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Haroon Phase 2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the properties of peptide hormones? How do they work?

A

Made from short-chain amino acids (size is anything from few AAs to small protein) - Pre-Made and stored in cell, released and dissolved into blood when needed - Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane - Bind to receptors on cell membranes, triggering a second messenger to be released within cell - very quick - Examples: Insulin, growth hormone, TSH, ADH

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2
Q

What are the properties of steroid hormones? How do they work?

A

Synthesised from cholesterol - Not stored in cell, released as soon as they are Made - Not water soluble - must be bound to transport proteins to travel in blood - Lipid soluble - can cross plasma membrane and Bind to receptor inside cell - slow response - Examples: Testosterone, oestrogen, cortisol

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3
Q

Tell me about catecholamine hormones (amino acid derived)

A

Synthesised from the amino acid tyrosine - Acts same way as peptide hormone - Large, hydrophilic, charged molecules - cannot diffuse through a plasma membrane, so released via exocytosis - Examples: Adrenaline, thyroxine

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4
Q

What are the cell types and their functions within the islets of langerhans in the pancreas?

A

Alpha cells - produce glucagon Beta cells - produce insulin and amylin Delta/D cells - produce somatostatin PP cells - produce pancreatic polypeptide

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5
Q

What are the classes of hormones?

A

Steroids - Peptides - Thyroid hormones - Catecholamines

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6
Q

Tell me about thyroid hormones 😎

A

released via proteolysis - T3 = triiodothyronine, T4 = thyroxine - Take a day to act - in blood bound to thyroglobulin binding protein (produced by liver)

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7
Q

What is the blood supply to the thyroid gland?

A

Superior Thyroid artery - off thyrocervical trunk (subclavian) - Inferior Thyroid artery - off external carotid artery

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8
Q

Where are the thyroid and parathyroid glands located?

A
  • Thyroid gland sits at C5-T1 - Two lobes connected by an isthmus - Parathyroid is 4 glands on the posterior surface of thyroid glands
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9
Q

What effect does parathyroid hormone have on the kidneys?

A
  • Increased conversion of 25-hydroxyvitamin D (inactive) to 1,25-dihydroxyvitamin D(active) - At the DCT: Increased Ca2+ reuptake and PO43- excretion
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10
Q

What effect does parathyroid hormone have on the gut?

A

Increased Ca2+ and PO43- absoroption

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11
Q

What hormones does the adrenal gland produce?

A

Adrenal cortex: - Zona glomerulosa - mineralocorticoids (eg: aldosterone) - Zona fasciculata - glucocorticoids (eg: cortisol) - Zona reticularis - adrenal androgens Adrenal medulla: - Catecholamines (eg: adrenaline)

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12
Q

Pathophysiology of T2DM

A

Peripheral Insulin resistance with partial Insulin deficiency - Decreased GLUT4 expression - impaired Insulin secretion - Lipid and beta amyloid deposits in pancreas, progressive b cell damage

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13
Q

Epidemiology of T2DM

A

Presents later on in life (usually 30+ years) - Males > females - People of Asian, African and Afro-Carribean ethnicity are 2-4x more likely to develop T2DM than white people

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14
Q

Clinical presentation of T2DM

A

Obese hypertensive older patient - Polydipsia - Nocturia - Polyuria - Glycosuria - Recurrent thrush

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15
Q

Diagnosis of T2DM

A

same as T1DM - Prediabetes exists this time

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16
Q

Risk factors for T2DM

A

Genetic link (stronger than T1DM) - Obesity - Alcohol excess - Hypertension - Gestational diabetes - PCOS - Drugs: corticosteroids, thiazides

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17
Q

Last line of treatment for T2DM if all else fails

A

Insulin treatment

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18
Q

Treatment for T2DM

A

Initial: Biguanide (metformin) Second line: Carry on Metformin and add either: - DPP-4 inhibitor - Pioglitazone - Sulfonylurea - SGLT-2 inhibitor

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19
Q

Epidemiology of Diabetic Ketoacidosis

A

4% of T1DM patients develop each year

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20
Q

Risk factors for DKA

A
  • Poorly managed/undiagnosed T1DM - Infection/illness - Characteristic in patients around 20 years old
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21
Q

Pathophysiology of DKA

A

Absolute immune deficiency = unrestrained lipolysis and gluconeogenesis and Decreased Peripheral glucose uptake - Not all glucose from gluconeogenesis is usable so converted to ketone bodies, which is acidic

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22
Q

Describe Kussmaul’s breathing

A

Deep and rapid breathing in acidosis to expel acidic carbon dioxide

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23
Q

Signs of DKA

A
  • Kussmaul’s breathing - Pear drop breath - Reduced tissue turgar (hypotension + tachycardia)
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24
Q

How to investigate DKA

A
  • Ketones > 3mmol/L - RPG > 11.1mmol/L (hyperglycemic) - pH < 7.3 or HCO3- < 15mmol - Urine dipstick glyosuria/ketonuria
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25
Q

What are common differentials of DKA?

A

HHS - Lactic acidosis - identical presentation, normal serum glucose and Ketones - Starvation ketosis - physiologically appropriate lipolysis

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26
Q

Treatment for DKA (in order)

A
  • ABCDE - IV fluids FIRST 0.9% saline - IV insulin 0.1units/kg/hour - once glucose level <14mmol add 10% glucose - Restore electrolytes, eg: K+
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27
Q

Symptoms of HHS

A

Generalised weakness and leg cramps - Confusion, lethargy, hallucinations, headaches - Visual disturbance - Polyuria and Polydipsia - Nausea, vomiting and abdo pain (more common in DKA)

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28
Q

Epidemiology of HHS

A
  • Less than 1% of diabetes admissions - 5-15% mortality Risk factors: - Infection - MI - Poor medication compliance
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29
Q

Pathophysiology of HHS

A
  • Rise in counter-regulatory hormones (glucagon, Ad, cortisol, GH) - Causes hyperglycaemia ans hyperosmolality - Electrolytes in blood overflow into urine -> excessive loss of water and electrolytes
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30
Q

Characteristics of HHS

A

Marked hyperglycaemia - hyperosmolality - Profound dehydration - Electrolyte abnormalities

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31
Q

Diagnosis of HHS

A

Diagnostic: - Hyperglycaemia ≥30mmol/L without a metabolic acidosis or significant ketonaemia - Hyperosmolality ≥320mOsmol/kg - Hypovolaemia Other tests: - Urine dipstick: heavy glycosuria - U+E: low total body K+, high serum K+

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32
Q

How can HHS be differentiated from Diabetic ketoacidosis?

A

DKA - T1DM - Patients younger and leaner - Ketoacidosis - Develops over hours to a day HHS - T2DM - No ketoacidosis - Significantly higher mortality rate - Develops over a longer time - days to a week

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33
Q

Treatment of HHS

A
  • IV fluid 0.9% saline - IV insulin only if there is ketonaemia or IV fluids aren’t working - LMWH to anticoagulate patient as they have thicker blood - Electrolyte loss (K+)
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34
Q

What are complications of HHS treatment with insulin?

A

Insulin-related hypoglycaemia - Hypokalaemia

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35
Q

Draw out the process of phosphate regulation physiology

A

img

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36
Q

What can pituitary tumours do?

A
  • Press local structures - eg: optic chiasm -> bitemporal hemianopia - Hypopituitism - Hyperpituitarism - acromegaly, Cushing’s disease, prolactinoma
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37
Q

Hormones secreted by the hypothalamus and what they stimulate from the anterior pituitary

A
  • GnRH -> FSH and LH - CRH -> ACTH - GHRH -> GH - TRH -> TSH - DA -> Prolactin
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38
Q

What is always given to unresponsive hypoglcyemic patients?

A

IM glucagon

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39
Q

Role of insulin

A
  • Increase peripheral glucose uptake - Glucose -> glycogen
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40
Q

Biphasic release of insulin

A
  1. Glucose binds to GLUT2 receptors of pancreas on b cells, stimulating insulin release 2. Insulin binds to peripheral insulin receptors: - Activates intracellular tyrosine kinases + cascane - Increase of Glut-4 channel expression on CSM
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41
Q

Posterior pituitary hormones

A

Oxytocin (paracentricular nucleus) - milk ejection + labour induction - Vasopressin (supraorbital nucleus)

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42
Q

What does vasopressin do?

A

Vasoconstricts blood vessels - Increased APO II expression in collecting duct - Increased aldosterone

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43
Q

Functions of cortisol

A
  • Increases protein and carb breakdown - Upregulates alpha 1 receptors on arterioles -> increased BP - Suppresses immune response - Increased osteoclast activity (osteoporotic) - Increased insulin resistance
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44
Q

Prediabetic states

A

FBG: 6.1-6.9 2nd post prandial: 7.8-11.0 HbA1c: 42-47 (6.0-6.4%)

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45
Q

First treatment for Type 2 diabetes and prediabetes before drugs

A

Lifestyle change - diet, exercise, modify RFs

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46
Q

Main complication of T2DM

A

Hyperosmolar hyperglycaemic state

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47
Q

Define T1DM

A
  • Absolute insulin deficiency, usually resulting from autoimmune destruction of the insulin-producing beta islet cells in the pancreas - Type 4 hypersensitivity
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48
Q

Which genes are linked with increased risk of developing T1DM?

A

HLA-DR2 and HLA-DQ3 or HLA-DR4 and HLA-DQ8

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49
Q

Environmental factors that can increase the risk of developing T1DM

A

Diet - Vitamin D deficiency - Early-life exposure to viruses associated with islet inflammation (eg: enteroviruses) - Decreased gut-microbiome diversity

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50
Q

Epidemiology of T1DM

A
  • Young (usually between 5-15 years) - Lean - North European descent - 10% of diabetes is type 1
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51
Q

Macrovascular complications of T1DM

A

Atherosclerosis, which leads to: - CVD - Stroke - Peripheral arterial disease

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52
Q

Microvascular complications of T1DM

A
  • Nephropathy - Retinopathy -> glaucoma, cataracts - Neuropathy -> diabetic foot disease
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53
Q

Other autoimmune conditions that can result from T1DM (most to least common)

A
  • Thyroid disease - Autoimmune gastritis - Pernicious anemia - Coeliac diease - Vitiligo - Addison’s disease
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54
Q

Psychological complications of T1DM

A
  • Anxiety - Depression - Eating disorders Also in children: - Behavioural and conduct disorders - Family/relationship difficulties - Risk-taking behaviour
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55
Q

Signs of T1DM

A
  • BMI < 25kg/m2 - Failure to thrive in children - Glove and stocking sensory loss - Reduced visual acuity - Diabetic retinopathy - Diabetic foot disease
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56
Q

Symptoms of T1DM

A

Polyuria - Polydipsia - Weigt loss - lethargy - Recurrent infections - Evidence of complications - eg: blurred vision or parasthesia

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57
Q

At what level of blood glucose can it no longer be absorbed?

A

10mmol/L Thirsty and develop polyuria - body attempts to remove excess glucose

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58
Q

At what level of Beta cell destruction does hyperglycaemia develop?

A

80-90%

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59
Q

Diagnosis of T1DM

A

Random blood glucose ≥11mmol/L Fasting blood glucose ≥7mmol/L - One abnormal value diagnostic in symptomatic patients - Two abnormal values diagnostic in asymptomatic patients

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60
Q

What is the most accurate test for T1DM?

A

HbA1C - measures glycated haemoglobin >48 mmol/mol or >6.5% suggest hyperglycaemia over 3 months

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61
Q

Optimal targets for glucose self monitoring

A
  • FBG: 5-7mmol/L on waking - Plasma glucose 4-7mmol/L before meals at other times of the day - If testing after meals: 5-9mmol/L at least 90 minutes after
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62
Q

How can T1DM be differentiated from Latent Autoimmine Diabetes in Adults (LADA)?

A
  • In LADA age of onset is >30 yrs - Low to normal C-peptide
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63
Q

How can T1DM be differentiated from Neonatal diabetes?

A

In neonatal diabetes: Genetic testing shows mutation in genes coding ATP K+ channel and insulin gene

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64
Q

How can T1DM be differentiated from Monogenic diabetes?

A

In monogenic diabetes: - C-peptide present - Autoantibodies absent

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65
Q

First line treatment for T1DM

A

Basal-Bollus regimen Basal - Long acting (either given twice or once daily) Bollus - Short before meals

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66
Q

Types of Insulin

A

Rapid: aspart, lisporo, novorapid, glulisine - short: regular Insulin - Intermediate: NPH (half a day) - Long: detemir, lantus, glargine

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67
Q

Pathophysiology of T1DM

A
  • Beta islet cell destruction - Hyperglycemia - Low cellular glucose (increased lypolysis and gluconeogenesis) - Hyperkalemia even though there is a low body K+ (enters cells via Na+/K+ ATPases)
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68
Q

Complications of DKA

A

Coma - Cerebral oedema - Thromboembolism - Aspiration pneumonia - Death - dehydration - MI

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69
Q

Presentation of hypokalaemia

A

Hypotonia - Hyporeflexia - Arrhythmias (especially AF) - Muscle paralysis and rhabdomyolysis

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70
Q

Aetiology of hypokalaemia

A

Decreased intake of potassium Increased excretion of potassium - Thiazides + loop diuretics - Renal disease - GI loss - Increased aldosterone (Conn’s syndrome) Potassium shifted to intracellular - Insulin - Salbutamol - (other drugs)

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71
Q

Treatment for hypokalaemia

A

K+ replacement - aldosterone antagonist (spironolactone) - Treat underlying cause - Other Electrolyte defficiencies

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72
Q

Diagnosis of hypokalaemia

A
  • Low K+ in U+E ECG: - Small inverted T waves - Prominent U waves - ST depression - PR prolongation
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73
Q

Definition of hyperkalaemia and hypokalaemia

A

Hyper ≥ 5mmol/L Emergency hyper = ≥ 6.5mmol/L Hypo < 3.5mmol/L

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74
Q

Presentation of hyperkalaemia

A

Muscle weakness and cramps - parasthesia - Palpitations - Tachycardia (Arrhythmias)

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75
Q

Aetiology of hyperkalaemia

A

Increased intake of potassium - IV therapy - Increased dietary intake Decreased excretion of potassium - AKI and CKD - Drugs (NSAIDs, spironolactone, ACE inhibitors) - Renal tubular acidosis (T4) - Addison’s disease Potassium shifted to extracellular - Metabolic acidosis/DKA - Rhabdomyolysis Other: trauma and burns

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76
Q

Effect of hyperkalaemia on types of muscle

A

Smooth Muscle cramping - Skeletal mucle weakness due to overcontraction - Cardiac arrythmias and arrest

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77
Q

Effect of hypokalaemia on types of muscle

A

Smooth Muscle constipation - Skeletal Muscle weakness and cramps - Cardiac arrythmias and Palpitations

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78
Q

Effect of hyperkalaemia on Insulin, pH and Beta 2 receptors

A
  • Insulin deficiency as not enough K+ flows into the cell - Acidosis (H+ in and K+ out) - Beta blocker - inhibits pumping of K+ into cell
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79
Q

Effect of hypokalaemia on insulin, pH and beta 2 receptors

A
  • Excess insulin as too much K+ flows into cell - Alkalosis (H+ out and K+ in) - B2 agonist - Increase B2 pumping of K+ into cell
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80
Q

Complications of hyperkalaemia

A

Cardiac arrhythmias and arrest - Hyperkalaemia is associated with broadening QRS complex

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81
Q

Aetiology of hypercalcaemia (90% of cases)

A

90%: - Hyperparathyroidism - Malignancy: bone mets, myeloma, PTHrP, lymphoma

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82
Q

ECG in hypercalcaemia

A

Short QTc

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83
Q

Symptoms of hypercalcaemia and hyperparathyroidism

A

Bones - excess resorption, ostopoenia - Stones - kidney - Groans - abdominal pain, constipation - Psychedelic moans - Confusion, Depression, Anxiety - Thrones - Polyuria and Polydipsia

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84
Q

How does hypercalcaemia affect muscles

A

Low muscle tone and contractions as Ca2+ inhibits fast Na+ influx

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85
Q

What happens to PTH in hypercalcaemia

A

It will decrease due to negative feedback (except in hyperparathyroidism)

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86
Q

Aetiology of hypocalcaemia

A

CKD (due to Decreased Vit D activation) - Severe Vit D deficiency - Primary hypoparathyroidism - Acute pancreatitis

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87
Q

Symptoms of hypocalcaemia and hypoparathyroidism

A

parasthesia - Tetany (involuntary Muscle contractions) - Chvostek sign - Trousseau sign

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88
Q

How does hypocalcaemia affect muscle?

A

Muscle spasms: hands, feet, larynx, premature labour

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89
Q

How does hypocalcaemia affect PTH?

A

Always Increases - Except in hypoparathyroidism

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90
Q

Difference between primary and secondary hyperthyroidism?

A

Primary: Pathology is in the Thyroid - Secondary: Pathology is in the hypothalamus/pituitary

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91
Q

TFTs for hyperthyroidism

A
  • Low TSH, high T4 = primary hyperthyroidism (Graves’) - High TSH, high T4 = secondary hyperthyroidism OR thyroid hormone resistance
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92
Q

Graves’ specific hyperthyroid signs

A

Exophithalmos or ephthalmoplegia - Pretibial myxedema due to deposits of mucin under the skin (may Also be seen in Hashimoto’s) - Thyroid acropachy

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93
Q

Epidemiology and risk factors of hyperthyroidism

A

Middle aged women - Family history - autoimmune diseases

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94
Q

De Quervain’s thyroiditis

A

Follows a viral prodrome and can Also present with a transient thyrotoxic state - Painful goitre with raised inflammatory markers. usually self limiting

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95
Q

Pathophysiology of Graves’ disease

A

immune system produces TSH receptor antibodies that mimic TSH and stimulate the TSH receptors on the Thyroid - Increased T3 Increases metabolic rate, CO, bone resorption and activates the sympathetic nervous system

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96
Q

Symptoms of hyperthyroidism

A

Heat intolerance and sweating - Weight loss - Palpitations - Oligomenorrhoea

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97
Q

What is toxic multinodular goitre? (also known as Plummer’s disease)

A

Nodules develop on the thyroid gland and produce excessive thyroid hormone

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98
Q

Symptoms of thyroid storm

A

NDV - abdo pain - Jaundice - Confusion, delirium or Coma

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99
Q

Diagnosis of hyperthyroidism

A

First line: TFT (thyroid function test) - Anti-TSH receptor antibodies positive in Graves’ - Anti TPO antibodies in 80% of cases (but much more in hypo) - Thyroid ultrasound

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100
Q

First line treatment for hyperthyroidism

A
  • Carbimazole - Blocks synthesis of T4 - Normal thyroid function after 4-8 weeks (euthyroidism) - SE: agranulocytosis, presents as sore throat/mouth ulcers - + beta blocker (eg: propanolol) alongside for rapid symptom relief
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101
Q

Second line treatment for hyperthyroidism

A
  • Propylthiouracil - Prevents T4->T3 conversion - Small risk of severe hepatic reaction, including death
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102
Q

Radioactive iodine treatment for hyperthyroidism

A
  • First line definitive treatment for Grave’s disease and toxic multinodulae goitre - Destroys excess thyroid tissue - Remission can take 6 months - Patient must not be pregnant or planning to get pregnant within 6 months, must also avoid close contact with children and pregnant women for 3 weeks - Also limit contact with anyone for several days after receiving the dose
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103
Q

Last resort treatment for hyperthyroidism

A

Surgery or radioactive iodine

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104
Q

How to stop patients from becoming hypothyroid after hyperthyroidism treatment

A

Give them levothyroxine

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105
Q

Most common cause of hypothyroidism in the developed world

A
  • Hashimoto’s thyroiditis - Autoimmune inflammation of the thyroid gland - initially cause a goitre - Associated with anti-TPO antibodies and antithyroglobulin antibodies
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106
Q

Most common cause of hypothyroidism in the developing world

A

Iodine deficiency

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107
Q

What is postpartum thyroiditis

A
  • Same mechanism as Hashimoto’s - Acute: presents during pregnancy - Resolves by itself within 1 year of symptoms
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108
Q

Other causes of hypothyroidism

A
  • DeQuervain’s thyroiditis - Post-thyroidectomy or post-radioiodine - Drugs; amiodarone, lithium, carbimazole
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109
Q

Causes of secondary hypothyroidism (pathology at pituitary gland)

A

Compression from a pituitary tumour - Sheehan syndrome - Drug: cocaine, Steroids, dopamime (all inhibit TSH secretion)

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110
Q

Symptoms of hypothyroidism

A

Cold intolerance - constipation - Weight gain - lethargy - Menorrhagia

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111
Q

Signs of hypothyroidism

A

Hair loss, dry and Cold skin- Bradycardia - goitre - Decreased deep tendon reflexes - Carpal tunnel syndrome

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112
Q

Diagnosis of hypothyroidism

A

TFT (Thyroid function test) - Anti-TPO antibodies high - Tyically anaemic (any Type)

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113
Q

TFTs for hypothyroidism

A

high TSH, Low T4 = Primary hypothyroid - Low TSH, Low T4 = Secondary hypothyroid - normal/Low TSH, Low T4 = hypopituitarism

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114
Q

Treatment for hypothyroidism

A

Levothyroxine (T4) - Titrate dose so you don’t induce iatrogenic hyperthyroidism

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115
Q

Complication of hypothyroidism

A

Myxedema coma - Often infection precipitated - Rapidly drops T4 - Loss of consciousness, heart failure

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116
Q

Treatment for myxedema coma

A

Levothyroxine - antibodies - Hydrocortisone

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117
Q

Types of thyroid carcinoma

A

Papillary - 70% - Follicular - 25% - Anaplastic (worst prognosisas as it metastasises the most) - Lymphoma - Medullary cell

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118
Q

Most common metastasis sites for thyroid carcinoma

A

Lung - 50% - bone - 30% - liver - 10% - Brain - 5%

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119
Q

How does thyroid carcinoma usually present?

A

as hard and irregular Thyroid nodules - may have local Compression (eg: hoarse voice)

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120
Q

Diagnosis of thyroid carcinoma

A

Fine needle Aspiration biopsy - TFTs - Thyroid ultrasound

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121
Q

Treatment for thyroid carcinoma

A
  • Papillary and follicular = thyroidectomy or radioactive iodine - Anaplastic = mostly palliative :(
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122
Q

Pathophysiology of Cushing’s syndrome

A

Chronic excess of cortisol released by the adrenal glands

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123
Q

Aetiology of Cushing’s syndrome

A

ACTH dependent causes - Cushing’s disease - Ectopic ACTH production - ACTH treatment ACTH independent causes - Iatrogenic (steroid use) - mc - Adrenal adenoma

124
Q

What is Cushing’s disease?

A

Pituitary adenoma secreting excess ACTH

125
Q

Signs of Cushing’s syndrome

A

Hypertension - Moon face - Central Obesity - abdominal striae - Buffalo hump (fat pad on upper back) - Proximal limb Muscle wasting - Ecchymoses and fragile skin

126
Q

Symptoms of Cushing’s syndrome

A

Bloating and Weight gain - Mood change - Increased susceptibility to Infection - Menstrual irregularity - Reduced libido - hyperglycaemia

127
Q

Pseudo-Cushing’s

A

Cushingoid features and abnormal cortisol levels, but not associated with HPA pathology - Common causes: alcohol excess, severe depression, obesity, pregnancy - Results in a false positive dexamethasone suppression test and 24hr free cortisol - Differentiated using an insulin stress test

128
Q

Diagnosis of Cushing’s syndrome

A

Dexamethasone suppression test or midnight salivary cortisol - If positive, test plasma ACTH to see If ACTH dependent - If independent, see If it is pituitary or ectopic GH release

129
Q

How to do dexamethasone suppression test

A
  • Measure cortisol at 12am, before giving dexamethasone - Measure cortisol 8 hours later, at 8am - Non-Cushing’s -> suppression >50nmol/L - Cushing’s -> little/no suppression
130
Q

Plasma ACTH test

A
  • Test at 9am - High = ACTH dependent cause -> Do high dose dexamethasone suppression test - Low = ACTH independent cause -> CT adrenals to look for pathology
131
Q

Treatment for Cushing’s syndrome caused by Cushing’s disease

A

Transsphenoidal resection or bilateral adrenalectomy

132
Q

Complication of bilateral adrenalectomy

A

Nelson’s syndrome - Pituitary tumour will continue to enlarge with no negative feedback from adrenals - High ACTH and skin hyperpigmentation

133
Q

Treatment for Cushing’s syndrome caused by adrenal adenoma

A

Tumour resection or unilateral adrenalectomy

134
Q

Treatment for Cushing’s syndrome caused by ectopic ACTH

A

Treatment of underlying cancer, such as surgical removal of SCLC

135
Q

Complications of Cushing’s syndrome

A

Osteoporosis - T2DM - Hypertension and ischaemic heart disease

136
Q

Primary adrenal insufficiency

A
  • Addison’s disease - Pathology is at the adrenal glands - Decreased producion of adrenocortical hormones (cortisol and aldosterone) - High ACTH, low adrenocortical hormones
137
Q

Secondary adrenal insufficiency

A

Pathology is in the pituitary - Inadequate ACTH released from pituitary - Leading to Low release of adrenocortical hormones from the adrenal gland - Low ACTH, Low adrenocortical hormones

138
Q

Why do patients with primary adrenal sufficiency present with bronzed skin?

A

High ACTH stimulates melanocytes, resulting in hyperpigmentation

139
Q

Aetiology of primary adrenal insufficiency

A
  • Developed world: Autoimmune adrenal destruction (21-hydroxylase present in 60-90% of people) - Developing world: TB (+ sarcoidosis)
140
Q

Risk factors for adrenal insufficiency

A

Female - adrenocortical antibodies - Other autoimmune disease

141
Q

Other causes of adrenal insufficiency

A

adrenal metastasis (Lung, liver, breast) - adrenal haemorrhage (eg: meningococcal septicaemia)

142
Q

Symptoms of adrenal insufficiency

A

Weight loss - Nausea and vomiting - lethargy and Generalised weakeness - Salt cravings

143
Q

Signs of adrenal insufficiency

A
  • Bronze hyperpigmented skin, particularly in palms (only in Addison’s) - Postural hypotension - Hypoglycaemia - Change in body hair distribution - Loss of pubic hair in women - Associated autoimmune condition
144
Q

Signs of adrenal crisis

A

Hyponatraemia - Hyperkalaemia - Profound fatigue - dehydration - Vascular collapse (Low BP)

145
Q

Treatment of Addisonian/adrenal crisis

A
  • Immediate 100mg hydrocortisone - IV solve + dextrose (if hypoglycaemia) - Without cortisol, you will die from adrenal crisis if you have an infection
146
Q

Diagnosis of adrenal insufficiency

A
  • First line: 8-9am cortisol - Gold standard: ACTH stimulation test (short Synacthen test) RESULTS - Low cortisol, high ACTH, poor response to synacthen = Primary adrenal insufficiency - Low cortisol, low/normal ACTH, poor response to synacthen = Secondary adrenal insufficiency OR hypopituitarism
147
Q

Other investigations for adrenal insufficiency

A
  • U+E to test for hyponatraemia and hyperkalaemia - Aldosterone:renin ratio - Adrenal CT or MRI - Test bloods for 21-hydrolase adrenal antibodies
148
Q

Treatment for Adrenal insufficiency

A

Hydrocortisone - glucocorticoid to replace cortisol - Fludrocortisone - mineralocorticioid to replace aldosterone If necessary - Double the dose of Hydrocortisone in trauma/Infection

149
Q

Tertiary adrenal insuffiiency

A

Caused by Inadequate CRH released by the hypothalamus - usually a result of Long term oral Steroids

150
Q

Acromegaly in children

A

Called gigantism - Occurs before epiphyseal fusion - hypopituitarism Causes inhibition of puberty as gonadotrophs cannot be released

151
Q

Aetiology of acromegaly

A

Functional pituitary adenoma

152
Q

Pathophysiology of acromegaly

A
  • Excess GHRH - GHRH -> GH -> High IGF-1 (produced by liver)
153
Q

Signs of acromegaly caused by space occupying lesion

A

Bitemporal hemianopia - headaches

154
Q

Signs of acromegaly to do with overgrowth of tissues

A

Prominent forhead and brow - Large nose, tongue, hands and feet - Large, protruding jaw - Arthritis

155
Q

Signs of acromegaly to do with GH causing organ dysfunction

A

Hypertrophic heart - Hypertension - impaired glucose tolerance - Colorectal cancer

156
Q

Other symptoms suggesting active raised growth hormone

A

Development of new skin tags - Profuse sweating

157
Q

Diagnosis of acromegaly

A
  • 1st line: IGF-1 serum levels (high) - Gold standard: OGTT: Oral glucose tolerance test (failure of GH suppression 2 hours post 75g glucose load)
158
Q

First line treatment for acromegaly

A

Transsphenoidal resection of pituitary adenoma

159
Q

Other treatments for acromegaly

A

Somatostatin analogue to block GH (eg: ocreotide) - Dopamine agonist (eg: bromocriptine) - GH antagonist (eg: pegvisomant) - Radiotherapy

160
Q

Complications of acromegaly

A

T2DM Caused by impaired glucose tolerance - Obstructive sleep apnoea - Cardiomyopathy - Hypertension - Arthropathy - Carpal tunnel syndrome

161
Q

Risk factors for hyperprolactinaemia

A

Females - high serum prolactin (released from lactotrophs in the ant. pituitary)

162
Q

Aetiology of hyperprolactinemia

A

Prolactinoma - Drugs (ecstacy)

163
Q

Symptoms of hyperprolactinoma

A

Secondary amenorrhoea - Galactorrhoea 🪐🌌 - Sexual dysfunction (M+F) - Gynecomastia, low testosterone

164
Q

Diagnosis of hyperprolactinemia

A
  • High serum prolactin - >1000mIU/L - or 500-1000mIU/L on two occasions
165
Q

Best treatment for hyperprolactinemia

A

Dopamine agonists - eg: cabergoline or bromocriptine - Massively shrinks Prolactinoma (tumour) as Dopamine is an inhibitor of prolactin

166
Q

Primary hyperparathyroidism

A

usually Caused by a Parathyroid adenoma - Causes hypercalcaemia

167
Q

Secondary hyperparathyroidism

A

Caused by Parathyroid hyperplasia - Secondary to CKD + Vit D deficiency

168
Q

Tertiary hyperparathyroidism

A

after many years of Secondary - most common cause is CKD - Glands act autonomously and release PTH regardless of Ca conc.

169
Q

Malignant causes of hyperparathyroidism

A

Neoplasms - (Squamous cell Lung cancer, breast, renal) - Secrete PTHrP, ectopically mimics PTH

170
Q

Diagnosis of primary hyperparathyroidism

A

high PTH - very high calcium - Low phosphate - high ALP

171
Q

Diagnosis of secondary hyperparathyroidism

A

high PTH - Low calcium - high phosphate - high ALP

172
Q

Diagnosis of tertiary hyperparathyroidism

A

high PTH - high calcium - high phosphate - high ALP

173
Q

Other tests for hyperparathyroidism

A

Xr KUB for kidney Stones - DEXA scan for bone density - U+E to assess renal function - short QT on ECG

174
Q

Treatment for hyperparathyroidism

A
  • Primary: Removal of PTH adenoma/parathyroidectomy of all 4 glands :( (most definitive) - Secondary and tertiary: Treat cause - Tertiary: Removal of parathyroid glands - Malignant: Remove tumour!
175
Q

Complication of hyperparathyroidism

A

Acute Severe hypercalcaemia - Give IV fluids + bisphosphonates

176
Q

Primary vs secondary hypoparathyroidism

A

Primary: PTH gland failure, a number of causes Secondary: After surgery (parathyroid/thyroid ectomy)

177
Q

Causes of primary hypoparathyroidism

A

Di George syndrome - Genetic - Radiation - autoimmune - Infiltration - Magnesium deficiency

178
Q

Pseudohypoparathyroidism

A
  • Very rare - End-organ PTH resistance due to defect in G protein signalling Associated with: - Low IQ - Short stature - Small 4th/5th metacarpals - Obesity
179
Q

What is the Chvostek sign?

A

Twitching of facial muscles when facial nerve is trapped over parotid

180
Q

What is the Trousseau sign?

A

Carpopedal spasm when tourniquet is applied to forearm

181
Q

Diagnosis of hypoparathyroidism

A

Low PTH - Low calcium - high phosphate - ECG = longer QTc

182
Q

Treatment for hypoparathyroidism

A

Calcium and Vitamin D suppements (AdCalD3)

183
Q

GH/IGF-I axis

A

img

184
Q

Insulin secretion by the beta cell

A

glucose enters via GLUT2 transporter - K+ channels close and depolarise cell membrane - calcium channels open and CA2+ enters cell and stimulates Insulin secretory granules - Insulin secreted

185
Q

Insulin action in muscle and fat cells

A

Insulin enters via Insulin receptors - Intracellular signalling cascades cause GLUT4 vesicles to integrate into plasma membrane - glucose enters cell via GLUT4 transporter

186
Q

Alpha vs beta islet of Langerhans cells

A

Alpha cells: glucagon - Increases hepatic glucose by increasing glycogenolysis and gluconeogenesis - Stimulates lipolysis and muscle breakdown - Reduces peripheral glucose output Beta cells: insulin - Suppresses hepatic glucose by decreasing glycogenolysis and gluconeogenesis - Suppresses lipolysis and breakdown of muscle - Increases glucose uptake into insulin sensitive tissues

187
Q

How can you get ketoacidosis in T2DM?

A

Happens later on in the disease - Because initially, micro secretions of Insulin are sometimes still present, inhibiting glucagon

188
Q

Symptoms of DKA

A

Nausea and vomiting - Weight loss - Drowsy/confused - abdominal pain

189
Q

Why are thiazolidinediones (pioglitazone) not commonly given as a diabetic drug?

A

Increase Weight - Increase risk of heart failure - Increase risk of fractures

190
Q

Advantages of basal insulin in T2DM

A

patient adjusts Insulin themselves, based on fasting glucose measurements - Carries on with oral therapy, combination therapy is common - Less risk of hypoglycaemia at night

191
Q

Advantages of premixed insulin in diabetes

A

Both basal and prandial together - can cover Insulin requirements though most of the day

192
Q

Disadvantages of pre-mixed insulin

A

Requires consistent meal and exercise pattern - cannot seperately Titrate individual Insulin components - Increased risk of nocturnal and fasting hypoglycaemia

193
Q

Causes of hypoglycaemia

A

Diabetic drugs: sulfonylureas or insulin - Non diabetic: oral, liver failure, Addison’s, increasing age

194
Q

Symptoms of hypoglycaemia on the brain

A

Cognitive dysfunction - Blackouts - Seizures - Comas - Psychological effects

195
Q

Treatment for hypoglycaemia

A

If not serious, food to release blood sugars - IV glucose or oral glucose gel - If no access, IM glucagon (only if alpha cells are working) - Check BM after 5 mins and if it’s increased give food

196
Q

Symptoms of hypoglycaemia on the heart

A

Increased risk of MI - Cardiac Arrhythmias

197
Q

Symptoms of hypoglycaemia on the musculoskeletal system

A

Falls - Accidents (inc. driving) - fractures - Dislocations

198
Q

Symptoms of hypoglycaemia on circulation

A

inflammation - blood coagulation abnormalities - Haemodynamic changes - Endothelial dysfunction

199
Q

Blood glucose of patient with hypoglycaemia

A

<3.5mmol/L

200
Q

Thyroid axis

A

img

201
Q

Diagnosis of pseudohyperparathyroidism

A

high PTH - Low calcium - high phosphate

202
Q

What does hypercalcaemia of malignancy do to PTH and phosphate levels?

A

PTH levels decrease - phosphate levels stay the same

203
Q

Other causes of hypercalcaemia (other than top 90%)

A

Multiple myeloma - Granulomatous diseases (eg: TB and sarcoidosis) - dehydration - Drugs

204
Q

How to calculate corrected calcium levels

A

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

205
Q

Why may serum calcium levels be inaccurate?

A

Low serum albumin Causes a Low total serum calcium - but this is Not a Low ionised calcium - Need to do corrected calcium equation

206
Q

Physiology of thyroid hormone production

A

iodine diffuses from Follicular Thyroid cells into the colloid (fatty empty space inbetween Follicular cells) - iodine binds to tyrosine residues on molecule thyroglobulin - Cleaved from Long chains to form T3 or T4(active)

207
Q

Physiology of thyroid hormone release

A

Supraventricular nucleus of hypothalamus releases TRH - TSH released from thyrotrophs in anterior pituitary - binds to TSH-receptors on Thyroid - Causes T3/T4 to diffuse from colloid to Follicular cells then to the bloodstream

208
Q

PTH regulation

A
  • Tightly regulated by body Ca2+ to prevent hyper/hypocalcaemia - Directly inhibited by calcitonin - from parafollicular C cells fo the thyroid
209
Q

Who would you not want to give carbimazole to?

A

Women wanting to get pregnant as it’s teratogenic (causes fetal abnormalities)

210
Q

Pathophysiology of hyperkalaemia

A

high K+ decreases action potential - Easier depolarisation - abnormal heart rhythms

211
Q

Diagnosis of hyperkalaemia

A
  • High K+ on U+Es ECG: - Absent P waves - Prolonged PR - Tall tented T waves - Wide QRS - Bradycardia
212
Q

Treatment for hyperkalaemia

A

If urgent: Calcium gluconate to stabilise cardiac membrane if there are heart problems, then insulin dextrose Non-urgent: Insulin (+dextrose)

213
Q

Aetiology of hyperaldosteronism

A

2/3 - Adrenal adenoma (Conn’s) 1/3 - Bilateral adrenal hyperplasia Also (rare): - Familial hyperaldosteronism type 1 and 2 - Adrenal carcinoma

214
Q

Secondary hyperaldosteronism

A

Excessive renin stimulates the adrenal glands to produce more aldosterone Causes: - Renovascular disease - Renin-secreting tumour

215
Q

Pathophysiology of hyperaldosteronism

A

excess aldosterone(😱) - Increased sodium and water reabsorption and potassium excretion in kidneys - Hypertension and Hypokalaemia

216
Q

Symptoms of hyperaldosteronism

A

Resistant Hypertension (unfixable with ACE inhibitors or beta blockers) - Hypokalaemia (lethargy Mood disturbance, parasthesia, Muscle cramps) - Polydipsia + Polyuria

217
Q

Diagnosis of hyperaldosteronism

A

1st line: Aldosterone:renin ratio High ratio = Primary (do CT) Low rato = Secondary Diagnostic: High serum aldosterone not suppressed with 0.9% IV saline or fludrocortisone Also: Hypokalaemic on U+E and ECG

218
Q

Treatment of hyperaldosteronism

A
  • Single benign adrenal tumour -> unilateral adrenalectomy - Bilateral adrenal hyperplasia -> Aldosterone antagonist (spironolactone)
219
Q

Two types of diabetes insipidus

A

Cranial - Low ADH secretion - Nephrogenic - Low response to ADH

220
Q

Aetiology of cranial diabetes insipidus

A

ADH gene mutation - pituitary adenomas - Brain infections - Idiopathic

221
Q

Aetiology of nephrogenic diabetes insipidus

A
  • Renal tubular acidosis - ADH-R mutation - Drugs (lithium) - Electrolyte disturbance
222
Q

Presentation of diabetes insipidus

A

Polyuria - Polydipsia - Hypernatremia - lethargy Confusion Coma - Severe dehydration

223
Q

How much urine a day will make you suspect diabetes insipidus?

A

Over 3L

224
Q

Water deprivation test for diabetes insipidus

A
  • No fluid for 8 hours - Normally serum osmolality stays normal, urine osmolality increase - DI = serum osmolality rises while urine osmolality unchanged
225
Q

Desmopressin test for diabetes insipidus

A

Cranial urine osmolality: After deprivation: Low After desmopressin: High Nephrogenic urine osmolality: After deprivation: Low After desmopressin: Low Primary polydipsia After deprivation: High After ADH: High

226
Q

Treatment for diabetes insipidus

A

Cranial - Desmopressin Nephrogenic - Thiazides (+ treat underlying cause)

227
Q

What are carcinoid tumours?

A
  • Poorly malignant tumours of enterochromaffin cells which produce 5-HT/serotonin - Mostly in the GI tract at the appendix and terminal ileum - Can also be in the lungs
228
Q

Carcinoid tumours vs syndrome

A

tumours - only the neoplastic cell, No/v little symptoms - syndrome - when tumour metastasises to the liver

229
Q

Presentation of carcinoid syndrome

A

Diarrhoea - Flushing - Tricuspid incompetence (valve lesion) - Right upper quadrant pain - Bronchospasm

230
Q

What does carcinoid syndrome tend to express?

A

Somatostatin receptors

231
Q

Diagnosis of carcinoid syndrome

A
  • High volume of 5-hydroxyindoleacetic acid (breakdown of serotonin) in urine - Metabolic panel and LFTs - Liver ultrasound to confirm metastases - CT/MRI to locate primary tumour
232
Q

Treatment for carcinoid syndrome

A

Surgically excise Primary tumour - Peri-operative ocreotide (SST analogue) infusion to block tumour hormones - for metastases: above + radiofrequency ablation

233
Q

Carcinoid crisis

A

Lif threatening - Treated with high dose SST analogue (octeotride)

234
Q

What is a phaeochromocytoma?

A

An adrenal medullar tumour of chromaffin cells that secrete catecholamines (NAd, Ad)

235
Q

Aetiology of phaeochromocytomas

A
  • 25% familial and associated with MEN 2a+2b - Neurofibromatosis 1 (tumours deposited along myelin sheath) - Von-Hippel Lindau disease
236
Q

Tumour patterns in phaeochromocytomas

A
  • 10% bilateral - 10% cancerous - 10% familial - 10% extra-adrenal (mc location: organ of Zuckerkandl at aortic bifurcation)
237
Q

Signs of phaeochromocytomas

A
  • Hypertension (90%) - Hypertensive retinopathy - Tachycardia
238
Q

Symptoms of phaeochromocytomas

A

Episodic headache - Profuse sweating - Palpitations - Anxiety

239
Q

Diagnosis of phaeochromocytoma

A
  • 24 hour urine metanephrine collection - Plasma free metanephrines - CT abdomen and pelvis
240
Q

Why are metanephrines measured to diagnose pheochromocytoma?

A

Adrenaline has a very short half life in blood (only a few minutes) - Metanephrines are a breakdown product of Adrenaline and have a longer half life

241
Q

Treatment of phaeochromocytoma

A

Peri-operative - Alpha blocker first (eg: phenoxybenzamine) - Then beta blocker (eg: atenolol, propanolol) - This prevents reactive vascoconstriction Surgical - Laproscopic adrenalectomy

242
Q

Pheochromocytoma hypertensive crisis

A
  • BP higher than 180/120 - Causes: XR contrast, TCA, opiates - First line treatment: phentolamine (alpha blocker)
243
Q

What is SIAD?

A

Overdiagnosed cause of hyponatremia - Inappropriately released ADH, dilute euvolemia - excess ADH = more water retention = compensatory Na+ excretion to maintain euvolemia

244
Q

Normal water sodium distribution vs SIADH

A

img

245
Q

Aetiology of SIAD

A

Cancers - SCLC and others - Infection/immunosuppression, eg: TB, pneumonia, meningitis - Abscesses - Drugs: SSRIs, carbamazepine, sulfonylureas - Head trauma

246
Q

Pathophysiology of SIAD

A

high ADH independent of RAAS - Increased vasoconstriction - APO-II expression of collecting duct - Lead to high BP - excess H2O retained means more dilute blood and more Na+ loss

247
Q

Symptoms of hyponatremia

A

vomiting - headache - Decreased GCS - Muscle weakness

248
Q

Symptoms of extreme hyponatremia

A

Seizures - Neurological complications - Brainstem herniation

249
Q

How can hyponatremia cause brain stem herniation?

A

Low Na+ means high compensatory H2O - enters skull, high ICP - Causes hyponatremic encephalopathy - risk of Brainstem herniating through foramen magnum (tentorial herniation)

250
Q

Diagnosis of SIAD

A

decrease in serum Na+ and normal serum K+ - high urine osmolality - skin turgor and jugular venous pressure test

251
Q

Differential diagnosis of SIAD

A

Na+ depletion - Give 0.9% saline - Na+ depletion -> serum will normalise - SIAD -> serum fails to normalise

252
Q

Treatment for hyponatraemia secondary to SIAD

A
  • Asymptomatic/mild symptoms: Fluid restrict; vaptans (vasopressin antagonist) - Severe symptoms: 3% hypertonic saline to concentrate blood
253
Q

Pathophysiology of craniopharyngioma

A
  • Squamous epithelial remnants of Rathke’s pouch - Benign, slow growing tumour infiltrates to surrounding structures - Mixed solid and cystic parts - Doesn’t spread to other parts of the body but puts pressure on suprasellar region of skull
254
Q

Adamantinous vs squamous papillary craniopharyngioma

A

Adamantinous: Cyst formation and calcification Squamous papillary: Well circumscribed

255
Q

Peak ages craniopharyngiomas occur

A
  • 5 to 14 years - 50 to 74 years
256
Q

Presentation of craniopharyngioma

A

raised ICP - Visual disturbances (Bitemporal hemianopia) - growth failure - Pit. hormone deficiency - Weight Increase

257
Q

How common are meningiomas?

A

Most common tumour of region after pituitary adenoma

258
Q

Cause of meningiomas

A

Complication of radiotherapy

259
Q

Complications of meningioma

A

loss of Visual acuity - Visual field defects - Endocrine dysfunction

260
Q

Testing gonadal axis: men

A
  • Low testosterone, high LH/FSH: Primary hypogonadism - Low testosterone, normal/low LH/FSH: Hypopituitarism - Low testosterone and low LH: Anabolic use Measure 9hr fasted testosterone (morning) and LH/FSH in pituitary disease
261
Q

Testing gonadal axis: women

A

Low oestradiol, high LH and FSH (FSH greater) = Pimary ovarian failure - Low oestradiol, normal/Low LH and FSH, oligo/amenorrhoea = hypopituitarism

262
Q

Normal gonadal levels in women

A

Before puberty: - Low oestradiol - Low LH/FSH Puberty: - Increased oestradiol - Increased pulsatile LH Post menarche: - Monthly menstrual cycle with LH/FSH - Mid-cycle surge in LH and FSH - Levels of oestradiol increases through cycle

263
Q

What to do after euthyroidism is achieved in hyperthyroid treatment

A

Maintenance carbimazole using either: - Titration block regimen - Block and replace regimen Complete remission achieved after 18 months of treatment (remission rate 50%)

264
Q

What does the pituitary gland control?

A

Thyroid - adrenal cortex - Testis - Ovary Not the adrenal medulla

265
Q

What hormones have a circadian rhythm

A
  • Cortisol - Testosterone - DHEA - 17OH Progesterone Not T4
266
Q

Which conditions do you need to rule out before confirming SIAD?

A

Hypothyroidism - Hypervolaemia - adrenal insufficiency - Diuretic use

267
Q

Which hormones suppress appetite?

A
  • Peptide YY - CCK - GLP 1 - Glucose
268
Q

What is the main adipose signal to the brain?

A

Leptin

269
Q

Treatment of chronic cases of SIAD

A

Furosemide - Vasopressin antagonist (tolvaptan) - Demeclocycline (inhibits ADH)

270
Q

Typical features of hypogonadism in males

A

Joint and muscular aches - Decreased sexual appetite - Decreased Hair growth - Asymptomatic

271
Q

What is satiety?

A

The physiological feeling of no hunger

272
Q

What does ghrelin do?

A

Stimulates hunger

273
Q

Risk factors of hyperthyroidism

A
  • Smoking - Stress - HLA-DR3 - Female 20-40 years - Other autoimmune diseases
274
Q

Epidemiology of hypothyroidism

A
  • Mainly >40 years - F>M 6:1
275
Q

High and low values for urine osmolality

A

< 300 = low >800 = high

276
Q

Cancers that can cause SIAD

A

SCLC (small cell carcinoma) - Prostate cancer - Pancreatic cancer - Lymphomas - cancer of the thymus

277
Q

What do long term corticosteroid medications lead to?

A
  • Suppression of the adrenal glands - Long term atrophy of the adrenal glands - can’t produce enough corticosteroids - Adrenal insufficiency if medication is stopped
278
Q

Differential diagnoses for presentation of polyuria and polydipsia

A

diabetes mellitus - diabetes insipidus - SIAD - Primary Polydipsia - hypercalcaemia

279
Q

Complications of adrenal insufficiency

A
  • Addisonian crisis (experiences by 40% of patients) - Cushing’s syndrome
280
Q

Signs of HHS

A

Reduced GCS - dehydration - Hemiparesis (can be confused for a stroke) - Seizures

281
Q

Why is there no acidosis in HHS?

A
  • Small amounts of circulating insulin in T2DM - So lipolysis doesn’t occur
282
Q

Complications of HHS

A

Cardiovascular - venous Thromboembolism, Arrhythmias, MI - Neuro - stroke and Seizures - AKI

283
Q

NICE diagnostic criteria for T1DM

A
  • Clinical features and evidence of hyperglycaemia - Ketosis - Rapid weight loss - < 50 years - BMI < 25 kg/m2 - Personal and/or family history of autoimmune disease
284
Q

Other treatments for T1DM after basal-bollus

A

Mixed Insulin regimen - Continuous Insulin infusion

285
Q

Mixed insulin regimen

A
  • A mixture of short or rapid acting and intermediate-acting insulin - Twice daily - For those who can’t tolerate multiple injections for basal bollus
286
Q

Continuous insulin infusion

A
  • If patient has disabling hypoglycaemia - or persistently hyperglycaemic (HbA1c > 69mmol/mol) on multiple injection insulin therapy
287
Q

Disadvantages of basal insulin in T2DM

A
  • Doesn’t cover meals - Best used with long-acting insulin analogues (expensive)
288
Q

Signs of T2DM

A

Acanthosis nigricans (fig.1) - Glove and stocking sensory loss - Diabetic Retinopathy - Diabetic foot disease

289
Q

Drugs that can cause hypercalcaemia

A

Thazides - Diuretics - Lithium - Excessive Vit D or a intake

290
Q

Treatment of hypercalcaemia

A

Aggressive IV fluids - Consider IV bisphosphonates If No response - Treat underlying cause

291
Q

Drugs that can cause hypocalcaemia

A

bisphosphonates - Phenytoin - Loop Diuretics - Cinacalcet

292
Q

Treatment of hypocalcaemia

A

oral calcium replacement or IV calcium gluconate - Treat the cause

293
Q

How to determine if hyperaldosteronism is unilateral or bilateral

A

Adrenal venous sampling - Measures the amount of corticosteroid secreted from each adrenal gland

294
Q

Epidemiology and risk factors of hyperparathyroidism

A
  • Female - Radiation therapy to neck - Severe Vit D or Calcium deficiences - Familial rare conditions: MEN1 and 2A
295
Q

Diagnosis of pseudohypoparathyroidism

A

high PTH - Low calcium - high phosphate Pseudopseudohypoparathyroidism Also exists, but levels for everything are normal

296
Q

General signs of hyperthyroidism

A

Postural tremor - Palmar erythema - Hyperreflexia - goitre - Lid lag and retraction

297
Q

Signs of thyroid storm

A
  • Hyperpyrexia, often >40°C - Tachycardia, often >140bpm, with or without atrial fib - Reduced GCS
298
Q

Diagnosis of thyroid storm

A

TFTs: high T3 and T4, suppressed TSH - ECG - blood glucose (perform in all patients with Reduced consciousness)

299
Q

Treatment of thyroid storm

A

High dose propylthiouracil and KI

300
Q

What is thyroid storm/thyrotoxic crisis?

A
  • Endocrine emergency often seen in patients with Graves’ disease or toxic multinodular goitre - Secondary to precipitating factor such as infection or trauma - 10-20% mortality
301
Q

Treatment for DeQuervain’s thyroiditis

A

NSAIDs for pain and inflammation - beta blockers for symptomatic relief

302
Q

Side effects of dopamine agonists such as bromocriptine

A

Impulsiveness, so can lead to addictions

303
Q

Link between acromegaly and prolactinoma

A

50% of acromegaly tumours are associated with prolactinoma

304
Q

ECG in hypocalcaemia

A

Longer QTc and ST segment

305
Q

Why can acromegaly cause sleep apnoea?

A

Pressure around the neck due to enlargement

306
Q

Side effects of other diabetic medication

A
  • SGLT-2 inhibitor - genitourinary infections - GLP-1 analogue - weight loss - Thiazide diuretics - weight gain

Haroon Phase 2A (14 decks)

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