Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > endocrine and metabolic > Flashcards

endocrine and metabolic Flashcards

1
Q

Define Addison’s disease

A

primary adrenal insufficiency caused by adrenal cortex destruction

  • low cortisol + elevated ACTH in response
  • low aldosterone
  • low adrenal androgens (DHEAP - dehydroepiandrosterone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of Addison’s disease

A
  1. TB
  2. autoimmune addison’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presenting symptoms of Addison’s

A
  • fatigue
  • hyperpigmentation (high ACTH+ high MSH => high )
  • GI (weight loss, loss of appetite, vomiting + nausea, abdominal pain)
  • dizziness
  • muscle weakness + cramps (electrolyte imbalance)
  • fever, headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Examination findings for Addison’s disease

A
  • postural hypotension (bp 20mmHg lower standing)
  • other autoimmune (vitiligo, pernicious anaemia, coeliac disease)
  • hyperpigmentation
  • loss of body hair on women (less androgens)
  • skin changes - darkening of elbows, under palms, gums
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Investigations + findings for Addison’s disease

A
  1. 9am serum cortisol (<100nmmol/L = likely adrenal insufficiency
    *cortisol= diurnal
  2. Bloods:
  • U&Es (low Na+, high K+)
  • FBC (anaemia)
  • Hypercalcemia
  • low glucose
  • TFTs (exclude hyperthyroidism)
  1. short Synacthen test (should in normals increase cortisol) - cortisol <500mmol/L in 30 mins = likely adrenal insufficiency
  • plasma renin/ aldosterone levels
  • serum DHEA-s (low)
  • autoantibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What factors can affect serum cortisol levels (other than addison’s disease)?

A
  • people working shifts (disrupts diurnal variation of cortisol)
  • pregnancy
  • oestrogen based medication (OCP/hormone replacement) - increases cortisol binding globulins increasing cortisol
  • people on long term corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Management for Addison’s disease

A
  • 3mg daily prednisilone OR 15-25mg 3/daily hydrocortisone (replace cortisol)
  • fludrocortisone (replace aldosterone)
  • DHEA replacement (unlicensed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What advice should be given to patients with Addison’s disease?

A
  • have a steroid warning card
  • carry emergency hydrocortisone
  • wear a medic-alert bracelet (take double steroid dosage when ill)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Features of Addison’s crisis

A
  • Hypotension
  • Hypovolemic shock (dehydration)- tachycardia
  • altered consciousness
  • seizures/convulsions
  • cardiac arrest (hyperkalemia)
  • severe vomiting/diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management of Addison’s crisis

A
  • IV fluid rehydration (replace Na+)
  • IV bolus hydrocortisone
  • dextrose to treat hypoglycaemia
  • treat cause (ABs for infection)
  • monitor (electrolyte levels/ vitals)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is cushing syndrome ?

A

high levels of cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of Cushings syndrome

A

ACTH dependant

  1. cushings disease (adrenal hyperplasia due to pituitary adenoma)- trea
  2. ectopic ACTH production -small cell lung cancer)

ACTH- independant

  1. ORAL STEROIDS
  2. adrenal adenoma
  3. adrenal nodular hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Presenting symptoms of Cushing’s syndrome

A
  • increased weight
  • mood change (depression)
  • proximal weakness
  • erectile dysfunction/ irregular menses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Examination findings of cushing’s syndrome

A
  • central obesity
  • moon face, red cheeks
  • buffallo hump
  • purple abdominal striae
  • poor wound healing
  • thin skin - bruises
  • osteoporosis (thin bones)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Investigations for cushing’s syndrome

A
  1. Bloods- U&Es, high glucose

2, High-sensitivity tests:

  • urinary free-cortisol
  • late-night cortisol (usually only high in morning unless cushings)
  • overnight dexamethasone suppression test
  • low dose dexamethasone suppression tests
  1. CT/MRI of adrenals, measure ACTH => ACTH dependant
    Pituitary MRI => ACTH independant
    lung cancer? => CXR, bronchoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of cushing’s syndrome

A
  1. stop steroids
  2. pre-surgery/ unfit
    - metyrapone (11b-hydroxylase inhbitor)
    - ketoconazole (17a-hydroxylase inhibitor => inhibitis cortisol/ aldosterone + sex-steroids)
    - drugs for osteoporosis
  3. surgery
    - pituitary adenoma => trans-sphenoidal adenoma resection
    - adrenal adenoma => surgical removal of tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mechanism + Side effects of metyrapone

A

Inhibits 11 hydroxylase enzyme and inhibits cortisol production

  • nausea, vomiting
  • hypoadrenalism (low mineralcorticoids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mechanism + Side effects of ketoconazole

A

Inhibits 17a hydroxylase enzyme and inhibits cortisol (+ sex steroids) production

  • nausea, vomiting
  • alopecia
  • liver damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

complications of cushing’s syndrome

A
  1. diabetes (high cortisol => high glucose)
  2. osteoporosis
  3. hypertension
  4. increased infection risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

prognosis for patients with cushing’s syndrome

A

untreated 5 yr survival - = 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define thyrotoxicosis

A

abnormally high levels of thyroid hormones in blood due to problem with HPT axis (hypothalamus-pituitary-thyroid)

=> Hyperthyroidisim (subset of thyrotoxicosis)

  • increased thyroid production from thyroid gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of thyrotoxicosis

A
  • Graves disease
  • Toxic multinodular goitre (from Plummer’s)
  • Early phase Thyroiditis - de Quervains/ post-partum/ hashimoto’s (most common in elderly)

Thyroiditis causes stored thyroxine to be released from thyroid gland=> causing brief early hyperthyroidism but as stores get used up => hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Define Graves disease

A

autoimmune condition where anti-TSH antibodies bind to TSH receptors on thyroid gland and activate thyroid gland => increased T3/T4 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Symptoms of Grave’s disease

A
  • weight loss + increased appetite
  • heat intolerance (hot)
  • diarrhoea
  • sweating
  • tremor
  • anxiety/ irritability
  • oligo/amenorrhoea
  • libido loss
  • weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Examination signs of Grave’s

A
  • palmar erythema
  • sweaty hands
  • thyroid acropachy (severe + painful finger/toe clubbing)
  • fine tremor
  • hair thinning
  • exopthalmos
  • opthalmoplegia (CN III,IV,VI palsy)
  • lid lag
  • goitre
  • gynaecomastia
  • tachycardia (AF most common arrythmia with thyrotoxicosis)
  • pre-tibial myxoedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Investigations of Grave’s

A

Bedside

  • ECG
  • glucose

Bloods

  • TFTs (raised T3/T4, low TSH)
  • FBC
  • U&Es
  • LFTs
  • autoantibodies (anti-TPO, anti-TSH receptor, anti-thyroglobulin)

Imaging

  • neck ultrasound
  • radioiodine uptake scan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Management of acute thyroid storm

A
  • IV fluids
  • beta-blockers (for tachycardia)
  • anti-thyroid drugs (propylthiouracil/ carbimazole)
  • IV steroids (hydrocortisone)
  • iodine/ pottassium iodide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Management of Grave’s (subacute)

A

First line:

  1. beta-blockers for tachycardia/anxiety/tremor/ palpitations + steroids-prednisilone
  • anti-thyroid drugs (carbimazole/ propylthiouracil) => 1yr
  • radioactive iodine

Surgery (usually in planning to get pregnant/ severe Graves/ ineffective first line/ suspect malignancy)

  • Thyroidectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Mechanism of antithyroid drugs (thionamides => propylthiouracil, carbimazole)

A
  1. inhibit thyroid peroxidase enzyme
  2. inhibit iodination of iodine
  3. inhibit iodination of thyroglobulin => no thyroxine synthesis

Side effects= rashes, agranulocytes (SEVERE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Complications of Grave’s

A
  • AF => strokes/ heart attacks
  • Congestive heart failure (elderly)
  • Untreated => osteroporosis
  • Elephantessis (RARE)
  • Orbitopathy (RARE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define Plummer’s => toxic multinodular goitre

A
  • benign tumour of thyroid gland => increased thyroxine production
  • Unilateral lump on one side
  • Radioactive iodine uptake on one side
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Define thyrotoxic storm

A

Extreme and sudden thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Symptoms of thyrotoxic storm

A
  • hyperpyrexia (fever)
  • hypertension
  • severe tachycardia (>140bpm)
  • confusion/ delerium
  • fainting
  • jaundice, nausea, abdominal pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Management of thyrotoxic storm

A
  • IV fluids
  • beta-blockers (for tachycardia)
  • anti-thyroid drugs (propylthiouracil/ carbimazole)
  • IV hydrocortisone
  • URGENT endocrinology review
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What can trigger thyrotoxic storm?

A
  • INFECTION
  • trauma
  • thyroid surgery
  • stroke
  • diabetic ketoacidosis
  • MI/ congestive heart failure
  • radioactive iodine replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

define hypothyroidism

A

syndrome caused by low levels of thyroid hormones (T3/T4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Causes of primary hypothyroidism (low T3/T4 + high TSH)

A
  • iodine deficiency (or XS)
  • Hashimoto’s thyroiditis (AUTOIMMUNE)
  • Post-surgery damage to thyroid gland (neck/thyroid)
  • iatrogenic (anti-thyroid drugs, iodine, amiodarone)
  • Transcient thyroiditis (de Quervains/viral, Post-partum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

causes of secondary hypothyroidism (low T3/T4 + low TSH)

A

pituitary dysfunction due to:

  • tumours
  • surgery/ trauma
  • pituitary infarction
  • infiltration (amyloidosis, sarcoidosis, haemachromotosis, TB)
  • Sheehan’s syndrome (pituitary necrosis due to post-partum haemorrhage)
  • drugs (cocaine, dopamine, glucocorticoids, metformin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

presenting symptoms of hypothyroidism

A

*everything slows down

  • slower metabolism=> weight gain
  • bradycardia
  • cold intolerance
  • fatigue
  • constipation
  • dry skin/ hair loss
  • weakness
  • depression, impaired concentration
  • menstrual irregularities

+ for secondary hypothyroidism

  • recurrent headaches/ vision changes
  • changes to other pituitary hormone levels- skin depigmentation (ACTH), galactorrhea (prolactin), erectile dysfunction/amennorrhea (LH/FSH), acromegaly (GH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

examination findings of hypothyroidism

A
  • hands (cold, bradycardia)
  • head/neck/ arms (puffy face, goitre, oedema, hair loss, dry skin, vitiligo, Thyroid pain (subacute thyroiditis)
  • chest (pericardial effusion, pleural effusion)
  • abdominal (ascites)
  • neurological (reduced deep tendon reflexes, signs of carpal tunnel)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is myxoedema coma + symptoms:

A

severe hypothyroidism seen in the elderly

  • hypothermia
  • hypoventilation
  • hyponatremia
  • heart failure
  • confusion
  • coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

investigations + findings for hypothyroidism

A

Bloods

  • Thyroid function tests (low T3/T4 +/- low TSH)
  • FBC + serum b12 ( check for associated normacytic anaemia)
  • U&Es- may have low sodium
  • high cholesterol (check for associated dyslipidaemia)
  • glycated HbA1c (check for associated diabetes)
  • check for coeliac disease (anti-transglutaminase antibody)
  • serum thyroid peroxidase antibodies (for autoimmune disease)
  • ultrasound of neck (look at goitre)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Management of hypothyroidism

A
  1. hypothyroidism => 50-100ug levothyroxine daily before food + monitor TSH (to normalise) every 3 months and adjust dose
    *in secondary hypothyroidism monitor using free T4 levels
  2. hypothyroidism during pregnancy- need higher levothyroxine dose to prevent neonatal complications (monitor TFTs more frequently)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why can the thyroid function tests still be abnormal in (suspected) hypothyroidism after adequate levothyroxine treatment

A
  • poor drug compliance (side effects)
  • interacting with other drugs
  • malabsorption of levothyroxine in gut (coeliac, pernicious anaemia, H. pylori gastritis, atrophic gastritis, IBD)
  • increased LT4 demands (weight gain/ pregnancy)
  • foods that reduce LT4 absorption (grapefruit, coffee, milk, soya)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Why does adrenal insufficiency need to be ruled out before prescribing levothyroxine?

A

as it can precipitate Addison’s crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Management of myxoedema coma

A
  • oxygen
  • rewarming
  • rehydration
  • IV T3 (faster action onset than T4)
  • IV hydrocortisone (for adrenocortical insufficiency)
  • treat underlying cause (e.g. infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

complications of hypothyroidism

A
  • myxoedema coma (80% mortality rate)
  • myxoedema madness (+ delusions/ psychosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Define hyperparathyroidism

A

XS production of PTH (by chief cells of parathyroid gland)

  • Primary - high PTH regardless of calcium levels (high Ca2+)
  • Secondary - high PTH in response to hypocalcemia (low Ca2+)
  • Tertiary- increased PTH in response to inital hypocalcemia, then autonomous secretion of PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Causes of hyperparathyroidism

A

Primary (high PTH)

  • parathyroid adenoma (80%)
  • parathyroid hyperplasia
  • parathyroid carcinoma
  • MEN syndromes

Secondary (low Ca2+ => high PTH)

  • chronic renal failure
  • Vit. D deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Presenting symptoms of hyperparathyroidism (hypercalcemia)

A

Primary

  • bone pain
  • renal calculi
  • abdominal pain, nausea, constipation, dyspepsia, anorexia
  • pscyhcic groans (depression, fatigue, impaired concentration)
  • polyuria, polydypsia
  • lethargy
  • pancreatitis, duodenal ulcers??

Secondary

  • could present with hypocalcemia signs (Convulsions, arrhytmias, tetany, parasthesia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Investigations for hyperparathyroidism

A

Bloods

  • U&Es- albumin
  • PTH (high)
  • serum calcium
  • serum phosphate (low)
  • LFTs- ALP
  • Vit D
  • calcium: creatinine ratio- differentiates primary hyperparathyroidism with familial hypercalciuric hypercalcemia (FHH)

Imaging

  • renal USS - check for stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Management of hyperparathyroidism

A

Primary

  • IV fluids
  • moderate calcium/ vit D intake
  • avoid thiazide diuretics (worsens hypercalcemia)
  • Surgery - partial/total parathyroidectomy

Secondary

  • treat cause- renal failure (dialysis?) / vit D deficiency (Ca2+/ Vit D supplements)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Complications of hyperparathyroidism

A
  • Primary => increased bone resporption, increased calcium reabsorption => HYPERCALCEMIA
  • Secondary => stimulates osteoclasts => osteitis fibrosa cystitis
  • Post-surgery => hypoPTH, hypoCa2+, hoarse voice (reccurent laryngeal nerve damage),
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Define hypoparathyroidism

A

low pTH production

  • Primary - Low pTH => low Ca2+
  • Secondary - high Ca2+ => low PTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Causes of hypoparathyroidism

A

Primary (low PTH, low Ca2+)

  • trauma
  • parathyroidectomy
  • thyroidectomy
  • hypomagnesium- chronic alcohol intake, XS diarrhoea, poor nutrition/ malabsoprtion
  • genetic mutations in CASR, GATA3

Secondary (high Ca2+ => low PTH)

  • malignancy (bone metastasis, multiple myeloma, lung Squamous CC)
  • thiazide diuretics
  • XS vit D (high calcitriol)
  • sarcoidosis
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Presenting symptoms of hypoparathyroidism

Primary -hypocalcemia

Secondary - hypercalcemia

A

Primary (low PTH => low Ca2+)

  • Convulsions
  • Arrhytmias
  • Tetany
  • Parasthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Examination findings of primary hypoparathyroidism (hypocalcemia)

A
  • Chovostek’s sign (ipsilateral facial twitch when cheek touched)
  • Trousseau’s sign (blood pressure cuff inflates, cause carpopedal spasm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Investigations for hypoparathyroidism

A

Bedside

  • ECG- prolonged QT interval (arrythmias)

Bloods

  • U&Es- albumin, creatinine (normal- unless renal failure)
  • serum calcium (low)
  • serum phosphorous
  • serum magnesium (low)
  • serum PTH (low)
  • Vit D (low)
  • LFTs- ALP
  • FBC

IMaging

  • renal imaging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Management of hypoparathyroidism

A

Primary (low PTH => low Ca2+)

  • Ca2+ / Mg2+ supplements
  • recombinant PTH
  • calcitirol supplements
  • thiazide diuretics (reduce the rate of urinary calcium excretion )
  • reduce PPI/Corticosteroids (reduce Ca2+ absorption), loop diuretics (increase Ca2+ excretion)

Secondary (high Ca2+ => low PTH)

  • treat cause
  • moderate Ca2+/ Vit D
  • reduce thiazide diuretics (worsen hypercalcemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Complications of hypoparathyroidism

A
  • hypocalcemia (CATs NUMB)
  • increased phosphate reabsorption
  • cataracts
  • renal stones/ insufficiency (hypercalcemia?)
    *
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

define hypercalcemia of malignancy

A

malignancy => hypercalcemia

62
Q

Differentials for hypercalcemia of malignancy

A
  • primary hyperparathyroidism (high PTH => high Ca2+)
  • hyperthyroidism
  • adrenal insufficiency
63
Q

Presenting symptoms of hypercalcemia of malignancy

A
  • risk factors (malignancy)
  • can have no signs of hypercalcemia
  • medication worsening hypercalcemia
  • polydypsia
  • polyuria
  • bone pain
  • nausea
  • constipation
  • confusion
  • fatigue
64
Q

Risk factors for hypercalcemia of malignancy

A
  • non-metastatic disease (humoral hypercalcemia) => releases PTH related peptide renal, ovarian, endometrial, squamous cell, breast
  • metastatic skeletal involvement (osteolytic hypercalcemia) => breast cancer, muliple myeloma
  • lymphoma (calcitriol- mediated hypercalcemia)
65
Q

What medications worsen hypercalcemia?

A
  • thiazide diuretics (reduce calcium excretion)
  • lithium
  • Ca2+ supplements
  • antacids
  • XS Vit D supplements
66
Q

Investigations for hypercalcemia of malignancy

A

Bedside

  • ECG- arrythmias (prolonged QT interval)

Bloods

  • U&Es - elevated creatinine (renal failure), albumin
  • serum calcium (high)
  • serum phosphorous (low)
  • serum intact PTH (high hyperparathyroidism)
  • serum PTH-related peptide (high in humoral hypercalcemia)
  • serum calcitriol (high in calcitriol-mediated hypercalcemia)
  • metabolic panel - elevated bicarbonate (malignancy)

Imaging

  • Skeletal screen- osteolytic lesions, pathological fractures, osteopenia
  • CXR- TB/sarcoidosis/lung cancer signs
67
Q

Management for hypercalcemia

A

Mild hypercalcemia/ asymptomatic

  • Treat malignancy
  • stop hypercalcemia exacerbating medication

Severe hypercalcemia/ symptomatic without AKI

  • IV fluids
  • BISPHOSPHONATES (stimulates osteoblasts) + calcitonin (reduces Ca2+)
  • Furosemide (loop diuretic)
  • Stop hypercalcemia exacerbating medication
  • Treat underlying malignancy

+ corticosteroid (if calcitriol-mediated hypercalcemia)

Symptomatic Hypercalcemia + AKI

  • renal dialysis
  • denusomab
68
Q

define Type 1 diabetes

A
  • autoimmune destruction of pancreatic-beta cells => no insulin production
  • prone to diabetic ketoacidosis (no background insulin so glucose converted to ketone bodies)
  • LADA - latent autoimmune diabetes of adults (slower progression to insulin dependance)
69
Q

cause of T1DM

A
  • genetic susceptibility + environmental trigger
  • genes (HLA DR3/4)
  • Autoantigens associated with T1DM (glutamic acid decarboxylase, insulin, insulinoma-associated protein 2)
70
Q

Presenting symptoms of T1DM

A
  • younger onset (<30)
  • osmotic diuresis (polyuria, polydypsia,nocturia)
  • tiredness
  • weight loss

Associated autoimmune conditions

  • vitiligo (skin condition)
  • addison’s (tan)
  • autoimmune thyroid disease
71
Q

Investigations for T1DM

A

Bedside

  • Urinalysis - glucose, ketones
  • Blood glucose (random/ fasting)
  • blood pressure (can repeat with ABPM/HBPM)

Bloods:

  • HbA1c (42- pre-diabetes, 48-diabetes)
  • FBC
  • U&Es
  • Lipid profile
  • anti-GAD/ islet cell autoantibodies
  • Urine albumin: creatinine ratio
  • Investigate DKA => capillary blood glucose, urine dipstick, ABG, FBC
72
Q

Management of T1DM

A

Glycaemic control

  • adjust insulin doses to exercise/meals (DAFNE-dose adjusted for normal eating)
  • calorie counting
  • illness increases insulin requirements

Basal-bolus regime

  1. Short acting insulin x3daily before meals (Lispro, Aspart)
  2. Long acting insulin x1daily (Glargine, Isophane)

Insulin pumps

Monitor/ screen for complications/ CVD risk factor management

Treat for hypoglycaemia => if reduced consiousness (50ml of 50% glucose IV) if conscious 50g of oral glucose

73
Q

define Type 2 diabetes mellitus

A
  • insidious onset (won’t know for many years)
  • resisitance to insulin + eventually impaired insulin secretion
  • hyperglycaemia but no acidosis (as there’s background insulin to suppress ketone body formation)
  • intermittent polyuria + polydypsia - assume they have prostate problems/UTIs
74
Q

pathophysiology of type 2 diabetes

A
  • months to years of hyperglycaemia
  • slow damage to endothelium
  • microvascular complications (retinopathy/nephropathy/neuropathy)
  • macrovascular damage (IHD/ CVA/paeriperal gangrene)
75
Q

risk factors for type 2 diabetes

A
  • obesity, inactivity (NEFAs => post-receptor defects)
  • hypertension
  • south-east asians
  • genetics- mutations in insulin receptors (MODY, mitochondrial diabetes)
  • chronic pancreatitis
  • endocrine disorders (Cushing, acromegaly, phaechromocytoma)
  • drugs (corticosteroids, atypical antipsychotics, TB drugs, SSRIs
  • autoimmune
  • renal failure
  • cystic fibrosis
  • PCOS
  • Werner’s syndrome
  • metabolic syndrome
76
Q

presenting symptoms of Type 2 diabetes

A
  • usually asymptomatic
  • osmotic diuresis (polyuria, polydypsia)
  • lethargy
  • can present with hyperglycaemic hyperosmolar state (HHS)
  • infections (infected diabetic foot, candidiasis)
77
Q

examination signs of type 2 diabetes

A

acanthosis nigricans

78
Q

investigations for type 2 diabetes

A

Bedside:

  • Urine dipstick- proteinurea/ albuminurea
  • blood glucose - random (>11) / fasting (>7) / 75g oral glucose tolerance (>11)
  • blood pressure

Bloods

  • HbA1c (42- pre-diabetes, 48-diabetes)
  • U&Es- urea/creatinine
  • lipid profile
  • eGFR (check renal function as complication)
  • urine albumin: creatinine ratio (microalbuminurea)
79
Q

How to measure osmotic pressure/ hyperosmolar state

A

osmolality= cations (Na + K) + anions (Cl + bicarb) + glucose + urea

= 2(cations/ Na + K) + glucose + urea

*as cations = anions

Normally = 295mM

80
Q

management for type 2 diabetes

A
  • Lifestyle modification - diet, exercise
  • Glycaemic control
  1. metformin (HbA1c >48)
    • sulphonylurea (gliclazide)/ SGLT-2 inhibitor (flozin)/ DPP-4 inhibitor (pioglitazone)
    • add another drug or INSULIN
  • BP control- ACE/ARB or CCB => A+C/D
  • Lipid management - atorvastatin 20mg (Q-risk >10%) or 80mg (IHD/CAD/PAD)
  • Antiplatelets - aspirin 75mg (if IHD/CVD/PAD)
81
Q

different medications for glycaemic control + side effects

A
  • metformin increases insulin sensitivity + weight loss (side effects = diarrhoea)
  • Sulphonylureas (gliclazide) - inhibit K+/ATPase in beta cells => Ca2+ influx => increase insulin release (side effects =weight gain)
  • Insulin/ insulin analogues
  • SGLT-2 inhibtors (flozin) => reduces glucose reabsorption + HF (side effects= UTIs/ thrush/ hypoglycaemia)
  • GLP-1 analogues (increase insulin release)
  • Gliptins/DPP4 inhibitors-stop GLP-1 breakdown => increased insulin release (side effects= flu/runny nose, allergy, joint pain)
82
Q

Complications of diabetes mellitus

A

Acute:

  • Diabetic ketoacidosis (T1DM)
  • Hyperosmotic osmolar state (T2DM)
  • hypoglycaemia -due to insulin treatment

Long-term:

  • Microvascular complications - glycosylation of basement membranes => leaky capillaries (retinopathy, neuropathy, nephropathy)
  • Macrovascular complication - atheroma development (peripheral vascular disease, IHD, Stroke/TIA)
  • Increased infection risk
83
Q

Define diabetic ketoacidosis

A
  • Increased ketone body production as there insufficient insulin to suppress it (e.g. in T1DM)
  • Diagnosed = metabolic acidosis (pH <7.3) + hyperglycaemia (>11mmol/L) + ketonaemia (>3mmol/L)
84
Q

Why does body increase ketone body production in T1DM?

A
  1. XS glucose but insufficent insulin to cause glucose uptake into cells
  2. body is starved
  3. so ketoacidosis is only mechanism of energy production
85
Q

symptoms + signs of DKA

A

Symptoms:

  • nausea/vomiting
  • abdo pain
  • drowsiness/ confusion/ coma
  • polyuria/polydypsia

Signs:

  • kussmaul breathing (deep, rapid breathing)
  • ketotic breath
  • signs of dehydration (dry mucous membranes)
86
Q

Investigations for DKA

A

Bedside

  • Capillary blood glucose (diabetes- glucose >11mmol/L)
  • Urinalysis (check ketonuria (>3mmol/L), glycosuria)

Bloods

  • FBC- raised WCC without infection =DKA
  • ABG- metabolic acidosis (pH <7.3)
87
Q

Management of DKA

A
  1. IV fluids (saline)
  • SBP <90 => 500ml bolus saline
  • SBP >90 => 0.9% saline IV fluids
  1. Fixed rate IV insulin infusion
  2. If K is low => KCL
  3. Include dextrose in saline if gluocse is <14mmol/L
  4. Monitor blood glucose, capillary ketones, urine ouput HOURLY
  5. Treat underlying cause- infection=> broad spectrum antibiotics
88
Q

What can trigger DKA/HSS other than diabetes?

A
  • surgery
  • infection- UTI
  • medication: wrong insulin dose/non-compliance, drugs that reduce insulin dose- chemotherapy, psychotics
  • MI/ STROKES
  • pancreatitis
89
Q

define Hyperosmolar hyperglycaemic state (HSS)

A
  • severe hyperglycaemia (>30mmol/L) without ketonemia/acidosis as some backrgound insulin present to suppress ketone body formation
  • more common in T2DM
90
Q

symptoms + signs of HSS

A

Symptoms:

  • nausea, vomiting
  • confusion/drowsy
  • coma
  • polyuria
  • severe dehydration (thirst)

Signs:

  • kussmaul breathing (deep, heavy breathing)
  • dry mucous membranes
  • dehydration signs (increased HR/RR, low bp)
91
Q

Investigations for HSS

A
  • urinalysis - no ketonuria (<3mmol/L)
  • blood glucose- HIGH GLUCOSE (>30mmol/L)
  • ABG - normal pH
92
Q

Management of HSS

A
  • IV fluids
  • Fixed rate IV insulin infusion
  • If K+ is low => KCL
  • Treat underlying cause
93
Q

complications of HSS

A
  • clots
  • SHOCK, coma
  • Stroke/ MI
  • brain swelling
94
Q

Risk factors for microvascular complications

A
  • poorly controlled hyperglycaemia
  • prolonged diabetes
  • hypertension
  • >70
  • CVD risk factors (type 2 diabetes)
  • dyslipidemia
95
Q

define diabetic nephropathy and it’s pathophysiology

A
  • microvascular complication of DM that leads to reduced renal function => chronic kidney disease
  • with albuminurea and reduced eGFR
  • progressive worsening of proteinurea

Pathophysiology:

  • hypertension => progressive proteinurea =>kidney failure
96
Q

symptoms of diabetic nephropathy

A
  • usually asymptomatic and present in later stage
  • swelling of extremeties (oedema)
  • lethargy
  • anorexia
  • fever
97
Q

Examination findings of diabetic nephropathy

A
  • hypertension
  • oedema
  • other microvascular complications (retinopathy/ neuropathy)
98
Q

Investigations for diabetic nephropathy

A

Bedside

  • urine dipstick- proteinurea
  • urinalysis: albumin:creatinine ratio (microalbuminuria) FIRST LINE

Bloods

  • FBC
  • U&Es - urea/creatinine
  • eGFR- reduced in later stage renal failure

Imaging:

  • kidney ultrasound (larger in diabetes => normal in nephropathy)
  • CT abdomen - rule out hydronephresis/ renal carcinoma/ renal stones
  • Magnetic resonance angiography - rule out renal artery stenosis

Other

  • kidney biopsy- GOLD-STANDARD but rarely done

glomerular changes (Kimmelstiel Wilson nodules, mesangial expansion, basement mebrane thickening)

99
Q

Management of diabetic nephropathy

A
  • ACE-inhibitor (inhibit RAAS system) => worsen creatinine immediately
  • Angiotensin receptor blocker (ARB- lorsartan)
  • diabetic control (control blood glucose)
  • Nutrition- low fat/cholesterol diet
  • Statins
  • Stop smoking

If bp not controlled with ACE-inhibitor/ARB => CCB/ thiazide diuretics

100
Q

Mechanism of ACE inhibitors/ Angiotensin 2 receptor blockers in diabetes

A
  • inhibit ACE (less angiotensin 1=> 2 conversion)
  • small fall in bp => reduces eGFR
  • reduction in microalbuminurea=> prevent end-stage renal failure

ACE inhibitor side effects= hyperkalemia

*worsens creatinine (increases) immediately (as GFR falls) if too much worsening stop ACE-inhibitor

101
Q

Why are ACE inhibitors not given in renal artery stenosis?

A
  • renal artery narrowed means flow is already low
  • With ACE inhibitor => fall in AT2
  • bp falls a lot => GFR falls a lot (0) => stops weeing

*STOP ACE INHIBITOR ASAP

102
Q

define diabetic neuropathy

A

microvascular complication of diabetes (type 1/2) that leads to peripheral nerve/ autonomic nerve dysfunction

  • affects vaso nervovum (vessels supplying nerves)
103
Q

Types of diabetic neuropathy

A
  1. diffuse neuropathy (peripheral polyneuropathy / autonomic neuropathy)
  2. Mononeuropathy
  3. Radiculopathy/ polyradiculopathy
104
Q

Pathogenesis of diabetic neuropathy

A

hypertension + hyperglycaemia

=>

  1. oxidative stress
  2. produce AGE (advanced glycated end products)
  3. hypoxia

=> activates pro-inflammatory cytokines

=> inflammation

=> neuropathy (inflammation of vaso nervovum= vessels supplying nerves)

105
Q

symptoms + signs of of diabetic neuropathy

A

peripheral nerve lesion (polyneuropathy)

  • glove-stocking sensory loss
  • reduced/ absent ankle reflex
  • painless injuries (foot ulcers)
  • pain (burning - worse at night)
  • burnining/tingling/numbness
  • loss of sensation (vibration, proprioception, temp)

autonomic neuropathy

  • tachycardia
  • bladder dysfunction- urinary frequency, urgency, nocturia, retention, incontinence
  • GI disturbance- difficulty swallowing, nausea/vomiting, constipation
  • postural hypotension => SUDDEN CARDIAC DEATH
  • erectile dysfunction + reduced libido + painful sex

radiculopathy

  • numbness/ tingling over dermatomal patterns (resolves in 4-6 months)

mononeuropathy (RARE)

  • motor loss (wrist drop, foot drop)
  • cranial nerve palsy (III => abducted, depressed eyes, droopy eyelid)
106
Q

Examination findings of diabetic neuropathy (foot)

A
  • absent/ reduced ankle jek reflexes = peripheral neuropathy
  • Monofilament used to investigate light touch (when it bends applying 10g of pressure) = peripheral sensory neuropathy
  • inspect foot - Clawed toes – increased pressure on metatarsal head, flexed toes, Greater risk of ulcers on big toe, Charcot foot = peripheral MOTOR neuropathy
  • Tachycardia/ hypotension - autonomic neuropathy
107
Q

investigations for diabetic neuropathy

A

Bedside:

  • blood glucose + HbA1c (check for undiagnosed diabetes)

Bloods:

  • HbA1c
  • FBC- Hb,WCC (exclude anaemia/inflammation)
  • LFTs (exclude hepatic disease)
  • U&Es (exclude renal disease)
  • lipid profile
  • TFTs (TSH) -exclude thyroid dysfunction
  • serum B12 - exclude deficiency

Imaging

  • corneal confocal microscopy - exclude severe disease

Other

  • Nerve conduction studies - reduced nerve conduction
  • Elecromyography (in asymmetry/ muscle weakness) - worse in severe disease
  • immunoelectrophoresis - exclude multiple myeloma
108
Q

management for diabetic neuropathy

A

polyneuropathy

  • without pain = glycaeminc control
  • with pain = 1. pregabalin/ gabapentin (treats nerve pain) + glycaemic control 2. antidepressant + glycaemic control 3. opioid analgesia + glycaemic control 4. Transcutaneous electrical nerve stimulation (TENS) or acupuncture

cranial neuropathies / Limb mononeuropathy

  • glycaemic control + supportive measures

autonomic neuropathy (treat symptoms)

  • with orthostatic hypotension => miodirine (antihypotensive) + glycaemic control + lifestyle (small,frequent meals, low salt, avoid abrupt body position changes)
  • gastroparesis (poor stomach emptying) => erythromycin/metoclopramide (ABs) + glycaemic control + low fat/fibre meals
  • diarrhoea => broad-spectrum ABs + glycaemic control
  • bladder dysfunction => bethanechol (parasympathetic stimulator) + glycamic control
  • erectile dysfunction => sildenafil(viagra- increases blood flow to penis) + glycaemic control
  • Diabetic foot= inspect foot, good footwear, avoid barefoot walking
  • ulcers => foot clinic (offload pressure, infected = antibiotics, revascularise, amputate)
109
Q

complications of diabetic neuropathy

A
  • foot ulcers
  • wound infection/ gangrene
  • silent MI (autonomic neuropathy)
  • death
  • charcot’s foot (abnormal pressure loading - as bones in foot are in the wrong place (+ fused together) => loss of joint space => CHANGE IN FOOT SHAPE + No pain) untreated => OSTEOLMYELITIS
110
Q

define hypoglycaemia

A

low levels of blood glucose (<3.6mmol/L)

  • impaired cognition when <3mmol/L
111
Q

causes of hypoglycaemia

A
  • Diabetics on insulin therapy

Recurrent hypoglycaemia

  • medication (anabolic steroids, ACE inhibitors, beta-blockers-mask tremor)
  • XS ALCOHOL
  • check diet (missed meals, reduced meals)
  • exercise routine (too intense)
  • incorrect dosing/ type of insulin
  • changes in insulin sensitivity
  • medical conditions (anorexia, hepatitis/cirrhosis, kidney disorders, Addison’s)
112
Q

presenting symptoms of hypoglycaemia

A

mild

  • palpitations
  • tremors
  • sweating

moderate

  • headaches
  • drowsiness
  • impaired vision
  • difficulty concentrating
  • confusion
  • behaviour change (children)

severe (3Cs)

  • convulsions
  • consciousness (loss of)
  • coma
113
Q

How to manage mild/moderate hypoglycaemia? (conscious/can swallow)

A
  1. oral glucose (short acting)- 200ml juice, 7 jelly beans, 4tsp sugar, 5 glucose tablets
  2. long acting complex carbohydrates
114
Q

How to manage severe hypoglycaemia (unconscious)

A
  • IM glucagon (1mg adults, 500ug children)
  • monitor blood glucose
115
Q

When to call 999 for patient with severe hypoglycaemia?

A
  • doesn’t respond to glucagon <10mins
  • IM glucagon not available
  • family/carers not trained in glucagon injection
  • taken alcohol => need IV glucagon
116
Q

How to manage nocturnal hypoglycaemia? (fatigue, hangover, headache)

A
  • monitor blood glucose at 2-3am (most likely to get hypoglycaemia)
  • have a snack before bed and keep short acting carbohydrate by bed
117
Q

How to prevent hypoglycaemia?

A
  • educate patient/family on symptoms + emergency treatment of hypoglycaemia
  • regularly monitor blood glucose
118
Q

Define Diabetes Insipidus

A

disorder of no AVP production/ insensitivity to AVP
=> large amounts of dilute urine (>3L/day)

119
Q

Types of Diabetes Insipidus

A

Cranial - no AVP production
Nephrogenic - insensitivity of collecting duct to AVP

120
Q

Causes of cranial DI

A
  • idiopathic
  • congenital (defects in AVP gene)
  • tumours (pituitary, craniopharyngioma, metastasis)
  • sarcoidosis
  • meningitis
  • vascular
  • trauma
  • hypophysectomy
  • autoimmune hypophysitis (pituitary gland inflammation)
121
Q

Causes of nephrogenic DI

A
  • idiopathic
  • inherited
  • metabolic (low K+, high Ca2+)
  • lithium
  • pyelonephritis
  • chronic renal disease
  • pregnancy
  • amyloidosis
  • hypercalciuria
122
Q

presenting symptoms of DI

A
  • polyuria
  • nocturia
  • polydipsia
  • children (enuresis/ bed-wetting ,sleep disturbance)
123
Q

signs of DI on examination

A

urine output <3L/day
if fluid intake < fluid output = dehydration (tachycardia, reduced tissue turgor, postural hypotension, dry mucous membranes)
- cause related (pituitary tumour = visual defect)

124
Q

Investigations for DI

A
  • Water deprivation test
    1. fluid deprive for 8hrs + measure urine + plasma osmolality + weigh patient hourly to monitor dehydration
    2. At 8 hours, stop test if urine osmolality >600mOsmol/kg
    or

Results= low urine osmolality

  • bloods (U&Es, Ca2+, increased plasma osmolality, decreased urine osmolality)
125
Q

When to stop water deprivation test?

A
  • fall in body weight >3%
126
Q

how to differentiate between cranial and nephrogenic DI with investigations

A
  • give desmopressin (ddAVP) after water deprivation test
    Results:
  • cranial => urine osmolality increases >50%
  • nephrogenic => urine osmolality rises <45%
127
Q

management for cranial DI

A
  • find cause (MRI)
  • give desmopressin
    for mild give carbamazepine (reduces effects of residual AVP)
128
Q

management of nephrogenic DI

A
  • sodium/ K+ restrictions help with polyuria
  • thiazide diuretics inhibits Na/Cl- transporters in DCT, causes compensatory increase in Na+ reabsorption from PCT
  • NSAIDs (lower urine volume and plasma Na+ by inhibiting prostaglandin synthesis)
129
Q

lesion in the optic chasm causes which visual field defect

A

bitemporal hemianopia

130
Q

lesion in the optic tract causes which visual field defect

A

homonymous hemianopia

131
Q

define pituitary tumours

A

tumours of the pituitary gland that can compress the pituitary gland and sometimes the optic chiasm => bitemporal hemianopia

  • non-functional
  • functional
132
Q

types of functional pituitary adenomas

A
  • acromegaly (high GH)
  • prolactinomas (high prolactin)
  • cushing’s disease (ACTH secreting tumour)
133
Q

symptoms of prolactinomas

A

Men

  • erectile dysfunction
  • loss of libido
  • infertility
  • galactorrhoea (rare)

Female

  • galactorrhoea
  • secondary amennorrhoea/ oligomennorrhea
  • infertility
  • loss of libido

General:

  • headaches
  • visual field defects (bitemporal hemianopia)
134
Q

Investigations for prolactinomas/ hyperprolactinemia

A
  • Pregnancy test
  • TFTs
  • basal prolactin level (if >6,000mU/L => prolactinoma)
  • MRI to check for prolactinoma
135
Q

Management for prolactinoma

A
  1. dopamine agonists (cabergoline, bromocriptine) FIRST-LINE
  2. Trans-sphenoidal surgery
136
Q

Other causes of hyperprolactinemia

A

Physiolgical:

  • pregnancy/ breast feeding (NORMAL)

Pathological:

  • Prolactinoma
  • Primary hypothyroidism
  • Pituitary stalk compression (other pituitary adenoma)
137
Q

signs + symptoms of acromegaly (ABCDEF)

A
  • A-arthritis
  • B- raised bp
  • C- carpal tunnel (due to nerve compression)
  • D- diabetes (insulin resistance)
  • E- enlarged hands, feet, face, TONGUE
  • F- visual field defect (compression of optic chiasm), prominent FOREHEAD
  • Sweating, thick,oily skin

*most GH-producing tumours also secrete prolacting => galactorrhoea, amenorrhoea

138
Q

Investigations for acromegaly

A
  • blood glucose
  • bloods: Ca2+, phosphate, lipid profile
  • IGF-1 levels (GH unreliable measurement)
  • MRI of pituitary/hypothalamus
  • check other pituitary hormone levels (prolactin, LH/FSH, ACTH)
139
Q

Management for acromegaly

A

Medical

  • somatastain analogues (inhibit GH) - ocreotide
  • dopamine agonists (bromocriptine, cabergoline)

Surgical:

  • trans-sphenoidal surgery
140
Q

Symptoms + signs of Cushings disease (ACTH secreting tumour)

A
  • moon face
  • centripetal obesity, buffalo hump
  • poor wound healing, easy bruising
  • striae
  • diabetes - osmotic symptoms (polyuria, polydypsia)
  • proximal muscle weakness + wasting

other pituitary adenoma associated symptoms:

  • headaches, visal field defects
  • prolactin => galactorrhea/ amennorrhea
141
Q

Investigations for Cushing’s disease (pituitary adenoma)

A
  • 9am serum cortisol
  • SynACTHen test
  • insulin induced hypoglycaemia (should increase cortisol)
142
Q

Management of Cushing’s disease (pituitary adenoma)

A
  • drugs: metyrapone, ketoconazaole
  • MRI
  • visual field assessment
143
Q

define obesity

A

XS fat usually due to energy intake > energy expenditure

  • Obesity I - BMI 30-35
  • Obesity II- BMI 35-40
  • Obesity III- BMI 40+

Higher waist circumference increases complications of obesity

144
Q

causes of obesity

A
  • Lifestyle - inactivity + poor diet (MOST COMMON)
  • Genetic - leptin deficiency
  • medication - insulin, sulphonylureas
  • Medical conditions (weight gain)
  1. hypothyroidism
  2. Cushing’s syndrome
  3. GH deficiency
  4. PCOS
  5. genetic=> hypogonadism (Prader-willis syndrome)
  6. hypothalamic dysfunction (tumour/trauma/surgery)
145
Q

Management of obesity

A
  1. Lifestyle interventions - structured activity/ diet
  2. Drugs - orlistat (reduces fat reabsorption) V expensive
  3. Refer Weight management services (cormorbidites)
  4. Bariatric surgery (first line for BMI >50, with significant cormorbidities)
146
Q

complications of obesity

A
  • diabetes
  • CVD
  • hypertension/ stroke
  • hyperlipidemia
  • asthma
  • depression
  • lower life expectancy
147
Q

Define thyroid nodules

A
  • abnormal growths of thyroid gland => single/ multi-nodular
  • usually benign
  • single nodules more likely to become malignant
  • more common in WOMEN
148
Q

types of thyroid cancer

A
  • papillary carcinoma (most common)- childhood radiation exposure
  • follicular carcinoma- low iodine intake
  • medullary carcinoma (MEN 2A/2B)
  • Anaplastic carcinoma
  • Lymphoma (RARE)
149
Q

Symptoms and signs of benign thyroid nodules

A
  • usually asymptomatic
  • can sometimes be painful (rarely => trachea compression => dyspnoea)
  • moves when water is swallowed
  • regional lymphadenopathy (if malignant)
  • sometimes causes hyperthyroidism symptoms
150
Q

Symptoms + signs of thyroid cancer (malignant nodule)

A

Signs:

  • single, irregular shape, hard and fixed nodule
  • painless, rapidly growing
  • cervical lymphadenopathy

Symptoms:

  • hoarse voice (compression of recurrent laryngeal nerve)
  • dysphagia (compression of trachea)
  • haemoptysis
  • airway obstruction
151
Q

Investigations for thyroid nodules

A

Bloods

  • TFTs (usually normal)

Imaging

  • Thyroid US
  • Radioiodine uptake scan
  • CT/MRI - check for spread if cancer

Other

  • Fine needle aspiration => check cytology (CANCER?)
152
Q

management of thyroid cancer

A
  1. thyroidectomy
  2. radioiodine to kill remaining thyroid gland
  3. levothyroxine treatment + monitor thyroglobulin

Year 3 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions