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1. Y5 Zero to finals MEDICINE > Endocrinology - my notes > Flashcards

Endocrinology - my notes Flashcards

1
Q

What does hypothalamus stimulate?

A

Pituitary gland

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2
Q

Anterior pituitary gland hormones release

A
  • Thyroid-stimulating hormone (TSH)* Adrenocorticotropic hormone (ACTH)* Follicle-stimulating hormone (FSH)* luteinising hormone (LH)* Growth hormone (GH)* Prolactin
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3
Q

Posterior pituitary hormones release

A
  • Oxytocin* Antidiuretic hormone (ADH)
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4
Q

Thyroid axis

A

Hypothalamus releases TRHTRH stimulates Anterior pituitary to release TSHTSH stimulates thyroid to release T3 and T4T3 and T4 suppress the release of TRH and TSH by acting on hypothalamus and pituitary

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5
Q

Adrenal axis

A

Hypothalamus releases corticotropin-releasing hormone. CRH stimulates anterior pituitary to release ACTHACTH stimulates adrenals to release cortisol* Cortisol supresses release of CRH and ACTH (in hypothalamus and anterior pituitary)

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6
Q

Which hormone has diurnal variation?

A
  • Cortisol (peaks in the morning, lowest in the evening)
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7
Q

Actions of cortisol

A
  • Increases alertness
  • Inhibits the immune system
  • Inhibits bone formation
  • Raises blood glucose
  • Increases metabolism
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8
Q

Growth hormone axis

A

Hypothalamus produces GHRHGHRH stimulates anterior pituitary to release GHGH stimulates the release of IGF-1 from the liver

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9
Q

Growth hormone actions

A
  • Stimulates muscle growth* Increases bone density and strength* Stimulates cell regeneration and reproduction* Stimulates growth of internal organs
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10
Q

Parathyroid axis

A

PTH is released from four PTH glands (in response to low Ca/ low Mg/ low phosphate)PTH increases serum calcium concentration1) PTH increases activity and numbers of osteoclasts in bone (resorption of Ca from bone into blood)2) PTH stimulates calcium reabsorption in the kidneys 3) PTH stimulates kidneys to convert D3 into calcitriol (Active form of vit D)* If serum Ca is high, PTH is suppressed

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11
Q

Role of Vit D

A

Hormone that promotes calcium absorption from food in the intestine

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12
Q

The renin-angiotensin-aldosterone system

A

Renin is released in the kidneyBlood vessels secrete more Renin in low BP/ less Renin in high BPRenin converts Angiotensinogen (released in liver) into Angiotensin IACE converts Angiotensin I into Angiotensin II (in the lungs)Angiotensin II stimulates the release of Aldosterone (from adrenals)* Aldosterone increases sodium and water reabsorption, increasing BP

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13
Q

Main role of renin-angiotensin-aldosterone

A

Regulate the BP

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14
Q

What is renin?

A

Enzyme released by juxtraglomerular cells in afferent arterioles in kidney

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15
Q

What is aldosterone?

A

Mineralcorticoid steroid hormone, acts on nephrons to:* Increase sodium reabsorption from the distal tubule* Increase potassium secretion from the distal tubule* Increase hydrogen secretion from the collecting ducts

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16
Q

2 groups of corticosteroid hormones

A
  • Glucocorticoids (e.g., cortisol)* Mineralocorticoids (e.g., aldosterone)
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17
Q

Primary glucocorticoid hormone

A

Cortisol, produced by adrenal glands

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18
Q

Cushing’s syndrome

A

Prolonged high levels of glucocorticoids in the body [Cushing disease + Alternative cause: use of exogenous corticosteroids (dexamethasone or prednisolone)]

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19
Q

Cushing’s disease

A

Pituitary adenoma secreting excess ACTH * This stimulates excess cortisol release from adrenals

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20
Q

Features of Cushing’s syndrome

A
  • Round, moon face* Central obesity* Abdominal striae (stretch marks)* Enlarged fat pad on the upper back (buffalo hump)* Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)* hirsutism* Easy bruising and poor skin healing* Hyperpigmentation
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21
Q

Hyperpigmentation in Cushing’s cause

A

High ACTH levels

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22
Q

Metabolic effects of Cushing’s syndrome

A
  • Hypertension* Cardiac hypertrophy* Type 2 diabetes* Dyslipidaemia (raised cholesterol and triglycerides)* Osteoporosis
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23
Q

Causes of Cushing’s syndrome

A
  • Cushing disease (pituitary adenoma releasing ACTH)* Adrenal adenoma (adrenal tumour secreting excess cortisol)* Paraneoplastic syndrome* Exogenous steroids
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24
Q

Paraneoplastic Cushing’s syndrome

A

ACTH is released from a tumour other than pituitary gland (ectopic ACTH)* Eg. small cell lung cancer

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25
Q

Dexamethasone suppression tests

A

Used to diagnose Cushing’s syndrome caused by endogenous problem (not used to look for exogenous steroids cause)

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26
Q

Normal dexamethasone response

A

Supressed cortisol due to negative feedback (dexamethasone negatively acts on hypothalamus, which reduces CRH – this causes negative feedback on pituitary, then reduces ACTH. Low CRH and ACTH result in low cortisol release from adrenals. – lack of cortisol suppression is cushings syndrome.

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27
Q

3 types of dexamethasone suppression test

A
  • Low dose overnight test- Low dose 48h test- High dose 48h test
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28
Q

Low dose overnight test

A

1mg dexa is given at night, cortisol checked in the morning; normal result is cortisol suppression

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29
Q

Low dose 48h test

A

0.5mg dexa is taken every 6h for 8 doses, starting at 9am.Cortisol is checked at 0h and 48h later Normal result: suppressed cortisol (abnormal is cushing syndrome)

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30
Q

High dose 48h test

A

2mg dexa taken every 6h for 8 doses starting at 9am. Cortisol checked at 0h and 48h later High dose supresses cortisol in cushing syndrome by pituitary adenoma (Cushing disease) but NOT in adrenal adenoma or ectopic ACTH

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31
Q

When is ACTH low?

A

When excess cortisol comes from adrenal tumour

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32
Q

When is ACTH high?

A

When it is produced by pituitary tumour or ectopic ACTH (small cell lung cancer)

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33
Q

high dose 48h test – cortisol supressed cause?

A

Cushing disease due to pituitary adenoma

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34
Q

High dose 48h test – cortisol not suppressed cause?

A

Adrenal adenoma or ectopic ACTH

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35
Q

Low dose dexa test/ high dose/ ACTH – normal pt

A

Cortisol low/ cortisol low/ ACTH high

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36
Q

Low dose dexa test/ high dose/ ACTH – adrenal adenoma

A

Not suppressed cortisol/ not suppressed/ low ACTH

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37
Q

Low dose dexa test/ high dose/ ACTH – pituitary adenoma

A

Not suppressed/ low cortisol/ high ACTH

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38
Q

Low dose dexa test/ high dose/ ACTH – ectopic ACTH

A

Not suppressed/ not suppressed/ high ACTH

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39
Q

Treatment in cushing syndrome

A
  • Trans-sphenoidal removal of pituitary adenoma- Surgical removal of adrenal tumour- Surgical removal of ectopic ACTH tumour
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40
Q

Nelson’s syndrome

A

ACTH producing pituitary tumour develops post surgical removal of adrenals and lack of cortisol (lack of negative suppression)

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41
Q

Metyrapone

A

Reduces production of cortisol in the adrenals, might be used in treating Cushing’s

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42
Q

Primary hyperthyroidism

A

Thyroid abnormal – produces excessive thyroid hormones. TSH is suppressed by high T3 and T4 causing a low TSH level.

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43
Q

Secondary hyperthyroidism

A

Pituitary abnormal – produces excessive TSH (pituitary adenoma), stimulating excess production of TSH from thyroid, and hence T3 T4 are raised

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44
Q

Primary hypothyroidism

A

Thyroid abnormal – increased thyroid hormone produced, hence TSH is raised, T3 and T4 are low.

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45
Q

Secondary hypothyroidism

A

Pituitary produces inadequate TSH (eg post surgical removal of pituitary), understimulation of thyroid, hence TSH, T3, T4 all low

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46
Q

Primary hyperthyroidisim tsh, t3/4 levels

A

TSH low, T3/4 high

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47
Q

Secondary hyperthyroidism

A

TSH high, T3/4 high

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48
Q

Primary hypothyroidism

A

TSH high, T3/4 low

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49
Q

Secondary hypothyroidism

A

TSH low, T3/4 low

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50
Q

Anti-thyroid perioxidase antibodies

A

Antibodies against the thyroid gland (most relevant thyroid autoantibody in autoimmune thyroid disease); Graves disease and Hashimoto thyroidits

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51
Q

Anti-thyroglobulin antibodies (anti-Tg)

A

Antibodies against thyroglobulin (protein produced in the thyroid). Might be present in healthy individuals but raised in Grave’s disease, Hashmioto’s thyroiditis, and thyroid cancer

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52
Q

TSH receptor antibodies

A

Autoantibodies that mimic TSH and bind to the TSH receptor – they stimulate thyroid hormone release and cause Grave’s disease.

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53
Q

Radioisotope scans – diffuse high uptake

A

Grave’s disease

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54
Q

Radioisotope scans – focal high uptake

A

Toxic multinodular goitre and adenomas

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55
Q

Radioisotope scans – cold areas, abnormally low uptake

A

Thyroid cancer

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56
Q

Hyperthyroidism

A

Over production of thyroid hormones, T3 and T4

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57
Q

Thyrotoxicosis

A

Abnormal and excessive quantity of thyroid hormones

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58
Q

Primary hyperthyroidism

A

Thyroid pathology, thyroid produces excessive thyroid hormones

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59
Q

Secondary hyperthyroidism

A

Due to pathology in hypothalamus or pituitary when pituitary produces too much TSH, stimulating thyroid to produce excessive thyroid hormone

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60
Q

Subclinical hyperthyroidism

A

Thyroid hormones are normal but TSH is suppressed

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61
Q

Grave’s disease

A

Autoimmune condition of primary hyperthyroidism, as TSH receptor antibodies stimulate TSH receptors to produce thyroid hormones

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62
Q

Toxic multinodular goitre (Plummer’s disease)

A

Nodules develop on thyroid and produce excessive thyroid hormones

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63
Q

Exophthalmos

A

Proptosis – bulging of eyes due to Grave’s (due to presence of TSH receptor antibodies behind eyes, that swell)

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64
Q

Pretibial myxodema

A

Deposits of glycosaminoglycans/mucin under skin, specific to Grave’s disease, due to TSH receptor antibodies

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65
Q

Causes of hyperthyroidism

A
  • G – Graves’ disease* I – Inflammation (thyroiditis)* S – Solitary toxic thyroid nodule* T – Toxic multinodular goitre
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66
Q

Thyroiditis

A

Initial hyperthyroid then hypothyroid

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67
Q

Causes of thyroiditis

A
  • De Quervain’s thyroiditis* Hashimoto’s thyroiditis* Postpartum thyroiditis * Drug-induced thyroiditis
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68
Q

Features of hyperthyroidism

A
  • Anxiety and irritability* Sweating and heat intolerance* Tachycardia* Weight loss* Fatigue* Insomnia* Frequent loose stools* Sexual dysfunction* Brisk reflexes on examination
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69
Q

Grave’s specific features

A

(due to presence of TSH receptor antibodies)* Diffuse goitre (without nodules)* Graves’ eye disease, including exophthalmos* Pretibial myxoedema* Thyroid acropachy (hand swelling and finger clubbing)

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70
Q

Solitary toxic thyroid nodule

A

Benign adenoma; Tx is surgical removal

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71
Q

De Quervain’s Thyroiditis

A
  • Thyrotoxicosis (excess T3/4, thyroid swelling, flu-like ilnness, raised ESR and CRP)* Hypothyroidism* Return to normal
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72
Q

What is a long term rish of De Quervain’s thyroiditis

A

<10% of pts remain hypothyroid

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73
Q

Tx for De Quervain’s Thyroiditis

A
  • NSAIDs for symptoms of pain and inflammation * Beta blockers for the symptoms of hyperthyroidism* Levothyroxine for the symptoms of hypothyroidism
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74
Q

Thyroid storm

A

/thyrotoxic crisis/ Rare representation of hyperthyroidism More severe presentation of hyperthyroidism (fever, tachy, delirium) – might need fluid resuscitation, anti-arrhythmic, and b blockers

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75
Q

Mx of thyroid storm

A

Carbimazole – 1st line, anti-thyroid, taken 12-18monthsPropylthiouracil – 2nd lineRadioactive iodineB blockerssurgery

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76
Q

Maintenance dose of carbimazole

A
  • Titrated to maintain normal thyroid levels- Higher dose of carbimazole to block all production and levothyroxine to replace thyroid hormones
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77
Q

SE of carbimazole

A

Pancreatitis

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78
Q

SE of propylthiouracil

A

Liver reactions and death

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79
Q

SE of anti-thyroid medications

A

(propylthiouracil, carbimazole) – agranulocytosis (v low WBC) – low immunity, presenting with sore throat

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80
Q

Radioactive iodine treatment

A

Drinking a single dose of radioactive iodine, proportion of thyroid cells is destroyed and there is a reduction in thyroid hormone production – remission is 6 months and thyroid is then ofter underactive requiring levothyroxine treatment

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81
Q

Rules of tx with radioactive iodine

A
  • No pregnancy or breastfeeding- No pregnancy within the next 6 months- No fathering within 4 months (men)- Limit contact with people afterward (especially pregnant and children)
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82
Q

B Blockers in thyroid storm

A

Block the adrenalin-related symptoms of hypothyroidism (propranolol)

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83
Q

Surgery in thyroid storm

A

Thyroidectomy; definitive treatment; pt then requires life long levothyroxine

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84
Q

Primary hypothyroidism

A

Thyroid produces inadequate t3 and t4 (thyroid hormones); low t3/4 cause no negative feedback so TSH raises.

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85
Q

Secondary hypothyroidism

A

Pituitary gland produces too little TSH which causes understimulation of t3/4 production. All 3 are low.

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86
Q

Most common cause for hypothyroidism

A

Hashimoto’s thyroiditis

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87
Q

Hashimoto’s thyroiditis

A

Autoimmune condition causing inflammation of the thyroid.

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88
Q

What antibodies are present in Hashimoto?

A

Anti TPO, anti Tg

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89
Q

Hyperthyroidism treatment

A
  • Carbimazole- Prophylthiouracil- Radioactive iodine- Thyroid surgery
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90
Q

Lithium and thyroid

A

Lithium inhibits the production of thyroid hormone; causing goitre and hypothyroidism

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91
Q

Amiodarone and thyroid

A

Causes hypothyroidism and thyrotoxicosis

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92
Q

Secondary hypothyroidism causes

A

Tumours (pituitary adenoma)Surgery to pituitarySheehan’s syndromeTraumaradiotherapy

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93
Q

Symptoms of hypothyroidism

A
  • Weight gain- Fatigue- Dry skin- Hair loss- Fluid retention - Heavy or irregular periods- Constipation
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94
Q

What causes goitre?

A

Iodine deficiency

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95
Q

Hashimoto thyroiditis and thyroid structure

A

Initially causes a goitre, then atrophy of thyroid

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96
Q

Mx of hypothyroidism

A

Oral levothyroxine (synthetic t4), titrated every 4 weeks

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97
Q

Alternative drug to levothyroxine

A

Liothyronine sodium (synthetic t3) when levothyroxine is not tolerated.

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98
Q

T1D

A

Pancreas is unable to produce adequate insulin (hence body cells can’t absorb glucose) -> hyperglycaemia

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99
Q

What viruses may trigger T1D

A

Coxsackie B Enterovirus

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100
Q

Hyperglycaemia symptoms

A
  • Polyuria (excessive urine)* Polydipsia (excessive thirst)* Weight loss (mainly through dehydration)Or diabetic ketoacidosis
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101
Q

Where are carbohydrates absorbed?

A

Small intestine

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102
Q

Ideal blood glucose concentration

A

4.4-6.1 mmol/L

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103
Q

Where is insulin produced?

A

Beta cells in Islets of Langerhans in pancreas

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104
Q

What kind of hormone is insulin?

A

Anabolic hormone (building hormone)

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105
Q

Actions of insulin

A

Reduces blood sugar:- Absorbs glucose into the cells- Causes muscle and liver to absorb glucose and store it as glycogen (glycogenesis)

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106
Q

Where is glucagon produced

A

By alpha cells in the Islets of Langerhans in the pancreas

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107
Q

Actions of glucagon

A

Responds to low blood sugar levels and stress and works to increase blood sugar levels – by acting on liver to break down the stored glycogen into glucose (glycogenolysis)- Also acts of liver to convert protein and fat into glucose (gluconeogenesis)

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108
Q

Ketogenesis

A

Production of ketones in event on insufficient glucose and exhausted glycogen stores (in fasting)- Liver takes fatty acids and converts them to ketones

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109
Q

Ketones

A

Water soluble fatty acids, they can cross blood prain barrier

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110
Q

Ketosis symptom

A

Acetone smell to breath

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111
Q

Pathophysiology of DKA

A

Consequence of inadequate insulin - T1D not adhering to insulin regime- T1D unwell with infection- Pt presenting with T1D for the first time

112
Q

Key features of DKA

A
  • Ketoacidosis* Dehydration * Potassium imbalance
113
Q

Ketoacidosis process

A

Liver produces ketone in low insulin state; levels of glucose and ketones increase and kidneys produce bicarbonate to counteract ketone acids. Over time blood becomes acidic (ketoacidosis)

114
Q

Dehydration in DKA

A

Glucose leaks into urine, then glucose in the urine draws more water by osmotic diuresis – this causes polyuria and severe dehydration +there is polydipsia.

115
Q

Potassium imbalance in DKA

A

Insulin drives potassium into cells – in DKA serum potassium may be high, bu total body potassium is low because no potassium is stored in cells – once insulin treatment starts, pts develop hypokalemia and arrythmia

116
Q

Presentation of DKA

A
  • Hyperglycaemia* Dehydration* Ketosis* Metabolic acidosis (with a low bicarbonate)* Potassium imbalance* Polyuria* Polydipsia* Nausea and vomiting* Acetone smell to their breath* Dehydration * Weight loss* Hypotension (low blood pressure)* Altered consciousness
117
Q

Diagnosing DKA

A
  • Hyperglycaemia (e.g., blood glucose above 11 mmol/L)* Ketosis (e.g., blood ketones above 3 mmol/L)* Acidosis (e.g., pH below 7.3)
118
Q

Mx of DKA

A
  • F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)* I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)* G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L* P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)* I – Infection – treat underlying triggers such as infection* C – Chart fluid balance* K – Ketones – monitor blood ketones, pH and bicarbonate
119
Q

Before stopping insulin and fluid in DKA

A
  • Ketosis and acidosis should have resolved* They should be eating and drinking* They should have started their regular subcutaneous insulin
120
Q

What is max rate of potassium infusion in normal circumstances?

A

10 mmol/h (risk of arrhythmia and cardiac arrest)

121
Q

What are the key complications in DKA treatment?

A
  • Hypoglycaemia (low blood sugar)* Hypokalaemia (low potassium)* Cerebral oedema, particularly in children* Pulmonary oedema secondary to fluid overload or acute respiratory distress syndrome
122
Q

How is insulin given in DKA?

A

Up to 20 mmol/h with central line

123
Q

Serum C peptide

A

Measure of insulin production

124
Q

Low serum C peptide

A

Low insulin production

125
Q

High serum C peptide

A

High insulin production

126
Q

Autoantibodies in T1D

A
  • Anti-islet cell antibodies * Anti-GAD antibodies* Anti-insulin antibodies
127
Q

Long term management

A
  • Subcutaneous insulin* Monitoring dietary carbohydrate intake* Monitoring blood sugar levels upon waking, at each meal and before bed
128
Q

Basal-bolus regime

A
  • Background, long-acting insulin injected once a day * Short-acting insulin injected 30 minutes before consuming carbohydrates (e.g., at meals)
129
Q

Lipodystrophy

A

Subcut fat hardens due to injections and can’t absorb insulin (must circulate injection sites)

130
Q

Insulin pump

A

Device that continuously infuses insulin (canula and site are rotated every 2-3 days)

131
Q

Advantage of insulin pump

A

Good at sugar control and more flexibility with eating and less injections

132
Q

Disadvantage of insulin pump

A
  • Difficulties learning to use the pump* Having it attached at all times* Blockages in the infusion set* A small risk of infection
133
Q

Tethered pumps

A

Devices with replaceable infusion sets and insulin

134
Q

Patch pumps

A

Sit directly on the skin without visible tubes, - when finished, entire pump is disposed and new one attached.

135
Q

Pancreas transplant

A

Implanting donor pancreas to produce insulin, original pancreas left in place to produce digestive enzymes

136
Q

Islet transplantation

A

Inserting donor islets into pt’s liver. Islet cells produce insulin; pt often still needs insulin therapy.

137
Q

Flash glucose monitor

A

FreeStyle Libre 2 – senson on the skin to measure glucose levels in the interstitial fluid in the subcut tissue. Pt swipes mobile phone over the sensor to collect reading. Sensors need replacing every 2 weeks.

138
Q

What is the issue with Flash glucose monitor

A

There is a 5 min delay which means capillary blood glucose is required if hypoglycaemia is suspected.

139
Q

Continuous glucose monitors

A

Similar to flash glucose, sensor on the skin monitors sugar levels, sends reading over bluetooth, no need to scan the sensor

140
Q

Closed-loop system

A

Called artificial pancreas. Combination of continuous glucose monitor and insulin pump. The system automatically adjusts itself.

141
Q

Short term complications of T1D

A
  • Hypoglycaemia* Hyperglycaemia (and diabetic ketoacidosis)
142
Q

Tx of hypoglycaemia

A

Rapid acting glucose (high sugar drink), then slower-acting carbohydrates to prevent sugar dropping. In severe cases: IV dextrose or IM glucagon.

143
Q

Long term complications of T1D

A

Chronic damage to endothelial cells of blood vessels, vessels are leaky and unable to regenerate. High glucose levels also cause immune dysfunction.

144
Q

Macrovascular complications of T1D

A
  • Coronary artery disease is a significant cause of death in diabetics* Peripheral ischaemia causes poor skin healing and diabetic foot ulcers* Stroke* Hypertension
145
Q

Microvascular complications of T1D

A
  • Peripheral neuropathy* Retinopathy* Kidney disease, particularly glomerulosclerosis
146
Q

Infection-related complications of T1D

A
  • Urinary tract infections* Pneumonia* Skin and soft tissue infections, particularly in the feet* Fungal infections, particularly oral and vaginal candidiasis
147
Q

T2D

A

Insulin resistance and reduced insulin production (+pancreas is fatigued over time)

148
Q

Complications of chronic hyperglycaemia

A
  • Microvascular- Macrovascular- Infectious complications
149
Q

Non modifiable risk factors for T2D

A
  • Older age* Ethnicity (Black African or Caribbean and South Asian)* Family history
150
Q

Modifiable risk factors for T2D

A
  • Obesity* Sedentary lifestyle* High carbohydrate (particularly sugar) diet
151
Q

Presenting features of T2D

A
  • Tiredness* Polyuria and polydipsia* Unintentional weight loss* Opportunistic infections (e.g., oral thrush)* Slow wound healing* Glucose in urine (on a dipstick)
152
Q

Acanthosis nigricans

A

Thickening and darkening of the skin (neck, axilla, groin), velvety appearance; present in insulin resistance

153
Q

Pre diabetes HbA1c

A

42-47 mmol/mol

154
Q

Type 2 diabetes HbA1c

A

> 48 mmol/mol (sample retaken 1 month later to confirm diagnosis)

155
Q

HbA1c targets in diabetics

A
  • 48 mmol/mol for new T2D* 53 mmol/mol for pts on >1 antidiabetic medication
156
Q

How often is HbA1c measured in a newly diagnosed pt

A

Every 3 to 6 months

157
Q

1st line Tx for T2D

A

Metformin

158
Q

Which pts need additional SGLT-2 inhibitor (dapagliflozin) after metformin?

A
  • If they have CVD or heart failure - QRISK >10%
159
Q

2nd line Tx for T2D

A

Sulfonylurea, pioglitazone, DPP4 inhibitor, SGLT2 inhibitor

160
Q

3rd line Tx for T2D

A

Either:- Metformin + 2nd line- Insulin

161
Q

When is GLP-1 mimetic (liraglutide) used?

A

When Triple therapy fails and BMI >35

162
Q

Metformin MOA

A

(biguanide)Increases insulin sensitivity Decreases glucose production by the liver No weight gain, No hypoglycaemia

163
Q

SE of metformin

A

GI symptoms (nausea and diarrhoea)Lactic acidosis 2ndary to AKI

164
Q

SE on standard release metformin

A

Try modified release metformin

165
Q

SGLT-2 inhibitors

A

-GLIFLOZIN (empagliflozin, canagliflozin, dapagliflozin, ertugliflozin)Blocks sodium glucose co transporter 2 protein in the proximal tubules so glucose is not reabsorbed from the urine and is excreted. - Improve heart failure, cause weight loss, reduces BP, lowers HbA1c

166
Q

Alternative action of SGLT-2 inhibitors

A

Reduces risk of CVD

167
Q

SGLT-2 inhibitors licenced for heart failure

A

Empagliflozin and dapagliflozin

168
Q

SGLT-2 inhibitors licensed for CKD

A

Dapagliflozin

169
Q

SE of SGLT-2 inhibitors

A
  • Glycosuria * Increased urine output and frequency* Genital and urinary tract infections (e.g., thrush)* Weight loss* Diabetic ketoacidosis, * Lower-limb amputation may be more common in patients on canagliflozin (unclear if this applies to the others)* Fournier’s gangrene (rare but severe infection of the genitals or perineum)
170
Q

Pioglitazone

A

thiazolidinedione. increases insulin sensitivity and decreases liver production of glucose. does not cause hypoglycaemia.

171
Q

Pioglitazone SE

A
  • Weight gain* Heart failure* Increased risk of bone fractures* A small increase in the risk of bladder cancer
172
Q

Sulfonylureas

A

Gliclazide Stimulates insulin release from the pancreas

173
Q

SE of sulfonylureas

A
  • Weight gain- Hypoglycaemia
174
Q

Glucagon like peptide 1

A

Glucagon like peptide 1

175
Q

What inhibits incretins?

A

Enzymes called dipeptidyl peptidase-4 DPP4

176
Q

Incretins

A

Hormones produced in the GI* Increasing insulin secretion* Inhibiting glucagon production* Slowing absorption by the gastrointestinal tract

177
Q

DPP4 inhibitors

A

Sitagliptin and alogliptin

178
Q

SE of DPP4 inhibitors

A

HeadacheAcute pancreatitis

179
Q

GLP 1 mimetics

A

Imitate GLP 1; exenatide, liraglutide

180
Q

SE of GLP 1 mimetics

A
  • Reduced appetite* Weight loss* Gastrointestinal symptoms, including discomfort, nausea and diarrhoea
181
Q

Rapid acting insulin

A

NovoRapid; start working after 10 min; last 4h

182
Q

Short acting insuling

A

Actrapid; start working in 30 mins and last 8h

183
Q

Intermediate acting insulins

A

Humulin I – start working in 1h and last 16h

184
Q

Long acting insulin

A

Levemir, Lantus – start working 1h and last 24h

185
Q

Combinations insulin

A

Contain rapid and intermediate acting (ratio of rapid to intermediate)* Humalog 25 (25:75)* Humalog 50 (50:50)* Novomix 30 (30:70)

186
Q

Complications of T2D

A
  • Infections (e.g., periodontitis, thrush and infected ulcers)* Diabetic retinopathy* Peripheral neuropathy* Autonomic neuropathy* Chronic kidney disease* Diabetic foot* Gastroparesis (slow emptying of the stomach)* Hyperosmolar hyperglycemic state
187
Q

T2D 1st line HTN tx

A

Ace inhibitor

188
Q

T2D with CKD and ACR >3mg/mmol

A

Start ACE inhibitor

189
Q

T2D with CKD and ACR >30mg/mmol

A

Start SGLT2 inhibitor on top off ACEi

190
Q

Erectile dysfunction in T2D

A

Give Phosphodiesterase 5 inhibitors (e.g., sildenafil or tadalafil)

191
Q

Gastroparesis in T2D tx

A

Prokinetic drugs (e.g., domperidone or metoclopramide)

192
Q

Tx For diabetic neuropathy (neuropathic pain)

A
  • Amitriptyline – a tricyclic antidepressant* Duloxetine – an SNRI antidepressant* Gabapentin – an anticonvulsant* Pregabalin – an anticonvulsant
193
Q

Hyperosmolar Hyperglycaemic State

A

Hyperosmolality (water loss), hyperglycaemia, and absence of ketones

194
Q

Tx of HSS

A

IV fluids

195
Q

Acromegaly

A

Excessive Growth hormone

196
Q

Where is Growth hormone produced?

A

By anterior pituitary

197
Q

Most common cause of growth hormone upregulation?

A

Pituitary adenoma (microscopic or macroscopic), lung or pancreatic cancer which secretes growth hormone releasing hormone or growth hormone

198
Q

Pituitary tumour pressing on optic chiasm

A

Bitemporal hemianopia

199
Q

Presentation of pituitary tumour

A

Space-occupying:* Headaches* Visual field defect (bitemporal hemianopia)

200
Q

How to diagnose acromegaly?

A

Test insulin-like growth-factor 1 (IGF1) – raised, means raised GH

201
Q

Additional features of excess growth hormone/acromegaly

A
  • Hypertrophic heart* Hypertension* Type 2 diabetes* Carpal tunnel syndrome* Arthritis* Colorectal cancer
202
Q

Excess growth hormone body features:

A
  • Prominent forehead and brow (frontal bossing)* Coarse, sweaty skin* Large nose* Large tongue (macroglossia)* Large hands and feet* Large protruding jaw (prognathism)
203
Q

How to diagnose pituitary adenoma?

A

MRI of the pituitary

204
Q

GH suppression test

A

Consume 75g glucose drink, GH tested at baseline and at 2h – the glucose should suppress the growth hormone – failure to suppress means Acromegaly

205
Q

Tx of pituitary tumour

A

Trans-sphenoidal surgery (through nose and sphenoid bone) to remove the tumour +- radiotherapy

206
Q

Why is testing GH unreliable?

A

Fluctuates throughout the day

207
Q

Somatostatin

A

Growth hormone-inhibiting hormone

208
Q

Medical options for reducing growth hormone

A
  • Pegvisomant is a growth hormone receptor antagonist given daily by a subcutaneous injection* Somatostatin analogues (e.g., octreotide) block growth hormone release* Dopamine agonists (e.g., bromocriptine) block growth hormone release
209
Q

Where is parathyroid hormone produced?

A

In chief cells in the parathyroid glands (in 4 corners of the thyroid), - produced in response to hypocalcaemia

210
Q

Dopamine

A

Where is parathyroid hormone produces?

211
Q

3 ways of PTH raising the blood calcium

A
  • Increasing osteoclast activity in bones (reabsorbing calcium from bones)* Increasing calcium reabsorption in the kidneys (less calcium is lost in urine)* Increasing vitamin D activity, resulting in increased calcium absorption in the intestines
212
Q

PTH and vit D

A

PTH acts on vit D to convert it to active form and absorb more calcium from the intestines

213
Q

Symptoms of hypercalcemia mnemonic

A

Stones, bones, groans, moans* Kidney stones* Painful bones* Abdominal groans (constipation, nausea and vomiting)* Psychiatric moans (fatigue, depression and psychosis)

214
Q

Primary hyperparathyroidism

A

Uncontrolled PTH production by parathyroid tumour – leads to increase in blood calcium

215
Q

Conn’s syndrome

A

Adrenal adenoma producing too much aldosterone

216
Q

Tertiary hyperparathyroidism

A

Occurs as a result of 2nd hyperparathyroidism – hyperplasia of the gland – when initial problem is corrected but still v high PTH produced – high PTH and hypercalcaemia

217
Q

High PTH and low/normal Ca

A

Secondary hyperparathyroidism

218
Q

High PTH and high Calcium

A

Primary hyperparathyroidism

219
Q

Key presenting feature of hyperaldosteronism

A

Hypertension

220
Q

Secondary hyperparathyroidism

A

Insufficient vit D or CKD reduce calcium absorption and cause hypocalcaemia. -> Hence more PTH is released. High PTH and low/normal serum Ca

221
Q

Where is renin released?

A

Juxtraglomerular cells in the afferent arterioles of the kidney

222
Q

What does ACE do ?

A

Converts angiotensin I to angiotensin II

223
Q

What is the role of Angiotensin II

A

Stimulates release of aldosterone from adrenal glands

224
Q

What is the role of juxtraglomerular cells?

A

Sense the blood pressure and release renin in response (low bp, more renin released; high bp , moless renin released)

225
Q

What does renin do?

A

Converts angiotensinogen (released by liver) to angiotensin I

226
Q

High PTH and high Ca

A

Tertiary hyperparathyroidism

227
Q

Causes of primary hyperaldosteronism

A
  • Bilateral adrenal hyperplasia (most common) * An adrenal adenoma secreting aldosterone (known as Conn’s syndrome)* Familial hyperaldosteronism (rare)
228
Q

Actions of aldosterone

A
  • Increase sodium reabsorption from the distal tubule* Increase potassium secretion from the distal tubule* Increase hydrogen secretion from the collecting ducts
229
Q

Secondary hyperaldosteronism

A

Due to excessive renin stimulating excessive aldosterone release

230
Q

How is renal artery stenosis confirmed?

A
  • Doppler ultrasound* CT angiogram* Magnetic resonance angiography (MRA)
231
Q

Primary hyperaldosteronism

A

Adrenal glands produce too much aldosterone

232
Q

Primary hyperaldosteronism blood test

A

High aldosterone and low renin

233
Q

What causes excessive renin?

A

Dispropitionaly lower pressure in the kidneys due to:* Renal artery stenosis* Heart failure* Liver cirrhosis and ascites

234
Q

How to check for primary/secondary hyperaldosteronism?

A

Aldosterone-to-renin ratio

235
Q

Ix on the effect of hyperaldosteronism

A
  • Raised blood pressure (hypertension)* Low potassium (hypokalaemia)* Blood gas analysis (alkalosis)
236
Q

Secondary hyperaldosteronism blood test

A

High aldosterone and high renin

237
Q

Ix for underlying cause of hyperaldosteronism

A
  • CT or MRI to look for an adrenal tumour or adrenal hyperplasia* Renal artery imaging for renal artery stenosis (Doppler, CT angiogram or MR angiography)* Adrenal vein sampling of blood from both adrenal veins to locate which gland is producing more aldosterone
238
Q

Mx of hyperaldosteronism

A
  • Eplerenone * Spironolactone
239
Q

Treating the underlying cause of hyperaldosteronism

A
  • Surgical removal of the adrenal adenoma * Percutaneous renal artery angioplasty via the femoral artery to treat renal artery stenosis
240
Q

Where is ADH secreted?

A

Posterior pituitary gland

241
Q

SIADH

A

Increased release of antidiuretic hormone from the posterior pituitary – it increases water reabsorption from urine, diluting blood and leading to hyponatremia

242
Q

Where does ADH work?

A

Collecting ducts in the kidneys

243
Q

Presentation of SIADH

A

Low sodium* Headache* Fatigue* Muscle aches and cramps* Confusion

244
Q

Where is ADH produced

A

Hypothalamus

245
Q

2 sources of too much ADH

A
  • Increased secretion by the posterior pituitary * Ectopic ADH, most commonly by small cell lung cancer
246
Q

What does SIADH result in?

A

Euvolaemic hyponatraemiaMore concentrated urine – high urine osmolality and high urine sodium

247
Q

How is diagnosis of SIADH made?

A

On clinical features:* Euvolaemia* Hyponatraemia* Low serum osmolality* High urine sodium* High urine osmolality

248
Q

Primary polydipsia

A

Excessive water consumption but low urine sodium and low urine osmolality

249
Q

Mx of SIADH

A
  • Admission if symptomatic or severe (e.g., sodium under 125 mmol/L)* Treating the underlying cause (e.g., stopping causative medications or treating the infection)* Fluid restriction* Vasopressin receptor antagonists (e.g., tolvaptan)
250
Q

Severe hyponatremia presentation

A

seizures and reduced consciousness.

251
Q

Why does Na need to be corrected slowly?

A

To prevent osmotic demyelination (Na concentration should not change more than 10 mmol/L in 24h)

252
Q

Causes of SIADH

A
  • Post-operative after major surgery* Lung infection, particularly atypical pneumonia and lung abscesses* Brain pathologies, such as a head injury, stroke, intracranial haemorrhage or meningitis* Medications (e.g., SSRIs and carbamazepine)* Malignancy, particularly small cell lung cancer* Human immunodeficiency virus (HIV)
253
Q

What is the fluid restriction in SIADH

A

Limiting fluid intake to 750-1000 ml

254
Q

Osmotic demyelination syndrome symptoms

A

1st phase: electrolyte imbalance, encelopathy, confusion, headache, vomiting, seizures2nd phase: demyelination, spastic quadriparesis, pseudobulbar palsy, cognitive and behavioural changes

255
Q

Osmotic demyelination syndrome

A

Central pontine myelinolysis – due to long term severe hyponatremia <120mmol/L treated too quickly

256
Q

2 causes of diabetes insipidus

A
  • A lack of antidiuretic hormone (cranial diabetes insipidus)* A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)
257
Q

What is diabetes insipidus

A

Kidneys are unable to reabsorb water and concentrate urine causing:* Polyuria (excessive amounts of urine) * Polydipsia (excessive thirst)

258
Q

Nephrogenic diabetes insipidus

A

Kidneys (collecting duct) does not respond to ADH

259
Q

Causes for nephrogenic diabetes insipidus

A
  • Medications, particularly lithium (used in bipolar affective disorder)* Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)* Hypercalcaemia (high calcium)* Hypokalaemia (low potassium)* Kidney diseases (e.g., polycystic kidney disease)
260
Q

Cranial diabetes insipidus

A

Hypothalamus does not produce ADH for the pituitary gland to secrete

261
Q

Causes of cranial diabetes insipidus

A
  • Brain tumours* Brain injury* Brain surgery* Brain infections (e.g., meningitis or encephalitis)* Genetic mutations in the ADH gene (autosomal dominant inheritance)* Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
262
Q

Presenting features of diabetes insipidus

A
  • Polyuria (producing more than 3 litres of urine per day)* Polydipsia (excessive thirst)* Dehydration* Postural hypotension
263
Q

Ix in diabetes insipidus

A
  • Low urine osmolality (lots of water diluting the urine)* High/normal serum osmolality (water loss may be balanced by increased intake) * More than 3 litres on a 24-hour urine collection
264
Q

Describe water deprivation test

A

Pt avoids all fluid for 8h; then urine osmolality is measured; if low then ADH/desmopressin is given and urine osmolality measured again after 4h

265
Q

How to diagnose diabetes insipidus?

A

Water deprivation test / (desmopressin stimulation test)

266
Q

Primary polydipsia water deprivation test

A

Urine osmolality:High after water deprivation; no desmopressin required

267
Q

Cranial DI water deprivation test

A

Urine osmolality:Low after water deprivation, high after desmopressin

268
Q

Mx of nephrogenic DI

A
  • Ensuring access to plenty of water* High-dose desmopressin* Thiazide diuretics* NSAIDs
269
Q

Phaeochromocytoma

A

Tumour of the adrenal glands that secretes unregulated amounts of catecholamines (Adrenaline) – tumour of chromaffin cells

270
Q

Nephrogenic DI water deprivation test

A

Urine osmolality:Low after water deprivation, low after desmopressin

271
Q

Dx of phaeochromocytoma

A
  • Plasma free metanephrines (have a longer half live than adrenaline)* 24-hour urine catecholamines* Ct or MRI to look at the tumour* Genetic testing
272
Q

Mx of cranial DI

A

Desmopressin

273
Q

What kind of hormone is adrenaline?

A

Catecholamine (stimulates sympathetic nervous system)

274
Q

Where is adrenaline produced?

A

Chromaffin cells in the medulla (middle part) of the adrenal gland

275
Q

Symptoms of phaeochromocytoma

A
  • Anxiety* Sweating* Headache* Tremor* Palpitations* Hypertension* TachycardiaSymptoms come in bursts when adrenaline is released
276
Q

Mx of phaeochromocytoma

A
  • Alpha blockers (e.g., phenoxybenzamine or doxazosin)* Beta blockers, only when established on alpha blockers* Surgical removal of the tumour
277
Q

Which genetic conditions are related to phaeochromocytoma

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

1. Y5 Zero to finals MEDICINE (13 decks)

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