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Phase 2A Conditions > Endocrinology conditions > Flashcards

Endocrinology conditions Flashcards

1
Q

Define diabetes mellitus type 1

A

Chronic hyperglycaemia due to insulin dysfunction

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2
Q

Clinical presentation of diabetes mellitus type 1

A

Usually presents in younger people with a 2-6 week history of polydypsia, polyuria, weight loss, polyphagia etc.

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3
Q

Pathophysiology of diabetes mellitus type 1

A

autoimmune destruction of pancreatic beta cells. No insulin secretion = uncontrolled hyperglycaemia (gluconeogenesis, glycogenolysis, lipolysis)
Polyuria = blood glucose exceeds renal tubular reabsorptive capacity leading to osmotic diuresis
Weight loss = due to fluid losses and muscle and fat breakdown

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4
Q

Aetiology of diabetes mellitus type 1

A

mutation of HLA/DR3/4

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5
Q

Epidemiology of diabetes mellitus type 1

A

typically presents younger <30

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6
Q

Diagnostic investigations in diabetes mellitus type 1

A

fasting glucose >7 mmol/L
random plasma glucose >11 mmol/L

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7
Q

Treatment for diabetes mellitus type 1

A

glycaemic control through diet and insulin

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8
Q

Define diabetes mellitus type 2

A

chronic hyperglycaemia due to insulin resistance

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9
Q

Clinical presentations of diabetes mellitus type 2

A

polydypsia, polyuria, weight loss, polyphagia

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10
Q

Pathophysiology of diabetes type 2 mellitus

A

polygenic- environmental factors triggers onset in genetically susceptible individuals. Beta cell mass reduced by 50% = low insulin secretion and resistance

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11
Q

Aetiology of diabetes type 2 mellitus

A

genetic susceptebility but no HLA link

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12
Q

Epidemiology of diabetes mellitus type 2

A

usually older onset >30
overweight

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13
Q

Diagnostic tests for diabetes mellitus type 2

A

HbA1c >48 mmol/L
fasting glucose >7 mmol/L
random glucose >11 mmol/L

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14
Q

Treatment of diabetes mellitus type 2

A

diet and lifestyle changes
biguanide (metformin)
sulfonylurea (gliclazide)
insulin

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15
Q

complications of diabetes mellitus

A

diabetic ketoacidosis
hyperosmolar hyperglycaemic state
neuropathy, nephropathy, retinopathy

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16
Q

Define graves disease

A

hyperthyroidism due to pathological stimulation of the TSH receptor

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17
Q

clinical presentation of graves disease

A

tachycardia
arrhythmia
diffuse goitre
bulging eyes
lid lag
extra-occular muscle swelling

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18
Q

pathophysiology of graves disease

A

thyroid stimulating immunoglobulins recognise and bind to the TSH receptors stimulating T3/4 production. Increased t3/4 causes negative feedback on pituitary = low TSH

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19
Q

epidemiology of graves disease

A

most common cause of hyperthyroidism

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20
Q

diagnostic tests of graves disease

A

TFTs, high T3/4, low TSH

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21
Q

treatment of graves disease

A

antithyroid drugs (Carbimazole)
thyroidectomy
radio-iodine therapy

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22
Q

complications of graves disease

A

thyroid storm
treat with propylthiouracil

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23
Q

define hashimotos thyroiditis

A

hypothyroidism due to aggressive destruction of thyroid cells

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24
Q

clinical presentation of hashimotos thyroiditis

A

thyroid gland may enlarge rapidly
occassionaly with dysponea or dysphagia from pressure on neck
hypothyroidism- fatigue, weight gain, bradycardia, constipation, depression

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25
Q

pathophysiology of hashimotos thyroiditis

A

aggressive destruction of thyroid cells by various cells and antibody mediated immune processes. Antibodies bind and block TSH receptors causing a decrease in thyroid hormone

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26
Q

aetiology of hashimotos thyroiditis

A

unkown- autoimmune

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27
Q

epidemiology of hashimotos thyroiditis

A

12-20 times more common in women
most common cause of hypothyroidism

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28
Q

diagnostic investigation of hashimotos thyroiditis

A

TFTs, low T3/4, high TSH

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29
Q

treatment of hashimotos thyroiditis

A

thyroid hormone replacement (levothyroxine)

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30
Q

complications of hashimotos thyroiditis

A

hyperlipademia, hashimotos encephaly

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31
Q

define hypothyroidism

A

reduced action of thyroid hormone

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32
Q

clinical presentation of hypothyroidism

A

goitre
depression
lethargy
weight gain
constipation

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33
Q

define primary hypothyroidism

A

disease associated with the thyroid itself (usually hashimotos, iodine deficiency etc) Low T3/4 and high TSH

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34
Q

define secondary hypothyroidism

A

disease associated with the pituitary or hypothalamus. Low T3/4 and low TSH. Caused by TSH deficiency, hypopituitarism, hypothalamic disorders.

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35
Q

treatment of hypothyroidism

A

levothyroxine

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36
Q

define transient hypothyroidism

A

disease associated with treatment withdrawal such as radioiodine treatment. Remits on its own

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37
Q

types of thyroid cancers

A

papillary
folicular
anaplastic
lymphoma
medullary
usually require total thyroidectomy, radioactive iodine, radiotherapy + possible lymph node dissection

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38
Q

define cushings disease

A

hypercortisolism
persistently and inappropriately elevated circulating cortisol

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39
Q

clinical presentation of cushings disease

A

obesity
moon face
thin skin
bruising
abdominal striae
hypertension

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40
Q

define cushings disease

A

when increased glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary

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41
Q

pathophysiology of cushings

A

many features due to protein catabolic effects

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42
Q

aetiology of cushings

A

ACTH dependent disease- increased ACTH from pituitary

Non-ACTH dependent- adrenal adenomas/carcinomas, excess glucocorticoid administration

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43
Q

epidemiology of cushings

A

higher incidence in diabetes
2/3rd are cushings disease

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44
Q

diagnostic tests for cushings

A

confirm raised cortisol
dexamethasone supression test
urinary free cortisol 24h
late night salivary cortisol
CT/MRI of pituitary

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45
Q

treatment of cushings

A

remove tumour
cortisol synthesis inhibition (metryapone, ketoconazole)

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46
Q

define acromegaly

A

overgrowth of all organ systems due to excess growth hormone (called gigantism in children)

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47
Q

clinical presentation of acromegaly

A

slow onset
large hands/feet
large tongue
prodtruding jaw

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48
Q

pathophysiology of acromegaly

A

growth hormone acts directly on tissues such as liver, muscles, bones, fat, as well as indirectly through IGF-1

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49
Q

aetiology of acromegaly

A

usually caused by a pituitary tumour

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50
Q

diagnostic tests for acromegaly

A

glucose tolerance test (IGF-1 raised, GH raised)

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51
Q

treatment for acromegaly

A

transphenoidal resection surgery
dopamine agonist (carbergoline)
somatostatin anologues + GH receptor antagonists

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52
Q

complications of acromegaly

A

hypertension
diabetes
bitemporal hemianopia

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53
Q

define conns syndrome

A

primary hyperaldosteronism
high aldosterone levels independent of rennin-angiotensin system

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54
Q

clinical presentation of conns syndrome

A

hypertension
hypokalemia

55
Q

define secondary hyperaldosteronism

A

hyperaldosteronism due to high renin levels

56
Q

pathophysiology of conns syndrome

A

aldosterone causes exchange of sodium and potassium in distal renal tubule
Increased aldosterone causes increased reabsorption of sodium + water and increased excretion of potassium

57
Q

aetiology of conns syndrome

A

adrenal adenoma secreting aldosterone or adrenal hyperplasia

58
Q

diagnostic test for conns sydndrome

A

plasma aldosterone (high) and renin levels

59
Q

treatment of conns syndrome

A

adenoma- surgical removal
hyperplasia- aldosterone antagonist (spiranolactone)

60
Q

define adrenal insufficiency

A

destruction of the adrenal cortex leading to a reduction in adrenal hormones

61
Q

primary adrenal insufficiency

A

problem with the adrenal gland itself- addisons disease

62
Q

clinical presentation of addisons disease

A

lehtargy
depression
tanned
tearful
hyperpigmentation
weight loss

63
Q

pathophysiology of addisons disease

A

autoimmune destruction of adrenal cortex = less cortical products = excess ACTH

excess ACTH stimulates melanocytes causing hyperpigmentation

64
Q

aetiology of addisons disease

A

organ specific antibodies
TB

65
Q

diagostic test for addisons disease

A

low sodium
high potassium
cortisol levels

66
Q

treatment of addisons disease

A

hormone replacement therapy (glucocorticoid= hydrocortisone)
(mineralcorticoid= fludrocortisone to replace aldosterone)

67
Q

secondary adrenal insufficiency

A

occurs when the pituitary gland doesn’t make enough of the hormone ACTH. The adrenal glands then don’t make enough cortisol.

68
Q

clinical presentation of secondary adrenal insufficiency

A

same symptoms as primary adrenal insufficiency but no hyperpigmentation because no excess ACTH to cause melanocyte stimulation

69
Q

aetiology of secondary adrenal insufficiency

A

hypothalamic/pituitary disease or from long term steroids

70
Q

diagnostic tests for secondary adrenal insufficiency

A

long ACTH test (synacthen test) to distinguish between primary and secondary adrenal insufficiency (primary = high ACTH, secondary = low ACTH)

71
Q

treatment of secondary adrenal insuffiency

A

just glucocorticoid replacement (hydrocortisone)
remove steroid use if necessary

72
Q

define adrenal hyperplasia

A

defective enzymes mediating the production of the adrenal cortex products

73
Q

clinical presentations of adrenal hyperplasia

A

salt loss
females = unambiguous genitalia
males = no signs at birth, slight hyperpigmentation and possible penile enlargement

74
Q

aetiology of adrenal hyperplasia

A

defective 21-hydrolase = disruption of cortisol synthesis
usually genetic

75
Q

pathophysiology of adrenal hyperplasia

A

Reduced activity of an enzyme required for cortisol production leads to chronic overstimulation of the adrenal cortex and accumulation of precursors proximal to the blocked enzymatic step.

76
Q

diagnostic tests for adrenal hyperplasia

A

ACTH stimulation test
precursors to cortisol are high but cortisol itself is low

77
Q

treatments for adrenal hyperplasia

A

glucorticoids (hydrocortisone)
control elctrolytes
NaCl replacement if salt loss

78
Q

define diabetes insipidus (Arginine Vasopressin Deficiency)

A

an uncommon disorder that causes an imbalance of fluids in the body. This imbalance leads you to produce large amounts of urine. It also makes you very thirsty

79
Q

clinical presentation of diabetes insipidus

A

polydypsia
polyuria
large volumes of dilute urine

80
Q

define cranial diabetes insipidus

A

hyposecretion of ADH
disease of the hypothalamus

81
Q

aetiology of cranial diabetes insipidus

A

surgery, trauma, tumour, genetic

82
Q

treatment of cranial diabetes insipidus

A

desmopressin (thiazide)

83
Q

define nephrogenic diabetes insipidus

A

insensitivity to ADH

84
Q

aetiology of diabetes insipdus

A

kidney damage, hypokalemia, hypercalcaemia, CKD

85
Q

treatment for nephrogenic diabetes insipidus

A

treat underlying cause

86
Q

diagnostic test of diabetes insipidus

A

water deprivation test
test urine volume
U&E
MRI

87
Q

define syndrome of inappropriate ADH (SIADH)

A

continued ADH secretion in spite of plasma hypotonicity and normal plasma volume

88
Q

clinical presentation of SIADH

A

nausea
irritability
headache
hyponatremia (because too much water retained which dilutes sodium)

89
Q

pathophysiology of SIADH

A

Increased ADH = increased water reabsorption in the distal nephron, producing a concentrated urine and diluted plasma (dilutes sodium)

90
Q

aetiology of SIADH

A

disordered hypothalamic-pituitary secretion
ectopic production of ADH
tumour
small cell lung cancer

91
Q

diagnostic test for SIADH

A

FBC
hyponatremia

92
Q

treatment of SIADH

A

fluid restriction in asymptomatic patients
IV saline in symptomatic patients

93
Q

define primary hyperparathyroidism

A

Primary hyperparathyroidism is when there’s a problem within the parathyroid gland itself, usually a benign (non-cancerous) tumour of the gland.

94
Q

clinical presentation of hyperparathyroidism

A

bones, stones, abdominal groans and psychic moans

95
Q

pathophysiology of hyperparathyroidism

A

parathyroid gland produces too much PTH

96
Q

aetiology of primary hyperparathyroidism

A

adenoma or hyperplasia

97
Q

diagnostic test for primary hyperparathyroidism

A

Urine test.
A 24-hour collection of urine can provide information on how well your kidneys work and how much calcium is passed in your urine.
hypercalcaemia

98
Q

treatment for primary hyperparathyroidism

A

surgical removal of adenoma or bisphosphenates

99
Q

define secondary hyperparathyroidism

A

result of another condition that lowers the blood calcium. This causes your parathyroid glands to overwork and produce high amounts of parathyroid hormone to maintain or restore the calcium level to the standard range.

100
Q

pathophysiology of secondary hyperparathyroidism

A

parathyroid gland becomes hyperplastic in response to hypocalcaemia

101
Q

aetiology of secondary hyperparathyroidism

A

any condition that causes hypocalcaemia)

102
Q

diagnostic test of secondary hyperparathyroidism

A

low serum calcium

103
Q

treatment for secondary hyperparathyroidism

A

calcium correction to prevent overcompensation of PTH

104
Q

define tertiary hyperparathyroidism

A

occurs when an excess of parathyroid hormone (PTH) is secreted by parathyroid glands, usually after longstanding secondary hyperparathyroidism.

105
Q

pathophysiology of tertiary hyperparathyroidism

A

autonomous secretion of PTH due to CKD. Keep producing PTH even after calcium correction.

106
Q

diagnostic test for tertiary hyperparathyroidism

A

blood- normal to high calcium
raised PTH

107
Q

aetiology of tertiary hyperparathyroidism

A

Develops from secondary.

108
Q

treatment of tertiary hyperparathyroidism

A

calcium mimetic
total or sub-total thyroidectomy

109
Q

define hypoparathyroidism

A

decreased PTH

110
Q

clinical presentation of hypoparathyroidism

A

increased excitability of muscles/nerves
numbness around mouth/extremeties
cramps
tetany
chovstek sign
trousseau sign

111
Q

pathophysiology of hypoparathyroidism

A

decreased PTH = decreased calcium reabsorption in kidneys, intestines etc

112
Q

aetiology of hypoparathyroidism

A

may be transient
most commonly follows neck surgery

113
Q

diagnostic tests for hypoparathyroidism

A

calcium and PTH levels low
phosphate high

114
Q

treatment of hypoparathyroidism

A

IV calcium
vitamin D analogue

115
Q

define hypercalcaemia

A

high serum calcium

116
Q

clinical presentations of hypercalcaemia

A

malaise
depression
bone pain
abdominal pain
constipation
short QT interval

117
Q

aetiology of hypercalcaemia

A

hyperparathyroidism
malignancy

118
Q

diagnostic test for hypercalcaemia

A

high serum calcium

119
Q

treatment for hypercalcaemia

A

loop diuretics to return calcium to normal
surgical removal in primary hyperparathyroidism

120
Q

define hypocalcaemia

A

low calcium

121
Q

clinical presentation of hypocalcaemia

A

increased excitability of muscles/nerves
numbness around mouth and extremities
cramps
tetany
chovestek sign
trousseau sign
QT prolongation

122
Q

diagnostic test for hypocalcaemia

A

high serum phosphate
low calcium
low PTH

123
Q

aetiology of hypocalcaemia

A

CKD usually
vit D deficiency
hypoparathyroidism

124
Q

treatment of hypocalcaemia

A

IV calium
vit d supplements

125
Q

define hyperkalemia

A

high potassium

126
Q

clinical presentation of hyperkalemia

A

few symptoms until it can cause an MI
tall tented t waves

127
Q

pathophysiology of hyperkalemia

A

renal impairment can cause potassium retention in nephron

128
Q

diagnostic tests for hyperkalemia

A

ecg
U&Es

129
Q

treatment of hyperkalemia

A

dietary potassium restriciton + loop diuretic

130
Q

define hypokalemia

A

low potassium

131
Q

clinical presentation of hypokalemia

A

usually asymptomatic
maybe muscle weakness
cardiac arrhythmias
t wave inversion

132
Q

aetiology of hypokalemia

A

usually caused by diuretics, V+D, hyperaldosteronism

133
Q

diagnostic test for hypokalemia

A

ecg
U&Es

134
Q

treatment with hypokalemia

A

treat underlying cause

Phase 2A Conditions (10 decks)

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