Year 3 Flashcards
IV Fluid Therapy
What are crystalloid and colloid fluid solutions?
*LOB: Define crystalloid and colloid fluid solutions and give examples of each
Crystalloid
Sodium Chloride
Ringers Lactate
Hartmanns
Hypertonic Saline
Colloid
Albumin
Hydroxyethyl starch
Gelatin
IV Fluid Therapy
Colloids: Gelatin, Albumin
M comparatively large, osmotically active molecules which do not readily cross semipermeable membranes, so their osmotic effect should ‘hold’ the infused volume in the intravascular compartment. and therefore increase circulating fluid
I To expand circulating volume in states of impaired tissue perfusion (including shock). However, compound sodium lactate and sodium chloride 0.9% are preferred.
C caution is required in heart failure, due to the risk of worsening cardiac output, and renal impairment, monitor fluid balance closely to avoid volume overload.
R IV Infusion
A promotes oedema. may increase LVent filling reducing cardiac output and precipitating pulmonary oedema.
Gelatins may cause hypersensitivity reactions, including anaphylaxis—another reason to prefer crystalloids, which are non-allergenic.
In managing a severely ill patient requiring large-volume fluid therapy, it is a good idea to use warmed fluids if possible, to avoid causing hypothermia.
IV Fluid Therapy
Compound sodium lactate (Hartmann’s solution)
M electrolyte composition approximates serum: 1 L contains Na+ 131 mmol, Cl– 111 mmol, K+ 5 mmol, Ca2+ 2 mmol, and lactate 29mmol. Lactate generates bicarbonate. As compound sodium lactate contains sodium in a concentration similar to extracellular fluid, the infused volume is largely retained in the extracellular water compartment
I To provide sodium and water for people unable to meet their water and electrolyte requirements orally (or by enteral tube). To expand circulating volume in states of impaired tissue perfusion (including shock). This may be done as a ‘fluid challenge’,
C Exercise caution during rapid infusion of IV fluid in patients with heart failure, due to the risk of pulmonary oedema. In renal impairment, monitor fluid balance closely to avoid overload. Conventional advice is to avoid compound sodium lactate in severe liver disease because of reduced capacity to metabolise lactate.
R The maximum rate of infusion using a pump is usually too slow for an effective fluid challenge.
A sodium in interstitium promotes oedema, may worsen cardiac output. Compound sodium lactate should not be mixed or infused with ceftriaxone, as may cause precipitation.
Can be used as your ‘standard’ sodium-based crystalloid solution.but cannot be used for potassium replacement
IV Fluid Therapy
Glucose (dextrose) - glucose 5%, 10%, 20% and 50%
M glucose content ensures it is initially isotonic with serum, so that it does not induce osmotic lysis of cells in the immediate vicinity of infusion. Glucose is rapidly taken up by cells and metabolised, leaving ‘free’ (hypotonic) water that distributes across all body water compartments
I To provide water for people unable to meet their water requirements orally (or by enteral tube), Severe hypoglycaemia, As a substrate fluid for IV insulin infusions., With insulin to treat hyperkalaemia. Reconstitution and dilution of drugs administered by injection or infusion.
C Giving IV glucose in thiamine deficiency can cause Wernicke’s encephalopathy. Administering hypotonic fluid in hyponatraemia may precipitate hyponatraemic encephalopathy.
R It is preferable, though, to use an infusion pump to control the rate and volume precisely.
The typical adult maintenance requirement for water is 25–30 mL/kg/day, some of which may be provided with a sodium-containing fluid (e.g. compound sodium lactate or sodium chloride 0.9%, to provide the daily sodium requirement) and the rest made up with glucose 5%
A Glucose 50% is highly irritant to veins and may cause local pain, phlebitis and thrombosis.
IV Fluid Therapy
Potassium, intravenous - potassium chloride (as an additive)
M In people unable to tolerate dietary intake, who are instead receiving their sodium and water requirement by IV infusion, potassium may be provided intravenously. For best effect,** IV potassium** is given with sodium chloride rather than glucose. This is because infusion of negatively charged Cl– ions promotes retention of K+ in the serum, whereas glucose may promote insulin release with resultant stimulation of Na+/K+-ATPase, shifting potassium into cells.
I Prevention of potassium depletion in people unable to meet their electrolyte requirements orally AND Treatment of established potassium depletion and hypokalaemia. (< 2.5 mmol/L), symptomatic or associated with electrocardiogram (ECG) changes.
C overcorrection leading to hyperkalaemia and a resultant risk of arrhythmias, irritant to veins
R infused no higher than 10 mmol/hr, due to the risks of venous irritation and cardiac toxicity.
AIV potassium has an additive effect with other potassium-elevating drugs, including oral potassium, aldosterone antagonists, potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin-receptor blockers.
For example, if you need to prescribe 10 mmol potassium in 500 mL of 0.9% sodium chloride, you might specify this as the total amount of potassium chloride in the bag (10 mmol), the concentration per litre (20 mmol/L) or the concentration as a percentage (0.15%). Which you use will depend on the requirements of the prescribing interface.
IV Fluid Therapy
Sodium chloride - sodium chloride 0.9%, sodium chloride 0.45%
M If you take in more sodium (like from a saline solution), the volume of ECF increases. a 0.9% sodium chloride solution has a sodium concentration similar to that of ECF, so when you receive this solution, the ECF increases by about the same amount as the volume of the solution given.
I To provide sodium and water for people unable to meet their water and electrolyte requirements orally, To expand circulating volume in states of impaired tissue perfusion (including shock, Reconstitution and dilution of drugs administered by injection or infusion.
C Caution is required with rapid IV infusions in heart failure, due to the risk of pulmonary oedema. The concentration of chloride in sodium chloride 0.9% (154 mmol/L) is significantly higher than that of ECF (about 100 mmol/L). This may cause hyperchloraemia which, in turn, promotes acidaemia.
R
A When reconstituting drugs, it is important to check its compatibility with the diluent. For example, amiodarone is incompatible with sodium chloride. Refer to local policies and product information.
When estimating maintenance fluid requirement, a simple rule of thumb is to infuse fluid at an hourly rate (in mL/hr) equal to body weight. This will provide 24 mL/kg/day of water, which is close to the 25–30 mL/kg/day recommended in guidelines. For example, for a 75-kg adult, you might prescribe sodium chloride 0.9% (1 × 500 mL bag) and glucose 5% (2 × 1 L bags), each infused at 75 mL/hr.
Sulfonylureas
Gliclazide, glimepride, glipizide
Statins
Atorvastatin, simvastatin, rosuvastatin, pravastatin
Hypertension: for first- or second-line treatment of hypertension, to reduce the risk of stroke, myocardial infarction, and death from cardiovascular disease.
➋ Chronic heart failure: for first-line treatment of all stages of heart failure, to improve symptoms and prognosis.
➌ Secondary prevention of major adverse cardiovascular events in people with ischaemic heart disease, cerebrovascular disease or peripheral vascular disease.
➍ Diabetic nephropathy and chronic kidney disease (CKD) with proteinuria: to reduce proteinuria and progression of nephropathy.
Mechanisms of action
ARBs have similar effects to angiotensin-converting enzyme (ACE) inhibitors, but instead of inhibiting the conversion of angiotensin I to angiotensin II, ARBs block the action of angiotensin II on the angiotensin type 1 (AT1) receptor. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion. Blocking its action reduces peripheral vascular resistance (afterload), which lowers blood pressure. It particularly dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD. Reducing aldosterone concentration promotes sodium and water excretion. This can help to reduce venous return (preload), which has a beneficial effect in heart failure.
ARBs can cause hypotension (particularly after the first dose), hyperkalaemia, and renal failure. The mechanism is the same as for ACE inhibitors. Renal artery stenosis presents a particular risk, as constriction of the efferent glomerular arteriole is required to maintain glomerular filtration. ARBs are less likely than ACE inhibitors to cause cough and angioedema, as they do not inhibit ACE, so do not affect bradykinin metabolism. They may therefore preferred in Black people of African or Caribbean origin, who are at higher risk of angioedema.
Methotrexate
Methotrexate
Methatrexate
M: inhibits dihydrofolate reductase which converts dietary folate to FH4 for DNA and protein synthesis. Actively dividing cells are particularly sensitive
Anti- inflammatory and immunosuppressive effects at a lesser value than anti-mitotic via G protein coupled receptors due to increased adenosine release.
I: for inflammatory disorders and for neoplastic disorders.
C: Tetarogenic, Aspirin, nsaid, pencillin, PPI, The risk of neutropenia is increased if methotrexate is combined with clozapine.
A: Mucosal damage, bone marrow suppression, toxicity from inadvertent daily administration. Folinic acid rescues normal cells from methotrexate
Why is Methotrexate intrethecal?
Methotrexate is a chemotherapy drug that is used to treat certain types of cancer and leukaemia. When given intrathecally, it prevents leukaemia cells entering the cerebrospinal fluid (CSF) around the spine and brain.
Metformin
Metformin
Type 2 diabetes, as the first-choice medication for control of blood glucose, used alone or in combination with other oral hypoglycaemic drugs (e.g. sulphonylureas, dipeptidylpeptidase-4 (DPP-4) inhibitors, sodium–glucose co-transporter 2 inhibitors) or insulin.
Metformin (a biguanide) lowers blood glucose primarily by reducing hepatic glucose output (glycogenolysis and gluconeogenesis) and, to a lesser extent, increasing glucose uptake and utilisation by skeletal muscle. It does not stimulate insulin secretion and therefore does not cause hypoglycaemia. The cellular mechanisms are complex, involving activation of adenosine monophosphate-activated protein kinase (AMP kinase). This is a cellular metabolic sensor, activation of which has diverse effects on cell functions. Its effects on glucose metabolism can be accompanied by other metabolic changes, notably modest weight loss, which can be a desirable side effect (see CLINICAL TIP).
Important adverse effects
Metformin commonly causes GI upset, including nausea, vomiting, taste disturbance, anorexia, and diarrhoea. Lactic acidosis has been associated very rarely with metformin use, although the evidence for this is largely derived from case reports. There is no strong evidence of an increased risk in general, but metformin may be a contributory factor in people who develop an intercurrent illness that causes metformin accumulation (e.g. renal impairment), increased lactate production (e.g. sepsis, hypoxia) or reduced lactate metabolism (e.g. liver failure).
Diuretics, thiazide and thiazide-like
Bendroflumethiazide, indapamide, chlortalidone
Thiazide diuretics (e.g. bendroflumethiazide) and thiazide-like diuretics (e.g. indapamide, chlortalidone) differ chemically but have similar effects and clinical uses. We refer to them here collectively as ‘thiazides’. Thiazides inhibit the Na+/Cl− co-transporter in the distal convoluted tubule of the nephron. This prevents reabsorption of sodium and its osmotically associated water. The resulting diuresis causes an initial fall in extracellular fluid volume. Over time, compensatory changes (e.g. activation of the renin–angiotensin system) tend to reverse this, at least in part. The longer-term antihypertensive effect may be mediated by vasodilation, the mechanism of which is incompletely understood.
HTN: Bendro, Chloratalidone
Take in morning so effect maximal in day
Corticosteroids, systemic
Dexamethasone, prednisolone, hydrocortisone
Dexamethasone
M: inding to glucocorticoid receptors in the cytoplasm of a cell, which then translocates to the nucleus.
I: Suppression of inflammatory and allergic disorders, local inflammation, short term inflammation, macular oedema, mild croup, congenital adrenal hyperplasia, overnight dexa supression test, adjunctive Tx of sus[ct bact MCD C: For all corticosteroids (systemic) Avoid live virus vaccines in those receiving immunosuppressive doses (serum antibody response diminished); systemic infection (unless specific therapy given)
Contra-indications, further information
With intra-articular use or intradermal use or intralesional use:
For further information on contra-indications associated with intra-articular, intradermal and intralesional preparations, consult product literature.
Contra-indicationsFor dexamethasone
With intravitreal use
Active ocular herpes simplex (in adults); active or suspected ocular infection (in adults); active or suspected periocular infection (in adults); rupture of the posterior lens capsule in patients with aphakia, iris or transscleral fixated intra-ocular lens or anterior chamber intra-ocular lens (in adults); uncontrolled advanced glaucoma (in adults)
A:Anxiety; behaviour abnormal; cataract subcapsular; cognitive impairment; Cushing's syndrome; electrolyte imbalance; fatigue; fluid retention; gastrointestinal discomfort; headache; healing impaired; hirsutism; hypertension; increased risk of infection; menstrual cycle irregularities; mood altered; nausea; osteoporosis; peptic ulcer; psychotic disorder; skin reactions; sleep disorders; weight increased
Calcium channel blockers
Amlodipine, felodipine, nifedipine, diltiazem, verapamil
Taken orally, CCB have a half life of 35-50 hours. They are prescribed for HTN, Angina, supraventricular arrythmia.
M: Calcium-channel blockers (less correctly called ‘calcium-antagonists’) interfere with the inward displacement of calcium ions through the slow channels of active cell membranes. They influence the myocardial cells, the cells within the specialised conducting system of the heart, and the cells of vascular smooth muscle. Thus, myocardial contractility may be reduced, the formation and propagation of electrical impulses within the heart may be depressed, and coronary or systemic vascular tone may be diminished.
I: Amlodipine HTN, Angina Dilitazem, Supraventricular arrhtymia Verapamil
C: Cardiogenic shock; significant aortic stenosis; unstable angina
R: Orally, only verapamil is IV option (arrythmia), MR shouldnt be crushed
A:Abdominal pain; dizziness; drowsiness; flushing; headache; nausea; palpitations; peripheral oedema; skin reactions; tachycardia; vomiting
Overdose
Features of calcium-channel blocker poisoning include nausea, vomiting, dizziness, agitation, confusion, and coma in severe poisoning. Metabolic acidosis and hyperglycaemia may occur. In overdose, the dihydropyridine calcium-channel blockers cause severe hypotension secondary to profound peripheral vasodilatation. For details on the management of poisoning, see Calcium-channel blockers, under Emergency treatment of poisoning.
Antihistamines (H1-receptor antagonists)
Cetirizine, fexofenadine, loratadine, chlorphenamine
Mechanism of Action (M):
H1 antihistamines block H1 receptors on cells, preventing histamine from binding and exerting its effects. This reduces allergic symptoms such as itching, swelling, and vasodilation, commonly seen in allergic rhinitis, conjunctivitis, and urticaria.
Indication (I):
Allergic rhinitis
Urticaria (hives)
Allergic conjunctivitis
Anaphylaxis (as part of combination therapy)
Other allergic conditions causing itching or swelling
Contraindication (C):
Severe liver impairment (for some antihistamines)
Use with caution in patients with glaucoma, prostate hypertrophy, or urinary retention
Cetirizine: Contraindicated in patients with severe renal impairment
Risk Factors (R):
Elderly (increased risk of sedation and confusion)
Use with other sedative medications
Patients with cardiovascular disease
Renal or hepatic impairment
Adverse Reactions (A):
Sedation (especially with first-generation antihistamines like chlorphenamine)
Drowsiness (common in first-generation; less so in newer agents like cetirizine, loratadine, and fexofenadine)
Dry mouth, blurred vision, and urinary retention (anticholinergic effects, more prominent with first-generation drugs)
Gastrointestinal discomfort, headache, dizziness
Cetirizine:
Less sedating than first-generation antihistamines but can cause mild drowsiness in some.
Requires dose adjustment in renal impairment.
Fexofenadine:
Non-sedating, making it a good choice for daytime use.
Generally has fewer interactions with other medications.
Loratadine:
Non-sedating and well-tolerated, often chosen for once-daily dosing.
Safe for most patients with mild liver or renal impairment but may require dose adjustment.
Chlorphenamine:
A first-generation antihistamine, causing more sedation and anticholinergic effects.
Used in more severe allergic reactions like anaphylaxis but typically avoided for regular allergy management due to sedation.
Cetirizine:
Useful for allergic rhinitis and urticaria, especially when mild drowsiness is not an issue or nighttime use is preferred.
Can be used for chronic allergies with some degree of renal function monitoring.
Fexofenadine:
Ideal for patients needing a non-sedating antihistamine, particularly for daytime management of hay fever or chronic urticaria.
Suitable for individuals with active lifestyles or driving needs.
Loratadine:
Good choice for once-daily use in allergic rhinitis or hives with minimal side effects.
Useful for patients requiring long-term allergy management without sedation.
Chlorphenamine:
Reserved for acute, severe allergic reactions (e.g., in anaphylaxis alongside adrenaline).
May also be used at night when sedation is desired or not problematic, but generally avoided for regular, daily allergy management.
Angiotensin-converting enzyme (ACE) inhibitors :
Ramipril, lisinopril, perindopril
Mechanism of Action (M):
ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to vasodilation, reduced blood pressure, and decreased aldosterone secretion, which reduces sodium and water retention, improving heart function.
Indication (I):
Hypertension (first-line treatment)
Heart failure (adjunct treatment)
Post-myocardial infarction (to improve survival and reduce heart failure risk)
Diabetic nephropathy (renal protective effects)
Chronic kidney disease (to reduce proteinuria)
Contraindication (C):
History of angioedema
Use with aliskiren in patients with diabetes or low eGFR
Pregnancy (due to risk of fetal harm)
Severe renal impairment without dose adjustments
Risk Factors (R):
Elderly (due to risk of hypotension, especially postural)
Renal impairment (increased risk of hyperkalemia and renal dysfunction)
Patients on diuretics or low-sodium diets (risk of first-dose hypotension)
Collagen vascular disease (increased risk of agranulocytosis)
Adverse Reactions (A):
Dry cough (due to bradykinin accumulation)
Hyperkalemia (especially in renal impairment or with potassium-sparing drugs)
Hypotension, especially after the first dose
Angioedema (can occur at any time during treatment)
Renal dysfunction (worsening of kidney function in some patients)
Fatigue, dizziness, headache
Differences Between Ramipril, Lisinopril, and Perindopril
Ramipril:
Often preferred for its once-daily dosing and longer half-life.
Indicated for a broad range of conditions, including hypertension, heart failure, and post-MI management.
Requires dose adjustment in renal impairment and elderly patients.
Lisinopril:
A longer-acting ACE inhibitor, usually taken once daily.
Commonly prescribed for hypertension, heart failure, and post-MI treatment.
Its fixed dosing for most renal impairment cases makes it a popular choice, but caution is advised in severe renal impairment.
Perindopril:
Has a longer half-life and is often prescribed for once-daily use.
Particularly useful in hypertension and chronic heart failure management.
Dose adjustments are required for renal impairment; it is also effective in patients at risk of ischemic heart disease.
When to Prescribe Each:
Ramipril:
A good first-line option for hypertension and heart failure.
Useful post-myocardial infarction for long-term cardiovascular protection.
Consider in patients who need a once-daily ACE inhibitor with a favorable renal protection profile.
Lisinopril:
Ideal for hypertension management, particularly when straightforward dosing and long-term therapy are needed.
Suitable for heart failure and post-MI patients, especially in those who tolerate the initial dose well.
Preferred when monitoring for renal impairment is straightforward.
Perindopril:
Best suited for patients with cardiovascular risk, particularly for hypertension and chronic heart failure.
Beneficial in ischemic heart disease and for patients requiring long-term vascular protection.
Use with caution in those with significant renal impairment, adjusting the dose as needed.
Angiotensin receptor blockers
Losartan, candesartan, irbesartan
Hypertension: for first- or second-line treatment of hypertension, to reduce the risk of stroke, myocardial infarction, and death from cardiovascular disease.
➋ Chronic heart failure: for first-line treatment of all stages of heart failure, to improve symptoms and prognosis.
➌ Secondary prevention of major adverse cardiovascular events in people with ischaemic heart disease, cerebrovascular disease or peripheral vascular disease.
➍ Diabetic nephropathy and chronic kidney disease (CKD) with proteinuria: to reduce proteinuria and progression of nephropathy.
Mechanisms of action
ARBs have similar effects to angiotensin-converting enzyme (ACE) inhibitors, but instead of inhibiting the conversion of angiotensin I to angiotensin II, ARBs block the action of angiotensin II on the angiotensin type 1 (AT1) receptor. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion. Blocking its action reduces peripheral vascular resistance (afterload), which lowers blood pressure. It particularly dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD. Reducing aldosterone concentration promotes sodium and water excretion. This can help to reduce venous return (preload), which has a beneficial effect in heart failure.
ARBs can cause hypotension (particularly after the first dose), hyperkalaemia, and renal failure. The mechanism is the same as for ACE inhibitors. Renal artery stenosis presents a particular risk, as constriction of the efferent glomerular arteriole is required to maintain glomerular filtration. ARBs are less likely than ACE inhibitors to cause cough and angioedema, as they do not inhibit ACE, so do not affect bradykinin metabolism. They may therefore preferred in Black people of African or Caribbean origin, who are at higher risk of angioedema.
Emergency drugs
Adrenaline
M potent agonist of the α1-, α2-, β1- and β2 adrenoceptors
bronchodilatation and suppresses inflammatory mediator release from mast cells, ; increases in heart rate, force of contraction, and myocardial excitability; vasoconstriction of vessels supplying skin, mucosa, and abdominal viscera
I Cardiac arrest (IV), Anaphylaxis (IM), Croup (nebuliser), Local vasoconstriction during endoscopy to control bleeding or premixd with local anaesthetics to increase effect
C may also precipitate angina, myocardial infarction, and arrhythmias, Co-administration with ▲ β-blockers may induce widespread vasoconstriction
R IV, IM, Nebuliser
A adrenaline-induced hypertension. It may cause anxiety, tremor, headache, and palpitations
In children with croup (laryngotracheitis), nebulised adrenaline is an unlicensed but widely recommended treatment for those whose condition has not responded adequately to a systemic corticosteroid.
Paracetamol
Paracetamol
M reduces the availability of oxidised COX-2, interfering in the prostaglandin synthesis pathway, interferes with transmission of pain signals between the spinal cord and higher centre. Reduces prostaglandin E2 (PGE2) concentrations in the thermoregulatory region of the hypothalamus, reducing fever.
I first-line analgesic for most forms of acute and chronic pain, AND an antipyretic that can reduce fever
C reduced in people at increased risk of liver toxicity, either because of increased NAPQI production chronic excessive alcohol use, inducing metabolising enzymes) or reduced glutathione stores (malnutrition, low body weight, severe hepatic impairment)
R PO as tablets, caplets, capsules, soluble tablets, and oral suspension. IV paracetamol solution may be infused neat over 15minutes or diluted in 0.9% sodium chloride or 5% glucose solution before administration, depending on the product.
A overdose, paracetamol causes liver failure as NAPQI accumulation causes hepatocellular necrosis, CYP inducers, e.g. phenytoin and carbamazepine, increase the rate of NAPQI production and therefore the risk of liver damage in paracetamol toxicity.
Cocodamol or co-dydramol contain paracetamol. DONT double dose
Alpha-blockers
Alpha-blockers : Tamsulosin, doxazosin, alfuzosin
Doxazosin is licensed both for benign prostatic enlargement and hypertension
Tamsulosin for benign prostatic enlargement only
M: are highly selective for α1-adrenoceptors found mainly in smooth muscle, including in blood vessels and the urinary tract (the bladder neck and prostate in particular). Stimulation induces contraction; blockade induces relaxation
causes vasodilation and a fall in blood pressure (BP) and reduces resistance to urine outflow from the bladder.
I a first-line medical option to improve lower urinary tract symptoms (LUTS) in benign prostatic enlargement, AND as an add-on treatment in resistant hypertension,
C avoid in existing postural hypotension. Omit existing anti hypertensive drugs. Ideally α-blocker treatment should be stabilised before starting a PDE-5inhibitor.
R PO advised bedtime.
A postural hypotension, dizziness, and syncope.
PDE-5inhibitor may be given (sildenafil) as those with BPH may experience erectile dysfunction.
Penicillins, antipseudomonal
Penicillins, antipseudomonal : Piperacillin with tazobactam (e.g. Tazocin®)
M broad spectrum of activity against a wide range of Gram-positive and Gram-negative bacteria (notably including Pseudomonas spp.) and anaerobes via β-lactamase inhibitor, high affinity to penicillin-binding proteins
I severe infections, Lower respiratory tract infection. Urinary tract infection, Intraabdominal infection, Skin and soft tissue infection.
Cpenicillin allergy, moderate/severe renal impairment.
R a powder to be reconstituted in 10mL sterile water or 0.9% sodium chloride. This is diluted further in 50–150mL of 0.9% sodium chloride or 5% glucose for IV infusion.
A GI upset is common, Less frequently, antibiotic-associated colitis occurs, hypersensitivity may occur
piperacillin–tazobactam contains about 11mmol Na+ and is infused in 50–150mL fluid (which may contain more sodium). Take this into account when determining the need for supplementary fluid and electrolyte therapy, particularly in people with heart failure or oedema.
Penicillins, narrow-spectrum
Penicillins, narrow-spectrum : Flucloxacillin, benzylpenicillin, phenoxymethylpenicillin
M Inhibit enzymes responsible for cross linking the peptidoglycans in bacterial cell wall - cell swells, cell lysis
P have beta lactam ring
ISTAPHOCOOCAL, Skin and soft tissue
Ostemyelitis and septic arthritis, Other infection - endo carditis
C Reduce dose renal failure
Allergy
Previous hepatotocxity
Reduce renal excretion of methotrexate - caution
A GI
Effects of allergy
Liver toxcity
Central nervous system toxcitity
Penicillins, broad-spectrum
Penicillins, broad-spectrum : Co-amoxiclav, amoxicillin
M inhibit enzymes responsible for cross-linking peptidoglycans, weakens the bacterial cell wall, reducing its ability to maintain an osmotic gradient, causing cell swelling, lysis, and death. Penicillins contain a β-lactam ring, which is responsible for their bactericidal
I Amoxicillin- including sinusitis, otitis media, community-acquired pneumonia, and urinary tract infection (UTI), and to eradicate Helicobacter pylori.
Co-amoxiclav is a common choice for severe, resistant, and hospital-acquired infections, including pneumonia, UTI, intraabdominal infection, cellulitis, and bone and joint infection.
C severe allergy to a β-lactam antibiotic, young people with a sore throat, as they can cause a rash with glandular fever, C. difficile infection, and in those with a history of penicillin-associated liver injury
R severe infection IV administration at a high dose, moderate orally at a lower dose
Available as capsules, tablets, and oral suspensions. Co-amoxiclav suspension may cause dental staining. IV preparations may be given by slow injection or infusion.
A GI upset is common, Less frequently, antibiotic-associated colitis occurs, hypersensitivity may occur. Acute liver injury (cholestatic jaundice or hepatitis) may develop during or shortly after co-amoxiclav
inactivated by bacterial penicillinases, and resistance is increasingly prevalent.
Opioids
Opioids : Strong (morphine, oxycodone); weak/moderate (codeine, dihydrocodeine, tramadol)
M agonism of opioid µ (mu) receptors in the central nervous system (CNS). leading to reduced neuronal excitability and pain transmission. BUT blunts response to hypoxia and hypercapnia, reduces respiratory drive and breathlessness.
I Acute pain, chronic pain if other analgesics are insufficient, breathlessness in palliative care, acute pulmonary oedema
C Avoid co-prescription with other sedating drugs including benzodiazepine and tricyclic antidepressants. Avoid in hepatic and renal failure and in older people. Do not give in respiratory failure other than palliative care.
R IV for rapid effect. A typical initial prescription is morphine 2–10mg IV, tailored to pain, age, and other individual factors. A common choice for mild pain is codeine (e.g. 30mg orally 4-hrly)
A Respiratory depression, euphoria, detachment, neurological depression, nausea, vomitting, pupillary constriction, constipation (reduced motility), itching (histamine release)
opioid withdrawal are the opposite of the clinical effects of opioids: anxiety, pain, and breathlessness increase; the pupils dilate; and the skin is cool and dry with piloerection (‘cold turkey’).
Anaesthetics, general
Anaesthetics, general : Propofol, thiopental, sevoflurane, nitrous oxide, ketamine
M Enhance the inhibitory action of γ-aminobutyric acid (GABA), particularly via GABAA receptor activation, and/or antagonise excitatory N-methyl-D-aspartate (NMDA) and nicotinic cholinergic receptors. This decreases cortical and thalamic activity, leading to varying degrees of unconsciousness, analgesia, and muscle relaxation
I induce reversible unconsciousness, (e.g. propofol) may be used at sub-anaesthetic doses to reduce discomfort from procedures that do not require full general anaesthesia, or as an infusion to improve tolerability of invasive ventilation in critical illness (sedation).
C enhances other drugs that supress conciousness and cardiorespiratory drive.
R Intravenous anaesthetics include propofol, thiopental, and ketamine, while inhalational anaesthetics include volatile liquids (e.g. sevoflurane) and simple gases (nitrous oxide)
IV anaesthetics are given by bolus injection to induce anaesthesia, and infusion to maintain anaesthesia (or sub-anaesthetic sedation)
A Supression of airway reflexes and respiratory drive, bradycardia, vasodlation, hypotension (ketamine hypertension), nausea and vomiting, propofol may cause pain on injection.
Anaesthetics, local
Anaesthetics, local : Lidocaine, bupivacaine, levobupivacaine
M reversibly inhibit voltage-gated sodium channels, prevents initiation and propagation of action potentials
I Surface anaethesia such as urinary catheterisation and venepuncture, local anaesthesia for suturing and lumbar puncture, regional anaesthesia/analgesia such as epidural, lidocaine second line for ventricular tachycardia
C Liver disease, cardiac failure (due to liver blood flow), duration of action can be overtly increased with vasoconstrictor (adrenaline)
R Urinary catheter- Instilagel. Subcuntaneous 1%- 3mg/kg, topical creams, plasters. NEVER IV
A stinging during administration, other affects are uncommon when care to avoid OD or IV administration. If OD- drowsiness, restlessness, tremor fits, hypotension, arrhythmia
Administer the local anaesthetic early, then complete any other preparatory work for your procedure. Wait 5minutes before testing the effect.
Antimuscarinics, genitourinary uses
Antimuscarinics, genitourinary uses : Solifenacin, oxybutynin, tolterodine
M bind to muscarinic receptors as competitive inhibitor of acetylcholine. promoting bladder relaxation increasing bladder capacity. May reduce urinary frequency, urgency, urge incontinence. Work in overactive bladder at antagnosim at M3 receptor.
I urinary frequency urgency and urge incontinence in overactive bladder
C Adverse with other antimuscarinics like tricyclic antidepressants, UTI, dementia (cognitive effect), caution in those at risk of intraocular pressure, caution with arrhythmia risk and urinary retention
R Immediate-release antimuscarinics should be taken at roughly equal intervals, with or without food. MR forms should be taken at a similar time each day and swallowed whole, not chewed.
A dry mouth, tachycardia, constipation, blurred vision, urinary retention may occur if there is bladder outflow obstruction. Oxybutiynin congnitive effects as ccrosses BBB acting at M1.
chewing gum good for dry mouth symptoms
Direct oral anticoagulants
Direct oral anticoagulants : Apixaban, rivaroxaban, edoxaban, dabigatran
M DOACs act on the final common pathway of the coagulation cascade: Factor X, Thrombin and Fibrin.
Dabigatran directly inhibits thrombin and the “xa” inhibit Factor Xa. And thus prevent fibrin formation.
I VTE for Tx and recurrence, Atrial Fibrilation to prevent stroke and systemic embolism in non-valvular AF associated with a risk factor
C Avoid in active clinically significant bleeding and those with risk of bleeding such as ulceration, cancer, recent surgery. Eliminates via CYP450 so reduce dose/ alternatives in those with hepatic and renal disease. Avoid in pregnancy and breastfeeding.
The anticoagulant effect is increased by macrolides, protease inhibitors, and fluconazole and decreased by rifampicin and phenytoin.
R PO. Rivaroxaban with food. Dabigatran cannot be crushed but ‘xa’ can.
A Bleeding including greater risk of GI bleeds (less intercranial risk than warfarin), anaemia, GI upset, dizziness, elevate liver enzymes.
In emergencies, dabigatran can be reversed with idarucizumab (a humanised monoclonal antibody fragment that binds to dabigatran and its metabolites). Apixaban and rivaroxaban can be reversed with andexanet alfa (a recombinant, modified form of human factor Xa that acts as a ‘decoy receptor’ for factor Xa inhibitors).
5 alpha reductase inhibitors
5 alpha reductase inhibitors: Finasteride, dutasteride
M Reduce size of prostate gland by inhibiting conversion of testosterone to dihydrotesterone but can take months for clinical difference to be seen. Hence second line
I Benign prostatic hyperplasia
Second line treatment after alpha blockers
C Pregnancy
R PO
A Impotence, Reduced libido, Gynaecomastia, Can be used to help male pattern baldness as adrogen inhibition can help hair growth
Nitrofuratoin
Nitrofuratoin
M Metabolised in bacterial cells by nitrofuran reductase
Damages the bacterial DNA and cause cell death
Active against - E coli (g -ve) and staphcoc (g +ve)
I Uncomplicated UTI first line treatment
Because:
Effective against most com uti patho
Reaches therapeutic conc in urine through rental excretion
Most bactericidal in acidic conditions - aka urine
C Pregnancy, Babies < 3 mo, Renal impairement as impaired excretion increase tox and reduce effectivity Caution with long term use
A GI upset
Hypersensitivity
Chronic pul reactions
Hepatisis and peripheral neuropathy in long term
Babies - haemolytic anaemia
Phosphodiesterase (type 5) inhibitors :
Phosphodiesterase (type 5) inhibitors : Sildenafil, tadalafil, vardenafil
M Phosphodiesterase inhibitor selective for type 5 This is mainly found in the SM of the corpus cavernosum of penis and arteries of lungs
I Erectile dysfunction, Primary pulmonary hypertension
CIf vasodilation is risky aka, Recent stroke, ACS, significant CVD, Severe renal or hepatic impairment, dont give or lower the dose
ARelated to the fact its a vasodilator
Flushing, Headaches, Dizzyness, nasal congestion
More serious, Hypotension, tachy, palpilations
If erection fails to subside - medical attention needed to prevent damage
Antiemetics, dopamine D2-receptor antagonists
Antiemetics, dopamine D2-receptor antagonists : Metoclopramide, prochlorperazine, domperidone
M D2 receptors in the main receptor in the ctz. Dop also relaxes stomach and lower esophagus and inhibs gastoduodenal effects
I Prophyaxis and treatment of nausea in many things but particulary reduced gut motilty
C Gastrointenintal obstructions
Perforation
Extrapyraminal side effects more common in under 25 so avoid
Dont combine with anti psycotics or dopmergic agents (park treatment)
A Diarrhoea
Extra pyrmindal sydrome
Acute dystonic reaction
Antiemetics, histamine H1-receptor antagonists
Antiemetics, histamine H1-receptor antagonists : Cyclizine, promethazine, cinnarizine
MH1 found in vomiting centre and in its comms with vestibular system
I Proph and treatment of nausea and vomiting particaully in motion sickness and vertigo
C Hepatic encephalopathy
Avoid patient suseptiable to anticholeric side effect aka men with prostatic hypertrophy
Sedation more if also on other sedative drugs
Anticholergic effects more pronounced in patients taking antimusc, bronch dilators
A Drowsiness
Dry throat and mouth
Tachy
Palpitations
Antiemetics, serotonin 5-HT3-receptor antagonists
Antiemetics, serotonin 5-HT3-receptor antagonists : Ondansetron, granisetron
M High density of 5ht in ctz and seratonin is key NT released by gut in response to emetogenic stimulation
I Nausea and vom, in context of GA and chemo
C May prolong qt so just be caution
Avoid taking with other drugs that prolong qt - antipsycotic, ssri
A Rare but constipation, diarrhoea, and headache
Benzodiazepines
Benzodiazepines : Diazepam, midazolam, lorazepam, chlordiazepoxide
M Targets γ-aminobutyric acid type A (GABAA) receptor in the brain. (Main inhibitory neurotransmitter) changes structure to facilitate binding odf GABA. Depressant effect on the synaptic transmission
reduced anxiety, sleepiness, sedation, and anticonvulsive effects.
I First line epilepsy and alcohol withdrawal. Sedation in palliatie care and inteventional procedures. Short term anxiety incl procedures.
C additive to those of other sedating drugs, including alcohol and opioids. CYP inhibitors (e.g. amiodarone, diltiazem, macrolides, fluconazole, protease inhibitors) may increase their effects.
R Oromucosal, IV,
A dose-dependent drowsiness, sedation, and coma. There is relatively little cardiorespiratory depression in benzodiazepine overdose (in contrast to opioid overdose), but loss of airway reflexes can lead to airway obstruction and death. If used repeatedly for more than a few weeks, a state of dependence
*Dont give Flumazenil- antagonist but can cause seizures that you cant fix becuase you block benzo receptor. *
Monoclonal antibodies
Monoclonal antibodies : Infliximab, adalimumab, denosumab, rituximab, omalizumab
MInfliximab & Adalimumab: Target TNF-α to reduce inflammation in autoimmune diseases.
Denosumab: Inhibits RANKL, reducing bone resorption by inhibiting osteoclast activity.
Rituximab: Binds to CD20 on B cells, leading to B-cell depletion.
Omalizumab: Binds IgE, reducing allergic responses.
IInfliximab & Adalimumab: Used in autoimmune diseases (e.g., rheumatoid arthritis, Crohn’s disease, psoriasis).
Denosumab: Treats osteoporosis, bone metastases, and hypercalcemia of malignancy.
Rituximab: Indicated for non-Hodgkin lymphoma, chronic lymphocytic leukemia, and some autoimmune conditions.
Omalizumab: Treats allergic asthma and chronic urticaria not controlled by antihistamines.
CAll: Avoid in active infections due to immunosuppressive effects.
Denosumab: Contraindicated in hypocalcemia.
Omalizumab: Contraindicated in patients with a history of severe hypersensitivity to the drug.
R Infliximab & Rituximab: IV infusion.
Adalimumab, Denosumab, & Omalizumab: Subcutaneous (SC) injection.
A Common: Infections (increased risk for all due to immunosuppression).
Infliximab & Adalimumab: Infusion or injection reactions, headache, nausea.
Denosumab: Hypocalcemia, osteonecrosis of the jaw, musculoskeletal pain.
Rituximab: Infusion reactions, cytopenias, risk of progressive multifocal leukoencephalopathy (PML).
Omalizumab: Injection site reactions, headache, rare risk of anaphylaxis.
Corticosteroids, inhaled: Beclomethasone, fluticasone, budesonide
Beclomethasone, fluticasone, budesonide
M interact with receptors in the cytoplasm- pro inflammatory IL, cytokines, chemokines are downregulated whilst antiinflammatory proteins are upregulated.
I: Asthma airway inflammation and shortterm control where B2 agonist is insufficient
C In COPD risk of pneumonia. Risk of paradoxical bronchospasm w wheezing. Systemic corticosteroid has adrenal suppression, osteoporosis and in children growth stunting.
If prescribed Cyp P450 inhibitors, inhibits inhaled corticosteroid metabolism (systemic symptoms)
R Metered-dose Inhaler (MDI) or dry powder inhaler (DPI). Beclamethasone ‘extrafine; is 3.5 times more potent than a standard inhaler, Fluticasone proprionate is 2 times more potent that budesonide
A changes in taste sensation and voice, oral candidiasis.
Corticosteroids, nasal: Beclometasone, mometasone, fluticasone.
Beclometasone, mometasone, fluticasone
Mhave antiinflammatory and vasoconstriction effects. in rhinitis this reduces mucosal inflammation, oedema and secretions.
I Prevention and tx of seasonal or perennial allergic rhinitis where antihistamines are insufficient, first line tx to shrink nasal polyps
C local adverse effects such as nasal irritation, epistaxis, pharyngisitis and change in sense of smell and taste. Occular adverse effects are rare. Systemic adverse effects are less common with mometasone and fluticasone as lesser bioavailability
R Nasal Spray with fixed drug per spray. starting dose 100mcg, once daily for mometasone and fluticasone or 12-hrly for beclometasone
A. DO NOT use in coexisting nasal infection, nasal trauma or surgery, avoid in Pulmonary TB
Corticosteroids, topical: Hydrocortisol, betamethasone, clobetasone
Hydrocortisol, betamethasone, clobetasone
M in skin suppresses inflammation during flares and reduces recurrence but not curative.
I Inflammatory skin conditions incl eczema and psoriasis to tx disease flares or control chronic disease where emollients alone are ineffective
Cdo not use in untreated bacterial, fungal or viral infection as this can worsen spread. Avoid for potent for use on face, genitals and axillae where the skin is thin or flexural
R potent (e.g. hydrocortisone 0.1%–2.5%), moderately potent (e.g. betamethasone valerate 0.025%) potent (e.g. betamethasone valerate 0.1%) or very potent (e.g. clobetasol propionate 0.05%).
A usually limited to site of application- skin thinning, striae, telangiectasia, contact dermatitis, worsening/spreading untreated infection. On face they can cause perioral dermatitis or acne. Withdrawal can occur with skin flare.
Emollients increase efficacy of topical corticosteroids so may allow a lower-potency drug to be used reducing adverse effects. Seperate application by 15 minuets to allow for absorption
Think as finger tip unit- 5mm tube should cover palms and fingers of both hands.
Corticosteroids, systemic: dexamethasone, prednisolone, hydrocortisone.
Dexamethasone, prednisolone, hydrocortisone.
M bind to cytosolic glucocorticoid receptors to regulate gene expression. modifies immune response. Upreg antiinfl. genes and downreg pro-infl. genes
I allergic or inflammatory disorders, anaphylaxis, exacerbations of asthma or COPD; suppression of AutoIx disease; reduce tissure damage in response to infection- bacterial meningitis, COVID19; some cancers or to reduce tumour associated swelling; hormone replacement in adrenal insufficiency or hypopituitarism.
C prescribe with caution in people with infection and children (suppress growth). Caution with NSAIDS as can increase risk of peptic ulceration and GI bleeding. Can increase hypokalaemia when used with B2 agonists, loop or thiazide diuretics. Efficacy can be reduced with cP450 inducers.
R Once-daily corticosteroid treatment should be taken in the morning, to mimic the natural circadian rhythm and reduce insomnia. antiinflammatory activity of hydrocortisone 100mg is approximately equivalent to prednisolone 25mg and dexamethasone 4mg. If PO inappropriate (ibd, anaphylaxis) IV hydrocortisone may be used.
A immunosuppresion risk of infection. metabolic effects of diabetes mellitus and osteoporosis. Increased catbaolism causes proximal muscle weakness and skin thinning. Mood and behavioural changes include insomnia, confusion, psychosis. Hypertension, hypokalaemia, oedema can result from mineralocorticoid actions.
Can suppress ACTH in prolonged tx this can cause adrenal atrophy. If then, corticosteroid is removed, adrenal crisis with CVS collapse may occur.
Can reduce immune response to vaccine.
β2-agonists: Salbutamol, formoterol, salmeterol, indaceterol.
salbutamol, formoterol, salmeterol, indacaterol
M B2 found in s.m of bronchi gut uterus and blood vessels. Stimulation leads to smooth muscle relaxation and bronchodilation. ALSO stimulates Na/K-ATPase pumps on cell membranes can be adverse or benefit as hyperkalaemia treatment
I Asthma (SABA) to relieve bronchospasm LABA added to Inhaled cortiocosteroids. COPD SABA relieves breathlessness and exercise limitation. If SABA inefficient, combine LABA or inhaled cortiocosteroid.
C LABA should only be used in asthma if inhaled corticosteroid part of therapy as LABA without is associated with increased asthma deaths. Caution in CVS disease as tachycardia may provoke angina or arrhythmia especially at high dose.
R inhaled as aerosol metered-dose or dry powder inhalers. In hospital tx regular nebulised therapy is used acutely. Inhalation via spacer also appropriate.
A tachycardia, palpitation, anxiety, tremor, headache. Hypokalaemia and elevated serum lactate at high doses. Promotes glycofenolysis so may cause hyperflycaemia. LABA can cause muscle cramps.
Spacers also reduce oropharyngeal deposition and therefore oral adverse effects.
Dipeptidylpeptidase-4 inhibitors: sitagliptin, linagliptin, alogliptin
sitagliptin, linagliptin, alogliptin
M Incretins such as GLP1 and GIP are released by the intestine throughout the day. Incretins are rapidly inactivated by hyrolysis by the enzymes DPP4. DPP4 inhibitors lower blood glucose by preventing incretin degradation and increasing plasma concentrations of their active forms. Actions are glucose dependents.
Less likely to cause hypoglycaemia than sulphonylurea.
IT2 diabetes,options for combination therapy with metformin if blood glucose not adequateky controlled or monotherapy if metformin is contraindicated/not tolerated.
C contra in people with hypersensitivity to the drug class. DO NOT use in tx of T1 diabetes or ketoacidosis. DO NOT use in pregnancy or breastfeeding. Caution in age > 80 and those with Hx of pancreatitis. Dose reduction advised in moderate to severe renal impairment. Saxagliptin avoid in hepatic impairment. Hypoglycaemia risk increased with coprescription of other antihyperglycaemics.
R PO t.d.s or fixed dose with metformin combination to time with metformin doses.
A GI upset, headache, nasopharyngitis, peripheral oedema. Hypoglycaemia can occur. Small risk of acute pancreatitis so stop drug if persistent abdo pain.
The efficacy of DPP-4 inhibitors is reduced by drugs that elevate blood glucose, e.g. prednisolone, thiazide, and loop diuretics.
no evidence that they reduce the risk of vascular complications.
