Endo Flashcards
cushings disease, acromegaly, phaeochromocytoma, osteomalacia, pagets disease of bone, osteoporosis, hyper and hypothyroid, diabetes, addisons
What are the 4 causes of cushings disease/ syndrome and the ACTH and cortisol /crh levels expected in each
1 cause: Exogenous - oral steroids
CAUSES
Cushing’s Syndrome
#1 cause: Exogenous - oral steroids: Cushing’s Syndrome
#2 cause: Endogenous – ACTH secreting pituitary
adenoma (most common), pituitary: Cushing’s Disease
#3 Pseudocushings –
stress/illness/alcoholism/depression
#4 Also consider ectopic ACTH production eg small cell lung cancer or adrenal adenoma
ACTH, Cortisol levels
Cushing’s disease: high ACTH, high cortisol
ectopic ACTH: high, ACTH, high cortisol
primary adrenal disease – low ACTH, high cortisol
Pseudocushings – high CRH, mildly high cortisol
What are the exam signs of cushings disease
EXAMINATION
- Central obesity
- Hypertensive, high blood glucose
- Plethora, moon face, buffalo neck hump
- Supraclavicular fat distribution
- Skin and muscle atrophy
- Bruises, violaceous striae
- Infection prone, poor healing
What are the IX - bloods, imaging for cushings disease
INVESTIGATIONS
Bloods:
- Pregnancy test (exclude in F)
- Blood glucose (elevated)
- 24-hour urinary free cortisol OR late-night
salivary cortisol tests to establish cortisol
levels - False positives in depression, obesity, alcohol excess.
- dexamethasone suppression tests
- (InCushing’s dexamethasone given at 11-12pm with 8-9am cortisol measured - normal pt suppressed morning cortisol, in cushings syndrome no cortisol suppression)
OR
plasma ACTH
- (if undetectable then 1*adrenal tumour, if high - pituitary or ectopic)
- if high Q6H 2mg dexamethasone for 48 hours suppression test: will cause >50% 9am cortisol fall in most pt with cushings but infrequently in ectopic
- CRH test (in pituitary disease cortisol rises, in ectopic it doesn’t)
Imaging:
- MRI pituitary, CT adrenals (looking for mass)
- don’t rely on imaging to localize source, as
many incidentalomas.
- Use localization laboratory tests.
- Inferior petrosal sinus sampling (elevated central: peripheral indicates central source).
Management of cushings disease in general and - For pituitary adenoma, adrenal adnoma, and ectopic
- Stop exogenous steroids
- Surgery or radiation therapy to remove pituitary, adrenal, or ectopic ACTH-producing tumors
Medication
- high protein intake and K administration / K sparing drugs such as spironolactone due to excess mineralocorticoid receptor stimulation by cortisol
somatostatin analogue: block ACTH secretion (pasireotide) + dopamine agonist cabergoline (block ACTH)
steroidogenesis adrenal inhibitor (ketaconazole)
glucocorticoid R antagonist (milfepristone)
- IV infusion etomidate inhibit b-hydroxylase to redue adrenal steroidogenesis: can be life saving for pt with fulminant symptoms
o Pituitary adenoma : trans-sphenoidal pituitary adenectomy. +/- radiation therapy
o Adrenal adenoma- adrenalectomy + med Tx before surgery:
o Ectopic- surgical resection of source +/- chemo/RTX. If disseminated - adrenal enzyme inhibitor - metyrapone, ketoconazole, mifepristone
Post-op hydrocortisone
What are complications of cushings disease before and after tx
- Increased vascular mortality
- HTN and hypokalaemia due to cortisol activating mineralocorticoid receptors
- Diabetes mellitus
- Osteoporosis: GC increased osteoblast and
osteoclast activity; interferes w Calcium absorp in GI tract. - nephrolithiasis
- Post Tx: adrenal insufficiency, central
hypothyroid, GH deficiency, Diabetes insipidus
definition of cushings disease/sndrome
Cushing syndrome is a constellation of clinical abnormalities caused by chronic high blood levels of cortisol or related corticosteroids.
Cushing disease is Cushing syndrome that results from excess pituitary production of adrenocorticotropic hormone (ACTH) secondary to a pituitary adenoma.
SE of ketaconazole, mifepristone, pasireotide
Pasireotide - hyperglycaemia
Mifepristone- hypokalaemia bc blocks corticosteroid, blocks action of steroid not lower its levels so monitoring hard
Ketaconazole - block corticosteroid,hepatotoxicity, QT prolongation and addisonian symptoms (adrenal insufficiency): eg, weakness, fatigue, orthostatic hypotension, hyperpigmentation).
Acromegaly definition and hx
DEFINITION
Increased secretion of GH (growth hormone) from:
- a pituitary tumour
- pituitary hyperplasia via ectopic GHR hormone from a carcinoid tumour
GH stimulates bone and soft tissue growth through
secretion of insulin like growth factor (IGI-1)
HISTORY
- Acroparaesthesia (tingling extremities)
- Shoes/rings not fitting, wonky bite, curly hair, altering appearance
- Amenorrhoea, decreased libido, headaches, increased sweating, snoring, arthralgia, backache
- OSA features
Examination and complications acromegaly
EXAMINATION
- Large hands and feet
- Tanned, acanthosis nigricans
Course face, wide nose, big supraorbital ridges
- Prognathism
- Macroglossia, spaced teeth
- Puffy lips, eyelids.
- Skin tags
- Goitre (increased vascularity)
- Proximal weakness, carpel tunnel bilateral (50%)
- Signs from pituitary mass; decreased vision, bitemporal hemianopia, seizures
COMPLICATIONS
- Impaired glc tolerance and DM
- Vascular – high BP, LVHypertorphy (+/- dilatation and CCF), arrhythmias,
- increased risk of IHD and stroke (? due to HTN +/- insulin resistance, GH-induced incr fibrinogen & decr protein S.
- Increased risk of colon cancer
Ix for acromegaly
INVESTIGATIONS
Bloods:
- Serum GH
- high glucose, high Ca and phosphate
- Don’t rely on random GH as secretion
pulsatile. Normally GH secretion is inhibited
by glucose, so perform OGTT, measuring GH
at 0,30,60,90,120 mins. If lowest GH is
>1ug/L acromegaly is confirmed.
Imaging:
- MRI to visualize pituitary fossa
Other:
- ECG
- ECHO
- Visual fields and acuity
- Old photos
Management & follow up of acromegaly
MANAGEMENT
1) Surgical removal of tumour (transsphenoidal) to reduce GH and IGF-1 to ‘safe’ levels
2) If surgery fails to correct hypersecretion, somatostatin analogues (GH inhibiting hormone) e.g. Octreotide
3) If resistant or intolerant to SSA, GH
antagonist e.g. Pegvisomant
Follow up
- Yearly GH, IGF-1, OGTT
- Yearly visual fields, vascular assessment, BMI,
photos
- Colonoscope consideration
phaeochromocytoma definition + presentation
DEFINITION
Catecholamine secreting neuroendocrine tumour of
adrenal medulla. Arise from sympathetic paraganglia cells, which are collections of chromaffin cells.
Extra-adrenal tumours are rarer, often found by
aortic bifurcation.
10% rule: 10% are malignant, 10% extra-adrenal,
10% bilateral, 10% familial.
PRESENTATION
- triad: episodic HA, sweating, tachycardia
- +/- HTN
- palpitations, skin sensations, flank pain,
visual changes, N/V/D
Ix (blood, imaging) + management + monitoring phaeochromocytoma
NVESTIGATIONS
Bloods
- plasma + 3 x 24hr urines for free metanephrines (elevated) & catecholamines (secreted intermittently)
- clonidine suppression test
MRI chest and abdo
- salt & pepper pattern
- MIBG (chromaffin seeking isotope) scan
MANAGEMENT
Medications
- a-blockade pre-op (phenoxybenzamine) used to avoid unopposed a-adrenergic stim.
- B-blocker after a blocker if heart disease or tachycardic.
- Need anesthetic consult.
Surgery
- Resection
MONITORING
- 24hr urine metanephrines 2/52 post-op, monitor BP
- lifelong f/u (malignant recurrence), genetic screening in younger patients (multiple endocrine metaplasia)
Osteomalacia definition, hx, exam and causes vs osteoporosis definition
DEFINITION osteomalacia
Normal bone mass + reduced mineral content.
Results in rickets if during bone growth,o steomalacia if after fusion of epiphysis. Basically, bones are soft.
Osteoporosis Definition: Loss in bone mass with normal mineral content. Bone loss is trabecular and cortical.
HISTORY and EXAMINATION
Bone pain, fractures (especially femoral neck),
proximal myopathy (waddling gait) due to vit D def
CAUSES
- Vitamin D Deficiency (most common)
- Calcium or phosphate deficiency
- Renal and Liver Disease
- Anticonvulsants
- High risk if low sun exposure (old people)
Ix of osteomalacia + management
INVESTIGATIONS
Bloods – low Ca and Phos, high alk phos and PTH,
low calcidiol, low vitamin D
Biopsy – bone biopsy shows incomplete mineralization
X-Ray – loss of cortical bone, non-displaced partial fractures.
MANAGEMENT
- Vitamin D and calcium supplements
(calcefort)
Pagets disease of bone definition, hx and exam and complications
DEFINITION
Increased bone turnover associated with increased
numbers of osteoblasts and osteoclasts leading to remodeling, bone enlargement, deformity,
weakness.
- cause unknown - genetic or viral trigger
HISTORY and EXAMINATION
- Asymptomatic (70%) – high ALP found incidentally
- Bone pain, joint pain – most common symptoms
- Pathological fractures
- Bony deformities of the pelvis, lumbar spine, skull,
and femur – usually affects a small number of bones, rest normal
- Abnormal gait
- Neurological symptoms
COMPLICATIONS
- Pathological fractures
- Osteoarthritis
- Nerve compression due to bone overgrowth (deafness, root compression)
- High output CCF
- Osteosarcoma
Ix and management paget disease of bone
INVESTIGATIONS
Bloods - Ca and Phosphate normal, alk phos raised
X-ray - shows localized enlargement, patchy cortical
thickening with osteolysis, sclerosis, deformity.
- Affinity for axial skeleton, long bones, skull.
MANAGEMENT
No cure
- Analgesia
- Alendronate (reduce pain)
- Sometimes surgery – osteotomy
- Lifestyle – Increase Ca diet, sun, exercise
Can screen those at high risk (fam history) with ALP
levels
Addisons disease; definition, and cause
DEFINITION
-primary adrenal insufficiency
-destruction of adrenal cortex = deficiency in
corticosteroids and mineralocorticoids
-anyone on steroids for long enough to suppress
adrenal glands is at risk
CAUSE
-80% autoimmune
-Tb (commonest worldwide)
-adrenal mets
-lymphoma
-exogenous steroids (although this is secondary
adrenal insufficiency)
Hx and exam Addisons disease + addisonian crisis
HISTORY
mineralocorticoid def:
- dehydration, hypotension : dizziness, faints , n&V abdopain
glucocorticoid def
- insulin sensitivity: hypoglycaemia, weakness, anorexia,
- myocardial weakness - reduced CO
^^ pit ACTH - increase melanocyte stim:
-pigmented palmar creases and buccal mucosa (but not in addisons 2nd to pituitary failure)
EXAMINATION
-pigmented palmar creases and buccal mucosa
-postural hypotension
-Addisonian crisis : under physiologic stress.
(profound weakness, severe abdomen very low BP, tachycardia, renal shutdown with azotemia, severe fever, shock.
Ix and treatment for addisons
INVESTIGATIONS
-low Na, high K (mineralocorticoid def)
-low glucose
-Synacthen test (synthetic ACTH) – measure cortisol before and after, should rise in healthy person but not in Addison’s
-serum ACTH – will be high in Addison’s
-adrenal autoantibodies – positive in autoimmune cases
-CXR – signs of Tb, or mets
TREATMENT
-replace steroids (hydrocortisone and
fludrocortisone in doses throughout day
-give IM hydrocortisone injection for crises
Risk factors for osteoarthritis - 12, + presenting complaint
Presentation
- Fragility fracture – fall from standing height or less
- Typically femoral neck , spine, greater trochanter, distal radius
Risk Factors
- Old age
- Family History
- Steroid Use (glucocorticoids inhibit osteoblasts + others)
- Hyperthyroid (increases bone turnover)/ hyperparathyroid/ calcinuria
- Alcohol + smoking
- Testosterone deficit F>M – (testosterone helps building bone)
- Thin (BMI <20)
- Early menopause (less estrogen – increased bone turnover and resorption)
- Renal failure (reduced vit D converted to active causes PTH increase to mobilise ca from bone to blood)
- or liver failure (mixed malnutrition, reduced vit D hydroxylation before kidney)
- Erosive/inflammatory bone disease like RA (systemic inflammation + steroid use)
- Dietary low calcium, malabsorption eg. coeliac (low vit D), T1DM (modulates osteoblast activity )
Ix, Scoring system and dx parameters for osteoporosis with potential secondary ix
Investigations
1. Bloods
- Ca, phosphate, ALP should be normal in osteoporosis
- Xray after a fracture : hypo chondral sclerosis, joint space narrowing, osteophytes, altered trabecular pattern, cortical thinning and increase radiolucency, joint
- Bone density DEXA scan in patients with
- low trauma fracture
- women <65 with 2 + risk factors
- women >65 with 1 risk factor
- prior to long term steroid use
- bone and remodelling disorders
Alternatively can use a fracture risk calculator – eg FRAX or Garvan Fracture Risk Calculator
FRAX score calculates the risk of osteoporotic fracture and hip fracture in next 10 years. IF >10% then advocate for BP treatment. Eligible for BP if hip fracture risk >3.5
- DIAGNOSIS is with T score (number of SD away from youthful average of bone mineral density)
- -1 to -2.5 is osteopenia – lifestyle advice
- > -2.5 is osteoporosis
If T score >2 consider : - renal function
- parathyroid hormone
- testosterone and SHBG in males
- LH and FSH
- Coeliac antibodies
- TSH
- Serum protein electrophoresis
Treatment - pharm and non pharm for osteoporosis with SE for bp
Non Pharmacological
- Quit smoking and reduce alcohol <2 drinks/day, >2 alcohol free days
- Weight bearing and balance exercises
- Ca and Vit D rich foods + sun exposure
- Home base fall prevention programme
Pharmacological
1. Supplemental Vitamin D if inadequate sun exposure/intake : colecalciferol 1.25mg monthly
2. Biphosphanate for pt >70 with T score -3 or less, minimal trauma fractures or prevention in long term steroid use
- Alendronate 70mg po weekly on empty stomach with water, upright for 30 minutes after .
- Fosamax plus one tab weekly has vit d added in already
- Monitoring : P1NP after 6 months– marker of bone turnover so if high not compliant, <35 is good
- CI: oesophageal abnormalities, can’t sit upright, hypocalcaemia
- Zolendronic acid infusion 5mg over 15 minutes annually
- CI is eGFR<35 ml/min, give vit D before infusion
- SE: osteonecrosis of jaw – check dentition before starting
- HRT –Raloxifene 60mg daily for women within 10 years of menopause + menopausal symptoms
- CI: MI, stroke, breast cancer, sex steroid responsive tumours, DVT - Recombinant PTH: teriparatide 20 mcg sub cut once daily for 18-24 months
- SA Indicated for T score <-3 with hx fo 2+ fractures or 1 fracture after year of bisphosphonate treatment
- CI: hypercalcaemia, GFR <35ml - Androgen replacement in hypogonadal men
- Denosumab in renal fracture on bisphosphonate but SA
Hx of hyperthyroid vs hypothyroid
Hyperthyroid
Diarrhoea, ↓weight, ↑ appetite, over-activity, sweats, heat
intolerance, palpitations, tremor, irritability, labile
emotions, oligomenorrhoea ± infertility.
Rare: psychosis, chorea, panic, itch, alopecia, urticaria.
Hypothyroid
Sleepy, tired, lethargic, ↓ mood, colddislike, weight ↑, constipation,
menorrhagia, hoarse voice,
↓memory/cognition, dementia,
myalgia, cramps, weakness.
Associations: Turner’s, Down’s, CF
Examination of hyperthyroid incl graves vs hypothyroid
Tachycardia, arrhythmia (AF, SVT), warm moist skin, fine
tremor, palmar erythema, thin hair, lid lag, lid retraction.
Goitre
Signs of Grave’s – exophthalmos, ophthalmoplegia,
pretibial myxoedema, thyroid acropachy, proximal myopathy, carpel tunnel. If eye disease, test VA and VF.
Hypothyroid
Bradycardia, cool dry palms, pallor, dull expression, puffy eyes, thin dry hair, goitre (diffuse or multinodular),
retrosternal percussion, Pemberton’s, ascites,
pleural/pericardial effusion, slow relaxing pulses. Knee and biceps hyporeflexia
Ix for thyroid
T3, T4, TSH.
Hyper – ESR, Ca, LFTs, normocytic anaemia.
Hypo – Chol, TG, macrocytic a.
Antibodies : Antithyroid Peroxidase (TPO) (H>G), TSH Receptor Antibody (G)
Ultrasound : cystic/solid, single nodule/multinodular
Isotope Scan:
cause (hot lesion => hyperthyroid, cold lesion =>20% malignant,
retrosternal goitre, ectopic thyroid tissue, metastasis
Causes of hyperthyroidism and causes of hypothyroidism
Hyperthyroidism
Graves
- IgG autoantibodies to thyrotropin receptor, react
with orbital antigens. Triggers like stress,infection.
Toxic MNG
- multiple thyroid hormone secreting nodules
Toxic Adenoma
- single thyroid hormone secreting nodule
Thyroiditis, initially
- Hashimoto’s, postpartum, subacute de Quervain’s
thyroiditis (post viral)
Drugs
- Amiodarone, levothyroxine
Hypothyroid
Acquired
- iodine deficiency, iatrogenic, (surgery, radioiodine,
carbimazole, lithium)
Autoimmune
- Primary Atrophic (lymphocyte infiltration, no goitre)
Hashimoto’s ( TPO antibodies)
Congenital hypothyroidism
Inflammation
Post-partum thyroiditis, subacute thyroiditis
Secondary
Hypopituitarism
managmeent hypothyroid vs hyper, + SE
Hyper
- Drugs - propranolol for palpitations
Carbimazole (15mg BD) or Propylthiouracil
(150mg BD)- Titrate to TFT’s. 12 - 18 months then withdraw.
SE: agranulocytosis - stop and urgent FBC if signs of infection.
Radioiodine - Most become hypothyroid post treatment.
Contraindicated in pregnancy and lactation and caution in active hyperthyroidism as risk of thyroid storm
Thyroidectomy - risk damage to recurrent laryngeal nerve and hypoparathyroidism
HYPO
Levothyroxine (T4) 50-100 μg od.
Check at 12 weeks then 6 weekly, aim to normalise TSH. If IHD or elderly start with 25 μg.
Liothyronine (T3) - small group pts defective in 5’deiodinase to cant convert to T4
Complications of hyperthyroid vs hypothyroid
HYPER
Severe: Thyrotoxic periodic paralysis + thyroid storm (fever, >200bpm), HF, angina, AF, osteoporosis,
ophthalmopathy, gynaecomastia,
HYPO
Pregnancy problems (eclampsia, anaemia, prematurity), heart disease, dementia.
What is the presentation symptoms of DM - different causes of T1 , T2 + others (3)
Presentation
-Symptoms of hyperglycaemia :
-Polydipsia, polyuria, thirst
-Unexplained weight loss
- Visual blurring
- Candida infection
- Lethargy
- Ketoacidosis
T1 - autoimmune usually symptomatic <35 yo
-T2: usually incidental or with complications
Other causes of diabetes
- Drugs: steroids, antipsychotics, thiazide diuretics , cocp
- Pancreatic: pancreatitis, cancer, destruction with haemochromatosis or CF, surgery
- Endocrine diseases: cushings, acromegaly, phaeochromocytoma, hyperthyroidism, pregnancy
Risk factors for T1 and T2 dm, Ix for T1 and T2 - cut offs for bloods for dx
For type 2 RF
- Family history of t2dm, gest dm
- BMI elevated, age, race
- Previous IGT or gest dm
- Hypertension
- Polycystic ovaries
IX Type 2
-HbA1c >50 = diabetes. >40 IGT - note unreliable in haemoglobinopathy, haemolysis, second & third trimesters
- Blood glucose – 2x Fasting blood glucose >7mmol or 2 hour post prandial glucose >11.1
- Urine or plasma ketones
- Urine protein to creatinine ratio
Type 2: high lipids, hypertension, high BMI
For type 1
RF : Autoimmune disease, coeliac, thyroid disease
IX
- low C peptide
- evidence of high b-hydroxybutyrate in blood or ketones in urine,
- positive Anti-GAD, anti Insulin antibody (IA2), Islet cell antibodies ICA, insulinoma antigen 2 (I2A) or anti ZnT8 antibodies
Pancreatic: low faecal elastase
Treatment of Type 2 dm - lifestyle, oral meds - moa, insulin regime
-150 min moderate intensity exercise / week
-Weight loss 5-10% - Green prescription
-Diet – reduce sugary beverages – consume high fibre
Oral medications
1. Metformin 500mg BD -> SE GI upset – DNV+ anorexia. CI: eGFR<30. Stop
2. + empagliflozin SGLT2 inhibitor
or dulaglutide (GLP-1 agonist),
vildagliptin (DPP4 inhibitor), sulfonylurea or pioglitazone
3. Can initiate insulin or combine 3 oral glucose lowering medicines or two oral + dulaglutide
- Insulin if despite oral therapy HbA1c >55 in young, >64 in old
- Basal insulin regimen is preferred option – once nightly injection
- – isophane intermediate
- insulin glargine (+ testing strips and needles).
- ‘Initial dosing is 0.1u/kg/day if older/liver or renal failure, 0.2u/kg/day if hba1c >64 + BMI >18
- Monitoring BSL before meals and before bed. Pt to reduce insulin dose by 10-20% if hypo (<4)with no cause. Uptitrate 2-3 units until targets reached
What are macrovascular complications of dm + treatment
Macrovascular
-Cardiovascular disease (MI)
-Cerebrovascular disease (TIA/Stroke)
-Peripheral vascular disease
Treatment
- Annual review of CVS risk factors
1.Hypertension: Ace or ARB – aim 130/80
2.Control lipids and triglycerides: statins +/- fibrates
3.Smoking cessation
4.Antiplatelet: aspirin prophylaxis if >CVS risk factors
What are the microvascular complications and treatment of DM - neuropathy separate card
Retinopathy: cotton wool spots, haemorrhage, neovascularisation
-2 yearly ophthalmology review
-Laser treatment - photocoagulation
-Screening for other disease – cataracts and glaucoma from vessel formation in the iris
Nephropathy
- Arteriolar disease causes glomerulosclerosis and ascending infections
o Microalbuminuria – urine alb:cr >30-300mg/day
–> Dipstick proteinuria– >300mg/day in nephrotic range –> end stage kidney disease
o Presents with dysuria, nocturia, oedema, hypertension
Treatment
1.Control BP
- Acei and ARB = renoprotective as soon as proteinuria
2.Treat UTI
3.Dietary protein restriction
4.Management of ESRF – peritoneal dialysis > haemodialysis which worsens retinopathy
diabetic neuropathy types (5) and treatment
Types
- Peripheral Symmetrical sensory neuropathy : glove and stocking loss of vibration > pain > temperature. Late stage loss of balance.
- Autonomic Neuropathy
-Gustatory sweating,- Gastroparesis – post prandial fullness and vomiting, nocturnal diarrhoea
- Cardiac denervation with tachycardia
- Postural hypotension
- Atonic bladder with incomplete emptying
- Sexual dysfunction
Acute painful neuropathy: burning pain worse at night, remits within 3-12 months of control
Mononeuropathy/mononeuritis multiplex:
- CN3 lesions (pupil sparing CN3 palsy , isolated VI,
- L4-S2 peroneal nerve (weakened dorsiflexion and eversion of foot, sensory deficit in anterolateral lower leg and first webspace)
- Median nerve carpal tunnel – paresthesia in radial palmar aspect , thumb abduction and opposition
Diabetic amyotrophy : painful asymmetrical wasting of quads, decreased knee reflex and improves with better control
Treatment of Neuropathy
Pain
- Amitriptyline + nortriptyline – note anticholinergic SE: dry mouth, dry eyes, urinary retention, hypotension)
- Gabapentin or carbamazepine for pain
- Orthotics + podiatry : regular foot checks
Treatment of Autonomic dysfunction
- Hypotension: TED stockings, advice
- Gastric paresis: metoclopramide or domperidone
Summary of f/up for diabetes
Follow up summary
- 3 monthly: BP + Hba1c, renal function and acr. Podiatrist review
- Annual weight, PVD and CVS status review
- Two yearly retinal screening
Blood sugar targets for treatment of type 2 and what to do if target not reached
BLOOD SUGAR TARGETS
- Pre breakfast <7, 2 hr post meal <10. Pre dinner <6-7.
- IF still no controlled do basal + meal time boluses – (10% of basal insulin up to 10 u of rapid acting before the largest meal )
- OR
- switching to biphasic insulin formation with rapid acting such as novomix 30 which is 2x daily injection before breakfast and dinner.
Reasons for hypoglycaemia in dm
Hypos
- On insulin or sulphonylureas
- Hypoglycaemia in previous stable diabetic on insulin therapy most commonly caused by:
o Decreased food intake, increased exercise or weight loss
o Injection errors, injection into lipohypertrophied sites
o Diabetic renal disease
Treatment of t1 Dm
TYPE 1 (+2 FOR dnS)
Diabetes Nurse Specialist involvement for education
- Re: sick day plans (withholding some meds), miss meals, travelling, managing hypos, monitoring, administration of insulin, use of medic alert bracelet, driving safely
Basal + boluses – need to carb count for boluses based on a previous unit insulin to carbohydrate ratio
