Pathophysiology and Pharmacology (MOA, Onset, Peak)

Alert - spontaneously aware of surroundings
Verbal- repsonds to voice
Painful- responds only ot painful stimulus
Unresponsive - no responce

Eye opening (1-4):
4. spontaneous
3. speech/sound
2.pain
1. nothing

Verbal responce (1-5):
5. Orientated
4. confused
3. inapropriate words
2. imcomprehensible sounds
1. nothing

Motor responce (1-5):
6. Obeys commands
5. localizes to pain
4. withdraws from pain
3. Flexion (decorticate)
2. Extension (decerebrate)
1. no response

≤8

-Pancrease
Insulin: lowers by driving sugar into cells
Glucagon: raises by triggering liver to release stored glycogen

glucose

too much insulin/oral hypoglycemic
missed meals
alcohol use
exercise
sepsis

agitation
diaphoresis
LOA altered

polyuria
polyphasia
tachycardia/tachypnea

Transduction- noxious stimulus ( mechanical, thermal, chemical) is converted into electrical signal by nocirepcepters (free nerve enedings throughout body)

Transmission- signal travels along peripheral nerves, up to spinal cord then brain

Perception- brain interprets signal as pain where mood, experiences, anxiety modulate severity

Modulation - body own descending pathways + analgesia dampen signal at multiple points

vomiting center in the medulla

altered LOA
combativeness
seizure-like
confusion

sits outside the blood-brain barrier, allowing it to directly sample circulating toxins, drugs, and metabolic byproducts in the blood
- major trigger pathway for nausea

The vestibular system (motion sickness)
The GI tract itself (irritation, distension)
Higher cortical centers (sight, smell, anxiety, pain)

yes- gravol

chemically induced, like alchohol or chemo

anything to do with movement

- bodys central stress responce system
Hypothalamus: signals stress
Pituitary gland: releases ACTH
Adrenal cortex: stimulated by ACTH
Cortisol: released into bloodstream

The surge of cortisol helps maintain blood pressure, blood glucose, and overall stress tolerance.

- Primary adrenal failure, pt cannot produce a cortisol surge on their own.

Effect of stress: Under physical stress (illness, injury, infection), they can rapidly decompensate into an adrenal crisis: hypotension, hypoglycemia, and shock.

Because you are replacing a hormone their body cannot produce in a crisis, rather than treating a new problem from scratch.

- opioids analgesic effects
side effect: respiratory depression

excess mu-receptor stimulation blunts the brainstem's response to rising Co2, pt stops breathing adequatly ( not from heart stopping but drive to breath dissapearing)

competitively displaces opiods from Mu receotors without activating itself, rapidly reversing respiratory depression

tightly binds to Mu receptors, while only partially activating them
- enought to relive withdrawl symptpms without producing sam overdose risk as full agonist

If the patient responds to dextrose or glucagon, they may receive oral glucose or other simple carbohydrate

The patient may receive oral glucose or other simple carbohydrates instead of dextrose or glucagon.

A final set of vital signs including blood glucometry must be attempted and documented.

gradually toward a level of awareness where the patient can safely consume carbohydrates on their own.

-Overcorrecting risks rebound hyperglycemia
- dextrose is irritating to peripheral veins

Dose & Reassessment: 15 g and every 15 min
Indications: Appropriate alternative if the patient is alert with only mild symptoms, or responds to dextroselucagon.

has to trigger liver to break down lgycogen stores first ( not instant fix)
- pt with depleted glycogen storage ( chornic alchol use, malnourishiment)

teo doses of the SAME medication (two dex or two glucagon)

onset: 1-2 min (IV)
peak: 3-5 min
duration: varible (depends on card intake)

- glucose in an injectable form
Absorbs directly into the bloodstream and immediatly availible as feul for glucose-dependent tisues ( most critically in the brain)

local vein irritation
rebound hyperglycemia
extravasation causing tissue damage

onset: 10-20 min (IM/IN)
peak: 20-30 min
duration: 60-90 min

- Naturally occurring pancreatic hormone that acts on liver cells to trigger glycogenolysis
Breakdown of stored glycogen into glucose, which is then released into the bloodstream

nausea/vomiting
headache
injection site discomfort

Because it has to work through the liver rather than delivering glucose directly into the bloodstream.

to try to blow off the large amounts of CO2 that they have so you dont send them into a huge catecholamine release

2 min intervals IV
0.08
0.08
0.08
0.08
Calls for a nice smooth wake up they tend to be less angry and it gives you a lot more time to blow off the CO2

respiratory depression, GCS 3, pinpoint pupils

≥ 10

methadones long half-life and buprenorphine strong receptor affinity ( interect unpredictably)

onset: 2-5 min (IM, IN, SC)
peak: 5-10 min
duration: 30-90 min

competitive opioid agonist?

binds to Mu receptors with high afinity physically deplacing already bound opioid molecules and rapidly reversing respiratory depression

shut down respiratory center because drug stops brain from blowing off Co2 + ability to breath

- acute withdrwals
- combativeness
- non-cardiogenic pulmonary edema

acute catecholamine surge triggered by sudden, severe opioid withdrawal leading to dry drowning

onset: 15-30 min
peak: 1-2 hours
duration:24+ ( up to 72)

partial mu-receptor agonist

Binds mu receptors with high affinity but only partially activates them—providing enough stimulation to relieve withdrawal symptoms without inducing severe respiratory depression or overdose risk.

-precipitated withdrwals
-headache
-nausea
- injection/site irritation

only 1

onset: within 1 hour
peak: 1-2 hours
duration: 8-12 hours

replaces missing hormone, restoring physiological effects, maintaining vascular tone, blood pressure and blood glucose level

hyperglycemia

Renal colic: Because it reduces intrarenal pressures.
Hip fracture: When the patient must remain supine and cannot tolerate PO medications due to being on their back.

work through different mechanism leading to better pain relif without risk

anti-inflamitory, smooth muscle relaxing effects target actual mechanism of colics pain more directly

onset: 30-60 min
peak: 1-2 hours
duration: 4-6 hours

act within CNS, inhibiting prostaglandin synthesis in brain + spinal cord with minimal periphral anti-inflammatory effects

hepatoxicity

onset: 30-60 min
peak: 1-2 hours
duration: 4-6 hours

non-selectively inhibts Cox 1+Cox2, reducing synthesis of prostaglandis responsible for pain, inflammation, and fever.

GI upset
increased bleeding risk
bronchospasm (asthmatics)

onset: 10-30 min
peak: 1-2 hours
duration: 4-6 hours

non-selectively inhibts Cox 1+Cox2, reducing synthesis of prostaglandis ( more potent/quicker onset)

GI upset
bleeding risk

over 450

1:9 with normal saline of D5W (IV)

onset: 10-15 min
peak: 30-60 min
duration: 4-8 hours

headache
constipation
QT prolongation

selectively blocks serotonin receptors both preiopherally on vagal nerve terminal in GI tract and centrally in chemoreptor trigger zone

onset: 20-30 min
peak: 1-2 hours
duration: 3-6 hours

sedation
drowsiness
dry mouth
agitation

blocks H1 receptors peripherally+centrally, and anticholinergic + antivertigo properties.

Anatomic Sites: Acts on the vestibular system and the chemoreceptor trigger zone (CTZ).
Clinical Efficacy: Particularly effective for nausea related to motion or vestibular causes, alongside its general antiemetic effect.

insulin, glucagon and cortisol

-raises it
- promites gluconeogenisus
-reduces glucose uptake in tissues

Glycogenolysis- breakdown of stored glycogen ( liver) into glucose
- triggered by glucagon and epinephrine
- fast

Gluconeogenesis- making brand new glucose from non-carbohydrate sources (liver)
- driven by cortisol + glucagon
- slow

nothing to break down anymore

- mostly type 1
absolute insulin deficiency, cells cant use glucose and body burns fat, making ketones + metabolic acidosis
onset: hours - days
signs: kussmals, fruity acitone breath, nausea, vomiting, abdominal pain, dehydration, tachycardia, altered LOA
triggers: infection, missing insulin, new diagnosis, MI

- mostly type 2
is enough insulin preventing ketosis, not enough to control glucose
onset: over days
signs: high glucose, dehydration, high osmolality, altered LOA

- rapid acting
- short acting
- immediate acting
- long acting

- Metformin: stimulates insulin release
- SGLT2 inhibitors: glucose excreated in urine
- DPP-4 inhibitors + GLP-1 agonits: boosts bodys own insulin responce
- Thiazolidinediones: improves insulin sensitivity

Adrenergic ( tachycardia, diphoresis, tremor, pallor, hunger)
Neuroglycopenic ( cofussion, combativeness, headahce, seizure)

peaked t-waves, widened QRS, flattened p waves, bradycardia

- Mu: analgesia, resp depression, euphoria, miosis, dependence
- Kappa: spinal analgesia, sedation, dysphoria, miosis
- Delta: analgesia, modulated mu effects

decreased LOA
slow/shallow respiration
pinpoint pupils
bradycardia
hypotension
dilated pupils

continued sedation
bradycardia
hypotension
skin wounds

morphine (x1), fentanyl (100x), carfentanil (10,000x)

35-45 mmhg
- sqaure rectengular, resturns to baseline

above 45 mmhg
- normal OR smal slow irregular

sharkfin

baseline doesn't return to zero

sudden jump in ETCO2

- sympathomimetic: agitation, tachycardia, hypertension, dilated pupils, diaphoresis
- anticholinergic: hot, dry, flushed, crazy
- cholinergic: SLUDGE/DUMBELS
- sedative-hypnotic: decreases LOA, depresed respirations

Fast touch stimulates inhibitory neurons in spinal cord.
- closes the gate

pelvis- 1-3 L
femur: 1-1.5 L
tib/fib: 500-1000 mL
humerus + forearm: 250-500 mL
ribs: 125 mL

1. expose
2. check 5 ps
3. control bleeding/dress ( if needed)
4. realign ( if needed)
5. imoblize
6. check 5 ps again
7. apply cold

chemical mediators cause vasodilation + increased capilary permiability, fluid leaks into tissue

platelet: stops platelets from sticking together
coagulants:

hemorrhage that cannot be controlled (hematemesis/GI bleed)

bones have rich blood supply

aspirin or clopidogrel

heparin, apixaban, warfrin

-rapid onset
- brain starved of primary feul instanly, causing acute medical emergency

-gradul onset
body slowly builds up high sugar + dehydration over time

turns on cell pumps that push sugar inside
at sam time
pushes potassium into cells, lower K in blood

Forces potassium out of the cells and into the blood
- test looks high, but body is depleted

Extremely high sugar creates thick, concentrated blood outside cells. which pulls water out of cells and moving water drags K out into blood stream

suddenly pushes all that potassium back into the cells.
Blood potassium levels plummet,

pivoting on a bent knee ( almsot always displaces laterally)

low cortisol/aldosterone
hypnatremia ( na)
hyperkalemia
low BP

high cortisol
higher blood pressure
high blood sugar
moon face

prim- adrenal gland failure ( low cortisol + low aldosterone + high ACTH)
secondary: pituitary/hypothalamus ( low cortisol + low ACTH)

- acts on kidneys
- retains sodium/water
-excretes potassium
- controls blood volume/pressure

hyperkalemia
severe fluid overload ( pulmonary edema)
acidosis
uremia

no BP or IV
direct pressure if bleeding

severe abdo pain + cloudy dialystate fluid

Acetaminophen + ibuprofen
Acetaminophen + ketorolac

Carbohydrate monosaccharide Generic: D10w. D50w

hyperglycemia agent
GlucaGen (IM), Baqsimi (intranasal).

opoid antagonsit
narcan

partail mu agonist
suboxone

non-opioid analgesic
tylenol

NSAID
advil/motrin

NSAID
toradol

antihistamine
gravol

5-HT3 receptor agonsit
zofran

glucocorticoiud
solu-cortef