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FINALS (all high yield study decks) > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is meant by catabolic metabolism?

A

larger molecules are broken down into smaller ones

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2
Q

What is meant by anabolic metabolism?

A

a larger molecule is made from smaller ones (e.g. storing)

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3
Q

What does autocrine mean?

A

Acts on the same cell it was released from

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4
Q

What does endocrine mean?

A

Acts on neighbouring cells

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5
Q

What does exocrine mean?

A

enters the bloodstream and acts on distant cells

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6
Q

What is meant by ‘neuroendocrine’?

A

neurons release hormones which enter the blood and travel to their target tissue

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7
Q

What is meant by ‘total plasma hormone’?

A

Free hormone + protein bound hormone

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8
Q

What connects the hypothalamus and the anterior pituitary?

A

capillary portal system

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9
Q

Which hormones are secreted by the posterior pituitary?

A

Vasopressin and oxytocin

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10
Q

Which part of the pituitary is an extension of neural tissue?

A

Posterior pituitary

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11
Q

Name the amine hormones

A

Catecholamines (adrenaline, dopamine)

Thyroid hormones

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12
Q

Name the steroid hormones

A
  • Sex steroids
  • HCG
  • Corticosteroids
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13
Q

What are steroid hormones derived from?

A

cholesterol

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14
Q

What is a primary endocrine disorder?

A

disorder arising from a defect in the tissue that secretes that hormones

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15
Q

What is a secondary endocrine disorder?

A

too much/too little from the pituitary

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16
Q

What is a tertiary endocrine disorder?

A

Hypothalamic defect

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17
Q

What are the growth drivers in infancy (0-2)?

A

Nutrition and insulin

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18
Q

What are the growth drivers in childhood (3-11)?

A

Growth hormone and thyroxine

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19
Q

What are the growth drivers in puberty (12-18)?

A

Growth hormones and sex steroids

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20
Q

What is the first sign of puberty in girls?

A

breast budding (Tanner stage B2)

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21
Q

What is the first sign of puberty in boys?

A

testicular enlargement (Tanner stage G2)

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22
Q

What is the normal age of pubertal onset in boys?

A

9-14

(below 9 is precocious and above 14 is late)

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23
Q

What is the normal age of pubertal onset in girls?

A

8-13

(below 8 is precocious and above 13 is late)

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24
Q

Who is offered bariatric surgery?

A

a BMII ≥ 40
or
BMI ≥ 35 with 1 or more health problems that are likely to improve upon weight loss

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25
Q

which pancreatic cells produce glucagon?

A

alpha

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26
Q

which pancreatic cells produce insulin?

A

Beta

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27
Q

Which pancreatic cells produce somastatin?

A

D cells

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28
Q

What is c-peptide?

A

a by-product of insulin production

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29
Q

What effect does insulin have on the body?

A

causes cells to absorb glucose and use it as energy.

causes liver and muscle cells to take up glucose and store it.

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30
Q

What effect does glucagon have on the body?

A

causes the liver to break down glucose stores (glycogenolysis)

tells the liver to change fats and proteins into glucose (gluconeogenesis

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31
Q

What are the sick day rules for insulin?

A

Don’t ever stop insulin, check blood glucose levels more often.

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32
Q

When must the DVLA be informed with regards to diabetes?

A

if you have diabetes managed with medications

If on insulin and likely to be for >3 months

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33
Q

What are the rules regarding driving and long car journeys for those with diabetes?

A

BM must be checked before driving and every 2 hours whilst driving

Must not drive if BM <5

If BM falls below 5 while driving, you must wait for at least 45 minutes after your BM has surpassed 5mmol/L

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34
Q

What is a healthy, non-diabetic HBA1c?

A

<42

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35
Q

What is the target HBA1c in diabetics not on medications which carry a hypo risk?

A

48 or less

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36
Q

What is the target HBA1c in diabetics on medications which carry a hypo risk?

A

53

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37
Q

what causes T1DM?

A

Autoimmune destruction of the pancreas

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38
Q

What is MODY?

A

subset of T1DM occurring in older patients

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39
Q

How often to those with T1DM need to check fngerprick BM?

A

Finger prick a least 4x daily (before each meal and before bed)

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40
Q

How does c-peptide measure in T1DM?

A

Low

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41
Q

what causes T2DM?

A

peripheral tissues become insensitive to insulin (this is insulin resistance) & the pancreas loses its ability to secrete high levels of insulin

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42
Q

Explain the stepwise management of T2DM

A

Management is stepwise

Diet & exercise
Metformin
Dual therapy (metformin + 1 from table)
Triple therapy (metformin +2 from table)

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43
Q

What are the3 features of DKA

A

Ketoacidosis, dehydration, potassium imbalance

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44
Q

Which tests cane used to diagnose DKA?

A
  • BM >11
  • Ketones > 3
  • pH < 7.3
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45
Q

What is the first line treatment of DKA?

A

Fluid

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46
Q

What must you be careful to avoid causing when treating DKA?

A

Cerebral oedema

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47
Q

What is the MOA of metformin?

A

Increases insulin sensitivity

Decreases glucose production by the liver

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48
Q

What are the side effects of metformin?

A

GI

Lactic acidosis secondary to AKI

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49
Q

What is the suffix of SGLT-2 medications?

A

-flozin

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50
Q

What is the MOA of SGLT-2 medications?

A

Increases urinary excretion of glucose

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51
Q

What are the side effects associated with SGLT-2 medications?

A

Hypoglycaemia & DKA
Weight loss
UTI/thrush/fournier’s
Lower limb amputation

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52
Q

What is the suffix associated with thiazolidinedones?

A

Increases insulin sensitivity

Decreases glucose production by the liver

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53
Q

What are the side effects associated with thiazolidinedones?

A

Weight gain
Heart failure
Bone fractures
Bladder cancer

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54
Q

What is the suffix of Sulfonylureas?

A

-zide

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55
Q

What is the MOA of Sulfonylureas?

A

Stimulates insulin release from the pancreas

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56
Q

What are the side effects associated with Sulfonylureas?

A

Weight gain
Hypoglycaemia

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57
Q

What is the suffix associated with DPP-4 inhibitors?

A

-gliptin

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58
Q

What is the MOA of DPP-4 inhibitors?

A

Incretin- Increase insulin secretion, inhibit glucagon production, slow absorption from GI tract

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59
Q

What are the side effects associated with DPP-4 inhibitors?

A

Headache
Pancreatitis

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60
Q

What is the suffix associated with GLP-1

A

-tide

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61
Q

What is the MOA of GLP-1?

A

Incretin- Increase insulin secretion, inhibit glucagon production, slow absorption from GI tract

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62
Q

What are the side effects associated with GLP-1?

A

Reduced appetite
Weight loss
GI

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63
Q

What is the first line antihypertensive in diabetics?

A

ACE inhibitors

64
Q

What drug is given in diabetics with CKD if albumin: creatinine > 3mg/mmol

A

ACE inhibitor

65
Q

What drug is given in diabetics with CKD if albumin: creatinine > 30mg/mmol

A

SGLT-2 inhibitor

66
Q

Name the significant side effects of poorly controlled diabetes?

A

Vascular
* Retinopathy
* Nephropathy
* Neuropathy

Erectile dysfunction

Depression

67
Q

What is the difference between cranial and nephrogenic diabetes insipidus?

A

Cranial DI = lack of antidiuretic hormone

Nephrogenic DI = lack of response to antidiuretic

68
Q

What causes cranial diabetes insipidus?

A

Brain pathology

69
Q

What causes nephrotic diabetes insipidus?

A

Lithium
High calcium
Low potassium
Polycystic kidney disease

70
Q

How is diabetes insipidus diagnosed?

A

Water depravation test

71
Q

In cranial diabetes inspidus, what result would you expect in

urine osmolality after water depravation

urine osmolality after desmopressin?

A
72
Q

In nephrogenic diabetes inspidus, what result would you expect in

urine osmolality after water depravation

urine osmolality after desmopressin?

A
73
Q

what is hyperosmolar, hyperglycaemic state?

A

Hyperosmolality
hyperglycaemia
absence of ketones

74
Q

How is hyperosmolar, hyperglycaemic state managed?

A

IV fluids

75
Q

Describe the hormonal axis for growth hormone

A

Growth hormone releasing hormone (stimulatory) Somatostatin (inhibitory)
->
Growth hormone (up or down regulated)
->
insulin-like growth factor-1 (IGF-1) from Liver

76
Q

What are the functions of growth hormone?

A

Increases blood glucose

Promotes growth

77
Q

What causes giantism?

A

Excessive growth hormone prior to closure of long bone epiphysis

78
Q

What causes acromegally?

A

Excessive growth hormone after closure of long bone epiphysis

79
Q

How is acromegaly diagnosed?

A

IGF-1 test then OGTT

80
Q

What is the most common cause of excessive growth hormone resulting in acromegaly?

A

pituitary adenoma

81
Q

How is a pituitary adenoma managed?

A

Trans-sphenoidal surgery

82
Q

What is the first line medical management of acromegallY?

A

octerotide (somatostatin analogue)

83
Q

describe the hormonal axis of sex hormones

A

Gonadotrophin releasing hormone
->
LH/FHS
->
oestrogen

84
Q

Why do children that have gone through precocious puberty have stunted growth?

A

long bones fuse early under influence of sex hormones.

85
Q

describe the hormonal axis of thyroid hormones

A

Thyrotropin releasing hormone
->
Thyroid stimulating Hormone
->
T3 & T4

86
Q

Which thyroid cells secrete calcitonin?

A

clear cell

87
Q

Which thyroid cells produce and secrete thyroid hormones?

A

Follicular cells

88
Q

What are the functions of thyroid hormones?

A

Metabolism and thermogenesis

Growth

controlling heart, muscle and digestive function

brain development

bone maintenance

89
Q

How can hyperthyroid be treated?

A

radioactive iodine
beta blockers (symptomatic)
antithyroid drugs (carbazole)
surgery

90
Q

Name the two main hyperthyroid presentations

A

Graves
Toxic multinodular goitre

91
Q

What antibodies are associated with Graves disease?

A

Anti-TSH & anti-TPO

92
Q

How does graves disease present

A

Classic hyperthyroid signs +
Pre-tibial myxoedema
Exophthalmos
Diffuse goitre

93
Q

What isotopic multi nodular goitre?

A

one or more nodules in the thyroid gland that make thyroid hormone without responding to the signal to keep thyroid hormone balanced

94
Q

How does toxic multi nodular goitre look on nuclerscintigraphy?

A

Patchy uptake

95
Q

How does thyroid storm (thyrotoxic crisis) present?

A

Fever
tachycardia
delirium
hyperthermia

96
Q

What are the two big side effects of carbamazepine?

A

agranulocytosis and pancreatitis

97
Q

What are the three main side effects of propyuracil?

A

severe liver reactions death
agranulocytosis

98
Q

What causes hashimotos thyroiditis?

A

Autoimmune attack of the thyroid gland

99
Q

What antibody is associated with hashimotos thyroiditis?

A

Anti-TPO

100
Q

How is hashimotos managed?

A

Give titrated levothyroxine (when pregnant, double the dose on 2/7days)

101
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

102
Q

How much iodine is required per year by the body?

A

50mg

103
Q

Name 3 foods high in iodine

A

milk, fish, seaweed

104
Q

What is Sheehans syndrome?

A

Avascular necrosis of pituitary due to massive blood loss

105
Q

What are the critical findings in myxoedema coma?

A

Critically low sodium
HYPOthermia

106
Q

What is Subacute (de Quervain’s) thyroiditis?

A

Temporary inflammation of thyroid gland triggered by viral infection (e.g. enteroviruses, coxsackie)

Thyrotoxic phase for 3-6 weeks followed by a period of hypothyroidism for 3-6 months

107
Q

what is the classic finding in subacute (De Quervains) thyroiditis?

A

PAINFULL goitre

108
Q

how is subacute (De Quervains) thyroiditis managed?

A

It itself limiting so treat symptoms

NSAIDs for goitre inflam
B-Blockers for thyrotoxic phase
Levothyroxine for hypothyroid phase

109
Q

What is the most common type of thyroid cancer?

A

Papillary

110
Q

describe the hormonal axis of parthyroid hormones

A

Serum calcium/phosphate/magnesium levels
->
parathyroid hormone (from PT gland)
->
increased intestinal absorption of calcium
increased kidney reabsorption of calcium
increased calcium reabsorption from bone

111
Q

What findings you see on skull x-ray in hyperparathyroidism?

A

Pepper pot skull

112
Q

How can primary, secondary and tertiary hyperthyroidism be differentiated in blood tests?

A
113
Q

How can hyperparathyroidism be managed?

A

Total parathyroidectomy

Calcimimetics

114
Q

Describe the hormone axis for prolactin

A

Thyrotropin releasing hormone ->
prolactin ->
stimulates breast tissue, inhibits ovulation

115
Q

How is prolactinoma diagnosed?

A

serum prolactin & MRI

116
Q

How’s prolacinoma managed?

A

dopamine agonists (cabergoline or bromocriptine)

Tran sphenoidal surgery

117
Q

name the area and what it produces

A
118
Q

What causes Congenital Adrenal Hyperplasia?

A

deficiency in the enzyme 21-hydroxylase

119
Q

How can Congenital Adrenal Hyperplasia present in babies?

A

Baby GIRLS are born with ambiguous genitalia

can have a salt-losing crisis and become very sick within the first few days of life

120
Q

Describe the hormonal axis of cortisol

A

Corticotrophin Releasing Hormone (CRH)
->
Adrenocorticotrophic hormone (ACTH)
->
Cortisol

121
Q

Describe the difference between Cushing’s disease and Cushing’s syndrome

A

Cushing’s syndrome = classic Cushing’s caused by everything but a tumour

Cushing’s disease = Cushing’s caused by a tumour

122
Q

How is Cushing’s diagnosed?

A

24 hour urinary cortisol or a dexamethasone suppression

123
Q

What causes Addisons disease?

A

Autoimmune destruction of the adrenal cortex causes hyposecretion of all adrenal steroid hormones (aldosterone, glucocorticoids and sex steroids)

124
Q

What is the autoantibody in Addison’s?

A

autoantibodies against 21-Hydroxylase

125
Q

What are the presenting features of Addison’s?

A

Hypotension, hyperkalaemia, hyponatremia
Hyperpigmentation

126
Q

What diagnostic test is used to identify Addison’s?

A

Short synacthen test (ACTH stimulation test)

127
Q

How is an addisonian crisis managed?

A

100mg IV hydrocortisone

128
Q

What is the chronic treatment of Addison’s disease?

A

Hydrocortisone and fludrocortisone

129
Q

What should people with Addison’s do to their medications when they have a short lived illness or are stressed?

A

double their glucocorticoid dose

130
Q

What should people with Addison’s do to their medications when they are seriously ill?

A

IV Hydrocortisone

131
Q

What is conn’s syndrome?

A

Excessive aldosterone from the zona glomerulosa (of the adrenal cortex) usually due to an adrenal tumour

132
Q

How does conns syndrome present?

A

hypertension, hyperpigmentation, lethargy

133
Q

How is conns syndrome tested for?

A

Aldosterone: Renin ratio

134
Q

How is conns syndrome managed?

A

Surgical resection of adrenal adenoma

135
Q

What is a pheochromocytoma?

A

neuroendocrine tumour, found in chromaffin cells of adrenal medulla which produces excessive adrenaline

136
Q

How does phaeochromocytoma present?

A

Hypertension resistant to anti-hypertensives
headaches
sweating
anxiety

137
Q

How is pheochromocytoma diagnosed?

A

Plasma free metanephrines

138
Q

How is pheochromocytoma managed?

A

surgical resection of tumour

Alpha blockers

139
Q

What genetic change is associated with pheochromocytoma?

A

RET

140
Q

What is a normal range calcium?

A

2.2-2.6 mM

141
Q

What are the two clinical signs of hypocalcaemia?

A

Trosseau’s sign = The involuntary contraction of the muscles of the hand and wrist that occurs after the compression of the upper arm with a blood pressure cuff

Chovstek’s Sign = The twitching of facial muscles that occurs when gently tapping an individual’s cheek in front of the ear

142
Q

How is calcium regulated?

A

Parathyroid hormone (increases calcium)

Calcitrol (increases calcium)

Calcitonin (decreases calcium)

143
Q

What causes Ricketts (osteomalacia)?

A

Vitamin D deficiency

144
Q

Howdoes hypercalcaemia present?

A

Stones, bones, abdominal moans, psychiatric groans

145
Q

How is hypercalcaemia managed?

A

Rehydration

IV Bisphosphonates

146
Q

What is SIADH?

A

Increased release of ADH from posterior pituitary

147
Q

What urine and serum changes does SIADH cause?

A

high urine osmolality
high urine sodium
low serum sodium

148
Q

What are the 3 most important causes of SIADH?

A

Post-operative
SSRI
small-cell lung cancer

149
Q

Why do you need to replace sodium slowly in patients with chronic hyponatraemia?

A

more than a 10mmol/L increase in 24 hours can cause osmotic demyelination syndrome

150
Q

What neoplasms are encompassed by MEN1?

A

Parathyroid hyperplasia and adenomas

Pancreatic and duodenal endocrine tumours

Pituitary adenoma (prolactinoma)

151
Q

What neoplasms are encompassed by MEN2A?

A

MEN1 features + parathyroid hyperplasia

152
Q

What gene is involved in MEN2A?

A

RET

153
Q

What neoplasms are encompassed by MEN2B?

A

Features of MEN1 & MEN2A + neuromas and skin abnormalities

154
Q
A
155
Q
A

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