Endocrine/Metabolism Flashcards
Thyroid Problems
Thyroid Problems
Hyperthyroidism/Thyrotoxicosis
Causes
Presentation
Investigation
Management
Complications
Causes
- Most common: Grave’s disease (autoimmune) - features of hyperthyroid +/- eye disease
- Toxic multinodular goitre (autonomously functioning thyroid nodules)
- Amiodarone
- Contrast (rare, normally in elderly w/ pre-existing thyroid disease BUT avoid iodinated contrast in pre-existing thyrotoxicosis)
Also seen in the acute phase of the following:
- Subacute (de Quervain’s thyroiditis)
- Post-partum thyroiditis
- Hashimoto’s thyroiditis (later -> hypo)
Presentation
General: Weight loss, manic restlessness, heat intolerance, palps/AF, sweating, diarrhoea, oligomenorrhoea, anxiety, tremor
*Only in Graves: *:
- eyes (30%): exophthalmol, ophthalmoplegia
- Pretibial myxedema (erythamatous, oedematous shin lesion b/l)
- Thyroid acropachy: clubbing, soft tissue swelling of hands/feet, periosteal new bone formation
Investigation
- TSH low, T4/T3 high
- Thyroid autoantibodies (Grave’s: TSH receptor stimulating antibodies (90%), anti-thyroid peroxidase Ab (75%))
- other: Thyroid scintigraphy (Grave’s: diffuse, homogenous, increased uptake of radioavtive iodine; Toxic multinodular goitre = patchy uptake)
Management
Grave’s (refer to secondary care)
- Symptomatic: Propanolol
- Ongoing:
- Carbimazole (alone for 12-18/12; or block + replace w/ levothyroxine for 6-9/12 (block+ replace has more side effects tho) (main SE: agranulocytosis)
- Radioiodine (if relapse w/ or resistant to above) SE: later hypothyroidism requiring replacement; can worsen eye disease. CIs: pregnancy, age <16yo.
Complications
Thyroid Storm
- Normally seen in established thyrotoxicosis
- Precipitants: surgery, trauma, infection, acute iodine load (eg. contrast)
- Features: fever >38.5C, tachy, confusion, agitation, n+v, HTN, HF, abnormal LFTs + jaundice
- Management:
- paracetamol + IV propanolol + treat cause
- Anti-thyroid meds (propylthiouracil)
- Lugol’s iodine
- Dexamethasone IV
Hypothyroidism
Causes
Presentation
Investigation
Management
Complications
Cause
Primary hypothyroidism (to do w/ thyroid):
- most common UK: Hashimotos (autoimmune, associated w/ addison’s, T1DM, pernicious anaemia, coeliac + MALT lymphoma)
- most common worldwide: iodine deficiency
- Subacute thyroiditis (de Quervain’s)
- Riedal thyroiditis
- Post-partum thyroiditis
- Drugs: lithium, amiodarone
- Thyroid tx: post-thyroidectomy or radioiodine
Secondary hypothyroid
- Pituitary failure
Presentation
- Weight gain, lethargy, cold intolerance, dry cold yellow skin, non-pitting oedema (eg. hands/face), dry coarse scalp hair, loss of lateral eyebrows, constipation, menorrhagia, hyporeflexia, carpal tunnel
- goitre (e.g. firm + non-tender in hashimotos)
Investigations
TFTs
- Primary hypothyroid (eg. hashimotos) - high TSH, low T4
- Secondary (eg. pituitary tumour) - low TSH + T4
Antibodies
- Anti Thyroid Peroxidase antibodies (90% of hashimotos)
Management
Levothyroxine
- SE: hyperthyroid, reduced bone mineral density, worsening of angina, AF
- Interactions: Iron + calcium carbonate (give 4 hours apart)
- Monitoring: TFTs 8-12/52 post-dose change, aim for normal TSH range
- Pregnancy: increase dose by 25-50mcg due to increased demands
Complications
Myxedema coma -> severe hypothyroid -> confusion, hypothermia -> life-threatening
- More common in autoimmune causes + >60s
- Management: IV thyroid replacement, IVI, IV steroids (until adrenal insufficiency ruled out), electrolyte correction+/– rewarming
What are the following thyroid disorders
- Post-partum thyroiditis
- Subacute (De Quervain’s Thyroiditis)
- Riedel’s Thyroiditis
- Sick Euthyroid Syndomre
- Subclinical Hypothyroidism
Post-partum Thyroiditis
- Initial hyperthyroidism –> hypothyroidism
- Likley autoimmune (presence of antithyroid Ab prior to pregnancy is big RF)
- Can present couple of months post-pregnancy. Most don’t need treatment + 80% have normal TFTs within 18months.
Subacute (de Quervain’s Thyroiditis)
- Occurs following viral infection
- consists of 4 phases: 1. hyperthyroid, painful goitre, raised ESR; 2. euthyroid. 2. hypothyroidism 4. return to normal
- Ix: scintigraphy: globally reduced uptake of iodine
- Mx: normally self-limiting w/ no need for tx (although some have steroids). Aspirin/NSADIs for pain.
Riedel’s Thyroiditis
- Hypothyroidism due to dense fibrous tissue replacing normal thyroi parenchyma
- -> hard, fixed, painless goitre
- normally in middl-age women + associated w/ retroperitoneal fibrosis
- Managed w/ steroids
Sick Euthyroid Syndrome
- Systemic illness –> hypothyroid
- Low/normal TSH and T3/T4
- Reversible on recovery from systemic illness + tx not normally needed
Subclinical Hypothyroidism
- 5% -> overy hypothyroid per year (higher risk if thyroid antibodies present)
- TSH raised BUT normal T3/T4 + no obvious symptoms
- if TSH >10 on 2 separate occassions 3/12 apart –> consider treatment
- If TSH 5.5-10: If <65 consider 6/12 trial thyroxine if symptoms or TSH 5.5-10 on 2 occassions. In older patients (esp >80) consider watch and wait strategy.
- If asymptomatic observe + repeat TFTs in 6/12
Adrenal Problems
- Adrenals release:
- Mineralocorticoids + Glucocorticoids
-Androgens
Adrenal Problems
Cushing’s
Pathophysiology (include difference between Cushing’s disease + syndrome)
Presentation
Investigations
Management
Complications
Pathophysiology
Syndrome = raised cortisol
Causes:
ACTH dependent:
- Cushing’s disease (80%) - pituitary ACTH secreting tumour -.adrenal hyperplasia
- Ectopic ACTH production eg. small cell lung ca
ACTH independent
- Iatrogenic: steroids
- adrenal adenoma
- Adrenal carcinoma (rare)
N.B. Pseudo-Cushings can mimic it, due to alcohol excess or severe depression -> false +ve dexamethasone supression or 24h free cortisol (insulin stress test can differentiate)
Presentation
- buffalo hump, abdominal striae + weight gain, moon face
- HTN, bone loss
- General lab: Hypernatraemia, Hypokalaemia + metabolic alkalosis, impaired glucose tolerance
Investigation
To confirm Cushing’s Syndrome
- Overnight dexamethasone supression test (morning cortisol spike NOT supressed in CS)
- 24h urinary free cortisol (raised)
Localisation Testing:
- 9am + midnight ACTH (if low ACTH then ACTH independent cause likley)
- High-dose dexamethasone supression test:
- w/ high doses Cushing’s disease (pituitary adenoma) will be supressed
- BUT ectopic ACTH syndrome will NOT be supressed
CRH stimulation:
- If pituiaty source then cortisol will rise
- If ectopic/adrenal then no change
Insulin Stress test
- differentiates true cushing from pseudo cushing
Management
- Treat the underlying cause
Addison’s Disease
Pathophysiology
Presentation
Investigation
Management
Complications
Pathophysiology
Autoimmune destruction of adrenals -> hypoadrenalism –> reduced cortisol + aldosterone
Other causes of hypoadrenalism: TB, mets (bronchial carcinoma), meningococcal sepsis (waterhouse-friderichsen syndrome), HIV, antiphospholipid syndrome, pituiary disorder (tumour, radiation)
Presentation
Low cortisol –>
- lethargy, weakness, anorexia, n+v, weight loss
- Hyperpigmentation (esp palmar creases) (due to ACTH rise + POMC)
- Hypoglycaemia
Low aldosterone –>
- hyponatraemia (-> salt craving), hyperkalaemia, hypotension (less water retention), metabolic acidosis
Other: vitiligo, loss of pubic hair in women
Typical presentation in questions: weakness, poor appetite, fatigue, weight loss, myalgia +/- vol depletion
-If presents in crisis: Shock, collapse, pyrexia
Investigation
- ACTH stimulation test (synacthen) = definitive Ix (cortisol measures before + 30mins after)
if cortisol >420 at 30mins = adequate adrenal response. If not = addison’s.
- If Synacthen not available (eg. primary case) –> 9am serum cortisol
- > 500 = addisons unliklkey
- <100 = definitiely abnormla
- 100-500 - needs synacthen
Management
- Glucocorticoid (hydrocortisone) + mineralocorticoid (fludrocortisone) replacement
- Need to double steroid dose during intercurrent illness
Primary Hyperaldosteronism
Pathophysiology/Causes
Presentation
Investigation
Management
Pathophysiology
- Raised aldosterone from adrenals
Causes:
- Bilateral Idiopathic Adrenal Hyperplasia (most common)
- Conn’s syndrome (adrenal adenoma)
- Adrenal carcinoma (v rare)
Presentation
- HTN
- Hypokalaemia (-> muscle weakness) + metabolic alkalosis
Investigation
1st line: Plasma aldosterone:renin
- high aldosterone w/ low renin (-ve feedback)
2nd: High resolution CT abdo + adrenal vein sampling
- differentiates unilateral adenoma + bilateral hyperplasia
Management
- Adrenal adenoma –> Surgery
- Bilateral adrenocortical hyperplasia –> aldosterone antagonist (eg. spironolactone)
Adrenal Crisis
- pathophysiology
- Presentation
- Investigation
- Management
**Pathophysiology **
- long term steroid uses supresses the HPA axis.
- Steroid deficiency without ability of adrenals to compensate (e.g. suddenly stopping or increased demand/illness) –> hypoglycaemia + shock
**
Presentation **
- Normally in addison’s w/ longterm steroid use
- Tachy, postural hypotension, oliguria, weakness, confusion, coma
- + hx of precipitant
Investigation
- Serum cortisol + ACTH (treat whilst awaiting result)
- Blood, urine, sputum culture, bloods
Management
- IV100mg Hydrocortisone
- IVI
- monitor BMs (hypo)
- Abx + treat underlying cause
- +/- fludrocortisone if adrenal cause (seek expert help)
Acromegaly
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Excess growth hormone in adulthood (pre-puberty -> gigantism)
Causes
- Pituitary adenoma (95%)
- Ectopic GnRH or GH production e.g. by pancreatic cancer
Presentation
- Coarse facial appearance, spade-like hands, increased shoe size, carptal tunnel
- Large tongue, proganthism, interdenal spaces
- Excessive sweating, oily skin (sweat gland hypertrophy)
- Other features of pituitary tumour: hypopituitarism, headache, bitemporal hemianopia, raised prolactin + galactorrhoea
- Complications: HTN, DM, cardiomyopathy, colorectal Ca
6% have MEN1
Investigation
1. Serum IGF-1 and serial GH levels (GH varies throughout the day)
- If serum IGF-1 raised then OGTT to confirm diagnosis:
- normally GH is supressed to <2 w/ hyperglycaemia
- In acromegaly there is no supressio - Pituitary MRI (?tumour)
Management
- Surgery
- If uncessful/unable: medication e.g. octreotide
- Radiotherapy
What are the following?
- MEN
- Kallmann’s Syndrome
MEN = Multiple Endocrine Neoplasia
Types
- 1. = 3Ps: Hyperparathyroidism; Pituitary tumours (eg. prolactinoma); Pancreas (insulinoma + gastrinoma -> recurrent peptic ulcers)
- 2a. = Medullary thyroid cancer and 2Ps - Hyperparathyroidism + Phaeochromocytoma
- 2b = medually thyroid cancer and 1P: phaeochromocytoma. (also marfinoid habitus + neuromas)
Kallmann’s Syndrome
- Delayed puberty due to hypogonadotrophic hypogonadism. X-linked recessive.
- Presentation: Anosmia, delayed puberty, male, cryptorchidism, low sex hormones + inappropriately low/normal FSH/LH
- Management: testosterone supplementation (+/- gonadotrophin supplements to -> sperm for fertility reasons)
What are the following?
- Prolactinoma
- Phaeochromocytoma
Prolactinoma
- Pituitary adenomas can be: micro (<1cm) or macro (>1cm) AND secretory (e.g. prolatinoma) or non-secretory
- Prolactinoma –>
- women:amenorrhoea, infertility, galactorrhoea, osteoporosis
- Men: impotence, loss of libido, galactorrhoea
- macroadenoma: headahce, bitemporal hemianopia, hypopituitarism
- Management: Most = dopamine agonist (eg. cabergoline or bromocriptine). Some = surgery (trans-sphenoidal)
N.B. other causes of raised prolactin:
- Pregnancy, oestrogen, stress, exercise, sleep, acromegaly, PCOS, hypothyroid, drugs (metoclopramide, domperidone, haloperidol, phenothiazides)
Phaeochromocytoma = rare catecholamine secreting tumour (can be associated w/ MEN II, neurofibromatosis)
- B/L in 10%; malignant in 10%, extra-adrenal in 10%
- Features; HTN, postural hypotension, headahce, palps, sweating, anxiety
- Test: 24h urinary collection of metanephrines
- Management:
- Initial stabilisation w/ alpha blockers (eg. phenoxybenzamine) and then Beta blockers. Then surgery.
Parathyroid Problems
Parathyroid Problems
Hyperparathyroidism
Causes
Presentation
Investigation
Management
Causes
Primary Hyperparathyroidism (associated w/ MENI and II) (hypercalcaemia + raised PTH due to overactivity)
- Solitary adenoma (80%)
- Hyperplasia (15%)
- multiple adenoma (4%)
- carcinoma (1%)
Secondary Hyperparathyroidism (Hypocalcaemia + reactive raised PTH)
e.g. Kidney failure, vit D deficiency
Tertiary Hyperparathyroidism (ongoing parathyroid hyperplasia after correcting underlying renal disorder in secondary cause) (Hypercalcaemia + raised PTH)
Presentation
Asymptomatic or
**Hypercalcaemia ** (primary/tertiary)
- Stones, moans, bones, groans
- Polyuria/dipsia, depression, anorexia, nausea, constipation, peptic ulceration, pancreatitis, bone pain/#, renal stones, HTN
Hypocalcaemia - normally muscle weakness, weak bones, rickets (if low vit d) etc rather than the acute hypocalcaemia features
Investigation
Primary: raised Ca2+, low phosphate, PTH (raised or normal)/
Secondary: normal/low Calcium, low Vit D, raised PTH, high or low phosphate
Tertiary: raised calcium, low vit D, high PTH, raised phosphate
Other investigations
- Technetium MIBI scan
- Pepperpot skull on X-ray
Management
Primary:
- Most =Total parathyroidectomy
- If unsuitable for surgery - cinacalcet (mimics action of calcium)
- (some can have conservative tx e.g. if Ca <0.25 above upper limit of normal AND patient >50 AND no evidence end-organ damage)
Secondary
- Phosphate binders + low phosphate diet
- Vit D replacmenet
- Calcimimetics e.g. cinacalcet
- +/- parathyroidectomy
Tertiary
- mostly = surgery
Hypoparathyroidism
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
Primary hypoparathyroidism (low PTH)
- low calcium, high phosphate, low PTH
- e.g. secondary to thyroid surgery
Pseudohypoparathyroidism (insensitive to PTH) - genetic disorder that mimics hypoparathyroidism
- associated w/ low IQ, short stature, short 4th/5th metacarpal
- low calcium, high phosphate, high PTH
- diagnosed by measuring urinary cAMP + phosphate following PTH infusion (neither rise in pseudohypoparathyroidism)
Pseudopseudohypoparathyroidism - genetic disorder that mimics pseudohypoparathyroidism
- Similar phenotype to above but normal biochemistry
Presentations (primary hyperparathyroidism)
- Tetany: muscle twitch, cramp, spasm
- Perioral paraesthesia
- Trosseau’s sign: carpal spasm when brachial artery occluded (inflating BP cuff)
- Chvostek’s sign: tapping parotid causes facial muscle twitch
- Chronic –> depression + cataracts
- ECG: prolonged QT
Management (primary)
- PO calcium + vit D replacement
- Thiazide diuretics (reduce urinary Ca loss)
- PTH replacement
Diabetes Insipidus
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
Low ADH/resistance to ADH –> polyuria, polydipsia, dehydration
- Cranial (low ADH) eg. congenital, head trauma, tumour, sheehans, meningitis
- Nephrogenic (insensitivty) eg. genetic, lithium, CKD, post-obstructive
Presentation
- Polyuria, polydipsia, dehydration, hypernatraemia
- Lethargy, thirst, weakness, irritability, confusion, coma, fits
Investigation
- Bloods, exclude DM
- Plasma:Urina osmol (urine = more dilute so excluded if >2:1 ratio)
8h water deprivation test
- normal - urine osmol >600
- DI - urine osmol low. Give desmopressin - if improve to >600 = central. If doesn’t make a difference= renal.
- MRI (?cranial cause)
Management
- IVI resus + manage hypernatraemia
- Central cause: Desmopressin + treat cause
- Nephrogenic: treat cause + bendroflumethiazide
SIADH
Pathophysiology
Presentation
Investigations
Management
Pathophysiology
- Too much SIADH –> hyponatraemia (dilutional)+ water retention
Causes:
- Malignancy: small cell lung, pancreas, prostate
- Neuro: stroke, subarachnoid or subdural
- Meningitis
- Infection: TB, pneumonia
- Meds: SSRI, TCAs, sulphonylureas, carbamazepine
Presentation
- Low urine output
- Hyponatraemia –> n+v, cramps, irritability, confusion, seizures, stupor, coma
Investigation
- Diagnosis: low serum osmol, raised urine osmol + Na
- Ix cause
Management
- correct hyponatraemia (slow to avoid central pontine myelinolysis)
-Mild-mod: Fluid restrict 1st line (+/- may need furosemide if overloaded or RF such as HF)
- Severe/unresponsive: Demeclocycline - reduces responsiveness of CD to ADH (although if due to malig often try to hold off tx as often resolves w/ management of underlying malignancy)
Give possible causes of gynaecomastia
Physiologic (puberty)
Low androgens e.g. Kallman’s, testicular failure (eg. post-mumps), testicular cancer
Raised oestrogen e.g. liver disease, ectopic secretion
Drugs e.g. spironolactone (most common drug cause), anabolic steroids, oestrogens, GnRH agonists
Hyperthyroidism
Haemodialysis (decreases testosterone:oestrogen ratio)
Hypoglycaemia
Causes
Presentation
Investigations
Management
Causes plasma <3.5mmol/l in most; or <4.0 in diabetics
Causes
- Insulinoma
- Liver failure
- Addison’s (hypoadrenalism)
- Alcohol
- meds: insulin, sulphonylureas
Presentation
- sweating, shaking, hunger, anxiety, nausea
- Weakness, vision change, confusion, dizziness
- Convulsion, coma
Investigations
If unexplained cause:
- Bloods: glucose, insulin C-peptide, ketones
Management
- conscious, oriented, able to swallow: 15-20mg quick acting carb, then once >4 give long acting carb
- conscious but confused/disoriented or unable to swallow: glucogel (then quick/slow acting carb; or glucagon/IV if not working)
- unconscious, seizure, ++agressive (or other methods failed) –> IV glucose 20% OR IM glucagon 1mg
(glucagon can only be given once)
Diagnosis and Classification of Diabetes
Diagnostic Criteria
To diagnose DIABETES:
Blood test criteria on 2 separate occassions OR 1 occassion if symptomatic
- Fasting glucose >/= 7.0mmol/l
- Random glucose OR OGTT >/= 11.1 mmol/l
- HbA1c >/= 48mmol/mol (6.5%)
N.B. HbA1c not as sensitive so cannot be used to rule out diabetes. AND cannot be used in: haemoglobinopathies or conditions which reduce rbc lifespan (falsely lowers HbA1c eg. sickle cell, haemolytic anaemia, spherocytosis, haemodialysis) or that raise rbc lifespan (falsely elevates eg. B12/folate def, IDA, splenectomy)
To diagnose Impaired Tolerance
Impaired fasting tolerance: >/= 6.1 but <7
Impaired glucose tolerance: OGTT >/= 7.8 BUT <11.1
(need both tests to rule out diabetes)
HbA1c 42-47 = prediabetes
Classification
- Type 1 (autoimmune destruction of B cells).
- LADA (latent autoimmune DM of adults) - subtype of type 1
- Type 2 (reduced secretion/resistance to insulin)
- MODY (maturity onset diabetes of the young) - subtype of type 2
- Gestational Diabetes
- Steroid Induced
- Other e.g. pancreatic Ca, cushing’s relaed
Type 1 Diabetes
Presentation
Management
Complications
Presentation
- Polyuria, polydipsia, weight loss
- blurred vision
- Thrush
- Fatigue
- Features of DKA: abdo pain, acetone breath, kausmall respiration etc.
- Tends to be younger patients w/ more acute onset than 2
Investigations
- Urine: glucose + ketones
Following if T1 suspected but clinical pres has atypical features (eg. >50yo, BMI >25, slow evolution/long prodrome)
- C-peptide low (because not enough insulin production)
- Diabetes specific antibodies +ve (insulin autoantibodies, islet cell antibodies, antibodies to glutamic acid decarboxylase)
N.B. HbA1c not that helpful in diagnosis
Management
Monitoring
- HbA1c every 3-6/12
- self-monitoring of BMs 4x a day. Target: 4-7 generally (or 5-7 on waking)
Insulin
-1st line: Basal - bolus regime w/ determir BD (base) + rapid-acting insulin analogues prior to meals (bolus)
Also consider adding metformin if BMI >25
Type 2 Diabetes
-Presentation
Investigation
Management
** Presentation **
Older onset, more insidiou, less associated w/ weight loss or DKA features
But otherwise similar to T1DM
- Investigation
- Can do antibodies and C-peptide to help differentiate from T1DM
-Management
HbA1c every 3-6/12 till stable, then every 6/12. (target depends on treatment)
Dietary/lifestyle advice - target HbA1c <48
Lifestyle + Meformin - target <48)
Hypoglycaemic agents target <53
How to decide on initial treatment (if needing meds)
- If low risk: Metformin
- If high risk: Metformin, then once established/titrated add SGLT-2 inhibitor (N.B. need to add this at any point if develops CVS disease) (e.g. -gliflozin
(risk: high CVD rish, prev CVD, HF)
If metformin is contraindicated
- high cvs risk –> SGLT-2 monotherapy
- low CVS risk - DPP-4 inhibitors (e.g -gliptin).or SGLT-2
Second-line management
- Add: DPP-4, pioglitazone, sulfonylurea, SGLT-2 (if NICE criteria met)
3rd line
- Add another drug from 2nd line
- OR start insulin
4th line
BMI >35 OR <35 but insulin not appropriate –> GLP-1 mimetic
Other Risk factor modifcation
- HTN management (same targets as normal)
-<80yo - clinic 140/90 (or home 135/85)
>80- clinic 150/90 (home 145/85)
- If QRISK >10% primary prevention - atorvastatin 20mg
Give common side effects and contraindications for the following hypoglycaemic drugs used in the management of T2DM
SGLT2 inhibitors e.g. -gliflozin
DDP4 inhibitors - gliptins
Thiazolidinediones
Sulphonylureas
GLP-1 Drugs e.g. exenatide
SGLT 2 inhibitors = -Gliflozin
1st line alongside metformin in CVS disease (otherwise need to meet NICE criteria to use it)
Side effects:
- Increased urinary + genital infection (due to glycosuria) - including fournier’s gangrene
- Normoglycaemic ketoacidosis
- Lower limb amputation (monitor feet)
DDP-4 - gliptins
- good if further weight gain would cause problems or if thiazolidinedione is contraindicated
- SEs: rarely can cause acute pancreatits
- CIs: HF, pancreatitis, CKD
Thiazolidinediones - glitazone
(N.B. rosiglitazone not used due to CVS risks)
SEs: weight gain, liver impairment, fluid retention, # risk, bladder cancer
CI: heart failure, bladder cancer
Sulphonylureas
- work by increasing pancreatic insulin secretion so only work if functional B-cells present
- SEs: hypoglycaemic episodes, weight gain, SIADH, marrow supression, hepatotoxicity, peripheral neuropathy
- CI: breastfeeding
Glucagon-like peptide 1 mimetics e.g. exenatide (SC)
- Consider adding to metformin + sulfonylurea if BMI >35 OR <35 w/ if insulin not acceptable
- SEs: nausea _ vomiting
- rarely linked w/ pancreatitis
Diabetic Ketoacidosis
Diagnosis
Presentation
Investigation
Management
Diagnosis
- Glucose >11 or known DM
- pH <7.3 OR Bicarb <15
- Ketones >3 or urine ++ on dip
Presentation
- Abdo pain, polyuria, polydipsia, dehydrration, kussmaul respiration, acetone breath
- Triggers: infection, missed insulin, MI
- N.B. children/young adults are at high risk of cerebral oedema from fluid resus in DKA so need to be monitored closely. Any suspicion needs CT head + senior r/v
Management
- IVI 0.9% NaCl
- Fixed rate insulin infusion 0.1unit/kg/hr (once glucose <15 can start 5% dex)
- Correct electrolytes - K+ (if infusion rate >20 -> cardiac monitoring)
- N.B. continue long-acting insulin whilst infusion running but stop short acting
Resolution: pH >7.3, ketones <0.6, bicarb >15. - once this occurs + patient E+D -> re-start sc insulin
