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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe endocrine action

A

Blood-borne, acts on distant sites

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2
Q

Describe paracrine action

A

Acts on adjacent cells

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3
Q

Describe autocrine action

A

Feedback on same cell that secreted the hormone

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4
Q

Give examples of fat-soluble hormones

A

-Steroids
-Thyroid hormones

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5
Q

Give examples of water-soluble hormones

A

-Peptides
-Monoamines

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6
Q

Describe 4 properties of water-soluble hormones

A

-Unbound
-Bind to surface receptor
-Short half-life
-Fast clearance

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7
Q

Describe 4 properties of fat-soluble hormones

A

-Protein bound
-Diffuse into cell
-Long half-life
-Slow clearance

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8
Q

What are the 4 hormone classes?

A

-Peptides
-Amines
-Iodothyronines
-Cholesterol derivatives + steroids

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9
Q

How are peptide hormones stored?

A

-Stored in secretory granules

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10
Q

How are peptide hormones released?

A

-Released in pulses/bursts

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11
Q

How are peptide hormones cleared?

A

-Cleared by tissue/circulating enzymes

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12
Q

What is the formation pathway for epinephrine?

A

Phenylalanine->Tyrosine->L-DOPA->Dopamine->Norepinephrine->Epinephrine

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13
Q

Describe thyroid hormone properties

A

-Not water soluble
-99% water bound

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14
Q

How are iodothyronines formed?

A

Iodine incorporated on tyrosine molecule

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15
Q

What is the base for thyroid hormone synthesis?

A

Colloid

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16
Q

How are T3 + T4 formed + where are they stored?

A

Formed by conjugation of iodothyronines
Stored in colloid

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17
Q

What are the 3 hormone receptor locations + what type of hormone acts there?

A

-Cell membrane-peptide
-Cytoplasm-steroid
-Nucleus-thyroid

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18
Q

What class of hormone is vit D?

A

Cholesterol derivative

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19
Q

What do adrenocortical + gonadal steroids do after entering cells

A

Pass into nucleus
-Become active metabolite
-Bind to cytoplasmic receptor

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20
Q

How do adrenocortical + gonadal steroids become inactivated?

A

Reduced + oxidised, or conjugated to glucoronide and sulphate groups in the liver

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21
Q

How do steroid hormones work?

A

-Diffuses through plasma membrane + binds to receptor
-Receptor-hormone complex enters nucleus
-Complex binds to GRE
-Binding initiates transcription of gene to mRNA
-mRNA directs protein synthesis

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22
Q

How can hormones be released?

A

Continuously or pulsatile

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23
Q

In what 3 ways can hormone release be stimulated?

A

-Humoral stimulus (change in levels of ions/nutrients)
-Neural stimulus-neural input
-Hormone stimulus-another hormone causes release

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24
Q

Name 3 hormones with diurnal rhythms

A

-Cortisol
-Prolactin
-GH

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25
Q

Name 5 ways in which hormone action can be controlled

A

-Hormone metabolism
-Hormone receptor induction/down regulation
-Synergism
-Antagonism

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26
Q

How does hormone metabolism control hormone action?

A

Increased metabolism to reduce function

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27
Q

How does hormone synergism control hormone action?

A

Combined effects of 2 hormones causes amplification

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28
Q

How does hormone antagonism control hormone action?

A

One hormone can oppose another

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29
Q

Where are oxytocin + ADH synthesised?

A

Hypothalamic neurons

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30
Q

Where are oxytocin + ADH stored?

A

Posterior pituitary

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31
Q

What hormones are produced in the anterior pituitary + where in the body do they act?

A

-TSH-thyroid
-ACTH-adrenal cortex
-FSH + LH-testes + ovaries
-GH-entire body
-Prolactin-mammary glands

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32
Q

What can pituitary dysfunction cause?

A

-Tumour mass effects
-Hormone XS
-Hormone deficiency

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33
Q

How does GH work + what does it act on?

A

-Acts on liver to produce IGFs

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34
Q

What effect does GH have?

A

-Increased cartilage formation + skeletal growth
-Increased protein synthesis, cell growth + proliferation

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35
Q

What are the direct metabolic effects of GH?

A

-Fat metabolism-increases fat breakdown + release
-Carb metabolism-increases blood glucose

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36
Q

Describe the hypothalamic-pituitary-thyroid axis

A

-Hypothalamus releases TRH which acts on anterior pituitary
-This releases TSH which causes thyroid to release hormones + positive feedback on hypothalamus

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37
Q

Where is T4 converted to T3?

A

Liver + muscle

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38
Q

What does TH do?

A

-Accelerates food, carb + fat metabolism
-Increases protein synthesis
-Increases ventilation rate
-Increases CO + HR
-Increases growth rate
-Helps foetal + postnatal brain devlopment

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39
Q

Where are the adrenal glands?

A

On top of kidneys

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40
Q

What are the parts of the adrenal glands?

A

Medulla + cortex

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41
Q

What are the layers of the adrenal cortex (out to in)?

A

-Zona glomerulosa
-Zona fasciculata
-Zona reticularis

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42
Q

How is BMI calculated?

A

weight (kg)/height (m2)

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43
Q

What is an underweight BMI?

A

<18.5

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44
Q

What is a normal BMI?

A

18.5-24.9

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45
Q

What is an overweight BMI?

A

25-29.9

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46
Q

What is an obese BMI?

A

30-39.9

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47
Q

What is a morbidly obese BMI?

A

> 40

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48
Q

What does weight regulation depend on?

A

-Environment
-Genes
-Normal fat mass
-Homeostasis system

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49
Q

Where is the hunger centre of the body?

A

Lateral hypothalamus

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50
Q

Where is the satiety centre of the body?

A

Ventromedial hypothalamic nucleus

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51
Q

How does leptin work?

A

-Binds to leptin receptor in hypothalamus
-Switches off appetite by:
-Inhibiting NPY/AgRP neurons + activating POMC neurons

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52
Q

What does peptide YY do?

A

Binds to inhibitory NPY receptors + inhibits gastric motility-reduces appetite

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53
Q

What secretes peptide YY?

A

Neuroendocrine cell sin ileum, pancreas + colon

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54
Q

What does CCK do?

A

Delays gastric emptying, contracts gallbladder + insulin release + via vagus-satiety

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55
Q

Which hormone causes satiety via the vagus?

A

CCK

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56
Q

What does ghrelin do?

A

-Stimulates release of GH + causes appetite

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57
Q

Where is ghrelin expressed?

A

Stomach

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58
Q

Name 4 hunger hormones that integrate with the hypothalamus

A

-NPY - Neuro peptide Y

-AgRP - Agouti-related peptide

-POMC - Pro-opiomelanocortin

-CART - cocaine and amphetamine regulated
transcript

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59
Q

How do leptin + insulin increase satiety + reduce appetite?

A

-Stimulate POMC/CART neurons
-Increases CART + alpha-MSH levels
-Inhibit NPY/AgRP neurons
-Decreases NPY + AgRP levels

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60
Q

How does ghrelin increase appetite?

A

-Stimulates NPY/AgRP neurons
Increases NPY + AgRP secretion

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61
Q

What are hunger hormone levels like in the fasted state? (NPY, glucose, insulin, ghrelin, leptin, alpha MSH, AgRP)

A

-High NPY
-Low glucose
-Low insulin
-High ghrelin
-Low leptin
-Low alpha MSH
-High AgRP

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62
Q

What 4 effects do incretins have?

A

-Blunting of glucagon
-Stimulation of beta cells to produce insulin
-Improve satiety
-Decrease gastric motility

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63
Q

What 4 things happen 5-10 mins after eating in a normal, healthy human?

A

-Glucose levels rise
-Stimulates insulin secretion
-Glucagon suppressed
-Lipolysis suppressed + non-esterified fatty acid levels fall

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64
Q

Where does ingested glucose go in a healthy human?

A

-40% to liver
-60% to periphery, mostly muscle
to replenish glycogen stores

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65
Q

What cells secrete insulin?

A

Beta cells in Islets of Langerhans in pancreas

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66
Q

What cells secrete glucagon?

A

Alpha cells in Islets of Langerhans in pancreas

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67
Q

What does insulin do?

A

Helps convert glucose into glycogen stores-reduces blood glucose

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68
Q

What does glucagon do?

A

Helps break down glycogen stores when blood glucose levels are low

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69
Q

What is the benefit of paracrine ‘crosstalk’ between alpha + beta cells?

A

Physiological response to the release of one e.g. local insulin release inhibits glucagon, this is lost in diabetes

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70
Q

How does glucose cause the release of insulin from beat cells?

A

-Glucose enters cell through GLUT2 transporter + is metabolised to ATP
-ATP binds to K+ channels + causes build up of K+
-This activates Ca+ channels and Ca+ rushes into the cell
-Ca+ activates vesicles which release insulin

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71
Q

Name 3 other hormones with similar effects to glucagon

A

-Adrenaline
-Cortisol
-GH

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72
Q

Define diabetes mellitus

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia

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73
Q

What can untreated diabetes mellitus lead to?

A

DKA - diabetic ketoacidosis
-HHS - hyperosmolar hyperglycaemic state

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74
Q

Name 5 key complications of untreated diabetes

A

-Diabetic retinopathy-vision loss + cataracts
-Diabetic nephropathy-CKD
-Stroke
-CVD
-Diabetic neuropathy-foot ulcers

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75
Q

Which type of diabetes includes gestational + medication induced?

A

Type 2

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76
Q

Name the 6 types of diabetes

A

-Type 1
-Type 2
-MODY (maturity onset diabetes of youth) aka monogenic
-Pancreatic diabetes
-Endocrine diabetes (acromegaly/Cushings)
-Malnutrition related

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77
Q

What causes type 1 diabetes?

A

-Autoimmune destruction of Beta cells

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78
Q

What antigen on Beta cells causes them to be targeted + destroyed in type 1 diabetes?

A

HLA antigens

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79
Q

What is chronic insulitis?

A

A chronic cell mediated immune process that leads to the destruction of beta cells + therefore reduced/stopped production of insulin

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80
Q

What is the first line Tx for type 2?

A

Metformin

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81
Q

Name 5 alternative Txs for type 2 (not metformin)

A

-Sulphonylureas
-DPP-IV inhibitors
-GLP 1 analogues
-SGLT-2 inhibitors
-Glitazones

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82
Q

Why doesn’t diabetic ketoacidosis happen in type 2?

A

-Rare as normally still have low levels of insulin suppressing catabolism + preventing ketogenesis

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83
Q

Name 3 causes of impaired insulin secretion in type 2?

A

-Lipid deposition in pancreatic islets stop normal secretion of insulin
-Also genetic predisposition to abnormalities in secretion
-Hyperglycaemia could also cause glucotoxicity + inhibit secretion

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84
Q

What are the types of insulin given called?

A

-Basal
-Bolus

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85
Q

What does basal insulin do?

A

Long-acting, should control blood glucose between meals + at night

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86
Q

What does bolus insulin do?

A

Given pre-meal, rapid acting to mimic normal physiology

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87
Q

Name the 3 most common approaches to insulin delivery schedules for diabetes

A

-Once-daily basal insulin (type 2)
-Twice-daily mix-insulin (type 1 + 2)
-Basal-bolus therapy (mostly type 1, some type 2)

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88
Q

What are the disadvantages of basal insulin with type 2?

A

-Doesn’t cover meals
-Best with long-acting insulin analogues-expensive

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89
Q

What are the advantages of basal insulin with type 2?

A

-Simple
-Less chance of hypos at night

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90
Q

What are the disadvantages for pre-mixed insulin?

A

-Not physiological
-Need constant meal + exercise pattern
-Higher risk nocturnal hypos

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91
Q

What are the 3 classes of hypoglycaemia?

A

-Lvl 1 - plasma glucose <3.9mmol, no symptoms
-Lvl 2 - PG <3
-Lvl 3-impaired cognitive function, assistance required

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92
Q

What are the pathophysiological effects of hypos on the brain?

A

-Blackouts
-Seizures
-Comas
-Psychological effects

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93
Q

What are the pathophysiological musculoskeletal effects of hypos?

A

-Falls
-Driving accidents
-Fractures
-Dislocations

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94
Q

What are the pathophysiological effects of hypos on the heart?

A

-Increased risk of MI
-Cardiac arrhythmias

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95
Q

What are the pathophysiological effects of hypos on the circulation?

A

-Inflammation
-Blood coagulation abnormalities
-Endothelial dysfunction

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96
Q

What are the autonomic symptoms of a hypo?

A

-Trembling
-Palpitations
-Sweating
-Anxiety
-Hunger

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97
Q

What are the neuroglycopenic symptoms of a hypo?

A

-Difficulty concentrating
-Confusion
-Weakness
-Drowsiness
-Vision changes
-Difficulty speaking

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98
Q

What are the non-specific symptoms of a hypo?

A

-Nausea
-Headache

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99
Q

Name 6 causes of hypoglycaemia

A

-Use of drugs/alcohol
-Sleeping
-Increased physical activity
-Increasing age
-Long duration diabetes
-Tight glycaemic control with repeated episodes of non-severe hypos

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100
Q

What are the 5 steps for treating hypos?

A

-Recognize symptoms
-Confirm need for Tx
-Treat with 15g fast-acting carbs
-Retest in 15 mins, check BG >4mmol/l + retreat if needed
-Eat a long-acting carb to prevent recurrence

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101
Q

How do you calculate corrected calcium?

A

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

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102
Q

What are the consequences of hyposcalcaemia?

A

-Paraesthesia
-Muscle spasm
-Seizures
-Basal ganglia calcification
-Cataracts
-ECG abnormalities

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103
Q

Name 2 signs associated with hypocalcaemia

A

-Chvostek’s
-Trousseau’s

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104
Q

What are the causes of hypocalcaemia?

A

-Vit D deficiency
-Hypoparathyroidism following surgery/radiation/genetic causes/immunodeficiency/magnesium deficiency

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105
Q

Name 5 symptoms of hypercalcaemia

A

-Thirst
-Polyuria
-Nausea
-Constipation
-Confusion->coma

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106
Q

Name 3 consequences of hypercalcaemia

A

-Renal stones
-ECG abnormalities e.g. short QT

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107
Q

What are the causes of hypercalcaemia?

A

-Malignancy (bone metastasis, myeloma, lymphoma)
-Primary hyperparathyroidism (with malignancy makes up 90%)
-Adrenal insufficiency
-Immobilisation etc

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108
Q

What is pseudoparathyroidism?

A

Resistance to PTH-end organs not responding but PTH produced + released normally

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109
Q

What is the effect of PTH on calcium?

A

Increases reabsorption

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110
Q

What is the effect of PTH on phosphate?

A

Decreases phosphate

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111
Q

What is the effect of PTH on bones?

A

Increases bone resorption, remodelling + formation

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112
Q

What are the consequences of primary hyperparathyroidism?

A

-Bone conditions e.g. osteoporosis
-Kidney stones
-Confusion
-Constipation
-Acute pancreatitis

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113
Q

What is the rhyme for symptoms of hyperparathyroidism?

A

-Bones-osteoporosis + osteitis fibrosa cystica
-Kidney stones
-Psychic groans-confusion
-Abdominal moans-constipation + pancreatitis

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114
Q

How does the anterior pituitary receive blood?

A

Through a portal venous circulation from the hypothalamus

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115
Q

What is the HPA axis?

A

Interaction between hypothalamus, pituitary + adrenal glands

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116
Q

What hormones are released by the anterior pituitary?

A

-TSH
-ACTH
-FSH
-LH
-GH
-Prolactin

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117
Q

What hormones does the posterior pituitary release?

A

-Oxytocin
-ADH

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118
Q

Describe the 3 steps of the thyroid axis

A

-Hypothalamus releases TRH
-TRH stimulates an. pituitary to release TSH
-TSH stimulates thyroid to release T3 + T4

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119
Q

How do the hypothalamus + anterior pituitary react to high levels of T3 + T4?

A

They suppress release of TRH + TSH-less T3 + T4 released

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120
Q

In what manner is cortisol released?

A

-In pulses throughout day + in response to stress
-Diurnal variation-peaks in early morning, lowest in evening prompting sleep

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121
Q

What is TRH?

A

Thyrotropin-releasing hormone

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122
Q

What is TSH?

A

Thyroid-stimulating hormone

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123
Q

What is T3?

A

Triiodothyronine

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124
Q

What is T4?

A

Thyroxine

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125
Q

What is CRH + what releases it?

A

-Corticotropin-releasing hormone
-Released by hypothalamus

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126
Q

What are the 3 steps of the adrenal axis?

A

-Hypothalamus releases CRH
-CRH stimulates ant pituitary to release ACTH
-ACTH stimulates adrenal glands to release cortisol

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127
Q

Name 5 actions of cortisol on the body

A

-Increased alertness
-Immune inhibition
-Bone formation inhibition
-Raised blood glucose
-Increased metabolism

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128
Q

What are the 3 steps of the GH axis?

A

-Hypothalamus produces GHRH
-GHRH stimulates pituitary to release GH
-GH stimulates liver to release IGF-1

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129
Q

Where is PTH released from?

A

4 parathyroid glands situated at 4 corners of thyroid gland

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130
Q

What is PTH released in response to?

A

-Low calcium
-Low magnesium
-Low phosphate

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131
Q

What does PTH do?

A

-Increases activity + number osteoclasts
-Stimulates Ca reabsorption in kidneys
-Stimulates kidneys to convert vit D to calcitriol
-All of these increase serum calcium

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132
Q

What 3 things can pituitary tumours cause?

A

-Pressure on local structures e.g. optic nerve
-Pressure on normal pituitary e.g. hypopituitarism
-Functioning tumour

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133
Q

Give 3 examples of functioning pituitary tumours

A

-Prolactinoma
-Acromegaly
-Cushing’s Disease

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134
Q

What are 4 local symptoms of a pituitary tumour?

A

-Headaches
-Visual field defects
-Cranial nerve palsies + temporal lobe epilepsy
-CSF rhinorrhoea

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135
Q

How do prolactinomas present?

A

-More common in women
-Loss of libido
-Visual field defect
Present with galactorrhoea/amenorrhoea/infertility

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136
Q

How are prolactinomas treated?

A

Dopamine agonist

137
Q

What is Cushing’s syndrome?

A

Prolonged high levels of glucocorticoids in the body

138
Q

What is Cushing’s disease?

A

A pituitary adenoma secreting XS ACTH which stimulates XS cortisol release

139
Q

What kinds of medication can cause Cushing’s?

A

Exogenous corticosteroids e.g. prednisolone or dexamethasone

140
Q

How does Cushing’s present on inspection?

A

-Round face
-Central obesity
-Abdominal striae (stretch marks)
-Enlarged fat pad on upper back
-Proximal limb muscle wasting
-Hyperpigmentation of the skin due to high ACTH

141
Q

What is the pneumonic for causes of Cushing’s?

A

CAPE

142
Q

What are the causes of Cushing’s Syndrome?

A

C-Cushing’s disease
A-adrenal adenoma
P-paraneoplastic syndrome
E-exogenous steroids

143
Q

What is acromegaly?

A

The result of XS GH

144
Q

What is the most common cause of unregulated GH secretion?

A

Pituitary adenomas

145
Q

How would acromegaly present on inspection?

A

-Frontal bossing (prominent forehead + brows)
-Coarse, sweaty skin
-Large nose, tongue, hands, feet
-Large protruding jaw

146
Q

What testicular volume indicates puberty?

A

> 3ml

147
Q

What is thelarche?

A

Breast development

148
Q

What ovarian volume suggests start of puberty?

A

> 2.8ml

149
Q

How does the vagina change in a pubertal/adult?

A

-Thickening epithelium
-pH change from neutral to acidic 3.8-4.2
-Secretion of whitish discharge in mths pre-menarche

150
Q

What effects does adrenarche have?

A

-Mild advanced bone age
-Axillary hair
-Oily skin
Mild acne
-Body odour

151
Q

Who most commonly has delayed puberty?

A

Boys

152
Q

When should you investigate delayed puberty in girls?

A

-No BD by 13
-More then 5yrs between BD + menarche
-No PH by 14
-No menarche by 15/16

153
Q

When should you investigate delayed puberty in boys?

A

-No testicular development by 14
-No pH by 15

154
Q

What is CDGP?

A

Constitutional delay of growth + puberty-extremes of normal physiologic variation, most common with family history of short stature + delayed puberty

155
Q

Give an example of a hypogonadotropic hypogonadism syndrome

A

Kallman syndrome

156
Q

Give 2 examples of hypergonadotropic hypogonadism syndromes

A

-Klinefelter’s syndrome
-Turner’s syndrome

157
Q

What is the karyotype for Turner’s?

A

45,X0

158
Q

What are the symptoms of Turner’s?

A

-Oedema of dorsa of hands, feet, neck at birth
-Webbing of neck
-Renal malformations e.g. horseshoe kidney
-Short stature
-recurrent otitis media

159
Q

What is the karyotype for Klinefelter’s?

A

47,XXY

160
Q

What are the symptoms of Klinefelter’s?

A

-Azoospermia
-Gynaecomastia
-Reduced PH
-Osteoporosis
-Tall stature
-Reduced IQ (in 40%)

161
Q

Why does diabetes insipidus occur?

A

-Lack of ADH
-Lack of response to ADH

162
Q

What is another name for ADH?

A

Vasopressin

163
Q

What are the presenting features of diabetes insipidus?

A

-Polyuria
-Polydipsia
-Dehydration
-Postural hypotension

164
Q

What is primary polydipsia?

A

When a patient has a normally functioning ADH system but drinks XS water. leading to XS urine production-not diabetes insipidus

165
Q

What are the 2 types of diabetes insipidus?

A

-Nephrogenic
-Cranial

166
Q

What is nephrogenic diabetes insipidus?

A

When collecting ducts of kidneys don’t respond to ADH

167
Q

What is cranial diabetes insipidus?

A

When the hypothalamus doesn’t produce ADH for pituitary to secrete

168
Q

Name 5 non-idiopathic causes of nephrogenic diabetes insipidus

A

-Meds e.g. lithium
-Genetic mutations
-Hypercalcaemia
-Hypokalaemia
-Kidney diseases e.g. PKD

169
Q

Name 6 non-idiopathic causes of cranial diabetes insipidus

A

-Brain tumours
-Brain injury
-Brain surgery
-Brain infections e.g. meningitis
-Genetic mutations
-Wolfram syndrome

170
Q

Where are vasopressin + oxytocin made?

A

In the paraventricular nucleus + supraoptic nucleus + transported to posterior pituitary

171
Q

Name 2 exogenous solutes that can affect osmolality

A

-Alcohol
-Methanol

172
Q

What is a normal osmolality?

A

282-295

173
Q

What is the most common cause of hyponatraemia?

A

Too much water, rather than salt loss

174
Q

What serum sodium indicates severe hyponatraemia?

A

<125mmol/l

174
Q

What serum sodium indicates hyponatraemia?

A

<135mmol/l

175
Q

What should a normal serum sodium be?

A

135-144mmol/l

176
Q

What are the symptoms of hyponatraemia?

A

-Headache
-Irritability
-N + V
-Mental slowing
-Unstable gait/falls
-Confusion/delirium

177
Q

What are the acute/chronic symptoms of hyponatraemia?

A

-Stupor/coma
-Convulsions
-Resp arrest

178
Q

What are the 4 ways hyponatraemia can be classified?

A

-Biochemical-mild, moderate, severe
-Symptoms-mild, moderate, severe
-Aetiology-Hypovolaemic, euvolaemic, hypervolaemic
-Acuity of onset-acute (<48hrs), chronic (>48hrs)

179
Q

What is SIAD?

A

Syndrome of Inappropriate Antidiuretic Hormone Secretion-too much ADH secreted

180
Q

What are the signs of SIAD?

A

-Low osmolality
-Low plasma sodium
-Wrong conc of urine
-Normal circulating vol, no oedema

181
Q

What are the causes of SIAD?

A

-CNS disorders e.g. meningitis, head injuries
-Tumours
-Drugs
-Res causes e.g. pneumonia, TB

182
Q

How do you manage SIAD?

A

-Diagnose + treat underlying
-Fluid restriction <1L/24hr
-Sometime demeclocycline/vaptan
-hypertonic slaien on ITU if fitting + N+ <115mmol/l

183
Q

What is ODS?

A

Osmotic demyelination syndrome-quick change in Na+ levels can cause demyelination of neurons

184
Q

What is hypothyroidism?

A

Insufficient T3 + T4 (thyroid hormones)

185
Q

What is primary hypothyroidism?

A

When the thyroid doesn’t produce enough T3 + T4, so negative feedback is absent + more TSH is produced. Raised TSH, low T3 + T4

186
Q

What is secondary hypothyroidism?

A

When the pituitary doesn’t produce enough TSH, so the thyroid isn’t stimulated to make T3 + T4. TSH, T3 + T4 are all low

187
Q

What is the most common cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis

188
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune condition causing inflammation of the thyroid

189
Q

What antibodies are associated with Hashimoto’s thyroiditis?

A

-Anti-thyroid peroxidase (anti-TPO)
-Anti-thyroglobulin (anti-TG)

190
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

191
Q

Name 4 Tx’s for hyperthyroidism that can cause hypothyroidism

A

-Carbimazole
-Proplythiouracil
-Radioactive iodine
-Thyroid surgery

192
Q

Name an element that inhibits the production of thyroid hormones + can cause a goitre + hypothyroidism

A

Lithium

193
Q

What is hypopituitarism?

A

Lack of pituitary hormones e.g. ACTH

194
Q

Name 5 causes of secondary hypothyroidism

A

-Tumours
-Pituitary surgery
-Radiotherapy
-Sheehan’s syndrome
-Trauma

195
Q

What are the symptoms of hypothyroidism?

A

-Weight gain
-Fatigue
-Dry skin
-Coarse hair + hair loss
-Fluid retention
-Heavy/irregular periods
-Constipation

196
Q

What causes Graves’ disease?

A

TSH-R antibodies (thyroid stimulating antibodies)

197
Q

What factors make you predisposed to thyroid conditions?

A

-Female
-Postpartum
-Stress
-High iodine intake
-Smoking

198
Q

What is goitre?

A

Palpable + visible thyroid enlargement

199
Q

Name 4 drugs that can cause hypothyroidism

A

-Iodine
-Lithium
-Thionamides
-Interferon alpha

200
Q

What is the main Tx for hypothyroidism?

A

Oral levothyroxine (synthetic T4, metabolised to T3 in the body)

201
Q

What is hyperthyroidism?

A

Over-production of T3 + T4 by the thyroid

202
Q

What is thyrotoxicosis?

A

Effects of the abnormal + XS T3/T4 in the body

203
Q

What causes primary hyperthyroidism?

A

Thyroid pathology-producing XS hormones

204
Q

What causes secondary hyperthyroidism?

A

Hypothalamic/pituitary pathology causing over-production of TSH, which then stimulates the thyroid to produce too much T3/T4

205
Q

What is subclinical hyperthyroidism?

A

Normal T3 + T4 levels but low TSH, symptoms are absent/mild

206
Q

What is Graves’ disease?

A

Autoimmune condition where TSH receptor antibodies stimulate TSH receptors on the thyroid + cause primary hyperthyroidism

207
Q

What is another name for Plummer’s disease?

A

Toxic multinodular goitre

208
Q

What is Plummer’s disease?

A

Condition where nodules develop on the thyroid gland + continuously produce XS thyroid hormones

209
Q

In what group of patients is Plummer’s disease most common?

A

Over 50s

210
Q

What is exophthalmos?

A

Bulging of the eyes caused by Graves’ disease. Inflammation, swelling + hypertrophy make eyes bulge out of sockets

211
Q

What is pretibial myxoedema?

A

Discolouration + waxy appearance of skin associated with Graves’ disease

212
Q

What causes pretibial myxoedema?

A

Deposits of glycosaminoglycans under the skin on the front of the leg that form as a reaction to TSH receptor antibodies

213
Q

What pneumonic can be used to remember causes of hyperthyroidism?

A

GIST

214
Q

What are the causes of hyperthyroidism (using GIST)?

A

G-Graves’ disease
I-Inflammation
S-Solitary toxic thyroid nodule
T-Toxic multinodular goitre

215
Q

Name the 4 types of thyroiditis

A

-De Quervain’s thyroiditis
-Hashimoto’s thyroiditis
-Postpartum thyroiditis
-Drug-induced thyroiditis

216
Q

What are the symptoms of hyperthyroidism?

A

-Anxiety + irritability
-Sweating + heat intolerance
-Tachycardia
-Weight loss
-Fatigue
-Insomnia
-Brisk reflexes on exam

217
Q

What are the 4 specific feature of Graves’ disease?

A

-Diffuse goitre (no nodules)
-Graves’ eye disease
-Pretibial myxoedema
-Thyroid acropachy (hand swelling + finger clubbing)

218
Q

What are the 4 types of goitre?

A

-Diffuse
-Multinodular
-Solitary nodule
-Dominant nodule

219
Q

What are the 3 mechanisms for hyperthyroidism?

A

-XS production of hormones
-Leakage of preformed hormone from thyroid
-Ingestion of XS hormone

220
Q

Name 4 drugs that can cause drug-induced hyperthyroidism

A

-Iodine
-Amiodarone
-Lithium?
-Radiocontrast agents

221
Q

What are 3 Tx’s for hyperthyroidism?

A

-Antithyroid drugs e.g. Carbimazole
-Radioiodine
-Surgery to remove thyroid (life-long Levothyroxien required)

222
Q

What is the most serious side effect of thionamides such as Carbimazole used to treat hyperthyroidism?

A

Agranulocytosis which manifests as sore throat, fever, mouth ulcers

223
Q

What happens to levels of thyroid hormones in the first trimester of pregnancy?

A

Rise in T3 + T4 production, causing inhibition of TSH

224
Q

How can hypothyroidism affect pregnancy?

A

-Gestational hypertension
-Placental abruption
-Post partum haemorrhage
-Low birth weight
-Preterm delivery
-Neonatal goitre

225
Q

How can hyperthyroidism affect pregnancy?

A

-Low birth weight
-Pre eclampsia
-Preterm delivery
-Risk of stillbirth/miscarriage

226
Q

What women are most at risk of post partum thyroiditis?

A

Those with:
-Type 1 diabetics
-Graves’ in remission
-Chronic viral hepatitis

227
Q

How do thyroid function test ranges change during pregnancy?

A

Ranges are lower

228
Q

What is a Rathke’s cyst?

A

Single layer of epithelial cells with cyst fluid-derives from remnants of Rathke’s pouch

229
Q

What are the symptoms of a Rathke’s cyst?

A

-Headache
-Amenorrhoea
-Hypopituitarism
-Hydrocephalus

230
Q

What is a craniopharyngioma?

A

Benign tumour derived from the squamous epithelial remnants of Rathke’s pouch

231
Q

What are the symptoms of a craniopharyngioma?

A

-Raised ICP
-Visual disturbances
-Growth failure
-Pituitary hormone deficiency
-Weight increase

232
Q

What can cause meningiomas?

A

Complications of radiotherapy

233
Q

What are the symptoms of meningiomas?

A

-Visual disturbance
-Endocrine dysfunction
-Visual field defects

234
Q

What is lymphocytic hypophysitis?

A

Inflammation of the pituitary gland due to an autoimmune reaction

235
Q

What are 3 signs that a pituitary tumour is aggressive?

A

-Large size
-Cavernous sinus invasion
-Lobulated suprasellar margins

236
Q

What controls the release of prolactin?

A

Negative control of dopamine

237
Q

Name 4 factors that could cause a raised prolactin level

A

-Stress
-Drugs e.g. antipsychotics
-Stalk pressure
-Prolactinoma

238
Q

Name 5 co-morbidities of acromegaly

A

-Hypertension/heart disease
-Sleep apnea
-Arthritis
-Insulin-resistant diabetes
-Cerebrovascular events + headaches

239
Q

What 3 things would be used to diagnose acromegaly?

A

-Clinical features
-GH levels
-IGF-I levels

240
Q

How is acromegaly treated?

A

-Trans sphenoidal pituitary surgery
-Radiotherapy
-Medical therapy e.g. dopamine agonists, somatostatin analogues, GH receptor antagonists

241
Q

How are prolactinomas managed?

A

Medical Tx e.g.
-Dopamine agonists

242
Q

What random plasma glucose indicates diabetes?

A

> 11.1 mmol/l

243
Q

What fasting plasma glucose indicates diabetes?

A

> 7.0 mmol/l

244
Q

What HbA1c indicates diabetes?

A

> 48 mmol/mol

245
Q

Name 6 presenting features of diabetes

A

-Thirst
-Polyuria
-Weight loss
-Fatigue
-Hunger
-Recurrent thrush/skin/chest infections
-Blurred vision

246
Q

Name 5 suggestive features of type 1 diabetes

A

-Onset in childhood/adolescence
-Lean body
-Acute onset osmotic symptoms
-Prone to ketoacidosis
-High levels of islet antibodies

247
Q

What 3 features indicate type 1 + immediate start of insulin Tx?

A

-Weight loss
-Short history of severe symptoms
-Moderate/large urinary ketones

248
Q

What is the most common ages for diagnosis of type 1?

A

5-15yrs

249
Q

Name 2 viruses that may be associated with type 1 diabetes

A

-Coxsackie B
-Enterovirus

250
Q

What is the normal range for blood glucose concentrations?

A

4.4-6.1 mmol/l

251
Q

What is ketogenesis + when does it occur?

A

-Production of ketones
-Occurs when glycogen stores are exhausted so liver converts f.a. to ketones to use as fuel

252
Q

How does type 1 diabetes cause ketoacidosis?

A

-Insulin not produced so glucose levels rise
-Ketones produced as fuel source instead
-Rise in ketones is so significant, kidneys can’t control it anymore by buffering blood
-Ketones are acidic-causes DKA

253
Q

What are the 3 key features of DKA?

A

-Ketoacidosis
-Dehydration
-Potassium imbalance

254
Q

In what 3 scenarios can DKA occur?

A

-Initial presentation of type 1
-Infection/illness of existing type 1 diabetic
-Non-adherence of insulin regime in existing type 1 diabetic

255
Q

How does type 1 cause dehydration?

A

-Hyperglycaemia overwhelms kidneys
-Causes glucose to leak into urine
-Glucose in urine draws water with it by osmotic diuresis
-Causes polyuria
-Causes severe dehydration + polydipsia

256
Q

How does DKA cause potassium imbalance?

A

-Insulin normally drives potassium into cells
-So lack of it = high serum potassium, but low body potassium
-When insulin Tx starts, patients can develop hypokalaemia which can lead to fatal arrhythmias

257
Q

What are the ranges for hyperglycaemia, ketosis + acidosis that indicate DKA?

A

-BG >11mmol/l
-Blood ketones >3 mmol/l
-pH <7.3

258
Q

What are first-line Txs for DKA?

A

-Fluid resuscitation
-Insulin infusion

259
Q

What pneumonic can be used for management of DKA?

A

FIG-PICK

260
Q

What are the principles of management for DKA, using FIG-PICK?

A

F-fluids (IV)
I-insulin
G-glucose, monitor BG + add glucose infusion when less than 14 mmol/l
P-potassium-add K to IV + monitor
I-infection, treat underlying triggers e.g. infection
C-chart fluid balance
K-ketones, monitor blood ketones, pH + bicarbonate

261
Q

What 3 factors must be present before Tx for DKA is stopped?

A

-Ketosis + acidosis resolved
-Eating + drinking
-Re-started regular subcutaneous insulin

262
Q

What are the main complications during Tx for DKA?

A

-Hypoglycaemia
-Hypokalaemia
-Cerebral oedema, particularly in children
-Pulmonary oedema

263
Q

Name 3 types of antibodies present in type 1 diabetes

A

-Anti-islet cell antibodies
-Anti-GAD antibodies
-Anti-insulin antibodies

264
Q

What serum levels can be used as a measure of insulin?

A

Serum C-peptide

265
Q

What is lipodystrophy + what can cause it?

A

-Hardening of the subcutaneous fat
-Can be caused by injecting in the same spot

266
Q

What are the advantages of insulin pumps?

A

-Better BG control
-More flexibility with eating
-Less injections

267
Q

What are the disadvantages of insulin pumps?

A

-Difficulties learning to use it
-Having it attached at all times
-Blockages in infusion set
-Small risk of injection

268
Q

What does HbA1c measure?

A

Glycated haemoglobin-reflects average glucose levels over previous 2-3mths (RBC lifespan of 4mths)

269
Q

Name 3 types of glucose monitor

A

-Capillary BG monitor (finger-prick test)
-Flash glucose monitor (sensor on skin, pass phone over to read)- 5 min lag time!
-Continuous glucose monitor (similar to flash monitors but connected to phone by bluetooth)

270
Q

Name 3 short-term complications of insulin + BG management

A

-Hypoglycaemia
-Hyperglycaemia
-DKA

271
Q

What effect can chronic hyperglycaemia have?

A

-Damages endothelial cells of blood vessels + makes them leaky
-Immune system dysfunction-prone to infection

272
Q

What is a closed loop system of Tx for type 1?

A

AKA artificial pancreas, combination of continuous glucose monitor + insulin pump, automatic communication + adjustment of insulin

273
Q

Name 4 macrovascular complications of poorly controlled diabetes

A

-Coronary artery disease
-Peripheral ischaemia-can cause foot ulcers
-Stroke
-Hypertension

274
Q

Name 3 microvascular complications of poorly controlled diabetes

A

-Peripheral neuropathy
-Retinopathy
-Kidney disease, particularly glomerulosclerosis

275
Q

Name 4 infection-related complications of poorly controlled diabetes

A

-UTIs
-Pneumonia
-Skin infections
-Fungal infections, particularly oral + vaginal candidiasis

276
Q

What is MODY?

A

Maturity-onset diabetes of the young, monogenic diabetes

277
Q

What is the inheritance pattern for MODY?

A

Autosomal dominant

278
Q

At what age is MODY diagnosed?

A

<25

279
Q

What mutations cause MODY + how do they work?

A

Hepatic nuclear factor (HNF) mutations alter insulin secretion, reduce beta cell proliferation

280
Q

What is the typical presentation for MODY?

A

-FH
-Young age
-Non-obese
-Neonatal hypoglycaemia

281
Q

Name 5 diseases of the exocrine pancreas that can cause diabetes

A

-Chronic pancreatitis
-Transient hyperglycaemia
-Hereditary haemochromatosis
-Pancreatic neoplasia
-Cystic fibrosis

282
Q

Name 3 endocrine causes of diabetes

A

-Acromegaly
-Cushings
-Pheochromocytoma

283
Q

Name 4 drugs that can cause drug-induced diabetes

A

-Glucocorticoids
-Thiazides
-Protease inhibitors
-Antipsychotics

284
Q

Name 3 causes of adrenal insufficiency

A

-Primary-Addison’s disease
-Secondary-Hypopituitarism
-Tertiary-suppression of HPA e.g. by steroids

285
Q

What are the signs + symptoms of adrenal insufficiency?

A

-Fatigue
-Weight loss
-Poor recovery from illness
-Adrenal crisis
-Headache
-Pigmentation + pallor
-Hypotension

286
Q

What family history might be indicative of adrenal insufficiency?

A

Autoimmunity, congenital disease

287
Q

What past history might be indicative of adrenal insufficiency?

A

-TB
-Post partum bleed
-Cancer

288
Q

How would you manage an adrenal crisis?

A

-Immediate hydrocortisone
-Fluid resuscitation

289
Q

What are sick-day rules for adrenal insufficiency?

A

-Always carry 10 x 10mg tablets hydrocortisone
-If unwell-double dose steroids
-If vomiting take emergency injection 100mg hydrocortisone
-Go to A&E/ring ambulance

290
Q

What levels should be checked if suspicion of adrenal insufficiency?

A

-Cortisol
-ACTH

291
Q

What are the aims of type 2 diabetes treatment?

A

-Manage blood glucose
-Reduce risk of comorbidities
-Weight loss

292
Q

What conditions/complications does type 2 diabetes Tx aim to manage?

A

-CVD
-CKD
-Microvascular complications

293
Q

What are the 4 pillars of diabetes mellitus management?

A

-Glycaemic management
-Blood pressure management
-Lipid management
-Agents with cardiovascular + kidney benefit

294
Q

Name 7 Tx options for type 2 diabetes

A

-Metformin
-Pioglitazone
-Insulin
-SGLT2 inhibitors
-Sulphonylureas
-DPP-4 inhibitors
-GLP-1 receptor agonists

295
Q

How does insulin help control type 2 diabetes?

A

Injected insulin promotes uptake storage in the liver + muscle

296
Q

How do SGLT2 inhibitors help control type 2 diabetes?

A

They remove XS glucose load

297
Q

How do metformin + pioglitazone help control type 2 diabetes?

A

Help body respond better to its own insulin

298
Q

How do sulphonylureas, DPP-4 inhibitors + GLP-1 receptors help control type 2 diabetes?

A

They stimulate the pancreas to secrete more insulin

299
Q

What HbA1c level indicates pre diabetes?

A

42-47 mmol/l

300
Q

What HbA1c level indicates diabetes?

A

48+ mmol/l

301
Q

What are the NICE targets for HbA1c levels for new type 2 diabetics?

A

-48 mmol/l for new diabetics
-53 mmol/l for patients on more then one antidiabetic medication

302
Q

What is first line Tx for type 2 DM?

A

Metformin

303
Q

When does NICE recommend adding an SGLT-2 inhibitor for type 2 DM?

A

-If patient has existing CVD/heart failure

304
Q

When does NICE recommend CONSIDERING adding an SGLT-2 inhibitor for type 2 DM?

A

QRISK score above 10%

305
Q

Name the 4 second lien Tx’s for type 2 DM

A

-Sulfonylurea
-Pioglitazone
-DPP-4 inhibitor
-SGLT-2 inhibitor

306
Q

What are 3rd line Ts options for type 2 DM?

A

-Triple therapy - metformin + 2 second line drugs
-Insulin therapy

307
Q

What might you do if triple therapy for DM type 2 fails and the patient’s BMI is over 35 kg/m2?

A

Could switch one drug to a GLP-1 mimetic

308
Q

What is a potential sig. side effect for SGLT-2 Tx?

A

Diabetic ketoacidosis

309
Q

How does metformin work?

A

It increases insulin sensitivity + decreases glucose production

310
Q

What kind of medication is metformin?

A

Biguanide

311
Q

Name the 2 main side effects of metformin

A

-GI symptoms e.g. pain, nausea + diarrhoea
-Lactic acidosis

312
Q

Give 3 examples of SGLT-2 inhibitors

A

-Empagliflozin
-Canagliflozin
-Dapagliflozin

313
Q

What do SGLT-2 inhibitors do?

A

The SGLT-2 protein reabsorbs glucose from urine back into blood so inhibitors block this action-increases glucose excreted in urine

314
Q

What can the use of SGLT-2 inhibitors in combination with insulin or sulfonylureas do?

A

It can cause hypoglycaemia

315
Q

What are SGLT-2 inhibitors?

A

Sodium-glucose co-transporter 2 protein inhibitors

316
Q

Name 6 side effects of SGLT-2 inhibitors

A

-Glycosuria
-Increased urine output + frequency
-Genital + urinary tract infections e.g. thrush
-Weight loss
-Diabetic ketoacidosis
-Fournier’s gangrene

317
Q

What are the main 2 side effects of SGLT-2 inhibitors?

A

-Lots of sugar passing through urinary tract = increased infections + genital thrush
-Diabetic ketoacidosis

318
Q

What does pioglitazone do?

A

Increases insulin sensitivity + decreases liver production of glucose

319
Q

Name 4 side effects of pioglitazone

A

-Weight gain
-Heart failure
-Increased risk of bone fractures
-Small increase in risk of bladder cancer

320
Q

What do sulfonylureas do?

A

Stimulate insulin release from pancreas

321
Q

Name the most common sulfonylurea

A

Gliclazide

322
Q

Name 2 side effects of sulfonylureas

A

-Weight gain
-Hypoglycaemia

323
Q

What are incretins?

A

Hormones produced by the GI tract + secreted in response to large meals, they act to reduce blood sugar

324
Q

Name 3 ways in which incretins reduce blood sugar

A

-Increase insulin secretion
-Inhibit glucagon production
-Slow absorption by GI tract

325
Q

What is the main incretin?

A

GLP-1 (glucagon-like peptide-1)

326
Q

Name the enzyme that inhibits GLP-1

A

DPP-4

327
Q

How do DPP-4 inhibitors help reduce blood sugar?

A

-DPP-4 inhibitors block action of DPP-4
-This increases incretin activity
-Incretins reduce blood sugar

328
Q

What are the main side effects of DPP-4 inhibitors?

A

-Headaches
-Low risk of acute pancreatitis

329
Q

What are GLP-1 mimetics?

A

Imitate action of GLP-1 (incretin that reduces blood sugar)

330
Q

What is first line Tx for type 2 diabetics to manage hypertension?

A

ACE inhibitors

331
Q

What is HHS?

A

Hyperosmolar hyperglycaemic state-rare, potentially fatal complication of type 2

332
Q

What 7 symptoms does HHS present with?

A

-Polyuria
-Polydipsia
-Weight loss
-Dehydration
-Tachycardia
-Hypotension
-Confusion

333
Q

Describe TSH, T3 + T4 levels for primary hyperthyroidism

A

TSH-Low
T3/T4-High

334
Q

Describe TSH, T3 + T4 levels for secondary hyperthyroidism

A

TSH-High
T3/T4-High

335
Q

Describe TSH, T3 + T4 levels for primary hypothyroidism

A

TSH-High
T3/T4-Low

336
Q

What is carcinoid syndrome?

A

Release of serotonin and other vasoactive peptides from carcinoid tumour (neuroendocrine tumour)

337
Q

How does carcinoid syndrome present?

A

Diarrhoea, flushing, palpitations, abdo pain, wheezing

338
Q

How do you treat carcinoid syndrome?

A

-Surgical resection
-Octreotide infusion
-Somatostatin analogue

Phase 2a (8 decks)

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