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FINALS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are features of Kallman syndrome?

A
  • Delayed pubtery
  • Hypogonadism
  • Loss of smell
  • Low sex hormones
  • Normal/above average height
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2
Q

How is Kallman syndrome managed?

A
  • Testosterone supplementation
  • Sex hormones supplementation for fertility
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3
Q

What is vitamin D deficiency associated with?

A

Hypocalcaemia

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4
Q

Patients with high calcium, low PTH with cancer risk factors?

A

Think malignancy

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5
Q

What hormones does anterior pituitary produce?

A

ACTH, TSH, LH, FSH, PRL. GH, MSH

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6
Q

What hormones does posterior pituitary produce?

A

ADH and oxytocin

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7
Q

What is the management of hypoglycaemia with impaired GCS?

A

IV Glucose if access

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8
Q

What characterises tertiary hyperparathyroidism?

A
  • extremely high PTH
  • moderately raised calcium
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9
Q

What is the management of new onset graves disease to control symptoms?

A
  • Propranolol
  • Carbimazole used to induce remission
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10
Q

Any change in vision for someone with thyroid eye disease needs what?

A

Urgent review by specialist

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11
Q

What is the target HBa1c for those on hypoglycaemic medications for T2DM?

A

53

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12
Q

What conditions make up MEN Type 2?

A

Medullary thyroid cancer, hypercalcaemia - parathyroid hyperplasia, phaeochromocytoma

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13
Q

What is the mode of action of orlistat?

A

inhibiting gastric and pancreatic lipase to reduce the digestion of fat

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14
Q

What should patients on long-term steroids do during intercurrent illness?

A

Double steroid doses

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15
Q

What adjunct can be used alongside orlistat for obese patients with one weight related co-mobidity?

A

Liraglutide

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16
Q

Subclinical hyperthyroidism is associated with what?

A

atrial fibrillation, osteoporosis and possibly dementia

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17
Q

What should be monitored to detect recurrence of medullary thyroid cancer?

A

Serum calcitonin

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18
Q

What is definitive management of primary hyperparathyroidism?

A

Total parathyroidectomy

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19
Q

What is primary hyperparathyroidism?

A

XS secretions of PTH resulting in hypercalcaemia.

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20
Q

When is primary hyperparathyroidism typically diagnosed?

A

Incidental finding of elevated serum Ca.

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21
Q

Causes of primary hyperparathyroidism?

A

85% parathyroid adenoma. Others: hyperplasia, multiple adenoma, carcinoma.

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22
Q

Primary hyperparathyroidism CP

A
  • 80% asymptomatic
  • ‘bones, stones, abdominal groans and psychic moans’
  • polydipsia, polyuria, depression, anorexia, nausea, constip, peptic ulcer, pacreatitis, bone pain/fracture, renal stones, HTN
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23
Q

Primary hyperparathyroidism associations

A

HTN, multiple endocrine neoplasia (MEN I and II)

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24
Q

Primary hyperparathyroidism Ix

A
  • Bloods
  • Technetium-MIBI subtraction scan
  • X-ray: pepperpot skull; osteoitis fibrosa cystica
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25
Q

Primary hyperparathyroidism bloods

A

Raised Ca, low phosphate,
PTH raised or normal (inappropriately given the raised calcium)

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26
Q

Primary hyperparathyroidism- when would conservative management be offered?

A

If the Ca is <0.25mmol/L above the limit of normal AND the pt is >50yrs AND there is no evidence of end organ damage

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27
Q

Primary hyperparathyroidism- what if the pt isn’t suitable for surgery?

A

May be treated with cinacalcet (a calcimimetirc that mimics the action of calcium on tissues by allosteric activation of calcium-sensing receptor)

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28
Q

What is primary hypoparathyroidism?

A

Decrease PTH surgery eg. secondary to thyroid surgery

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29
Q

Primary hypoparathyroidism Mx

A

Alfacalcidol

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30
Q

Calcium and phosphate in primary hypoparathyroidism?

A

Low calcium, high phosphate

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31
Q

Main symptoms of hypoparathyroidism are secondary to what?

A

Hypocalcaemia (so CP is same as hypocalcaemia)

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32
Q

Pseudohypoparathyroidism?

A

Target cells being insensitive to PTH; due to abnormality in G protein; associated with low IQ, short stature, shortened 4th and 5th metacarpals.

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33
Q

Pseudohypoparathyroidism electrolyte levels?

A

Low calcium, high phosphate, high PTH

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34
Q

Pseudohypoparathyroidism diagnosis?

A

Infusion of PTH then measure urinary cAMP and phosphate levels. In hypoparathyroidism it’ll increase. In psuedohypoparathyroidism type I they won’t increase but in type II only cAMP rises.

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35
Q

Pseudopseudohypoparathyroidism?

A

Similar phenotype to pseudohypoparathyroidism but normal biochemistry

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36
Q

Confusion, hypothermia, hyporeflexia, bradycardia, seizures and signs of hypothyroidism?

A

Myoxedema coma

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37
Q

Patients with type I diabetes and a BMI > 25 should be considered for what?

A

Metformin alongside insulin

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38
Q

Asymptomatic patients with abnormal HbA1c/fasting glucose need what?

A

Second abnormal reading

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39
Q

hypothyroidism + goitre + anti-TPO triad suggests what?

A

Hashimotos thyroiditis

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40
Q

Thyrotoxicosis with tender goitre and raised ESR?

A

Subacute thyroiditis (De Quervains)

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41
Q

What are sick day rules for T1DM?

A
  • Insulin should not be stopped
  • Increased frequency of checking blood sugars
  • Drink atleast 3L fluids
  • Replace meals with carbohydrate drinks if appetite is reduced
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42
Q

What are sick day rules for T2DM?

A
  • Stop oral hypoglycaemics and restart once eating and drinking is back to normal for 24-24 hours
  • Do not stop insulin if using
  • Monitor blood glucose more frequently as needed
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43
Q

Which drugs can cause galactorrhoea?

A
  • Metoclopramide, domperidone
  • Haloperidol
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44
Q

Who should diabetic foot problems be referred to?

A

Local diabetic foot centre

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45
Q

What does a patchy uptake on nuclear scintigraphy suggest?

A

Toxic multinodular goitre

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46
Q

Long term steroid use can lead to what?

A

Avascular necrosis

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47
Q

Steroids can cause what in the muscles?

A

Proximal myopathy

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48
Q

Which hormones are decreased in response to stress?

A
  • Insulin
  • Testosterone
  • Oestrogen
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49
Q

What are the features of sick euthyroid syndrome?

A

Low T3/T4 with normal TSH during acute illness

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50
Q

What imaging should be done for those with suspected Cushings syndrome?

A

CT adrenal glands

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51
Q

Cushing’ syndrome?

A

Prolonged high levels of glucocorticoids in body (CORTISOL).

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52
Q

Cushing’s disease?

A

Cause of cushing’s syndrome. When a pituitary adenoma secreting XS ACTH stimulates XS cortisol release from adrenal glands.

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53
Q

Causes of Cushing’s syndrome?

A
  • ACTH independent causes= Iatrogenic (corticosteroid therapy), adrenal adenoma (adrenal tumour secreting XS cortisol)
    -ACTH dependent causes= pituitary adenoma secreting XS ACTH (CUSHING’s DISEASE), paraneoplastic syndrome (eg. small cell lung ca secreting ACTH)
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54
Q

Cushing’s syndrome CP?

A

Round puffy face (moon face), central obesity, abdo striae, proximal muscle wasting, hirsutism, hyperpigmentation of skin if Cushing’s disease (high ACTH levels), depression, insomnia

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55
Q

Metabolic effects of Cushing’s syndrome?

A
  • hypokalaemic metabolic alkalosis
  • impaired glucose tolerance
  • HTN, DMT2, cardiac hypertrophy, osteoporosis, dyslipidaemia (raised cholesterol and triglycerides)
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56
Q

Body’s normal response to dexamethasone?

A

Suppressed cortisol due to -ve feedback on hypothalamus. Reduces corticotropin releasing hormone (CRH) output. The lower CRH and ACTH levels result in low cortisol output by adrenal glands.

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57
Q

What is the response to dexamethasone in somebody with Cushing’s syndrome?

A

Lack of cortisol suppression

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58
Q

Why does a high level of ACTH cause skin pigmentation?

A

Stimulates melanocytes in skin to produce melanin.
Pigmentation= Cushing’s disease or ectopic ACTH.
No pigmentation= adrenal adenoma or exogenous steroids.

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59
Q

Cushing’s syndrome Ix?

A

1) low-dose overnight dexamethasone supression test= if cortisol not supressed then…
- high-dose 48hr test= if cortisol suppressed (ACTH high) then Cushing’s disease (pituitary adenoma), if not suppressed then adrenal adenoma (ACTH low) or ectopic ACTH (ACTH high).

2) Also do 24hr urinary free cortisol
3) CT adrenals if not suppressed and ACTH low
4) U&Es may show low K+ if adrenal adenoma also secreting aldosterone

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60
Q

Cushing’s syndrome Mx?

A
  • Transphenoidal resection of pituitary adenoma
  • Surgical resection of adrenal adenoma/ectopic ACTH source
  • If not possible= adrenalectomy + life long steroid replacement therapy
  • occasionally Metyrapone used to reduce production of cortisol in adrenals
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61
Q

Nelson’s syndrome?

A

Development of ACTH-prouding tumour following surgical removal of both adrenals glands due to lack of cortisol and -ve feedback. Causes skin pigmentation (high ACTH), bitemporal hemianopia and lack of other pituitary hormones.

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62
Q

Pseudo-Cushings?

A

Mimics cushings. Often due to alcohol XS or severe depression. Causes false +ve dexamethasone supression test or 24hr urinary free cortisol. Insulin stress test may be used to differentiate.

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63
Q

2nd line medication for obese patient with T2DM?

A

DPP-4 inhibitors as least likely to cause weight gain

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64
Q

What would be seen on thyroid scintigraphy for someone with De Quervains thyroiditis? (the Ix)

A

Reduced iodine uptake

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65
Q

Peptic ulceration, galactorrhoea, hypercalcaemia all suggest what?

A

MEN type 1(pancreas, parathyroid, pituitary)

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66
Q

Glucocorticoid therapy can induce what?

A

Neutrophilia

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67
Q

What would be the urine osmolality for someone with primary polydipsia?

A

-Initially low
- After fluid deprivation: High

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68
Q

What features would be atypical for suspected T1DM?

A
  • Age > 50
  • BMI > 25
  • Slow progression of hyperglycaemia
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69
Q

What tests should patients undergo if atypical presentation of T1DM?

A
  • C peptide and diabetic autoantibodies
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70
Q

What is the treatment of a thyrotoxic storm?

A
  • Beta blockers, IV fluids, propylthiouracil and steroids
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71
Q

What should women with hypothyroidism do when they are pregnant?

A

Increase thyroid hormone replacement by upto 50%

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72
Q

Presentation of HHS

A

1) Hypovolaemia
2) Hyperglycaemia
3) Significantly raised serum osmolarity
4) Absence of ketoacidosis.

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73
Q

What blood sugars suggest impaired fasting glycaemia?

A

Between 6.1 and 6.9

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74
Q

What are the target blood sugars for T1DM?

A

Waking - 5-7
Other times: 4-7

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75
Q

What can worsen thyroid eye disease in patients with Graves?

A

Radioiodine treatment

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76
Q

What does a raised C-peptide help to distinguish?

A

Raised - T2DM
Low = T1DM

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77
Q

Management of subclinical hypothyroidism?

A

Check TPO antibodies

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78
Q

If 3 diabetic drugs are not helping, what should be done?

A

Switch one of them for a GLP-1 e.g. exenatide

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79
Q

Side effect of piogliotazone

A

Peripheral oedema

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80
Q

Patient who have 2 hypoglycaemic episodes need what?

A

Surrender driving licence

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81
Q

How should steroid doses be altered during illness with Addisons?

A

Glucocorticoid e.g. hydrocortisone -> doubled
Fludrocortisone -> kept the same

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82
Q

What are the diabetic specific autoantibodies?

A

anti-GAD

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83
Q

Which diabetes med increases risk of bladder cancer?

A

Thiazolidinedione e.g Pioglitazone

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84
Q

Over replacement with thyroxine increases the risk of what?

A

Osteoporosis

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85
Q

Fluids resuscitation in DKA?

A

1L of IV 0.9% NaCl over 1 hour - if systemic BP >90
500ml of IV 0.9% NaCl over 5 mins if systemic BP <90

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86
Q

What would be the expected metabolite results in Cushings?

A

Hypokalaemia with metabolic alkalosis

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87
Q

Erratic blood glucose control, bloating and vomiting

A

Gastroparesis

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88
Q

What should every person with insulin be given for emergencies?

A

Glucagon kit

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89
Q

Headaches, amenorrhoea, visual field defects suggests what?

A

Prolactinoma

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90
Q

Thyrotoxicosis with tender goitre?

A

De Quervains thyroiditis

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91
Q

Elevated prolactin with secondary hypothyroidism and hypogonadism?

A

Non-functioning pituitary adenoma

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92
Q

increased TSH levels and normal T4 suggests what?

A

Poor compliance with thyroxine

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93
Q

What can mimic Cushings disease?

A

Excess alcohol consumption

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94
Q

Increased plasma 17-hydroxyprogesterone levels is suggestive of what?

A

Congenital adrenal hyperplasia

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95
Q

Primary vs secondary hyperaldosteronism?

A

If renin is high, secondary cause is likely i.e. renal artery stenosis

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96
Q

hyponatraemia, reduced plasma osmolality and increased urine osmolality suggests what?

A

SIADH

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97
Q

Acromegaly?

A

XS GH secondary to a pituitary adenoma in over 95% of cases.

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98
Q

Symptoms of acromegaly?

A
  • Spade like hands and feet
  • Frontal bossing
  • Macroglossia
  • Headaches
  • Bitemporal hemianopia
  • Sleep disturbances
  • Carpal tunnel
  • HTN
  • increased shoe size
  • sweaty oily skin (sweat gland hypertrophy)
  • 6% have MEN-1
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99
Q

What is the main cause of death in patients with acromegaly?

A

CVD

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100
Q

Cx of Acromegaly?

A

HTN, diabetes, cardiomyopathy, colorectal cancer

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101
Q

Ix for Acromegaly?

A
  • 1st= serum IGF-1 levels; if raised then…
  • Diagnostic test= Oral glucose tolerance test (shows no supression of GH)
  • MRI may show pituitary tumour
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102
Q

Why are GH levels not diagnostic for acromegaly?

A

They vary throughout the day

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102
Q

How do somatostain analogues work for acromegaly?

A

Inhibits GH release

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102
Q

Acromegaly Mx

A
  • 1st= trans-sphenoidal resection of pituitary adenoma
    if inoperable unsuccessful…
    -Somatostatin analogues e.g ocreotide
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103
Q

What are some signs of hypothyroidism?

A
  • Dry hair/skin
  • Goitre
  • Mental slowness
  • Ataxia
  • Peripheral neuropathy
  • Slow/relaxing reflexes
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104
Q

What are some signs of hyperthyroidism?

A
  • Tachycardia
  • AF
  • Goitre
  • Palmar erythema
  • Brisk reflexes
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105
Q

Hashimotos vs Graves antibodies

A

Graves - anti TSH reception antibodies
Hashimotos - anti TPO antibodies

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106
Q

Where does thyroid gland originate from embryologically?

A

Foramen caecum

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107
Q

What are symptoms of neuroglycopenia?

A
  • Coma
  • Seizures
  • Drowsiness
  • Confusion
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108
Q

What are causes of hypoglycaemia in non-diabetic patients?

A
  • Liver failure
  • Addisons
  • Alcohol binging
  • Pituitary insufficiency
  • Insulin secreting tumour
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109
Q

What happens to periods with hypo and hyperthyroidism?

A

Hypo - heavy periods
Hyper - irregular/no periods

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110
Q

Low vit D, low serum calcium, low serum phosphate, raised ALP and raised PTH

A

Osteomalacia

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111
Q

Osteomalacia

A

Softening of bones 2 to low vit D leading to decreased bone mineral content. (Called rickets in children).

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112
Q

Causes of osteomalacia

A

Vit D def (malabsorption, lack of sunlight, diet); CKD, drug induced (anticonvulsants), inherited, liver cirrhosis, coeliac

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113
Q

Features of osteomalacia

A

Bone pain, bone/muscle tenderness; fractures (femoral neck); proximal myopathy (waddling gait).

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114
Q

Osteomalacia Ix

A
  • Bloods
  • X-ray: translucent bands (Looser’s zones/psudeofractures)
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115
Q

Osteomalacia Mx

A

vit D supplmentation (loading dose initally) and Ca supp if dietary Ca inadequate

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116
Q

What is latent autoimmune diabetes of adulthood and maturity onset diabetes of the young?

A

LADA - Late onset T1DM - usually aged 30-50
MODY - earl onset T2DM - usually under 25

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117
Q

What cardiac manifestations can occur with carcinoid syndrome?

A
  • Pulmonary stenosis and tricuspid insufficiency
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118
Q

Management of an incidental pituitary mass?

A

Lab investigations to assess hormone hypersecretion/hypopituitarism

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119
Q

What is alcoholic ketoacidosis?

A

A euglycemic form of ketoacidosis occurring in alcoholics
- When they don’t eat and they become malnourished, they start breaking down ketones
- Presents with metabolic acidosis, elevated ketones and normal/low glucose
- Tx with IV saline and thiamine

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120
Q

Depression, nausea, constipation, bone pain

A

Primary hyperparathyroidism

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121
Q

Diabetic ketoacidosis?

A

Cx of DMT1 or be the first presentation of it. Extreme stress may cause patients with DMT2 to develop DKA.

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122
Q

DKA pathophysiology?

A

Caused by uncontrolled lipolysis which results in XS of free fatty acids that are converted to ketone bodies

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123
Q

Most common precipitating factors of DKA?

A

infection, missed insulin doses, MI

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124
Q

DKA CP?

A
  • abdo pain
  • polyuria, polydipsia, dehydration
  • Acetone-smelling (pear drop smelling) breath
  • Kussmaul respiration (deep hyperventilation)
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125
Q

DKA diagnostic criteria

A
  • glucose >11mmol/l or known DM
  • pH <7.3
  • bicarb <15mmol/l
  • ketones >3mmol/l or urine ketones ++ on dip
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126
Q

DKA Mx: fluid replacement?

A

0.9% sodium chloride initially eg. 1000ml over 1st hour.

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127
Q

DKA Mx: insulin?

A

IV infusion of 0.1unit/kg/hr. Once blood glucose <14 then 10% dextrose infusion started at 125ml/hr in addition to the 0.9% sodium chloride regime

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128
Q

DKA Mx: correction of electrolyte disturbances?

A

KCl may needed to be added to the replacement fluids. Serum K often high on admission but total body K low, K falls following insulin treatment.

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129
Q

If the rate of potassium infusion is greater than 20mmol/hr then what may be required?

A

Cardiac monitoring

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130
Q

Example of a DKA fluid replacement regime for pt with systolic BP on admission 90mmHg and over?

A

0.9% NaCl 1L= 1000ml over 1st hr
0.9% NaCl 1L with KCl= 1000ml over next 2hrs
0.9% NaCl 1L with KCl= 1000ml over next 2hrs
0.9% NaCl 1L with KCl= 1000ml over next 4hrs
0.9% NaCl 1L with KCl= 1000ml over next 4hrs
0.9% NaCl 1L with KCl= 1000ml over next 6hrs

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131
Q

Most pts with DKA deplete how many litres?

A

5-8

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132
Q

DKA Mx

A
  • fluid replacement
  • insulin
  • correction of electrolyte disturbance
  • long-acting insulin continued and short-acting stopped
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133
Q

Potassium guidelines in DKA?

A
  • > 5.5mmol/l (in first 24hrs)= no replacement
  • 3.5-5.5= 40mmol/L infusion solution of potassium
  • <3.5= senior review
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134
Q

What is an important complication of fluid resus in DKA in children?

A

Cerebral oedema. So use SLOW infusion for children and young adults (18-25yrs).

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135
Q

When to start dextrose infusion in DKA?

A

When blood glucose is <14

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136
Q

DKA resolution is defined as what?

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
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137
Q

In DKA, ketonaemia and acidosis should have been resolved within…

A

24hrs. If not get senoir review.

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138
Q

What when DKA resolution criteria met?

A
  • if pt eating and drinking then switch to subcut insulin
  • review by diabetes specialist nurse prior to discharge
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139
Q

Cx of DKA or the treatment?

A
  • gastric stasis
  • thromboembolism
  • arrhythmias secondary to hyperkalaemia/iatrogenic
  • hypokalaemia
  • iatrogenic due to incorrect
  • fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
  • acute respiratory distress syndrome
  • AKI
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140
Q

What do children/young adults need following fluid resus in DKA?

A

1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. Usually 4-12hrs following starting Mx. If suspicion: senior review and CT head

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141
Q

Vit D deficiency vs CKD as cause of hyperparathyroidism

A

Vit d - low calcium and phosphate
CKD - low calcium but raised phosphate

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142
Q

What differentials for SIADH must be considered

A

Severe hypothyroidism + adrenal insufficiency

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143
Q

What is Klinefelters syndrome?

A
  • 47 XXY
  • Tall and slender male with small testes and gynaecomastia
  • Low testosterone with raised FSH:LH
  • Managed with HRT + regular monitoring for polycythaemia and DEXA scans for bone mineral density
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144
Q

Microvascular vs macrovascular complications of diabetes?

A

Micro - nephropathy, neuropathy, retinopathy
Macro - CVD/Stroke, MI, PVD

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145
Q

What is the pathophysiology of DKA?

A

Insulin deficiency produces glucose production in the liver;
lipolysis also occurs; fatty acids are broken done to form ketone
bodies which produce a metabolic acidosis

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146
Q

What should patients taking steroids be made aware of?

A
  • carry steroid card
  • medic alert bracelet
  • know how to change dose for sick days
  • carry emergency IM hydrocortisone
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147
Q

What sensation will be affected first in diabetic neuropathy?

A

Vibration

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148
Q

What findings may be present with diabetic neuropathy on feet?

A
  • Joint deformity
  • Painless ulcer
  • Diminished reflexes
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149
Q

Vomiting in poorly controlled diabetic patient?

A

Think gastroparesis

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150
Q

carpal tunnel syndrome can be associated with what?

A

Acromegaly

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151
Q

What is the most common complication of thyroid eye disease?

A

Exposure keratopathy

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152
Q

What is the management of de Quervains thyroitidits?

A

Conservative with analgesia. If severe then steroids.

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153
Q

What is the most common cause of Cushings syndrome?

A

Pituitary tumour secreting ACTH (Cushings disease)

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154
Q

What can cause low HbA1c?

A

Sickle cell/G6PD
Hereditary spherocytosis
Haemodialysis

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155
Q

Splenectomy can cause what?

A

Raised Hba1c

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156
Q

What is the key parameter to monitor in HHS?

A

Serum osmolality

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157
Q

How to differentiate between unilateral and bilateral sources of aldosterone excess?

A

High res CT
If normal, adrenal venous sampling

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158
Q

Moderate-severe aortic stenosis is a C/I to what?

A

ACE inhibitors

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159
Q

hypertension, hypokalaemia, and metabolic alkalosis

A

Conn’s syndrome

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160
Q

What is Conn’s?

A

Primary hyperaldosteronism

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161
Q

Causes of Conn’s?

A
  • bilateral idiopathic adrenal hyperplasia: (70%)
  • adrenal adenoma
  • unilateral hyperplasia
  • familial hyperaldosteronism
  • adrenal carcinoma
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162
Q

Features of Conn’s?

A

HTN, hypokalaemia and metabolic alkalosis

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163
Q

Conn’s Ix?

A
  • 1st: plasma aldosterone/renin ratio= high aldosterone levels, low renin levels (negative feedback due to sodium retention from aldosterone)
  • Then CT abdo and adrenal vein sampling: uni adenoma or bilateral hyperplasia
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164
Q

What patient’s should be screened for Conn’s?

A
  • hypertension with hypokalemia
  • treatment-resistant hypertension
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165
Q

Management of myoxedemic coma?

A

Thyroxine + Hydrocortisone

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166
Q

Conn’s Mx?

A
  • laparoscopic adrenalectomy= adrenal adenoma
  • aldosterone antagonist e.g. spironolactone= bilateral adrenocortical hyperplasia
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167
Q

Management of thyroid storm?

A

Beta blockers, propylthiouracil and hydrocortisone

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168
Q

How should HHS fluids be given?

A

Slow infusion

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169
Q

Which diabetic medication is approved in CKD?

A

DPP inhibitors

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170
Q

What enzyme is deficient in congenital adrenal hyperplasia?

A

21-hydroxylase

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171
Q

What serum marker is raised in CAH?

A

17-OH progesterone

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172
Q

How does CAH present?

A
  • Ambiguous genitalia
  • Acne
  • Hirsutism
  • Delayed puberty
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173
Q

How is CAH managed?

A
  • Glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) replacement
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174
Q

If patients are asymptomatic for DM, what do you need?

A

2 abnormal readings

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175
Q

What are side effects of gliotazones?

A
  • Weight gain
  • Increased risk of fractures
  • Fluid retention
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176
Q

Iron tablets/calcium carbonate tablets can have what effect?

A

Reduced absorption of levothyroxine -> give 4 hours apart

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177
Q

How does Cushing’s disease present on dex suppression test?

A

ACTH and cortisol suppressed

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178
Q

What time gap should be kept when titrating metformin doses?

A

1 week

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179
Q

Which cancer is Hashimotos thyroiditis associated with?

A

MALT lymphoma

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180
Q

Thyrotoxicosis can lead to what?

A

high output cardiac failure

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181
Q

When should treatment with statins be discontinued?

A

If serum transaminase concentrations rise to 3 times the upper limit of reference ranges

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182
Q

Why does Cushing’s cause tanned appearance?

A

ACTH has a stimulatory effect on the melanocytes due to affinity for the MSH receptor

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183
Q

Why does impaired hypoglycaemia awareness occur?

A

neuropathy of parts of the autonomous nervous system

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184
Q

Management of subclinical hypothyroidism

A

TSH > 10 - Consider thyroxine if this is present on 2 separate occasions atleast 3 months apart
TSH 5.5-10 - Consider 6 months of thyroxine if <65 and there are symptoms of hypothyroidism
If asymptomatic/older - watch and wait

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185
Q

What do each of the zones of the adrenals produce?

A

Zona glomerulosa - Mineralocorticoids - Aldosterone
Zona fasciculata - Glucocorticoids - Cortisol
Zona reticularis - Androgens
Medulla - Adrenaline/Noradrenaline

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186
Q

hyperkalaemic, hyponatraemic, hypoglycaemic metabolic acidosis

A

Adrenal Crisis - Addisons

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187
Q

How quickly should ketones fall in DKA?

A

Atleast 0.5 per hour

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188
Q

What are primary causes of hypogonadism?

A
  • Trauma
  • Mumps
  • Iatrogenic
  • Klinefelter’s syndrome
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189
Q

What is the most common thyroid cancer?

A
  • Papillary
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190
Q

What is the management of non adrenal adenoma hyperaldosteronism?

A

Spironolactone

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191
Q

Which cells of pancreas are affected in diabetes?

A

Beta pancreatic islet cells

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192
Q

What genetic mutations might T1DM have?

A

HLA-DR3/4

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193
Q

What time should serum cortisol be taken?

A

9am

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194
Q

Treatment of choice for toxic multinodular goitre?

A

Radioactive iodine

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195
Q

Osteoporosis in a man?

A

Check testosterone

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196
Q

What is the management of Addisonian crisis?

A
  • Hydrocortisone
  • 1L Saline
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197
Q

How do DPP-4 inhibitors work?

A

Increase incretin levels by reducing their peripheral breakdown

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198
Q

How should the dose of hydrocortisone be taken in someone with Addisons?

A

Majority in first half of the day

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199
Q

What should be corrected before giving bisphosphonates?

A

Hypocalcaemia
Vit D deficiency

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200
Q

Patient >75 with fragility fracture?

A

Start bisphosphonate without needing to do DEXA

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201
Q

What dose of glucose gel should be given to a patient with a low blood sugar?

A

10-20g

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202
Q

Which HTN drug an cause sexual dysfunction?

A

Thiazide-like diuretics e.g indapamide

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203
Q

How long should metformin be discontinued for after CT with contrast?

A

48 hours

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204
Q

In primary prevention of CVD, what should the non-HDL cholesterol reduce by?

A

> 40% within the first 3 months

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205
Q

What should be done after treatment with bisphosphonates for 5 years?

A

Repeat DEXA and FRAX and stop if score <-2.5

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206
Q

Which diabetes medication is linked to Fournier’s gangrene (necrotising fasciitis of the genitals)?

A

SGLT-2 inhibitors

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207
Q

What is the investigation of choice for suspected insulinoma?

A

72 hour fast

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208
Q

Ferrous sulphate can interact with what?

A

Levothyroxine

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209
Q

Management of hyperglycaemia in someone who has started enteral feeding?

A

Insulin

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210
Q

Management of steroid induced diabetes?

A

Sulfonylureas e.g. gliclazide

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211
Q

Primary amenorrhoea?

A

Failure to establish mentruation by 15yrs but normal secondary sexual characteristics; or by 13yrs with no characteristics

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212
Q

Secondary amenorrhoea?

A

Cessation of menstruation for 3-6m in women with normal regular menses or 6-12m in women with previous oligomenorrhoea

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213
Q

Causes of primary amenorrhoea

A

Gonadal dysgenesis eg. Turner’s (common); testicular feminisation; congenital malformations of genital tract; functional hypothalamic amenorrhea eg. 2 to anorexia; imperforate hymen; congenital adrenal hyperplasia

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214
Q

Causes of secondary amenorrhoea (after excluding pregnancy)

A

hypothalamic amenorrhoea eg. 2 to stress, XS exercise; PCOS; hyperprolactinaemia; premature ovarian failure; thyrotoxicosis; Sheehan’s; Asherman’s

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215
Q

Amenorrhoea Ix

A
  • urinary or serum bHCG
  • FBC, U&E, coeliac screen, TFTs
  • prolactin
  • oestradiol
  • androgen levels (raised in PCOS)
  • gonadotrophins= low means hypothalamic cause, raised suggest ovarian problem (premature ovarian failure) or gonadal dysgenesis eg. Turner’s
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216
Q

Amenorrhoea Mx

A

-TUC
- Primary: with primary ovarian insufficiency due to gonadal dysgenesis eg. Turner’s then HRT eg. to prevent osteoporosis ect.

217
Q

What is gynaecomastia?

A

Abnormal amount of breast tissue in males caused usually by increased oestrogen:androgen ratio.

218
Q

Causes of gynaecomastia?

A
  • physiological: normal in puberty
  • syndromes with androgen deficiency: Kallman’s, Klinefelter’s
  • testicular failure: e.g. mumps
  • liver disease
  • testicular cancer e.g. seminoma secreting hCG
  • ectopic tumour secretion
  • hyperthyroidism
  • haemodialysis
  • drugs
219
Q

Drug causes of gynaecomastia?

A
  • spironolactone (most common)
  • cimetidine
  • digoxin
  • cannabis
  • finasteride
  • GnRH agonists e.g. goserelin, buserelin
  • oestrogens, anabolic steroids
220
Q

Very rare drug causes of gynaecomastia?

A
  • tricyclics
  • isoniazid
  • calcium channel blockers
  • heroin
  • busulfan
  • methyldopa
221
Q

What is dysmenorrhoea?

A

XS pain during menstrual period. Primary and secondary.

222
Q

Primary dysmenorrhoea?

A

No underlying pelvic pathology. Partially due to EX endometrial prostaglandin production.

223
Q

Primary dysmenorrhoea features?

A

up to 50% women, usually within 1-2yrs of menarche.
- pain just before or within few hrs or period starting
- usually lasts 72hrs and improves as menses progress
- suprapubic cramping pains which may radiate to back or down thigh
- vomiting, nausea, fatigue, dizziness

224
Q

Primary dysmenorrhoea Mx

A
  • NSAIDs eg. ibuprofen and mefenamic acid= inhibit prostaglandin production
  • 2nd: COCP
225
Q

Secondary dysmenorrhoea?

A

Result of underlying pathology and develops many yrs after menarche

226
Q

Secondary dysmenorrhoea feature?

A

Pain usually starts 3-4 days before onset of period
- dyspareunia
- not really related to menstruation but this exacerbates pain

227
Q

Causes of secondary dysmenorrhoea?

A

Endometriosis, adenomyosis, PID, copper coil, fibroids.

228
Q

Mx for secondary dysmenorrhoea

A

Refer to gynaecology for investigation

229
Q

Red flags for dysmenorrhoea

A
  • +ve preg test and vag bleeding
  • ascites/pelvic/abdo mass
  • abnormal cervix on pelvic exam
  • persistent intermenstrual or postcoital bleeding with features of PID
230
Q

What is Addison’s disease?

A

Primary adrenal insufficiency. Autoimmune destruction of adrenal glands. Most common cause of hypoadrenalism (80% cases).

231
Q

What does Addison’s result in?

A

Reduced cortisol (glucocorticoid) and aldosterone (mineralocorticoid) being produced.

232
Q

Addison’s CP?

A
  • lethargy, weakness, weight loss, N&V
  • salt craving
  • hyperpigmentation (esp palmar creases)
  • vitilligo
  • loss of pubic hair in women
  • hypotension
    hypoglycaemia
  • may be hyponatraemia and hypokalaemia
233
Q

When should Addison’s be considered?

A
  • persistent non-specific symptoms (of addisons)
  • hypothyroidism if symptoms worsen when thyroxine is started
  • DMT1 with recurrent unexplained hypoglycaemic episodes
  • other autoimmune conditions
  • low Na or high K levels
234
Q

Addisonian crisis CP

A

hypotension, hypovolaemic shock, acute abdo pain, vomiting, reduced consciousness

235
Q

Addison’s Ix?

A
  • Inital:
  • 8-9am serum cortisol
  • urea & electrolytes.
  • GOLD (confirm diagnosis): Synacthen test (adrenocorticotrophic hormone simulation)
236
Q

What do the 9am serum cortisol levels mean?

A
  • <100nanomol then admit to hospital as adrenal insuff highly likely.
  • 100-500 then refer to endo for Ix
237
Q

What autoantibodies may be common in Addison’s?

A

Adrenal cortex autoantibodies or 21-hydroxylase antibodies

238
Q

Normal response to ACTH simulation test (Synacthen test)?

A

Cortisol levels increase to more than 500nanomol/L after 30-60mins.
If adrenal insfuficiency: serum cortisol levels don’t repsond to tetracosactide but adrenal cortex already receiving max stimulation from endogenous ACTH.

239
Q

Addison’s Mx?

A

Hydrocortisone for glucocorticoid replacement and fludrocortisone for mineralcorticoid replacement.

240
Q

Important information to tell someone who has Addison’s?

A
  • INCREASE corticosteroid during physical stress eg. illness, injury or surgery to prevent adrenal crisis: DOUBLE glucocortiocid and keep fludrocortisone dose same
  • Recognise symptoms of adrenal crisis
  • Carry steroid emergency card
241
Q

Causes of Addisonian crisis?

A

Current illness or stress.

242
Q

Mx of Addisonian crisis

A

IM or IV hydrocortisone and admit to hospital

243
Q

Primary vs secondary adrenal insufficeny?

A
  • Primary (Addison’s)= adrenal glands don’t make enough cortisol and aldosterone
  • Secondary= pituitary doesn’t make enough ACTH
244
Q

What is ACTH (adrenocorticotropic hormone)?

A

Produced by pituitary gland that regulates cortisol and androgen production. When released it triggers adrenal glands to produce C and A.

245
Q

Causes of primary hypoadrenalism (Addison’s)?

A
  • Autoimmune (most)
  • congenital adrenal hyperplasia
  • TB
  • Metastases eg. bronchial carcinoma
  • meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
  • HIV
  • antiphospholipid syndrome
246
Q

Causes of secondary hypoadrenalism?

A
  • pituitary disorders eg. tumours, irradiation, infiltration
  • long term administration of corticosteroids
247
Q

Diabetes insipidus (DI)?

A

Decreased secretion of antidiuretic hormone (ADH) from pituitary (cranial DI) or insensitivity to ADH (nephrogenic DI).

248
Q

Causes of cranial DI

A
  • idiopathic
  • post head injury
  • pituitary surgery
  • craniopharyngiomas
  • infiltrative= sarcoidosis, histiocytosis X
  • DIDMOAD (DM, Optic Atrophy and Deafness- Wolfram’s syndrome)
  • haemochromatosis
249
Q

Causes of nephrogenic DI

A
  • genetic
  • electrolytes= hypercalcaemia, hypokalaemia
  • lithium
  • demeclocycline
  • tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
250
Q

Genetic causes of nephrogenic DI

A
  • affects the vasopressin (ADH) receptor
  • or mutation in gene that encodes the aquaporin 2 channel
251
Q

How does lithium cause nephrogenic DI?

A

Desensitised the kidney’s ability to respond to ADH in collecting ducts

252
Q

CP of DI

A

polydipsia and polyuria

253
Q

DI Ix

A
  • high plasma osmolality, low urine osmolality
  • urine osmolality of >700mOsm/kg excludes diabetes insipidus
  • water deprivation test
254
Q

DI Mx: nephrogenic

A

thiazides and low salt/protein diet

255
Q

DI Mx: crainial

A

Desmopressin

256
Q

What is the water deprivation test (desmopressin stimulation test)?

A

Used to evaluate pts who have polydipsia.
1. prevent pt drinking water 8hrs before test
2. measure urine osmolality
3. if urine osm low, then synthetic ADH (Desmopressin) is given
4. re-measure urine osm 2-4hrs later

257
Q

Water deprivation test: primary polydipsia

A
  • urine osm after water deprivation= high
  • urine osm after desmopressin= N/A

rules out DI

258
Q

Water deprivation test: cranial DI

A
  • urine osm after water deprivation= low
  • urine osm after desmopressin= high

pt lacks ADH, kidneys still capable of responding to ADH. Initially urine osm low as continues to be diluted by XS water lost in urine. After des given, kidneys respond by reabsoring water and concentrating water so urine osm high.

259
Q

Water deprivation test: nephrogenic DI

A
  • urine osm after water deprivation= low
  • urine osm after desmopressin= low

pt unable to respond to ADH so both low.

260
Q

Hyperosmolar hyperglycaemic state (HHS)?

A

Medical emergency, usually elderly with DMT2 and up to 20% mortality.

261
Q

What does HHS result in?

A

Hyperglycaemia results in osmotic diuresis, severe dehydration and electrolyte def.

262
Q

HHS pathophysiology

A

hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion

263
Q

HHS clinical presentation

A
  • comes on over many days (DKA hrs) so dehydration and metabolic distrubances more extreme
  • Cx of volume loss= polyuria, polydipsia, dehydration
  • systemic= lethargy, N&V
  • neurological= altered consciousness, focal neuro deficits
  • haematological= hypervidcosity (MI, stroke, peripheral arterial thrombosis)
264
Q

What is typically seen in HHS for diagnosis?

A
  • hypovolaemia
  • hyperglycaemia= >30
  • raised serum osmolarity= >320mosmol/kg
  • no hyperketonaemis= <3
  • no acidosis= bicarb >15 or pH >7.3 (can occur due to lactic acidosis or renal impairment however)
265
Q

How to calculate serum osmolarity in HHS?

A

2 * Na+ + glucose + urea

266
Q

HHS Mx

A
  • fluid replacement
  • insulin= should not be given unless blood glucose stops falling while giving IV fluids
  • VTE prophylaxis
267
Q

HHS Mx: fluid replacement?

A
  • fluid loss estim 100-200ml/kg
  • IV 0.9% sodium chloride
  • 0.5-1L/hr
  • Monitor K+ levels and add to fluids if needed
268
Q

HHS Cx?

A

Vascular due to hyperviscosity eg. MI, stroke

269
Q

When do most children achieve day and night continence by?

270
Q

Enuresis?

A

Involuntary discharge of urine by day or night or both in child 5yrs+, in absence of congenital or acquired defects of NS or urinary tract.

271
Q

Nocturnal enuresis?

A
  • Primary= never achieved sustained continence at night
  • Secondary= after child has been previously dry at night for >6m
272
Q

Causes of primary nocturnal enuresis?

A

sleep arousal difficulties, polyuria, bladder dysfunction

273
Q

Causes of secondary nocturnal enuresis?

A

diabetes, UTI, constipation, psychological problems

274
Q

Causes of primary nocturnal enuresis with daytime symptoms?

A

overactive bladder, congenital malformations, neuro disorders, UTI, chronic constipation

275
Q

RFs for nocturnal enuresis

A

FHx, male, delay in attaining bladder control, obesity, ADHD, autism, anxiety

276
Q

Important points to ask in nocturnal enuresis history?

A
  • daytime symptoms?
  • previously dry at night without assistance for 6m?
277
Q

Nocturnal enuresis Mx?

A
  • advice: lifting and waking, fluid intake, toilet before bed. If infrequent (<2 times week) or <5yrs then reassure that usually resolves without Mx and wait-and-see approach
  • 1st= enuresis alarm AND positive reward system (eg. star charts) for agreed behaviour eg. using toilet before bed rather than dry night
  • 2nd= desmopressin for short term eg. sleepover or if alarm ineffective.
278
Q

Common (>1 in 10) causes of polyuria

A
  • diuretics, caffeine and alcohol
  • DM
  • lithium
  • HF
279
Q

Infrequent (1 in 100) causes of polyuria

A
  • hypercalcaemia
  • hyperthyroidism
280
Q

Rare (1 in 1000) causes of polyuria

A
  • chronic renal failure
  • primary polydipsia
  • hypokalaemia
281
Q

Very rare (<1 in 10000) causes of polyuria

A

Diabetes insipidus

282
Q

Hyperthyroidism?

A

Pathologically increased thyroid hormone production and secretion by thyroid gland

283
Q

Thyrotoxicosis?

A

Clinical manifestation of XS thyroid hormone due to any cause, incl. hyperthyroidism

284
Q

Primary hyperthyroidism?

A

When thyrotoxicosis is caused by abnormality of thyroid gland eg. Graves’ or a nodular goitre

285
Q

Pathophysiology of primary hyperthyroidism?

A

When thyroid-stimulating hormone (TSH) is suppressed below normal reference range and free thyroxine (FT4) and/or free triiodothyronine (FT3) concs are high

286
Q

Pathophysiology of subclinical hyperthyroidism

A

TSH low and T4/T3 normal

287
Q

Thyrotoxicosis without hyperthyroidism?

A

Thyrotoxicosis without thyroid gland overacitivity, normally transiet due to thyroiditis or XS levothyroxine.

288
Q

Cx of hyperthyroidism

A

thyrotoxic crisis, Graves orbitopathy, compression symptoms from large goitre, AF, HF

289
Q

Causes of primary, secondary and tertiary hyperthyroidism?

A

1= thyroid pathology eg. Graves, thyroid adenoma, toxic multinodular goitre

2= pituitary pathology eg. XS iodine

3= hypothalmic

290
Q

Hyperthyroidism CP

A

T.remor
H.eart rate increase
Y.awning
R.estlessness
O.ligomenorrhoea
I.rritability
D.iarrhoea
I.ntolerance to heat
S.weating
M.uscle wasting

PAINLESS GOITRE, anxiety, WEIGHT LOSS, sinus tachy, features of graves

291
Q

Graves’ disease CP

A
  • orbitopathy: XS eye watering, eyelid retraction or lid lag, proptosis, double vision, changes in visual acuity or colour vision
  • non-pitting pretibial myxoedema
  • thyroid bruit
292
Q

DeQuervains?

A

After upper resp infection. Thyroid PAINFUL

293
Q

Hyperthyroidism Ix?

A

TFTs:
- Primary= TSH low, T3 & T4 high
- Subclinical= TSH low, T3 & T4 normal
- Secondary= TSH high, T3 & T4 high
- Repeat TFTs after 3m to confirm

  • TRAb (TSH receptor antibodies) if suspect Graves
  • ESR & CRP ?thyroiditis
294
Q

Hyperthyroidism Mx

A
  • Beta blocker for andrenergic symptoms
    • Carbimazole
  • definitive Mx: radioactive iodine or thyroid surgery
295
Q

Monitoring of carbimazole?

A

FBC and LFTs before starting

296
Q

Graves’ Mx

A

Sunglasses, IV methylprednisolone, surgical decompression

297
Q

Hypothyroidism?

A

Thyroid hormone (thyroxine T4 and tri-iodothyronine T3 def)

298
Q

Primary hypothyroidism (overt)

A

TSH high, T3 & T4 low

299
Q

Secondary hypothyroidism

A

TSH low/normal, T3 & T4 low

300
Q

Subclinical hypothyroidism

A

TSH high, T3 & T4 normal

301
Q

Tertiary hypothyroidism

A

TSH low, T3 & T4 low, TRH low

302
Q

Causes of primary hypothyroidism

A
  • autoimmune thyroiditis (Hashimotos)
  • iodine def
  • post-ablative therapy or surgery
  • drugs
  • Subacute thyroiditis (de Quervain’s)
  • transient thryoiditis
  • thyroid infiltrative disorders
303
Q

What drugs can cause hypothyroidism?

A

Amiodarone, lithium, carbimazole

304
Q

Cause of secondary hypothyroidism

A

Pituitary eg. tumour. Associated with Down’s, Turner’s and coeliac.

305
Q

Causes of teritary hypothyroidism

A

Hypothalamic

306
Q

Cx of hypothyroidism

A

dyslipidaemia, metabolic syndrome, CHD, stroke, HF, neuro and cognitive impairments, adverse maternal & fetal outcomes in preg

307
Q

Hypothyroidism CP

A

B.readycardia
R.eflexes relax slowly
A.taxia
D.ry thin hair and skin
Y.awning
C.old intolerance
A.scites
R.ound puffy face
D.epression
I.mmobile ileus (constipation)
C.ongestive HF

WEIGHT GAIN, PAINLESS GOITRE

308
Q

Hypothyroidism Ix

A
  • TFTs
  • TPOAb (thyroid peroxidase antibodies) if ?autoimmune cause
  • FBC and B12: pernicious anaemia
  • HbA1c
  • coeliac serology
    serum lipids
309
Q

Hypothyroidism Mx

A

Levothyroxine (T4).
Refer to endo if pregnant, postpartum planning pregnancy or already diagnosed with postpartum thyroiditis.

310
Q

Levothyroxine dose?

A

50-100mcg od starting.
If >50yrs, severe hypothy or IHD then start inital at 25mcg od then titrate slowly.

311
Q

Therapeutic goal for levothyroxine?

A

TSH 0.5-2.5mU/l

312
Q

Following change in levothyroxine dose, when should TFTs be checked?

A

After 8-12w

313
Q

Levothyroxine S/E?

A

hyperthyroidism, reduced BMD, worsening angina, AF

314
Q

Levothyroxine interactions?

A

Iron, calcium carbonate.
Absorption of thyroxine reduced so give 4hrs apart

315
Q

Hashimoto’s thyroiditis: hashitoxicosis?

A

Transient thyrotoxic state

316
Q

Diabetes mellitus type 1 and 2 classification?

A

Fasting plasma glucose >7
Random plasma glucose >11
HbA1c >48

317
Q

DMT1 cause?

A

Absolute insulin def resulting from autoimmune destruction of insulin producing pancreatic beta cells of the islets of Langerhans.

318
Q

Cx of DMT1: microvascular

A

retinopathy, nephropathy, neuropathy

319
Q

Cx of DMT1: macrovascular

A

MI, stroke, PAD

320
Q

Cx of DMT1: metabolic

A

DKA, hypoglycaemia (<3.5)

321
Q

Other Cx of DMT1?

A

Depressions, eating disorders, risk of other autoimmune conditions eg. thyroid, coeliac, pernicious anaemia, addison’s

322
Q

How do pts with DMT1 typically present?

A

Early life, unwell- possibly in DKA

323
Q

When should you suspect DMT1 in children/young adult?

A

hyperglycaemia +
polyuria, polydipsia, weight loss, XS tiredness

324
Q

DMT1 clinical diagnosis?

A

Hyperglycaemia + 1 or more:
- ketosis
- weight loss
- <50yrs (>rarer)
- BMI <25 (>rarer)
- FHx or personal history of autoimmune disease

325
Q

DMT1 Ix?

A
  • clinical + urine dip for glucose and ketones + fasting and random glucose + HbA1c
  • Can do c-peptide levels= typically low
  • diabetes specific autoantibodies= distinguish between T1 & T2 eg. anti-GAD in T1
326
Q

DMT1 Mx

A

Subcut insulin

327
Q

DMT2 cause?

A

Persistent hyperglycaemia caused by combination of deficient insulin secretion and resistance to the action of insulin.

328
Q

DMT2 RFs?

A

obesity, inactivity, diet, FHx, Asian, African, Afro-Caribbean, long-term corticosteroids, Hx gestational diabetes

329
Q

DMT2 Cx

A

Same as T1

330
Q

When to suspect DMT2?

A
  • persistent hyperglycaemia
  • polydipsia, polyuria, weight loss, tiredness, enuresis, impaired growth in children, acanthosis nigricans (suggesting insulin resisitance)
331
Q

Mx of DMT2

A
  • Individualised care plan
  • Education, support, advice in lifestyle
  • Screening for complications
  • Lifestyle Mx
  • Medication if lifestyle not sufficient
332
Q

DMT2 antidiabetic medication?

A

1st: metformin standard release (not at CVD risk) or metformin standard relase + SGLT2 inhibitor (risk of CVD.
- if GI disturbance with metformin then switch to metformin modified release

2nd: + sulfonylurea, pioglitazone or DPP-4 inhibitor (‘gliptin’)

3rd: dual therapy not worked= consider insulin based therapy (with or without other drugs). Can also try triple therapy= + sulfonylurea, pigoglitazone or DPP-4 in.

4th: triple therapy not working with metformin + 2 other drugs, switch one of the drugs to GLP-1 mimetri eg. exenatide (SC)

333
Q

DMT2: how often should HbA1c be measured?

A

3-6m until stable then 6mthly

334
Q

DMT2 ‘sick day rules’ advice?

A

Stop medication except insulin

335
Q

Diabetes Ix to check blood glucose?

A
  • finger prick
  • fasting or random blood glucose
  • HbA1c
  • oral glucose tolerance test
336
Q

Side effects of insulin?

A

Hypoglycaemia, weight gain, lipodystrophy

337
Q

Insulin mechanism of action

A

direct replacement for endogenous insulin

338
Q

Metformin mechanism of action

A

increases insulin sensitivity; decreases hepatic gluconeogenesis

339
Q

Metformin side effects

A

GI upset, lactic acidosis. Can’t be used in pts with eGFR <30

340
Q

Sulfonylureas mechanism of action?

A

Stimulate pancreatic beta cells to secrete insulin

341
Q

Sulfonylureas side effects?

A

Hypoglycaemia, weight gain, hyponatraemia, SIADH

342
Q

DPP-4 inhibitors (gliptins) mechanism of action?

A

Increase incretin levels which inhibit glucagon secretion

343
Q

DPP-4 inhibitors (gliptins) side effects?

A

Increased risk of pancreatitis

344
Q

Thiazolidinediones mechanism of action?

A

Activate PPAR-gamma receptor in adipocytes to promoite adipogenesis and fatty acid uptake

345
Q

Example of Thiazolidinediones?

A

pioglitazone

346
Q

Thiazolidinediones side effects?

A

Weight gain, fluid retention, fractures

347
Q

SGLT-2 inhibitors (-gliflozins) mechanism of action?

A

reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

348
Q

SGLT-2 inhibitors (-gliflozins) side effects?

A

UTI, weight loss, increased risk of lower-limb amputation so monitor feet

349
Q

SGLT-2 inhibitors (-gliflozins) example?

A

canagliflozin, dapagliflozin

350
Q

GLP-1 agonists (-tides) mechanism of action?

A

Incretin mimetic which inhibits glucagon secretion

351
Q

GLP-1 agonists (-tides) side effects?

A

N&V, pancreatitis, weight loss

352
Q

Prediabetes?

A

This term is used for patients who don’t yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years. They, therefore, require closer monitoring and lifestyle interventions such as weight loss

353
Q

Gestational diabetes?

A

Some pregnant develop raised glucose levels during pregnancy. This is important to detect as untreated it may lead to adverse outcomes for the mother and baby

354
Q

Maturity onset diabetes of the young (MODY)?

A

A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

355
Q

Latent autoimmune diabetes of adults (LADA)?

A

The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM

356
Q

What else can cause diabetes?

A

Any pathological process which damages the insulin-producing cells of the pancreas may cause diabetes to develop. eg. chronic pancreatitis and haemochromatosis.

357
Q

What drugs can cause raised blood glucose levels?

A

Glucocorticoids

358
Q

BP target for diabetics?

A

140/90mmHg

359
Q

What should be avoided in diabetics with uncomplicated HTN as they may cause insulin resistance/impair insulin secretion?

A

Beta blockers

360
Q

DMT1 blood glucose targets?

A

5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day

361
Q

DMT1 types of insulin?

A
  • Multiple daily injection basal-bolus insulin regimens
    eg. twice-daily insulin detemir
  • Rapid-acting insulin analogues injected before meals
362
Q

DMT2: what should be done before starting a patient with CVD risk of SGLT-2 inhibitors?

A

Metformin should be esablished and titrated up before starting.

363
Q

DMT2: when should a SGLT-2 inhibitor be started?

A

Start SGLT-2 at any point if pt develops CVD, QRISK >10 or HF.

364
Q

If triple therapy not tolerated then when should you consider switching one of the drugs for GLP-1 mimetic?

A
  • BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
  • BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
  • only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
365
Q

Advice to give muslims who are diabetic during Ramadan?

A
  • eat meal containing long-acting carbs at Suhoor
  • check blood glucose levels
  • if taking metformin, split to 1/3 dose at Suhoor and 2/3 dose at Iftar
  • take once daily sulfonylureas at Iftar
366
Q

Why should a patient on insulin not stop it if they are sick?

A

risk of DKA

367
Q

Presentation of diabetic foot?

A
  • neuropathy
  • ischaemia: absent foot pulses, reduced ABPI, intermittent claudication
  • ulceration, Charcot’s arthropathy, cellulitis
368
Q

How often to screen for diabetic foot?

A

Anuually. If moderate or high risk (problems other than simple calluses) then follow up regularly at diabetic foot centre

369
Q

Contraindications to metformin?

A

CKD (eGFR <30); recent MI, sepsis; having iodine-containing x-ray contrast media; alcohol abuse

370
Q

2 main types of impaired glucose regulation?

A
  • impaired fasting glucose (IFG): due to hepatic insulin resistance
  • impaired glucose tolerance (IGT): due to muscle insulin resistance
371
Q

What implies impaired fasting gluocse?

A

a fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l

372
Q

What is impaired glucose tolerance defined as?

A

fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

373
Q

What should people with impaired fasting glucose be offered?

A

oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT

374
Q

What is diabetic nephropathy?

A

Commonest cause of end-stage renal disease in world; 33% pts with DMT1 have it by 40yrs

375
Q

Pathophysiology of diabetic nephropathy?

A
  • Changes to haemodynamics of glomerulus, leads to increased glomerular capillary pressure.
  • Non-enzyme glycosylation of basement membrane
376
Q

Histological changes in diabetic nephropathy?

A

BM thickening, capillary obliteration, mesangial widening. Nodular hyaline areas develop in glomuli-Kimmelstiel-Wilson nodules.

377
Q

Modifiable RFs for diabetic nephropathy?

A

Hypertension
Hyperlipidaemia
Smoking
Poor glycaemic control
Raised dietary protein

378
Q

Non-modifiable RFs for diabtic nephropathy?

A

Male sex
Duration of diabetes
Genetic predisposition (e.g. ACE gene polymorphisms)

379
Q

Screening for diabetic nephropathy how often?

380
Q

How do you screen for diabetic nephropathy?

A

Urinary albumin:creatinine ratio (ACR), early morning specimin.
ACR>2.5= microalbuminuria

381
Q

Diabetic nephropathy Mx

A
  • dietry protein restriction
  • tight glycaemic control
  • BP control (aim <130/80)
  • ACE in or ARB
  • control dyslipidaemia eg. statins
382
Q

Diabetic nephropathy- when to start ACE or ARB?

A

if urinary ACR 3+

DONT use dual therapy.

383
Q

How many stages of diabetic nephropathy?

384
Q

Diabetic nephropathy stage 1?

A
  • hyperfiltration: increase in GFR
  • may be reversible
385
Q

Diabetic nephropathy stage 2 (silent or latent phase)

A
  • most don’t develop microalbuminuria for 10yrs
  • GFR remains elevated
386
Q

Diabetic nephropathy stage 3 (incipient nephropathy)

A
  • microalbuminuria (albumin excretion 30-300mg/day, dipstick neg)
387
Q

Diabetic nephropathy stage 4 (overt nephropathy)

A
  • persistent proteinuria (albumin excretion >300, dip +ve)
  • HTN present
  • Histology= diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
388
Q

Diabetic nephropathy stage 5

A
  • end stage renal disease, GFR <10
  • renal replacement therapy needed
389
Q

Diabetic nephropathy in DMT1 vs DMT2

A

DMT2 same stages as T1 but may progress at different timescale- quicker to later stag

390
Q

Diabetic neuropathy?

A

Sensory loss NOT motor loss

391
Q

Diabetic neuropathy: peripheral neuropathy typical sensory loss pattern?

A

Glove and stocking distribution.
Lower longs affected 1st due to length of sensory neurone affecting this area.
Painful neuropathy is common.

392
Q

Diabetic neuropathy Mx

A
  • pain Mx clinics
  • 1st: amitriptyline, duloxetine, gabapentin or pregabalin
  • 2nd: + another
  • localised neuropathic pain eg. post-herpetic neuralgia= topical capsaicin
393
Q

Diabetic neuropathy: what can be used as ‘rescue therapy’ for exacerbations of neuropathic pain?

394
Q

Diabetic neuropathy: 2 types?

A

Peripheral neuropathy and GI autonomic neuropathy

395
Q

Diabetic GI autonomic neuropathy?

A
  • gastroparesis
  • chronic diarrhoea (at night)
  • GORD
396
Q

Diabetic GI autonomic neuropathy: gastroparesis?

A
  • secondary to autonomic neuropathy
  • CP: erratic blood glucose control, bloating and vomiting
  • Mx: metoclopramide, domperidone or erythromycin (prokinetics)
397
Q

Diabetic GI autonomic neuropathy: GORD caused by what?

A

decreased lower oesophageal sphincter pressure

398
Q

When does a patient need primary prevention for hyperlipidaemia?

A

QRISK= 10+
DMT1
CKD is eGFR <60
Most people over 60yrs ideally

399
Q

Primary prevention for hyperlipdaemia?

A

Atorvastatin 20mg od. If not fallen by >=40% then titrate up to 80

400
Q

Secondary prevention for hyperlipidaemia (known IHD, CVD, PAD)?

A

Atorvastatin 80mg od

401
Q

QRISK may underestimate CVD risk in what populations?

A
  • pts treated for HIV
  • serious mental health problems
  • meds causing dyslipidaemia: antipsychotics, corticosteroids, immunosuppressants
  • autoimmune disorders/systemic inflam disorders eg. SLE
402
Q

When to consider possibility of familial hypercholesterolaemia?

A
  • total cholestrol >7.5
  • personal or FHx of premature CHD (event before 60yrs in person or first degree relative)
403
Q

Atorvastatin 20mg should be offered to T1 diabetics who are…

A
  • > 40yrs
  • diabetes >10yrs
  • established nephropathy
  • or other CVD RFs
404
Q

In CKD what should be done before increasing a dose of atorvastatin?

A

Consult renal specialist

405
Q

Follow up after starting pt on a statin?

A

at 3m:
- repeat full lipid profile

406
Q

When following a pt up, what if the non-HDL cholesterol has not fallen by at least 40%?

A

Talk about concordance and lifestyle changes with pt. Consider increasing atorvastatin up to 80mg.

407
Q

What is xanthelasma?

A

Yellowish papules and plaques commonly seen on eyelid

408
Q

What is xanthelasma appearance caused by?

A

Localised accumulation of lipid deposits. Also seen in pts without lipid abnormalities

409
Q

Mx of exanthelasma?

A

Surgical excision, topical trichloroacetic acid, laser therapy or electrodesiccation

410
Q

Palmar xanthoma?

A
  • remnant hyperlipidaemia
  • may less commonly be seen in familial hypercholesterolaemia
411
Q

Eruptive xanthoma?

A

Due to high triglyceride levels and present as multiple red/yellow vesicles on extensor surfaces (elbows, knees)

412
Q

Causes of eruptive xanthoma?

A
  • familial hypertriglycerdaemia
  • lipoprotein lipase def
413
Q

Tendon xanthoma, tuberous xanthoma and xanthelasma?

A
  • familial
  • hypercholesterolaemia
    remnant hyperlipidaemia
414
Q

Mechanism of action of statins?

A

Inhibit action of HMG-CoA reductase (rate limiting enzyme in hepatic cholesterol synthesis)

415
Q

Aim of treatment in secondary prevention (statins)?

A

LDL-C level of 2.0 mmol per litre or less, or non-HDL-C levels of 2.6 mmol per litre or less

416
Q

Aim of treatment in primary prevention (statins)?

A

greater than 40% reduction in non-HDL-C levels.

417
Q

Before starting lipid modification therapy, what baseline bloods should be performed?

A
  • non-fasting lipid profile
  • LFTs
  • Renal function
  • HbA1c
  • creatine kinase
  • TFTs
418
Q

Adverse effects of statins?

A
  • myopathy: myalgia, myositis, rhabdomyolysis
  • liver impairment (check LFTs 3m and 12m)
  • increase risk intracerebral haemorrhage
419
Q

Statin contraindications

A
  • pregnancy
  • macrolides (erythromycin, clarithromycin)
420
Q

When should statins be taken?

A

At night- majority of cholestrol synthesis takes place here.

421
Q

Causes of hypoglycaemia

A
  • insulinoma
  • self administration fo insulin
  • liver failure
  • Addison’s
  • alcohol
    -nesidioblastosis (beta cell hyperplasia)
422
Q

What is insulinoma?

A

Increased ratio of proinsulin to insulin

423
Q

How does alcohol cause hypoglycaemia?

A

Causes XS insulin secretion.
Affects pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion.

424
Q

Hormonal response to hypoglycaemia?

A

decrease insulin secretion, increase glucagon secretion. GH and cortisol released but later.

425
Q

Sympathoadrenal response to hypoglycaemia?

A

increased catecholamine-mediated (adrenergic) and acetylcholine-mediated (cholinergic) neurotransmission in the peripheral autonomic nervous system and CNS

426
Q

Blood glucose conc <3.3mmol/L cause what?

A

Autonomic symptoms due to release of glucagon and adrenaline

427
Q

Blood glucose conc <2.8 cause what?

A

neuroglycopenic symptoms due to inadequare glucose supply to the brain

428
Q

CP of pt with blood glucose <3.3?

A

sweating, shaking, hunger, anxiety, nausea

429
Q

CP of pt with blood glucose <2.8?

A

weakness, vision changes, confusion, dizziness

430
Q

CP of pt with severe hypoglycaemia?

A

Convulsion, coma

431
Q

Mx of hypoglycaemia in community?

A
  • oral glucose 10-20g in liquid, gel or tablet form
  • or quick acting carb eg. GlucoGel or Dextrogel
  • Hypokit may be prescribed (glucagon for IM or SC injection at home)
432
Q

Mx of hypoglycaemia in hospital?

A
  • if pt is alert, then quick acting carb
  • unconcious: SC or IM glucagon or IV 20% glucose solution
433
Q

Types of bariatric surgery?

A
  • Primarily restrictive operations
  • Primary malabsorptive operations
  • Mixed operations
434
Q

Bariatric surgery: types of restrictive operations?

A
  • laparoscopic-adjustable gastric banding (LAGB): fewest Cx but less weight loss
  • Sleeve gastrectomy (stomach reduced to 15% of orginial)
  • Intragastric balloon (max 6m)
435
Q

Bariatric surgery: example of malabsorptive operation?

A

biliopancreatic diversion with duodenal switch (if BMI >60)

436
Q

Bariatric surgery: example of mixed operations (restrictive and malabsorptive)?

A

Roux-en-Y gastric bypass surgery

437
Q

First line bariatric surgery in pts with BMI 30-39kg/m2?

A

laparoscopic-adjustable gastric banding (LAGB)

438
Q

Underweight BMI

439
Q

Normal BMI

440
Q

Overweight BMI

441
Q

Obese class 1, 2 & 3 BMI

A

1= 30-35
2= 35-40
3= >40

442
Q

Medical Mx for obesity

A

Orlistat or liraglutide

443
Q

What is the mechanism of action of Orlistat?

A

Pancreatic lipase inhibitor

444
Q

Criteria for using orlistat for obesity?

A
  • BMI 30+ or 25+ with RFs
  • continued weight loss eg. 5% at 3m
  • <1yr use
445
Q

What is Liraglutide?

A

Glucagon-like-peptide (GLP-1) mimetic used for weight loss and DMT2 Mx. Once daily SC.

446
Q

Criteria for using Lireaglutide for obesity?

A

BMI 35+
or prediabetic hyperglycameia (HbA1c 42-47)

447
Q

Pituitary adenoma?

A

Benign tumour of pituitary gland. Common but mainly never found (asymptomatic) or incidental finding).

448
Q

How are pituitary adenomas classified?

A

Size and hormonal status

449
Q

Microadenoma size?

450
Q

Macroadenoma size?

451
Q

Secretory/functioning adenoma?

A

Produces an XS of a particular hormone

452
Q

Non-secretory/functioning adenoma?

A

Does not produce hormone to XS

453
Q

Most common type of pituitary adenoma?

A

Prolactinoma.
Then non-secreting adenomas, then GH-secreting and ACTH-secreting adenomas

454
Q

How do pituitary adenomas typically cause symptoms?

A

XS hormone, depletion of a hormone, stretching of the dura within/around pituitary fossa (eg. headaches) or compression of the optic chiasm.

455
Q

Examples of pituitary adenoma causing XS hormone?

A
  • Cushing’s disease: XS ACTH
  • Acromegaly: XS GH
  • Amenorrhoea/galactorrhoea: XS prolactin
456
Q

Example of pituitary adenoma causing depletion of a hormone?

A

due to compression of normal pituitary gland.
Eg. non-functioning tumours: hypopituitarism

457
Q

What CP does a pituitary adenoma compressing the optic chiasm cause?

A

Bitemporal hemianopia due to crossing nasal fibres

458
Q

What is a pituitary incidentaloma?

A

When they are incidental finding on neuroimaging eg. microadenoma.

459
Q

Pituitary adenoma Ix?

A
  • pituitary blood profile (GH, prolactin, ACTH, FSH, LSH, TFTs)
  • visual field testing
  • MRI brain with contrast
460
Q

Pituitary adenoma differential diagnoses?

A

pituitary hyperplasia
craniopharyngioma
meningioma
brain metastases
lymphoma
hypophysitis
vascular malformation (e.g. aneurysm)

461
Q

First line Mx for non-functioning adenomas?

A

transsphenoidal surgery due to their compressive symptoms

462
Q

Primary Mx for most pituitary adenomas?

A
  • transsphenoidal surgery
463
Q

If medical therpy is used for pituitary adenoma Mx, what would be used for prolactinomas? GH-secreting adenomas? ACTH secreting adenomas?

A
  • P= dopamine agonists eg. cabergoline
  • GH= somatostatin analogues eg. octreotide or GH-recept antag eg. pegvisomant
    -ACTH= cortisol synthesis inh eg. ketoconaxole and neuromodulators eg. pasireotide
464
Q

When is radiotherapy indicated for pituitary adenomas?

A

For residual or recurrent tumours post-surgery

465
Q

Thyroid eye disease?

A

Affects 25-50% pts with Graves. Autoimmune response causes orbital inflam causing collagen and glycosaminoglycan deposition in muscles.

466
Q

RFs for thyroid eye disease?

A

Smoking, radioiodine treatment

467
Q

Thyroid eye disease CP

A

conjunctival oedema, optic disc swelling, inability to close eyelids- dry eyes- risk of exposure keratopathy.

468
Q

Mx of thyroid eye disease?

A

smoking cessation, topical lubricants to prevent corneal inflamm caused by exposure, steroids, radiotherapy, surgery

469
Q

Cx of thyroid eye?

A

Exposure keratopathy, optic neuropathy, strabismus and diplopia

470
Q

Primary aim of investigating thyroid nodules?

A

To exclude thyroid cancer (5% of nodules)

471
Q

Thyroid nodules Ix?

A

Ultrasonography

472
Q

Benign and malignant causes of thyroid nodules?

A

B= mutlinodular goitre, thyroid adenoma, Hashimotos, cysts.

M= papillary carcinoma, lymphoma

473
Q

Toxic multinodular goitre?

A

thyroid gland containing a number of autonomously functioning thyroid nodules resulting in hyperthyroidism. Nuclear scintigraphy reveals patchy uptake.

474
Q

Mx for toxic multinodular goitre?

A

Radioiodine therapy

475
Q

Phaeochromocytoma?

A

tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline).

About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

476
Q

Phaeochromocytoma basics?

A

bilateral in 10%

malignant in 10%

extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

477
Q

Phaeochromocytoma features?

A

typically episodic (relate to periods when tumour is secreting adrenaline)

HTN (may be sustained)
headaches

palpitations

sweating

anxiety

478
Q

Phaeochromocytoma Ix?

A

24 hr urinary collection of metanephrines

479
Q

Phaeochromocytoma Mx?

A

Surgery is the definitive management.

The patient must first however be stabilized with medical management:
- alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

480
Q

Phaeochromocytoma pathophysiology?

A

Adrenaline is produced by the chromaffin cells in the medulla (middle part) of the adrenal glands. Adrenaline is a catecholamine hormone that stimulates the sympathetic nervous system and is responsible for the “fight or flight” response.

A phaeochromocytoma is a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline. In patients with a phaeochromocytoma, the adrenaline tends to be secreted in bursts, giving intermittent symptoms.

481
Q

How is cortisol produced?

A

CRH produced by hypothalamus -> stimulates anterior pituitary to produce ACTH -> acts on adrenals -> cortisol produced by zona fasiculata layer in adrenal cortex

482
Q

When is cortisol usually secreted?

A

throughout the day, peaks at 6am

  • also in response to stress= fight or flight; hypoglycaemia; infections; caffeine, sleep deprivation
483
Q

Main function of cortisol

A

steroid hormone (glucocorticoid) that helps regulate metabolic and immune pathways

484
Q

How does cortisol help regulate the immune response eg. as it is released in response to infection?

A

promotes overall anti inflamm state by inhibiting: prostaglandins, leukotrienes and interleukin-2 production by WBCs (P & L products of inflam)

485
Q

How does cortisol help with hypoglycaemia?

A

Promotes gluconeogenesis in liver= this is production of new glucose. Also increases insulin resistance in tissues so insulin less effective at moving glucose into cells so blood glucose increases.

Also stimulates proteolysis: breakdown of proteins into amino acids in muscles, these are substrates for gluconeogenesis

486
Q

How does cortisol play a role in maintaining BP?

A

up-regulates alpha1 adrenergic receptors in blood vessels which causes vasoconstriction

487
Q

How does cortisol decrease bone formation?

A

inhibits new production by osteoblasts, suppresses Ca absorption and decreases production of type I collagen

488
Q

Functions of cortisol?

A

1) anti-inflam
2) stimulates metabolic pathways (lipolysis, gluconeogenesis and proteolysis) to maintain normal glucose concs
3) maintains BP
4) improves brain performance
5) decreases bone formation

489
Q

What stimulates ACTH secretion?

A
  • throughout day, peaks at 6am
  • stress= infection, hypoglycaemia, low BP

(as acts on adrenals to produce glucocorticoids eg. cortisol)

490
Q

Glucocorticocoid example?

491
Q

ACTH functions?

A
  • act on adrenals to secrete glucocorticoids eg. cortisol
  • acts on melanocortin receptor 1 (responsible for skin pigmentation) so if ACTH XS get bronzing of skin
492
Q

Diuresis?

A

XS urine production

493
Q

2 actions of ADH?

A

water retention and vasocontriction
- these increase BP

494
Q

XS sweating eg. on hot day leads to what?

A

dehydration and so increased blood osmolarity (same amount of solutes but less water)

495
Q

What detect changes in osmolarity?

A

osmoreceptors in supraoptic nuclei of hypothalamus

496
Q

What is the thirst response that happens when blood osmolarity increases (eg. dehydrated)?

A

1) osmoreceptors in supraoptic nuclei of hypothalamus detect the change
2) water moves out of aquaporin 4 channels in cells into the blood by osmosis
3) osmolarity past 290-300 causes neurons to fire action potentials that signal hypothalamus to trigger the thirst response

497
Q

Role of ADH when blood osmolarity increases?

A

1) ADH released by posterior pituitary
2) act on vasopressin receptor 2 in kidneys (distal convoluted tubule and collecting ducts of the nephrons)
3) when ADH binds to receptors, a G protein inside the cell gets activated that then signals adenylyl cyclase to convert ATP to cAMP
4) increased cAMP signals cells to produce more aquaporin 2 (water channels)= allows water to travel out lumen of tubule, into cells lining nephron then into blood
5) dilutes blood (like drinking water)

498
Q

How does ADH respond to low blood volume?

A

1) low blood volume = low BP
2) low BP detected by baroreceptors near carotid artery in neck and arch of aorta
3) signals ADH secretion
4) causes vasocontriction and water retention

2) also the renin angiotensin system

499
Q

Role of renin when there is low blood volume?

A

2) baroreceptors in afferent artery of kidneys (juxtaglomerular cells)
3) cause kidneys to secrete enzyme renin
3) renin converts angiotensinogen in the liver to angiotensin I
4) angiotensin converting enzyme (ACE) in the lungs then concerts angiotensin I to angiotensin II
5) angiotensin II stimulates more ADH production in hypothalamus
6) ADH causes vasocontriction and water retention

500
Q

How does ADH (vasopressin) maintain blood pressure and plasma osmolarity?

A

1) acts on vasopressin receptor 2 in distal convoluted tubule and collecting ducts of the nephron to increase water reabsorption through aquaporins= decreases blood osmolarity

2) acts on vasopressin receptor 2 in walls of blood vessels to cause vasoconstriction and increase in peripheral resistance= increase BP
(baroreceptors and release of renin)

501
Q

What happens when blood pressure decreases and renin-angiotensin-aldosterone system is activated?

A

1) baroreceptors in juxtaglomerular cells in afferent arteriole (next to glomerulus in kidney) detect this

2) causes enzyme renin to be released by kidney

3) renin converts angiotensinogen (in liver) to angiotensin I

4) angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II

5) angiotensin II causes vasocontriction of blood vessels, an increase in ADH (P.Pituitary) and the production of aldosterone in the kidneys

6) ADH increases thirst and water reabsoption as well as vasoconstriction and increasing peripheral resistance

7) late response of RAAS: aldosterone helps regulate sodium balance by acting on cells that line distal tubules and collecting ducts

8) aldosterone gets into these cells and bind its receptor which increases the expression (levels) of sodium/potassium ion pump

9) this pump pushes sodium
and water into blood and potassium into cells

502
Q

Electrolyte disturbance in pts with intense activation of RAAS?

A

hypokalaemia (sodium potassium pump activated by aldosterone pulls K into cells and pushes Na and H20 into blood)

503
Q

Decrease in BP can be detected by what?

A

baroreceptors of the carotid sinus or aortic arch; juxtaglomerular cells; or macula densa cells sensing less Na and Cl flowing through the tubules

causes kidneys to secrete renin

504
Q

Role of aldosterone?

A

sodium and water retention

and increased elimination of K

505
Q

What when baroreceptors in juxtaglomerular cells are stretched (due to increase BP) vs when collapsed (from low BP)?

A

stretched= inhibit renin release

collapsed= stimulate renin release

506
Q

How do mechanoreceptors (baroreceptors) in carotid sinus and aortic arch measure BP and help regulate BP?

A

stretched= sympathetic NS will be downregulated

collapsed= SNS will be activated

sympathetic nerves stimulate b1 adrenergic receptors on JG cells to stimulate renin

507
Q

How to macula densa cells help regulate BP?

A

they are chemoreceptors that sense when GFR increases or decreases based on the quantity of Na and Cl ions flowing through tubule

1) BP rises= renal blood flow and so GFR increases
2) so means more fluid reaching macula densa
3) if decreased fluid then the MD cells send signal to JG cells in afferent arteriole (signal is prostaglandins) to stimulate renin

so NSAIDs can block prostaglandin signal and impair response of kidney to reduce BP

508
Q

Role of angiotensin II?

A

1) vasoconstriction of blood vessels
2) production of aldosterone in kindey
3) release of ADH by posterior pituitary
4) thirst response= signals tp hypothalamus to increase thirst

509
Q

How does aldosterone increase BP?

A

increases water & sodium retention, and increases the elimination of potassium

  • acts on cells lining the distal tubules and collecting ducts, causes increased expression (levels) of Na/K ion pump which pushes sodium and water into blood and pulls K into cells
510
Q

Summary of how ADH responds to low BP?

A

1) water retention= acts on vasopressin receptor 2 in distal convoluted tubule and collecting ducts of nephron to increase water reabsorption through aquaporins= decreasing blood osmolality
2) vasocontriction and increase in peripheral resistance

511
Q

Thirst response?

A

angiotensin II signals to hypothalamus or
osmoreceptors detect change (increase osmolality) in supraoptic nuclei of hypothalamus, causes neurons to fire action potentials that signal to hypothalamus to increase thirst

512
Q

3 things that detect low BP?

A

1) baroreceptors in juxtaglomerular cells that stimulate renin release

2) baroreceptors in carotid sinus & aortic arch that will collapse= stimulates sympathetic NS= sympathetic nerves stimulate b1 adrenergic receptors on JG cells to stimulate renin production

3) macula densa cells (chemoreceptors) sense decreased GFR (& so decreased fluid) so send signal to JG cells to stimulate renin release (signal is prostaglandins)

513
Q

Why can NSAIDs impair kidneys response to low BP?

A

block prostaglandin signals from macula densa cells (detect low BP) to JG cells that stimulate release of renin

514
Q

What hormones does the hypothalamus secrete?

A

Act on anterior pituitary:
- Stimulatory hypothalamic hormones= TRH, CRH, GnRH, GHRH
- Inhibitory hormones= GHIH (somatostatin) and prolactin inhibiting factor (dopamine)

Act on posterior pituitary:
- ADH (vasopressin) and oxytocin

515
Q

Anterior vs posterior pituitary?

A

Anterior= hypothalamic hormones act on and stimulates anterior pituitary to produce and release its own hormones

Posterior= stores hormones in Herring bodies (ADH and oxytocin produced by hypothalamus)

516
Q

What in the hypothalamus produces ADH and oxytocin that is stored in posterior pituitary?

A

paraventricular and supraoptic nuclei of hypothalamus

517
Q

TRH?

A

Thyrotropin releasing hormone

518
Q

Thyrotropin releasing hormone?

A

hypothalamus produces TRH -> acts on anterior pituitary and stimulates it to make thryoid stimulating hormone (TSH) -> acts on thyroid -> increase in thyroid hormone production

519
Q

CRH?

A

corticotropin releasing hormone

520
Q

Corticotropin releasing hormone?

A

hypothalamus produces CRH -> acts on AP -> ACTH -> acts on adrenals -> cortisol

521
Q

Growth hormone releasing hormone?

A

hypothalamus makes GHRH -> AP -> GH production -> acts on long bones and other tissues

522
Q

Increased levels of plasma cortisol inhibit…

A

ACTH production in anterior pituitary through negative feedback to decrease cortisol production

523
Q

GHRH?

A

growth hormone releasing hormone

524
Q

GnRH?

A

gonadotropin releasing hormone

525
Q

Gonadotropin releasing hormone?

A

hypothalamus makes GnRH
-> AP -> gonadotrophins (FSH and LH) -> acts on gonads:
1) regulate production and maturation of gametes (testes= sperm, ovaries= oocytes)
2) stimulates production of sex hormones= testosterone, oestrogen, progesterone

  • females= oestrogen spikes before ovulation, makes AP more sensitive to GnRH so surge of FSH and LH to stimulate ovulation (+ve feedback)
526
Q

GHIH?

A

growth hormone inhibiting hormone (somatostatin)

527
Q

Growth hormone inhibiting hormone (somatostatin)?

A

GHIH also made in GI tract (and hypothalamus), tells AP to produce less GH

528
Q

Prolactin inhibiting factor (dopamine)?

A

prolactin inhibiting factor (dopamine) -> AP -> inhibits prolactin production

during breastfeeding= suckling signals to hypothalamus -> haults production of PI factor so prolactin is produced

529
Q

ADH (vasopressin) stands for?

A

anti diuretic hormone

530
Q

ADH (vasopressin) use?

A

released by posterior pituitary when blood osmolarity increased or blood volume decreased -> vasoconstriction of blood vessels and water retention (& Na) from urine -> decreases osmolarity and increases BP

531
Q

Oxytocin?

A

released by posterior pituitary during motherhood / small amounts following social interaction (hug, orgasm)

  • dilates cervix, stimulates uterine contractions during childbirth, causes breast muscles to contract to eject milk
532
Q

Pineal gland?

A

behind hypothalamus and pituitary

pinealocytes make and release melatonin (mostly at night)

533
Q

Melatonin?

A

regulates circadian rhythm (tells us when to sleep and wake)

534
Q

3 things that make up the thyroid gland that secrete hormones?

A

1) follicular cells= T3 and T4 (most of T4 converted to T3 as T3 increases basal metabolism rate)

2) parafollicular cells= calcitonin

3) parathyroid gland (4 total, 2 each lobe)= parathyroid hormone

535
Q

Role of calcitonin and PTH (secreted in thyroid)?

A

involved in calcium, bone and phosphate metabolism

levels regulated by calcium blood levels

536
Q

Structure of adrenal glands and what hormones they secrete?

A

Medulla (centre)= adrenaline and noradrenaline

Cortex (outer) 3 layers:
1) zona Glomerulosa (outer)= mineralcorticoids eg. aldosterone
2) zona Fasiculata= glucocorticoids eg. cortisol
3) zona Reticularis (inner)= sex hormone precursors

537
Q

Main hormones secreted in adrenals?

A

1) aldosterone secreted when BP low or increased blood K -> water and Na retention and increased elimination of K

2) cortisol secreted during fight or flight alongside adrenaline and noradrenaline by medulla

538
Q

2 parts of the pancreas?

A

Exocrine part= secretes digestive enzymes into duodenum

Endocrine part= Beta cells (secrete insulin) and Alpha cells (glucagon)

539
Q

Pancreas response to hyperglycaemia?

A

B cells secrete insulin -> binds to receptors on all cells in body so they take in glucose for energy -> decreases blood glucose after eating

540
Q

Pancreas response to hypoglycaemia?

A

Alpha cells secrete glucagon -> binds to receptors on liver cells -> releases enzymes to break down glycogen (bodys glucose store) in liver -> released as glucose into blood to increase blood glucose

FINALS (37 decks)

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