Endocrine Flashcards
What is type 1 diabetes?
autoimmune destruction of the beta cells in the pancreas that produce insulin so there is an absolute deficiency in insulin and persistent hyperglycaemia state
What are the risk factors for type 1 diabetes?
genetic predisposition
family history of autoimmunity e.g. thyroid disease, Addisons, coeliac, pernicious anaemia, vitiligo
How does type 1 diabetes present?
- poluria
- polydipsia
- weight loss
- prolonged tiredness
+ blurred vision, increased skin infections, acutely unwell in DKA
How is type 1 diabetes clinically diagnosed in adults and children?
ADULTS: hyperglycaemia + >1 of ketosis, weight loss, <50 y/o, BMI <25, FH of autoimmunity
CHILDREN: hyperglycaemia + polyuria/ polydipsia / weight loss/ tiredness
How is type 1 diabetes diagnosed by hyperglycaemia?
random blood glucose >11.1 mol/l
fasting blood glucose >7 mmol/l
HbA1C >48
or urine dip (glucose ++)
What are the microvascular complications of diabetes?
- RETINOPATHY - cataracts, diabetic maculopathy, glaucoma
- NEUROPATHY - “glove and stocking” distribution of peripheral neuropathy, vibration first sense to lose
- NEPHROPATHY - leads to HTN and CKD
What are the macrovascular complications of diabetes?
- CARDIOVASCULAR DISEASE - high risk
- CEREBROVASCULAR DISEASE - stroke risk
- PERIPHERAL ARTERIAL DISEASE - cause “diabetic foot” , ulcers
Apart from micro/macro vascular, what are the other complications of diabetes?
- autonomic dysfunction - ED, bladder retention, postural hypotension, diarrhoea, autonomic gastroparesis
- increased risk of infections e.g. vaginal thrush
- metabolic complications e.g. hypo, DKA, hyperosmolar lipidaemia, metabolic syndrome, dyslipidaemia
- psychological effects - depression, reduced QoL, eating disorders , anxiety
- other autoimmune conditions - coeliac, Addisons, vitiligo, pernicious anaemia, RA
How is type 1 diabetes managed with medication?
INSULIN THERAPY
- need mix of short acting insulin (novorapid, actrapid) and long acting insulin (detemir)
- SE: weight gain, hypoglycaemia, lipodystrophy
- individual care plan
What should be told to a type 1 diabetic when managing their care?
- attend DAFNE course (insulin education)
- testing random blood glucose 4 x a day and before each meal and before bed
- more frequent management if ill, exercise, stress, during pregnancy
What is a type 1 diabetics target for blood glucose?
on waking up: 5-7 mmol/l
before meals and throughout the day: 4-7 mmol/l
What is included in the annual review of type 1 diabetics?
- HbA1C (every 3-6 months) - target <48 mmol/l
- Blood pressure
- U&E
- ophthalmology eye check
- foot check
- assess for depression
- inspect injection sites
What is defined as hypoglycaemia?
blood glucose < 4mmol/l
List the risk factors for hypoglycaemia?
too much insulin
missed a meal / too few carbohydrates
unplanned exercise
How does hypoglycaemia present?
sweating trembling anxious agitated/ restlessness pallor confused nausea drowsy blurred vision weakness
How is hypoglycaemia managed?
- give 15g starchy carbohydrates / sugary drink
- repeat blood sugar in 15 minutes
- if still low and symptomatic, glucagon injection IM
What is diabetic ketoacidosis?
- decreased insulin
- reduced uptake of glucose into the cells
- hyperglycaemic state
- osmotic diuresis -> potassium depletion
- increased protein catabolism
- increased lipolysis -> excess of free fatty acids -> converted to ketone bodies
List the risk factors for ketoacidosis?
I - insulin missed
I - infection
I - intoxication
I - infarction/ ischaemia (MI)
+ pregnancy, surgery, periods, drugs (illegal, steroids)
How does diabetic ketoacidosis present?
abdominal pain, nausea and vomiting polyuria, polydipsia confusion, loss of consciousness Kussmaul breathing acetone breath
How is diabetic ketoacidosis confirmed?
- high plasma ketones >3mmol/L
- hyperglycaemia - plasma glucose >7 mmol/L
- metabolic acidosis
- urine dip: ketone ++, glucose ++
How is diabetic ketoacidosis managed?
- ABCDE
- IV fluids - 1L 0.9% saline in first hour -> 1L 0.9% saline with KCL over next 2 hours
- IV insulin 0.1 unit/kg/ hr + potassium
- once glucose <15 mmol/L, infusion of 5% dextrose added
What is type 2 diabetes?
insulin resistance and insulin deficiency caused by destruction of beta cells in the pancreas
List the risk factors for type 2 diabetes?
family history obesity sedentary lifestyle high calorific diet ethnic group - south asians, afro Caribbean hypertension PCOS history of gestational diabetes
When is pre diabetes diagnosed and how is it managed?
if HbA1c 42-47, then diabetes is likely to develop in the next few years
“Impaired Glucose Tolerance “ confirmed by oral glucose tolerance test of 7.1 - 11.1 mmol/l
offer lifestyle advice: weight loss, reduce sugar in diet, exercise, smoking cessation, managed hypertension
How does type 2 diabetes present?
often incidental finding and symptoms less obvious
polyuria
polydipsia
tiredness
weight loss
recurrent/ prolonged infection and healing
When Is type 2 diabetes diagnosed?
random plasma glucose > 11mmol/l
HbA1C >48 mmol/l
How is type 2 diabetes managed in terms of lifestyle and advice?
- lifestyle: weight loss, reduce sugar in diet, exercise, manage BP, statin if cV risk
- DESMOND course
- blood glucose control: aim for 4-7 fasting glucose, HbA1C measured every 3-6 months
What is 1st line treatment for type 2 diabetes? (+ mechanism and side effects)
METFORMIN
= increases insulin sensitivity
SE: GI upset, lactic acidosis, impaired renal function
if metformin ineffective, what is added for dual therapy?
SULFONYLUREA e.g. gliclazide
= increases the amount of insulin produced by the pancreas
SE: weight gain, hypoglycaemia, peripheral neuropathy
aim: HbA1C <53 mmol/mol
What are 3rd line options in type 2 diabetic management?
PIOGLITAZONE
= increases insulin sensitivity
SE: weight gain, bladder cancer, osteoporosis , fluid retention (caution in HF)
DPP4 INHIBITORS e.g. gliptins
= increases incretin levels and inhibits glucagon secretion to increase insulin (decrease appetite)
SE: GI upset, flu like symptoms
if triple therapy is not tolerated/ ineffective in type 2 diabetes, what is used?
insulin therapy
indicated if BMI <35 and triple therapy ineffective
SE: weight gain, hypoglycaemia, lipodystrophy
What are the risk factors for hyperosmolar hyperglycaemic state?
infection MI dehydration thiazide and loop diuretic poor control elderly
What is the pathology behind hyperosmolar hyperglycaemic state?
- hyperglycaemia
- osmotic diuresis
- hyperosmolaltiy
- causes fluid shift of water into intravascular compartment
- severe dehydration
What is the criteria for hyperosmolar hyperglycamic state?
- hypovolaemia
- high serum osmolality >320 mosmol/kg
- high hyperglycaemia >30
How does hyperosmolar hyperglycaemia present?
severe dehydration confusion altered mental state LOC \+/- seizures, delirium, cerebral oedema
How is hyperosmolar hyperglycaemia managed?
- MEDICAL EMERGENCY
- ABCDE
- IV fluids 3-6L over 12 hours of 0.9% saline
- normalise blood sugars (insulin)
How is hyperthyroidism caused?
AUTOIMMUNE (graves disease) antibodies cause overstimulation of the thyroid gland so there is increased production of thyroid hormones T4 and T3 (but TSH suppressed)
List possible triggers for Graves disease?
smoking
e.coli infection
stress
high iodine intake
How does hyperthyroidism present?
GENERAL: sweating, heat intolerance, fatigue
HEART: palpitations, AF, heart failure
GYNAE: oligomenorrhoea
GI: diarrhoea, weight loss, increased appetite
NEURO/PSYCH: anxiety, tremors, restlessness
MSK: reduced bone mineral density
What are the signs of Graves disease?
- EYE SIGNS - lid lad, ophthalmoplegia, exophthalmos (pop out eyes)
- PRETIBIAL MYXOEDEMA (erythematous oedematous lesions above lateral malleolus)
- THYROID ACROPACHY (clubbing)
What is aN emergency complication of hyperthyroidism?
THYROID STORM
S+S: tachycardia, fever, sweating, trembling, agitation, confusion, confusion, goitre
How is a thyroid storm managed?
- iV Carbimazole / propiletheouracil (better in pregnancy)
- resus: oxygen, fluids, NG tube
- IV propanolol
- IV hydrocortisone
How is hyperthyroidism confirmed?
- low TSH
- high T4 and T3
- thyroid autoantibodies e.g. anti TPO, anti TSH
- ultrasound of thyroid
How Is hyperthyroidism managed?
- Carbimazole - inhibit production of thyroid hormones
- propanolol - bloco circulating thyroxine and immediate relief of symptoms
- lubricant eye drops - ease eye irritation
What are the side effects/ precautions with Carbimazole?
agranulocytosis, teratogenic, acute pancreatitis
what is the conservative management for hyperthyroidism?
- refer to ophthalmology to assess eyes
- annual thyroid function tests
- follow up after starting medication
- refer to thyroid specialist
- advice to stop smoking
- refer to endocrinologist if trying for baby
if medication is not working and relapse of symptoms in hyperthyroidism, how can it be managed?
- radioiodine
2. thyroidectomy
What is hypothyroidism?
impaired production of thyroid hormone (T4 and T3)
What are the primary (95%) causes of hypothyroidism?
- AUTOIMMUNE hashimotos thyroiditis **
- deficiency of iodine **
- radio iodine treatment or surgery
+ DeQuervains, atrophic hypothyroidism, riedels thyroiditis, postpartum thyroiditis, drugs (lithium, amiodarone)
What are the main features indicating hashimotos autoimmune hypothyroidism?
GOITRE * = painless, rubbery, irregular surface, nodular mass in thyroid
anti TPO and anti Tg autoantibodies
What are the features of de Quervains hypothyroidism?
subacute: PAINFUL goitre and raised ESR
after viral infection
first presents with hyperthyroidism and then drops
diagnosed by thyroid scintigraphy and reduced uptake of iodine 131
What are the secondary causes of hypothyroidism?
= insufficient production of TSH due to hypothalamic or pituitary problems
e.g. isolated TSH deficiency, neoplasia, radiotherapy or trauma to hypothalamus or pituitary,
How does hypothyroidism present?
B- bradycardia
R- reflexes slow (delayed tendon reflex)
A-ataxia
D- dry thin skin and hair
Y- yawn (fatigue)
C- cold intolerance
A- ascites, peripheral oedema
R- round face - weight gain, decreased appetite
D- depression
I- immobile
C- concentration loss
+ menorrhagia, fertility issues (still birth), carpal tunnel, CVD
When does myxoedema coma occur?
in elderly when primary hypothyroidism presents with adrenal insufficiency and too low T3/T4
seizures, hypothermia, decreased consciousness, hypoventilate
RX: IV levothyroxine + IV hydrocortisone + resp support
What would you see on TFTs in hypothyroidism?
primary: high TSH, low T3/T4, ANTI TPO and anti Tg
secondary: low TSH, low T3/T4
How is hypothyroidism treated?
levothyroxine (T4) 50-100mcg + annual TFTs
Which hormones does the anterior pituitary gland produce?
Growth hormone -> stimulates liver to produce IGF-1
Prolactin -> stimulates growth of mammary glands and lactation
FSH/LH -> stimulates release of testosterone and oestrogen from testes/ ovaries
ACTH -> stimulates adrenal cortex to release glucocorticoids and androgens
TSH -> acts of thyroid gland to produce thyroid hormones
Which hormones doe the posterior pituitary gland produce?
supraoptic nucleus -> vasopressin -> acts on kidneys
paraventricular nucleus -> oxytocin -> acts on breasts and uterus
How is the adrenal divided and what does it produce?
- adrenal medulla (derived from ectodermal neural crest tissue)
- > contains phaeochromocytes which secretes adrenaline and noradrenaline -> control autonomic NS - adrenal cortex (derived from embryonic mesoderm)
- > produces steroid hormones (mineralocorticoids, glucocorticoids) and androgens
Where and which hormones are produced in the adrenal cortex?
renin/ angiotensin act on -> zona glomerulosa -> aldosterone -> electrolyte imbalance and regulate blood volume
ACTH act on -> zona fasciculata -> cortisol -> deals with metabolism and stress
ACTH act on -> zone reticularis -> DHEAS -> helps make sex hormones
What is acromegaly?
excess of growth hormone due to an anterior pituitary adenoma
How is growth hormone regulated?
- hypothalamus produces somatostatin and GNRH
- acts on anterior pituitary gland
- produces growth hormone
- acts on liver to produce IGF-1
- this stimulates soft tissue and skeletal growth
What are the symptoms/ signs of acromegaly?
FACIAL FEATURES: prominent nasolabial folds, large nose, large jaw, large tongue, prominent supraorbital ridge, enlarged head circumference, interdental spaces, frontal bossing
spade like hands and feet, wide feet/ increase in shoe size
SKIN: excessive sweating, oily skin
NERVE: peripheral neuropathy, carpal tunnel
GU: sexual dysfunction, galactorrhea
What are the signs of a pituitary tumour?
headache bitemporal hemianopia (compression of optic chiasm) hypopituitarism (abdo pain, thirst, fatigue, anaemia, loss of libido)
What are the possible complications of acromegaly?
hypertension
diabetes , glucose intolerance (GH is anti-insulin so insulin resistance develops)
cardiomyopathy, CV disease (most common cause of death)
osteoarthritis
sleep apnoea
How is acromegaly diagnosed?
1) oral glucose tolerance test * -no suppression of GH (rapid increase in blood glucose should depress GH secretion)
2) pituitary MRI* - diagnose pituitary adenoma
3) random GH levels
4) serum IGF1 raised
How is acromegaly managed?
- transphenoidal surgery
2. somatostatin analogue e.g. octreotide - directly inhibit release of GH
What is cushings syndrome?
chronic excess glucocorticoids (cortisol)
How is cushings syndrome caused?
- CUSHINGS DISEASE - pituitary adenoma stimulating adrenal cortex to secrete excess cortisol and loss of negative feedback system (+ pigmented skin **)
- prolonged treatment with steroids e.g. IBD, asthma, RA, post transplant
- small cell lung cancer - ectopic ACTH production
- adrenal adenoma - ACTH independent
When can pseudo cushings occur and how can you differentiate between cushings disease?
caused by: alcohol excess, severe depression
insulin stress test differentiates
What are the main features of cushings syndrome?
weight gain: central obesity, buffalo hump, moon face, purple striae , hyperglycaemia
hirsutism: acne, facial hair, red cheeks,
steroids: thin skin, thin skin, easy bruising, proximal muscle weakness, slow wound healing
What are the complications of cushings?
osteoporosis diabetes depression, insomnia hypertension heart failure metabolic syndrome impaired immunity
How is cushings syndrome diagnosed?
- overnight dexamethasone suppression test **
if cortisol not suppressed: steroid therapy, ACTH syndrome likely
if cortisol suppressed by high doses dexamethasone: cushings disease - 24 hr urinary free cortisol high
- plasma ACTH
if low= adrenal cause -> CT adrenal glands
How is cushings disease managed?
transphenoidal pituitary adenomectomy or pituitary irradiation?
SE: NELSONS SYNDROME (enlargement of pituitary gland and development of adenomas)
What is Addisons disease?
primary insufficiency of the adrenal cortex characterised by deficient secretion of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
What are the causes of insufficiency of corticosteroids and mineralocorticoids?
PRIMARY: autoimmune Addisons disease => progressive autoantibody destruction of the adrenal cortex so reduced cortisol and aldosterone produced
SECONDARY: tumour, TB, meningococcal septicaemia, autoimmune adrenalitis => inadequate secretion of pituitary hormones so decrease stimulation of adrenal glands
What are the clinical features of Addisons disease?
” thin tanned tired tearful and tumbling”
GI: nausea and vomiting, abdo pain , crave salty foods, anorexia, weight loss
NEURO: depression, lethargy, dizziness
POSTURAL HYPOTENSION
SKIN/MSK: bronze pigmentation, vitiligo, loss of pubic hair, skeletal muscle weakness
describe the features of addisonian/ adrenal crisis ?
cause: stress, infection, long term steroid therapy WITHDRAWAL
acute deficiency of gluocorticoids and mineralocorticoids
- hypovolaemia
- hypoglycaemia
- hypotensive shock
How is an addisonian crisis managed?
- iV hydrocortisone - then continue 6 hourly until stable
- IV fluids (FLUID BOLUS)
- cardiac and electrolyte monitoring
How is Addisons diagnosed?
- ACTH (synacthen) stimulation test - confirms Addisons if cortisol doesn’t rise rapidly (<550nmol/l after 30 mins)
- U&E: hypoglycaemia, Hyperkalemia, hyponatraemia
- adrenal autoantibodies e.g. anti 21 hydroxyls
- 9am serum cortisol levels
How is Addisons treated?
hydrocortisone and fludrocortisone lifelong
patient education: carry steroid cards, how to adjust in illness (double hydrocortisone, same fludrocortisone as cortisol increases in stress response)
What are the side effects of long term steroid therapy?
easy bruising, thin skin, weight gain, osteoporosis, hyperglycaemia
What are the causes of hyperaldosteronism?
PRIMARY: Conns syndrome : adenoma of the zona glomerulosa which secrets aldosterone
SECONDARY: renal artery stenosis, excess diuretic therapy, congestive heart failure, nephritic syndrome, cirrhosis with ascites
What are the clinical features of conns syndrome?
hypertension
hypernatraemia
hypokalaemia - muscle cramps, weakness, paraesthesia
metabolic alkalosis
+ polyuria, polydipsia
How is conns syndrome diagnosed?
- U&E - hypernatraemia, hyponatraemia
- high blood pressure
- raised aldosterone
- low renin levels —> aldosterone: renin >800 confirms diagnosis
How is conns syndrome managed?
surgery to remove adenoma + spironolocatone 4 weeks prior to surgery
What are the causes of raised prolactin?
- prolactinoma: benign adenoma associated with MEN1
- hypothyroidism
- physiological: pregnancy, stress, exercise
- drugs: anti psychotics *, TCA, SSRI
How does a prolactinoma present in women?
galactorrhea
oligomenorrhoea, amenorrhoea
hirsutism: male pattern hair growth, increase muscle bulk
+ headache, bitemporal hemianopia, visual loss, hydrocephalus, loss of appetite
How does a prolactinoma present in men?
reduced libido
reduced hair growth
ED
+ headache, bitemporal hemianopia, visual loss, hydrocephalus, loss of appetite
How is a prolactinoma diagnosed?
- raised prolactin levels
- MRI pituitary
- TFTs to exclude hypothyroidism
How is a prolactinoma managed?
- dopamine agonist e.g. bromocriptine
dopamine has inhibitory effect on prolactin production - transphenoidal surgery
What are the side effects of dopamine agonists?
impulsive behaviours
sleepiness
hypotension
What is diabetes insipidus?
deficiency of ADH secretion preventing osmotic control of kidneys
Explain how ADH is secreted, where and its actions
- osmoreceptors in the hypothalamus detect an increased serum osmolality (concentration of solutes)
- ADH is secreted by supraoptic nucleus in the hypothalamus
- ADH released by the posterior pituitary gland
- travels to kidneys and binds to ADH receptors on distal convulated tubules
- causes Aquaporin2 channels to be inserted into the tubules
- causes more water reabsorption back into the circulation and bloodstream
- concentres the urine and decreases serum osmolality
What are the possible causes of diabetes insipidus?
CRANIAL DI: deficiency of ADH due to damage of hypothalamus or pituitary
idiopathic, head injury, pituitary surgery, craniopharyngiomas, haemochromatosis , Sheehans syndrome (pituitary infarction after PPH)
NEPRHOGENIC DI: insensitivity to ADH in the kidneys
tubulo interstitial disease ( pyelonephritis, sickle cell disease), genetic, drugs (lithium), Hypercalcaemia, CKD
How does diabetes insipidus present?
polyuria polydipsia dehydration nocturia distended bladder
How is diabetes insipidus diagnosed?
- high plasma osmolality
2. ADH stimulation test - distinguish between cranial and nephrogenic DI CAUSES
How is nephrogenic diabetes insipidus managed?
- thiazide diuretics
2. low salt and protein diet
What is SIADH (syndrome of inappropriate ADH secretion)
excessive secretion of ADH causing excessive water retention and dilution of blood and hyponatraemia
What are the causes of SIADH?
- malignancy - small cell lung cancer ***, pancreas, prostate
- neurological - stroke, meningitis, SAH, encephalitis
- infection - TB, pneumonia
- hypothyroidism
- drugs - carbamazepine, sulfonylureas, SSRI, amitriptyline, vincristine
How does SIADH present?
symptoms of hyponatraemia (more symptomatic when acute, chronic hyponatraemia asymptomatic mostly)
MILD: nausea, vomiting, malaise, headaches
MODERATE: weakness, muscle cramps, lethargy, ataxia
SEVERE: coma, seizures, loss of consciousness, confusion
How is SIADH diagnosed?
- serum osmolality low
- urine osmolality high
- hyponatraemia
- high Na in urine
How is SIADH managed?
correct slowly as want to prevent central pontine myelinolysis
- fluid restrict 1-1.5L/ day
- Na given and monitored every 2 hours
What is a pheochromocytoma?
neuroendocrine tumour (usually unilateral and benign) of the adrenal medulla which produces catecholamines (adrenaline and noradrenaline)
What is associated with pheochromocytoma?
MEN 2
familial
Von Hippel Lindau syndrome
neurofibromatosis
How does pheochromocytoma present?
excess secretion of adrenaline and noradrenaline so…
dangerous hypertension ** causing headaches **
sweating
trembling
palpitations
tachycardia
anxiety
What are the complications of pheochromocytoma?
heart failure arrhythmias e.g. SVT MI dilated cardiomyopathy stroke death !
How is pheochromocytoma diagnosed?
- 3x 24 hr urinary samples of plasma free catecholamines
2. high levels of VMA in urine
How is pheochromocytoma managed?
- alpha blockers e.g. phenoxybenzamine
- then beta blockers given
- surgical excision of benign tumour
What is carcinoid syndrome?
due to carcinoid tumour or mets in the liver releasing SEROTONIN into the circulation
what are the features of carcinoid syndrome?
flushing ** diarrhoea hypotension bronchospasm R side heart failure/ valve stenosis
How is carcinoid syndrome managed?
somatostatin analogues e.g. octreotide
What are the causes of hypocalcaemia?
with a low PTH: hypoparathyroidism , parathyroid surgery
with a high PTH: pseudohypoparathyroidism, vitamin D deficiency , hypomagnesaemia
other: CKD, pancreatitis, rhabdomyolysis
What are the symptoms of hypocalcaemia?
paraesthesia - tingling in fingers, toes, mouth muscle cramps depression carpopedal spasm tetany - severe sign
What are the signs of hypocalcaemia?
Trousseaus sign - when inflate BP cuff, look for carpopedal spasm
Chvosteks sign - tap over facial nerve and induce facial spasm
How is hypocalcaemia diagnosed and assessed?
- U&E - low adjusted calcium
- ECG - prolonged QT
- serum PTH
- serum magnesium
How is hypocalcaemia managed acutely?
if severe/ seizures/ tetany -> IV calcium gluconate 10ml 10%
if mild/ moderate - oral calcium
How is hypocalcaemia managed long term?
oral calcium and vitamin D
What are the causes of Hypercalcaemia?
- primary hyperparathyroidism *
- malignancy * - squamous cell lung cancer, bony mets, breast, myeloma
+ sarcoidosis, TB, Addisons, pheochromocytoma, dehydration, pagets disease of the bone, drugs (thiazines, vit D)
What are the symptoms of hypercalcaemia?
ABDOMINAL MOANS - constipation, nausea and vomiting, abdominal pain
THRONES - polyuria, polydipsia, dehydration
STONES - renal colic and stones
PSYHIC OVERTONES - depression, confused, memory loss
+ weakness, proximal myopathy, fatigue, osteoporosis, arrhthymias
How is hypercalcaemia investigated?
- U&E - high serum Ca
- ECG - short QT interval
- serum PTH - high in hyperparathyroidism
- alk phos - high in bony mets, low in myeloma
+ x ray, albumin, calcitonin ( high in B cell lymphoma)
How is acute hypercalcaemia managed?
- IV fluids 3-4 L 0.9% saline
- loop diuretic
- IV bisphosphonates
- treat cause
What are the causes of hyperkalaemia?
AKI, CKD renal tubular acidosis DKA (metabolic acidosis) Addisons drugs - potassium sparing diuretics, ACE-I, ARBs, NSAIDs, digoxin, ciclosporin blood transfusion rhabomyolysis
How does hyperkalaemia present?
fatigue
weakness
flaccid paralysis
palpitations and chest pain
How is hyperkalaemia investigated?
- U&E - high potassium
- ABG- metabolic acidosis
- review medications
- ECG
List the ECG changes in hyperkalaemia?
tall tented t waves
absent p waves
wide QRS
VF !!!!***
How is hyperkalaemia managed?
- ABCDE
- IV 10ml 10% calcium gluconate - stabilises cardiac membrane
- insulin actrapid / 10% dextrose infusion in 250ml over 15 mins - shift potassium from extracellular to intracellular
- nebulised salbutamol
What are the causes of hypokalaemia?
vomiting (alkalosis)
thiazide and loop diuretics (alkalosis)
diarrhoea (acidosis)
cushings and conns syndrome
How does hypokalaemia present?
muscle weakness
constipation
hypotonia
What are the signs on ECG of hypokalaemia?
prominent u waves
prolonged PR interval
ST depression
How is hypokalaemia managed?
mild/ moderate: oral sandoK supplements 2040mmol x2/4 daily
severe: IV potassium + ECG monitoring
What are the causes of hypernatraemia?
dehydration - diarrhoea, vomiting, severe burns, inadequate fluid intake, excessive exercise/ sweating
diabetes insipidus
drugs and excess saline - IV abx, IV sodium bicarbonate, hypertonic dialysis, loop diuretics
How does hypernataemia present?
lethargy irritable doughy skin hyperreflexia myoclonic jerk confusion signs of dehydration
How is hypernatraemia managed?
- treat cause
- correct 0.5 mmol/hour and fluids
- monitor fluid status and monitor electrolytes
List drugs that can cause weight gain?
A- anti psychotic A - anti depressants e.g. TCA, mirtazepine A - anti histamines e.g. certrizine A - anti convulsants e.g. lithium B - beta blocker C - corticosteroids C - contraceptives e.g. depo-provera D - diabetic medication e.g. insulin, sulfonylurea, pyoglitazone
Which conditions cause weight Gain / obesity?
hypothyroidism
Cushings syndrome
PCOS
what are the possible complications of obesity?
type 2 diabetes ** hypertension ** CVD - MI, angina , stroke pregnancy risks - infertility, gestational diabetes, macrosomia, shoulder dystocia endometrial, breast and colorectal cancer sleep apnoea GORD gallstones , fatty liver disease osteoarthritis
How is obesity managed?
- diet advice - 600 kcal deficit, low fat, high wholewheat carbs, low sugar, limit alcohol
- exercise - 30 mins moderate 5x/week
- medication - orlistat
- bariatric surgery - gastric band, bypass
Which medication is used to help weight loss in obesity and when is it given?
ORLISTAT= pancreatic lipase inhibitor
indicated if BMI >30, BMI >28 + RF
stopped after 3 months if not lost 5% of body weight
what are the side effects of orlistat?
flatulence, diarrhoea, incontinence, abdo pain, oily stool
What is the criteria for metabolic syndrome?
- truncal obesity/ BMI >30
- blood pressure: systolic >130, diastolic >85
- reduced HDL
- high triglycerides
- fasting glucose >6.1 mmol/l -> prediabetes
what are the causes of metabolic syndrome?
OBESITY ***
sedentary lifestyle
smoking
What are some of the causes of gynaecomastia?
LOW TESTOSTERONE
klinefelters, mumps
HIGH OESTROGEN
obesity, seminoma , oestrogen secreting tumour, hyperthyroid
prolactinoma
MEDICATION
finasteride (inhibit testosterone), anabolic steroids, anti psychotics, digoxin, spironolactone
Describe parathyroid hormones action when serum calcium is low
- calcium in the blood is low
- chief cells in the parathyroid gland secrete parathyroid hormone which have 3 actions:
- BONE: stimulate osteoclasts and inhibit osteoblasts so bone is broken down and releases Ca into the blood
- KIDNEY: decreases Ca excretion in the urine and also activates vitamin D which increases Ca absorption
- INTESTINE: calcitriol stimulates intestine to absob more Ca from the food
- results in calcium levels raising
Describe what happens if serum calcium is high
- parafollicular cells in the thyroid gland activated to release calcitonin
- acts on the BONE to inhibit osteoclast and stimulate osteoblast so Ca is removed from blood and used to build new bone
- calcium leves decrease
What is the cause of primary hyperparathyroidism?
benign adenoma of the parathyroid gland (85%) **
+ carcinoma of the parathyroid gland, hyperplasia
Who is primary hyperparathyroidism associated with?
post menopausal elderly women
MEN 1/2
hypertension
How does primary hyperparathyroidism present?
80% asymptomatic and found on bloods
HYPERCALCAEMIA - “abdominal groans, stones, thrones and psychotic moans” (constipation, thirst, abdo pain, renal stones, peptic ulcers, osteoporosis, confusion, memory loss, polyuria)
What is seen on the bloods for primary hyperparathyroidism?
high PTH
high Ca
low phosphate
x-ray: pepper pot skull
MRI scan
How is primary hyperparathyroidism treated?
watch and wait if mild: monitor PTH and Ca levels, increase fluids, low Ca diet , Cincalet
if HIGH calcium, symptomatic: surgical excision of adenoma
What are the possible complications with parathyroid surgery?
damage of the recurrent laryngeal nerve
hypothyroidism
symptomatic hypocalcaemia
“hungry bone syndrome”
How is secondary hyperparathyroidism caused?
as a result of low calcium (usually due to CKD*, vitamin D deficiency, inadequate Ca in diet) there is parathyroid gland hyperplasia
What would you see on the bloods for secondary hyperparathyroidism?
high pTH
low Ca
high phosphate
low vitamin D
How does secondary hyperparathyroidism present?
CKD + bone pain
low vitamin D + osteomalacia + fracture
How is secondary hyperparathyroidism treated?
- correct Vit D deficiency
- phosphate binders
- cinacalet
what causes tertiary hyperparathyroidism ?
after secondary hyperparathyroidism and correction of calcium, there is still parathyroid gland hyperplasia so continues secreting parathyroid hormone at high levels
what would you see on the bloods of tertiary hyperparathyroidism?
high PTH
high Ca
high phosphate
high Alk Phos
What are the causes of hypoparathyroidism?
- PRIMARY HYPOPARATHYROIDISM
= surgery to thyroid/ parathyroid gland, DiGeorges syndrome, alcohol, Wilsons/ hereditary haemochromatosis - PSEUDO HYPOPARATHYROIDISM
= target cells insensitive to PTH
low IQ, short stature, short 4th and 5th metatarsal - PSEUDOPSEUDO HYPOPARATHYROIDISM
similar to pseudo but normal biochemical
What would you do to diagnose pseudo hypoparathyroidism?
urinary cAMP and phosphate levels after a PTH infusion - will not rise
How does primary hypoparathyroidism present?
hypocalcaemia features (tetany, carpopedal spasm, paraesthesia, muscle cramps, depression, Trousseaus sign, Chvosteks sign)
What would you see on bloods for primary hypoparathyroidism?
low PTH low Ca high phosphate low Mg ECG - prolonged QT
How is primary hypoparathyroidism treated?
diet rich in calcium and vit D
calcium and vIt D suppléments
How does nephropathy occur in T1DM?
hyperglycaemia damages and causes thickening of the glomerular basement membrane and increase in mesangial cells
How does glucagon work?
increases the concentration of glucose in the blood by promoting glycogenolysis and gluconeogenesis
which antibodies are found in hyperthyroidism?
anti TPO
anti TSH
which antibodies are found in hypothyroidism?
anti TPO
anti Tg
How does goitre occur?
increase in TSH so increases cellularity and hyperplasia of thyroid gland
list the tissues derived from ectoderm?
adrenal medulla CNS hair, teeth nose eyes nails
List the tissues derived from endoderm?
stomach intestines liver pancreas bladder respiratory epithelium
List the tissues derived from mesoderm?
adrenal cortex muscle bone cartilage kidneys heart testis
list the functions of cortisol
gluconeogenesis lipolysis reduce stress anti inflammatory protein synthesis
List the functions of aldosterone
- vasoconstriction
2. up regulate Na/K pump at DCT to increase Na and water reabsorption and excrete K
Summarise MEN and its associations
MEN 1 - (3 P’s) - Parathyroid (hyperparathyroidism), Pancreas (insulinoma, gastrinoma), Pituitary -> MEN1 gene
MEN 2A/B - parathyroid, phaemochromocytoma, medullary thyroid cancer -> RET oncogene
How is toxic multi nodular goitre treated?
radioactive iodine
List the different types of steroids?
HIGH mineralocorticoid activity, MINIMAL glucocorticoid -> fludrocortisone
HIGH mineralocorticoid, HIGH glucocorticoid -> hydrocortisone
LOW mineralocorticoid activity , HIGH glucocorticoid -> prednisolone
MINIMAL mineralocorticoid activity , HIGH glucocorticoid -> dexamethasone
What are the electrolyte disturbances in cushings syndrome?
hypokalaemia
metabolic alkalosis
where is thyroid derived from embryonically?
foramen caecum
describe the oral glucose tolerance test?
- pt fasts overnight
- given drink of 75g sugar in morning
- BM taken before and 120 mins after drink
- blood glucose >11.1 mmol/L after drink = diabetes
If taking regular steroids, what advice should be given?
carry steroid cards
wear medic alert bracelet
side effects of long term steroids
know how to adjust steroids in infection
