Miidterm 2 Flashcards
1
Q
Crystalloids
A
- contain water plus: electrolytes (e.g. Na+, K+, Cl-) and small molecules (e.g. glucose, lactate)
- do not contain proteins/large molecules (colloids)
- to treat dehydration- volume loss or maintenance
- used as replacement/maintenance fluids: compensate for insensible fluid losses (e.g. NS), to replace fluids (e.g. NS), to manage specific fluid and electrolyte disturbances (e.g. Ringers lactate), promote urinary flow (e.g. NS), expand plasma volume (e.g. 3% NaCl)
2
Q
Examples of crystalloids
A
- Normal saline (0.9% sodium chloride)- only fluid used with administration of blood cell products
- half normal saline (0.45% sodium chloride)
- hypertonic saline (3% sodium chloride)
- Lactated Ringer’s
- D5W
- Normosol/Plasmalyte
3
Q
Crystalloids: Indications
A
- acute liver failure
- acute nephrosis
- burns
- hypovolemic shock
- renal dialysis
- many other conditions
4
Q
Crystalloids: Adverse Effects
A
- edema- peripheral or pulmonary (fluid overload)
- many dilute plasma proteins
- effects may be short-lived
- many other effects
5
Q
Colloids
A
- increase COP (colloid osmotic pressure)
- move fluid from interstitial compartment to plasma compartment
- “plasma volume expanders”- restore BP, for situations with low BP
- initiate diuresis e.g. removal ascites in patients with portal hypertension
6
Q
Examples of colloids
A
- dextran 40 or 70 (big glucose polymers)
- hetastarch/hydroxyethyl starch (HES)- synthetic, derived for cornstarch
- modified gelatin
- albumin (from human donors)- plasma protein in blood
7
Q
Colloids: indications
A
- trauma
- burns
- sepsis
- hypovolemic shock- low volume, tissues cannot be perfused
8
Q
Colloid vs crystalloids
A
- no clear advantage of one over the other
- debate is ongoing
- colloids more expensive
9
Q
Colloid: Adverse effects
A
- usually safe- concerns in renal failure
- may cause altered coagulation- bleeding
- no oxygen-carrying capacity
10
Q
Blood and blood products
A
- most expensive and least available fluid because they require human donors
- whole blood
- RBC products carry oxygen
- increase supply of various products e.g. clotting factors from plasma
- platelets- not typically from whole blood donation, useful for people that cannot make enough platelets
11
Q
Blood products: Indications
A
- packed RBCs and whole blood: to increase oxygen-carrying capacity, anemia, substantial hemoglobin deficits, blood loss > 25% of total blood volume
- fresh frozen plasma (FFP): can be stored for long time when frozen, increase clotting factor levels in clients with demonstrated deficiency= coagulation disorder e.g. disseminated intravascular coagulation (DIC) and for patients that have had surgery and are continuously bleeding (missing coagulation factors)
- cryoprecipitate and plasma protein factors (PPF) e.g. fibrinogen, factor VIII, prothrombin complex concentrates
12
Q
Blood products: adverse effects
A
- transfusion reaction- ways to avoid these reactions: blood type and cross-match
- transmission of pathogens to recipient (hep B and C, HIV)
13
Q
Client care for fluids
A
- administer colloids slowly
- monitor for fluid overload and possible heart failure
- monitor closely for signs of transfusion reactions
14
Q
Crystalloids advantages
A
- few side-effects
- low cost
- wide availability
15
Q
Crystalloids disadvantages
A
- short duration of action
- may cause edema
16
Q
Colloids advantages
A
- longer duration of action
- less fluid required to correct hypovolemia
17
Q
Colloids disadvantages
A
- higher cost
- may cause volume overload
- may interfere with clotting
- risk of anaphylatic reactions
18
Q
Electrolytes
A
- Principal ECF electrolytes: sodium (Na+) and chloride (Cl-)
- Principal ICF electrolyte: potassium (K+)
- Others: calcium, magnesium, phosphorus
19
Q
Potassium is responsible for…
A
- skeletal muscle contraction
- transmission of nerve impulses
- regulation of heartbeat
- maintenance of acid-base balance
20
Q
Potassium
A
- most abundant positively charged electrolyte inside cells
- 95% of body’s potassium is intracellular
- normal ECF- 3.5 to 5 mmol/L
- potassium levels are critical to normal body function
- obtained from foods: fruit, fish, vegetables, poultry, meats, diary products
- excess dietary potassium excreted via kidneys (impaired kidney function leads to higher serum levels, possibly toxicity)
21
Q
Hypokalemia
A
- deficiency of potassium (<3.5 mmol/L)
- excessive potassium loss (rather than poor dietary intake)
- causes: vomiting, diarrhea, muscle weakness and/or lethargy, cardiac dysrhythmias (irregular pulse), paralytic ileus (decrease in bowel motility)
22
Q
Hyperkalemia
A
- excessive serum potassium level >5 mmol/L
- causes: cardiac rhythm irregularities (leading to possible ventricular fibrillation and cardiac arrest), muscle weakness, paralysis, paresthesia (tingling)
- treatment: IV sodium bicarbonate, calcium salts, dextrose with insulin, sodium polystyrene sulfonate (Kayexalate) or hemodialysis to remove excess potassium
23
Q
Client care for potassium
A
- parenteral infusions of potassium must be monitored closely- rate should not exceed 10 mmol/hour, never give as an IV bolus or undiluted
- oral forms of potassium: must be diluted in water or fruit juice to minimize GI distress or irritation, monitor for compliants of nausea, vomiting, GI pain, or GI bleeding
24
Q
Sodium
A
- most abundant positively charged electrolyte outside cells
- normal concentration outside cells is 135 to 145 mmol/L
- dietary intake of sodium chloride: salt, fish, meats, foods flavored or preserved with salt
25
Sodium is responsible for...
- control of water distribution
- fluid and electrolyte balance
- osmotic pressure of body fluids
- participates in acid-base balance
26
Hyponatremia
- sodium loss or deficiency
- serum levels < 135 mmol/L
- symptoms: lethargy, stomach cramps, hypotension, vomiting, diarrhea, seizures
- causes: same causes as hypokalemia, prolonged diarrhea or vomiting, or renal disorders
27
Hypernatremia
- sodium excess
- serum levels > 145 mmol/L
- symptoms: edema, hypertension, red, flushed skin, dry, sticky mucous membranes, increased thirst, elevated temperature, decreased urine output
- causes: kidney malfunction, inadequate water consumption and dehydration
28
Sodium: Indications
- treatment or prevention of sodium depletion when dietary measures are inadequate
- mild: treated with oral sodium chloride and/or fluid restriction
- severe: IV normal saline or lactated Ringer's solution
29
Sodium: adverse effects
- oral administration: nausea, vomiting, cramps
- IV administration: venous phlebitis
30
Client care for sodium
- monitor serum electrolyte levels during therapy
- monitor infusion rate, appearance of fluid or solution, infusion site
- observe for infiltration, other complications of IV therapy
31
Nociception
detection of noxious stimuli or stimuli that are capable of damaging tissue
32
Pain
an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
33
Pain: 4 processes
1) transduction
2) transmission
3) perception
4) modulation
34
Acute pain
- sudden in onset
- usually subsides once treated
35
Chronic pain
- usually more than 6 weeks and can be long lasting
- persistent or recurring
- often difficult to treat: mild, musculoskeletal pain, deep pain, neuropathic pain, chronic pain of indeterminate cause
36
Neuropathic pain
- pain induced by injury to or disease of the somatosensory system
- resulting from nerve injury or infections of the nervous system e.g. phantom limb pain, trigeminal neuralgia, shingles (postherpetic neuralgia), diabetic neuropathy
- develops slowly, outlasts healing of original injury
- allodynia, hyperalgesia, causalgia (burning)
37
Sources of pain
- somatic- superficial
- visceral- vascular, respiratory
- referred- occurs in area away from the real cause
- cancer- breakthrough
- phantom- after amputation, still feel pain
- neuropathic
- psychogenic
- central
38
Medication for pain: Analgesic
- selectively blocks the sensation of pain without blocking other symptoms or loss of consciousness
- most commonly used drugs
39
Medication for pain: Anesthetic
- local anaesthetic blocks nerve conduction and all local sensations (including pain)
- general anaesthetics cause loss of sensations and unconsciousness
40
What does analgesia do for the cause of pain?
- addressing pain without addressing the cause means the underlying cause continues
- cause has not gone away because you have reduced sensation of pain
41
Opioids
morphine-like action compounds- bind to opioid receptors on nerve endings
42
Opiate
any drug derived from opium e.g. morphine, codeine
43
Codeine
- effect of codeine is from its conversion of codeine --> morphine
- codeine is poor to act on opioid receptors, so most of its effect is when it converts to morphine
44
Receptor sites
- properties of different opioid drugs due to: affinity and activation for different opioid receptor subtypes
- all opioid analgesics are full agonists or partial agonists at mu and/or kappa receptors
45
Mu receptors
- analgesia
- brain (cortex, medulla, thalamus, limbic system, amygdala) and spinal cord
46
Kappa receptors
- analgesia- brain and spinal cord
- dysphoria and hallucinations
47
Pharmacological properties of opioids
- analgesia (mu and kappa receptors)
- sedation and 'mental clouding'
- euphoria and tranquility (delta and mu receptors) involves central dopaminergic pathways
- antitussive- depresses cough reflex by acting on a cough centre in the medulla
- depression of respiratory centre (mu-receptors) direct effect on brainstem respiratory centre
- nausea, vomiting stimulation of chemoreceptor trigger zone of the medulla
- miosis (pin point pupil) (mu and kappa receptors) excitatory action of the parasympathetic nerve innervating the pupil
- tolerance and serious dependence (mu receptors)
- constipation (mu and delta receptors) increase GI muscle tone to point of spasm, increase tone of anal sphincter
- postural hypotension inhibition of baroreceptor reflex
- dilation of cutaneous blood vessels (warm skin) may involve release of histamine and lead to sweating and itching
- urinary urgency but difficulty in urination inhibits urinary voiding reflex
- biliary colic and epigastric distress tone increases in sphincter of Oddi, increases in bile duct (increases pain of gall stones)
48
Opioids analgesics
- morphine
- oxycodone
- codeine
49
Opioid analgesics: indications
- alleviate mild to moderate to severe pain
- depending on the opioid used
- often given with adjuvant analgesic agents to assist with pain relief
50
Opioids are also used for...
- cough centre suppression (codiene)- antitussive
- treatment of diarrhea (loperamide)- e.g. trade name= Imodium
- balanced anaesthesia (fentanyl)
51
Morphine
- acute and chronic pain- less successful when used for chronic pain but still one of the best analgesics for this
- other analgesics compared to morphine- "the standard", equianalgesic doses of other opioids
- primarily on mu opioid receptors (strong agonist)- brain and spinal cord
- versatile- IV, IM, SC, PO, intrathecal
52
Metabolism of morphine
- t1/2= 2-4 hours
- extensive liver metabolism
- inactivation
- first pass metabolism
53
Pregnancy/breast feeding morphine
- risk exists for physical dependence
- crosses placenta
- enters breast milk
54
Pharmacological properties of morphine
- analgesia (mu and kappa receptors)
- sedation and 'mental clouding'
- euphoria and tranquility (delta and mu receptors) involves central dopaminergic pathways
- antitussive- depresses cough reflex by acting on a cough centre in the medulla
- depression of respiratory centre (mu-receptors) direct effect on brainstem respiratory centre
- nausea, vomiting stimulation of chemoreceptor trigger zone in area postrema of the medulla
- miosis (pin point pupil)
- tolerance and serious dependence (mu receptors)
- constipation (mu and delta receptors) increase colonic tone to point of spasm, increase tone of anal sphincter
- postural hypotension inhibition of baroreceptor reflex
- dilation of cutaneous blood vessels (warm skin)
- urinary urgency but difficulty in urination
- biliary colic and epigastric distress
55
Analgesics and cancer pain
- chronic pain: requires fixed schedule around-the-clock (ATC) treatment- opioids, NSAIDs, adjuvants
- breakthrough pain- transient episodes of pain while chronic pain is controlled, access to rescue medication
56
NSAIDs
the most common non-narcotic analgesic
57
Adjuvants
- antidepressants e.g. amitriptyline (Elavil)
- antiseizure drugs e.g. carbamazepine
- glucocorticioids
58
Morphine: contraindications and cautions
- severe asthma or other respiratory insufficiency (respiratory depression)
- hepatic dysfunction
- elevated intracranial pressure (ICP)- exacerbates condition
- pregnancy
59
Opioid analgesics: adverse effects
- respiratory depression- #1 serious adverse effect (slowing of breahting pattern, more shallow breathing )
- CNS depression- possible coma
- nausea and vomiting- greatest on 1st dose, then decreases
- constipation- no tolerance development
- hypotension- dilation of peripheral arteries and veins (histamine release)
- histamine release- itchiness, rash, dilation of peripheral arteries and veins
- urinary retention
- diaphoresis (sweating) and flushing
- pupil constriction (miosis)
60
Opioid analgesics: interactions
CNS depressants have cumulative effects e.g. antipsychotics, antihistamines, sedatives (benzodiazepines, barbiturates) and ethanol
- do not mix opioids with other CNS depressants --> increases chances of respiratory depression
61
Codeine
- moderate opioid analgesics
- less analgesia and respiratory depression- liver metabolism to morphine, antitussive
- often combined: acetaminophen in Tylenol 1, 2, 3, 4 (increases in dose of codeine per tablet as you go from 1-->4), acetylsalicyclic acid in '222's' or '292'
62
Oxycodone (oxycontin or percodan)
- risks not as high as morphine
- metabolism required for activation
- abuse potential
- widely used in combination with acetaminophen (Percocet)
- used for mild-moderate levels of pain
63
Opioid antagonists
- naloxone (narcan), naltrexone
- used for complete or partial reversal of opioid-induced respiratory depression
- naloxone on its own does not do anything if the overdose is not on opioids - no harm on trying it
64
Naloxone
- shorter half-life (~2h) than morphine and some other opioids
- IV/IM/SC/nasal administration- IM or nasal in naloxone rescue kits
65
Treating opioid addiction
- methadone program- strong opioid, subtly different properties than heroine, slow acting compound with long half-life, no same high but calming down of cravings for long period of time
- buprenorphine and naloxone (suboxone)- SL tablet, alternative to methadone
66
Opioid tolerance
- a common physiological result of chronic opioid treatment
- tolerance to respiratory depression, pin point pupils, analgesia etc.
67
Opioids- physical dependence
- state that develops in which an abstinence syndrome will occur if a drug is abruptly withdrawn
- drug must be administered to maintain normal function
- occurs with other unrelated drug classes- withdrawal symptoms specific to drug
- on abrupt discontinuation or when an opioid antagonist is administered e.g. narcotic withdrawal- very unpleasant but not dangerous
68
Physical dependence and addiction
- physical dependence is not the same as addiction (substance dependence syndrome)
- tolerance and physical dependence are both part of the body's response to the presence of drug
69
Opioid analgesics: implications
- oral forms should be taken with food to minimize gastric upset
- withhold dose and contact physician if there is a decline in the client's condition or if vital signs are abnormal - esp if reps rate is < 12 breaths/min
- respiratory depression may be manifested by: respiratory rate of < 12 per min, dyspnea, diminished breath sounds, shallow breathing
- constipation: very common, take with adeqaute fluid and fibre intake, stool softener (docusate) and/or stimulant (senna) daily
- orthostatic hypotension- instruct to change positions slowly
70
Tissue injury causes the release of...
- prostaglandins
- bradykinin
- histamine
- leukotriennes
- serotonin
71
Local mediators cause..
vasodilation, increased vascular permeability, chemotaxis, pain
72
NSAIDs: Mechanism of action
- blocking either or both cyclooxygenase (COX= enzymet that converts arachidonic acid into prostanoids) enzymes- COX-1 and COX-2
- limits the undesirable inflammatory effects of PGs and related substances
73
NSAIDs
large and chemically diverse group of drugs with the following properties:
- analgesic
- anti-inflammatory
- antipyretic
74
NSAIDs: Indications
- relief of mild to moderate pain
- osteoarthritis, rheumatoid arthritis and juvenille rheumatoid arthritis
- acute gout (a form of arthritis)
- various bone, joint and muscle pain
- dysmenorrhea
- fever
- many other conditions
75
Non-selective NSAIDs
- Examples: acetylsalicyclic acid (ASA)- Aspirin and ibuprofen (motrin, Advil)
- inhibit COX-1 and COX-2
- alleviate mild to moderate pain
- inflammatory disorders
- suppress inflammation but pose risk of serious harm
76
Acetylsalicylic acid (ASA, Aspirin)
- standard NSAID against which all others are compared
- 'Aspirin' from acetalation spiraea
- anti-inflammatory, analgesic, antipyretic
- antiplatelet (only NSAID used for this purpose)
- ASA is different to other NSAIDs- irreversibly inhibits COX
- all other NSAIDs reversibly inhibit COX
77
ASA (Aspirin) contraindications and cautions
- pregnancy- in late trimester connected with low weight, intracranial bleed and even death
- almost all bleeding disorders, hemophilia
- discontinue 1 week before operation
- caution in renal dysfunction
78
All NSAIDs adverse effects
- gastrointestinal- gastric ulceration (erosions), dyspepsia (discomfort in stomach), heartburn, epigastric distress, nausea
- GI bleeding
- Renal- reduction in creatinine clearance, acute tubular necrosis with renal failure
- blockade of platelet aggregation- bleeding problems
- inhibition of prostaglandin-mediated renal function
- hypersensitivity reactions
78
ASA (Aspirin) Adverse Effects
- influenza and chickenpox in kids/teens due to possibility of Reye's syndrome
- vomiting
- liver damage
- CNS problems (encephalopathy)- confusion, seizures, coma
79
NSAIDs- salicylate toxicity
- ASA, Na salicylate, Mg salicylate
- Adults: tinnitus and hearing loss
- Children: hyperventilation (CNS stimulation)
80
ASA (Aspirin) interactions
- increased bleeding with anticoagulants
- glucocorticoids- gastric ulcers
- Non-ASA NSAIDs- reduce antiplatelet effects of ASA, do not mix NSAIDs if ASA used for antiplatelet effect
81
Non-ASA NSAIDs
- ASA-like drugs with fewer GI, renal and hemorrhagic effects than ASA (aspirin)
- 20+ non-ASA NSAIDs available (all similar, but for unknown reasons, patients tend to do better on one drug or another)
- inhibit COX-1 and COX-2: inhibition is reversible (unlike with ASA)
- do not protect against MI and stroke
82
COX-2
responsible for inflammatory mediators
83
COX-2 inhibitor example
celecoxib (celebrex)- "sulfa" drug
84
Selective COX-2 inhibitors
- just as effective as traditional NSAIDs in suppressing inflammation and pain
- perhaps lower risk for GI adverse effects- but higher than not taking the drug
- can impair renal function and cause hypertension and edema
- increased risk of MI and stroke
85
Misoprostol (Cytotec)
synthetic prostaglandin, used in combination with NSAIDs to reduce ulceration
86
NSAIDs- antipyretic
- antipyretic (reduce fever)
- inhibit prostaglandin E2 production within the area of the brain that controls temperature
87
NSAIDs: Client implications
- before beginning therapy, assess for conditions that may be contraindications to therapy, especially: GI lesions or peptic ulcer disease, bleeding disorders
- notify if GI pain occurs or evidence of GI bleeding
- clients should watch closely for the occurrence of any unusual bleeding, such as in stool- dark or black color, tarry
- enteric-coated tablets should not be crushed or chewed
- salicylates are NOT to be given to children under age 12- Reye's syndrome- Absolutely critical
88
Gout
- painful inflammatory disorder seen mainly in men
- symptoms result from the deposition of uric acid crystals in joints
- recurrent inflammatory disorder characterized by hyperuricemia and episodes of severe joint pain, typically in the large toe
89
Antigout agents
- allopurinol
- colchicine
- probenecid, sulfinpyrazone
90
Allopurinol
- to prevent attacks
- reduces production of uric acid
- xanthine oxidase (enzyme that leads to the formation of uric acid from breakdown products of DNA) inhibitor
- prophylactic use
91
Colchicine
- used for acute attacks
- reduces inflammatory response to the deposits of urate crystals
92
Probenecid and sulfinpyrazone
increase excretion of uric acid in urine
93
Rheumatoid Arthritis
- systemic disease across the lifespan
- autoimmune and inflammatory disorder
- attack of synovium
- joint swelling, pain, systemic symptoms
- eventual fusing of bones
94
Antirheumatoid arthritis medications
- drugs intended to suppress inflammation- NSAIDs, symptomatic relief only
- DMARDs: disease modifying antirheumatic drugs- slow onset of action up to several weeks, slow progression of disease
95
DMARDs: Methotrexate
- most common
- alone or in combination with other drugs
- also used in cancer chemotherapy (in larger doses)
96
DMARDs: Immunological agents (biologics)
- antibodies against inflammatory mediators e.g. cytokines
- infliximab (remicade), adalimumab (humira)
97
Other rheumatoid arthritis drugs
- glucocorticoids: short term use
- other immunosuppressant drugs: gold salts
98
Acetaminophen e.g. Tylenol
- analgesic
- antipyretic- reduce fever, inhibition prostaglandin E2 production within the area of the brain that controls temperature
- little to no anti-inflammatory effects (not a NSAID)
- no antiplatelet effect
- alternative for those who cannot take NSAID products
- inhibits COX but only a COX present in CNS
- no peripheral therapeutic sites of action
- absence of adverse effects associated with NSAIDs- no GI ulceration, excessive bleeds
- maximum 4000 mg per day for adult- 2400 mg for 11-12 years, sliding scale based on age/weight, extreme caution in alcohol abusers
- single ingredient- tabs are 325 mg, 500 mg, 650 mg, maximum reached quickly
- tylenol 1,2, 3, or 4
99
Contraindications of acetaminophen
- severe hepatic disease
- severe renal disease
- alcoholism
- drug allergy
100
Acetaminophen: Toxicity
- OTC and prescription- can be lethal in overdose
- overdose- whether intentional or due to chronic unintentional misuse, hepatic necrosis (drug-induced hepatitis)
- long-term ingestion of large doses also causes nephropathy
101
Acetaminophen: Overdose
- recommended antidote- acetylcysteine (mucomyst), mucolytic used usually to decreased viscosity of bronchial secretion
- protects liver from acetaminophen- induced damage- max protection within 8-10 hours (IV or PO), give even in late presentation @ 24 h
102
Acetaminophen should not be taken in the presence of..
- liver dysfunction, chronic alcoholism
- possible liver failure or severe renal disease
- when taking other hepatotoxic drugs
103
Respiratory conditions
- asthma
- COPD: emphysema, chronic bronchitis
- cystic fibrosis (CF)
- acute respiratory distress syndrome (ARDS)
104
Bronchial asthma
- recurrent and reversible shortness of breath
- occurs when lung airways narrow: bronchospasms, inflammation of the bronchial mucosa (edema)
105
Respiratory tract drugs: Bronchodilators
- beta 2-adrenergic agonists (salbutamol)
- anticholinergics (ipratropium bromide)
- xanthine derivatives (theophylline/aminophylline)
106
Respiratory tract drugs: Anti-inflammatory
- for asthma and COPD
- glucocorticoids- budesonide (Pulmicort)
- leukotriene modifiers- (montelukast)
107
Bronchodilators: beta-agonists
- sympathomimetic bronchodilators
- stimulate bronchial smooth muscle beta 2- adrenergic receptors: short-acting beta agonists (SABA) e.g. salbutamol, long-acting beta agonists (LABA)
- LABA- longer duration of action, not used for rescue
108
Beta-agonists: mechanism of action
- dilation of airways: activation of smooth muscle beta 2-receptors
- relaxes smooth muscles of the airway and results in bronchial dilation
- increased airflow
109
Beta-agonists: indications
- relief of bronchospasm related to asthma, COPD, and other pulmonary diseases
- treatment of: acute attacks (quickly reduce airway constriction), prevent attacks (chronic management, exercise-induced)
- not used to prevent asthma long-term that is more glucocorticoids
110
Beta-agonists: adverse effects that are common to all
- cardiac stimulation- tachycardia (bc it activates beta 1 receptors too in the heart)
- tremors - caused by epinephrine
- restlessness, insomnia (CNS stimulation)
111
Beta-agonists: adverse effects for salbutamol
- beta receptor effects e.g. muscle tremor, CNS (anxiety, nausea)
- decrease receptor selectivity- stimulates beta 1 adrenergic receptors in heart --> increased HR, palpitations, chest pains, angina
- if use inhaled form too frequently- inhaled form has lower concentration than PO
- more likely with oral preparations
112
Care implications bronchodilators: beta-agonists
- encourage measures that promote good state of health in order to prevent, relieve, or decrease symptoms of asthma/COPD --> avoid exposure to conditions that precipitate bronchospasms (smoking, allergens, stress, air pollutants)
- adequate fluid intake
- monitor for therapeutic effects: decreased dyspnea, decreased wheezing, restlessness, and anxiety, improved respiratory patterns with return to normal rate and quality, improved activity tolerance
113
Bronchodilators: anticholinergics
- ipratropium (Atrovent)
- prevent bronchoconstriction (fixed schedule use)
- not used alone for acute exacerbations
- poorly absorbed- will not get anticholinergic effects in other parts of the body
- can affect locally and not affect systemic- good thing
- use of drug is not for rescue but to keep symptoms under control (morning and night)/maintenance
114
Anticholinergics: adverse effects
- dry mouth or throat (cough): inhaler- some goes down respiratory tract and some stays in mouth, constant dry mouth because drug sticks to receptors on salivary glands
- systemic effects are minimal
115
Bronchodilators: methylxanthines
- example= caffeine (similar effects)
- theophylline (oral)
- aminophylline (more water-soluble form of theophylline, IV admin)
- bronchodilation: bronchial smooth muscle relaxation
- quick relief of bronchospasm- greater airflow into and out of the lungs
116
Methylxanthines: adverse effects
- CNS stimulation: anxiety, insomnia, seizures
- CV stimulation: palpitations (increased force of contraction/fast HR), sinus tachycardia (increased HR), ventricular dysrhythmias
- GI distress- nausea, vomiting
117
Methylxanthines: interactions
- increased effects of theophylline- Ciprofloxacin --> inhibits liver CYP metabolism
- large amounts of caffeine can intensify adverse effects
- decreased effects of theophylline- liver enzyme inducers e.g. phenytoin, phenobarbital (antiseizure drugs)
118
Care implications: methylxanthines
- stay away from caffeine
- encourage reporting: palpitations, nausea and/or vomiting, weakness or dizziness, chest pain, convulsions
119
Anti-inflammatory drugs: glucocorticoids
- many drugs in group- similar action to cortisol (adrenal steroid hormone), high dosing for immunosuppressant effect
- steroid drugs- structure based on cholesterol
- some drugs used for respiratory diseases
- inhaled- used for chronic asthma and COPD- oral/IV for severe/short-term treatment
- not symptomatic relief of asthmatic attacks- but keeps it under control
- inhaled forms reduce systemic effects
- may take several weeks for full therapeutic effect
120
Glucocorticoids: mechanism of action
many mechanisms:
- reduces inflammatory mediators (prostaglandins, LTs, etc.)
- decrease production of cytokines
- reduces infiltration and activity of inflammatory cells (e.g. eosinophils, other leukocytes)
- reduces edema (capillary permeability)
121
Inhaled glucocorticoids
- budesonide (pulmicort)
- combination preparations: glucocorticoid + long-acting beta 2-agonist (LABA) e.g. budesonide + formoterol (Symbicort)
- lasts many hours
- LABA rarely given alone, exacerbates asthma alone
122
Inhaled glucocorticoids: fluticasone
- used alone (Flovent)
- used in combination= Advair diskus- combo with long-acting beta 2- agonist salmeterol
123
Inhaled glucocorticoids: indications
prophylaxis treatment of: asthma, COPD (with LABA)
124
Inhaled glucocorticoids: adverse effects
- limited to mouth
- oral fungal infections*
- pharyngeal irritation
- coughing
- dry mouth
- systemic effects are rare due to low doses used for inhalation therapy
125
Care implications: inhaled glucocorticoids
- avoid if have candida in sputum
- may slow growth in children- but does not reduce adult height
- possible bone loss- weight bearing exercise
- if require beta-agonist bronchodilator and corticosteroid inhaler --> bronchodilator should be used several minutes before the glucocorticoid to provide bronchodilation before administration of the glucocorticoid
- teach clients to gargle and rinse the mouth with water afterward to prevent the development of oral fungal infections
126
Leukotrienes
released in immune responses from (e.g. mast cells, eosinophils) in asthma
127
Leukotrienes cause
- inflammation
- bronchoconstriction
- mucus production
- leukocyte recruitment
128
Leukotriene modulators
- suppress leukotriene effects:
prevent smooth muscle contraction of the bronchial airways, decrease mucus secretion, prevent vascular permeability, decrease neutrophil and other leukocyte infiltration to the lungs, preventing inflammation
- inflammation in lungs is reduced: asthma symptoms relieved
- leukotriene receptor antagonists: montelukast (generally well tolerated)
- leukotriene synthesis inhibitor: zileuton (liver injury and CYP inhibition)
129
Leukotriene modulators: indications
- prophylaxis and chronic treatment of asthma in adults and children- montelukast in children ages 2 and older
- not for acute asthmatic attacks
130
Care implications: leukotriene modulators
- ensure that the drug is being used for chronic management of asthma, not acute asthma- on a continuous schedule
- improvement should be seen in 1 day- 1 week
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Histamine effects
mast cells (and others) release histamine and other substances- symptoms of allergic reactions
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Antihistamines
- histamine receptor antagonists- drugs that compete with histamine for receptor site
- two histamine receptor subtypes: H1* and H2
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Histamine-mediated disorders
- allergic rhinitis (hay fever, mould and dust allergies)
- anaphylaxis
- angioedema
- drug fevers- usually young children
- insect bite reactions
- urticaria (redness and itching)
134
Histamine vs antihistamine: Cardiovascular effects
- histamine: dilation of small blood vessels and increased permeability, swelling (fluid from plasma into interstitial fluid)
- antihistamine: reduce dilation of blood vessels, reduce increased permeability of blood vessels
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Histamine vs antihistamine: Exocrine gland effects
- histamine: stimulate salivary, lacrimal, and bronchial secretions
- antihistamine: reduce salivary, lacrimal and bronchial secretions
136
Antihistamines- other uses
skin:
- reduce capillary permeability
- wheal-and-flare formation
- itching (pruritus)
137
Antihistamines: indications
- palliative, not curative, treatment: nasal allergies, seasonal or perennial allergic rhinitis (hay fever), allergic reactions
- motion sickness
- sleep disorders
138
2 types of antihistamines
- traditional
- nonsedating/peripherally acting
139
Traditional antihistamines
- older drugs
- antagonists of H1 receptors: peripherally (reduce respiratory/eye symptoms), centrally (CNS: cause sedation)
- have anticholinergic effects- drying effect that reduces nasal, lacrimal gland secretions, salivary
- used in nighttime relief (bc cause sleepiness)
- example= diphenhydramine (Benadryl)
140
Traditional antihistamines: adverse effects
anticholinergic effects:
- dry mouth (reduced salivary secretions)
- difficulty urinating
- constipation
- changes in vision (dilated pupils, blurred vision)
141
Nonsedating/peripherally acting antihistamines
- developed to eliminate unwanted adverse effects- mainly sedation
- work peripherally- fewer CNS adverse effects
- longer duration of action (increases adherence)
- 2 benefits over traditional antihistamines:
(1) no drowsiness bc does not work on CNS
(2) long-acting
- examples: Loratadine (Claritin)
142
Antihistamines: nursing implications
use of traditional antihistamines:
- instruct clients to report excessive sedation, confusion or hypotension
- avoid driving or operating heavy machinery
- do not consume alcohol or other CNS depressants
143
Productive cough
congested, removes excessive secretions
144
Nonproductive cough
dry cough
145
Cough
- most of the time, coughing is beneficial: removes excessive secretions, removes potentially harmful foreign substances
- in some situations, coughing can be harmful- e.g. after hernia repair surgery
146
Antitussives
- drugs used to stop or reduce coughing
- used only for nonproductive coughs
- common OTC antitussive: dextromethorphan (Benylin)- synthetic opioid-like compound, does not produce morphine-like effects
147
Antitussives: mechanism of action
- opioids: suppresses the cough reflex, acts in cough centre of medulla
- examples: codeine
148
Antitussives: indications
used to stop cough reflex when the cough is nonproductive and/or harmful
149
Antitussives: adverse effects
- codeine: sedation, nausea, vomiting, lightheadedness, constipation, typical opioid effects
- dextromethorphan (benylin): not as good of an antitussive as codeine, dizziness, drowsiness, nausea, much less than CNS effects of codeine
150
Antitussive agents: nursing implications
- report of any of the following symptoms: cough that lasts more than a week, persistent headache, fever, rash
- antitussive agents are for nonproductive coughs
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Hypertension
- unknown cause: essential, idiopathic, or primary hypertension, 90% of the cases
- known cause: secondary hypertension, 10% of the cases
152
Antihypertensive drugs: categories
- angiotensin-converting enzyme (ACE) inhibitors
- angiotensin II receptor blockers (ARBs)
- calcium channel blockers (CCBs)
- diuretics
- beta-adrenoceptor blockers
- vasodilators
- adrenergic agents
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Antihypertensive drugs: ACE inhibitors (ACEIs)
- large group of safe and effective drugs
- often used as first-line agents for HF and hypertension
- often combined with a thiazide diuretic or calcium channel blocker
- e.g. Captopril (Capoten)- shortest half-life of the prils
154
ACE inhibitors: indications
- hypertension: may be used alone or with other agents (CCB, diuretics), renal protective effects in clients with diabetes
- slows progression of left ventricular remodelling after an MI
155
ACE inhibitors: mechanism of action
- prevents Ang II vasoconstriction: reduces peripheral resistance (afterload)
- prevents aldosterone release: reduce salt and water reabsorption
- also prevent the breakdown of bradykinin
156
ACE inhibitors: Adverse effects
- dry, nonproductive cough: problematic for some patients, reverses when therapy is stopped
- first-dose hypotensive effect may occur
- possible hyperkalemia
157
ACE inhibitors: interactions
K supplements and K-sparing diuretics (ACEI already increases potassium)
158
Contraindications of ACE inhibitors
contraindicated in pregnancy
159
Angiotensin II Receptor Blockers: ARBs
- similar to ACEIs (but not identical)- do not cause a dry cough, generally not combined with ACEIs
- e.g. Losartan (Cozaar)
- alternative for those who cannot tolerate ACE inhibitors
- contraindicated in pregnancy
160
Angiotensin II Receptor Blockers: Mechanism of Action
- block receptors that angiotensin II activates
- blocks Ang II-mediated vasoconstriction
- blocks release of aldosterone
161
Angiotensin II Receptor Blockers: Indications
- hypertension
- adjunctive agents for the treatment of HF (heart failure)
- may be used alone or with other agents: CCB, diuretics
162
Calcium Channel Blockers (CCBs) examples
- diltiazem (cardiac + vascular)
- verapamil (cardiac + vascular)
- Diphydropyridines- DHPs (vascular selective)- amiodipine, nifedipine
163
CCBs on cardiac muscle
- block cardiac muscle Ca channels
- alters electrical activity of cardiac muscle cells- SA, AV nodes and cardiac muscle
164
CCBs on vascular muscle
- inhibits Ca entry into arteriolar vascular smooth muscle cells- cause relaxation
- decreased peripheral resistance- decreased BP
165
CCBs: Verapamil/Diltiazem Adverse Effects
- cardiovascular: hypotension (dizziness), flushing, peripheral edema
- GI: constipation, nausea
- Other: rash, dermatitis
166
CCBs: DHPs Adverse Effects
- cardiovascular: hypotension (dizziness), palpitations, tachycardia, flushing, peripheral edema
- GI: very little constipation
- other: rash, dermatitis
167
Beta-adrenergic receptor blockers (antagonists)
- act in the periphery, mainly heart: beta 1-blockade, block norepinephrine/epinephrine action in heart
- reduce heart rate
- decrease force of heart muscle contraction: reduce stroke volume
- avoided in patients with asthma
- e.g. metoprolol
168
Beta-blockers indications
- hypertension
- HF
- angina
- dysrhythmias
169
Antihypertensive: Client implications
- drugs should not be stopped abruptly- may cause rebound hypertensive crisis, and perhaps lead to stroke
- client should: avoid smoking, avoid eating foods high in sodium e.g. tinned soups, packaged meals, follow other lifestyle recommendations
- instruct clients to change positions slowly to avoid syncope (fainting) from postural hypotension
- patients should avoid aggravating low blood pressure e.g. hot tubs, showers, or baths, hot weather, prolonged sitting or standing, intense physical exercise, alcohol ingestion
170
Angina
- chest pain
- supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart= pain
171
Types of Angina
- stable angina (angina pectoris)- predictable e.g. exercise, excitement
- unstable angina- occurs without activity
- variant angina (prinzmetal's angina)- coronary artery vasospasm
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Antianginal drugs
- Therapeutic goals: relieve the pain of a current attack, prevent angina (limit the number of angina attacks)
- broad treatment goals: (1) improve blood flow in coronary circulation, (2) reduce heart muscle metabolic demands (3) both
- e.g. organic nitrates
- combination therapies: nitrates + CCBs, nitrates + b-blockers, CCBs + b-blockers, nitrates + CCBs + b-blockers
173
Organic nitrates
- available forms: sublingual, oral capsules/tablets, intravenous solutions, ointments, transdermal patches, translingual sprays
- cause vasodilation- relaxation of vascular smooth muscles
- dilate coronary arteries- increased coronary blood flow, useful in variant angina
- reduced cardiac preload (relax veins) and afterload (relax systemic arteries)
- decrease preload- dilate veins, decreases stroke volume, CO and BP
- decrease afterload- arteriolar vasodilator (decrease TPR) and so decrease BP
174
Preload
- stress on ventricular wall before systole
- volume of blood in ventricles end of diastole/before systole
175
Afterload
- resistance heart has to pump against
- determined by arteriolar pressure
176
Organic nitrates: Nitroglycerin
- large first-pass effect
- SL (not PO) for symptomatic treatment
- patch/PO for prevention of angina
- IV form used for BP control in perioperative hypertension, treatment of HF, ischemic pain, pulmonary edema associated with acute MI, and hypertensive emergencies
177
Organic nitrates: isosorbide mononitrate
- prolonged action for prophylaxis
- oral (high bioavailability)
178
Organic nitrates: adverse effects
- headache: classic and predictable in almost all patients, usually diminish in intensity and frequency with continued use
- postural hypotension: some peripheral edema due to pooling of blood in venous system
- reflex tachycardia: partially offsets beneficial effects, may combine with beta-blocker
179
Organic nitrates: tolerance
develops over a single day
180
Client implications: nitroglycerin
- proper technique and guidelines for taking sublingual nitroglycerin- never to chew or swallow SL form
- nitrate topical ointments and transdermal forms- site rotation, removal of old medication (reduce tolerance by removing topical forms at bedtime, and applying new doses in the morning, allowing for a nitrate-free period)
181
Beta-blockers antagonists examples
- atenolol
- metoprolol
- propanolol
182
Beta-blockers: mechanism of action
- decrease HR= decrease cardiac work, decreases myocardial oxygen demand
- decrease myocardial contractility= decrease cardiac work, decreases myocardial oxygen demand
183
Beta-blockers
long-term prevention of angina- not for acute exacerbations of angina
184
Beta-blockers: adverse effects- cardiovascular
bradycardia, hypotension second-or third-degree heart block; heart failure
185
Beta-blockers: adverse effects- metabolic
altered glucose and lipid metabolism
186
Beta-blockers: adverse effects- CNS
dizziness, fatigue, mental depression, lethargy, drowsiness, unusual dreams
187
Beta-blocks: adverse effects- Other
Impotence, wheezing, dyspnea
188
Client implications: beta-blockers
- clients taking beta-blockers should monitor pulse rate daily and report any rate lower than 60 bpm
- medications should never be abruptly discontinued --> rebound hypertensive crisis, physical dependence
- long-term prevention of angina- not for acute exacerbations of acute
189
Calcium channel blockers examples
- diltiazem
- verapamil
- nifedipine
190
Calcium channel blockers: mechanism of action
- reduce myocardial contractility (negative inotropic action)
- cause peripheral arterial vasodilation
- decreased myocardial oxygen demand
191
Calcium channel blockers: indications
- first line agents for treatment of: angina, hypertension, supraventricular tachycardia
192
Client implications: calcium channel blockers
constipation is a common problem: adequate fluids and eat high-fibre foods
