256 COURTNEY > SDLP Qs > Flashcards
SDLP Qs Flashcards
Selectivity
Narrowness of the drugs range of action on particular Receptors, Cellular Processes and Tissues
Potency
Amount required for a given effect
More potent the drug, the lower the dose required
Specificity
Referring to the repationship between the chemical structure of the drug and its Pharmacological actions within the body.
Alkaloids
Organic nitrogen containing compounds
Bitter tasting - include caffeine, nicotine and morphine
Carbohydrates
Organic compounds containing Carbon, Hydrogen and Oxygen
Include Inulin - used in kidney function tests
Glycosides
Typew of Carbohydrates
Includes digoxin
Hydrocarbons
Found in Plants
Include Fats, Waxes and oils
Phenols
Active Plant Compounds
Compound containing a hydroxel group linked to a benzene ring
Include- aspirin or flavouring agents
Steroids
Organic compounds containing 4 carbon atom rings
Include oestrogenic hormones for contraception
Oils
Viscous liquids derived from petroleum (high in hydrocarbon content)
Can be flammable
Includes respiratory medications
Chemical names
Description of the drugs chemical/ molecular composition.
Official name not used by public.
Often too long and not understood for selling purposes
Generic names
Suggested by manufacturer and approved by drug regulating authority, what nurses look up in mims
Derived from chemical name but complies with drug group name (ie penicillins etc)
Trade names
Particular brand of each drug
Name is trade marked by particular company
Advertising is carried out in this stage
4 categoriesof drug classification
There are several but the main 3 are: Clinical indication The body system The mechanism of action (Pharmacodynamics and pharmacokinetics)
Schedule 1
Blank for future use
Classifying herbal/natural remedies
Schedual 2
Pharmacy Only
Most cough/cold suppressants
Antihistamines
Schedual 3
Pharmacist Only
Asthma aerosols
Antivirals (cold sores)
Schedual 4
Prescription Only
Antibiotics
Hormonal contraceptives
Injections
Antidepressants
Schedual 5
Caution
Household poisons
Most head lice lotions
Schedual 6
Posion
Household Pesticides and solvents
Schedual 7
Dangerous Poison
Commercial pesticides and solvents (varying in strength)
Arsenic solutions
Schedual 8
Controlled Drug
Opioids (morphine, methadone, codeine, cocaine, ketamine) and cannabis extracts
Schedual 9
Prohibited Substances
Heroin and most recreational drugs (including alcohol and tobacco)
Pharmacokinetics
Branch of pharmacology concerned with the movement of drugs within the body (absorption, distribution and elimination)
Absorption
Process by which unchanged drug proceeds from site of admin into the blood.
All sites use this apart from IV
Dissolution
(Process of dissolving) Process by which a drug goes into a solution and becomes available for absorption
Diffusion
Involves the movement of a substance from a region of high concentration to lower concentration until equilibrium is established either sode of the membrane
Active transport
Movement of a substance across a cell membrane into a region of higher concentration, assisted by enzymes and requires energy
Bioavailability
The proportion of the administered dose that reaches the systemic circulation intact
Distribution
Th process of reversible transfer of a drug between one location and another (one of which is usually the blood)
Metabolism
Breaking down a substance to yeild energy
Elimination
Irreversible loss of a drug from the site of measurment by metabolism and excretion
Therapeutic Range
The range of concentration having a high probability of producing the desired therapeutic effect and low probability of producing adverse effects
Clearance
Volume of plasma that gets filtered of a drug per unit and time
Includes renal excretion and filtration
List and discuss the factors that affect the rate of drug absorption
N, Bf, S, F
1- NATURE OF THE ABSORBING MEMBRANE
the more vast the surface area = the
greater the drug absorption + the more
rapid its effects
2- BLOOD FLOW
rich bs = quicker absorption, lower =
delayed absorption
3- SOLUBILITY OF DRUG
drugs that are able to be placed in a
solution increased the solubility of that
drug
4- FORMULATION
process where different chemical
substances are combined to produce
final product (eneteric coating)
LIST the routes of medication administration and discuss the advantages and disadvantages of each
Oral/enteral - (admin via mouth/anus &
includes the GI tract)
Ad= most comm used, safe + convienient
Dis= slow, unreliable (chg in GI tract)
Subcutaneous - (admin beneath skin into
subcut fatty layer or dermis)
Ad= can prov, sustained effect
Dis= slow, only 4 non-irritating agents
Intramuscular - (injec direct into muscle)
Ad= rapid due to great tissue blood flow
Dis= may not be equal - obese/ emaciated
Intravenous - (injection directly into veins)
Ad= most rapid route, immed response
Dis= adverse effects (admin slowly)
Intrathecal - (directly into space bt spinal cord
& subarachnoid spance)
Ad= bypases BBB
Dis= absorption is slow
Epidural - (admin within spinal cord/dura mat)
Ad= rapid pain relief & dosnt knock pt out
Dis= if left 2 long, cant be done + weakness
Intraosseous - (injected into bone marrow)
Ad= if iv access not avail. Entry pt in2 BS
Dis= pain, fractures from long term use
Inhalation - (admin locally to ensure normal
exchange of O2 and CO2 occurs)
Ad= fast, lrg surface area/lungs, alveolar
membrane is thin (rich capil network)
Dis= only produces a local effect
Topical - (applied topically to skin, mucus
membranes)
Ad= rapid absorption
Dis= only produces local affect
Discuss the 2 natural barriers that prevent medication from crossing into affected areas
BBB = protects brain from any potentially toxic/ damaging substances as well as pathogens. Prevents diffusion of ions and water soluble compounds from blood to brain. Does allow lipid soluble drugs such as general anasthetics into the brain and CSF. Conditions such as meningitis can be serious as this interferes with this protective process.
Placental Barrier = seperates the blood vessels from the mother and the fetus. However it does not provide complete protection. Protective mechanisms - placental enzymes that metabolise substances, inactivating them as they travel towards the embryo from maternal circulation.
List the factos that may impact on drug metabolism
G, Ef, A+G, Ds, Hc
Genetics
Environmental Factors
(drugs, diet, alcohol, smoking)
Age and Gender
Disease States
Hormonal Changes (pregnancy)Define Renal excretion
The volume of the plasma that gets filtered of a drug per unti and time.
(Influenced by GF, TS & TR)
Facilitates transfer of drugs from blood to urine, whereas unbound/free drugs (protein bound substances) cannot be filtered hence they are reabsorbed.
Biliary Excretion
Drugs collected/excreted via the Bile
Which is delivered to the duodenum and removed in the in the faeces
Pulmonary excretion
Excreting drugs via the lungs
Depends on the rate and depth of respiration
Used in alcohol breath tests
Exercises that promote deep breathing (increasing cardiac output and increaidng blood flow to the lungs) is advised.
Excretion via the sweat and saliva
Relatively unimportant because this process is slow and represents only a minor proportion of total excretion.
May be responsible for adverse effects such as dermatitis and skin rashes
Excretion via Breats Milk
Drugs that cross the epithelium of the mammary glands and are excreted in breast milk. There is a risk of infant exposure that depends on the maternal plasma drug concentration and the amount ingested by the infant.
Can cause failure to thrive and adverse effects
Identify the 4 levels of evidence in nursing
1- meta analysis = evidence from systemic review of all relevant randomised controlled clinical trials
2- evidence from at least 1 properly designed randomly controlled clinical trial
3- evidence from well-designed non-randomised trials
4- evidence frok case series
Describe two reasons why new drugs become available and why existing drugs may become unavailable
New - bcos of the new chemical industries & pharmacological techniques developed; meaning that new drugs dont have to just be from natural sources
Exsisting - bcos better drugs are being developed,
because (in comparison to newer drugs) are generally less effective and more dangerous, become obsolete (not produced),
when a deficiency is identified in the drugs quality, safety or efficiency
Disease may become less prevalent which can be problematic due to pts who have been on these for a while and of whom are intolerant or unresponsive to other drugs (+tolerance)
List the 6 actions in the safe administration of medication (6 steps)
Apn + pdh 6R Ed+rac iaptdt (ae) Essom Ep+coc
1 - properly assess pts needs & past drug Hx
2 - use the 6 rights
3 - ensure documentation & records are correct
4 - identify any problems to drug therapy
(adverse reactions)
5 - ensure safe storage of the medications
6 - educating pt about meds and ensuring
continuity of care
List the 4 sections that must be included on an authorised prescription
1- Superscription = date and pt information
2- Inscription = specifying ingredients + drug
info
3- Subscription = directions to pharmacist (ie
Instructions on the formula or how
much to give of a particular drug)
4- Signiture = instructions how to admin and
signiture
Abbreveations bd IV prn g mane nocte tds IM
bd - twice daily IV - intravenous (into a vein) prn - as/when required g - gram (unit of measurement) mane - morning nocte - night tds - 3 times a day IM - intramuscular (into muscle)
Eneteric coating is used to: (4 reasons)
Pdocsdbgs
Pdodbirti
Pn+vibdis
Pdaod
1- prevent decomposition of chemically
sensitive drugs by the gastric secretions
2- prevent dilution (less concentrated) of the
drug before it reaches the intestine
3- prevent N+V induced by the effect of the
drug in the stomach
4- to provide delayed action of the drug
Describe the 3 methods by which therapeutic drug monitoring is carried out
1- observing pts progress (measuring levels of
drug in th body to ensure right dosage)
2- observing any changes in signs/symptoms
(Monitoring BP when hypertensives admin)
3- observing/watching for any adverse drug
reactions (checking WBC count in cancer
pts - cytotoxic therapy)
List the common ingredients found in Antacids and the possible adverse reactions associated
Antacids are chemical compounds that buffer/neutralize hydrochloric acid in the stomach thereby increasing pH.
Ingredients - aluminum, hydroxide, calcium, carbonate, magnesium salts, and sodium bicarbonate
Reactions- beltching, flatulence, constipation, abdominal distension, metabolic alkalosis, diarrhoea, chalky taste, feacal impaction
Discuss the mechanism of action of Proton Pump Inhibitors (PPI)
And discuss why the duration of their pharmacological effects are longer than their plasma half lives
End in “azole” (Omeprazole)
PPI suppress gastric acid secretions (reduce production of acid) by blocking the enzyme in the wall of the stomach that produces acid. The reduction of acid prevents ulcers and allows adequate time for healing.
When drug molecules bind to proton pump (hydrogen, potassium ATPase enzyme system), the final step of acid production is stopped.
In regards to the drugs effects extending its plasma half life = the irreversible inhibitory action on the enzyme system in the wall of the stomach (H, P, ATPase) explains why it excedes its half life. When admin is ceased, acid secretion is restored by synthesizing new H,P,ATPase
Discuss the areas of the brain that control the need to vomit and discuss the stimuli that increase nausea (that induce vomiting)
Vomiting is the coordinated response between 2 areas:
1- the sensory nerve cells of the 4th
ventricle of the brain (CTZ-
chemoreceptor trigger zone)
2- the vomiting centre (emetic cntre)
located in the medulla (recieves info
from the CTZ & organs such as the GI
tract)
The CTZ itself cannot induce vomiting, but is stimulated by smells, strong emotion, severe pain, increased ICP, Motion sickness, toxic reactions to drugs, GI disease, radiation treatments and chemo.
Discuss the action of Metoclopramide in N+V, and explain why some ppl may experience extrapyramidal adverse effects
Metoclopramide has both Central and Peripheral actions.
Centrally- it blocks dopamine receptors in the
CTZ
Peripherally- it accelerates gastric emptying, reduced reflux from the duodenum and stomach into the oesophagus.
They enhance motility (filling/emptying or moving of stomach contents) of the upper GI tract.
Extrapyramidal effects = could occur due to its possible interaction with many CNS antidepressants, causing serious drug reactions resulting in parkinsonian effects
Discuss the mechanisms of action for the 4 different types of laxatives
(BL, FSA, SL, OL)
1- Bulk Laxatives = absorb water and increase
the volume, bulk and moisture of non-
absorbable intestinal contents thereby
distending the bowel & initiating reflex bowel
activity
2- Faecal Softening Agents = disperse wetting
agents that facilitate mixture of water and
fatty substances within the faecal mass
producing soft faeces
3- Stimulated Laxatives = promote
accumulation of water and increase
peristalsis in the colon by irritating the
sensory nerve endings in the mucosa
4- Osmotic Laxatives = are not absorbed, but
exert an osmotic effect by increasing the
volume of fluid in the lumen
What potential problems are associated woth ppl self medicating with OTC drugs?
Although considered relatively safe, issues=
Self diagnosis (mask condit & delay treatm)
Adverse Affects
Drug Interactions (capable of producing both
desired and undesirable
effects; 2 much = toxicity)
Labelling (confusing or 2 small =unsafe use)
Potency/Efficiency (more potent=less requir)
Combination (drugs cont subst not necessary
for pts symptoms)
What are the potential risks for ppl taking complamentry or alternative therapies?
Not backed up with Evidence Not clear in regards to safety/efficiency Can be more of a Placebo effect Economic harm (wasting money) Adverse reactions Delay in obtaining effective treatment Contaminated products False/misleading advertising
Factors that affect airway efficiency
Bronchoconstriction (narrowing of airway) Bronchodilation (widening of airway) Mucociliary Transport (mucokinesis)
Obstruction, increased mucus production/ phlegm, inflammation, immune/allergic responses, trauma, muscle spasms of the trachea/bronchi etc
Droplet sizes and area affected and uses
LARGE - >40um, upper airway, keeps area
(nose + trachea) moist & loosens
secretions
MEDIUM - 8-15um, deposited in bronchi +
bronchiols
SMALL - 2-4um, alveolar ducts/sacs, pts with
tiny fibres or asbestos dust in lungs
VERY SML- 0-6um, unlikely to be deposited,
will most likely be exhaled.
What causes Oxygen Toxicity and what are the signs and symptoms?
OT - is an inflammatory response brought on by prolonged exposure to 80-100% oxygen.
Can cause destruction of the alveolar-capillary membranes of the respiratory tract.
Symptoms = Substernal distress (ache/burning
sensation behind sternum)
Respiratory distress with
decreased vital capacity
(decreased max posbl exhal)
N+V, restlessness, tremours,
twitching, paraesthesias (pins
+ needles) convulsions, dry
hacking cough
Outline the steps involved in administrating respiratory medications via an inhaler correctly
1- take cap off, hold puffer upright +shake well
2- breathe out slowly & gently (without
emptying lungs)
3- place mouthpiece between teeth without
biting and close lips around
4- tilt head back slightly
5- while breathing in slowly, press down on
cannister
6- continue to breath deeply
7- take puffer away and hold breath for as long
as possible
8- breathe out gently
9- restore cap
(Don’t point inhaler towards cheek or roof of mouth)
Define the following
Expectorants, Mucolytics, & Cough
Suppressants
Expectorants - drugs that aid in the removal
(swallowing or spitting out) of sputum
phlegm from the bronchial passages
(chronic bronchitis)
Mucolytics - drugs that help disintegrate
mucus, facilitating removal of mucus/
other exudates from lung, bronchi,
trachea by drainage, coughing, spitting,
swallowing etc (cystic fibrosis)
Cough Suppressants - are used for non
productive (dry/hacking) coughs that are
inadequately controller by OTC meds.
Objective is to decrease intensity and
frequency of cough, yet permit adequate
drainage/ elimination of secretions/
exudates.
List the 3 classes of hormones that the adrenal glands are responsible for synthesising and discuss their primary functions
Glucocorticoids- (cortisone) have important
metabolic, anti inflammatory and
immunosuppressant effects (useful in
preventing asthma- corticosteroid not a
bronchodilator)
Corticosteroids are the chemically modified
drugs to resemble the bodys natural
glucocorticoids (prednisone/prednisolone)
Mineralcorticoid - (aldosterone) help maintain
blood volume, promote retentionI of
sodium and water and increaee urinary
secretion of potassium and hydrogen
ions (affect electrolyte levels and
homeostasis)
Androgens- are the metabolic precursors to the
sex hormones
Describe the mechanism of the anti-inflammatory and immunosuppressant actions of glucocorticoids
Anti-inflamm = decrease all vascular and
cellular events in an inflammatory response
(decreasing neutrophils and release of
proteolytic enzymes)
Immunos = decrease number of components
involved in an immune/allergic response in
the blood (# of lymphocytes, plasma cells,
eosinophils, and T + B lymphocytes,
macrophages, monocytes)
Expain the advantages of local admin of glucocorticoids and four specialised agent, formulations and uses
Local Admin = allows lower doese to be used
Less systemic adverse effects
& more rapid/direct actions
4 Agents = topical, inhaled, injected & oral.
Formulations = prednisolone,
methylprednisolone,
betamethasone,
dexamethasone
What is Glyceryl Trinitrate and what additional instructions should be given regarding their use?
GT = very effective drug used in the treatment of angina bcos of their dilating effects on veins and arteries.
They decrease venous return which aids in decreasing myocardial oxygen demand.
Additional Instructions = they are rapidly absorbed/metabolised, can cause drug interactions (alcohol, anti hypertensives, and vasodilators), result in decreased BP when sitting, can cause (due to vasodilation) headaches, dizziness, orthostatic hypotension, N+V, agitation, facial flushing, palpitations, dry mouth, rash and blurred vision.
What is the Renin-angiotensin-aldosterone system? (RAAS)
The RAAS is responsible for the regulation of BP by either increasing or decreasing the blood volume theough modulation of the renal function (ie kidneys) (neg feedback model)
Abnormal activation = HPoTN, CVD
Major effector molecules = renin, angiotensin II and the mineral corticoid Aldosterone.
When blood flow to the kidneys decreases, renal arterial pressure also decreases.
This causes a release in Renin into circulation.
Which initiates the transformation of angiotensin to form AT1 (weak vasoconstrictor)
This can then be converted by the ACE enzyme to AT2 (potent vasoconstrictor).
By constricting arteriols, this increases peripheral resistance in which increases BP.
AT2 also acts on the adrenal cortex to stimulate the release/secretion of Aldosterone, which promotes reabsorption of sodium in the kidneys and excretion of potassium. The increased sodiuk increases osmotic pressure in the plasma = release of ADH = increased reabsorption of water from renal tubules = increase in BP.
AT2 has vascular effects by decreasing sensitivity and impaires insulin secretion (increasing risk of metabolic syndrome and type two diabetes)
What 4 drugs affect the RAAS system and how does each group work?
Renin Inhibitors -
Inhibits the development of renin that is
responsible for the conversion of
angiotensinogen to AT1 (blocks receptor
action)
ACE Inhibitors -
(Angiotensin receptor enzyme) blocks ACE
necessary for converting AT1 - 2.
ARBs -
(Angiotensin receptor blockers) inhibit AT2
(block vasoconstrictor effects rather than
broader effects of ACE Inhibitors)
Aldosterone Receptor Antagonists-
Block aldosterone production & secretion.
List the anti-atherosclerotic (agents that prevent clogging of arteries/ hardening of vessels) properties of HMG-CoA reducase inhibitors (statins) used in reducing LDL (low density lipoproteins)
Have beneficial effects on endothelial funct
Modify inflammatory responses
Decrease platelet aggregability (clumping that
could cause thrombus/clot)
Modifies thrombus/clot formation
Stabalises anthersclerotic plaques
Decreases smth muscle migration and
proliferation
Increases fibrinolytic activity (prevents blood
clots from growing/bec. problematic)
Decreases markers in inflammation
Decreases coronary heart disease risk
Define the 4 serious side effects of ‘statin’ medications related to muscle toxicity.
Mylagia -
Pain/discomfort in proximal muscles
Characteristics - ADR, dose related,
& reversible.
Myopathy -
Disease/pain in muscle tissue r/t elevated
creatine kinase levels
Characteristics - dose related, affects
proximal limbs, muscle fibre necrosis
Myositis -
Inflammation & degeneration of muscle
tissue/ weakness with/without elevated CK
levels
Characteristics - dose related, variation in
muscle fibre size and inflamm
Rhabdomyolysis -
Destruction of muscle cells and presence of
myoglobin in urine, muscle pain and
swelling + elevated CK levels
Characteristics - rare, acute renal failure
may occur & can be fatal
Discuss the current evidence of the effectiveness of omega 3 fatty acids in the treatment of hypertriglyceridaemia (an excess of triglycerides in the blood)
Consumption of these oils decreases the incidence of ischemic heart disease and sudden death from myocardial infarction (also prolongs life of MI survivors)
Can decrease BP and HR, plus platelet aggregation and antidysrhythmic effects (preventing/relieving irregularities in the force and rhythm of the heart)
Can also decrease the incidence in coronary heart disease.
Explain the roles that Insulin and Glycagon have in the body
Insulin - is the bodys main fuel storage
hormone. It is secreted in response to high
glucose levels in the blood (hyperglycemia).
It ensures tissues have sufficient chemical
substrates for energy, storage and repair.
There is always a low basal rate circulating
but is released due to increased stimuli.
(Facilitates removal of glucose frm blood &
promotes storage if not needed)
Glucagon - is secreted in reponse to low BSL
(hypoglycemia) and is named ‘anti-insulin’.
Acts to stimulate hepatic glycogenolysis
(breakdown of glycogen) and
gluconeogenisis (generation of new glucose
from non carb molecules such as aa and
glycerol portion of fats).
Low BSL = glucagon is released
High BSL = insulin is released (stimulates
glucose uptake and inhibits
gluconeogenesis and further release of
glucagon)
List the signs and symptoms of Hypoglycemia and Hyperglycemia and list how to treat each condition
Hypo = (low BSL) confusion, dizziness, shaky,
hunger, headaches, irritability,
pounding heart, racing pulse, pale,
sweaty, weak
Treatment - eat something sugary, &
then follow it up with something more
slowly absorbed such as a complex
carb. In extreme cases, glucagon can
be admin via pen/injection.
Hyper = (high BSL) high levels of sugar in urine
(waste product), frequent urination,
increased thirst, fruity smelling
breathe (ketoacidosis).
Treatment - take insulin dose, or
exercise to lower BSL. Monitor and
check urin for ketone levels ane
decrease food intake.
Why are benzodiazepines preferred over older hypnotic agents?
(More advantages than older agents)
Decreased fatality rates following acute toxicity and overdose
Lower potential for abuse
More favourable adverse effects
Fewer potentially serious drug interactions
And increased availability
Describe the manifestation and management of benzodiazepine overdose
Manifests as CNS depression
Ranging from confusion & drowsiness theough to coma, hypotonia (low muscle tone), HYPoTN, and respiratory depression.
Overdose is not usually life threatening, unless multiple other drugs have been taken.
Supprtive treatment is needed (maintenance of airway and oxygen, monitoring of vital signs and promoting diuresis by admin IV fluids. Hypotension will need monitoring
Describe the 4 types of seizures and give examples of the appropriate antiepileptic agents
Grand Mal/ Generalized Tonic/Clonic Seizures
Characterised by an aura (sense of seizure
coming/preparation), sudden loss of
consciousness & motor control.
Tonic - spasm & increased muscle tone +
stiffening. Clonic - muscular contractions &
rapid jerking, decreased awareness.
Drugs- phenytoin (dec excitability of CNS) +
Barbiturates for sedation
Petit Mal/ Absence Seizures (asian child)
Temporary lapses in consciousness that
lasts a few seconds. Dosnt involve muscle
movements. Pt gets spaced out look.
Drugs- agent that will alter sodium calcium.
channels and indirectly increase
GABA.
Partial Seizures (simp or comp) (child couch)
Alterations in consciousness, unusual
stereotyped movement, changes in
temperament, confusion, feelings of
unreality & can evolve into generalised
grand mal. Can exhibit apathy/lethargy.
Drugs- carbamazepine, phenytoin, sodium
valproate
Myoclonic Seizures (girl on bed)
Myo= muscle, clonic= contrac/jerking
Bilaterally symmetrical muscle jerks
(twitches or tics). More like grand mal, pt
can be unconscious.
Drugs- phenytoin, clonazepam, primidone +
sodium valproate.
Status epilepticus
Permanant state (seizures dont stop for pt to rest or recover between episodes)
List the characteristics considerd desirable in the ideal antiepileptic drug
Highly effective but low incidence of toxicity.
Effective against more than 1 type of seizure or
for mixed seizures.
Long acting
Non sedating
Inexpensive (long term use)
Does not result in development of tolerance.
What are the following drugs used for?
Antiepileptic/ anticonvulsants
Antipsychotics
Antimanics
Antidepressants
Antiepileptic/ anticonvulsants
Seizures
Antipsychotics
(Typical and atypical) psychotic conditions.
Antimanics
Bipolar (lithium)
Antidepressants
Depression (TCAs, SSRIs, MAOIs)Define the extrapyramidal conditionsand their possible treatments
Akathisia Dystonia Drug-Induced Parkinsonism Tardive Dyskinesia Neuroleptic Malignant Syndrome
Akathisia
Motor restlessness, pt unable to sit/stand
still, feels urgent need to move, pace, rock
or tap foot.
Treatment- decrease dose or switch to
another atypical med. can also
admin anti-parkinson drug.
Dystonia
Muscle spasms (+ locked muscles) of the
face, tongue, neck, jaw, or hands.
Hyoerextension of neck and trunk or
arching of back.
Treatment- decrease dose, switch to
another med, admin
benztropine IM or IV. Is an
emergency situation as can
cause blocked airway.
Drug-Induced Parkinsonism
Similar to parkinson’s disease; shuffling
gate, drooling, tremours, increased rigidity.
Can include fine movements of fingers.
Treatment- admin anti-parkinson drug, or
switch to a newer atypcial agent.
Tardive Dyskinesia
Oral or facial dyskinesias (abnormal
involuntary muscle movements around the
mouth, lip smacking, darting tounge,
constant chewing movement or tics) can be
irreversible- prevention is crucial. Pt is
aware & can also be axial (trunk + limbs).
Treatment- decrease dose or cease
neuroleptic asap
Neuroleptic Malignant Syndrome
Rare but potentially fatal adverse effect for
pts on typical antipsychotics. Can occur
months/years after starting treatment but
then progresses rapidly over 1-3 days.
Involved increased temp, muscle rigidity,
altered LOC, and impaired autonomic
homeostasis (increased BP, fever, sweating
etc)
Treatment- req withdrawal from drug,
hydration and sometimes a
dopamine agonist plus another
agent to control muscle
spasms.
What is seratonin syndrome and what drugs can this occur with?
SS- excessive stimulation of the 5-HT (seratonin) receptors by seratonergic drugs.
Characterized by changes in mental state (confusion, delirium, hypomania), GI tract effects (diarrhoea), neuromuscular hyperactivity, autonomic instability, sweating, fever, shivering.
Occurs commonly when MAOIs are combined with SSRIs. (Must be stopped immediately as can be fatal)
Can require hospitalization for CVS or temp stabilization, sedation, and hydration. (Seratonin antagonists admin)
Explain what a Tyramine Reaction is and what education would be necessary in regards to the pts meds and foods to avoid?
TR- reaction from eating certain food whilst on
an MAOI in which causes Headaches, N
+V, Palpitations & High BP.
Tyramine is an aa essential in the regulation of BP. But is found in many foods such as;
Aged cheeses
Aged/cured/pickeled Meats/fish
Veggies - over ripe avos, broad beans
Fruit - figs, banana & raisins
Alcoholic beverages
These foods should be avoided at all costs or eaten in very small amounts when fresh.
Why is the amount of Caffeine consumed by a pt a concern?
Name 3 illnesses/conditions that may be induced/ exacerbated by chronic consumption of caffeine.
Caffeine is a natural substance found in our bodys -in the form of methylxanthine- that is a metabolite base used in adrenaline.
In increased amounts consumed, may increase awareness, but may also induce insomnia and heart dysthymias.
In large amounts, caffeine can mimic certain neurotransmitters (increase CaMP Levels) and can block neuro modulators.
Can also effects/stimulate the CNS system in which can cause effects on the respiratory, CV and musculoskeletal systems.
3 conditions = insomnia, atrial fibrillation and hypertension (+ ulcers)
Define Drug Misuse and Drug Abuse
Drug Misuse
Is when the amount taken is causing harm
to the individual, family or wider
community.
Drug Abuse
Is the self admin of a drug in chronically
excessive quantities, in a manner that
deviates from the approved patterns.
Results in both physical and psychological
harm. Generally obtained in illegal ways.
Define (in relation to Tolerance)
Psychological dependence
Physical dependence
Addiction
Tolerance
Psychological dependence
(In our brain)
Behavioral pattern characterized by out of
control cravings for the pleasure of the
drugs effects. Denial and excessive drug
use and continual use despite personal
social/legal situations
Physical dependence
(Body needs the drug)
Intense disturbances when administration of
the drug ceases (withdrawal syndrome).
Makes us physically unwell.
Addiction
(Obsession with obtaining the drug)
Behavioral pattern pf drug use
characterized by an overwhelming
involvement with the procurement and use
of that drug. Can cause pt to relapse into
dependance.
Tolerance
(Affects decrease, so need more to acheive
same affect)
Physical state in which repeated use/doses
causes decreased effects in which dosages
need to be increased to maintain the same
effects (long term use)
Signs and symptoms of drug intoxication;
Cannabis Cocaine Opioids Barbiturates & general CNS depressants Amphetamines Hallucinogenic agents
Cannabis (depressant)
Tachycardia & postural hypotension
Red eyes, distortions of perception +
memory, dry mouth & throat, panic,
disorientation and hyperemesis (severe
prolonged vomiting)
Cocaine (stimulant)
Increases stimulation, euphoria, increased
BP & HR, anorexia, insomnia, agitation. In
overdose- increased temp, hallucinations,
seizures, and death.
Opioids (depressant)
Decreased BP & respirations, hypercapnia
(increased CO2 in blood), fixed/pinpoint
pupils, coma, pulmonary oedema,
hypothermia and rhabdomyolysis
(destruction of muscle cells)
Barbiturates & general CNS depressants
Decrease BP & respirations, ataxia, slurred
speech, confusion, decreased tendon
reflexes, sleepiness, coma and shock
Amphetamines & MDMA/ecstasy (stimulants)
Increased BP, tachycardia, other cardiac
arrhythmias, hyperactive tendon reflexes,
dilated pupils (reactive to light),
perspiration, shallow respirations,
circulatory collapse, hallucinations,
paranoid euphoria, and delirium.
Hallucinogenic agents (both stim + depress)
Increased BP, hyperactive tendon reflexes,
piloerection, perspiration, pupils dilated
(reactive to light), anxiety, distortion of
body image and perception, delusions and
hallucinations.
What are the pharmacological effects that ethanol (alcohol) has on the CNS, CV, & GI systems and then name 3 major drug interactions associated
CNS- depressant; inhibits transmission of
nerve impulses at synapses.
CV- depressant; of vascular neurons (causing
flushing) and rapid heat loss. Chronic use=
HoTN, arrhythmias and cardiomyopathy
(disease of heart muscle).
GI- stimulant; stimulates secretions of gastric
juices rich in acid and of saliva. Chronic
use= nutritional deficiencies, gastritis,
pancreatitis and hepatic cellular damage.
3 major drug interactions = ethanol interacts
with many prescription and OTC drugs
such as antidepressants, antipsychotics,
antianxiety, antihistamines, opioid
analgesics, warfarin, anticholinergics and
caffeine.
