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Phase 2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Why is type 2 diabetes a public health issue?

A
  • Preventable and increasing prevelance
  • Common cause of mortality, disability, co-morbidity, reduced quality of life
  • Major inequalities in prevelence and outcomes including BME communities and poorer outcomes
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2
Q

What are the 4 steps to reduce the impact of type 2 diabetes?

A
  1. Identifying people at risk
  2. Preventing diabetes
  3. Diagnosing diabetes earlier
  4. Effective management and supporting self management
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3
Q

Who is at risk of diabetes?

A
  • Everyone due to obesogenic environment
  • Sedentary job, sedentary leisure activities
  • Diet high in calorie dense foods/ low in fruit and veg, pulses and wholegrains
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4
Q

What are the factors of the obesogenic environment?

A
  • Physical environment e.g. TV remote controls, lifts, car culture
  • Economic environment e.g. Cheap TV watching, expensive fruit and veg
  • Sociocultural environment e.g. safety fears, family eating patterns
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5
Q

List some mechanisms that maintain obesity

A
  • Physical/psychological- more weight= more difficult to exercise
  • Psychological- Low self esteem and guilt, comfort eating
  • Socioeconomic= Reduced opportunities, employment, relationships
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6
Q

Who is at risk of type 2 diabetes?

A
  • Age, sex, ethnicity, family history
  • Weight, BMI, waist circumference
  • History of gestational diabetes
  • Hypertension or vascular disease
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7
Q

How is diabetes/ pre-diabetes tested for?

A
  • HbA1c
  • Random capillary blood glucose
  • Random venous blood glucose
  • Fasting venous blood glucose
  • Oral glucose golerance test
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8
Q

What is the diagnostic threshold for diabetes?

A

FBG ≥ 7.0 OR 2 hr Glu ≥ 11.1 mmol/l

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9
Q

List some methods of preventing diabetes

A

Sustained increase in physical activity
Sustained change in diet
Sustained weight loss

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10
Q

When is diabetes screened for?

A
  • Screening as part of NHS health check
  • Screening as part of CHD prevention
  • Screening at review of hypertension management
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11
Q

List some methods of self-care for diabetes

A

Self monitoring
Diet- Support for changing eating patterns
Exercise- Support for increasing physical activity
Drugs- Support for taking medication
Education- Professionals/ expert patients
Peer support

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12
Q

What is the difference between endocrine and exocrine glands?

A

Endocrine glands pour secretions directly into the bloodstream, whereas exocrine glands use ducts

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13
Q

Where do endocrine hormones act?

A
  • Blood borne= Act at distant sites
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14
Q

Where do paracrine hormones act?

A
  • Act on nearby adjacent cells
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15
Q

Where do autocrine hormones act?

A
  • Feedback on same cell that secreted hormone (acts on itself)
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16
Q

Describe the properties of water-soluble hormones

A
  • Transported unbound
  • Bind to surface receptors on cell
  • Short half life
  • Cleared fast
  • Often stored in vesicles
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17
Q

Describe the properties of fat-soluble hormones

A
  • Transported bound to protein
  • Diffuse into cells
  • Have a long half-life
  • Are cleared slowly
  • Often synthesised on demand (e.g. Steroids)
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18
Q

What are the classes of hormones?

A
  • Peptides
  • Amines
  • Iodothyronines
  • Cholesterol derivatives and steroids
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19
Q

What is the difference between an endocrine gland and an exocrine gland?

A

Endocrine glands secrete substances/hormones directly into the bloodstream
Exocrine glands secrete substances/hormones into a duct before they enter the bloodstream

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20
Q

Acromegaly is the result of an overproduction of which pituitary hormone?

A

Growth Hormone

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21
Q

Adrenal insufficiency can be divided into primary insufficiency and secondary insufficiency, give 2 examples of each.

A

Primary: Addison’s, Surgical removal, Trauma, TB, Infarction, Invasion from tumour, ACTH resistance/blocking antibodies
Secondary: Steroids, Congenital, Corticiotropin releasing hormone deficiency, Trauma (fracture base of skull), Radiotherapy, Surgery, Neoplasm

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22
Q

Describe 2 investigations appropriate for diagnosing a patient with Cushing’s Disease

A

24hr urine collection

Blood cortisol test following dexamethasone

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23
Q

Explain on a cellular level how hyperglycaemia leads to insulin secretion

A

Hyperglycaemia leads to increase glucose uptake by cells
Glucose metabolism leads to increased levels of ATP within cell
Increased ATP causes K+ channels to close
Causes depolarisation of cell membrane
Ca2+ channels open and Ca2+ enters cell
Increased Ca2+ in cell causes exocytosis of insulin-containing vesicles
Insulin released by Pancreatic Beta cells / cells in Islets of Langerhans

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24
Q

Give 3 blood tests with values that are diagnostic for Diabetes Mellitus

A

Random plasma glucos = Score >11mmol/L
Fasting plasma glucose = Score > 7mmol/L
HbA1c = Score > 48

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25
Q

Give 2 examples of microvascular and macrovascular complications of DM

A 
Microvascular= Retinopathy, Neuropathy 
Macrovascular= CVD, Cerebrovascular disease, Peripheral artery disease
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26
Q

Miranda, 35 year old lady presents to the GP complaining of weight loss, feeling hot all the time, diarrhoea and a tremor. When you examine her pulse is 92 bpm. She has goitre, palmar erythema and bulging eyes.
What condition do you suspect Miranda has?

A

Hyperthyroidism/ Grave’s Disease

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27
Q

Describe the levels of TSH, T3, T4 of a patient with Grave’s disease

A

TSH low, T3 raised, T4 raised

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28
Q

Name the thyroid autoantibodies also found on a patient with Graves disease’s blood test?

A

Thyroglobulin and anti-thyroid peroxidase antibodies

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29
Q

What are 2 treatment options for a patient with Grave’s disease?

A

Carbimazole
Beta Blockers
Radio Iodine therapy
Thyroidectomy

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30
Q

Give 5 signs of a patient with Hashimoto’s Thyroiditis?

A 
Bradycardia 
Reflexes relax slowly 
Ataxia 
Dry/thin hair + skin 
Yawning/drowsiness/coma 
Cold hands 
Ascites 
Round puffy face 
Defeated Demeanour 
Immobile
Round ‘moon’ face
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31
Q

What medication is used to treat hypothyroidism?

A

Synthetic Levothyroxine (T4)

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32
Q

Name the 2 hormones produced by the posterior pituitary gland.

A

Antidiuretic Hormone

Oxytocin

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33
Q

What are the 2 main symptoms of patients with Diabetes Insipidus?

A

Polyuria

Polydipsia

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34
Q

Patient presents with palpitations, headache, episodic sweating. Blood tests reveal raised plasma catecholamines.
What condition does this patient have?

A

Phaeochromocytoma

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35
Q

Which cells produce catecholamines

A

Cromaffin cells

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36
Q

Where are cromaffin cells found?

A

Adrenal medulla

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37
Q

What visual field defect would make you suspect a patient has a pituitary tumour?

A

Bitemporal hemianopia

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38
Q

Where does the anterior pituitary receive blood from?

A

Portal venous circulation of hypothalamus

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39
Q

When does growth hormone release peak?

A

At night

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40
Q

What is synergism?

A

Combined effects of two hormones amplified

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41
Q

Where is the pituitary gland?

A

A pocket of the sphenoid bone in the pituitary fossa.
Sits inferior to optic chiasm. On either side lies the cavernous sinuses
Connected to the hypothalamus via the infundibulum

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42
Q

What are the hormones produced by the anterior pituitary?

A 
TSH
ACTH
FSH
LH
Growth hormone
Prolactin
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43
Q

What are the functions of thyroid hormone?

A

Accelerates food metabolism
Increases protein synthesis
Enhances fat metabolism
Increase in ventilation rate
Increase in cardiac output and heart rate
Brain development during foetal life and postnatal development
Growth rate accelerated

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44
Q

What does the adrenal cortex’s zona glomerulosa produce?

A

Mineralocorticoids e.g. aldosterone

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45
Q

What does the adrenal cortex’s zona fasiculata produce?

A

Glucocorticoids e.g. Cortisol androgens

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46
Q

What does the adrenal cortex’s zona reticularis produce?

A

Androgens e.g. androstenedione and DHEA

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47
Q

What does the adrenal medulla produce?

A

Epinephrine and norepinephrine

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48
Q

What happens as part of the short-term stress response?

A
  • Heart rate increases
  • Blood pressure increases
  • Bronchioles dilate
  • Liver converts glycogen to glucose and releases glucose into blood
  • Metabolic rate increases
  • Blood flow changes (reducing digestive and urinary flow)
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49
Q

What happens as part of the long term stress response?

A
  • Kidney retain sodium and water
  • Blood vol and pressure rise
  • Blood glucose increases
  • Immune system suppressed
  • Proteins and fats are converted to glucose
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50
Q

What hormone acts on leydig cells, and what do they produce?

A
  • LH acts on leydig cells

- Produces testosterone

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51
Q

What hormone acts on sertoli cells, and what do they produce?

A
  • FSH acts on sertoli cells

- Produces androgen-binding protein and inhibin

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52
Q

What are the hypophysiotropic hormones?

A
  • Corticotropin releasing hormone
  • GHRH
  • Thyrotropin releasing hormone
  • Gonadotropin releasing hormone
  • Dopamine
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53
Q

What hormone inhibits release of GHRH?

A

Somatostatin

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54
Q

What hormone inhibits release of prolactin?

A

Dopamine

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55
Q

What is appetite?

A

Desire to eat food

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56
Q

What is satiety?

A

Feeling of fullness- disappearance of appetite after a meal

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57
Q

What is the BMI range for being underweight?

A

<18.5

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58
Q

What is the normal BMI range?

A

18.5-24.9

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59
Q

What is the overweight BMI range?

A

25.0-29.9

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60
Q

What is the obese BMI range?

A

30.0-39.9

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61
Q

What is the morbidly obese BMI range?

A

> 40.0

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62
Q

What hormones/ chemicals/ Factors act to decrease appetite?

A
  • Leptin
  • Insulin
  • POMC
  • CCK
  • Peptide YY
  • GLP
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63
Q

What hormones/ Chemicals/ Factors act to increase appetite?

A
  • Ghrelin

- Olfactory, gustatory, congestive and visual stimuli

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64
Q

What are the actions of cholecystokinin?

A
  • Delays gastric emptying
  • Gall bladder contraction
  • Insulin release
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65
Q

What are the actions of ghrelin?

A
  • Stimulates GH release

- Stimulates appetite

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66
Q

List some complications of obesity?

A
  • Type II diabetes
  • Hypertension
  • Coronary artery disease
  • Stroke
  • Osteoarthritis
  • Obstructive sleep apnoea
  • Carcinoma= Breast, endometrium, prostate, colon
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67
Q

What are the actions of parathyroid hormone?

A
  • Increased Ca2+ reabsorption in the kidney
  • Increased 1 alpha-hydroxylation of 25-OH vitamin D in the kidney
  • Decreased phosphate reabsorption in the kidney
  • Increased bone remodelling
  • Indirectly increases Ca2+ reabsorption in the intestine
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68
Q

What are the consequences of hypocalcaemia?

A 
Paraesthesia
Muscle spasm
Seizures 
Basal ganglia calcification
Cataracts 
ECG abnormalities (long QT)
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69
Q

How do you calculate corrected calcium?

A

Total serum calcium + 0.02 x(40-serum albumin)

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70
Q

What is Chvostek’s sign?

A

Tap over facial nerve and look for spasm of facial muscles

Shown in hypocalcaemia

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71
Q

What is Trousseau’s sign?

A

Inflate the blood pressure cuff to 20mmHg above systolic for 5 mins and it will cause a characteristic spasm of the hand
Shown in hypocalcaemia

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72
Q

What are the causes of hypoparathyroidism?

A
  • Genetics – recessive, dominant, X-linked
  • Autoimmune – isolated, polyglandular type 1
  • Infiltration of the parathyroid glands by iron overload
  • Surgery - parathyroidectomy
  • Radiation
  • Magnesium deficiency
  • Syndrome= Di George, HDR, Kenney-Caffey
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73
Q

What is pseudohypoparathyroidism?

A

Resistance to parathyroid hormone

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74
Q

What are the clinical features of pseudohypoparathyroidism?

A 
Short stature
Obesity 
Round faces
Mild learning difficulties
Short fourth metacarpals
Other hormone resistance
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75
Q

What are the symptoms of hypercalcaemia?

A 
Thirst
Polyuria
Nausea
Constipation
Confusion
Can lead to coma
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76
Q

What are the consequences of hypercalcaemia?

A

Renal stones

ECG abnormalities

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77
Q

What are the causes of hypercalcaemia?

A

Malignancy
Primary hyperparathyroidism
Thiazides
Sarcoidosis

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78
Q

What are the consequences of primary hyperparathyroidism?

A

Bones- Osteitis fibrosa cystica, osteoporosis
Kidney stones
Psychic groans- confusion
Abdominal moans- Constipation, acute pancreatitis

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79
Q

What are the PTH, calcium, and phosphate levels in vit D deficiency?

A 
PTH= High
Calcium= Low
Phosphate= Low
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80
Q

What are the PTH, calcium, and phosphate levels in hypoparathyroidism?

A 
PTH= Low
Calcium= Low
Phosphate= High
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81
Q

What are the PTH, calcium, and phosphate levels in pseudohypoparathyroidism?

A 
PTH= High
Calcium= Low
Phosphate= High
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82
Q

What are the PTH, calcium, and phosphate levels in primary hyperparathyroidism?

A 
PTH= High
Calcium= High
Phosphate= Low
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83
Q

What is diabetes mellitus?

A

Syndrome of chronic hyperglycemia due to relative insulin deficiency, resistance or both.

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84
Q

What are normal parameters for blood glucose?

A

3.5-8.0mmol/L

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85
Q

Why can’t the brain use free fatty acids for energy?

A

FFAs cannot cross the BBB

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86
Q

What are the actions of insulin?

A
  • Decreases glycogenolysis and gluconeogenesis
  • Increases glucose uptake
  • Suppresses lipolysis, and breakdown of muscles
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87
Q

Where is insulin produced?

A

Beta cells of the islets of langerhans

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88
Q

What is C peptide?

A

proinsulin is formed of C peptide and insulin

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89
Q

What does a lack of C peptide in the blood show?

A

That the insulin present in the blood is synthetic not natural

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90
Q

What are the actions of glucagon?

A
  • Increases glycogenolysis and gluconeogenesis
  • Reduces peripheral glucose uptake
  • Stimulates peripheral release of gluconeogenic precursors
  • Stimulates lipolysis and muscle glycogenolysis and breakdown
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91
Q

Where is GLUT-1 and what is its role?

A

Enables basal NON-INSULIN-STIMULATED glucose uptake into many cells

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92
Q

Where is GLUT-2 and what is its role?

A

Found in beta-cells of the pancreas. Transports glucose into the beta-cell - enables these cells to sense glucose levels

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93
Q

Where is GLUT-3 and what is its role?

A

Enables non-insulin-mediated glucose uptake into brain neurons & placenta

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94
Q

Where is GLUT-4 and what is its role?

A

Mediates much of the peripheral action of insulin. It is the channel through which glucose is taken up into muscle and adipose tissue cells following stimulation of the insulin receptor.

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95
Q

List some conditions which diabetes can be secondary to

A

Pancreatic= Pancreatectomy, chronic pancreatitis, haemochromatosis
Endocrine= Acromegaly and Cushing’s disease
Drug induced

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96
Q

Briefly explain the GH, IGF-1 axis

A

GHRH is produced by the hypothalamus, which causes the pituitary to release more GH. GH triggers the liver to produce more IGF-1, which then reduces the amount of GH released. Somatostatin can be released by the hypothalamus and inhibit GH.

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97
Q

What are the 3 vital signs of presentation of pituitary tumour?

A
  • Pressure on local structure
  • Pressure on normal pituitary
  • Functioning tumour
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98
Q

What can pressure on local structures due to a pituitary tumour cause?

A
  • Bitemporal hemianopia
  • IIIrd nerve palsy
  • Headaches
  • Hydrocephalus
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99
Q

What can pressure on the pituitary due to a pituitary tumour cause?

A

Hypopituitarism= Pale, no body hair, central obesity

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100
Q

What can functioning pituitary tumours cause?

A
  • Prolactinoma
  • Acromegaly
  • Cushing’s disease
How well did you know this?
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2
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101
Q

How are prolactinomas treated?

A

Dopamine agonist

102
Q

What is the typical presentation of a prolactinoma?

A
  • Galactorrhoea
  • Amenorrhoea
  • Infertility
  • Loss of libido
  • Visual field defects
103
Q

What can hypothyroidism in pregnancy lead to?

A
  • Pre-eclampsia
  • Low birth weight
  • Neonatal goitre
  • Placental abruption
  • Post partum haemorrhage
  • Preterm delivery
104
Q

List some groups that are targeted for screening in hypothyroidism in pregnancy?

A
  • Age >30
  • BMI >40
  • Personal or family history
  • Goitre
105
Q

What can hyperthyroidism in pregnancy lead to?

A
  • IUGR
  • Low birth weight
  • Pre eclampsia
  • Preterm delivery
  • Risk of stillbirth or miscarriage
106
Q

What is fetal thyrotoxicosis?

A

When thyroid autoantibodies cross the placenta leading to transplacental transfer of TSH-R autoantibodies

107
Q

List the features of maturity-onset diabetes of the young

A
  • Usually diagnosed <25
  • Autosomal dominant
  • Non-insulin dependent
  • Single gene defect altering beta cell function
  • Tend to be non-obese
  • Sensitive to sulphonyurea
108
Q

If a patient with diabetes is C peptide negative, which type will they likely have?

A
  • Type 1

Type 2 and MODY are C peptide positive

109
Q

List some types of diabetes

A 
Type 1 and 2
MODY
Permanent neonatal diabetes 
Maternally inherited diabetes and deafness
Inflammation of the pancreas
Cystic fibrosis
110
Q

A 21 year old woman has diabetes. She has a BMI of 20, and hasn’t taken her insulin for a year, but has not had ketoacidosis. What type of diabetes is she likely to have?

A

Maturity onset diabetes of the young

111
Q

A 50 year old man has a family history of diabetes, and is not insulin dependent. He has a BMI of 38. What type of diabetes is he likely to have?

A

Type 2 diabetes

112
Q

List some common thyroid diseases

A 
Hyperthyroidism
Hypothyroidism
Goitre 
Graves' disease 
Thyroiditis 
Autoimmune thyroid disease
113
Q

What is goitre?

A

A palpable and visible thyroid enlargement

114
Q

How can autoimmune thyroid disease be diagnosed?

A
  • Thyroglobulin antibodies

- TPO antibodies

115
Q

What is the cause of graves’ disease?

A

Thyroid stimulating antibodies that may cross the placenta

116
Q

What are the 3 mechanisms for increased levels of thyroid hormone

A

Overproduction of thyroid hormone
Leakage of preformed hormone from thyroid
Ingestion of excess thyroid hormone

117
Q

What are the causes of hyperthyroidism?

A
  • Graves’ disease
  • Toxic multinodular goitre
  • Toxic adenoma
  • Congenital hyperthyroidism
  • Thyroiditis
  • Iodine induced
118
Q

What are the clinical features of hyperthyrodism?

A 
Weight loss
Tachycardia
Hyperphagia
Tremor
Fatigue
Anxiety
Heat intolerance
Sweating
Diarrhoea
Menstrual disturbance
119
Q

List some Graves’ disease specific clinical signs

A

Diffuse goitre, thyroid eye disease, acropachy

120
Q

List a multinodular goitre specific clinical sign

A

Multinodular goitre (Large thyroid)

121
Q

What is the biochemistry of primary hyperthyroidism?

A

High T4
High T3
Suppressed TSH

122
Q

What is the biochemistry of secondary hyperthyroidism?

A

High T4
High T3
High TSH

123
Q

How is hyperthyroidism diagnosed?

A

Biochemistry (T3, T4, TSH)
Clinical history and physical signs
Supporting investigations- thyroid antibodies, isotope uptake scan

124
Q

What are the possible treatments of hyperthyroidism?

A
  • Beta blockers for rapid control of symptoms
  • Carbimazole
  • Radioactive iodine
  • Thyroidectomy
125
Q

What are causes of hypothyroidism in an adult?

A

Hashimoto’s thyroiditis
Thyroidectomy
Iodine deficiency
Certain drugs

126
Q

What are the causes of hypothyroidism in a child?

A

Neonatal hypothyroidism
Resistance to thyroid hormone
Isolated TSH deficiency

127
Q

What are the clinical features of hypothyroidism?

A 
Weight gain
Fatigue 
Dry, rough skin
Menstrual disturbance
Constipation
Cold intolerance
Oedema 
Low in mood
128
Q

How is hypothyroidism diagnosed?

A
  • Increased TSH, decreased T4, decreased T3

- Positive TPO antibodies in Hashimoto’s

129
Q

How is hypothyroidism treated?

A
  • Synthetic L-thyroxine

- Requirements vary according to cause

130
Q

What is a circadian rhythm?

A

Physical, mental and behavioural changes that follow a daily cycle

131
Q

When are cortisol levels the highest?

A

First thing in the morning

132
Q

What is adrenal insufficiency?

A

A condition in which the adrenal glands do not produce adequate amounts of steroid hormone

133
Q

List some causes of adrenal insufficiency?

A

Primary – Addison’s Disease
Secondary – Hypopituitarism
Tertiary – Suppression of HPA

134
Q

What are the symptoms of adrenal insufficiency?

A 
Fatigue
Weight loss
Poor recovery from illness
Adrenal crisis
Headache
135
Q

What are the risk factors for adrenal insufficiency?

A
  • Past history of TB, cancer or postpartum bleed

- Family history

136
Q

What are the signs of adrenal insufficiency?

A

Pigmentation and pallor

Hypotension

137
Q

What is the biochemistry of adrenal insufficiency?

A 
Low Na, high K
Eosinophilia
Borderline elevated TSH
Cortisol < 100 nmol/L
ACTH >22 pmol/ L= Primary
ACTH <5 pmol/L = Secondary
Elevated renin in primary
138
Q

What is the treatment for adrenal insuffiency?

A
  • Replace aldosterone with fludrocortisone
  • Hydrocortisone 2/3 times daily
  • Mineralocorticoid treatment in adrenal failure
  • Androgen replacement?
139
Q

What are the clinical features of adrenal crisis?

A 
Hypotension and cardiovascular collapse
Fatigue 
Fever
Hypoglycaemia
Hyponatraemia and hyperkalaemia
140
Q

What is the treatment for an adrenal crisis?

A

Immediate hydrocortisone 100mg IV, IM.
Fluid resuscitation
Regular hydrocortisone.

141
Q

What is a craniopharyngioma?

A

A tumour of the squamous epithelial remnants of rathke’s pouch

142
Q

What are the clinical features of a craniopharyngioma?

A

A benign tumour that infiltrates surrounding structures

Raised ICP, Visual disturbances, growth failure, pituitary hormone deficiency

143
Q

What is rathke’s pouch?

A

an evagination at the roof of the developing mouth in front of the buccopharyngeal membrane – gives rise to the anterior pituitary

144
Q

What is a meningioma?

A

A common tumour of the pituitary region

145
Q

What are the clinical features of a meningioma?

A

Loss of visual acuity, endocrine dysfunction and visual field defects

146
Q

What is lymphocytic hypophysitis?

A

Inflammation of the pituitary gland due to autoimmune reaction

147
Q

What are the common clinical features of pituitary tumours?

A 
Visual changes (Bitemporal hemianopia)
Endocrine dysfunction
148
Q

What are the clinical features of GH deficiency?

A

Short stature
Abnormal body composition
Reduced muscle mass
Poor quality of life

149
Q

What are the clinical features of LH/FSH deficiency?

A

Hypogonadism
Reduced sperm count
Infertility
Menstruation problems

150
Q

What are the clinical features of ACTH deficiency?

A

Adrenal failure

Decreased pigmentation

151
Q

What are the clinical features of ADH deficiency?

A

Diabetes insipidus

  • Polyuria
  • Polydipsia
152
Q

In a 70kg man, how many L of fluid are there?

A

42L

153
Q

How many L of fluid are present in the extracellular fluid in a 70kg man?

A

14L

154
Q

How many L of fluid are present in the intravascular fluid of a 70kg man?

A

3.5L

155
Q

How many L of fluid are present in the interstitial fluid of a 70kg man?

A

10.5L

156
Q

How many L of fluid are present in the intracellular fluid of a 70kg man?

A

28L (2/3 of total body water)

157
Q

What is the main cation found in the intracellular fluid?

A

K+

158
Q

What is the main cation found in the extracellular fluid?

A

Na+

159
Q

What is the main anion found in the extracellular fluid?

A

Cl-

160
Q

What is the main anion found in the intracellular fluid?

A

PO4 3-

161
Q

What controls the release of vasopressin?

A
  • Osmoreceptors in hypothalamus controls release day to day

- Baroreceptors in brainstem and great vessels release ADH in emergencies

162
Q

What is the action of vasopressin?

A

Vasopressin binds to V2 receptors on the renal collecting duct principal cells. This causes translation of the aquaporin 2 receptor channels, causing more reabsorption of water.

163
Q

What is osmolality?

A

The concentration of solutes per kilo (normally 282-295 mOsmol/K)

164
Q

What is the difference between nephrogenic and cranial DI?

A 
Cranial= Lack of vasopressin
Nephrogenic= Resistance to action of vasopressin
165
Q

What are the causes of cranial diabetes insipidus?

A 
Idiopathic 
Trauma 
Tumours 
Genetic 
Vascular – aneurysms, infarction
166
Q

What are the causes of nephrogenic diabetes insipidus?

A 
Osmotic diuresis
Drugs
Renal failure
Metabolic 
Familial
167
Q

How is diabetes insipidus diagnosed?

A

Measure urine vol (DI unlikely if urine vol <3L/day)
Check renal function and serum calcium
Inappropriately dilute urine for plasma osmolality
Water deprivation test

168
Q

How is Diabetes insipidus treated?

A
  • Treat underlying conditions

- Desmopressin

169
Q

What is the limits of severe hyponatraemia?

A

serum sodium <125mmol/l

170
Q

What is normal serum sodium?

A

135-144mmol/L

171
Q

If a patient is hyponatraemic, and is fluid overloaded, what are the possible causes?

A

Inappropriate IV fluids
Congestive cardiac failure
Cirrhosis of liver

172
Q

If a patient is normovolaemic and hyponatraemic, what is a possible cause?

A

SIADH

173
Q

What are the symptoms of hyponatraemia?

A 
Headache
Lethargy
Anorexia
Abdominal pain
Weakness
Confusion/ hallucinations
174
Q

What are the tests that should be done for hyponatraemia?

A 
Plasma osmolality
Urine osmolality 
Plasma glucose
Urine sodium
Assessment of cortisol
175
Q

If a patient has hyponatraemia, why must salts not be replaced rapidly?

A

Risk of osmotic demyelination

176
Q

What is the definitive sign of female puberty onset?

A

Menarche

177
Q

What is the definitive sign of male puberty onset?

A

First ejaculation

178
Q

What are the effects of androgens during puberty?

A 
Girls= Pubic and axillary hair 
Male= Pubic hair growth, external genitalia, enlargement of larynx and laryngeal muscles
179
Q

What are “tanner stages”?

A
  • A scale that defines physical measurements of development based on external primary and secondary sex characteristics
180
Q

What is therlarche, and what induces it?

A

Breast development

Induced b oestrogen

181
Q

What is precocious puberty?

A

Onset of secondary sexual characteristics before 8 years (girls), 9 years (boys)

182
Q

What is delayed puberty?

A

Absence of secondary sexual characteristics by 14 years (girls), 16 years (boy)

183
Q

What is adrenarche?

A

Maturational process of the adrenal gland. Causes mild advanced bone age, axillary hair, oily skin, mild acne, body odour

184
Q

How is precocious puberty treated?

A

GnRH agonist

185
Q

What can cause precocious puberty?

A

Idiopathic
Pituitary tumour
External hGC producing tumour

186
Q

What are some laboratory investigations for delayed puberty?

A 
Complete red blood count
U + E, renal, LFT
LH, FSH
Testosterone/ oestradiol
Thyroid function, prolactin
Karyotyping in girls for Turner syndrome
187
Q

What is hypogonadism?

A

Reduction or absence of hormone secretion of the gonads

188
Q

What is the biochemical process of primary female hypogonadism?

A
  • Oestrogen goes down
  • Lack of feedback
  • LH and FSH increase
189
Q

What is the biochemical process of primary male

hypogonadism?

A
  • Testosterone goes down
  • Lack of feedback
  • LH and FSH increase
190
Q

What is the biochemical process of secondary female hypogonadism?

A
  • LH and FSH low
  • No response to feedback
  • Oestrogen decreases
191
Q

What is the biochemical process of secondary male hypogonadism?

A
  • LH and FSH low
  • No response to feedback
  • Testosterone decreases
192
Q

What is the karyotype of someone with turner syndrome?

A

45, X0

193
Q 
Which of the following is not under control of the pituitary? 
A) Thyroid
B) Adrenal cortex
C) Adrenal medulla
D) Testis
E) Ovary
A

Correct answer= C

194
Q

Which of the following statements is false?
A) The pituitary gland lies in the sella turcica
B) The weight of the pituitary gland is around 0.5g
C) ACTH is secreted from the pituitary during stress
D) The pituitary regulates calcium metabolism
E) The anterior and posterior pituitary are distinct on an MRI scan

A

Correct answer= D

195
Q 
In men all the following are mainly produced in the adrenal cortex except?
A. DHEAS
B. Testosterone
C. Aldosterone
D. 17-OH progesterone
E. Androstenedione
A

Correct answer= B

196
Q

Which of the following regarding AVP is false?
A. AVP levels have a linear relationship with serum osmolality
B. It is produced in the pituitary gland
C. It stimulates reabsorption of water in the collecting duct of the nephron
D. In hypotension baroreceptors predominantly activate ADH production and secretion
E. Further AVP production is no longer effective once urine osmolality has reached a plateau

A

Correct answer= B

197
Q 
Where is growth hormone’s main site of action to stimulate IGF1 release?
A. Bone
B. Liver
C. Adrenal cortex
D. Muscle
E. Pancreas
A

Correct answer= B

198
Q 
The following are typical features of excess growth hormone secretion except?
A. Polyuria
B. Joint pains
C. Sweating
D. Hypotension
E. Headaches
A

Correct answer= D

199
Q 
The following hormones all have a circadian rhythm except?
A. Cortisol
B. Testosterone
C. DHEA
D. 17OH progesterone
E. Thyroxine (T4)
A

Correct answer= E

200
Q 
Typical features of cortisol deficiency include the following except?
A. Hypotension
B. Muscle aches
C. Weight loss
D. Hyperglycaemia
E. Lethargy
A

Correct answer= D

201
Q 
A 38 year old lady presented with weight gain, menorrhagia and constipation. She is most likely to be suffering from?
A. Cushing’s syndrome
B. Addison’s disease
C. Primary hypothyroidism
D. Graves disease
E. Acromegaly
A

Correct answer= C

202
Q

Which test would you likely want to perform in a patient with proximal muscle weakness, purple striae and thin skin?
A. Synacthen test
B. Overnight dexamethasone suppression test
C. Insulin tolerance test
D. Glucagon test
E. Skin allergy tests

A

Correct answer= B

203
Q 
A 24 year old girl presented with hirsutism, oligomenorrhoea and acne. What test would you likely carry out from the ones below?
A. Ultra sound adrenals
B. Ultra sound ovaries
C. MRI ovaries
D. CT scan adrenals
E. Prolactin
A

Correct answer= B

204
Q 
A 54 year old gentleman presented with hyponatraemia. All the following conditions need excluding before confirming SIADH except?
A. Hypothyroidism
B. Hypervolaemia
C. Euvolaemia
D. Adrenal insufficiency
E. Diuretic use
A

Correct answer= C

205
Q

A 66 year old gentleman had a serum sodium of 124 mmol/l, serum osmolality 265 mmol/l and a urine sodium of 52 mmol/l. What would you like to perform first?
A. Chest X-ray
B. CT brain
C. Skin turgor and jugular venous pressure test
D. Thyroid function tests
E. Synacthen test

A

Correct answer= C

206
Q 
The following are most likely causes of SIADH except?
A. Multiple sclerosis
B. Lung abscess
C. Subdural haemorrhage
D. Lymphoma
E. Cerebrovascular accident
A

Correct answer= A

207
Q 
A 28 year old presented with a microprolactinoma. What is the most unlikely symptom?
A. Galactorrhoea
B. Oligomenorrhoea
C. Decreased sexual appetite
D. Headaches
E. Visual field defects
A

Correct answer= E

208
Q 
The following suppress appetite except:
A. Peptide YY
B. Ghrelin
C. CCK
D. GLP1
E. Glucose
A

Correct answer= B

209
Q 
The main adipose signal to the brain is
A. CCK
B. Neuropeptide y
C. Leptin
D. Agouti-related peptide
E. Adiponectin
A

Correct answer= C

210
Q

A 65 year old lady is diagnosed with SIADH. Her sodium is 123mmol/l. What is your first line of management?
A. If she is symptomatic I will treat with fluid restriction
B. If she is asymptomatic I will treat with hypertonic saline
C. If she is asymptomatic I will treat with fluid restriction
D. If she is asymptomatic I will repeat the sodium level the next day
E. If she is asymptomatic I will give normal saline

A

Correct answer= C

211
Q

A patient with Addison’s disease presents with a chest infection. What do you do?
A. Omit his steroids to avoid immunosuppression
B. Stop his steroids as they have precipitated a chest infection
C. Double his steroid dose whilst unwell
D. Keep him on his usual steroid dose
E. Not of the above

A

Correct answer= C

212
Q 
The following tests are typical of secondary hypogonadism
A. Low LH; High testosterone
B. Low LH; Low testosterone
C. High prolactin; high testosterone
D. Low FSH; Low prolactin
E. None of the above
A

Correct answer= B

213
Q 
Typical features of hypogonadism in a male include the following except:
A. Decreased sweating
B. Joint and muscular aches
C. Decreased sexual appetite
D. Decreased hair growth
E. Asymptomatic
A

Correct answer= A

214
Q

A patient has a noon testosterone level below the normal range. What will you do?
A. Treat with testosterone gel
B. Repeat the test at 0900h and check for symptoms
C. Repeat the test at noon to keep things equal
D. Refer to endocrinology
E. Ignore it

A

Correct answer= B

215
Q 
The first line treatment for a patient with a symptomatic prolactinoma is usually:
A. Radiotherapy
B. Transphenoidal surgery
C. Dopamine agonists
D. Transfrontal surgery
E. Somatostatin analogues
A

Correct answer= C

216
Q 
Typical visual field defect of a patient with a large pituitary mass is
A. Unilateral quadrantanopia
B. Bitemporal hemianopia
C. Complete unilateral visual field loss
D. Complete bilateral visual field loss
E. None of the above
A

Correct answer= B

217
Q

Satiety is
A. The physiological feeling of no hunger
B. Inhibited by activation of POMC neurons
C. The physiological feeling of hunger
D. Induced by ghrelin release
E. Enhanced by Agoutirelated peptide

A

Correct answer= A

218
Q 
The centres of appetite regulation in the brain are mainly found in the:
A. Pituitary
B. Cerebellum
C. Hypothalamus
D. Basal ganglia
E. Brain cortex
A

Correct answer= C

219
Q

At what level is the thyroid found?

A

C5-T1

220
Q

What do C cells produce?

A

Calcitonin

221
Q

What is the main function of the thyroid?

A

Production of thyroid hormone

222
Q

What are the general functions of thyroid hormone?

A

Increases metabolism
Oxygen/energy consumption
Thermogenesis

223
Q

A 35 year old female presents with a non-tender, painless rubbery goitre with symmetrical enlargement. She is feeling low of mood, has been gaining weight and is constipated. What is it likely to be?

A

Hashimotos disease leading to hypothyroidism

224
Q

What is myxoedema coma?

A

A rare life threatening state of severe hypothyroidism

225
Q

How does myxoedema coma present?

A

Impaired mental status, hypothermia, hypoglycaemia, hypotension, myxoedema, elevated CK

226
Q

How is myxoedema coma treated?

A

IV levothyroxine, IV hydrocortisone, oxygen, gradual rewarming, glucose

227
Q

What is a thyroid storm?

A

A rare but life threatening acute exacerbation of hyperthyroidism

228
Q

How do patients with a thyroid storm present?

A

Hyperpyrexia with profuse sweating
Tachycardia
Vol depletion secondary to diarrhoea, vomitting
Severe agitation

229
Q

How is thyroid storm treated?

A

PTU (Antithyroid medication)

Symptom treatment

230
Q 
What type of enzyme converts T4 to T3 peripherally 
A) Deiodinases
B) Triiodinases
C) TPO
D) Iodine Dehydrogenase
A

Correct answer= A

231
Q 
Which one of these would most likely be found in graves disease
A) TSH high, T3 and T4 low
B) TSH high, T3 and T4 high
C) TSH low, T3 and T4 high 
D) TSH low, T3 and T4 low
E) TSH, T3 and T4 normal
A

Correct answer= C

232
Q 
Which one of these is not a symptom of hyperthyroidism
A) Diarrhoea
B) Weight loss
C) Palpitations
D) Cold intolerance 
E) Irritability
A

Correct answer= D

233
Q

A 30 yo female presents to A and E. On examination she is agitated, pyrexial and tachycardic. She recently suffered a severe viral infection. She has a PMHx of Graves’. What does she have, and what 4 medications would be prescribed?

A

She has a thyroid storm

PTU
Beta blocker
Steroids
Potassium iodide

234
Q 
Which condition is characterised by a diffusely reduced uptake on a radioiodine scan of the thyroid
A) Grave's
B) Toxic adenoma
C) De Quervain's thyroiditis
D) Iodine deficiency
A

Correct answer= C

235
Q

What is HLA DD3/4 associated with?

A

T1DM

236
Q

Describe in simple terms the relationship between Thyroid Stimulating Hormone (TSH) and Circulating thyroxine levels

A

The two are in balance with a negative feedback loop. A reduction in circulating thyroxine will lead to an increase in TSH. Similarly if thyroxine levels go too high it will act on the pituitary to cause a reduction in TSH.

237
Q

Give 4 classical symptoms of hyperthyroidism

A
  • Weight loss despite increased appetite
  • Heat Intolerance
  • Sweating
  • Diarrhoea
  • Tremor
  • Irritability
  • Emotional lability and potential psychosis
  • Itch
  • Oligomennorhoea
238
Q

What Units is Body Mass Index (BMI) expressed in and at what BMI would an individual be considered to be obese?

A

The units of BMI are kg/m2

Obesity is classified as a BMI equal to, or greater than 30 kg/m

239
Q

Pituitary tumors cause clinical effect in 3 main ways – what are they?

A
  • Pressure on local structure
  • Pressure on normal pituitary
  • Functioning tumour
240
Q

What pituitary hormone excess would cause the following symptoms and signs?
Galactorrhoea/amennorhoea/infertility and lack of Libido

A

Prolactin

241
Q

What pituitary hormone excess would cause the following symptoms and signs?
Truncal weight gain with increased fat around the neck (buffalo hump), stretch marks and easy bruising

A

Adrenocorticotropic hormone

242
Q

What pituitary hormone excess would cause the following symptoms and signs?
Enlarged hands and feet, protruding brow and chin, excess sweating, deeper voice

A

Growth Hormone

243
Q

What are the commonest biochemical abnormalities found on blood investigations in Addisons disease and why?

A
  • Raised Sodium and reduced potassium due to reduced Aldosterone secretion
  • Metabolic Acidosis due to the link between sodium and H+ ion management in the kidney. Increased sodium loss leads to increased H+ retention in the serum. This is also due to reduced aldosterone secretion
  • Decreased Glucose due to reduced cortisol
  • Raised Calcium due to volume depletion and increased release into the extracellular space
244
Q

What is the commonest cause of addisonian crisis and what is the most important initial treatment for it?

A

The commonest cause is abrupt cessation of long term steroid treatment either by choice or due to concurrent illness preventing the use of oral steroids.
The most important initial treatment is Hydrocortisone

245
Q

What is hypoparathyroidism, and what biochemical abnormalities would you see?

A

Due to gland failure – causes reduced calcium with normal/raised phosphate and normal alkaline phosphatase

246
Q

What is secondary hypoparathyroidism and what biochemical abnormalities would you see?

A

Due to an external cause - commonest cause is surgical damage leading to reduced calcium with normal/raised phosphate and normal alkaline phosphatase

247
Q

What is pseudohypoparathyroidism and what biochemical abnormalities would you see?

A

– Peripheral resistance to parathyroid hormone – causes reduced calcium, raised phosphate, normal or raised alkaline phosphatase

248
Q

Malignancy affecting the bones can often cause hypercalcaemia. Give four common clinical symptoms of hypercalcaemia

A
  • Weakness
  • Tiredness
  • Dehydration
  • Renal Stones
  • Fractures due to osteopaenia/osteoporosis
  • Abdominal pain (constipation/pancreatitis)
  • Depression/confusion
249
Q

Diabetes Mellitus and Diabetes Insipidus have 2 key symptoms in common – what are they?
What simple urine test can help differentiate them?

A

Both can cause Polyuria and Polydipsia however dip testing the urine for glucose can assist the diagnosis differentiation as diabetes mellitus will show glycosuria.

250
Q

Define Type 1 and Type 2 diabetes in terms of their pathophysiology

A
  • Type 1 Diabetes Mellitus is due to insulin deficiency secondary to selective destruction of insulin secreting pancreatic β cells.
  • Type 2 Diabetes Mellitus is due to reduced insulin secretion and peripheral insulin resistance
251
Q

What is the most appropriate first line drug treatment for Type 2 diabetes and how does it act?

A

Metformin is the most appropriate first line agent. It acts by decreasing hepatic glucose production, decreasing intestinal absorption of glucose, and improving insulin sensitivity by increasing peripheral glucose uptake and utilization.

252
Q

Give 4 common complications of diabetes – especially if poorly controlled.

A
  • Neuropathic pain
  • Autonomic neuropathy (e.g. orthostatic hypotension, erectile dysfunction, constipation)
  • Peripheral sensory loss and consequences (Charcot joints, falls, traumatic ulceration)
  • Peripheral vascular disease
  • Retinopathy
  • Nephropathy

Phase 2a (31 decks)

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