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66 Cards in this Set

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Pharmacological treatment of thyrotoxicosis?

MOA?
THIONAMIDES:
1. Methimazole (MMI, Tapazole®)
2. Carbimazole (Neomercazole®)
3. Propylthiouracil (PTU)

Drug of choice in Aust = Neomercazole®

MOA = block activity of peroxidase
--> prevent organification of I-
--> prevent coupling of DIT/MIT to form T3/T4

PTU also blocks 5'-deiodinase (which converts T4 to T3)
Indications and contraindications, advantages and disadvantages for radioactive iodine in thyrotoxicosis?
Does the thyroid status of the Pt matter?
INDICATIONS: newly diagnosed Graves', relapsed Graves', toxic nodular hyperthyroidism

CONTRAINDICATIONS: pregnancy!!

ADV: effective cure, outpatient, easily applicable, reduced goitre

DISADV: slow effect over months, permanent hypothyroidism in >60% pts, deferral of pregnancy for 6mo

NB: Pt should be euthyroid before commence treatment
Indications and contraindications, advantages and disadvantages of SURGERY in thyrotoxicosis?
Does the thyroid status of the Pt matter?
ABSOLUTE INDICATIONS: thyroid cancer, obstructive symptoms
RELATIVE INDICATIONS:
failure or non-compliance with medical treatment, large goitre, pregnancy if clinically sig. drug side effects

ADV: rapid control hyperthyroidism, 100% cure

DISADV: invasive, expensive, permanent hypothyroidism, pain, scarring, complication risk (hypoparathyroidism, recurrent laryngeal n.)
carbimazole
anti-thyroid drug
brand name = neomercazole
Anti-thyroid drug regime
Therapy for hyperthyroidism generally starts at a high daily dose of 15 - 40mg continued until the patient has normal thyroid function, and then reduced to a maintenance dose of 5 - 15mg. Treatment is usually given for 12 - 18 months followed by a trial withdraw.
proylthiouracil
PTU = anti-thyroid drug
Treatment options hyperthyroidism
1. Anti-thyroid drugs
2. Radioactive iodine
3. Surgery
Treatment for hypothyroidism
Thyroxine (levothyroxine)
Treatment options for pituitary tumour
1. surgery
2. radiotherapy
3. medical therapy
medical therapy for prolactinoma.
MOA?
dopamine receptor agonists (cabergoline).

MOA = binds D2 receptors. Inhibits synthesis and release of prolactin
cabergoline = ?
potent dopamine receptor agonist on D2 receptors.
First-line agent in the management of prolactinomas
octreotide = ?
Somatostatin analogue. Inhibits growth hormone. Also decreases tumour size of GH-secreting adenoma
medical therapy for GH-secreting adenoma?
Octreotide (somatostatin analogue)
medical therapy for corticotropin-secreting adenoma?
Ketoconazole (=anti-fungal agent that inhibits adrenal steroidogenesis). Not effective LT treatment. Usually reserved for patients unsuitable for surgery, or whose tumour has recurred post-surgery/radiation.
Ketoconazole = ?
anti-fungal agent that inhibits adrenal steroidogenesis
Radiation therapy for pituitary tumours. When and how is it used?
used in patients with recurrent or incompletely excised tumours, or patients that are unable to tolerate trans-sphenoidal surgery or medical therapy.

can be delivered by conventional external beam techniques, stereotactic radiosugery techniques, or isotope-labelled radiopharmaceuticals
route used for surgical excision of pituitary adenoma? when wouldn't you use this route?
Transphenoidal microsurgery.

May have to use a transcranial route if tumour has extended into subfrontal, retrochiasmatic or middle cranial fossae
describe route of administration for the following:
1. steroids
2. thyroid hormone
3. insulin
4. testosterone
5. gonadal steroids
6. DDAVP (desmopressin)
1. steroids = oral
2. thyroid hormone = oral
3. insulin = subQ injection, pump
4. testosterone = depot IM injection
5. gonadal steroids = transdermal
6. DDAVP = intranasal spray, solution, oral
DDAVP= ?
Desmopressin (trade names: DDAVP, Stimate, Minirin) is a synthetic replacement for vasopressin
Addison's disease treatment
Gluucocorticoid dose is 25 mg cortisone acetate mane and 12.5 mg nocte to mimic diurnal rhythm. Cortisone acetate is given at a minimum of two doses per day in Addison's disease. The half life of cortisone acetate is not long enough to sustain a once a day dose. In active individuals a third (midday) dose may be required.

PLUS fludrocortisone dose which is generally fixed
Atosibar = ?
oxytocin antagonist used to prevent premature birth
syntocinon = ?
Synthetic oxytocin - used to induce labour or induce ejection of the placenta after birth
Glucocorticoid and mineralocorticoid relative potency of:
hydrocortisone
dexamethasone
prednisone
betamethasone
hydrocortisone G=1, M=1
prednisone G=4, M=0.25
betamethasone G=25, M<0.01
dexamethasone G=30-40, M<0.01
give doses of prednisone and dexamethasone equivalent to 20mg hydrocortisone
20mg hydro
= 5mg pred
= 0.5mg dex
what do you give in emergency anaphylaxis
endogenous hydrocortisone IV
what steroid do you give to prevent cerebral oedema?
dexamethasone
what are the basal needs of hydrocortisone per day?
when does this increase?
20-25mg
mild illness x2-3
major stress x10
management of hypoglycaemia if conscious
"15 rule"
15g fast acting CHO (7 jelly beans, 150mL soft drink, 100mL glucozade, 3 tsp honey)

15g complex CHO (1 pce fruit, 1 slice bread, 2 buscuits)

15 mins later - re check BGL and if still low, give more fast acting
management of hypoglycaemia if unconscious
IV injection 50% glucose (20-25mL)
IV injection glucagon
then 15g complex CHO once awake
after treatment of severe hypoglycaemia, what do you do if BGL are then really high?
BGL may rebound - do NOT treat hyperglycaemia aggressively in the first 24-48 hrs
rapid acting insulin = ?
analogues, absorbed rapidly, injection immediately before food, less likely to cause hypo
acting time = 2-3 hrs
onset = 0-20 mins

brands = Apidra, NovoRapid, Humalog
short acting insulin = ?
solution of human insulin
onset of action w/in 30 min
Duration 6-8 hrs

brands = Actrapid, Humulin R
intermediate acting insulin = ?
isophane aka NPH insulin
(complex of insulin bound to protamine which is a non-immunogenic fish protein)
insulin released gradually into tissues
onset = 1.5hr
duration up to 24hr
differs bw brands

Brands = protaphane, humulin NPH
Long acting insulin = ?
human insulin complexed with zinc
rarely used - replaced by analogues
very long acting insulin = ?
analogue, replaced long-acting
there are 2: glargine and detemir
24 hr duration
peak 3-14 hours

Glargine = Lantus
chemically modified so insoluble after injection

Detemir = Levemir
insulin binds to albumin from which it is slowly released
management DKA
rehydration
restore normoglycaemia (insulin)
look for infection
replace K+ to prevent hypokalaemia
monitor K+, glucose, HCO3-, creatinine hourly
treatment candidiasis
topical, poorly absorbed antifungals
= IMIDAZOLE group, or AMPHOTERIUN

or single oral dose imidazole

occ. IV for serious infection
treatment cellulitis
oral or IV? why?
Oral therapy. For staph: FLUCLOXACILLIN or DICLOXACILLIN monotherapy.

Or can use cephalexin (didn't really understand what you're supposed to use)

more severe or strep --> phenoxymethylpenicillin

can give IV if unsuitable for oral, vital signs indicate septicaemia, rapidly progressing, immobile
pharmacological treatment of obesity?
1. Phentermine (duromine)
2. Orlistat (Xenical)
3. Sibutramine (Meridia)
phentermine = ?
chemically related to amphetamine - works predominantly on noradrenaline to reduce appetite.
central stimulant --> HTN, tachycardia, nervousness, headache, insomnia, tremor
orlistat = ?
pancreatic lipase inhibitor
reduces the absorption of fat by roughly 30%
not absorbed in bloodstream, not an appetite suppressant.
can't eat high-fat meal or get incontinence and greasy stools.
average weight loss 7-8%
sibutramine = ?
combination noradrenaline and serotonin reuptake blocker.
no serotonin-releasing action therefore pharmacologically more like SSRIs.
weight loss av. 5-8%
has been ass'd with incr. BP - shouldn't be used in people with poorly controlled HTN
oral hypoglycaemic therapy classes
1. Sulphonylureas
2. Biguanides
3. alpha-glucosidase inhibitors
4. meglitinides
5. thiazolidinediones
6. DPP-4 inhibitors
Sulphonylureas = ?

SE?
potentiate glucose-stimulated insulin release.
combine with sulfonylurea receptors of beta-cells.
close potassium channels (like glucose!)
depol of cell
calcium influx
insulin released

SE= weight gain, hypoglycaemia
Biguanides = ?

SE?
Contraindications?
Adv?
Metformin is the only one currently available.
increased glucose uptake into skeletal muscle and fat
appetite suppression (?gastric irritation)
decreased intestinal glucose absorption
decreased gluconeogenesis

DOES NOT STIMULATE INSULIN

SE= transient nausea, diarrhoea. Also LACTIC ACIDOSIS - check renal fn

CONTRA = significant renal failure (excreted entirely by kidneys)

ADV = prevents weight gain, may assist weight loss
metformin = ?
Biguanide oral hypoglycaemic agent
T/F metformin stimulates insulin release
FALSE
T/F big side effect of metformin is risk of hypoglycaemia
false
alpha-glucosidase inhibitors = ?

SE?
most widely used = ACARBOSE!
inhibit enzyme that breaks down dietary complex carbs to sugars.
reduces quantity of glucose available for abs'n across intestinal wall.
less effective - use in combination with sulphonylureas or metformin

SE = not well tolerated --> abdo distension, pain, flatulence
first line OHA?
metformin
meglitinides = ?
only drug = REPAGLINIDE

stimulate same R as sulphonylureas but at diff site.
actions/se similar to sulphonylureas

short acting take bd
thiazolidinediones = ?

SE = ?
Act on PPAR-g (peroxisome proliferator receptors) in fat cells.

can cause SUBSTANTIAL WEIGHT GAIN
DPP-4 inhibitors = ?
Dipeptidyl dipeptidase inhibitors - they INHIBIT the activity of the enzymes that break down INCRETINS!

incretins = gut hormones GLP-1 and GIP. These incretins normally stimulate insulin-mediated glucose release from the pancreas following an oral glucose load.

GLP-1 also inhibits secretion of glucagon, inhibits gastric emptying and thus delays glucose absn
melatonin
light dark cycle regulation

sleep disorders, blind persons
budenoside, ciclesonide
long term asthma

action of GCS
fluticasone
long term asthma

action of GCS
metyrapone
Dx of adrenal insufficiency, sometimes Tx of cushings

inhibits cortisol synthesis via 11 β hydroxylase
what makes steroid myopathy worse?
9-α fluorinated corticosteroids


changing to prednisone produces improvement
Prostaglandin synthetase inhibitors
Abnormal uterine bleeding

inhibit synthesis of prostaglandin, also interfere with myometrial prostaglandin E2 binding
Tranexamic acid (antifibrinolytic)
Abnormal uterine bleeding

inhibit plasminogne activator
Norethisterone
Abnormal uterine bleeding

Is a progesterone, can be used in combo or stand alone
Dydrogesterone
Abnormal uterine bleeding
Depo Provera
Abnormal uterine bleeding/contraception

progesterone only contraceptive
Implanon
inhibit ovulation

abnormal bleeding, contraception
Danazol
abnormal uterine bleeding

inhibits endometrial proliferation causing endometrial atrophy

androgenic side effects
Goserelin, Nafarelin
(GnRH agonist)


initial agonist of pituitary, followed by 'exhaustion' --> hypogonadotrophic hypogonadism


long term use complicated by decreased bone mass