Endocrine Flashcards
definition of hypoglycemia
< 3.3
what is Whipple’s triad for hypoglycaemia
symptoms of hypoglycemia, blood glucose level low, resolve of symptoms after blood glucose level back to normal
causes of hypoglycemia in known diabetes
hypoglycaemia (using sulphonylureas eg gliclazide, insulin)
dec glucose delivery (missed meal, fasting)
inc glucose utilisation (exercise)
dec endogenous glucose production (alcohol)
inc insulin sensitivity (weight loss)
dec insulin clearance (renal failure)
pregnancy - tight control
causes of hypoglycemia in non-diabetes
pituitary insufficiency - low ACTH
Addison’s disease - low BP, low NA, high K, low aldosterone and ACTH
exogenous drugs (quinine, chloroquine, B-blocker overdose, valproate, aspirin, insulin)
post-meal hypoglycemia
liver disease
Immune Hypo (anti-insulin Ab, or Hodgkins)
non-pancreatic neoplasm (small cell, fibroma, sacroma)
NIPH syndrome - noninsulinoma pancreatogenous hypoglycaemia (islet cell hyperplasia)
starvation + malnutirition
hypothyroidism (myxoedema coma)
symptoms of hypoglycaemia
lethergy weakness sweating shaking tingling lips and tongues uhnger palpitations headache double visions difficulty concentrating slurred speech confusion change in behavior coma
what scale is used to represent the symptoms of hypoglycaemia
Edinburgh hypo scale - 11 most common hypoglycaemic symptoms
Autonomic nervous system
- sweat
- palpitation
- shaking
- hunger
Neuroglycaemic
- confusion/drowsy
- dec GCS
- slurred speech
- odd behaviour
- incoordination
General
- malaise
- Nausea
what are the investigations for hypoglycaemia
- blood glucose < 3.3
- Bloods: FBC/UE/LFT, blood glucose, HBA1c, serum insulin
- C peptide (elevated if endogenous insulin production – either insulinoma or sulfonylurea use)
- Beta-hydroxybutyrate - < 2.7 mmol/L, low = diagnosis of mesenchymal tumour
- serum sulfonylurea
- TSH – hypothyroidism can cause hypoglycaemia
- serum cortisol – pituitary insufficiency
management of hypoglycemia if GCS is 15
If GCS15:
- Fast acting sugar: 7/8 jelly babies (not chocolate), 10-20g dextrogel. and
- Long acting: 2 toast/ cereal
- Check BG after 15mins- aim for 5- repeat x3 above management until normal
- BM<3 then 1mg IM glucagon.
GCS<15: assume they cant swallow or IV access cannot rapidly established
- 75ml 20% glucose / 150ml 10% glucose IV or 1mg IM glucagon.
- Check after 15mins- aim for 5 x3 until normal.
pathophysiology of DKA
- Ketoacidosis occurs in starvation states and produces acetone.
- In DM a lack of insulin means that glucose cannot be used, pushing the body into the starvation state.
- A lack of insulin stimulates the release of glucagon from the alpha cells which stimulate glycogen breakdown, gluconeogenesis, release of free fatty acid which are converted by the liver to ketones. = HIGH KETONES.
- Excess glucose excreted by kidneys due to osmotic diuresis = HIGH URINE GLUOCSE.
- lipolysis ketogenesis and metabolic acidosis = METBAOLIC ACIDOSIS.
what are the clinical features of the first presentation of DKA in a T1DM?
sudden onset weight loss ployuria polydipsia non-specific abdo pain drowsy confusion Kussmauls' breathing Ketoci breath N+V dehydration inc urination (osmotic diuresis)
usually due to alcohol intake (because alcohol inc insulin in the blood stream and so less insulin to get glucose into cells)
what are some of the causes of DKA
4Is
infection - UTI, RTI, skin
Infarction - MI, stroke, GI tract, peripheral vasculture
INsufficient insulin
intercurrent illness - many underlying conditions precipitate or aggravate DKA
what are the diagnostic criteria for DKA
BLood glucose > 11
Ketone - urine 2+ or blood > 3mmol/L
Metabolic acidiosis - pH < 7.3 +/- HCO < 15mmol/L
what are some investigations for DKA
FBC - WCC U&E - inc urea, creatinine, dehydration LFT CRP amylase blood glucose blood culture HbA1c.
ABG/VBG - metabolic acidosis, dec bicarb
Urine dip +/- MCS - for infection, ketones, protein, glucose
find infection ECG (exclude MI, tall tented in hyperK) CXR - RTI infection MSU Pregnancy test
beware of pseduohyponatreamia - for every 4mmol dec of glucose –> 1 mmol dec in Na+
what are the 9 steps for treating DKA
ABCDE
• SpO2, ECG, BP/HR, 2 large bore cannulas
1) diagnosis – pH, Ketones, BM
2) immediate treatment
a. 1L 0.9% NaCl over 1 hour if BP > 90
b. If BP < 90, 500ml bolus stat, max 2L if BP still low, call criteria outreach
c. start IV insulin – 50 unites quick releasing insulin in 49.5 ml NaCl 0.9% to give 0.1 unit/ml solution via syringe driver at 0.1units/kg/hour
d. call diabetes speciliast team
3) call critical care for review if
a. venous bicarb < 5 or pH < 7.1
b. drowsy (GCS < 12 or abnor AVPU)
c. pregnant
d. heart failure
e. oliguria or anuria
f. sat < 92% on air
g. persistent hypotension < 90 systolic after 2 L
h. K+ < 3.5mmol/L on admission
4) Essential investigations – as mentioned above
5) Insulin – fixed rate insulin (0.1 unites/kg/hour) + continue long acting insulin
6) IV fluids
a. 1L NaCl 0.9% over 1 hour then
b. 1L NaCl 0.9% over 2 hours then
c. 1L NaCl 0.9% over 2 hours then
d. 1L NaCl 0.9% over 4 hours
e. when glucose < 14 mmol/L continue IVI +/- KCL + 10% glucose 125ml/Hour
7) potassium (start after 2nd IV fluids not resus fluid)
a. if <3.5 senior review (>40 mmol/litre maybe necessary)
b. 3.5-5.5 40mmol KCl per litre of NaCl
c. >5.5 – none
8) Monitoring
a. re-assess hourly for first 4-6 hours
b. check vital signs hourly
c. consider catheter if clinical evidence of poor LV or renal function
d. consider NGT if drowsy
e. treat underlying causes for DKA
f. give LMWH to all (thromboprophylaxis)
g. treatment target
i. blood glucose falls of >3mmol / L / hour until < 14
ii. cap ketones fall of at least 0.5mmol / litre / hour until <0.6
iii. venous bicarbonate rises of > 3 mmol/ litre . hour until > 15
iv. if not improving, inc rate of insulin infusion by 1 unit / hour every hour
9) After recovery
a. transfer to SC insulin if pt able to eat and drink well and pH > 7.3 or blood ketones < 0.6 mmol/L
what is the function of insulin
it moves glucose from bloodstream into cells for energy consumption
which cells is destroyed in T1DM
beta cells of islet of Langerhans in the pancreas
symptoms of T1DM
acute onset
25-50% present with DKA
thin (low BMI)
4Ts - thirst, toilet, thinner, tired
genital itchy or frequent episodes of thursh
wounds heal slowly, boils
recurrent/prolonged infections
what is the investigation regimen of suspect T1/2DM with symptoms
singe episode of test of the following:
fasting blood glucose > 7 or
random blood glucose >11.1 or
2 hour fasted glucose > 11.1 (after 75g of glucose) or
HbA1c of 48
also
1) HbA1c
2) FBC - chronic anaemia, elevated WCC
3) U&Es - baseline renal function
4) TFTs
5) LFT
6) tissue transglutaminase (tTG)
what is the investigation regimen of suspect T1/2DM without symptoms
2 sperate episodes of testing (2 wk apart) of the following:
fasting glucose > 7 or
random glucose > 11 or
HbA1c > 48 on 2 occasions
also
1) HbA1c
2) FBC - chronic anaemia, elevated WCC
3) U&Es - baseline renal function
4) TFTs
5) LFT
6) tissue transglutaminase (tTG)
differentials for T1DM
LADA - latent autoimmune diabetes of adulthood
MODY - Maturity Onset Diabetes of the Young
T2DM
dibaetes insipidus
UTI
what are the different treatment regimen of T1DM
basal-bolus
insulin pump
2 injections per day
1 injection per day
when will basal-bolus (multiple daily injections) regimens be beneficial for patients
good physiological management
can be flexible to those with varied meal/exercise
only for those who can do multiple injections per day
when is insulin pump insulin treatment regimen used
when MDI fails
when is 2 injections per day regimen used?
rarely used nowadays
good for those unable to give multiple injections
what is the SICK day rule for Diabetes?
management of blood glucose during sickness
1) Sugar - sugar measurement inc, frequency every 2-3 hrs
2) I - Insulin = keep taking it
3) C - keep taking carbohydrate and fluids
4) K = measure ketones (4 hours)
drink at least 3 L of fluid
what is the essential mechanism for T2DM
peripheral resistance to insulin –> blood unable to break down glucose into energy properly
clinical features of T2DM
- Gradual Onset
- Polydipsia (thirst)
- Polyuria, esp nocturia
- Often obese (high BMI)
- Lethargy, blurred vision
- Genital itching (pruritius vulvae), frequent episodes of thrush, UTI
- unintentional weight loss
- DKA rare
- Wounds that heal slowly, boils
- Recurrent/prolonged infections
Treatment for T2DM
• 1st step lifestyle + aim for HbA1c of < 48
• 2nd step metformin if HbA1c > 48 + aim for < 48
• 3rd step/1st intensification if HbA1c > 58 dual therapy & aim for HbA1c < 53
o metformin + DPP-4i
o metformin + pioglitazone
o metformin + SU
o metformin + SGLT-2i
• 4th step/2nd intensification if HbA1c > 58 triple therapy & aim for HbA1c < 53
o metformin + SU + DDP-4i or pioglitazone or SGLT-2i
o metformin + SU + GLP-1
if not tolerate the above combination and have BMI > 35 and specific psychological and other medical problems associated with obesity
BMI >35 and insulin would not be suitable
BMI < 30 and South Asian
• 5th step/3rd intensification Insulin (refer for this)
complications of T2DM
HHS microvascular disease Macrovascular disease inc BP cataracts fatty liver disease
When is the management for ACR > 2.5 in men or 3.5 in women?
ACEi or ARB and maintain BP <130/80
pathophysiology of diabetic foot disease
diabetes causes nerve damage - causes infection and charcoat’s
diabetes causes PVD - ulcers and gangrene
what are the 3 main types of diabetic foot disease?
1) Charcoat’s Arthropathy - refers to progressive degeneration of the weight-bearing joint, a process marked by bony destruction, bone resorption and eventually deformity due to loss of sensation
2) diabetic foot infection - caused by repetitive foot trauma which becomes infected
3) diabetic foot ulcer - caused by repetitive foot trauma due to lack of sensation
clinical features of charcoat’s arhtorpahty
pain redness swelling deformity (skin intact) maybe associated with foot ulcer
clinical features of diabetic foot infections
fever pain red swollen hot to touch purulence
maybe able to see some break in the skin
clinical features of diabetic foot ulcers
eroded ulcer
commonly found on pressure points
can results in dry or wet gangrene
when will you refer a patient with diabetic foot disease
for all diabetic foot pathology refer within 1 day
life-threatening limb injury (refer immediately)
- ulceration with fever
- ulceration with limb ischaemia
- concern of osteomylitis
- gangrene
investigation for charcot’s foot
weight bearing X-ray of foot and ankle
consider MRI
investigation for diabetic foot infection
FBC + blood glucose
soft tissue or bone sample from base of the debrided wound
if this cannot be obtained take a deep swab
consider X-ray
investigation for diabetic foot ulcer
assess using SINBAD Size ischaemia neuropahty Bacterial infection area depth
management of charcoat’s foot
acute - monitor treatment usinf foot skin temperature difference in both feet and serial X-rays
1st line - non-removable offloading device
2nd line - removable offloading device
management of diabetic foot infection
start abx
reassess in 1-2 days when improvement should be seen
consider x-ray to assess full extend of the body
management of diabetic foot ulcer
nonremovable casting off loading
control infectio n and ischemia
wound debridement
wound dressing
management of limb ischaemia
refer to vascular
revascularisation - bypass
angioplasty
stent
what are the causes of hyperthyrodisim
grave’s disease
toxic multi-nodular goitre
amiodarone
what are the causes of hypothyroidism
7 in total
Hashimoto's thyroiditis Subactue Hypothyroditis - *de Quervain's Iodine deficiency lithium Riedel's thyroiditis postpartum thyroiditis amiodarone
definition of Graves’ Disease
Autoimmune hyperthyroidism causes by stimulation of the thyroid by TSH receptor antibodies.
Aetiology of Graves’ Disease
• Autoimmune: reason for autoimmunity is unknown, 80% genetics and 20% environmental
RF for Graves’ Disease
female
Fhx
tobacco use
clinical features of Graves’ Disease
Systemic
- heat intolerance
- sweating
- weight loss
- palpitations
- tremor
- tachycardia
- anxiety/depression
- SOB
- hair loss
- moist, smooth skin
- dirrhoea
Eye
- upper lid retraction
- exophthalmos
- optic neuropathy
other
- irregular menstruation, often amenorrhea
- loss of libido
- oncycholysis - detachment of nail from nailbed
- cardiac flow murmur - due to inc flow of blood through the heart valve
- palmar erythema
- proximal muscle weakness
- toxic diffuse goitre
- thyroid acropachy
- pretibial myxoedema
Investigation for Graves’ Disease
TSH (suppressed)
serum free or total T4 - elevated
serum free or total T3 - elevated
thyroid isotope scan - diffuse uptake
radioactive iodine/technetium uptake - elevated
TSH receptor antibodies - +ve
thyroid USS - goitre/enlarged
CT/MRI of orbit – may show muscle thickening
Skin biopsy – may show thyroid dermopathy
management of acute thyroid storm of Graves’ Disease
High dose antithyroid (carbimazole or polythiouracil or thiamazole )
corticosteroids (Hydrocortisone)
beta-blocker (propranolol - congestive heart failure)
iodine solution with supportive care.
+/- Cholestyramine (bile acid to reduce enterohepatic circulation of thyroid hormones)
lithium – to reduce thyroid hormone reduce
• supportive care cooling, correction of volume, resp support
what is acute thyroid storm?
volume depletion, congestive heart failure, confusion, N+V
when can acute thyroid storm occur
after radioactive iodine therapy due to release of stores of thyroid hormone
or at any time
management of non-acute Graves’ Disease
- 30% spontaneous remission
- block and replace therapy - carbimazole titration/carbimazole + levothyroxine replacement
- +/- propranolol
- Definitive Rx: radioactive iodine or thyroidectomy +/- prednisolone + levothyroxine after surgery/iodine
- +/- methylprednisolone (for orbitopathy)
- +/- Triamcinolone acetonide topical (for dermopathy)
SE of antithyroid meds
agranulocytosis - leukopenia
what is another name for Adrenocortical insufficiency?
Addison’s Disease - where adrenal glands do not produce enough steroids (cortisol and aldosterone)
what is secondary adrenal insufficiency
inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release.
this is a result of loss or damage to the pituitary gland
common cause = Sheehan syndrome
what are the most common causes of primary adrenal insufficiency?
Addison’s Disease
in developed countries - Autoimmune
in endemic countries - TB
what are the most common causes of tertiary adrenal insufficiency?
steriods uses - steriod causes the suppression of hypothalamus and so less corticotrophic releasing hormone is released to stimulate the pituitary gland which intern stimulates the adrenocorticotrophic hormone to stimulate the adrenal glands to produce cortisol and alderstone
what are some of the less common causes of Addison’s Disease
1) infection - Pesudomonas aeruginosa, meningococcal infection, systemic fungal infection secondary to HIB infection
2) malignancies - lung, breast, stomach, colon, melanoma and lymphoma
clinical features of Addison’s Disease
fatigue anorexia reduced libido abdo pain cramps
salt craving
Bronze hyperpigmentation to skin - ACTH stimulate melanocytes to produce melanin
hypotenison
investigation of Addison’s Disease
- U&E : hyponatraemia, hyperkalaemia, hypercalcaemia
- blood urea – elevated due to hypovolaemia
- FBC – anaemia
- Early morning cortisol
- Short syancthen (ACTH) test: synathcen given to patient and blood cortisol measured at baseline, 30 mins and 60 minutes. A failure of cortisol level to rise (double or remain below <497) indicates primary adrenal insufficiency (Addison’s)
- Addison’s : ACTH (high), cortisol level low
- ACTH level (> 22)
- plasma aldosterone (reduced)
- plasma renin activity – elevated
- 80% autoimmune: Adrenal cortex antibodies and 21 hydroxylase antibodies
- CT/MRI adrenals – after biochemical diagnosis has been confirmed
management of acute addisonian crisis
hydrocortisone - replaces cortisol
on-going management of Addison’s Disease
replace cortisol - hydrocortisone or prednisolone or cortisone
replace aldosterone - fluticasone
in periods of illness/stress - double dose (normally the body produce more cortisol during period of stress)
carry steroid card and emergency ID
dehydroepiandrosterone - replace androgen in women with dec libido
a complication of Addison’s disease?
Addisonian crisis - potentially life-threatneing presentation
- triggered by infection or trauma
- can be 1st presentation
- reduced consciousness, hypotension, hypoglycaemia, hyponatraemia, hyperkalemia
- treat without Ix
- rex - IV hydrocortisone 100mg stat then 100mg every 6 hr
- correct hypoglycaemia
careful monitoring of electrolytes and fluid balance
what are the causes of primary hypothyroidism
hashimoto’s thyroiditis -autoimmmune
Sub-acute de Quervain thyroiditis - viral
Postpartum thyroiditis
underdevelopment
ecoptic hypoplastic gland
seondary to hyperthyroidism treatment - carbimazole, lithium and amiodarone
radiation
iodine deficiency - added to food such as table salt
what are the causes of secondary hypothyroidism - hypothalamic disorder
giloma surgery radiotherapy infarction infiltrative - TB, syphilis, sarcoid, hemochromatosis retinods
what are the causes of secondary hypothyroidism - pituitary disorder
pituitary adenoma surgery radiotherapy infarction Sheehan's syndrome infiltrative - TB, syphilis, sarcoid, amyloidosis, hemochromatosis
what are the RF for hypothyrodisim
female middle age FHx autoimmune disorders down syndrome primary pulmonary hypertensions MS
clinical features of hypothyroidism
weight gain fatigue cold intolerance menorrhagia constipation depression - poor concentration bradycardia / low BP dry skin carpal tunnel syndrome coarse hair and hair loss loss of material 1/3 of the eyebrow goitre fluid retention (oedema, pleural effusion, ascites) proximal myopathy myxoedema - severest form as mucoplysaccharides accumulate below the skin and cause facial features to thicken hyporeflexia
investigation for hypothyroidism
serum TSH serum T3/T4 serum cholesterol - elevated FBC - normocytic anaemia fasting blood glucose - elevated serum creatine kinase - elevated Hashimotos- antithyroid peroxidase antibodies and anti-Tg antibodies
management of hypothyroidism
- Levothyroxine (synthetic T4) – dose titrated till TSH levels are normal
- Measure TSH levels monthly till stable, then check 4-6 weeks, then annually
what is primary hyperparathyroidism
it is when the parathyroid glands secrete too much parathyroid hormone which causes derangement of Ca2+
what is secondary hyperparathyroidism
it is when any disorder that causes an initial low state of Ca2+ which causes excretion of parathyroid hormone from parathyroid glands
what is the function of parathyroid glands
regulates serum calcium and phosphate levels
also play a part in bone metabolism
how does PTH hormone affect serum calcium and calcium phosphate
when Ca2+ is low, PTH is released from the pararthyriod gland
PTH acts on kidney, bone and small intestine
kidney - PTH causes the release of Calcitriol ( 1,25-(OH)2D) which acts on the kiney to reduce excretion of Ca2+
Bone - PTH and calcitorol both causes releases of Ca2+ and phosphate
Small intestine - PTH and Calcitriol in absorption of Ca2+
the over results
- inc serum Ca2+
- dec serum phosphate
what is tertiary hyperparathyroidism?
occurs after prolong secondary hyperparathyroidism. Glands become autonomous to producing excessive PTH due to hyperplasia of the gland, even after cause of hypocalcemia has been corrected.
what are the causes of primary hyperparathyroidism
parathyroid adenoma - 85%
carcinoma - small cell lung cancer
MEN1/MEN 2a
external neck irradiation
what are the causes of secondary hyperparathyroidism
CKD
malabsorption
Vit D deficiency
others - crohn’s coeliac, following bypass surgery, chronic pancreatitis, fat malabsorption.
clinical features of primary hyperthyroidism
Bones, stones, abdominal groans, psychic moan, thrones
- excessive Ca2+ resoprtion - osteopenia/osteoporosis
- excessive Ca2+ excretion - renal calculi
- hypercalcemia - proximal myopathy, anorexia, N+V, abdo pain, constipation
- polyuria, polydipsia, dehydration
- depression, dementai, confusion, inability to concentrate, memory problems
clinical features of secondary hyperthyroidism
o features of chronic renal failure – discoloured skin, bruising, pruritis, evidence of fluid overload (lung rales, pericardial rub and peripheral), elevated BP, fatigue, náusea, poor concentration and myoclonus
o featutes of malabsorption
o muscle cramps and bone pain
o perioral tingling or paresthaesia in fingers or toes
o Chvostek’s sign – tapping on the face just anterior to the ear and seeing a twitching of muscles around the mouth – neuromuscular excitability
o Trousseau’s sign - Inflating blood pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyper extension of the fingers and flexions of the thumb - neuromuscular excitability
o features of rickets in children – bowed legs or knock knee
o fratures
investigation for hyperparathyroidism
- Albumin adjusted serum calcium- supressed secondary, raised in primary and tertiary (+ renal failure)
- PTH – elevated. (measure if calcium is indicative)
- Phosphate – supressed primary, raised in secondary and tertiary
- 24-hour urinary calcium excretion – high in primary and low in secondary
- 25-hydroxyvitamin D (25(OH)D) – low
- UE- assess kidney function.
- DEXA – risk of osteoporosis
- XR – salt and pepper pot skull
- Tc-99m sestamibi scanning + USS – to locate the parathyroid mass and to plan for surgery
differential for hyperparthyroidism
familial hypocalciuric hypercalcaemia
hyperclacaemia of malignancy
multiple myeloma
sarcoidosis
osteomalacia
osteoporosis
paget’s disease
management of primary hyperthyroidism
surveillance if mild check serum creatinine and calcium level every 6 months 3 sites DEXA study - 1-2 years U&e every 6 months BP - every 6 months correct it
treatment for primary hyperparathyroidism
Surveillance if mild
Check serum creatinine and calcium levels every six months
3 site DEXA study – 1-2 years
UE- every six months
Blood pressure – every six months
if symptomatic (kidney, renal calcali, bone disease) parathyroidectomy
if asymptomatic + age < 50 or dec eGFR, bone density < -2.5, 24 hour urinary Ca2+ > 400 parathyroidectomy
bisphosphonate as adjunct
Correct vitamin D deficiency.
Avoid dehydration
Avoid thiazide diuretics
treatment for secondary hyperparathyroidism
Treat underlying disease
Correct vitamin D deficiency – ergocalciferol (Vit D + Ca2+)
treat malabsorption with supplement
Treat CKD: calcium supplementation, correction of vitamin D deficiency
Phosphate restriction +/- phosphate binders (sevelamer, lanthanum, calcium acetate)
Vitamin D analogues
Calcimimetics (e.g. cinacalcet) – stop the production of PTH.
Bisphosphonates – reduced fracture risk.
• last resort - parathyroidectomy
what can cause malignant hypercalcaemia
occurs in 10-20% of cancer due to imbalance between bone resorption + Ca2+ excretion most common cancers - breast - prostate - squamous cell - NSCLC lung - kidney - multiple myeloma - causes punched out lesion - lytic - lymphoma
pathophysiology of malignant hypercalcaemia
1) Transforming growth factor Alpha (TGFA) - cell growth stimulator and replication that is produced by many tumour cells. It is a powerful stimulator of bone resorption (Osteoclasts)
2) Parathyroid hormone related peptides (PTHrP) - tumour associated protein that mimics PTH, stimulating bone absorption and inc plasma Ca2+ - breast cancer
symptoms of malignant hypercalcaemia
- Boans (pain, fractures), moans (lethargy), groans (abdo pain, vomit), thrones (constipation, polyuria), stone
- General: dehydration, weakness, fatigue/malaise, drowsiness
- CNS: hyporeflexia, confusion, seizure, proximal neuropathy, coma
- GIT: weight loss, nausea, vomiting, constipation, ileus, dyspepsia, polydipsia (thirst)
- GU: Polyuria
- Cardiacbradycardia, short QT, wide T wave, prolonged PR, arrhythmia (HTN), arrest
- Late Confusion, Drowsiness, Fits, Coma
INvestigations for malignant hypercalcaemia
- GCS
- Bloods: Serum Ca corrected for albumin, U&E, Alk Phos, PTH level, serum PTHrP, serum phosphorus. serum calcitriol, serum 25-hydroxyvitamin D
- ECG: Qt shortening
Mx of malignant hypercalcaemia
• Saline 1L 4hrly for 24hrs then
• 1L 6hrly for 48-72hrs with K+ and mild dose furosemide if risk of fluid overload. About 3L per day.
• IV bisphosphonates (pamidronate 60-90mg/zoledronic acid)
• If arrythmias/ seizures: calcitonin (normal physiological hormone to reduce absorption of Ca2+ in kidney + inc osteoblast activity) + corticosteroids (this combination help lower serum Ca)
o SC/IM calcitonin at 4units/kg 12hrly with oral prednisolone 40mg PO
what level of serum Ca2+ will you consider aggressive treatment of malignant hypercalcemia
Ca2+ < 3 = rehydrate with IVI
Ca2+ > 3 = 3L of fluids, consider fureosemide and stop thiazide diuretics
causes of hyperlipidaemia
can be acquired or genetics disorder
- diets
- DM
- obesity
- lack of exercise
- CKD
- hypothyroidism
- pregnancy
- FHX
- drugs - steriods
clinical features
mostly asymptomatics but can also presents in acute blockage of vessels eg MI and strokes
1) tendon xanthoma - yellow deposits of cholesterol near joints
2) Xanthelasma - yellow deposition of cholesterol underneath the skin
3) corneal arcus
investigation for hyperlipidaemia
lipid panel
- over cholesterol > 5 mmol/L
- HDL cholesterol (bad cholesterol) > 1 mmol/L in men, > 1.2 in female
- LDL (good cholesterol) > 3
Non- HDL cholesterol > 4
TC:HDL > 6
if want to find out causes - fasting glucose, TSH, U&Es, serum albumin/LFT
management of hyperlipidaemia
primary prevention - atorvastatin 20mg
secondary prevention - atorvastatin 80mg
