Endocrinology AS Flashcards
Diabetes Mellitus definition
Multisystem disorder due to an absolute or relative lack of endogenous insulin –> Metabolic and vascular complications
Type 1 DM
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
T2DM?
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
Diagnosis of symptomatic diabetes?
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
Diagnosis of Asymptomatic diabetes?
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.
What is a OGTT?
- Only needed if borderline fasting or random glucose measurements
What is normal fasting glucose?
<6.1 (<41)
What is impaired fasting glucose defined as?
- 1-6.9 fasting (42-47)
- These patients should be recommended diet and exercise.
What is diabetes defined as on fasting glucose?
> 7 (>48)
What is normal in a 75g OGTT?
<7.8
What is impaired glucose tolerance
7.8-11
What is diabetes on OGTT?
> 11.1
What are secondary drug causes of DM?
Drugs: Steroids, anti-HIV, atypical neuroleptics, thiazides
what are secondary pancreatic causes of DM?
CF, chronic pancreatitis, HH, pancreatic Ca
What are secondary endo causes of DM?
Phaeo, Cushings (increases blood sugar), Acromegaly, hyperthyroidism
Other: glycogen storage
What is metabolic syndrome?
- 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
Conservative management of diabetes?
- MDT
GP, endorinologist, surgeons, specialist nurses, dieticians, chiropodists, fellow patients (education groups)
The 4Cs of diabetes monitoring?
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
Lifestyle modifications for Diabetes Mellitus?
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
Management of diabetes - Oral hypoglycaemics - first line after lifestyle modification?
Aim HbA1c <6.5% / 48mmol
- Lifestyle Modification: delays
- 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)
Management of diabetes - Oral hypoglycaemics - after metformin?
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.
What dual therapy do you use if metformin is not suitable?
- 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.
What is 3rd line treatment for diabetes mellitus
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.
What if third-line is ineffective for DM?
- 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.
What are the principles of insulin?
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)
What are the common insulin regimes?
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).
Management of insulin during illness?
- 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
Side effects of insulin?
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
What are the complications of diabetes?
Hyperglycaemia: DKA, HONK Hypoglycaemia Infection Macrovascular: MI, CVA Microvascular
Macrovascular complications of diabetes?
MI: may be silent due to autonomic neuropathy
PVD: Claudication, foot ulcers
CVA: Strokes
Management of Macrovascular complications?
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.
Diabetic Foot
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.
Management of diabetic foot?
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.
Microvascular complications of diabetes
Diabetic nephropathy
Diabetic neuropathy
Diabetic retinopathy
Diabetes complications - Diabetic nephropathy
Pathophysiology
- Hyperglycaemia –> nephron loss and glomerulosclerosis
Features of diabetic nephropathy?
Microalbuminuria
- urine albumin:Cr (ACr) >30 mg/Mm
- If present –> ACEi/ARA
- Refer if UCR >70
Diabetic Retinopathy
- Microvascular disease –> Retinal ischaemia –> increased VEGF
- Increased VEGF –> new vessel formation
Presentation of diabetic retinopathy?
- Retinopathy and maculopathy
- Cataract
- Rubeosis iris: new vessels on iris –> glaucoma
- CN palsies
Diabetic retinopathy and maculopathy?
- 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
Stages of diabetic retinopathy?
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
Diabetic Neuropathy pathophysiology?
Pathophysiology
- Metabolic: glycosylation, ROS, sorbitol accumulation
- Ischaemic: loss of vasa nervorum
Types of diabetic neuropathy?
- Symmetrical sensory polyneuropathy
- Mononeuropathy/Mononeuritis multiplex (isolated cranial or peripheral nerve)
- Femoral neuropathy/amyotrophy(radiculopathy)
- Autonomic neuropathy
Diabetic Neuropathy - Symmetric sensory polyneuropathy?
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
Diabetic Neuropathy - Mononeuropathy/Mononeuritis multiplex
- Progressive motor and sensory deficit in the distribution of specific peripheral nerves.
- Numbness and weakness
- Pain
Eg of CN3/6 palsies
Diabetic Neuropathy - Femoral neuropathy/amyotrophy
Painful asymmetric weakness and wasting of quads with loss of knee jerks
Dx: nerve conduction and electromyography
Diabetic Neuropathy - Autonomic neuropathy?
- Postural hypotension - Rx: fludrocortisone
- Gastroparesis –> Early satiety, GORD, bloating
- Diarrhoea: Rx with codeine phosphate
- Urinary retention
What is the pathogenesis of DKA?
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
Precipitants of DKA?
- Infection/stress ± Stopping insulin
- New T1DM
Presentation of DKA?
- Abdo pain + vomiting
- Gradual drowsiness
- Sighing Kussmaul hyperventilation
- Dehydration (sunken eyes, poor skin turgor)
- Ketotic breath
Signs of diabetes
- Polyuria
- Polydipsia
Diagnosis of DKA?
- Acidosis (increased AG): ph <7.3 (± HCO3 <15mM)
- Hyperglycaemia: >11.1 mM (or known DM)
- Ketonaemia: >3mM (>++ on dipstick)
Investigations for DKA?
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
Why Hyponatraemia in DKA?
- 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
Why should you avoid rapid decreased in insulin once glucose normalised in DKA?
Glucose decreases faster than ketones and insulin is necessary to get rid of ketones
Why is amylase up in DKA?
Amylase is up due to extrapancreatic sources or pancreas itself.
Why do you get hyperchloraemic metabolic acidosis after management of DKA?
Excretion of ketones –> loss of potential bicarbonate
Management of DKA?1st step
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
Management of DKA?2nd step?
- 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
Management of DKA? 3rd step?
Insulin infusion
- Actrapid 0.1u/kg/h (6u if no weight, max 15u)
Management of DKA? 4th step
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
Monitoring required for DKA?
- 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
Resolution of DKA?
- 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.
Transfer to SC insulin + provide education?
- 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.
Complications of DKA?
- 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.
What is a hyperosmolar non-ketotic coma?
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)
Metabolic derangement in HONK?
Marked dehydration and glucose >30mM (hypovolaemia).
No acidosis (no ketogeneisis) Osmolality >320mosmol/kg.
Ketones can be high but normally. No acidosis.
Complications of HONK?
Occlusive events are common: DVT, Stroke
Give LWMH
Management of HONK?
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.
Define Hypoglycaemia: Whipple’s Triad?
- 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.
How to you classify symptoms of hypoglycaemia?
- Autonomic: 2.5-3
- Neuroglycopenic: <2.5
What are the autonomic symptoms of hypoglycaemia?
- Sweating
- Anxiety
- Hunger
- Tremor
- Palpitations
What are the neuroglycopenic symptoms of hypoglycaemia ?
- Confusion
- Drowsiness
- Seizures
- Personality change
- Focal neurology
- Coma (<2.2)
Causes of a fasting hypoglycemia?
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
Investigations of hypoglycaemia?
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.
On administration of insulin
Diagnosis of hypoglycaemia: a hyperinsulinaemic hypoglycaemia?
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.
Diagnosis of hypoglycaemia: a decreased insulin with no ketones?
- Non-pancreatic neoplasms (secrete IGF-II which is like insulin)
- Insulin receptor antibodies
Diagnosis of hypoglycaemia: a decreased insulin, increased ketones?
- Alcohol binge with no food
- Pituitary insufficiency/ Addison’s due to a failure to respond to hypoglycaemia.
What is an insulinoma?
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
Causes of a post-prandial hypoglycaemia?
Dumping post-gastric bypass
Management of hypoglycaemia if alert and orientated?
Rapid acting: Lucozade
Long acting: toast, sandwich
Management of hypoglycaemia if drowsy/confused but swallow intact: Buccal Carb?
Hypostop/Glucogel
Consider IV access.
IF IV access give 100ml 20% glucose IV .
Management of hypoglycaemia if unconscious or concerned with swallow: IV dextrose
100ml 20% glucose IV
Management of hypoglycaemia if deteriorating/refractory/insulin-induced/no access?
- 1mg glucagon IM/SC
Won’t work in drunks + short duration of effect (20 mins). - May get rebound hypoglycaemia (insulin release may)
Define thyrotoxicosis?
The clinical effect of increased T4, usually from gland hyperfunction.
Symptoms of hyperthyroidism
- Diarrhoea
- Increased appetite but
decreased weight - Sweats, heat intolerance
- Palpitations
- Tremor
- Irritability
- Oligomenorrhoea ± infertility
Signs in the hands of hyperthyroidism
- Fine tremor
- Fast/irregular pulse
- Warm, moist skin
- Palmer erythema
- Bruit in thyroid (TSH)
Signs in the face of hyperthyroidism?
Thin hair
Lid lag
Lid retraction
Signs in the neck of hyperthyroidism?
Goitre or nodules
Specific hyperthyroidism signs in the eyes for Graves? Ophthalmopathy?
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.
Other Grave’s specific signs apart from ophthalmopathy?
- 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
Investigations of thyrotoxicosis?
- 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
Most common cause of thyrotoxicosis?
Graves 60% of cases of thyrotoxicosis Prev: 0.5% Sex: F>>M= 9:1 Age: 40-60 yrs.
Features of Graves’?
- Ophthalmopathy and dermopathy and thyroid acropachy
Triggers for Graves?
Stress, infection, child-birth
Disease associations with Graves?
- T1DM
- Vitiligo
- Addison’s
Name some other causes (apart from Graves) of thyrotoxicosis?
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
Management of hyperthyroidism - Medical
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
Big side-effect of carbimazole?
Agranulocytosis (1/2000), Rash (1/200). Must warn patients
Radiological treatments of hyperthyroidism?
Most become hypothyroid
CI: pregnancy, lactation
Surgical treatment of hyperthyroidism?
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
What are the features of a thyroid storm?
Develops in untreated or partially treated patient. Caused by a precipitate
- Recent thyroid surgery or radio-iodine
- Infection
- MI
- Trauma
Management of a thyroid storm?
- Fluid resuscitation + NGT
- Bloods: TFTs + cultures if infection suspected
- Propranolol PO/IV
- 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
- Manage cause
Epidemiology of hypothyroidism?
Incidence 4/1000 / yr
Sex: F>M = 6:1
Age >40yrs.
Symptoms of hypothyroidism?
Lethargy Cold intolerance decreased appetite but increased weight Constipation Menorrhagia Decreased mood
Signs of hypothyroidism?
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
Causes of primary hypothyroidism?
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
Causes of post-surgical hypothyroidism?
Thyroidectomy
Radioiodine
Causes of secondary hypothyroidism?
Hypopituitarism.
Replacement steroid therapy is required prior to thyroxine.