PPCS1 Flashcards
Morphine
Powerful analgesic, binds to specific opioid receptors in the brain & spinal cord. Mainly mu - reduces sensation of pain, creates feeling of euphoria & causes sedations. Can cause side effects- rest depression & constipation. Also kappa- lesser degree- pain relief with less euphoric feeling. Can cause dysphoria & hallucinations. Weak effect on delta receptors- smaller role in pain relief- contribute to modulation of mood & emotional responses.
Contra-indications:
Children >1
Resp depression (adults >10rpm children >20 rpm)
Hypotension (systolic >90mmHg)
Head inj with significant impaired level of consciousness (below P/ below gcs 9)
Known hypersensitivity to morphine
10mg/10ml dosage iv/io- 10mg repeat dose after 5 mins 10mg- max dose 20mg slow injection eg 2mg per min diluted with 9ml sodium chloride
IM/sub cut- 10mg undiluted repeat after 60 mins 10mg - max dose 20mg
Oral- 10-20mg - 10mg/5ml repeat dose 60mins 20mg- max dose 40mg
Naloxone
An opioid antagonist- blocks opioid receptors mainly mu receptors- prevents morphine and other opioids binding- quickly reversed effects and the dangerous side effects eg reap depression
Contra-indications- neonates born to opioid addicted mothers
400mcg/1ml
Dose- iv/io/im- 400mcg every 3 mins max dose 4000mcg
Cardiac arrest- 400mcg, then repeat dose 800mcg every 1 minute max dose- 10000 mcg
A short half life so needs to be given repeatedly
Salbutamol
Selective beta 2 adrenoceptor agonist. Stimulates beta 2 receptors in the lungs - bronchodilation, beta 2 receptors in smooth muscle of skeletal muscle arteries- peripheral tremors, beta 2 receptors in the uterus causing relaxation. Small affinity to beta 1 receptors in the heart- mild tachycardia. Reduces mucus production without affecting cillary transport & has moistening effects. Older adults- beta 2 in lungs less sensitive to slb- not as many beta 2 receptors.
5mg/2.5ml nebulised repeat dose every 5 mins, no max dose
Ipratropium bromide
Muscarinic receptor antagonist. Anti-muscarinic. Normally neurotransmitter acetylcholine binds to muscarinic receptors on post-synaptic membrane on bronchiole smooth muscle nerves- causes airways to constrict. IPR binds to receptors and blocks receptors - bronchodilation.
500mcg/2ml - 1 dose
Adrenaline
Stimulates multiple adrenergic receptors throughout the body- alpha 1 & 2 beta 1 & 2 receptors. Can cause competing effects.
Strongly activates alpha 1 primarily in blood vessels- vasoconstriction particularly in skin & peripheral areas - increase blood pressure.
Beta 1 receptors in heart- increases HR & force of each contraction.
Beta 2 in blood vessels supplying skeletal muscles- vasodilation - counteracts alpha 1- increase blood flow & reduce systemic vascular resistance. Beta 2 in airways - bronchodilation- improve breathing.
Alpha 2- inhibits noradrenaline- reduce BP & HR- not strong enough to counteract effects of alpha 1 & beta 1 receptors.
1:1000 1mg- dosage 500mcg (0.5ml) every 5 minutes- no max dose
Glucagon
When blood sugar drops glucagon is released from alpha cells in islets of langahan in the pancreas- travels to liver which stores glucose in form of glycogen. Glucagon signals the liver to break down glycogen back into glucose. Glucose released into blood stream & increases blood sugar levels, giving body energy.
If pt not eaten much the liver may not have much stored glycogen so response of glucagon may be less.
1mg in a vial max dose - 1mg
Contra- pheochromocytona
Should not be given IV due to vomiting
Furosemide
Acts on a part of the kidney ‘Loop of Henley’ - in nephron which controls how much water & sodium the body keeps or gets rid of. Furosemide blocks the reabsorption of sodium & chloride (salt) by preventing them to the absorbed back into the body- forces kidneys to send them out in the urine- when salt excreted in urine water follows it. More salt loss = more water loss -> increased urine output & reduces fluid build up in the body. Furosemide relieves symptoms of fluid overload eg swelling in the legs & lungs, reduces BP.
20mg/2ml - dose is 40mg iv over 2 mins - 1 dose only
Contra- reduced gcs with liver cirrhosis
Carcinogenic shock
Severe renal failure with anuria
Children under 18
Aspirin
Non steroidal anti-inflammatory drug- blocks action of enzyme ‘cyclooxygenase’. Normally COX metabolises aracadonic acid into prostaglandins which cause pain, swelling, redness, pyrexia. Blocking action of cox prevents these symptoms. COX also metabolises aracadonic acid into thromboxains which stimulate platelets to stick together - pre hospital aspirin is used to reduced clot formation with suspected ACS. Blocking of COX 2 is associated with pain relief, swelling & pyrexia. COX 1 blocking prevents thromboxains. Aspirin tends to block COX 1 more than other subtypes.
Ibuprofen
Non-steroidal anti-inflammatory drug. Blocks cyclooxygenase 2 reducing pain, swelling, redness & pyrexia.
Corticosteroids
Hydrocortisone, prednisolone, dexamethasone. Steroid anti-inflammatory drugs. Act like a large bolus of cortisol which adrenal glands on top of the kidneys normally produce. Corticosteroids rapidly converts to lipocortin an antagonist to enzyme phospholipase a2- blocking action. Normally phospholipase metabolises phospholipids from broken & damaged cells creating inflammatory precursor aracadonic acid- further metabolised by lipoxygenase to make leukotrines (bronchoconstriction) & cyclooxygenase to make prostaglandins (pain, swelling, redness, pyrexia) and thromboxains which cause clot formation from platelets.
Corticosteroids reduce effects of inflammation.
Diazepam & midazolam
Benzodiazepines- bind to specific benzodiazepine receptor on the chloride channels of nerve cells. Nerve cells require high level of intracellular voltage for action potential. - seizures = many action potentials. When benzodiazepine binds to receptors it causes the channel to open & let in negatively charged chloride into the cell- lowers voltage (hyperpolarises cell) less likely for action potential & stopping seizures.
Chloephenamine
Antihistamine- histamine 1 receptor antagonist. In allergic response histamine is released from mast cells which bind to histamine 1 receptors causing vasodilation (erythema)-> increases permeability of blood vessels = swelling. Histamine excites nociceptors causes itching. Chlorphenamine blocks histamine 1 receptors- symptoms reduce- doesn’t reduce amount of histamine that is released or already present.
Anti emetics
Ondansatron is 5ht3 receptor antagonist AKA serotonin receptor antagonist. Serotonin receptors are on chemoreceptor trigger zone in medulla oblongata in brain stem. If receptors are stimulated by seretonin, chemoreceptor trigger zone sends signal to muscarinic receptors on vomiting centre in the pons.
Same for metacloprimide- dopamine 2 receptor antagonist also on chemoreceptor trigger zone.
Atropine
Anticholinergic/ cholinergic receptor antagonist.
Cholinergic receptors are stimulated by acetylcholine - muscarinic & nicotinic.
Muscarinic found on smooth muscle eg lungs. Nicotinic found on skeletal muscle.
Cholinergic receptors that are stimulated in the heart cause bradycardia.
Atropine blocks receptors- increasing HR.
Adrenaline vs noradrenaline
Adrenaline is a hormone released from adrenal cortex in adrenal glands.
Noradrenaline is the main neurotransmitter in the sympathetic nervous system.
Both bind to adrenergic receptors eg beta 2 but adrenaline has better effect.
Amiodarone
Class 3 anti-arrhythmic. Blocks potassium channels in cardiac cells- prolonging repolarisation phase. Prolongs action potential duration, increases refractory period of cardiac cells. Helps prevent abnormal electrical signals which cause arrhythmia.
VQ mismatch
VQ ratio = the amount of air reaching the alveoli in 1 minute vs the amount of blood that circulates to the alveoli in 1 minute.
Normal= 4:5= 0.8
Air reduced/blood reduced= mismatch.
Bad ventilation eg 2:5=0.4 -> low VQ mismatch
Bad perfusion eg 4:3= 1.3 -> high VQ mismatch.
Pulmonary Embolism
Clots in the lung often originate from DVT. Well’s criteria to assess DVT/PE
Can travel up the ascending vena cava into right side of the heart then into the lungs.
Clots can also form from AF- blood turbulence & stasis, then moving to the lungs.
A clot in situ increased pressure in pulmonary circulation (pulmonary hypertension)
Can be spotted on ECG- peaked P waves
S1,Q3,T3 presentation.
The area of the lung affected will not be able to participate in gaseous exchange= hypoxic.
Bronchiectasis
A chronic lung condition- airways damaged & permanently widened from ongoing inflammation, infection or underlying conditions which cause damage to the walls of the airways (emphysema)
Over time= thickening & scarring of airway walls
Fibrosis reduces elasticity - harder to clear mucus effectively -> widening damage.
Lungs lose normal shape- widening bronchi- traps mucus - persistent infections as bacteria can thrive.
As disease progresses, more tissue is damaged-> gaseous exchange is impaired- reduced surface area & thickened alveoli walls = less oxygen can enter blood -> SOB, reduced exercise tolerance.
Asthma
Chronic resp condition characterised by hypersensitivity in the airways- overreact to triggers leading to inflammation, swelling & bronchoconstriction = DIB.
Intrinsic - non allergic triggers eg cold air, exercise, resp infections, stress
Extrinsic- allergens, eg pollen, dust mites, animal dander & certain foods- provokes immune response.
Antigen provokes adaptive immune response- reacts with immunoglobulin on mast cells causes release of histimine (increase blood vessel permeability), kinins (inflammatory mediators & cause vasodilation& smooth muscle contraction- bronchoconstriction) & prostoglandins (vasoconstriction, lower BP & reduce perfusion to the lungs)
Irritation from inflammation- stimulates vagus nerve from coughing = reflex of bronchoconstriction & bronchospasm - air becomes stuck.
Forced expiration causes bronchioles to collapse.
Residual volume starts to increase - difficulty taking deep breath in= hypoxia, arrhythmias & CNS depression.
Over time demand for more oxygen leads to metabolic & respiratory acidosis
Hypoxia leads to vasoconstriction in pulmonary vessels-> increases work load to right side of the heart.
Emphysema
Cigarette smoke & pollution causes a release of neutrophils (type of blood cell).
Neutrophils release enzyme elastase which break down elastin (protein which gives airway elasticity). Alpha 1 antitripsin inhibits elastase, cigarette smoke inhibits alpha 1 antitripsin.
Emphysema pts have increased lung compliance making it easy to breath in but an active process to breath out due to lack of elastic recoil. Breathe out through pursed lips to maintain positive pressure in lungs to aid gaseous exchange & stop the lungs from collapsing.
Chronic bronchitis
Cigarette smoke causes constant irritation in the lungs causing inflammation & a reduction in airway aperture. Pts cough a lot leading to stimulation of the vagus nerve leading to further bronchoconstriction.
To try & create more oxygen carrying capabilities the kidneys secrete more erythropoietin to encourage the bone marrow to produce more red blood cells = polycythaemia, engorges circulation leading to bloated plethric look.
Circulation sluggish - longer to replenish oxygen, pt looks cyanosed.
COPD
Umbrella term- emphysema, chronic bronchitis, bronchiectasis.
Problem with gas exchange, VQ mismatch, reduced surface area for gas exchange, mucus build up from hyperplasia & hypertrophy of goblet cells, increased diffusion distance for gas exchange, hypoxic drive, pulmonary fibrosis, damage to cilia, airway inflammation & irritation, cough, hypoxia- reflex vasoconstriction, excessive coughing- reflex bronchoconstriction.
