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Phase 2a > endocrine > Flashcards

endocrine Flashcards

1
Q

What 3 conditions can pituitary adenomas cause?

A

Cushings
Acromegaly
Prolactinoma

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2
Q

Aetiology of acromegaly

A

Pituitary somatotroph adenoma in about 95% to 99% of cases
Also but rare: increased GHRH from hypothalamic tumours, ectopic GHRH and GH from nonendocrine tumours

all causes lead to increased and unregulated GH

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3
Q

Risk factors for acromegaly

A

Prior history of pituitary tumour

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4
Q

What does IGF-1 do?

A
  • Promotes cellular metabolism
  • Prevents cell death
  • Increases rate of cell division and differentiation
  • Stimulates AA uptake into muscle cell (helps with growth)
  • Stimulates growth in length in long bones (stimulates osteoblasts and chondrocytes activity)
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5
Q

Direct effects of GH

A
  • Tissue growth due to stimulation of metabolism
  • Lipolysis
  • Promotes gluconeogenesis in liver and glycogen breakdown
  • Increases insulin resistance in tissues, leading to increase in blood glucose levels (diabetogenic)
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6
Q

Indirect effects of GH

A

Stimulates steady release of Insulin-like growth factor 1 in liver, skeletal muscles, bones and kidneys

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7
Q

How is GH released?

A

Hypothalamus secretes GHRH
GHRH binds to receptor on somatotroph on anterior pituitary
Somatotroph releases GH

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8
Q

When are GH and GHRH normally released?

A

GHRH is normally released in pulsatile manner across day and peaks after you fall asleep
GH released in response to stimuli via GHRH, e.g. hypoglycaemia, adrenaline, puberty

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9
Q

What are the key features of acromegaly?

A

Acral enlargement (hands, feet, legs, arms etc..)
Morphological facial changes and coarse features

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10
Q

Symptoms of acromegaly caused by excess GH and IGF-1

A
  • Morphological changes
  • Acral enlargement
  • Respiratory: sleep apnoea, airway obstruction
  • Hypertension, arrhythmias, congestive heart failure
  • Metabolic: impaired glucose tolerance, DM
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11
Q

Symptoms of acromegaly caused by prolactin co-secretion

A
  • Decreased libido
  • Infertility
  • Amenorrhoea, oligomenorrhoea
  • Galactorrhoea
  • Erectile dysfunction
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12
Q

Symptoms of acromegaly from tumour effects

A
  • Headaches
  • Visual field defects
  • Cranial nerve palsies
  • Pituitary stalk compression: signs and symptoms of hypopituitarism
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13
Q

Differential diagnoses for acromegaly

A

acromegaloidism
pseudo-acromegaly

both have normal IGF-1s

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14
Q

How would you treat acromegaly?

A

Trans-sphenoidal surgery to remove pituitary adenoma
Somatostatin analogue (octreotide) second line if surgery not successful

third line GH receptor antagonist

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15
Q

How would you monitor acromegaly?

A

Lifelong monitoring of GH and IGF-1
Monitoring of complications

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16
Q

Complications of acromegaly

A

Sleep apnoea and airway obstruction
Hypertension and heart disease
Impaired glucose tolerance and diabetes mellitus
Arthritis
Carpal tunnel

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17
Q

First line investigations for acromegaly

A

Serum IGF-1: should be raised
OGTT: GH not suppressed in acromegaly.

(testing GH unreliable as fluctuates across day)

Can also do an MRI for pituitary adenoma

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18
Q

What is the basic pathophysiology of acromegaly?

A

usually caused by over-secretion of growth hormone from a pituitary adenoma
excess GH acts on liver to produce IGF-1

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19
Q

What does insidious onset mean? + example

A

any disease that comes on slowly and does not have obvious symptoms at first

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20
Q

When is acromegaly usually diagnosed?

A

Mean age 44
Insidious onset means 4-7 years after initial symptoms

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21
Q

What is the definition of Cushing syndrome?

A

clinical manifestation of pathological hypercortisolism from any cause

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22
Q

What is Cushing’s disease?

A

hypercortisolism caused by an ACTH-secreting pituitary adenoma

most common cause of endogenous cushing syndrome

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23
Q

What is the epidemiology of cushing syndrome?

A

2-3 cases per mil
CS 3x more common in women than men
CD 3:1 to 5:1 female-male predominance
Can occur in any age but most common between 20-50

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24
Q

What is the aetiology of cushing syndrome?

A

Exogenous corticosteroid exposure: most common cause of CS
ACTH secreting pituitary tumours (cushing’s disease): cause of 70-80% of endogenous CS
Adrenal adenomas with unregulated secretion of cortisol: cause 10% of endogenous
Autonomous adrenal cortisol overproduction
Ectopic ACTH-secreting tumours (rare)

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25
Q

What is ACTH dependent Cushing syndrome?

A

conditions that have high or inappropriately normal ACTH levels stimulating adrenal cortisol overproduction, e.g. pituitary adenomas and ectopic tumours

HIGH ACTH

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26
Q

What is ACTH independent Cushing syndrome?

A

excessive cortisol secretion by the adrenal glands despite a suppressed ACTH level, e.g. adrenal adenomas and carcinomas

LOW ACTH

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27
Q

What are the risk factors for Cushing syndrome?

A

exogenous corticosteroid use
pituitary adenoma
adrenal adenoma
adrenal carcinoma

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28
Q

How does the HPA axis work?

A

hypothalamus makes CRH
CRH stimulates pituitary to make ACTH
ACTH stimulates zona fasciculata of adrenal cortex to secrete cortisol

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29
Q

What are the effects of cortisol?

A
  • Increases plasma glucose levels (breaks down proteins into AAs to be taken to the liver, also stimulates gluconeogenesis in liver)
  • Stimulate lipolysis in adipose tissue
  • Immunosuppression
  • Anti-inflammation
  • Protein and fat metabolism
  • Bone metabolism – acts on trabecular bone to limit osteoblast activity to make new bone
  • Regulate calcium absorption from GI tract
  • Regulate behaviour, mood, and cognition through activity on the CNS
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30
Q

What is the negative feedback of cortisol?

A

Inhibits production of CRH
Reduces sensitivity of Ant Pit to CRH, which reduces ACTH release

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31
Q

What can endogenous Cushing syndrome be divided into?

A

ACTH dependent: high ACTH levels stimulate the adrenal glands to produce glucocorticoids, normally from pituitary adenomas

ACTH independent: excess glucocorticoid secretion from the adrenal glands occurs despite low ACTH levels, normally from adrenal adenoma

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32
Q

What are some clinical findings of cushing syndrome?

A

Progressive proximal muscle weakness
Bruising without obvious trauma
Facial plethora or rounding
Violaceous striae
Supraclavicular fat pad
Dorsocervical fat pad

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33
Q

What are the symptoms of cushing syndrome?

A

Weakness
Facial fullness
Weight gain
Low mood
Decreased libido
Polydipsia, Polyuria
Increased frequency of infection

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34
Q

What are the first line investigations for cushing syndrome?

and what results would you expect for CS

A
  • 1 mg overnight dexamethasone suppression test: positive test is morning cortisol >50 nanomol/L (>1.8 micrograms/dL)
  • 24-hour urinary free cortisol (not in renal failure): >50 micrograms/24 hour
  • late-night salivary cortisol: elevated
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35
Q

What are the differential diagnoses for Cushing syndrome and what do they not have?

A

Obesity and metabolic syndrome

Neither have: facial plethora, unexplained bruising, proximal muscle weakness, violaceous striae, supraclavicular fullness, and osteoporotic fractures

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36
Q

How would you manage Cushing’s disease?

A

transsphenoidal resection of the causative pituitary adenoma

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37
Q

How would you manage exogenous cushing syndrome?

A

Glucocorticoid treatment
Reduce meds dose where possible

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38
Q

What are some complications of cushing syndrome?

A

Hypertension
Diabetes
Obesity
Metabolic syndrome
Osteoporosis

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39
Q

How would you monitor cushing syndrome?

A

Standard testing of complications
Screening for remission (e.g. late night salivary cortisol)

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40
Q

What does basal insulin do in the treatment of diabetes?

A

keep blood glucose levels at consistent levels during periods of fasting

long acting insulin

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41
Q

What is bolus insulin in the treatment of DM?

A

insulin that is specifically taken at meal times to keep blood glucose levels under control following a meal

short acting insulin

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42
Q

Examples of long acting basal insulin

A

insulin detemir, degludec, or glargine

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43
Q

Examples of short acting bolus insulins

A

insulin lispro, aspart, or glulisine

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44
Q

Why should patients alternate injection sites for insulin in DM?

A

Injecting into the same spot can cause lipodystrophy, where the subcutaneous fat hardens
Areas of lipodystrophy do not absorb insulin properly from further injections.
Patients should cycle their injection sites.

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45
Q

What plasma glucose should adults with T1DM aim for?

A
  • On waking: 5-7 mmol/L
  • Before meals and fasting: 4-7 mmol/L
  • After meals: 5-9 mmol/L
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46
Q

What plasma glucose should children and u18s with T1DM aim for?

A
  • On waking and before meals: 4-7 mmol/L
  • After meals: 5-9 mmol/L
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47
Q

How regularly would you measure HbA1c in children and adults?

A

Children: every 3 months
Adults: every 3-6 months

aim for 48mmol/mol or lower

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48
Q

What are the short term complications of T1DM?

A

Hypo
DKA

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49
Q

What are some long term complications of T1DM?

A

Cardiovascular disease
Diabetic retinopathy
Diabetic nephropathy
Diabetic foot
Leg ulcers
Risk of depression and EDs

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50
Q

What are some risk factors for T1DM?

A
  • genetic predisposition, especially variation in HLA region involved in immune response
  • having close relative with T1DM
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51
Q

Definition of T1DM

words not values

A

metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency

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52
Q

Definition of T1DM

investigations

A

Symptoms and random plasma glucose > 11.1 mmol/l
Fasting plasma glucose > 7.0 mmol/l
HbA1c > 48 mmol/mol
No symptoms - OGTT (75g glucose) fasting > 7 or 2h value > 11.1 mmol/l

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53
Q

What is the aetiology of T1DM?

A

Combination of genetic predisposition and an autoimmune process that results in gradual destruction of the beta cells of the pancreas, leading to absolute insulin deficiency

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54
Q

Pathophysiology of T1DM

A

autoimmune pancreatic beta-cell destruction (sub-clinical for a while)
insulin deficiency
unable to utilise glucose in peripheral muscle and adipose tissues
stimulates the secretion of counter-regulatory hormones (glucagon, adrenaline, cortisol, and GH).
promote gluconeogenesis, glycogenolysis, and ketogenesis in the liver

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55
Q

Symptoms of T1DM

A

Polydipsia and polyuria
Unintentional weight loss
Hyperglycaemia
Tiredness
May present with DKA

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56
Q

First line investigations for T1DM

in children, adults use clinical diagnosis

A

random plasma glucose: ≥11.1 mmol/L
fasting plasma glucose: ≥7 mmol/L
2-hour plasma glucose: ≥11.1 mmol/L
HbA1c: ≥48 mmol/mol

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57
Q

Differentials of T1DM

A

Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Latent autoimmune diabetes in adults (LADA)
Type 2 diabetes

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58
Q

What is primary hyperthyroidism?

A

thyroid is behaving abnormally and producing excessive thyroid hormone

pathology of thyroid

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59
Q

What is secondary hyperthyroidism?

A

pituitary gland produces too much TSH, stimulating the thyroid gland to produce excessive thyroid hormones

pathology of hypothalamus or pituitary

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60
Q

What is hyperthyroidism?

A

over-production of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), by the thyroid gland

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61
Q

What is thyrotoxicosis?

A

effects of an abnormal and excessive quantity of thyroid hormones in the body

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62
Q

What is the most common cause of hyperthyroidism?

A

Graves

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63
Q

What are the symptoms 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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64
Q

Who should be given levothyroxine therapy?

A

all symptomatic patients with overt primary hypothyroidism

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65
Q

Symptoms of myxoedema coma

life-threatening state where severe hypothyroidism worsens

A

hypothermia
change in mental status
hypotension
bradycardia
hypoventilation
diffuse non-pitting oedema

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66
Q

Who does myxoedema coma normally effect and what’s the mortality rate?

A

occurs in older people and is usually precipitated by an underlying medical illness.
mortality rate: 25% to 60%

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67
Q

Definition of hypothyroidism

A

Thyroid hormones levels abnormally low
Leads to a generalised slowing of metabolic processes

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67
Q

What is myxoedema coma?

A

extreme manifestation of (usually untreated) hypothyroidism
Life-threatening complication
Even with treatment in ICU, can be fatal

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68
Q

Difference between primary and central (secondary) hypothyroidism

A

Primary: High TSH, low T3/T4, thyroid dysfunction
Secondary (central) from pituitary/ HT abnormality: underproduction of TSH

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69
Q

How common is central hypothyroidism in all hypothyroidism cases?

A

Rare, less than 1%

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70
Q

What is the epidemiology of hypothyroidism?

A

Higher in women and increases with age
Prevalence of 0.2% to 5.3% in gen pop

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71
Q

What is the most common cause of primary hypothyroidism globally?

A

Iodine deficiency

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72
Q

What is the most common cause of hypothyroidism in iodine sufficent areas?

A

Hashimoto’s

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73
Q

Aetiology of primary hypothyroidism

A

Iodine deficiency
Hashimoto’s
Less common: damage to thyroid gland (thyroidectomy, radiotherapy)
Medications such as: amiodarone, lithium, thionamides

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74
Q

Aetiology of central (secondary) hypothyroidism

A

Pituitary disease: most commonly adenoma
Dysfunction of hypothalamus

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75
Q

Risk factors for primary hypothyroidism

A

iodine deficiency
female
ages 30-50
family history of autoimmune thyroiditis
autoimmune disorders
treatment for thyroid disease, e.g. graves
post-partum thyroiditis
Turner’s and Down’s syndromes (as autoimmune thyroiditis is more common)
radiotherapy to head and neck
amiodarone or lithium use

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76
Q

What are the risk factors for central hypothyroidism?

A

presence of pituitary mass lesions
multiple endocrine neoplasia (MEN) type I
head and neck irradiation
traumatic brain injury (TBI)

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77
Q

What is the normal axis for thyroid hormones?

A
  • Hypothalamus releases TRH
  • Anterior pituitary releases TSH
  • Thyroid releases T3 and T4
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78
Q

What does T3 do?

A
  • speeds up cell basal metabolic rate
  • Increases cardiac output
  • Increase bone reabsorption
  • Activates symp NS
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79
Q

What is lacking in central hypothyroidism?

A

Inadequate levels of TSH so thyroid is understimulated

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80
Q

What are the key presentations of hypothyroidism?

A

presence of risk factors
weakness
fatigue
cold intolerance

Often insidious and non-specific symptoms

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81
Q

Signs of hypothyroidism

A

Dry coarse skin, hair loss and cold peripheries.
Puffy face, hands and feet (myxoedema).
Bradycardia.
Delayed tendon reflex relaxation.
Carpal tunnel syndrome.
Serous cavity effusions - eg, pericarditis or pleural effusions

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82
Q

Symptoms of hypothyroidism

A
  • Fatigue
  • constipation
  • weight gain
  • depression
  • menstrual irregularity
  • dry or coarse skin
  • deeper, hoarse voice
  • bradycardia and hypertension
  • delayed relaxation of tendon reflexes
  • hair loss
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83
Q

What are the first line investigations for hypothryoidism?

A

TFTs:
high TSH (primary), low TSH (secondary/tertiary), low T4 and T3

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84
Q

Apart from TFTs, what investigations should you consider for hypothyroidism?

A

Free serum T4: low
FBC
Fasting glucose
Serum cholesterol

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85
Q

Differentials for primary hypothyroidism

A

Central or secondary hypothyroidism
Depression
Alzheimer’s dementia
Anaemia

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86
Q

Differentials for central hypothyroidism

A

Fibromyalgia
EMS
Primary hypothyroidism
Iodine deficiency

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87
Q

How would you treat hypothyroidism?

A

Levothyroxine

look at pituitary pathology in central

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88
Q

How would you monitor hypothyroidism?

A

When first starting levothyroxine, measure TSH 4-12 weeks later
Then yearly
If symptomatic, consider measuring T4

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89
Q

Complications of hypothyroidism

A

Angina: if high initial dose of levothyroxine in patients with coronary artery disease
Osteoporosis
Myxoedema coma
Pregnancy complications
Atrial fibrillation
Iatrogenic thyrotoxicosis from levothyroxine
Adrenal crisis in patients on levothyroxine with untreated adrenal insufficiency

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90
Q

What is a prolactinoma?

A

benign, prolactin-producing tumour of the pituitary gland

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91
Q

What is the epidemiology of prolactinomas?

A

50% of pituitary adenomas
more frequent in women between 20 and 50 years old (esp during childbearing years)

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92
Q

Aetiology of prolactinomas

A

anterior pituitary lactotroph tumours
majority occur sporadically

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93
Q

What are the risk factors for prolactinomas?

A

Female, age 20-50
Weaker:
- MEN-1 (genetic predis)
- If in men, age 30-60
- Familial isolated pituitary adenoma

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94
Q

Difference between micro and macro prolactinomas

A

Microprolactinomas – smaller than 10 mm
Macroprolactinomas – larger than 10 mm

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95
Q

What can hypersecretion of prolactin cause?

A

secondary hypogonadism via its inhibitory effects on GNRH

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96
Q

How do prolactinomas cause bitemporal hemianopia?

A

Macroprolactinomas can compress meninges and optic nerves at optic chiasm

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97
Q

What are the key presentations of prolactinomas?

A
  • amenorrhoea or oligomenorrhoea
  • infertility
  • galactorrhoea
  • loss of sexual desire (libido)
  • erectile dysfunction
  • visual deterioration (e.g., temporal hemianopia)
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98
Q

What are the first line investigations for prolactinomas?

A

serum prolactin: elevated, greater than 5000 mIU/L (250 micrograms/L)
pituitary MRI
computerised visual-field examination: looking for hemianopia

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99
Q

Differentials for prolactinomas

A

Non-functioning pituitary macroadenomas
Drug-induced hyperprolactinaemia
Primary hypothyroidism
Renal insufficiency
Pregnancy
PCOS

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100
Q

How would you treat a prolactinoma?

A

Primary treatment is dopamine agonists to inhibit prolactin and reduce lactotroph volume.
Secondary treatment for macro is transsphenoidal surgery

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101
Q

What is the goal of treatment for prolactinomas?

A

suppress and normalise prolactin levels, and reduce tumour size

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102
Q

How would you monitor a prolactinoma?

A

Monitor serum prolactin
Annual MRI (more regular in macro or increasing serum prolactin levels)
Regular visual field exams in patients with visual disturbance
Pituitary axes tested every 3-6months (e.g. TFTs) in macro

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103
Q

What are some complications of prolactinomas?

A

Visual field disturbance
Anterior pituitary failure and/or diabetes insipidus post transsphenoidal surgery
Hypopituitarism after radiotherapy (therefore RT not used)

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104
Q

What is the definition of hypercalcaemia?

A

a serum calcium concentration of 2.6 mmol/L or higher, on two occasions, following adjustment (correction) for the serum albumin concentration

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105
Q

Epidemiology of hypercalcaemia

A

Small % of cancer patients
Patients with hyperparathyroidism

90% of cases of hypercal caused by malignancy or primary hyperparathyroi

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106
Q

Aetiology of hypercalcaemia

A

Primary hyperparathyroidism or malignancy in 90% of cases
Also but rare
* Thiazides: increase renal absorption
* Lithium
* Hyperthyroidism
* Sarcoidosis
* Familial hypocalciuric / benign hypercalcaemia
* Immobilisation
* Milk-alkali syndrome
* Adrenal insufficiency
* Phaeochromocytoma

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107
Q

What does PTH do?

A
  • Binds to receptors on osteoblasts and release cytokines (increases mobilisation of calcium from bone)
  • Binds receptors on tubular cells on proximal tubules in kidneys
  • Binds to principal cells on distal convoluted tubule and increase calcium reabsorption
  • Helps body convert precursor to active vitamin D by activating 1 alpha hydroxylase enzyme
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108
Q

What are the symptoms of hypercalcaemia?

A

Bone pain
Polydipsia, polyuria
Confusion
Coma
Renal stones
Short QT

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109
Q

What are the key presentations of hypercalcaemia?

A

Bones: bone pain, suggesting mets in long bones
Stones: renal stones
Groans: abdo pain, constipation, nausea
Moans: psych symptoms, depression, confusion, irratability

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110
Q

What are the first line investigations for hypercalcaemia?

A

total serum calcium/ serum ionised calcium (not when testing for hyperparathyroidism) = elevated
asymptomatic, mild or moderate: arrange for serum ca again in a week

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111
Q

Gold standard investigation for hypercalcaemia

A

Serum calcium

avoid prolonger torniquet when taking bloods

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112
Q

Differentials of hypercalcaemia

A

Primary hyperparathyroidism
Multiple myeloma
Malignancy

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113
Q

How would you monitor hypercalcaemia?

A

Serum calcium levels
Estimated GFR
Creatinine
DEXA scan every 2-3 years

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114
Q

Complications of hypercalcaemia

A

Osteoporosis
Transient flu-like syndrome due to bisphosphonate treatment
Acute kidney injury (AKI)
Acute pancreatitis
Cardiac arrhythmias
Seizures
Coma

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115
Q

What is the prognosis for cancer patients with hypercalcaemia?

A

Poor as it often indicates advanced stage, e.g. 2-3 months prognosis

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116
Q

What does PTHrP do in malignancy?

A
  • stimulates osteoclastic resorption
  • inhibits osteoblast formation of bone
    (resulting in excessive calcium release from the skeleton)
  • acts in the kidney to reduce calcium clearance, further increasing calcium levels in the blood.
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117
Q

Risk factors for hypercalcaemia of malignancy

A

Multiple myeloma: via osteolytic metastases
Breast cancer: via PTHrP and osteolytic metastases
Lung cancer (squamous cell carcinoma): via PTHrP
Renal cancer: via PTHrP
Thyroid cancer (squamous cell carcinoma): via PTHrP
Lymphomas (all types): via calcitriol

Thiazides, lithium

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118
Q

Aetiology of hypercalcaemia of malignancy

A

Bone mets releasing calcium, especially myeloma
Parathyroid hormone related peptide (PTHrP)
Lymphoma: can convert inactive vitD into active (tumour activating lots of vitD)

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119
Q

What is Calcitriol (1,25-dihydroxyvitamin D)-mediated hypercalcaemia associated with?

A
  • Lymphomas (of all types)
  • Granulomatous disease (such as active sarcoidosis) or tuberculosis
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120
Q

Risk factors for hyperthyroidism

A

Family history.
High iodine intake
Smoking
Trauma to the thyroid gland (including surgery).
Toxic multinodular goitre
Childbirth
Highly active antiretroviral therapy

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121
Q

What is goitre?

A

a swelling in the neck resulting from an enlarged thyroid gland

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122
Q

What can increase thyroid hormone lead to?

metabolism

A

Increased BMR

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123
Q

Symptoms of hyperthyroidism

A

Weight loss despite hyperphagia
Anxiety and change in mental state
Weakness and fatigue
Diarrhoea
Sweating
Tremor
Heat intolerance
Menstrual disturbance
Loss of libido

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124
Q

Aetiology of hyperthyroidism

A

Graves
Thyroiditis (destruction of thyroid cells and release of hormone)
Toxic multinodular goitre
Drug induced
TSH secreting pituitary adenoma

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125
Q

Signs of hyperthyroidism

A

Palmar erythema.
Sweaty and warm palms.
Fine tremor
Lid lag
Goitre
Hair thinning

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126
Q

What tests would you run for hyperthyroidism?

A

TFTs: elevated T3/T4, suppressed TSH
After confirmed: TSH receptor antibody

consider serum free T4/3

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127
Q

How would you treat hyperthyroidism?

A

Antithyroid drugs: carbimazole or propylthiouracil (thionamides)
radio-iodine and surgical (not really used)

beta blockers for immediate treatment

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128
Q

What’s a complication of untreated/ severe hyperthyroidism?

A

Thyroid storm

sudden life-threatening flare up of symptoms

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129
Q

Differentials for hyperthyroidism

A

Phaeochromocytoma and any cause of weight loss

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130
Q

What are some precipitating factors for DKA?

A

Infection/ Physiological stress
Discontinuation of insulin (unintentional or deliberate)
Inadequate insulin
CVD, e.g. stroke or MI
Drug treatments, e.g. steroids, thiazides or SGLT2 inhibitors

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131
Q

What 3 features characterise DKA?

A

Hyperglycaemia
Ketonaemia
Acidosis

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132
Q

What are the ketone levels for ketonaemia in DKA?

A

3mmol

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133
Q

Lab results to diagnose DKA

A

blood glucose is >11.0 mmol/L
blood ketones are >3.0 mmol/L or ketonuria (2+ or more on standard urine sticks)
bicarbonate (HCO3 -) is <15.0 mmol/L, and or venous pH is <7.3

must all be present

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134
Q

What investigations would you order for DKA and what would they show?

A

venous blood gas: shows metabolic acidosis with raised anion gap
blood ketones: >3.0 mmol/L
blood glucose: >11.0 mmol/L
urea and electrolytes: hyponatraemia and hyperkalaemia are common but hypokalaemia is an indicator of severe DKA
full blood count: leukocytosis

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135
Q

What are some differentials for DKA?

A

Hyperosmolar hyperglycaemic state (HHS)
Lactic acidosis
Starvation ketosis
Alcoholic ketoacidosis

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136
Q

What would you monitor in the first 6 hours with DKA?

A
  • hourly blood glucose and hourly blood ketones.
  • Perform a venous blood gas for pH, bicarbonate, and potassium at 60 minutes, 2 hours, and 2 hourly thereafter
  • GCS hourly
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137
Q

Symptoms of DKA

A

Polyuria
Polydipsia
Nausea and vomiting
Weight loss
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of an underlying trigger (i.e. sepsis)

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138
Q

Basic pathophysiology of DKA

A

Lipolysis: fat is broken down into ffa
liver turns ffa into ketone bodies
Ketone bodies can be used for energy but also increase acidity of the blood
Acidic blood and lack of insulin leads to more potassium outside of cells (hyperkalaemia)
Severe DKA, K+ excreted and depleted so hypokalaemia

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138
Q

What are the 2 key points in managing DKA?

A

correct dehydration evenly over 48hours
give a fixed rate insulin infusion

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139
Q

What is important in management of DKA, apart from correcting dehydration and insulin?

A
  • Avoid fluid boluses to minimise the risk of cerebral oedema
  • Treat underlying triggers
  • Prevent hypoglycaemia
  • Add potassium to IV fluids and monitor serum potassium closely.
  • Monitor for signs of cerebral oedema.
  • Monitor glucose, ketones and pH
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140
Q

Complications of DKA

A

Children with DKA are at high risk of developing cerebral oedema
Hypokalaemia
Hypoglycaemia
ARDS

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141
Q

Risk factors for T2DM

A
  • Obesity, especially central (truncal) obesity.
  • Lack of physical activity.
  • Ethnicity
  • History of gestational diabetes.
  • Impaired glucose tolerance and fasting glucose.
  • Drug therapy - eg, combined use of a thiazide diuretic with a beta-blocker.
  • Low-fibre, high-glycaemic index diet.
  • Metabolic syndrome.
  • PCOS
  • Family history
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142
Q

What tests would you order to diagnose T2DM and what results would you expect?

A

fasting plasma glucose: ≥7.0 mmol/L
HbA1c: ≥48 mmol/mol
2-hour post-load glucose after 75 g oral glucose: ≥11.1 mmol/L
random plasma glucose: ≥11.1 mmol/L

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143
Q

What arae symptoms that all diabetic patients can present with?

A

Polyuria
Polydipsia
Lethargy
Boils
pruritus vulvae
frequent, recurrent or prolonged infections

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144
Q

Differential diagnoses for T2DM

A

Pre-diabetes
T1DM
Gestational diabetes
Latent autoimmune diabetes in adults (LADA)
Monogenic diabetes
Ketosis-prone diabetes

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145
Q

What are the HbA1c values for pre-diabetes?

A

42 – 47 mmol/mol

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146
Q

When would someone with T2DM need to self-monitor blood glucose?

A
  • On insulin
  • Evidence of hypoglycaemic episodes
  • On oral medication that may increase their risk of hypoglycaemia while driving or operating machinery
  • pregnant, or is planning to become pregnant.
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147
Q

Aetiology of T2DM

A

Impaired insulin secretion and insulin resistance

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148
Q

What would you check before starting someone with T2DM on an SGLT2 inhibitor?

A

If they are at increased risk of DKA

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149
Q

What are the components of the annual diabetic review?

A
  • HbA1c
  • BP and bloods
  • Urine test
  • Cholesterol
  • Weight and BMI
  • Eye screening for retinopathy
  • Foot exam
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150
Q

What are possible complications of T2DM?

A

diabetic kidney disease
impaired vision
lower extremity amputation
dementia/cognitive decline
CVD
congestive heart failure (CHF)
Stroke
infection
periodontal disease
treatment-related hypoglycaemia
Hyperosmolar hyperglycaemic state

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151
Q

Symptoms of T2DM

A

Polyuria
Polydipsia
Lethargy
Boils
pruritus vulvae
frequent, recurrent or prolonged infections
Slow wound healing
Glucose in urine
Acanthosis nigricans

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152
Q

What is the first line treatment for T2DM?

A

Standard release metformin

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153
Q

What would you try if someone was experiencing GI side effects on standard release metformin?

A

Modified release metformin

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154
Q

Apart from metformin, what other pharmacological options are available for T2DM?

A
  • A DPP‑4 inhibitor
  • Pioglitazone
  • A sulfonylurea
  • An SGLT2 inhibitor

oral agent + basal insulin also used

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155
Q

What is the aetiology of HHS?

A

MI, stroke
Infection
Poor diabetic control, first presentation of DM
AKI
Burns
Hypo and hyperthermia
PE
Cushings

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156
Q

What is HHS?

A

Rare but potentially fatal complication of T2DM
glucose ≥30 mmol/L
Hyperosmolarity, high blood glucose and absence of ketones

Hyperosmolar hyperglycaemic state

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157
Q

What are the risk factors for HHS?

A

infection
inadequate insulin or oral antidiabetic therapy
acute illness in a known patient with diabetes
nursing home residents
sedatives
medications: thiazides, corticosteroids, beta-blockers and didanosine

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158
Q

What has higher mortality rates, HHS or DKA?

A

HHS
Mortality rates of 5-20%, increases significantly if age 70+

10 fold higher

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159
Q

How does adrenaline contribute to hyperglycaemic states?

A
  • induce insulin resistance
  • decrease insulin production and secretion
  • increase lipolysis, ketogenesis, and volume depletion
160
Q

What is the basic pathophysiology of HHS?

A

Evolves over several days
- Osmotic diuresis leads to hypernatraemia
- Inadequate water intake and excess water loss leads to hypovolaemia
- Progress decline in GFR, aggravating hyperglycaemia
- Adrenaline released and contributes

161
Q

Is there any insulin secretion in HHS?

A

Yes, more than DKA so may suppress ketogenesis
Not enough to regulate hepatic glucose

162
Q

What are some signs of dehydration?

A

dry mouth
decreased skin turgor
sunken eyes

163
Q

What investigations would you order for HHS and what would they show?

A

Blood glucose: ≥30 mmol/L
Blood ketones: negative/low (not DKA)
Venous blood gas: mild acidosis
Serum osmolarity: ≥320 mmol/kg
urea, electrolytes, and creatinine
FBC
ECG

164
Q

What are some differential diagnoses for HHS?

A

Diabetic ketoacidosis (DKA)
Lactic acidosis
Alcohol ketoacidosis
Ingestion of toxic substances
Paracetamol overdose

165
Q

What are the main goals of treating HHS?

A

Correction of dehydration, hyperglycaemia and hyperosmolality, electrolyte imbalance, and increased ketonaemia

166
Q

What’s the first thing you would do to treat HHS?

A

Start IV fluids (before insulin)

167
Q

How would you monitor HHS?

A

Hourly blood glucose for the first 24 hours
Hourly sodium, potassium, urea, and calculated serum osmolality for the first 6 hours
Continue cardiac monitoring if necessary

168
Q

Why isn’t basal NPH insulin used now as much as detemir, etc..

A

Would rise in the blood and only last around 12-13 hours
Newer ones last the whole 24 hours (degludec lasts up to 2-3 days)

169
Q

What is level 1 hypoglycaemia in diabetes?

A

<3.9 mmol/L
Should alert patient to hypo

170
Q

What is level 2 hypoglycaemia in diabetes?

A

serious biochemical
<3.0 mmol/L

171
Q

What is severe hypoglycaemia?

A

Any episode that requires help from someone else, e.g. passing out, patient has impaired cog function

172
Q

What is non-severe hypoglycaemia?

A

Cognitive function only mildly impaired so patient can self-treat

173
Q

What are the symptoms of hypoglycaemia?

A

irritability
shakiness
sweating
tremor
palpitations
tachycardia
feeling warm
anxiety
nausea
hunger
pallor

174
Q

What are some autonomic symptoms of diabetic hypoglycaemia?

A

trembling, palpitations, sweating, anxiety, hunger

175
Q

What are some neuroglycopenic symptoms of diabetic hypoglycaemia?

A

confusion
weakness
drowsiness
difficulty concentrating
dizziness
vision changes
difficulty speaking

176
Q

How does impaired awareness of hypoglycaemia occur in diabetics?

A

recurrent episodes of hypoglycaemia
activation of the SNS and adrenaline can become impaired
takes a lower blood glucose for adrenaline to be released and patient to be made aware of hypo
risk of severe hypo

177
Q

What is the pathophysiology behind diabetic hypoglycaemia?

A

Patient is taking exogenous insulin which isn’t controlled by feedback in body
As duration of diabetes increases, glucagon secretion in response to hypo is impaired
Impaired awareness as adrenaline secretion also impaired so happens at lowering blood glucose

178
Q

Risk factors for diabetic hypoglycaemia

A

T1DM
Diabetes treatment
Poor glycaemic control
Previous episodes of hypo
Age <6 or >60
Impaired awareness
Early pregnancy in diabetics

179
Q

What can cause diabetic hypoglycaemia?

A

altered eating patterns
taking more insulin than usual
engaging in more activity than usual

180
Q

At what blood glucose level would beta cells stop producing insulin in a non-diabetic person?

A

4.6mmol

181
Q

At what blood glucose level would glucagon be made in a non-diabetic person?

A

3.8mmol

182
Q

At what blood glucose level would adrenaline be secreted to alert a person to hypoglycaemia?

normal circumstances

A

3.5mmol

183
Q

What investigation should you do for someone with suspected hypoglycaemia?

A

Blood glucose
<3.9 mmol/L

184
Q

What are some differential diagnoses for diabetic hypoglycaemia?

A

hypoglycaemia due to non-diabetic drugs
sepsis
hypothyroidism
hypopituitarism
primary adrenal insufficiency

185
Q

How would you manage hypoglycaemia?

A

Confirm diagnosis with blood glucose
Give glucose orally
Re-check the patient’s blood glucose after 10-15 minutes and repeat administration of glucose until the hypoglycaemia has resolved
Treat underlying cause

186
Q

How would you monitor hypoglycaemia acutely?

A

Re-check the patient’s blood glucose after 10-15 minutes and repeat administration of glucose until the hypoglycaemia has resolved

187
Q

How would you monitor episodes of hypoglycaemia in the long term?

A

Assess any episodes of hypoglycaemia (both confirmed and suspected) and the possibility of impaired awareness of hypoglycaemia at each patient visit

188
Q

What are some complications of hypoglycaemia?

A

Falls, especially in older patients
Impaired awareness of hypo
Neurological and psychological impacts

189
Q

What are some neuro/psych complications of hypoglycaemia?

A

cognitive impairment
increased risk of dementia
negative effect on mental health including depression

190
Q

How can you primary prevent hypoglycaemia in diabetics?

A

Educate patients and carers
Patients on antidiabetic therapy should carry carbohydrates at all times
Check glucose level before exercising

191
Q

What does the zona glomerulosa of the adrenal gland make?

A

Mineralcorticoids
e.g. aldosterone

192
Q

What is primary adrenal insufficiency?

A

destruction or dysfunction of the adrenal gland resulting from intrinsic diseases of the adrenal cortex and leading to impairment in steroid hormone synthesis and secretion

193
Q

What is made in the zona fasciculata of the adrenal gland?

A

cortisol + other glucocorticoids

194
Q

What is made in the zona reticularis of the adrenal gland?

A

androgens (sex hormones)

195
Q

What is the most common cause of primary adrenal insufficiency in developed countries?

A

Autoimmune
(antibodies against 21-hydroxylase)

196
Q

What does adrenal medulla make?

A

Catecholamines

197
Q

What are the symptoms of primary adrenal insufficiency?

A

Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdominal pain
Depression
Reduced libido

198
Q

What are the main causes of primary adrenal insufficency?

A

Autoimmune
TB
Metastatic malignancies

199
Q

How much of the adrenal cortex needs to be destroyed in order to cause the clinical symptoms?

A

Approx 90%

200
Q

What are the clinical signs of primary adrenal insufficency?

A

Hyperpigmentation
Hypotension
Loss of pubic and armpit hair (in women)

201
Q

What is primary adrenal insufficiency also known as?

A

Addisons

when not acute

202
Q

Why would women be at an increased risk of developing primary adrenal insufficiency?

A

Most common cause is autoimmune which women are more susceptible to

203
Q

What would happen in PAI if the zona glomerulosa was destroyed?

A

aldosterone falls:
hyperkalaemia, hyponatraemia (low BP), hypovolaemia, metabolic acidosis

204
Q

What would happen in PAI if the zona fasciculata was destroyed?

A

cortisol falls:
low blood glucose in times of stress
overactive pituitary gland (as no negative feedback) produces precursor to MSH and hyperpigmentation

205
Q

What would happen in PAI if the zona reticularis was destroyed?

A

androgen levels fall (less significant for men as testes produce lots)
loss of pubic and armpit hair, loss of libido

206
Q

What are the main risk factors for primary adrenal insufficiency?

A

Female
Known autoimmune disease (e.g. T1DM, pernicious anaemia, rheumatoid arthritis)
Adrenal haemorrhage
Adrenocortical autoantibodies

207
Q

What investigations would you run for PAI?

A
  • Short synacthen test: no rise in cortisol in response to administered ACTH
  • Morning serum cortisol: <140 nanomols/L (low) – this test can be falsely normal
  • Plasma ACTH: high
  • Serum electrolytes: low sodium, high potassium
208
Q

What does the short synacthen test do?

A

Tests for primary adrenal insufficiency by giving synthesised ACTH and measuring cortisol levels

in PAI, cortisol would not rise

209
Q

What are the differentials for PAI?

A

Adrenal suppression due to the use of glucocorticoid
Secondary AI
Anorexia nervosa
Hyperthyroidism
Haemochromatosis

210
Q

What is the treatment for primary adrenal insufficiency?

A

Oral glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) replacement for life

211
Q

How do you monitor primary adrenal insufficiency?

A

Annual history, exam and tests (FBC, electrolytes, BP etc…)

212
Q

What are the complications of PAI?

A

Adrenal crisis
Osteoporosis

213
Q

Symptoms of adrenal crisis

A

Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

214
Q

What is secondary adrenal insufficiency?

A

inadequate adrenocorticotropic hormone (ACTH) and a lack of stimulation of the adrenal glands, leading to low cortisol.

215
Q

What can cause secondary adrenal insufficiency?

A

Loss or damage to pituitary gland

216
Q

What is teritary adrenal insufficiency?

A

results from inadequate corticotropin-releasing hormone (CRH) release by the hypothalamus

217
Q

What can cause tertiary adrenal insufficiency?

A

long-term oral steroids, causing suppression of the hypothalamus

218
Q

What is Conn’s syndrome?

A

an adrenal adenoma producing too much aldosterone

219
Q

What is primary aldosteronism?

A

when the adrenal glands are directly responsible for producing too much aldosterone

Conn’s: adrenal adenoma

220
Q

What is the aetiology of primary aldosteronism?

A

Adrenal adenoma (Conn’s)
Adrenal hyperplasia
Familial hyperaldosteronism

221
Q

What does aldosterone do?

A
  • Increase sodium reabsorption from the distal tubule
  • Increase potassium secretion from the distal tubule
  • Increase hydrogen secretion from the collecting ducts
222
Q

What are the risk factors for primary aldosteronism?

A

Family history of primary aldosteronism
Family history of early onset hypertension and stroke

223
Q

What is the main presentation of primary aldosteronism?

A

Hypertension

224
Q

What may be present in a patient with primary aldosteronism?

A

Hypertension.
Hypokalaemia (usually <3.5 mmol/L, although 70% of patients may be normokalaemic).
Metabolic alkalosis

225
Q

What symptoms may be present in a patient with primary aldosteronism?

A

Hypertension
nocturia, polyuria
lethargy
mood disturbance (irritability, anxiety, depression)
difficulty concentrating

226
Q

What does low renin and high aldosterone indicate on a anldosterone/renin ratio?

A

Primary aldosteronism

227
Q

What does high renin and high aldosterone indicate on a anldosterone/renin ratio?

A

Secondary aldosteronism

228
Q

Why would you do an adrenal CT/MRI?

A

Look for adenoma

229
Q

What tests would you run for primary aldosteronism (Conn’s)?

A

aldosterone-to-renin ratio (ARR)
U&E: plasma potassium may be normal/low, hypernatraemia

230
Q

What test can localise the cause of primary aldosteronism?

A

Selective adrenal venous sampling

231
Q

What are 2 aldosterone antagonists that may be used to treat primary aldosteronism?

A

Eplerenone
Spironolactone

232
Q

What are some differentials for primary aldosteronism?

A

Primary hypertension
Renal stenosis

233
Q

What is the most common cause of secondary hypertension?

A

Hyperaldosteronism

234
Q

How would you manage primary aldosteronism?

A

Aldosterone antagonists: Eplerenone, Spironolactone
Surgical removal of the adrenal adenoma

235
Q

What are some complications of primary aldosteronism?

A

Stroke
MI
Heart failure
Impaired renal function
Drug-induced hyperkalaemia

236
Q

What is cranial diabetes insipidus?

A

decreased secretion of ADH, issue in HT or PG
reduces the ability to concentrate urine and so causes polyuria and polydipsia

237
Q

What is nephrogenic diabetes insipidus?

A

decreased ability to concentrate urine because of resistance to ADH in the kidney.

the collecting ducts of the kidneys do not respond to ADH

238
Q

What is dipsogenic diabetes insipidus?

(aka primary polydipsia)

A

caused by a primary defect in osmoregulation of thirst
can be psychological, drinking too much water

239
Q

What is gestational diabetes insipidus?

A

results from degradation of vasopressin by a placental vasopressinase
associated with increased complications of pregnancy

Placenta produces vasopressinase causing ADH breakdown, starting in week 8 and can continue until 2 months after giving birth

240
Q

What are the 4 types of DI?

A

Cranial
Nephrogenic
Gestational
Dipsogenic

cranial and nephrogenic are main ones

241
Q

Why is ADH useful in hypovalaemic shock?

A

In high concentrations, ADH can act on the blood vessels to increase peripheral vascular resistance, the result of which is increased blood pressure

242
Q

When is ADH (AVP) secretion increased?

A

states of increased plasma osmolality
increases total blood volume

243
Q

What can cause nephrogenic DI?

A

Medications, particularly lithium
Genetic mutations in the ADH receptor gene
Hypercalcaemia
Hypokalaemia
Kidney diseases

244
Q

What can cause cranial DI?

A

Brain tumours, injury or surgery
Brain infections (e.g., meningitis or encephalitis)
Genetic mutations in the ADH gene
Wolfram syndrome

245
Q

What are the main symptoms in diabetes insipidus?

A

Polyuria and nocturia
Polydipsia
No glycosuria
Postural hypotension

246
Q

What signs would you see in DI?

A

Hypernatraemia
Signs of dehydration

247
Q

What is the definition of hyperkalaemia?

A

serum potassium level ≥5.5 mmol/L (abnormally high)

248
Q

What is mild hyperkalaemia?

A

potassium 5.5 to 5.9 mmol/L

249
Q

What is moderate hyperkalaemia?

A

potassium 6.0 to 6.4 mmol/L

250
Q

What is severe hyperkalaemia?

A

potassium ≥6.5 mmol/L

251
Q

What are the risk factors for hyperkalaemia?

A

Kidney dysfunction
Heart failure
Certain meds affecting RAAS: ACEi, ARBs, NSAIDs, aldosterone antagonists
Liver disease
Tissue breakdown
DM

252
Q

What drugs can cause hyperkalaemia?

A

ACEi
ARBs
Aldosterone antagonists (spironolactone)
LMWH
NSAIDs
Calcineurin inhibitors

253
Q

How does hyperkalaemia present?

A

Often asymptomatic or non-specific symptoms: fatigue, paraesthesia, muscle cramps

254
Q

What investigations would you order for hyperkalaemia?

A

FBC (serum potassium) and repeat if any uncertainty
ABG
ECG

255
Q

What changes would you see on an ECG for hyperkalaemia?

A

peaked T waves
shortened QT interval
lengthened PR interval
absent P wave
widened QRS

256
Q

What is the differential for hyperkalaemia?

A

pseudohyperkalaemia
a repeated test would show if pseudo or not

257
Q

What could cause pseudohyperkalaemia in a lab result?

A

Haemolysis during sampling
Prolonged tourniquet
Trauma when collecting sample
Long storage time of sample
Excessive cooling of sample

258
Q

How do you treat hyperkalaemia?

A

Insulin drives potassium from the extracellular space to intracellular space
Dextrose is required to prevent hypoglycaemia while on insulin
Calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias

259
Q

Complications of hyperkalaemia

A

Cardiac dysrhythmias
Severe muscle weakness/ paralysis
Renal tubular acidosis

260
Q

What is the definition of hypokalaemia?

A

serum potassium level <3.5 mmol/L

261
Q

What are the values for moderate and severe hypokalaemia?

A

Moderate: 2.5 to 3 mmol/L
Severe: <2.5 mmol/L

262
Q

Why do changes in serum potassium impact the cardiovascular and neuromuscular systems?

A

The ratio of intracellular to extracellular potassium determines, in part, the cellular membrane potential.

Therefore small changes in the extracellular potassium level can have large effects on function

263
Q

Why does alkalosis cause potassium to enter cells?

A

hydrogen ions leave the cells and potassium enters into cells to maintain electroneutrality

can cause hypokalaemia and be seen in sodium bicarbonate treatment of metabolic acidosis

264
Q

What can cause hypokalaemia?

A

Decreased K intake
Increased K entry into cells
Increased K excretion

265
Q

What can cause decreased potassium intake in hypokalaemia?

A

Rapid weight loss
Diuretic therapy

266
Q

What are some reasons for increased potassium entry into cells in hypokalaemia?

A
  • elevated extracellular pH, e.g. in alkalosis,
  • increased beta-adrenergic activity: by catecholamines, or beta-adrenergic agonists like salbutamol. These increase Na-K-ATPase activity.
  • Increased availability of insulin: insulin increases Na-K-ATPase activity
267
Q

What are some reasons of increased potassium excretion in hypokalaemia?

A

GI losses: vomiting, villous adenoma
Increase loss in urine: diuretics, mineralocorticoid excess
Increased loss through sweating

268
Q

How does hypokalaemia present?

A

Mild is asymptomatic
More severe may having muscle weakness, paraesthesia and constipation

269
Q

First line investigations for hypokalaemia

A

Basic metabolic panel (Na, K, glucose, urea, creatinine, bicarb)
ECG
Urine electrolytes and creatinine

270
Q

What ECG changes are seen in hypokalaemia?

A

ST depression
decrease in amplitude of T wave
increase in amplitude of U waves

271
Q

Differentials for hypokalaemia

A

D&V
Eating disorder
DKA
HHS
Laxative and bowel cleansing agent use

272
Q

How do you treat hypokalaemia?

A

Potassium replacement
Manage underlying cause

273
Q

What are some possible complications of hypokalaemia and its treatment?

A

Cardiac arrhythmias
Abnormal renal function
Iatrogenic hyperkalaemia

274
Q

What is the normal range of potassium ECF (serum)

A

3.5-5mmol

275
Q

What is the normal range for serum sodium?

A

135-145mmol

276
Q

What is hypernatraemia?

A

Serum sodium higher than 145mmol

277
Q

Risk factors for hypernatraemia

A

inability to drink water/limited access to water
Extremes of age
renal concentrating defect
GI disorders
insensible water losses
diabetes insipidus
drugs: lithium, laxatives, loop diuretics
large salt intake or administration
TBI
primary hypodipsia

main: inability to drink water or concentrate urine, high urine/stool output

278
Q

What can cause hypernatraemia?

A

M – medications/meals
O – osmotic diuresis
D – diabetes insipidus
E – excessive water losses
L – low water intake

free water losses, inadequate water intake, sodium overload

279
Q

What can cause hypovolaemic hypernatraemia?

A

Diuretics
Dehydration (D&V, burns)
HHS

280
Q

Symptoms of hypernatraemia

A

Signs of hypovolaemia
CNS dysfunction: weakness, lethargy, confusion
Increased thirst

281
Q

First line investigations for hypernatraemia

A

serum electrolyte panel with glucose, urea, and creatinine
urine osmolality – if DI suspected
serum osmolality – if DI suspected

282
Q

What is the aim of management for hypernatraemia?

A

replace any fluid deficit and correct the serum sodium at a suitable rate

283
Q

What is a risk of correcting serum sodium too quickly in hypernatraemia?

A

Cerebral oedema

284
Q

Does hyponatraemia only occur in fluid overload?

A

No
Can occur in volume depletion, volume overload, or euvolaemia

285
Q

What is the most common electrolyte imbalance?

A

hyponatraemia

286
Q

What is normal serum sodium?

A

135-145 mmol/L

287
Q

What are some risk factors for hyponatraemia?

A

older age
hospitalisation
SSRIs
thiazide diuretics
MDMA

288
Q

What is severe hyponatraemia?

A

serum sodium < 125 mmol/l

289
Q

Difference between acute and chronic hyponatraemia

A

Acute: over less than 48 hours
Chronic: after 48 hours

290
Q

What are some signs of volume overload?

A

Oedema and/or ascites
Rales or crackles on lung auscultation
Significant weight gain
Raised jugular venous pressure

291
Q

What can cause low urine sodium and how is this treated?

A

D&V
Burns
Pancreatitis
Diuretics

Treated: give saline

292
Q

In hypovolaemic hyponatraemia, what can cause this with a normal urine sodium?

and how is it treated?

A

Diuretics
Addisons
Cerebral salt wasting

saline replacement

293
Q

What can cause hypovolaemic hyponatraemia?

A

GI fluid loss
Pancreatitis
Cerebral salt wasting
Mineralcorticoid deficiency (addison’s)

294
Q

What can cause hypervolaemic hyponatraemia?

A

Congestive heart failure
Cirrhosis
Nephrotic syndrome
AKI/CKD

295
Q

What can cause euvolaemic hyponatraemia?

A

Thiazide diuretics and SSRIs
SIADH
High fluid intake

296
Q

How do you treat acute hyponatraemia?

A

hypertonic 3% saline

297
Q

How does T2DM pathophysiology cause the symptoms seen?

A

Insulin resistance, receptors are not working as effectively.
High blood glucose for longer periods of time.
Pancreas secretes more insulin.
Glucose travels to kidneys and is secreted out, resulting in glucosuria and osmotic diuresis, leading to polyuria.
Can lead to dehydration and HHS.
Dehydration stimulates brain to drink more -> polydipsia

298
Q

Pathophysiology of T2DM

A

Tissues become insulin resistant
More insulin secreted from beta cells (hyperplasia and hypertophy)
Beta cells also secrete amylin
Higher blood glucose for longer periods of time
Beta cells cannot sustain and eventually die so less insulin out and more hyperglycaemia

299
Q

What can cause increase thyroid hormone levels?

A
  • overproduction thyroid hormone
  • leakage of preformed hormone from thyroid
  • ingestion of excess thyroid hormone
300
Q

What does thyrotoxicosis increase?

A

BMR

301
Q

What are some signs of hyperthyroidism?

A

Palmar erythema.
Sweaty and warm palms.
Fine tremor
Lid lag
Goitre
Hair thinning

302
Q

What are the symptoms of hyperthyroidism?

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss and hyperphagia
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Menstrual disturbance
Lid lag and stare
Brisk reflexes on examination

303
Q

What would TFTs show in hyperthyroidism?

A

elevated T3/T4, suppressed TSH

304
Q

What is a differential for hyperthyroidism?

A

Phaeochromocytoma and any cause of weight loss

305
Q

How do you manage hyperthyroidism?

A

Antithyroid drugs: carbimazole or propylthiouracil (thionamides

306
Q

What is Grave’s disease?

A

an autoimmune thyroid condition associated with hyperthyroidism

307
Q

What investigations would you do for Grave’s and hyperthyroidism?

A

TFTs: serum T3, T4, TSH
TSH receptor antibodies

308
Q

Symptoms of Grave’s disease

A

heat intolerance + sweating
weight loss
palpitations
tremor
diffuse goitre
orbitopathy

309
Q

How do osmoreceptors act in dehydration?

diabetes insipidus physiology

A

Osmolality is increase and osmoreceptors detect this
Trigger thirst
Water in, osmolality decreases

310
Q

How does ADH secretion work?

Diabetes insipidus physiology

A

ADH is produced in supraoptic nucleus
Causes vasoconstriction and an increase in BP - secreted in high osmolality

311
Q

How does ADH act on the kidneys?

DI physiology

A

ADH acts on collecting ducts and DCT of nephrons
Binds to AVPR2 causing aquaporins to inbed on apical cell surface
Water can move out of tubule lumen into cells and back into blood
Blood dilutes and returns osmolality to normal

312
Q

What is pathologically happening in DI?

A

Too little water is reabsorbed in kidneys, causing polyuria
There is less water in blood, increasing osmolality and osmoreceptors trigger thirst, causing polydipsia

313
Q

What test is used to confirm DI?

A

Water deprivation test
Urine osmolality would remain inappropriately low as can’t concentrate urine even in dehydration

314
Q

Apart from a water deprivation test, what other investigations should be used in diabetes insipidus?

A

Urine osmolality: low
Serum osmolality: normal/high
Serum sodium, potassium and glucose

315
Q

First line treatment for cranial DI

A

Desmopressin
Check sodium every 3 months for risk of hyponatraemia

316
Q

How would you manage nephrogenic DI?

A

Desmopressin not as effective
High dose DDAVP
Ensure adequate fluid intake to match output
Stop any nephrogenic drugs

317
Q

Differentials of diabetes insipidus

A

Psychogenic polydipsia
Diabetes mellitus
Diuretic use

318
Q

What needs monitoring in diabetes insipidus?

A

Serum sodium

319
Q

How does vitamin D become activated?

A

7-dehydrocalciferol produced in skin in response to UV + gained through diet
Moves to liver and becomes 25-hydroxyvitamin D
1 alpha hydroxylase enzyme in kidneys converts to 1,25-dihydroxy vit D (calcitriol)

320
Q

Effect of 1,25-dihydroxy vit D on calcium

A

GI tract: increases absorption
Kidneys: increases reabsorption
Bone: Increases release of calcium

321
Q

What has an effect on calcium levels in blood?

A

Active vitamin D and PTH increase
Calcitonin decreases

322
Q

How does calcitonin decrease calcium levels?

A

Limits release from bone
Decreases reabsorption in kidney

323
Q

What happens in PTH mediated hypercalcaemia?

A

impaired receptors and suppression of PTH

324
Q

What happens in calcitriol mediated hypercalcaemia?

A

overexpression of 1-alpha hydroxylase, the enzyme responsible for converting 25-hydroxyvitamin D to calcitriol.

Excessive production of calcitriol
Resulting in increased intestinal absorption of calcium and increased osteoclast activity

325
Q

How would you treat severe hypercalcaemia?

A

IV saline
IV bisphosphonates or subcut denosumab

326
Q

What can cause hypocalcaemia with inappropriately low serum PTH?

A
  • Developmental parathyroid disorders
  • Destruction of parathyroid glands
327
Q

What can cause hypocalcaemia with secondary hyperparathyroidism?

A
  • Vitamin D deficiency/ resistance
  • Inadequate ultraviolet B light exposure, poor diet, malabsorption
  • Chronic renal disease, enzyme-induced drug resistance to PTH
  • Pseudohypoparathyroidism
  • Hypomagnesaemia
  • Mutations in vitamin D receptor (mutations in 1-alpha hydroxylase enzyme)
328
Q

Risk factors for hypocalcaemia?

A

Vitamin D deficiency.
A parathyroid disorder or parathyroid gland surgery.
Thyroid removal surgery (thyroidectomy).
Family history of genetic conditions e.g. genetic vitamin D disorder or DiGeorge syndrome

329
Q

What signs are seen in hypocalcaemia?

A

Chvostek’s sign: Twitch of innervated muscles when tapping over facial nerve
Trousseau’s sign: Inflate the blood pressure cuff to 20 mm Hg above systolic for 5 minutes, forms characteristic shape

330
Q

What are the symptoms of hypocalcaemia?

A

Parathesia
Muscle spasms: hands, feet, larynx, premature labour
Seizures
Basal ganglia calcification if chronic
Cataracts
Long QT interval

331
Q

What is the first line investigation for hypocalcaemia?

A

Serum total calcium levels, adjusted for albumin

332
Q

Differentials of hypocalcaemia

A

Vit D deficiency
Hypoparathyroidism + pseudo
CKD
Hypomagnesaemia

333
Q

Management of hypocalcaemia

A

Mild/moderate: oral calcium
Severe: IV calcium gluconate

334
Q

What is SIADH?

A

Increased inappropriate ADH release, leading to euvolaemic hypotonic hyponatraemia

335
Q

What happens in normal physiology when osmolality is reduced from more water intake?

A

ADH is reduced
Urine becomes more dilute
Osmolality returns to normal

336
Q

What is the pathophysiology in SIADH?

A

Excessive ADH
Increased water reabsorption in the collecting ducts
Blood diluted
Less aldosterone and excess water leads to hyponatraemia (still euvolaemic)

337
Q

Why do patients with SIADH have high urine osmolality and high urine sodium?

A

urine becomes more concentrated as the kidneys excrete less water

338
Q

What is type A SIADH?

A

Unregulated release of lots of ADH, independent of osmolality levels

339
Q

What is type B SIADH?

A

Constant moderate release of ADH, milder increase than type A

340
Q

What is type C SIADH?

A

a baseline plasma sodium concentration that is stable, but lower than normal

341
Q

What is type D SIADH?

A

pseudo-SIADH, low levels of ADH but increased urine osmolality

342
Q

What can cause SIADH?

A

Drugs: SSRIs, NSAIDS, carbamazepine
Pulmonary: infection, small cell lung cancer
Malignancy: lung, Gi, GU cancers
CNS disorders: e.g. trauma, MS
Post-operative

Main causes: SSRIs, post-op, small cell lung cancer

343
Q

Risk factors for SIADH

A

age >50 years
pulmonary conditions (e.g., pneumonia)
nursing home residence
malignancy
meds: SSRIs, carbamazepine, NSAIDs
CNS disorders

344
Q

Symptoms of SIADH

A

Headache
Nausea
Muscle aches and cramps
Severe: seizures and confusion

Coming from hyponatraemia which risks cerebral oedema

345
Q

What investigations should be done for SIADH and what would they show?

A

Serum sodium and osmolality: low
Urine sodium and osmolality: high

Diagnosis made off clinical features too: euvolaemic hyponatraemia

346
Q

Differentials for SIADH

A

Volume changes (hypo/hyper)
Pseudohyponatraemia
Cerebral salt wasting
Renal failure

347
Q

Management of SIADH

A

Correction of hyponatraemia
Fluid restriction
Vaptans (e.g. tolvaptan) in certain patient groups

348
Q

What is hypoparathyroidism?

A

Relative or absolute deficiency of plasma PTH synthesis and secretion

349
Q

What is pseudohypoparathyroidism?

A

A resistance to PTH
Not an issue with PTH, bones and kidneys don’t respond

350
Q

What does a decrease in PTH (hypoparathyroidism) lead to?

A
  • Decreased renal calcium reabsorption
  • Increased renal phosphate reabsorption
  • Decreased bone turnover
  • Decreased formation of active vitamin D

low calcium, high phosphate

351
Q

What is the most common cause of hypoparathyroidism?

A

Post-surgical (75%), e.g. surgical treatment for hyperparathyroidism

352
Q

What can cause hypoparathyroidism?

A

Post surgical (commonest cause, 75%)
Radiation induced damage
Genetic, e.g. with DiGeorge syndrome (a developmental abnormality)
Autoimmune
Infiltrative, e.g. haemachromatosis

353
Q

Pathophysiology of hypoparathyroidism

A

Low PTH leads to low calcium and high phosphate
Hypocalcaemia makes neurones more excitable causing involuntary muscle contraction (chvostek’s and trousseau’s sign). Also impairs cardiac output
High phosphate and low calcium can lead to calcification of the eye lens and basal ganglia

354
Q

Symptoms of hypoparathyroidism

as a result of hypercalcaemia

A

Muscle twitches/cramps
Paraesthesias
Poor memory
Dry, brittle nails
Cataracts

355
Q

What would an ECG show for hypocalcaemia?

A

Prolonged QT interval

356
Q

What investigations would you do for hypoparathyroidism?

A

Serum calcium, phosphorus, albumin
Plasma intact PTH

Vit d, magnesia, ECG also

357
Q

Differentials of hypoparathyroidism

A

CKD
Vitamin D deficiency
Pseudohypoparathyroidism

358
Q

How do you manage hypoparathyroidism?

A

Calcium and vitamin D supplements
In chronic can give human recombinant parathyroid hormone

359
Q

What is primary hyperparathyroidism?

A

overproduction of PTH, independent of calcium level
often due to a tumour, 80% of time a parathyroid adenoma

360
Q

What can cause primary hyperparathyroidism?

A

benign adenoma in 80% of cases
hyperplasia
parathyroid carcinoma (very small amount of cases)

361
Q

What is the pathophysiology of primary hyperparathyroidism?

A

PTH secretion is not suppressed by high calcium levels.
Excessive PTH leads to over-stimulation of bone resorption, kidneys to reabsorb calcium and to convert active form of vitamin D

All result in hypercalcaemia and low phosphate.
Neurones are less excitable, slower muscle contractions.
Also can lead to hypercalciuria and dehydration

362
Q

What is secondary hyperparathyroidism?

A

elevation of PTH secondary to hypocalcaemia

363
Q

What is tertiary hyperparathyroidism?

A

When secondary hyperparathyroidisim is treated, hyperplasia of PT gland and baseline parathyroid hormone production remains inappropriately high

364
Q

What are the main causes of secondary hyperparathyroidism?

A

CKD
malabsorption syndromes
chronic inadequate exposure to sunlight

365
Q

Risk factors for secondary hyperparathyroidism

A
  • ageing
  • chronic kidney disease
  • vitamin D deficiency
  • nutritional deficiency (especially absence of dairy products and fish)
366
Q

Risk factors for primary hyperparathyroidism

A
  • female sex
  • age ≥50 (increases with age, especially post-menopausal)
  • family history of PHPT
  • multiple endocrine neoplasia (MEN) 1, 2A, or 4
  • lithium treatment
367
Q

Symptoms of primary hyperparathyroidism

A
  • Fatigue
  • Myalgia
  • Hypercalciuria
368
Q

Symptoms of secondary hyperparathyroidism

A
  • Muscle cramps
  • Bone pain
  • Signs of hypocalcaemia
369
Q

What investigations would you run for hyperparathyroidism?

A

serum calcium
serum intact PTH

370
Q

Differentials of primary hyperparathyroidism

A
  • hypercalcaemia of malignancy
  • Multiple myeloma
  • Milk-alkali syndrome
371
Q

Differential diagnosis of secondary hyperparathyroidism

A

Primary HPT

372
Q

How do you manage hyperparathyroidism?

A

Primary: Parathyroidectomy
Secondary: treat underlying cause

373
Q

What is a phaeochromocytoma?

A

A tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla
secretes unregulated and excessive amounts of adrenaline in bursts

374
Q

What causes phaeochromocytoma?

A

Most are sporadic but can be familial
Genetic conditions associated with:
- Multiple endocrine neoplasia type 2
- Von Hippel-Lindau
- Neurofibromatosis type 1

375
Q

What is the triad of symptoms for phaeochromocytoma?

A

Palpitations
Headaches
Diaphoresis

episodic spells of symptoms

376
Q

What investigations are carried out for phaeochromocytoma?

A

Serum free metanephrines
24-hour urine catecholamines

377
Q

Differentials of phaechromocytoma

A

Anxiety and panic attacks
Hypertension
Hyperthyroidism
Carcinoid syndrome
Cardiac arrhythmias

378
Q

What is the management of phaeochromocytoma?

A

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

379
Q

What is a complication of phaeochromocytoma?

A

Hypertensive crisis

380
Q

How does thyroid cancer usually present?

A

asymptomatic thyroid nodule detected by palpation or ultrasound

381
Q

What is the most common endocrinological malignancy?

A

thyroid cancer

382
Q

What cells do thyroid cancers derive from?

A

thyroid follicular epithelial cells or parafollicular neuroendocrine cells of the thyroid

383
Q

What are the risk factors for thyroid cancer?

A

head and neck irradiation
female sex

384
Q

What investigations should be ordered for thyroid cancer?

A

TSH
ultrasound, neck
fine-needle aspiration

385
Q

Differential diagnosis of thyroid cancer

A

Benign thyroid nodule

386
Q

What do neuroendocrine cells release?

A

Serotonin
Histamine
Bradykinin
Prostaglandins

387
Q

Why does carcinoid syndrome occur?

A

occurs due to release of serotonin and other vasoactive peptides into the systemic circulation from a carcinoid tumour

388
Q

Pathophysiology of carcinoid syndrome from neuroendocrine tumours

A

NE tumours
- Produce and secrete large amounts of hormones
Mets in liver
- Leads to liver dysfunction, harder to metabolize hormones, allowing build up and symptoms

389
Q

What causes the symptoms of carcinoid syndrome?

A

Increased bradykinin and histamine cause vasodilation and flushing
Increased serotonin can cause thickening of collagen in heart valves, leading to heart dysfunction (tricuspid regurgitation)
Extensive fibrosis can impair kidney function

390
Q

Symptoms of carcinoid syndrome

A

flushing
diarrhoea
wheeze
palpitations
telangiectasia
abdominal pain

391
Q

What is the normal pathway of serotonin

(physiology of carcinoid)

A

serotonin is synthesised from tryptophan
metabolised by monoamine oxidase to 5-hydroxyindoleacetic acid, which is subsequently secreted in the urine
some stays in circulation

392
Q

How is carcinoid syndrome diagnosed?

A

elevated levels of urinary 5-hydroxyindoleacetic acid Chromogranin A is often elevated in the presence of liver metastases

393
Q

What investigations should be ordered for carcinoid syndrome and what would they show?

A

serum chromogranin A/B: elevated
urinary 5-hydroxyindoleacetic acid: elevated

394
Q

Differential diagnoses of carcinoid syndrome

A

Irritable bowel syndrome
Crohn’s disease
Menopause
Asthma

395
Q

How does somatostatin affect serotonin?

A

Binds to surface of neuroendocrine cells and inhibits release of serotonin

396
Q

How would you treat carcinoid syndrome?

A

Somatostatin analogues
Surgical resection of tumour

397
Q

Complications of carcinoid syndrome

A

Carcinoid heart disease
Pellagra
Intestinal bleeding
Bowel obstruction

398
Q

How much insulin and dextrose is given for hyperkalaemia?

A

10 units of insulin with 25g of dextrose

399
Q
A

Phase 2a (14 decks)

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