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Phase 2a medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the definition of diabetes mellitus?

A

Disorder of carbohydrate metabolism characterised by hyperglycaemia due to relative insulin deficiency, resistance or both

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2
Q

What range should normal blood glucose be in?

A

3.5-8.0 mmol/L

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3
Q

What measurements need to be detected in bloods for a person to be diagnosed with diabetes?

A

Random plasma glucose > 11 mmol/L
Fasting plasma glucose > 7 mmol/L
HbA1c of 48 mmol/mol
2 hour postprandial > 11.1 mmol/L

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4
Q

What is the difference between type 1 and type 2 diabetes?

A

Type 1 is insulin deficiency, autoimmune

Type 2 is insulin resistance/relative insulin deficiency

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5
Q

What are the epidemiological differences between type 1 and type 2 diabetes?

A

Type 1
- Often presents in childhood, peak incidence at puberty
- Increasing prevalence
- Increased prevalence of those of Northern European ancestry
Type 2
- Common in all populations with affluent lifestyle
- Increasing incidence (ageing population, increasing obesity)
- Presents in adulthood > 40
- More prevalence in South Asia, African nad Caribbean ancestry

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6
Q

Other than type 1 and type 2, name 3 other types of diabetes

A

Maturity onset diabetes of youth, pancreatic diabetes, endocrine diabetes, malnutrition related diabetes, drug induced

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7
Q

Give 5 risk factors for developing type 1 diabetes

A

Northern European ancestry (particularly Finnish), family history, having another autoimmune condition, diet, enteroviruses, vitamin D deficiency, recreational drug use, alcohol, steroids

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8
Q

Give 5 risk factors for developing type 2 diabetes

A

Genetics, male, increasing age, obesity, lack of exercise, Asian, high calorie intake

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9
Q

What is the pathophysiology of type 1 diabetes?

A
  • Autoimmune destruction of beta cells leads to insulin deficiency
  • Chronic insulitis ensues
  • Continued breakdown of liver gylcogen, unrestrained lipolysis and skeletal muscle breakdown, increased in hepatic glucose output and suppression peripheral glucose uptake
  • Increased urinary glucose losses as renal threshold exceeded
  • Perceived stress leading to increased cortisol and adrenaline
  • Catabolic state leading to increasing levels of ketones (lack of glucose and fat breakdown) and muscle loss
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10
Q

What is the pathophysiology of type 2 diabetes?

A
  • Insulin resistance post-receptor and progressive failure of insulin secretion
  • Impaired insulin action leading to reduced muscle and fat uptake after eating
  • Failure to suppress lipolysis and high circulating FFAs - depositing in islets of Langherhan’s leading to further impairment of insulin secretion
  • Increased glucose levels in blood leads to damage - prevents NO release from endothelial cells so vessel lumen remains small = increased BP
  • Hyperglycaemia and lipid excess toxic to beta cells = loss of beta cells
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11
Q

What occurs during diabetic ketoacidosis?

A

State of uncontrolled catabolism

  • Rise in ketones
  • Glucose and ketones excreted in urine leads to osmotic diuresis and falling circulatory blood volume
  • Ketones acidic so lower blood pH, impairs Hb ability to bind to O2
  • Reduced glucose = increased FFA oxidation = increased acteyl-CoA production = increased ketones exceeding ability of peripheral tissues to oxidise them
  • Vicious circle of dehydration, hyperglycaemia and increasing acidosis eventually leading to circulatory collapse and death
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12
Q

What are the symptoms of ketoacidosis?

A 
Polyuria and polydipsia
Nausea and vomiting
Weight loss
Weakness
Abdominal pain
Drowsiness/confusion
Hyperventilation as respiratory compensation
Fruity breath
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13
Q

What are the risk factors for developing ketoacidosis?

A 
Stopping insulin
Infection
Surgery
MI
Pancreatitis
Undiagnosed diabetes
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14
Q

What occurs when someone develops hyperosmolar hyperglycaemic state?

A
  • Endogenous insulin levels reduced but still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production
  • Severe dehydration, decreased level of consciousness, hyperglycaemia, hyperosmolality, no ketones in blood/urine, coma, bicarbonate not lowered
  • Treat with insulin
  • Fluid replacement and restore lost electrolytes
  • Low molecular weight heparin
  • Risk of cerebral oedema
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15
Q

What are the risk factors of developing hyperosmolar hyperglycaemic state?

A

Infection, consumption of glucose rich foods, concurrent medication eg thiazide diuretics or steroids

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16
Q

How might someone with type 1 diabetes present?

A 
Lean, polydipsia, polyuria
Weight loss and fatigue
Ketosis
Nocturia, ketonuria, glycosuria
Dehydration
Decreased appetite 
Blurred vision
Hunger
High levels of islet autoantibodies
Short history of severe symptoms
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17
Q

How might someone with type 2 diabetes present?

A 
Overweight in abdominal area
Polydipsia, polyuria
Ketosis
Older
Gradual onset
Often able to control by diet, exercise and oral medication
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18
Q

How is diabetes diagnosed?

A

Random plasma glucose/fasting plasma glucose/2 hours postprandial/HbA1c
If symptomatic require only 1 abnormal
If asymptomatic require 2 abnormal
Microalbuninuria - kidney disease?
FBC, U&Es, fasting blood for cholesterol and triglycerides
Blood pH

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19
Q

Give 3 differential diagnoses of diabetes

A

Pancreatitis, trauma/pancreatectomy, neoplasia of pancreas, acromegaly, Cushing’s, Addison’s

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20
Q

How is type 1 diabetes treated?

A 
Insulin - basal/bolus
Educate to self-control doses
Phone for support
Modify diet and avoid binge drinking
Make sure to change injection sites
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21
Q

How is type 2 diabetes treated?

A 
Weight loss and exercise
Statins 
BP control
1st drug - metformin
Dual therapy of metformin with DDP4 inhibitor/ploglitazone/sulphonylurea/SGLT-2i
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22
Q

Give 5 complications of diabetes

A

Hypoglycaemia
Microvascular - retinopathy, nephropathy, neuropathy
Macrovascular - strokes, renovascular disease, limb ischaemia, heart disease, erectile dysfunction, hypertension
Staphylococcal skin infections
DKA

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23
Q

What is impaired glucose tolerance?

A

Abnormal 2 hours post-prandial
BUT glucose level not high enough to be diabetic
Insulin resistance

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24
Q

What is impaired fasting glucose?

A

Abnormal fasting glucose
BUT glucose level not high enough to be diabetic
Insulin resistance

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25
Q

What is diabetic nephropathy?

A

Glomerular damage due to diabetes
Main cause of end stage renal disease
Major risk factor for CVD

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26
Q

What are the risk factors for diabetic nephropathy?

A

Poor BP control

Poor glycaemic control

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27
Q

What occurs during diabetic nephropathy?

A 
Progressive decline in renal function
Prevents kidney filtration
Glomerulus changes
Increase of glomerular injury
Filtration of proteins = proteinuria
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28
Q

What is the presentation of diabetic nephropathy?

A

Progressive decline in kidney function, proteinuria

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29
Q

How is diabetic nephropathy diagnosed and treated?

A

Diagnosis - kidney function test, amount of albumin in urine
Treatment - BP control, glycaemic control
Proteinuria control and cholesterol control

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30
Q

What is diabetic neuropathy?

A

Irreversible nerve damage due to hyperglycaemia
Occurs in 1 in 5 patients with diabetes
Can lead to foot ulceration

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31
Q

What are the risk factors for diabetic neuropathy?

A

Poor glycaemic control, hypertension, smoking, HbA1c changes, duration of diabetes, BMI, trigylcerides, high total cholesterol

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32
Q

How does diabetic neuropathy present?

A

Pain - burning, pins and needles, worse at night
Autonomic - diarrhoea, incontinence, constipation, erectile dysfunction
Insensitivity - foot ulceration, infection, amputation, falls
Glove and stocking
No significant motor deficit

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33
Q

How is diabetic neuropathy diagnosed and treated?

A

Diagnosis - 10gm monofilament, neurotips, tuning fork, ankle reflexes
Treatment - good glycaemic control, tricyclic antidepressants/SSRIs, anticonvulsants, opioids, IV lignocaine, capsaicin
Transcutaneous nerve stimulation/acupuncture
Psychological interventions

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34
Q

What is diabetic retinopathy?

A

Damage to blood vessels of light sensitive tissue in eye causing blindness

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35
Q

What are the risk factors for diabetic retinopathy?

A

Poor glycaemic control, long durational diabetes, hypertension, insulin treatment, pregnancy, higher HbA1c

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36
Q

What occurs in diabetic retinopathy?

A
  • Blood vessel leakage
  • Occlusion
  • Pericyte loss and smooth muscle cell loss
  • Micro-aneurysms adjacent to or upstream of capillary non-perfusion
  • Thickened basement membrane
  • Loss of junctional contact between endothelial cells
  • Glial cells grow down capillaries
  • Ischaemia/occlusion
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37
Q

How is diabetic retinopathy diagnosed and treated?

A

Diagnosis - eye screening once per year for early detection

Treatment - laser therapy to stabilise changes (doesn’t improve sight)

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38
Q

What are the risks of laser eye treatment?

A 
Difficulty with night vision
Loss of peripheral vision
Tunnel vision
Temporary drop in acuity
Vitreous haemorrhage
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39
Q

How does metformin (biguandie) work?

A
  • Reduces gluconeogenesis in liver

- Increases glucose uptake and ultilisation in skeletal muscle (increased insulin sensitivity)

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40
Q

What are the side effects of metformin?

A 
Hypoglycaemia
GI disturbances (anorexia, diarrhoea, nausea) - weight loss
Lactic acidosis in renal disease, hepatic disease and HF
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41
Q

What is the action of sulphonyl-ureas? And give some examples

A

Stimulate B cells to secrete insulin
Glicalazide
Glipizide

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42
Q

What are contraindications of sulphonyl-ureas?

A

Pregnancy and breastfeeding as can cross placenta and enter breast milk causing hypoglycaemia in newborns

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43
Q

What are the side effects of sulphonyl-ureas?

A 
Hypoglycaemia
Weight gain (stimulate appetite)
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44
Q

What is the action of DPP4 inhibitors? And give an example

A

Inhibit DPP4, increasing effect of incretins that stimulate insulin secretion
Incretins - group of hormones released after eating and augment secretion of insulin
Don’t cause weight gain/loss
Sitagliptin

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45
Q

What is the action of gliazones? And give an example

A

Enhance uptake of fatty acids and glucose

Pioglitazone

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46
Q

What are the side effects of gliazones?

A 
Fluid retention (increases Na+ reabsorption) - may worsen HF
Weight gain (fluid retention and fat gain)
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47
Q

How does hypoglycaemia develop?

A

Too much insulin/oral hypoglycaemic agents leading to insufficient glucose to brain

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48
Q

What are the signs and symptoms of hypoglycaemia?

A

Odd behaviour (aggression)
Sweating (fight/flight)
Raised pulse
Seizures

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49
Q

How is hypoglycaemia diagnosed and treated?

A

Blood glucose level
Glucose (food/IV infusion)
Glucagon

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50
Q

What is the definition of Graves’ disease?

A

Hyperthyroidism
Excessive stimulation of TSH receptor which stimulates thyroid to produce more hormone and grow larger (goitre)
AKA - thyrotoxicosis - excess thyroid hormones in blood

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51
Q

What are the causes of thyrotoxicosis?

A

Overproduction of thyroid hormone
Leakage of preformed hormone from thyroid (destroyed follicular cells by infection/autoimmune)
Ingestion of excess hormone

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52
Q

Epidemiology of hyperthyroidism?

A

2-5% of women with have at some time
20-40 mainly
2 diseases account for majority of causes
2/3 cases Graves’

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53
Q

Name 3 other conditions that can cause hyperthyroidism

A

Toxic multi-nodular goitre
Toxic adenoma
Ectopic thyroid tissue
Exogenous (iodine/T4 excess)

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54
Q

Name 5 risk factors for developing Graves’

A

Female, family history, E coli/gram-negative bacterial infections (contain TSH binding sites), smoking, stress, high iodine levels, autoimmune disease

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55
Q

What is the pathogenesis of Graves’?

A
  • Serum IgG antibodies called TSH receptor stimulating antibodies bind to TSH receptors in thyroid
  • Stimulates production of T3/4 behaving like TSH
  • Excess secretion of thyroid hormones and hyperplasia of thyroid follicular cells (diffuse goitre)
  • Similar auto-antigen can result in retro-orbital inflammation - Graves’ opthalmopathy
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56
Q

Give 5 general symptoms and signs of hyperthyroidism

A

Symptoms - palpitations, diarrhoea, weight loss, oliomenorrhea/infertility, heat intolerance, tremor, behavioural change, hyperkinesis, muscle wasting, anxiety, sweats, Signs - diffuse goitre, lid lag and stare, atrial fibrillation, tachycardia, thin hair, onycholysis

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57
Q

Give 2 symptoms specific to Graves’

A

Graves’ ophthalmopathy - eye discomfort, grittiness, increased tear production, photophobia, diplopia, protruding eye
Thyroid acropachy - clubbing, finger and toe swelling

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58
Q

How is hyperthyroidism diagnosed?
How is Graves’ diagnosed?
Give a differential diagnosis

A

TFTs - TSH suppressed (only in primary), T3/4 raised
TPO and thyroglobulin antibodies present
Ultrasound thyroid
Graves’ - TSH receptor stimulating antibodies
Differential - mild cases of anxiety

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59
Q

How is hyperthroidism treated?

A

Beta-blockers
Anti-thyroid drugs - propylthiouracil/oral carbimazole
Radioactive iodine
Surgery - thyroidectomy

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60
Q

What is hypothyroidism?

What is myxoedema?

A

Underactivity of thyroid gland

Under production of thyroid hormone

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61
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary - reduced T4 and T3

Secondary - reduced TSH from anterior pituitary - hypopituitarism

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62
Q

Give some examples of causes of primary hypothyroidism

A

Primary atrophic hypothyroidism, Hashimoto’s thyroiditis, iodine deficiency, post-thyroidectomy/radioiodine/antithyroid drugs, lithium/amiodarone

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63
Q

Give 5 epidemiology facts about hypothyroidism

A

Endemic in iron deficient areas
More common in women
Incidence increases with age
Associated with other autoimmune diseases
Associated with Turner’s and Down’s syndrome, cystic fibrosis, primary billiary cirrhosis and ovarian hyper-stimulation

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64
Q

How does goitre form?

A

The pituitary gland will detect low thyroid levels so it produces more TSH which will stimulate TSH receptors on thyroid resulting in thyroid enlargement

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65
Q

What is autoimmune hypothyroidism?

A

Antithyroid antibodies lead to lymphoid infiltration of gland and eventually atrophy and fibrosis
No goitre

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66
Q

What is Hashimoto’s thyroiditis?

A

Form of autoimmune hypothyroisism
Produces atrophic changes with regeneration resulting in goitre formation due to lymphocytic and plasma cell infiltration
Normally feels firm and rubbery
Thyroid peroxidase present in high titres
Levothyroixine - may shrink goitre

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67
Q

What is post-partum thyroiditis?

A

Observed after pregnancy
Modifications in immune system necessary in pregnancy and histologically lymphocyte thyroiditis
Can proceed to permanent hypothyrodism

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68
Q

What is iatrogenic thyroiditis?

A

From thyroidectomy or radioactive iodine treatment

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69
Q

What drugs may induce thyroiditis?

A

Carbimazole, lithium, amiodarone (can also cause hyper), interferon

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70
Q

What is iodine deficiency thyroiditis?

A

Lack of iodine in diet
Euthyroid or hypothyroid depending on severity
Borderline hypothyroidism leading to TSH stimulation and thyroid enlargement in face of continuing iodine deficiency

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71
Q

What are the symptoms of hypothyroidism?

A

Hoarse voice, goitre, constipation, cold intolerant, weight gain, menorrhagia, myalgia, weakness, tired, low mood, dementia, oedema

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72
Q

What are the signs of hypothyroidism?

A

BRADYCARDIC
Bradycardia, Reflexes relax slowly, Ataxia, Dry/thin hair/skin, Yawning, Cold hands, Ascites, Round, puffy face, Defeated demeanour, Immobile, Congestive heart failure

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73
Q

How is hypothyroidism diagnosed?

What is a differential diagnosis of hypothyroidism?

A

TFTs - serum TSH high (increases to make thyroid work again), TSH inappropriately low for low T3/4 (secondary)
Serum free T4 low
Thyroid antibodies
Blood tests
- Anaemia
- Raised serum aspartate transferase levels
- Increased serum creatine kinase
- Hypercholesterolaemia
- Hyponatraemia due to increased ADH and impaired free water clearance
Differential - ageing

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74
Q

How is hypothyroidism treated?

A

Hormone replacement
Monitoring
- Primary - dose titrated until TSH normalises
- Secondary - TSH always low, T4 monitored

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75
Q

What are the complications of hypothyroidism?

A

Myxoedema coma
Severe hypothyroidism - confusion, coma
Hypothermia, cardiac failure, hypoventilation, hypoglycaemia, hyponatraemia
Medical emergency - IV/oral T3 and glucose infusion, gradual rewarming

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76
Q

What is Cushing’s disease?

A

Chronic, excessive and inappropriately elevated levels of circulating plasma cortisol resulting from inappropriate ACTH secretion from pituitary due to a tumour
Most common cause oral steroids

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77
Q

What other things could cause high levels of cortisol?

A

Cushing’s syndrome, ectopic ACTH production, ACTH treatment for asthma, adrenal adenoma

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78
Q

What is the pathophysiology of high levels of cortisol?

A

Excess cortisol resulting from either excess ACTH or by ingesting excess glucocorticoids or from neoplasms in adrenals that stimulate zone reticularis to release more cortisol

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79
Q

What are the symptoms of Cushing’s?

A

CUSHING
Cataracts, Ulcers, Skin (striae), HTN, hyperglycaemia, Infections increase, Necrosis, Glucosuria
Aesthetic things
Central obesity, plethoric complexion - ruddy, swollen, moon face, mood change - depression, lethargy, irritability, psychosis, acne, buffalo hump, hirsutism

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80
Q

How is Cushing’s diagnosed?

A

Careful drug history
Random plasma cortisol
Overnight dexamethasone suppression test - should send negative feedback to pituitary and hypothalamus leading to decreased ACTH and reduced cortisol
Urine free cortisol over 24 hours
If no suppression - 48 hour dexamethasone suppression test
CT/MRI for tumour
Distinguish pituitary cause from ectopic ACTH production
If cortisol responds to CRH - Cushing’s

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81
Q

What is a differential diagnosis of Cushing’s?

A

Pseudo-Cushing’s syndrome - alcohol excess, resolves after 1-3 weeks of alcohol abstinence

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82
Q

What is the treatment of high cortisol?

A

Stop steroids
Cushing’s - surgical selective removal of adenoma, bilateral adrenalectomy, radiotherapy
Adrenal adenoma/carcinoma - adrenalectomy
Ectopic ACTH - surgery, drugs to inhibit cortisone sythesis

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83
Q

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

A

Syndrome - excess cortisol, loss of hypothalamix pituitary axis feedback, loss of circadian rhythm
Disease - all that caused by pituitary adenoma

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84
Q

What is acromegaly?

What is gigantism?

A

Excess GH production in adults

Excess production in children before fusion of epiphyses of long bones

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85
Q

What is the epidemiology of acromegaly?

A

Rare - 3 per million/year
Equal prevalence between women and men
Incidence highest in middle age 40+

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86
Q

What are the risk factors and causes of acromegaly?

A

Risk factors - MEN-1

Aetiology - benign pituitary GH-producing adenoma, hyperplasia

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87
Q

What is the pathophysiology of acromegaly?

A

GH - pulsatile release
Stimulated by GHRH, ghrelin
Inhibited by somatostatin, high glucose
Exerts effects via IGF-1 or directly on tissues to induce metabolic changes
Increased secretion due to pituitary tumour or ectopic carcinoid tumour
Stimulates skeletal and soft tissue growth giving rise to giant-like symptoms
Local expansion of tumour can lead to compression of surrounding structures resulting in headaches and visual field loss

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88
Q

How does acromegaly present? - Symptoms

A

Headaches, excessive sweating, visual deterioration, snoring, wonky bite, increased weight, decreased libido, amenorrhea, arthralgia and backache, acroparaesthesia

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89
Q

How does acromegaly present? - Signs

A

Skin darkening, coarsening of face with wide nose, rings tight, deep voice, large tongue, increased size of hands and feet, puffy lips, eyelids and skin, obstructive sleep apnoea

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90
Q

What co-morbidites accompany acromegaly?

A

Impaired glucose tolerance, DM, sleep apnea, hypertension, LV hypertrophy, cardiomyopathy, arrhythmia, IHD, stroke, colon cancer, arthritis

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91
Q

How is acromegaly diagnosed?

A

High glucose, calcium and phosphate
Plasma GH levels - should be undetectable (but remember pulsatile secretion)
Glucose Tolerance Test - diagnostic if no suppression of glucose
IGF-1 - raised and doesn’t fluctuate so diagnostic
Visual field exam
MRI scan pituitary
ECHO for cardiomyopathy
Old photos - changes
Serum prolactin raised

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92
Q

How is acromegaly treated?

A 
Trans-sphenoidal surgery - remove tumour and correct tumour suppression
Somatostatin analogues
GH receptor antagonists
Dopamine agonist
Radiotherapy
Stereotactic radiotherapy
Gamma knife, LINAC or proton beam
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93
Q

What is Conn’s syndrome?

A

Excess production of aldosterone independent of renin-angiotensin-aldosterone system
Results in increased sodium and water retention (increased BP) and decreased renin release
Primary hyperaldosteronism
Rare

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94
Q

What are the causes of Conn’s?

A

Adrenal adenoma that secretes aldosterone

Hyperaldosteronism - bilateral adrenocortical hyperplasia

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95
Q

What are the risk factors of Conn’s?

A

Hypertension

  • Under 35 with no FH
  • Malignant hypertension
  • Hypokalaemia before diuretic therapy
  • Resistant to conventional antihypertensives
  • Unusual symptoms
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96
Q

How does Conn’s syndrome present?

A

Often asymptomatic
Hypertension - can be associated with renal, cardiac and retinal damage if severe
Hypokalaemia - weakness/cramps, paraesthesia, polyuria, polydipsia, constipation

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97
Q

How is Conn’s diagnosed?

A

Hypokalaemic ECG - flat T waves, ST depression, long QT
Serum hypokalaemia
Plama aldosterone:renin ratio - raised (decreased renin)
Increased plasma aldosterone levels not suppressed with 0.9% saline infusion or fludrocortisone administration
CT and MRI adrenals
U&E

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98
Q

What is a differential diagnosis for Conn’s?

A

Secondary hyperaldosteronism - excess renin stimulating aldosterone release
Caused by reduced renal perfusion due to
- Renal artery stenosis, accelerated hypertension, diuretics, congestive heart failure, hepatic failure

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99
Q

How is Conn’s treated?

A

Laproscopic adrenalectomy, aldosterone antagonist - oral spironolactone for 4 weeks pre-op to control BP and K+

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100
Q

What is Addison’s disease?

A

Primary hypoaldrenalism (can also be caused by TB)
Destruction of entire adrenal cortex resultin in mineralocorticoid (aldosterone), glucocorticoid (cortisol) and sex steroid deficiency
Very rare 0.8 per 100,000
Can be fatal
More common in women

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101
Q

What is secondary hypoadrenalism?

A

Issue with pituitary glands leading to lack of release of products from adrenal glands

102
Q

What are risk factors for Addison’s disease?

A

Autoimmune adrenalitis - destruction of adrenal cortex by adrenal autoantibodies
TB, adrenal metastases, long term steroid use (prevents ACTH release via negative feedback), opportunistic infections in HIV, adrenal haemorrhage/infarction

103
Q

What are the risk factors in secondary hypoadrenalism?

A

Long term steroid therapy leading to suppression of pituitary-adrenal axis
Decreased ACTH production from hypothalamic-pituitary disease

104
Q

How does Addison’s disease present?

A

Hyperpigmentation (increased CRH and ACTH)
Lethargy, depression, anorexia, weight loss, vitiligo, nausea and vomiting, diarrhoea, constipation, abdominal pain, impotence/amenorrhoea, postural hypotension, lean build, dizzy, dehydration
Tanned, Tired, Toned, Tearful

105
Q

How is Addison’s diagnosed?

A

Bloods - hyponatraemia and hyperkalaemia (aldosterone), hypoglycaemia (cortisol), hypoaldosteronism, low cortisol, uraemia, hypercalcaemia, eosinophilia (lack of anti-inflammatory effects from cortisol), anaemia
Short ACTH stimulation test - cortisol will remain low
21-hydroxylase adrenal antibodies
9am ACTH levels
AXR/CXR

106
Q

How is Addison’s treated?

A 
IV hydrocortisone (cortisol replacement), IV 0.9% saline, glucose infusion if hypoglycaemia, replace steroids with daily 3x to mimic rhythm
Fludrocortisone to replace aldosterone
Adrenal crisis - IV hydrocortisone immediately and fluids
107
Q

What are the symptoms of adrenal crisis?

A

Nausea, vomiting, abdominal pain, muscle cramps, confusion

Shock

108
Q

How is secondary hypoadrenalism diagnosed and treated?

A

Diagnosis - ACTH levels low and mineralocorticoid production intact
Treatment - wean off steroids slowly and adrenals will recover
Oral hydrocortisone

109
Q

What is diabetes insipidus?

A

Passage of large volumes (> 3L/day) of dilute urine due to impaired water reabsorption in kidney either due to reduced ADH secretion from posterior pituitary (cranial DI) and impaired response of kidney to ADH (nephrogenic DI)

110
Q

What is the epidemiology of DI?

A

2-5% women at some time

Mainly between 20-40

111
Q

What are the differences in causes between cranial DI and nephrogenic DI?

A

Cranial - pituitary tumour, head trauma

Nephrogenic - drug induced

112
Q

What is the main risk factor for developing DI?

A

Family history

113
Q

Why do patients with DI become dehydrated?

A

Reduced ADH secretion or impaired response to ADH resulting in significant water losses resultin g in dilute urine

114
Q

How does DI present?

A

Polyuria - 15L in 24 hours
Polydipsia
Hypernatraemia due to water loss in excess of Na loss
Dehydration - impaired consciousness

115
Q

What are the symptoms of hypernatraemia?

A

Lethargy, thirst, weakness, irritability, confusion, coma, fits

116
Q

How is DI diagnosed?

A

Urine volume measured
Blood glucose to exclude DM
Water deprivation test - determine whether kidneys continue to produce dilute urine despite dehydration, measure serum and urine osmolality, urine vol and body weight hourly for 8 hours during fasting and w/o fluids
Cranial DI - MRI of head and test anterior pituitary
Desmopressin (ADH analogues) to differentiate

117
Q

What differential diagnoses could be made other than DI?

A

DM - osmotic diuresis secondary to glycosuria
Hypokalaemia
Hypercalcaemia

118
Q

How is cranial DI treated?

A

Treat cause - synthetic analogue of ADH - desmopressin

119
Q

How is nephrogenic DI treated?

A

Treat cause - usually renal disease
Thiazide diuretics (bendroflumethiazide)
NSAIDs - lower urine volume and plasma Na+ giving prostaglandin synthase

120
Q

What is SiADH?

A

Syndrome of inappropriate seretion of ADH
Continuous secretion of ADH despite plasma being very dilute leading to retention of water and excess blood volume and thus hyponatraemia

121
Q

What is the epidemiology of SiADH?

A

2-5% of women at some time

20-40 years

122
Q

What are the possible causes of SiADH?

A 
Tumours
CNS - meningitis, head trauma
Pulmonary lesions
Metabolic causes
Drugs
123
Q

What is the pathophysiology of SiADH?

A

Excess release of ADH results in increased insertion of aquaporin 2 channels in apical membrane of collecting duct
Excess water retention which will dilute blood plasma resulting in hyponatraemia as Na+ conc will decrease

124
Q

What are the symptoms of SiADH?

A 
Same as hyponatraemia
Anorexia/nausea and malaise
Weakness and aches
Reduction in GCS and confusion with drowsiness
Fits and coma
Concentrated urine
125
Q

How is SiADH diagnosed?

A 
Low serum Na+
Euvolaemia - normal blood volume
High urine Na+ > 30 mmol/L
Low plasma osmolality
High urine osmolality
Normal renal, adrenal and thyroid function
126
Q

How is SiADH treated?

A

Treat underlying cause where possible
Restrict fluid intake to 500-1000ml daily to increase Na conc
Hypertonic saline - prevents brain swelling
Oral demeclocycline daily - induces nephrogenic DI (inhibits ADH)
Vasoprssin antagonist - oral tolvaptan
Salt and loop diuretic - oral furosemide

127
Q

What are the measurements that denote hyponatraemia?

A

Serum Na < 135 mmol/l
Biochemical severe - serum Na < 125 mmol/l
Normal serum Na 137-144mmol

128
Q

What are the moderate (125-129 mmol/l) symptoms of hyponatraemia?

A 
Headache 
Irritability
Nausea/vomiting
Mental slowing
Unstable gait/falls
Confusion.delerium
Disorientation
129
Q

What are the severe (<125 mmol/l) symptoms of hyponatraemia?

A

Stupor/coma
Convulsions
Respiratory arrest

130
Q

What is the difference between acute and chronic hyponatraemia?

A

Acute - within 48 hours, rapid correction safer and may be necessary, may occur after subarachnoid haemorrhage
Chronic - CNS adapts, correction must be slow < 8mmol/24 hours

131
Q

How do you investigate hyponatraemia?

A 
Plasma osmolality low
High urine osmolality
Plasma glucose
Urine sodium
Urine dip test for proteins
TSH
Cortisol
Consider alcohol
TFTs
Assessment of underlying causes
Review drugs
132
Q

What is hyperkalaemia?

A

Serum K+ > 5.5 mmol/L

Serum K+ > 6.5 mmol/L = medical emergency

133
Q

What causes hyperkalaemia?

A

Decreased excretion - AKI or oligouric renal failure (v small amount of urine produced), drugs (ACEi, potassium sparing diuretics, NSAIDs), Addison’s disease (adrenal insufficiency, low aldosterone)
Redistribution - intracellular to extracellular - DKA, metabolic acidosis, tissue necrosis or lysis
Increased load - potassium chloride, transfusion of stored blood

134
Q

What happens during hyperkalaemia?

A

When K+ levels rise, reduces difference in electrical potential between cardiac myocytes and outside cells meaning threshold for action potential significanly decreased resulting in increased abnormal action potentional = abnormal heart rhythms = ventricular fibrillation and cardiac arrest

135
Q

What are the symptoms of hyperkalaemia?

A

Asymptomatic until high enough to cause cardiac arrest
Fast, irregular pulse, chest pain, weakness, light headedness
Muscle weakness and fatigue (over contraction)
Associated with metabolic acidosis
Kussmaul’s respiration

136
Q

What is could cause a false positive in hyperkalaemia?

A

Haemolysis from venepuncture or K+ release from abnormal RBCs in blood disorders
Contamination with K+ EDTA anticoagulant in FBC bottles
Thrombocythaemia - K+ leaks out of platelets during clotting

137
Q

How is hyperkalaemia diagnosed?

A

Serum K+

Progressive ECG abnormalities - tall, tented T waves, small P waves, wide QRS complexes

138
Q

How is hyperkalaemia treated?

A

Non-urgent
- Treat underlying cause
- Review medications
- Dietary K+ restriction
- Polystyrene sulfonate resin binds to K+ in gut reducing absorption
Urgent
- Stabilise cardiac membrane - IV 10 ml 10% calcium gluconate reducing excitability of cardiomyocytes
- Drive K+ into cells - insulin (glucose uptake brings K+ with it) with glucose to avoid hypoglycaemia
- IV or nebulised salbutamol (increases B2 pumping of K+ into cell)

139
Q

What is hypokalaemia?

A

Serum K+ < 3.5 mmol/L

Serum K+ < 2.5 mmol/L - medical emergency

140
Q

What causes hypokalaemia?

A

Increased excretion - thiazide diuretics, loop diuretics, increased aldosterone secretion (Conn’s), liver/heart failure
Exogenous mineralocorticoids
Renal disease
Reduced dietary intake
Redistribution to cells - beta-agonists
GI losses - vomiting, severe diarrhoea, laxative abuse

141
Q

How does hypokalaemia present?

A 
Muscle weakness
Cramps
Hypotonia
Hyporeflexia
Tetany - spasms
Palpitations
Light headedness -arrhythmias
Constipation
142
Q

How is hypokalaemia diagnosed?

A

Serum K+

ECG - small/inverted T waves, prominent U waves, long PR interval, depressed ST segments

143
Q

How is hypokalaemia treated?

A

Treat underlying cause
Acute can resolve on own - remove initiated factor
Mild
- K+ supplements
- If on thiazide diuretics move to K+ sparing diuretics
Severe
- IV K+ cautiously, no more than 20mmol/h

144
Q

What happens in hyponatraemia?

A

Low Na+ causes water conc gradient out of cell

Increased leakage of ICF causes hyperpolarisation of myocyte membrane decreasing myocye excitiability

145
Q

What is the action of parathyroid hormone?

A

Increased bone resorption by osteoclasts
Increased intestinal calcium reabsorption
Activates 1,25-dihydroxyVD in kidney
Increased calcium reabsorption and phosphate excretion in kidney

146
Q

What are the causes of hyperparathyrodism?

A

80% solitary adenoma
20% parathyroid hyperplasia
Rare - parathyroid cancer
Secondary to hypocalcaemia - chronic kidney disease, VD deficiency, GI disease

147
Q

How does hyperparathyroidism present?

A

Hypercalcaemia - weak, tired, depressed, thirsty, renal stones
Bone resorption - pain, fractures, osteoporosis
Hypertension

148
Q

What investigations need to be done in hyperparathyroidism?

A

Bloods
- Primary: increased PTH, increase Ca, decreased phosph
- Secondary: increased PTH, decreased Ca, increased phosph
- Tertiary: increased everything
Increased 24 hour urinary calcium excretion
DEXA bone scan - osteoporosis

149
Q

How do you treat hyperparathyroidism?

A

Fluids
Surgically treat underlying cause
Bisphosphonates

150
Q

What are the causes of hypoparathyroidism?

A 
Autoimmune destruction of PT glands
Congenital
Surgical removal (secondary)
Mg deficiency
VD deficiency
151
Q

What are the symptoms of hypoparathyroidism?

A 
Same as hypocalcaemia
SPASM
Spasms
Peripheral paraesthesia
Anxious
Seizures
Muscle tone increases
152
Q

How do you treat hypoparathyroidism?

A

Ca supplements
Calcitriol
Synthetic PTH

153
Q

What is pseudohypoparathyroidism?

A

Decreased response to PTH
Blood shows low Ca, high PTH
Treat as normal hypoparathyroid

154
Q

What is hypercalcaemia?

A

When serum calcium is above normal

10.5-12 mg/dL

155
Q

What can cause hypercalcaemia?

A 
Occurs more in elderly women
Primary hyperparathyroidism
Secondary hyperparathyroidism
Tertiary hyperparathyroidism
Malignancies
Thiazide diuretics
Vitamin D analogues
Lithium administration
156
Q

How does primary hyperparathyroidism cause hypercalcaemia?

A

Excess PTH secretion and production and so hypercalcaemia

157
Q

How does secondary hyperparathyroidism cause hypercalcaemia?

A

Physiological compensatory hypertrophy of all parathyroids resulting in excess PTH due to hypocalaemia that occurs in CKD and vitamin D deficiency
Due to diet/GI disease

158
Q

How does tertiary hyperparathyroidism cause hypercalcaemia?

A

Occurs after many years of hyperparathyroidism that occurs from CKD or vit D deficiency
Causes glands to act autonomously having undergone hyperplastic or adenomatous change resulting in excess PTH secretion unlimited by feedback control
Most often seen in chronic renal failure
Treating disease so calcium high

159
Q

How does malignant hpyerparathyroidism cause hypercalcaemia?

A

PT-related protein produced by some squamous cell lung cancer, breast and renal carcinomas (myeloma and non-Hodgkin’s lymphoma)
- Mimic PTH resulting in hypercalcaemia
- PTH low as PT-related protein not detected
Bone infiltration resulting in calcium mobilisation in multiple myeloma and secondary bone metastases
Production of osteoclastic factors by tumours
Excessive calcium intake

160
Q

How does hypercalcaemia present?

A

BONES - pain, fractures, osteopenia/osteomalacia/osteoporosis
STONES - excess calcium, renal colic from renal calculi, biliary stones
GROANS - abdominal pain, malaise, nausea, constipation, polydipsia, calcium deposition in renal tubules, dehydration, confusion, risk of cardiac arrest
MOANS - depression, anxiety, cognitive dysfunction, insomnia, coma

161
Q

How is primary hyperparathyroidism diagnosed?

A

High PTH
High calcium
Low phosphate

162
Q

How is secondary hyperparathyroidism diagnosed?

A

High PTH
Low calcium
High phosphate

163
Q

How is tertiary hyperparathyroidism diagnosed?

A

High PTH
High calcium
High phosphate

164
Q

How is malignant hyperparathyroidism diagnosed?

A 
Low/undetectable PTH from PT-like protein resulting in hypercalcaemia
Low albumin
Increased alkaline phosphatase (severe hyperparathyroidism)
Protein electrophoresis for myeloma
Renal function test
TSH to exclude hyperthyroidism
X-ray
Ultrasound
PT ultrasound
Radioisotope scanning
CT/MRI
DXA bone scan
ECG - tented T, short QT
165
Q

How is hypercalcaemia caused by hyperparathyroidism treated?

A

Treat underlying cause - with surgery
Acute severe hypercalcaemia medical emergency
- Rehydrate with IV 0.9% saline to prevent stones
- Bisphosphonates after rehydration
- Serum U&Es after 48 hours
- Glucocorticoid steroids
Chemotherapy

166
Q

How do you find the cause of the hypercalcaemia?

A

Corrected calcium levels mild increase in hyperparathyroidism and PTH high
Corrected calcium levels severe increase in cancer and PTH low

167
Q

What is hypocalcaemia?

A

Deficiency of serum calcium

Less than 2.1 mmol/l

168
Q

When is hypocalcaemia seen?

A

Hypoparathyroidism
Spans all ages
Common in hospitalised patients and common on ITU wards

169
Q

What can cause hypocalcaemia?

A 
Primary hypoparathyroidism (high phosph)
Secondary hypoparathyroidism
Tertiary hypoparathyroidism
Pseudohypoparathyroidism
Pseudopseudohypoparathyroisim
Secondary to increased serum phosphate levels
Vitamin D deficiency (low phosph)
Reduced PTH function
Acute pancreatitis (low phosph)
Osteomalacia (low phosph)
CKD (high phosph)
170
Q

How does vitamin D deficiency cause hypocalcaemia?

A

Results in less calcium absorption

Due to reduced UV exposure, malabsorption, anti-epileptic drugs

171
Q

How does CKD cause hypocalcaemia?

A

Inadequate production of active vitamin D and renal phosphate retention
Results in micro-precipitation of phosphate in tissues

172
Q

How does reduced PTH function cause hypocalcaemia?

A

Low PTH due to parathyroid gland failure
Primary hypoparathyroidism
Calcium low and phosphate high
Primary hypoparathyroidism

173
Q

What can cause hypoparathyroidism?

A

After parathyroidectomy or thyroidectomy surgery
Radiation
Hypomagnesaemia - required for PTH secretion

174
Q

How does pseudohypoparathyroidism cause hypocalcaemia?

A

Syndrome of end-organ resistance to PTH due to a mutation in Gs alpha-protein
Low calcium, high PTH

175
Q

How does hypocalcaemia present?

A

Parasthesia - pins and needles
Muscle spasms
Basal ganglia calcification
Cataracts
ECG abnormalities
Undermineralised bone with pseudofractures
Increased excitability of muscles and nerves
Papilloedema
SPASMODIC
Spasms, Peripheral paraesthesia, Anxious, irritable, irrational, Seizures, Muscle tone increases in smooth muscles (wheeze), Orientation impaired and confusion, Dermatitis, Impetigo herpetiformis, Chvostek’s sign, Cataract, Cardiomyopahty

176
Q

What is Chvostek’s sign?

A

Tap over facial nerve and look for spasms of facial muscles

177
Q

What is Trousseau’s sign?

A

Inflate BP cuff to 20mmHg above systolic for 5 mins

Hand will start to form into spasm

178
Q

How is hypocalcaemia diagnosed?

A 
Chvostek's sign
Trousseau's sign
Serum urine and creatinine and eGFR for renal disease
PTH levels in serum
PT antibodies
Vitamin D
Magnesium
X-ray metacarpals (pseudohypoparathyroidism)
ECG - long QT
179
Q

What could a differential diagnosis of hypocalcaemia be?

A

Hypoalbuminaemia - low total serum calcium but not ionised calcium, work out corrected calcium
Alkalosis
Potassium and magnesium deficiency
Hyperventilation

180
Q

How do you work out corrected calcium?

A

Total serum calcium + 0.02 (40-serum albumin)

181
Q

How is hypocalcaemia treated?

A

Calcitonin - decreases plasma calcium and phosphate
Bisphosphonates - reduce osteoclast activity
Acute - hospital admission, IV calcium gluconate over 30 mins with ECG
Vit D deficiency - oral cholecalciferol or adcal, ineffective in hypoparathyroidism as PTH needed to convert vit D3 - 1,25 dihydroxyvitamin D
Hypoparathyroidism - calcium supplements, calcitriol

182
Q

What is hyperprolactaemia?

A

Increased secretion of prolactin
Commonest hormonal disturbance of the pituitary
More common in women
Presents earlier in women with menstrual disturbance and later in men with erectile dysfunction

183
Q

Give 4 potential causes of hyperprolactaemia?

A

Prolactimona - tumour of pituitary resulting in excess prolactin release
Pituitary stalk damage - results in less dopamine so there is no inhibition of prolactin
Drugs - most common, metoclopramide or ecstasy
Physiological - pregnancy, breast feeding, stress

184
Q

What is the pathophysiology of hyperprolactaemia?

A

Prolactin secreted by anterior pituitary
Inhibited by dopamine from the hypothalamus
Raised prolactin leads to lactation and inhibition of gonadotropin releasing hormone resulting in reduced LH/FSH and thus reduced testosterone and oestrogen

185
Q

How does hyperprolactaemia present?

A

Amenorrhoea/oligomenorrhoea
Infertility
Galatorrhoea - spontaneous flow of milk from breasts in both males and females
Low libido
Low testosterone in men
Erectile dysfunction and reduced facial hair in men
Local effect of tumour - headache, visual defects
CSF leak

186
Q

How is hyperprolactaemia diagnosed?

A

Measure basal prolactin level - will be very high

187
Q

How is hyperprolactaemia treated?

A

Medical approaches are more efficent that surgical
Dopamine agonists - massive tumour shrinkage, macroadenoma shrinkage = sight saving
Microadenoma usually responds to small doses just once/twice a week

188
Q

What is a non-functioning pituitary adenoma?

A

Benign growth in the pituitary gland that doesn’t produce excess hormones in blood and isn’t cancerous
15% of all pituitary adenomas

189
Q

How does a non-functioning pituitary adenoma present?

A 
Tumour mass effects
Hormone excess
Hormone deficiency
Local mass effects
- Visual field defects
- Cranial nerve palsy and temporal lobe epilepsy
- Headaches
- CSF rhinorrhoea
190
Q

How is a non-functioning pituitary adenoma diagnosed?

A

Hormonal tests - test the different axes
Tumour mass effects and abnormal hormonal tests - MRI
Test normal pituiart function - may have borderline deficiecny of one or all, circadian rhythms

191
Q

How do you test the pituitary-thyroid axis?

A

Primary hypothyroid - raised TSH, low Ft4
Hypopituitary - low Ft4 with normal/low TSH
Graves disease (toxic) - suppresses TSH, high Ft4
TSHoma (rare) - High Ft4, normal/high TSH
Hormone resistance - high Ft4 with normal/high TSH

192
Q

How do you test the gonadal axis in men?

A

Primary hypogonadism - low T, raised LH/FSH
Hypopituitary - low T, normal/low LH/FSH
Anabolic use - low T and suppressed LH
Measure 0900 fasted T and LH/FSH in pituitary disease

193
Q

How do you test the gonadal axis in women?

A

Before puberty - oestradiol low/undetectable, low LH and FSH (FSH slightly higher then LH)
Puberty - pulsatile LH increases and oestradiol increases
Post-menarche - monthly menstrual cycle with LH/FSH, mid-cycle surge LH/FSH and levels oestradiol increase throughout cycle
Primary ovarian failure (menopause) - high LH/FSH (FSH > LH), low oestradiol
Hypopituitary - olio or amenorrhoea with low oestradiol and normal/low FSH/LH

194
Q

How do you test the HPA axis?

A

Circadian rhythm
Measure 0900h cortisol and synacthen
Primary AI - low cortisol, high ACTH, poor response to synacthen
Hypopituitarism - low cortisol, low/normal ACTH, poor response to synacthen

195
Q

How do you test the GH/IGF1 axis?

A 
GH secreted in pulses with greatest pulses at night and low/undetectable levels between pulses
GH levels fall with age, low in obesity
Measure IGF-1 and GH stimulation test
- Insulin stress test
- Glucagon test
196
Q

How do you measure prolactin levels?

A 
Under negative control of dopamine
Stress hormone
Measure prolactin or cannulated prolactin (3 samples over an hour to exclude stress of venepuncture)
May be raised due to 
- Stress
- Drugs - antipsychotics
- Stalk pressure
- Prolactinoma
197
Q

How do you test hormonal axis using dynamic testing?

A

Dexamethasone suppression test - Cushing’s
Oral glucose GH suppression test - Acromegaly
CRH stimulation - Cushing’s
TRH stimulation - TSHoma
GnRH stimulation - gonadotrophin deficiency
Insulin-induced hypoglycaemia - GH/ACTH deficiency
Glucagon test - GH deficiency
Useful for further evaluation to test pituitary reserve/pituitary hyperfunction

198
Q

How is non-functioning pituitary adenoma treated?

A

Hormone replacement therapies
Surgery - if sight threatening
Radiotherapy
Medications

199
Q

What is precocious puberty?

A

Early puberty

Considered early puberty at ages 8 in girls and 9 in boys

200
Q

What is the epidemiology of precocious puberty?

A

Incidence of 1 in 5,000 to 10,000
90% patients female
Females tend to be idiopathic and otherwise healthy
Males - high chance it’s a brain tumour

201
Q

How is precocious puberty classified?

A

True precocious puberty - starts at pituitary, activation of hypothalamus activating GnRH system begins puberty, activation of HPG axis
- Stimulated LH:FSH ratio > 1
Precocious puberty - secreting tumours in gonads, brain, liver, retroperitoneum, mediastinum
- Stimulated LH:FSH ration < 1
- Not activation of HPG axis - could even be suppressed as hormones being produced by gonads will shut doesn HPG axis

202
Q

What are the causes of true precocious puberty?

A 
GnRH dependent
Idiopathic in girls
Boys - consider brain tumour
CNS tumours
CNS disorders - developmental abnormalities, encephalitis, brain abcess, hydrocephalus
Secondary central precocious puberty
Psychosocial
203
Q

What are the causes of precocious pseudo-puberty?

A

Increased androgen secretion - congenital adrenal hyperplasia, virilising neoplasm, Leydig cell adenoma
Gonadotrophin secreting tumours - chorioepitheliomas, germinoma, hepatoma
Ovarian cyst
Oestrogen secreting neoplasm
Hypothyroidism
Iatrogenic or exogenous sex hormones

204
Q

How is precocious pseudo-puberty diagnosed?

A 
Differential diagnosis
True
- Stimulation pubertal range
- Stimulated LH:FSH ratio > 1
Precocious 
- Stimulated pre-pubertal range or suppression
- Stimulated LH:FSH ratio < 1
205
Q

How is precocious puberty treated?

A

GnRH super-agonist the suppress pulsatility of GnRH secretion
Improves final height
Lowers risk of sexual abuse in children

206
Q

Name an example of a biguanide

A

Metformin

207
Q

What are biguanides used for?

A

To treat DMT2 as first choice medication for control of blood glucose, alone or in combination with other hypoglycaemics such as sulphonyl ureas or insulin

208
Q

How do biguanides work?

A

Lower blood glucose by increasing response to insulin
Suppresses hepatic glucose production (glycogenolysis and gluconeogenesis), increases glucose uptake and utilisation by skeletal muscle and suppresses intestinal glucose absorption
DOESN’T cause hypoglycaemia as does not stimulate pancreas
Reduces weight gain and can induce weight loss, which can prevent worsening of insulin resistance

209
Q

What are the main adverse effects of biguanides?

A

GI disturbance - may contribute to weight loss
Lactic acidosis can occur in intercurrent lines such as renal or hepatic impairment or cardiac failure
Contraindicated in severe renal impairment and should be withheld in AKI and severe tissue hypoxia, used with care in hepatic impairment and alcohol intoxication
Can interact with IV contrast media so withheld before these investigations
Use with caution with other drugs that may impact renal function eg ACEI diuretics or NSAIDs
Prednisolone, thiazide and loop diuretics elevate blood glucose and may reduce efficacy of metformin

210
Q

Name an example of a sulphonylurea

A

Gliclazide

211
Q

What are sulphonylureas used for?

A

DMT2 as single agent to control blood glucose and reduce complications where metformin contraindicated/not tolerated
Can be used in combination with metformin and other hypoglycaemics in uncontrolled glucose levels

212
Q

How do sulphonylureas work?

A

Lower blood glucose by stimulating pancreatic insulin secretion
Block ATP dependent K+ channels in pancreatic beta cell membranes, causing depolarisation of cell membrane and opening of voltage gates Ca2+ channels, stimulating insulin secretion
Only effective in patients with residual pancreatic function

213
Q

What are the main adverse effects of sulphonylureas?

A

GI disturbance occurs infrequently, more serious hypoglycaemia especially when used with other hypoglycaemic medication
Rare hypersensitivity reactions and cause hepatic toxicity, rash and fever and haematological abnormalities
Use with care in hepatic and renal impairment and in people at increased risk of hypoglycaemia
Efficacy reduced by prednisolone, thiazide and loop diuretics which increase glucose

214
Q

Name an example of a glitazone

A

Pioglitazone

215
Q

What are glitazones used for?

A

DMT2, alone if metformin contraindicated or in combination with metformin/sulphonylurea when glucose levels uncontrolled

216
Q

How do glitazones work?

A

Activate peroxisome proliferator-activated receptors which bind FFAs and induce genes that enhance insulin action in skeletal muscle, adipose tissue and liver
Increases peripheral glucose uptake and utilisation and reduces hepatic gluconeogenesis
Increases storage of fatty acids in adipocytes, decreasing amount present in circulation
Less risk of hypoglycaemia as does not stimulate pancreas

217
Q

What are the main adverse effects of glitazones?

A

Increased fracture risk, peripheral oedema, anaemia and mild weight gain
Increased risk of bladder cancer
Lower risk of hypoglycaemia than other agents but risk increased in combination
Contraindicated in HF, DMT1 and diabetic ketoacidosis
Used with care in hepatic impairment

218
Q

What are the different types of insulin?

A 
Insulin aspart
Insulin glargine
Biphasic insulin
Soluble insulin
Isophane insulin
219
Q

What is insulin used for?

A

Insulin replacement in people with DMT1 and control of blood glucose in those with DMT2 where oral hypoglycaemic treatment inadequate or poorly tolerated
IV in diabetic emergencies such as diabetic ketoacidosis and hyperglycaemic hyperosmolar state

220
Q

How does insulin work?

A 
Stimulates glucose uptake from circulation into tissue and increases use of glucose as energy source
Stimulates glycogen, lipid and protein synthesis and inhibits gluconeogenesis and ketogenesis
Rapid acting (insulin aspart), short acting (soluble insulin), intermediate acting (isophane insulin) and long acting (insulin glargine)
Biphasic insulin contains mixture of rapid and intermediate acting
221
Q

What are the main adverse effects of insulin treatment

A

Hypoglycaemia which can cause lipohypertrophy if administed by injection in same site
Care in renal impairment as increased risk of hypoglycaemia
Combinations with other hypoglycaemic agents increases risk of hypoglycaemia and use with corticosteroids increases the dose required to have to same effects

222
Q

Name an example of a thyroid replacement hormone

A

Levothyroxine

223
Q

What are thyroid replacement hormones used in?

A

Primary hypothyroidism and hypothyroidism secondary to hypopituitarism

224
Q

How do thyroid replacement hormones work?

A

Regulate metabolism and growth preventing effects of hypothyroidism
Thyroixine (T4) converted to active triiodothyronine T3 in target tissues
Levothyroxine synthetic T4

225
Q

What are the main adverse effects of thyroid replacement hormones?

A

Hyperthyroidism symptoms - GI disturbance, cardiac arrhythmias, neurological tremors
Increased HR and metabolism and precipitate cardiac ischaemia so used with care in CAD
Corticosteroid therapy must be initiated alongside levothyroixineif patient has hypopituitarism to avoid Addisonian crisis
GI absorption reduced
by antacid, Ca2+ and iron
Increased dose required with cytochrome 450 inducers such as carbamazepine
Increase insulin or other hypoglycaemic requirements in diabetes and enhance effects of warfarin

226
Q

Name an example of an antithyroid drug

A

Carbimazole

227
Q

What are antithyroid drugs used in?

A

Graves’ disease as long term treatment

Taken before thyroid surgery to lower hormone levels

228
Q

How do anti-thyroid drugs work?

A

Prevents thyroid peroxidase enzyme from coupling and iodinating the tyrosine residues on thyroglobulin, reduces production of thyroid hormones T3 and 4
Relief of clinical symptoms slow as large store of preformed T3 and 4 must be depleted before and effect seen - can be months

229
Q

What are the main adverse effects of anti-thyroid drugs?

A

Rashes and pruritus common, treated with anti-histamines, more rarely and severely can be bone marrow suppression and resultig neutropenia and agranulocytosis
Care in patients with past or current blood disease or liver impairment
CYP450 enzyme inhibitor so drugs metabolism by this eg warfarin may become toxic if does not lowered

230
Q

Name an example of a growth hormone receptor antagonist

A

Pegvisomant

231
Q

What are growth hormone receptor antagonists used for?

A

Treatment of acromegaly if pituitary tumour cannot be controlled with surgery or irradiation
Administered as a powder solution injection

232
Q

How do growth hormone receptor antagonists work?

A

Block action of growth hormone at the growth hormone receptor to reduce the production of IGF-1

233
Q

What are the main adverse effects of growth hormone receptor antagonists?

A 
Reactions at injection site
GI disturbance
Hypoglycaemia, chest pain, hepatitis
Increased GH levels - reduces feedback
Use with care in diabetics and patient with malignant tumours or liver impairment
234
Q

Name an example of a vasopressin antagonist

A

Tolvaptan

235
Q

What are vasopressin antagonists used for?

A

Treatment of euvolaemic (SIADH) and hypervolaemic hyponatraemia

236
Q

How does vasopressin antagonists work?

A 
Inhibit vasopressin-2 receptor so increases fluid excretion
Causes aquaresis (exretion of H2O with NO electrolyte loss) leading to increases Na+ in hyponatraemia
237
Q

What are the main adverse effects of vasopressin antagonists?

A

GI disturbance, headache, increased thirst, insomina
Hypersensitivity reactions
Contraindicated in hypovolaemic hyponatraemia and severe renal impairment
Can interact with statins and cause serious muscle problems
Side effects increased with macrolides
Can cause enhanced effects of benzodiazepines and digoxin when used together

238
Q

What do statins do?

A

HMG-CoA reductase inhibitors

Enzyme responsible for cholesterol biosynthesis

239
Q

Name 3 examples of statins

A

Atorvastatin
Lovastatin
Simvastatin
Fluvastatin

240
Q

Name an example of a vasopressin analogue

A

Desmopressin

241
Q

What are vasopressin analogues used for?

A

Treatment of cranial diabetes insipidus

Also used to distinguish cranial and nephrohenic diabetes insipidus

242
Q

How do vasopressin analogues work?

A

Replace endogenous vasopressin that is missing in cranial diabetes insipidus
Works on renal collecting duct by binding to V2 receptors, which signal aquaporin 2 to be inserted into the collecting duct apical membrane and thus increase water reabsorption from the usrine

243
Q

What are the main adverse effects of vasopressin analogues?

A

Headaches, facial flushing, nausea, seizures
Hyponatraemia
Contraindicated in moderate to severe renal impairment and patients with hyponatraemia
Use with tricyclic antidepressants, SSRIs, NSAIDs, opioid analgesics should be monitored carefully as may increase risk of water intoxication with hyponatraemia

244
Q

Name an examples of an adrenal corticosteroid inhibitor

A

Metyrapone

245
Q

What are adrenal corticosteroid inhibitors used for?

A

Diagnosis of adrenal insufficiency

Control cortisol hypersecretion in Cushing’s

246
Q

How to adrenal corticosteroid inhibitors work?

A

Metyrapone blocks cortisol synthesis by reversibly inhibiting steroid 11 beta-hydroxide enzymes
Enzyme normally stimulates adrenocorticotrophic hormone secretion and increases plasma 1–deoxycortisol level that is metabolised to cortisol - inhibiting enzyme leads to a reduction in cortisol

247
Q

What are the main adverse effects of adrenal corticosteroid inhibitors?

A

GI disturbance, headache, dizziness and drowsiness
Hirsutism can occur because of excess androgen precursors created
Contraindicated in adrenal cortical insufficiency and patients taking corticosteroids
Use in care in patients on paracetamol as liver damage can be increased, and insulin or other hypoglycaemics as side effects may be increased
Corticosteroid, oestrogen and phenytoin can reduced effectiveness

248
Q

Name 3 examples of synthetic corticosteroids

A

Bethamethasone
Prednisone
Prednisolone
Methyprednisolone

249
Q

What are steroids used for?

A

Decreasing inflammation and reducing activity of immune system
Treat a variety of inflammatory diseases

250
Q

What are the main adverse effects of steroids?

A 
Acne
Easy bruising
High BP
Increased appetite, weight gain
Hirsutism
Insomnia
Osteoporosis
Stomach irritation/bleeding
Restlessness
Lower resistance to infection
Swollen, puffy face
Water retention
Worsening of diabetes

Phase 2a medicine (13 decks)

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