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Phase 2a BASICS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Where is insulin and glucagon secreted from?

A

secreted from alpha and beta cells in the islets of langerhans in the pancreas

alpha cells- glucagon
beta cells- insulin

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2
Q

What is type 1 diabetes mellitus?

A

autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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3
Q

When does type 1 DM usually present?

A

age 5-15

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4
Q

Describe the pathophysiology of type 1 diabetes mellitus.

A
  • autoantibodies attack beta cells in islets of langerhans
  • leads to insulin deficiency
  • hyperglycaemia
  • continuous breakdown of glycogen from the liver causes glycosuria
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5
Q

What is the medical term for sugar in the urine?

A

glycosuria

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6
Q

Who is most at risk of T1 DM?

A
  • Northern European people
  • patients already suffering with autoimmune disease
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7
Q

What are the signs and symptoms of T1 DM?

A

The classic triad: polydipsia, polyuria, weight loss

usually a short history of severe symptoms

may present with ketosis

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8
Q

What is the medical term for extreme thirstiness?

A

polydipsia

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9
Q

What is ketosis?

A

the burning of fat for energy instead of glucose

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10
Q

How is T1 DM diagnosed?

A

fasting plasma glucose > 7mmol/L or random plasma glucose > 11.1mmol/L

if patient is symptomatic only need one raised plasma glucose reading

if patient asymptomatic need 2 abnormal readings on different occasions

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11
Q

What is the treatment for T1 DM?

A

basal-bolus insulin treatment

basal - insulin that is injected once or twice a day always

bolus - insulin that is injected specifically before a mean

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12
Q

What antibodies have been found to be associated with T1 DM?

A

anti GAD
pancreatic islet cell Ab
islet antigen-2 Ab
ZnT8

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13
Q

Describe the pathophysiology of T2 DM.

A
  • repeated exposure to high levels of glucose leads to repeated release of insulin which makes cells resistant to effects of insulin
  • over time beta cells become fatigued and damaged from overuse and start to produce less
  • continues pancreatic fatigue leads to chronic hyperglycaemia
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14
Q

What are the risk factors of T2 DM?

A

obesity/ inactivity
alcohol excess
asian males
age
hypertension
family history

gestational diabetes

steroid use
Cushing’s syndrome
chronic pancreatitis

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15
Q

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

A

slower onset that type 1

polydipsia
polyuria
glycosuria
blurred vision
polyphagia

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16
Q

What is the term for extreme hunger?

A

polyphagia

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17
Q

How is T2 DM diagnosed?

A

similar to T1 except for HbA1c test

  1. HbA1c - GOLD STANDARD
    HbA1C > 48mmol/mol - diabetes
    HbA1c 42-47 mmil/mol - prediabates
  2. Blood tests
    random plasma glucose > 11.1mmol/L
    fasting plasma glucose > 7 mol/L
  3. Oral glucose tolerance test
    fasting > 7 mol/L
    2 hrs after glucose > 11.1 mol/L
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18
Q

What is the management of type 1 diabetes?

A

1st line- lifestyle changes
- weight loss
- dietary advice (high complex carbs, low fat)
- smoking cessation
- exercise
- blood pressure control

2nd line- metformin
used if newly diagnosed patient have blood glucose above 48mmol/L after lifestyle modifications

3rd line- dual therapy of metformin with sulfonylurea/ pioglitazone/ DPP-4 inhibitor/ SGLT-2 inhibitor

4th line- if still not working, insulin

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19
Q

How does metformin treat diabetes?

A

increases sensitivity to insulin

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20
Q

How does sulphonylurea treat diabetes?

A

increases insulin secretion

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21
Q

What is diabetic ketoacidosis?

A

complete lack of insulin results in high ketone production

medical emergency

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22
Q

In which patients do we tend to see diabetic ketoacidosis?

A

it’s the most common way that children with a new diagnosis of T1 DM present

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23
Q

Describe the pathophysiology of diabetic ketoacidosis.

A

occurs when body does not have enough insulin to use and process glucose

  • complete absence of insulin
  • unrestrained production of glucose and decreased peripheral glucose uptake
  • hyperglycaemia
  • osmotic diuresis
  • dehydration
  • peripheral lipolysis for energy
  • increased free fatty acids
  • fatty acids oxidised to acetyl coA
  • production of ketones leads to acidosis
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24
Q

What is the direct effect of ketones on the body?

A

anorexia and vomiting

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25
Q

What are the causes/ risk factors of diabetic ketoacidosis?

A
  • untreated T1DM/ interruption of insulin therapy
  • undiagnosed DM
  • infection/ illness
  • myocardial infarction
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26
Q

What is the presentation of diabetic ketoacidosis?

A

extreme diabetes symptoms plus:
- nausea and vomiting
- weight loss
- confusion/ drowsiness, potential coma
- Kussmaul’s breathing
- ‘pear drop’ breath
- abdo pain

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27
Q

What is Kaussmaul’s breathing?

A

an abnormal breathing pattern characterised by rapid, deep breathing at a consistent pace

characteristic of diabetes-related ketoacidosis (DKA)

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28
Q

How is diabetic ketoacidosis diagnosed?

A

blood test:
hyperglycaemia (blood glucose > 11mmol/L)
ketosis (blood ketones > 3mmol/L)

arterial blood gas:
acidosis (pH < 7.3 and/or bicarbonate < 15 mmol/L) - ABG

urine dipstick:
glycosuria, ketonuria

U+Es:
raised urea + creatinine

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29
Q

What is the treatment for diabetic ketoacidosis?

A
  • immediate abc management
  • replace fluid loss with IV 0.9% saline
  • IV insulin
  • restore electrolytes
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30
Q

What are the potential complications of diabetic ketoacidosis?

A

cerebra oedema (leading to coma, death)

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31
Q

Why can insulin treatment for DKA cause hypokalaemia and why is it dangerous?

A

insulin decreases potassium levels in the blood by redistributing K+ into cells via increased sodium potassium pump activity

causes low serum K+ levels - hypokalaemia

low levels of K+ can cause arrhythmia and weakness

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31
Q

Why can insulin treatment for DKA cause hypokalaemia and why is it dangerous?

A

insulin decreases potassium levels in the blood by redistributing K+ into cells via increased sodium potassium pump activity

causes low serum K+ levels - hypokalaemia

low levels of K+ can cause arrhythmia and weakness

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32
Q

Why is polyphagia a symptom/ sign of diabetes mellitus?

A

although glucose is high in blood it cannot enter cells

cells are starved of energy

body undergoes lipolysis and proteolysis which leaves patients hungry

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32
Q

Why is polyphagia a symptom/ sign of diabetes mellitus?

A

although glucose is high in blood it cannot enter cells

cells are starved of energy

body undergoes lipolysis and proteolysis which leaves patients hungry

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33
Q

What is HHS?

A

hyperosmolar hyperglycaemia state

marked hyperglycaemia and hyperosmolality

serious complication of T2 DM- medical emergency

usually no ketosis

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34
Q

Describe the pathophysiology of hyperosmolar hyperglycaemic state.

A
  • insulin levels are sufficient to inhibit hepatic ketogenesis BUT insufficient to inhibit hepatic glucose production
  • hyperglycaemia results in osmotic diuresis with loss of sodium and potassium
  • severe volume depletion results in a significant raised serum osmolarity resulting in hyper viscosity of blood
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35
Q

What causes hyperosmolar hyperglycaemic state?

A

untreated/ undiagnosed T2DM

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36
Q

What are the signs and symptoms of HHS?

A

Extreme diabetes symptoms plus…

  • fatigue/ lethargy
  • nausea and vomiting
  • altered consciousness
  • headaches
  • papilloedema
  • dehydration
  • hypotension
  • tachycardia
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37
Q

How is HHS diagnosed?

A

severe hyperglycaemia:
random plasma glucose > 30mmol/L
glycosuria on dipstick

hyperosmolality

unlike DKA- no significant acidosis or ketosis

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38
Q

What is the treatment for HHS?

A

fluid replacement with 0.9% saline

VTE prophylaxis (high risk due to dehydration) - LMW heparin e.g. enoxaprin

IV insulin if high levels of ketones or treatment not working

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39
Q

What are the complications of HHS?

A

hyperviscosity may cause:
stroke
MI
PE

high dose insulin therapy may cause:
insulin related hypoglycaemia
treatment related hypokalaemia

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40
Q

What is hypoglycaemia?

A

blood glucose levels below 3 mmol/L

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41
Q

Describe the pathophysiology of hypoglycaemia.

A
  • blood glucose is taken up by cells, leading to drop in blood glucose levels
  • this stimulated alpha cells to produce glucagon and reduce production of insulin from beta cells
  • decreased blood glucose increases production of adrenaline, GH and cortisol
  • all of these mechanism act to rapidly increase blood glucose

the pathophysiology of hypoglycaemia depends on its cause and an interruption to one of the above mechanisms

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42
Q

What does the thyroid gland secrete?

A

thyroxine (T4)
triiodothyronine (T3)

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43
Q

What is hypothyroidism?

A

a clinical effect of lack of thyroid hormones

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44
Q

What is the difference between primary and secondary hypothyroidism?

A

primary:
abnormally reduced thyroid function

secondary:
pituitary fails to produce enough TSH

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45
Q

What are the causes of primary hypothyroidism?

A

most common cause: Hashimoto’s thyroiditis

radiotherapy
de quervain’s thyroiditis
dietary iodine deficiency

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46
Q

Which conditions are associated with hypothyroidism?

A

downs syndrome
turners syndrome
coeliac disease

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47
Q

How do patients with hypothyroidism present?

A

weight gain
lethargy
cold intolerance
menorrhagia
constipation
dry scalp

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48
Q

What investigations confirm a diagnosis of hypothyroidism?

A

1st line: thyroid function tests (TFTs)

primary - high TSH, low T4
secondary - low TSH, low T4

elevated antithyroid peroxidase antibodies

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49
Q

How is hypothyroidism treated?

A

levothyroxine

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50
Q

What is Hashimoto’s thyroiditis?

A

an autoimmune disease in which the thyroid gland is attacked causing primary hypothyroidism

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51
Q

Describe the pathophysiology of Hashimoto’s thyroiditis.

A

antithyroid antibodies attack thyroid tissue causing progressive fibrosis (low T4, high TSH)

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52
Q

What is the treatment for Hashimoto’s thyroiditis?

A

levothyroxine

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53
Q

What is hyperthyroidism?

A

the clinical effect of excess thyroid hormone

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54
Q

What is the difference between primary and secondary hyperthyroidism?

A

primary- abnormal increased thyroid function

secondary- abnormal increased TSH production

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55
Q

What is the main cause of hyperthyroidism?

A

Graves’ disease- accounts for approx. 70% of cases

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56
Q

What are the causes of hyperthyroidism?

A
  • Graves’ disease (most common)
  • toxic multi nodular goitre
  • iodine excess
  • thyroiditis
  • amiodarone use
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57
Q

How does hyperthyroidism present?

A

weight loss
heat intolerance
palpitations
sweating
pretibial myxoedema
diarrhoea
oligomenorrhoea
anxiety
tremor

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58
Q

How is hyperthyroidism diagnosed?

A

1st line: thyroid function tests (TFTs)
will show high T4 and low TSH

antibodies present: TSH-receptor antibodies

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59
Q

What is the treatment for hyperthyroidism?

A

Depends on the cause

  1. Drug management
    - 1st line: carbimazole (blocks synthesis of T4)
    - 2nd line: propylthiouracil (prevents T4 to T3 conversion)
    - beta blockers (rapid symptom relief of tremor etc)
  2. Radioiodine treatment (beta particles used to cause ionisation of thyroid cell, may exacerbate thyroid eye disease)
  3. Surgery (thyroidectomy)
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60
Q

What is Graves’ disease?

A

autoimmune destruction of the thyroid gland resulting in hyperthyroidism

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61
Q

What causes Graves’ disease?

A

autoimmune disease
can be caused by MS drug alemtuzumab

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62
Q

Describe the pathophysiology of Graves’ disease.

A

IgG autoantibodies are directed against the thyrotropin (TSH) receptor

they bind and activate the receptor, causing autonomous production of thyroid hormones

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63
Q

How does Graves’ disease present?

A

All symptoms of hyperthyroidism plus:

thyroid eye disease:
- bulging eyes (exophthalmos)
- extra ocular muscle palsy (ophthalmoplegia)
- eyelid retraction

thyroid acropatchy (triad of digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation)

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64
Q

How is Grave’s disease diagnosed?

A

Same as hyperthyroidism
TFTs- high T4 and low TSH

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65
Q

How is Graves’ disease treated?

A

The same as hyperthyroidism:

  1. Drug management
    - 1st line: carbimazole (blocks synthesis of T4)
    - 2nd line: propylthiouracil (prevents T4 to T3 conversion)
    - beta blockers (rapid symptom relief of tremor etc)
  2. Radioiodine treatment (beta particles used to cause ionisation of thyroid cell, may exacerbate thyroid eye disease)
  3. Surgery (thyroidectomy)
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66
Q

What is De Quervain’s thyroiditis?

A

aka subacute granulomatous thyroiditis
inflammation of thyroid gland resulting in the rapid swelling of the thyroid gland, painful and uncomfortable

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67
Q

What causes De Quervain’s thyroiditis?

A

often occurs following a viral infection

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68
Q

Describe the pathophysiology of De Quervain’s thyroiditis.

A

4 phases:

phase 1 - lasts 3-6 weeks
hyperthyroidism, painful goitre, raised ESR

phase 2- lasts 1-3 weeks
euthyroid (normal function)

phase 3- weeks to months
hypothyroidism

phase 4
thyroid structure and function returns to normal

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69
Q

How does De Quervain’s thyroiditis present?

A

neck/ jaw/ ear pain
difficulty eating
tend, firm, enlarged thyroid
fever
palpitations

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70
Q

What investigations confirm a diagnosis of De Quervain’s thyroiditis?

A

Elevated:
total T4
T3
T3 resin uptake
free thyroxine index
CRP

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71
Q

What is the treatment of De Quervain’s thyroditis?

A

hyperthyroid phase: NSAIDS and corticosteroids for pain
hypothyroid phase: usually not treatment but if severe hypothyroidism occurs may give small dose of levothyroxine

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72
Q

What is an acute diagnosis for a patient with an episode of hyperthyroidism followed by an episode of hypothyroidism?

A

De Quervain’s thyroiditis

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73
Q

What are the four main types of thyroid cancer?

A

papillary
follicular
anaplastic
medullary

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74
Q

What are the risk factors of thyroid cancer?

A

head and neck radiation exposure
female sex

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75
Q

How does thyroid cancer present?

A

palpable thyroid nodule

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76
Q

How is thyroid cancer diagnosed?

A

1st line: ultrasound neck

fine needle biopsy

laryngoscopy

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77
Q

What is the treatment for thyroid cancer?

A

total thyroidectomy followed by radioactive iodine ablation and suppression of TSH

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78
Q

What are the possible complications of total thyroidectomy?

A

increased risk of recurrent laryngeal nerve damage or hypoparathyroidism

thyroid storm

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79
Q

What type of thyroid cancer has the best and worst prognosis?

A

Best: papillary

Worst: anaplastic, median survival 3-8 months

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80
Q

What is a thyroid storm?

A

AKA thyrotoxic crisis

the severe end of the spectrum of thyrotoxicosis and is characterised by compromised organ function

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81
Q

What are the potential causes of a thyroid storm?

A

Graves’ disease
post thyroidectomy
infection/ trauma
MI
DKA
pregnancy
iodine
abrupt cessation of thyroid drugs

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82
Q

How does a thyroid storm present?

A

fever
cardiovascular disfunction
profuse sweating
tachyarrhythmias
nausea and vomiting

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83
Q

Describe the pathophysiology of a thyroid storm.

A

clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones, usually caused by hyperthyroidism

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84
Q

How is a thyroid storm diagnosed?

A

completely suppressed TSH and high thyroxine
diagnosed with clinical presentation

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85
Q

How is a thyroid storm treated?

A

1st line: antithyroid treatment- carbimazole

hydroscortisone- treats possible relative adrenal insufficiency, decreased T4 to T3 conversion

gold standard: thyroidectomy

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86
Q

Describe the basic anatomy of the thyroid gland.

A

two lobes (left and right) connected by the central isthmus

wrapped around the cricoid cartilage

butterfly shape

blood supply from the inferior and superior thyroid artery

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87
Q

What hormones are secreted by the anterior pituitary?

A
  • adrenocorticotropic hormone (ACTH)
  • growth hormone (GH)
  • luteinising hormone (LH)
  • follicle-stimulating hormone (FSH)
  • prolactin
  • thyroid-stimulating hormone (TSH)
88
Q

What hormones are secreted by the posterior pituitary?

A
  • anti-diuretic hormone (ADH)
  • oxytocin
89
Q

What hormone is secreted from the pars intermedia of the pituitary gland?

A

melanocyte-stimulating hormone

90
Q

What is the function of ACTH?

A

stimulates the adrenal glands to secrete steroids (e.g. cortisol)

91
Q

What is the function of GH?

A

regulates growth, metabolism and body composition

92
Q

What is the function of LH and FSH?

A

These are the gonadotropins

act on ovaries/ testes to stimulate sex hormone production and egg/ sperm maturity

93
Q

What is the function of prolactin?

A

stimulates milk production in mammary glands

94
Q

What is the function on TSH?

A

stimulates thyroid gland to secrete thyroid hormones

95
Q

What is the function of ADH/ vasopressin?

A

controls water balance and blood pressure

96
Q

What is the function of oxytocin?

A

stimulates uterine contractions during labour and milk secretion during breast feeding

97
Q

What is the function of melanocyte-stimulating hormone?

A

acts on cells in the skin to stimulate the production of melanin

98
Q

Where are posterior pituitary hormones made?

A

hypothalamus

99
Q

What is a pituitary adenoma?

A

a benign growth on the pituitary gland

100
Q

What are the 3 categories of pituitary adenoma?

A

prolactinoma
acromegaly
Cushing’s syndrome

101
Q

What is Cushing’s syndrome?

A

long term exposure to excessive cortisol hormone released by adrenal glands

102
Q

What are causes of Cushing’s syndrome?

A

2 classes:

ACTH dependent (rare):
- ACTH secretion from pituitary adenoma
- ectopic ACTH production from small cell lung cancer

ACTH independent:
- Iatrogenic- steroid use (e.g. prednisolone)
- adrenal adenoma

103
Q

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

A

Cushing’s syndrome that occurs as a result of a pituitary tumour is called Cushing’s disease

104
Q

How does Cushing’s disease present?

A

round moon face
central obesity
abdominal striae
buffalo hump
proximal limb muscle wasting
mood change
ammenorhea/ irregular periods
acne
hirsutism

105
Q

What is ammenorhea?

A

absence of a period in women

106
Q

What is hirsutism?

A

when women have excessive dark/ coarse hair in a male-like pattern (face/ chest/ back)

107
Q

How is Cushing’s syndrome diagnosed?

A

1st line: raised random plasma cortisol

gold standard: dexamethasone suppression test- cortisol will not be suppressed in Cushing’s

other tests:
24hr urinary free cortisol
MRI brain (for pit. adenoma)
chest CT (for small cell lung cancer)
abdominal CT (for adrenal tumour)

108
Q

Why can you not make a diagnosis of Cushing’s off the random plasma cortisol alone?

A

can be misleading as cortisol is raised depending on illness, time of day, stress etc and will influence results

109
Q

What is the treatment for Cushing’s syndrome?

A

depends on the underlying cause

if cause is:

  • iatrogenic- stop steroids
  • Cushing’s disease- trans-sphenoidal surgery to remove pituitary adenoma
  • adrenal adenoma- adrenalectomy
  • ectopic ACTH production- surgery to remove neoplasm is can be located and hasn’t metastasised

cortisol synthesis inhibition drugs: metyrapone, ketoconazole

110
Q

What are the potential complications of Cushing’s syndrome?

A

hypertension
cardiovascular diasease
osteoporosis
diabetes mellitus

111
Q

What is acromegaly?

A

release of excess growth hormone (GH) causing overgrowth of all systems

112
Q

What are the causes of acromegaly?

A
  • 99% due to pituitary adenoma
  • (rarely) secondary to a malignancy that secretes ectopic GH (e.g. lung cancer)
113
Q

Describe the pathophysiology of acromegaly.

A

GHRH is released from the hypothalamus and stimulates release of GH from anterior pituitary

this results in excessive production of insulin-like growth factor (IGF-1) which is responsible for inappropriate growth

this stimulates bone and soft tissue growth

114
Q

How does acromegaly present?

A

large spade-like hands a feet
prominent forehead and brow
large tongue
increased jaw size- “prognathism”
bitemporal hemianopia
acroparaesthesia (tingling and numbness of arms/ legs)
arthralgia (joint pain)
profuse sweating
headache

115
Q

What inhibits the release of GH?

A

somatostatin
high levels of glucose
dopamine

116
Q

How is acromegaly diagnosed?

A

1st line: insulin-like growth factor (IGF-1) raised
gold standard: oral glucose tolerance test, no suppression of GH (as there usually would be in this test)

MRI brain for pituitary adenoma to assess size and extent

117
Q

How is acromegaly treated?

A

gold standard- trans-sphenoidal surgery of pituitary tumour if present/ surgical removal of other cancer if causing acromegaly

if surgery not possible, use medications to block GH:

2nd line: somatostatin analogue e.g. ocreotide
3rd line: GH receptor analogue e.g. pegvisomant
4th line: dopamine agonist e.g. cabergoline/ bromocriptine

118
Q

What are the potential complications of acromegaly?

A

erectile dysfunction
type 2 diabetes
heart disease
hypertension
arthritis

119
Q

Who generally has high prolactin levels?

A

pregnant women and new mothers

120
Q

What is a prolactinoma?

A

benign adenoma of the pituitary gland producing excess prolactin

121
Q

What cells make prolactin?

A

lactotrophs

122
Q

What are the risk factors for prolactinoma?

A

female
20-40 years old

123
Q

What are the causes of hyperprolactinaemia OTHER THAN prolactinoma?

A

non-functioning pituitary tumour- compresses pituitary stalk and stops inhibition of prolactin release

antidopaminergic drugs

124
Q

Describe the pathophysiology of prolactinoma.

A

hypersecretion of prolactin causes secondary hypogonadism

this is due to its inhibitory effects on gonadotropin-releasing hormone

125
Q

What are the two types of prolactinoma?

A

micro:
tumour < 10mm diameter on MRI
most common - 90% of cases

macro:
tumour > 10mm diameter on MRI

126
Q

How does prolactinoma present in males and females?

A

males:
- low testosterone
- erectile dysfunction
- reduced facial hair
- low libido

females:
- amenorrhoea
- oligomenorrhoea
- infertility
- galactorrhea
- low libido

127
Q

Why does prolactinoma cause infertility in women?

A

high prolactin inhibits ovulation in women due to its effect on GnRH

128
Q

What investigations are used to diagnose prolactinoma?

A

1st line- serum prolactin levels
(elevated if prolactinoma)

2nd line- pituitary MRI
(to detect adenoma)

129
Q

What is the treatment of prolactinoma?

A

medical approach more efficient than surgical approach unlike other pituitary adenomas

1st line- dopamine agonists, oral cabergoline/ bromocriptine
2nd line- HRT e.g. oestrogen

130
Q

Why are dopamine agonists used to treat prolactinoma?

A

dopamine inhibits prolactin release, so we want to stimulate the release of dopamine to shrink the prolactinoma

131
Q

What type of molecule is aldosterone?

A

mineralocorticoid

132
Q

What does aldosterone do to the kidney?

A

it acts on the kidney to:
- increase sodium reabsorption from the distal tubule
- increase potassium excretion from the distal tubule

133
Q

Where are Sertoli cells found?

A

the testes

134
Q

What is Conn’s syndrome?

A

primary hyperaldosteroneism due to an aldosterone producing adenoma of the adrenal gland

135
Q

What is primary hyperaldosteroneism?

A

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

136
Q

What is secondary hyperaldosteroneism?

A

when excessive renin stimulates the adrenal glands to produce more aldosterone

137
Q

How can you differentiate between primary and secondary hyperaldosteroneism?

A

by measuring serum renin levels

primary- serum renin will be low as it is suppressed by high BP
secondary- serum renin will be high

138
Q

What are the causes of primary hyperaldosteroneism?

A

bilateral adrenal hyperplasia (70%)
Conn’s syndrome- aka adrenal adenoma

139
Q

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

A

often asymptomatic but can present with:

hypertension
headaches
hypokalaemia
nocturia, polyuria, polydipsia

140
Q

What are the investigations for Conn’s syndrome?

A

FBC/ U+E/ LFT:
low plasma potassium
aldosterone- renin ratio - high

CT/ MRI to locate adrenal lesions

gold standard- selective adrenal venous sampling

141
Q

What is selective adrenal venous sampling?

A

a test used to determine whether autonomous hormone production is unilateral or bilateral

only unilateral can be treated with surgery

142
Q

What is the treatment for Conn’s syndrome?

A

1st line: aldosterone antagonists
SPIRONOLACTONE/ eplerenone
controls BP and K+ levels

laparoscopic adrenalectomy

143
Q

What is the aim of treatment of Conn’s syndrome?

A

lower blood pressure, decrease aldosterone levels and resolve electrolyte imbalance

144
Q

What is Addison’s disease?

A

primary adrenal insufficiency

the adrenal glands are damaged which results in reduced cortisol and aldosterone

145
Q

What are the causes of Addison’s disease?

A

autoimmune adrenalitis - most common in developed countries
TB - most common worldwide

146
Q

What causes secondary adrenal insufficiency?

A

loss/ damage of the pituitary gland

147
Q

What is tertiary adrenal insufficiency?

A

results from inadequate CRH released from the hypothalamus, usually due to long term oral steroid use causing suppression of the hypothalamus

148
Q

How does adrenal insufficiency present?

A

non-specific symptoms

fatigue
weight loss
nausea
vomiting
abdo pain
hypotension

key symptoms: hyperpigmentation especially in palmar crease for Addison’s

149
Q

How is adrenal insufficiency diagnosed?

A

1st line: U+E’s
low sodium- due to low aldosterone
high potassium- due to low aldosterone
low cortisol
ACTH- high in Addison’s, low in secondary insufficiency
Addisons: high renin, low aldosterone

Gold standard: short synacthen test (ACTH stimulations test) gives low cortisol and high ACTH

150
Q

How is adrenal insufficiency managed?

A

hydrocortisone to replace cortisol
fludrocortisone to replace aldosterone

151
Q

What is the potential complications of Addison’s disease?

A

Addisonian Crisis (AKA adrenal crisis)

152
Q

Why is it dangerous to stop steroids abruptly?

A

causes adrenal insufficiency

153
Q

What is SIADH?

A

syndrome of inappropriate ADH

inappropriately large amount of ADH secretion causes water to be reabsorbed in the collecting duct

154
Q

What are the causes of SIADH?

A
  • idiopathic
  • post-operative from major surgery
  • infection (atypical pneumonia and lung abscesses)
  • iatrogenic (thiazide diuretics, antipsychotics, SSRIs, NSAIDS)
  • malignancy (particularly small cell lung cancer)
155
Q

What is the pathophysiology of SIADH?

A
  • ADH is produced in the hypothalamus and secreted by the posterior pituitary
  • it stimulates water reabsorption from the collecting ducts in the kidneys
  • excessive ADH results in excessive water reabsorption in the collecting ducts
  • this dilutes sodium in the blood causing hyponatraemia
  • this is usually not significant enough to cause a fluid overload therefore you end up with “euvolaemic hyponatraemia”
  • the urine becomes more concentrated and less water is excreted by the kidneys, therefore patients with SIADH have a “high urine osmolality” and “high urine sodium”
156
Q

How does SIADH present?

A

symptoms largely due to hyponatraemia:

headache
fatigue, confusion
muscle aches and cramps

if hyponatraemia severe- seizures and reduced consciousness

157
Q

How is SIADH diagnosed?

A

usually a diagnosis of exclusion

  • U+E: hyponatraemia
  • urine sodium and osmolality: high
  • negative short synachen test: excludes adrenal insufficiency
  • no diarrhoea/ vomiting
  • no history of diuretic use
  • no AKI/ CKD
158
Q

How is SIADH managed?

A

establish and treat underlying cause

most common iatrogenic so stop causative medications if possible

fluid restriction to correct hyponatraemia

vasopressin receptor agonist for chronic SIADH, e.g. tolvapan

159
Q

What are the types of diabetes insipidus?

A

cranial and nephrogenic

160
Q

What is diabetes insipidus?

A

a disease characterised by either the decreased secretion of ADH from the posterior pituitary (cranial DI) or an insensitivity to ADH (nephrogenic DI)

161
Q

What type of diabetes insipidus is most common?

A

cranial

162
Q

What are the causes of cranial diabetes insipidus?

A

idiopathic
brain tumours
head injury
brain infection (meningitis, encephalitis, tuberculosis)
neurosurgery, radiotherapy

163
Q

What are the causes of nephrogenic diabetes insipidus?

A

inherited- mutations (most common)
iatrogenic- lithium (used in bipolar disorder)
systemic disease (e.g. CKD)
electrolyte disturbance (hypokalaemia, hypercalcaemia)

164
Q

What is the difference nephrogenic and cranial diabetes insipidus?

A

cranial- when the hypothalamus does not produce ADH for the pituitary gland to secrete

nephrogenic- when the collecting ducts of the kidneys do not respond to ADH

165
Q

How does diabetes insipidus present?

A

polyuria
polydipsia
dehydration
postural hypotension
hypernatraemia

166
Q

How is diabetes insipidus diagnosed?

A

Gold standard: water deprivation test
in DI- continue to produce large amounts of dilute urine
then desmopressin test to establish cranial or nephrogenic

167
Q

What is the main clinical features that distinguishes diabetes insipidus and diabetes mellitus?

A

there should not be glycosuria in diabetes insipidus

168
Q

What is the treatment for diabetes insipidus?

A

if possible, treat underlying cause
in mild cases- rehydration

cranial- desmopressin (synthetic ADH)
nephrogenic- thiazide diuretics

169
Q

What is desmopressin?

A

synthetic ADH/ vasopressin

170
Q

What is the potential complication of diabetes insipidus?

A

severe hypernatraemia

171
Q

What is hyperparathyroidism?

A

the excessive secretion of parathyroid hormone (PTH)

172
Q

What are the categories of hyperparathyroidism?

A

primary, secondary and teriary

173
Q

What is primary hyperparathyroidism?

A

tumour/ hyperplasia of the parathyroid glands leading to addition secretive tissue

results in excess PTH production thus hypercalcaemia

174
Q

What causes primary hyperparathyroidism?

A

80% due to solitary adenoma

20% due to hyperplasia of glands

<0.5% due to parathyroid cancer

175
Q

What is the most common type of hyperparathyroidism?

A

primary hyperparathyroidism

176
Q

What is secondary hyperparathyroidism?

A

when insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones causing hypocalcaemia

this causes parathyroid gland to release more PTH and becomes hyperplastic to further increase excess PTH secretion

177
Q

What is tertiary hyperparathyroidism?

A

usually occurs after prologues secondary hyperparathyroidism

the glands become autonomous, producing excessive PTH even after the cause of hypocalcaemia has been corrected

no response to negative feedback

178
Q

What causes secondary hyperparathyroidism?

A

CKD
low vitamin D

179
Q

What causes tertiary hyperparathyroidism?

A

prolonged secondary hyperparathyroidism which has most likely been caused by long-standing kidney disease

180
Q

What are the risk factors for hyperparathyroidism?

A

elderly women who have gone through menopause

having prolonged calcium or vitamin D deficiency

181
Q

How does hyperparathyroidism present?

A

‘stones, bones, groans and moans’

painful bones
renal stones
constipation, nausea, vomiting
fatigue, depression, psychosis

182
Q

How is hyperparathyroidism diagnosed?

A

primary- raised calcium
secondary- low serum calcium, high PTH
tertiary- raised calcium, raised PTH

SCANS:
bones- dexa scan for osteoporosis (salt and pepper scans)
stones- ultrasound for kidney to find stones
groans- abdominal x-ray showing renal calculi or nephrocalcinosis
detect adenomas via radioisotope scanning

183
Q

How is hyperparathyroidism treated?

A

primary- surgical removal of adenoma, prescribe bisphophates
secondary- treat vitamin D and calcium deficiency, or kidney transplant if CKD
tertiary- total/ subtotal parathyroidectomy, and cinacalcet (calcimimetic- increases sensitivity of parathyroid cells to calcium, thereby causing less PTH secretion)

184
Q

What is hypocalcaemia?

A

low serum calcium levels < 8.5mg/dL or <2.20 mmol/L

185
Q

What are the causes of hypocalcaemia?

A

hypoparathyroidism (post thyroid/ parathyroid surgery)
pseudohypoparathyroidism
vitamin D deficiency
hyperventilation
drugs
malignancy
toxic shock

186
Q

How does hypocalcaemia present?

A

muscle spasms
cramps
tetany
seizures

187
Q

How is hypocalcaemia diagnosed?

A

blood calcium < 8.5 mg/ dL
ECG- prolonged QT interval (arrhythmia)

188
Q

How is hypocalcaemia treated?

A

acute management of severe hypocalaemia- intravenous calcium gluconate or calcium chloride

vit D supplementation for persistant hypocalcaemia

189
Q

What are the complications of hypocalcaemia?

A

seizure
cardiac arrest
long QT syndrome

190
Q

What is hypercalcaemia?

A

serum calcium > 2.6 mmol/L

191
Q

What are the causes of hypercalcaemia?

A

hyperparathyroidism
malignancy
sarcoidosis
thyrotoxosis
drugs

192
Q

How does hypercalcaemia present?

A

bones, stone, moans and groans- basically exactly the same as hyperparathyroidism

painful bones
renal stones
abdominal pain (groans)
psychiatric moans (depression, anxiety)

and SHORT QT ON ECG

193
Q

How is hypercalcaemia diagnosed?

A

fasting serum calcium and phosphate samples both high
serum PTH- elevated
ultrasound if pointing towards hyperparathyroidism
24hr urinary calcium

194
Q

How is hypercalcaemia treated?

A

rehydration with saline
then rehydration with bisphosphonates
loop diuretics like furosemide sometimes used

195
Q

What is hypokalaemia?

A

serum potassium < 3.5 mmol/L

196
Q

What causes hypokalaemia without alkalosis/ acidosis?

A

decreased potassium intake
increased potassium entry into cells
increased potassium excretion
magnesium depletion
hyperaldosteronism

197
Q

What causes hypokalaemia with acidosis?

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated DKA

198
Q

What causes hypokalaemia with alkalosis?

A

vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome

199
Q

How does hypokalaemia present?

A

muscle weekness
hypotonia
hyporeflexia
cramps
tetany
palpitations
light headedness
arrhythmias
constipation

200
Q

What are the ECG changes in hypokalaemia?

A

small/ inverted T waves
prominent U waves
long PR interval
depressed ST segment

201
Q

How is hypokalaemia diagnosed?

A

metabolic panel
ECG
U+Es

202
Q

Why are U+Es useful in hypokalaemia?

A

differentiated between renal and non-renal causes

203
Q

How is hypokalaemia treated?

A

mild: oral replacement, consider IV
severe: IV replacement 40mmol KCL in 1L 0.9 NaCl

204
Q

What are the complications of hypokalaemia?

A

cardiovascular: chronic heart failure, acute MI, arrythmias

muscle: weakness, rhabdomyolysis, depression of deep tendon reflexes

205
Q

What is hyperkalaemia?

A

serum potassium > 5.5 mmol/L

206
Q

What are the causes of hyperkalaemia?

A

increased intake
increased production
reduced excretion
redistribution (intracellular to extracellular)

207
Q

How does hyperkalaemia present?

A

muscle weakness/ paralysis
fast irregular pulse
chest pain
light headedness

208
Q

How does the ECG look for hyperkalaemia?

A

tall, tented T waves
small P waves
wide QRS complex
ventricular fibrillations

209
Q

How is hyperkalaemia diagnosed?

A

metabolic panel
ECG
U+Es

210
Q

How is hyperkalaemia treated?

A

CAN CAUSE LIFE-THREATENING ARRYTHMIAS

If ECG changes- stabilise cardiac membrane with IV calcium gluconate

If no ECG changes, shift potassium into cells with combines insulin/ dextrose infusion + nebulised salbutamol

remove potassium from body with calcium resonium, loop diuretics, dialysis

211
Q

What is carcinoid syndrome?

A

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

212
Q

What is the chemical name for serotonin?

A

5-hydroxytryptamine

213
Q

What is a carcinoid tumour?

A

type of neuroendocrine tumour that grows from neuroendocrine cells

214
Q

What are the causes of carcinoid syndrome?

A

most commonly arises from GI tract, following by lungs, liver, ovaries, thymus

  • small intestine malignancy (most common)
  • appendix most common GI tract site
  • liver most common site for metastases
215
Q

How does carcinoid syndrome present?

A

flushing
diarrhoea
abdominal cramps
bronchospasm (wheezing, asthma)
fibrosis (heart valve dysfunction, palpitations)

216
Q

How is carcinoid syndrome diagnosed?

A

1st line: urinary 5-hydroxyindoleacetic acid test - elevated

CXR + chest/ pelvic MRI/ CT - locate primary tumours

217
Q

How is carcinoid syndrome treated?

A

SURGERY:
resection of tumour is only cure for carcinoid tumours so it is vital to find primary tumour

SOMATOSTATIN ANALOGUES:
octreotide

debulking, embolisation, or radio frequency ablation for hepatic metastases/ masses can decrease symptoms

218
Q

Why is ocreotide used to treat carcinoid syndrome?

A

blocks release of tumour mediators and counters peripheral effects

Phase 2a BASICS (6 decks)

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