Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2 3. Endocrinology > Endocrine pharmacology > Flashcards

Endocrine pharmacology Flashcards

1
Q

Where do peptide hormones bind?

A

extracellular receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do steroid hormones bind?

A

intracellular receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where do thyroid hormones bind?

A

nuclear receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is pharmacokinetics

A

what an individual does to a drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is pharmacodynamics?

A

what a drug does to an individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the factors of pharmacokinetics?

A
  • absorption
  • distribution
  • metabolism
  • excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the factors of pharmacodynamics?

A
  • receptor binding
  • action on ion channels
  • action on enzymes
  • cytotoxic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does prolactin do?

A

stimulate lactation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is prolactin secreted?

A

lactotrophs in anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is prolactin regulated?

A

under tonic inhibition by dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how can prolactin levels be changed?

A

anything that alters/inhibits dopamine levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the result of hyperprolactinaemia?

A

hypogonadotrophic hypogonadism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What drugs can effect prolactin?

A

any drug interfering with dopamine action

  • antipsychotics
  • antiemetics
  • antidepressants
  • opiates
  • H2 receptor antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is galactorrhoea?

A
  • milky discharge from the nipples
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a microprolactinoma?

A

<1cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a macroprolactinoma?

A

> 1cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is prolactinoma treated?

A
  • dopamine D2 agonists (1st line)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name commone dopamine agonists?

A
  • cabergoline
  • quinagolide
  • bromocriptine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is vasopressin?

A
  • Antidiuretic hormone (peptide)
  • secreted from posterior pituitary
  • regulating serum osmolarity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is ADH released?

A

in response to low plasma volume/ increased serum osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are V1 receptors and what are their actions?

A
  • in vascular smooth muscle

- vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where are V2 receptors found and what are their actions?

A
  • distal tubule

- aquaporin channels to reabsorb water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name a vasopressin therapy

A
  • desmopressin

synthetic analogue, no vasoconstricting effects, longer half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Briefly describe the physiology of the thyroid hormones

A

hypothalamus secreted thyrotropin releasing hormone, which acts on the pituitary to release thyroid stimulating hormone, which acts on the thyroid to release thyroxine (T4) and triiodothyronine (T3)

T4 predominant peripherally. Can convert to T3 (active)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is maintenance therapy for cranial diabetes insipidus given?

A

Oral - bioavailability low, therefore high doses are required
o Sublingual
o Intranasal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is acute therapy for diabetes insipidis given?

A

Subcutaneous
o Intramuscular
o Intravenous (variceal bleeding/shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name a T4 drug

A

Levothyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How should Levothyroxine be taken?

A

Daily dose, advised to be taken in the morning on an
empty stomach

Incomplete gastric absorption – can be affected by other medication
o Not advised to combine with PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does levothyroxine work?

A
  • travels bound to protein
  • metabolised to T3

long half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the treatment options of thyroid disorders?

A
  • drugs
  • radiation
  • surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Name types of anti-thyroid drugs

A

Thionamides:

  • carbimazole
  • propylthiouracil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the features of carbimazole

A

Drug of choice
o Absorbed well from gut and converted to methimazole via first pass metabolism
o Half-life of methimazole is 12-15 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the features of propylthiouracil

A

PTU
Less active and shorter half-life so higher doses twice daily are required
o Usually second line
o Associated with some liver toxicity
o NB: Better safety data in pregnancy than carbimazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is a side effect of thionamides?

A

agranulocytosis (low white cell count)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe the mechanism of action of anti-thyroid drugs

A

Reduce thyroid hormone synthesis
o Inhibit iodide oxidation
o Inhibit iodination of tyrosine
o Inhibit coupling of iodotyrosines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why should management of thyroid medication be monitored?

A

It can take a few weeks to reduce circulating hormones

o Repeat analysis of thyroid function is normally done a few months after commencing treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the additional features of PTU?

A

also reduces conversion of T4 to T3 peripherally giving some more acute effects
o More beneficial in e.g. a thyroid storm
o Limits the metabolic effects of the hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Name non-thionamide treatments for hyperthyroidism

A

Beta-blockers – overactive thyroid hormones effectively increase SNS over activity

Potassium iodide
o Reduces thyroid hormone release acutely, used in thyroid storm and pre-operatively

Radioactive iodine
o Takes a few months for the gland to become underactive
o 80-90% of patients will subsequently become hypothyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe glucose homeostasis

A

Insulin secreted from pancreatic beta cells in response to serum glucose allows glucose entry into
adipose tissue and muscle

  • Gluconeogensis primarily in liver allows glucose into circulation, inhibited by insulin
  • Counter-regulatory hormones include glucagon, cortisol, growth hormone  stimulate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the causes of T2DM?

A
  • insulin resistance

- impaired insulin secretion

41
Q

Why does insulin resistance occur?

A

Usually develops due to combination of lifestyle and
genetic factors
o Insulin signalling impaired at cellular level

42
Q

Why does impaired insulin secretion occur?

A

Initial hyperinsulinaemia no longer able to cope with resistance, beta cell failure

43
Q

What are the 1st line treatments for T2DM?

A
  • metformin
  • sulphonylurea (if not tolerant to metformin or weight loss/osmotic symptoms)

In addition to lifestyle measures

44
Q

What is the 2nd line treatment for T2DM?

A

Add one of:

  • sulphonylurea
  • thiazolidinediones
  • DPP-IV inhibitor

to 1st line, in addition to lifestyle measures

45
Q

What are the 3rd line treatments for T2DM?

A

Add or substitute with one of:

  • thiazolidinediones
  • DPP-IV inhibitor
  • injectable insulin
  • GLP-1 agonists
46
Q

Which T2DM medications are insulin sensitisers?

A
  • biguanides (metformin)

- thiazolidinediones

47
Q

Which T2DM medications increase insulin?

A
  • sulphonylureas
  • GLP-1 agonists
  • DPP-4 inhibitors
  • insulin
48
Q

What T2DM medications increase glucose in urine

A
  • SGLT2 inhibitors
49
Q

Describe the pharmacokinetics of metformin

A

Rapidly absorbed
o Half-life 2-5 hours initially taken OD, but can be increased to 2 or 3x
o Typical dose = 1g/day
o Excreted unchanged by kidneys

50
Q

Describe the pharmacodynamics of metformin

A

Inhibits mitochondiral glycerophosphate dehydrogenase in liver, activates AMPK

Reduced hepatic gluconeogenesis and acts as an insulin sensitiser

51
Q

What are the side effects of metformin?

A

GI side effects

52
Q

Name a type of biguanide

A

metformin

53
Q

Name sulphonylureas

A
  • gliclazide
  • glipizide
  • glibenclamide
54
Q

Describe the pharmacokinetics of suphonylureas

A

Well absorbed, peak plasma concentration within 2-4 hours
o Metabolised by liver, but important role of the kidneys
(contraindicated in patients with end-stage renal failure)
o Duration of action up to 24 hours
o Usually given 2x daily

55
Q

Describe the pharmacodynamics of sulphonylureas

A

Bind to receptor on beta cells, inhibit KATP channels and permit increased insulin secretion

56
Q

What are the side effects of sulphonylureas?

A

Increased circulating insulin, but there is a risk of hypoglycaemia (this can limit their use)

57
Q

Name thiazolidinediones

A
  • pioglitazone

- rosiglitazone

58
Q

What is the use of thiazolidinediones?

A

used to treat insulin resistance associated with diabetes

59
Q

What are the pharmacokinetics of Thiazolidinediones?

A

Rapidly absorbed
o Extensive hepatic metabolism
o Pioglitazone is excreted in bile

60
Q

What are the pharmacodynamics of Thiazolidinediones?

A

PPARγ agonists
o increase transcription of insulin senstising genes
o PPARγ is a nuclear receptor expressed in adipose tissue, muscle, liver

61
Q

What are the side effects of thiazolidinediones?

A
  • increased adipogenesis => associated with weight gain
  • increased long bone fractures
  • fluid retention
  • potentially bladder cancer
62
Q

Describe the incretin system

A

Gut hormones GLP-1 and GIP enhance insulin secretion in response to oral glucose

Broken down by DPP-4

These drugs increase insulin secretion

63
Q

Name GLP-1 agonists

A
  • exenatide

- liraglutide

64
Q

Describe features of GLP-1 agonists

A

Subcutaneous injection (peptide)
o Based on exendin-4 from Gila monster venom (kills prey by hypoglycaemia)
➢ Increased insulin secretion and weight loss (GI side effects are tolerable (nausea), and also
decrease food intake)
(Should not cause hypoglycaemia)

65
Q

Name DPP-4 inhibitors

A
  • sitagliptin

- linagliptin

66
Q

Describe the uses of DPP-4 inhibitors

A

Linagliptin is commonly used in patients with low renal function (CKD 4/5)
o Oral administration, prevent endogenous GLP-1 breakdown

67
Q

Name SGLT2 inhibitors

A
  • canagliflozin
  • dapagliflozin
  • empagliflozin
68
Q

Describe the pharmacokinetcs of SGLT2 inhibitors

A
  • oral, once daily

- half life 10-13 hours

69
Q

Describe the pharmacodynamics of SGLT2 inhibitors

A

Inhibit SGLT2 transporter which normally reabsorbs glucose in proximal convoluted tubule
o Increase glucose excretion

70
Q

What are the side effects of SGLT2 inhibitors

A

Potential risk of volume depletion and UTI

➢ Lowers glucose without causing hypoglycaemia

71
Q

What is the function of insulin in the liver?

A
  • Decrease gluconeogenesis

- Increase glycogen synthesis

72
Q

What is the function of insulin on skeletal muscle?

A
  • Increased glucose transport via GLUT 4

- Increase glycogen synthesis

73
Q

What is the function of insulin on adipose tissue?

A
  • Increased glucose transport via GLUT 4

- Increase lipogenesis and decrease lipolysis

74
Q

What are the different delivery methods of insulin?

A

Subcutaneous injection, most common with pre-filled pens/cartridges
 Continuous subcutaneous insulin infusion (insulin pumps) - more common in children
 Intravenous - during acute illness (e.g. DKA)
 Intramuscular - rare

75
Q

Describe regulation of glucocorticoid and mineralcoricoid release

A

Hypothalamus > cortocotrophin releasing hormone (CRH)

Pituitary >adrenocorticotrophic hormone (ACTH)

Adrenal > cortisol
> Aldosterone is also controlled by RAAS/[K+]

76
Q

Describe the circulation of glucocorticoids

A

Steroid hormones are protein bound in circulation (cortisol
binding globulin) and bind intracellular receptors before entering
the nucleus

77
Q

Describe the systemic effects of glucocorticoids

A

1) anti-inflammatory by inhibiting transcription of genes for
proinflammatory cytokines
2) Reduced T-lymphocytes
3) Counter-regulatory metabolic effects – gluconeogenesis,
increase adiposity
4) Improve alertness (circadian rhythm)
5) Mineralocorticoid effect

78
Q

Which drug is physiologically closest in preparation to cortisol?

A

hydrocortisone

79
Q

What is dexamethasone used for?

A

severe swelling

80
Q

Describe routes of administration of glucocorticoids

A 
o Topical
o Nasal
o Inhaled
o Oral
o Subcutaneous
o Intramuscular
o Intravenous
81
Q

What is aldosterone?

A

a mineralcorticoid stimulated by angiotensin II, ACTH and potassium

82
Q

What is the action of aldosterone

A

Main action on Na/K pump - stimulates sodium and water reabsorption and loss of potassium

83
Q

Why can aldosterone not be given orally?

A
  • metabolised in the liver
84
Q

What is fludrocortisone?

A

oral mineralocorticoid used in Addison’s disease and postural hypotension

85
Q

Name mineralcorticoid receptor antagnosts

A
  • spironalactone

- eplerenone

86
Q

What is the mechanism of action of spironalactone?

A

Competitive antagonist at MR, androgen and progesterone receptors

87
Q

What are the side effects of spironalactone?

A

gynaecomastia, hyperkalaemia

88
Q

What is Eplerenone?

A

Selective MR antagonist, no observed anti-androgen effects

89
Q

What are the clinical uses of mineralcorticoid receptor antagonists?

A

Primary aldosteronism (Conn Syndrome)
heart failure
hypertension

90
Q

What is the action of PTH?

A

maintains calcium levels and can govern bone density

91
Q

What are bisphosphonates?

A

Used to treat osteoporosis, Paget’s disease, metastatic bone disease,
etc.
➢ Reduce bone resorption

92
Q

Name common bisphosphonates

A
  • adendronate
  • pamidronate
  • zolendronate
  • risedronate
93
Q

What are the pharmacokinetics of bisphosphonates?

A

Oral or intravenous administration, depending on preparation, free drug excreted by kidney
o Alendronate oral once weekly on an empty stomach with large glass of water, upright, 30
minutes before breakfast
(Specific instructions because the oral forms can be poorly tolerated)

  • Zolendronate intravenous once yearly
94
Q

What are the pharmacodynamics of bisphosphonates?

A

Carbon substituted pyrophosphate

o Bind to bone and inhibit osteoclast activity

95
Q

List other osteoporosis treatments

A
  • calcium & vit D
  • denosumab
  • teriparatide
  • strontium ranelate
  • HRT
  • SERMs
96
Q

What is denosumab

A

monoclonal antibody that inhibits RANK ligand which signals to osteoclasts, therefore
reduces resorption, subcutaneous injection every 6 months

97
Q

What is teriparatide

A

recombinant parathyroid hormone, binds to osteoblasts to increase bone formation, requires subcutaneous injection as it is a peptide

98
Q

What is strontium ranelate

A

stimulates osteoblasts and inhibits osteoclasts

99
Q

What are SERMs?

A

bind to oestrogen receptor and decreases bone resorption

Phase 2 3. Endocrinology (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions