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Phase 2A Tom > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Define type 1 diabetes

A

Type 1 diabetes mellitus is a metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency.

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2
Q

What is the epidemiology for type 1 diabetes?

A
  • Accounts for 5-10% of all patients with diabetes.
  • More common amongst Europeans.
  • Causes more than 85% of diabetes in under 20s.
  • Highest incidents amongst 10–14-year-olds.
  • Incidence increasing by 3% yearly
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3
Q

What is the genetic aetiology of type 1 diabetes?

A

Some human leukocyte polymorphisms can increase susceptibility to the disease.(HLA-DR gene)

In susceptible people environmental factors may lead to immune-mediated destruction of beta cells.

Coeliac disease may have link

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4
Q

What is the environmental aetiology of type 1 diabetes?

A

Much higher rates in Europe may indicate environmental factors no known specific ones.

Vitamin D can be protective

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5
Q

What virus is believed to have a link to type 1 diabetes?

A

Human enterovirus

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6
Q

What are the risk factors for type 1 diabetes?

A

Family history

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7
Q

What is the usual physiological cause of type 1 diabetes?

A

Destruction of pancreatic beta cells (that produce insulin)

Up to 90% of people have autoantibodies

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8
Q

How long does beta cells destruction occur for before symptoms usually start to present for type 1 diabetes?

A

Months to years

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9
Q

What % of beta cells need to be destroyed before symptoms usually appear for type 1 diabetes?

A

80-90%

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10
Q

What happens as a result of low insulin levels?

A

Due to insulin deficiency glucose can’t be utilised from muscle and adipose.

Stimulates secretion of glucagon (adrenaline, cortisol, and growth hormone)

So increased Lipolysis, = weight loss

More glucose in urine - Polyuria and Polydipsia

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11
Q

What does the secretion of glucagon (adrenaline, cortisol, and growth hormone) result in? (Type 1 diabetes)

A

Gluconeogenesis, Glycogenolysis and ketogenesis.

Patients as a result present with ketoacidosis and hyperglycaemia.

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12
Q

What are the most common key presentations of type 1 diabetes?

A
  • Hyperglycaemia (above 11.1).
  • Polyuria (passing urine frequently).
  • Polydipsia (drinking water frequently)
  • Tiredness
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13
Q

What are some other common key presentations of type 1 diabetes?

A

young age, weight loss, blurred vision, nausea, and vomiting, Abdo pain,

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14
Q

What are the first line investigations for children in type 1 diabetes?

A
  • Random plasma glucose (above 11)
  • Fasting plasma glucose (above 7)
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15
Q

What are the first line investigations for adults in type 1 diabetes?

A
  • Hyperglycaemia (above 11.1) (random plasma glucose) - one of Ketosis, Rapid weight loss, Age <50 years, BMI <25 kg/m², personal and/or family history of autoimmune disease this is for adults
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16
Q

What is the gold standard test for diagnosing type 1 diabetes in children?

A

Glycohemoglobin test (HbA1c)

Reflects the degree of hyperglycaemia over the preceding 3 months greater than 6.5% (48 mmol/mol) indicates diabetes

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17
Q

What are other diagnostic tests you do to confirm a diagnosis of type 1 diabetes?

A
  • Plasma or urine ketones,
  • C-peptide,
  • Autoimmune markers
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18
Q

What are some differential diagnoses of type 1 diabetes?

A

Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Type 2 diabetes

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19
Q

What is the management of type 1 diabetes?

A

o Basal-bolus insulin (insulin glargine s/c)
o Pre-meal insulin correction dose
o Amylin analogue (pramlintide)
2nd line: fixed insulin dose

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20
Q

What is the difference between Basal and Bolus insulin dosing for Diabetes?

A

The two main ways to take insulin are bolus and basal.

Bolus insulin is the quick-acting delivery that you often take before mealtimes.

Basal insulin is longer-acting and helps keep your glucose levels steady day and night

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21
Q

What is the main medical drug given to treat T1DM?

A

Using a combination of long-acting insulin (insulin detemir, degludec, or glargine) for basal dosing,

and rapid-acting insulin (insulin lispro, aspart, or glulisine) for bolus dosing

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22
Q

What are the side effects of insulin?

A

hypoglycaemia, weight gain, lipodystrophy

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23
Q

What would you monitor for patients with diabetes?

A

Measure HbA1c levels every 3 months in children and every 3-6 months in adults
Make sure level is under 6.5% (48 mmol/mol)

Also monitor BP and kidney function

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24
Q

What are the short-term complications associated with type 1 diabetes?

A

Death due to ketoacidosis

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25
Q

What are some microvascular complications of diabetes?

A

Peripheral neuropathy- nerves in the body’s extremities, such as the hands, feet and arms, are damaged
Retinopathy- damage to vessels in the eye
Kidney disease, particularly glomerulosclerosis

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26
Q

What are some macrovascular complications of diabetes?

A

Coronary artery disease is a major cause of death in diabetics
Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
Stroke
Hypertension

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27
Q

What are the long-term complications associated with type 1 diabetes?

A
  • Microvascular: retinopathy, peripheral or autonomic neuropathy
  • Cardiovascular disease, diabetic kidney disease.
  • Potential for depression and eating disorder#
  • Foot amputations
  • Blindness
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28
Q

Define type 2 diabetes

A

A progressive disorder defined by deficits in insulin secretion and insulin resistance that lead to abnormal metabolism and related metabolic derangements

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29
Q

What percentage of diabetes cases are type 2?

A

90%

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30
Q

What is the epidemiology of type 2?

A

OLDER! >30 years of age. Often overweight around the abdomen
- More prevalent in South Asian, African and Caribbean ancestry

Common is all populations enjoying an affluent lifestyle
More common in males

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31
Q

By how much cases of type 2 diabetes have increased since 1980

A

4%

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32
Q

What is the aetiology of type 2 diabetes?

A

Genetic

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33
Q

What are some risk factors for type 2 diabetes?

A

Ageing
high BMI
gestational diabetes
non-white ancestry
polycystic ovary syndrome
hypertension

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34
Q

What BMI is overweight?

A

25-29.9

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35
Q

What BMI is considered obese?

A

> 30

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36
Q

What is the pathophysiology for type 2 diabetes?

A

Insulin resistance affects primarily the liver, muscle, and adipocytes,
It is characterized by complex derangements in cellular receptors, intracellular glucose kinase function, and other intracellular metabolic processes
Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less.

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37
Q

How does type 2 diabetes cause damage to blood vessels and nerves?

A

Glycated end products accumulating in tissues damages them.

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38
Q

What are the key presentations for type 2 diabetes?

A

Hyperglycaemia with presence of risk factors

E.g., Overweight, certain ethnic groups, age

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39
Q

What are some signs of type 2 diabetes?

A

High blood glucose levels

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40
Q

What are symptoms of type 2 diabetes?

A

Polydipsia
Polyuria
candidal infections,
skin infection,
UTIs,
fatigue,
blurred vison
uncommon symptoms

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41
Q

What are first line investigations for type 2 diabetes?

A

Fasting glucose, 2-hour post load glucose (75g orally) random plasma glucose

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42
Q

What is the gold standard test for type 2 diabetes?

A

HbA1c

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43
Q

What are some differential diagnosis for type 2 diabetes?

A

Type 1 diabetes, other types e.g. gestational, adolescent

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44
Q

What is the initial management for type 2 diabetes?

A

1st lifestyle changes plus agree glycaemic (HbA1c) target
Adjunct of BP and lipid management

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45
Q

What is the management for acute type 2 diabetes?

A

HbA1c is above target 1st metformin plus lifestyle measures, cardiovascular risk reduction, and specific considerations

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46
Q

How would you manage type 2 diabetes?

A

Every 3 to 6 months (tailored to individual needs), until the patient’s HbA1c is stable on unchanging therapy *
Every 6 months once the patient’s HbA1c level and blood glucose-lowering therapy are stable.

First-line is metoformin

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47
Q

When should a second anti-diabetic drug be added to the use of metformin?

A

When HBA1c rises above 58mmol/mol despite maximum dose of metformin

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48
Q

How does metformin work?

A
  • Metformin which increases the rate of gluconeogenesis in the liver??????? tom i think this is the exact opposite of what it does
  • Increases cell sensitivity to insulin
  • Helps with weight issues
  • reduces CVS risk in diabetes
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49
Q

What are some other anti-diabetic drugs?

A
  • Sulfonylureas (gliclazide) they promote insulin secretion but only work in people with functional B-cells. Risk of hypoglycaemia and weight gain. Increased risk of CVD when used as a monotherapy
  • Dipeptidyl peptidase-4 inhibitor (DPP-4i) (incretins): they are hormones produced in the GI tract which increase Increase insulin secretions, Inhibit glucagon production, Slow absorption by the GI tract
  • SGLT-2 inhibitors “-gliflozin”, such as empagliflozin, canagliflozin and dapagliflozin- it inhibits glucose reabsorption from the the urine into the blood
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50
Q

What is a basal bolus that is given in type 1 DM and sometimes in bad T2DM

A

Givng a dose before each meal in order to miminc the effect of insulin released

So three times a day

eg. Insulin Inspiro, or Insulin Aspart

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51
Q

What insulin medication pattern do you see in T2DM

A

Just once a day, (Basal) sometimes twice (BD)

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52
Q

What else would you monitor in a patient with type 2 diabetes?

A

Measure blood pressure at least once a year in an adult with type 2 diabetes without previously diagnosed hypertension or renal disease.

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53
Q

What are some low likelihood complications associated with type 2 diabetes?

A

Diabetic kidney disease, impaired vision, lower extremity amputation

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54
Q

What are the most likely complications associated with type 2 diabetes?

A

Cardiovascular disease, congestive heart failure, stroke.
Diabetic ketoacidosis if very poorly managed

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55
Q

Why are you more at risk of infections if you have type 2 diabetes?

A

Hyperglycaemia impairs immune function

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56
Q

How years on average is someone’s life shortened by type 2 diabetes?

A

Men lose 5.8 years women lose 6.8 years

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57
Q

What is ketoacidosis?

A

Diabetic ketoacidosis (DKA) is characterized by a biochemical triad of hyperglycaemia (or a history of diabetes), ketonemia, and metabolic acidosis, with rapid symptom onset.

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58
Q

What is the main cause of ketoacidosis?

A

Uncontrolled/undiagnosed diabetes

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59
Q

What is the pathophysiology of ketoacidosis?

A

Reduced insulin concentration and insulin counter regulatory hormones leads to hyperglycaemia and electrolyte imbalance.

Insulin deficiency leads to release of fatty acids (lipolysis), hepatic fatty acid oxidation and increased formation of ketone bodies (hydroxybutyrate and acetoacetate (most common)).

This results in ketonemia and acidosis

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60
Q

What are the key presentations of ketoacidosis?

A

Patients with known diabetes who are experiencing nausea, vomiting, abdominal pain, hyperventilation, dehydration and reduced consciousness
Or patients with suspected diabetes and these symptoms

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61
Q

What are the common symptoms of ketoacidosis?

A

Nausea, vomiting, abdominal pain, hyperventilation, dehydration and reduced consciousness

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62
Q

What are some biochemical signs of ketoacidosis?

A

Hyporkalaemia, high plasma osmolarity, blood ketones.

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63
Q

What are some other symptoms of ketoacidosis?

A

Acetone smell on breath
Hypothermia

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64
Q

What is the first line investigation for ketoacidosis?

A

Venous blood gas greater

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65
Q

What blood PH indicates mild to moderate ketoacidosis?

A

Below normal but above 7

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66
Q

What blood PH indicates severe ketoacidosis?

A

Below 7

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67
Q

What is the gold standard test for ketoacidosis?

A

Urinary analysis

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68
Q

What other tests would you order for a patient with ketoacidosis?

A

ECG, pregnancy test

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69
Q

What are some differential diagnoses for diabetic ketoacidosis?

A
  • Hyperosmolar hyperglycaemic state,
  • Latic acidosis (order serum lactate).
  • Starvation/alcoholic ketoacidosis
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70
Q

How would you treat ketoacidosis?

A
  1. Give a fluid bolus of 500 mL of normal saline (0.9% sodium chloride) over 10 to 15 minutes if the initial systolic blood pressure (SBP) is <90 mmHg.
  2. Give IV insulin to lower blood glucose
  3. Add potassium to the second litre of intravenous fluid if serum potassium is ≤5.5 mmol/L. As giving insulin lowers potassium
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71
Q

How would you monitor ketoacidosis?

A
  • order hourly blood glucose and hourly blood ketones.
  • Perform a venous blood gas for pH, bicarbonate, and potassium at 60 minutes, 2 hours and then every 2 hours after
  • Assess GCS
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72
Q

What are some complications associated with ketoacidosis?

A
  • Hypokalaemia (due to high dose insulin therapy)
  • Arterial/venous thrombotic events
  • Cerebral oedema (main cause of death)
  • ARDS (occurs when too much fluid is given)
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73
Q

What is the prognosis for a patient with ketoacidosis?

A

0.67% mortality

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74
Q

What is Hyperosmolar hyperglycaemic state?

A

A profound state of hyperglycaemia and hyperosmolarity and volume depletion in the absence of ketoacidosis more commonly a side effect of T2DM

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75
Q

What is the epidemiology of HHS?

A
  • Usually occurs in the elderly but is more recognised in younger patients
  • Average age is 60
  • Often the first presentation of T2DM (20-30% of cases)
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76
Q

What causes HHS?

A
  • Usually triggered by an infection. Due to the relative lack of insulin, coupled with a rise in cortisol, growth hormone, glucagon there is a profound rise in glucose
  • The excessive glucose leads to massive osmotic diuresis within the kidneys with loss of Na and K.
  • There is profound dehydration which leads to the viscosity of the blood increasing the risk of DVT and stroke and MI
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77
Q

What are the signs of HHS?

A
  • Reduced GCS - reduced consciousness/ coma
  • Dehydration - tachycardia and hypotension, dry mucous membranes, reduced skin turgor
  • Could be confused for a stroke - e.g. hemiparesis
  • Seizures
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78
Q

What are the investigations for HHS?

A

Laboratory glucose, urea & electrolytes blood test (electrolyte derangement and AKI due to dehydration), ABG/VBG (hyperglycaemia without a metabolic acidosis) and a blood or urinary ketone level.

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79
Q

What is the diagnostic criteria for HHS?

A
  • Hyperglycaemia > 30 without hyperketonaemia and acidosis
  • Hyperosmolarity >320
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80
Q

What is the treatment for HHS?

A
  • IV fluid (0.9% saline)- results in reduction in osmolality and glucose. Insulin not always required
  • Potassium replacement
  • Anti-coagulant
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81
Q

What is Graves’ disease?

A

An autoimmune disease associated with hyperthyroidism

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82
Q

What are some other causes of Hyperthyroidism?

A

Toxic adenoma
Toxic multinodular goitre

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83
Q

What is the cause of Graves’ disease?

A

TSH (thyroid-stimulating hormone) receptor antibodies cause the hyperthyroid syndrome and underlie the extrathyroidal manifestations.

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84
Q

Describe the epidemiology of Graves’ disease

A
  • 2.5% prevalence.
  • More common in older age groups.
  • 6 times more common in women.
  • 20-50 cases per 100,000 per year
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85
Q

Is graves’ disease more common in men or women?

A

Women (6x more likely)

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86
Q

What is the aetiology of Graves’?

A

TSH receptor antibodies
Combination of genetic and environmental risk factors.
No specific genes but HLA linked.

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87
Q

What 2 autoantibodies are found in 75% of patients with Graves’ disease

A

Thyroglobulin and thyroid peroxidase.

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88
Q

What are some risk factors for Graves’?

A
  • Family history of autoimmune disease (HLA-DR3)
  • Tobacco use
  • Female sex
  • Radiation
  • High iodine intake (increases TRH)
  • Lithium therapy
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89
Q

What is the pathophysiology of Graves?

A
  1. TSH receptor antibodies bind to thyroid
  2. This causes increased thyroid hormone production
  3. The increased production leads to thyroid hypertrophy
  4. Symptoms occur as result of increase in thyroid hormone
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90
Q

What are the key presentations for Graves’/hyperthyroidism?

A
  • Presence of risk factors
  • Heat intolerance + increased sweating
  • Weight loss
  • Palpitations
  • Goitre
  • Orbitopathy
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91
Q

What are some signs of Graves?

A
  • Elevated TSH receptor antibodies
  • Suppressed TSH levels
  • Elevated T3 and T4
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92
Q

What are some other symptoms associated with Graves/hyperthyroidism?

A
  • Irritability
  • Cardiac flow murmur
  • Moist velvety skin
  • Scalp hair loss
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93
Q

What is the first line investigation for Graves?

A
  • Serum TSH (levels will be surppressed)
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94
Q

What is the gold standard test for Graves disease?

A
  • Presence of TSH receptor antibodies
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95
Q

What are some other tests you can do to make a diagnosis of Graves?

A
  • Serum T3 and T4
  • Thyroid isotope scan
  • Ultrasound of thyroid
  • Pregnancy test
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96
Q

What are some differential diagnosis for Graves?

A
  • Toxic nodular goitre,
  • Pregnancy related,
  • TSH producing pituitary adenoma
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97
Q

What are some side effects of Antithyroid drugs (thionamides)

A

Rash (most common)
hepatitis
vasculitis
Agranulocytosis (most serious side effect)- sore throat fever, mouth ulcers

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98
Q

What is the main goal when treating Graves?

A
  • To normalise thyroid function parameters

There is nothing done to counteract autoimmune aspect

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99
Q

How would you treat Graves?

A
  • Antithyroid medications- decreases synthesis of of new thyroid hormone (carbimazole)
  • Radioactive Iodine
  • Thyroid ablation
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100
Q

How would you monitor Graves?

A

Measure TSH levels at 6 week intervals until levels are stable

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101
Q

What are some complications associated with Graves?

A
  • AF
  • Congestive heart failure
  • Bone mineral loss
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102
Q

What risk associated with Graves?

A

Cardiovascular problems

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103
Q

What are the four main types of thyroid cancer?

A
  • Follicular
  • Anaplastic
  • Medullary
  • Papillary

FAMP

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104
Q

What percentage of thyroid cancers do the 4 main types make up?

A

98%

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105
Q

Is thyroid cancer more common in men or women?

A

Women

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106
Q

What is the most common age to be diagnosed with thyroid?

A

45-54

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107
Q

What is the prevalence of thyroid cancer?

A

15.8 per 100,000

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108
Q

What are risk factors for developing thyroid cancer?

A
  • Head and neck irradiation
  • Female sex
  • Genetic factors
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109
Q

What is the most common pathophysiology of
a papillary carcinoma?

A
  • Papillary carcinoma tends to spread to local lymph nodes
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110
Q

What is the common pathophysiology of a follicular tumour?

A
  • Follicular and Hurthle cells often spread haematogenous.
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111
Q

How does anaplastic thyroid cancer spread?

A
  • Anaplastic thyroid cancer is a rare, aggressive, undifferentiated carcinoma with a high propensity for local invasion and metastatic spread.
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112
Q

What are the key presentations for thyroid cancer?

A
  • Presence of risk factors
  • Palpable thyroid nodule
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113
Q

What are some symptoms of thyroid cancer?

A
  • Hoarseness
  • Tracheal deviation
  • Dyspnoea
  • Dysphagia
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114
Q

What is a first-line investigation for thyroid cancer

A

Normal TSH with reduced thyroid function

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115
Q

What is the gold standard test for thyroid cancer?

A

Fine-needle biopsy

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116
Q

What is a differential diagnosis for thyroid cancer?

A

A benign thyroid nodule

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117
Q

How would you manage a follicular tumour?

A

The standard approach is surgery followed by radioactive iodine ablation and suppression of TSH for most patients

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118
Q

How would you manage a medullary tumour?

A

Total thyroidectomy

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119
Q

How would you treat an anaplastic tumour?

A

Total thyroidectomy and if that is not possible then with chemo/radio therapy

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120
Q

How would you treat a thyroid lymphoma?

A

With radio and chemotherapy

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121
Q

What are some disease related complications of thyroid cancer?

A
  • Airway obstruction
  • Secondary tumours
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122
Q

What are some complications of a thyroidectomy?

A
  • Hypoparathyroidism due to damage to parathyroid glands
  • Recurrent laryngeal nerve damage
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123
Q

What is the prognosis for a papillary/follicular carcinoma?

A

> 90% 10 year survival rate
- medullary is slightly worse due to more metastasis

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124
Q

What is the prognosis for a anaplastic thyroid tumour?

A

Average survival of a few months after diagnosis

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125
Q

What is the prognosis for a medullary tumour?

A

80% 5 year survival rate

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126
Q

What is the prognosis for a primary thyroid lymphoma?

A

<50% 5 year survival rate

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127
Q

What is Cushing’s syndrome?

A

Cushing syndrome is the clinical manifestation of pathological hypercortisolism from any cause.

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128
Q

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

A

Exogenous corticosteroid exposure

For example taking steroids e.g., prednisone

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129
Q

What is the difference between Cushing’s syndrome and Cushing’s disease

A
  • Cushing’s syndrome disease is pathological hypercortisolism from any cause.
  • Cushing’s disease is hypercortisolism caused by a endogenous source e.g., pituitary adenoma
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130
Q

What is the incidence of Cushing’s syndrome per year

A

0.7-2.4 per million population

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131
Q

Is Cushing’s syndrome more common in men or women?

A

Women, Cushing’s disease is also more common in women

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132
Q

What is the most likely age range to be diagnosed with Cushing’s?

A

20-50

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133
Q

What is the most common cause of Cushing’s disease?

A

Pituitary adenomas- make up 70-80% of all cases

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134
Q

What % of Cushing’s disease is caused by pituitary adenomas?

A

70-80%

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135
Q

What % of pituitary adenomas result in excessive ACTH production?

A

10%

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136
Q

What % of Cushing’s disease is caused by adrenal adenomas?

A

10%

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137
Q

Name 2 other causes of Cushing’s disease?

A
  • Ectopic neuroendocrine tumours (usually masses in the lungs)
  • Adrenal carcinoma
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138
Q

What is ACTH-dependant Cushing’s disease?

A

overproduction of ACTH which stimulates adrenal gland to secrete more cortisol.

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139
Q

What two types of tumour are ACTH-dependant causes of Cushing’s disease?

A

Pituitary adenoma, ectopic neuroendocrine ACTH secreting tumours

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140
Q

What is ACTH-independant Cushing’s disease

A

When there is excessive cortisol production without high levels of ACTH

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141
Q

What are the 6 hormones secreted by the anterior pituitary?

A

Adrenocorticotrophic hormone (ACTH)
Thyroid-stimulating hormone (TSH)
Luteinising hormone (LH)
Follicle-stimulating hormone (FSH)
Prolactin (PRL)
Growth hormone (GH)

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142
Q

What are the two hormones secreted by the posterior pituitary?

A

Oxytocin
Anti-diuretic hormone (ADH)

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143
Q

What two types of tumour are ACTH-independent causes of Cushing’s disease?

A

Adrenal adenomas and adrenal carcinomas

144
Q

How does Cushing’s cause disease?

A
  • The clinical manifestations is due to excess tissue exposure to cortisol.
  • The degree to which symptoms present is due to the amount of excess.
145
Q

What cause of Cushing’s is most likely to be severe and abrupt in its presentation?

A

Ectopic ACTH secretion from neuroendocrine tumours

146
Q

What are some key presentations associated with Cushing’s?

A
  • Presence of risk factors
  • Facial plethora (redness)
  • Weight gain
  • Supraclavicular fulness, torso weight gain but weak arms
  • Absence of pregnancy, alcoholism, malnutrition
147
Q

What are some key signs of Cushing’s?

A

Increased serum glucose, elevated cortisol in saliva, high urinary cortisol

148
Q

What are some symptoms associated with Cushing’s?

A
  • Hypertension
  • Weight gain
  • Glucose intolerance
  • Premature osteoporosis
  • Decreased libido
  • Muscle weakness
  • Facial rounding
  • Acne

think of a bloke with massive fat stomach and face, really skinny limbs and really stressed

149
Q

How many key investigations are there you can do to confirm a diagnosis of Cushing’s?

A

4

150
Q

What are the 4 main diagnostic tests for Cushing’s?

A
  1. Late night salivary cortisol (4nmol)
  2. 1mg overnight dexamethasone suppression test (50 nmol/litre),
  3. 24 hour urinary free cortisol.
  4. 48- hour 2 mg dexamethasone suppression testing
151
Q

How do you perform a late night salivary cortisol test?

A
  • Samples are collected by saturating a collection swab with saliva or by passively drooling into a collection tube between 11 p.m. and midnight.

Sampling should be done on 2 separate nights

152
Q

Why is the salivary test performed at night?

A

This is when cortisol levels are at their lowest. Will give the most accurate baseline figure

153
Q

What is the 1mg overnight dexamethasone test

A

Patient is given 1 mg of dexamethasone at 11 p.m., and a plasma cortisol level is obtained the following morning at 8 a.m

154
Q

What value would indicate Cushing’s?

A

morning cortisol >50 nanomol/L

155
Q

What is a positive result for the 24 hour urinary free cortisol?

A

> 50 micrograms/24 hour

156
Q

What is the difference between the low and high dose dexamethasone tests?

A

This higher dose is enough to suppress the cortisol in Cushing’s syndrome caused by a pituitary adenoma (Cushing’s disease), but not when it is caused by an adrenal adenoma or ectopic ACTH.

157
Q

What other test would be performed on a patient with suspected Cushing’s?

A

Pregnancy test

158
Q

What are some differntial diagnosis of Cushing’s

A
  • Obesity
  • Metabolic syndrome
  • Pregnancy

Lack of facial plethora, bruising weakness and osteoporosis

159
Q

How would you treat Cushing’s disease?

A

First line : If an adenoma remove adenoma as that is the cause.

Adjunct: If only mild use or very severe (before surgery) use a steroidogenesis (pasireotide) inhibitor or a glucocorticoid receptor antagonist (mifepristone).

Monitor cortisol levels after removal of pituitary adenoma. May require hormone replacement due to dysfunction of HPA

160
Q

How would you monitor Cushing’s?

A

Recurrence of adrenocorticotrophic hormone-dependent Cushing syndrome is common, with at least a 5% to 26% risk of recurrence at 5 years.

Patients who have achieved remission should be screened periodically (every 6-12 months) for recurrence of disease.

161
Q

What are some complications associated with Cushing’s?

A

CVD, Hypertension, Diabetes, Osteoporosis

162
Q

What is the prognosis for untreated Cushing’s?

A

5 year survival of 50%

163
Q

What is Hypothyroidism?

A

The deficiency of thyroid hormones, which leads to a generalised slowing of metabolic processes.

164
Q

What is primary hypothyroidism?

A

The failure of the thyroid gland to produce thyroid hormones.

165
Q

What is secondary/central hypothyroidism?

A

Arises from an anatomical or functional disorder of the pituitary gland and/or the hypothalamus.

166
Q

What % of hypothyroidism cases are caused by primary hypothyrodism?

A

99%

167
Q

What is the epidemiology of hypothyroidism?

A
  • More common in women
  • More common in white people
  • Incidence increases with age
168
Q

What is the most common cause of primary hypothyroidism?

A

Hashimoto’s thyroiditis (8-9 times more likely in women)

169
Q

Name some other causes of hypothyroidism (non-drug related)

A
  • Damage or destruction of the thyroid gland from thyroidectomy,
  • Radioactive iodine therapy for Graves’ disease
  • Nodular goitre,
  • Radiotherapy for head and neck cancer.
  • Sarcoidosis and haemochromoatosis
170
Q

Name some drugs that can cause hypothyroidism

A

lithium, amiodarone, interferon alpha

171
Q

What can cause transient primary hypothyroidism?

A
  • Sub-acute granulomatous (De Quervain’s
  • Post partum
172
Q

Name some risk factors for hypothyroidism

A

Iodine deficiency, female, middle age, family history, hyper treatment, turners and down syndrome.

173
Q

Describe the pathophysiology of Hashimoto’s thyroiditis

A
  • T3 and T4 create negative feedback loop with TSH so low levels of T3 and T4 equal elevated TSH
  • In autoimmune lymphocytes, Thyroglobulin and thyroid peroxidase antibodies invade the thyroid causing damage (High iodine makes thyroid more antigenic).
    This means less T4 and T3 are produced resulting in the clinical symptoms
174
Q

How do some drugs cause hypothyroidism?

A

Amiodarone contains iodine, which interferes with thyroid hormone synthesis.
Lithium interferes with thyroid hormone synthesis and release.

Both are reversible

175
Q

What are the key presentations for hypothyroidism?

A

Risk factors.
Lots of non-specific features e.g., tiredness but don’t know why, weakness

176
Q

What are some signs of primary hypothyroidism?

A

High levels of TSH but low T3 and T4.

177
Q

What are the signs of secondary hypothyroidism?

A

Low TSH and low T3 and T4.

178
Q

Name some symptoms of hypothyroidism?

A
  • Fatigue
  • Weight gain
  • Cold intolerance
  • Constipation
  • Menstrual disturbance
  • Dry rough skin
  • Bradycardia
  • Oedema
  • Delayed muscle reflexes
179
Q

What would be the first line investigations for hypothyroidism?

A

Serum TSH
Free T4

180
Q

Name 3 differential diagnosis for hypothyroidism?

A

Depression
Alzheimer’s
Anaemia

All have normal TSH levels

181
Q

What is the main treatment for hypothyroidism?

A

L-thyroxine (levothyroxine)

182
Q

How should you monitor patients with hypothyroidism?

A

Levothyroxine has a long half-life, TSH levels should be measured 4-12 weeks after dose change.

183
Q

What changes should be made during pregnancy?

A

Pregnancy requires increased dose of levothyroxine

184
Q

What are some side effects of L-thyroxine

A

Angina, resistant hypothyroidism, AF, osteoporosis.

185
Q

What are some complications of untreated hypothyroidism?

A

myxoedema coma (older patients) , complications in pregnancy

186
Q

What is acromegaly?

A

Acromegaly is a rare, chronic disease caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma.

187
Q

What is crucial when treating acromegaly?

A

Early recognition but the disease has an insidious onset

188
Q

When is acromegaly most likely to be diagnosed?

A

Middle age

189
Q

What is the most common cause of acromegaly?

A

Pituitary somatotroph adenoma (95-99%)

Prolactin is co-secreted in 25% of cases

190
Q

What is another potential cause of acromegaly?

A

Neuroendocrine tumours

191
Q

What gene mutation is shown in 30-40% of pituitary somatotroph adenomas?

A

GNAS1

192
Q

Describe the pathophysiology of acromegaly

A
  • Dysregulation of hormones and transcription factors lead to growth of tumours
  • Pituitary somatotroph adenomas secrete excess GH
  • GH binds to liver which causes the release of insulin growth factor 1 (IGF-1)
  • IGF-1 causes symptoms
193
Q

What are the key presentations of acromegaly?

A
  • Coarsening of facial features (enlarged nose, jaw - Enlargement, separation of teeth)
  • Thickening skin
  • Carpal tunnel
  • Joint pain,
  • Alterations of sexual function
  • Headaches
194
Q

What are some signs of acromegaly?

A

Elevated IGF-1, elevated GH

195
Q

What are some symptoms of acromegaly?

A

Fatigue, hypertension, organmegaly, increased appetite, headaches

196
Q

What are first line investigations of acromegaly?

A

Serum IGF-1 test
Serum GH test

197
Q

What is the gold standard test for diagnosing acromegaly?

A

Oral glucose tolerance test (lack of supressed GH)

198
Q

What is a differential diagnosis of acromegaly?

A

Pseudo-acromegaly clinical features but all tests will be normal

199
Q

How would you manage acromegaly?

A

For enclosed pituitary tumour surgery will be the first option.

SSA somatostatin analogue (octreotide).
Dopamine agonist in some groups

200
Q

How would you monitor acromegaly?

A

lifelong monitoring of growth hormone and insulin-like growth factor 1 (IGF-1) levels

201
Q

What are complications associated with untreated acromegaly?

A

Cardiac complications, hypertension, sleep apnoea, diabetes, pre-cancerous colon polyps, carpal tunnel syndrome

202
Q

What is the prognosis for a patient diagnosed with acromegaly?

A

2-3 time higher chance of mortality then general population

203
Q

What is Conn’s syndrome?

A

Primary aldosteronism (PA) is the most common specifically treatable and potentially curable form of hypertension.

204
Q

What is aldosterone?

A

Aldosterone is a mineralocorticoid, a steroid hormone released from the zona glomerulosa of the adrenal cortex

Causes sodium to be reabsorbed through ENaC to be pumped into the blood by the sodium/potassium pump.

In exchange, potassium is moved from the blood into the principal cell of the nephron. This potassium then exits the cell into the renal tubule to be excreted into the urine.

205
Q

What % of hypertension cases are caused by Conn’s?

A

It accounts for at least 5% of hypertensive patients

206
Q

What causes unilateral Conn’s and what % of cases does it make up?

A

Benign cortical adenomas correctable by unilateral laparoscopic adrenalectomy

Accounts for 30% of cases

207
Q

What causes bilateral Conn’s and what % of cases does it make up?

A

Bilateral adrenal hyperplasia in which hypertension responds well to aldosterone antagonist medicines.

Accounts for 70% of cases

208
Q

Name a form of genetically inherited PA

A

familial hyperaldosteronism type I (FH-I)

209
Q

What are some risk factors for PA

A

Familial history of PA, family history of early onset hypertension/stroke

210
Q

Explain the pathophysiology of Conn’s

A

Aldosterone production is excessive to the body’s requirements, and autonomous to the RAAS.

This results in excessive Na+ absorption which leads to hypertension and suppression of RAAS and in severe cases low K+ (hypokalaemia) and metabolic acidosis (22%) of cases

211
Q

What are some microvascular complications of diabetes?

A

Peripheral neuropathy- nerves in the body’s extremities, such as the hands, feet and arms, are damaged
Retinopathy- damage to vessels in the eye
Kidney disease, particularly glomerulosclerosis

212
Q

What are some microvascular complications of diabetes?

A

Peripheral neuropathy- nerves in the body’s extremities, such as the hands, feet and arms, are damaged
Retinopathy- damage to vessels in the eye
Kidney disease, particularly glomerulosclerosis

213
Q

What are key presentations for Conn’s?

A

Hypertension, presence of risk factors, 20-70 years of age.

214
Q

What are signs of PA?

A

Low potassium, high aldosterone to renin ratio

215
Q

What are some symptoms of PA

A

Polyuria, lethargy, mood disturbance, difficulty concentrating

216
Q

What are some investigations for getting a diagnosis of PA?

A

Plasma potassium- won’t be low only present in 20% of cases
Aldosterone /renin ratio

217
Q

What further tests could be done for a patient with suspected PA?

A

Genetic testing, adrenal CT, fludrocortisone suppression test

218
Q

What are some differential diagnosis for PA?

A
  • Idiopathic Hypertension- aldosterone/renin ratio will be normal.
  • Renal artery stenosis
  • Liddle syndrome- hypokalaemia and low renin but also low aldosterone levels
219
Q

How can you manage a patient with PA?

A

1st line: Unilateral adrenalectomy/bilateral adrenalectomy

adjunct preoperative aldosterone antagonists
adjunct postoperative aldosterone antagonists

220
Q

How would you monitor a patient who has undergone an adrenalectomy?

A

Plasma electrolytes, and aldosterone and renin levels should be monitored every 6 to 12

221
Q

How would you monitor a patient who is treating their PA through the use of aldosterone antagonists?

A

Electrolytes and renal function should be monitored regularly (e.g., every 3 to 6 months), watching for development of hyperkalaemia (for patients on medication)

222
Q

What are the complications associated with Conn’s?

A

Untreated: Stroke, MI, heart failure, AF, impaired renal function
Treatment: aldosterone antagonist induced hyperkalaemia

223
Q

What is the prognosis for PA?

A

Surgery leads to cure of hypertension in 50% to 60% of carefully selected patients
Medication leads to improved control of hypertension in most cases

224
Q

What is Addison’s/primary adrenal insufficiency?

A

A disorder that results from intrinsic diseases that affect the cortex of the adrenal gland.

This results in impairment in the synthesis of all steroids.

225
Q

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

A

Zona glomerulosa- mineralocorticoids (aldosterone)
Zona fasciculata- glucocorticoids ( Cortisol)
Zona reticularis- dehydroepiandrosterone (DHEA)

226
Q

What is secondary/central adrenal insufficiency

A

When the hormones are not secreted due to lack of ACTH release from pituitary/CRH from the hypothalamus.
Mineralocorticoids (aldosterone) are maintained

227
Q

What is the epidemiology of Addison’s in the UK?

A

300-350 new cases a year
Women are at greater risk of developing an autoimmune disease
Therefore in the UK the predominant cohort is women

228
Q

What is the predominant cause of Addison’s in developed countries?

A
  • In developed countries 75-95% of cases are autoimmune
  • In 90% of these cases 21-hydroxylase autoantibodies are present
  • Is often associated with other autoimmune endocrine disorders
229
Q

What is the main cause of Addison’s worldwide?

A

TB

230
Q

What are some risk factors for developing Addison’s ?

A

Female sex, adrenocortical autoantibodies, adrenal haemorrhage, autoimmune diseases, coeliac disease

231
Q

Describe the process in which Addison’s causes symptoms?

A
  • Symptoms are a result of decreased production of main adrenal steroids
  • This is a result of destruction of the 3 layers of the cortex or disruption of the synthesis of these hormones

Approximately 90% of the cortex needs to be destroyed for symptoms to appear

232
Q

What can cause the destruction of the adrenal cortex?

A
  • Autoimmune process (adrenalitis)
  • Infection (TB)
  • Infiltrating diseases (amyloidosis hemochromatosis)
  • Tumours

Haemorrhage within the adrenals can also result in acute destruction

233
Q

What are the key presentations of Addison’s?

A
  • Hyperpigmentation
  • Anorexia/weight loss
  • Fatigue
  • Salt craving
234
Q

What are the signs of Addison’s?

A
  • Postural hypotension
  • Lowered serum cortisol
  • Increased ACTH (only in primary)
  • Elevated urea and creatine
235
Q

What are some other symptoms of Addison’s?

A
  • Vomiting
  • Axillary and pubic hair loss
236
Q

What are some first line investigations for Addison’s?

A
  • Na+ low and K+ high (result of reduced aldosterone)
  • Morning serum cortisol (>140 low)
  • Plasma ACTH (>12 high)
237
Q

What is the gold standard test for diagnosing Addison’s?

A

ACTH stimulation test of cortisol ( exclude Addison’s if serum cortisol is greater than 550 after stimulation)

238
Q

What would some other tests be for Addison’s?

A

Antibodies (presence of 21-hydroxylase) , CT or MRI of adrenals

239
Q

What would some other test be for addisons?

A

Antibodies (presence of 21-hydroxylase) , CT or MRI of adrenals

240
Q

What are some differential diagnosis of Addison’s?

A

Hemochromatosis
Hyperthyroidism
Anorexia nervosa

241
Q

How should Addison’s be managed?

A
  • Oral glucocorticoid and mineralocorticoid replacement on diagnosis (hydrocortisone is the preferred steroid)
  • Give prasterone if reduced libido

Note dose may need to be increased during pregnancy

242
Q

What is an Addisonian crisis?

A
  • Patients present in shock
  • increased HR, vasoconstriction, postural hypotension, weak and confused
  • Occurs in undiagnosed Addison’s or someone who has forgotten meds
  • Hypoglycemia

Can occur in acute bilateral adrenal haemorrhage

Can look like hypoglycaemia

243
Q

How would you treat an Addisonian crisis?

A
  • 100mg IV hydrocortisone
  • IV fluids to support BP
  • Correct glucose
244
Q

What should be monitored in a patient with Addison’s

A
  • Fatigue and increasing pigmentation suggests insufficient dosage
  • Weight gain and facial plethora suggest excess ( Cushing’s disease)
245
Q

What are some complications of Addison’s?

A

Secondary Cushing syndrome, adrenal crisis, osteoporosis due to glucocorticoid replacement , treatment related hypertension and hypokalaemia

246
Q

What is SIADH?

A
  • Syndrome of inappropriate antidiuretic hormone is when too much ADH is secreted
  • Characterised by hypotonic hyponatremia, concentrated urine and euvolemic state
247
Q

What can cause SIADH?

A
  • Drugs: SSRI, amiodarone, NSAIDs
  • Pulmonary processes: Pulmonary infections and lung cancers
  • Malignancy: GI, GU, Lymphomas, sarcomas
  • CNS disorders: infections, brain trauma
248
Q

What stimulates ADH release?

A
  • Osmotic pressure is the most sensitive stimulus
  • Arterial pressure reduction also stimulates ADH release
249
Q

How does SIADH cause problems?

A
  • ADH binds to AVP v2 receptors and this results in aquaporin 2 channels on the collecting duct membrane
  • Too much ADH results in too many channels resulting in hyponatremia and suppression of RAAS
250
Q

What are the key presentations of SIADH?

A
  • Low Na+ and low osmolarity with the absence of: hypo/hypervolemia, Addison’s, hypothyroidism
251
Q

What are the symptoms of SIADH?

A
  • Headache
  • Seizure
  • Mental state change
  • Concentrated urine
252
Q

How would you diagnose SIADH?

A
  • Concentrated urine (>20 Na+) with hyponatremia and low plasma osmolarity
253
Q

What are the 4 different types of SIADH?

A

Type A: unregulated release of arginine vasopressin (AVP). Approximately 30% of patients. Marked increase in plasma AVP levels that fluctuate in a manner unrelated to changes in plasma osmolarity/sodium during infusion of hypertonic saline.

Type B: slow leak of AVP. Approximately 30% of patients. Milder increase in plasma AVP in comparison to type A. Plasma AVP remains stable during hypertonic saline infusion and only rises when serum sodium levels reach normal range.

Type C: Approximately 30% of patients. Low AVP levels during hyponatremic state; however, AVP levels rise inappropriately during hypertonic saline infusion before hyponatremia is corrected.

Type D: pseudo-SIADH. Approximately 10% of patients. Low or undetectable AVP. Low levels of AVP during hyponatremic state with apparent normal osmoregulation of AVP release. Antidiuresis occurs through an alternative mechanism, one of which is nephrogenic syndrome of inappropriate diuresis (SIADH), a genetic disorder characterized by gain-of-function mutation of vasopressin 2 (V2) receptor.

254
Q

How would you treat SIADH?

A
  • Treat the underlying cause and restrict fluid
  • Consider salt loop diuretic if severe
  • Vasopressin receptor antagonists (tolvaptans)
255
Q

What is a complication of SIADH?

A

Central pontine myelinolysis- too much sodium due to treatment and brain compensation

256
Q

What are some differential diagnosis of SIADH?

A

Hypo/hypervolemia
Cerebral salt-wasting
Renal failure
Addison’s
Hypothyroidism

257
Q

What is diabetes insipidus?

A

Diabetes insipidus is a metabolic disorder characterised by an absolute or relative inability to concentrate urine, resulting in the production of large quantities of dilute urine

258
Q

What % of cases of DI are genetic?

A

<10%

259
Q

What are the 4 different types of DI?

A

Central acquired- pituitary affected
Central genetic- pit affected
Nephrogenic acquired- collecting duct affected
Nephrogenic inherited- collecting duct affected

260
Q

What can cause central acquired DI?

A

pituitary surgery, craniopharyngioma, post-traumatic brain injury, pituitary stalk lesion autoimmune disorder, CNS infections, meds

261
Q

What can cause central genetic DI?

A

malformations in hypo/pituitary, wolfram syndrome

262
Q

What can cause nephrogenic genetic DI?

A

Mutations in the AVPR2

263
Q

What can cause nephrogenic acquired DI?

A

Medications (lithium + can be irreversible), systemic disease

264
Q

What is the difference between central and nephrogenic DI?

A
  • Central DI results from any condition that impairs the production, transportation, or release of AVP.
  • Nephrogenic DI results from conditions that impair the renal collecting ducts’ ability to respond to AVP.
265
Q

What are the key presentations of DI?

A

History of pit/family, history of lithium therapy, polyuria, increased thirst

266
Q

What are some signs of DI?

A

Hypernatremia

267
Q

What are some first line investigations for DI?

A

Low urine osmolality, high serum osmolality, serum Na+

268
Q

What are the gold standard tests for diagnosing DI?

A
  • Water deprivation test- urine will fail to concentrate
  • ADH stimulation test (used to distinguish between central and nephrogenic)
269
Q

What are some differential diagnosis of DI?

A

Psychogenic polydipsia
Diabetes mellitus
Diuretic use

270
Q

How would you treat central DI?

A

Use long acting synthetic ADH (DDAVP) also useful for pregnancy related

271
Q

How would you treat nephrogenic DI?

A

Nephrogenic is harder to treat
high dose DDAVP can be partially effective,

fix underlying issue if possible, Low sodium diet can be effective

272
Q

What are some complications of DI?

A

Hypernatremia, thrombosis, bladder and renal dysfunction, iatrogenic hyponatremia

273
Q

What is primary hyperparathyroidism (pHPT)?

A

PHPT is an endocrine disorder in which autonomous overproduction of parathyroid hormone (PTH) results in derangement of calcium metabolism.

274
Q

Describe the epidemiology of pHPT

A

Affects 1 in 500 women
Affects 1 in 2000 men
50 and 60 year olds are the most affected group

Incidence has gone up because of more testing and incidental findings

275
Q

What is the main cause of pHPT?

A

80% of cases are caused by a single benign adenoma

276
Q

Name some other causes of pHPT?

A

Carcinoma, lithium, irradiation. Also multiple adenomas and PT hyperplasia.

277
Q

What % of cases are inherited?

A

5-10%

278
Q

Describe the pathophysiology of pHPT

A

In normal physiology high calcium levels suppress PTH secretion.

However in pHPT high levels of calcium do not suppress release. This leads to more bone resorption, Vit D activation and GI absorption this leads to hypercalcaemia.

279
Q

What are the key presentations of pHPT?

A

Symptoms often not related to hypercalcemia itself but related to effect on key target organ.

For example osteoporosis/osteopenia. Or renal stones.

280
Q

What are the signs of pHPT?

A

High serum calcium (albumin adjusted)
Elevated/inappropriately normal PTH

281
Q

What are some symptoms of pHPT?

A

Fatigue
Poor sleep
Myalgias
Anxiety
Depression
Memory loss
Pancreatitis
Ulcers
Constipation
polyuria
polydipsia `

282
Q

What the first line investigations for pHPT?

A

Measure serum calcium and PTH

Also measure phosphate levels which will be low.

283
Q

Name some differential diagnosis for pHPT?

A

Familial hypocalciuric hypercalcaemia
Humoral hypercalcaemia
Multiple myeloma

284
Q

Name the management of pHPT?

A

Parathyroid surgery for most patients especially asymptomatic . (Parathyroidectomy). Consider Vit D sup.

285
Q

What are some complications of pHPT/treatment of it?

A

Neck haematoma, recurrent laryngeal nerve injury, hypocalcaemia following surgery .

Osteoporosis/osteopenia , bone fractures, nephrolithiasis

286
Q

What is the prognosis for pHPT?

A

75% have stable disease for up to 10 years asymptomatic
Parathyroidectomy has a cure rate of over 95%

287
Q

What is secondary hyperparathyroidism (sHPT)

A

Secondary hyperparathyroidism (SHPT) is elevation of parathyroid hormone (PTH) secondary to hypocalcaemia.

288
Q

What are the main causes of sHPT?

A

CKD results in low levels of activated Vit D. This is detected by receptors causes increase in PTH.

Crohn’s, coeliac diseases with fat malabsorption will result in decreased absorption of Vit D and Calcium.

Lack of exposure to sunlight.

Also diminished dietary intake of calcium increased calcium loss or increased metabolic requirement

289
Q

What % of patients with CKD are at risk of sHPT?

A

80%

290
Q

What % of the population have severe Vit D deficiency?

A

7%

291
Q

Describe the pathophysiology of sHPT?

A

Vit d2 and d3 found in food and by exposure to sunlight. Undergoes two hydroxylations one in liver to 25 hydroxyvitamin D. Then in kidney to 1-25-dihydroxyvitamin D. (does not occur in CKD)

In gut this increases absorption of calcium and also helps with bone resorption.

Any reason stated above can cause low calcium levels and thus an increase in PTH

292
Q

What are the key presentations of sHPT?

A

Neuromuscular irritability. Numbness and paraesthesia in the fingers and toes. Muscle cramps or seizures .

293
Q

What are some signs of sHPT?

A

Chvostek’s sign (tapping on the face just anterior to the ear produces twitching of muscles around the mouth)

Trousseau’s sign (inflating a blood-pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyperextension of the fingers, and flexion of the thumb)

294
Q

What are some first line investigations for diagnosing sHPT?

A

Serum calcium (low) and serum PTH (high) and High phosphate

295
Q

What other tests might you perform on a patient with expected sHPT?

A

Serum creatinine and urea to assess kidney function

296
Q

How would you treat sHPT?

A

If malabsorption related manage the disease and consider UV exposure and Vit D sup

If sunlight exposure use UV and consider Vit D sup

297
Q

Name some complications of sHPT?

A

Osteodystrophy, osteoporosis , calciphylaxis

298
Q

What is tertiary hyperparathyroidism?

A

Prolonged secondary. Everything will be high phosphate calcium and PTH

299
Q

What is Hypoparathyroidism (HPPT)?

A

A disorder caused by relative or absolute deficiency of plasma parathyroid hormone (PTH) synthesis and secretion.

This leads to low albumin-corrected serum total calcium and elevated serum phosphate

300
Q

What is the main cause of HPPT?

A

Post surgery (in 80% of cases)
Either surgery to parathyroid or recurrent laryngeal nerve

301
Q

What are some other causes of HPPT?

A

DiGeorge syndrome and other genetic conditions
Can be caused by hypomagnesemia

302
Q

Name a risk factor for HPPT that isn’t surgery?

A

Alcoholism

303
Q

What are the key presentations of HPPT?

A

Muscle twitches
Paraesthesia
Poor memory

304
Q

What are signs of HPPT?

A

Irregular heart beat
Chvostek’s sign
Trousseau sign

305
Q

Name some first line investigations for HPPT

A

Serum calcium and albumin. Make sure PTH levels are assessed to rule out secondary hyperparathyroidism

306
Q

What other tests would you perform for HPPT?

A

Low Magnesium as this exacerbates the problem

Liver function: Consider possible haemochromatosis, Wilson’s disease, or chronic alcohol abuse.

Urine calcium and creatinine suggest autosomal dominant if elevated

307
Q

What are some differential diagnosis of HPPT?

A

Low Vit D
Hypomagnesaemia
Hypalbuminaemia
CKD

308
Q

How would you manage HPPT?

A

If acute treat with IV calcium with ECG monitoring as too fast replacement can cause cardiac arrhythmia

Oral calcium if asymptomatic

Chronic oral calcium plus calcitriol

309
Q

What are some complications of HPPT?

A

Ectopic calcifications, renal insufficiency, renal stones. Cardiac problems

Chronic hypocalcaemia impairs left ventricular contractility.

310
Q

What is hypercalcaemia of malignancy?

A

When tumours in the body cause hypercalcaemia

311
Q

In what percentage of patients with cancer does hypercalcaemia occur?

A

20-30%

312
Q

What are the different types of hypercalcaemia caused by malignancy?

A
  • Humoral hypercalcaemia (accounts for 80%)
  • Local osteolytic (accounts for 20%)
  • Hypercalcemia mediated by release of PTH/1,25-dihydroxyvitamin D ( accounts for less than 1%) (lymphomas or TB or sarcoidosis)
313
Q

What tumours are the main cause of humoral hypercalcaemia?

A

Renal cancer, ovarian cancer, breast cancer, endometrial cancer, human T-lymphotropic virus-associated lymphoma , squamous cell carcinoma

314
Q

What tumours are the main cause of osteolytic hypercalcaemia?

A

Breast and multiple myeloma

315
Q

Describe the pathophysiology of humoral hypercalcaemia?

A

Tumour secretion of parathyroid hormone-related peptide (PTHrP) leads to activation of osteoclastic bone resorption and suppression of osteoblastic bone formation. This results in skeletal release of calcium and subsequent hypercalcemia.

PTHrP also acts at the level of the kidney to reduce calcium clearance, as well as to reduce the renal phosphorus threshold, leading to hypophosphaturia and hypophosphatemia.

316
Q

Describe the pathophysiology of osteolytic hypercalcaemia?

A

Tumours release cytokines (e.g. IL-1 and IL-6), chemokines, and PTHrP which leads to increased osteoclastic bone resorption, and to increased release of calcium into the serum that overwhelms the kidney’s capacity to clear calcium

317
Q

What are the key presentations of hypercalcaemia of malignancy?

A

History of malignancy and signs and symptoms of hypercalcemia

318
Q

What are the symptoms of hypercalcaemia of malignancy?

A
  • Neuropsychiatric changes e.g., fatigue, confusion,
  • Muscle weakness,
  • Polyuria,
  • Polydipsia
  • GI disturbances
319
Q

What are some differential diagnosis of hypercalcaemia of malignancy?

A

Primary hyperparathyroidism
Hyperthyroidism
Sarcoidosis
TB

320
Q

How would you treat hypercalcaemia?

A

If acute and severe treat with intravenous normal saline and intravenous bisphosphate

Consider use calcitonin or furosemide if severe

Treat underlying malignancy if possible

321
Q

What are some complications of hypercalcaemia?

A

Bisphosphate induced flu like syndrome.
AKI
Coma
Acute pancreatitis

322
Q

What would hypercalcaemia show on an ECG?

A

The ST segment is short or absent and the duration of the corrected QT interval is decreased

323
Q

What causes hypocalcaemia?

A

No parathyroid/dysfunction
Following drug treatment
Severe illness, tumour lysis, acute pancreatitis

324
Q

How would you treat hypocalcaemia?

A

With calcium gluconate. ECG is recommended as dysrhythmia can occur

325
Q

What are the complications associated with hypocalcaemia?

A

Respiratory failure
Cardiac arrythmias

326
Q

What effect does hypocalcaemia have on an ECG?

A

Hypocalcaemia typically prolongs the Q-T interval and may lead to complete heart block.

327
Q

What is defined as moderate hyperkalaemia?

A

Serum potassium between 5-6 mmol/L

328
Q

What is defined as significant hyperkalaemia?

A

Serum potassium greater than 6. Greater than 6.5 requires urgent intervention

329
Q

What are the two main causes (pathophys) of HK?

A
  1. Increased intake of potassium in association with decreased renal output. Rare for this to occur with proper renal function. But can happen with normal intake and poor renal function (especially diabetes)
  2. Decreased cellular entry of potassium or increased exit of potassium from cells.
    ( Diabetes+ during metabolic acidosis. )
330
Q

Name some causes of HK (diseases and drugs)?

A

ddison’s disease due to lack of aldosterone.
A number of drugs can cause this e.g., K+ sparing diuretics and ACE inhibitors
Rhabdomyolysis
Excess k+ therapy
Massive blood transfusion
Burns
Metabolic acidosis

331
Q

What are the key presentations of HK?

A

Chest pain, weakness, palpitations, and light-headedness. With abnormal ECG.

332
Q

What effect does HK have on an ECG?

A
  • Fast irregular pulse.
  • Tall tented T-waves in ECG.
  • Small/no p-waves
  • Wide QRS complex
333
Q

What tests would you perform on a patient with suspected HK?

A

Basic metabolic panel.
Serum calcium, FBC and an ECG

334
Q

How would you treat a patient with HK and K+ levels below 6.5 mmol/L

A

Polystyrene sulfonate resin (binds to K+ in gut and lowers over a few days)

335
Q

How would you treat a patient with HK and k+ levels above 6.5 mmol/L

A
  • First give calcium chloride (which is cardioprotective). May need to repeat in 5-10 mins. Will protect for 30-60 mins but won’t lower k+ levels
  • Use insulin and glucose to lower K+ levels as insulin will force K+ into cells.
  • Can also use salbutamol to lower K+ levels further
336
Q

What are the complications associated with untreated hyperkalaemia?

A

Myocardial hyperexcitability leading to ventricular fibrillation and cardiac arrest.

337
Q

What is defined as moderate hypokalaemia (HPK)?

A

Potassium levels between 2.5-3 mmol/L

338
Q

What is defined as severe HPK?

A

Potassium levels below 2.5 mmol/L

339
Q

What can cause HPK?

A
  • Diuretics, vomiting/diarrhoea,
  • Pyloric stenosis,
  • Cushing’s/ steroids/ACTH,
  • Conn’s syndrome,
  • Alkalosis,
  • Renal tubular failure
340
Q

What are the symptoms of HPK?

A
  • Muscle weakness,
  • Cramps, palpitations,
  • Light headiness,
  • Constipation
341
Q

What are some signs of HPK?

A

Hypotonia, hyporeflexia, tetany

342
Q

What are the effects of HPK on an ECG?

A

Small T-waves, with prominent U waves. A long PR interval.

343
Q

What tests would you conduct on a patient with suspected HPK?

A

Basic metabolic panel (includes serum sodium, potassium, glucose, chloride, bicarbonate, urea, and creatinine).
ECG.

Urine electrolytes and creatinine can be useful for determining aetiology

344
Q

High levels of what would indicate long standing HPK?

A

HC03-

345
Q

How would you treat mild HPK?

A

Give an oral K+ supplement and review after 3 days. If due to diuretic consider K+ sparing one.

346
Q

How would you treat severe HPK?

A

Give IV k+ no more than 20mmol/h and not more concentrated than 40mmol/L otherwise can cause cardiac arrest.

347
Q

What is carcinoid syndrome?

A

A tumour of the neuroendocrine cells that results in excessive release of certain hormones

348
Q

Where are most carcinoid tumours found?

A

The GI tract

349
Q

What is carcinoid syndrome?

A

A build up of hormones produced by the neuroendocrine cells and the liver can no longer metabolise them

350
Q

What are the symptoms of carcinoid syndrome?

A
  • Diarrhoea
  • SOB
  • Flushing
  • Itching
  • Hepatic pain
  • Fibrosis of heart valves
  • Bronchoconstriction
    Symptoms are worsened by stress and alcohol as these stimulate the neuroendocrine cells
351
Q

What are the investigations for carcinoid syndrome?

A
  • 24 hr urine 5-hydroxyindoleacetic acid: show increased levels
  • Chest X-ray/ chest or pelvis MRI/ CT: to identify location
  • Plasma chromogranin A: reflects tumour mass
  • Ostreoscan: injected radiolabelled somatostatin analogue, octreotide, to bind to the increased number of somatostatin receptors on tumour cells.
352
Q

What is the management of carcinoid syndrome?

A
  • Decreasing emotional stress and alcohol consumption
  • Somatostatin analogues: e.g. octreotide, inhibit hormone release
  • Surgical resection
  • Debulking embolisation or radiofrequency ablation of hepatic metastases: can help with symptoms
353
Q

What is pheochromocytoma?

A

A tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla that classically presents with headaches, diaphoresis, and palpitations in the setting of paroxysmal hypertension

354
Q

What are the symptoms of Pheochromocytomas?

A
  • Headache,
  • palpitations,
  • resistant/young age hypertension,
  • Impaired glucose tolerance.
  • Cold sweats (diaphoresis)
355
Q

What is the treatment of Pheochromocytomas?

A
  • If hypertensive crisis give antihypertensive agents (calcium channel blockers)
  • Alpha blockers phenoxybenzamine or doxazosin
355
Q

Tests for pheochromocytomas?

A

Plasma free metanephrines
24-hour urine catecholamines

356
Q

What can cause Pheochromocytomas?

A

Multiple endocrine neoplasia type 2 (MEN 2)
Neurofibromatosis type 1
Von Hippel-Lindau disease

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