Endocrinology Flashcards
(135 cards)
1
Q
Hormones released by anterior vs posterior pituitary gland and their function?
A
Anterior:
→ FSH/LH = gamete production
→ TSH = T3/T4 production
→ PRL = milk production, breast development
→ GH = IGF production
→ ACTH = glucocorticoid production
Posterior:
→ ADH = water balance
→ oxytocin = uterine contractions
2
Q
Outline the thyroid hormonal axis?
A
- Hypothalamus secretes TRH
- Pituitary gland secretes TSH
- Thyroid gland secretes T3 and T4
- T4 -ve feedback on hypothalamus/pituitary
3
Q
Ratio of T4:T3 production and clinical relevance?
A
20:1
T4 is a better indicator of thyroid function
4
Q
Cause of primary vs secondary hyper/hypothyroidism?
A
Primary = thyroid abnormality
Secondary = hypothalamus or pituitary abnormality
5
Q
Typical TFTs for primary and secondary hypothyroidism and hyperthyroidism?
A
Primary hypothyroidism = high TSH, low T3/T4
Primary hyperthyroidism = low TSH, high T3/T4
Secondary hypothyroidism = low TSH, low T3/T4
Secondary hyperthyroidism = high TSH, high T3/T4
6
Q
Typical TFTs for subclinical hypothyroidism vs subclinical hyperthyroidism vs sick euthyroid?
A
Subclinical hypothyroidism = high TSH, normal T3/T4
Subclinical hyperthyroidism = low TSH, normal T3/T4
Sick euthyroid = low or normal TSH, low T3/T4
7
Q
Investigation for thyroid nodule?
A
Thyroid US +/- biopsy
8
Q
Features of hypothyroidism vs hyperthyroidism?
A
Hypothyroidism = cold, weight gain, fatigue, dry skin/hair, constipation, menorrhagia, carpal tunnel
Hyperthyroidism = warm, weight loss, restlessness, anxiety, tremor, palpitations, hyperhidrosis, diarrhoea, oligomenorrhoea, thyroid acropachy
9
Q
Triad of thyroid acropachy?
A
Digital clubbing
Swelling of hands and feet
Periosteal new bone formation
10
Q
Most common cause of hypothyroidism in the developed world vs developing world?
A
Developed world = hashimoto’s thyroiditis
Developing world = iodine deficiency
11
Q
Features of Hashimoto’s thyroiditis and associated antibodies?
A
Hypothyroid symptoms
Firm, non-tender goitre
PMH autoimmune disease
Antibodies = anti-TPO and anti-Tg
12
Q
Cancer linked to Hashimoto’s thyroiditis?
A
MALT lymphoma
13
Q
Treatment for hypothyroidism and dosing guidance?
A
Levothyroxine:
→ elderly or CVD = 25mcg
→ everyone else = 50-100mcg
→ increase dose by 25-50mcg in pregnancy
14
Q
Monitoring of levothyroxine?
A
TFTs monitored 8-12 weeks after dose change
Aim for TSH 0.5-2.5
15
Q
Typical TFTs of patient with poor levothyroxine compliance and explain?
A
High TSH, normal T3/T4
→ patient takes medication just before blood test
→ thyroxine (T4) is normal
→ TSH lags reflecting chronic low levels
16
Q
Drugs which reduce levothyroxine absorption and advice?
A
Iron, calcium
Take 4 hours apart
17
Q
Management of subclinical hypothyroidism?
A
Offer levothyroxine if:
→ TSH > 10
→ TSH 5.5-10 and symptomatic
18
Q
Management of myxoedema coma (hypothyroid crisis)?
A
IV fluids + IV levothyroxine + IV corticosteroid
19
Q
Hypothyroidism after a post-partum haemorrhage?
A
Sheehan syndrome
20
Q
Most common cause of hyperthyroidism?
A
Grave’s disease
21
Q
Features of Grave’s disease and assocated antibodies?
A
Hyperthyroid symptoms
Eye disease e.g. exophthalmos
Pretibial myxoedema “orange peel skin”
Thyroid acropachy
Antibodies = anti-TSH receptor and anti-TPO
22
Q
Investigation and feature of Grave’s disease?
A
Thyroid scinctigraphy
Globally increased iodine uptake
23
Q
Key lifestyle risk factor for Grave’s disease?
A
Smoking
24
Q
Treatment for hyperthyroidism?
A
1st line = carbimazole (1st choice) or propylthiouracil (2nd choice)
2nd line = radioiodine therapy
3rd line = surgery
N.B. propanolol is used to block adrenergic symptoms
25
Management of hyperthyroidism during pregnancy?
1st trimester = propylthiouracil
2nd trimester onwards = carbimazole
26
Major side effect of carbimazole and PPU?
Agranulocytosis
27
Phases and features of subacute (De Quervain's) thyroiditis?
Phase I = hyperthyroidism, painful goitre, flu-like symptoms, raised inflammatory markers e.g. ESR, CRP
Phase II = euthyroid
Phase III = hypothyroidism
Phase IV = euthyroid
28
Investigation and feature of subacute (De Quervain's) thyroiditis?
Thyroid scintigraphy
Globally reduced iodine uptake
29
Main drug associated with thyrotoxicosis?
Amiodarone
30
Features of thyrotoxicosis?
Fever
Tachycardia
Hypertension
Confusion, agitation
Heart failure (especially in elderly)
31
Management of thyrotoxicosis?
IV propanolol + IV hydrocortisone + propylthiouracil
N.B. IV digoxin if heart failure
32
Investigation, feature and management of toxic multinodular goitre?
Thyroid scintigraphy
Patchy increased iodine uptake
Management = radioiodine therapy
33
Types of thyroid cancer and most common?
Papillary (most common)
Follicular
Medullary
Anaplastic
Lymphoma
34
Thyroid cancer associated with young females, elderly females, MEN 2, lymph node invasion, vascular invasion, raised calcitonin?
Young females = papillary
Elderly females = anaplastic
MEN 2 = medullary
Lymph node invasion = papillary
Vascular invasion = follicular
Raised calcitonin = medullary
35
Management of papillary and follicular carcinoma?
Total thyroidectomy + radioiodine
36
Outline the parathyroid-thyroid hormone axis?
- Parathyroid gland senses low calcium
- Chief cells secrete PTH
- PTH increases calcium
- Thyroid gland senses high calcium
- C-cells secrete calcitonin
- Calcitonin decreases calcium and has negative feedback on parathyroid gland
37
How does PTH increase and calcitonin decrease calcium levels?
PTH = (1) activates osteoclasts, (2) increases calcium re-absorption in kidneys and (3) triggers calcitriol (active vitamin D) formation which increases gut calcium absorption
Calcitonin = inhibits osteoclasts
38
Features of hypercalcaemia?
Bone pain
Renal stones
Constipation
Pancreatitis
Polydipsia/polyuria
Depression
39
Cause of primary vs secondary vs tertiary hyperparathyroidism?
Primary = excess PTH secretion
Secondary = increased PTH secretion in response to low calcium
Tertiary = autonomous PTH secretion after prolonged secondary cause, usually CKD
40
Blood test features of primary vs secondary vs tertiary hyperparathyroidism?
Primary = normal/high PTH, high calcium, low phosphate
Secondary = high PTH, low calcium, high phosphate
Tertiary = high PTH, high calcium, low phopshate, high ALP
41
X-ray features of hyperparathyroidism?
"Pepperpot" skull
Osteopenia
Osteitis fibrosis cystica
42
Management of hyperparathyroidism?
1st line = total parathyroidectomy
2nd line = calcimemetic (e.g. cinacalcet)
43
Most common cause of hypoparathyroidsm?
Parathyroid injury during thyroid/neck surgery
44
Management of hypoparathyroidism?
Vitamin D analogue e.g. alfacalcidol
45
Features of hypocalcaemia?
Tetany e.g. cramps, parasthaesia
Trosseau's sign (carpal spasm)
Chvostek's sign (facial twitch)
Psychological disturbance e.g. depression
46
Which electrolyte is vital for maintaining calcium levels and clinical relevance?
Magnesium
→ patient not responding to calcium and vitamin D supplements should have magnesium checked
47
Features of MEN 1, MEN 2a and MEN 2b?
MEN 1 = (3 Ps) parathyroid tumour, pituitary tumour, pancreatic tumour
MEN 2a = (1 M, 2 Ps) medullary carcinoma, parathyroid tumour, phaeochromocytoma
MEN 2b = (2 Ms, 1 P) medullary carcinoma, marfanoid habitus, phaeochromocytoma
48
Features of a phaeochromocytoma?
Hypertension
Headaches
Flushing
Anxiety
Palpitations
49
Investigation and management of a phaeochromocytoma?
Investigation = 24hr urinary metanephrines
Management = alpha-blocker (e.g. phenoxybenzamine) BEFORE beta-blocker (e.g. propanolol) + surgery
50
Classification of pituitary adenomas?
Microadenoma (< 1cm) or macroadenoma (> 1cm)
Functioning (secretory) or non-functioning (no secretion)
51
Features of pituitary adenoma?
Hormonal excess
Hormonal deficit
Headaches
Bitemporal hemianopia
52
Most common cause of hypopituitarism vs hyperpituitarism?
Hypopituitarism = compression of pituitary gland via non-secretory adenoma
Hyperpituitarism = secretory adenoma
53
Investigation for hypopituitarism and explain?
Insulin stress test
→ insulin given, GH and cortisol measured
→ normally GH and cortisol should rise
→ low response indicates hypopituitarism
54
Most common type of secretory adenoma?
Prolactinoma
55
What normally inhibits prolactin release?
Dopamine
56
Features of prolactinoma?
Pituitary adenoma symptoms
Amenorrhea
Galactorrhoea
Infertility
Erectile dysfunction
57
Investigation and management of a prolactinoma?
Investigation = MRI
1st line = dopamine agonist e.g. cabergoline, bromocriptine
2nd line = trans-sphenoidal surgery
58
Second most common cause of secretory adenoma?
GH adenoma
59
What normally inhibits GH release?
Somatostatin
60
Features of acromegaly?
Pituitary adenoma symptoms
Large "spade-like" hands/feet
Protruding jaw and brow
Interdental spaces
Hyperhidrosis
61
Investigations and management of acromegaly?
Investigation = serum IGF-1, OGTT if IGF-1 raised
1st line = trans-sphenoidal surgery
2nd line = somatostatin analogue (e.g. ocreotide)
3nd line = GH antagonist (e.g. pegvisomant), dopamine agonist (e.g. bromocriptine)
62
Types of corticosteroids hormone, where they are produced in the adrenal glands and example?
Glucocorticoids (zona fasciculata) = cortisol
Mineralocorticoids (zona glomerulosa) = aldosterone
63
List side effects of glucocorticoids?
Osteoporosis
Peptic ulcers
Steroid psychosis
Hyperglycaemia
Cushing's syndrome
Proximal myopathy
Immunosuppression
Glaucoma, cataracts
Stunted growth in kids
64
List side effects of mineralocorticoids?
Fluid retention
Hypertension
Hypokalaemia
65
Effect of cortisol vs aldosterone vs ADH on the kidneys?
Cortisol and aldosterone = water and Na retention, K excretion
ADH = water retention, Na and K excretion
66
Cushing's vs hyperaldosteronism vs Addison's?
Cushing's = excess CORTISOL
Hyperaldosteronism = excess ALDOSTERONE
Addison's = lack of CORTISOL AND ALDOSTERONE
67
Classification of Cushing's syndrome causes?
ACTH-dependent e.g. pituitary adenoma, ectopic ACTH
ACTH-independent e.g. adrenal adenoma
68
Features of Cushing's syndrome?
Moon face
Hirsutism
Central obesity
Abdominal striae
Buffalo hump
Thin limbs
Hypertension
Osteoporosis
69
Investigations of Cushing's syndrome?
Overnight low-dose DST
Low-dose 48 hour DST
High-dose 48 hour DST
70
High-dose DST results for Cushing's causes?
ACTH suppressed, cortisol not = adrenal adenoma
ACTH and cortisol suppressed = pituitary adenoma
ACTH and cortisol not suppressed = ectopic ACTH
71
Management of Cushing's syndrome?
Steroid blocker (e.g. metyrapone) + surgery
Replacement steroids post-surgery
72
Most common causes of primary aldosteronism?
Bilateral adrenal hyperplasia
Adrenal adenoma (Conn's syndrome)
73
Features of hyperaldosteronism?
Polydipsia/polyuria
Headaches
Hypertension
Hypokalaemia
74
Investigations for primary hyperaldosteronism?
Plasma aldosterone:renin ratio
Imaging e.g. CT abdomen
Adrenal vein sampling (to differentiate between unilateral or bilateral pathology)
75
Aldosterone:renin ratio results in primary vs secondary hyperaldosteronism?
Primary = high aldosterone, low renin
Secondary = high aldosterone, high renin
76
Management of primary hyperaldosteronism?
Adrenal adenoma = surgery
Bilateral adrenal hyperplasia = aldosterone antagonist e.g. spironolcatone
77
Most common cause of congenital adrenal hyperplasia?
21-hydroxylase deficiency
78
Most common cause of primary hypoadrenalism?
Addison's disease
79
Features of Addison's disease?
Weight loss
Fatigue
Salt craving
Hyperpigmentation
Hypotension
Hypoglycaemia
Hyponatraemia/hyperkalaemia
80
Why can Addison's present with hypoglycaemia?
Cortisol normally increases blood sugar
81
Investigations and management for Addison's disease?
Investigations = short Synacthen test
Management = hydrocortisone + fludricortisone
82
Guidance for unwell patients on steroids?
Glucocorticoid dose should be doubled
Mineralocorticoid dose should stay the same
83
Management of Addisonian crisis?
IM or IV hydrocortisone
IV saline 0.9% (dextrose if hypoglycaemic)
84
What is pre-diabetes ("impaired glucose tolerance") and clinical values?
Impaired fasting glucose (6.1-6.9) or
Impaired glucose tolerance (7.8-11.0)
85
Cause of T1DM vs T2DM?
Type 1 = absolute insulin deficiency caused by autoimmune destruction of pancreatic beta cells
Type 2 = relative insulin deficiency caused by insulin resistance
86
Main features of diabetes?
Polydipsia/polyuria
Weight loss (type 1)
Obesity (type 2)
87
Investigations and clinical values for T2DM?
If patient is symptomatic:
→ random glucose or OGTT ≥ 11.1
→ fasting glucose ≥ 7.0
→ HbA1c ≥ 48.0
If patient is asymptomatic:
→ above must be demonstrated on 2 occasions
88
HbA1c monitoring guidance and targets?
Monitor every 6 months once stable
Lifestyle changes +/- metformin = 48.0
Other anti-diabetic drugs = 53.0
89
What can interfere with HbA1c interpretation and examples?
Conditions which shorten RBC lifespan e.g. sickle-cell disease
Conditions which prolong RBC lifespan e.g. IDA, splenectomy
90
Drug options for T2DM?
1st line = metformin (+ SGLT-2 inhibitor if known CVD or QRISK > 10%)
2nd line = add DPP-4 inhibitor or pioglitazone or sulfonylurea or SGLT-2 inhibitor
3rd line = metformin + dual therapy of above or insulin
4th line = switch a medication for a GLP-1 mimetic
91
HbA1c level which would prompt addition of 2nd line therapy?
≥ 58.0
92
NICE guidance for insulin in T2DM?
Start with isophane insulin (intermediate-acting)
93
Antidiabetic medications associated with hypoglycaemia?
Sulphonyureas
DPP-4 inhibitors
GLP-1 mimetics
Insulin
94
Metformin mechanism of action and side effects?
Mechanism of action = increases insulin sensitivity, decreases hepatic gluconeogenesis
Side effects = GI upset, lactic acidosis
95
Metformin prescribing guidance?
Should be titrated up slowly (to reduce GI upset)
If not tolerated, offer modified-release metformin
96
SGLT-2 inhibitor examples, mechanism of action and side effects?
Examples = dapagliflozin, empagliflozin
Mechanism of action = inhibits glucose reabsorption in the kidneys
Side effects = weight loss, GU infection
97
Sulfonylurea examples, mechanism of action and side effects?
Examples = gliclazide, glipizide
Mechanism of action = increases insulin production
Side effects = weight gain, hypoglycaemia
98
Pioglitazone mechanism of action and side effects?
Mechanism of action = reduces peripheral insulin resistance
Side effects = weight gain, hepatotoxic, heart failure, increased risk of bladder cancer
99
DPP-4 inhibitor examples, mechanism of action and side effects?
Examples = sitagliptin, alogliptin
Mechanism of action = prevents incretin breakdown
Side effects = GI upset, hypoglycaemia
100
GLP-1 mimetic examples, mechanism of action and side effects?
Examples = liraglutide, exenatide
Mechanism of action = increases insulin secretion, inhibits glucagon secretion
Side effects = weight loss, N&V, hypoglycaemia, pancreatitis
101
Outline sick day rules for diabetes mellitus?
- Check blood sugar 4 hourly (or more)
- Keep well hydrated (aim for 3L/day)
- Take ALL diabetic medications
→ hold metformin if dehydrated
102
Main factors leading to diabetic foot disease?
Diabetic neuropathy
Peripheral arterial disease
103
Drug options for diabetic neuropathy?
1st line = amitriptyline, duloxetine, pregabalin, gabapentin
2nd line = another of the above options
N.B. tramadol can be used for exacerbations
104
Drug options for gastroparesis?
Metaclopramide
Domperidone
Erythromycin
105
Diabetic nephropathy screening and management?
Yearly albumin:creatinine ration (ACR)
ACR > 3 = ACEi/ARB
106
Osmolality calcuation?
2(Na) + glucose + urea
107
Outline the pathophysiology of Hyperosmolar Hyperglycaemic State (HHS)?
- Hyperglycaemia increases serum osmolality
- Body compensates by increased glycosuria
- Water follows into urine down osmotic gradient
- Polyuria leading to volume depletion
108
Features of HHS?
Progresses over days/weeks
Type 2 diabetics (mostly)
Polyruria/polydipsia
Confusion, fatigue, N&V
109
Biochemical features of HHS?
Hyperglycaemia
Raised serum osmolality
110
What inhibits lipolysis and clinical relevance?
Insulin
→ T2DM patients still have some insulin so HHS does not present with ketoacidosis
111
Management of HHS?
IV fluid replacement
Do not give insulin unless blood glucose stops falling whilst giving IV fluids
112
Complication of giving insulin in HHS?
Cerebral pontine myelinolysis
113
Investigations and clinical values for T1DM?
If patient is symptomatic:
→ random glucose or OGTT ≥ 11.1
→ fasting glucose ≥ 7.0
If patient is asymptomatic:
→ above must be demonstrated on 2 occasions
114
Why is HbA1c not recommended for diagnosing T1DM?
May not reflect a rapid blood glucose increase
115
Additional blood test features of T1DM?
Low C-peptide
Anti-GAD, anti-islet cell, insulin antibody
116
T1DM autoantibodies?
Anti-GAD
Anti-islet cell
Insulin antibody
117
Management of T1DM?
MDI basal-bolus regime (rapid/short mealtime bolus + intermediate/long basal)
118
Give examples of rapid, short, intermediate and long acting insulin?
Rapid = aspart (NovoRapid), lispro (Humalog)
Short = Actrapid, Humulin S
Intermediate = isophane
Long = determir (Levemir), glargine (Lantus)
119
Insulin side effects?
Weight gain
Hypoglycaemia
Lipodystrophy
120
Management of hypoglycaemia?
Mild = 10-20g oral glucose or other fast-acting carbohydrate
Severe = IV dextrose + SC or IM glucagon
121
DVLA diabetes guidance?
- Must inform DVLA if taking insulin
- Check blood sugars within 2 hours of driving and every 2 hours during long journeys
- Surrender licence if 1 (group 2) or > 1 (group 1) hypoglycaemic episode requiring medical assistance in the past 12 months
122
Outline the pathophysiology of DKA?
- Lack of insulin leads to uncontrolled lipolysis
- Adipose tissue breaks down into fatty acids
- Fatty acids hydrolysed in the liver to ketones
- Ketones consume HCO3 leading to acidosis
123
Features of DKA?
Polydipsia/polyuria
Abdominal pain
Kussmaul's breathing
Acetone-smelling breath
Drowsiness, coma
124
Biochemical features of DKA?
Severe hyperglycaemia
Raised serum osmolality
Hyperketonaemia
Metabolic acidosis
Hypokalaemia
125
Management of DKA?
IV 0.9% saline
IV insulin 0.1 unit/kg/hour
→ once glucose < 14.0 add IV 10% dextrose
Correct serum potassium
Continue normal long-acting insulin
126
Complication of fluid replacement in DKA?
Cerebral oedema
127
What is maturity-onset diabetes of the young, inheritance and most common form?
T2DM in patients < 25
Autosomal dominant
MODY 3
128
Types of diabetes inspidus and cause?
Cranial = lack of ADH secretion
Nephrogenic = insensitivity to ADH
129
Water deprivation and DDAVP test results for cranial vs nephrogenic DI?
Cranial = low urine osmolality after water deprivation, high urine osmolality after DDAVP
Nephrogenic = low urine osmolality after water deprivation, low urine osmolality after DDAVP
130
Management of DI?
Cranial = DDAVP (desmopressin)
Nephrogenic = low salt diet, thiazide diuretics
131
Normal urine osmolality before and after DDAVP in patient with polydipsia/polyuria?
Primary polydipsia e.g. excessive drinking
132
General guidance for diabetic management pre- and post-op?
- Variable rate insulin if poor glycaemic control or long surgery meaning more than one missed meal
- Otherwise, patients should just require their dosage (insulin and/or oral agents) adjusted
133
Only antidiabetic drug which should be omitted on the day of surgery?
SGLT-2 inhibitor
134
How to manage once daily vs twice daily insulin pre- and post-op?
OD = reduce by 20% (day before + day of)
BD = no change (day before), half morning dose and normal evening dose (day of)
135
Sex hormone levels in Klinefelter's vs Kallman's vs androgen insensitivity?
Klinefelter's = high LH, low testosterone
Kallman's (primary amenorrhoea) = low LH, low testosterone
Androgen insensitivity = high LH, normal/high testosterone
