot and breaking of bones but can’t feel due to neuropathy), pes cavus, claw toes (extension of MTPJ and flexion of IPJ due to diabetic foot)
  • Injury or infection over pressure points
  • Ulcers: painless, punched-out, metatarsal heads, calcaenium

Charcot’s is a localised inflammatory condition leading to varying degrees and pattern of bone destruction, subluxation, dislocation and deformity.

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33
Q

Management of diabetic foot?

A

Prevention

  • Education about foot care is fundamental in the prevention of gangrene.
  • Good glycaemic control prevents both macro- and micro-vascular complications
  • Regular screening: fundoscopy, ACR, foot checks.
Conservative 
- Daily foot inspection (e.g with mirror) 
- Comfortable/therapeutic shoes
- Regular chiropody (remove callus) 
- Wound care
Medical 
- Management of infection: benpen + fluclox ± metronidazole
Surgical
- Abscess or deep infection
- Spreading cellulitis
- Gangrene
- Suppurative arthritis

Screen for ischaemia and neuropathy.

All those with moderate to high risk should be followed up regularly by local diabetic foot centre.

Therefore any patient that has a problem other than simple calluses should be followed up in local diabetic foot centres.

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34
Q

Microvascular complications of diabetes

A

Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy

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35
Q

Diabetes complications - Diabetic nephropathy

A

Pathophysiology

- Hyperglycaemia –> nephron loss and glomerulosclerosis

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36
Q

Features of diabetic nephropathy?

A

Microalbuminuria

  • urine albumin:Cr (ACr) >30 mg/Mm
  • If present –> ACEi/ARA
  • Refer if UCR >70
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37
Q

Diabetic Retinopathy

A
  • Microvascular disease –> Retinal ischaemia –> increased VEGF
  • Increased VEGF –> new vessel formation
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38
Q

Presentation of diabetic retinopathy?

A
  • Retinopathy and maculopathy
  • Cataract
  • Rubeosis iris: new vessels on iris –> glaucoma
  • CN palsies
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39
Q

Diabetic retinopathy and maculopathy?

A
  • Commonest cause of blindness up to 60yrs
  • Refer if pre-proliferative retinopathy/maculopthy
  • Ix: fluorescein angiography (for macula) /imaging of fundus
  • Rx: laser photocoagulation
    Management
  • Intravitreal anti-VEGF and consider macular laser laser therapy.
  • Also urgent pan-retinal photocoagulation of high risk proliferate
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40
Q

Stages of diabetic retinopathy?

A

Background Retinopathy

  • Dots: Microaneurysms
  • Blot haemorrhages
  • Hard exudates: yellow lipid patches (hard)

Pre-proliferative retinopathy

  • Cotton-wool spots (retinal infarcts - white fluffy)
  • Venous beading
  • Haemorrhages

Proliferative

  • New vessels
  • Pre-retinal or vitreous haemorrhage

Maculopathy

  • Decreased acuity may be only sign
  • Hard exudates within one disc width of macula (where fovea sits)

Management

  • Intravitreal anti-VEGF and consider macular laser laser therapy.
  • Also urgent pan-retinal photocoagulation of high risk proliferate
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41
Q

Diabetic Neuropathy pathophysiology?

A

Pathophysiology

  • Metabolic: glycosylation, ROS, sorbitol accumulation
  • Ischaemic: loss of vasa nervorum
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42
Q

Types of diabetic neuropathy?

A
  • Symmetrical sensory polyneuropathy
  • Mononeuropathy/Mononeuritis multiplex (isolated cranial or peripheral nerve)
  • Femoral neuropathy/amyotrophy(radiculopathy)
  • Autonomic neuropathy
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43
Q

Diabetic Neuropathy - Symmetric sensory polyneuropathy?

A

Glove and stocking: length-dependent (therefore feet 1st)
- Loss of all modalities
Absent ankle jerk
Absent ankle jerk
Numbness, tingling, pain (worse at night)

Management

  • Paractamol
  • Amitriptyline, Gabapentin, SSRI, pregabalin or duloxetine.

Use Tramadol as rescue therapy for exacerbation of neuropathic pain.

Amitriptylline is normally first choice but given history of BPH better to avoid amitriptylline due to risk of urinary retention. Anti-muscarinic effects.

  • Capsaicin cream
  • Baclofen
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44
Q

Diabetic Neuropathy - Mononeuropathy/Mononeuritis multiplex

A
  • Progressive motor and sensory deficit in the distribution of specific peripheral nerves.
  • Numbness and weakness
  • Pain
    Eg of CN3/6 palsies
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45
Q

Diabetic Neuropathy - Femoral neuropathy/amyotrophy

A

Painful asymmetric weakness and wasting of quads with loss of knee jerks
Dx: nerve conduction and electromyography

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46
Q

Diabetic Neuropathy - Autonomic neuropathy?

A
  • Postural hypotension - Rx: fludrocortisone
  • Gastroparesis –> Early satiety, GORD, bloating
  • Diarrhoea: Rx with codeine phosphate
  • Urinary retention
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47
Q

What is the pathogenesis of DKA?

A

Hyperglycaemia

Ketogenesis

  • decreased insulin –> increased stress hormone and glucagon
  • decreased glucose utilisation in tissues+ increased fat B-oxidation
  • Increased fatty acids from tissues –> increased ATP + generation of ketone bodies

Dehydration

  • Decreased insulin –> decreased glucose utilisation + increased gluconeogenesis –> severe hyperglycaemia
  • Osmotic diuresis –> dehydration
  • Also, increased ketones –> vomiting

Acidosis

  • Dehydration –> renal perfusion
  • Hyperkalaemia
  • Ketones
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48
Q

Precipitants of DKA?

A
  • Infection/stress ± Stopping insulin

- New T1DM

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49
Q

Presentation of DKA?

A
  • Abdo pain + vomiting
  • Gradual drowsiness
  • Sighing Kussmaul hyperventilation
  • Dehydration (sunken eyes, poor skin turgor)
  • Ketotic breath

Signs of diabetes

  • Polyuria
  • Polydipsia
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50
Q

Diagnosis of DKA?

A
  • Acidosis (increased AG): ph <7.3 (± HCO3 <15mM)
  • Hyperglycaemia: >11.1 mM (or known DM)
  • Ketonaemia: >3mM (>++ on dipstick)
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51
Q

Investigations for DKA?

A

Urine: ketones and glucose, MCS
Cap glucose and ketones
VBG: acidosis + increased K (due to extracellular shift of potassium due to insulin insufficiency, acidiaemia). Na is low due to osmotic reflux from intracellular to extracellular space due to hyperglycaemia

Total body potassium conc is low due to diuresis.

Bloods: U+E, FBC, Glucose, Cultures, Magnesium, elevated anion gap, serum osmolality.

CXR: Evidence of infection

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52
Q

Why Hyponatraemia in DKA?

A
  • Osmolar compensation for hyperglycaemia - water moving into where sugar is, leading to a dilutional hyponatraemia.
    If there is little water, means hypernatraemia.
  • Increased or normal Na indicates severe dehydration
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53
Q

Why should you avoid rapid decreased in insulin once glucose normalised in DKA?

A

Glucose decreases faster than ketones and insulin is necessary to get rid of ketones

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54
Q

Why is amylase up in DKA?

A

Amylase is up due to extrapancreatic sources or pancreas itself.

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55
Q

Why do you get hyperchloraemic metabolic acidosis after management of DKA?

A

Excretion of ketones –> loss of potential bicarbonate

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56
Q

Management of DKA?1st step

A

In HDU

  • Rehydrate
  • Insulin infusion
  • Potassium replacement

Fluid
- 0.9% saline infusion via large bore cannula
SBP <90 –> 1L stat + more until SBP >90
SBP >90 –> 1L over 1h

Then: 
1L over next 2hrs (1L with potassium chloride) 
1L/2h, (with potassium chloride) 
1L/4h, (with potassium chloride) 
1L/4h, (with potassium chloride) 
1L/6h (with potassium chloride)
  • Switch to 5% dex 1L/8hr with 0.45% saline when glucose <11.1mM, to avoid hypoglycaemia
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57
Q

Management of DKA?2nd step?

A
  • Insulin therapy corrects hyperosmolarity + acidaemia decreased plasma conc of potassium by driving it into cells.
  • Potassium chloride/phosphate
    20-30 mEq/L/hour IV infusion.

-Please start this on the 2nd bag of fluid.
>5.5 –> nil
3.5-5.5mM –> 40mmol/L
<3.5 –> consult senior for review

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58
Q

Management of DKA? 3rd step?

A

Insulin infusion

- Actrapid 0.1u/kg/h (6u if no weight, max 15u)

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59
Q

Management of DKA? 4th step

A

Assessment

  • Hx + full examination
  • Capillary, urine, blood, imaging

Additional measures

  • Urinary catheter (aim: 0.5ml/kg/hr
  • NGT if vomiting or decreased GCS
  • Thromboprophylaxis with LMWH
  • Refer to specialist diabetes team
  • Find + treat precipitating factors
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60
Q

Monitoring required for DKA?

A
  • Hrly capillary glucose and ketones
  • VBG @ 60 mins, 2hr, and then 2hrly
  • Plasma electrolytes 4hrly

Aims

  • decreased ketones by >0.5 mM/h or increased HCO3 by >3mM/h
  • decrease plasma glucose by <3mM/h
  • Maintain K in normal range. Normally DKA will lead to hyperkalaemia due to H+ being pushed in cells to normalise acidaemia. Following on from this, when insulin in administered, K+ is driven into cells, so hypokalaemia.
  • Avoid hypoglycaemia
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61
Q

Resolution of DKA?

A
  • Ketones <0.3 mM + venous pH >7.3
  • transfer to sliding scale if not eating
  • Transfer to SC insulin when eating and drinking

When converting - see how much they use in 24hr, 2/3 given, then 10 units split in morning, afternoon, evening.

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62
Q

Transfer to SC insulin + provide education?

A
  • When biochemically resolved and eating
  • Start long-acting insulin the night before
  • Give short-acting insulin before breakfast
  • Stop IVI 30 mins after short acting

Education

  • ID precipitating factors and provide action plan
  • provision of ketone meter with education on use.
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63
Q

Complications of DKA?

A
  • Cerebral oedema: excess fluid administration
    Commonest cause or mortality
  • Aspiration pneumonia
  • Hypokalaemia
  • Hypoglycaemia
  • Hypophoshataemia –> resp and skeletal muscle weakness/ ARDS
  • Thromboembolism
  • hyperchloraemic acidosis - loss of ketoanions needed for bicarb regen, increased reabsorption of chloride secondary to intensive admi of chloride fluids.
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64
Q

What is a hyperosmolar non-ketotic coma?

A

HHS - characterised by

  • profound hyperglycaemia,
  • hyperosmolality
  • volume depletion in the absence of significant ketoacidosis.

Severe hyperglycaemia, dehydration and renal failure, mild/absent ketonuria.

The insulin conc in these patients is sufficient to suppress lipolysis and ketogenesis.

Cause- Infection, non-adherence, corticosteroids, thiazide diuretics, beta-blockers

The patient

  • usually T2DM, often new presentation
  • Usually older
  • Long hx (e.g 1 week)
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65
Q

Metabolic derangement in HONK?

A

Marked dehydration and glucose >30mM (hypovolaemia).

No acidosis (no ketogeneisis) 
Osmolality >320mosmol/kg.

Ketones can be high but normally. No acidosis.

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66
Q

Complications of HONK?

A

Occlusive events are common: DVT, Stroke

Give LWMH

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67
Q

Management of HONK?

A

Rehydrate with 0.9% NS over 48hr 0
- May need ~9L
- Wait 1hr before starting insulin (sliding scale) - variable rate for uncontrolled diabetes.
May not be needed
Start low to avoid rapid changes in osmolality 1-3u/hr
Consider potassium therapy

  • Look for precipitant
    MI, infection, bowel infarct.
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68
Q

Define Hypoglycaemia: Whipple’s Triad?

A
  • Low plasma glucose <3mM
  • Symptoms consistent with hypoglycaemia
  • Relief of symptoms by glucose administration

Insulin produced in beta cells of pancreas. Central to regulating carbs and fat metabolism.

Pro-insulin is formed and cleaved to form insulin and c-peptide.

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69
Q

How to you classify symptoms of hypoglycaemia?

A
  • Autonomic: 2.5-3

- Neuroglycopenic: <2.5

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70
Q

What are the autonomic symptoms of hypoglycaemia?

A
  • Sweating
  • Anxiety
  • Hunger
  • Tremor
  • Palpitations
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71
Q

What are the neuroglycopenic symptoms of hypoglycaemia ?

A
  • Confusion
  • Drowsiness
  • Seizures
  • Personality change
  • Focal neurology
  • Coma (<2.2)
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72
Q

Causes of a fasting hypoglycemia?

A

EXPLAIN

  • usually insulin or sulfonylurea management in a known diabetic (exercise, missed meal, OD)
  • Exogenous drugs (quinine sulphate, aspirin pentamidine, quinine sulphate, ACEi).
  • Pituitary insufficiency (failure of cortisol)
  • Liver failure
  • Addison’s
  • Islet cell tumours (insulinomas - neuroendocrine tumours)
  • Immune (insulin receptor Abs: Hodgkin’s)
  • Non-pancreatic neoplasm: fibrosarcoma
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73
Q

Investigations of hypoglycaemia?

A

72hr fast with monitoring
Bloods
- Glucose, (at conclusion of 72hrs -every 6 hours with finger stick blood sugar).

  • insulin (measure when glucose <3.3 or end of 72hr fast. Should be undetectable. Elevated value = factitious
    hypoglycaemia or insulinoma.
  • C-peptide = elevated if insulin is endogenous. INappropriate elevation of c-peptide suggests either insulinoma or sulfonylurea.
  • If insulin in raised when you have glycaemia this is not a physiological reaction, should have very low insulin to put glucose back into the blood.
  • Therefore if high insulin and high c-peptide, endogenous insulin is coming from somewhere, either gliclazide (sulfonylurea). Cannot be exogenous insulin as this doesnt raise C-peptide.
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74
Q

On administration of insulin

Diagnosis of hypoglycaemia: a hyperinsulinaemic hypoglycaemia?

A

Drugs
- Increased C-pep: Sulfonylurea. Increasing the endogenous levels on insulin with C-peptide.

  • Normal C-pep: insulin
    Insulinoma.

C-peptide does not fall on admin of insulin if the patient has an insulinoma as endogenous levels are not reduced.

C-peptide levels fall on admin of insulin if self-medication. This is because on administration of insulin, his endogenous insulin drops, therefore C-peptide also drops.

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75
Q

Diagnosis of hypoglycaemia: a decreased insulin with no ketones?

A
  • Non-pancreatic neoplasms (secrete IGF-II which is like insulin)
  • Insulin receptor antibodies
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76
Q

Diagnosis of hypoglycaemia: a decreased insulin, increased ketones?

A
  • Alcohol binge with no food

- Pituitary insufficiency/ Addison’s due to a failure to respond to hypoglycaemia.

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77
Q

What is an insulinoma?

A

Path: 95% benign B-cell tumour usually seen with MEN1
Pres: fasting/exercise induced hypoglycaemia
Ix:
- Hypoglycaemia + increased insulin
- Exogenous insulin doesn’t suppress C-pep
- MRI, EUS pancreas

Manangement
- Excision

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78
Q

Causes of a post-prandial hypoglycaemia?

A

Dumping post-gastric bypass

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79
Q

Management of hypoglycaemia if alert and orientated?

A

Rapid acting: Lucozade

Long acting: toast, sandwich

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80
Q

Management of hypoglycaemia if drowsy/confused but swallow intact: Buccal Carb?

A

Hypostop/Glucogel
Consider IV access.

IF IV access give 100ml 20% glucose IV .

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81
Q

Management of hypoglycaemia if unconscious or concerned with swallow: IV dextrose

A

100ml 20% glucose IV

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82
Q

Management of hypoglycaemia if deteriorating/refractory/insulin-induced/no access?

A
  • 1mg glucagon IM/SC
    Won’t work in drunks + short duration of effect (20 mins).
  • May get rebound hypoglycaemia (insulin release may)
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83
Q

Define thyrotoxicosis?

A

The clinical effect of increased T4, usually from gland hyperfunction.

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84
Q

Symptoms of hyperthyroidism

A
  • Diarrhoea
  • Increased appetite but
    decreased weight
  • Sweats, heat intolerance
  • Palpitations
  • Tremor
  • Irritability
  • Oligomenorrhoea ± infertility
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85
Q

Signs in the hands of hyperthyroidism

A
  • Fine tremor
  • Fast/irregular pulse
  • Warm, moist skin
  • Palmer erythema
  • Bruit in thyroid (TSH)
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86
Q

Signs in the face of hyperthyroidism?

A

Thin hair
Lid lag
Lid retraction

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87
Q

Signs in the neck of hyperthyroidism?

A

Goitre or nodules

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88
Q

Specific hyperthyroidism signs in the eyes for Graves? Ophthalmopathy?

A

Autoimmune response against the autoantigen (TSH receptor) –> retro-orbital inflammation. Inflammation results in glycosaminoglycan and collagen deposition in the muscles.

  • Exophthalmos
  • Ophthalmoplegia: Esp up-gaze palsy (failure)
  • Eye discomfort and grittiness
  • Loss of the colour red
  • Photophobia and decreased acuity (dangerous)
  • Chemosis
  • Most worrying is corneal involvement.

Other worrying signs are proptosis, corneal involvement, sight loss due to optic nerve involvement.

Dangerous - inability to close the eyes.
Loss of visual acuity

Smoking is the most important modifiable risk factor for development of thyroid eye disease.

Can use radiotherapy, steroids or surgery.

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89
Q

Other Grave’s specific signs apart from ophthalmopathy?

A
  • Dermopathy: pre-tibial myxoedema - excess glycosaminoglycans in tissue of legs, with plaques or scaly nodules. Overlying discoloured skin.
  • Thyroid acropachy (digital clubbing, soft tissue swelling of hands and feet, periostitis)

Only lid retraction
odt tissue involvement
Proptosis
Extra-ocular involvemnt

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90
Q

Investigations of thyrotoxicosis?

A
  • TFT: Decreased TSH, increased T4/T3
  • Abs: TSH receptor (diagnostic), TPO (less specific to Graves, also in Hashimoto’s).
  • Increase Ca due to thyroid hormone mediated increase in bone resorption, increased LFTs
  • Isotope scan
    Increased in Graves
    Hot+cold thyroiditis
  • Ophthalmopathy: acuity, fields, movements
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91
Q

Most common cause of thyrotoxicosis?

A 
Graves
60% of cases of thyrotoxicosis 
Prev: 0.5% 
Sex: F>>M= 9:1
Age: 40-60 yrs.
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92
Q

Features of Graves’?

A
  • Ophthalmopathy and dermopathy and thyroid acropachy
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93
Q

Triggers for Graves?

A

Stress, infection, child-birth

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94
Q

Disease associations with Graves?

A
  • T1DM
  • Vitiligo
  • Addison’s
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95
Q

Name some other causes (apart from Graves) of thyrotoxicosis?

A

Toxic multinodular goitre = Plummer’s disease

  • Autonomous nodules develop on background multinodular goitre
  • Elderly and iodine-deficient areas
  • Iodine scan shows hot nodules

Manage with radioactive iodine.

Toxic adenoma

  • solitary hot nodules ± producing T3/T4
  • Most nodules are non-functional

Thyrotoxic phase of Thyroiditis

  • de Quervain’s
  • Hashimoto’s
  • Subacute lymphocytic

Drugs

  • Thyroxine
  • Amiodarone
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96
Q

Management of hyperthyroidism - Medical

A

Medical management of symptoms - B-B (propranolol 40mg/6h)

  • Anti-thyroid: carbimazole/(inhibits TPO) or
    Titrate according to TFTs or block and replace.

In Graves’ Rx for 12-18 mo then withdraw - 50% relapse then move to surgery or radioiodine

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97
Q

Big side-effect of carbimazole?

A

Agranulocytosis (1/2000), Rash (1/200). Must warn patients

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98
Q

Radiological treatments of hyperthyroidism?

A

Most become hypothyroid

CI: pregnancy, lactation

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99
Q

Surgical treatment of hyperthyroidism?

A

Treat prior to surgery with antithyroid drugs until euthyroidism is achieved

Thyroidectomy
- May be preferred in woman planning pregnancy
- Complications
Recurrent laryngeal N.damage –> hoarseness
Hypoparathyroidism
Hypothyroidism

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100
Q

What are the features of a thyroid storm?

A

Develops in untreated or partially treated patient. Caused by a precipitate

  • Recent thyroid surgery or radio-iodine
  • Infection
  • MI
  • Trauma
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101
Q

Management of a thyroid storm?

A
  1. Fluid resuscitation + NGT
  2. Bloods: TFTs + cultures if infection suspected
  3. Propranolol PO/IV
  4. Carbimazole/methimazole or propylthiouracil then

Lugol’s Iodine 4hr later to inhibit thyroid (escape from Wolff-Chaikoff effect)
5. Hydrocortisone - blocks conversion of T4 to T3

  1. Manage cause
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102
Q

Epidemiology of hypothyroidism?

A

Incidence 4/1000 / yr
Sex: F>M = 6:1
Age >40yrs.

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103
Q

Symptoms of hypothyroidism?

A 
Lethargy 
Cold intolerance
decreased appetite but increased weight 
Constipation 
Menorrhagia
Decreased mood
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104
Q

Signs of hypothyroidism?

A 
Cold hands
Bradycardia
Slow-relaxing reflexes
Dry hair and skin 
Puffy face
Goitre
Myopathy, neuropathy
Ascites
Myxoedema 
- SC tissue swelling in severe hypothyroidism
Typically around eyes and dorsum of hand
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105
Q

Causes of primary hypothyroidism?

A

Primary?

  • Atrophic thyroiditis
  • Hashimoto’s thyroiditis
  • Subacute thyroiditis (post-partum)
  • Post de Quervain’s thyroiditis
  • Iodine deficiency (commonest worldwide)
  • Drugs: Carbimazole, amiodarone (contains iodine), lithium (stop drug entirely)
  • Congenital: thyroid agenesis
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106
Q

Causes of post-surgical hypothyroidism?

A

Thyroidectomy

Radioiodine

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107
Q

Causes of secondary hypothyroidism?

A

Hypopituitarism.

Replacement steroid therapy is required prior to thyroxine.

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108
Q

What is atrophic thyroiditis? (part of Hashimotos, but without Goitre)

A

Thyroid antibodies +ve: anti-TPO, anti-TSH.
Lymphocytic infiltrate –> atrophy (no goitre)
Associations
- Pernicious anaemia
- Vitiligo
- Endocrinopathies

109
Q

What is hashimoto’s thyroiditis?

A
  • TPO +ve
  • Atrophy + regeneration –> goitre
  • May go through initial thyrotoxicosis phase
  • May be euthyroid or hypothyroid
110
Q

Investigations for hypothyroidism?

A
  • Increased TSH, decreased T3/T4
  • Increased MCV ± normochromic anaemia
  • Increased triglyceride + increased cholesterol
  • Check prolactin levels (PRL- secreting pituitary adenoma)
  • Hyponatraemia (SIADH)
  • Increased CK if associated with myopathy
  • Abs: Anti-TPO and TSH

MUST Do a Short synACTHen test.

111
Q

Management for hypothyroidism?

A

Short synACTHen test for addison’s/

  • Levothyroxine - must take early in the morning at 6am.
    1.7 microgram/kg/day.
    30 mins before food as it’s absorption may affect food.
    Titrate to normalise TSH
    Enzyme inducers increase thyroxine metabolism

Clinical improvement takes ~2 weeks.

Check for other AI disease: E.g Addison’s, PA

For older patients or those with cardiac disease, severe hypothyroidism or patients over 50 the initial starting dose should be 25mcg od.
Other patients should start at 50-100mcg.

Check after 8-12 weeks.

Increased dose if pregnant.

May cause hyperthyroidism, reduced bone mineral density, worsening of angina, AF.

Management is aiming to normalise the TSH.

112
Q

What is a myxoedema coma?

A
  • Looks like hypothyroidism
  • Hypothermia
  • Hypoglycaemia
  • Heart failure: bradycardia and decreased BP
  • Coma and seizures
113
Q

Precipitants of Myxoedema coma?

A

Radioiodine
Thyroidectomy
Pituitary surgery
Infection, trauma, MI, stroke

114
Q

Management of myxoedema coma?

A
  • Blood: TFTs, FBC, U+E, Glucose, cortisol
  • Correct any hypoglycaemia
  • T3/T4 IV slowly (may ppt myocardial ischaemia
  • Hydrocortisone 100mg IV
  • Rx hypothermia and heart failure
115
Q

Benign thyroid disease - Simple goitre features and management?

A 
Diffuse painless goitre 
Mass effect: 
- dysphagia
- Stridor
- SVC obstruction

Usually euthyroid, may –> hypothyroidism

Causes: iodine deficinecy, autoimmune, (goitrogens (sulphonylureas) or hereditary.

Manage - thyroxine and/or thyroidectomy if pressure symptoms.

116
Q

Benign thyroid disease - Multinodular goitre features and signs?

A
  • Evolves from long-standing simple goitre.
  • Mass effects
  • Euthyroid or subclinical hyperthyroidism

As for simple goitre

Treat with thyroxine, total or subtotal thyroidectomy if pressure symptoms.

Mainly concerned about thyroid pressure symptoms.

117
Q

Benign thyroid disease - Plummer’s Disease - Toxic multinodular goitre signs and features?

A
  • Multinodular goitre
  • Thyrotoxicosis
  • Uneven iodine uptake with hot nodule

Caused by an autonomous nodule developing on a background of a multinodular goitre

Management is with anti-thyroid drugs such as carbimazole, then surgical treatment such as total or subtotal thyroidectomy.

118
Q

Benign thyroid disease - Graves’ disease features and signs

A 
DIFFUSE goitre with bruit
Ophthalmopathy 
Dermopathy
Thyrotoxicosis
Assoc with other AI disease (TiDM, PA) 
Increased uptake on radionucleotide scan

Caused by autoimmune (T2 hypersensitivity)
- Anti-TSH receptor

Management of Graves

  • Propanolol
  • Carbimazole
  • Radioiodine
  • Thyroidectomy
119
Q

Benign thyroid disease - Hashimoto’s thyroiditis signs and features?

A
  • Diffuse PAINLESS goitre
  • May have transient thyrotoxicosis, then hypothyroidism
  • Associated with AI disease (TIDM, PA)

Caused by autoimmune (T2+T4) - anti-TPO, -Tg.

Management with levothyroxine.

120
Q

Benign thyroid disease - de Quervain’s thyroiditis signs and features

A
  • Diffuse PAINFUL goitre
  • Preceding viral URTI common
  • Thyrotoxicosis –> hypo –> eu
  • Decreased iodine uptake on thyroid scintigraphy.

Caused by a viral Coxsackie or autoimmune

Management is usually self-limiting. Thyroid pain managed with aspirin or other NSAIDs.
In more severe cases steroids are used.

121
Q

Benign thyroid disease - Subacute lymphocytic signs and features?

A

Diffuse painless goitre
May occur post-partum
Thyrotoxicosis –> hypo –> eu

Normally autoimmune in origin

Self-limiting management.

122
Q

Benign thyroid disease - Follicular adenoma signs and features?

A

Single thyroid nodule ± thyrotoxicosis (majority are cold)
May get pressure symptoms

Management is with a hemithyroidectomy

123
Q

Benign thyroid disease - Thyroid cysts signs and features?

A

Solitary thyroid nodule
Asymptomatic or pressure symptoms
Can –> localised pain due to cyst bleed.

Management with aspiration or excision.

124
Q

Malignant Thyroid disease - What is Papillary carcinoma?

A
  • 80% frequency total thyroid malignancy
  • associated with irradiation
  • Normally young (20-40yrs old)
  • Origin from follicular cells
  • Thyroglobulin tumour marker

Associated with lymphadenopathy.

Spreads nodes and lung
- JDG node = lateral aberrant thyroid.

Marker = Antibodies to thyroglobulin.

125
Q

Management of papillary thyroid carcinoma?

A

Total thyroidectomy
± node excision
± radioiodine
T4 to suppress TSH

> 95% 10yrs.

126
Q

What is follicular thyroid carcinoma + management?

A

10% frequency

  • F>M = 3:1
  • Age 40-60
  • Cell origin is the follicular cells and Thyroglobulin is the tumour marker.

Spread is from the blood –> bones and lungs

Management is through total thyroidectomy + T4 suppression +radioiodine

> 95% 10yrs.

127
Q

What are the 4 types of thyroid malignancy?

A

Papillary
Follicular
Medullary
Anaplastic

128
Q

What is medullary thyroid carcinoma and its management?

A
  • 5% of all thyroid malignancy
  • 30% are familial through MEN2 (medullary = MEN)
  • Affects MEN: young, and can also be sporadic: 40-50.
  • Origin is from the parafollicular C-cells and use CEA and calcitonin markers.
129
Q

Management of medullary thyroid carcinoma

A
  • Do Phaeo screen pre-op
  • Thyroidectomy
  • Nodal clearance
  • Consider radiotherapy
130
Q

What is anaplastic malignant thyroid disease?

A

Rare
F>M = 3:1 (ana)

Age >60 (ana)

Cell origin = Undifferentiated follicular cells
Rapid growth + aggressive: local, LN and blood.

131
Q

Management of anaplastic thyroid disease?

A

Usually palliative
May try thyroidectomy + radiotherapy
<1% 10yr survival.

132
Q

Management of lymphoma of the thyroid?

A

5%
Lymphocytes cell origin from a MALToma in Hashimoto’s.

Chemo-radiotherapy as management.

133
Q

What is the presentation for malignant thyroid disease?

A
  • Non-functional (cold)
  • Painless neck mass
  • Cervical mets
  • Compression symptoms
    Dysphagia
    Stridor
    SVC obstruction
134
Q

What is the presentation for malignant thyroid disease?

A
  • Solitary
  • Solid
  • younger
  • Male
  • Cold
  • Risk factors: Radiation exposure
135
Q

Indications for thyroid surgery for a malignant disease?

A
  • Pressure symptoms
  • Relapse hyperthyroidism (<1 failed drug management)
  • Carcinoma
  • Comesis
136
Q

Practicalities of thyroid surgery?

A

Render euthyroid pre-op with antithyroid drugs

  • Stop 10 days prior to surgery (they increase vascularity)
  • Alternatively just give propranalol

Check for phaeo in medullary carcinoma
Laryngoscopy: check vocal cords pre-and post-op.

137
Q

Complications of thyroid surgery - early?

A

Early
- Reactionary haemorrhage -> haematoma (<1%)
Can –> airway obstruction
Can anaesthetist and remove wound clips
Evacuate haematoma and re-explore wound.

  • Laryngeal oedema
    Damage during intubation or surgical manipulation
    Can –> increase airway obstruction
  • Recurrent laryngeal nerve palsy (0.5%)
    Right RLN more common (oblique ascent)
    Damage to one –> hoarse voice
    Damage to both –> obstruction needing tracheostomy
  • Hypoparathyroidism (2.5%
  • -> decreased Ca2+ –> Chvostek’s and Trousseau’s (carpopedeal spasm during BP cuff inflation). Chvostek’s tapping sign.
138
Q

Complications of thyroid surgery - late?

A
  • Keloid scar
  • Hypothyroidism
  • Recurrent hyperthyroidism
139
Q

Physiology of hyperparathyroidism?

A

PTH secreted in response to decrease Ca and causes

  • Increased osteoclast activity
  • Increase Ca and decreased PO4 reaborption in kidney
  • Increased 1a-hydroxylation of 25OH- Vit D3
140
Q

What is the presentation of hyperparathyroidism?

A 
Increase Calcium? 
- Stones
Renal stones
Polyuria and polydipsia (nephrogenic DI) 
Nephrocalcinosis
- Bones
Bone pain
Pathological #
- Moans
Depression
- Groans
Abdo pain
n/v and constipation
Pancreatitis 
PUD (increased fastrin secretion) 
- Other
- Increased BP ( check Ca2_ in all with HTN)
141
Q

What are the causes of primary hyperparathyroidism?

A

Solitary adenoma: 80%
Hyperplasia: 20%
PArathyroid Ca: <0.5%

142
Q

What is the investigations of primary hyperparathyroidism, what will you see?

A

Bloods: Increased Ca2+ and increased PTH, increased ALP, decreased PO4.

PTH can be inappropriately normal

ECG: Decreased QT –> Bradycardia –> 1st degree block

X-ray: osteitis fibrosa cystica –> Phalangeal erosions.

DEXA: osteoporosis

143
Q

Management for primary hyperparathyroidism

A

General

  • increase fluid intake
  • Avoid dietary Ca2+ and thiazide (increased serum Ca)

First line - Parathyroidectomy if symptomatic. (elevated Ca, hypercalciuria, nephrolithiasis, age <50, T score lower than -2.5).
In urgent cases consider hydration with saline. Bisphosphonates and loop diuretics to increase calcium excretion.

Look for scar which is in the crease of neck.

Surgical: excision of adenoma

  • Hypoparathyroidism
  • Recurrent laryngeal N. palsy
144
Q

Causes of secondary hyperparathyroidism?

A

Vitamin D deficiency

Chronic renal failure

145
Q

Investigations and signs of 2ndry HyperPTH?

A

increased PTH, decrease Ca, increase PO4, increased ALP, Decreased Vit D.

146
Q

Management of secondary hyperparathyroidism?

A
  • Correct cause
  • Phosphate binders
    With Ca: calcichew
    W/O Ca: sevelamer
  • Vit D: calcitriol, ergocalciferol, cholecalciferol (inactive)

Calcium carbonate - 210/1300 mg/day.

Indication for surgery = bone pain, persistent pruritus, soft tissue calcification.

147
Q

What is tertiary hyperparathyroidism?

A
  • Prolonged 2 HPT –> autonomous PTH secretion.

Allow 12 months following transplant as many cases will resolve.

Total parathyroidectomy.

  • Increased Ca, Increased PTH, decreased PO4, Increased ALP.
148
Q

What causes hypoparathyroidism?

A

Decreased PTH due to gland failure

149
Q

What is the presentation of decreased Ca –> SPASMODIC?

A
  • Spasms (carpopedal = Trousseau’s sign)
  • Perioral paraesthesia
  • Anxious, irritable
  • Seizures
  • Muscle tone increased - colic, wheeze, dysphagia
  • Orientation impaired (confusion)
  • Dermatitis
  • Impetigo herpetiformis (decreased Ca + pustules in pregnancy)
  • Chovsteks, cardiomyopathy (increased QTc –> Torsades de Pointes)
150
Q

Causes of hypoparathyroidism?

A 
Autoimmune - Isolated autoimmune hypoparathyroidism
Congenital: DiGeorge
- Cardiac abnormality
- Abnormal facies
- Thymic aplasia
- Cleft palate
- Hypocalcaemia
- Chr 22

Iatrogenic

  • Surgery
  • Radiation

Hypomagneasemia - Required for both PTH section + action on target tissues.
May cause hypocalcaemia + render patient unresponsive to treatment with calcium + Vit D.

151
Q

Investigations for hypoparathyroidism?

A

decreased Ca, increased PO4, decreased PTH, normal ALP.

152
Q

Management of hypoparathyroidism?

A

Ca supplements
Calcitriol

In emergency - Infuse Calcium at a Ca <1.88 alongside magnesium.

Thiazide diuretics can reduce the rate of urinary calcium excretion.

153
Q

What is pseudohypoparathyroidism?

A
  • Failure of target organ response to PTH
  • Symptoms of hypocalcaemia
  • Short 4th and 5th metacarpals, short stature
  • Investigtions = decreased Ca, increased PTH

Management = Ca + calcitriol

154
Q

What is pseudopseudohypoparathyroidism?

A

Normal maternal receptors in kidney –> Normal biochem.

Abnormal paternal receptors in body –> psuedohypoparathyroidism phenotype.

155
Q

What is Cushing’s Syndrome?

A

Clinical state produced by chronic glucocorticoid excess

Consider pseudo-Cushings in alcoholics or in severe depression. False positive dexamethasone suppression test. Thought to be excess alcohol decreased liver’s ability to clear cortisol.

Differentiate with insulin stress test to differentiate true and pseudo-Cushing’s.

156
Q

Features of Cushing’s Syndrome? - Catabolic Effects

A
  • Proximal myopathy
  • Striae
  • Bruising
  • Osteoporosis
157
Q

Features of Cushing’s Syndrome? - Glucocorticoid Effects

A

DM

Obesity

158
Q

Features of Cushing’s Syndrome? - Mineralocorticoid Effects

A

HTN

Hypokalaemia

159
Q

Appearance of a person with Cushing’s Syndrome?

A
  • Moon face
  • Acne and hirsuitism
  • Interscapular and supraclavicular fat pads
  • Centripetal obesity
  • Striae
  • Thin limbs
  • Bruising
  • Thin skin
160
Q

What is ACTH-independent CUshing’s?

A
  • Decreased ACTH due to -ve feedback.

- No suppression with any dose of dexamethasone.

161
Q

Causes of ACTH independent Cushing’s Syndrome?

A
  • Iatrogenic steroids: commonest cause
  • Adrenal adenoma/Ca: carcinoma often –> virilisation
  • Adrenal nodular hyperplasia
  • Carney complex: LAME syndrome:
  • myxomatous neoplasms, cardiac, endocrine, cutaneous and neural
  • pigmented lesions of the skin and mucosae, including the rarely occurring epitheloid blue nevus.
  • McCune-Albright
162
Q

What is ACTH- Dependent Cushing’s?

A

ACTH is raised

163
Q

Causes of ACTH-Dependent Cushing’s

A

Cushing’s Disease

  • Bilateral adrenal hyperplasia from ACTH-secreting pituitary tumour. MRI pituitary does not rule out Cushing’s Disease. Often too small.
  • Cortisol suppression with high-dose dex

Ectopic-ACTH

  • SCLC
  • Carcinoid tumour
  • Skin pigmentation, metabolic alkalosis, weight loss, hyperglycaemia
  • No suppression with any dose of dex.
  • Characteristically presents with very low potassium level.
164
Q

Investigations for Cushing’s Syndrome?

A

Cushings can present with a hypokalaemic metabolic alkalosis - aldosterone acts on sodium hydrogen channels in kidney.

1st: 24hr urinary free cortisol
- Late night serum or salivary cortisol (>50micrograms/24hr)
Highest @ 9AM, lowest @ midnight (elevated)

then check ACTH levels (if low = adrenal source = cushings syndrome. If high pituitary/ectopic).

Then: - Dexamethasone suppression test

Low dose is to differentiate patients with CS from those who do not have CS.

High dose - distinguish patients with Cushing’s disease (Suppressed) from those with ectopic ACTH (not suppressed).

  • ACTH (but ACTH degrees v quick after venepuncture to determine whether this is ACTH dependent or independent
  • localisation: CT, MRI
  • DEXA scan

Bilateral inferior petrosal sinus vein sampling - best test to confirm pituitary vs ectopic) .

CRH stimulation - if pituitary source then cortisol rises
If ectopic/adrenal then no change in cortisol.

165
Q

Management of Cushing’s?

A
  • Disease?: Trans-sphenoidal excision
  • Adrenal adenoma/Ca: Adrenelectomy
  • Ectopic ACTH: tumour excision, metyrapone (inhibits cortisol synthesis).
166
Q

What is Nelson’s Syndrome?

A 
Rapid enlargement of a pituitary adenoma following bilateral adrenelectomy for Cushing's syndrome .
- Not typically performed nowadays. 
- Presentations 
Mass effect: bitemporal hemianopia
Hyperpigmentation

Removal of both adrenal glands eliminates the production of cortisol, and the lack of cortisol’s negative feedback can allow any pre-existing pituitary adenoma to grow unchecked.

Production of the ACTH leading to increased MSH and hyperpigmentation.

167
Q

What is primary hyperaldosteronism?

A

Excess aldosterone independent of the RAS

168
Q

Features of primary hyperaldosteronism?

A
  • Hypokalaemia: weakness, hypotonia, hyporeflexia, cramps
  • Paraesthesia
  • HTN
169
Q

Causes of primary hyperaldosteronism?

A
  • Bilateral adrenal hyperplasia (70%)
  • Adrenocortical adenoma (30%): Conn’s Syndrome.
  • Adrenocortical carcinoma?
170
Q

Investigations for primary hyperaldosteronisM?

A
  • U+E: increased Na, Decreased K, Alkalosis
  • Take care with diuretics, hypotensives, laxatives, steroids
  • Aldosterone: renin ratio: increased with primary. High aldosterone, low renin.
  • ECG: flat/inverted T waves, U waves, depressed ST segment, prolonged PR and QT intervals (hypokalaemia)
  • Adrenal CT/MRI -
171
Q

Management of primary hyperaldosteronism?

A

Conn’s: Laparoscopic adrenalectomy

Hyperplasia: spironolactone, eplerenone (aldosterone antagonists)

2nd line is laparoscopic adrenalectomy

172
Q

Secondary hyperaldosteronism?

A

Due to increased renin from decreased renal perfusion?

173
Q

Causes of secondary hyperaldosteronism?

A
  • RAS (renal artery stenosis)
  • Diuretics
  • CCF
  • Hepatic failure
  • Nephrotic syndrome

Investigations
- Aldosterone: renin ratio normal.

Management of RAS
- anti HTN with captopril, enalapril but not if bilateral?
- + aspirin
2nd line is renal artery stenting

174
Q

What is Bartter’s Syndrome?

A
  • AR
  • Blockage of NaCl reabsorption in loop of Henle (as if taking frusemide)
  • Congenital salt wasting –> RAS activation –> hypokalaemia and metabolic alkalosis
  • Normal BP
175
Q

What is primary adrenal insufficiency?

A

Addison’s - Destruction of adrenal cortex –> glucocorticoid and mineralocorticoid deficiency

176
Q

Causes of Addison’s

A

Primary = TB, addison’s

Secondary - Low ACTH - Pituitary failure. Doesn’t present with the hyperpigmentation.

  • Autoimmune destruction: 80%
  • TB: worldwide most common
  • Metastasis: lung, breast, kidney
  • Haemorrhage: Waterhouse-Friedrichson - Adrenal haemorrhage following massive meningitis.
  • Congenital: CAH
177
Q

Symptoms of Adrenal insufficiency

A
  • Weight loss + anorexia
  • Nausea, abdo pain, diarrhoea, constipation
  • Lethargy, depression
  • Hyperpigmentation: buccal mucosa, palmar creases
  • Postural hypotension –> Dizziness, faints
  • Hypoglycaemia
  • Vitiligo
  • Addisonian crisis
178
Q

Investigations for Adrenal Insufficiency?

A

Bloods

  • Decreased Na, increased K
  • Decreased glucose
  • Decreased Ca
  • Anaemia
  • Morning serum cortisol

Short SYnACTHen test

  • Cortisol before and after tetracosactide
  • Exclude Addison’s if increased cortisol (measure the amount of cortisol produced).
  • increased 9am ACTH (usually Low)

Other tests: 21-hydroxylase Abs: +Ve in 80% of AI disease
Plasma renin and aldosterone
CXR: evidence of TB
AXR: adrenal calcification

8am cortisol: no morning elevation suggests Addison’s
Short Synacthen test
- Exclude addison’s disease if cortisol rises to adequate level

Long Synacthen test
- Diagnose Addison’s disease if cortisol does not rise to adequate levels

179
Q

Management of Adrenal insufficiency?

A

Replace

  • Hydrocortisone
  • Fludrocortisone

Advice

  • Don’t suddenly stop steroids
  • Increased steroids during intercurrent illness, injury. Double hydrocortisone dose, same fludrocortisone dose.

Hydrocortisone - 2/3 dose. Patients typically require 20-30mg per day. Majority given in the morning dose.

  • Wear a medic-alert bracelet

F/up
- Watch for autoimmune disease

180
Q

What is secondary adrenal insufficiency?

A

ie. Hypothalamus or pituitary failure

Causes

  • Chronic steroid use –> suppression of HPA axis
  • Pituitary apoplexy/Sheehan
  • Pituitary microadenoma

Features

  • Normal mineralocorticoid
  • No pigmentation
181
Q

What is an Addisonian Crisis?

A

Presentation

  • Shocked: Increased HR, postural drop, oliguria, confused.
  • Hypoglycaemia
  • Hyponatraemia
  • Hyperkalaemia
  • Usually known Addisonian or chronic steroid user.
182
Q

Precipitants to an addisonian crisis?

A
  • Infection
  • Trauma
  • Surgery
  • Stopping long-term steroids
  • Pregnancy due to immune-regulatory changes following pregnancy.
183
Q

Management of an Addisonian Crisis?

A
  • Bloods: Cortisol, ACTH, U+E, - Cultures
  • Check CBG: glucose may be needed
  • Hydrocortisone 100mg IV 6hrly
  • IV crystalloid - normal saline over 30-60 mins or with dextrose if hypoglycaemic.
  • Repeat hydrocortisone 6hrly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action.
  • Septic Screen
  • Treat underlying cause
184
Q

What is a Phaeochromocytoma?

A
  • Catecholamine-producing tumours arising from sympathetic paraganglia
  • Usually found in adrenal medulla
  • Extra-adrenal phaeo’s found by aortic bifurcation.
185
Q

What is the rule of 10s in Phaeochromocytoma?

A

10% malignant
10% extra-adrenal
10% bilateral
10% part of hereditary syndrome

186
Q

Phaeo’s are associated with which hereditary syndromes?

A

MEN2a and 2b

  • Neurofibrimatosis
  • Von HIppel-Lindau: RCC + cerebellar signs
187
Q

Presentation of phaeochromocytoma?

A
  • Triad: episodic headache, sweating and tachycardia
  • Other adrenergic features Increased BP, palpitations
    Anxiety
    Headache, tremor, dizziness
    Anxiety
    D/v, abdo pain
    Heat intolerance, flushes

May have precipitant

  • Straining, abdo palpation
  • Exercise, stress
  • B-b, IV contrast, TCAs, GA.
188
Q

Investigations for phaeo?

A
  • 24hr urine catecholamines, metanephrines, normetanephrines, creatinine.
  • plasma catecholamines, metanephrines, normetanephrines,
  • Also Vanillylmandelic acid
  • Abdo CT/MRI
  • MIBG Scan
189
Q

Management of Phaeo?

A

Non-hypertensive crisis? Non malignant
Do alpha-blockage first, then B-blockade pre-op.

Give alpha first. After 24hrs then give B-Blocker.

  • Phenoxybenzamine (alpha 2 blockade). Phaeochromocytoma = give PHenoxybenzamine before beta-blockers.
  • Then monitor BP post-op for decreased BP.

Then offer atenolol 25-100mg.

Then surgical excision of the tumour (adrenelectomy)

If malignant - Surgical debulking and then use MIBG.

If monotherapy - consider labetalol as this is both alpha and beta blockade.

190
Q

How to manage a HTN crisis in a phaeo?

A

Features of HTN crisis

  • pallor
  • Pulsating headache
  • Feeling of impending doom
  • very high BP (>180)
  • increased ST and cardiogenic shock

Management
- Phentolamine 2-5mg IV (a-block) or labetalol 50mg IV
- repeat to safe BP
Phenoxybenzamine 10mg/PO when BP controlled.
- elective surgery after 4-6 weeks to allow full alpha-blockage and volume expansion

191
Q

Define MEN?

A

Multiple Endocrine Neoplasia

  • Functioning hormone tumours in multiple organs
  • all autosomal dominant
192
Q

What does MEN1 Consist of?

A

3 Ps

  • Pituitary adenoma: prolactin or GH
  • Parathyroid adenoma/hyperplasia: ABNORMAL CALCIUM GIVE AWAY.
  • Pancreatic tumours: gastrinoma or insulinoma

May also present with Zollinger-Ellison syndrome = multiple gastroduodenal ulcers. High dose PPI

Most commonly present with Hypercalcaemia

193
Q

What does MEN2A consist of?

A

2 Ps PPT

Thyroid Medullary Carcinoma
Parathyroid
Phaeochromocytoma - PHAEO is the give away

194
Q

What does MEN2B consist of?

A

MMP

Thyroid Medullary carcinoma
Phaeochromocytoma
Marfanoid habitus

195
Q

What is the Carney Complex/LAME syndrome?

A 
- Lentigenes: spotty skin pigmentation 
\: Differential: peutz-jehgers
- Atrial Myxoma 
- Endocrine tumours: pituitary, adrenal hyperplasia
- Schwannomas
196
Q

What is Peutz-Jegher’s

A

Mucocutaneous freckles on lips, oral mucosa and palms
GI hamartomas: obstruction
Pancreatic endocrine tumours
Increased risk of cancer: CRC, pancreas, liver, lungs, breast

197
Q

Von Hippel-Lindau?

A
  • renal cysts
  • Bilateral renal cell carcinoma
    Haemangioblastomas - often in the cerebellum –> cerebellar signs
  • Phaeochromocytoma
  • pancreatic endocrine tumours
198
Q

Neurofibromatosis NF1?

A 
Dermal neurofibromas
Cafe-au-lait spots
Lisch nodules
Axillary freckling
Phaeochromocytomas
199
Q

What is Schmidt’s syndrome?

A
  • Polygenic
  • Addisons
  • Thyroid disease: hypothyroidism or Graves
  • T1DM

Polyendocrine Syndromes

200
Q

Causes of hypopituitarism?

A

Hypothalamic

  • Kallmann’s (anosmia + GnRH Deficiency)
  • Tumour
  • Inflammation, infection, ischaemia

Pituitary stalk?

  • Trauma
  • Surgery
  • Tumour (craniopharyngioma)

Pituitary

  • Irradiation
  • Tumour
  • Ischaemia: apoplexy, Sheehan’s
  • Infiltration: HH, amyloid
201
Q

What are the most common causes of panhypopituitarism?

A

Surgery
Tumour
Irradiation

202
Q

What are the features of panhypopituitarism?

A

Hormone deficiency
- GH: central obesity, atherosclerosis, decreased CO, decreased strength
- LH/FSH
M: decreased libido, ED, decreased hair growth
F: decreased libido, amenorrhoea, breast atrophy
- TSH: hypothyroidism (prolactin excess can cause TRH reduction and therefore TSH reduction).
- ACTH: secondary adrenal failure

203
Q

Investigations for hypopituitarism?

A

Basal hormone tests?
Dynamic pituitary function tests?
- Insulin test –> increased cortisol and increased Growth hormone in response to hypoglycaemia
- GnRH –> Increased LH/FSH
- TRH –> Increased T4 and increased PRL.

MRI brain

Management is by treating underlying cause and hormone replacement.

204
Q

What % of intracranial tumours are pituitary tumours?

A

10%

205
Q

Classification of pituitary tumours?

A

Microadenoma <1cm
Macroadenoma >1cm

Secretory function - secretory/functioning vs non-secretory/functioning adenoma.

206
Q

What is the pathology of pituitary tumours?

A
  • Most are non-secretory
  • 50% produce PRL
  • Others produce GH or ACTH?
207
Q

Features of pituitary tumours? Mass effect features?

A

Mass effects

  • Headache
  • Visual field defect: bitemporal hemianopia
  • CN palsies: 3,4,5,6 (pressure on cavernous sinus)
  • Diabetes insipidus
  • CSF rhinorrhoea
208
Q

Hormone effects of pituitary tumours?

A

PRL –> galactorrhoea, decreased libido, amenorrhoea, erectile dysfunction (this is because increased PRL goes to decreased GnRH –> decreased LH and FSH)

GH –> Acromegaly

ACTH –> Cushing’s Disease

209
Q

Investigations for pituitary tumours?

A

MRI
Visual field tests
Hormones: PRL, IGF, ACTH, Cortisol, TFTs, LH/FSH
Suppression test

210
Q

Management of pituitary tumours?

A

Replace hormones
- Prolactinoma - Give Dopamine Agonist = Cabergoline/bromocriptine
Treat hormone excess

Surgical - transsphenoidal pituitary adenomectomy.

  • pre-op hydrocortisone
  • Post-op dynamic pituitary test
211
Q

What is pituitary apoplexy?

A

Rapid pituitary enlargement due to bleed into a tumour
- Mass effect
Headache, meningism, decreased GCS
Bitemporal hemianopia
- CVS collapse due to acute hypopituitarism
- Rx: Urgent hydrocortisone 100mg IV.

212
Q

What is a craniopharyngeoma?

A
  • Originates from Rathke’s pouch
  • Commonest childhood intracranial tumour
  • growth failure
  • Calcification seen on CT/MRI
213
Q

Causes of hyperprolactinoma?

A

Excess pituitary production

  • Pregnancy, breastfeeding
  • Prolactinoma (PRL >5000)
  • Hypothyroidism (increased TRH)

Disinhibition by compression of pituitary stalk (stalk effect compression of dopamine)

  • Pituitary adenoma
    Most common type and produce an excess of prolactin. Non-secreting adenomas are next most common, the GH secreting and then ACTH secreting adenomas.

-Craniopharyngioma

Dopamine antagonists (commonest cause)

  • Antiemetics: metoclopramide
  • Antipsychotics: risperidone, haldol
214
Q

Symptoms of hyperprolactinaemia?

A
  • Amenorrhoea
  • Infertility
  • Galactorrhoea
  • Decreased Libido
  • ED
  • Mass effect from prolactinoma
215
Q

Investigations for hyperprolactinaemia?

A
  • Basal PRL: >5000 = prolactinoma
  • Pregnancy test, TFTs
    MRI
216
Q

Management of hyperprolactinaemia?

A

1st line: cabergoline or bromocriptine
Da agonist, decreased PRL secretion and decreased tumour size
SE: nausea, postural hypotension lung fibrosis

2nd line: trans-sphenoidal excision
- If visual or pressure symptoms don’t respond to medical management.

217
Q

Acromegaly causes?

A
  • Pituitary acidophil adenoma in 99%
  • Hyperplasia from GHRN secreting carcinoid tumour
    GH stimulates bone and soft tissue growth through increased IGF1
218
Q

Symptoms of acromegaly?

A
  • Acroparaesthesia
  • Amenorrhoea, decreased libido
  • Headache
  • Snoring
  • Sweating
  • Arthralgia, back ache
  • Carpal tunnel (50%)
219
Q

Signs of acromegaly? Hands

A
  • Spade-like
  • Thenar wasting
  • Boggy sweaty palms (if active)
  • Increased skin fold thickness
  • Carpal tunnel: decreased sensation + thenar wasting.

Check for raised ICP (look for bitemporal hemianopia)
- 3 Gs
Gynaecomastia, goitre, glycosuria

220
Q

Signs of acromegaly? Face

A
  • Prominent supraorbital ridges
  • Scalp fold: cutis verticis gyrata
  • Coarse face, wide nose, big ears
  • Prognathism: look from side
  • Macroglossia
  • Widely-spaced teeth
  • Goitre
221
Q

Other features of acromegaly

A
  • Puffy, oily, darkened skin
  • Proximal weakness + arthropathy
  • Pituitary mass effect: bitemporal hemianopia
222
Q

Complications of acromegaly?

A

Endocrine

  • Impaired glucose tolerance (40%)
  • Diabetes (15%)

Cardiovascular

  • increased BP
  • LVH
  • Cardiomyopathy
  • Increased IHD and increased stroke

Neoplasia
- Increased risk of CRC

Could be part of MEN1

223
Q

Investigations of acromegaly?

A
  • Increased IGF1 is now first line.

Increased glucose, increased Ca,
- increased PO4

  • Glucose tolerance test
    GH fails to suppress with glucose in acromegaly (not first line anymore)
  • Visual fields and acuity
  • MRI
224
Q

Management for acromegaly?

A

1st line: trans-sphenoidal excision
2nd line: somatostatin analogues - octreotide (increased risk of gallstones) - if tumours or surgery fail to achieve remission of acromegaly.
3rd line: GH antagonist - pegvisomant
4th line: radiotherapy

225
Q

Diabetes insipidus symptoms?

A

Polyuria
Polydipsia
Dehydration
Hypernatraemia: lethargy, thirst, confusion, coma.

Nephrogenic vs central

226
Q

Causes of cranial diabetes insipidus?

ADH defective release

A 
Idiopathic
Congenital: wolfram syndrome
Tumours
Trauma
Vascular: haemorrhage (Sheehan's) 
Infection: meningoencephalitis
Infiltration: sarcoidosis
227
Q

Causes of nephrogenic diabetes insipidus?

Kidney is resistant or insensitive.

A

Congenital
metabolic: decreased K, Increased Ca.
Drugs: Lithium, demecleocycline, vaptans
Post-obstructive uropathy

228
Q

Investigations of Diabetes Insipidus

A

Diagnosis - Water deprivation test
- Deprived of fluids for 8hrs, serum osmolality, urine volume and urine osmolality measured. +Ve if there is a suboptimal response in urinary concentration.
- Desmopressin stimulation test (to distinguish nephrogenic from central.
BLoods: U+E, Ca, glucose
Urine and plasma osmolality
- A low urine osmolality in conjunction with high serum osmolality strongly suggests DI.
- Exclude DI if U:P osmolality >2 (concentration)

229
Q

Differential for Diabetes Insipidus?

A

DM
Diuretics or Lithium
Primary Polydipsia

230
Q

Management of Diabetes Insipidus?

A

Cranial:

Find cause: MRI brain
Desmopression PO

Nephrogenic: treat cause

231
Q

Sexual characterisitcs - Hirsuitism causes?

A 
Familial
Idiopathic
Increased androgens 
- Ovary: PCOS
- Adrenal: CUshings, adrenal Ca
- Drugs: steroids
232
Q

Features of PCOS?

A

Features
- 2nd oligo/amenorrhoea –> Infertility
Obesity
Acne, hirsuitism

US: bilateral polycystic ovaries
Hormones: increased testosterone, decreased SHBG, increased LH:FSH ratio

Management

  • Metformin
  • COCP
  • Clomifene for infertility
233
Q

Gynacomastia causes?

A
  • Cirrhosis
  • Hypogonadism
  • Hyperthyroidism (increased ratio of oestrogen to androgen - increased in SHBG)
  • Oestrogen - or HCG producing tumours: e.g testicular
  • Drug: spiro, digoxin, oestrogen
234
Q

Erectile dysfunction causes?

A

Organic causes

  • Smoking
  • ETOH
  • DM
  • Endo: hypogonadism, hyperthyroidism, increased Prolactin
  • Neuro: MS, autonomic neuropathy, cord lesion
  • Pelvic surgery: bladder, prostate
  • Penile abnormalities: Peyronie’s disease.
235
Q

Patient with T2DM has STEMi and is on simvastatin, gliclazide and metformin. How should he be managed in CCU?

A

Stop metformin and gliclazide. Start IV insulin infusion.

Benefits of tight glycaemic control following MI. Manage hyperglycaemia in patients admitted to hospital for an ACS by keeping blood glucose below 11. Consider dose-adjusted insulin infusion with monitoring of blood glucose.

236
Q

Thyroid gland

A 
Inspect 
Palpate
LAN 
Percuss behind sternum
Auscultate (thyroid bruit)
237
Q

Causes of thyrotoxicosis

A 
Graves 
TMnG
Adenoma
Viral/postpartum thyroiditis
Amiodarone
238
Q

Endocrine causes of HTN?

A

Hyperaldosteronism: conn’s CAH
- Low potassium

Phaeochromocytoma - phenoxybenzamine followed by propanolol

239
Q

Nelson’s syndrome

A

Pituitary enlargement following bilateral adrenalectomy - high ACTH and pigmentation.

240
Q

Vit D deficiency

A

Fatigue
Proximal myopathy
Muscle aches and pain

241
Q

Non-PTH causes of hypercalcaemia

A

Hyperthyroidism
Malignancy:
PTHrP - SCC of breast, lung
- Multiple myeloma - old man with back pain (could be Paget’s - check the Alk Phos) - look at total protein
- Mets - bone pain, Ca sign
- Prostate Ca - PSA.
- Sarcoidosis - increased 1,25 dihydrox Vit D - in granulomata of the lungs - action of interferon. Polyuria/Polydipsia.

Bradycardia - Artificially elevated by calcium, high BP. Reflex sinus brady.

242
Q

Osteoporosis

A

At risk groups (PM, Steroids, Immobilie, chronic inflammatory conditions)
Check BMD, Vit D
- Exclude osteomalaica

High risk/post fracture -

  • bisphosphonates (Stand 30 mins after). No Need for DEXA.
  • Very poor oral absorption - stand up, big glass of water
  • Ulcer
  • CI in osteomalacia
243
Q

Types of corticosteroids

A
  • Minimal glucocorticoid activity, high MC activity = Fludrocortisone
  • Glucocorticoid activity, high mineralocorticoid activity, = Hydrocortisone
  • Predominant glucocorticoid activity, low mineralocorticoid activity = Prednisolone
  • Dexamethasone = least amount of mineralocorticoid.

Hyrocortisone:
G 1, M 1.

Prednisolone:
G 4, M 0.8.

Fludricortisone:
G 15, M 150

Aldosterone:
G 0, M 500

Dexamethasone:
G 40, M 0’

244
Q

Glucocorticoid side-effects

A
  • endocrine: impaired glucose regulation, increased
  • appetite/weight gain, hirsutism, hyperlipidaemia
  • Cushing’s syndrome: moon face, buffalo hump, striae
  • musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
  • immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis
  • psychiatric: insomnia, mania, depression, psychosis. Rare cause of prednisolone is to cause steroid psychosis.
  • gastrointestinal: peptic ulceration, acute pancreatitis
    ophthalmic: glaucoma, cataracts
    suppression of growth in children
    intracranial hypertension
    neutrophilia
245
Q

Mineralocorticoid side-effects

A

fluid retention

hypertension

246
Q

Subclinical hypothyroidism

A

Watch and wait

TSH is between 4 - 10mU/L and the free thyroxine level is within the normal range
if < 65 years with symptoms suggestive of hypothyroidism, give a trial of levothyroxine. If there is no improvement in symptoms, stop levothyroxine
‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’
if asymptomatic people, observe and repeat thyroid function in 6 months

TSH is > 10mU/L and the free thyroxine level is within the normal range
start treatment (even if asymptomatic) with levothyroxine if <= 70 years
'in older people (especially those aged over 80 years) follow a 'watch and wait' strategy, generally avoiding hormonal treatment'
247
Q

Pituitary incidentaloma

A

If found within the sellar, lab investigations must be done to determine if it is functional or non-functional.

248
Q

Gynaecomastia drugs?

A

DISCO

Digoxin
Isoniazid
Spironolactone
Cimetidine
Other (e.g. oestrogens, cannabis, finasteride)

CODES

C: cirrhosis
O: obesity
D: digoxin
E: oestrogen
S: spironolactone
249
Q

Sick euthyroid?

A

Common in unwell, elderly patients and often need no treatment.

Abnormal TFTs are very common in elderly patients when they are unwell.

IN the majority of cases TSH is within the normal range (inappropriately normal given the low thyroxine and T3).

250
Q

MODY

A

Maturity onset diabetes of the young. Type Hepatic Nuclear Factor 1 Alpha.
HNF1a accounts for 70% of MODY cases.

Sulphonylureas (gliclazide) are the optimal treatment in HNF1a-MODY

MODY = T2DM in patients < 25 yrs old. Typically inherited as an autosomal dominant condition.

MODY 3 = HNF1 alpha associated witH HCC.

MODY 2 = Defect in glucokinase gene.

MODY 5 = Liver and renal cyst.

Typically in patients <25.
A family history of early onset diabetes is often present.
Ketosis is not a feature at presentation.
Patients with the most common form are very sensitive to suphonylureas, insulin is not usually necessary.

251
Q

Gastroparesis

A

Erractic blood glucose control, bloating and vomtiing .

Can occur in diabetics due to neuropathy of the vagus nerve, causing abnormal gut movement.

Metoclopramide is a pro-kinetic drug that can improve gastric emptying.

252
Q

Causes of raised prolactin?

A

Prolactin is secreted by the anterior pituitary gland. Dopamine acts as the primary prolactin releasing inhibitory factor and hence dopamine agonist such as bromocriptine may be used to control galactorrhoea.

Pregnancy 
Prolactinoma 
Physiological
PCOS 
Primary hypothyroidism
Phenothiazines, metocloPramide, domPeridone.
253
Q

Thiazolidinediones?

A

Pioglitazone - insulin into the zone.

Reduces peripheral insulin resistance.

PPAR gamma receptor.

SE: Increased risk of bladder cancer. Weight gain, liver impairment: LFTs, fliud retention. Risk of fractures, bladder cancer.

Absolute contraindiation to heart failure due to fluid retention

254
Q

SGLT-2 inhibitor?

A

‎Canagliflozin · ‎Empagliflozin · ‎Dapagliflozin

Prevents the reabsorption of glucose from the proximal renal tubule, resulting in more glucose being secreted in the urine.

SE: Genital infections, DKA. such as thrush.

255
Q

Biguanides?

A

Metformin - GI upset, lactic acidosis

256
Q

GLP-1 mimetics?

A

Exenatide

SE: Nausea, vomiting, pancreatitis.

257
Q

Congenital adrenal hyperplasia?

A

AR disorders
Affecting steroid biosynthesis
Response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH
ACTH stimulates production of adrenal androgens that may virilize a female infant.

21-hydroxylase deficiency
11-beta hydroxylase deficiency
17-hydroxylase deficiency

258
Q

Sulphonylureas + side effects

A

Gliclazide

Increase insulin secretion.

SE: hypoglycaemic episodes and weight gain

Can also lead to hyponatraemia 2ndry to SIADH, bone marrow suppression, hepatotoxicity, peripheral neuropathy.

Avoid in breastfeeding and pregnancy.

259
Q

Orlistat + MOA

A

Pancreatic lipase inhibitor

Inhibits pancreatic lipases.

Orlistat is a pancreatic lipase inhibitor used in the management of obesity. Adverse effects include faecal urgency/incontinence and flatulence. A lower dose version is now available without prescription (‘Alli’). NICE have defined criteria for the use of orlistat. It should only be prescribed as part of an overall plan for managing obesity in adults who have:
BMI of 28 kg/m^2 or more with associated risk factors, or
BMI of 30 kg/m^2 or more
continued weight loss e.g. 5% at 3 months
orlistat is normally used for < 1 year

260
Q

Sitagliptin class + MOA

A

Dpp-4 inhibitors. Give to patients who are obese.

Reduce the breakdown of incretins, which thereby decreass glucagon secretion.

261
Q

Klinefelter’s syndrome?

A

XXY

features

  • Often taller than average
  • Lack of secondary sexual characteristics
  • small, firm testes
  • infertile
  • Gynaecomastia
  • Elevated gonadotrophin
262
Q

LADA?

A

Latent autoimmune diabetes of adulthood.

despite the presence of islet antibodies at diagnosis of diabetes, the progression of autoimmune -cell failure is slow.

In contrast to type 2 diabetes, patients are typically younger and without an increased body habitus. In contrast to type 1 diabetes, insulin is not usually required in the early stages of the disease.

Diagnosis may be aided through a Glutamic Acid Decarboxylase (GAD) Autoantibodies test and evidence of other autoimmune diseases.

263
Q

Stress response to surgery: Hormones that increased

A 
GH
Cortisol
Renin
ACTH
Aldosterone
Prolactin 
ADH
Glucagon

ACTH and growth hormone (GH) is stimulated by hypothalamic releasing factors, corticotrophin releasing factor (CRF) and somatotrophin (or growth hormone releasing factor)
Perioperative increased prolactin secretion occurs by release of inhibitory control
Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) does not change significantly
ACTH stimulates cortisol production within a few minutes of the start of surgery. More ACTH is produced than needed to produce a maximum adrenocortical response.

Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).
The usual negative feedback mechanism fails and concentrations of ACTH and cortisol remain persistently increased.
The magnitude and duration of the increase correlate with the severity of stress and the response is not abolished by the administration of corticosteroids.
The metabolic effects of cortisol are enhanced:

An important vasopressor and enhances haemostasis
Renin is released causing the conversion of angiotensinogen to angiotensin I
Angiotensin II formed by ACE on angiotensin 1, which causes the secretion of aldosterone from the adrenal cortex. This increases sodium reabsorption at the distal convoluted tubule

264
Q

Stress response to surgery; hormones that decreased?

A

Insulin - Steroids oppose the action of insulin and stimulate hepatic gluconeogenesis.
Testosterone
Oestrogen

265
Q

Neuroblastoma?

A

Raised urinary vanillylmandelic acid and homovanillic acid levels

266
Q

Acarbose

A

Decreased glucose absorption in the gut.

267
Q

Galactorrhea?

A

Caused by Chlorpromazine - antipsychotic

268
Q

DM Sick day rules

A

ncrease frequency of blood glucose monitoring to four hourly or more frequently
Encourage fluid intake aiming for at least 3 litres in 24hrs
If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis

Imperial Medicine Year 3 (35 decks)

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