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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What’s the difference between endocrine and exocrine?

A

endocrine- glands pour secretions into bloodstream
exocrine- glands pour secretions though a duct to site of action

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2
Q

What happens to TSH if you remove the thyroid/ thyroid is under active?

A

TSH will increase/ be elevated

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3
Q

What happens to TSH if you have an overactive thyroid?

A

TSH decreased

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4
Q

What happens to FSH and LH after menopause?

A

increases

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5
Q

What are the diseases of the pituitary?

A

benign pituitary adenoma
craniopharygioma
trauma
apoplexy/ sheehans (bleeding)
sarcoid/ TB

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6
Q

How big is the pituitary?

A

1cm in diameter

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7
Q

How do pituitary tumours present?

A
  1. PRESSIRE OF LOCAL STRUCTURE
    bitemporal hemianopia (double vision)
    headache
    CSF leakage
  2. PRESSURE ON NORMAL PITUITARY
    hypopituitarism
  3. FUNCTIONING TUMOUR
    prolactinoma
    acromegaly and gigantism
    Cushing’s disease
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8
Q

What is Cushing’s disease?

A

too much cortisol

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9
Q

What is acromegaly?

A

too much growth hormone

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10
Q

How do you tell the difference between CSF leakage from nose and snot?

A

CSF has glucose in it

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11
Q

How does somebody with a hypopituitary present?

A

pale
no body hair
central obesity

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12
Q

What happens if you have excess GH as a child? Why only in a child?

A

gigantism

tumour on pituitary presses on it and causes hypothyroidism meaning that the child won’t go through puberty (no testosterone secretion, etc)

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13
Q

How does acromegaly present?

A

big hands
big jaw
excess sweating
big heart

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14
Q

What is galactorrhea?

A

a milky nipple discharge unrelated to the normal milk production of breast-feeding

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15
Q

Can both men and women get prolactinomas?

A

Yes

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16
Q

Symptoms of prolactinomas?

A

galactorrhea
infertility
loss of libido
visual field defect

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17
Q

How quickly does acromegaly progress?

A

slow onset

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18
Q

Symptoms of Cushing’s?

A

main symptoms is weight gain, ulcers, stretch marks, easy bruising

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19
Q

What does an orchidometer measure?

A

testicular volume in mL

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20
Q

What is normal pre-pubertal testicular volume?

A

1-3 mL

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21
Q

What is normal testicular volume for an adult male?

A

15-25mL

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22
Q

What is thelarche?

A

breast development signalling first visible change of puberty

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23
Q

What induces thelarche?

A

oestrogen

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24
Q

How long do thelarche last?

A

3 years approx

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25
Q

What are you looking for on a pelvic ultrasound?

A

check for mullerian structures
morphology of uterus
morphology of ovaries

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26
Q

What are mullerian structures?

A

structures found in the female fetus that eventually develop into a woman’s reproductive organs

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27
Q

What causes growth of pubic and axillary hair in girls?

A

adrenal androgens and ovarian androgens

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28
Q

What is adrenarche?

A

maturation of adrenal glands, zona reticularis is formed

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29
Q

What happens if adrenarche happens in children?

A

mild advanced bone age
axillary hair
oily skin
mild acne
body odour

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30
Q

Which children most commonly experience adrenarche?

A

obese children

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31
Q

What is the name for early puberty?

A

precocious puberty

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32
Q

What are the types of precocious puberty?

A

true precocious puberty
precocious pseudopuberty

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33
Q

What is the gender distribution of true precocious puberty?

A

90% female
10% male

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34
Q

Why is it alarming if a male child has true precocious puberty?

A

he is likely to have a brain tumour

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35
Q

How do you differentiate between diagnosis of true precocious puberty and precocious pseudopuberty?

A

GnRH (LHRH) test

inject GnRH

If amount of of FSH and LH rises - true precocious puberty

If amount of TSH and LH stays the same - precocious pseudopuberty

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36
Q

What is the treatment for precocious puberty?

A

GnRH superagonist to suppress pulsatility of GnRH secretion

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37
Q

In what percentage of children does delayed puberty occur?

A

3% of children

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38
Q

What are the effects of delayed puberty?

A

psychological problems
defects in reproduction
reduced peak bone mass
delay in acquisition of sex characteristics

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39
Q

What’s the average size for an adult penis?

A

12-14cm

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40
Q

What is CDGP?

A

constitutional delay of growth and puberty

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41
Q

What is the most common cause of delayed puberty?

A

CDGP

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42
Q

What are the hormones of the anterior pituitary?

A

adrenocorticotrophic hormone (ACTH)
thyroid-stimulating hormone (TSH)
luteinising hormone (LH)
follicle-stimulating hormone (FSH)
prolactin (PRL)
growth hormone (GH)
melanocyte-stimulating hormone (MSH)

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43
Q

What are the hormones of the posterior pituitary?

A

anti-diuretic hormones (ADH)
oxytocin

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44
Q

What are the possible co-morbidities associated with acromegaly?

A

arthritis
headache
arthritis
insulin-resistant diabetes
sleep apnoea
hypertension
heart disease

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45
Q

How does acromegaly affect life expectancy?

A

reduces average life expectancy by approx 10 years

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46
Q

What is the difference in the way water-soluble and fat-soluble hormones interact with the cell?

A

water-soluble hormones bind to a surface receptor, fat-soluble hormones diffuse into the cell

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47
Q

Whats the difference in half-life of water-soluble and fat soluble hormones?

A

water-soluble: short half life
fat-soluble: long half life

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48
Q

Whats the difference in transport of water-soluble and fat soluble hormones?

A

water-soluble: unbound
fat-soluble: protein bound

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49
Q

Whats the difference in clearance of water-soluble and fat soluble hormones?

A

water-soluble: fast
fat-soluble: slow

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50
Q

What is the difference in the water peptides/ monoamine hormones are stored vs steroids?

A

peptides/ monoamines- stored in vesicles
steroids- synthesised on demand

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51
Q

What is paracrine?

A

cellular secretions/ signals that act on adjacent cells

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52
Q

What is autocrine?

A

cellular signals/ secretions that feedback on the same cell that created the hormones

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53
Q

How big are peptide hormones?

A

variable- 3 to 180 amino acids

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54
Q

What type of hormone is insulin?

A

peptide

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55
Q

How does insulin exert its effect?

A
  • insulin binds to receptor
  • causes phosphorylation of intracellular tyrosine residues associated with the receptor
  • this offsets the tyrosine kinase signal transduction pathway inside cell
  • leads to decreased plasma glucose
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56
Q

By what mechanisms does the action of insulin decrease blood glucose?

A
  • translocation of glut-4 transporter to plasma membrane and influx of glucose
  • glycogen synthesis in the liver
    -glycolysis
  • fatty acid synthesis in liver and adipose tissue
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57
Q

What are catecholamines?

A

type of neurohormone

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58
Q

What are the catecholamines and where are they secreted from?

A

adrenaline and noradrenaline: adrenal medulla
dopamine: hypothalamus

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59
Q

What are the catecholamines and where are they secreted from?

A

adrenaline and noradrenaline: adrenal medulla
dopamine: hypothalamus

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60
Q

What receptors do adrenaline and noradrenaline act upon?

A

adrenoreceptors

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61
Q

What are the two lodothyronines?

A

tyroxine (T4) and triiodothyronine (T3)

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61
Q

What are the two lodothyronines?

A

tyroxine (T4) and triiodothyronine (T3)

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62
Q

Where is T4 produced?

A

thyroid gland

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63
Q

Where is T3 produced?

A

20% of T3 in circulation is secreted directly by thyroid gland, other 80% is T4 that has been converted to T3 after it leaves the thyroid gland

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64
Q

What enzyme converts T4 to T3?

A

iodothyronine deiodinase

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65
Q

What are the two classes of steroid hormones?

A

corticosteroids
sex (gonadal) steroids

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66
Q

What are the classes of corticosteroids?

A

glucocorticoids
mineralocorticoids

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67
Q

What are the classes of sex steroid?

A

androgens
oestrogens
progestogens

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68
Q

What are steroid hormones derived from?

A

cholesterol

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69
Q

How is cholesterol converted to each steroid hormone?

A
  • cholesterol converted to pregnenolone
  • pregnenolone converted to progesterone
  • progesterone converted to cortisol in the adrenal glands
  • progesterone converted to androstenedione then to testosterone in the ovaries or testes
  • testosterone converted to estradiol in the ovaries
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70
Q

How are steroid hormones transported around the body?

A

vitamine D binding protein

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71
Q

Where is glucose stored?

A

liver

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72
Q

What do muscles use for fuel?

A

free fatty acids

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73
Q

What happens if glucose gets too high?

A
  1. inhibition of glucagon secretion
  2. stimulation of insulin release
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74
Q

Where is insulin and glucagon secreted?

A

islets of langerhans in the pancreas
insulin- beta cells
glucagon- alpha cells

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75
Q

Why is it getting more difficult to differentiate between T1 and T2 diabetes?

A

Because of increased levels of obesity, T2DM is being diagnosed in younger patients including children

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76
Q

What are microvascular complications of T1DM?

A

In UK, 30% of T1DM patients will develop diabetic nephropathy

Nephropathy tends to lead to retinopathy and severe neuropathy which massively affects quality of life

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77
Q

What is nephropathy?

A

deterioration of kidney function
can end up in kidney failure (end stage renal disease)

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78
Q

Define type 1 diabetes mellitus

A

autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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79
Q

When do T1DM usually present?

A

age 5-15

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80
Q

What percentage of diabetes is T1DM?

A

10%

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81
Q

What is glycosuria?

A

sugar in the urine

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82
Q

What are the risk factors for T1DM?

A

Northern European
Autoimmune disease
Family History

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83
Q

What are the signs and symptoms of T1DM?

A
  • “classic triad”: polydipsia, polyruria, weightloss (BMI < 25)
  • short history of severe symptoms
  • possibly presents with ketosis
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84
Q

What is the name for extreme thirstiness?

A

polydipsia

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85
Q

What is the name for frequent urination?

A

polyuria

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86
Q

How is T1DM diagnosed?

A

Either:
- fasting glucose >= 7.0 mmol/L
- random glucose >= 11.0 mmol/L
- HbA1c >= 6.5% (48 mmol/mol)

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87
Q

What is important to remember about diagnosing diabetes using HbA1c?

A

a value less that 6.5% DOES NOT exclude diabetes as this test is not as sensitive as fasting samples in detecting diabetes

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88
Q

What is the treatment for T1DM?

A

insulin, short or long acting

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89
Q

How long does short and long acting insulin work for?

A

short: 4-6 hrs
long: 12-24 hrs

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90
Q

Which antibodies can you check for in T1DM?

A

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

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91
Q

Why does T2DM occur?

A

patients gradually become insulin resistant AND/OR beta cells fail to secrete enough insulin

non-insulin dependent and progresses from impaired glucose tolerance

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92
Q

What causes T2DM?

A
  • reduced insulin secretion/ increased insulin resistance
  • gestational diabetes
  • steroids
  • Cushing’s
  • chronic pancreatitis
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93
Q

What are the risk factors of T2DM?

A
  • lifestyle: obesity, inactivity, calorie and alcohol excess
  • higher prevalence in asian men
  • > 40yrs age
  • hypertension
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94
Q

What are the signs and symptoms of T2DM?

A

polydipsia
polyuria
glycosuria
central obesity
slower onset
blurred vision

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95
Q

What are the investigations for T2DM?

A

Exactly the same as type 1:

Either:
- fasting glucose >= 7.0 mmol/L
- random glucose >= 11.0 mmol/L
- HbA1c >= 6.5% (48 mmol/mol)

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96
Q

Describe first line management of T2DM

A

1st line- lifestyle changes
- dietary advice (high complex carbs, low fat)
- smoking cessation
- decrease alcohol intake
- encourage exercise
- regular blood glucose and HbA1c monitoring

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97
Q

Describe second line management of T2DM

A

2nd line- medication

  1. METFORMIN (e.g. biguanide)
  2. If HbA1c remains high then DUAL THERAPY with metformin:
    - DPP4 inhibitor
    - Sulphonylurea (e.g. gliclazide)
    - pioglitazone
  3. If still high = TRIPLE THERAPY with metformin
  4. Insulin
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98
Q

How does metformin work and what type of patients suit it best?

A

increases sensitivity to insulin, decreases hepatic gluconeogenesis

first choice in overweight patients as it can cause a slight weight decrease

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99
Q

How does sulphonylurea treat T2DM?

A

increases insulin secretion

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100
Q

What are the notable side effects of metformin?

A

gastrointestinal upset
lactic acidosis

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101
Q

Why is sulphonylurea becoming less popular as a 2nd line treatment for T2DM?

A

causes weight gain

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102
Q

What are the notable side effects of sulphonylurea?

A

hypoglycaemia
weight gain
hyponatraemia

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103
Q

Give 2 examples of sulphonylureas

A

gliclazide
glimepiride

104
Q

What is DKA?

A

diabetic ketoacidosis- complete lack on insulin resulting in ketone production

105
Q

What causes DKA?

A

unrelated/ undiagnosed type 1 diabetes
infection/ illness

106
Q

Describe the pathophysiology of DKA

A
  1. absence of insulin causes hyperglycaemia and increased ketones
  2. hyperglycaemia causes osmotic diuresis- dehydration
  3. glucose and ketones escape in urine
  4. circulating ketones are acidic and cause acidosis
107
Q

What is the direct effect of ketones on the body?

A

anorexia and vomiting

108
Q

What are the signs and symptoms of diabetic ketoacidosis?

A

extreme diabetes symptoms plus:
nausea and vomiting
weight loss
confusion and reduced mental state
lethargy
abdominal pain
Kussmaul’s breathing
‘pear drop’ breath
hypotension
tachycardia

109
Q

What is kussmaul’s breathing?

A

fast, deep breaths that occur in response to metabolic acidosis

110
Q

What investigations can be done to confirm diabetic ketoacidosis?

A
  • random plasma glucose > 11mmol/L
  • plasma ketones >3mmol/L
  • blood pH <7.35, or bicarb <15mmol/L
  • urine dipstick: glycosuria, ketonuria
  • serum U+E:
    -raised urea and creatinine
    -decreased total K+, increased serum K+
111
Q

What is the treatment for diabetic ketoacidosis?

A
  1. ABC management
  2. replace fluid- 0.9% saline IV
  3. IV insulin
  4. restore electrolytes (e.g. K+)
112
Q

What is HHS?

A

hyperosmolar hyperglycaemic state

113
Q

What causes HHS?

A

untreated/ undiagnosed T2DM
infection/ illness

114
Q

What are the signs and symptoms of HHS?

A

extreme diabetes symptoms plus:
confusions and reduced mental state
lethargy
severe dehydration

115
Q

What investigations confirm a diagnosis of HHS?

A
  • random plasma glucose > 11mmol/L
  • urine dipstick: glycosuria
  • high plasma osmolality
  • U+E
    • decreased total body K+
    • increased serum K+
116
Q

What is the treatment for HHS?

A
  • replace fluid- 0.9% saline
  • insulin- AT LOW RATE OF INFUSION
  • restore electrolytes
  • low molecular weight heparin (LMWH)
117
Q

Why must patients with HHS be given insulin at a low rate of infusion?

A

patients with HHS have a high sensitivity to insulin

requires a low infusion rate to prevent cerebral oedema caused by glucose being lowered too quickly

118
Q

What is hypoglycaemia?

A

low plasma glucose causing impaired brain function

119
Q

What is neutropenia?

A

abnormally low concentration of neutrophils

120
Q

What glucose value signals hypoglycaemia?

A

3.9 mmol/L

121
Q

What is hyperthyroidism?

A

clinical effects of too much thyroid hormone

122
Q

What is the difference between primary and secondary hyperthyroidism?

A

primary- abnormal increased thyroid function
secondary- abnormal increased TSH production

123
Q

What are the causes of hyperthyroidism?

A
  • 65-75% caused by GRAVES DISEASE
  • toxic multi nodular goitre
  • toxic adenoma
  • metastatic follicular thyroid cancer
  • iodine excess

secondary cause: TSH secreting pituitary tumour

124
Q

What is the ratio of F:M diagnosed with Graves disease?

125
Q

Who is affected by hyperthyroidism?

A

mostly young women aged 20-40

126
Q

What are the risk factors for hyperthyroidism?

A

smoking
stress
HLA-DR3
other autoimmune diseases (T1DM, Addisons, vitiligo)

127
Q

What are the signs and symptoms of hyperthyroidism?

A

hot and sweaty
diarrhoea
hyperphagia
weight loss
palpitations
tremor
irritability
anxiety/ restlessness
oligomenorrhoea
goitre

128
Q

What is goitre?

A

swelling of thyroid gland causing lump in the front of the neck

129
Q

What is hyperphagia?

A

abnormally big desire for food/ excessive eating

130
Q

What is oligomenorrhoea?

A

abnormal menstruation involving infrequent periods

131
Q

Which investigations confirm a diagnosis of hyperthyroidism?

A
  • Thyroid function tests (TFTs) showing increased T4/ T3, plus:

primary: decreased TSH
secondary: increased TSH

  • Thyroid autoantibodies (anti-TSHR)
  • ultrasound and CT head
132
Q

What is the treatment for hyperthyroidism?

A
  1. DRUG MANAGEMENT
    a) beta blockers (rapid symptom relief)
    b) 1st line: carbimazole
    c) 2nd line: propylthiouracil
  2. RADIOIODIDE
  3. TYROIDECTOMY
133
Q

How does carbimazole and propylthiouracil treat hyperthyroidism?

A

carbimazole- blocks synthesis of T4

propylthiouracil- prevents T4 to T3 conversion

134
Q

What are the consequences of untreated hyperthyroidism during pregnancy?

A
  • intrauterine growth resistance (IUGR)
  • pre eclampsia
  • preterm delivery
  • risk of stillbirth/ miscarriage
135
Q

How does Graves disease cause hyperthyroidism?

A

IgG antibodies bind to TSH receptors to increase T4/ T3 production

136
Q

What are the symptoms of Graves disease?

A

hyperthyroidism symptoms plus:
- thyroid eye disease
- pretibial myxoedema
- thyroid acropachy

137
Q

What are the features of thyroid eye disease?

A

eye retraction
periorbital swelling
proptosis/ exophthalmos (bulging eyeballs)

138
Q

What percentage of patients with Graves disease have thyroid eye disease?

139
Q

How does thyroid acropachy present?

A

clubbing
painful finger and toe swelling
periosteal reaction (bone growth)

140
Q

What is hypothyroidism?

A

clinical effects of lack of thyroid hormone

141
Q

What is the difference between primary and secondary hypothyroidism?

A

primary: abnormally low thyroid function

secondary: abnormally low TSH production

142
Q

What are the causes of hypothyroidism?

A
  1. AUTOIMMUNE: Hashimotos inflammation = goitre), Primary atrophic hypothyroidism (atrophy = no goitre)
  2. OTHER PRIMARY: iodine deficiency, drugs (antithyroid drugs, iodine, lithium), post thyroidectomy/ radio iodine)
  3. SECONDARY: hypopituitarism
143
Q

How many people are diagnosed with hypothyroidism every year?

A

4 in every 1000 people

144
Q

Who is most commonly affected by hypothyroidism?

A

affects F:M in a ratio of 6:1
mainly > 40 yrs old

145
Q

What are the signs and symptoms of hypothyroidism?

A

fatigue
weight gain
loss of appetite
cold
lethargy
constipation
low mood/ depression
menorrhagia
goitre

146
Q

What is the treatment for hypothyroidism?

A

levothyroxine (T4)

147
Q

List the hormones of the anterior pituitary

A
  • adrenocorticotropic hormone (ACTH)
  • growth hormone (GH)
  • luteinising hormone (LH)
  • follicle-stimulating hormone (FSH)
  • prolactin
  • thyroid-stimulating hormone (TSH)
148
Q

List the hormones of the posterior pituitary

A
  • anti-diuretic hormone (ADH)
  • oxytocin
149
Q

Where is melanocyte-stimulating hormone produced and what does It do?

A

pars intima- part of pituitary between anterior and posterior

acts on cells in skin to stimulate production of melanin (pigment which prevents against UV radiation)

150
Q

Where are the hormones released from the posterior pituitary produced?

A

hypothalamus

151
Q

What is another name for ADH?

A

vasopressin

152
Q

What does ACTH do?

A

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

153
Q

What does GH do?

A

regulates growth, metabolism and body composition by acting on liver, bones, adipose tissue and muscles

154
Q

What does LH and FSH do? What are they collectively called?

A

gonadotrophins

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

155
Q

What does prolactin do?

A

stimulates milk production in mammary glands

156
Q

What does TSH do?

A

stimulates thyroid gland to secrete thyroid hormone

157
Q

What does ADH/ vasopressin do?

A

controls water balance and blood pressure

158
Q

What does oxytocin do?

A

stimulates uterine contractions during labour and milk secretion during breast feeding

159
Q

What is Cushing’s syndrome?

A

long term exposure to excessive cortisol hormone released by adrenal glands

160
Q

What is the difference between a syndrome and a disease?

A

A disease typically has a defining cause, distinguishing symptoms and treatments. A syndrome is a group of symptoms that may not have a definite cause.

161
Q

What are the two types of causes of Cushing’s syndrome

A

ACTH dependent and ACTH independent

162
Q

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

A

Cushing’s disease is a specific type of Cushing’s syndrome resulting from a pituitary tumour

163
Q

What are the ACTH dependent causes of Cushing’s syndrome?

A
  • Cushing’s disease- ACTH secreting from pituitary adenoma
  • Ectopic ACTH production from small cell lung cancer
164
Q

What are the ACTH independent causes of Cushing’s syndrome?

A
  • latrogenic- steroid use (most common)
  • adrenal adenoma
165
Q

What are the signs and symptoms of Cushing’s?

A

moon face
central obesity
buffalo hump
acne
hypertension
striae
hirsutism
weight gain

166
Q

What is striae?

A

stretch marks

167
Q

What is hirsutism?

A

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

168
Q

What investigations are used for Cushing’s?

A
  1. random plasma cortisol- raised
  2. overnight dexamethasone suppression test- cortisol will not be suppressed in Cushing’s
  3. urinary free cortisol (24hr)
  4. plasma ACTH
169
Q

What is the treatment for Cushing’s?

A

treatment depends on the underlying cause:

  • latrogenic: stop medications if possible
  • Cushing’s disease: removal of pituitary adenoma (transsphenoidal surgery)
  • adrenal adenoma: adrenalectomy

cortisol inhibition drugs:
metyrapone
ketoconazole

170
Q

What is acromegaly?

A

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

171
Q

What are the causes of acromegaly?

A
  • 99% of cases caused by pituitary adenoma
  • secondary to a malignancy that secretes ectopic GH (e.g. lung cancer)
172
Q

What are some complications of acromegaly?

A

erectile dysfunction
diabetes mellitus

173
Q

What are the signs and symptoms of acromegaly?

A

prominent forehead and brow
increased jaw size
large hands, nose, tongue, feet
bitemporal hemianopia
profuse sweating
lower pitch of voice
obstructive sleep apnoea

174
Q

What investigations are used for acromegaly?

A

1st line: insulin like growth factor 1 test - raised
gold standard: oral glucose tolerance test
other tests: random serum GH raised, MRI of pituitary fossa

175
Q

What is the treatment for acromegaly?

A

1st line- transsphenoidal resection surgery (if cause is adenoma)
2nd line- somatostatin analogue e.g. ocreotide
3rd line- GH receptor antagonist e.g. pegvisomant
4th line- dopamine agonist e.g. cabergoline

176
Q

What is transsphenoidal resection?

A

most common way to remove pituitary tumours

tumour removed via the sphenoid sinus, accessed through the nose

177
Q

What is a prolactinoma?

A

benign adenoma of pituitary gland producing excess prolactin

178
Q

What causes prolactinoma?

A

cause is unknown but there is a genetic association

179
Q

What is hyperprolactinaemia?

A

too much prolactin in the blood of men and women who aren’t pregnant

180
Q

What are some causes of hyperprolactinaemia other than prolactinoma?

A

non-functional pituitary tumour (compresses pituitary stalk hence no inhibition of prolactin release)

antidopaminergic drugs

181
Q

What are the 2 classifications of prolactinoma?

A

micro- tumour < 10mm diameter on MRI (most common, accounts for 90% of cases)

macro- tumour > 10mm diameter on MRI

182
Q

Why does prolactinoma cause galactorrhoea?

A

increased release of prolactin can cause galactorrhea by stimulating milk production from mammary gland as well as inhibiting FSH and LH

183
Q

What are the signs and symptoms of prolactinoma?

A

visual field defect
headache
menstrual irregularity
infertility
galactorrhea

184
Q

What investigations are used to diagnose prolactinoma?

A

prolactin levels
head CT

185
Q

What is the treatment for prolactinoma?

A
  • gold standard: transphenoidal resection surgery
  • 1st line: dopamine agonists: bromocriptine/ cabergoline
186
Q

Why are dopamine agonists used to treat prolactinoma?

A

dopamine has an inhibitory effect on prolactin

187
Q

What is Conn’s syndrome?

A

primary hyperaldosteronism due to an aldosterone producing adenoma

188
Q

Describe the pathophysiology of Conn’s syndrome

A

excess production of aldosterone independent of renin-angiotensin system:
- high sodium and water retention
- increased potassium excretion in kidneys
- low renin release

189
Q

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

A

hypertension
hypokalaemia
nocturia
polyuria
mood disturbance

190
Q

What investigations can confirm a diagnosis of Conn’s syndrome?

A
  • aldosterone-renin ratio blood test: increased
  • plasma potassium: reduced
  • U+E
191
Q

What is the treatment for Conn’s syndrome?

A
  • 1st line: spironolactone (pre-op controls BP and K+ levels)- if hyperplasia
  • gold standard: laparoscopic adrenalectomy- if adenoma

Aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance

192
Q

What is Addison’s disease?

A

primary adrenal insufficiency

193
Q

Describe the pathophysiology of Addison’s disease

A

destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

194
Q

What are the causes of Addison’s disease?

A
  • autoimmune destruction (80% of cases in UK + developed countries)
  • TB (most common cause worldwide)
  • adrenal metastases
195
Q

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

A

tanned
lean
fatigue
pigmented palmar creases
postural hypotension
often diagnosed late

196
Q

What investigations can confirm a diagnosis of Addison’s disease?

A
  • 1st line:
    U+E confirms hyponatraemia, hypokalaemia
    Blood glucose confirms hypoglycaemia
  • Gold standard:
    Short SynACTHen test (ACTH stimulation test) presents with low cortisol, high ACTH
  • Plasma renin and aldosterone:
    high renin, low aldosterone
197
Q

What are some less commonly used test that can also confirm a diagnosis of Addison’s disease?

A
  • adrenal CT or MRI
  • 2l-hydroxylase adrenal autoantibodies- is positive in autoimmune diseases in more than 80% of cases
198
Q

What is the treatment for Addison’s disease?

A

replace steroids depending on signs and symptoms:
hydrocortisone- replaces cortisol
fludrocortisone- replaces aldosterone

treat underlying cause and warn against abruptly stopping steroids

199
Q

What does SIADH stand for?

A

syndrome of inappropriate ADH

200
Q

What is SIADH?

A

inappropriately large amounts of ADH secretion causing water to be reabsorbed in collecting duct

201
Q

What are the causes of SIADH?

A
  • post-operative from major surgery
  • infection (atypical pneumonia and lung abscess)
  • head injury
  • medications (thiazide diuretics)- most common cause
202
Q

What are the signs and symptoms of SIADH?

A

very non-specific
headache
nausea
fatigue
muscle cramps
confusion
severe hyponatraemia

203
Q

What investigations can confirm a diagnosis of SIADH?

A

DIAGNOSIS BY EXLCUSION
- U+E shows hyponatraemia
- high urine sodium
- high urine osmolality

Causes of hyponatraemia that need to be excluded:
- -ve short SynACTHen test- exclude adrenal insufficiency
- no diarrhoea, no vomiting
- no history of diuretic use
- no AKI/CKD

204
Q

How is SIADH managed?

A

treat underlying cause:
stop causative medicine
fluid restriction
tolvaptan (ADH receptor blocker)

205
Q

What is hyperkalaemia?

A

blood potassium level > 5.5mmol/L

206
Q

What are the causes of hyperkalaemia?

A

3 categories:

IMPAIRED EXCRETION:
- AKI/CKD
- drug affect (ACEi, NSAIDS, beta blockers)
- renal tubular acidosis
- addison’s disease (low aldosterone)

INCREASED INTAKE:
- IV K+ therapy
- increased dietary intake

SHIFT TO EXTRACELLULAR:
- metabolic acidosis
- rhabdomyolysis
- decreased insulin
- tumour lysis syndrome

207
Q

How does metabolic acidosis cause hyperkalaemia?

A

cells switch H+ for K+ to reduced acidosis

208
Q

Why does tumour lysis syndrome cause hyperkalaemia?

A

the intracellular contents (including potassium) are released

209
Q

What are the symptoms of hyperkalaemia?

A

fatigue
light-headedness
chest pain
palpitations

210
Q

What are the signs of hyperkalaemia?

A

arrhythmia (potential cardiac arrest)
reduced power and reflexes
flaccid paralysis
signs of underlying cause

211
Q

How will hyperkalaemia present on an ECG?

A
  • small/ absent p waves
  • prolonged PR interval (> 200ms)
  • wide QRS interval (> 120ms)
  • TALL TENTED T WAVES
212
Q

What investigations are used to confirm a diagnosis of hyperkalaemia?

A

ECG
bloods- FBC, U+E

213
Q

What is the treatment for hyperkalaemia?

A
  • ABC
  • cardiac monitoring
  • calcium gluconate- to protect myocardium
  • insulin and dextrose or nebuliser salbutamol - drives K+ intracellularly
  • treat underlying cause
214
Q

What is hypokalaemia?

A

blood potassium < 3.5mmol/L

215
Q

What are the causes of hypokalaemia?

A

3 categories:

INCREASED EXCRETION
- renal disease
- drug effect (thiazide, loop diuretics, laxatives)
- GI loss (D+V)
- Conn’s Syndrome

DECREASED INTAKE:
- dietary deficiency/ fasting
- liquorice abuse

SHIFT TO INTRACELLULAR:
- metabolic alkalosis
- drug effect (insulin, B2 agonists (SABAs and LABAs)

216
Q

What are the symptoms of hypokalaemia?

A

can be asymptomatic
fatigue + light headedness
weakness
cramps
palpitations
constipation

217
Q

What are the signs of hypokalaemia?

A

arrhythmia
hypotonia
hypereflexia
muscle paralysis
rhabdomyolysis

218
Q

How does hypokalaemia present on an ECG?

A
  • prolonged PR interval
  • ST depression
  • flat T waves
  • prominent U waves
219
Q

What investigations are used to confirm a diagnosis of hypokalaemia?

A

ECG
Bloods- FBC, U+E

220
Q

What are the two types of diabetes insipidus?

A

cranial
nephrogenic

221
Q

What are the symptoms of diabetes insipidus?

A

polyuria
polydipsia
dehydration

222
Q

Describe the pathophysiology of diabetes insipidus

A

caused by impaired water reabsorption from the kidneys

large volumes of dilute urine due to reduced ADH due to:

impaired secretion from posterior pituitary (cranial) OR impaired response of the kidney to ADH (nephrogenic)

223
Q

What are the causes of cranial diabetes insipidus?

A

can be idiopathic
congenital
tumour
trauma
infection

224
Q

What are the causes of nephrogenic diabetes insipidus?

A

inherited
metabolic (low potassium, high calcium)
drugs (lithium)
chronic renal disease

224
Q

What are the causes of nephrogenic diabetes insipidus?

A

inherited
metabolic (low potassium, high calcium)
drugs (lithium)
chronic renal disease

225
Q

How is diabetes insipidus diagnosed?

A

gold standard: 8hr water deprivation test to diagnose, then desmopressin test to establish if cranial or nephrogenic

other possible investigation: cranial MRI

226
Q

What is the treatment for diabetes insipidus?

A

treat underlying cause, mild cases can just undergo rehydration

cranial- desmopressin (synthetic ADH) to replace ADH
nephrogenic- if cause persists, give bendroflumethiazide

227
Q

What is desmopressin?

A

synthetic ADH

228
Q

What is hyperparathyroidism?

A

excessive secretion of parathyroid hormone (PTH)

229
Q

What are the categories of hyperparathyroidism?

A

PRIMARY- 1 parathyroid gland produced excessive PTH

SECONDARY- increased secretion of PTH to compensate hypocalcaemia

TERTIARY- autonomous secretion of PTH even after correction of calcium deficiency due to chronic kidney disease (CKD)

230
Q

What are the causes of primary hyperparathyroidism?

A

80% caused by adenoma
20% caused by hyperplasia of all glands

231
Q

What are the causes of secondary hyperparathyroidism?

A

chronic kidney disease (CKD)
low vitamin D

232
Q

What causes tertiary hyperparathyroidism?

A

develops from prolonged secondary hyperparathyroidism

233
Q

What are the signs and symptoms of hyperparathyroidism?

A

Bones, Stones, Moans, Groans, Hypercalcaemia

Bones- bone pain
Stones- renal calculi (kidney stones)
Moans- psychic moans (depression)
Groans- abdominal moans
Hypercalcaemia

234
Q

What investigations can be used to confirm a diagnosis of hyperparathyroidism?

A

PTH/ BONE PROFILE: high PTH, high calcium, low phosphates

PRIMARY- raised calcium
SECONDARY- low serum calcium, high PTH
TERTIARY- raised calcium + raised PTH

Can also do a DEXA scan X-ray which will show “salt and pepper” degradation of bone, and an ultrasound to look for kidney stones

235
Q

How is hyperparathyroidism managed?

A

“watchful waiting”

PRIMARY- surgical removal of adenoma, give bisphosphates
SECONDARY- calcium correction, treat underlying cause
TERTIARY- cinacalet (calcium mimetic), total/ part thyroidectomy

236
Q

What is hypoparathyroidism?

A

reduced PTH production
primary- due to gland failure
secondary- other causes

237
Q

What are the causes of hypoparathyroidism?

A

PRIMARY- failure of gland caused by:
autoimmune destruction
congenital (DiGeorge Syndrome)

SECONDARY-
surgical removal of thyroid gland
decreased magnesium (required for PTH secretion)

238
Q

What is DiGeorge Syndrome?

A

22q11 deletion

239
Q

What are the risk factors for hypoparathyroidism?

A

other autoimmune disorders

240
Q

Describe the pathophysiology of hypoparathyroidism

A

low PTH results in hypocalcaemia and hyperphosphateaemia which makes neurons more excitable

241
Q

What are the symptoms of hypoparathyroidism?

A

acronym: CATS go numb

Convulsions
Arrhythmias
Tetany
Spasm
Numbness

242
Q

What is tetany?

A

involuntary contraction of muscles

243
Q

What are the signs of hypoparathyroidism?

A
  • Chvostek’s sign- facial nerve tap induces spasm
  • Trousseau’s sign- BP cuff causes wrist flexion and fingers to pull together
244
Q

What investigations confirm a diagnosis of hypoparathyroidism?

A

Bloods- bone profiling
- decreased calcium
- increased or normal phosphate
- decreased PTH

ECG:
prolonged QT and ST segments

245
Q

What is the role of basal insulin in T1DM?

A

controls glucose levels between meals and at night
concentration can be adjusted as needed between 5-7mmol/L

246
Q

What is the role of bolus insulin?

A

manage glucose according to carbohydrate intake and pre-meal glucose

247
Q

Where is PTH secreted from?

A

chief cells in parathyroid gland

248
Q

How does PTH act on bone to increase serum calcium?

A

stimulates osteoclasts to release ionic calcium for reabsorption

249
Q

What hormone regulates the decrease in serum calcium?

A

calcitonin

250
Q

Where does calcitonin secretion occur?

A

c-cells in the thyroid, stimulated by increased serum calcium

251
Q

What is a normal level for serum calcium?

A

2.2 to 2.6 mmol/L

252
Q

What calcium levels would indicate hypocalcaemia?

A

mild-moderate: 1.9-2.2 mmol/L
severe: < 1.9 mmol/L

253
Q

What calcium levels would indicate hypocalcaemia?

A

mild-moderate: 1.9-2.2 mmol/L
severe: < 1.9 mmol/L

254
Q

Prolactinoma is a tumour of what cell type?

A

lactotroph

255
Q

Prolactinoma is a tumour of what cell type?

A

lactotroph

256
Q

What makes up the HPA axis?

A

hypothalamus
pituitary
adrenals

257
Q

What makes up the HPA axis?

A

hypothalamus
pituitary
adrenals

Phase 2a (18 decks)

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