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MRCS Physiology > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

Types of hormones

A

Steroids (from cholesterol)
Peptides
Altered amino acids (e.g. thyroid hormones made up of 2 tyrosine residues)

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2
Q

3 main types of receptors that hormones bind to

A

Receptors on cell surface: usually protein/peptide hormones –> conformational change –> second messengers –> modify cell response

Cytoplasmic receptors: steroid hormones –> receptor-hormone complex enters nucleus and binds to specific area of DNA to stimulate translation of protein

Nuclear receptors: thyroid hormone receptors found in cell nucleus; thyroid hormone enters cell with receptor and then enters nucleus to exert its effects

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3
Q

Where does the hypothalamus lie?

A

In the forebrain in the floor of the third ventricle

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4
Q

How is the hypothalamus linked to the pituitary?

A

Via a hypophyseal stalk

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5
Q

Where is the anterior pituitary (adenohypophysis) derived from?

A

Derived from the ectoderm, an outpouching of tissue from the oral cavity

Linked to hypothalamus via hypophyseal portal system

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6
Q

Where is the posterior pituitary (neurohypophysis) derived from?

A

Derived from a downgrowth of neural tissue

Continuous with hypothalamus

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7
Q

What are the nuclei in the posterior pituitary?

A

Paraventricular (produce oxytocin)

Supraoptic (produce ADH)

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8
Q

Causes of SIADH

A

Cancer (esp. SCLC, also pancreas, prostate)

Neuro: stroke, SAH, subdural haemorrhage, meningitis/encephalitis/abscess

Infections: TB, pneumonia

Drugs: Analgesics (opioids, NSAIDs), Barbiturates, Cyclophosphamide/Chlorpromazine/CBZ, Diuretics (thiazides), sulfonylurea, SSRI, TCA, vincristine

Others: PEEP, porphyria, alcohol withdrawal

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9
Q

Causes of pituitary deficiency

A

Infection: meningitis, encephalitis

Cerebral tumours

Radiation

Trauma i.e. frontal skull

Pituitary apoplexy: bleeding into pituitary tumour

Sheehan’s syndrome: infarction after PPH

Sarcoidosis

Rare congenital deficiencye.g. Kallman syndrome (FSH and LH deficiency)

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10
Q

What type of epithelium is the outer layer of the thyroid?

A

Cuboidal epithelium

surrounding colloid which is where the thyroid hormones are stored

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11
Q

What lie between the follices of the thyroid gland and what do they produce?

A

Parafollicular C-cells which secrete calcitonin

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12
Q

Hormones of the thyroid gland and their functions

A

T3 triiodothyronine = major hormone ACTIVE in target cells

T4 thyroxine = most prevalent form in PLASMA, less biologically active than T3

Calcitonin = lowers plasma Ca

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13
Q

Synthesis of thyroid hormones

A

Active pumping of iodide ions from extracellular space into follicular epithelium (thyroid actively concentrates iodide to 25x plasma conc)

Iodide ions enter colloid and oxidised to IODINE by PEROXIDASE

Iodine combine with tyrosine contained in thyroglobulin to form either 1 MT (monoiodotyrosine) or 2 DT (diiodotyrosine)

1 MT and 2 DT in thyroglobulin undergo coupling to either T3 or T4

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14
Q

How many months of reserves of hormones does a normal thyroid gland have?

A

3 months

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15
Q

Mechanism of action of thionamides (carbimazole, propylthiouracil)

A

Competitive inhibitor of peroxidase, blocking oxidisation of iodide to iodine

Block coupling of iodotyrosine

PTU = also inhibits peripheral deiodination of T4

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16
Q

Mechanism of action of anion inhibitors (e.g. perchlorate)

A

Competitive inhibition of iodine uptake

discontinued as can cause aplastic anaemia

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17
Q

Mechanism of action of iodide (e.g. Lugol’s solution)

A

Block binding of iodine with tyrosine residues, inhibiting hormone release

Decrease size and vascularity of thyroid gland

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18
Q

What is sick euthyroid syndrome?

A

Acute illness resulting in abnormal thyroid function markers without actually affecting thyroid function

LOW TSH, LOW T3/4

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19
Q

Changes in sick euthyroid syndrome

A

Decreased amount of binding proteins and their affinity
Decreased peripheral conversion of T4 to T3
Decreased TSH

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20
Q

Where is calcium stored?

A

99% in bone

Intracellular

Extracellular = normal levels between 2.2-2.6mmol/L, ~50% is protein-bound

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21
Q

Role of calcitonin

A

Inhibit intestinal Ca absorption
Inhibit osteoclast activity + stimulate osteoblast
Inhibit renal tubular absorption of Ca and phosphate

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22
Q

Why is Mg important in Ca metabolism?

A

Mg is required both for PTH secretion and its action on target tissues

HypoMg may both cause hypoCa and render pts unresponsive to Tx with Ca and vit D supplementation

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23
Q

How much Mg does the body contain and where is it stored?

A

1,000mmol

50% in bone
50% in muscle, soft tissues, ECF

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24
Q

What is the commonest cause of hyperCa in hospitalised pts?

A

Malignancy

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25
Q

What is the commonest cause of hyperCa in the community?

A

Primary hyperPTH (parathyroid adenoma ~80%)

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26
Q

Causes of hyperCa

A

Main = malignancy, primary hyperPTH

Less common = sarcoidosis, drugs (thiazides, lithium), Paget’s, vit A/D toxicity, thyrotoxicosis, MEN syndrome, milk alkali syndrome, immobilisation

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27
Q

What is free Ca level affected by?

A

pH (increased in acidosis)

Plasma albumin concentration

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28
Q

ECG changes in hyperCa

A

Shortening of QTc interval

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29
Q

When is urgent Mx of hyperCa indicated?

A

Ca >3.5mmol/L
Reduced consciousness
Severe abdo pain
Pre-renal failure

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30
Q

Mx of hyperCa

A

IV fluid resus with 3-6L of 0.9% NaCl in 24 hours

+/- calcitonin (quickest onset of action but short duration - tachyphylaxis - hence only given with 2nd agent)

+/- medical therapy (usually if corrected Ca >3.0)

Prednisolone if sarcoidosis, myeloma or vit D intoxication`

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31
Q

Examples of IV bisphosphonates

A

IV pamidronate = most potent, SE fever, leucopenia

IV zoledronate = response lasts 30 days, used for cancer-associated hyperCa

(bisphosphonates are analogues of pyrophosphate)

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32
Q

Effects of hypophosphataemia

A

Confusion
Convulsions
Muscle weakness (acute hypophosphataemia can lead to significant diaphragmatic weakness and delay weaning from a ventilator in ITU pt)

LEFT SHIFT of oxyHb curve = decreased O2 delivery to tissues (due to reduction in 2,3-DPG)

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33
Q

Causes of hypophosphataemia

A 
HyperPTH
Vit D deficiency
TPN (refeeding syndrome)
DKA
Alcohol withdrawal
Acute liver failure
Paracetamol OD (phosphaturia)
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34
Q

Causes of hyperphosphataemia

A

Chronic renal failure (causing itching)
Tumour lysis syndrome
Myeloma

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35
Q

What type of cells does the adrenal medulla contain?

A

Chromaffin cells (specialised sympathetic post-ganglionic neurons)

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36
Q

What stimulates hormone release from the adrenal medulla?

A

ACh release from splanchnic nerves innervating the medulla

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37
Q

What does the adrenal medulla produce?

A

Main:
Epinephrine (adrenaline) = bind to beta-receptors
Norepinephrine (NA) = bind to alpha-receptors

Dopamine
Beta-hydroxylase (enzyme involved in catecholamine synthesis)
ATP
Opioid peptides (metenkephalin, leuenkephalin)

38
Q

Which enzymes inactivate the adrenal hormones once they are released?

A

Catechol-O-methyl transferase
Monoamine oxidase

present in liver and kidney

39
Q

Which part of the kidney tubule does aldosterone act on?

A

Distal convoluted tubule

40
Q

What is cortisol bound to?

A

90% of cortisol protein-bound, 10% active

75% transcortin
15% albumin

41
Q

What stimulates cortisol release?

A 
ACTH
Circadian rhythm: high in morning
Stress
Trauma, burns
Infection
Exercise
Hypoglycaemia
42
Q

Actions of cortisol

A

Metabolic (opposite to insulin): glycogenolysis, gluconeogenesis, lipolysis, breakdown of proteins

CV effects: necessary for vasopressors to increase vascular tone

CNS: euphoria

Anti-inflammatory: decrease immunocompetent cells and macrophages, stimulate lipocortin synthesis in WBCs

Immunosuppressive: decrease T cell no. and function, decrease B cell clonal expansion, decrease basophils and eosinophils

Decrease protein in bones
Increase gastric acid
Increase neutrophils/plt/RBCs
Inhibit fibroblast activity

43
Q

Action of lipocortin

A

Inhibit phospholipase A2 and hence prevent formation of inflammatory mediators e.g. prostaglandins, leukotrienes, plt-activating factor (PAF)

44
Q

Commonest enzyme defect in congenital adrenal hyperplasia (CAH)

A

21-hydroxylase

45
Q

Rule of 10 of phaeochromocytoma

A

10% malignant
10% bilateral
10% arise from outside adrenal medulla
10% part of MEN syndrome

46
Q

Actions of norepinephrine > epinephrine

A

Alpha 1 = increased gluconeogenesis, increased BP, increased tone in GI sphincters, bronchoconstriction

Alpha 2 = decreased insulin secretion

47
Q

Actions of epinephrine > norepinephrine

A

Beta 1 = increased HR and cardiac contractility

Beta 2 = increased glycogenolysis, increased insulin and glucagon secretion, increased K+ uptake by muscle, bronchodilatation

Beta 3 = increased lipolysis

48
Q

What stimulates GH release?

A 
Hypoglycaemia = potent (+ inhibit somatostatin)
Anxiety, pain
Hypothermia
Haemorrhage
Trauma
Fever
Exercise
49
Q

Actions of GH

A

Increased glycogenolysis, protein synthesis, amino acid uptake into cells
Increased lipolysis and release of FFAs
Decreased glucose uptake by cells
Decreased LDL cholesterol

50
Q

Where are exocrine secretions produced in the pancreas?

A

The pancreatic acini

51
Q

Where are endocrine secretions produced in the pancreas?

A

The islets of Langerhans

52
Q

3 main hormones produced by islets of Langerhans

A

Insulin (beta cells) - 70% total secretions
Glucagon (alpha cells)
Somatostatin (delta cells)
Pancreatic polypeptide (F cells)

53
Q

What is the half-life of insulin in the circulation?

A

Very short, 5-10min

54
Q

What is insulin broken down by?

A

Liver

Kidneys

55
Q

What is insulin stored as?

A 
Glycogen = liver, skeletal muscles
Triglycerides = adipocytes
56
Q

Structure of insulin

A

Human insulin protein has 91 amino acids
Molecular weight 5,808 Da
Dimer of A-chain and B-chain linked by disulfide bonds

57
Q

Synthesis of insulin

A

Proinsulin (precursor) formed by RER

Proinsulin cleaved to form insulin and C-peptide

Insulin stored in secretory granules and released in response to Ca

58
Q

Factors INCREASING insulin release

A 
Hyperglycaemia
Raised fatty acids and ketone bodies
PARASYMPATHETIC stimulation
Amino acids (arginine, leucine)
Gastrin, CCK, secretin, GIP
Prostaglandins
Drugs e.g. sulphonylureas
59
Q

Factors DECREASING insulin release

A 
SYMPATHETIC stimulation
Alpha-adrenergic drugs
Dopamine
Serotonin
Somatostatin
60
Q

Actions of insulin

A 
Promote glucose and aa uptake into cells
Glycogenesis
Glycolysis
Protein synthesis
Lipogenesis

Inhibit lipolysis

61
Q

What stimulates somatostatin release?

A

Increased plasma glucose and amino acids

Increased plasma glycerol

62
Q

Effects of somatostatin

A

Inhibit release of insulin and glucagon

Decrease GI motility, secretion and absorption

63
Q

4 systems involved in body’s response to injury

A

Sympathetic NS
Acute phase system
Endocrine response
Vascular endothelium

64
Q

Types of pancreatic endocrine tumours

A 
Insulinoma (75%)
Gastrinoma (Zollinger-Ellison)
Vipoma
Glucagonoma
Somatostatinoma
65
Q

Classic presentation of insulinoma

A

Whipple’s triad =
Hypoglycaemic symptoms
Reduced blood sugar levels during these periods
Relief with IV glucose

~10% malignant

66
Q

Features of gastrinoma

A

Gastric hypersecretion
Diarrhoea
Widespread peptic ulceration

> 50% malignant

67
Q

Features of Vipoma

A

Severe watery diarrhoea
HypoK
Achlorhydria (absent HCl)

68
Q

Features of glucagonoma

A

Secondary DM
Anaemia
Weight loss
Characteristic rash = necrolytic migratory erythema

75% malignant

69
Q

Features of somatostatinoma

A

DM
Cholelithiasis
Steatorrhoea

70
Q

What are the SYSTEMIC effects of the acute phase response to injury?

A 
Fever
Increased HR and RR
Increased vascular permeability and vasodilatation (hence decreased BP)
Immune cell activation
Increased leukocyte adhesion
71
Q

Vascular endothelial response to trauma

A

Increased adhesion molecule expression to attract neutrophils

Nitric oxide production causing vasodilatation

Endothelins oppose action of NO

Platelet-activating factor (PAF) released in response to cytokines (e.g. IL-1, TNF-alpha), stimulating plt aggregation and vasoconstriction

72
Q

Clinical changes in response to trauma and surgery

A

Hypovolaemia (third space losses)

Decreased water and Na excretion (due to aldosterone and ADH release)

Fever

Leukocytosis

Decreased albumin

Increased K (from cell death)

73
Q

Metabolic changes in response to trauma and surgery

A

Ebb phase = initial response, phase of reduced energy expenditure, lasts ~24hrs

Flow phase = CATABOLIC phase, hyperglycaemia, negative nitrogen balance, increased O2 consumption, lipolysis

74
Q

Metabolic changes in response to trauma and surgery

A

Ebb phase = initial response, phase of reduced energy expenditure, lasts ~24hrs

Flow phase = CATABOLIC phase, hyperglycaemia, negative nitrogen balance, muscle protein loss, increased O2 consumption, lipolysis

75
Q

Respiratory changes in response to trauma and surgery

A

Increased RR –> resp alkalosis

Affects O2 dissociation curve –> harder for O2 to dissociate into tissues

76
Q

Hormones that are INCREASED in stress response

A 
GH
ACTH, cortisol
Renin, aldosterone
ADH
Prolactin
Glucagon
77
Q

Hormones that are DECREASED in stress response

A

Insulin
Testosterone
Oestrogen

78
Q

Hormones that have NO CHANGE in stress response

A

TSH

LH, FSH

79
Q

Medical Mx of thyroid storm

A

ABC: high-flow O2, IV access and fluids
If suspect infection = treat with empirical Abx

High-dose PTU (prevent peripheral conversion of T4 to T3)

Lugol’s iodine 1hr after PTU given (block release of stored T3 and T4)

Hydrocortisone (as per PTU action)

Beta blocker (for symptomatic relief)

80
Q

How is diagnosis of phaeochromocytoma confirmed?

A

Biochem = 24h acidified urine sample for VMA (vanillylmandelic acid - breakdown product of catecholamines)

Imaging = CT and MRI (latter preferred), or radio-isotope MIBG scans

81
Q

List of acute phase proteins

A 
CRP
Procalcitonin
Ferritin
Fibrinogen
Alpha-1 antitrypsin
Caeruloplasmin
Serum amyloid A
Haptoglobin
Complement
82
Q

List of NEGATIVE acute phase proteins

A 
Albumin
Transthyretin (formerly prealbumin)
Transferrin
Retinol binding protein
Cortisol binding protein

Liver decreases the production of these proteins during the acute phase response

83
Q

What level of CRP at 48hrs post-op suggest evolving complications?

A

CRP >150

84
Q

What does CRP bind to in bacterial cells and on cells undergoing apoptosis after being synthesised in the liver?

A

Phosphocoline

85
Q

What stimulates glucagon release?

A 
Hypoglycaemia
Increased catecholamines and plasma amino acids
Sympathetic NS
ACh
CCK
86
Q

What inhibits glucagon release?

A

Somatostatin
Insulin
Increased FFAs and ketones
Increased urea

87
Q

Causes of hypoMg

A 
Diuretics
TPN
Diarrhoea
Alcohol
HypoK, hypoCa
88
Q

Where are PTH receptors found?

A

Kidneys

Bone

89
Q

Half-life of PTH in plasma

A

4 minutes

90
Q

Effects of PTH

A

Bone = Binds to OSTEOBLASTS which signal to osteoclasts to resorb bone and release Ca

Kidney = active reabsorption of Ca and Mg from DCT, decrease reabsorption of phosphate

GI via kidney = increase intestinal Ca absorption by increasing activated vit D

MRCS Physiology (6 decks)

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