Endocrinology Flashcards
What is Addison’s? Describe the key presenting features and the treatment
Autoimmune destruction of adrenal glands = reduced cortisol and aldosterone
Signs and sx: (picture a shrivelled person)
-lethargy, weakness, n&v, weight loss, ‘salt-craving’
-hypoglycaemia, hypotension
-hyperpigmentation (esp palmar creases), vitiligo, loss of pubic hair in women
-hyponatraemia and hyperkalaemia (sometimes)
crisis: collapse, shock, pyrexia
Tx:
hydrocortisone to replace cortisol
fludrocortisone to replace aldosterone
(the hydrocortisone dose is split with the majority given in the first half of the day)
Addison’s patient with intercurrent illness →
double the glucocorticoids, keep fludrocortisone dose the same
What is the cause of Addisonian crisis in patients with poorly controlled HIV? Tx?
Cytomegalovirus (CMV)-related necrotising adrenalitis
Give IV hydrocortisone first and then fluid replacement
Thyrotoxicosis is excess circulating T3 and T4. What symptoms might someone present with? Tx?
- sx include heat intolerance, palpitations, anxiety, fatigue, weight loss, muscle weakness
- tx is carbimazole - high dose for 6 weeks then reduced, can cause agranulocytosis (immunodeficiency)
Why is dexamethasone good for raised ICP secondary to brain tumours?
It combines high glucocorticoid (anti-inflammatory) activity with minimal mineralocorticoid (fluid-retention) effects
Side effects of long term systemic corticosteroids?
- Cushing’s syndrome
- weight gain
- immunosuppression
- increased risk of osteoporosis, fractures, and avascular – necrosis of fem. head
- risk of intracranial hypertension
- can cause neutrophilia
What can be seen on ABG in Cushing’s?
hypokalaemic metabolic alkalosis (excess ACTH lowers K+ )
In suspected T1DM, what atypical factors would prompt you to consider additional tests?
age 50 years or above, BMI of 25 kg/m² or above, slow evolution of hyperglycaemia or long prodrome
What is MODY? How should it be treated?
Maturity-onset diabetes of the young: autosomal-dominant disease
- development of T2DM in patients younger than 25 years old
- C-peptide remains in the normal range and beta-cell antibodies are -ve
Treatment is a sulfonylurea
How will C peptide levels differ in T1 and T2 diabetes?
C-peptide will be low in individuals with type 1 diabetes mellitus (as the pancreas is not making enough insulin precursor, which breaks down to form C-peptide and insulin), and normal or high in individuals with type 2 mellitus.
what are the HbA1c targets in T2DM?
48 mmol/mol or 53 mmol/mol in patients with drugs that may cause hypoglycaemia e.g. sulfonylureas
What is the stepladder of tx for T2DM?
You can titrate up metformin (slowly) and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol, but should add a second drug if the HbA1c rises to 58 mmol/mol.
metformin + DPP-4 inhibitor
metformin + pioglitazone
metformin + sulfonylurea
metformin + SGLT-2 inhibitor
When should modified release metformin be used?
in patients who cannot tolerate metformin due to gastrointestinal symptoms such as diarrhoea
What drug should be added to metformin (in T2DM management) if the patient has existing CVD, HF or a risk of developing either?
Gliflozins should be added if the patient has existing CVD, HF or a risk of developing either bc helps glucose control and sodium simultaneously
What is the first line tx for all hypertensive diabetic patients ?
ARBs
Who should you never give gliptins to?
Patients with pancreatitis
Who should you avoid gliclazides in?
Patients with a raised BMI
What are the diabetes sick day rules?
when unwell, If a patient is on insulin, they must not stop it due to risk of DKA. They should continue their normal insulin regime but ensure that they are checking their blood sugars frequently
Key points:
- Check BM more regularly
- Aim to drink 3L of fluid per day
- Sugary drinks should be used only if pt is struggling to eat normally
- Phone should be nearby in case of emergency
How do patients in DKA present?
Presents with abdo pain, hyperventilation (Kussmaul respiration) and acetone on the breath
Bloods show metabolic acidosis and hyperglycaemia (‘unrecordable’ blood glucose always means that the blood sugar is high rather than low)
How should DKA be treated?
- isotonic saline should be used initially, even if the patient is severely acidotic
- then fixed rate IV insulin at 0.1ml /kg/hr
- electrolytes should be corrected
- long acting insulin should be started and short acting should be stopped
How is DKA resolution measured? What if it doesn’t resolve?
- pH >7.3 and
- blood ketones < 0.6 mmol/L and
- bicarbonate > 15.0mmol/L
If the ketonaemia and acidosis have not been resolved within 24 hours then the patient should be reviewed by a senior endocrinologist
What is the first line tx for diabetic neuropathy?
What other treatments are available?
amitriptyline, duloxetine, gabapentin or pregabalin
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems
What are the key features of Grave’s disease on examination and on investigation?
On examination:
Smooth enlarged non tender goitre (tender would be viral thyroiditis)
Exophthalmos (proptosis) and chemosis (bulging, swollen eyes)
pretibial myxoedema, clubbing
On investigation:
+ve TSH receptor stimulating antibodies
On thyroid scintigraphy will see diffuse inc. uptake of iodine
what is first line for 1. immediate control of symptoms and 2. maintaining euthryoidism in Grave’s disease?
- propanolol
- Carbimazole - particularly if there is marked thyrotoxicosis and the patient is elderly/has underlying CVD
What malignancy is Hashimoto’s associated with?
MALT lymphoma
Give the 3 key features of Hashimoto’s (autoimmune) thyroiditis
Hashimoto’s= hypothyroidism + goitre (firm non-tender) + anti-TPO antibodies
What is the most common metabolic condition in cancer patients?
Hypercalcaemia
Most common cause of hypercalcaemia?
Malignancy is the most common cause of hypercalcaemia in hospitalised patients and primary hyperparathyroidism is the most common cause in non-hospitalised patients
What is the most useful test to determine cause of hypercalcaemia? How is it treated?
Most useful test in hypercalcaemia- PTH level
U&Es to confirm, then rehydration with saline, then bisphosphonates if needed
What is the pathophysiology of Hyperosmolar Hyperglycaemic State?
What 3 features are classical? What symptoms would a patient present with?
Hyperglycaemia > osmotic diuresis > vol depletion
1.) Severe hyperglycaemia
2.) Dehydration and renal failure
3.) Mild/absent ketonuria
Extreme dehydration, N+V, ALOC, fatigue
What are the main risk factors for HHS?
Usually elderly pts
New diagnosis of T2DM / poor tx compliance
Infection
High dose steroids
MI
Stroke/ thromboembolism
How do you confirm a diagnosis of HHS? How do you treat?
Diagnosis:
Hypovolaemia
Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
Tx:
- Give fluids first ( e.g. 0.9% saline over 48hours )
- Replace electrolyte losses
- Gradually normalise blood glucose
Hypothermia, hyporeflexia, bradycardia, confusion and seizures- diagnosis? Tx?
Myxoedemic coma- complication of untreated hypothyroidism
Tx with IV thyroid replacement , IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded) and fluids
Side-effects of thyroxine therapy?
hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation
What substances interact with levothyroxine and alter absorption?
Iron / calcium carbonate tablets can reduce the absorption of levothyroxine - should be given 4 hours apart
What is Whipple’s triad?
Suggestive of insulinoma
- Symptoms and signs of hypoglycemia
- Plasma glucose < 2.5 mmol/L
- Reversibility of symptoms on the administration of glucose
C peptide will not fall when insulin administered
Summarise the 3 key types of multiple endocrine neoplasia
MEN type 1: 3 Ps
- Parathyroid: hyperparathyroidism due to parathyroid hyperplasia (most common)
- Pituitary
- Pancreas: e.g. insulinoma, gastrinoma
MEN type 2a: 2 Ps + RET gene
- Parathyroid (60%)
- Phaeochromocytoma
(+ Medullary thyroid cancer)
MEN type 2b : 1 P + RET gene
- Phaeochromocytoma
(+ Medullary thyroid cancer, marfanoid body habitus, neuromas )
What is the course of action for a child with a palpable abdominal mass or unexplained enlarged abdominal organ?
refer very urgently (<48hr) for specialist assessment for neuroblastoma and Wilms’ tumour
raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels may be seen
calcification may be seen on abdominal x-ray
Phaeochromocytoma is a rare catecholamine secreting tumour (adrenaline and noradrenaline). How does it typically present?
How do you test for it? How do you manage it?
triad of sweating, headaches, and palpitations in association with severe hypertension
24 hr urinary collection of metanephrines
Surgery is the definitive management. The patient must be stabilized first with medical management:
alpha-blocker (e.g. phenoxybenzamine), then
beta-blocker (e.g. propranolol)
Should thyroid replacement drugs be given at an altered dose in pregnancy?
Yes
Women with hypothyroidism may need to increase their thyroid hormone replacement dose by up to 50% as early as 4-6 weeks of pregnancy due to increased metabolic demand
Primary hyperaldosteronism can present with hypertension, hypernatraemia, and hypokalemia, and maybe also a metabolic alkalosis.
What are the 2 causes?
How are they diagnosed?
How are they treated?
Caused by bilateral adrenal hyperplasia (most common) or Conns (adrenal adenoma) not by excessive stimulation by renin.
Plasma aldosterone:renin ratio is first line investigation
Tx is spironolactone (for BAH) or surgery (Conns)
Symptoms of hypercalcaemia?
“painful bones, renal stones, abdominal groans, and psychic moans,”
Painful bones are the result of abnormal bone remodelling due to overproduction of PTH.
Symptoms of hypocalcaemia?
hyperexcitability of NMJ (bc increases sodium entry into neurones which causes depolarisation) which increases likelihood of AP.
- Pins and needles, tetany, paralysis and convulsions
Depression, nausea, constipation, bone pain →
→ ?primary hyperparathyroidism
How does hyperparathyroidism present?
presents w/ symptoms of hypercalcaemia
raised calcium and PTH and low phopshate on blood tests
pepperpot skull on X-ray
association w/ htn
What is the primary cause of hyperparathyroidism and how is it treated?
Primary cause: solitary adenoma
Definitive tx : parathyroidectomy
- in patients who don’t qualify for surgery cinacalcet can be used - this is a calcimimetic drug that mimics the action of calcium on the parathyroid gland & increases the sensitivity of calcium receptors on parathyroid cells, reducing PTH levels
Excess prolactin can present as impotence, loss of libido, and galactorrhoea in men and amenorrhea and galactorrhea in women. What are the causes?
Causes - the p’s
pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metoclopramide, domperidone
Problems with gliflozins?
They are contraindicated in pts with recurrent thrush bc they increase glucose secreted in the urine
They are also linked to necrotising fasciitis (Fourniere’s gangrene)
What should be prescribed and avoided in T2DM when weight loss desired?
Can use SGLT-2 bc often have weight loss as a side effect
Avoid glitazones ( can cause weight gain)
How is sick euthyroid (low thyroxine and T3) treated?
Sick euthyroid (low thyroxine and T3) is common in unwell, elderly patients and often needs no treatment, especially with no hx of thyroid disease
Wait for current illness to resolve and repeat tests
What is De Quervain’s thyroiditis? How is it treated?
Subacute thyroiditis often triggered by viral infection
initial hyperthyroidism, painful goitre, raised ESR and globally reduced uptake of iodine-131
then euthyroid
then hypothyroidism
Usually self limiting, but naproxen can be given for pain
What is the approach for subclinical hypothyroidism in the elderly?
watch and wait
treat if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart
Hyperinsulinemia with high C peptide levels?
Gliclazide overdose
Other drugs such as exogenous insulin would not raise C peptide levels bc C peptide is released as insulin is formed from pro-insulin
PMH of hypothyroidism and hard painless lump on neck→
Thyroid lymphoma ( Hashimoto’s predisposes to this type of malignancy)
Major risk factor for Grave’s?
SMOKING
Tachycardia, htn and fever in someone with a hx of hyperthyroidism→
thyroid storm! 🌩
They may also have jaundice and altered mental state
Often triggered by infection
Tx for thyroid storm?
Tx = beta blockers (e.g. IV propanolol), thionamides(anti-thyroid drugs e.g. propylthiouracil) and corticosteroids (e.g. hydrocortisone)
What is Toxic multinodular goitre?
Appearance on nuclear scintigraphy?
Tx?
Toxic multinodular goitre = multiple autonomously functioning thyroid nodules causing hyperthyroidism
Patchy uptake of iodine
Tx= radioiodine therapy
Describe diabetic neuropathy
Diabetes typically leads to sensory loss and not motor loss. Sensory loss typically results in a ‘glove and stocking’ distribution, with the lower legs affected first
How does gastrointestinal autonomic neuropathy present in diabetics?
Gastroparesis:
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)
Chronic diarrhoea (often occurs at night)
GORD:
caused by decreased lower esophageal sphincter pressure
What is the pathophysiology of diabetic retinopathy?
Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
How is diabetic retionopathy classified?
Patients are typically classified into those with non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy.
Describe the changes seen in non-proliferative diabetic retinopathy
Mild NPDR:
1 or more microaneurysm
Moderate NPDR:
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots (‘soft exudates’ - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA)
Severe NPDR:
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
Describe the changes seen in proliferative diabetic retinopathy
retinal neovascularisation (new blood vessel formation) - may lead to vitreous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
Describe the changes seen in diabetic maculopathy
based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM
How is diabetic retinopathy managed?
optimise glycaemic control, blood pressure and hyperlipidemia and regular review by ophthalmology for all patients
Non-proliferative retinopathy:
regular observation
if severe/very severe consider panretinal laser photocoagulation
Proliferative retinopathy:
panretinal laser photocoagulation
intravitreal vascular endothelial growth factor inhibitors
(examples include ranibizumab, they slow progression of proliferative diabetic retinopathy and improve visual acuity)
if severe or vitreous haemorrhage: vitreoretinal surgery
Maculopathy:
if there is a change in visual acuity then intravitreal VEGF inhibitors
Diabetic foot disease occurs secondary to 2 main problems. What are they?
neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin
peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia
How does diabetic foot disease present?
neuropathy: loss of sensation
ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
All patients with diabetes should be screened for diabetic foot disease on at least an annual basis. What is involved in screening?
screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse
screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot
How is diabetic foot disease managed?
All patients who are moderate or high risk (I.e. any problems other than simple calluses) should be followed up regularly by the local diabetic foot centre.
How are venous leg ulcers managed?
Doppler ultrasound looks for presence of reflux and duplex ultrasound looks at the anatomy/ flow of the vein
Management: 4 layer compression banding after exclusion of arterial disease or surgery
If fail to heal after 12 weeks or >10cm2 skin grafting may be needed
Causes of hypoglycaemia?
insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
alcohol
- (causes exaggerated insulin secretion : mechanism is thought to be due to the effect of alcohol on the pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion)
Presentation of hypoglycaemia?
blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline:
Sweating
Shaking
Hunger
Anxiety
Nausea
blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:
Weakness
Vision changes
Confusion
Dizziness
How should hypoglycaemia be managed?
in the community (for example, diabetes mellitus patients who inject insulin):
Initially, oral glucose 10-20g should be given in liquid, gel or tablet form
or a quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
in a hospital setting:
If the patient is alert, a quick-acting carbohydrate may be given
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given
Alternatively, IV 20% glucose solution may be given through a large vein
What are Trousseau’s sign and Chvostek’s sign in hypocalcaemia?
Trousseau’s sign
carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
wrist flexion and fingers are drawn together
seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people
Chvostek’s sign
tapping over parotid causes facial muscles to twitch
seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people
Causes of hypocalcaemia?
vitamin D deficiency (osteomalacia)
CKD
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
How is hypocalcaemia managed?
acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
How is hypercalcaemia managed?
The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days
How does hypokalaemia present?
muscle weakness, hypotonia
hypokalaemia predisposes patients to digoxin toxicity - care should be taken if patients are also on diuretics
Causes of hypokalaemia with alkalosis?
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Causes of hypokalaemia with acidosis?
diarrhoea
renal tubular acidosis
partially treated diabetic ketoacidosis
carbonic anhydrase inhibitors (acetazolamide)
Causes of hyponatraemia with urinary sodium > 20 mmol/L?
Sodium depletion, renal loss (patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure
Patient who are euvolaemic:
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism
Causes of hyponatraemia with urinary sodium < 20 mmol/L?
Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum
Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Symptomatic hyponatraemia should be monitored in a HDU and can be corrected with hypertonic saline. How should chronic asymptomatic hyponatraemia be managed?
If a hypovolemic cause is suspected:
normal, i.e. isotonic, saline (0.9% NaCl)
if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia
if the serum sodium falls an alternative diagnosis such as SIADH is likely
If a euvolemic cause is suspected:
fluid restrict to 500–1000 mL/day
consider medications:
demeclocycline
vaptans
If a hypervolemic cause is suspected:
fluid restrict to 500–1000 mL/day
consider loop diuretics
consider vaptans
Risk of correcting hyponatraemia too quickly?
central pontine myelinolysis- ‘locked in’ syndrome
Describe the presentation of Cushing’s syndrome.
What may be seen on ABG?
rounded face, central obesity w abdominal striae, dorsocervical fat pad, proximal limb muscle wasting
hypertension, hyperglycaemia
cardiac hypertrophy
depression and insomnia
osteoporosis
poor skin healing / easy bruising
A hypokalaemic metabolic alkalosis may be seen
Give the 4 causes of Cushing’s syndrome
Exogenous steroids
Adrenal adenoma
Cushing’s disease (pit. tumour releasing ACTH)
Paraneoplastic- ectopic secretion of ACTH e.g. from SCLC
Explain the low dose (overnight) dexamethasone suppression test (1mg dexamethasone)
This is the 1st line investigation in suspected Cushing’s
dexamethasone exerts negative feedback on the hypothalamus and pituitary (acts like cortisol) so cortisol levels should go down
If the cortisol level is not suppressed, then it is being produced outside of the normal hormonal axis, and Cushing’s syndrome can be diagnosed
A high dose test should then be performed to determine the cause
Explain the possible results of a high dose dexamethasone suppression test (8mg dexamethasone)
In Cushing’s disease (pit. adenoma) the pituitary still shows some response to negative feedback , so both cortisol and ACTH will be suppressed by the high dose of dexamethasone.
With an adrenal adenoma, the cortisol level will not be suppressed as it is being produced independently, but ACTH will be suppressed due to negative feedback on the pituitary.
With ectopic secretion of ATCH, neither cortisol nor ACTH will be suppressed because they are both being secreted from somewhere else.
What investigations might be used in Cushing’s other than the suppression tests?
24h urinary free cortisol
FBC- raised white cells
Electrolytes- K+ may be low if aldosterone also being secreted by adrenal adenoma
MRI brain for pit. tumour
Chest CT for SCLC
Abdo CT for adrenal tumours
How is Cushing’s treated?
trans-sphenoidal removal of pituitary tumour
surgical removal of an adrenal tumours or SCLC tumours
Give the ranges for the different BMI categories
Underweight: < 18.49
Normal : 18.5 - 25
Overweight : 25 - 30
Obese class 1 : 30 - 35
Obese class 2 : 35 - 40
Obese class 3 : > 40
Which hormone is measured to assess response to tx in Hashimoto’s?
TSH
Target range: TSH value 0.5-2.5 mU/l
What is the most common type of thyroid cancer? Prognosis?
papillary carcinoma - 70% of the cases
Typical presentation: young female with a neck lump with tendency to spread to cervical lymph nodes early
it has an excellent prognosis.
What is the next step if the CT scan is inconclusive in suspected primary hyperaldosteronism?
Adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia in primary hyperaldosteronism
What is the first line tx for a prolactinoma?
Cabergoline - dopamine agonist
What antibodies are useful to distinguish between type 1 and type 2 diabetes?
Diabetes specific antibodies- Antibodies to glutamic acid decarboxylase (anti-GAD)
First line investigation for acromegaly?
Serum IGF-1 levels
The OGTT test is recommended to confirm the diagnosis if IGF-1 levels are raised.
What is the first line insulin regimen in newly diagnosed adults with T1DM?
basal–bolus using twice‑daily insulin detemir
What conditions can cause lower than expected Hba1c?
Conditions that decrease the lifespan of RBCs
Sickle-cell anaemia
G6PD deficiency
Hereditary spherocytosis
What conditions can cause higher than expected Hba1c?
Conditions that increase the lifespan of RBCs
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
Cause of hypothyroidism with low TSH and low T4?
Secondary hypothyroidism- pituitary insufficiency is most likely and therefore an MRI of the gland should be performed.
Complications of DKA?
gastric stasis
thromboembolism
arrhythmias (K+)
iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury
N.B: children/young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment
Which hormones are reduced in stress response?
Insulin
Testosterone
Oestrogen
Most common cause of primary hyperparathyroidism?
solitary adenoma
What are the criteria for a diagnosis of Type 2 diabetes?
If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
What range implies impaired fasting glucose (IFG )?
A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l
Should be offered an OGTT to check for diabetes
Why is it so important to monitor response to tx in HHS?
Rapid changes of serum osmolarity are dangerous and can result in cardiovascular collapse and central pontine myelinolysis (CPM).
What range implies impaired glucose tolerance (IGT)?
Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour between 7.8 mmol/l - 11.1 mmol/l
What is the protocol when a patient with Addison’s has a vomiting bug?
A person with Addisons’ who vomits should take IM hydrocortisone until vomiting stops
What causes impaired hypoglycaemia awareness in patients with long-standing diabetes?
In a patient with long-standing type 1 diabetes, impaired hypoglycaemia awareness is most commonly due to neuropathy of parts of the autonomous nervous system.
Describe the TSH and T4 levels in:
1.Thyrotoxicosis (e.g. Graves’ disease)
2.Primary hypothyroidism (primary atrophic hypothyroidism)
3. Secondary hypothyroidism
4.Sick euthyroid syndrome (common in inpatients)
5. Subclinical hypothyroidism
6. Poor compliance with thyroxine
7. Steroid therapy
TSH T4
1. Low High
2. High Low
3. Low Low
4. Low Low (T3 is particularly low in these patients too)
5. High Normal
6. High Normal
7. Low Normal
Hyponatraemia and hyperkalaemia in a patient with lethargy is highly suggestive of….
ADDISON’S!!!
When should blood glucose be checked in relation to driving in insulin- dependent diabetics?
When should blood glucose be checked generally day to day ?
Before driving and every 2 hours regardless of whether they have eaten or not
In type 1 diabetics, at least 4 times a day, including before each meal and before bed
What is pseudo-Cushing’s? How can it be investigated?
condition that mimics Cushing’s syndrome
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate
A 19-year-old lady is admitted to ITU with severe meningococcal sepsis. She is on maximal inotropic support and a CT scan of her chest and abdomen is performed. The adrenal glands show evidence of diffuse haemorrhage.
What is the diagnosis?
Waterhouse- Friderichsen syndrome
This is often a pre-terminal event and is associated with profound sepsis and coagulopathy.
Erratic blood glucose control, bloating and vomiting→ ?
Gastroparesis
Can occur in diabetics due to neuropathy of the vagus nerve, causing abnormal gut movement.
anosmia in a boy with delayed puberty→ ?
Kallmann’s syndrome
- a cause of delayed puberty secondary to hypogonadotropic hypogonadism
- X-linked recessive
- low sex hormones and low/normal LH and FSH
First step in management if a post-menopausal woman with normal calcium levels has a fracture?
Put them on bisphosphonates- no need for a DEXA scan
once blood glucose is < 14 mmol/l in DKA what should be added?
an infusion of 10% dextrose should be started at 125 mls/hr in addition to the saline regime
