1
Q
CNS Neurotransmitters
A
Receptor determines action of NT
(ie, NTs are excitatory or inhibitory, and communication is complex between neurons, but the receptor itself determines the action of NT)
2
Q
What specific characteristics must a substance have to cross the blood-brain barrier (BBB)?
A
BBB formed by endothelial cells and astrocytes that limits movement of substances into CNS
In order to cross, substances must be lipophilic and able to diffuse easily
3
Q
Basal nuclei (basal ganglia) function
A
Regulates starting and stopping of skeletal muscle movements
Assists with starting and stopping of some cognitive functions associated with memory, learning and planning
4
Q
Extrapyramidal System
A
Modulates motor activities associated with alpha motor neurons including reflex arcs, postural control and complex movements like walking
Tracts move through brainstem into spinal cord
Signals carried along these tracts are influenced by activity of basal nuclei
5
Q
The Three D’s
A
Delerium - Acute onset, can be treated
* Altered state of consciousness
* Assessed using the CAM (see Care Plans)
Patients disoriented and fluctuating levels of consciousness.
Depression - Gradual onset, can be treated
* Look for signs, such as low self-esteem.
* Can coexist with other medical diagnoses. Need lifestyle modifications or ECC for fever cases
Dementia - Gradual onset, might be treated
* Memory loss and decline in cognitive function.
* Progresses slowly over months or years. Certain types are not fully reversible, but some can be caught and treated early (like vitamin deficiencies)
6
Q
Geriatric Pharmacokinetics
A
Absorption –> Distribution –> Metabolism –> Excretion
Absorption: not affected significantly, maybe minor changes, like decreased gastric acid production, reduced GI motility, and this can impact some drugs
Distribution:
↘️ total body water
↗️ body fat
↘️ serum albumin
* older adult have less water in body, so some drug concentrations can be higher, and needs to be adjusted.
* Also, body fat up means slower metab.
Serum albumin decreased
Metabolism:
↘️ hepatic blood flow and metabolizing enzymes
* slower metab. so slower drug clearance, –> drugs have longer durations of action
Excretion:
↘️ renal function
* Reduced GFR, kidney clears meds slower.
7
Q
Medications to treat primary symptoms - Cholinesterase Inhibitors
A
Cholinesterase inhibitors = donepezil, rivastigmine, galantamine
These drugs stop the breakdown of acetylcholine, which is an important neurotransmitter in memory and cognition.
* SO, since breakdown is reduced, it increases how much is available in the synapse.
Show modest improvement in cognition, function, and behaviour.
Response: 1/3 improve, 1/3 stabilize, 1/3 have no response.
Does not prevent the progression of underlying disease
8
Q
Medications to treat primary symptoms - Memantine
A
Glutamate is a transmitter in the brain that is affected by Alzheimer’s Disease.
Blocks the pathological effects of abnormal glutamate release.
Allows for better function of the impaired brain.
Indicated for moderate to severe Alzheimer’s.
Trials show slowing in cognitive and functional decline, as well as ↘️ in agitation.
9
Q
Risks associated with acute care admissions for patients with dementia.
A
- Inability to communicate symptoms
- Mismanagement due to staff lack of information, poor understanding, time and bed pressures, inadequate training
- Information gathering difficult for staff – sometimes relies heavily on external source that may not be readily available, particularly ‘out of hours’
- Environmental changes - multiple ward moves, patients and staff
- Cluttered ward layouts, poor signage, other hazards
- Inappropriate prescribing.
- Inadequate pain recognition and control
- Procedures – e.g. catheter, NGT, blood tests, IV lines
- Poor supervision on the ward
10
Q
What are the potential consequences of “risky” acute care admissions for dementia patients?
(Related to previous “Risks” card)
A
- Delayed diagnosis
- ↗️ incidence of delirium, falls and fractures, malnutrition, dehydration, hospital acquired infections, and iatrogenic illness
- ↗️ length of stay
- ↗️ subsequent admission to long-term care (institutionalization)
- ↗️ mortality
11
Q
How to work with pts with Dementia
A
Show them you care/validate:
* Be mindful of tone of voice, facial expressions, word choices, gestures.
* Be able to listen to criticism, complaints, and sadness without invalidating, retaliating, or withdrawing.
MIScommunication can occur when:
* Eyeglasses are not being worn or are dirty
* Hearing aids aren’t in, or batteries are dead
* Dentures are out, unable to access nutrition
The DOs:
* Respect and dignity
* Explain clearly, keep short.
* Maintain eye contact
* Look directly at person, get their attention
* Be realistic in expectations
* Paraphrase and use calm, reassuring tone
* Encourage talk about things they are familiar with
* Therapeutic touch
The DON’Ts:
* No baby talk
* No complicated words
* Don’t NOT explain things that you are about to do
* Don’t Talk over distracting environment
* Don’t Provoke
* Don’t disregard you own non-verbals
* Don’t shout/talk too fast
* Don’t touch without permission
12
Q
Describe the specific neurotransmitter imbalance in the striatum during Parkinson’s Disease.
Also, what is the normal physiology?
A
Normal Physiology: The striatium receives excitatory input from the cortex
* Mediated by the excitatory neurotransmitter, glutamate
There is a loss of inhibitory dopamine input from the substantia nigra (the neurons die), which fails to balance the excitatory glutamate input from the cortex.
13
Q
Pathophysiology of Parkinson’s Disease (PD)
A
Death of dopamine-producing neurons projecting from the substantia nigra to the striatum.
14
Q
Define the four characteristic motor problems of PD.
A
Degenerative disease in which dopamine-producing neurons in the basal ganglia die
* Neurons projecting from substantia nigra to striatum are affected
* Reduction in DA in this pathway leads to characteristic motor problems
- Resting Tremor
- Cogwheel Rigidity
- Akinesia/Bradykinesia
- Postural Instability.
15
Q
Treatment of PD
A
Since Dopamine neurons are deteriorating then replace dopamine to restore balance
* Increasing available dopamine
* Give dopamine agonists
Levodopa/carbidopa: A first line therapy (many Neurologist will delay until symptoms are bothersome)
* Levodopa is the amino acid precursor to dopamine
* Carbidopa inhibits peripheral decarboxylation of levodopa so that enough can cross the blood brain barrier
DA doesn’t cross BBB, but levodopa DOES cross the BBB.
Agonist will stimulate receptors for what’s remaining.
16
Q
Levodopa/carbidopa
A
First-line treatment for PD
Pharmacokinetics:
* When given as immediate release product
* Half 1-1.5 hours
* Slow-release product allows for few daily doses
Clinical effects:
* Improves bradykinesia and rigidity
* (SO, Tremor can improve, but bradykinesia and rigidity really improve)
Long-term adverse effects
* “Wearing off” phenomenon
* “on-off” phenomenon ( sudden unpredictable changes in mobility)
* Dyskinensias (involuntary movements, associated with long-term Levodopa use)
17
Q
What is the “75mg/day” rule for Carbidopa?
A
At least 75mg/day is required to effectively inhibit peripheral dopamine decarboxylase and allow levodopa to cross the BBB.
18
Q
Dopamine Agonists
A
Available Agents
- Bromocriptine
- Pergolide
- Pramipexole (also used for restless leg)
- Ropinirole (also used for restless leg)
Clinical Pharmacology
- Directly stimulate dopamine receptors
1. * D2 receptor agonists
2. * Bromocriptine and pergolide are also ergot derivatives and also are D1 partial antagonists
- Used as initial therapy or adjunctive to Levodopa (to reduce off time or prolong on-time)
19
Q
Anticholinergics (for PD)
A
Typical agents
* Trihexyphenidyl
* Benztropine
* others
Clinical Pharmacology
* Block muscarininc receptors in the striatum
* Reduces striatal activity
Modest effect on treating symptoms
* More beneficial for tremors
great for tremor, but less beneficial for bradykinesia.
–> More used for tremors he said
20
Q
Amantadine (for PD)
A
Clinical Pharmacology
* Enhances dopamine release
* Blocks reuptake
* Stimualtes receptors
Clinical Effects
* Improves tremor, rigidity, and bradykinesia
* Adjunctive therapy in advanced disease
* Possible initial therapy for mild disease
21
Q
Contrast “Simple Partial” vs. “Complex Partial” seizures.
A
Simple: No loss of consciousness; regional motor or non-motor symptoms.
Complex: Altered level of consciousness, often preceded by an aura.
22
Q
Define the PD “wearing off” and “on-off” phenomena.
A
Wearing off: Loss of drug effect at the end of a dosing interval.
On-off: Sudden, unpredictable periods of poor mobility (off) and good mobility (on).
23
Q
Primary indication for using COMT inhibitors (e.g., Entacapone, Tolcapone) in PD?
A
They are used as adjuncts to Levodopa/Carbidopa to increase the half-life and availability of levodopa.
Clinical Pharmacology
* Blocks the metabolism of dopamine and levodopa therefore can increase availability of levodopa
* Improves half-live of levodopa = lengthens time taken to break them down
24
Q
Differentiate between a “simple partial” and “complex partial” seizure.
A
Simple: No loss of consciousness; symptoms are regional (motor or sensory).
Complex: Altered level of consciousness, often preceded by an aura.
25
What are the characteristics of an "absence seizure"?
Staring spells and transient loss of consciousness, typically lasting only a few seconds; common in children.
26
What are the three primary Cholinesterase inhibitors used for Alzheimer’s symptoms, and what is their mechanism?
Donepezil, rivastigmine, and galantamine.
They stop the breakdown of acetylcholine to modestly improve cognition and behavior.
27
Indication and mechanism for Memantine in Alzheimer’s treatment?
Indicated for moderate to severe cases.
It blocks the pathological effects of abnormal glutamate release to slow cognitive and functional decline.
28
Describe the primary pathophysiology of Parkinson’s Disease.
Degenerative death of dopamine-producing neurons in the basal ganglia (specifically projecting from the substantia nigra to the striatum)
29
What is the purpose of Carbidopa when combined with Levodopa?
It inhibits the peripheral decarboxylation of levodopa, allowing enough levodopa to cross the blood-brain barrier.
30
Clinical pharmacology and primary use of Anticholinergics (e.g., Benztropine) in Parkinson’s?
They block muscarinic receptors in the striatum to reduce activity. They have a modest effect and are most beneficial for treating tremors.
31
Multiple Sclerosis (MS): its early signs and pharmacotherapy
A neurodegenerative autoimmune disease characterized by demyelination of neurons.
Early signs:
* muscle weakness
* visual disturbances
* paresthesia
* bladder control issues.
Pharmacotherapy:
* Focus is modifying progression of disease and managing symptoms
* Immunomodulators are commonly used as therapy
32
Seizures --> Convulsions
Convulsions:
* Not synonymous with seizures
* Involuntary, violent spasms of large skeletal muscles of face, neck, arms, and legs
**All convulsions are seizures but not all seizures are convulsions**
33
Temporal Lobe Epilepsy/ Seizures
## Footnote
the three phases
Seizures have a beginning, middle, and end
**Aura:** Beginning. Sometimes, the warning or aura is not followed by any other symptoms.
**Ictus**: The middle of the seizure may take several different forms.
* the aura may simply continue or it may turn into a complex partial seizure or a convulsion.
**Post-ictal**: The end to a seizure represents a transition from the seizure back to the individual’s normal state. This period is referred to as the “post-ictal period” (an ictus is a seizure)
* Post-ictal is the recovery phase of brain --> patient is confused, fatigued or confused sometimes.
34
Types of Seizures
Partial (focal) seizures:
* Usually occur in limited portion of brain
* Symptoms may vary depending on part of brain affected
* Two types: Simple or Complex
Generalized seizures
* Multiple foci that spread abnormal neuronal discharges across both hemispheres of the brain simultaneously
* Four types: Absence, Atonic, Tonic-Clonic, Myoclonic
35
Types of Seizures: Partial (Focal)
Simple partial
* Regional symptoms
* Motor – can be tonic, clonic, atonic or repeated motions
* Non-motor – autonomic, behavioural, cognitive, sensory, emotional changes (fear and anxiety)
Complex partial (focal impaired awareness)
* Altered level of consciousness, often with aura
* May be motor, sensory and autonomic symptoms
36
Types of Seizures: Generalized
Absence seizures
* Staring, transient loss of consciousness
* Used to be called *petit mal*
* Usually in children, last a few seconds
Atonic seizures
* Drop attacks, clients stumble/fall for no reason
Tonic-clonic (aka *grand-mal*)
* Aura, intense muscle contraction, loss of consciousness
* Most common type
* There may be warning, or aura
Myoclonic
* Contraction of major muscles, jerky motion, no loss of consciousness
* can involve one group of MM or entre body, conciseness usually reserved.
37
What is **Status Epilepticus** and its primary risk.
A series of generalized seizures without full recovery of consciousness between them, or a continuous electrical seizure lasting 30+ minutes.
The main risk is respiratory arrest leading to hypoxia and brain damage.
38
Emergency nursing interventions for Status Epilepticus?
MEDICAL EMERGENCY
* **FIRST PRIORITY** --> ABCDEFG (ABCs and Don't Ever Forget the Glucose)
* Oxygen & Airway device/intubation inserted between seizures (lateral decubitus, nasal trumpets, O2, suction)
* Maintain IV access!!
* Hydration IV using glucose for hypoglycemia (high metabolic demand during seizure)
* cerbyx, Ativan, Valium IV
* Concurrent watch for reversable cause
---------
Treatment:
* May have to anesthetize with short acting barbiturate to stop seizure
* Serum levels of anti- seizure meds
* Cardiac/respiratory depression may be life-threatening
* Cerebral edema can occur
39
What is the first-line pharmacologic treatment for Status Epilepticus (Medical Emergency)?
Choice dependent on many factors:
* Type of seizure, medical history, results of EEG and other diagnostic tests
IV Lorazepam (Ativan) or Diazepam (Valium).
40
Why is IV Glucose administered during a prolonged seizure?
To treat hypoglycemia caused by the high metabolic demand of the seizure.
41
Name the four mechanisms of action for anti-seizure drugs.
1. Increasing GABA receptor stimulation
2. Reducing Na+ influx into neurons
3. Reducing Ca+2 influx into neurons
4. Blocking glutamate receptors
42
Drugs that Stimulate GABA Receptors
Barbiturates (i.e. pentobarb, phenobarb)
* indicated primarily for tonic-clonic seizures, but also used as sedative, hypnotic and general anaesthetic purposes
Benzodiazepines (i.e. diazepam, lorazepam)
* Indicated primarily for absence and myoclonic seizures but also used as anxiolytic and sedative
* Often used in combination with other drugs
Gabapentin – indicated for partial seizures
43
Drugs That Reduce Na+ Influx
Desensitize Na+ channels thereby delaying opening of channels and reducing excitability of neurons *(SO, Stabilizes hyperactive neurons)*
Hydantoins (i.e. phenytoin)
* Indicated for all seizures except absence
Phenytoin-like drugs
* Carbamezapine – indicated for tonic-clonic and partial
* Valproate – indicated for absence and tonic-clonic; also for bipolar disorder
44
Drugs that Reduce Ca+2 Influx
Succinimides are most commonly used in this category
Indicated primarily for **absence seizures**
Reduce Ca+2 influx which reduces NT release by neurons, reducing the excitability of post-synaptic neurons
45
What is the mechanism and primary side effect of the Ketogenic diet for seizures?
Who is a candidate?
Switches primary energy source from glucose to ketones (fats).
Side effects: lack of weight gain, high cholesterol, constipation, kidney stones, and acidosis.
----------
Who is a candidate?
* In general, individuals with uncontrolled seizures that have failed at least two medications for seizure control can be considered for this therapy.
* Research shows that it is more effective for certain seizures types. These include infantile spasms, Doose Syndrome, Rett Syndrome, and tuberous sclerosis complex.
46
Importance of Client Adherence in Seizure Treatments
Following directions for administering anti-seizure medications ensures best chance to manage seizure activity
Irregular dosing (missed dosing, doubling up) increases likelihood of seizure activity, occurrence of adverse effects
Adherence can be improved by client documentation of drug administration and alterations, and responses in a “seizure diary”
* What happened before (change in mood or behaviour, time of day, etc), during (changes in LOC, whether can talk or understand you), and after the event (response to voice, LOC, alert/oriented, how long seizure lasted)
* Be detailed
47
Sleep Disorders - Insomnia
**Sleep-onset:** Difficulty falling asleep.
**Sleep-maintenance:** Difficulty staying asleep.
**Sleep-offset:** Waking up too early.
**Non-restorative sleep**: Adequate sleep but sleepy during day
Can be associated with forms of anxiety (depression, manic disorders, chronic pain)
48
Sleep Disorders - Narcolepsy
**Narcolepsy** – severe daytime sleepiness
* Client may also fall asleep at inappropriate times
* Other symptoms: cataplexy, hypnagogic hallucinations, muscular paralysis, automatic behaviour
49
Drug Classes Used to Treat Anxiety and Sleep Disorders
**CNS depressants**
* Benzodiazepines
* Barbiturates
* Other agents
* **Zopiclone** --> IDEALLY used for the short-term (7-14 days) treatment of insomnia in adults
* Inhibition of GABAA activity leads to a calming, sedative, and hypnotic effect, promoting sleep
* Similar action to benzodiazepines but chemically distinct
Act on a continuum in terms of effects
* Anxiolytic – reduce anxiety
* Sedative – promote relaxation
* Hypnotic – promote sleep*
## Footnote
Main one is Zopiclone, he wanted to highlight this med. It is short-term, you usually don’t take it for life.
50
Benzodiazepines
Tolerance develops with repeated use
Dependency can develop as well
Decrease time to fall asleep for clients with insomnia, reduce sleep interruptions
Interactions
* Respiratory depression can occur when mixed with other CNS depressants (alcohol, certain histamines, opioids)
51
Barbiturates
Used less commonly now for anxiety and insomnia compared to benzodiazepines
Used as anti-seizure, IV anaesthetic
Dependence – both psychological and physiological dependence occur; withdrawal is severe and can be fatal
Mechanism of action – same as for benzodiazepines; bind GABAA receptors causing opening of its Cl- channels
* enhance GABA activity, increase neura excitibility
. . . . . .
PARADOXICAL DRUG REACTIONS
* A drug reaction that causes an outcome that is exactly opposite from the outcome that would be expected from the drug's known actions
* ex. Barbs have paradoxical excitement (normal fucntion is CNS/resp. depression)
52
The "Barbiturate Ceiling Effect" and its danger.
Tolerance develops to CNS/sedative effects but NOT to respiratory depression.
Increasing the dose to feel the effect can lead to fatal respiratory arrest.
53
Selective Serotonin Reuptake Inhibitors (SSRIs)
Mechanism of Action
* Prevent reuptake of 5HT, primarily
* Therapeutic effects associated with increased sensitivity of post-synaptic receptors, usually 4 – 6 weeks after start of treatment
* Same efficacy as TCAs and MAO inhibitors
= improve mood and emotional status in pts with depression.
54
Signs of Serotonin Syndrome
Definition: Serotoneric overactivity in patients with exposure to serotonergic drugs
Risk factors: overdose, switching 5HT drugs without tapering, using multiple 5HT drugs.
.
Signs/Symptoms:
* **Autonomic dysfunction** (Hyperpyrexia (high fever), hyperthermia, HTN, mydriasis (dilated pupils), Diaphoresis, tachycardia, diarrhea, N/V)
* **Neuromuscular Excitibility** (Hyperreflexia, myoclonus, rigidity, tremor, clonus)
* **Altered mental status** (anxiety, confusion, delirium, psychomotor agitation, seizure, coma)
* ataxia
-------------
Ataxia: neurological sign representing a lack of muscle control and coordination, leading to clumsy, unsteady movements, often resulting from damage to the cerebellum. It affects gait, balance, speech, and eye movement
55
Monoamine Oxidase Inhibitors
Indication:
* Depression, for clients that do not respond to TCAs or SSRIs
* Equal efficacy to TCAs and SSRIs but smaller margin of safety
. . . ..
e.g., Selegiline
Mechanism of Action
* By inhibiting MAO, more NE, DA or 5HT is available for release by the neuron/ released into synapse to stimulate receptors
## Footnote
not first line, it’s more because patients not responding to TCAs or SSRIs
56
Monoamine Oxidase Inhibitors: Drug-Drug Interactions
Insulin and oral hypoglycemic
* Enhances hypoglycemia
Antihypertensive agents
* Profound hypotension
When used with SSRIs --> Serotonin syndrome
Foods containing tyramine
* MAO inhibitors prevent breakdown of dietary tyramine
* Tyramine promotes release of NE which causes acute hypertension, palpitations, occipital headache, flushing, sweating, nausea
57
Atypical Antidepressants have uses beyond depression
Duloxetine is also indicated for fibromyalgia and other nerve pain disorders (e.g., diabetic peripheral neuropathy).
Bupropion is used in smoking cessation.
Atomoxetine and methylphenidate are commonly used in ADHD.
Trazodone is more often used as a sedative / sleep aid.
58
Pathophysiology of Bipolar Disorder
Biological, hormonal, genetic, and environmental components
Focus on the levels and function of neurotransmitters in the limbic system
* **Mania **associated with too much NE and glutamate or too little inhibitory NTs such as GABA
Associated with impaired levels of NE, 5HT, and DA in the limbic system
59
Lithium Carbonate: Monitoring requirements
Action: uncertain, crosses cell membranes, altering sodium transport, not protein bound
**NARROW THERAPETIC RANGE**
.
Side effects: thirst, metallic taste, increased frequency or urination, fine head-and-hand tremor, drowsiness, and mild diarrhea
.
Blood lithium levels, creatinine (kidney function), CBC, and thyroid hormones (T3/T4/TSH)
* lithium toxicity—severe diarrhea, vomiting, drowsiness, muscular weakness and lack of coordination, withhold
* Thyroid function may be altered usually after 6 to 18 months. Observe for dry skin, constipation, bradycardia, hair loss, and cold intolerance.
.
Avoid during pregnancy.
60
Positive vs. Negative symptoms of Schizophrenia
Schizophrenia: A type of psychosis in which clients exhibit a set of diverse symptoms over time. Can see alternating hyperactivity and stupor, indifference or detachment toward life, abnormal thoughts, thought processes, etc.
**Positive:** Hallucinations, delusions, paranoia, disorganized speech, movement disorders (additions to behavior).
**Negative:** Lack of emotion, social withdrawal, lack of pleasure/emotion in daily activities/hygiene, reduced or repetitive speech (subtractions from behavior).
**Cognitive Symptoms:** often not noticed as part of condition until positive or negative behaviours emerge. Significant learning and memory problems, decreased ability to concentrate.
61
Antipsychotic Drugs
First-generation antipsychotics
* Includes phenothiazines and non-phenothiazines
* Effective but with many adverse effects
* **Neuroleptic** – term given to CNS drug that can cause Parkinson-like symptoms
62
Adverse Effects of Antipsychotic Drugs
Extrapyramidal Side Effects: (on READING)
1. Acute Dystonia: Sustained muscle spasms (neck, tongue).
2. Akathisia: Subjective restlessness/discomfort.
3. Pseudo-Parkinsonism: Tremors, shuffling gait.
4. Tardive Dyskinesia: Involuntary face/tongue movements (long-term use).
.
**Neuroleptic** Malignant Syndrome (NMS)
* High fever, diaphoresis
* Muscle rigidity
* Tachycardia, blood pressure fluctuations
* Treat with muscle relaxants, antipyretics
63
Acute Dystonia
Is a medical emergency.
Dystonic movement result from a slow sustained muscular spasm that lead to an involuntary movement.
Can involve neck, jaw, tongue & entire body (opisthotonus)
There is also involvement of eyes leading to upward lateral movement of known as occulogyric crisis.
64
Akathisia
A subjective feeling of muscular discomfort that can cause patients to be agitated, restless , and feel generally dysphoric.
* Feel hella disconfirm, feel like wanting to crawl out of their skin. Can present as worsening psychosis, but is different.
Treated with propanolol, benzodiazepines, and clonidine.
65
Tardive Dyskinesia
It is a delayed one with abnormal , irregular movements of the muscles of the head , limb & trunk.
Characterized by chewing ,sucking , grimacing and perioral movements.
. . . . .
Shows up maybe years after use of meds, and is irreversible
Monitoring is key here, if TD is suspected, think about switching to second gen or atypical antidepressant
66
Neuroleptic Malignant Syndrome (NMS)
Rare but serious
Onset is often in first 10 days of treatment.
Rapid onset of severe motor, mental & autonomic disorders.
Prominent muscular symptom is muscular tonicity.
Stiffness of the muscles in throat & chest may cause dysphasia & dyspnea.
Treatments: supportive care, cooling, benzodiazepines
67
Substance Use Disorder and Addiction - CNS Depressants
Group of drugs that cause client to feel sedated, relaxed; controlled under CDSA due to their addictive potential.
.
Physical and psychological dependance, and tolerance builds with prolonged use.
.
Sedatives (Barbiturates Benzodiazepines)
* slurred speech, loss of coordination, apathetic, sleepy, disoriented
Opioids (Morphine Meperidine Fentanyl Oxycodone)
* euphoria, extreme pleasure, slowed cardiovascular and respiratory function, decreased GI motility
Ethyl Alcohol (Ethanol)
* relaxation, sedation, memory impairment, loss of coordination, decreased inhibition, poor judgment, flushed skin
68
CIWA for Alcohol Withdrawal
Understand the process to assessing a patient using the CIWA protocol.
What types of questions would you ask to assess for each symptom?
* **Nausea/Vomiting** - nausea, dry heaves, vomiting
* **Tremors** - moderate/severe with/without arms extended
* **Anxiety** - anxious, gaurded, acute panic state
* **Agitation** - fidgety/restless, pacing , thrashing
* **Paroxysmal Sweats** - palms/forehead moist, drenching
* **Orientation** - to date/place/person
* **Tactile Disturbances** - itch, numbness, P&N, burning, hallucinations
* **Auditory Disturbances** - startling, harsh, hallucinations
* **Visual Disturbances** - sensitivity to, hallucinations
* **Headache** - none to severe
69
Substance Use Disorder and Addiction - Cannabinoids
Most frequently used class of addictive substances, derived from Cannabis sativa
.
THC is responsible for most of the psychoactive properties in cannabinoids
.
DO NOT cause physical dependance, ONLY psychological dependance. Tolerance does NOT build.
* decreased coordination, disconnected thoughts, paranoia, euphoria, bloodshot eyes
* Ex. Marijuana, Hashish
70
Substance Use Disorder and Addiction - Hallucinogens
Produce an altered, dream-like state of consciousness; all are Schedule 1 drugs, no medial use
.
Prototype substance is LSD
.
NO physical or psychological dependance, but yes DOES build tolerance.
* laughter, visions, deep personal insights, religious revelations, afterimages, bright lights, vivid colours
* EX. LSD, Mescaline, MMDA, PCP, Ketamine, Psilocybin
71
Substance Use Disorder and Addiction - CNS Stimulants
Example: Cocaine
.
Increase the activity of the CNS; some available by prescription (e.g., Adderall / Ritalin)
.
Serious addiction potential (both physical and pyschological), and builds tolerance.
* Increased blood pressure and respiratory rate euphoria, alertness, confidence, restlessness, anxiety
* EX. Cocaine, Caffeine, Amphetamines, Methylphenidate
72
Substance Use Disorder and Addiction - Nicotine
Strongly addictive, highly carcinogenic
Can cause effects to those nearby as well
Some effects similar to CNS stimulants
.
YES physical, psychological dependace, YES tolerance builds.
* Increased alertness and focus, relaxation, lightheadedness, increased HR and blood pressure
73
Substance Use Disorder and Addiction - Inhalants
Vaporize or form a gas at room temperature
.
Usually placed in paper/plastic bag or soaked in cloth and inhaled
.
Some can be easily found
.
NO physical or psychological dependance, UNKNOWN tolerance effects.
* Lightheadedness, drowsiness, exhilaration, euphoria, hallucinations
* EX. Adhesives and glues, aerosol, cleaning agents, solvents, fuels, nitrous oxide
74
Substance Use Disorder and Addiction - Anabolic Steroids
Unlike other substances; effects may be delayed for weeks, months *(Effects can take weeks to months to develop, which makes the pattern of addiction a bit different than other drugs)*
.
Provide a boost in athletic performance, similar to testosterone *(mimics testosterone)*
Long-term effects can cause the opposite
.
NO physical or psychological dependence, NO tolerance built
* Substance adds to skeletal muscle mass and increased strength at first
75
Liver Function Tests: ALT vs. AST vs. ALP vs. GGT
**ALT:** More liver-specific than AST.
* High serum levels in acute hepatitis (300-1000U/L)
* Moderate elevation in alcoholic hepatitis (100-300U/L)
* Minor elevation in cirrhosis, hepatitis C and non-alcoholic steatohepatitis (NASH) (60-100U/L)
* Appears in plasma many days before clinical signs appear
* *A normal value does **not always indicate** absence of liver damage*
* Obese but otherwise normal individuals may have elevated ALT levels
**AST**: Marker of hepatocellular damage.
* This enzyme leaks out of those damages cells and show up in the blood.
* High serum levels are observed in: Chronic hepatitis, cirrhosis and liver cancer
**ALP**: A non-specific marker of liver disease
* Produced by bone osteoblasts (for bone calcification)
* Present on hepatocyte membrane
* Moderate elevation observed in: Infective hepatitis, alcoholic hepatitis and hepatocellular carcinoma
* High levels are observed in: Extrahepatic obstruction (obstructive jaundice) and intrahepatic cholestasis
* Very high levels are observed in: **Bone diseases**
**GGT:** Highly sensitive for detecting alcohol abuse.
* Used for glutathione synthesis* (glutathione is critical for toxin clearance in body, deals with toxins, cleans body, idk etc.)*
* Moderate elevation observed in: Infective hepatitis and prostate cancers
* GGT is increased in alcoholics despite normal liver function tests
* Highly sensitive to detecting alcohol abuse
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Liver Function Tests: Other
Measures of liver cell failure; production:
* Low serum albumin
* Prolonged prothrombin time (PT) (synthetic function)
Ultrasonography, CT scans, and MRI: evaluate liver structures
Angiography: visualizes the hepatic or portal circulation
Liver biopsy: used to obtain tissue specimens for microscopic examination
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Disorders of the Hepatobiliary System - Jaundice
* Excessive destruction of red blood cells
* Impaired uptake of bilirubin by the liver cells
* Decreased conjugation of bilirubin
* Obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or extrahepatic bile ducts
* Main cause = Hyperbilirubinemia
Ie. Build up of uncongugated bilirubin, block from flowing out, so pretty much hella bilirubin on blood.
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Differentiate the three categories of Jaundice
**Prehepatic:** Excessive RBC hemolysis (unconjugated bilirubin).
* liver just can’t handle all this on time
**Intrahepatic:** Liver damage affecting uptake/conjugation (conjugated bilirubin).
* directly liver can’t deal with it, often conjugated, but issue is excreting it.
**Posthepatic:** Obstruction of bile flow (conjugated bilirubin).
* obstructive flow of bile (gallstones, strictures, tumours, blcokign the duct), so bilirubin was conjugated, it just can’t get out and builds up in the blood stream.
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What is Asterixis?
A "flapping tremor" indicating severe hepatocellular dysfunction or failure.
Is one of the assessments for patients with Hyperbilirubinemia (jaundice).
Asterixis is main test: tell patient to put hands out as if trying to stop a bus, and you will see their hands tremble. “flapping tremors”
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Disorders of the Hepatobiliary System - Hepatic Cirrhosis
| Pathophysiology
Cirrhosis literally means permanent scarring
.
Although several factors have been implicated in the etiology of cirrhosis, **alcohol consumption** is considered the major causative factor. Cirrhosis occurs with greatest frequency among alcoholics. Although nutritional deficiency with reduced protein intake contributes to liver destruction in cirrhosis.
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Other factors may play a role, including exposure to certain **chemicals or infectious** . Twice as many men as women are affected. Most patients are between 40 and 60 years of age.
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Three Types of Hepatic Cirrhosis
| The three types
Cirrhosis is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver.
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There are three types of cirrhosis or scarring of the liver:
1. **Alcoholic cirrhosis**, in which the scar tissue characteristically surrounds the portal areas. This is most frequently due to chronic alcoholism and is the most common type of cirrhosis.
2. **Post necrotic cirrhosis**, in which there are broad bands of scar tissue as a late result of a previous bout of acute viral hepatitis. (eg, hepatitis A, B, C, D, or E)
3. **Biliary cirrhosis**, in which scarring occurs in the liver around the bile ducts. This type usually is the result of chronic biliary obstruction and infection; it is much less common than the other two types.
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Disorders of the Hepatobiliary System - Portal Hypertension
Portal hypertension occurs when blood flow through the liver is obstructed, leading to a buildup of pressure in the portal vein, which carries blood from the digestive organs to the liver.
* **Ascites:** a buildup of fluid in the abdomen, which is a common complication of cirrhosis, the most frequent cause of portal hypertension
* **Esophageal varices:** dilated submucosal distal esophageal veins connecting the portal and systemic circulations
* **Splenomegaly:** increased pressure in the portal vein (which carries blood from the digestive organs to the liver) can cause the spleen to enlarge (splenomegaly) due to blood congestion and increased splenic blood flow
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Complications of Portal Hypertension in Cirrhosis and how to treat . . .
Ascites (fluid in abdomen)
* **Paracentesis**: procedure performed, a needle is inserted into the peritoneal cavity to obtain ascitic fluid.
* fluid is drained using negative pressure. (therapeutic paracentesis) Releasing pressure can relieve pressure and allow easier breathing, activity, etc. BUT --> fluid will re-accumulate
Esophageal Varices (dilated veins)
Splenomegaly (enlarged spleen)
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Medical Management of Cirrhosis
The management of the patient with cirrhosis is usually based on the **presenting symptoms**. For example, antacids are prescribed to decrease gastric distress and minimize the possibility of GI bleeding.
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**Vitamins and nutritional supplements** promote healing of damaged liver cells and improve the general nutritional status. (since some are poorly absorbed with liver damage)
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**Potassium-sparing diuretics** (spironolactone) may be indicated to decrease ascites, if present. (since these pt are already at risk of electrolyte imbalances)
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Disorders of the Hepatobiliary System - Hepatitis
Hepatitis is an inflammation of the liver that is caused by a variety of infectious viruses and noninfectious agents leading to a range of health problems, some of which can be fatal. There are five main strains of the hepatitis virus, referred to as types A, B, C, D and E.
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The **acute** illness usually subsides gradually over a 2- to 12-week period, with complete clinical recovery in 1 to 4 months depending on the type of hepatitis
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Causes:
* Autoimmune disorders
* Reactions to drugs and toxins (drug-induced hepatitis; e.g.: acetaminophen)
* Infectious disorders (Malaria, infectious mononucleosis, salmonellosis, and amebiasis)
* Hepatotropic viruses that primarily affect liver cells or hepatocytes (Direct cellular injury and induction of immune responses against the viral antigens)
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Name the three periods of Acute Viral Hepatitis
1. **Prodromal:** Malaise, myalgia, arthalgia, lethargy, N/V, diarrhea, chills/fever, RUQ pain, pruritus, rising AST/ALT.
2. **Icterus**: Follows 1. by 1-2 weeks. Jaundice (rise in bilirubin, severe pruritis, liver tenderness, dark urine, clay-colored stools.
3. **Convalescent:** Disappearance of jaundice, return of appetite.
AND ALSO,
.4. **Carrier State:** Infection with HBV and HCV can produce a carrier state (so it stays in the body and continues damaging the body over tiem --> can lead to worse outcomes, like cancer)
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Types of Anesthesia
**Local anesthesia:**
* Loss of sensation to limited body area, no LOC changes, few adverse effects and risks compared to general anesthesia
**General anesthesia**
* Loss of sensation throughout whole body
* Loss of consciousness
* Used for major surgical procedures
**Regional anesthesia**
* Similar to local but affects a larger area
* Ex. Epidural, nerve block
. . . . .
**Monitored anesthesia care (MAC)**
* Uses sedatives, analgesics, and low dose drugs
* Allows client to remain responsive and breathe without assistance
* Used during diagnostic procedures, minor surgeries
* Moniter: oxygen saturation, LOC, airway patency.
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Local Anesthetic Administration
| Five Methods of Local Anesthetic Administration
Organized as:
"Route
* Formulation/Method
* Description"
**Topical** (surface)
* Creams, sprays, suppositories, drops, and lozenges
* Applied to mucous membranes including the eyes, lips, gums, nasal membranes, and throat; very safe unless absorbed
**Infiltration** (field block)
* Direct injection into tissue immediate to the surgical site
* Drug diffuses into tissue to block a specific group of nerves in a small area close to the surgical site
**Nerve block**
* Direct injection into tissue that may be distant from the operation site
* Drug affects nerve bundles serving the surgical area; used to block sensation in a limb or large area of the face
**Spinal**
* Injection into the cerebrospinal fluid (CSF)
* Drug affects large, regional area such as the lower abdomen and legs
**Epidural**
* Injection into epidural space of spinal cord
* Most commonly used in obstetrics during labour and delivery
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Local Anesthetics - Mechanism of Action and Pharmacokinetics
**Mechanism of Action**
* Prevents conduction of action potentials by blocking sodium channels
* Affects both sensory and motor neurons
**Pharmacokinetics**
* Onset and duration of drug action can be difficult to control
* Onset depends on drug's ability to diffuse in tissues to surrounding nerves
* Termination depends on blood flow to the region
* **Epinephrine**, a vasoconstrictor, is sometimes given extend duration of anesthetic by reducing perfusion of tissue
* **Sodium bicarbonate**, an alkaline agent, is sometimes given to raise the pH of a tissue
* Local anesthetics are** less effective in acidic pH**
* pH of tissue can be more acidic during bacterial infections
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Local Anesthetics - Esters
**Benzocaine** is most commonly used agent
Sunburns, insect bites, hemorrhoids, HIVES
Mechanism – prevent conduction of action potential along affected neurons by blocking sodium channels
* Esters are fast acting and short lived.
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Why is Epinephrine added to local anesthetics?
It acts as a vasoconstrictor to reduce blood flow (perfusion), which extends the duration of the anesthetic.
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Why is Sodium Bicarbonate added to local anesthetics?
It is an alkaline agent used to raise tissue pH, making the anesthetic more effective (anesthetics work poorly in acidic/infected tissue)
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Principles of General Anesthesia
* Loss of sensation to whole body, accompanied by loss of consciousness
* Used for procedures for longer procedures or when local anesthetics are not suitable
* Ideal is for client to be induced quickly to surgical anesthesia and to recover full function quickly when anesthetic is discontinued
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Inhaled General Anesthetics
Indication – maintain surgical anesthesia following administration of IV agents
Mechanism – thought to stimulate GABA receptors in brain, depressing activity of neurons
Classes:
* (laughing) Gas – nitrous oxide
* **Volatile Liquids** – halothane, isoflurane, sevoflurane,
* Liquids that vaporize at low temperatures and pressures
* Anesthesia machine delivers precisely controlled amounts
* Typically depress cardiovascular and respiratory function; can increase sensitivity of heart to catecholamines resulting in cardiac dysrhythmias
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Intravenous Anesthetics
* Often used in combination with inhaled anesthetics so that doses can be reduced, to minimize risk of adverse effects
* Provide better muscle relaxation and analgesia than inhaled agents
* Can be used independently for short procedures
* Includes benzodiazepines, opioids and barbiturates, as well as other agents (propofol, ketamine)
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Adjuncts to Anesthesia
Purpose of adjuncts is to enhance anesthesia, or to minimize potential adverse effects of anesthesia in pre- and post-operative conditions
Pre-operative medications:
* Reduce anxiety (sedatives)
* Reduce gastric acid, salivary and airway secretions (anticholinergics)
Intraoperative medications
* Reduce pain (analgesics – opioids)
* Increase muscle relaxation (neuromuscular blocking agents); promote flaccid paralysis
* Depolarizing (has the initial twitches)
* Non-depolarizing (does not)
Post-operative medications
* Antiemetics (5HT receptor antagonists)
* Increase GI motility (cholinergic agents)
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Adjuncts to Anesthesia – Neuromuscular Blocking Agents (NMBAs)
**Depolarizing Agents** (i.e. succinylcholine)
* Bind Ach receptors at neuromuscular junction (NMJ) causing muscle fasciculations (result of depolarization)
* Skeletal muscles do not repolarize resulting in flaccid paralysis
* Rapidly metabolized by pseudocholin-esterase thus duration of action is short
**Non-depolarizing Agents** (i.e. pancuronium)
* Binds Ach receptors at NMJ but does not depolarize leading to flaccid paralysis
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Contrast Depolarizing vs. Non-depolarizing NMBAs (Neuromuscular Blocking Agents)
**Depolarizing** (Succinylcholine): Causes muscle fasciculations (twitching) followed by flaccid paralysis.
**Non-depolarizing** (Pancuronium): Binds receptors without depolarizing, leading directly to flaccid paralysis.
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Critical Nursing Note for NMBAs
They cause paralysis but do NOT provide sedation or analgesia. The patient can still feel and hear everything unless other agents are given.
