Final Exam Topics Flashcards
1
Q
Define Pharmacotherapeutics
A
the use of drugs to treat, cure, prevent disease
2
Q
define pharmacokinetics
A
the journey of the drug through the body / what the body does to the drug
3
Q
define pharmacodynamics
A
what the drug does to the body
4
Q
what is the absorption of a drug?
A
absorption is the movement of drug from site of administration to systemic circulation (blood flow)
5
Q
what is the bioavailability of a drug (definition)
A
bioavailability (F) is the proportion of a drug dose that you administer that reaches systemic circulation
how much of it actually gets into the blood stream
example: if you swallow a 100mg pill and 70mg is eliminated from the body, only 30mg reaches systemic circulation meaning that F = 30%
6
Q
what type of drug administration are always 100% bioavailable?
A
intravenous drugs
7
Q
what factors can influence bioavailability from peripheral tissues?
A
- regional blood flow
- type of tissue (fat, muscle, bone, etc.)
- drug’s chemical properties
- limitation of physiologic transport processes
8
Q
what is lipophilic?
A
a fat soluble drug
crosses cell membranes easily
* same for molecules w/ neutral electric charge (nonpolar / non-ionized)
9
Q
what is hydrophilic?
A
water soluble drug
does not cross cell membranes easily
* same for molecules w/ pos or neg charge (polar, ionized)
10
Q
what is the first pass effect?
A
when the drug is absorbed in the stomach and enters the blood stream via the portal vein but goes straight to the liver to get metabolized. whatever the liver lets through is what gets into our systemic circulation and starts helping us.
11
Q
how does acidity (pH) affect drug absorption
A
drugs are either weak acids or weak bases
best absorbed in their non-ionized state
12
Q
what is the definition of distribution
A
movement of drug from systemic circulation to peripheral tissues
the drug is in the blood stream now!
13
Q
what is volume distribution (Vd) of a drug
A
the relative extent to which a drug moves to other body compartments
14
Q
what is a small Vd
A
≤ 0.25L/kg
drug remains mostly in blood stream
15
Q
what is a mid-range Vd
A
0.25 - 0.7 L/kg
16
Q
what is a large Vd
A
> 0.7 L/kg
drug distributes extensively to cells/tissues (peripheral compartment)
17
Q
what type of Vd do fat and water soluble drugs have
A
water soluble drugs have a small Vd
fat soluble drugs have a large Vd
18
Q
what type of drugs cross the BBB easier?
A
Fat-soluble drugs cross the BBB more easily because the barrier’s tightly packed cells are more permeable to lipids, allowing easier diffusion. Water-soluble drugs require specific transport, making entry harder
19
Q
Factors that increase Volume of Distribution (Vd)
A
- Higher Lipid Solubility: Fat-soluble drugs easily cross cell membranes.
- Lower Plasma Protein Binding: Less binding allows more drug to enter tissues.
- Greater Peripheral Tissue Binding: Strong affinity for tissues increases distribution.
20
Q
define metabolism in pharmacology
A
biochemical transformation of a drug to form a metabolite that is usually less active and/or more water soluble than the parent drug
(easier for body to eliminate)
21
Q
What occurs in Phase I of drug metabolism?
A
Types: Oxidation, reduction, hydrolysis
Function: Adds functional groups (-OH, -COOH, -SH, -O, -NH2) to drugs
Outcome: Prepares drugs for Phase II, often decreasing potency or inactivating the drug.
22
Q
What occurs in Phase II of drug metabolism?
A
Types: Conjugation reactions
Function: Attaches large polar molecules (e.g., glucuronic acid, sulfate)
Outcome: Increases water solubility for easier excretion; less susceptible to liver dysfunction.
23
Q
what enzyme is phase 1 metabolism mediated by?
A
Cytochrome-P (CYP)-450
24
Q
What are the effects of substrates, inducers, and inhibitors on CYP450 enzyme activity?
A
Substrates: Molecules metabolized by CYP450 enzymes.
Inducers: Increase CYP450 activity, enhancing metabolism and clearance of substrates, potentially reducing drug effectiveness.
Inhibitors: Decrease CYP450 activity, slowing metabolism of substrates, leading to greater drug exposure and increased risk of side effects or toxicity.
25
define elimination in pharmacology
removal of drug or metabolite from body without further chemical change
26
how are most drugs eliminated
through the kidney and urine
other ways include: bile, sweat, spit, breast milk, exhalation
27
what is clearance (CI) in pharmacology
volume of blood that is cleared of a drug per unit time
it is a rate
28
how many half-lives for a drug to be removed from the body
4-5 half-lives
1 half life - 50%
2 - 75%
3 - 87.5%
4 - 93.75%
5 - 96.86%
29
how do agonist vs. antagonist drugs interact with receptors in order to work?
agonist drugs = activate receptors and enhance it's effects
antagonist drugs = block receptors and inhibiting their effects
30
what do B1 receptors control?
heart rate
norepinephrine (NE) is an endogenous B1 agonist (binds to/activates receptor and increases HR)
metoprolol is a B1 antagonist (binds to receptor but doesn't activate and prevents NE from binding = decreases HR)
31
B1 and B2 receptors connect where?
B1 = heart
B2 = lungs
32
What are the differences between threshold dose and ceiling effect?
Threshold Dose: Minimum dose required to produce a measurable effect; below this dose, the drug has no significant effect.
Ceiling Effect: Maximum effect a drug can produce; after this point, increasing the dose does not enhance the therapeutic effect and may increase side effects.
33
Explain down-regulation and up-regulation
down-regulation: constantly exposed to a drug so the body stops sending receptors to not have as much of a reaction
up-regulation: not exposed as often to the drug so the body sends more receptors in order to have a reaction
34
Therapeutic Index
measure of drug's safety - ratio between toxic dose and effective dose. **BELOW <0.25 IS TOXIC STOP THE DRUG
35
Characteristics of a High TI?
safer bc larger gap between effective and toxic dose, no high risk of toxicity
36
Characteristics of a Low TI?
requires careful monitoring as the therapeutic dose is close to the toxic dose.
37
ADRs vs. ADEs vs. Side Effects?
ADRs: unintended, undesirable response to a drug that doesn't include human error or non-adherence
ADEs: ADRs + errors (prescribing, dosing, administration)
Side Effects: minor well-known ADR of a drug, doesn't change management
38
Drug Toxicity
medical emergency - go to hospital to treat and reduce toxicity
39
Drug Tolerance
how well someone tolerates the drug/if it works the way it should
slowly increasing the dose based on how the person responds and if they were on like 5mg then doesn’t work so they go up to 10mg
40
Risk Factors for / What Leads to ADEs
Drug itself, poly-pharmacy, genetic polymorphisms, drug-disease, age, prescriber factors, non-adherence, medication errors, drug-drug interactions, drug allergies
41
Type I Drug Allergy Reaction Symptoms
Anaphylaxis - IgE mediated - Immediate
Pulmonary: dyspnea, cyanosis, bronchospasm, edema, cough, respiratory arrest
Cardiac: tachycardia, hypotension, arrythmia
Skin: erythema, puritis, urticarial
GI: N/V/D
can be life threatening
discontinue immediately and seek emergency services - epi-pen
42
Type II Drug Allergy Reaction Symptoms
IgG/IgM Cytotoxic - delayed by several days/weeks
hemolytic anemia, thrombocytopenia, leukopenia
Life threatening
discontinue drug - self resolves
43
Type III Drug Allergy Reaction Symptoms
autoimmune - inflammatory cascade - 1-3 weeks
serum sickness, drug induced systemic lupus erythematosus
arthritis/arthalgia
fever/malar rash
discontinue drug: prognosis is excellent and self-resolves
44
Type IV Drug Allergy Reaction Symptoms
cell mediated hypersensitivity
symptoms: contact dermatitis - rash
discontinue offending agent and can use steroids
45
Urticarial rashes occurs with what Types?
Types I and III
46
Non-urticarial rashes occurs with what Types?
Types I, II, IV
47
What drug allergy types are possibly life threatening?
Types I and II
48
Polypharmacy
use of multiple medications in someone with comorbidities.
49
Polymorphisms
genetic variations in the DNA sequence - variations that affect how individuals metabolize and respond to drugs.
often influences drug efficacy, safety, and likelihood of ADRs.
50
Nonadherence
pt who failed to meet treatment targets described being prescribed appropriate therapy bc they dont take their meds
51
Changes with age and drugs?
balance/gait - ability to compensate for ADE
changes in body comp - fat soluble drugs
CNS - ADE vs. age?
GI - decreased motility / absorption/sensitivity
***Hepatic/Renal Function - decreased clearance of meds
skin - thinning / absorption changes of topical meds
52
Drug-Drug interactions
Combination of 2 drugs causing synergistic or diminished effects
53
Food-Drug interactions
Combination of drug and food leads to synergistic or diminished effect of drug
54
What is the classification of ADRs?
ABCDEF
Augumented Pharmacologic Effects
Bizarre Effects
Chronic Effect
Delayed effects
End of treatment effects
Failure of Therapy
55
Augumented Pharmacologic Effects
overreactive response to what the drug does - reduce the dose if this happens.
Type of reaction: dose-related response
features: related to pharnacologic action, predictable, common, low mortality
Management: reduce to lowest tolerated dose
56
Bizarre Effects
type of reaction: non-dose related
features: occurs unpredictably, serious, high mortality, uncommon
management: Discontinue immediately and avoid drug class.
57
Chronic Effects
type of reaction: dose/time related
features: only occurs with chronic use, not after 1 dose.
management: limit length of treatment - discontinue and may need to taper down dose
58
Delayed Effects
time related reaction
uncommon, usually dose related, effects occur AFTER treatment ended
often intractable - treat symptomatically -- avoid known teratogens in pregnant women
59
End-of-Treatment Effects
type of reaction: withdrawal
features: uncommon, effects occur immediately after discontinuation, effects may be what drug was treating
management: stress important of adherence to pts and taper drug when discontinuation is desired
60
Failure of Therapy
Type of reaction: dose-related
Features: common, no response despite appropriate dose, may be caused by drug interactions or genetic difference
Management: increase dosage, switch to different drug
61
What are Pharmacy Databases?
Clinical Pharmacology, Micromedex, LexiDrug/Comp
62
What are Dietary/Herbal Databases?
Natural Medicine / Nat Med Pro
63
What are Open Access Resources?
Physician's Desk Reference
64
What is the database for Medical AI?
Open Evidence
65
What Databases are not Recommended?
Epocrates, Google, ChatGPT, etc.
66
key characteristics of sympathetic nervous system?
- increases function of organs
- once on, usually results in more massive/diffuse response thru multi-organ systems
-**ganglia usually found near spinal cord or target area
-**1:15 preganglionic:postganglionic
-**NE + EPI
67
key characteristics of parasympathetic nervous system?
- slows down function of organs
- once on, usually specific organ system
-**ganglia usually found in organ/tissue
-**1:1 preganglionic:postganglionic
-**ACh
68
Parasympathetic Ganglion
Pre/Post-Ganglionic Neurotransmitter: ACh
Ganglionic Receptor: Nicotinic
Effector Cell Receptor: Muscarinic
Functions: slows HR, bronchocontrict, increases digestion, stimulates urination, constricts pupils, increases salivation+tears
69
Sympathetic Ganglion
Pre/Post-Ganglionic Neurotransmitter: NE + EPI
Ganglionic Receptor: Nicotinic
Effector Cell Receptor: Alphas, Betas adrenergic receptors
Functions: incr. HR, bronchodilate, decreases digestion, inhibits urination, dilates pupils, incr. glucose release
70
Define Direct Agonist
the drug does something that you want it to do - binds directly with the receptor
71
define indirect agonist
does what you want it to but doesn't bind directly with that receptor
72
define antagonists
whatever you want the drug to do, it does the opposite
e.g. you have bad stomachache so you take prilosec -- body stops producing acid
73
what do direct cholinergic agonists do
mimics acetylcholine and binds directly to muscarinic receptor
74
what do indirect cholinergic agonists do
meds that stop/inhibit cholinesterase enzyme that increases Ach at post-synaptic cholinergic receptor
goes thru enzyme first
75
what are common cholinergic stimulant side effects (ADRs)?
as dose increases, # and intensity of ADRs can increase
- increase in SLUD (saliva, lacrimation (tears), urination, defecation)
- decreased HR
- increased sweating (sweating because you're not in the AC!)
76
what are common anti-cholinergic stimulant ADRs
- decreased SLUD (saliva, lacrimation(tears), urination, defecation)
- increased HR
- decreased sweating (not sweating bc you're in AC!)
- risk of falls in elderly (orthostasis)
77
how do anticholinergics work?
blocks acetylcholine from stimulating / going to the muscarinic receptor
78
in what cases/diagnoses would an anticholinergic be prescribed?
- IBD
- cardiology: bradycardia
- motion sickness
- overactive bladder
- asthma/COPD
79
most common anticholinergic for motion sickness?
scopolamine (skin patch)
80
most common anticholinergic for overactive bladder?
oxybutynin
81
what do a1 agonists usually work on and how?
arteries, BP most likely
causes vasoconstriction which can increase BP (dangerous!)
82
when are a1 agonists used?
- primarily used in shock states as a last resort
**phenylephrine
83
what are adverse drug reactions for a1 agonists?
- oral agents (sudafed) should not be used in CVD
- raises BP
- nasal spray - do not use for more than 3 days due to rebound congestions
84
what do a2 agonists usually work on and how?
works on muscle spasticity
complete opposite of a1 agonist -- it is a vasodilator and lowers BP
85
when are a2 agonists used?
primarily used to treat HTN or muscle spasticity
86
what specific a2 agonist agents used for HTN and ADHD?
HTN and ADHD
- Clonidine
87
when are a1 antagonists used and how do they work?
they work on the arteries and blocks the receptors
used as a last line of treatment for HTN and first line of treatment for BPH. also migraines.
88
when are B1 agonists used?
shock states and acute heart failure (dobutamine - increases CO)
89
where do B2 agonists work on?
in the lungs, bronchioles to dilate
90
what do mixed a1/b1 agonists work on and what do they do?
arteries (a1) and heart (b1) and increases HR and BP. Increases norepinephrine + epinephrine.
Also helps ADHD
91
when are B antagonists used?
most common autonomic nervous system medication
used in:
- CVD/post-MI
- tachy-arrythmias
- HTN
- HF
92
what is selective vs non-selective?
selective - primarily B1 selectivity
non-selective - effects mostly B1 but some B2. could cause bronchoconstriction
93
what changes affect PK and PD
- age
- renal function
- liver dysfunction
- overweight
- low weight/malnourished
94
Diuretic PT Considerations
muscle weakness/cramping (hypokal/mag), hyperreflexia/numbess (hyperkal), orthostatic hypotension, dehydration
95
Beta-Blocker PT Considerations
During exercise HR and CO may be depressed enough to reduce exercise capacity
Masks symptoms of hypoglycemia
96
Direct Vasodilator PT Considerations
vasodilation/edema
may antagonize cryotherapy
effects increased by thermotherapy
97
ACE Inhibitor/ARB PT Considerations
hypotension
hyperkalemia
98
CCB Dihydropyridine PT Considerations
hypotension, dizziness, headache, peripheral edema
99
CCB Non-Dihydropyridine PT Considerations
hypotension, bradycardia, headache, fatigue, dizziness
100
Nitrates PT Considerations
sublingual 5-10min before activity
thermotherapy can cause vasodilation may lead to syncope
orthostatic hypotension
dizziness
101
Antiarrhythmic Agent PT Considerations
may reduce exercise tolerance
may precipitate arrhythmias in some patients
faintness/dizziness
102
Thiazide Diuretics job
primary BP lowering
103
Loop Diuretics
very potent, may lower BP but not used to manage. seen in getting peripheral edema out in HF.
104
Potassium Sparing Diuretic
very gentle diuretic and sometimes used to raise someone's potassium and can use in HF
105
What PT interventions are contraindicated for patients on anti-coagulants
debridement, deep tissue massage, upper cervical manipulation
106
Statin PT considerations
myopathy and muscle aches - be concerned
pts w liver disease may not be able to take statins
107
What is pre-prandial glucose testing?
Pre-prandial glucose testing measures blood glucose levels before eating to monitor and manage blood sugar levels, especially in diabetes
108
Why is pre-prandial glucose testing important?
Assesses effectiveness of diabetes treatments.
Monitors basal glucose levels.
Helps adjust insulin dosing and other therapies
109
How should pre-prandial glucose testing be performed?
Use a glucometer or CGM.
Test after at least 8 hours of fasting for accurate fasting/pre-prandial results.
Record and track trends for healthcare review
110
what is empiric therapy
may be one or multiple agents to give sufficient coverage
an "educated guess"
samples are good but takes several days for results
111
routes of administration for antibiotics?
topical, oral, intramuscular, IV, intravitreal (into the eye), or combination
112
what is drug resistance
bacteria evolve mechanisms to survive antibiotics
can occur if antibiotics are overprescribed, not thoroughly finished
113
What is the difference between Gram-positive and Gram-negative bacteria?
Gram-positive bacteria have a thick peptidoglycan layer and appears purple 2° retaining the stain, while Gram-negative bacteria have a thin peptidoglycan layer and appears pink 2° being counterstained with safranin.
114
What role does peptidoglycan play in bacterial cells?
provides structural rigidity to the bacterial cell wall.
115
examples of diseases caused by gram-positive bacteria?
strep throat, staph infections
116
examples of diseases caused by gram-negative bacteria?
e. coli and salmonella
117
hy are Gram-negative bacteria often more resistant to antibiotics?
Their outer membrane acts as a barrier that can make it difficult for antibiotics to penetrate.
118
What is the significance of lipopolysaccharides (LPS) in Gram-negative bacteria?
LPS can be toxic when released into the body, contributing to disease.
119
What is a bactericidal agent?
a type of antibiotic that kills bacteria directly.
120
What is a bacteriostatic agent?
an antibiotic that inhibits bacterial growth and reproduction but does not directly kill the bacteria.
121
How do bactericidal and bacteriostatic agents differ in their mechanism of action?
Bactericidal agents disrupt essential processes, leading to bacterial cell death, while bacteriostatic agents interfere with protein synthesis or other functions to prevent bacteria from multiplying.
122
When might a bacteriostatic agent be preferred over a bactericidal agent?
Bacteriostatic agents are often preferred in cases where the immune system can effectively clear the infection after bacterial growth is inhibited.
123
What are the classes of antibiotics affecting cell wall synthesis?
Examples: Penicillins (e.g., Amoxicillin), Cephalosporins (e.g., Cefazolin), Vancomycin
Action: Inhibit the formation of the bacterial cell wall, leading to cell lysis and death.
124
What are the classes of antibiotics affecting the cell membrane?
Examples: Polymyxins (e.g., Polymyxin B)
Action: Disrupt the integrity of the bacterial cell membrane, causing leakage of cellular contents and cell death.
125
What are the classes of antibiotics affecting protein synthesis?
Examples: Tetracyclines (e.g., Doxycycline), Macrolides (e.g., Azithromycin), Aminoglycosides (e.g., Gentamicin)
Action: Inhibit bacterial ribosomes, preventing protein synthesis, which is essential for bacterial growth and reproduction.
126
What are the classes of antibiotics affecting folate metabolism?
Examples: Sulfonamides (e.g., Bactrim)
Action: Inhibit the bacterial enzyme involved in folate synthesis, disrupting nucleic acid synthesis and bacterial growth.
127
What are the classes of antibiotics affecting bacterial DNA synthesis?
Examples: Fluoroquinolones (e.g., Ciprofloxacin)
Action: Inhibit DNA gyrase and topoisomerase IV, enzymes necessary for DNA replication, leading to bacterial cell death.
128
What is CAM?
natural products, traditional chinese medicine, homeopathic meds, mind/body practice
129
what % of patients using CAM don't tell their PCP and why?
1/3 due to fear of judgment, it's natural, and thinks it doesn't matter
130
what is the DHSEA?
dietary supplement health and education act 1994
allows FDA oversight for suppements, but FDA has burden of proving unsafe after marketing (recalls)
131
rules for advertising supplements/CAMs?
can't claim any effects that are a feature of drugs
must be supported by objective scientific evidence
nonspecific claims (promotes digestive health etc) are allowed
132
what are the two databases we can use for CAM
american botanical counsel and databases
natural medicines database
133
is there a genetic link to ADHD
yes
134
risk factors for ADHD?
fam. history
FAS
lead poisoning
maternal smoking
meningitis
poor parent-child relationships
135
how long must ADHD symptoms be present for diagnosis
6 months
136
diagnosis requirements for ADHD?
have symptoms before age 7
+
have ≥ 6 inattention/hyperactivity symptoms
+
symptoms present in more than 1 setting
+
symptoms persist for at least 6 months
137
symptoms of inattention for ADHD?
makes careless mistakes and lacks attention to detail
aversion to activities that require prolonged attention
easily distracted
forgetful
fails to finish projects
138
symptoms of hyperactivity for ADHD?
fidgets/squirms in seat
leaves seat inappropriately
challenge with playing quietly
interrupts others
139
ADHD and addictive behavior?
increased risk for substance use disorder (SUD) by 2x, associated with:
nicotine, alcogol, cocaine
140
treatment guidelines for kiddos with ADHD?
behavioral therapy first, then medication
141
what are the first line of medications for ADHD?
stimulants
risk of diversion
142
first line of meds for kiddos with ADHD aged 4-5?
methylphenidate **only if behavioral therapy doesn't work
143
first line of meds for kiddos with ADHD aged 6-11?
FIRST LINE: stimulants
Second line: atomoxetine, ER guanfacine, ER clonidine
144
first line of meds for kiddos with ADHD aged 12-18?
ADHD meds (unspecific in slide)
145
contraindications for ADHD stimulant meds?
tourette's (either fam diagnosis or personal diagnosis)
tics
glaucoma
severe anxiety
MAOI use
146
ER vs IR drugs
ER = extended release
- less frequent dosing + longer onset
IR = immediate release
- less expensive, shorter duration of action, decreased risk for growth retardation
147
which adhd drugs have a high misuse potential
methylphenidate, dexmethylphenidate, amphetamine salts, dextroamphetamine
148
which adhd drugs have a med/low misuse potential
long acting/ER methylphenidate
149
which adhd drugs have a medium misuse potential
amphetamine salts (adderall VR)
Dextroamphetamine (Dexedrine Spansule)
150
which adhd drugs have a low misuse potential
Methylphenidate patch (Daytrana)
Lisdexamfetamine (Vyvanse)
Dexmethylphenidate (Focalin XR)
151
how often to titrate ADHD drugs?
every 3-7 days
152
common ADRs for stimulants ADHD?
decreased appetite
wt loss
stomach ache/headache
rebound sx
irritability/nervousness
153
less common ADRs for stimulants ADHD
dysphoria
zombie-like state
tics
HTN
abnormal pulse
hallucinations
growth retardation
154
ADHD stimulant warnings?
psychosis, mania, aggression, violence, severe anxiety/panic attacks
decrease dose or stop all together
155
PT considerations for ADHD?
break appointment/tasks into smaller segments
structured schedule
remove distractions
***do not apply direct heat over skin patches and check to see if patch came loose at end of session
156
PT considerations for endocrinological issues?
diabetes = chronic pain, loss of limbs, possible cardiac
thyroid probs = can lead to increased risk of general health deficits
osteoporosis = loss of bone density increases risk of fractures
exercise contraindicated in ketosis signs
may work with overweight pts
157
Type I Diabetes
Affects children and young adults
accounts for 5% of all diabetes cases
158
Type II Diabetes
adult onset
90-95% of all diabetes cases
159
gestational diabetes
10% of pregnant women
increases risk of developing TII diabetes later on
160
major T1 characteristics
occurs when pancreas is unable to produce enough insulin
requires insulin therapy
tends to develop at a young age
161
major T2 characteristics
occurs due to insulin resistance (when body doesn’t respond well to it)
can be managed with lifestyle mods if dx early
developed at an older age
162
Sx of both T1/T2?
frequent urination
increased thirst
extreme hunger
unintentional wt loss
fatigue
blurry vision
slow healing sores/wounds
tingling sensation in hands/feet
163
macrovascular complications from diabetes
MI
Stroke
PAD
164
microvascular complications from diabetes
foot ulcers (amputations)
retinopathy (vision loss)
neuropathy (chronic nerve pain)
nephropathy (dialysis)
165
hypOglycemic symptoms
sweating
pallor
irritability
hunger
lack of coordination
sleepiness
166
hypERglycemic symptoms
dry mouth
increased thirst
weakness
HA
blurred vision
frequent urination
167
what can lead to hypOglycemia?
- medications = taking too many or not on schedule
- exercice can exacerbate but reversed by glucose intake
*one of highest reasons elderly go to ER
168
what can lead to hypERglycemia?
nonadherence
non-optimized therapy
169
how to manage hypOglycemia?
glucose = <70 take a fast acting sugar source:
- 4oz fruit juice or soda
- 3-5 glucose tablets
- 6-7 lifesavers
test blood after 15min, if sugar still low then repeat until normal
170
when to call 911 for blood glucose?
if pt is unconscious or blood glucose is <50 and glucagon (rescue medication) should be given immediately
171
is hyperglycemia dangerous?
no severe sx until serious probs develop over time
172
what is hypOthyroidism
underactive thyroid gland - not enough thyroid hormones produced (T3 & T4)
173
causes of hypOthyroidism
autoimmune dx such as hasimoto's
thyroid surgery
radiation
certain meds
iodine deficiency
174
what is hypERthyroidism
overactive thyroid gland producing too much thyroid hormones (T3 & T4), TSH lower than normal.
175
causes of hypER thyroidism
graves disease
radiation
certain meds
176
symptoms of hypOthydroidism?
cold intolerance
wt gain
constipation
decreased sweating
depression/irritability
177
symptoms of hypERthyroidism
wt loss or gain
increased sweating
nail thickening/flaking
heat intolerance
nervousness/anxiety
racing heart
diarrhea
178
symptoms that both hyper/hypothyroidism share?
fatigue
insomnia
hair loss
179
target range for T4, serum and TSH?
T4, serum = 4.5-11.2 mcg/dL
TSH = 0.4 - 6.0 MIU/L
180
drug of choice for hypothyroidism?
levothyroxine
181
what is a thyroid storm?
decompensated hyperthyroid which can be life threatening
caused by nonadherence, trauma, surgery, or infection
182
treatment for thyroid storm?
beta-blockers
steroids
antithyroid meds + iodide therapy
cooling blankets / ice and antipyretics
183
PT considerations for thyroid problems?
cardiovascular/respiratory dysfunction can be precipitated w/ exercise
extended warm up / several minutes rest between resistive sets, 5min cool down to avoid hypotension
*these patients are typically higher risk for osteoporosis*
184
what is osteoporosis
weakened bones that become fragile and more prone to fractures. loss of bone mass.
185
what causes osteoporosis
aging
hormonal changes (esp. in post-menopausal women)
insufficient calcium/vitamin D intake
fam. history
certain meds such as long-term corticosteroid use
186
2 ways to determine risk for osteoporosis
fracture risk assessment tool (FRAX) - identifies risk of osteoporotic fx over 10 yrs in postmenopaus. women & men >50yrs old
Bone Mineral Density (BMD) scan - women >65 men >70. creates T score.
*normal = >-1, osteopenia = -1 - -2.4, osteoporosis = < -2.5*
187
two supplements to help with osteoporosis
calcium & vitamin D
188
when is treatment initiated for osteoporosis
when T-score is < -2.5. can initiate when score is -1 - -2.4 and FRAX score is >20%
189
what are the 6 classes of osteoporosis meds
1. biphosphonates
2. estrogen agonists / antagonists products
3. calcitonin
4. parathyroid hormones
5. rankl inhibitor
6. romosozumab
190
PT considerations for osteoporosis?
higher risk of fractures
wt bearing exercise can help strengthen/prevent falls
orthostatic hypotension is a concern w/ several meds
191
what is GERD
movement of gastric contents into esophagus
caused by relaxation of lower esophageal sphincter
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what is PUD
peptic ulcer disease
ulcers in upper Gi tract
causes: h. pylori, NSAIDs, stress
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Antacid "OIAs"
Use: neutralize gastric activity (primarily for acid reflux)
Dosing: frequent
Side Effects: minimal (constipation from aluminum/calcium, diarrhea from magnesium)
Interactions: binds to other drugs/reduces effectiveness
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Histamine-2 Receptor Antagonists "OIAs"
Uses: Inhibit histamine, gastrin, and ACh stimulated acid release; helps with basal and meal-related acids.
Dosing: Usually once to twice a day dosing.
Side Effects: Diarrhea, dizziness, muscle pain, rashes; Cimetidine has multiple drug interactions.
Interactions: Upregulation of receptors may diminish effectiveness with long-term use; cessation may lead to rebound acid secretion.
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Proton Pump Inhibitors (PPIs) "OIAs"
Uses: Irreversibly inhibit the H+/K+-ATPase pump on parietal cell membrane, stopping the final step of acid secretion; very effective at healing ulcers and preventing stress ulcer formation.
Dosing: Once daily dosing; need an acidic environment to function.
Side Effects: Similar to H2 Blockers; concerns with long-term use include decreased calcium absorption and increased risk for infection.
*concern w/ longterm use causes decrease in calcium absorption/increased risk of infection*
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neural mechanism for N/V - CTZ
chemoreceptor trigger zone
Senses toxins and drugs in blood and cerebrospinal fluid.
Involves dopamine, serotonin (5HT3), neurokinin, and opioid receptors.
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neural mechanism for N/V - vestibular
Responsible for motion sickness.
Involves muscarinic and histamine-1 receptors
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how do anticholinergics work for nausea
binds to ACh receptors in vestibular nuclei to block messages in vomiting center
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how do neuroleptic drugs work for nausea
similar to antipsychotic agents - blocks dopamine in CTZ
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how do antihistamines work for nausea
H1-blocking agents that inhibit vestibular input to the CTZ, blocks Ach binding to H1 in vestbiular nuclei
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how do prokinetic drugs work for nausea
block dopamine at CTZ - side use stimulate peristalsis in the stomach
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how do serotonin blockers work for nausea
blocks serotonin receptors in GI tract, CTZ, and vomiting center
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what is diarrhea
frequent passage of loose stools, either acute or chronic
mostly due to electrolyte imbalances in intestinal tract
chronic diarrhea have underlying GI conditions
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how do adsorbents work for diarrhea
coats GI tract, binds to diarrhea causing bacteria and reduces irritation providing relief
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how do opiates (lite) work for diarrhea
decreases GI motility and propulsion by increasing absorption of electrolytes and water
reduces pain w/ diarrhea
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what is constipation
movement disorder of colon/rectum = infrequent and painful defecation of sense of incomplete evacuation
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how do bulk-forming laxatives work for constipation
increases water absorption to soften/bulk up stool and stimulates paristalsis
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how do emollient laxatives work for constipation
facilitate water and fat absorption into the stool, reabsorption of water back into the body is blocked
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how do hyperosmotic laxatives work for constipation
works in large intestine by drawing fluid into colon
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how do saline laxatives work for constipation
increases osmotic pressure by increasing electrolyte and water concentrations in small bowel. increases peristalsis but with watery stools
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how do stimulant laxatives work for constipation
stimulates enteric nervous system and peristalsis.
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what to keep in mind if a patient is taking biphosphonates?
stand or sit up for 30min after taking it
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what is step 1 of the WHO Pain Ladder?
when a pt rates their pain 1-3/10
they can take NSAIDs
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what is step 2 of the WHO Pain Ladder?
when a pt rates their pain around 4-7/10
can take weak opioids
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what is step 3 of the WHO Pain Ladder?
when a pt rates their pain around 8-10/10
can take strong opioids
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what is step 4 of the WHO Pain Ladder?
typically surgery, pts have nerve blocks, epidurals, etc. *not anything with PT
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difference in dosing with aspirin for pain vs. platelets?
higher dose for pain, lower for platelets
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Characteristics of COX-1?
physiological housekeeping role (whole body maintenance)
- vascular homeostasis
- GI blood flow
- renal blood flow/function
- proliferation of intestinal mucousa
- platelet function
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Characteristics of COX-2?
as needed role
- inflammation
- fever
- pain
- ovulation
- placental function
- uterine contractions
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if someone has/had cardiovascular issues, what NSAID should they take and why?
Naproxen as it has the lowest cardiotoxicity risk of all NSAIDs
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which NSAIDs have potentially less GI toxicity?
Cox-2 semi selective (Diclofenac + Nabumetone)
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what is the most common NSAID used for OA and RA?
Celecoxib
decreases pain/swelling and increases function
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ADRs to keep in mind for all NSAIDs?
Blackbox warning - GI and cardiovascular toxicity. Renal toxicity.
Cox 1 = GI, renal, cardio hematologic, kidneys - increases salt excretion
Cox 2 = pregnancy concerns, can put someone into labor
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Pharm prevention treatment for NSAID-induced ulcers?
Histamine-2 Receptor Antagonists or Proton Pump Inhibitors
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Monitoring sequence for NSAID-induced nephrotoxicity?
get baseline levels before starting NSAID treatment
monitor urine output, serum creatinine, BUN
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Why should NSAIDs be avoided in those with previous cardiovascular issues?
can cause an increased risk of cardiovascular thrombotic events including MI and stroke. even with short term use and may begin within a few weeks of starting NSAID treatment. greater for those who already have heart disease.
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Drug interactions with NSAIDs ?
DIs with:
- anticoagulants (bleeding risk)
- corticosteroids (increased GI toxicity)
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special considerations / who should avoid NSAIDs?
heart disease
pre-existing renal dysfunction
pregnancy (avoid in 3rd trim, consider avoiding in 1st trim.)
elderly
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difference between local/general anesthetic?
local = specific portion of body, less systemic side effects, decrease pain but increase risk of falls
general = nervous system depression (reversible), various meds used (IV or inhaled), sedation, 4 stages
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ideal characteristics of general anesthesia?
rapid onset, skeletal muscle relaxation, minimum toxic side effects, rapid recovery, amnesia, analgesia
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what is stage 1 of general anesthesia?
analgesia
decrease pain, induce drowsiness
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what is stage 2 of general anesthesia?
delirium
excitement
loss of consciousness
irregular/rapid breathing
increased BP
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what is stage 3 of general anesthesia?
surgical anesthesia
regular, even, deep breathing
skeletal muscle relaxation
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what is stage 4 of general anesthesia?
medullary paralysis
respiratory paralysis
death
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are inhaled anesthetics lipid or water soluble?
lipid soluble, there's a hangover effect where it sticks to fat tissue.
anesthetics that are highly soluble in blood have a slower onset
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ADRs for inhaled anesthetics?
tachycardia
arrhythmia
muscle rigidity
increased BP/HR
hepatotoxicity
nephrotoxicity
increased ICP
decreased RR
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what is propofol infusion syndrome?
A rare, fatal condition from prolonged/high-dose propofol use.
Features: Metabolic acidosis, rhabdomyolysis, cardiac/renal failure.
Risk: High dose >48 hrs, critical illness.
Management: Stop propofol, supportive care.
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In what order are the anesthetic medications given?
premeds first
paralytics ONLY AFTER sedation
opioids, benzos before IV or inhaled anesthetics are at discretion of anesthetic team
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what are the therapeutic concerns of treating someone post-sedation?
hangover effect (weakness, lethargy)
excess mucous and secretion
abdominal distention
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regional vs local anesthesia?
local = small part of the body such as tooth or area of skin
regional = larger part of body (distal to injection), arm/leg
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what is LAST and how do you treat it?
local anesthetic systemic toxicity
treat with lipid rescue
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do topical anesthetic agents have risk of systemic toxicity?
yes
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what to keep in mind regarding topical anesthetic agents?
do not apply heat over a patch
still risk for systemic toxicity as it's well absorbed from mucous membranes
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what causes headaches associated with intrathecal administration?
altered CSF pressure
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What is salvage chemotherapy, and when is it used?
High-dose chemo used for relapsed or refractory cancer.
Goal: Prolong survival, achieve remission in patients unresponsive to standard therapy
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What are neoadjuvant vs. adjuvant chemotherapy?
Neoadjuvant: Before surgery/radiation to shrink tumors.
Adjuvant: After surgery/radiation to eliminate residual cancer cells.
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What is CAR-T therapy?
T-cells harvested, re-engineered to express chimeric antigen receptors (CARs), and reinfused.
Targets specific cancer antigens (e.g., CD19 in leukemia/lymphoma)
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How is nausea and vomiting (CINV) managed?
Before chemo: 5HT3 antagonists (ondansetron) give meds to prevent acute and anticipatory
After chemo: cannabinoids after chemo to treat or prevent delayed CINV
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What are the 3 phases of cancer patient care?
During treatment: Focus on tolerance and response.
Recovery: Rebuild strength, manage late effects.
Advanced cancer: Quality of life improvements.
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What are the 3 phases of chemotherapy-induced nausea and vomiting (CINV)?
Acute: Within 24 hours of chemotherapy.
Delayed: Occurs 24–48 hours after chemotherapy.
Anticipatory: Triggered by prior negative experiences or anxiety about chemotherapy
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What are secondary malignancies?
Cancers caused by mutagenic effects of prior chemo.
Commonly leukemia or lymphoma; typically harder to treat
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What is extravasation, and why is it dangerous?
Definition: Leakage of chemotherapy drugs into surrounding tissues during IV administration.
Effects: Tissue damage, large open wounds
Occurs with only some chemotherapy - Vesicants: Vincristine
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What are the signs/symptoms of Extravasation?
pain, redness, burning, pallor, no blood return, edema, decreased IV flow or flush
