Quiz 2 Flashcards
(192 cards)
1
Q
Why 10 shooters of hard alcohol within an hour can cause alcohol poisoning?
A
- The body metabolizes alcohol at a fixed rate of 20 mg/dL/hr
- After 10 shooters, the alcohol exceeds the liver’s ability to clear it (risk of alcohol toxicity–> poison)
2
Q
What else do we know about alcohol’s elimination rate?
A
- It’s zero kinetics elimination
- it’s being metabolized at a fixed ratw
3
Q
Half life
A
time required for (maximum concentration) Cmax drug plasma concentration to decrease by one half (by 50%)
- half life is known per each drug
4
Q
What do we know about drugs that have higher half-life?
A
- Since they have higher half-life drugs this then means that we will require less frequent dosing since the drug stats in the blood stream longer
5
Q
Pharmacodynamics
A
The study of what a drug does to the body. It focuses on the mechanisms through which it causes its effect
6
Q
Once a drug is distributed – where does it cause the therapeutic effect?
A
- It either binds directly to the drug ie.) Anti-infectives like antibiotics
OR - It binds to the receptors (6 major types)
7
Q
Know that drug-receptor binding is:
A
- *saturable: only limited # of receptors; once all are occupied increasing the drug dose won’t increase the effect. (more saturated= more therapeutic)
-
dynamic: increases (agonists) or suppresses (antagonists) existing processes.
** drugs only change existing processes and NOT create a new one** - *reversible drug can attach and detach from the receptor
8
Q
*Receptor Affinity
A
How well a drug binds to its receptor
- the strength/ length of binding
- it is specific, saturable and reversible
9
Q
*Drug Efficacy
A
effectiveness
*Degree to which a drug induces maximum therapeutic effect
10
Q
Potency
A
-How much of the drug is required! Amount!
11
Q
What is considered a more potent drug?
A
Whichever has smaller doses needed to achieve the same effect ( a more potent drug)
*Eg. Drug A 20 mg & Drug B 10 mg = Drug B potency is higher!
12
Q
*Agonist
A
activates the receptor to it’s max potential→ strongest possible effect
- has high affinity and high efficacy
- mimics the endogenous substance
13
Q
Endogenous Substance
A
inside the body substance; can be hormones, neurotransmitters, signalling molecules
- some drugs”mimics” the endogenous substance in the body
14
Q
Morphine mimics the effects of endogenous substance such as endorphins. What does it tell us?
A
- Morphine acts as natural pain killers, creating a sense of well- being and reducing pain
15
Q
Primary (aka Full) agonist
A
Full agonist activates the receptor to its max potential-> strongest possible effect
16
Q
Partial Agonist
A
-lower efficacy; good when we dont want cell to get used to that receptor
- maximum response is smaller even if all receptors occupied.
ie.) Buprenorphrine
17
Q
Partial Agonist in a presence of Primary Agonist
A
- Partial agonist can become Antagonist.. because the partial agonist can compete for those receptors
- this can prevent the full agonist from working fully
18
Q
Inverse agonists
A
Induce the opposite effect of naturally binding substance.
ie.) Caffeine; is an inverse agonist and promotes increased alertness and wakefulness
Adenosine: promotes sleep and relaxation when it binds to receptors.. However when Caffeine binds to adenosine receptors (it induce the opposite effect)
19
Q
Antagonists
A
Drug ‘blocks’ the receptor site to prevent endogenous or endogenous-like substance from binding
20
Q
Does Antagonist work in cellular activity?
A
No, it does not
- All it does it it blocks the receptor site so that “endogenous” or “endogenous - like substance” is prevented from binding
21
Q
Can we take as many Naloxone when we have an opioid receptors?
A
Of course we can! Again, the Naloxone does not induce or inhibit any cellular activity. But instead it displaces the opioid receptors
22
Q
What are the 6 major receptor types?
A
- G-protein (GPCR)
- Ion channels
- Nuclear receptors
4 & 5. Enzyme types - Non-enzyme
‘JAK-STAT’
23
Q
- G-protein
A
most common in terms of full agonist drugs
-stimulates G-protein & second messenger systems = sympathomimetic stimulation
24
Q
Which one is more specific n regards to receptors?
A
- Epinephrine is more specific- due to a wider adrenergic receptors???
- Norepinephrine: less specific???
25
What does "sympathomimetic circulation" and what will we see when a drug causes this?
- it mimics the Sympathetic Nervous System
-↑HR, ↑BP, ↑BGC, bronchodilation,pupils dilate, vasoconstriction (in terms of general periphery→ to redirect blood flow to skeletal muscles, heart and lung
26
Epinephrine
- higher affinity for Beta 2 receptors
-increases HR, bronchodilates and increases blood flow to muscles and skin (while constricting blood vessels in less critical areas like skin)
27
Norepinephrine
- higher affinity for A1 receptors
- leads to vasoconstriction (narrowing of blood vessels)
28
2.) Ion channels
gates that control the movement of electrolytes (ions like sodium, potassium and calcium) into and out of cells.
29
Depolarization
ion channels open, ions flow into the cell, making it more positively charged
30
Repolarization:
ion channels close or ions flow out, the cell returns to it’s resting negative charge.
31
What drug do we ought to know- closes ion channels?
Lidocaine
32
What happens if a drug closes ion channels?
no action potential => no cellular depolarization => no pain transduction (no pain sensation)
33
3.) Nuclear receptors
aka ‘steroid’ receptors
- often drugs are lipophilic; thus they can enter the cell directly and make a change
- most bind in cytoplasm= change cell fx via DNA
34
*4&5. Enzyme binding
- Intracellular enzyme and Transmembrane enzyme
35
*Intracellular enzymes
- operate inside the cell, often activated by signs received through receptors on the cell membrane.
36
*Transmembrane enzymes
act as receptor themselves or part of receptor systems, bridging events outside the cell to cellular responses inside.
37
Non-enzyme Transmembrane
Acts in cellular signaling pathways,mediating responses to external stimuli without requiring enzymatic activity
*Eg. JAK-STAT receptors (e.g. used by interferons)
38
Drug tolerance
- aka Down-regulation
-receptor de-sensitization OR decreased number of viable receptors to a substance
; this means we need more drugs required for the same response
(addictive substance, opiates, benzodiazepines)
39
Drug resistance
Many variations of kinetic alterations
- drug either is metabolized at a faster rate (therefore less bioavailable and therefore less effective)
40
Non-deleterious (side effects)
Unwanted effects that are not harmful or damaging to the body
ex.) drowsiness
41
Deleterious (TOXIC)
Harmful effects caused by a drug-> due to excessive dosage or prolonged use
ex.) liver damage
42
Factor influencing patient response (Clinical factors)
-Age, weight
-Present health disorder -Other disease entities , -Client drug compliance
43
Factors Influencing Pt Response (Administration)
- Drug Form
- Route of Drug Administration
- Multiple drug therapy
- Drug interactions
44
Factors Influencing Pt Response (Pharmacokinetics)
- Absorption
- Distribution
-Metabolism (t1/2)
-Excretion
45
Factors Influencing Pt Response (Pharmacodynamics)
- Onset, peak, and duration
- Therapeutic range (Therapeutic window)
- Side effects, adverse reactions (assess!)
46
How do age and weight affect dosing and drug metabolism?
Age and weight significantly impact how drugs are metabolized in the body. Children and the elderly often metabolize drugs differently than adults due to variations in body composition, organ function, and enzyme activity. Children may have faster metabolism for some drugs, requiring different dosages, while the elderly may have slower metabolism, increasing the risk of drug accumulation and side effects.
47
How can current illnesses or conditions alter drug effectiveness or how the body handles the drug?
Current health disorders can influence how drugs are absorbed, distributed, metabolized, and excreted. For instance, liver or kidney diseases can impair drug metabolism and excretion, leading to higher drug levels in the body and increased risk of toxicity.
48
In what ways can co-existing health conditions impair drug metabolism and excretion?
: Co-existing health conditions, such as chronic diseases (e.g., diabetes, hypertension, heart disease), can impair drug metabolism and excretion. For example, liver disease can reduce the liver's ability to metabolize drugs, while kidney disease can impair the excretion of drugs, leading to drug accumulation and potential toxicity. Additionally, interactions between multiple medications used to treat co-existing conditions can affect drug metabolism and effectiveness.
49
How does patient compliance with taking the drug as prescribed (correct dose, time, and frequency) impact treatment outcomes?
Patient compliance is crucial for the effectiveness of treatment. Taking the drug as prescribed ensures that the medication reaches and maintains the therapeutic levels needed to treat the condition. Non-compliance, such as missing doses, taking incorrect doses, or not following the prescribed frequency, can lead to suboptimal therapeutic outcomes, worsening of the condition, and potential drug resistance.
50
How does the form of a drug (tablet, injection, liquid, etc.) impact its administration and absorption?
The form of a drug affects how it is administered and absorbed by the body. For example, tablets and capsules are absorbed more slowly as they need to dissolve in the stomach,
- while liquid forms are absorbed more quickly. Injections deliver the drug directly into the bloodstream, resulting in rapid absorption and effect. The choice of drug form can influence the onset, duration, and effectiveness of the medication.
51
How does the route of administration (oral, intravenous, topical, etc.) affect the drug's absorption and effectiveness?
The route of administration determines how quickly and efficiently a drug is absorbed and takes effect.
-Oral administration is convenient but may be slower due to digestion. - -Intravenous administration delivers the drug directly into the bloodstream for rapid effect.
-Topical administration targets specific areas of the body with minimal systemic absorption.
52
What are the potential interactions and challenges when taking several medications simultaneously?
Taking multiple medications can lead to potential interactions where one drug affects the action of another. These interactions can enhance or reduce the effectiveness of the drugs and may increase the risk of side effects.
53
How does one drug affect the action of another when taken together?
Drug interactions occur when one drug influences the action of another, either enhancing or diminishing its effects. This can happen through various mechanisms, such as altering the absorption, metabolism, or excretion of the drugs
54
Onset
How long it takes for the drug to start working
55
Peak
When the drug is its max effect
56
Duration
How long the drug’s effects last
57
Therapeutic range (Therapeutic window)
The concentration of the drug in the blood that produces the desired effect without causing toxicity
58
Side effects
mild and expected
59
Adverse reactions
Severe and harmful
60
There are genetic differences affecting ADME: (in Absorption)
Genetic differences-> affect the function of transport proteins in the gut-> changing how much drug enters the bloodstream
61
Poor Metabolizer:
- Has little or no enzyme activity-> leads to slower drug breakdown
- Increase toxicity (for active drugs): the drug builds up in the body due to poor metabolism
- Reduce Efficacy (of prodrugs). ie.) Codeine (needs to me metabolized into its active from but due to poor metabolism, it stays inactive)
62
Intermediate metabolizer
Reduced enzyme activity
Less severe effects than poor metabolizers
63
Normal metabolizer
- Typical enzyme activity
- Drugs behave as expected
64
Rapid metabolizer
-Higher than normal enzyme activity
- The drugs are metabolized quickly; potentially reducing effectiveness
65
Ultrarapid metabolizer
Extremely high enzyme activity .
- drugs is cleared too quickly
- Risk of toxicity: Prodrug (activated too quickly into high levels)
66
How will a poor metabolizer affect prodrug? ie.) Codeine
- Reduce effectiveness of the prodrug (takes a while to metabolize and turn it into active form)
67
How will a ultrarapid metabolizer affect prodrug? ie.) Codeine
Risk of toxicity (gets activated too quickly into high levels)
68
decreased CYP2D6 (liver enzyme)... how will this affect metabolism?
decreased CYP2D6 enzyme= reduced metabolism of specific drugs, risk of toxicity + reduced metabolism of prodrugs such as:
(eg.) Codeine) risk of low efficacy
69
Pregnancy category A
-Appropriate human studies- no risk
- drug is safe during pregnancy ie.) certain vitamins at recommended dose
70
Pregnancy category B
Insufficient human studies, but animal research suggests safety or:
Animal studies: safe
Human studies:
No adequate studies
71
Pregnancy category C
Animal studies:
Fetal harm
Human studies:
No adequate studies
- No studies for both
*drug should only be used if the potential benefits outweigh the risks
72
Pregnancy category D
Human studies, with/without animal research show fetal risks, but the drug is important to some women to treat their conditions
73
Pregnancy category X
- Fetal risks are evident; there are no situations where the risk/benefit justifies use
- Studies in humans and animals have showed fetal risks
-Strictly contraindicated in pregnancy **
74
Pregnancy Pharmacotherapy (1)
Altered GI function:
- delayed GI emptying (stomach takes longer to empty its content into the intestines
- Decreased acidity (some drugs require acidic environment -->absorption may be less efficient)
75
Pregnancy Pharmacotherapy (2)
- Higher blood volume
- higher blood flow to placenta ( increases to supply 02 nutrients to the fetus)
- higher HR: heart pump's faster
- decreased PBB: since there's an increase in blood- this dilutes the concentration of plasma proteins resulting in a lower overall binding capacity for drugs
- higher GFR: kidneys work harder because we have more blood
76
FYII.. about drugs and pregnancy:
- most drugs taken by the mother can cross the placenta and reach the fetus (bc we have tons of blood that cross the placenta)
- drug can be passed through breast milk while breastfeeding
77
What type of characteristics make drug more likely to cross the placenta or transfer into breastmilk?
- High Vd drugs
- Absorption + Distribution Characteristics:--> lipophilic, small, non-ionized, drugs that are unbound by PPB.
78
Which meds are not recommended during breastfeeding?
Ibuprofen, Opioids (codeine, oxycodone, morphine)
79
how do we calculate pediatric pharmacotherapy (0-18 yrs of age)
typically calculated based on the child’s weight
80
What age is considered as "Pediatric pharmacotherapy"?
0-18 yrs of age
81
Pediatric blood volume is:
80ml/kg of body weight
- much lower than adult
- therefore blood loss can have much larger impact on an adult
- less albumin (if they have less blood)--> careful dosaging
82
Pediatrics Pharmacotherapy:
- Education for caregivers is important
- Make sure that meds are stored in child proof containers (to avoid poisoning)
83
Organ fx: neonates and young ingants
- body is still developing→ drug metabolism are not yet fully developed + underdeveloped kidneys
84
CrCl:
kidneys ability to filter creatinine
85
Urine output:
help assess kidney function and electrolyte balance.
86
Liver enzymes
high levels of ALT and AST are indicators if liver health→
-elevated levels indicate liver damage/ dysfunction.
87
Liver
responsible for metabolizing (breaking down) drugs and other substances
88
Kidneys
responsible for filtering waste and eliminating substances from the body
89
Underdeveloped liver and kidneys in neonates and young infants are at risk for:
- processing drugs more slowly--> leading to a longer duration of effects and potential toxicity
90
Older Adult Pharmacotherapy: (1)
- decreased peristalsis, acidity, elimination: slower movement of food/ drugs through the digestive tract
- decreased GFR: can lead to slower drug elimination, causing drugs to accumulate (increasing toxicity)
- shallow resps: reduced lung capacity
91
Older Adult Pharmacotherapy: (2)
- Lower albumin (affects PPB): means that there will be more free- bound, increasing drug potency and toxicity.
- Decreased CO (affects distribution): lower heart efficiency reduces blood flow (affecting how drugs are delivered to organs and tissues)--> can delay drug onset; and prolong drug effects (due to slower metabolism and elimination)
- *Lower total body water due to lower muscle mass & alterations in metabolism: aging leads to less muscle mass and total body H20--> this will result to risk for dehydration (affects plasma volume; decreases GFR= risk for toxicity
92
Why is dehydration play a role for Older Adults?
- Dehydration (affects plasma volume)--> decreased GFR.
- Decreased GFR= risk for toxicity; because slower filtration of the drug
93
What are the things that can affect medication intake for older adults?
- Hearing, vision, cognitive impairments
- memory issues
- underuse (not taking enough meds/ skipping doses)
- misuse(incorrect use of meds)
- overuse (too much meds leads to multiple side effects)
94
Polypharmacy
multiple medication
95
Risk for polypharmacy?
- increasing the risk of drug interactions, side effects and confusion.
96
*ASA (Aspirin)
A common pain reliever and fever reducer.
- Toxic effects:
Can cause stomach bleeding, ringing in the ears (tinnitus), breathing problems, confusion, and even kidney failure.
-Severe cases:
Can lead to seizures, coma, or death.
97
*ASA (Aspirin)
A common pain reliever and fever reducer.
- Toxic effects:
Can cause stomach bleeding, ringing in the ears (tinnitus), breathing problems, confusion, and even kidney failure.
-Severe cases:
Can lead to seizures, coma, or death.
98
*Tylenol (Acetaminophen)
Used for pain relief and fever reduction.
-Toxic effects:
Too much can damage the liver, causing nausea, vomiting, abdominal pain, and jaundice (yellowing of the skin/eyes).
-Severe cases:
Can lead to liver failure and death without treatment.
99
*Opioids (strong painkillers)
ie.) Oxycodone, Fentanyl
- Toxic effects:
Can slow or stop breathing, cause extreme drowsiness, pinpoint pupils, and unconsciousness.
-Severe cases:
Overdose can be fatal without quick treatment (Narcan/Naloxone can reverse effects).
100
*Benzodiazepines (Anti-anxiety medication & sedatives)
ie.) Xanax (alprazolam), Valium (diazepam)
-Toxic effects:
Can cause drowsiness, confusion, slow breathing, and unconsciousness.
*Dangerous when mixed with alcohol or opioids—increases risk of overdose.
101
*Alcohol (ETOH)
Found in beer, wine, liquor, and some medications.
-Toxic effects:
Can cause slurred speech, confusion, vomiting, breathing problems, and unconsciousness.
-Severe cases:
Can slow or stop breathing, cause coma, or lead to death.
102
*THC (Tetrahydrocannabinol) -> cannabis, marijuana
The active ingredient in marijuana (weed, edibles, vapes, etc.).
-Toxic effects:
Can cause anxiety, paranoia, hallucinations, nausea, vomiting, and an increased heart rate.
- Severe cases:
Rare, but some people experience extreme agitation or prolonged vomiting (cannabinoid hyperemesis syndrome).
103
*Cocaine (stimulating drug)
A highly addictive stimulant drug that increases energy and alertness.
Toxic effects: Can cause a fast heart rate, high blood pressure, severe sweating, confusion, and seizures.
Severe cases:
Can lead to a heart attack, stroke, or sudden death.
104
Common nursing errors
*Dose errors (incorrect dosage)
*Crushing of enteric-coated tablets or sustained-release tablets
*Late charting
*Rushing (not checking all the rights, every time)-->.6 rights of administration
105
Clinical procedure in toxicity (overdose): ‘stabilize & analyze’
A- Airway
B- Breathing
C- Circulation
D- Disability
E- Exposure
106
A & B (Airway & Breathing)
-assess patency: check if the airway is open?
- effort: stuggling to breathe
- rate: breathing too fast or too slow?
- colour: is the skin turning blue (cyanosis)
107
C (Circulation)
- assess blood flow and perfusion.
- LOC: is the pt awake or unresponsive?
- Consider IV fluids? if pt is in shock or dehydrated.
- Sympathomimetics meds: may be given to increase HR, BP, vasoconstrict the peripheral bv, bronchodilation and pupil dilation
108
D (Disability)
- assess for neurological & organ dysfunctions and treat as needed.
- apnea, seizures, cardiac arrythmias, hyperthermia
109
Apnea
patient has stopped breathing-> artificial ventilation is needed
110
Seizures
- can be caused by certain drug overdoses.
Tx may include: lorazepam, diazepam
111
Cardiac arrhythmias
Some drugs (e.g., cocaine, opioids) cause dangerous heart rhythm
112
Hyperthermia
high body temp
113
E (Exposure
- Identify the drug/ substance and initiate tx
114
How do we identify drug/ substance?
- Patient’s Health History
- Lab toxicology (urine, serum)
115
Urine toxicology screen
Detects recent drug use
116
Serum (blood) toxicology
Measures drug levels in the bloodstream to assess severity and risk of toxicity
117
How do we assess patterns of signs and symptoms specific to certain drug overdoses
Toxidromes
118
What is toxidromes?
Characterized by a specific group of symptoms that help healthcare providers identify the type of poisoning→ provide appropriate tx
119
Cholinergic
excessive salivation, lacrimation, urination, diarrhea and bradycardia
120
Sympathomimetic
symptoms like increased HR, BP + dilated pupils
121
*ASA (Aspirin): Overdose Toxidrome
*Confusion: altered mental state
*Tachycardia:fast heart rate
*Tachypnea:fast breathing
*Hyperthermia: high body temp
*Diaphoresis: excessive sweating
*Vomiting:GI distress
122
Diaphoresis
excessive sweating
123
*Acetaminophen (Tylenol): Overdose Toxidrome
*Abdominal pain: liver damage
*Loss of appetite: early sign of toxicity
*Nausea/vomiting: GI distress
*Diaphoresis: excessive sweating
*Somnolence: excessive drowsiness
124
*Opioids (Fentanyl, Codeine, Morphine, Oxycodone, Heroin, ….)
- Are CNS depressants that slow breathing, heart rate, and brain activity
- *Bradypnea/Apnea: Slow or stopped breathing (life-threatening!)
*Bradycardia: slow heart rate
*Somnolence/Coma: severe drowsiness, unresponsiveness, or coma
****Pupils constricted : Very small pupils-> key sign of opioid overdose
125
*Cocaine (& other stimulants)
*Agitation, tremors: restlessness, shaking, anxiety, paranoia
*Tachycardia: ast heart rate
*Tachypnea: rapid breathing
*Hyperthermia
*Diaphoresis
**Pupils dilated: Large pupils-> key sign of stimulant overdose
126
Is there an ADME that we can use for Cannabis?
No, there is not!
127
What is cannabis?
- Depressant: reduced neural activity and slow body fx (calm/ relaxation)
-Hallucinogen: alter perception, mood, and cognitive processes
-Stimulant: boost energy levels and improve alertness
128
Cannabis Toxidrome
-VS changes: tachycardia, hypertension
- seizures
-nausea & vomiting
- acute psychosis (hallucinations, paranoia, delusions)
- LOC changes: agitation (restlessness, confusion), coma
129
Cannabis ROA
Inhalation: 15-30 mins onset; 50% bioavailability
PO: 1-2 hr onset; delayed effect and can lead to overdose risk if taken too much and too fast; 20 % bioavailability (due to first pass)
130
THC "tetrahydrocannabinol"
- has psychoactive effects
causes CNS & VS instability
- binds to receptors causing that "euphoria effect", altered perception, anxiety, paranoia, increase HR and hallucinations
131
CBD ((Cannabidiol)
modulates (reduces) effect of THC at receptors
- changes the shape of the receptor so THC binds less effectively
132
How does THC and CBD differ from each other?
THC produces the psychoactive effect
CBD: modulates/ reduces effect of THC at receptors.
133
Tx of Cannabis:
- it is supportive
- Tx focuses on managing symptoms
134
Treatment (Algorithms)
Algorithms : step-by-step medical guidelines used to quickly decide on the best treatment.
ie.) Hypertension with antihypertensives, respiratory depression with Intubation to ensure 02 delivery
135
How do we utilize ADME in tx?
- If a drug is metabolized slowly, it might require prolonged monitoring and supporting care
- If a drug is eliminated by the kidneys, doctors may give IV fluids or dialysis to help remove it faster?
136
What do we do first? give antidote or stabilize the pt?
- First, stabilize the pt
- Second: Give antidote
137
Antidote
substance that neutralize, reverse, or stop the toxic effects in the body
138
seizures tx with
Benzodiazepines:
Stops seizure and calms brain overactivity
139
hypertension tx with
Antihypertensives:
Lowers BP to prevent stroke or heart attack
140
respiratory depression tx with
intubation: ensures O2 delivery
141
psychosis tx with
Antipsychotics:
Calms hallucinations and paranoia
142
What is out activated agent?
Activated Charcoal- fine, highly porous black powder made from carbon-based materials.
143
What does Activated Charcoal do?
- it binds to toxic drugs in the stomach and prevent their absorption into the bloodstream
144
How is Activated Charcoal- drug complex eliminated?
The drug-charcoal complex is then eliminated through stool (feces).
145
Agents Poorly Absorbed by Activated Charcoal:
- Cyanide
-Ethanol
-Ethylene Glycol
-Iron
-Isopropanol
-Lithium
-Methanol
-Strong Mineral Acids & Alkali
146
Well Absorbed by Activated Charcoal (that we've talked about in class)
- ASA, Antidepressants, Antihistamines, Aspirin, Other Salicylates, Benzodiazepines, Beta-blockers, Other Opioids, Digitalis, Furosemide, Indoemethacin, other NSAIDS, Methotrexate, NSAIDS, Paracetamol*, Tetracyclines,
147
What does poorly absorbed by Active charcoal tells us?
- It tells us that having alternative tx or interventions are often required for poisoning/ overdose
148
Provide an example where "inducing metabolism" will help with overdose tx?
- Tx of Tylenol toxicity
149
Glutathione
-a natural liver enzyme + neutralizes toxic substances in the body.
- the liver needs Glutathione to safely break down Tylenol
150
What is there depletion of during Tylenol toxicity?
- there is depletion of Glutathione, thus leading to toxic build up (liver can no longer protect itself from harmful by products)
151
What forms when Tylenol is broken down?
NAPQI (N-acetyl-p-benzoquinone imine
152
How does Glutathione and NAPQI work?
Normally, Glutathione neutralizes NAPQI, so it doesn’t cause harm.
But in Tylenol overdose, there isn't enough Glutathione left to stop NAPQI.
153
What is NAC? (n-acetylcysteine/acetylcysteine
a Glutathione enzyme precursor
- Helps the body produce more Glutathione
- Restores Glutathione that was depleted by Tylenol
154
Which Phase of Tylenol metabolism does NAC enhance?
Phase 2 metabolism
155
Algorithm to treat an Acetaminophen
- used in hospitals to determine when and how to treat an Acetaminophen overdose based on time since ingestion acetaminophen levels.
156
Algorithm for Acetaminophen: less than 4hrs since overdose
- consider activated charcoal
- if levels are high:consider NAC
157
Algorithm for Acetaminophen:
more than 4-8 hrs:
- check paracetamol level; if level not obtained before 8 hrs after ingestion --> start NAC
158
Algorithm for Acetaminophen: more than 8-24hrs
- start NAC immediately
- if level is high; continue NAC and if level below tx: stop NAC
159
Algorithm for Acetaminophen: more than 24hrs
- Start NAC
- Check AST/ALT levels (liver function)
160
How does Alcohol affect CNS?
In low doses: relaxation, reduced anxiety
In high doses: loss of coordination, slurred speech, unconsciousness.
161
Alcohol as GABA agonist:
- Alcohol binds to GABA receptors, enhancing relaxation and sedation
162
GABA (gamma-aminobutyric acid)
GABA is the brain’s calming neurotransmitter.
163
Alcohol as Glutamate Inhibitor
- Alcohol blocks glutamate
- leading to slowed brain function, poor
coordination, and memory loss (blackouts)
164
Alcohol.. inhibits ADH
- blocks ADH; thus producing more urine
- this can lead to dehydration, electrolyte imbalance (cause headaches, dizzines and hangover symptoms)
165
3 ways that alcohol acts on one' s body
- Inhibits ADH ( leads to diuresis= urine production)
- GABA agonist (enhancing relaxation + sedation)
- Glutamate inhibitor (slows brain function)
166
Alcohol Chronic Use:
will cause GABA receptors numbers to increase; requiring higher doses of alcohol to feel the same effects
167
alcohol dehydrogenase
enzyme that metabolizes ETOH
168
Tx for Alcohol Overdose?
- Metadoxine: to induce alcohol dehydrogenase
- IV fluids: help with dehydration + electrolyte imbalances
169
Metadoxine
- Speeds up alcohol metabolism
-Induces alcohol dehydrogenase metabolism
170
Symptons of an Alcohol Poisoning Emergency:
- Slow or irregular breathing
- Low body temperature
- Vomiting
- Seizures
- Unconsciousness and can’t be woken up
171
Main fx of the liver:
- Metabolism:
- Detoxification
- Bile production
- Blood sugar regulation
-Protein synthesis
-Storage
- Immune function
172
Main fx of the liver:Metabolism
Processes nutrients, fats,
carbohydrates, and proteins for
energy and storage
173
Main fx of the liver:Detoxification
Breaks down and removes toxins, drugs, and alcohol from the blood
174
Main fx of the liver: Bile production
Produces bile, which helps digest
and absorb fats in the small
175
Main fx of the liver: Blood sugar regulation
Stores and releases glucose (sugar) to keep blood sugar levels stable
176
Main fx of the liver: Protein synthesis
-makes important proteins like
albumin (for blood pressure) and clotting factors (for blood clotting)
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Main fx of the liver: Storage
- Stores vitamins (A, D, E, K, B12)
and minerals (iron, copper) for
later use
178
Main fx of the liver: Immune function
Helps fight infections by removing bacteria and toxins from the blood
179
What happens when liver is compromised:
- Toxins build up:
- Fat digestion fails:
- Blood sugar swings
-Protein production stops
180
Hepatic vein
- Carries "clean" blood from the liver back to the heart.
181
What happens when hepatic vein is compromised?
- Blood backs up in the
liver, causing congestion
and swelling
- Increases risk of liver
damage due to poor drainage
182
Portal vein
Brings nutrient-rich blood from the intestines to the liver for processing
183
What happens when portal vein is compromised?
- Portal hypertension (high pressure in portal vein occurs)
184
What happens is there is high pressure in portal vein--> blood backs up into tissues, intestines, stomach, esophagus?
- Ascites
185
Opioid receptor antagonist
- A drug that blocks opioid receptors to stop opioid effects.
186
Tx drug for Opioid?
- Narcan (Naloxone)
187
Tx for Alcohol Overdose?
- Metadoxine: to induce alcohol dehydrogenase
- IV fluids: help with dehydration + electrolyte imbalances
188
Tx Narcan (Naloxone)
- only blocks to prevent drug-receptor activity from happening; but does not alter anything--> it is safe to give.
189
Tx Benzodiazepine toxicity:
- GABA receptor antagonist
Tx Drug: Flumazenil, IV
190
Innate immunity
- born with
- non-specific
191
Examples of Innate Immunity
- eg.) skin
- Mucus & cilia (in the nose/lungs)
- Stomach acid-> kills bacteria in food
- Tears & saliva-> contain enzymes that break down bacteria
192
What type of cells are part of the innate immune system?
