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Jonathan's Endocrine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the effect of early growth hormone deficiency?

A

dwarfism, but growth is in proportion

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2
Q

Where is growth hormone released from?

A

anterior pituitary

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3
Q

Which hormones influence the secretion of GH?

A

GHRH, Ghrelin, and somatostatin

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4
Q

What is the action of growth hormone?

A

stimulate the liver to release IGF-1, the effector growth hormone

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5
Q

What are the three ways in which the growth hormone axis can go wrong?

A

GH insensitivity - liver cannot respond
Secondary deficiency - Pituitary doesn’t produce GH
Tertiary deficiency - hypothalamus not stimulated, no GHRH

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6
Q

What’s the replacement drug for growth hormone? What’s the method of administration?

A

Somatotropin

IV injection, because it’s a peptide with zero oral bioavailability

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7
Q

How often does a patient need to inject somatotropin if the person needs replacement therapy?

A

daily or multiple times a day, because of the short half life

Peptides are not bound to carrier protein

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8
Q

T/F GH can cause reduction in T4 level

A

True, there is interaction between the GH and TSH release

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9
Q

Why do GHRH and ghrelin have synergetic response?

A

they work on the same pathway. GHRH elevates cAMP while Ghrelin elevates Ca2+ level

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10
Q

In what situations do we use IGF-1 replacement therapy

A

When the patient is GH-insensitive or when patient has anti-GH antibody

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11
Q

What’s the side effect of using IGF-1 therapy

A

hypoglycaemia, because of the insulin like behaviour

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12
Q

What causes acromegaly

A

excessive level of GH, so the face becomes chunky and hands/feet grow out of proportion

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13
Q

What are the options for treating acromegaly?

A

remove tumour (if it’s the cause)
reduce GH release
inhibit GH action

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14
Q

how do we reduce GH release?

A

use somatostatin analogue (inhibit action of pituitary)

dopamine agonist

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15
Q

what’s the name of the drug inhibiting GH action?

A

pegvisomant - a GH antagonist

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16
Q

How can we use somatostatin analogue to identify tumours

A

tumours are very rich in somatostatin2 receptors
use tagged somatostatin analogue, and tumours will accumulate radioactive SST and internalise receptors. We then use imaging to find the tumour

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17
Q

What is the disadvantage of use somatostatin as a acromegaly therapy?

A

it has a very short half life, rapidly broken down by enzymatic cleavage and renal elimination

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18
Q

What’s the strategy in modifying the SST analogue?

A

add D-amino acids to prevent enzymatic breakdown

make the molecule smaller also prevents some enzymatic action

19
Q

What are the two modified SST drugs?

A

Octreotide

Lanreotide

20
Q

Why is glycine at codon 120 on the human GH gene necessary?

A

GH needs to bind to two receptors. Any substitution at 120 will allow binding on site 1, but any side chain will prevent binding of site 2, hence stopping dimerisation and activation

21
Q

What is the use of PEGylation

A

increase size to reduce renal filtration
improve solubility
decrease accessibility for proteolytic enzymes

22
Q

What’s the disadvantage of PEGylation?

A

it tends to reduce some activity as PEG gets in the way. In GH, PEG occurs at lysine, which interferes with binding site 1

23
Q

How many mutation on GH does pegvisomant have?

A

9

24
Q

What are the drug treatment for Graves’

A

radioactive iodine to ablate the thyroid or use carbimazole

25
Q

What’s the action of carbimazole

A

inhibit thyroid peroxidase

26
Q

What’s the additional effect of using propylthiouracil instead of carbimazole

A

It blocks conversion of T4 to T3 as well, but you have to take 2-4 doses a day

27
Q

Propylthiouracil and carbimazole are both thioamines. What are the side effects of thioamines?

A

possible goitre
agranulocytosis
hepatotoxicity (propylthiouracil only)

28
Q

What are the drugs to treat Hashimoto?

A

Liothyronine (T3)

Thyroxine (T4)

29
Q

How does T3 interact with cortisol?

A

cortisol inhibits conversation of T4 to T3

T3 inhibits cortisol production

30
Q

When is liothyronine preferred over thyroxin?

A

when treating severe hypothyroid and myxoedma coma

31
Q

why is there usually poor compliance for patients taking thyroxine?

A

there is a slow accumulation and onset of action

32
Q

where are the three peaks of cortisol release?

A

wake up time
mid day
early evening

33
Q

How is cortisol excreted?

A

it gets converted to cortisone in the kidney and then excreted

34
Q

Which enzyme coverts cortisol to cortisone?

A

11-b-hydroxysteroid-dehydrogenase 2 (HSD2)

35
Q

Where does cortisone get activated?

A

in the liver by HSD1

36
Q

Why doesn’t cortisol have effect on aldosterone receptors when it has higher affinity?

A

HSD2 is a physiological ligand to aldosterone receptor. Cortisol is converted to cortisone when it is in contact with the receptor

37
Q

Why is it hard to diagnose acute adrenocortical insufficiency?

A

the presenting signs are often nonspecific

38
Q

Why do patients need extra cortisol doses during infection?

A

normal cortisol level goes up during illnesses

39
Q

What’s the incentive to be compliant when being placed on cortisol therapy?

A

overdose can lead to weight gain

40
Q

what’s the most common iatrogenic complication of cortisol therapy

A

Cushing syndrome

41
Q

What are the two internal pathways associated with steroid action?

A

trans-activation (dimerisation and response to GREs)

Trans-repression (inhibit AP-1 and NF-kB)

42
Q

How do we minimise adrenal suppression?

A

avoid long-lasting drugs
alternate day dosing
morning dosing to mimic physiological rhythm

This will allow for ACTH secretion and recover atrophic cells

43
Q

How is ciclesonide better than the previous generation of glucocorticoids?

A

it is given as a pro drug. it is also lipophilic with low oral bioavailability. Hence there is low system effect

Jonathan's Endocrine (9 decks)

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