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Endocrinology Flashcards

1
Q

endocrine abnormality and features of acromegaly

A

excess growth hormone secondary to pituitary adenoma

rare - caused by ectopic GHRH/GH production by tumours

Features
coarse facial appearance, spade-like hands, increase in shoe size
large tongue, prognathism, interdental spaces
excessive sweating and oily skin: caused by sweat gland hypertrophy
features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases → galactorrhoea
6% of patients have MEN-1

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2
Q

investigations and results in acromegaly

A

serum IGF-1 - raised
also used to monitor disease

OGTT - confirms diagnosis
no suppression of GH (should be <2)

pituitary MRI may demonstrate tumour

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3
Q

management of acromegaly

A

trans-sphenoidal surgery - first line tx

if inoperable/surgery unsuccessful may need medication
somatostatin analogue e.g., octreotide - inhibits GH

pegvisomant - GH recdeptor antagonist

dopamine agonist - bromocriptine

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4
Q

definition and features of addison’s disease

A

AI destruction of adrenal glands causing hypoadrenalism - reduced cortisol and aldosterone

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

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5
Q

non-addisonian causes of hypoadrenalism

A

primary causes
tuberculosis
metastases (e.g. bronchial carcinoma)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
antiphospholipid syndrome

secondary causes
pituitary disorders (e.g. tumours, irradiation, infiltration)

Exogenous glucocorticoid therapy

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6
Q

investigation findings in addison’s disease

A

ACTH stimulation test - short synacthen test

Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM

9am serum cortisol may also be useful
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

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7
Q

managing addison’s disease

A

glucocorticoid and mineralocorticoid replacement therapy

hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day - double in intercurrent illness

fludrocortisone - stays the same in illness

hydrocortisone for injection for adrenal crisis

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8
Q

causes of an addisonian crisis

A

sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)

adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)

steroid withdrawal

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9
Q

management of an addisonian crisis

A

hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

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10
Q

cause and features of
bartter’s syndrome

A

inherited AR cause of severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter (NKCC2) in the ascending loop of Henle - similar to taking massive dose of furosemide

usually presents in childhood, e.g. Failure to thrive
polyuria, polydipsia
hypokalaemia
normotension
weakness

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11
Q

use and moa of carbimazole

A

management of thyrotoxicosis - 6w high dose until pt euthyroid

blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

may cause agranulocytosis
crosses placenta but may be used in low doses in pregnancy

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12
Q

relationship between magnesium and calcium

A

magnesium required for PTH secretion and its action on target tissues - may result in hypocalcaemia and cause poor response to calcium/VD supplementation

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13
Q

types of congenital adrenal hyperplasia

A

AR disorders affecting steroid biosynthesis - resulting low cortisol causes high ACTH secretion, stimulating adrenal androgen production

21-hydroxylase deficiency (90%)
11-beta hydroxylase deficiency (5%)
17-hydroxylase deficiency (very rare)

usually screened for, ACTH stimulation testing used to confirm diagnosis

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14
Q

features of 21-hydroxylase deficiency

A

virilisation of female genitalia
precocious puberty in males
60-70% of patients have a salt-losing crisis at 1-3 wks of age

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15
Q

11-beta hydroxylase deficiency features

A

virilisation of female genitalia
precocious puberty in males
hypertension
hypokalaemia

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16
Q

features of congenital hypothyroidism

A

screened for with heel-prick at 5-7 days

Features
prolonged neonatal jaundice
delayed mental & physical milestones
short stature
puffy face, macroglossia
hypotonia

If not diagnosed and treated within the first four weeks it causes irreversible cognitive impairment

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16
Q

17-hydroxylase deficiency features

A

non-virilising in females
inter-sex in boys
hypertension

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17
Q

types corticosteroid drugs

A

high mineralocorticoid activity - fludrocortisone

high mineralocorticoid - hydrocortisone

glucocorticoid - prednisolone

v high glucocorticoid - dexamethasone, betamethasone

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18
Q

S/E of glucocorticoids

A

endocrine - impaired glucose regulation, weight gain, hirsuitism, hyperlipidaemia

cushing syndrome

MSK - osteoporosis, prox myopathy, AVN femoral neck

immunosuppression

psychiatric - insomnia, mania

GI - peptic ulcers, acute pancreatitis

ophthalmic - glaucoma, cataracts

growth suppression

neutrophilia

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19
Q

mineralocorticoid S/E

A

fluid retention
hypertension

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20
Q

causes of cushing syndrome

A

ACTH dependent causes - cushing disease (80%) - pituitary tumour screning ACTH causing adrenal hyperplasia
ectopic ACTH production from SCLC

ACTH independent causes - exogenous, more common
iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)

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21
Q

what is pseudo-cushings and how to differentiate

A

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

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22
Q

tests to confirm cushingss syndrome

A

hypokalaemic metabolic alkalosis and impaired glucose tolerance

overnight (low-dose) dexamethasone suppression test - most sensitive test, first-line to test for Cushing’s syndrome - morning cortisol spike notsuppressed

24 hr urinary free cortisol
two measurements are required

bedtime salivary cortisol
two measurements are required

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23
Q

how is high dose dexamethasone suppression test used

A

cortisol and ACTH suppressed - cushings disease

cortisol and ACTH not suppressed - ectopic ACTH

cortisol not suppressed, ACTH suppressed - cushings syndrome due to other cause

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24
Q

features of DKA

A

abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
acetone-smelling breath (‘pear drops’ smell)

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24
Q

antibodies present in T1DM

A

Antibodies to glutamic acid decarboxylase (anti-GAD) (80%)

Islet cell antibodies (ICA, against cytoplasmic proteins in the beta cell) (70-80%)

Insulin autoantibodies (IAA) - presence reduces with age

Insulinoma-associated-2 autoantibodies (IA-2A)

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25
Q

typical features of T1DM patient

A

young, acute onset, recent weight loss, DKA features, ketonuria common

ketosis
rapid weight loss
age of onset below 50 years
BMI below 25 kg/m²
personal and/or family history of autoimmune disease

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26
Q

diagnostic criteria for diabetes

A

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)

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27
Q

HbA1c figures for diabetes diagnosis

A

a HbA1c of greater than or equal to 48 mmol/mol (6.5%)

a HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes

if asymptomatic - repeat test to confirm diagnosis

misleading HbA1c results can be caused by increased red cell turnover

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28
Q

definition of impaired fasting glucose and impaired glucose tolerance

A

impaired fasting glucose = >6.1, <7

impaired glucose tolerance - fasting glucose <7, OGTT 2h > 7.8, <11.1

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29
Q

managing type 1 diabetes (pharmacological and monitoring)

A

insulin - due to absolute deficiency, SC
basal-bolus insulin - multiple daily injection
twice-daily insulin detemir
rapid acting insulin analogues before meals

add metformin if BMI >25

HbA1c measurement every 3-6m - target <48

self monitoring glucose 4x/day

blood glucose targets - 5-7 on waking, 4-7 before meals

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29
Q

managing type 2 diabetes

A

oral metformin

+ SGLT2 - if CVD

sulfonylureas (gliclazide) - stimulate pancreatic b cells to secrete insulin

gliptins (DPP4 inhibitors) - inhibits glucagon secretion

pioglitazone (thiazolidinediones) - promote adipogenesis

HbA1c measurement every 3-6m - target <48

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30
Q

GLP 1 drugs

A

exenatide - GLP1 mimic - increase insulin secretion, inhibit glucagon secretion - weight loss

sitagliptin - DPP4 inhibitors - increase incretin levels by reducing breakdown -

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31
Q

sick day rules for type 1 diabetes

A

if on insulin - do not stop due to risk of diabetic ketoacidosis
frequent checking of blood glucose
maintain normal meal pattern and drinkk >3L fluid

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32
Q

sick day rules for type 2 diabetes

A

temporarily stop some oral hypoglycaemics during acute illness
restart medication once person feeling better and drinking for 24-48h

metformin - stop if risk of dehydration (reduce risk of lactic acidosis_
sulfonylurea - increase risk of hypo
SGLT-2 inhibitors - check for ketones and stop treatment if unwill/risk of dehydration
GLP-1 receptor agonists - stop if risk of dehydration
monitor blood glucose more frequently

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33
Q

causes of diabetic foot disease

A

neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin

peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia

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34
Q

how does diabetic foot disease present

A

neuropathy: loss of sensation

ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication

complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangren

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35
Q

what happens during diabetic ketoacidosis

A

uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

causes: infection, missed insulin doses and myocardial infarction.

Features
abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)

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36
Q

diagnostic criteria for diabetic ketoacidosis

A

Key points
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick

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36
Q

managing diabetic ketoacidosis

A

fluid replacement - DKA pt usually deplete 5-8l
use isotonic saline

insulin - 0.1unit/kg/hr
once blood glucose <14mmol/l start 10% dextrose at 125ml/hr

usually K+ is high - should fall following insulin tx - may cause hypokalaemia thus may need to add replacement K+ 20mmol/hr

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37
Q

features of diabetic neuropathy

A

peripheral - sensory loss, not motor loss - glove and stocking, lower legs affected first due to the length of the sensory neurons supplying this area, may be painful
mx - amitriptyline, duloxetine, gabapentin, pregabalin

gastrointestinal autonomic neuropathy - gastroparesis, bloating, vomiting, chronic diarrhoea, GORD
mx - metoclopramide, domperidone

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38
Q

features of androgen insensitivity syndrome

A

46 XY

X-linked recessive condition. Defect in androgen receptor results in end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype.

Rudimentary vagina and testes present but no uterus. Testosterone, oestrogen and LH levels are elevated

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39
Q

features of 5-a reductase deficiency

A

46 XY

Autosomal recessive condition. Results in the inability of males to convert testosterone to dihydrotestosterone (DHT).

Individuals have ambiguous genitalia in the newborn period. Hypospadias is common. Virilization at puberty.

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40
Q

features of female pseudohermaphroditism

A

46XX

Individual has ovaries but external genitalia are male (virilized) or ambiguous. May be secondary to congenital adrenal hyperplasia

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40
Q

features of male pseudohermaphroditism

A

46XY
Individual has testes but external genitalia are female or ambiguous. may be secondary to androgen insensitivity syndrome

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41
Q

features of true hermaphroditism

A

46XX or 47XXY

Very rare, both ovarian and testicular tissue are present

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42
Q

DVLA rules for diabetes mellitus

A

insulin users cannot hold HGV licence

DVLA rules
no severe hypoglycaemic event in prev 12m
full hypoglycaemic awareness
adequate condition control with regular blood glucose monitoring
undertand risks of hypoglycaemia

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43
Q

causes of inaccurate HbA1c interpretation

A

The level of HbA1c is dependent on:
red blood cell lifespan
average blood glucose concentration

lower than expected HbA1c
Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
Haemodialysis

higher than expected HbA1c
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

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44
Q

features of graves disease

A

most common cause of thyrotoxicosis
usually seen in F 30-50y

thyrotoxicosis
eye signs (30% of patients) - exophthalmos, ophthalmoplegia
pretibial myxoedema
thyroid acropachy, a triad of: digital clubbing, soft tissue swelling of the hands and feet, periosteal new bone formation

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45
Q

investigation findings in graves disease

A

TSH receptor stimulating antibodies (90%)
anti-thyroid peroxidase antibodies (75%)

thyroid scintigraphy
diffuse, homogenous, increased uptake of radioactive iodine

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46
Q

management of graves disease

A

propranolol - blocks adrenergic effects

carbimazole - start at 40mg and reduce to maintain euthyroidism - continue for 12-18m

radioiodine treatment - for patients who relapse
C/I - pregnancy for 4-6m, <16y
post-radioiodine, patients may become hypothyroid

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47
Q

indications for growth hormone therapy

A

GH given SC, discontinue if poor response in 1st year of therapy

proven growth hormone deficiency
Turner’s syndrome
Prader-Willi syndrome
chronic renal insufficiency before puberty

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48
Q

features of hashimoto’s thyroiditis

A

chronic autoimmune thyroiditis - autoimmune disorder assx with hypothyroidism, with transient thyrotoxicosis in acute phase

Features
features of hypothyroidism
goitre: firm, non-tender
anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies

assx with other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo and MALT lymphoma

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48
Q

causes of hypercalcaemia

A

Primary hyperparathyroidism

malignancy
sarcoid
VD intoxication
acromegaly
thyrotoxicosis

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49
Q

causes and definition of hyperosmolar hyperglycaemic state

A

medical emergency with significant mortality

hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion and electrolyte deficiencies

presents in elderly with T2DM

precipitated by intercurrent illness, dementia, sedative drugs

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50
Q

features of hyperosmolar hyperglycaemic state

A

comes on over days with more extreme dehydration and metabolic disturbances

consequences of volume loss
clinical signs of dehydration
polyuria
polydipsia

systemic
lethargy
nausea and vomiting

neurological
altered level of consciousness
focal neurological deficits

haematological
hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)

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51
Q

diagnostic markers for HHS

A

hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 – acidosis can occur due to lactic acidosis or renal impairment)

52
Q

management of HHS

A

fluid replacement - fluid loss of 100-220ml/kg - give normal saline 0.5-1L/.hour
monitor K+

insulin - dont give until blood glucose stops falling with IV fluids

VTE prophylaxis due to hyperviscosity

53
Q

causes of hypoglycaemia (non diabetes)

A

insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
alcohol - exaggerates insulin secretion

54
Q

physiological response to hypoglycaemia

A

hormonal response - reduced insulin secretion, increased glucagon secretion

sympathoadrenal response - increased catecholamine-mediated (adrenergic) and acetycholine-mediated (cholinergic) neurotransmission in peripheral ANS and CNS

55
Q

features of hypoglycaemia

A

BM <3.3 mmol/L - autonomic symptoms due to release of glucagon and adrenaline
Sweating
Shaking
Hunger
Anxiety
Nausea

blood conc <2.8mmol/L - causes neuroglycopenic symptoms due to inadequate glucose supply to brain
Weakness
Vision changes
Confusion
Dizziness

56
Q

management of hypoglycaemia

A

if alert (out or in hospital)
oral glucose 10-20g - liquid, gel or tablet form, glucogel, dextrogel

unconscious or unable to swallow - SC or IM glucagon

IV 20% glucose in large vein

57
Q

definition and features of primary hypoparathyroidism

A

reduced PTH secretion (e.g., secondary to thyroid to surgery) causing low calcium and phosphate

tx - alfacalcidiol

58
Q

symptoms of hypoparathyroidism

A

tetany: muscle twitching, cramping and spasm
perioral paraesthesia

Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic

Chvostek’s sign: tapping over parotid causes facial muscles to twitch

if chronic: depression, cataracts

ECG: prolonged QT interval

59
Q

definition and features of pseudoparathyroidism

A

target cells insensitive to PTH
Associated with low IQ, short stature, shortened 4th and 5th metacarpals

low calcium, high phosphate, high PTH

diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH

hypoparathyroidism - raise cAMP and phosphate
pseudoparathyroidism only cAMP rises or doesnt rise

60
Q

features of pseudopseudohypoparathyroidism

A

similar phenotype to pseudohypoparathyroidism but normal biochemistry

61
Q

causes of hypothyroidism

A

hashimoto’s thyroiditis - most common cause, AI disease

Subacute thyroiditis (de Quervain’s)

Riedel thyroiditis

After thyroidectomy or radioiodine treatment

Drug therapy (e.g. lithium, amiodarone or anti-thyroid drugs such as carbimazole)

Dietary iodine deficiency

62
Q

causes of secondary hypothyroidism

A

From pituitary failure

Other associated conditions
Down’s syndrome
Turner’s syndrome
coeliac disease

63
Q

features of hypothyroidism

A

general - weight gain, lethargy, cold intolerance

skin - dry, cold, yellow skin, non-pitting oedema, dry coarse scalp hair

GI - constipation

gynaecological - menorrhagia

neurological - reduced deep tendon reflexes, carpal tunnel

64
Q

doses of levothyroxine therapy

A

cardiac disease or >50y - start on 25mcg OD

normal patients - 50-100mcg OD

after changing thyroxine - do TFTs after 8-12w

goal - to normalise TSH level

dose in pregnancy - increase by 25-50mcg

65
Q

side effects of thyroxine therapy

A

hyperthyroidism: due to over treatment

reduced bone mineral density

worsening of angina

atrial fibrillation

Interactions
iron, calcium carbonate
absorption of levothyroxine reduced, give at least 4 hours apart

66
Q

function of insulin

A

Secreted in response to hyperglycaemia
Glucose utilisation and glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss
Increases cellular uptake of potassium (via stimulation of Na+/K+ ATPase pump)

67
Q

when is the insulin stress test used

A

used in investigation of hypopituitarism

IV insulin given, GH and cortisol levels measured
with normal pituitary function GH and cortisol should rise

68
Q

types of insulin therapy

A

Rapid-acting insulin analogues - bolus dose (novorapid, humalog)

Short-acting insulins - bolus dose - actrapid (soluble)

Long-acting insulins - levemir OD/BD, lantus OD

premixed intermediate acting with rapid acting - novomix

69
Q

side effects of insulin therapy

A

hypoglycaemia - give insulin treated pt glucagon kit

Lipodystrophy - atrophy or lumps of SC fat

70
Q

features of an insulinoma

A

a neuroendocrine tumour deriving mainly from pancreatic islets of Langerhans - most common pancreatic endocrine tumour

hypoglycaemia sx, rapid weight gain
high insulin
high proinsulin:insulin ratio
high c peptide

71
Q

investigation and management of insulinoma

A

Diagnosis
supervised, prolonged fasting (up to 72 hours)
CT pancreas

Management
surgery
diazoxide and somatostatin if patients are not candidates for surgery

72
Q

definition of kallman syndrome

A

cause of delayed puberty secondary to hypogonadotropic hypogonadism (failure of GnRH secreting neurons to migrate to hypothalamus)
X linked recessive trait

73
Q

features of kallman syndrome

A

‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
normal/tall

74
Q

management of kallman syndrome

A

testosterone supplementation
gonadotrophin supplementation may result in sperm production if fertility is desired later in life

75
Q

features of klinefelter’s syndrome

A

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 but low testosterone

diagnosed by karyotype

76
Q

definition of liddle’s syndrome

A

rare autosomal dominant condition
causes hypertension and hypokalaemia alkalosis

caused by increased sodium reabsorption

77
Q

moa of meglitinides

A

increase pancreatic insulin secretion
often used for patients with an erratic lifestyle
adverse effects include weight gain and hypoglycaemia (less so than sulfonylureas)

78
Q

definition of MODY

A

monogenic diabetes
autosomal dominant inheritance pattern
onset <25y
impairment in insulin secretion with minimal or no defects in insulin action
not driven by lifestyle factors

79
Q

features of MODY

A

mild non-ketotic hyperglycemia, detected incidentally
normal weight

MODY should be suspected in individuals with persistent, asymptomatic hyperglycemia detected before the age of 25, without the typical features of Type 1 or Type 2 diabetes.

80
Q

features of MEN type 1

A

pituitary

parathyroid - hyperparathyroidism due to parathyroid hyperplasia

pancreas - insulinoma, gastrinoma

MEN1 gene

81
Q

features of MEN type IIa

A

parathyroid

medullary thyroid cancer

phaeochromocytoma

RET oncogene

82
Q

features of MEN type IIB

A

medullary thyroid cancer

phaeochromocytoma

marfanoid body habitus

RET oncogene

83
Q

features of myxoedema coma

A

confusion and hypothermia

84
Q

treatment of myxoedema coma

A

IV thyroid replacement
IV fluid
IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
electrolyte imbalance correction
sometimes rewarming

85
Q

definition of neuroblastoma

A

7-8% of childhood malignancies

the tumour arises from neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system

median onset 20m

86
Q

features of neuroblastoma

A

abdominal mass
pallor, weight loss
bone pain, limp
hepatomegaly
paraplegia
proptosis

87
Q

investigation findings in neuroblastoma

A

raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels
calcification may be seen on abdominal x-ray
biopsy

88
Q

medical management of obesity

A

orlistat - pancreatic lipase inhibitor
adverse effects - faecal urgency/incontinence and flatulence
used if BMI >28 with risk factors or >30

liraglutide - GLP1 mimetic used when BMI >35

89
Q

hormone profile of primary hyperparathyroidism

A

high Ca
low PO4
normal/high PTH

Urine calcium : creatinine clearance ratio > 0.01

90
Q

causes of primary hyperparathyroidism

A

due to solitary adenoma (80%), multifocal disease occurs in 10-15% and parathyroid carcinoma in 1% or less

91
Q

hormone profile of secondary hyperparathyroidism

A

high PTH, low or normal Ca, high PO4, low VD

92
Q

cause of secondary hyperparathyroidism

A

Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications

92
Q

causes of tertiary hyperparathyroidism

A

result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause

features: Metastatic calcification
Bone pain and / or fracture
Nephrolithiasis
Pancreatitis

93
Q

hormone profile of tertiary hyperparathyroidism

A

normal or high Ca
high PTH
low/normal PO4
low/normal VD
high ALP

94
Q

Indications for surgery in secondary (renal) hyperparathyroidism

A

Bone pain
Persistent pruritus
Soft tissue calcifications

95
Q

definition of phaeochromocytoma

A

a rare catecholamine secreting tumour

10% familial, may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

bilateral in 10%
malignant in 10%
extra-adrenal in 10%

96
Q

features of phaeochromocytoma

A

episodic sx

hypertension (around 90% of cases, may be sustained)
headaches
palpitations
sweating
anxiety

97
Q

investigations and management of phaeochromocytoma

A

24 hr urinary collection of metanephrines

alpha blocker e.g. phenoxybenzamine
then beta blocker e.g. propranolol

98
Q

definition and classification of pituitary adenoma

A

a benign tumour of the pituitary gland - common

usually incidental findings

classified according to:
size (a microadenoma is <1cm and a macroadenoma is ≥1cm)
hormonal status (a secretory/functioning adenoma produces an excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess)

prolactinoma - most common type
can be non-secreting

99
Q

how do pituitary adenomas cause symptoms

A

excess of a hormone e.g., cushings
depletion of a hormone - compression of normal functioning pituitary gland
stretching of dura within/around pituitary fossa causing headaches
compression of optic chiasm

100
Q

investigations needed for pituitary adenoma

A

a pituitary blood profile (including GH, prolactin, ACTH, FSH, LSH and TFTs)
formal visual field testing
MRI brain with contrast

101
Q

some thyroid problems in pregnancy

A

increase in TBG in pregnancy causes an increase in total thyroxine but doesnt affect free thyroxine level

Untreated thyrotoxicosis increases the risk of fetal loss, maternal heart failure and premature labour

graves disease - most common cause of thyrotoxicosis in pregnancy

propylthiouracil

102
Q

managing hypothyroidism in pregnancy

A

thyroxine is safe during pregnancy
serum thyroid-stimulating hormone measured in each trimester and 6-8 weeks post-partum
women require an increased dose of thyroxine during pregnancy
by up to 50% as early as 4-6 weeks of pregnancy
breastfeeding is safe whilst on thyroxine

103
Q

definition and causes of primary hyperaldosteronism

A

most common cause - bilateral idiopathic adrenal hyperplasia (60-70%)

adrenal adenoma: 20-30% of cases
unilateral hyperplasia
familial hyperaldosteronism
adrenal carcinoma

104
Q

features of primary hyperaldosteronism

A

hypertension

hypokalaemia e.g. muscle weakness

metabolic alkalosis

105
Q

investigation findings in primary hyperaldosteronism

A

plasma aldosterone/renin ratio - shows high aldosterone levels and low renin levels

high-resolution CT abdomen and adrenal vein sampling - differentiates between unilateral and bilateral causes of excess

106
Q

management of primary hyperaldosteronism

A

adrenal adenoma: surgery (laparoscopic adrenalectomy)

bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

107
Q

function of prolactin

A

Stimulates breast development (both initially and further hyperplasia during pregnancy)
Stimulates milk production

decreases GnRH pulsatility at the hypothalamic level

108
Q

regulation of prolactin

A

constant inhibition by dopamine

Increases secretion
thyrotropin releasing hormone
pregnancy
oestrogen
breastfeeding
sleep
stress
drugs e.g. metoclopramide, antipsychotics

Decreases secretion
dopamine
dopaminergic agonists

109
Q

regulation of calcium by PTH

A

calcium levels in the blood fall, which is detected by the parathyroid gland

chief cells secrete PTH into the blood

calcium is released from bone and reabsorbed from the renal tubules, causing its level to rise

increased calcium levels are detected by the parathyroid gland, which decreases PTH secretion

110
Q

definition and clinical findings of riedel’s thyroiditis

A

rare cause of hypothyroidism - dense fibrous tissue replacing the normal thyroid parenchyma

hard, fixed, painless goitre
seen in middle-aged women
associated with retroperitoneal fibrosis

111
Q

moa of SGLT2 inhibitors and examples

A

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

canagliflozin, dapagliflozin and empagliflozin.

112
Q

side effects of SGLT2 inhibitors

A

urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

Patients taking SGLT-2 drugs often lose weight, which can be beneficial in type 2 diabetes mellitus.

113
Q

definition of sick euthyroid syndrome

A

everything (TSH, thyroxine and T3) is low. In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3).

114
Q

phases in subacute thyroiditis

A

occurs post-viral infection, presents with hyperthyroidism

phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal

115
Q

investigation findings and management of subacute thyroiditis

A

Investigations
thyroid scintigraphy: globally reduced uptake of iodine-131

Management
usually self-limiting - most patients do not require treatment
thyroid pain may respond to aspirin or other NSAIDs
in more severe cases steroids are used, particularly if hypothyroidism develops

116
Q

definition of subclinical hyperthyroidism

A

normal serum free thyroxine and triiodothyronine levels

thyroid stimulating hormone (TSH) below normal range (usually < 0.1 mu/l)

117
Q

causes of subclinical hyperthyroidism

A

multinodular goitre, particularly in elderly females
excessive thyroxine may give a similar biochemical picture

118
Q

management of subclinical hyperthyroidism

A

TSH levels often revert to normal - therefore levels must be persistently low to warrant intervention
a reasonable treatment option is a therapeutic trial of low-dose antithyroid agents for approximately 6 months in an effort to induce a remission

119
Q

definition of subclinical hypoothyroidism

A

TSH raised but T3, T4 normal
no obvious symptoms

risk of progressing to overt hypothyroidism is 2-5% per year (higher in men)
risk increased by the presence of thyroid autoantibodies

120
Q

management of subclinical hypoothyroidism

A

TSH >10 and free thyroxine in range 2 time 3 months apart - offer levothyroxine

TSH 5.5-10 and free thyroxine in range 2 time 3 months apart - <65y offer 6m trial of levothyroxine OR if sx of hypothyroidism

if >80y - watch and wait

if asymptomatic people, observe and repeat thyroid function in 6 months

121
Q

function of sulfonylureas

A

oral hypoglycaemic drugs which increase pancreatic insulin secretion

S/E - hypoglycaemic episodes (more common with long-acting preparations such as chlorpropamide)
weight gain

122
Q

function of thiazolidinediones

A

agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance

Adverse effects
weight gain
liver impairment: monitor LFTs
fluid retention

123
Q

types of thyroid cancer

A

papillary - 70% - young F
follicular
medullary
anaplastic
lymphoma

124
Q

management of thyroid cancer

A

total thyroidectomy
followed by radioiodine (I-131) to kill residual cells
yearly thyroglobulin levels to detect early recurrent disease

125
Q

causes of thyroid eye disease

A

autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation - glycosaminoglycan and collagen deposition in the muscles

smoking - big risk factor

126
Q

features of thyroid eye disease

A

the patient may be eu-, hypo- or hyperthyroid at the time of presentation
exophthalmos
conjunctival oedema
optic disc swelling
ophthalmoplegia
inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy

127
Q

causes of thyroid nodule

A

Multinodular goitre
Thyroid adenoma
Hashimoto’s thyroiditis
Cysts (colloid, simple, or hemorrhagic)
carcinoma

128
Q

clinical features of thyroid storm

A

fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test

TSH down, T4 and T3 up
thyroid autoantibodies

129
Q

management of thyroid storm

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

130
Q

causes of thyrotoxicosis

A

Graves’ disease
toxic nodular goitre
acute phase of subacute (de Quervain’s) thyroiditis
acute phase of post-partum thyroiditis
acute phase of Hashimoto’s thyroiditis (later results in hypothyroidism)
amiodarone therapy
contrast

131
Q

features of thyrotoxicosis

A

General
Weight loss
‘Manic’, restlessness
Heat intolerance

Cardiac
palpitations, tachycardia
high-output cardiac failure may occur in elderly patients, a reversible cardiomyopathy can rarely develop

Skin
Increased sweating
Pretibial myxoedema: erythematous, oedematous lesions above the lateral malleoli
Thyroid acropachy: clubbing

Gastrointestinal
Diarrhoea

Gynaecological
Oligomenorrhea

Neurological
Anxiety
Tremor

132
Q

definition of toxic multinodular goitre

A

a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism

nuclear scintigraphy reveals patchy uptake

treatment - radioiodine therapy

133
Q

results of the water deprivation test

A

psychogenic polydipsia - urine osm start lowish, no change

cranial DI - urine osm start low, end high

neph DI - urine osm start low, end low

Finals (27 decks)

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