CLIN SKILLS: Endocrine Disorders Flashcards
(32 cards)
1
Q
causes of hyperthyroidism
A
- graves disease/diffuse toxic goitre (most common)
- thyroid nodules (Plummer’s disease/toxic nodular goitre)/adenoma producing excess thyroid hormones
- INITIAL phase of thyroiditis > leakage of stored hormones into blood
2
Q
PRIMARY causes of hypothyroidism
A
- with goitre: LATE phase of thyroiditis (hormone stores are depleted after leakage into bloodstream), amiodarone, iodine imbalance (high OR low) in HEALTHY PEOPLE
- without goitre: idiopathic atrophy, congenital aplasia, radiotherapy, lingual thyroid (small and underdeveloped), resistance to TSH
3
Q
why can amiodarone cause hypothyroidism
A
- contains high levels of iodine
4
Q
effect of iodine imbalance on thyroid
A
- low iodine: can’t make T3/T4 = loss of -ve feedback to anterior pituitary = excess TSH = thyroid overstimulation = growth of follicle cells = goitre (but still can’t produce T3/T4 = hypothyroidism)
- high iodine in HEALTHY ppl: inhibition of thyroid hormone synthesis to prevent toxicity = hypothyroidism
- high iodine in ppl with autonomous thyroid tissue (nodule/tumour) = uncontrolled thyroid hormone production = hyperthyroidism
5
Q
secondary and tertiary causes of hypothyroidism
A
- secondary: pituitary lesions
- tertiary: hypothalamic lesions
6
Q
causes of goitre
A
- majority idiopathic
- puberty or pregnancy
- graves disease
- amiodarone
- thyroiditis
- iodine deficiency
7
Q
complications of goitre + examination findings
A
- retrosternal extension may cause obstruction, e.g.:
- of venous drainage (+ve Pemberton’s sign)
- of blood supply to head = dizziness, fainting
- of trachea = dyspnoea
- of oesophagus = dysphagia
8
Q
Sx of hyperparathyroidism
A
- stones – renal stones (sometimes polydipsia or polyuria without stones)
- bones – osteopenia, pseudogout, muscle weakness
- groans (GIT) – nausea, constipation, peptic ulcer, pancreatitis
- moans (including psychological) - lethargy, drowsiness, confusion, psychosis
9
Q
examination findings for parathyroidism
A
- mental state
- bony tenderness
- proximal muscle weakness
- HTN
- pseudogout
10
Q
Sx of hypoparathyroidism
A
- muscle spasms (carpopedal, facial grimacing, laryngospasm, convulsions),
- intestinal cramps
- arrhythmia
- depression/psychosis
11
Q
2 tests for hypocalcaemia
A
- Chvostek’s sign: tap over facial nerve in front of the ear. if +ve, ipsilateral mouth twitch
- Trousseau’s sign: inflate sphygmomanometer to above systolic pressure. if +ve, within 4 minutes, will cause carpopedal spasm (opposition of thumb, extension of IP joints and flexion MCP joints) which resolves when cuff deflated
12
Q
causes of hypocalcaemia
A
- hypoparathyroidism after thyroidectomy
- malabsorption
- vit D deficiency
- CKD
- acute pancreatitis
- pseudohypoparathyroidism
- Mg2+ deficiency
13
Q
Sx of Cushing’s syndrome
A
- round, moon-shaped, plethoric (red) facies
- acne due to androgenic properties
- HTN, oedema
- redistribution of fat to trunk, face, abdomen
- proximal muscle weakness & wasting due to protein breakdown
- skin striae (stretch marks) and ecchymoses (bruising) due to protein breakdown
- polyuria + polydipsia
- amenorrhoea
- hyperglycaemia
14
Q
most common causes of Cushing’s syndrome
A
- exogenous administration of steroids or ACTH
15
Q
Sx of Addison’s disease (adrenal insufficiency)
A
- malaise
- LOW
- depression
- hypoglycaemia
- N&V due to increased K+ and H+
- muscle weakness due to increased K+ and H+
- abdominal pain, diarrhoea, constipation due to electrolyte imbalance
- postural hypotension due to less aldosterone = loss of Na+
- pigmentation (and vitiligo) due to excess ACTH
16
Q
features of acromegaly
A
- coarse, prominent facial features:
- prognathoid jaw
- prominent nose & forehead
- thickened lips & large tongue
- ‘spade-shaped’ hands
- excessive sweating and greasy skin
- kyphosis
- HTN: GH causes fluid retention
- bitemporal hemianopia (pressure on optic nerve) due to GH-secreting pituitary tumour
- carpal tunnel syndrome: GH causes fluid retention
- impaired glucose tolerance
17
Q
2 types of hyperthyroidism
- onset
- changes to thyroid gland
- presence of exophthalmus
- cause
A
- diffuse toxic goitre (Graves’ disease): onset at 20-60 yrs, thyroid gland uniformly enlarged, exophthalmus, autoimmune
- toxic nodular goitre: onset > 50 yrs, 1 or more nodules with uneven enlargement, no exophthalmus, caused by benign nodule
18
Q
graves’ disease
A
- autoantibodies activate thyroid gland = increased synthesis of thyroid hormones
19
Q
how to Dx hyperthyroidism
A
- check for high serum thyroxine and low TSH (b/c -ve feedback) levels
- then check for TSHR autoantibodies to see whether it’s Graves’ disease (diffuse toxic goitre) or toxic nodular goitre
20
Q
primary vs secondary hyperthyroidism
A
- primary: increased T3/T4 but decreased TSH due to functional -ve feedback
- secondary: increased T3/T4 but increased TSH - suggests pituitary (2˚) or hypothalamic (3˚) dysfunction
21
Q
central vs nephrogenic diabetes insipidus
A
- central: decreased secretion of ADH by posterior pituitary
- nephrogenic: kidney resistant to ADH
22
Q
type 1 diabetes mellitus
- onset
- age of onset
- body size
- ketoacidosis
- pathophys
- endogenous insulin
A
- sudden onset
- children
- thin/normal body build
- ketoacidosis common (hyperventilation to compensate, sweet-smelling breath)
- autoimmune destruction of B cells in pancreas = can’t make insulin
- low/absent endogenous insulin
23
Q
type 2 diabetes mellitus
- onset
- age of onset
- body size
- ketoacidosis
- pathophys
- endogenous insulin
A
- gradual onset
- adults
- often obese
- ketoacidosis rare - instead HHS (hyperosmolar hyperglycaemic state)
- compromised insulin signalling pathway, impairing GLUT4 translocation = impaired glucose uptake
- insulin may be normal, increased or decreased
24
Q
why do diabetics produce ketone bodies?
A
- insulin deficiency = decreased glucose uptake in cells
- instead, fatty acids undergo B-oxidation to form acetyl-coA
- acetyl-coA forms ketone bodies b/c can cross BBB > broken back down into acetyl-coA, enter krebs cycle and produce ATP
- increased FAs = DKA
25
why do diabetics get polydipsia?
- insulin deficiency = decreased glucose uptake in cells = too much in blood
- causes increased filtration of glucose but PCT can't reabsorb it all = stays in urine (glycosuria)
- glucose draws water and Na+ into urine = decreased blood volume and pressure = polydipsia
26
why do diabetics experience fatigue and LOW
- decreased insulin = decreased protein synthesis = low muscle mass = fatigue + LOW
27
complications of untreated diabetes mellitus
- glucose binds to proteins, forming advanced glycation end products (AGEs) = cause widespread inflammation and risk of infection
- macrovascular: atherosclerosis > IHD, CVA, peripheral vascular disease
- microvascular: retinopathy, nephropathy, neuropathy (won't feel when you get hurt > gangrene)
28
BGL suggestive of diabetes
- >11.1 mmol/L
29
3 features of oral GTT suggestive of diabetes
- higher BGL baseline
- higher BGL peak following insulin drink
- delayed return to baseline
30
what is HbA1c
- % of Hb that is bound to glucose
- marker for long-term (3 month) glycaemic control
- <6% is good
31
C-peptide test for diabetes
- insulin = proinsulin + C-peptide
- C-peptide does not affect BGL + has a much longer 1/2 life
- can use to differentiate b/n type I and II DM since type I involves a loss of insulin secretion so will have less C-peptide
- can also use to determine staging + progression of T2DM
32
LADA (latent autoimmune diabetes in adults)
- autoantibodies attack B cells in pancreas but develops really slowly so can appear as type II
