Cardiac Medications
The specific drug that prevents clotting by inhibiting Vitamin K
Warfarin (Coumadin)
Prostaglandins, Bradykinin, Substance P, and the release of Potassium (K+) are all chemical mediators released from damaged cells during this first step of nociception, where a noxious stimulus is converted into an electrical signal.
Transduction
Also known as a "toxic fingerprint"
Toxidrome
10gtts/mL is this kind of drip set
Macro Drip Set
A drug that blocks the effect of another drug
Antagonist
The classification of a drug that can cause digitalis effect/toxicity
Cardiac Gylcoside
The three medications that can be given as per the ALS PCP Analgesia Medical Directive
Acetaminophen, Ibuprofen, Ketorolac
These 3 neurotransmitters are all broken down by monoamine oxidase (MAO)
Norepinephrine, Serotonin, Dopamine
Hypotonic solutions cause blood cells to do this
Swell
In cholinergic overdoses, this enzyme is blocked from breaking down ACh
Acetylcholinesterase
Along with ADP, this component is key to the process of initiating platelet aggregation
Thromboxane (TxA2)
The four processes involved in nociception
1. Transduction
2. Transmission
3. Modulation
4. Perception
Characterized by a thiamine deficiency and the triad of: an ataxic gait, confusion and abnormal eye movements
Wernicke's Encephalopathy
The ALS PCS "Indication" for the intravenous medical directive
The actual or potential need for intravenous medication OR fluid therapy
The two types of Cholinergic Receptors
Muscarinic and Nicotinic
This type of drug acts on the distal tubules and blocks chloride pumps. (Give the name of the drug as well).
Thiazide Diuretic (HCTZ)
This describes the use of agents that have differing onset of action or duration of action to maximize pain relief, as well as to minimize episodes of breakthrough pain
Rational Polypharmacy
Na+ and K+ channel blockages can occur in this type of overdose, resulting in prolonged QRS (arrhythmias)
Tricyclic Antidepressants Overdose
The TKVO rate for an adult patient
30 to 60 mL/hr
These two physiological events occur during an ASA overdose, name in order of occurrence
Respiratory Alkalosis and Metabolic Acidosis
The FULL process of the RAAS to increase BP...
Drop in BP => Renin produced by JG Cells => Converts Angiotensinogen from Liver to Angiotensin I => ACE from Lungs converts Angiotensin I to Angiotensin II => Angiotensin II causes vasconstriction of arterioles and hits receptors on adrenal cortex => aldosterone released and promotes increased Na+ and H2O reabsorption => Increase BP
Describe the process for pain, specifically the 3 neuron pathway.
Break it down to the most detail you can.
Nociceptor (pain receptor) sends signal through dorsal nerve root--Goes through the dorsal gray horn--Synapse occurs with a 2nd order neuron--Crosses through white matter and travels up spinal cord--Synapse occurs in thalamus (relay station) = 3rd order neuron--Then goes to the cerebral cortex
Alcohol Dehydrogenase converts Ethyl Alcohol into this and Methyl Alcohol into this.
H20 + CO2
Formic Acid
The per minute drip rate for a patient with an IV running with a macrodrip (10 gtts/mL) set. The patient’s chart indicates that he is to be given 2000 cc of normal saline in 8 hours (to two decimal spots)
41.66 gtts/min
The amount of mL you would push for a patient with an order of 2 mg per kg of Norepinephrine I.V. is to be administered. There is pre-mixed syringe of (400mg/10ml) and the patient weights 110 lbs (to one decimal spot)
2.5mL