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miscellaneous pharmacology lectures Flashcards

1
Q

how do we define diabetes?

A

fasting glucose level: >7.8mmol/L

post-meal glucose >11.1.mmol/L

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2
Q

what are some of the adverse effects of insulin therapy?

A

lipoatrophy: associated with porcine injections
lipohypertrophy: at site of injection
weight gain: as a result of insulin injection
hypoglycaemia
antibody formation
hypersensitivity reactions
somogy rebound hyperglycaemia (usually results from excessive insulin injection)

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3
Q

what is tolbutamide?

A

a short acting sulphonylurease
- acts by blocking ATP sensitive potassium channels
drugs increase insulin release in response to glucose

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4
Q

what is glibenclamide?

A

this is a long acting sulphoylurease
acts by blocking ATP sensitive potassium channels
drugs increase insulin release in response to glucose

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5
Q

what are the mechanism of actions of sulphonylureas?

A

they block ATP sensitive K channels
this causes depolarisation of the cells, and intracellular release of calcium
this mediates calcium dependant insulin release

examples: tolbutamide and glibenclamide

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6
Q

what are the unwanted side effects of sulphonyulreas?

A

weight gain is a major issue (hence only used in non-obese patients as first line of therapy)
lack of selectivity to K+ channels - interactions with cardiac channels
hypoglycaemia

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7
Q

what is metformin?

A

a biguanide, which increases insulin receptor sensitivity but has no effect on insulin secretion

  • causes increase in glucose uptake by tissue
    suppresses hepatic gluconeogenesis
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8
Q

what are the side effects associated with metformin?

A 
lactic acidosis 
GI effects (can be avoided if the dose is gradually increased) 
reduces B12 absorption

NO DANGER OF HYPOGLYACEMIA

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9
Q

what type of patients is metformin used with?

A

obese patients

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10
Q

what is pioglatozone an example of

A

thiazolenediones

  • those activate PPAR receptors
  • act on hormone response elements in the promoter region of the insulin target genes
  • mostly act on adipose tissue
  • increase fatty acid uptake (which reduces the amount available for other tissue, and this increases tissue sensitivity to insulin)
  • reduces hepatic glucose output
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11
Q

what are the side-effects associated with thiazolenediones?

A

weight gain
water retention (Can potentiate heart failure)
takes unto three months for their maximal effect to work

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12
Q

what are exenatide and Gliptins?

A

those are GLP-1 mimetic and enhancer

  • those increase the beta receptor sensitivity to glucose post meals and they’re responsible for the post-prandial increase in insulin levels
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13
Q

what is diabetic ketoacidosos?

A

this is a complication of hyperglycaemia associated with type 1 diabetes

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14
Q

what drugs are used for hyperthyroid?

A

carbmizole
propylthiouracil (only use if carbmizole is not tolerated)

propanolol can be used to control the tachycardia, agitation and tremor associated with the condition
guanthenidine can be used to elevate the exthalmpos

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15
Q

what is carbmizole?

A

this is a perioxidase inhibitor which is used in the treatment of hyperthyroid disease

side effects include: agranulocytosis, GI upsets and rays

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16
Q

what is propylthiouracil?

A

this is a peroxidase inhibitor, preventing iodination, used in the treatment of hyperthyroid disease
also prevents peripherial de-iodination of T4–>T3
causes more frequent agranulocytosis

only preserved for use when carbimazole is not tolerated

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17
Q

what is the treatment of hypothyroid

A

levothryoxine is used

t3 is only reserved for myoexdema
t4 is given by danger of angina and heart failure with overdose

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18
Q

what are the possible causes of drug induced hypothryoid?

A

lithium and amidarone

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19
Q

what is familial hyperlipoproteinaemia?

how is it treated?

A

this is a type I hyperlipidaemia

  • caused by decreases lipoprotein lipase
  • causes increase in chylomicrons
  • treated by diet control
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20
Q

how is familial hyperlipoproteinaemia treated?

A

by diet control

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21
Q

what is familial hypercholestedalemia?

A

this is a type IIa hyperlipidaemia

  • caused by LDL-R receptor deficient
  • causes an increases in LDL
  • treated using sequestrates, statins and niacin
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22
Q

what is combined hyperlipidaemia?

A

this is type IIb hyperlipidaemia

caused by: LDL-r deficiency, and increased ApoB

causes:

  • increases LDL
  • increased VLDL
  • increased triglycerides

treated:

  • statins
  • niacin
  • fibrates
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23
Q

how is familial hypercholesteraemia treated?

A

using statins, sequestrants and niacin

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24
Q

what is type familial disbetalipoproteinaemia?

A

this is a type III hyperlipidaemia

caused by:
- ApoE deficiency 
causes:
- increase in IDL 
treatment:
- fibrates
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25
Q

how is combined hyperlipidaemia treated?

A

statins, niacins and fibrates

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26
Q

what is familial hyperlipidaemia

A

this is a type IV hyperlipademia

caused by:
- increased VLDL production and clearance
causes:
- increased VLDL

treated:
fibrates and niacins

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27
Q

how is familial disbetalipoproteinaemia treated?

A

fibrates

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28
Q

familial hypertriglyceridaemia

A

type V hyperlipidaemia

caused by:
- increases VLDL production and clearance

causes:

  • increases VLDL
  • increased chylomicrons

treatment:

  • niacins
  • fibrates
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29
Q

what is the treatment for familial hyperlipidaemia?

A

fibrates and niacin

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30
Q

what is the treatment for familial hypertriglyceridaemia?

A

fibrates and niacin

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31
Q

how do the fibrates work?

A

they work because they’re PPAR-A agonists, this increases the lipoprotein lipase activity (therefore lipoprotein lipase catabolism)

  • causes an increase in HDL
  • decrease in LDL
  • decrease in VLDL
  • also increase fatox in muscle and liver
  • reduces serum TAG
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32
Q

what are the side-effects associated with fibrates?

A

those are muscle inflammation (this risk increases further if used with statins)

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33
Q

how do the niacins work?

A

those work by reducing hepatic VLDL synthesis

  • they have the largest effect on increasing HDL synthesis
  • they also are the only drugs that work on ApoA protein
  • reduce LDL, cholesterol and TAG (by inhibiting their peripheral metabolisation)
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34
Q

when are niacins used? and why?

A
  • they’re now rarely used this is because of their prostaglandin mediated side effects including palpitation, dizziness and flushing
  • although it use in combination with other drugs can reduce those side effects
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35
Q

how do cholesterol absorption inhibitors work?

A

those work by inhibiting cholesterol absorption from the gut -

this increases cholesterol excretion and causes an increase in LDL-R which reduces plasma LDL
- reduces TAG and increases HDL also

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36
Q

when is ezetimibe used?

A

this is used in hypercholesteramia?

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37
Q

how do the statins work?

A

nthey block HMG-COA (this reduces hepatic cholesterol synthesis) by blocking the rate limiting step
- this causes an increase in LDL-R expression (this reduces plasma LDL levels which is the main way they work)

tolerance can result by liver up regulating enzyme levels, all drugs which mainly work by up regulating LDL-R will not work with patients with familial hypercholestaremia

38
Q

which drugs inhibit hepatic VLDL synthesis?

A

niacin

39
Q

which drugs act as ligands to the PPAR-A receptor?

A

fibrates

40
Q

which drugs reduce hepatic cholesterol synthesis?

A

the statins

41
Q

which drug has the largest effect on HDL?

A

niacins

42
Q

how do bile binding resins work?

A

those are powders in liquid

  • they’re not absorbed from the gut (so all their side-effects limited to the gut)
  • the increase bile acid excretion (because reduces its enterohepatic circulation)
  • more cholesterol is metabolised to form bile
  • LDL-R upregulation (causes reduction in LDL plasma levles)
43
Q

when are the side-effects of statins worsened?

A

when taken in combination with fibrates and niacins

44
Q

what is torecetrapin?

A

this is a CEPT inhibitor
prevents formation of LDL from HDL (trial halted because of cardiovascular events)
increase in HDL and lowering in LDL (anacetrapib)

45
Q

what are the evidence for statin use?

A

the s4 study:

-increases life -expectancy in patients with arthrogenic cardiovascular disease

46
Q

what is the evidence for the use of ezetimibe?

A

ENHANCE TRIAL:

  • no additive effect when used with statins to increase life=expectancy in hypercholesteraemias
  • but did reduce LDL
47
Q

when are ezetimibes used?

A

they’re used in cases of hypercholesteraemias
- mild - monotherpay
severe- with statins

48
Q

what is the affect of ACE inhibitors on the foetus?

A

renal damage

49
Q

what is affect of amino glycosides on the foetus?

A

damage to the VIIIth cranial nerve

50
Q

what is the affect of cocaine on the foetus?

A

limb and urinary tract defects and congenital heart disease

51
Q

what are the affects of ethanol on the foetus?

A

foetal alcohol syndrome, craniofacial defects, growth retardation, characteristically abnormal corpus callosum

52
Q

what is the effect of phenytoin on the foetus?

A

cleft lip and palate

53
Q

what is the effect of tetracycline on the foetus?

A

discoloured teeth and altered bone growth

54
Q

what is the affect of thalimode on the foetus?

A

phocomelia

55
Q

what is the affect of valproic acid on the foetus?

A

spina bifida

56
Q

what is the affect of an insult at 21-22 days of gestation

A

absence of external ears and paralysis of cranial nerves

57
Q

what is effect on an insult on the 24-27th day of gestation

A

phocomelia maximal effect arms

58
Q

what is the effect of an insult during 28th - 29th day of gestation?

A

phocomelia affecting the legs

59
Q

what is the effect of an insult during the 34-36th day of gestation?

A

hypoplastic thumbs and anorectal stenosis

60
Q

what are the toxicity associated with paracetamol?

A

liver failure

61
Q

what is the toxicity associated with amino glycosides?

A

deafness

62
Q

what is the toxicity associated with tetracycline?

A

damage to teeth

63
Q

what is the toxicity associated with gentamicin?

A

concentrating in renal tubules leads to nephrotoxicity

64
Q

what is the toxicity associated with sulphonamide?

A

crysalluria (because of low solubility)

65
Q

what is the toxicity associated with methanol

A

optic nerve damage

66
Q

what is the toxicity associated with chloroquine?

A

melanin affinity - retinal toxicity

67
Q

what is the antidote for opiate toxicity?

A

naloxone

68
Q

what can ethanol be used as an antidote for?

A

methanol posioning

69
Q

what can oximes be used as an antidote for?

A

for organophosphates

70
Q

how can paracetamol toxicity treated?

A

by using methionine

71
Q

what are non-pulastile GnRH agonists used for?

A

precious puberty
endometriosis
sex-hormone dependant tumours

72
Q

what are pulsatile GnRH agonists used for?

A

stimulate ovulation in infertility

73
Q

what are goseralin and buseralin an example of?

A

GnRH analogues

74
Q

what are the side-effects associated with GnRH analogues?

A

vasomotor symptoms
reduction in bone density
withdrawal bleeding

75
Q

what is menotrophin used in?

A

used in female infertility caused by pituitary insufficiency or do not respond to clomiphene (causes LH/FSH release)

also used in cryptorchidism

76
Q

what are peripheral oestrogen antagonists used for?

A

tamioxifen - used in the treatment of oestrogen dependant breast cancers

77
Q

what are central oestrogen antagonists used for?

A

e. g. clomiphene
- used to treat PCOS
- used to block oestrogen receptors at the pituitary and hypothalamus, therefore induce ovulation

78
Q

how is PCOS caused infertility treated?

A

use of metformin and clomiphene

79
Q

what is danazol

A

specifically inhibits gonadtrophin secretion (a derivative of the synthetic norethisterone)

80
Q

how is the combined pill used?

A

taken for 21 days and stopped for 7 days (sugar pill)

  1. oestrogen prevents follicular maturation by inhibiting FSH
  2. progestrone prevents ovulation by inhibiting LH
  3. progestrone causes the formation of hostile cervical mucus preventing sperm penetration
  4. progestrone causes the formation of glandular epithelium in the endometrium so that it is not-suitable for implantation

contains: norethisterone and ethinylestradiol

81
Q

how is the mini-pill used?

A

taken continuously

  1. progestrone prevents ovulation
  2. progesterone makes cervical mucous hostile
  3. progesterone makes endometrium non-suitbale for implantation
82
Q

what are the advantages of the COC?

A
  • reduced dysmenorrhea and menorrhagia
  • reduces risk of PID
  • reduces risk of ovarian and endometrial cancer (because of progesterone)
  • very reliable
  • reversible
83
Q

what are the advantages of using the mini-pill?

A
  • used when there is absolute contra-indication to oestrogen (e.g. thrombi-emobolim) or smoker over 35
  • used when oestrogen would interfere with lactation
84
Q

what are the overall effects of the contraceptive pill?

A

increased risk of CVD

    • increased BP
    • MI in smokers

increased risk of stroke in those with migraines especially with auras

higher incidence of thromboembolism

85
Q

when is HRT used?

A

in women with primary pituitary failure
in PM with vasomotor and urogenital symptoms
useful in prevention of osteoporosis

86
Q

what are the dangers of HRT?

A
  • increases risk of breast cancer
  • oestrogen has an affect on blood coagulation, so increases chance of thromboembolism
  • increased risk of CVD
87
Q

give examples of androgenic agonists

A

fluoxymestrone:

  • used in hypogonadism
  • used in delayed puberty

nandrolone:
- used as an anabolic steroid

88
Q

what are the side effects associated with androgenic agonists?

A
  • CVD
  • Virlisation
  • anabolic effects
  • acne
  • increased BP
  • interaction with warfarin
89
Q

give examples of androgeric antagonists, what are they used for?

A

prostate cancer

flutamide:
- prevents testosterone binding and DT

cyproterone:
- 
bicalutamide:
- prostate cancer and hirtusim 
both drugs are partial agonists in the periphery and hypothalamus
90
Q

how is gonatrophin therapy used?

A

used in women who lack pituitary function
- treatment with mentrophin (FSH>LH)
or recombinant human follitropin FSH

then chorionic gonadotrophin is given (LH) to induce ovulation

multiple pregnancies can easily occur

in male hypogonadotrophin hypogonadism: both gonadotrophins sometimes given to stimulate spermatogenesis and androgen release

Pharmacology (17 decks)

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