HNN215 medications

exam revision

non-narcotic analgesics (non-opioid) MOA

inhibits the cyclooxgenase enzyme in the CNS, which reduces the production of prostaglandins, reducing the feeling of pain

• panadol

• paracetamol

cyclooxyrgenase

an enzyme that helps create chemicals that cause inflammation and pain

prostaglandins

chemicals that promote inflammation, pain and fever

adverse effects of non-narcotics

• liver toxicity

• renal damage

• allergic reactions

nursing considerations for non-narcotics

• monitor liver function

• education on dosing

• monitor signs of toxicity

• renal function monitoring

Non-Steriodal Anti-Inflammatory Drugs (NSAIDS) MOA

reducing inflammation and pain by blocking the enzyme cyclooxygenase

• aspirin

• ibuprofen

adverse effects of NSAIDS

• gastrointestinal damage and bleeding (impair protective effect on stomach lining)

• kidney damage

• cardiovascular damage

• allergic reactions

nursing considerations for NSAIDS

• monitor for signs of GIT bleeding

• monitor kidney function

• asses cardiovascular status

• encourage lowest effective dose

Narcotic Analgesics MOA

acts by binding to opioid receptors in the CNS, therefore inhibiting transmission of pain signals and altering the emotional response to pain

• codeine

• fentanyl

• oxycodone

• morphine

adverse effects of narcotics

• respiratory depression (affect respiratory centres in the brain)

• addiction and dependence

• constipation and n+v

• drowsiness

• tolerance

nursing considerations for narcotics

• monitor respiratory function

• assess for signs of overdose

• encourage bowel regimens to prevent constipation

prescription order requirements

1. patient identification (full name, date of birth and URN)

2. allergies and adverse reactions alert

3. date medication is prescribed

4. medication name

5. slow release ticked where applicable

6. route

7. dose

8. frequency of dose

9. administration times

10. prescribers signature

11. prescribers name

steady state concentration

the time at which the concentration of a drug remains stable when the drug is given consistently

• providing drug before it is needed to maintain in the effective window

aim of steady state concentration

stop the duration of action from decreasing below minimum range and providing no analgesic relief

benefit of regular dosing

• helps maintain steady analgesic relief and prevents pain from becoming difficult to manage

• reduces the risk of rebound pain

anti viral MOA

inhibits the viral replication by interfering with the viral DNA and RNA synthesis

• acylovir

• oseltamivir

adverse effects of anti virals

• hepatoxicity

• nephrotoxicity

• CNS effects

nursing considerations for anti virals

• monitor liver and kidney function

• adequate hydration

• educate on adherence

anti fungal MOA

inhibits fungal cell membrane synthesis, leading to cell death

• flunconazole

• amphotericin

adverse effects of anti fungals

• hepatoxicity

• nephrotoxicity

• infusion reactions

nursing considerations for anti fungals

• monitor renal and liver function

• adequate hydration

• educate of drug interactions

macrolides (antibacterial) MOA

inhibits bacterial protein synthesis by binding to to 50S ribosomal subunit

• erythromicin

• azithromycin

• clarithromycin

adverse effects of macrolides

• GIT disturbances

• superinfections

• increased QT interval by altering conduction of the heart

• hepatoxicity

nursing considerations for macrolides

• assess liver function

• monitor QT prolongation

• educate for food interactions

aminoglycosides (anti-bacterial) MOA

inhibits bacterial protein synthesis by binding to 30S ribosomal subunit

• gentamicin

adverse effects of aminoglycosides

• nephrotoxicity

• ototoxicity

• neuromuscular blockade

nursing considerations for aminoglyosides

• monitor renal function

• monitor hearing

• serum drug levels

• peak and trough levels

beta lactams (anti-bacterials) MOA

inhibit bacterial wall synthesis, leading to bacterial cell death

• penicilin

• cephalosporins

• carbopenems

adverse effects of beta lactams

• allergic reaction

• GIT disturbances

• superinfections

nursing considerations for beta lactams

• avoid rapid infusion

• monitor renal and hepatic function

• note either with food or empty stomach

glycopeptides (anti-bacterials) MOA

inhibits bacterial wall synthesis, effective against Gram positive bacteria

• vancomycin

adverse effects of glycopeptides

• nephrotoxicity

• rapid infusion reactions

nursing considerations for glycopeptides

• monitor renal function

• monitor hearing

• avoid rapid infusion

• monitor trough levels in pts with renal impairment

antimicrobial resistance

the ability of microorganisms to evolve and become resistant to drugs

beta 2 agonists MOA

relaxes bronchial smooth muscles and dilates airways by stimulating beta-2 adrenergic receptors

short acting

• albuterol

• levalbuterol

long acting

• salmetrol

• formoterol

adverse effects of beta 2 agonists

• tachycardia

• tremors

• hypokalemia (low potassium)

• palpitations

• brochospasms

nursing considerations for beta 2 agonists

• monitor heart rate

• monitor potassium levels

• assess respiratory status

• use in conjunction with inhaled corticosteroids for acute conditions

anticholingerics MOA

blocks acetylcholine from binding to muscarinic receptors, leading to bronchodilation and reduced mucus production and reducing parasympathetic activity

short acting

• ipratopium

long acting

• tiotropium

adverse effects of anticholingerics

• dry mouth (reduced secretions)

• blurred vision

• tachycardia

• constipation

• urinary retention (reduced bladder tone)

nursing considerations for anticholingerics

• adequate hydration

• monitor urinary function

• monitor intraocoular pressure

inhaled corticosteriods MOA

binds to receptors in airway cells, leading to suppression of inflammatory mediators

adverse effects of inhaled corticosteroids

• oral thrush

• hoarseness and sore throat

• bone thinning

• cartaracts

nursing considerations for inhaled corticosteroids

• rinse mouth after use

• monitor for signs of infection and adrenal supression

systemic corticosteroids MOA

binds to receptors in airway cells, leading to suppression of inflammatory mediators

• prednisone

• methylprednisone

adverse effects for systemic corticosteroids

• weight gain

• hyperglycaemia

• fluid retention

• risk of infection

nursing considerations for systemic corticosteroids

• administer with food to decrease gastric irritation

• taper off gradually to avoid adrenal insufficiency

paediatric medication challenges

• absorption → GI absorption rates differ due to immaturity of the digestive system. the pH is higher, affecting the solubility of medications

• distribution → higher percentage of body water and lower body weight compared to adults (larger body surface) impacts the distribution of water soluble and fat soluble drugs

• metabolism → liver enzymes responsible for drug metabolism are immature, leading to slower or incomplete metabolism

• excretion → kidney function is immature, leading to reduced clearance of medication

beta blockers MOA

block beta adrenergic receptors in the heart, depressing SA node rate and slowing AV conduction, thereby reducing heart rate, blood pressure and cardiac contractility

• antenolol

• metoprolol

adverse effects of beta blockers

• bradycardia

• hypotension

• bronchospasm

• alteration of glucose metabolism

nursing considerations for beta blockers

• avoid abrupt discontinuation to reduce rebound hypertension

• may mask signs of hypoglycaemia

• monitor heart rate and blood pressure

• monitor for signs of respiratory distress

digoxin (antiarrhythimc) MOA

inhibits the NA+/K+ pump in heart cells, which increases intracellular sodium levels, enhancing myocardial contractility

adverse effects of digoxin

• worsening of arrhythmia

• narrow therapeutic range

• CNS disturbnaces

• nausea and vomiting

• renal impairment

nursing considerations for digoxin

• assessing for signs of digoxin toxicity due to narrow therapeutic range

• assessment of renal function

• assess electrolyte levels

amiordarone MOA

blocks potassium channels responsible for repolarisation, therefore prolonging repolarisation and increasing refractory, meaning the heart is less likely to develop or continue abnormal electrical impulses

adverse effects for amiodarone

• worsen arryhthmias

• central nervous system toxicity

• pulmonary toxicity

nursing considerations for amiodarone

• close monitoring of vital signs, electrolyte levels, ECGs and chest x-rays

• monitor respiratory function

calcium channel blockers MOA

inhibit the influx of calcium ions through calcium channels in the heart and smooth muscle, resulting in vasodilation and a decrease in myocardial contractility and conduction

• amlodipine

• diltiazem

• verapamil

adverse effects of calcium channel blockers

• vasodilatory effects (headache, flushing, dizziness, hypotension and bradycardia)

• oedema (due to vasodilation)

nursing considerations for calcium channel blockers

• monitor vital signs

• avoid rapid infusion to prevent sudden hypotenison

• further depress cardiac function in those with heart failure

potassium

serum potassium levels: 3.5-5

hyperkalaemia

characterised by level above 5

• renal injury

• potassium sparing diuretics

• excessive potassium intake

hypokalaemia

characterised by level below 3.5

• excessive gastrointestinal losses

• renal losses (diuretics)

• inadequate intake

magnesium

serum magnesium levels: 1.6-2.6

hypermagnesaemia

characterised by level above 2.6

• renal insufficiency or disease

• excessive intake antacids/laxatives

• excess magnesium administration

hypomagnesaemia

characterised by serum levels below 1.6

• chronic alcoholism

• GI losses

• impaired absorption

loading dose

a larger than normal dose of medication given to rapidly achieve therapeutic range drug levels in the body

ACE inhibitors MOA

block the angiotensin-converting enzyme (ACE), preventing conversion of angiotensin I to angiotensin II, therefore reducing induced vasoconstriction and thus lowering blood pressure

• catopril

• enalapril

• perindopril

adverse effects of ACE inhibitors

• reduce systemic vascular resistance (hypotension, dizziness, headache)

• renal impairment

• hyperkalaemia

• non-productive cough

nursing considerations for ACE inhibitors

• monitor renal function

• monitor electrolyte levels

vasodilators (nitrates) MOA

release nitrous oxide in smooth muscles, resulting in decreased intracellular calcium, vasodilation and promoting blood flow and reducing preload on the heart

• nitroglycerin

adverse effects of vasodilators

• vasodilatory effects (hypotension, flushing, palpitations, fainting

• headache

• tachycardia

nursing considerations for vasodilators

• avoid sudden position changes

• monitor chest pain relief

• monitor blood pressure

lipid lowering agents (statins) MOA

inhibits HMG-CoA reductase, which is involved in cholesterol synthesis, thus decreasing production of LDL cholesterol

• atorvastatin

• rosuvastatin

adverse effects for lipid lowering agents

• muscle pain (myopathy)

• GI symptoms

• hepatoxicity

nursing considerations for lipid lowering agents

• assess liver function

• more effective taken in the evening

• avoid abrupt stopping

oral anticoagulants

• warfarin

• aspirin

aspirin MOA

inhibits COX 1, preventing the formation of thromboxane A2, thus inhibiting platelet aggregation

warfarin MOA

inhibits vit K reductase, reducing activation of vit K dependent clotting factors, preventing clot formation

adverse effects of oral anticoagulants

• bleeding

• GI upset

• hepatic dysfunction

• skin necrosis

nursing considerations for oral anticoagulants

• monitor for signs of bleeding

• monitor GI issues, advise coated aspirin to reduce gi irritation

• take dose at the same time each day

• reduce food rich food with vit K

injectable anticoagulants MOA

binds to antithrombin III, enhancing its ability to inactivate Factor XA and thrombin, preventing the conversion of fibrinogen to fibrin

• heparin

• enoxaparin

adverse effects for injectable anticoagulants

• bleeding

• bruising

• thrombocytopenia → drop in platelets

the clotting cascade

1. Extrinsic Pathway:

   • Tissue damage → TF + Factor VII → Activation of Factor X → Common pathway.

2. Intrinsic Pathway:

   • Blood vessel damage → Factor XII → Factor XI → Factor IX + Factor VIII → Activation of Factor X → Common pathway.

3. Common Pathway:

   • Activation of Factor X → Factor Xa + Factor V → Prothrombinase → Prothrombin to Thrombin → Fibrinogen to Fibrin → Formation of clot.

loop diuretics MOA

inhibit sodium and chloride reabsorption in the loop of henle, increasing urine output and reducing fluid overload

adverse effects of loop diuretics

• hypokalaemia

• hypotension

• ototoxicity

nursing considerations for loop diuretics

• monitor potassium levels

• assess for signs of dehydration

thiazide diuretics MOA

inhibit sodium and chloride reabsorption in the distal convoluted tubule, promoting fluid loss and lowering blood pressure

adverse effects of thiazide diuretics

• hypokalaemia

• hyponatraemia

• hyperglycaemia

nursing considerations for thiazide diuretics

• monitor blood pressure and electrolytes

• advise patient to eat potassium rich foods

potassium sparing diuretics MOA

inhibit sodium reabsorption and potassium excretion, preserving potassium levels

adverse effects of potassium sparing diuretics

• hyperkalaemia

• dizziness

• fatigue

antacids MOA

neutralises stomach acid my increasing hydrochloric acid pH, providing symptomatic relief for heart burn and acid reflux, by reducing acidity that irritates the oesophagus

• magnesium hydroxide

• aluminium hydroxide

adverse effects of antacids

• electrolyte imbalances

• constipation or diarrhoea

• abdominal discomfort

nursing considerations for antacids

• they reduce the affect of other medications, therefore take them seperately

• encourage adequate hydration

H2 agonists MOA

reduce gastric acid secretion by competitively binding to histamine receptors on parietal cells, preventing histamine from stimulating acid production

• ranitidine

• famotidine

adverse effects of H2 agonists

• dizziness and confusion

• GI issues

• potential for bacteria growth

nursing considerations for H2 agonists

• assess renal function for dose adjustments

• educate on proper use and not to exceed recommended dosages

proton pump inhibitors MOA

inhibit the proton pump in the parietal cells of the stomach, preventing gastric acid secretion

• omeprazole

• esomeprazole

• lansoprazole

adverse effects of proton pump inhibitors

• nutrient deficiencies

• increased risk of infection

nursing considerations for proton pump inhibitors

• regular monitoring of renal function

• limit long term use

• advise taking before meals for better efficacy