Download Endocrinology Drug List

NAME OF DRUG
TYPE
MECHANISMS OF ACTION
USES
PHARMACOKINETICS
SIDE-EFFECTS OF DRUG
 Hypopituitary disorders
 Just like normal GH
 GH deficiency in children (adults)
 Administer subcutaneous/IM,
daily or 4-5 times a week
 Metabolised by liver/kidneys
 Half life = 20mins (short) but
actions take longer 
transcription of proteins etc.
 Absorption and maximal
plasma conc 2-6hrs, peak IGF 1
levels after 20hrs.
 Resistance can develop after
about a year.
 Intercranial hypertension
 Headaches
 Increased incidence of leukaemia
 Lipotrophy at injection site.
 In adults, increased risk of CV and
cancer susceptibility, soft tissue
growth  cardiomegaly.
 Acts as dopamine,
decreasing prolactin
and somatostatin
secretion
 Hyperprolactinaemia
 Hypersomatotrophinism
 Used in short term before pituitary surgery,
or long term treatment in ppl not controlled
by other means.
 Same as bromocriptine




 Nausea, vomiting, abdominal
cramps, dyskinesias, psychomotor
excitation, postural hypotension,
vasospasm (esp fingers and toes)
 1-2 per week, oral
 half life v long >45 hours
 Same as bromocriptine but less
pronounced
 Distributed in ECF
 Metabolised by liver and
kidneys
 Half life = 2-4 hours
 Administer subcutaneous/IM 3
times daily.

 GI tract disturbances
 initial reduction in insulin
secretion
 transient hyperglycaemia
 gall stones
Human recombinant
GH
 Hyperpituitary disorders
Dopamine
receptor agonist
Bromocriptine
1 a day, oral
Highly plasma bound (93%)
Half life =7 hours
Hepatic metabolism
Dopamine
receptor agonist
(DA2 receptor)
 Same as
bromocriptine
Somatostatin
analogue
 Acts as somatostatin,
inhibiting production
of prolactin and
somatotrophin
 Hyperprolactinaemia
 Hypersomatotrophinism
 Used in short term before pituitary surgery,
or long term treatment in ppl not controlled
by other means.
Lithium, DMCT
Vasopressin v2
receptor
antagonists
 antagonise v2
receptors, stopping
vasopressin action
 used to treat syndrome of inappropriate
ADH (SIADH) which is too much vasoperssin
 Agonist at v2
receptors in kidneys,
acts like vasopressin
Desmopressin
(DDAVP)
V2 receptor
agonist – these
are much more
sensitive to this
than VP in
kidneys, but not in
heart, so reduce
sideeffects
 Cranial diabetes insipidus (not enough
vasopressin being made)
 Nocturnal enuresis (weeing at night)
 Haemophilia (make more fViii and vWF)





Administered orally or nasally
Retained in ECF
Half life = 5 hours
Hepatic/ renal metabolism
Has longer effect than VP =
more powerful






 Inhibit Na+/Clresorption in distal
convoluted tubule 
compensatory
mechanism to
 Treatment of nephrogenic Diabetes
Insipidus – cant just give VP analogue as the
kidney wont react to this
 This is PARADOXICAL





Given oral
Onset – 1-2hr
DoA: 8-12hr
Excretion – tubular secretion
N.B. competes with uric acid
 K+ loss, Metabolic Alkalosis
 Diabetes Mellitus – Inhibits insulin
secretion
 Reduced loss of Ca+ in urine
Cabergoline
Octreotide
Thiazides

Abdominal pain
Headaches
Nausea
Fluid retention
Hyponatraemia
No heart problems – not as
effective on those v2 receptors
NAME OF DRUG
TYPE
MECHANISMS OF ACTION
USES
PHARMACOKINETICS
SIDE-EFFECTS OF DRUG
increase Na+
resorption in proximal
tubule  more water
resorption in proximal
tubule  reduced
urine volume
Oxytocic –
increased motility
and decreased
bleeding

oxytocic

Prostaglandin
derivative (PGE2)
= vasodilator
 Stimulates
contractions
throughout pregnancy
and induces cervical
ripening
 Vasoconstrictor
 INDUCES CERVICAL RIPENING AT TERM
 INDUCTION OF ABORTION (intravaginally as
gel or tablet)
 To control post partum haemorrhage in ppl
resistant to oxytocin/ergometrine
 Given IM
 Blocks uterine
progesterone
receptors 
detachment of
blastocyst and
reduced hCG
production 
reduced progesterone
production by corpus
leuteum  decidual
 ABORTION Softens and dilates cervix prior
to suction abortion, and causes therapeutic
abortion with gemeprost.
 Oral administration
 Distribution: Enters cells but
limited plasma protein binding
 Metabolism = hepatic
 Excretion is by bile, into faeces
 Half life = 2—40 hours
Oxytocin
Ergometrine
Dinoprostone
15 methyl –
PGE2alpha
 Induction of labour at term, needs careful
control as causes v strong contractions of
uterus and dilation of cervix
 Prevention of post partum haemorrhage by
vasoconstriction of umbilical arteries and
veins.
 Facilitation of milk let down by contraction
of myoepithelial cells in mammary glands.
Nasal spray
 Increased tone of myometirum 
prolonged stronger contractions, but these
aren’t rhythmic so only used in end of 2nd
stage/3rd stage of labour
 Constriction of b. vessels, stops bleeding
 Distribution = ECF
 Half life = 5 mins very short
 Metabolised in liver kidneys
and also plasma (as is placental
derived enzyme)
 Compromised placental exchange
(02, nutrients) by vasoconstriction
 Uterine rupture by crazy
contraction s
 Hypotension and tachycardia
(transient)
 Water intoxication as is
antidiuretic
 Routine administration is IM
 Give IV if high risk of
haemorrhage
 Oral for post partum atony
 Half life = 3-4 hours, longer
than oxytocin
 Hepatic metabolism






Carboprost
Progesterone
receptor
antagonists
Mifepristone
Abortifacients
Abdominal pain
Hypertension
Angina pain
Nausea/vomiting
Cant give to ppl with preeclampsia
or vascular disease
 Potentiate actions of oxytocin 
dangerous contractions
 N, V, diarrhoea
 Pyrexia (fever)
 Hypotension (vasodilator)
 Potentiate actions of oxytocin 
dangerous contractions
 N, V, diarrhoea
 Pyrexia (fever)
 Hypertension (vasoconstrictor)
 Vaginal bleeding, headache
NAME OF DRUG
Tocolytics
TYPE
B2 adenoceptor
agonists, reduce
motility
MECHANISMS OF ACTION
breakdown &
increased uterine
prostaglandin
production.
 Receptor activation
increases intracellular
cAMP  relaxation of
uterine muscle 
delay of premature
labour
USES
PHARMACOKINETICS
SIDE-EFFECTS OF DRUG
 Delay of premature labour


 analogue
 used in hypothyroidism as replacement
therapy.
 Levothyroxine is usually drug of choice as is
T4 so more long acting, liothyronine sodium
is T3 so used in myxoedema coma as IV
(emergency)
 hyperthyroidism
 isotope of iodine,
taken up into thyroid
gland, emits B
particles (v short
range) and destroys
gland
 inhibit
thyroperoxidase, so
inhibit T3/T4
synthesis and
secretion
 hyperthyroidism
 T3 half life is 6days, peak effect
after 9 days, prohormone
 T3 halflife of 2-5 days, peak
effect 1-2 days
 Almost 100% bound to plasma
proteins, mainly thyroxine
binding globulin (TBG)
 give as single oral dose
 radioactive half life = 8 days
 must be isolated to avoid
pregnant women and children
 Massive amounts of
iodine causes
inhibitory response,
inhibiting h2o2
production
 Used to prepare hyperthyroid pts for
surgery
 In severe thyrotoxic crisis (thyroid storm)
 Orally active
 Half life = 6-15 hours
 Metabolised by liver, excreted
in urine
 Crosses placenta and milk, has
bad effects on babies/ children
 30x normal daily requirement
 Given orally
 Mex effects after 10 days
continuous administration (use
up stores of T3 and T4 first)







 Stops 11deoxycortisol 
cortisol, and 11deoxycosterone 
corticosterone.
 Treat some cushings syndrome – inoperable
tumours.
 Control symptoms of cushings syndrome
before surgery, to regain health state.
 Orally active
 N, V , D, sedation
 Hypertension as deoxycortiserone
accumulates and turns into
aldosterone  salt retention 
hypertension.
 Hyper and hypo thyroid disorders
Levothyroxine
sodium/liothyronine
sodium
Replacement
T4/t3
Radioiodine
Thiourylenes
(carbimazole or
propylthiouracil=
PTU)
Thiourylenes
(takes long time
for effect as have
stores of T3 and
T4
Usually potassium
iodide
Iodide
 Hyperadrenal disorders
Steroid inhibitor,
Inhibits 11 bhydroxylase.
Metyrapone
 Hyperthyroidism – reduces CV system,
diffuses toxic goitre, exophthamic goitre,
used whilst waiting for surgery or
radioactive iodine to work
 can cause hypothyroidism if too
much destroyed
Rashes (common)
Headaches
Nausea
Jaundice
Joint pain
Granulocytopenia/agraulocytosis
Allergic reaction  rash, fever
angiooedema.
NAME OF DRUG
Trilostane
Ketoconazole
TYPE
USES
SIDE-EFFECTS OF DRUG
 Cushings syndrome
 Primary aldosteronism
 Reduction of sex steroid hormone
production
 Orally active
 N, V , D
 FLUSHING
 Cushings syndrome
 Orally active
Steroid inhibitor, i
 Inhibits cholesterol to
pregnenolone, VERY
TOXIC
 Adrenocortical carcinoma (malignant)
 Prostatic cancer (malignant – need to
replace corticosteroids!)
 Orally active





N, V , D, liver damage
Alopecia, ventricular tachycardias
Gynacomastia, oligospermia
Reduced androgen production
Same as ketoconazole
Aldosterone
receptor
antagonists
 Prodrug canrenone
 competitive
antagonist of
aldosterone receptor.
 CONN’S DISEASE
 Antialdosterone effect, therefore blocks
Na+ resorption and k+ excretion in kindey =
potassium sparing diuretic.
 Orally active
 Highly protein bound
 Metabolised in liver




Menstrual irregularities
Gynaecomastia
Gi tract irritation
Don’t give if renal/hepatic disease
 Used for short term
administration.
 90-95% bound to plasma
protein corticosteroid binding
globulin (CBG)
 Half life = 1 hr, duration of
action = 8 hr.
 Binds to CBG
 Hepatic metabolism, excreted
in bile and urine
 Half life = 1.5 hrs, duration of
action =12hr.
 Binds WEAKLY to ALBUMIN
only, so can be active in blood.
 Half life =1.5 hrs, duration of
action = 40hours.
To minimise unwanted effects:
 Administer locally if possible
(oral/im rather than iv)
 Use glucocorticoid selective
steroid.
 Withdraw steroids slowly
 Use ACTH in children to avoid the
growth suppression caused by
steroids.
 Pts should carry a steroid card
 Given orally
 Used as aldosterone is not
effective orally.
 Orally active
 If trying to suppress ACTH,
dexamethasone 1 per day, or
 Neonatal kidney is quite
insensitive to this, so need higher
doses in children
 Dexamethasone impairs growth so
don’t give to children
 Long high dose treatment 
Steroid inhibitor,
inhibits
cytochrome p450
 Adrenal steroids as anti inflammatories and immunosuppressives
Corticosteroid,
 Acts as corticosteroid
 ANTIINFLAMMATORY/IMMUNOSUPRESSIVE
mineralocorticoid
THERAPY = asthma, inflam conditions of
actions at high
skin,eye,ear,joints, autoimmune/inflame
Cortisol/
doses
disease like rheumatoid arthritis, prevent
hydrocortisone
rejection after organ/bone marrow
transplants.
 NEOPLASTIC DISEASE (abnormal
proliferation of cells) = in combination with
Corticosteroid and  4-5 times more active
cytotoxic drugs eg: leukaemia, to reduce
weak
on corticosteroid
cerebral oedma in pts with brain tumours,
mineralocorticoid
receptors than
Prednisolone
part of anti emetic treatment with chemo,
activity
cortisol
elevate mood in terminally ill pts.
 PREGNANCY = mature foetal lung in
V high
 40 x more active on
preterm births –helps produce surfactants.
corticosteroid
corticosteroid
activity, no
Dexamethasone
receptors than
mineralocorticoid
cortisol.
action
 Therapeutic and replacement therapy with adrenal steroids
analogue of
 Acts as aldosterone
aldosterone
Fludrocortisone
Hydrocortisone/
dexamethasone
PHARMACOKINETICS
 One of the first steps,
so stops aldosterone,
corticosterone,
cortisol and sex
steroids.
 This is first step, so
blocks production of
EVERYTHING
Steroid inhibitor,
inhibits 3bhydroxysteroid
dehydrogenase
Aminoglutethamide
Spironolactone
MECHANISMS OF ACTION
Cortisol analogues

 In deficiency of aldosterone (primary /
secondary adrenocortical failure)
 Congenital adrenal hyperplasia (salt losing)
 Primary/secondary adrenocortical failure
 Acute adrenocortical failure = emergency
treatment IV/IM infusion, every 6 hrs +
With prolonged glucocorticoid
excess/steroid treatment can
cause iatrogenic cushings sydrome
NAME OF DRUG
TYPE
MECHANISMS OF ACTION
USES
PHARMACOKINETICS
SIDE-EFFECTS OF DRUG
saline for rehydration and glucose.
 Congenital adrenal hyperplasia (CAH) –
replace cortisol, and also suppress ACTH
and adrenal androgen production by
massive doses of these.
hydrocortisone 2-3 x a day.
 Wont have normal stress
response, so if have minor
illness need 2-3 x norm dose,
surgery = much higher doses.
iatrogenic adrenal insufficiency by
switching of HPA axis, so if need to
come off, wean them off gradually
to restart natural system.

 Natural oestrogen, produced in pregnancy,
may protect against multiple sclerosis in
fetus


 Orally active
 70% OF CIRCULATING
OESTROGENS ARE BOUND TO
PLASMA PROTEINS
 Conjugated, hydrolysed to
normal oestrogen in tissues.
 Orally active

 DRUG OF CHOICE


 Increases blood clotting factors 
increased incidence of
thromboembolic disease
 Proliferation of endometrium
increased risk of cancer (reduced if
progesterone coadministered)
 Discomfort to breasts, increased
risk of breast cancer
 Na+ & water retention by kidneys
 oedema and weight gain
 Hypertension, nausea, headaches
 Can act on chemoreceptor trigger
zone and cause nausea at high
doses (like morning sickness)
 Change in structure,
so it acts on
progesterone
receptors not
androgen receptors.


 Orally active
 Metabolised to other
biologically active steroids eg:
testosterone, oestrogen
 May need co administration of
oestrogen to prevent the
adrogenic effects of the
metabolites.



Progestogen:
 Thickens cervical mucus (inhospitable to
sperm)
 Suppress menstrual cycle by fb to hyp & pit
Oestrogen:
 Upregulates sensitivity of progestogen
receptors.
 Counteracts androgenic effects of P
 Contributes to –ve fb to hyp and pit






 Oral contraceptives, HRT and SERMS
Oestriol
Oestrone sulphate
Oestrogen
treatment drug
Ethinyl oestradiol
Transdermal skin
patches
Testosterone
analogues
Progesterone and its
analogues
Combined oral
contraceptives
Progestogens eg:
Norethisterone
Progestogens eg:
MEDROXYPROGESTERONE
ACETATE
Orally active
oestrogen (ethinyl
oestradiol) +
progestogen
(norethisterone)
 Semi synthetic oestrogen (has
ethinyl group added)
 Orally active
 Resistant to metabolism
 Avoids first pass metabolism
 Oestrogens readily cross
membranes into blood
Poorly absorbed
Rapidly metabolised by liver
Given IM in oily vehicle
Excreted in urine
Orally active
Take for 21 days, stop for 7
days
 Can be monophasis (same
conc throughout) or triphasic
(3 step wise changes in conc)

NAME OF DRUG
TYPE
MECHANISMS OF ACTION

Progesterone only
contraceptives
Emergency
contraception
Morning after pill
Hormone
replacement
therapy
Combined O & P
(prescription only)
or P alone (over
counter)
 Stops implantation,
causes shedding of
endometrium
O only – in women
without uterus
O + P in everyone
else

Anti cancer drug
 Selective oestrogen
receptor modulating
drug
 Don’t have the typical
steroid structure
 Actions are TISSUE
SELECTIVE.
 ‘designer oestrogens’
 bind to receptors
and are either
oestrogenic or
antioestrogenic there.
Tamoxifen
Raloxifene
Treatment and
protection of
postmenopausal
osteoporosis
Fertility drug with
some HRT effects
Clomiphere
Tibolone
USES
PHARMACOKINETICS
 When oestrogens are contradicted = CVS
problems, thrombosis, before major
surgery, during lactation (as oestrogens
could cross in milk)
 After unprotected sex
 Oral administration
 Can use Depot-Provera
(medroxyprogesterone) for
long acting use.
 2 doses, 12 hrs apart
 Begin asap (within 72hrs)
 Prevents 75-85% of
pregnancies which might occur







Advantages (licensed for):
Control vasomotor symptoms in 90%
Delays osteoporosis
Advantages (possible, not licensed for):
Reduces symptoms of alzheimers
V small risk reduction of colon cancer
Antioestrogenic in breast tissue (oestrogen
dependent breast cancer treatment)
Oestrogenic effects in:
 Liver  lowers cholesterol
 Bone  increases bone density
 Endometrial tissue  hyperplasia
 Agonist in bone, antagonist in breast and
uterus.
 Reduced risk of vertebral fractures and
breast cancer
 Binds to oestrogen receptors and stops neg
fb to HPA so increase in secretion of GnRH,
LH, FSH.

 Can give orally (1st pass
metabolism)
 Intranasal spray, intravaginal
oestrogens, transdermal HRT.
 By giving it locally, try to avoid
systemic side effects



Synthetic
prohormone =
designer HRT

 Oestrogeninc, progesterogenic and weak
androgenic actions.
 As effective as HRT for relieving vasomotor
symptoms, increases bone density

Androgen therapy

 Primary hypogonadism/primary testicular
failure
 Secondary hypogonadism
 Will increase lean body mass, muscle size,
strength, bone density, libido
 WILL NOT RESTORE FERTILILTY
 Can be:
 Orally active androgens
 Transdermal delivery/topical
gels
 Monthly/3monthly injections
 Subcutaneous implant
SIDE-EFFECTS OF DRUG

 N & V – if vomit, will need a repeat
dose, and anti emetics
 Non known risks if unsuccessful
 Caution – cannot terminate
established pregnancy
 Increased risk of endometrial
carcinoma
 Increased risk of breast cancer
after 5 yrs of use
 Increased risk of gallstone, CVA,
venous thromboembolism.
 Endometrial changes 
hyperplasia, polyps, cancer
 Bone pain if have bone metastases
 Hot flushes
 Menstrual irregularities
 GI disturbances
 Increased risk of fatal stroke and f
venous thromboembolism
 Doesn’t reduce vasomotor
symtoms
 Ovarian hyperstimulation,
abdominal discomfort
 Hot flushes &
 Endometriosis
 N AND V, headache
 Not drug of choice until more tests
done (link to endometrial and
breast cancer)
 Endocrine Infertility
Testosterone
 Masculinisation/virilisation
 Salt and water retention, weight
gain, oedema due to aldosterone
like activity at high levels – caution
with heart and kidney disease
 Acne
NAME OF DRUG
TYPE
GnRH
MECHANISMS OF ACTION
USES
PHARMACOKINETICS
SIDE-EFFECTS OF DRUG
 Stimulates pituitary to
produce LH & FSH 
testosterone
 For fertility in Hypothalamic – pituitary
diseases, IF PITUITARY IS INTACT.

 IIF PITUITARY NOT INTACT, GIVE
LH AND FSH  TESTOSTERONE.

 DIABETES MELLITUS TYPE 1
Soluble = short acting
NPH = immediate acting
Or combination


 HYPOGLYCAEMIA
 Lispro/novorapid  rapid
onset, short duration, so can
eat instantly
 Glargine  long acting, flat
24hr profile
 Rapidly absorbed glucose
(solution/tablets) + complex
carbs to maintain levels
 If unconscious  IM/ IV
 Calcium chloride = IV
 Calcium gluconate = orally
active, IV in sever
hypocalcaemic tetany
 Calcium chloride = vasodilation,
cutaneous burnin g feeling,
decreased bp so give slowly
 Calcium gluconate = doesn’t cause
gastric irritation
 Increase in non minerosteoid
formation
 Gastric pain and GI upsets
 Osteophagitis and bone pain

 Orally active but poorly
absorbed so take on empty
stomach
 Can remain for yrs/months in
bone where it is absorbed
 Excreted in urine
unmetabolised

 Pagets disease – relieves bone pain and
neurological components
 Osteoporosis – post menopausal and
glucocorticoid induced
 Hypercalcaemias
 Given subcutaneously or IM
injection for Pagets
 Intranasally for the others
 Can develop resistance
(antibody formation)





 Diabetes Mellitus
Insulin analogues
Glucose

Glycaemia drugs for  Metformin = acts on insulin resistance in liver. Very effective. Unwanted effects = Gi side effects.
DIABETES MELLITUS  Acarbose = alpha glucosidose inhibitor  prolonged sugar absorption.
 Thiazzolidinediones = act on insulin in adipocytes
TYPE 2
 Metabolic bone disorders
Calcium chloride,
calcium gluconate

Sodium etidronate
Alendronate
 Indirectly stimulates
osteoblast activity
Calcium salts
Bisphosphates/
Diphosphates
 Tamoxifen, raloxifene, ethinyl oestradiol
 OSTEOPOROSIS (reduced bone mass and
disolation of bone microstructure)
 HYPOCALCAEMIAS (dietary insufficiencies,
malabsorption, hypoparathyroidism,
hypocalcaemic tetany)
 CARDIAC DYSRHYTHMIAS (severe
hyperkalaemia)
 Paget’s disease
 Manage hypercalcaemias
 Delay bone metastases in cancer treatment
 In osteoporosis
Oestrogen receptor
ligands
Calcitonin
Peptide hormone
made by
parafollicular cells
 Decreases plasma Ca+
levels
 Decreases 1 alpha
hydroxylase in kindey
 Inhibits osteoclasts
 Increased risk of breast and
endometrial cancer
 Minor GI problems
Inflam reaction at site of injection
Nausea, vomiting
Facial flushing
Tingling sensation in hands
Unpleasant taste in mouth
NAME OF DRUG
Vit d
TYPE
Fat soluble
vitamin. Enhances
transcription of
ca+ transporter
protein so ca+ and
po34 absorption is
increased.
MECHANISMS OF ACTION
 Maintains ca+ and
regulates cell growth
 Most potent form is
CALCITRIOL = 1,25
(02) D3.
 Can use
ERGOCALCIFEROL to
prevent osteomalacia
and rickets
USES
 Osteomalacia and rickets
 Disorders of vit d absorption
 Hypocalcaemias associated with
hypoparathyroidism
 Osteodystrophy due to chronic renal failure
and decreased calcitrol production (cant
give them ergocalciferol as they cant
convert it in the kidney)
PHARMACOKINETICS

SIDE-EFFECTS OF DRUG
