Passmed- Endocrinology Flashcards

1
Q

oral hypoglycaemic agents that treats DMT2. Works by increasing insulin sensitivity. Side effects=hypoglycaemia, fluid retention, elevated LFTs.

A

pioglitazone (aka glitazone)

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2
Q

“bones, stones, groans and psychic moans”:
polydipsia, polyuria
peptic ulceration/constipation/pancreatitis
bone pain/fracture
renal stones
depression
hypertension
80% due to adenoma
raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
pepperpot skull

A

primary hyperparathyroidism

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3
Q

average blood glucose (sugar) levels for the last two to three months. Measurement used to check for diabetes. If it is 42-46 you have prediabetes, discuss exercise and diet with pt.

A

HbA1c

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4
Q
hashimoto's thyroiditis--
iodine deficiency
lithium
postpartum thyroiditis--
Riedel's thyroiditis
Subacute thyroiditis (de Quervain's)--
amiodarone
A

causes of hypothyroidism

– = may have brief hyperthyroid/thyrotoxic phase initially, followed by longer hypothyroid phase.

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5
Q

Grave’s Disease(eye disease only in 30%)
toxic multinodular goitre
amiodarone

A

causes of hyperthyroidism

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6
Q

side effects of which medications?
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
neutrophilia

A

glucocorticoids (steroids).

Very high glucocorticoid activity, minimal mineralocorticoid activity=Dexamethasone, Betamethasone
Predominant glucocorticoid activity, low mineralocorticoid activity=Prednisolone
Glucocorticoid activity, high mineralocorticoid activity= Hydrocortisone
Minimal glucocorticoid activity, very high mineralocorticoid activity= Fludrocortisone

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7
Q

side effects of which medications?
fluid retention
hypertension

A

mineralocorticoids(steroids).

Very high glucocorticoid activity, minimal mineralocorticoid activity=Dexamethasone, Betamethasone
Predominant glucocorticoid activity, low mineralocorticoid activity=Prednisolone
Glucocorticoid activity, high mineralocorticoid activity= Hydrocortisone
Minimal glucocorticoid activity, very high mineralocorticoid activity= Fludrocortisone

e.g. would want to give dexamethasone for patients with raised intracranial pressure secondary to brain tumours.

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8
Q

hypertension
hypokalaemia
alkalosis
bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases
high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
…what is the disease?

A

Conn’s syndrome (aka Primary Hyperaldosteronism)

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9
Q

numerous distinct syndromes involving tumors of the endocrine glands. They are inherited autosomal dominant disorders. The term “xxx” is used if two or more endocrine tumors types, known to occur as part of one of the defined “xxx” syndromes, occurs in a single patient and there is evidence for either a causative mutation or hereditary transmission.

A

xxx=MEN, multiple endocrine neoplasia. There are 3 main types of MEN:
MEN type 1= 3 P’s(Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia; Pituitary (70%); Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration))
MEN type 2a= 2 P’s (Parathyroid (60%); Phaeochromocytoma(adrenals) +Medullary thyroid cancer
MEN type 2b=Phaeochromocytoma(adrenals) +medullary thyroid cancer)

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10
Q

Oral hypoglycaemic drugs used to treat DMT2. They work by increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. Side effects: hypoglycaemic episodes, weight gain.

A

Glicazide (sulfonylureas)

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11
Q

The standard HbA1c target in type 2 diabetes mellitus is …?mmol/mol

A

48 mmol/mol

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12
Q
one of the top five causes of cancer in children, accounting for around 7-8% of childhood malignancies. The tumour arises from neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system.
Features:
abdominal mass
pallor, weight loss
bone pain, limp
hepatomegaly
paraplegia
proptosis
A

neuroblastoma

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13
Q
not enough of the hormone cortisol and, often, not enough aldosterone as well. Usually due to autoimmune disease.
high plasma potassium(hyperkalaemia)
high urinary sodium
hyperpigmentation
depression/irritability
sexual dysfunction
abdo/joint/muscle pain
low BP
decreased appetite and weight loss
extreme fatigue
diagnosed via ACTH stimulation test: cortisol does not rise in this ACTH stimulation test. In a healthy person, they would rise after administration of synthetic ACTH.
A

Addison’s Disease (primary adrenal insufficiency)

(in seocndary adrenal insufficiency, the ACTH stimulation test would show the same results for that of a person with primary adrenal insufficiency, however they may appear normal at early stages in the disease as the adrenal glands have not yet atrophied enough to stop being able to produce cortisol in response to synthetic ACTH).

Primary= ACTH high, cortisol and aldosterone levels low.
Secondary=ACTH low, lowering levels of cortisol over course of disease.

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14
Q

Metabolic acidosis is associated with it.
ECG changes seen include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole.

Causes of this problem:
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison's disease
rhabdomyolysis
massive blood transfusion
A

Hyperkalaemia
Plasma potassium levels are regulated by a number of factors including aldosterone, acid-base balance and insulin levels.

Metabolic acidosis= because hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule.

  • beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment
  • *both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by inhibition of aldosterone secretion
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15
Q
Causes of XXX with alkalosis:
vomiting
thiazide and loop diuretics
Cushing's syndrome
Conn's syndrome (primary hyperaldosteronism)
Causes of XXX with acidosis:
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis

Magnesium deficiency may also cause XXX.

A

XXX=Hypokalaemia

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16
Q
Increased synthesis:
Lesch-Nyhan disease
myeloproliferative disorders
diet rich in purines
exercise
psoriasis
cytotoxics
Decreased excretion:
drugs: low-dose aspirin, diuretics, pyrazinamide
pre-eclampsia
alcohol
renal failure
lead
A

Hyperuricaemia (high uric acid levels in the blood)
Can lead to gout (treated with allopurinol).

Increased levels of uric acid may be seen secondary to either increased cell turnover or reduced renal excretion of uric acid. Hyperuricaemia may be found in asymptomatic patients who have not experienced attacks of gout

Hyperuricaemia may be associated with hyperlipidaemia and hypertension. It may also be seen in conjunction with the metabolic syndrome

17
Q

what is first line therapy for patients with hypercalcaemia?

A

IV fluid therapy

18
Q
Features:
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG: prolonged QT interval

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 drawn together. Seen in around 95% of patients with XXX.

Chvostek’s sign= tapping over parotid causes facial muscles to twitch. Seen in around 70% of patients with XXX.

A

XXX=hypocalcaemia

19
Q

Causes of raised ALP? (alkaline phosphatase)

A

liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
hyperparathyroidism
renal failure
physiological: pregnancy, growing children, healing fractures

high ALP and high calcium= Bone metastases, Hyperparathyroidism.
high ALP and low calcium=Osteomalacia, Renal failure.

20
Q

high ALP and high calcium are signs of what?

A

high ALP and high calcium= Bone metastases, Hyperparathyroidism.

21
Q

high ALP and low calcium are signs of what?

A

high ALP and low calcium=Osteomalacia, Renal failure.

22
Q

The diagnosis of XXX can be made by either a plasma glucose or a HbA1c sample. Diagnostic criteria vary according to whether the patient is symptomatic (polyuria, polydipsia etc) or not.

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, then what?

A

XXX=Type 2 Diabetes Mellitus

the above criteria apply but must be demonstrated on two separate occasions (rather than one).

23
Q

Answer the following:

1) a HbA1c of greater than or equal to 48 mmol/mol (6.5%) means what…?
2) a HbAlc value of less than 48 mmol/mol (6.5%) means what…?

A

1) …a diagnosis of diabetes mellitus.

2) … this result does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes)

24
Q

Give some examples f when HbA1c cannot be used for diagnostic purposes.

A
Conditions where HbA1c may not be used for diagnosis:
haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)
25
Q

what is “impaired glucose tolerance” (IGT)?

A

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

OGTT=oral glucose tolerance test

26
Q

What should be done if you are found to have an impaired fasting glucose?
(A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)).

A

‘People with IFG(impaired fasting glucose) should then be offered an OGTT to rule out a diagnosis of diabetes.

A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT.’

27
Q

Features
lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia
reduced cortisol and aldosterone

A

Addison’s Disease (autoimmune destruction of adrenal glands).
Primary hypoadrenalism.

Other causes of primary hypoadrenalism are:
TB, HIV, antiphospholipid syndrome, metastases, etc.

28
Q

Presentation: typically presents with confusion and hypothermia. It is defined as severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs. It is a medical emergency with a high mortality rate.

A

myxoedma coma

29
Q

Presentation: variable among patients. Patients may exhibit symptoms of sympathetic activation, such as anxiety, hyperactivity, tremor, dyspnoea or cardiovascular symptoms such as atrial fibrillation. Low TSH levels.

A

thyrotoxicosis

30
Q

Presentation: may manifest with autonomic symptoms such as hunger, sweating, tachycardia and neuroglycopenic symptoms such as confusion and behavioural changes.

A

hypoglycaemia

31
Q

Classic presentation: includes polyuria, polydipsia, vomiting, dehydration and, if severe, an altered mental state, including coma. Other symptoms include weight loss, lethargy, Kussmaul respiration (deep hyperventilation) and acetone smell (like pear drops) on the breath.

A

diabetic ketoacidosis

32
Q

Classic presentation includes syncope, hypoglycaemia, nausea and vomiting with characteristic electrolyte disturbances: hyponatraemia, hyperkalaemia (mild), hypercalcaemia and raised urea.

A

addisonian crisis