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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define hyperthyroidism

A

Excess thyroid hormones
Primary = abnormal overproduction of thyroid hormones / increased thyroid function
(Secondary = abnormal overproduction of TSH)

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2
Q

Describe the epidemiology of hyperthyroidism

A

Mainly affects younger women (20-40yrs)
Grave’s disease prevalence = 0.5%

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3
Q

What are the causes of hyperthyroidism?

A

Grave’s disease (autoimmune) = 75% of hyperthyroidism
Toxic multinodular goitre
Toxic adenoma
Metastatic follicular thyroid cancer
Iodine excess (e.g. contrast media)
*Secondary cause = TSH-secreting pituitary adenoma

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4
Q

What are the risk factors for hyperthyroidism?

A

Female sex
Smoking
Family history
Other autoimmune conditions
Low iodine intake

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5
Q

What are the associations of hyperthyroidism?

A

Other autoimmune conditions (T1DM, Addison’s disease, vitiligo)

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6
Q

Describe the pathophysiology of hyperthyroidism

A

High levels of T3 increases metabolism, cardiac output, bone resorption, and activates sympathetic nervous system

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7
Q

What are the signs/symptoms of hyperthyroidism?

A

Weight loss
Hyperphagia (increased appetite)
Tachycardia
Sweating
Heat intolerance
Diarrhoea
Menstrual disturbances
Tremor
Irritability
Anxiety/restlessness
Lid lag + stare

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8
Q

What investigations are needed in hyperthyroidism?

A

TFTs = high T4/T3, low TSH (secondary = high for both)
Thyroid antibodies = TSH-receptor Abs or thyroid peroxidase Abs (indicate Grave’s disease)
Isotope uptake scan (to detect nodular disease)

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9
Q

What are the treatments of hyperthyroidism?

A

Drugs = beta-blockers (control symptoms), antithyroid drugs (e.g. carbimazole - blocks T4 synthesis)
Radioiodine = 131I emits beta particles to ionise thyroid cells, causing DNA damage (many become hypothyroid)
Surgery = usually total thyroidectomy (need thyroid replacement after, risk to recurrent laryngeal nerve causing hoarseness)

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10
Q

What are the complications of hyperthyroidism?

A

Heart failure
Angina
AF
Ophthalmopathy
Thyroid storm (sudden flare up)

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11
Q

Describe the pathophysiology of Grave’s disease

A

IgG autoantibodies bind to TSH receptors to increase T4/T3 production, also react with orbital autoantigens

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12
Q

Other than those of hyperthyroidism, what are the additional symptoms of Grave’s disease?

A

Thyroid eye disease - inflammation causes eyelid retraction, periorbital swelling, bulging eyes
Pretibial myxoedema - swelling and changes to the skin on lower legs
Thyroid acropachy - clubbing and painful toe/finger swelling, periosteal reactions (bone growth)

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13
Q

Define hypothyroidism

A

Low levels of thyroid hormones
Primary = absence/dysfunction of thyroid gland
(secondary = pituitary dysfunction/abnormal low TSH production)

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14
Q

Describe the epidemiology of hypothyroidism

A

Most affects women >40 yrs old

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15
Q

What are the causes of hypothyroidism?

A

Hashimoto’s thyroiditis (autoimmune: inflammation -> goitre)
Primary atrophic hypothyroidism (autoimmune: no goitre)
Iodine deficiency (dietary, common cause world wide)
Drugs (anti-thyroids, iodine, lithium)
Post-thyroidectomy/radioiodine
Postpartum hypothyroidism
*secondary cause = pituitary/hypothalamic dysfunction

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16
Q

What are the risk factors for hypothyroidism?

A

Female sex
Family history
Other autoimmune conditions
Medication/surgery for hyperthyroidism

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17
Q

What are the association for hypothyroidism?

A

Other autoimmune conditions (T1DM, Addison’s, vitiligo)
Turner’s and Down’s syndromes
Genetic defects in hormonal synthesis

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18
Q

Describe the pathophysiology of hypothyroidism

A

Low levels of T3 are not enough to increase metabolic rate for normal body functions

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19
Q

What are the sings/symptoms of hypothyroidism?

A

BRADYCARDIC:
Bradycardia
Reflexes (relax slowly)
Ataxia (cerebellum)
Dry, thin skin/hair
Yawning/drowsiness
Cold hands w/wo low temperature
Ascites w/wo non-pitting oedema
Round/puffy face
Defeated demeanour
Immobile (weakness)
Cardiac failure

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20
Q

What investigations are needed for hypothyroidism?

A

TFTs = low T4/T3, high TSH (secondary = low for both)
Thyroid antibodies = thyroid peroxidase Abs (indicate Hashimoto’s)

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21
Q

What are the treatments of hypothyroidism?

A

Levothyroxine (LT4) - synthetic T4

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22
Q

What are the complications of hypothyroidism?

A

Impaired quality of life (from fatigue + other symptoms)
Cardiovascular - CHD, stroke, heart failure
Reproductive - infertility, pregnancy/birth complications
Cognitive impairment (attention, memory, speed)

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23
Q

Define type 1 diabetes mellitus

A

Absolute insulin deficiency causing persistent hyperglycaemia

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24
Q

Describe the epidemiology of type 1 diabetes mellitus

A

Usually presents age 5-15 (but can be at any age)
8% of diabetes is type 1

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25
Q

What is the cause of type 1 diabetes mellitus?

A

Autoimmune destruction of insulin-producing beta-cells of the pancreas

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26
Q

What are the risk factors for type 1 diabetes mellitus?

A

Genetic (a heritable polygenic disease)
Environmental (diet, vitamin D deficiency, early-life exposure to certain viruses)

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27
Q

What are the associations of type 1 diabetes mellitus?

A

Personal and family history of autoimmune diseases

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28
Q

Describe the pathophysiology of type 1 diabetes mellitus

A

Loss of beta-cells from the pancreas and failure of insulin secretion leads to:
- reduced peripheral glucose uptake causing hyperglycaemia
- continuous breakdown of glycogen in liver (gluconeogenesis) causing hyperglycaemia, ketoacidosis, and glycosuria
- unrestrained lipolysis and skeletal muscle breakdown

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29
Q

What are the signs/symptoms of type 1 diabetes mellitus?

A

Polydipsia (increased thirst)
Polyuria (increased urination)
Weight loss (BMI < 25)
Excessive tiredness
May present with ketosis

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30
Q

What investigations are needed for type 1 diabetes mellitus?

A

Random plasma glucose > 11mmol/L
Fasting plasma glucose > 7mmol/L

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31
Q

What are the treatments of type 1 diabetes mellitus?

A

Insulin and insulin analogues
Short-acting (4-6h) to long-acting (12-24h)
Different regimens…
- multiple injection basal-bolus = short-acting before meals + once (or more) daily long-acting
- mixed (biphasic) = 1/2/3 injections of short/intermediate mix of insulin
- continuous subcutaneous infusion (insulin pump) = programmed to deliver insulin through needle/cannula, gives personalised basal rate + higher infusion at meal times

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32
Q

What are the complications of type 1 diabetes mellitus?

A

Macrovascular = increased risk of cardiovascular disease, stroke, and peripheral vascular disease (narrowing of blood vessels -> reduced blood flow -> slow wound healing -> diabetic foot disease)
Microvascular =
-retinopathy (damaged blood vessels of the retina -> vision loss)
- nephropathy (damaged vessels in the kidney -> proteinuria, increased CVD risk)
- neuropathy (nerve damage -> sensory loss, typically glove and stocking distribution, pain, diabetic foot disease, also autonomic neuropathy -> autonomic dysfunction)
DIABETIC KETOACIDOSIS

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33
Q

Define type 2 diabetes mellitus

A

Insulin resistance and relative insulin deficiency causing persistent hyperglycaemia

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34
Q

Describe the epidemiology of type 2 diabetes mellitus

A

Increasing to epidemic proportions, commonly diagnosed >40yrs old, but increasingly onset at younger ages (childhood)

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35
Q

What are the causes of type 2 diabetes mellitus?

A

Genetic and environmental factors leading to insulin resistance
Insulin deficiency due to loss of function of beta-cells/progressive insulin secretion failure

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36
Q

What are the risk factors for type 2 diabetes mellitus?

A

Obesity + lack of exercise
Family history
Asian, African, Afro-Caribbean ethnicities
High glycaemic index diet (e.g. sugary drink/food)
Age >40yrs
Drug treatments (e.g. steroids)
PCOS

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37
Q

What are the associations of type 2 diabetes mellitus?

A

Hypertension
Drug treatments (e.g. statins, steroids)
PCOS
Metabolic syndrome

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38
Q

Describe the pathophysiology of type 2 diabetes mellitus

A

Impaired insulin action leads to reduced glucose uptake in muscle/fat, and failure to supress lipolysis, leading to high circulating free fatty acids

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39
Q

What are the signs/symptoms of type 2 diabetes mellitus?

A

Polydipsia
Polyuria
Glycosuria
Blurred vision
Central obesity
*slower onset, may be asymptomatic

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40
Q

What are the investigations needed for type 2 diabetes mellitus?

A

Random plasma glucose > 11mmol/L
Fasting plasma glucose > 7mmol/L
HbA1c > 48 mmol/L

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41
Q

What are the treatments for type 2 diabetes mellitus?

A

INITIAL = lifestyle modification (diet, weight control, exercise)
1st line = metformin (increases insulin sensitivity)
If HbA1c is still high, the dual therapy = metformin +…
- DPP4 inhibitor (extends duration of GLP-1, so stimulates insulin secretion e.g. sitagliptin)
- SGLT2 inhibitor (blocks glucose reabsorption in kidney, increases glycosuria so risk of yeast infections e.g. empagliflozin)
- thiazolidinedione (activate glucose uptake gene, increases insulin sensitivity e.g. pioglitazone)
- sulphonylureas (stimulate insulin release e.g. gliclazide)
If HbA1c still high, triple therapy, then insulin

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42
Q

What are the complications of type 2 diabetes mellitus

A

Macrovascular = increased risk of cardiovascular disease, stroke, and peripheral vascular disease (narrowing of blood vessels -> reduced blood flow -> slow wound healing -> diabetic foot disease)
Microvascular =
-retinopathy (damaged blood vessels of the retina -> vision loss)
- nephropathy (damaged vessels in the kidney -> proteinuria, increased CVD risk)
- neuropathy (nerve damage -> sensory loss, typically glove and stocking distribution, pain, diabetic foot disease, also autonomic neuropathy -> autonomic dysfunction)
HYPEROSMOLAR HYPERGLYCAEMIC STATE

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43
Q

Define diabetic ketoacidosis

A

A medical emergency and serious complication of T1DM, characterised by…
- hyperglycaemia
- raised plasma ketones
- metabolic acidosis

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44
Q

What are the causes of diabetic ketoacidosis?

A

Treatment errors (stopped/reduced insulin dose)
Infection/illness (e.g. myocardial infarction)
Undiagnosed/untreated T1DM

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45
Q

Describe the pathophysiology of diabetic ketoacidosis

A

In the absence of insulin…
- unrestrained gluconeogenesis and decreased peripheral glucose uptake leads to hyperglycaemia
- peripheral lipolysis increases circulating free-fatty acids, which are oxidised to Acetyl-CoA and form ketone bodies, leading to acidosis

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46
Q

What are the signs/symptoms of diabetic ketoacidosis?

A

Extreme polydipsia and polyuria
Nausea + vomiting
Hyperventilation (Kussmaul breathing)
Weight loss
Confusion
Abdominal pain
Dehydration
Tachycardia
Hypotension

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47
Q

What are the investigations needed in diabetic ketoacidosis?

A

Random plasma glucose > 11mmol/L
Plasma ketone > 3mmol/L
Blood pH < 7.35 / HCO3- < 15mmol/L
Urine dipstick showing glycosuria and ketonuria
Serum U+E = raised urea and creatinine
Decreased total K+, increased serum K+

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48
Q

What is the treatment for diabetic ketoacidosis?

A

ABC emergency management
1st = rehydrate with 0.9% saline IV
Then give IV insulin
Then replace electrolytes (K+)
+ treat underlying cause

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49
Q

What are the complications of diabetic ketoacidosis?

A

Cerebral oedema (occurs if rehydrated too quickly, children are more at risk)
Thromboembolism (venous/arterial, occurs because of dehydration)
Aspiration pneumonia (in drowsy/comatose patients)
Death

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50
Q

Define hyperosmolar hyperglycaemic state

A

A medical emergency and serious complication of T2DM, characterised by…
- hyperglycaemia
- hyperosmolality

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51
Q

What are the causes of hyperosmolar hyperglycaemic state?

A

Untreated/undiagnosed T2DM
Infection/illness

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52
Q

Describe the pathophysiology of hyperosmolar hyperglycaemic state

A

Low insulin causes increased gluconeogenesis, leading to hyperglycaemia
Hyperglycaemia leads to osmotic diuresis, causing dehydration
*there is still enough insulin to inhibit ketogenesis, so ketosis in HHS is rare

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53
Q

What are the signs/symptoms of hyperosmolar hyperglycaemic state?

A

Extreme polydipsia and polyuria
Confusion/reduced mental state
Severe dehydration
Weakness + lethargy
Hypotension
Tachycardia

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54
Q

What are the investigations needed for hyperosmolar hyperglycaemic state?

A

Random plasma glucose >11mmol/L
Plasma osmolality = high (>320mosmol/kg)
Urine dipstick = glycosuria
U+E = decreased total K+, increased serum K+

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55
Q

What are the treatments for hyperosmolar hyperglycaemic state?

A

ABC emergency management
Rehydrate with 0.9% saline IV
Insulin (at low infusion rate) if glucose doesn’t fall quickly enough, or if ketonaemia/uria
Replace electrolytes (K+)
Can give prophylactic low-molecular weight heparins to prevent complications

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56
Q

What are the complications of hyperosmolar hyperglycaemic state?

A

Seizures, coma, death
Thromboembolisms
Cerebral oedema (if rehydrated too quickly)

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57
Q

Define acromegaly

A

Excessive secretion of growth hormone (GH), which causes the overgrowth of all organ systems, bones, joints, and soft tissues
*gigantism = excess GH occurring before puberty ends, causing increased linear growth

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58
Q

Describe the epidemiology of acromegaly

A

Diagnosis is usually in 40s, mean duration of symptoms = 8yrs

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59
Q

What are the causes of acromegaly?

A

Pituitary adenoma (secreting GH) = 99%
Rare = ectopic GH from non-endocrine tumours (e.g. lung cancer)

60
Q

What are the associations of acromegaly?

A

Familial causes associated with other endocrine disorders (e.g. multiple endocrine neoplasia type 1)

61
Q

Describe the pathophysiology of acromegaly

A

GH stimulates the production of insulin-like growth factor 1 (IGF-1) in the liver, which is the main tissue mediator of the actions of GH, and stimulates protein synthesis in the muscle, bones, and fat

62
Q

What are the signs/symptoms of acromegaly?

A

Enlargement of hands, feet, nose, tongue, jaw (prognathism)
Excessive sweating
Obstructive sleep apnoea
Lower pitched voice
Headaches
Visual field defects (bitemporal hemianopia)

63
Q

What investigations are needed for acromegaly?

A

1st line = IGF-1 (raised)
Confirmed with glucose tolerance test (glucose should cause GH to fall)
Random serum GH = raised (not recommended)
MRI scan of pituitary + hypothalamus

64
Q

What are the treatments of acromegaly?

A
  1. transsphenoidal resection surgery
  2. somatostatin analogue (e.g. octreotide) - inhibits high levels of growth hormone
  3. GH-receptor antagonists (e.g. pegvisomant)
  4. dopamine agonist (e.g. cabergoline) - improves GH and IGF-1 levels, can shrink tumours
65
Q

What are the complications of acromegaly?

A

Hypertension, CHD, cardiac failure, cerebrovascular disease
Increased risk of colon/thyroid cancer
Hyperprolactinaemia and deficiencies in other pituitary hormones
Hypopituitarism after surgery
Impaired glucose tolerance + diabetes
Psychological problems

66
Q

Define prolactinomas and hyperprolactinaemia

A

Prolactinomas are a benign, prolactin-producing tumour of the pituitary gland, causing excess prolactin production and hyperprolactinaemia

67
Q

Describe the epidemiology of prolactinomas and hyperprolactinaemia

A

More common in women

68
Q

What are the causes of prolactinomas and hyperprolactinaemia?

A

Prolactinomas = unknown cause, some genetic associations
Hyperprolactinaemia = pregnancy, breastfeeding, stress, non-functioning tumour compressing pituitary stalk (so no inhibition of prolactin release), antidopaminergic drugs

69
Q

What are the associations of hyperprolactinaemia?

A

Hypothyroidism
PCOS
Cushing’s syndrome
Sarcoidosis
*significant risk of prolactinoma enlargement in pregnancy

70
Q

Describe the pathophysiology of prolactinomas and hyperprolactinaemia

A

Microadenoma (<10mm) or macroadenoma (>10mm), leading to inhibited secretion of gonadotrophins and can stimulate lactation

71
Q

What are the sings/symptoms of prolactinomas and hyperprolactinaemia?

A

In women…
- galactorrhoea
- amenorrhea/oligomenorrhoea
- low libido
- hirsutism
- infertility
In men…
- galactorrhoea, gynaecomastia
- erectile dysfunction
- low libido
- loss of facial hair
- late presentation with osteoporosis, atherosclerosis
Pressure effects from tumour…
- headaches
- bitemporal hemianopia

72
Q

What are the investigations for prolactinomas and hyperprolactinaemia?

A

Basal serum prolactin >5000mU/L indicates true prolactinoma (avoiding stressful venepuncture)
Thyroid function tests
Rule out pregnancy
MRI of pituitary

73
Q

What are the treatments of prolactinomas and hyperprolactinaemia?

A
  1. Dopamine agonist (e.g. cabergoline) - reduced prolactin levels, shrink tumours
  2. Transsphenoidal resection surgery if no response to other treatment
74
Q

What are the complications of prolactinomas and hyperprolactinaemia?

A

Hypogonadism causes osteoporosis, reduced/in-fertility, erectile dysfunction
Tumour size can cause visual loss

75
Q

Define diabetes insipidus

A

The passage of large volumes of dilute urine due to impaired water secretion by the kidneys, because of…
- reduced ADH secretion from the posterior pituitary (cranial DI / ADH deficiency)
- impaired sensitivity to ADH in the kidney (nephrogenic DI / ADH resistance)

76
Q

What are the causes of diabetes insipidus?

A

Cranial…
- idiopathic
- trauma
- infection (encephalitis, meningitis)
- inflammation (neurosarcoidosis, granuloma)
- congenital (autosomal dominant, rarely autosomal recessive)
Nephrogenic..
- idiopathic
- metabolic (hypercalcaemia, hypokalaemia)
- drugs (lithium)
- chronic kidney disease
- inherited (X-linked V2 receptor defect, autosomal recessive aquaporin 2 defect)

77
Q

What are the risk factors of diabetes insipidus?

A

Family history
Had brain surgery/head injury
Having a metabolic disorder
Taking medications which damage kidneys
Associated conditions/illnesses

78
Q

Describe the pathophysiology of diabetes insipidus

A

Impaired water reabsorption from the kidney leading to the excretion of large volumes of dilute urine

79
Q

What are the signs/symptoms of diabetes insipidus?

A

Polyuria (>3L/day)
Polydipsia
Dehydration

80
Q

What are the investigations needed for diabetes insipidus?

A

24hr urine volume > 3L
Fluid deprivation test (8 hours), followed by desmopressin test
- in cranial DI… urine osmolality will be low but increase after desmopressin
- in nephrogenic DI… urine osmolality will be low and not increase after desmopressin
Hypertonic saline infusion and measurement of ADH
MRI of pituitary, hypothalamus etc.
Renal tract ultrasound (check for obstructive complication

81
Q

What are the treatments of diabetes insipidus?

A

Cranial DI = treat underlying cause, desmopressin (to replace ADH), mild cases = rehydration
Nephrogenic DI = avoid drugs causing the problem, correct metabolic abnormalities, high-dose desmopressin, combination treatment with thiazide diuretic (e.g. Bendroflumethiazide)

82
Q

What are the complications of diabetes insipidus?

A

Desmopressin can worsen myocardial ischemia, and increase risk of heart attack
Patients with genetic causes are prone to bladder dysfunction

83
Q

Define SIADH

A

Syndrome of inappropriate antidiuretic hormone - inappropriate over-secretion of ADH, causing large amount of water to be reabsorbed in the collecting duct

84
Q

What are the causes of SIADH?

A

After major abdominal/thoracic/neuro surgery
Infection (pneumonia + abscess)
Head injury (haemorrhage, stroke)
Medications (opiates)
Malignancy (ectopic source e.g. lung carcinoma)

85
Q

Describe the pathophysiology of SIADH

A

Too much ADH is released when in shouldn’t be, increasing the expression of aquaporin-2 so that more water is reabsorbed in the collecting duct of the kidney, leading to increased total body water and decreased plasma osmolality

86
Q

What are the signs/symptoms of SIADH?

A

Headache
Nausea
Fatigue
Muscle cramps
Confusion
*all non-specific symptoms of severe hyponatraemia

87
Q

What are the investigations needed for SIADH?

A

Urinalysis: high sodium (>20mmol/L) and osmolality (>100mosmol/kg)
U+Es: low plasma sodium (<125mmol/L) and osmolality (<260mosmol/kg)
Need to rule out other causes of hyponatraemia: SynACTHen test = -ve to exclude adrenal insufficiency, no AKI/CKD, no history of diuretic use, diarrhoea, or vomiting

88
Q

What are the treatments for SIADH?

A

Treat underlying cause
Fluid restriction
Tolvaptan (ADH receptor blocker - promotes water excretion without the loss of electrolytes)

89
Q

Define Cushing’s syndrome

A

Long-term exposure to excessive levels of exogenous or endogenous glucocorticoids (cortisol)

90
Q

Describe the epidemiology of Cushing’s syndrome

A

Prevalence varies in different ethnic and cultural groups depending on the use of steroid-based therapies
Higher prevalence in patients with a combination of obesity/T2DM/hypertension
Cushing’s syndrome caused by adrenal/pituitary tumour is more common in women, mostly aged 25-40

91
Q

What are the causes of Cushing’s syndrome?

A

Exogenous use of glucocorticoids/iatrogenic = most common cause
Endogenous causes are split into ACTH dependent…
- excessive ACTH from pituitary adenoma (Cushing’s disease) = 80% of cases
- ectopic ACTH-producing tumours = 20% of cases
or ACTH independent…
- adrenal adenoma = 60%
- adrenal carcinoma = 40%

92
Q

What are the associations of Cushing’s syndrome?

A

Conditions requiring steroid therapy (e.g. COPD, hay fever, atopic asthma, IBD, MS)

93
Q

Describe the pathophysiology of Cushing’s syndrome

A

Chronic glucocorticoid excess
Loss of normal feedback mechanisms of HPA axis
Loss of circadian rhythm of cortisol secretion (usually highest on waking)

94
Q

What are the signs/symptoms of Cushing’s syndrome?

A

Central obesity, buffalo hump
Face fullness, moon face
Weight gain
Skin changes: acne, striae, easy bruising, hirsutism
Hypertension
Gonadal dysfunction (irregular menses, erectile dysfunction)
Mood changes (depression, lethargy, psychosis)
Proximal muscle wasting/weakness
Osteoporosis
Impaired immune function: increased infection, poor healing
Hyperglycaemia (diabetes, polydipsia, polyuria)

95
Q

What are the investigations needed for Cushing’s syndrome?

A
  • 24 hour urinary free cortisol = raised cortisol in 2/3 collections confirms Cushing’s syndrome
  • Overnight dexamethasone suppression test = 1mg of dexamethasone given at night, cortisol measured next morning (cortisol won’t be supressed in Cushing’s syndrome)
  • Midnight cortisol levels = should be low due to circadian rhythm, but will remain high in Cushing’s syndrome
  • Plasma ACTH = to confirm cause
  • MRI/CT for suspected tumours
96
Q

What is the treatment for Cushing’s syndrome?

A

Depends on the cause…
- iatrogenic = stop medications if possible
- Cushing’s disease = transsphenoidal surgery to remove pituitary adenoma
- Adrenal tumours = surgical removal
Drugs…
- enzyme inhibitors for cortisol synthesis = metyrapone, ketoconazole

97
Q

What are the complications of Cushing’s syndrome?

A

Hypertension
Osteoporosis
Diabetes and impaired glucose tolerance
Impaired immunity, opportunistic infections
Death from vascular disease (MI/stroke), uncontrolled diabetes, infections

98
Q

Define adrenal insufficiency and Addison’s disease

A

Primary = Addison’s disease: adrenal insufficiency caused by the destruction of the adrenal gland
(secondary = adrenal insufficiency caused by insufficient production of ACTH in the pituitary, due to long-term use of corticosteroids, or disorders of the pituitary/hypothalamus)

99
Q

Describe the epidemiology of Addison’s disease

A

Most common age of onset = 30-50yrs, women affected more than men

100
Q

What are the causes of Addison’s disease?

A

Autoimmunity (80% of cases in the UK)
TB (commonest cause worldwide)
Congenital adrenal hyperplasia (commonest cause in children)
Adrenal metastases (e.g. lung, breast, renal cancer)

101
Q

What are the associations of Addison’s disease?

A

Autoimmune conditions (T1DM, vitiligo, etc.)

102
Q

Describe the pathophysiology of Addison’s disease

A

Destruction of the adrenal cortex leads to reduced production of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
ACTH production will increase due to the lack of negative feedback from cortisol

103
Q

What are the signs/symptoms of Addison’s disease?

A

Fatigue
Weight loss
Vomiting + diarrhoea
Abdominal pain
Headache
Postural hypotension
Lean
Tanned
Pigmented palmar creases + buccal mucosa
Shock (in adrenal crisis)

104
Q

What are the investigations needed for Addison’s disease?

A

Serum cortisol <100nmol/L (measures in morning when cortisol is highest due to Circadian rhythm)
U+Es = hyponatraemia, hyperkalaemia
May have low glucose, high calcium, high TSH, high renin
Diagnosis confirmed with synthetic-ACTH stimulation test (synacthen)
- 250mg of synthetic-ACTH given IV/IM, after 30 mins cortisol < 500nmol/L (low) = Addison’s
Test for adrenal antibodies to confirm autoimmune cause

105
Q

What is the treatment for Addison’s disease?

A

Replace steroids…
- hydrocortisone to replace cortisol
- fludrocortisone to replace aldosterone
In adrenal crisis… immediate high dose of IV hydrocortisone, fluid to support BP, glucose if needed
If unwell with flu/fever… double steroid dose

106
Q

What are the complications of Addison’s disease?

A

Adrenal crisis -> shock, stroke, cardiac arrest
Adverse maternal and neonatal outcomes
Reduced quality of life
Premature ovarian insufficiency

107
Q

Define Conn’s syndrome

A

Primary hyperaldosteronism due to an aldosterone producing adenoma

108
Q

What are the causes of Conn’s syndrome?

A

Aldosterone-producing adenoma (causes 2/3 of hyperaldosteronism cases)
Other causes of primary hyperaldosteronism include adrenocortical hyperplasia, adrenal carcinoma

109
Q

Describe the pathophysiology of Conn’s syndrome

A

Excess production of aldosterone, independent of renin-angiotensin system, leading to…
- high sodium and water retention
- increased potassium excretion in kidneys
- low renin release

110
Q

What are the signs/symptoms of Conn’s syndrome?

A

Hypertension
Heart arrhythmias (AF)
Fatigue
Muscle cramps, weakness, paraesthesia
Hypokalaemia
Polyuria + nocturia
Excessive thirst
Mood disturbance (e.g. anxiety/depression)
Difficulty concentrating, memory loss

111
Q

What are the investigations needed for Conn’s syndrome?

A

Aldosterone-renin ratio: increased
Plasma potassium: reduced

112
Q

What are the treatments for Conn’s syndrome?

A

1st line: spironolactone (aldosterone antagonist - controls BP and potassium levels)
Gold standard: laparoscopic adrenalectomy

113
Q

Define hyperparathyroidism

A

Excessive secretion of parathyroid hormone (PTH) due to…
- primary = one (or more) parathyroid gland(s) producing excess PTH
- secondary = increased secretion of PTH in response to hypocalcaemia because of kidney/bowel/liver disease

114
Q

Describe the epidemiology of hyperparathyroidism

A

Primary hyperparathyroidism is more common in women, diagnosed 50-60 y/o

115
Q

What are the causes of hyperparathyroidism?

A

Primary…
- 80% = single benign adenoma
- 20% = 4 gland hyperplasia
- 0.5% = malignant
Secondary…
- most commonly due to CKD
- also vitamin D deficiency/malabsorption
Tertiary…
- prolonged secondary causes

116
Q

What are the association of hyperparathyroidism?

A

CKD
Vitamin D deficient osteomalacia/rickets
Gastrointestinal malabsorption
Multiple endocrine neoplasia syndromes

117
Q

Describe the pathophysiology of hyperparathyroidism

A

Primary…
- raised PTH increases its affects = increased release of calcium and phosphate from bones, increased reabsorption of calcium and decreased reabsorption of phosphate in kidneys, increased vitamin D production
- overall = increase of calcium and decreased phosphate in blood
Secondary…
- low levels of calcium cause an appropriately raised PTH, due to negative feedback
- increased affects of PTH (as above)
Tertiary…
- raised PTH is an inappropriate response (as calcium is raised, so PTH is not limited by feedback control)
- increased affects of PTH (as above)

118
Q

What are the signs/symptoms of hyperparathyroidism?

A
  • bones = pain, osteoporosis
  • stones = renal calculi (kidney stones)
  • groans * = abdominal groans (e.g. nausea, vomiting, constipation, pancreatitis)
  • moans * = physic moans (e.g. confusion, depression)
    also: hypertension
    *not present in secondary hyperparathyroidism as caused by hypercalcaemia
119
Q

What are the investigations needed for hyperparathyroidism?

A

Albumin-adjusted serum calcium = high in primary and tertiary, low in secondary
PTH = high in all types
Phosphate = low in primary, high or low in secondary, usually high in tertiary
DEXA scan = shows loss of bone density
Ultrasound of renal tract to check for stones

120
Q

What are the treatments for hyperparathyroidism?

A

Primary = removal of adenoma/hyperplastic glands, increase fluid intake, vitamin D analogues, bisphosphate to reduce chance of fractures
Secondary = treat underlying cause, calcium supplements, vitamin D analogues, cinacalcet (mimics calcium)
Tertiary = cinacalcet, total/partial parathyroidectomy

121
Q

What are the complications of hyperparathyroidism?

A

Hypercalcaemia -> coma, death
After surgery… hypoparathyroidism, damage to recurrent laryngeal nerve -> hoarseness

122
Q

Define hypoparathyroidism

A

Reduced secretion of parathyroid hormone (PTH), characterised by…
- hypocalcaemia
- hyperphosphatemia
- low/inappropriately normal levels of PTH

123
Q

What are the causes of hypoparathyroidism?

A

Autoimmune
Surgery/radiation
Magnesium deficiency
Congenital syndromes (e.g. DiGeorge’s)
Genetic faults in PTH or calcium receptor genes
Defects in PTH action (PTH resistance = pseudohypothyroidism)

124
Q

What are the risk factors for hypoparathyroidism?

A

Other autoimmune disorders

125
Q

Describe the pathophysiology of hypoparathyroidism

A

Low levels of PTH leads to decrease bone resorption (less release of calcium), decreased calcium and increased phosphate reabsorption in kidneys, and decreased vitamin D production, so overall decrease in calcium and increase in phosphate in blood

126
Q

What are the signs and symptoms of hypoparathyroidism?

A

Due to hypocalcaemia…
- muscle pains and spams (laryngospasm)
- paraesthesia (burning/tingling/numbness) or face, fingers, toes
- carpopedal spasm (fingers pull together + wrist flexion when brachial artery compresses)
- Chvostek’s sign (tapping facial nerve causes facial muscle spams)

127
Q

What are the investigations needed for hypoparathyroidism?

A

Serum calcium = low
Serum phosphate = high
PTH = low
Alkaline phosphate = normal
ECG = prolonged QT interval
U+Es (to exclude CKD)
Vitamin D (check for deficiency as cause of hypocalcaemia)

128
Q

What are the treatments of hypoparathyroidism?

A

Calcium supplements
Vitamin D analogues (calcitriol)
Synthetic PTH replacement

129
Q

What are the complication of hypoparathyroidism?

A

Laryngospasm -> airway obstruction
Prolonged QT interval -> syncope, arrythmias, death
Calcium deposits -> kidney stones
Stunted growth, malformed teeth, mental impairment if untreated in childhood

130
Q

Define hyperkalaemia

A

Plasma potassium in excess of 5.5mmol/L

131
Q

Describe the epidemiology of hyperkalaemia

A

More common in men, more at risk in very young/old

132
Q

What are the causes of hyperkalaemia?

A

Impaired excretion:
- acute kidney injury (AKI)
- chronic kidney disease (CKD)
- drugs affecting renal function (e.g. ACEi, NSAIDs)
- renal tubular acidosis
- Addison’s disease (due to low aldosterone)
Increased potassium in circulation:
- excess K+ therapy
- increased dietary intake
- tissue breakdown (burns, tumour lysis syndrome, rhabdomyolysis)
Shift from intracellular to extracellular:
- metabolic acidosis
- diabetic ketoacidosis (decreased insulin)
- drugs (e.g. digoxin toxicity)

133
Q

What are the associations of hyperkalaemia?

A

Addison’s disease (primary adrenal insufficiency)
Diabetes (risk of DKA, likely to be on ACEi)
Tumour lysis syndrome
Rhabdomyolysis

134
Q

What are the signs/symptoms of hyperkalaemia?

A

Fatigue
Weakness
Chest pain
Palpitations
Arrhythmias
Bradycardia
Tachypnoea
Depressed or absent tendon reflexes
Flaccid paralysis (weakness of limbs, muscles of respiration and swallowing)

135
Q

What are the investigations needed for hyperkalaemia?

A

Bloods… FBC, U+Es, plasma glucose, arterial blood gas (to check for metabolic acidosis)
ECG… small/absent P waves, prolonged PR interval, wide QRS interval, peaked T waves

136
Q

What is the treatment for hyperkalaemia?

A

In emergency (K+ > 7mmol/L, or any rise with abnormal ECG)…
- ABC emergency management
- give calcium gluconate to protect the myocardium (doesn’t treat K+ levels)
- give insulin to stimulate intracellular shift of K+ (salbutamol will have the same effect)
- treat underlying cause, if persisting remove excess K+ using polystyrene sulfonate resin
In non-emergency…
- treat underlying cause
- can use polystyrene sulfonate resin to prevent GI absorption of K+

137
Q

What are the complications of hyperkalaemia?

A

Death (most fatal cases are complicated by AKI)

138
Q

Define pseudohyperkalaemia

A

This is an artefactual result where the patient is well but the potassium is unexpectedly high due to…
- prolonged tourniquet time
- difficult venepuncture
- patient had fist clenched
- use of wrong anticoagulants (potassium EDTA)
- delayed analysis (stored too long)
- test tube haemolysis (tube shaken/blood squirted through needle)
Any doubt = repeat test urgently

139
Q

Define hypokalaemia

A

Plasma potassium below 3.5 mmol/L

140
Q

Describe the epidemiology of hypokalaemia

A

More common in women, elderly most at risk

141
Q

What are the causes of hypokalaemia?

A

Increased loss…
- renal disease
- Conn’s syndrome (high aldosterone)
- thiazide or loop diuretic
- diarrhoea + vomiting
- laxatives
- burns
- increased sweating
- activation of RAAS (e.g. Gitelman’s syndrome)
Decreased intake…
- dietary deficiency
- fasting
- anorexia nervosa
Shift from extracellular to intracellular…
- alkalosis (metabolic/respiratory)
- drugs (e.g. insulin, glucose, beta-2 agonists)

142
Q

What are the associations of hypokalaemia?

A

Heart failure
Nephrotic syndrome
Alcoholism (multifactorial)
Conn’s syndrome
Gitelman’s syndrome

143
Q

What are the sings/symptoms of hypokalaemia?

A

Fatigue
Muscle weakness + pain
Tetany
Hypotonia
Hyporeflexia
Constipation
Palpitations
Arrhythmias

144
Q

What investigations are needed for hypokalaemia?

A

Bloods… U+Es, FBC, glucose, bicarbonate
Urinary… low potassium if due to poor intake, shift to intracellular, GI loss, high potassium if due to renal loss (also measure sodium and osmolality)
ECG… ST depression, flat T waves, prominent U waves

145
Q

What are the treatments for hypokalaemia?

A

If mild/low risk of complications… treat underlying cause, dietary supplements, oral K+ replacement
If severe… IV K+ replacement using KCl (slowly, low concertation)

146
Q

What are the complications of hypokalaemia?

A

Cardiac arrhythmias and sudden cardiac death
Abnormal renal function (e.g. nephrotic diabetes insipidus)
Iatrogenic hyperkalaemia

Phase 2a (14 decks)

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