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Y2 - my own > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

How do we diagnose Cushing’s?

A

Free cortisol in urine and low dose dexamethasone suppression test.

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2
Q

What are two main changes we seen in diabetic nephropathy?

A

Proteinuria

Hypertension

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3
Q

GLUT 4 is activated by insulin. True or false?

A

True; pumps glucose into the cell.

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4
Q

Can fat be converted to glucose?

A

No. Triglycerides are broken down into glycerol and NEFAs. GLYCEROL can be made into glucose.

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5
Q

Which is the last method of energy use - really only used in survival?

A

Degrading protein.

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6
Q

What is the order in which we use energy?

A

Glucose, then FAs, then ketones.

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7
Q

Why can fatty acids not be used by the brain?

A

Cannot cross the BBB. The brain instead uses ketones.

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8
Q

What is acetoacetate?

A

A ketone: will be used by the brain when there is not enough glucose.

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9
Q

Does insulin signal the fed or fasted state?

A

Fed state.

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10
Q

How does insulin influence ketone production?

A

Insulin decreases ketone production.

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11
Q

Why do we see glycosuria in diabetes?

A

Low insulin so glucose is not being taken up by cells.

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12
Q

How do we treat ketoacidosis?

A

Give insulin. Insulin lowers ketones.

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13
Q

Kussmaul breathing is characteristic of….?

A

Diabetic ketoacidosis. = deep, shallow breathing.

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14
Q

In which Diabetes do we see diabetic ketoacidosis?

A

T1DM; DO produce enough insulin in t2dm, but cells to reduce glucose are resistant.

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15
Q

How does insulin work?

A

Increases insulin sensitivity.

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16
Q

What is the cutoff for high fasting glucose levels?

A

> 7.0mmol/L

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17
Q

Which Diabetes has a stronger familial history?

A

t2dm.

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18
Q

Gliclazide is what type of Diabetic medication?

A

Sulphonylurea

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19
Q

Metformin is what type of Diabetic medication?

A

Biguanide

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20
Q

Give x3 causes of DKA

A

Diabetic ketoacidosis:

  1. Unknown
  2. infection
  3. no insulin
  4. new diagnosis of T1DM.
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21
Q

Give x5 clinical features of DKA

A 
Polydipsia (increased thirst)
Polyuria (increased urination)
Sweating
Abdominal pain
Glycosuria, ketonuria
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22
Q

Where will you see Kussmaul’s breathing?

A

Diabetic ketoacidosis.

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23
Q

Give x3 metabolic defects with insulin deficiency

A

Proteolysis
Lipolysis
Glycogenolysis

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24
Q

Which structure is at the base of the hypothalamus?

A

The arcuate nucleus

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25
Q

Which are the two populations which stimulate/ inhibit food intake?

A

[In the arcuate nucleus]:
Stimulatory: NPY (neuropeptide Y), Agrp.
Inhibitory: POMC (pro-opiomelanocortin).

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26
Q

What affect does POMC have on appetite?

A

It inhibits appetite.

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27
Q

Could stimulation or inhibition of POMC cause obesity?

A

Inhibition of POMC; POMC works to inhibit appetite after sufficient food intake.

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28
Q

What is the relationship between leptin and body fat?

A

high body fat = high leptin (as compensation). Otherwise leptin is a satiety hormone.

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29
Q

Which hormone activates POMC?

A

Leptin; wants to signal satiety.

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30
Q

Which hormone resistance is obesity associated with?

A

Leptin resistance

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31
Q

Give two ways the patient may present with low leptin:

A

Hyperphagia

Fertility problems

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32
Q

What affect can insulin have on food intake?

A

Lower food intake

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33
Q

Which is the special functional group on Ghrelin?

A

A fatty acid.

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34
Q

Which neuron group does Ghrelin stimulate?

A

Stimulates the NPY/Agrp neurones; a hunger hormone

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35
Q

Which hormone has an opposite effect to Ghrelin - how so?

A

PYY;

Stimulates POMC
Inhibits NPY/Agrp.

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36
Q

What effect does PYY have on appetite?

A

Inhibits appetite.

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37
Q

What does GLP-1 stand for and what does it do?

A

Glucagon-like peptide 1.

Has an incretin effect.

38
Q

If something has an incretin role, what does it do?

A

Stimulate insulin release.

39
Q

What is Liraglutide?

A

GLP-1 receptor agonist = increases insulin and increases satiety = used as a weight loss treatment

40
Q

What is the difference between osteoporosis and osteomalacia?

A 
Osteoporosis = reduction in mass of bones
Osteomalacia = softening of bones
41
Q

What can a DEXA scan show you?

A

Bone density - used to assess osteoporosis

42
Q

What is the difference between primary and secondary hyperparathyroidism?

A 
Primary = problem with the Parathyroid gland itself; potential tumour.
Secondary = may be compensatory high PTH due to low calcium in bone.
43
Q

What is the main side effect of metformin?

A

bloating, diarrhoea, nausea.

44
Q

What is the main side effect of statins?

A

Muscle pain

45
Q

What diabetes class are Gliptins?

A

DPP-4 Inhibitors.

46
Q

What diabetes class is gliflozin?

A

SGLT-2 Inhibitor

47
Q

What diabetes class is Metformin?

A

Biguanide

48
Q

What diabetes class is gliclazide?

A

Sulphonylurea

49
Q

Which diabetes class treatments are given together and why?

A

GLP-1 agonists and DPP4 inhibitors (prevents breakdown of GLP-1 agonists)

50
Q

How do GLP-1 agonists work?

A

Increase insulin secretion and increase satiety.

51
Q

What are the choices of drug treatment in acromegaly?

A

Somatostatin analogues to reduce growth.

52
Q

Desmopressin is usually given in which form?

A

As a nasal spray (for majority)

53
Q

Desmopressin is used to treat cranial diabetes insipidus. True or false.

A

True.

54
Q

Which has a shorter half life - T3 or T4?

A

T3

55
Q

What is Plummer’s disease?

A

Toxic nodule producing thyroxine.

56
Q

Why will a large dose of iodine cause short term hypothyroidism?

A

; Wolff-Chaikoff effect. An autoregulation mechanism where the thyroid rapidly reduces thyroxine production. Used prior to surgery for patients with hyperthyroidism.

57
Q

Why will an overdose of thyroxine in a normal individual cause lid lag?

A

Causes contraction of the Muller muscle.

58
Q

Which is the first therapeutic step in treating phaeochromocytomas?

A

Alpha blockade

59
Q

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

A

Cushing’s disease is due to a pituitary origin.

60
Q

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

A

Cushing’s disease is due to a pituitary origin.

DP

61
Q

Spirinolactone is a diuretic. Fludrocortisone is a corticosteroid. What are each of their effects on aldosterone receptors?

A

Aldosterone receptor antagonist

Aldosterone receptor agonist

62
Q

What are fludrocortisone, hydrocortisone and dexamethasone?

A

Glucocorticoids.

63
Q

Does NPY stimulate or inhibit food intake?

A

Stimulates; the Agrp/NPY neuronal population

64
Q

Do we see hyperpigmentation in Addison’s or Cushing’s?

A

Both; both have high levels of ACTH!

65
Q

Is Ghrelin a hunger or fasting hormone?

A

A hunger hormone = stimulates Agrp/NPY.

66
Q

Where is GLP-1 produced?

A

From L cells in the gut

67
Q

What does the ‘Ethinyl’ in estradiol mean?

A

Makes it orally active so it does not undergo first pass metabolism.

68
Q

What are the LH levels like during menopause?

A

High; low oestrogen.

69
Q

hCG acts on which receptors?

A

LH receptors

70
Q

What must the sperm undergo to be able to penetrate the egg?

A

Capacitation

71
Q

Does fertilisation need an oestrogen or progesterone dominated environment?

A

Progesterone dominated environment

72
Q

Give x3 signs of Acromegaly

A

Frontal bossing, prognathism, enlargement of supraorbital ridges.

73
Q

What is the relationship between IGF-1 and GH?

A

Growth hormone controls production of IGF-1.

74
Q

Which main hormone is raised in acromegaly?

A

IGF-1

75
Q

Why do we give DDAVP rather than ADH directly to patients with DI? (not DM, DI!)

A

DDAVP is selective for v2 receptors in kidney. ADH would stimulate v1 receptors also

76
Q

Which form of cortisol do we give primarily in Addison’s?

A

Hydrocortisone

77
Q

Which cortisol substitute is given as an aldosterone analogue?

A

Fludrocortisone

78
Q

When will metryrapone be used?

A

In Cushing’s; steroidogenesis inhibitor. Also, ketoconazole.

79
Q

What is the daily dose of hydrocortisone and which chunks?

A

20mg a day. x3 a day in 10mg, 5mg and 5mg divisions.

80
Q

What do hormone levels look like in pregnancy?

A

High oestrogen, low LH, low FSH.

81
Q

If PTH is raised due to calcium levels being low, what type of hyperparathyroidism is it?

A

Secondary

82
Q

What is primary hyperparathyroidism?

A

When PTH AND Ca2+ are high

83
Q

The brain is mineralised by what?

A

Calcium phosphate - hydroxyapatite crystals.

84
Q

What are osteocytes?

A

Mature bone cells - former osteoblasts.

85
Q

Which bone borders the lacrimal bone on a diagram?

A

The ethmoid bone

86
Q

What is the name of the posterior suture of the brain?

A

The lambdoid suture

87
Q

Name the three branches of the trigeminal nerve

A 
V1 = Opthalmic (sensory)
V2 = Maxillary (sensory)
V3 = Mandibular (sensory and motor)
88
Q

How many cranial nerves enter the middle cranial fossa?

A

4; 2 enter the anterior cranial fossa, 4 enter the middle cranial fossa and 6 the posterior cranial fossa.

89
Q

Which cranial nerve pass through the supraorbital fissure?

A

Oculomotor, trochlear, trigeminal (v1 division) and abducens.

90
Q

Which two cranial nerves pass through the internal acoustic meatus?

A

Facial and vestibulococchlear nerve.

91
Q

What is the name of the bone which has a greater and lesser wing?

A

The sphenoid bone

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