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Pass Medicine Endocrinology

Terms in this set (41)

features of diabetic ketoacidosis
abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath ('pear drops' smell)
diagnostic criteria for diabetic ketoacidosis
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick
management of diabetic ketoacidosis
fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially.

insulin: an intravenous infusion should be started at 0.1 unit/kg/hour. Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started

correction of hypokalaemia
complications of diabetic ketoacidosis and its treatment
- gastric stasis
- thromboembolism
- arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
- iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
- acute respiratory distress syndrome
- acute kidney injury
side effects of glucocorticoids
- endocrine: impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia
- Cushing's syndrome: moon face, buffalo hump, striae
- musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
- immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis
- psychiatric: insomnia, mania, depression, psychosis
- gastrointestinal: peptic ulceration, acute pancreatitis
- ophthalmic: glaucoma, cataracts
suppression of growth in children
intracranial hypertension
acromegaly management
Trans-sphenoidal surgery is first-line treatment for acromegaly in the majority of patients

Dopamine agonists
for example bromocriptine
now superseded by somatostatin analogues
- effective only in a minority of patients

Somatostatin analogue
for example octreotide
effective in 50-70% of patients
may be used as an adjunct to surgery

Pegvisomant
GH receptor antagonist - prevents dimerization of the GH receptor
once daily s/c administration
very effective - decreases IGF-1 levels in 90% of patients to normal
doesn't reduce tumour volume therefore surgery still needed if mass effect
Cushing's disease
results from increased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary, often caused as a result of a pituitary adenoma.
Cushings triad
a set of three clinical signs irregular respirations, bradycardia and systolic hypertension resulting from raised intracranial pressure
Cushing's syndrome
a collection of signs and symptoms due to prolonged exposure to cortisol - Cushing's disease is a specific type of Cushing's syndrome characterised by increased ACTH production of because of a pituitary adenoma (or sometimes due to excess production of hypothalamus CRH).
ACTH dependent causes of Cushing's syndrome
Cushing's disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
ectopic ACTH production (5-10%): e.g. small cell lung cancer
ACTH independent causes of Cushing's syndrome
iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)
pseudo Cushing's
mimics Cushing's
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
causes of gynaecomastia
physiological: normal in puberty
syndromes with androgen deficiency: Kallman's, Klinefelter's
testicular failure: e.g. mumps
liver disease
testicular cancer e.g. seminoma secreting hCG
ectopic tumour secretion
hyperthyroidism
haemodialysis
drugs
drugs that can cause gynaecomastia
spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
gonadorelin analogues e.g. Goserelin, buserelin
oestrogens, anabolic steroids
typical exam presentation of primary hyperparathyroidism
stereotypically seen in elderly females with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level
causes of primary hyperparathyroidism
80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma
features of primary hyperparathyroidism
bones, stones, abdominal groans and psychic moans'
- polydipsia, polyuria
- peptic ulceration/constipation/pancreatitis
- bone pain/fracture
- renal stones
- depression
- hypertension
Ix in primary hyperparathyroidism
raised calcium, low phosphate
PTH may be raised or normal
technetium-MIBI subtraction scan
pepperpot skull is a characteristic X-ray finding of hyperparathyroidism
treatment for 1º hyperparathyroidism
the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
calcimimetic agents such as cinacalcet are sometimes used in patients who are unsuitable for surgery
two things that can lower an HbA1c reading
lower average blood glucose concentration and a shorter red cell life span.
blood disorders that lower HbA1c
Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
blood disorders that raise the HbA1c
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
Klinefelter's syndrome
karyotype 47, XXY

Features
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia - increased incidence of breast cancer
elevated gonadotrophin levels

Diagnosis is by chromosomal analysis
papillary thyroid cancer
65%, generally young females. Metastasis to cervical lymph nodes. Thyroglobulin can be used as a tumour marker. Characteristic Orphan Annie eyes on light microscopy. Good prognosis
follicular thyroid cancer
20%, generally women >50 years old. Metastasis to lung and bones. Thyroglobulin can be used as a tumour marker. Moderate prognosis
medullary thyroid cancer
5%, sporadic or part of MEN2 syndrome. It originates from the parafollicular cells which produce calcitonin - can be used as a tumour marker.
MEN 1 syndrome
Pituitary adenoma, parathyroid hyperplasia, pancreatic tumours
MEN 2 syndrome
Parathyroid hyperplasia, medullary thyroid carcinoma, phaeochromocytoma
hyperosmolar hyperglycaemic state characterised by
1.) Severe hyperglycaemia
2.) Dehydration and renal failure
3.) Mild/absent ketonuria

confirmed by:
Dehydration
Osmolality >320mosmol/kg
Hyperglycaemia >30 mmol/L with pH >7.3, bicarbonate >15mmolL and no significant ketonenaemia <3mmol/L
complications of hyperosmolar hyperglycaemic state
rhabdomyolysis,
venous thromboembolism,
lactic acidosis,
hypertriglyceridaemia,
renal failure,
stroke
and cerebral oedema
precipitants of hyperosmolar hyperglycaemic state
New diagnosis of type 2 diabetes
Infection
High dose steroids
Myocardial infarction
Vomiting
Stroke
Thromboembolism
Poor treatment compliance
Dapagliflozin
sodium-glucose transport protein 2 (SGLT2) inhibitor

reversibly inhibit sodium-glucose co-transporter 2 (SGLT2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

Examples include canagliflozin, dapagliflozin and empagliflozin

Important adverse effects include
genital infection (secondary to glycosuria)
diabetic ketoacidosis
Maturity onset diabetes of the young (MODY)
A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
Latent autoimmune diabetes of adults (LADA)
The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM
Addison's disease features
lethargy, weakness, anorexia, nausea & vomiting, weight loss, 'salt-craving'
hyperpigmentation (especially palmar creases), vitiligo, loss of pubic hair in women, hypotension
crisis: collapse, shock, pyrexia
differentiating between T1 and T2 DM
Consider measuring C-peptide after initial presentation if there is difficulty distinguishing type 1 diabetes from other types of diabetes. Be aware that C-peptide concentrations have better discriminative value the longer the interval between initial presentation and the test.

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
hormones reduced in stress response
Insulin
Testosterone
Oestrogen

Stress response is associated with: substrate mobilization, muscle protein loss, sodium and water retention, suppression of anabolic hormone secretion, activation of the sympathetic nervous system, immunological and haematological changes.
hormones increased in the stress response
GH
cortisol
renin
ACTH
aldosterone
prolactin
ADH
glucagon
causes of raised prolactin
the Ps
pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metocloPramide, domPeridone, haloPeridol
features of excess prolactin
men: impotence, loss of libido, galactorrhoea
women: amenorrhoea, galactorrhoea
treatment ladder for T2DM
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