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Endocrine System Flashcards

1
Q

What are the 3 layers of the adrenal cortex?

A

Zona Glomerulosa
Zona Fasciculate
Zona Reticularis

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2
Q

Which part of the adrenal gland are glucocorticoids (like cortisol) produced in?

A

zona fasciculata

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3
Q

Which part of the adrenal gland are Mineralocorticoids (like aldosterone) produced in?

A

Zona glomerulosa

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4
Q

Which part of the adrenal gland are Androgens (like testosterone precursor) produced in?

A

Zona reticularis

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5
Q

Somatostatin is released from the ___ cells in the pancreas

A

delta

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6
Q

Where can delta cells be found?

A

Pancreas, stomach, duodenum, and the jejunum

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7
Q

What is the function of somatostatin in the pancreas?

A

acts to inhibit the release of exocrine enzymes, glucagon, and insulin

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8
Q

Sources of Somatostatin

A

Delta cells of the pancreas, pylorus and duodenum

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9
Q

What is somatostatin also known as?

A

growth hormone inhibiting hormone (GHIH).

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10
Q

Function of stomatostain

A

Inhibits growth hormone secretion

Inhibits insulin and glucagon secretion

Decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion

Inhibits trophic effects of gastrin

Stimulates gastric mucous production

Somatostatin analogs are used in the management of acromegaly, as they inhibit growth hormone secretion

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11
Q

Somatostatin increases secretion of :

A

fat, bile salts and glucose in the intestinal lumen

glucagon

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12
Q

Somatostatin decreases secretion of :

A

Insulin

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13
Q

Alpha-cells release ____

A

glucagon

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14
Q

Beta cells release ____

A

Insulin

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15
Q

S cells release ____

A

secretin

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16
Q

PP cells release __________________

A

pancreatic polypeptide

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17
Q

What is the half life of insulin in the circulation of a normal healthy adult?

A

Less than 30 minutes

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18
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)

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19
Q

The symptoms of polyuria, nocturia, and chronic thirst, combined with a pre-existing history of chronic kidney disease (CKD) stage 4 (eGFR of 30-15ml/min/1.73m²) suggests ________________________

A

nephrogenic diabetes insipidus (DI).

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20
Q

Nephrogenic DI results from renal insensitivity to ______________________, preventing the concentration of urine.

A

anti-diuretic hormone (ADH)

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21
Q

Causes of nephrogenic DI

A

CKD, nephrotoxic drugs, and metabolic disturbances

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22
Q

Why is there low urine osmolality after both fluid deprivation and desmopressin in nephrogenic DI?

A

This lack of ADH sensitivity results in an inability to concentrate urine even if a patient is hypovolaemic, therefore producing a low urine osmolality even during water deprivation. Furthermore, as the kidneys are insensitive to ADH, they will not respond to desmopressin (synthetic ADH) and urine osmolality will once again be low.

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23
Q

Why is low urine osmolality after fluid deprivation but high after desmopressin occur in cranial DI?

A

This lack of ADH results in an inability to concentrate urine even if a patient is hypovolaemic, therefore producing a low urine osmolality even during water deprivation. However, as the kidneys are unaffected by cranial DI, they will respond to desmopressin (synthetic ADH) to produce concentrated urine

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24
Q

RFs for cranial DI

A

head trauma, localised infections, and post-radiotherapy

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25
Exogenous insulin administration is characterised by ____________
elevated serum insulin levels with low C-peptide levels.
26
Insulinomas are typically associated with the Whipple triad:
hypoglycaemia, symptoms relieved by glucose, and low blood glucose during symptoms.
27
What is an insulinoma?
Pancreatic tumour that secretes insulin autonomously, leading to hypoglycaemia. However, these tumours also secrete C-peptide along with insulin.
28
Causes of hypoglycaemia
insulinoma - increased ratio of proinsulin to insulin self-administration of insulin/sulphonylureas liver failure Addison's disease alcohol causes exaggerated insulin secretion mechanism is thought to be due to the effect of alcohol on the pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion nesidioblastosis - beta cell hyperplasia
29
What is the hormonal response to hypoglycaemia?
the first response of the body is decreased insulin secretion. This is followed by increased glucagon secretion. Growth hormone and cortisol are also released but later.
30
What is the sympathoadrenal response to hypoglycaemia?
increased catecholamine-mediated (adrenergic) and acetylcholine-mediated (cholinergic) neurotransmission in the peripheral autonomic nervous system and in the central nervous system
31
Blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline :
Sweating Shaking Hunger Anxiety Nausea
32
blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:
Weakness Vision changes Confusion Dizziness
33
Severe and uncommon features of hypoglycaemia include:
Convulsion Coma
34
Hypoglycaemia; Insulin (HIGH) + C-peptide (HIGH) =
Endogenous insulin production = Insulinoma, Sulfonylurea use/abuse
35
Hypoglycaemia; Insulin (HIGH) + C-peptide (LOW) =
Exogenous insulin administration = Exogenous insulin overdose, Factitious disorder
36
Hypoglycaemia; Insulin (LOW) + C-peptide (LOW) =
Non-insulin-related cause = Alcohol-induced hypoglycaemia, Critical illness (e.g., sepsis), Adrenal insufficiency, Growth hormone deficiency, Fasting/starvation
37
Community management of Hypoglycaemia
Initially, oral glucose 10-20g should be given in liquid, gel or tablet form Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel. A 'HypoKit' may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
38
Hospital management of Hypoglycaemia
If the patient is alert, a quick-acting carbohydrate may be given (GlucoGel or Dextrogel) If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given. Alternatively, intravenous 20% glucose solution may be given through a large vein
39
Metabolic Syndrome
a clustering of cardiovascular disease risk factors whose underlying pathophysiology is related to insulin resistance and visceral/central obesity.
40
Consequences of Metabolic Syndrome
- Strokes - Non-insulin dependant diabetes - Cardiovascular disease - Cancers - including breast, colon and endometrial - Polycystic ovarian syndrome - Obstructive sleep apnea - Fatty liver - Gall stones - Mental health problems
41
What is Leptin?
Leptin is thought to play a key role in the regulation of body weight. It is produced by adipose tissue and acts on satiety centres in the hypothalamus and decreases appetite. More adipose tissue (e.g. in obesity) results in high leptin levels.
42
Leptin stimulates the release of _____
melanocyte-stimulating hormone (MSH) and corticotrophin-releasing hormone (CRH).
43
Low levels of leptin stimulates the release of
neuropeptide Y (NPY)
44
What is Ghrelin?
Where as leptin induces satiety, ghrelin stimulates hunger. It is produced mainly by the P/D1 cells lining the fundus of the stomach and epsilon cells of the pancreas. Ghrelin levels increase before meals and decrease after meals
45
Primary hyperparathyroidism is caused by _______________resulting in hypercalcaemia.
excess secretion of PTH
46
46
47
In ____% of cases of Primary Hyperparathyroidism a parathyroid adenoma is responsible
85
48
Causes of primary hyperparathyroidism
85%: solitary adenoma 10%: hyperplasia 4%: multiple adenoma 1%: carcinoma
49
Around ____% of patients who have primary hyperparathyroidism are asymptomatic and are diagnosed on routine blood tests.
80
50
The symptomatic features of primary hyperparathyroidism may be remembered by the mnemonic:
'bones, stones, abdominal groans and psychic moans'
51
Sx of primary hyperparathyroidism
polydipsia, polyuria depression anorexia, nausea, constipation peptic ulceration pancreatitis bone pain/fracture renal stones hypertension
52
Associated conditions with primary hyperparathyroidism
hypertension multiple endocrine neoplasia: MEN I and II
53
What inhibits the release of prolactin?
Dopamine acts as the primary prolactin releasing inhibitory factor
54
Ix for primary hyperparathyroidism
bloods raised calcium, low phosphate PTH may be raised or (inappropriately, given the raised calcium) normal technetium-MIBI subtraction scan x-ray findings pepperpot skull osteitis fibrosa cystica
55
X ray findings for primary hyperparathyroidism
pepperpot skull osteitis fibrosa cystica
56
Tx of primary hyperparathyroidism
the definitive management is total parathyroidectomy conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage patients not suitable for surgery may be treated with cinacalcet, a calcimimetic a calcimimetic 'mimics' the action of calcium on tissues by allosteric activation of the calcium-sensing receptor
57
What can be given to control galactorrhoea?
dopamine agonists such as bromocriptine may be used to control galactorrhoea.
58
Features of excess prolactin in men and women
men: impotence, loss of libido, galactorrhoea women: amenorrhoea, galactorrhoea
59
Causes of raised prolactin
prolactinoma pregnancy oestrogens physiological: stress, exercise, sleep acromegaly: 1/3 of patients polycystic ovarian syndrome primary hypothyroidism (due to thyrotrophin releasing hormone (TRH) stimulating prolactin release)
60
Drugs that cause raised prolactin
metoclopramide, domperidone phenothiazines haloperidol very rare: SSRIs, opioids
61
Aldosterone is secreted from the____________
zona glomerulosa
61
Juxtaglomerular cells release _____, (they are found in the nephron).
renin
62
Pulmonary endothelium produces ____, (produced in the lungs)
ACE
63
The chromaffin cells of the adrenal medulla secrete the ________________________
catecholamines noradrenaline and adrenaline.
64
Chvostek's sign is seen in ________ due to increased irritability of the peripheral nerves
hypocalcaemia
65
Primary hypoparathyroidism
decrease PTH secretion e.g. secondary to thyroid surgery* low calcium, high phosphate
66
Primary hypoparathyroidism is treated with _______
alfacalcidol
67
The main symptoms of hypoparathyroidism are secondary to hypocalcaemia:
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
68
ECG for hypocalaemia
prolonged QT interval
69
Gold standard for diagnosing insulinoma
72-hour fast is the gold standard for diagnosing Insulinoma
70
Primary hyperaldosteronism (Conn's Syndrome) can present with _____________
hypertension, hypernatraemia, and hypokalemia
71
________ is important in maintaining potassium balance as it binds to and activates Na+/K+ pumps.
Aldosterone
72
What is the most common cause of Primary Hyperaldosteronism?
bilateral idiopathic adrenal hyperplasia
73
Causes of Primary hyperaldosteronism
bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases adrenal adenoma: 20-30% of cases unilateral hyperplasia familial hyperaldosteronism adrenal carcinoma
74
Features of Primary hyperaldosteronism
hypertension increasingly recognised but still underdiagnosed cause of hypertension hypokalaemia e.g. muscle weakness this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients, and is more common with adrenal adenomas metabolic alkalosis
75
First line Ix for primary hyperaldosteronism
aldosterone/renin ratio ; should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone) following this a high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess if the CT is normal adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia
76
Management of primary hyperaldosteronism
adrenal adenoma: surgery (laparoscopic adrenalectomy) bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
77
DKA is caused by uncontrolled __________ which results in an excess of free fatty acids that are ultimately converted to ketone bodies
lipolysis
78
Aldosterone causes _______reabsorption and ________excretion.
sodium ; potassium
79
A lack of aldosterone would result in the following biochemical abnormality: ____________ And ___________
hyperkalaemia & hyponatraemia
80
Primary hyperaldosteronism can present with hypertension, _____natraemia, and ______kalemia
hyper ; hypo
81
Mnemonic for the causes of hypercalcaemia:
CHIMPANZEES C alcium supplementation H yperparathyroidism I atrogentic (Drugs: Thiazides) M ilk Alkali syndrome P aget disease of the bone A cromegaly and Addison's Disease N eoplasia Z olinger-Ellison Syndrome (MEN Type I) E xcessive Vitamin D E xcessive Vitamin A S arcoidosis
82
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