Pharmacology Flashcards
ACE inh
rami”pril”
Dilate arteries and veins by blocking angiotensin II formation and inhibiting bradykinin metabolism. This vasodilation reduces arterial pressure, preload and afterload on the heart.
Down regulate sympathetic adrenergic activity by blocking the facilitating effects of angiotensin II on sympathetic nerve release and reuptake of norepinephrine.
Promote renal excretion of sodium and water (natriuretic and diuretic effects) by blocking the effects of angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosterone secretion. This reduces blood volume, venous pressure and arterial pressure.
Inhibit cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction
Calcium channel blocker
amlodi”pine” acts on the smooth muscle of the vascular smooth muscle (arterial not venous) to reduce contraction.
nitrates
isosorbide mononitrate promotes NO mediated dilation of the venous system.
A blockers
used fro benign prostate hyperplasia
doxasin negative ionotrope, and cause vasoconstriction of the veins especially when the patient stands.
medication given in alcohol withdrawal
chlordiazepoxide
drugs that can contribute to dysphagia
oesophageal tone: ca channel blockers and nitrates
PUD: NSAIDS, asprin, steriods, and bisphosphonates
mechanism of action of asprin
irreversible inhibitor of the enzyme cyclooxygenase which synthesises inflammatory mediators including platelet aggregator A2. Platelets have no nuclei so cannot reverse this action by procudcing more COX. Aspirin’s action is reversed by platelet production
mechanism of action of clopidogrel
irreversibly blocks the ADP receptor on pletlet cell membranes that prevents binding to fibrogen and inh platelet aggregation.
Abcixmab mechanism of action
also tirofiban works the same way to reversibly block fibrogen binding to the glycoproteins r IIB/IIIa on the platelet cell membranes that mediate platelet aggregation,
bivalirudin mechanism of action
is a direct thrombin inh and used as an alternative to heparin
what are the indications for an exercise stress test?
possibility of coronary artery disease and the benefit of angioplasty. patients ECG and bp are measured along with symptoms ST depression greater than 2 mm exertional angina, ST elevation greater than 1 mm
30% of positive results are false positives
what are you looking for in a stress echogram
give dobutamine looking for hypokinetic movement in ischemia
hyperkinetic movement is normal
this is used for patients who are not fit for traditional stress test or immobile
salbutamol
selective B agonist
acts on the G protien coupled receptor activating adenylate cyclise and increasing the formation of camp leading the relaxation of smooth muscle cells
ipratropium
antimuscarinic/ anticolinergic antagonizes muscarinic receptors in the airways preventing parasympathetic muscular contraction. often used in COPD but less often in asthma
combivent
mixture of salbutamol and ipratropium bromide
inhaled corticosteroids mechanism of action
affecting the intracellular production of various proteins to reduce inflammation response in the airways
cycline mechanism of action and use
antihistamine and antimuscarinic that blocks actylcholine rectors in the vestibular and vomiting centres
use in post op nausea, bowel obstruction nausea *ANTIKINETIC
and also raised ICP
metoclopramide MOA and use
agonist properties at the 5HT4 receptor and antagonist properties at D2 receptors
PROKINETIC DO NOT use in bowel obstruction and use with caution in parkinson’s patients
used in causes of delayed gastric emptying.
odansetron MOA and use
5HT3 receptor antagonist acts on receptors of the gut and chemoreceptors trigger zone useful for chemo induced and post op vomiting
haloperidol MOA and use
antagonist of dopamine (D2) receptors found in the chemoreceptor trigger zone and myenteric plexus of GIT
drug induced and metabolic causes of vomiting and also raised ICP
what are the cautions and contraindications for NSAIDs
contraindicated in asthma
history of anaphylaxis with NSAIDS
previous or active peptic ulcers
severe heart failure
COX2 SHOuld not be used in ischeamic heart disease, cerebralvascular disease or PAD increased risk of thromboembolic events
caution in:
cogulation defects
renal cardiac and hepatic impairment
during pregnancy or breastfeeding- in utero can cause closure of the ductus arteriosus
elderly patients have risk of bleeding and renal failure
indications for AAA surgery repair
symptomatic
greater than 5.5 cm
if it is growing greater than 1 cm per year
indapamide
thiazide like diuretic used for HTN or decompensative heart failure
alendronate
bisphosphanate drug used for bone disease
what three medications predispose a patient to peptic ulcers?
NSAIDS
bisphosphonates
steriods
what medications should you put on hold in a patient with oligouria or a worsening kidney function
NSAIDS ACE inh diuretics and abx (gent, vanc,)
MOA of biguanides
decrease hepatic uptake and increase peripheral glucose uptake
MOA of glitazones
activate peroxisome proliferator activated receptor gamma
nuclear transcription factor increasing LPL and fatty acid transporter protein 1 transcription involved in lipid metabolism
increasing perpheral insulin sensitivity
MOA of sulphonylureas and meglitinides
increased insulin secretion by blocking the K ATP channel in the pancreatic B cells causeing deploratization and ca entry leading to increased insulin production.
MOA of gliptins
competively inhibit the DPP4 enzyme that normally inactivates glucagon like peptide and incretin that stimulates insulin secretion and inhibits glucagon release.
a- glucosidase inh. MOA
decrease glucose reabsorption in the intestine.
Warfarin side effects
heamorrhage nausea and vomiting purple toes and skin necrosis hepatic dysfunction pancreatitis
What is the INR target range for patients with proven DVT?
2-3
