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Year 2 Revision > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the arterial supply of the adrenal glands?

A

Superior adrenal artery from the inferior phrenic artery

Middle adrenal artery from the abdominal aorta

Inferior adrenal artery from the renal arteries

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2
Q

What is the name of the fascia that surrounds the adrenal glands?

A

Perinephric fascia

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3
Q

What is the venous drainage of the adrenal glands?

A

Right adrenal vein into the IVC

Left adrenal vein into the left renal vein

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4
Q

What is the nervous supply of the adrenal glands?

A

Coeliac plexus and abdominopelvic splanchnic nerves.

Sympathetic innervation is from T10-L1 spinal segments.

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5
Q

Name the different auto-antibodies associated with type 1 Diabetes Mellitus.

A

IAA, IA2, ICA, GAD65, ZnT8

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6
Q

What genes are associated with type 1 DM?

A

HLA-DR3/4
PTPN22
IL2RA

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7
Q

Name some environmental factors which increase risk of type 1 DM.

A

Enteroviruses, rotavirus, bacteria, early introduction of cow’s milk and cereals, vitamin D deficiency, some chemicals and drugs.

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8
Q

Describe the different types of available insulin (include what they are used for, when they would be taken)

A

Short acting soluble - injected 30 mins before a meal, peak effect 2-4 hours, used for IV infusion of ketoacidosis and insulin pump.
Short acting analogue - given immediately before, during or after a meal, onset of effect 30 mins after injection.
Long acting - prolonged release, taken once or twice daily with a meal for convenience.

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9
Q

From what embryological tissue is the pancreas derived from?

A

Endoderm

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10
Q

Is the pancreas retroperitoneal?

A

Yes

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11
Q

What vertebral level is the pancreas located?

A

L1/L2

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12
Q

What type of epithelium lines the ducts of the pancreas?

A

Cuboidal to columnar lining

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13
Q

What type of cells make up the islets of langerhans? What hormones do these different cells prdoduce?

A

β cells – insulin
α cells – glucagon
δ cells cells – somatostatin

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14
Q

What is acute pancreatitis.

A

A life-threatening condition of sudden onset where damage to pancreatic tissue releases dangerous digestive enzymes directly into the surroundings.

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15
Q

What is chronic pancreatitis? What condition can it lead to?

A

A condition following repeated episodes of acute damage where you get scarring and loss of normal tissue. Can lead to secondary diabetes.

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16
Q

What can a malignant tumour in the head of the pancreas present with? Where does this cancer commonly spread to?

A

Obstructive jaundice because it blocks the common bile duct.
Stomach, duodenum, transverse colon, liver, major vessels.

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17
Q

What are the embryological origins of the adrenal glands?

A

Cortex - mesoderm

Medulla - ectoderm

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18
Q

Describe the anatomical location of the adrenal glands.

A

Situated above upper poles of the kidneys, in the retroperitoneal space.

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19
Q

Name the three layers of the cortex of the adrenal glands and what these layers produce.

A

Outer - Zona glomerulosa - mineralocorticoids - aldosterone and deoxycorticosterone
Middle - Zona fasciculata - glucocorticoids - cortisol and corticosterone
Inner - zona reticularis - Adrenal androgens - DHEA and androstenedione

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20
Q

What hormones does the medulla of the adrenal glands produce?

A

Catecholamines - Adrenaline and NorAdrenaline

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21
Q

What is an adrenal adenoma?

A

A benign tumour of the adrenal cortex.

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22
Q

What hormones can be produced in excess due to an adrenal adenoma?

A

Cortisol (cushing’s syndrome)
Aldosterone (conn’s syndrome)
Adrenal androgens

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23
Q

Which of these conditions is most likely to result in excess production of hormones: adrenal adenoma or adrenal cortical carcinoma?

A

Adrenal adenoma

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24
Q

Name 2 causes of atrophy of the adrenal cortex.

A

Iatriogenic - long term administration of corticosteroids

Autoimmune destruction - addison’s disease

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25
Q

What disorder of the adrenal gland can cause excessive production of catecholamines and is an important cause of secondary hypertension?

A

Phaeochromocytoma - a rare tumour of the adrenal medulla.

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26
Q

What is the prevalence of type 1 DM, type 2 DM and MODY?

A

Type 1 - 0.5%
Type 2 - 5%
MODY - 0.1%

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27
Q

Name the different types of diabetes.

A 
Type 1
Type 2
MODY
Gestational 
Secondary
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28
Q

What are potential secondary causes of diabetes?

A
  • Pancreatitis
  • Cystic Fibrosis
  • Haemochromatosis
  • Steroid-induced
  • Acromegaly (excessive GH)
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29
Q

Which types of diabetes are insulin deficient and which are insulin resistant?

A 
Insulin deficient:
Type 1
MODY
Pancreatitis 
Cystic fibrosis 
Haemochromatosis 
Insulin resistant:
Type 2
Gestational 
Steroid-induced
Acromegaly
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30
Q

What other autoimmune diseases are associated with type 1 DM?

A

Thyroid disease (hypo/hyper)
Coeliac disease
Addison’s disease

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31
Q

Mutations in what genes can cause MODY?

A

HNF-1α
Glucokinase
HNF-4α
HNF-1β

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32
Q

Give a brief description of how carbohydrate is digested.

A

Starch is broken down into glucose, maltose and dextrins in the mouth with salivary α-amylase.
Starch and dextrins are broken down into dissacharides by pancreatic α-amylase. Brush border enzymes maltase, sucrase and lactase break down dissacharides into monsaccharides.

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33
Q

In what organs is active transport of glucose via SGLUT1 and SGLUT2 sodium co-transporters required?

A

Required in the intestine to absorb from the gut lumen and in the kidney to reabsorb from the filtrate.

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34
Q

What sites are GLUT-2 transporters expressed?

A

Liver, pancreatic beta cell, small intestine, kidney.

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35
Q

What sites are GLUT-4 transporters expressed?

A

Skeletal and cardiac

muscle, adipocytes

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36
Q

What sites are GLUT-3 transporters expressed?

A

Brain, placenta, testes.

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37
Q

What sites are GLUT-5 transporters expressed?

A

Small intestine, sperm

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38
Q

Where are GLUT-1 receptors located?

A

Everywhere

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39
Q

What 2 things stimulates GLUT-4 translocation in muscle and adipose tissue?

A

Insulin binding to it’s receptor on muscle cells or adipocytes.
In muscle cells, exercise. (independent of insulin)

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40
Q

What are the 5 fates of glucose within a cell?

A 
Production of ATP
Glycogenesis 
Storage of lipid
Synthesis of pentoses (for DNA/RNA)
Synthesis of glycolipids and glycoproteins
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41
Q

What is the first step that glucose has to undergo in a cell for every potential fate?

A

Phosphorylation to glucose-6-phosphate by hexokinases I-IV.

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42
Q

Where is glucokinase (hexokinase IV) expressed?

A

In the pancreatic beta-cells and the liver.

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43
Q

What is the committed step for glycolysis?

A

Phosphofructokinase-1

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44
Q

What is the net gain of ATP in respiration?

A

36 ATP

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45
Q

What is the net gain of ATP in glycolysis?

A

2 ATP

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46
Q

What enzyme is required for the final step of glycogenesis?

A

Glycogen synthase

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47
Q

What enzyme is required to change glygogen back into glucose-1-phosphate in glycogenolysis?

A

Glycogen phosphorylase

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48
Q

Define gluconeogenesis.

A

The synthesis of glucose from a

non-carbohydrate source, i.e. lactate, pyruvate, glycerol, certain amino acids (NOT fatty acids)

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49
Q

Where does gluconeogenesis occur?

A

Mainly in the liver, kidney with prolonged starvation.

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50
Q

What enzymes are required for gluconeogenesis?

A

PEPCK
Fructose 1,6 bisphosphatase
Glucose-6-phosphatase

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51
Q

What hormones stimulate gluconeogenesis?

A

Glucagon, adrenaline

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52
Q

What are the actions of insulin?

A

Glycogen synthesis in the liver.
Glycogen synthesis in the muscle.
Uptake of glucose by muscle and adipose tissue.
Synthesis of fatty acids and triglycerides.
Inhibition of gluconeogenesis and glycogenolysis and lipolysis.

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53
Q

What are the actions of glucagon?

A

Glycogenolysis in the liver.

Gluconeogenesis in the liver.

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54
Q

Define type 2 diabetes mellitus.

A

A progressive disorder defined by deficits in insulin secretion and action that leads to hyperglycaemia that is less marked than in type 1 diabetes.

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55
Q

What are the risk factors for developing type 2 DM?

A 
Obesity
Increasing age
Family history
History of gestational diabetes
Physical inactivity 
Hypertension
Dyslipidaemia 
South Asian/Afro-Caribbean ethnicity 
Known CV disease
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56
Q

What symptoms may a patient with type 2 DM present with?

A 
Polydipsia
Polyuria
Blurred vision
Fatigue
Weight Loss (less extreme because of obesity)
Polyphagia (excessive hunger)
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57
Q

Describe the macrovascular complications of type 2 DM.

A

Diabetes is a risk factor for developing atherosclerosis and therefore increases risk of:
MI
Stroke
Gangrene

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58
Q

How should CV risk factors in diabetes mellitus be targeted?

A 
Glucose lowering therapy
Hypertension treatment
Smoking cessation
Lipid therapy
Aspirin
Weight loss 
Reduced alcohol intake
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59
Q

Describe the pathophysiology of T2DM.

A

Liver, muscle and adipose tissue become insensitive to insulin, associated with obesity - adipokines: leptin, adiponectin, TNF- α, resistin.
Impaired insulin secretion due to hyperglycaemia (glucose toxicity) and amylin infiltration of β-cells, glucokinase defects and pancreatic beta cell transcription factor mutations.

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60
Q

List the drugs used to treat T2DM and state their mechanism of action.

A

Metformin – inhibits G6Pase and PEPCK so reduces rate of gluconeogenesis
Sulphonylureas – act on beta cells, promote insulin secretion
SGLT2 inhibitors – reduce reabsorption of glucose
Proglitazone – reduces insulin resistance
GLP-1 agonists – increase insulin secretion, decrease glucagon secretion
DPP-4 inhibitors – they inhibit the inactivation of GLP-1 which increases insulin secretion

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61
Q

What are the 3 steps in the disease progression of T2DM?

A
  1. Insulin resistance
  2. Hyperinsulinemia
  3. Hyperglycaemia
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62
Q

What is the pathophysiology of microvascular disease?

A

Capillary damage - thickening and damage to vessel walls leading to leakage of albumin and other proteins.
Metabolic damage - nerve, kidney and retina do not need insulin to take up glucose, excess glucose enters pylol pathway > reactive oxygen species builds up.

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63
Q

What are some of the early and late stage features of diabetic retinopathy?

A 
Early -
Damage to small vessel wall
Micro-aneurysms 
Dot haemorrhages
Hard exudates – yellowy spots
Cotton wool spots

Late -
Neovascularisation
Vitreous haemorrhage
Macular oedema

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64
Q

How is diabetic retinopathy prevented and treated?

A 
Prevention:
Glycaemic control
Stop smoking
Blood pressure control
Retinal screening 
Treatment:
Address risk factors
Ophthalmic review -
Laser
VEGF inhibitors 
Vitrectomy
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65
Q

What are the early and late stages of diabetic nephropathy?

A 
Early steps:
Renal hypertrophy, increase in GFR
Afferent arteriole vasodilates – leads to increased glomerular pressure, thickened GBM, capillary damage, endothelial cell stress
End result = leakage of protein into urine (microalbuminuria) 
Later steps:
Progressive glomerulosclerosis 
Glomeruli destroyed 
Progressive proteinuria 
Renal failure
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66
Q

How is diabetic nephropathy prevented and treated?

A

 Screen for microalbuminuria every year from diagnosis
 ACE inhibitor or Angiotensin II receptor blocker – if microalbuminuria present. Helps prevent progression of macroalbuminuria
 Aggressive CV risk reduction
 Improve glycaemic control
 Refer to renal clinic

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67
Q

Name some of the different forms of diabetic neuropathy.

A

Peripheral (sensory) neuropathy
Autonomic neuropathy
Mononeuritis multiplex
Diabetic amyotrophy

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68
Q

What changes occur in diabetic neuropathy?

A

Sorbitol accumulation
Capillary damage and occlusion of vasa nervorum
Axonal degradation due to ischaemia

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69
Q

What are some of the signs and symptoms of diabetic neuropathy?

A

Loss of feeling
Tingling
Aching/burning/lancinating pain
Diminished vibratory perception
Decreased knee and ankle reflexes
Reduced protective sensations i.e. pressure, pain, temperature
Diminished proprioception of feet and toes

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70
Q

What forms of lipid can you get in the diet?

A

Triglycerides, cholesterol and phospholipids

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71
Q

What is the structure of triglyceride?

A

Glycerol + three fatty acids attached on with ester bonds.

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72
Q

Describe the process of lipid digestion.

A

Occurs in the small intestine, large lipid droplets are emulsified into smaller droplets with bile salts, smaller lipid droplets broken down with bile salts, pancreatic lipase and colipase to form water soluble micelles of FA and MAG.

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73
Q

Describe the process of lipid absorption.

A
  1. Micelles absorbed into intestinal cell and TAG reformed.
  2. TAG packaged with cholesterol. lipoprotein and other lipids to form chylomicrons
  3. Chylomicrons released into lymphatic system by exocytosis.
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74
Q

What is the function of lipoprotein lipase?

A

Hydrolyses the triglyceride component of lipoproteins i.e. chylomicrons

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75
Q

Fat metabolism: how do TAG and FAs get into the plasma and how do they get out?

A

In: fatty acid synthesis, dietary lipids, TAG from adipose tissue.
out: formation of ketone bodies, phospholipids, TAG in adipose tissue, β-Oxidation

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76
Q

What enzyme is required for breakdown of triglyceride (lipolysis)?

A

Hormone sensitive lipase

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77
Q

What are the effects of insulin and noradrenaline/adrenaline on lipid metabolism?

A

Insulin: stimulates FA synthesis, TAG synthesis, suppresses lipolysis.
Nor(adrenaline): stimulates lipolysis.

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78
Q

Explain the potential effect of elevated FA (lipotoxicity)?

A

Impaired insulin action, hyperglycaemia and T2DM.

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79
Q

Name some DPP-4 inhibitors.

A

Sitagliptin, vildagliptin

80
Q

Name some GLP-1 receptor agonists.

A

Exenatide, liraglutide.

81
Q

In normal renal glucose handling, what percent of glucose is reabsorbed by SGLT2?

A

90%

82
Q

Name some SGLT2 inhibitors.

A

Dapagliflozin

Canagliflozin

83
Q

What would you expect to find in the blood in DKA RE pH, bicarb levels, glucose levels?

A

Metabolic acidosis (<7.3)
Low bicarbonate
Hyperglycaemia

84
Q

What are the main features of diabetic ketoacidosis?

A

Hyperglycaemia
Dehydration
Ketoacidosis
Potassium depletion

85
Q

Explain why ketone levels increase and pH decreases in DKA?

A

Insulin deficiency promotes lipolysis and a product of the process is ketones. Increased ketones causes the pH to become more acidic.

86
Q

In DKA are the levels of the following compounds high or low: Hydrogen ion, bicarbonate, CO2?

A

H+ - high
Bicarb - low
CO2 - low (due to respiratory compensation.)

87
Q

Is DKA a metabolic or a respiratory acidosis?

A

Metabolic acidosis.

88
Q

Adrenaline, cortisol and growth hormone counter the action of insulin. How do they work?

A

Promote gluconeogenesis, lipolysis, glycogenolysis inhibition of peripheral glucose uptake.

89
Q

How is DKA treated?

A

IV fluid, IV insulin (+10% dextrose if BM<14), IV potassium.
Supportive treatment i.e. NG tube, antiemetics, precipitating causes.

90
Q

What is Hyperosmolar hyperglycaemic state (HHS)?

A

Complication of type 2 diabetes where hyperglycaemia results in high osmolarity without significant ketoacidosis.

91
Q

What conditions does HHS make you at risk of?

A

Central pontine mylinolysis and cerebral

oedema due to large fluid shifts

92
Q

HHS treatment is very similar to the treatment of DKA. How does it differ?

A

IV fluid replacement should be slow and steady.
Plasma glucose will fall with fluid alone, IV insulin starts when plasma glucose stable. Less aggressive replacement of potassium required as the shift is less pronounced than in DKA.

93
Q

What supportive treatments are used in HHS?

A

Anticoagulants because venous thrombosis common.

94
Q

What is the difference between DKA and HHS?

A 
DKA:
• Short history
• Patient <65y, usually
type 1 DM
• No residual insulin
• Hyperglycaemia
• Dehydration
• Acidosis
• Patient usually alert
HHS:
• Insidious history
• Patient >65y, usually
type 2 DM
• Residual insulin
• Profound
hyperglycaemia
• Significant
dehydration and
hypernatraemia
• No acidosis
• Patient often drowsy
95
Q

Describe the microstructure of the thyroid gland.

A

Made up of follicles consisting of a single layer of cells surrounding a lumen filled with colloid.

96
Q

Describe how thyroid hormones are synthesised in the thyroid gland.

A
  1. Iodide is transported into follicular cells via the sodium-iodide transported which is TSH dependent.
  2. Iodine moves to apical surface and transported into follicular lumen via prendrin.
  3. Enzyme peroxidase oxidises iodide into iodine.
  4. Iodine binds on to tyrosine groups on thyroglobulin to form MIT and DIT.
  5. Two DITs fuse together to form T4 and one MIT and one DIT fuse together to form T3.
  6. The hormones are taken back into follicular cells via pinocytosis and lysosomes free them from thyroglobulin.
  7. T3 and T4 diffuse across basement membrane into blood stream.
97
Q

How are thyroid hormones transported in the bloodstream? Why do they need to be bound?

A

Bound to thyroid binding globulins (TBGs)/albumin/transthyretin. Because they are lipid and so cannot travel freely in the bloodstream.

98
Q

Which of T3 or T4 is secreted in greater quantities by the thyroid? Which is more active? What happens to T4 when it reaches the target tissues?

A

T4 is secreted in greater quantities. T3 is more active. T4 is converted to T3 at the target tissues in a process called 5’deiodination.

99
Q

What proportion of thyroid hormones are free and bound?

A
  1. 5% bound

0. 5% free

100
Q

Describe how thyroid hormone production is regulated with a negative feedback loop.

A

TRH produced by the hypothalamus. TRH stimulated the anterior pituitary gland to produce TSH. TSH stimulates the thyroid gland to produce T3 and T4. T3 and T4 inhibit the production of TRH and TSH.

101
Q

What is the effect of T3 and T4 on body tissues?

A

Increases basal metabolic rate. Produces heat. Promotes energy production by increasing the number of mitochondria.
Important for growth and development in children.
Increases heart rate, bone turnover, lipid and glucose consumption, sensitivity to catecholamines, brain development.

102
Q

How do thyroid hormones act on their target tissues?

A

Thyroid hormones are hydrophobic so act so can diffuse through the cell membranes of target tissues. Thyroid hormone receptors are nuclear (found within the nucleus) and when bound can cause gene transcription.

103
Q

What is the clinical condition of a patient with low TSH and low T4?

A

Secondary hypothyroid

104
Q

What is the clincal condition of a patient with high TSH and low T4?

A

Primary hypothyroid.

105
Q

What is the clinical condition of a patient with low TSH and high T4?

A

Primary hyperthyroid

106
Q

What is the clinical condition of a patient with normal to mildly low TSH and T3 proportionally lower than T4?

A

Sick euthyroid

107
Q

Define hyperthyroidism and list its causes.

A 
Excess thyroid hormone. 
Causes:
Autoimmune: grave's disease
Toxic adenoma
Multi-nodular goitre 
Thyroiditis
Excess administration of thyroxine.
108
Q

What are the clinical manifestations of thyrotoxicosis (excess thyroid hormone for any reason)?

A 
Weight loss
Tremor
Palpitations
Tachycardia 
Hypertension
Sweating 
Diarrhoea 
Heat intolerance
109
Q

Describe some symptoms specific to grave’s disease.

A

Dysthyroid eye disease - proptosis (bulging eyes), lid retraction, periorbital oedema, diplopia (double vision).

Dermopathy - pretibial myxoedema (orange peel skin) and thryoid acropachy (soft tissue swelling of hands and finger clubbing).

110
Q

What are the treatment options for thyrotoxicosis?

A

Thiamides - carbimazole, propylthiouracil
Beta blockers - only treat symptoms, don’t lower hormone levels.
Radioiodine therapy
Surgery - removal of all or part of the thyroid gland.

111
Q

How does radioiodine therapy on the thyroid work and what are the short and long term consequences?

A

Destroys thyroid tissue by beta emisson. Short term consequences - must be isolated for 3 weeks after treatment, may worsen eye disease, can’t conceive for at least 4 months.
Long term - potential hypothyroidism in the future.

112
Q

What risks are associated with thyroid surgery?

A

Haemorrhage, recurrent laryngeal nerve palsy, hypothyroidism, hypoalcaemia.

113
Q

What are the clinical manifestations of hypothyroidism?

A 
Weight gain
Bradycardia
Lethargy
Tiredness
Dry skin
Depression
menorrhagia - abnormally heavy menstrual bleeding
Cold intolerance
Possible goitre
114
Q

What are some of the causes of hypothyroidism?

A 
Autoimmune: Hashimoto's
Thyroiditis
Thyroidectomy
Following radioiodine therapy
Drug induced - lithium, sunitib
Severe iodine deficiency 
Pituitary disease - secondary
115
Q

How is hypothyroidism treated?

A

Levothyroxine 1.7-2.0mg/kg/day
Best taken on an empty stomach
Start slowly in elderly and in those with cardiac disease
Avoid taking with PPIs, ferrous sulphate or calcium.

116
Q

Describe how grave’s disease caused thyrotoxicosis.

A

Auto-antibodies bind to the TSH receptor and overstimulate the production of T3 and T4. The autoantibodies are long acting - they stay bound to the receptor and continually cause production of thyroid hormones.

117
Q

Describe how Hashimoto’s disease causes hypothyroidism.

A

Anti-TPO antibodies destroys thyroid gland. Lymphoid infiltration of the gland with eventual atrophy and fibrosis.

118
Q

What percentage of men and women in the population are affected by thyroid disease?

A

Women: 5%
Men: 0.5 %

119
Q

How is thyroid disease investigated?

A

Measure:
Free T4
TSH

120
Q

What hormones are produced by the hypothalamus that go on to stimulate the pituitary?

A 
Growth hormone releasing hormone (GHRH)
Gonadotrophin releasing hormone (GRH)
Cortiotrophic releasing hormone (CRH)
Thyroid releasing hormone (TRH)
Dopamine
121
Q

What hormones are produced by the pituitary after being stimulated by hypothalamic hormones?

A 
Growth hormone
FSH/LH
Adrenocorticotrophic hormone
Thyroid stimulating hormone (TSH)
Prolactin
122
Q

Describe the growth hormone axis.

A

Growth hormone negatively feeds back to both the anterior pituitary and the hypothalamus.
IGF-1 negatively feeds back to the anterior pituitary and the hypothalamus.
Stress, exercise, sleep, hypoglycaemia all positively feed back to the hypothalamus.

123
Q

Describe the hypothalamic-pituitary-adrenal axis.

A

Time of day, illness and stress stimulate the hypothalamus to produce CRH, this stimulates the anterior pituitary to produce ACTH which acts on the adrenal cortex to produce cortisol and androgens. Cortisol and androgens feed back negatively to the hypothalamus and pituitary.

124
Q

Describe the hypothalamic-pituitary-gonadal axis in males.

A

GnRH produced by hypothalamus which acts on the pituitary to produce LH and FSH. LH acts on Leydig cells in testes to produce testosterone. FSH works on Sertoli cells in testes to produce inhibin. Testosterone and inhibin both negatively feedback the pituitary and the hypothalamus. Testosterone positively feed backs to the sertoli cells.

125
Q

Describe the hypothalamic-pituitary-gonadal axis in females.

A

GnRH produced by hypothalamus which acts on the pituitary to produce LH and FSH which act on the ovary to produce oestradiol, progesterone and inhibin. Inhibin negatively feeds back to the hypothalamus and pituitary, oestradiol and progesterone positively and negatively feedback to the hypothalamus and pituitary.

126
Q

Describe the lactotroph axis.

A

Hypothalamus produces dopamine which suppresses the anterior pituitary’s production of prolactin. Oestrogen stimulates the anterior pituitary to produce prolactin.

127
Q

What does the posterior pituitary produce?

A

ADH, oxytocin.

128
Q

What is the role of oxytocin?

A

Important in labour and breast feeding.

Stimulates cervical dilatation and uterine contractions. Let down reflex in mammary glands, stimulated by suckling.

129
Q

Name some clinical disorders of the pituitary gland.

A

Diabetes insipidus - lack of ADH produced by posterior pituitary.
Pituitary tumours
Anterior pituitary hormone excess.
Hypopituitarism

130
Q

How does ADH work?

A

Binds to AVPR2 receptor on the basolateral membrane of kindey collecting ducts, inserts aquaporin channels and increased renal water reabsorption.

131
Q

What are the clinical features of diabetes insipidus (DI)?

A

Polyuria, polydipsia, nocturia, passage of large volumes>3L/day of dilute urine.

132
Q

What are the causes of diabetes insipidus (DI)?

A 
Cranial: ADH deficiency - idopathic, genetic, trauma, tumours, infections, inflammatory conditions of posterior pituitary. 
Nephrogenic:
ADH resistance
Genetic (AVPR2 mutation)
Secondary to drugs, renal disease.
133
Q

How is DI diagnosed?

A

Water deprivation test: deprive patients of fluid for 8h, measure plasma and urine osmolality every 2-4h. Then give synthetic ADH and reassess urine osmolality. With cranial DI osmolality should go up with synthetic ADH, with nephrogenic DI, ADH should have no effect on urine osmolality.

134
Q

How is DI treated?

A

Cranial - Desmopressin (synthetic ADH), monitor plasma and urine osmolality, can be given nasally, orally, with injection.
Nephrogenic - treat underlying cause, high doses of desmopressin.

135
Q

How would you manage a prolactinoma?

A

Dopamine agonists or surgery if the tumour is large and affects vision.

136
Q

How would you diagnose acromegaly?

A

Glucose tolerance test
IGF-1 level
Pituitary MRI

137
Q

How would you treat acromegaly?

A

Surgery
Medical therapy - somatostatin analogues to suppress GH secretion.
Radiotherapy

138
Q

What is hypopituitarism? How is it treated?

A

A failure of the anterior pituitary gland function affecting all the axis or just one.
Replacement of all hormones, cortisol firstly.

139
Q

Any drugs affecting dopamine can cause hyperprolactinaemia (abnormally high levels of prolactin). Give examples of such drugs.

A 
Antipsychotics
Antiemetics
Antidepressants 
Opiates
H2 receptor agonists
140
Q

How would you treat a hyperprolactinaemia?

A

First line dopamine agonists i.e. cabergoline

Surgery if tumour is large and affecting vision

141
Q

What are the different ADH receptors in the body and where are they found?

A

AVPR1A - found in vascular smooth muscle, cause vasoconstriction
AVPR2 - found in kidney tubules, cause reabsorption of water.

142
Q

How is desmopressin (the ADH analogue) different to ADH itself?

A

It only acts on the kidney tubules, not the vasular smooth muscle and it has a longer half-life.

143
Q

How is cortisol produced?

A

In response to ACTH binding to its G-protein coupled receptor, there is an increase in cAMP, activation of PKA and influx of Ca2+. This causes rapid cholesterol delivery to mitochondria and switching on of genes for steroidogenic enzymes. Cortisol is produced as a result.

144
Q

What are the physiological effects of cortisol?

A 
Oppose the action of insulin, increases blood glucose. 
Gluconeogenesis
Lipolysis in adipose tissue
Glycogenolysis
Glycogen synthesis in late fasting
Breakdown of skeletal muscle protein
Immune suppression
Memory, learning, mood
145
Q

How is aldosterone produced?

A

Produced in the zona glomerulosa, catalysed by aldosterone synthase. Produced in response to low blood volume, increased levels of plasma angiotensin II, increased extracellular K+.

146
Q

What are the actions of aldosterone?

A

Acts in the distal kidney tubule and collecting duct. Causes upregulation of Na/K+ pumps on the basolateral surface. Causes recruitment of ENaC transporters in the apical membrane, increasing sodium and water reabsorption and potassium excretion. These things increase blood volume and pressure.

147
Q

What different tests can be used to diagnose adrenal insufficiency?

A
  1. Suspicious biochemistry - Low Na+, high K+, hypoglycaemia
  2. Short synACTHen test:
    Measure cortisol levels before and 30 minutes after an IV ACTH injection. Normal: baseline >250nmol/L, post injection >480 nmol/L.
  3. ACTH levels - should be increased, causes skin pigmentation
  4. Renin/aldosterone levels - should be increased renin, decreased aldosterone
  5. Adrenal autoantibodies
148
Q

What different tests can be used to diagnose cortisol excess?

A
  1. Dexamethasone suppression testing - dexamethasone reduces ACTH production and therefore cortisol production by negative feedback. It should render cortisol undetectable unless you have cortisol excess.
  2. 24 hour urinary cortisol
  3. Late night salivary cortisol
149
Q

How do you distinguish between endogenous and iatriogenic cortisol excess?

A

Endogenous - increased urinary and plasma cortisol.

Iatriogenic - decreased urinary and plasma cortisol.

150
Q

What is the difference between primary and secondary adrenal insufficiency?

A

Primary is a failure of the adrenal cortex, secondary is a failure of the pituitary gland.
With secondary adrenal insufficiency, no skin pigmentation due to ACTH and aldosterone production remains in tact.

151
Q

What are some of the causes of primary adrenal insufficiency?

A

Addison’s disease (autoimmune)
Adrenal TB/malignancy
Congenital adrenal hyperplasia

152
Q

What are some of the causes of secondary adrenal insufficiency?

A

Due to lack of ACTH stimulation
Pituitary/hypothalamic disorders
Iatriogenic (due to excess steroid use.)

153
Q

What are the clinical features of addison’s disease?

A 
Weight loss
Fatigue
Dizziness
Low blood pressure
Vomiting, diarrhoea, abdominal pain
Skin pigmentation
154
Q

How is adrenal insufficiency managed?

A

Hydrocortisone tablets to replace cortisol

Fludrocortisone to replace aldosterone

155
Q

What measures should be taken to ensure the safety of patient’s on long term steroid therapy?

A

Education about sick day rules when steroid doses should be increased.
Carrying steroid treatment card to show to health care providers.
Wearing identification as someone who has adrenal insufficiency and is on steroid treatment.

156
Q

What are the clinical features of Cushing’s syndrome?

A 
Buffalo hump
Hypertension
Thin skin
Thin arms and legs
Increase in abdominal fat
Striae 
Easy bruising
Poor wound healing
Moon face
Facial plethora
157
Q

What are the different causes of ACTH dependent and ACTH independent Cushing’s syndrome?

A 
ACTH dependent:
Pituitary adenoma - Cushing's disease 
Ectopic ACTH
Ectopic CRH 
ACTH independent:
Long term glucocorticoid treatment 
Adrenal adenoma 
Adrenal carcinoma 
Nodular hyperplasia
158
Q

How is cortisol excess managed?

A 
Surgery:
Transsphenoidal pituitary surgery
Laparoscopic adrenalectomy 
removal of ACTH source
Medical:
Metyrapone/ketoconazole - inhibit cortisol production.
159
Q

What is congenital adrenal hyperplasia?

A

An autosomal recessive condition where there is a lack of 21-hydroxylase activity leading to a deficiency in cortisol, aldosterone and an increase in adrenal androgens.

160
Q

What other autoimmune conditions are associated with Addison’s disease?

A

T1DM, pernicious anaemia, autoimmune thyroid disease.

161
Q

What conditions could require long term steroid use?

A

Asthma, rheumatoid arthritis, IBS, transplants.

162
Q

What is the most common cause of cortisol excess?

A

Iatriogenic cushing’s syndrome - caused by prolonged high dose steroid use.

163
Q

What is the potential long term effect of prolonged steroid use?

A

Chronic suppression of ACTH production leads to adrenal atrophy and cortisol insufficiency. Must not be taken off steroids suddenly but gradual withdrawal if have been on them for 4-6 weeks.

164
Q

What are the clinical features of primary aldosteronism?

A

Significant hypertension, hypokalaemia, alkalosis

165
Q

What are the causes of primary aldosteronism?

A

Adrenal adenoma or bilateral adrenal nodules.

166
Q

What tests can be done to diagnose primary aldosteronism?

A

Biochemistry - elevated aldosterone and lowered renin.
Suppression testing - IV saline load
Adrenal CT

167
Q

How is primary aldosteronism treated?

A

If adrenal adenoma - unilateral laparoscopic adrenalectomy
If bilateral adrenal hyperplasia - mineralocorticoid receptor antagonists i.e. spironolactone. Or amiloride, blocks Na reabsorption from the kidney.

168
Q

What is a phaeochromocytoma?

A

A rare tumour of the medulla of the adrenals causing excess catecholamines.

169
Q

What type of cells is the adrenal medulla made up of?

A

Chromaffin cells.

170
Q

What are all steroid hormones derived from?

A

Cholesterol

171
Q

What is the rate limiting step in the production of cholesterol?

A

HMG-CoA reductase

172
Q

ADH is produced in response to…

A

Decreased plasma volume - sensed by baroreceptors in the atria, carotids and veins
Increased plasma osmolality - sensed by osmoreceptors in the hypothalamus

173
Q

Apart from ADH production, what mechanism increases blood water concentration.

A

Thirst

174
Q

Briefly describe how the RAAS system works to increase blood volume.

A

Renin produced by JGA in kidney in response to reduced blood volume. Renin converts angiotensinogen from the liver into angiotensin I, ACE converted angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction, aldosterone release, ADH secretion, stimulates activity of Na+/H+ exchanger, increasing sodium and water reabsorption.

175
Q

What level of serum sodium is considered hyponatraemia?

A

Serum sodium<135mmol/L

176
Q

Name some of the causes of hypovolaemic hyponatraemia.

A 
Renal loss:
Diuretic excess
Aldosterone deficiency
Salt losing nephritis 
Renal tubular acidosis
Extrarenal loss:
Vomiting
Diarrhoea 
Third degree burns
177
Q

Name some of the causes of euvolaemic hyponatraemia?

A 
Glucocorticoid deficiency
Hypothyroidism 
Pain
Psychiatric disorders
Drugs
Syndrome of inappropriate ADH secretion
178
Q

Name some of the causes of hypervolaemic hyponatraemia?

A

Nephrotic syndrome
Cardiac failure
Cirrhosis
Acute and chronic renal failure

179
Q

Syndrome of inappropriate ADH (SIADH) is the commonest cause of low plasma sodium; it is due to increased body water. What causes it?

A

Cancer - lung/lymphoma/leukaemia
Chest disease - pneumonia
CNS disorders - infection, injury
Drugs - opiates, thiazides, anti-convulsants, PPIs, anti-depressants.

180
Q

How is SIADH diagnosed?

A

Hyponatraemia with low inappropriate plasma osmolality
Urine osmolality>plasma osmolality
Urine sodium>20mmol/L
No pituitary, thyroid, adrenal or renal insufficiency.
No recent diuretic use.

181
Q

What conditions of the brain can be caused by a sudden decrease in sodium and a sudden increase in sodium?

A

Increase? - Cerebral oedema

Decrease? - osmotic demyelination syndrome

182
Q

What are the worsening clinical features of hyponatraemia as plasma Na falls?

A 
Often asymptomatic
Mild confusion
Gait instability
Marked confusion
Drowsiness
Seizures
183
Q

How is severe and acute hyponatraemia managed differently to less severe/chronic hyponatraemia?

A

Severe and acute (unconscious or seizures) - give infusion of hypertonic (3%) saline. Can increase quickly.
Less severe/chronic -
Try to establish cause, usually fluid restriction is correct management, increase slowly. 2nd line can consider AVPR2 antagonists (vaptans)

184
Q

Hypernatraemia is usually due to dehydration. What are the main causes?

A

Severe burns or sepsis - sweating and insensible loss
GI loss
Diabetes insipidus
Osmotic diuresis due to hyperglycaemia

185
Q

How is hypernatraemia managed?

A

Treat underlying cause, try to estimate total body water deficit to guide fluid regime. Avoid rapid correction - aim for a decrease in sodium of 10mmol/L in 24 hours. Concern is cerebral oedema. Use IV 5% dextrose.

186
Q

Where are the sources of calcium in the body?

A

GI tract - absorbed throughout small intestine from dietary sources. Vit D dependent.
Bones - calcium reservoir, plasma calcium altered via osteoblasts and osteoclasts.
Kidney - free Ca filtered by glomerulus, 97-99% reabsorbed.

187
Q

What effect does vitamin D (calcitriol) have on calcium homeostasis?

A

Increases GI absorption
Increases bone resorption
Increases renal reabsorption

188
Q

What effect does parathyroid hormone have on calcium metabolism?

A

Increase in plasma calcium concentration concentration.
Bone resorption leads to release of calcium into plasma, increased calcium reabsorption in kidney, increased calcitriol formation leading to increased GI absorption.

189
Q

What effect does parathyroid hormone have on phosphate metabolism?

A

Bone resorption leading to release of phosphate into plasma, increased phosphate excretion in the kidney. Net effect: no change or decrease in phosphate.

190
Q

What percentage of circulating calcium is free and what percentage is bound?

A

55% bound to albumin or other substances

45% free

191
Q

What are the clinical features of hypercalcaemia?

A

Polyuria, polydipsia, nephrolithiasis, anorexia, nausea, vomiting, constipation, pancreatitis, muscle weakness, bone pain, osteoporosis, confusion, fatigue, coma.

192
Q

What ECG changes are present in hypercalcaemia?

A

Shortened QTc interval

Bradycardia

193
Q

What are the causes of hypercalcaemia?

A

Primary hyperparathyroidism - usually due to adenoma
Malignancy -
Breast, lung or multiple myeloma or bone metastases.
If PTH low then malignancy likely. If high or normal, primary hyperparathyroidism.

194
Q

How is hypercalcaemia managed?

A

For mild, treat hypovolamia with isotonic (0.9%) saline infusion.
Bisphosphonates - Zolendronic acid, used in malignancy.
Calcitonin
Glucocorticoids
Parathyroidectomy

195
Q

What are the symptoms of acute hypocalcaemia?

A

Tetany - increased neuromuscular excitability, peri-oral numbness, muscle cramps, tingling of hands/feet. If severe: carpopedal spasm, layngospasm, seizures.
Cardiac complications - dysrhythmia, hypotension.

196
Q

What are the causes of hypocalcaemia?

A 
Low PTH - following parathyroid surgery, autoimmune hypoparathyroidism.
High PTH - 
Vit D deficiency
Chronic renal failure
Drugs
Hypomagnesaemia
197
Q

How is hypocalcaemia treated?

A 
IV calcium replacement if tetany or cardiac manifestations 
May also need magnesium infusion 
Chronic management:
Vit D 
Oral calcium salts

Year 2 Revision (15 decks)

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