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MRCS Physiology > Endocrine System > Flashcards

Endocrine System Flashcards

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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
What is the commonest cause of hyperCa in the community?
Primary hyperPTH (parathyroid adenoma ~80%)
26
Causes of hyperCa
Main = malignancy, primary hyperPTH Less common = sarcoidosis, drugs (thiazides, lithium), Paget's, vit A/D toxicity, thyrotoxicosis, MEN syndrome, milk alkali syndrome, immobilisation
27
What is free Ca level affected by?
pH (increased in acidosis) Plasma albumin concentration
28
ECG changes in hyperCa
Shortening of QTc interval
29
When is urgent Mx of hyperCa indicated?
Ca >3.5mmol/L Reduced consciousness Severe abdo pain Pre-renal failure
30
Mx of hyperCa
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`
31
Examples of IV bisphosphonates
IV pamidronate = most potent, SE fever, leucopenia IV zoledronate = response lasts 30 days, used for cancer-associated hyperCa (bisphosphonates are analogues of pyrophosphate)
32
Effects of hypophosphataemia
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)
33
Causes of hypophosphataemia
``` HyperPTH Vit D deficiency TPN (refeeding syndrome) DKA Alcohol withdrawal Acute liver failure Paracetamol OD (phosphaturia) ```
34
Causes of hyperphosphataemia
Chronic renal failure (causing itching) Tumour lysis syndrome Myeloma
35
What type of cells does the adrenal medulla contain?
Chromaffin cells (specialised sympathetic post-ganglionic neurons)
36
What stimulates hormone release from the adrenal medulla?
ACh release from splanchnic nerves innervating the medulla
37
What does the adrenal medulla produce?
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
Which enzymes inactivate the adrenal hormones once they are released?
Catechol-O-methyl transferase Monoamine oxidase present in liver and kidney
39
Which part of the kidney tubule does aldosterone act on?
Distal convoluted tubule
40
What is cortisol bound to?
90% of cortisol protein-bound, 10% active 75% transcortin 15% albumin
41
What stimulates cortisol release?
``` ACTH Circadian rhythm: high in morning Stress Trauma, burns Infection Exercise Hypoglycaemia ```
42
Actions of cortisol
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
Action of lipocortin
Inhibit phospholipase A2 and hence prevent formation of inflammatory mediators e.g. prostaglandins, leukotrienes, plt-activating factor (PAF)
44
Commonest enzyme defect in congenital adrenal hyperplasia (CAH)
21-hydroxylase
45
Rule of 10 of phaeochromocytoma
10% malignant 10% bilateral 10% arise from outside adrenal medulla 10% part of MEN syndrome
46
Actions of norepinephrine > epinephrine
Alpha 1 = increased gluconeogenesis, increased BP, increased tone in GI sphincters, bronchoconstriction Alpha 2 = decreased insulin secretion
47
Actions of epinephrine > norepinephrine
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
What stimulates GH release?
``` Hypoglycaemia = potent (+ inhibit somatostatin) Anxiety, pain Hypothermia Haemorrhage Trauma Fever Exercise ```
49
Actions of GH
Increased glycogenolysis, protein synthesis, amino acid uptake into cells Increased lipolysis and release of FFAs Decreased glucose uptake by cells Decreased LDL cholesterol
50
Where are exocrine secretions produced in the pancreas?
The pancreatic acini
51
Where are endocrine secretions produced in the pancreas?
The islets of Langerhans
52
3 main hormones produced by islets of Langerhans
Insulin (beta cells) - 70% total secretions Glucagon (alpha cells) Somatostatin (delta cells) Pancreatic polypeptide (F cells)
53
What is the half-life of insulin in the circulation?
Very short, 5-10min
54
What is insulin broken down by?
Liver | Kidneys
55
What is insulin stored as?
``` Glycogen = liver, skeletal muscles Triglycerides = adipocytes ```
56
Structure of insulin
Human insulin protein has 91 amino acids Molecular weight 5,808 Da Dimer of A-chain and B-chain linked by disulfide bonds
57
Synthesis of insulin
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
Factors INCREASING insulin release
``` Hyperglycaemia Raised fatty acids and ketone bodies PARASYMPATHETIC stimulation Amino acids (arginine, leucine) Gastrin, CCK, secretin, GIP Prostaglandins Drugs e.g. sulphonylureas ```
59
Factors DECREASING insulin release
``` SYMPATHETIC stimulation Alpha-adrenergic drugs Dopamine Serotonin Somatostatin ```
60
Actions of insulin
``` Promote glucose and aa uptake into cells Glycogenesis Glycolysis Protein synthesis Lipogenesis ``` Inhibit lipolysis
61
What stimulates somatostatin release?
Increased plasma glucose and amino acids | Increased plasma glycerol
62
Effects of somatostatin
Inhibit release of insulin and glucagon | Decrease GI motility, secretion and absorption
63
4 systems involved in body's response to injury
Sympathetic NS Acute phase system Endocrine response Vascular endothelium
64
Types of pancreatic endocrine tumours
``` Insulinoma (75%) Gastrinoma (Zollinger-Ellison) Vipoma Glucagonoma Somatostatinoma ```
65
Classic presentation of insulinoma
Whipple's triad = Hypoglycaemic symptoms Reduced blood sugar levels during these periods Relief with IV glucose ~10% malignant
66
Features of gastrinoma
Gastric hypersecretion Diarrhoea Widespread peptic ulceration >50% malignant
67
Features of Vipoma
Severe watery diarrhoea HypoK Achlorhydria (absent HCl)
68
Features of glucagonoma
Secondary DM Anaemia Weight loss Characteristic rash = necrolytic migratory erythema 75% malignant
69
Features of somatostatinoma
DM Cholelithiasis Steatorrhoea
70
What are the SYSTEMIC effects of the acute phase response to injury?
``` Fever Increased HR and RR Increased vascular permeability and vasodilatation (hence decreased BP) Immune cell activation Increased leukocyte adhesion ```
71
Vascular endothelial response to trauma
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
Clinical changes in response to trauma and surgery
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
Metabolic changes in response to trauma and surgery
Ebb phase = initial response, phase of reduced energy expenditure, lasts ~24hrs Flow phase = CATABOLIC phase, hyperglycaemia, negative nitrogen balance, increased O2 consumption, lipolysis
74
Metabolic changes in response to trauma and surgery
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
Respiratory changes in response to trauma and surgery
Increased RR --> resp alkalosis Affects O2 dissociation curve --> harder for O2 to dissociate into tissues
76
Hormones that are INCREASED in stress response
``` GH ACTH, cortisol Renin, aldosterone ADH Prolactin Glucagon ```
77
Hormones that are DECREASED in stress response
Insulin Testosterone Oestrogen
78
Hormones that have NO CHANGE in stress response
TSH | LH, FSH
79
Medical Mx of thyroid storm
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
How is diagnosis of phaeochromocytoma confirmed?
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
List of acute phase proteins
``` CRP Procalcitonin Ferritin Fibrinogen Alpha-1 antitrypsin Caeruloplasmin Serum amyloid A Haptoglobin Complement ```
82
List of NEGATIVE acute phase proteins
``` Albumin Transthyretin (formerly prealbumin) Transferrin Retinol binding protein Cortisol binding protein ``` Liver decreases the production of these proteins during the acute phase response
83
What level of CRP at 48hrs post-op suggest evolving complications?
CRP >150
84
What does CRP bind to in bacterial cells and on cells undergoing apoptosis after being synthesised in the liver?
Phosphocoline
85
What stimulates glucagon release?
``` Hypoglycaemia Increased catecholamines and plasma amino acids Sympathetic NS ACh CCK ```
86
What inhibits glucagon release?
Somatostatin Insulin Increased FFAs and ketones Increased urea
87
Causes of hypoMg
``` Diuretics TPN Diarrhoea Alcohol HypoK, hypoCa ```
88
Where are PTH receptors found?
Kidneys | Bone
89
Half-life of PTH in plasma
4 minutes
90
Effects of PTH
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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