Cleaning IV port – vigorously scrub and allow a few seconds for port to air dry
Assess for infiltration
Always scrub IV port before and after administration
Continuously clamp simultaneously while flushing IV during the last round of flushing
IV
IM
SubQ
IV push
Assessing the head and neck
-
Inspection
Palpation of temporal artery (bilateral symmetry)
Maseter Muscle
TMJ (clicking sensations)
Pathophysiology of Seizers
-
Glutamate pathway vs GABA pathway
1. Glutamate pathway first
a. Membrane depolarization begins, Na+ influx, inside of membrane becomes
positive. Flow of action potential reaches hillock, voltage gated Ca2+ channels
open.
b. Influx of Ca2+ enters axon terminal, binds to SV2A receptors on vesicle
membrane for vesicle transport fusion to presynaptic terminal.
c. Release of glutamate proceeds into synapse, binding to two receptor types of
the postsynaptic terminal:


AMPA receptors
NMDA receptors
d. Entrance of continuous cations into the cell becomes promoted by the opening
of these receptors once activated by glutamate neurotransmitters.
e. Continuous cation influx promotes a continuous action potential from one nerve
cell to another as each membrane becomes depolarized since the
intramembrane is becoming more and more positive as cations flow in.
f.
This trigger of cascading action potentials leads to an excessively increased level
of electrical activity in the brain called a seizer
2. Gamma Amino-butyric Acid pathway Begins after
a. Glutamate synthesis from mitochondria in nerve cell body, released to activate
vesicle transport of GABA neurotransmitters to release for binding to GABA
receptors on postsynaptic cell from step 1.
b. Gaba binds to GABA-A receptors to create chloride synthesis into cell in attempts
to make the cell more negative and less positive (hyperpolarization), for seizure
prevention.
c. GABA NTs are then reuptake by reuptake auto receptors, then broken down into
cell for parts into
Pulmonary Disease
-
COPD
o Risk factors
 Smoking
 Environmental exposure
 Silica
 Dust
 Air pollutants
 Alpha 1 anti-trypsin deficiency
 (Autosomal disease)
Chronic Bronchitis and Emphysema coexist
Chronic Bronchitis (cellular obstruction)
-
Mucus builds up
o Mucus glands and goblet Cells
 Mucus production
 Hypertrophy
 Hyperplasia
Ciliary dysfunction
-
Mucus builds up over time results in ciliary obstruction on goblet cells, less motility,
leading to over accumulation of mucus in airway
Airway obstruction
Air trapping
- Mucus builds up leads to mucus plugs
o O2 concentration decreases in alveoli as mucus acts as a plug, leading to air
trapping. Gas exchange occurs, but CO2 unable to adequately return to alveoli
and out the lungs
Hypoxemia (PO2 lowered)
Hypercapnia (PCO2 increased)
-
More CO2 build up via airway occlusion amongst forced expiration
o Leading to CO2 overload in blood capillary and alveoli
o Eventual gas exchange diminished
o CO2 perfusion from capillary to alveoli reduces, causing CO2 build up in capillary
resultant of occluded airway from mucus plug
o O2 is decreased from mucus plug and more lowered O2 levels as CO2 increases
 Hypoxemia (PO2 lowered)
 Hypercapnia (PCO2 increased)
Increased Risk of Pneumonia
-
Homafas influenza
Moraxella Catarrhalis
Asthma (Chronic inflammatory disorder of airways)
- Promotes recurrent episodes of wheezing, breathlessness, chest tightness, and cough
o Associated with variable airflow obstruction
o Reversable spontaneously
o Reversable with treatment
May be seasonal or year-round depending on exposure to allergen
-
Cockroaches
Furry Animals
Fungi
Molds
Risk Factors
- Genetic
o 3 conditions making up an Atopic Triad
 Asthma


-
Atopic Dermatitis (Exema)
Allergic Rhinitis
Pollen
Samters triad
- Asthma
- Nasal Polyps
- ASA Sensitivity
Teratogenous drugs – pregnancy
-
-
Drugs are chemicals that cause change or an alteration of pathways
o Pharmacotherapeutics
 Study of how drugs are used to prevent or treat a diagnosed disease
Genetic variability can alter drugs
o Adverse effects
o Toxic affects
Nurses responsibility
- Expected reaction vs Adverse and Toxic reaction
- Side effects and treatment management
- Pretreatment of side effects for expected side effects that are a cause of initial
treatment
- Patient education before during and after is very important
- Assessing drug effect
- Monitoring overall patient care plan
Care plan example page 04 – table 1.1 in chapter 1
Diet history
Medication history
Diet history
Lifestyle habits
Which medications can and cannot be combined with each other?
Drug parameters – verifying correct range of indicated assessment levels per patient MAR
(Could be BP, Vitals, Inspection, objective or subjective based, pain level, urine output,
measurable forms of obtaining data, texture, size, volume, and frequency of body fluids).
What is Steven Johnson Syndrome?
Natural Sources of Drugs
- Plants
o Synthetic version of the active chemical found in a plant
-
-
o Main component of growing alternative therapy
Animal products
o Used to replace human chemicals that are not produced because of disease or
genetic problems
o Genetic Engineering
o Many are prepared synthetically
o Are they culturally appropriating for the patient based off where they come
from?
Inorganic compounds
Salts
Synthetics
Organic based
Clinical trials for drug approval
Preclinical trials
- Chemical tested on laboratory animals
Phase 1 Studies
- Chemicals tested on human volunteers
Phase 2 Studies
- Drug used in vast clinical market
Phase 3 Studies
- Drug in vast clinical market
FDA approval
- If approved may be patented and marketed
Phase IV studies
- Continual evaluation
Pregnancy Risk Factors for drugs
Category A – no history of demonstrated risks to the fetus in the first trimester
Category D – has the greatest risk
Controlled Substances (Schedule 1 – Schedule 5 drugs)
-
Schedule 1 class drugs have highest risk for chemical dependency
o “Dispense as written” is written on drug labels that have narrow safety margins