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Endocrinology Flashcards

1
Q

What is the definition of diabetes mellitus?

A

Impaired production or response to insulin, resulting in raised blood glucose levels.

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2
Q

What are the classifications of diabetes?

A

Type 1, type 2, gestational, other specific types (e.g. MODY).

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3
Q

Is T1D insulin dependent or independent?

A

Insulin dependent.

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4
Q

What are the symptoms of T1D?

A

Polydipsia, polyuria, weight loss and fatigue.

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5
Q

What are the long term complications of diabetes (T1D and T2D)?

A

Macrovascular: coronary artery disease, peripheral artery disease, stroke, hypertension.
Microvascular: retinopathy, nephropathy, neuropathy, diabetic foot.
Infections: UTIs, pneumonia, skin & soft tissue, fungal.

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6
Q

Insulin secretion is dependent on what?

A

Glucose uptake by GLUT2 receptors, which stimulates insulin release from beta cells.

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7
Q

What are the actions of insulin?

A

Insulin binds to its receptor causing movement of GLUT4 receptors to the cell surface, stimulating glucose uptake into the cell.
Insulin causes decreased hepatic production of glucose (gluconeogensis and glycogenolysis).
Insulin also causes increased peripheral glucose uptake (glucose transport, glycogenesis).

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8
Q

What is the common presentation of T2D?

A

Asymptomatic detected on routine testing.
Or polydipsia, polyuria and complications e.g. infected foot.

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9
Q

What are normal blood glucose levels in a non diabetic?

A

Before meals: 4.0-5.9 mmol/L
90 mins after meals: < 7.8 mmol/L

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10
Q

What are target blood glucose levels in a type 1 diabetic?

A

Before meals: 4.0-7.0 mmol/L
90 mins after meals: 5.0-9.0 mmol/L

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11
Q

What are the target blood glucose levels in a type 2 diabetic?

A

Before meals: 4.0-7.0 mmol/L
90 mins after meals: < 8.5 mmol/L

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12
Q

What are normal, prediabetes and diabetes HbA1c levels?

A

Normal: < 42 mmol/mol
Prediabetes: 42-47 mmol/mol
Diabetes: 48 mmol/mol or greater

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13
Q

What is the role of insulin and where is it produced?

A

Insulin causes uptake of glucose into cells for energy and causes muscle and liver cells to uptake glucose from the blood and store it as glycogen (glycogenesis). Insulin also inhibits glycogenolysis, gluconeogenesis and lipolysis. It is produced from the beta cells of the pancreatic islets of langerhans in response to high blood glucose levels.

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14
Q

What is the role of glucagon and where is it produced?

A

Glucagon causes the liver to break down glycogen into glucose (glycogenolysis). It also stimulates gluconeogensis (production of glucose from fats and proteins) in the liver. Glucagon is produced by the alpha cells of the pancreatic islets of langerhans in response to low blood glucose levels and stress.

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15
Q

What is ketogenesis?

A

Ketogenesis occurs when there is insufficient glucose supply in cells and glycogen stores are exhausted. The liver converts fatty acids into ketones. Ketones are water soluble so can cross the BBB and used by the brain for energy. Ketones are normally buffered so the blood doesn’t become acidotic, but in patients with T1D with extreme hyperglycaemic ketosis it results in metabolic acidosis (diabetic ketoacidosis).

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16
Q

What is T1D?

A

Autoimmune destruction of beta cells in pancreatic islets of langerhans resulting in insulin deficiency and hyperglycaemia.

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17
Q

What is the typical onset of T1D?

A

Children and adolescents.

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18
Q

Which viruses are linked to T1D development?

A

Coxsackie B virus and enterovirus.

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19
Q

Which auto-Abs are involved in T1D pathophysiology?

A

Anti-GAD and islet cell Abs (ICA).

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20
Q

Which HLA genes are linked to T1D?

A

HLA-DR3 and HLA-DR4.

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21
Q

What causes weight loss in T1D?

A

Fluid loss and muscle/fat breakdown.

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22
Q

Which tests would you do for suspected T1D?

A

Random blood glucose level, urine dipstick, laboratory glucose, HbA1c, auto-Abs screen, C-peptide.

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23
Q

Describe the different types of insulin regimes

A

Basal bolus: long acting insulin in evening and short acting insulin 3x per day 30 mins before meals.
1, 2 or 3 injections per day: mix of both short and intermediate acting insulin (70/30).
Insulin pump: injects short acting insulin through a cannula inserted under the skin.

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24
Q

Why should patients cycle their injection sites of insulin?

A

Because lipodystrophy can occur which prevents absorption of insulin.

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25
Q

How is diabetes monitored?

A

HbA1c measured every 3-6 months.
Capillary blood glucose 4 times per day (one before each meal and one before bed).
Flash glucose monitoring (libre) measures glucose of interstitial fluid.
Diabetic review - injection site, retinopathy, nephropathy, diabetic foot, CV risk factors, thyroid disease.

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26
Q

What are the acute complications of T1D?

A

Hypoglycaemia and DKA.

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27
Q

What causes hypoglycaemia in diabetic patients?

A

Secondary to insulin or suphonylureas, not enough carbohydrates or not processing carbohydrates properly (D+V).

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28
Q

What are the symptoms of hypoglycaemia?

A

Hunger, tremor, sweating, palpitations, anxiety, irritability, dizziness and pallor.
Serious (< 2.8 mmol/L) - decreased consciousness, seizures, coma and death.

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29
Q

How would you manage hypoglycaemia?

A

Oral: rapid acting glucose (e.g. lucozade) and slower acting carbohydrates (e.g. biscuits/toast).
Severe cases: IV dextrose and IM glucagon.

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30
Q

What are the precipitating factors for DKA?

A

First presentation of T1D, poor diabetic control (not taking insulin), intercurrent illness e.g. infection.

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31
Q

What are the 3 features of DKA?

A

Hyperglycaemia (> 11 mmol/L).
Ketonaemia (> 3 mmol/L).
Acidosis (HCO3- < 15 mmol/L or venous pH < 7.3).

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32
Q

What is the pathophysiology of DKA?

A

Lack of insulin leads to hyperglycaemia. This is exacerbated by glycogenolysis, gluconeogensis and increased hormone secretion (cortisol, glucagon and GH). Lipolysis occurs leading to free FA, which are then converted into ketones. Build up of ketones in the blood causes acidosis. Excess glucose is filtered into the urine, causing osmotic diuretics, leading to polyuria and dehydration. As insulin normally drives potassium into the cell, there is high serum potassium but low total body potassium. Treatment with insulin can lead to hypokalaemia and arrhythmias.

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33
Q

What are the symptoms and signs of DKA?

A

Polydipsia, polyuria, N+V, acetone smell to breath, dehydration, hypotension, altered consciousness, abdominal pain and kussmaul breathing.

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34
Q

How would you manage DKA?

A

IV fluids, insulin infusion, glucose monitoring, potassium monitoring, treat infections, fluid balance chart and ketone monitoring.

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35
Q

When should HbA1c be used with caution?

A

Conditions interrupting erythropoiesis (e.g. EPO use, iron deficiency), haemoglobinopathies, glycation (e.g. CKD, alcoholism), red cell survival (e.g. haemolysis, splenectomy).

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36
Q

Is HbA1c appropriate for diagnosis of diabetes in children/young people?

A

No - also not appropriate in pregnancy.

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37
Q

What is the role of incretins?

A

Incretins are hormones produced by the GI tract. They’re secreted in response to large meals and act to decreased blood glucose. They increase insulin secretions, inhibit glucagon production and slow absorption by GI tract. GLP-1 is an incretin. DPP-4 is an enzyme that inhibits incretins.

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38
Q

What are the risk factors for T2D?

A

Non-modifiable: age, ethnicity (black, Chinese, south Asian), FHx/genetics, low birth weight, PCOS, Hx of GDM.
Modifiable: obesity, sedentary lifestyle, high carbohydrate diet, medications (e.g. corticosteroids).

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39
Q

What is the pathophysiology of T2D?

A

Insulin resistance: related exposure to glucose and insulin —> cells become insulin resistant —> more insulin is required to produce an effect —> failed glucose uptake —> chronic hyperglycaemia.
Insulin deficiency: high glucose levels toxic to beta cells —> beta cell depletion and pancreatic fatigue —> decrease insulin secretion.

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40
Q

What is involved in the oral glucose tolerance test (OGTT)?

A

Baseline fasting plasma glucose measured prior to breakfast in the morning. Then give 75g glucose drink and measure plasma glucose 2 hours later.

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41
Q

What is the diagnostic criteria for pre-diabetes?

A

HbA1c: 42-47 mmol/mol.
Impaired fasting glucose - fasting glucose: 6.1-6.9 mmol/L.
Impaired glucose tolerance - plasma glucose at 2 hours: 7.8-11.1 mmol/L.

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42
Q

What is the management for pre-diabetes?

A

Education and lifestyle changes - no medication. Potentially reversible with weight loss and exercise.

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43
Q

What is the diagnostic criteria for T2D?

A

HbA1c: > 48 mmol/mol.
Random glucose: > 11 mmol/L.
Fasting glucose: > 7 mmol/L.
OGTT: > 11 mmol/L.

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44
Q

What is the management for T2D?

A

Education and lifestyle changes —> low glycaemic, high fibre diet, exercise, weight loss, stop smoking, decrease alcohol intake, manage other diseases (e.g. hypertension, hyperlipidaemia, CVD).
Monitor for complications.
Monitor HbA1c and blood glucose levels.
Medication: 1st line (metformin), 2nd line (metformin + sulfonylurea/pioglitazone/DPP-4 inhibitor/SGLT-2 inhibitor), 3rd line (metformin + 2 drugs above OR metformin + insulin).

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45
Q

What are the acute complications of T2D?

A

Hypoglycaemia and hyperosmolar hyperglycaemic state (HHS).

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46
Q

What are the characteristics of HHS?

A

Hypovolaemia, hyperglycaemia, absent ketonaemia, high osmolarity.

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47
Q

What is the pathophysiology for HHS?

A

Relative insulin deficiency and elevated counter-regulatory hormones (e.g. cortisol, glucagon, GH) —> reduced glucose utilisation, increased gluconeogensis, increased glycogenolysis —> hyperglycaemia —> osmotic diuresis.

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48
Q

What are the symptoms of HHS?

A

Polydipsia, polyuria, N+V, muscle cramps, weakness, altered mental state, seizures, coma.

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49
Q

What is the management of HHS?

A

Fluid resuscitation, IV insulin infusion, electrolyte replacement, cardiac monitoring.

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50
Q

What are the complications of HHS?

A

MI, thrombotic events (hyperosmolar state —> hyperviscosity of blood), cerebral oedema.

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51
Q

Describe the role of bariatric surgery in the management of T2D

A

Bariatric surgery among T2D patients improves micro- and macrovascular complications. Post-operative weight loss and better glycaemic control. Effects on tissue-specific insulin sensitivity, beta cell function and incretin responses. Remission of diabetes in some patients.

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52
Q

What is metabolic syndrome?

A

Combination of diabetes, hypertension and obesity.

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53
Q

How would you treat diabetic nephropathy?

A

ARB/ACEi, SGLT2 inhibitor, statins.
Hypertension and glycaemic control.

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54
Q

What is the general treatment for diabetic foot ulcers?

A

Offloading, control of foot infection, control of ischaemia, wound debridement and wound dressings.

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55
Q

What is the relationship between mental health problems/eating disorders and T1D?

A

Diabetic patients can develop an unhealthy relationship or fixation with food because their disease is linked to diet, weight and body image. E.g. skipping insulin to lose weight, binge eating to make themselves vomit, food restriction, or over-exercising. Up to 30% of patients with T1D have an eating disorder.

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56
Q

What was the outcome of the diabetic control and complications trial (DCCT) on glycaemic control targets and progression of T1D complications?

A

The study showed that patients with T1D who keep their blood glucose levels as close to normal as safely possible with intensive diabetes treatment as early as possible in their disease have fewer diabetic complications compared to those on conventional treatment.

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57
Q

Why is carbohydrate counting important in T1D?

A

It means that insulin dose can be individually matched to your carbohydrate intake, leading to better glycaemic control.

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58
Q

Why is there increased CVD risk in T1D?

A

Accelerated atherosclerosis from inflammation.

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59
Q

How would you manage CV risk in patients with T1D?

A

Insulin, statins, BP control, aspirin and lifestyle changes.

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60
Q

Describe the role of transplant interventions in the management of T1D

A

Pancreatic islets cell transplant - beta cell replacement therapy. Available on NHS on a specific criteria.

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61
Q

Short-acting insulin is also known as…

A

Regular or soluble insulin.

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62
Q

Long-acting insulin mimics what type of insulin secretion?

A

Background secretion.

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63
Q

What is the insulin to carbohydrate ratio?

A

For every 10g carbohydrate you need 1 unit of insulin.

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64
Q

What are the pharmacological and surgical interventions for obesity?

A

Drugs - orlistat and liraglutide.
Bariatric surgery.

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65
Q

Why is HbA1c not recommended as a diagnostic test for patients with suspected T1D?

A

Because it may not reflect a recent rapid rise in blood glucose and results take longer than with serum glucose testing.

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66
Q

What is the relationship between obesity and the development of T2D?

A

Adipose tissue releases pro-inflammatory cytokines leading to insulin resistance. Increased waist circumference is associated with increased risk of developing T2D.

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67
Q

Describe tiered services in obesity management

A

Tier 1 - behavioural.
Tier 2 - lifestyle, diet, nutrition.
Tier 3 - MDT approach, weight management clinics, medical management.
Tier 4 - bariatric surgery.

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68
Q

What is the classification of obesity (BMI)?

A

Class 1: 30-34.9
Class 2: 35-39.9
Class 3: 40+

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69
Q

How would manage obesity?

A

Education, very low calorie diet, exercise programme, orlistat, liraglutide, bariatric surgery.

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70
Q

How does orlistat reduce weight in obesity?

A

Inhibits GI lipase, impairing absorption.

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71
Q

What is the role of leptin?

A

Suppresses appetite, secreted by adipose tissue.

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72
Q

What is the role of ghrelin?

A

Stimulates appetite, secreted by stomach.

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73
Q

Which hormones are released by the anterior pituitary?

A

TSH, ACTH, FSH, LH, GH and prolactin.

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74
Q

Which hormones are produced by the posterior pituitary?

A

Oxytocin and ADH.

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75
Q

Describe the thyroid axis

A

Hypothalamus releases TRH, which stimulates anterior pituitary to release TSH, which stimulates thyroid to released T3 and T4. T3 and T4 negatively feedback on TRH and TSH.

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76
Q

Describe the adrenal axis

A

Hypothalamus releases CRH, which stimulates anterior pituitary to release ACTH, which stimulates the adrenal cortex to release cortisol. Cortisol negatively feedbacks suppressing release of CRH and ACTH.

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77
Q

What is the role of cortisol in the body? When is it secreted?

A

Inhibits immune system, inhibits bone formation, raises blood glucose, increases metabolism and increases alertness (stress hormone).
Diurnal variation —> cortisol peaks early in morning and lowest in the late evening.

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78
Q

Describe the growth hormone axis

A

GHRH released by hypothalamus, stimulates GH to be released from anterior pituitary, which stimulates release of IGF-1 from liver. IGF-1 stimulates bone growth, muscle growth and cell regeneration and reproduction. Somatostatin inhibits GH secretion.

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79
Q

Describe the parathyroid axis

A

PTH released from parathyroid glands in response to low serum calcium, low magnesium and high serum phosphate. PTH increases serum calcium via increasing osteoclast activity causing reabsorption of calcium from bone into blood. PTH also increases calcium reabsorption in kidneys. PTH stimulates activation of vitamin D in kidneys which promotes calcium absorption in small intestine. High serum calcium suppresses PTH release (negative feedback) to reduce serum calcium level.

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80
Q

Describe RAAS system

A

Renin secreted by juxtaglomerular cells in afferent arterioles in kidneys in response to low BP. Renin converts angiotensinogen (released by liver) into angiotensin 1. ACE (released by lungs) converts angiotensin 1 into angiotensin 2. Angiotensin 2 causes vasoconstriction, increases sympathetic activation and increases ADH secretion. Angiotensin 2 also stimulates aldosterone release from adrenal gland. Aldosterone increases sodium reabsorption and in turn water reabsorption (and increases potassium secretion). This all acts to increase BP.

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81
Q

What are the functions of thyroid hormones?

A

Stimulate metabolic rate, positive inotropic and chronotropic effects on heart, involved in growth and development.

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82
Q

Which is the active thyroid hormone?

A

T3.
Conversion of T4 —> T3 in muscle, liver, kidney and brain.

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83
Q

Which hormone is used to screen for thyroid disease?

A

TSH.
If TSH is abnormal then T3 and T4 are measured.

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84
Q

Describe TFT results for primary hyperthyroidism

A

TSH: low
T3 & T4: high

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85
Q

Describe TFT results for secondary hyperthyroidism

A

TSH: high
T3 & T4: high

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86
Q

Describe TFT results for subclinical hyperthyroidism

A

TSH: low
T3 & T4: normal

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87
Q

Describe TFT results for primary hypothyroidism

A

TSH: high
T3 & T4: low

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88
Q

Describe TFT results for secondary hypothyroidism

A

TSH: low
T3 & T4: low

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89
Q

Describe TFT results for subclinical hypothyroidism

A

TSH: high
T3 & T4: normal

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90
Q

Anti-TPO Abs are present in which diseases?

A

Grave’s disease and Hashimoto’s thyroiditis.

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91
Q

Anti-thyroglobulin Abs are present in which diseases?

A

Grave’s disease, Hashimoto’s thyroiditis and thyroid cancer.

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92
Q

TSH receptor Abs are present in Grave’s disease. How do they cause hyperthyroidism?

A

Ab mimic TSH by binding to its receptor stimulating thyroid hormone release.

93
Q

How can the thyroid gland be imaged?

A

Ultrasound —> thyroid nodules.
Radioisotope scan —> hyperthyroidism and thyroid cancer.

94
Q

What is the difference between hyperthyroidism and thyrotoxicosis?

A

Hyperthyroidism is the overproduction of thyroid hormones due to an overactive thyroid gland. Whereas thyrotoxicosis is the abnormal/excessive amount of thyroid hormones in the body.

95
Q

What are the main causes of hyperthyroidism?

A

Grave’s disease: autoimmune condition where TSH receptor Abs stimulate increased T3 and T4 production.
Toxic multinodular goitre: nodules develop on thyroid gland, leading to excessive thyroid hormone secretion.
Solitary toxic thyroid nodule: single abnormal thyroid nodule releasing thyroid hormones.
De Quervain’s thyroiditis: viral infection with fever, neck pain, dysphasia and hyperthyroidism. Self-limiting disease treated with NSAIDs and beta blockers.

96
Q

What are the general clinical features of hyperthyroidism?

A

Anxiety, irritability, sweating, heat intolerance, tachycardia, weight loss, fatigue, tremor, loose stools, sexual dysfunction, goitre, hair loss.

97
Q

What are the specific features of Grave’s disease?

A

Exophthalmos, lid retraction, lid lag, pretibial myxoedema.

98
Q

What is the management of hyperthyroidism?

A

Carbimazole (1st line): decreases thyroid hormone formation by decreasing uptake of iodine by thyroid.
Propylthiouracil (2nd line): inhibits thyroid peroxidase.
Radioactive iodine: radiation destroys thyroid cells decreasing thyroid hormone production.
Beta blockers: propranolol, symptom control.
Thyroidectomy.

99
Q

What are the causes of hypothyroidism?

A

Hashimoto’s thyroiditis: autoimmune inflammation of thyroid gland by anti-TPO Abs and anti-thyroglobulin Abs.
Iodine deficiency.
Secondary to hyperthyroid treatment.
Medications e.g. lithium and amiodarone.
Postpartum thyroiditis.
Congenital hypothyroidism.
Secondary hypothyroidism: pituitary adenoma.

100
Q

What are the clinical features of hypothyroidism?

A

Weight gain, fatigue, dry skin, coarse hair, hair loss, cold intolerance, goitre, bradycardia, depression, fluid retention, heavy or irregular periods, constipation, reduced libido.

101
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (synthetic T4).

102
Q

What are the symptoms of hypercalcaemia?

A

Stones, bones, abdominal groans and psychiatric moans.
Also polyuria and polydipsia.

103
Q

What are the causes of primary hyperparathyroidism?

A

Uncontrolled PTH secretion from a tumour of parathyroid glands (parathyroid adenoma).
High PTH and hypercalcaemia.

104
Q

What are the causes of secondary hyperparathyroidism?

A

Vitamin D deficiency or CKD cause hypocalcaemia, so parathyroid reacts by secreting more PTH, which leads to hyperplasia of gland overtime.
High PTH and low/normal calcium.

105
Q

What are the causes of tertiary hyperparathyroidism?

A

Occurs when secondary hyperparathyroidism continues for a long time leading to parathyroid hyperplasia and baseline PTH level increases. Treatment of secondary hyperparathyroidism but PTH remains inappropriately high.
High PTH and hypercalcaemia.

106
Q

What are the most common types of thyroid cancer?

A

Papillary carcinoma (most common) and follicular carcinoma.

107
Q

What are the clinical features of thyroid cancer?

A

Thyroid nodules (hard, non-mobile, non-tender), unexplained hoarseness or stridor with goitre, cervical lymphadenopathy, sore throat, dysphasia.

108
Q

What is the management for thyroid cancer?

A

Thyroidectomy, radioactive iodine, radiotherapy and chemotherapy.

109
Q

What are the 3 layers of the adrenal cortex and what do they secrete?

A

Zona glomerulosa —> mineralocorticoids e.g. aldosterone.
Zona fasciculata —> glucocorticoids e.g. cortisol.
Zona reticularis —> androgens e.g. DHEA.

110
Q

Which cells of the adrenal medulla secrete catecholamines e.g. A/NA?

A

Chromaffin cells.

111
Q

Describe adrenal steroid synthesis pathway

A

Cholesterol is the main precursor. Cholesterol converted into pregnenolone, which is then converted to DHEA. DHEA is the precursor to testosterone and oestradiol. Pregnenolone can also be converted into aldosterone.

112
Q

What is the most common cause of secondary hypertension?

A

Renal disease

113
Q

Which hormones does Addison’s disease affect and how?

A

Damage to the adrenal gland reduces both cortisol and aldosterone secretion.

114
Q

What are the common causes of Addison’s disease?

A

Autoimmune adrenalitis and TB infective adrenalitis (developing world).

115
Q

How can immune checkpoint inhibitors cause adrenal insufficiency?

A

Immune checkpoint inhibitors cause activation of the immune system (to kill cancer cells), but the immune cells can attack the adrenal glands or pituitary causing adrenalitis.

116
Q

What are the clinical features of Addison’s disease?

A

Fatigue, abdominal pain, decreased libido, N+V, postural hypotension, hyperpigmentation, depression, anorexia, dehydration, pubic and armpit hair loss.

117
Q

Describe features of adrenal crisis and management

A

Decreased consciousness, confusion, hypotensive shock, hypoglycaemia, hyponatraemia, hyperkalaemia, dehydration, N+V, pyrexia.
Management: IV hydrocortisone, IV fluids.

118
Q

What are ACTH and steroid hormone levels like in Addison’s disease?

A

ACTH high, cortisol low, aldosterone low.

119
Q

How would you investigate for Addison’s disease?

A

Hyponatraemia, short synacthen test, ACTH levels, adrenal auto-Abs.

120
Q

What is characteristic of Addison’s disease in the short synacthen test?

A

Failure of cortisol to rise less than double the baseline at 30 and 60 mins.

121
Q

Which 2 drugs would you prescribe for a patient with Addison’s disease?

A

Hydrocortisone and fludrocortisone.

122
Q

Describe the aetiology of secondary adrenal insufficiency and it’s hormone levels

A

Caused by pituitary pathology such as pituitary adenoma, infection, ischaemia or radiotherapy.
Low ACTH, low cortisol.
Management: hydrocortisone.

123
Q

Describe the aetiology of tertiary adrenal insufficiency and it’s hormone levels

A

Hypothalamus suppression such as from long-term oral steroid use.
Low CRH, low ACTH, low cortisol.

124
Q

Cushing’s syndrome vs. Cushing’s disease

A

Cushing’s syndrome is the result of any cause of excess glucocorticoid exposure (ACTH dependent or ACTH independent).
Cushing’s disease is specifically caused by increased ACTH secretion e.g. pituitary adenoma.

125
Q

What are the causes if Cushing’s syndrome?

A

Exogenous glucocorticoids (most common), pituitary/adrenal adenoma, paraneoplastic Cushing’s (increase ACTH release from cancer).

126
Q

Describe the characteristic features of Cushing’s

A

Round moon face, central obesity, abdominal striae, buffalo hump, proximal limb muscle wasting, easy bruising, poor healing skin, amenorrhoea, hypertension, cardiac hypertrophy, hyperglycaemia, depression, insomnia, osteoporosis, hirsutism.

127
Q

Describe the findings of low dose dexamethasone suppression test

A

Cushing’s syndrome: increased/normal cortisol.

128
Q

Describe the results of high dose dexamethasone suppression test

A

Pituitary adenoma: decrease ACTH, decrease cortisol.
Adrenal adenoma: decrease ACTH, increase/normal cortisol.
Ectopic ACTH: increase ACTH, normal/increase cortisol.

129
Q

Treatment of Cushing’s syndrome?

A

Treat cause: gradual removal of glucocorticoids, tumour removal.

130
Q

What are the 2 clinical findings of hyperaldosteronism?

A

Hypertension and hypokalaemia.

131
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia and Conn’s syndrome (adrenal adenoma).

132
Q

What are the causes of secondary hyperaldosteronism?

A

Renal artery stenosis/obstruction leading to excessive renin secretion due to drop in kidneys BP.

133
Q

Is serum renin high or low in primary hyperaldosteronism?

A

Low.

134
Q

Is serum renin high or low in secondary hyperaldosteronism?

A

High.

135
Q

What are the investigations for hyperaldosteronism?

A

Renin/aldosterone ratio, BP, U&Es, blood gas, abdominal CT/MRI, renal Doppler ultrasound.

136
Q

Which drug would you give to someone with hyperaldosteronism?

A

Aldosterone antagonist e.g. spironolactone.

137
Q

What is a phaeochromocytoma?

A

Tumour of chromaffin cells in adrenal medulla, increasing the secretion of adrenaline.

138
Q

What are the causes of phaeochromocytoma?

A

Sporadic or hereditary (MEN2, VHL syndrome, neurofibromatosis type 1).

139
Q

Why do the signs and symptoms of phaeochromocytoma fluctuate and what are they?

A

They fluctuate because adrenaline is secreted from the tumour in bursts.
Anxiety, sweating, headache, hypertension, palpitations, tachycardia, paroxysmal AF, dyspnoea and tremor.

140
Q

How would you diagnose a phaeochromocytoma?

A

24 hour urine catecholamines.
Plasma free metanephrines.
CT/MRI.

141
Q

What are the management options of a phaeochromocytoma?

A

Alpha blockers e.g. phenoxybenzamine, beta blockers and adrenalectomy.

142
Q

How would you reduce the risk of a hypertensive crisis from anaesthesia or surgery in a patient with a phaeochromocytoma?

A

Optimise BP control.

143
Q

What are the causes of acromegaly?

A

Excessive GH secretion:
- pituitary adenoma.
- ectopic GHRH or GH secretion from cancer (lung/pancreatic).

144
Q

Acromegaly vs gigantism

A

In childhood excessive GH secretion causes your bones to increase in size leading to increased height (before epiphyseal plate fusion), which is termed gigantism. Whereas, in adulthood, excessive GH secretion causes tissues to increase in size but not bones, so a change in height isn’t characteristic of acromegaly.

145
Q

What are the clinical features of acromegaly?

A

Bitemporal hemianopia, frontal bossing, large ears & nose, macroglossia, large hands & feet, prognathism.
Cardiac hypertrophy, hypertension, T2D, colorectal cancer.
Also new skin tags and profuse sweating.

146
Q

How would you investigate for acromegaly?

A

IGF-1, OGTT (high glucose suppresses GH) and brain MRI.

147
Q

What is the surgical and medical management for acromegaly?

A

Surgical: trans-sphenoidal removal of pituitary tumour.
Medical: GH antagonists, somatostatin analogues, dopamine agonists.

148
Q

What is the function of ADH and when is it released?

A

ADH (aka vasopressin) is released by the posterior pituitary in response to high plasma osmolarity. It acts on the DCT and collecting ducts to increase water reabsorption independent of sodium via insertion of aquaporin channels onto luminal membrane.

149
Q

What are the 2 causes of diabetes insipidus?

A

Nephrogenic - collecting ducts don’t respond to ADH.
Cranial - hypothalamus doesn’t produce ADH.

150
Q

What are the main symptoms of diabetes insipidus?

A

Polydipsia and polyuria.

151
Q

What is the diagnostic test for diabetes insipidus?

A

Water deprivation test.

152
Q

What is the treatment for diabetes insipidus?

A

Desmopressin (synthetic ADH).

153
Q

What are the investigations for SIADH?

A

Bloods: U&Es (hyponatraemia), serum osmolality (low).
Urine: urinary osmolality (high), urine sodium (high).
Examination: euvolaemia.
Exclusion of other causes of hyponatraemia e.g. Addison’s, dehydration, diuretics, excessive water intake, CKD or AKI.
Establish cause e.g. chest X ray.

154
Q

What is a complication of rapid correction of hyponatraemia?

A

Central pontine myelinolysis (osmotic demyelination syndrome)

155
Q

Management for SIADH?

A

Treat cause e.g. remove medications.
Fluid restriction.
Tolvaptan (ADH receptor blocker).

156
Q

What medications have a role in the aetiology of hypophysitis?

A

Immune checkpoint inhibitors.

157
Q

What are the causes of hypopituitarism?

A

Pituitary adenomas, craniopharyngiomas, empty sella syndrome, hypophysitis, pituitary apoplexy, Sheehan’s syndrome, radiotherapy or surgery.

158
Q

What are the clinical features of hypopituitarism?

A

Headaches, amenorrhoea, galactorrhoea, visual field defects, short stature/faltering growth, infertility, cold intolerance, weigh gain, erectile dysfunction/reduced libido.

159
Q

What are the investigations for hypopituitarism?

A

Serum electrolytes, serum & urine osmolarity, early morning cortisol, ACTH levels, TFTs, IGF-1, LH, FSH, testosterone, oestradiol, short synacthen test, insulin tolerance test and CT/MRI pituitary.

160
Q

How would you manage hypopituitarism?

A

Treat underlying cause. Hormone replacement therapy.

161
Q

What are the clinical features associated with hyperprolactinaemia?

A

Amenorrhoea, reduced libido, erectile dysfunction, gynaecomastia.

162
Q

Investigations for prolactinomas?

A

Pregnancy test, serum prolactin, pituitary MRI.

163
Q

Management for prolactinomas?

A

Dopamine agonists (dopamine inhibits prolactin) and trans-sphenoidal removal of pituitary tumour.

164
Q

What does MEN syndrome stand for?

A

Multiple endocrine neoplasia syndrome.

165
Q

Describe MEN type 1

A

Caused by a mutation in MEN 1 tumour suppressor gene and is characterised by primary hyperparathyroidism, pituitary adenoma and pancreatic tumours.

166
Q

Describe MEN type 2

A

Caused by a mutation in RET proto-oncogene and is characterised by primary hyperparathyroidism, phaeochromocytomas and medullary thyroid cancer. Divided into MEN 2A and MEN 2B.

167
Q

Management of hypercalcaemia

A

Calcitonin, calcimimetics, bisphosphonates, IV fluids

168
Q

At what BMI should obese patients be referred for bariatric surgery?

A

40-50 kg/m^2

169
Q

What are the types of bariatric surgery?

A

Laparoscopic -adjustable gastric banding (first-line).
Sleeve gastrectomy.
Intragastric balloon.
Biliopancreatic diversion with duodenal switch (BMI > 60).
Roux-en-Y gastric bypass surgery.

170
Q

How often should blood glucose be monitored in T1D?

A

At least 4 times a day, including before each meal and before bed.

171
Q

Name a specific feature of Grave’s disease that would distinguish it from general hyperthyroidism

A

Exophthalmos

172
Q

DVLA and diabetes

A
  • Patients on insulin can drive a car as long as they have good hypoglycaemic awareness, not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months and no relevant visual impairment. Must notify DVLA.
  • Patients on tablets don’t need to notify DVLA.
  • Patients on insulin who want to apply for a Group 2 (HGV) licence need to complete a VDIAB1I form.
173
Q

Describe the presentation of myxoedema coma

A

Confusion and hypothermia.

174
Q

What is an important complication of fluid resuscitation in DKA, especially in young patients?

A

Cerebral oedema

175
Q

Describe common complications of papillary and follicular thyroid cancer

A

Papillary - spread to cervical lymph nodes.
Follicular - high calcitonin (calcitonin made by parafollicular cells).

176
Q

Name a side effect of Pioglitazone other than weight gain

A

Fluid retention

177
Q

A 32-year-old man is prescribed a 5-day course of amoxicillin following a diagnosis of community acquired pneumonia (CURB-65 score of 1). He has a past medical history of type 1 diabetes mellitus, which is well controlled with an insulin basal-bolus regime.

What action should be taken with regards to this patients insulin therapy?

A

Continue their normal insulin regime but ensure that they are checking their blood sugars frequently.

178
Q

What can cause pseudo-Cushing’s syndrome?

A

Alcohol excess, severe depression.

179
Q

What is the fixed rate insulin infusion rate for DKA?

A

0.1 unit/kg/hour

180
Q

What is the most common cause of primary hyperparathyroidism?

A

Solitary parathyroid adenoma

181
Q

What is the first line medication for thyroid storm?

A

IV propranolol

182
Q

Describe the radioiodine uptake in Grave’s disease

A

Diffuse, oncreased, homogenous uptake.

183
Q

Describe radioiodine uptake in toxic nodular goitre

A

Areas of intense uptake interspersed with some reduced activity.

184
Q

Describe radioiodine uptake in subacute thyroiditis (De Quervain’s thyroiditis)

A

Faint diffuse uptake.

185
Q

Describe radioiodine uptake in toxic adenoma

A

A single hot nodule with the rest of the gland suppressed.

186
Q

What is the initial management of DKA?

A

Isotonic saline

187
Q

What is the standard target HbA1c level in T2D?

A

48 mmol/mol

188
Q

At what HbA1c level should a second drug be added for the management of T2D?

A

> 58 mmol/mol

189
Q

What is the first line management for T2D?

A

Metformin OR Metformin + SGLT-2 inhibitor (if high risk CVD or chronic HF).

190
Q

If metformin is not tolerated because of GI side effects, which medication can be trialled next?

A

Modified-release metformin

191
Q

What are the BP targets for patents with T2D?

A

The same as patients without diabetes:

  • < 80: 140/90 mmHg (clinic) or 135/85 mmHg (ABPM).
  • > 80: 150/90 mmHg (clinic) or 145/85 mmHg (ABPM).
192
Q

What is the first line medication for hypertension in patients with T2D?

A

ACEi or ARB (if black)

193
Q

What is the first line insulin regime in newly diagnosed T1D?

A

Basal-bolus regime: a rapid-acting insulin analogue, such as NovoRapid, at meal times in conjunction with a long-acting basal insulin-like detemir (Levemir), which is delivered subcutaneously twice daily.

194
Q

What is the function of aldosterone?

A

Increases Na+ reabsorption (increasing BP) and increases K+ excretion.

195
Q

What is the first line investigation for suspected primary hyperaldosteronism?

A

Plasma aldosterone/renin ratio

196
Q

Describe the uptake in nuclear scintigraphy for toxic multinodular goitre

A

Patchy uptake

197
Q

What is the treatment of choice for toxic multinodular goitre?

A

Radioiodine therapy

198
Q

What should happen to the levothyroxine dose in pregnant women with hypothyroidism?

A

Increase their levothyroxine dose by up to 50% as early as 4-6 weeks of pregnancy.

199
Q

What should happen to a patients regular insulin whilst they’re being treated for DKA?

A

Continue long-acting insulin but stop short-acting insulin.

200
Q

Thyrotoxicosis can lead to which cardiac sequela?

A

High output HF

201
Q

What blood gas finding would you expect with Cushing’s syndrome?

A

Hypokalaemic metabolic alkalosis

202
Q

Outline the side effects of glucocorticoids

A
  • Endocrine: impaired glucose regulation! increased appetite/weight gain, hirsutism, hyperlipidaemia.
  • Cushing’s syndrome: moon face, buffalo hump, striae.
  • Musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head.
  • Immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis.
  • Psychiatric: insomnia, mania, depression, psychosis.
  • Gastrointestinal: peptic ulceration, acute pancreatitis.
  • Ophthalmic: glaucoma, cataracts.
  • Suppression of growth in children.
  • Intracranial hypertension.
  • Neutrophilia.
203
Q

Outline the side effects of mineralocorticoids

A
  • Fluid retention.
  • Hypertension.
204
Q

Describe the sick day rules for patients on long-term steroids

A

Patients should have their doses doubled during intercurrent illness.

205
Q

Why should patients on long-term steroids not have them abruptly withdrawn?

A

As it may precipitate an Addisonian crisis.

206
Q

How often should insulin-dependent diabetics check their blood glucose whilst driving?

A

Every 2 hours

207
Q

Management for myxedema coma?

A

IV corticosteroids, IV fluids and IV thyroid replacement.

208
Q

How does myxoedema coma typically present?

A

With confusion and hypothermia.

209
Q

What Abs are most commonly associated with Grave’s disease?

A

TSH receptor stimulating Abs

210
Q

Thyroid acropachy (seen in Grave’s) is a triad of:

A
  • Digital clubbing
  • Soft tissue swelling of the hands and feet
  • Periosteal new bone formation
211
Q

Treatment of thyrotoxicosis in pregnancy

A
  • Propylthiouracil in first trimester.
  • Then switch to carbimazole.
212
Q

Why are there increased levels of total thyroxine in pregnancy (but doesn’t affect free thyroxine level)?

A

Because there is an increase in levels of thyroxine-binding globulin (TBG).

213
Q

What parameter is most important for measuring treatment success for DKA with insulin?

A

Blood ketones

214
Q

Treatment of HHS

A
  • Fluid resuscitation
  • Insulin when blood glucose stops falling
215
Q

How can alcohol bingeing affect ADH secretion?

A

It suppresses ADH in the posterior pituitary leading to polyuria

216
Q

Management of DKA

A
  1. If patient is shocked - IV fluid resuscitation with 500ml NaCl 0.9% over 15 mins. If patient isn’t shocked - 1L NaCl 0.9% over 1 hour.
  2. No insulin immediately.
  3. FRIII - 0.1unit/kg/hr. When blood glucose is <= 14 mmol/L then switch to VRIII (GKI).
  4. KCl added to NaCl 500ml bag.
  5. Continue long acting insulin in DKA.
217
Q

What should you monitor with DKA?

A
  1. Blood ketones
  2. Blood glucose
  3. Bicarbonate
218
Q

Which hypoglycaemic agent can be used as a monotherapy for T2D in patients with severe renal impairment (GFR < 30)?

A

Sulfonylureas e.g. gliclazide

219
Q

What is the most common drug cause of gynaecomastia?

A

Spironolactone

220
Q

What are the two most common causes of hypercalcaemia?

A
  1. Primary hyperparathyroidism
  2. Malignancy (e.g. PTHrP from squamous cell lung cancer, bone mets, myeloma)
221
Q

Poor compliance with levothyroxine

A
  • Increased TSH
  • Normal T4
222
Q

Erratic blood glucose control, bloating and vomiting

A

Gastroparesis

223
Q

Treatment of thyrotoxic storm

A

Beta blockers, propylthiouracil and hydrocortisone

224
Q

What is the most common endogenous cause of Cushing’s syndrome?

A

Pituitary adenoma

225
Q

Which hypoglycaemic agent is associated with increased risk of bladder cancer?

A

Pioglitazone

226
Q

Describe the key features of hypocalcaemia

A
  • Perioral paraesthesia
  • Cramps
  • Tetany
  • Convulsions/seizures
227
Q

What is the management of severe hypocalcaemia (carpopedal spasm, tetany, seizures or QT prolongation)?

A

IV calcium gluconate

228
Q

What is the first line management of hypercalcaemia?

A

IV fluids

Metabolic (6 decks)

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