Medicine/Surgery - Endocrine Flashcards
What is DKA and its main causes?
Diabetic ketoacidosis
Mainly complication of T1
causes: illness, infection, UTI, pregnancy, surgery, MI, insulin dosing issues (forgetting/purposefully not taking), eating disorders
Describe the pathophysiology of DKA
No insulin in the body to utilise the glucose
Glucose broken down by beta-oxidation instead producing acidic ketone bodies
These ketone bodies lower pH of blood causing metabolic acidosis
Kidneys are overwhelmed by XS ketones and glucose = osmotic diuresis
What are the following biochemical features in DKA?
1) Na
2) K
3) urinary ketones
4) plasma ketones
5) BM
6) ABG
1) Na low (as the hyperglycaemia leads to the osmotic shift of water from the intracellular -> extracellullar space and Na goes too?)
2) K low (as the hyperglycaemia leads to the osmotic shift of water from the intracellular -> extracellullar space and K goes too?)
3) Urinary ketones (high)
4) Plasma ketones (>3)
5) BM (>11)
6) ABG (metabolic acidosis)
How might a patient in DKA present
dehydrated, hypotensive tachycardic cold compensatory Kussmaul breathing pear-drop breath delirium/coma polyuria, polydipsia weak cramps abdominal pain blurred vision
How would you investigate DKA?
Bloods: FBC, CRP, U&E, BM, ABG Blood cultures Urine culture/dipstick ECG CXR
What is the diagnosis of DKA based on the triad of?
Acidaemia (low pH)
High glucose >11
High plasma ketones >3 (or 2+ on dipstick!)
How is DKA treated?
IV access 0.9% saline + 50U insulin (IV) Once BM <15, start 5% dextrose IV May need potassium chloride replacement depending on hypokalaemia severity Consider thromboprophylaxis
Define HHS and its causes
hyperglycaemic hyperosmolar state
Features of: hyperglycaemia, hypovolaemia, hyperosmolality WITOHUT acidosis/ketones
also called HONK (hyperosmolar non-ketotic state)
Usually T2DM complication
Infection, drugs (steroids), CV events, sepsis, MI
What is the pathophysiology of HHS and its signs/symptoms
Some residual insulin production in T2DM therefore no B-oxidation of ketoacidosis
Develops more insidiously meaning the hyperglycaemia and dehydration are more profound
Hx will be ~1 week
Fts: confusion, dehydration
What are the following biochemical features in HHS?
1) plasma ketones
2) BM
3) ABG
1) plasma ketones - <3
2) BM much higher e.g. >30
3) ABG = usually pH >7.3
What investigations are carried out for HHS?
Bloods: FBC, CRP, U&E, BM, ABG Blood cultures Urine culture/dipstick ECG CXR
How is HHS treated?
IV 0/9% saline
May add insulin once BM has plateaued
Thromboprophylaxis/urinary catheter
Define hypoglycaemia and its causes
BM of <2.8 in non-insulin treated individual or <4 in an insulin treated pt
Mainly as a complication of insulin therapy
Causes in diabetics:
- increased physical activity
- missed meals
- accidental insulin overdose
Causes in non-diabetics:
EX - exogenous drugs
P - pituitary insufficiency (e.g. lack of cortisol, cannot oppose the effects of insulin!)
L - liver failure
A - Addison’s (causing lack of cortisol)
I - Islet cell tumour (making XS insulin)
N - non-pancreatic neoplasm (making insulin-like hormone)
What are the S/Sx of hypoglycaemia?
Related to glucose deprivation: delirium, drowsy, speech difficulties, nausea, headache
Related to ANS activation: sweating, anxiety, hunger, tremor, palpitations
How is hypoglycaemia investigated?
FBC BM Insulin levels C-peptide Ketones
How is hypoglycaemia treated?
if BM <4 10g oral glucose (wait 10 mins, if BM still <4 then repeat) (give oral glucose up to 3 cycles) ?IM glucagon
What are the rules with hypoglycaemia and the DVLA?
Notify DVLA if taking insulin
BMs should be >5 to drive
Only drive 2hrs at a time
If >1 hypoglycaemic attack has occurred whilst awake in the last year, then you are not allowed to drive at all
Describe the basal bolus insulin regimen
- long acting insulin given at night
- rapid infusion given 3x a day (once before each meal)
Describe the bi-basal (twice daily) insulin regimen
- at breakfast a mix of intermediate+short/rapid insulin is given, and then the same before dinner
What is the pathophysiology of T2DM?
Acquired resistance to the effects of insulin initially (?chemicals released from adipose tissue?? or high dietary carbohydrate?)
Pancreas tries to compensate by going into overdrive
Eventually insulin deficiency occurs
What are the S/Sx of T2DM
TTTT UTI/candida Poor concentration/mood changes Dry mucous membranes Postural hypotension Visual changes Headaches... Acanthosis nigricans
What are the WHO criteria for diagnosing DM?
1) venous glucose readings of
- BM >7 (fasting)
- BM >11.1 (random)
- HbA1C >48
2) symptomatic
3) HbA1C >48
Describe the management of T2DM
Lifestyle: diet, weight, smoking cessation, less alcohol, exercise (can increase insulin sensitivity)
Pharmacological:
Monotherapy -> metformin
Dual therapy -> add sulphonylurea/thiozoladinedone/SGLT2i/GLP1
Triple therapy -> add DPP-4/insulin
Name two reasons as to why a patient may have a falsely high HbA1c reading:
Post splenectomy (reduced RBC turnover and cells are exposed to glucose for a longer time)
Medications e.g. opioids
Define metabolic syndrome
Central obesity (BMI > 30) plus 2 of:
- DM
- HTN (>130/85)
- Hyperlipidaemia
- Fasting glucose >5.6
Describe IGT
Impaired glucose tolerance
Fasting BM normal but 2-hrs post glucose measurement is high
Usually impaired GLUT4 expression on muscle leading to impaired 1st and 2nd phase insulin secretion
5% can progress to T2DM
Describe IFG
Fasting glucose high but 2hr post-glucose measurement normal
Normally hepatic issue with impaired 1st phase insulin secretion
5% can progress to T2DM
Describe the pathophysiology of T1DM
Autoimmune destruction of pancreatic islets and B cells
Leads to severe insulin deficiency
Due to genetics (HLA-DR3/4) + environmental factors (cows milk, lack of vit D…)
Common autoantibodies: IAA, IA2, GAD (glutamic acid decarboxylate)
Describe the S/Sx of T2DM
TTTT UTI/candida Poor concentration/mood changes Dry mucous membranes Postural hypotension Visual changes Headaches... Acanthosis nigricans
Define the cut off values for ‘pre-diabetes’
Combination of IGT + IFG
Random BM 7.8-11.1
Fasting BM 6.1-7
Describe autoimmune polyendocrine syndrome
Triad of:
- T1DM
- Addison’s
- Autoimmune thyroiditis
What will the C-peptide measurement be like in T1DM?
Very low!
What is the treatment regimen for T1DM?
SC insulin (basal bolus or biphasic)
Target HBA1C <53!!!!!!
Address all RFx
Only curative option = islet cell/pancreatic transplantation
Describe the pathophysiology underlying diabetic micro/macrovascular complications
Poorly controlled DM
High blood glucose -> leads to vessel inflammation and atherosclerosis
Thickening of capillary basement membranes
Microvascular damage = localised response to generalised vascular injury
Describe the main macrovascular complications and their treatment
Coronary -> MI/infarction (4x greater risk)
Cerebral -> TIA/stroke (2x greater risk)
Peripheral -> claudication/ischaemia
Management: BP control, reduce RFx (diet, smoking, exercise), statins, aspirin
Describe the main microvascular complications and their treatment
Treatment = good glycaemic control!!!
- Retinopathy (annual screening)
- Peripheral neuropathy (analgesia, gabapentin, vibration/sensory testing)
- Nephropathy (optimise BP and BM control)
- Autonomic neuropathy (e.g. may need catheter)
- Diabetic feet (foot screening, appropriate footwear)
- Mononeuropathy (altered motor/sensory function)
Define gestational DM and its pathophysiology
Any degree of insulin insensitivity which occurs with onset or pregnancy
Carbohydrate intolerance occurs as placenta produces hormones making you resistant to insulin
The insulin needs during pregnancy are increased and the pancreas cannot keep up with demands -> hyperglycaemia
Describe causes of secondary DM
Genetics (Down syndrome, Turners, Kleinfelters)
Pancreatic disease (cancer, pancreatitis)
Endocrinopathies (Cushing’s, phaeochromocytoma)
Immunosuppressants (steroids)
Drugs (antipsychotics)
Define monogenic diabetes and its three main features
Also called MODY Non-insulin requiring DM that develops <25yrs Caused by single gene mutation Inheritance pattern is normally AD 3 main features: - run in families - <25yrs onset - managed with diet, exercise, oral hypoglycaemics (+/- insulin)
Describe diabetes insipidus
XS quantities of dilute urine (>3L) and thirst every day
Low serum gravity and osmolality
Hypernatraemia
Either cranial (not enough ADH made) or nephrogenic (kidneys not responsive to ADH)
How is diabetes insipidus diagnosed?
8hr water deprivation test (to try and stimulate natural ADH release)
Collect urine every 2hrs and measure urine volume and osmolality, and plasma osmolality and body weight
If plasma osmolality is high and urine osmolality is low, then work out if cranial/nephrogenic:
Give desmopressin and measure urine osmolality over the next 4 hrs:
- if urine becomes more concentrated (higher osmolality) -> cranial issue
- if not = nephrogenic issue
How is diabetes insipidus treated?
Give desmopressin if cranial
Treat polyuria with thiazide diuretics
Remove the underlying cause e.g. tumour
Which is the active thyroid hormone (T3/4?)
T3!!
T4 can be converted into T3 in the periphery
Describe causes of hypothyroidism
Hashimotos most common (anti-thyroid peroxidase enzyme which converts I2 -> Io in colloid filled lumen before T3/4 are made (autoimmune!)
Iatrogenic (lithium, PTH, carbimazole)
De-quervians (subacute thyroiditis -> where a hypothyroid phase can follow the hyper phase)
Primary atrophic hypothyroidism (diffuse lymphocytic infiltration of thyroid gland leading to atrophy)
Congenital
Secondary = hypopituitarism
What are the signs/symptoms of hypothyroidism?
BRADYCARDIA! Bradycardia Reflexes relax slowly Ataxia Dry hair/skin Yawning (tired) Cold intolerance Ascites/oedema Round puffy face Defeated demeanour (low mood) Immobile Anaemia Loss lateral 1/3 eyebrow Constipation Infertility Goitre Pretibial myxoedema
How is hypothyroidism investigated
Bloods: TFTs. autoantibodies (anti-TPO)
low cholesterol and high Na (due to ADH release)
Radioactive iodine uptake tests
How is hypothyroidism treated?
Levothyroxine (synthetic T4) (MAY CAUSE ANGINA so taper dose in CAD)
Amiodarone -> has an iodine rich structure
Describe the causes of hyperthyroidism
Graves (autoimmune, most common) - autoantibodies made against TSH receptor Thyroid adenoma Drug induced Multinodular goitre Ectopic thyroid tissue De Quervians (viral infection causing high T3/4) Amiodarone Iatrogenic
Secondary - pituitary adenoma
What are the S/Sx of hyperthyroidism?
Tachycardia Warm moist skin Tremor Palmar erythema Thin hair Lid retraction/lag Goitre Thyroid bruit Weight loss Diarrhoea Heat intolerance Hungry... Pretibial myxoedema Thyroid acropatchy (HYPER ONLY!) Thyroid eye disease in Grave's only -> exophthalmos, ophthalmoplegia
How is hyperthyroidism investigated?
TFTs Autoantibodies Bloods (?infection/de Quervians) Radioactive iodine uptake test Check eyes FNA neck lump Imaging
How is hyperthyroidism treated?
Carbimazole
PTU (propylthiouracil)
Block and replace regimen -> carbimazole + levothyroxine
Surgery Radioactive iodine (BUT may worsen eye disease)
Why should aspirin be avoided in hyperthyroidism
Displaces T3/4 from protein carriers, increasing levels of circulating T3/4
Name a side effect of PTU/carbimazole
Agranulocytosis and neutropenic sepsis!
Name and describe 5 causes of benign thyroid disease
Diffuse goitre = iodine deficiency, graves, hashimotos
Multinodular goitre = cause unclear
Cyst = fluid filled swelling treated with FNA/surgery
Solid nodule = e.g. benign follicular adenoma
Thyroglossal cyst = fluid filled sac resulting from incomplete closure of thyroglossal duct in embryology, a painless midline cyst
Name some complications of thyroid surgery (lobectomy or thyroidectomy)
Recurrent laryngeal nerve damage
Parathyroid gland damage
Tracheal damage
Thyrotoxic crisis (after handling the gland)
Describe thyroid cancer presentation and its 5 main types
Commonly presents as an asymptomatic nodule detected by USS/palpation in females 30-40yrs
PeopleFallMainlyLiftingApparatus
Papillary (younger pts) Follicular (middle aged pts) Medullary (of parafollicular cells which make calcitonin) Lymphoma Anaplastic
What is the role of calcitonin
The role of calcitonin is to oppose the function of PTH and reduce serum Ca levels by
- (bone) Inhibits OC activity
- (kidney) Reduces renal reabsorption of calcium
Define hyperparathyroidism and its causes
Raised PTH
Causes: 80% solitary adenoma, 20% gland hyperplasia, rarely cancer
Cause is not always clear!
Describe the normal function of PTH hormone
PTH release from parathyroid gland in response to low serum Ca
Acts on:
1) Bone (increase OC activity and reduce OB activity)
2) Kidneys (increase a-1-hydroxylase activity, so more vit D production and more Ca reabsorption in the DCT)
3) Gut (more Ca absorption from food)
Describe S/Sx of hyperparathyroidism
Bones - OP, pain, # Stones - renal stones Moans - depression, low mood Groans - abdominal pain Thrones - constipation HTN
How is hyperparathyroidism investigated?
Bloods: PTH, Ca, Vit D, U&E, LFT
Review drugs
Imaging -> DEXA, USS, X-ray
How is hyperparathyroidism treated?
Surgical -> parathyroidectomy
Medical -> bisphosphonates, lower Ca intake, cinacalcet (enhances the sensitivity of the calcium sensing receptor and lowers PTH levels), if secondary then vit D replacement, lots of fluids to reduce stone formation
Describe complications of parathyroidectomy
Haematoma
Vocal cord damage
Transient hypoparathyroidism and hypocalcaemia
Ca/Vit D supplementation
Describe hypoparathyroidism and its causes
Reduced PTH secretion
Can be due to gland failure but most commonly iatrogenic
Causes:
(primary)
iatrogenic, congenital, wilsons disease (gland gets infiltrated with copper), haemochromatosis
(secondary)
radiation, surgery, hypomagnesaemia
What are the signs/symptoms of hypocalcaemia?
SPASMODIC Spasms Perioral paraesthesia Anxiety/irritable Seizures Muscle tone increased Orientation poor/confused Dermatitis Impetigo herpetiformis Chvostek's sign (tapping facial nerve causes muscle hyperreactivity/spasm) Trosseau sign -> spasm of hand/forearm when BP cuff tightened
How is hypoparathyroidism investigated?
24hr urine Ca/creatinine collection Bloods: FBC, LFT, TFT, ABG Gene sequencing Renal imaging ECG (as low Ca can prolong QTc)
How is hypoparathyroidism treated?
Ca supplementation
Synthetic PTH
Vit D
Describe the zones of the adrenal gland and what is made in each
Cortex: salt, sugar, sex
- zona glomerulosa -> makes MC (aldosterone)
- zone fasciculata -> makes GC (cortisol) + some androgens
- zone reticularis -> makes GC (cortisol) + mainly androgens
Medulla: part of sympathetic NS with chromaffin cells makes catecholamines (A/NA)
Describe hormones released in the HPA axis of the adrenal glands
Hypothalamus = CRH Pit = ACTH Adrenals = Aldosterone/CORTISOL/androgens!
Describe Addison’s disease
Primary cause of adrenal insufficiency
Autoimmune destruction of adrenal cortex
low cortisol and aldosterone
causes K retention and Na loss
What is the most common secondary cause of adrenal insufficiency?
Iatrogenic! (long term steroid therapy suppresses the pituitary-adrenal axis)
What are S/Sx of adrenal insufficiency?
Anorexia and weight loss Tired, tearful Depression Low BP Dizzy/fainting Tanned skin Dark buccal mucosa
Describe the functions of cortisol
Pancrease (opposes insulin) Adipose (increases lipolysis) Liver (increases gluconeogenesis and glucagon action) Muscle (more proteinolysis) Bone (less oB activity)
How is adrenal insufficiency investigated?
Bloods:
- low BM
- Low Na and high K (due to low aldosterone)
- high ACTH
- high renin (RAAS trying to make more aldosterone)
- adrenal autoantibodies
Short synACTHen test to diagnose:
- measure plasma cortisol before and after
- try and stimulate cortisol release
- if no rise in cortisol = Addison’s
How is adrenal insufficiency treated?
Steroids and do not delay!
GC = hydrocortisone
MC = fludrocortisone
Give high steroid dose in morning and low dose at night to mimic diurnal release
Sick day rules -> double steroid doses, and always carry steroid warning card!
Describe Addisonian crisis and how it is treated
low Na, high K, high BM
Can occur with previous steroid use which suddenly stops!
Tx: IV hydrocortisone and fluids (may use dextrose to lower BM)
What is hypopituitarism and describe its possible causes
Reduced secretion of the ANTERIOR pituitary hormones
Aetiologies can be NEOPLASTIC, vascular, infective, iatrogenic
3 areas can be affected: Hypothalamus, pituitary stalk, pituitary gland
In what order are the hormones depleted in hypopituitarism?
1st to last GH FSH/LH Prolactin TSH ACTH
Describe the S/Sx of hypopituitarism based on the hormones that are lost:
GH -> obesity, atherosclerosis, OP, hypoglycaemia
FSH/LH -> reduced fertility and libido, oligomenorrhoea, OP, breast atrophy
Prolactin -> absent lactation
TSH -> hypothyroid!
ACTH -> adrenal insufficiency!
What investigations should be carried out for hypopituitarism?
Blood: GH/IGF1 (longer half life)/OGTT LH/FSH/oestradiol/testosterone Prolactin (will be raised as loss of dopamine inhibitory effect) TSH/T3/T4 Cortisol/short synACTHen test
Imaging:
MRI of pituitary
How is hypopituitarism treated?
Endocrine referral and hormone replacement
- steroids
- thyroxine
- testosterone/oestrogen
- gonadotrophin
- somatotrophin!!! (replace GH)
What is a phaeochromocytoma
Catecholamine producing adrenal medulla tumour
Rule of 10’s: 10% familial, 10% bilateral, 10% ectopic, 10% malignant
25% associated with genetic conditions: VHL, MEN
Tumour is almost always of the adrenal medulla but can be extra-adrenal (paragangliomas) but rare
What are the S/Sx of a phaeochromocytoma and how it is investigated?
TRIAD: episodic headaches, sweating, tachycardia, HTN!!!
Investigate:
- urinary catecholamines (A/NA) -> NOTE can be false + in stressed pts
- Imaging -> CT abdo, MIBG scan chromaffin isotope)
- BP
- Genetic testing
- Family screening
How is a phaeochromocytoma treated?
SURGERY!
Alpha blockade first (to avoid crisis from unopposed alpha-adrenergic stimulation if B-blockade was carried out first) e.g. with doxazosin
Then B blockade (bisoprolol)
Encourage salt intake
What are MEN syndromes?
multiple endocrine neoplasia syndromes
Formation of functioning, hormone producing tumours in multiple organ systems
Describe MEN1
3Ps
- pituitary tumour
- parathyroid tumour
- pancreatic tumour
Describe MEN2a
TAP!
- thyroid medullary carcinoma
- adrenal phaeo
- parathyroid hyperplasia
Describe MEN2b
Similar to MEN2 (- thyroid medullary carcinoma - adrenal phaeo - parathyroid hyperplasia) + marfan appearance!
What is Cushings syndrome/disease and describe its 4 aetiologies
Syndrome = clinical state created due to XS cortisol Disease = cushings syndrome caused by an PITUITARY adenoma!! (XS ACTH release)
Causes:
1) ACTH dependent (pituitary adenoma, ectopic ACTH/CRH)
2) ACTH independent (adrenal adenoma/carcinoma)
3) Iatrogenic (steroids!)
4) Other causes of high cortisol -> obesity, XS alcohol
What are the S/Sx of cushings?
central obesity hirsuitism proximal myopathy moon face buffalo hump easy bruising acne hypertension striae ED poor wound healing depression/mood changes
How is cushings investigated?
Look at medications (?steroids)
1) Establish if there is XS cortisol
a) salivary measurment
b) urinary cortisol/creatinine ratio
2) Carry out dexamethasone suppression testing
= if cortisol suppressed then it is an issue at the level of the adrenal, and if not there is too much ATCH being produced
3) Localise the source of the ACTH:
- undetectable after dexamethasone test = adrenal issue
- high ACTH = ectopic or pituitary cause (use CT/MRI to find ectopic source)
How is cushings disease managed?
Surgery:
Pituitary surgery -> transphenoidal adenectomy
Laraposcopic bilateral adrenalectomy
Removal of ectopic tumours
Medical:
Pasireotide (a GH analogue to reduce ACTH release)
What is Conn’s syndrome?
XS aldosterone production independent of the RAAS system, due to an ADRENAL ADENOMA
May also be bilateral adrenal hyperplasia or adrenal carcinoma
What are the S/Sx of Conns?
XS aldosterone
- increased ENaC insertion in DCT
- more Na and water reabsorbed into the body and more K lost
- hypertension, hypokalaemia, weakness
How is Conns investigated?
Aldosterone measured (will be high)
Renin (low)
A/R ratio >35
How is Conns treated?
Medical: Spironolactone or amiloride (aldosterone antagonists which are K sparing)
Surgical: laparoscopic adrenalectomy
Describe acromegaly and how it is investigated
XS GH secretion (99% due to pituitary tumour, 1% ectopic)
Different from gigantism as it occurs post-puberty when bones have fused, whereas gigantism starts in childhood
Usually a macroadenoma which causes high GH and increased IGF-1 release from the liver
Fts: sweating, acroparaesthesia, headache, altered facial features, increased ring/hat/shoe size, visual impairment, cardiomegaly, reduced libido, increased interdental space
Investigate:
- OGTT and measure IGF-1 (glucose load should reduce GH/IGF1 production)
- MRI
Describe hyperprolactinaemia and its 5 causes
XS prolactin production
5Ps
- prolactinoma (the most common cause) = can be micro or macro
- PCOS
- pharmacological (antipsychotics reduce dopamine)
- physiological (sleep, stress, sex)
- pregnancy
What are the S/Sx of hyperprolactinaemia and how is it investigated?
S/Sx:
galactorrhoea, ED, headaches, mass effect, visual changes, amenorrhoea
Investigate:
measure all AP hormones
CT/MRI
Visual field assessment
Describe PCOS and its proposed aetioloy
clinical +/- biochemical signs of hyperandrogenism
oligo/anovulation
Cause unclear, complex hormone imbalance, primary issue with pituitary gland
Obesity + genetics -> ?insulin resistance -> increased insulin production which increases androgen release and there is higher free testosterone leading to hirsuitism and oligo-ovulation
What are the S/Sx of PCOS
Irregular/no periods Difficulty getting pregnant Excessive hair: face, back, chest, buttocks Weight gain Hair thinning Oily/acne prone skin
Describe primary gonadal failure, its causes and how it presents
In males = failure of testes to produce sperm/testosterone/both
Due to testicular failure, trauma, Kleinfelters…
S/Sx: slow growth, small testes/phallus in children
in adults: low mood, low libido, gynaecomastia, weight gain, small testes +/- abnormal consistency
How is male gonadal failure investigated?
Bloods: low testosterone, high prolactin…
Sperm analysis: 1-3 days after last ejaculation, at least 20 million sperm with 50% mobile and 30% normal morphology
Describe Kleinfelters syndrome
XXY (male genetic disorder)
Extra X interferes with development meaning testes produce less testosterone
Either the mothers egg/fathers sperm has an extra
Shy child, slower development, gynaecomastia, small testes, dyslexic
Define obesity and factors affecting it
BMI >30 Majority due to lifestyle factors Hormones may also play a part: Leptin -> secreted from adipose tissue when substrate is plentiful, causes satiety and increased substrate utilisation Ghrelin -> released to increase appetite
Associated with many comorbidities
How is obesity managed?
Lifestyle!!!
Psychological therapy
Pharmacological: e.g. orlistat
Bariatric surgery
What is the definition of hyperkalaemia and name some of its causes
-K >6.5mmol/L
Emergency as can cause myocardial hyperexcitability -> VF -> cardiac arrest
Causes: Increased intake + renal failure Addison's disease (low Na and high K) K sparing diuretics Rhabdomyolysis Large blood transfusion Burns Drugs (ACEi)
What are the features of hyperkalaemia?
Fast irregular pulse (?VF)
chest pain
weakness
light headed
On ECG:
- tall tented T waves
- small P waves
- large PR interval
- wide QRS complex
Describe reasons for false hyperkalaemia readings
The EDTA K+ antagonist in the FBC bottles can contaminate other bottles -> so do U&E > FBC
Delayed lab analysis and RBCs leak K
Thrombocythaemia (K leaks out of platelets during clotting)
Describe the urgent treatment of hyperkalaemia
URGENT = means there is evidence of myocardial hyperexcitability
1) IV calcium gluconate (to stabilise cardiac membrane)
2) IV insulin + glucose (insulin causes K to move into cells)
3) Salbutamol (causes intracellular K shift)
4) Definitive Tx: dialysis to remove K+
5) Calcium resonium (work over a few days to reduce K uptake from the gut)
Describe the non-urgent treatment of hyperkalaemia
NON-URGENT = means there is no evidence of myocardial hyperexcitability
1) treat the underlying cause
2) medication review
3) calcium resonium (work over a few days to reduce K uptake from the gut)
Describe hypokalaemia and its causes
K <2.5mol/L
Causes may include increased K+ secretion:
GI -> votiting, villous adenoma
Renal -> diuretics, increased cortisol/aldosterone
Skin -> burns, eczema, psoriasis
Others: steroids conns renal tubule failure liquorice abuse -> overstimulation of MR receptors, XS aldosterone...
How does hypokalaemia present and what are its ECG features
Muscle weakness Hypotonic Hyporeflexia Cramps Tetany Palpitations Light headed Constipation
ECG:
- long PR interval
- small/inverted T waves
- prominent U wave
- depressed ST segment
How is hypokalaemia treated?
1) correct Mg levels
2) if mild: oral supplementation, swap thiazide diuretics for K sparing ones
3) if severe give IV K+ (no more than 20mmol/hr at a concentration no greater than 40mmol/L)
Define hypernatraemia and its causes
Na >145mmol/L
Causes: normally DEHYDRATION, but can be:
Hypovolaemic -> GI loss (vomiting, diarrhoea), renal (diuretics, osmotic diuresis), skin (burns, sweating)
Euvolaemic -> reduced fluid intake, DI, fever
Hypervolaemic -> hyperaldosteronism, hypertonic saline
What are the S/Sx of hypernatraemia/hyponatraemia
Lethargy Thirst Weakness Irritability Confusion Coma Fits Dehydration
How is hypernatraemia treated?
Water/rehydration
IV glucose -> which the liver rapidly metabolises leaving only H2O (i.e. to rehydrate if not possible orally)
Define hyponatraemia and name some of its causes
Serum Na <135mmol/L
Can be:
Hypervolaemia = cardiac failure, nephrotic syndrome, cirrhosis, renal failure
Euvolaemic = SIADH
Hypovolaemic due to renal loss = Addison’s, renal failure, XS diuretics, diabetes
Hypovolaemic due to extra-renal loss = D&V, burns, SB obstruction, trauma…
How is hyponatraemia investigated?
Assessment of fluid status is key to determine:
- serum osmolality
- urine osmolality
- urinary [Na]
Carry out short synACTHen test to rule out Addison’s
How is hyponatraemia treated?
1) Restrict fluids
2) Treat the underlying disorder e.g. heart/liver failure
3) Slowly rehydrate with 0.9% saline
4) ?ADH receptor antagonists (promote water loss without electrolyte loss but are expensive)
What complication can occur if hyponatraemia is corrected too quickly with IV rehydration?
Central pontine myelinolysis (pontine demyelination!) -> now has a new name = ODS (osmotic demyelination syndrome)
Describe hypermagnesaemia, name some causes and features:
Mg >2.9 (although rarely requires treatment unless >7.5)
Causes: renal failure, iatrogenic (XS antacids)
Fts (if severe): neuromuscular depression, reduced BP, reduced HR, hyporeflexia, CNS/respiratory depression, coma
Describe hypomagnesaemia, name some causes and features:
Mg <0.9
Causes: diuretics, severe diarrhoea, alcohol, other electrolyte imbalances (low Ca, K, PO4)
Presents: ataxia, paraesthesia, tetany, arrhythmias
Treatment: Mg salts
What ECG changes are seen in hypomagnaesaemia?
Wide QRS QTc prolongation Peaked T waves (mild) Diminished T waves (more severe) PR prolongation (more severe)
What are the functions of calcium?
Development of bone/teeth Muscle contraction Blood coagulation Hormone secretion Cell membrane depolarisation Intracellular messenger
Define hypercalcaemia and its causes
Serum Ca >2.6mmol/L Causes: dehydration cuffed specimen hyperparathyroid bony mets thyrotoxicosis lithium myeloma XS vitamin D sarcoidosis
What are the S/Sx of hypercalcaemia
Bones - OP, pain, # Stones - renal stones Moans - depression, low mood Groans - abdominal pain Thrones - constipation HTN
On ECG - reduced QT interval
How is hypercalcaemia treated?
Treat underlying cause
1) correct dehydration
2) bisphosphonates (reduce OC activity)
3) loop diuretics (promote calciuria)
4) further management -> steroids (if sarcoidosis), chemotherapy (if malignancy)
Define hypocalcaemia and its causes
Ca <2.2mmol/L Causes: hypoparathyroid CKD Vit D deficiency Osteomalacia pancreatitis resp alkalosis overhydration low Mg
Describe S/Sx of hypocalcaemia
SPASMODIC Spasms Perioral paraesthesia Anxiety/irritable Seizures Muscle tone increased Orientation poor/confused Dermatitis Impetigo herpetiformis Chvostek's sign (tapping facial nerve causes muscle hyperreactivity/spasm) Trosseau sign -> spasm of hand/forearm when BP cuff tightened
ECG -> can prolong QTc
How is hypocalcaemia treated?
Calcium PO
IV calcium gluconate
What is SIADH and its causes
syndrome of inappropriate ADH release Causes hyponatraemia (dilutional effect)
Causes: malignancy CNS disorders chest disease endocrine disease drugs (opiates, SSRIs) other
What are the criteria needed to diagnose SIADH
Concentrated urine
low plasma Na
low plasma osmolality
How is SIADH treated?
Treat the cause
restrict fluids
consider diuretics if severe
ADH receptor antagonists (vaptans) - but expensive so not generally used
