-
ECL cells
- entero chromaffin like
- in body/fundus of stomach
- secrete HCL
-
G Cells
- in antrum of stomach
- secrete Gastrin
-
parietal cells
- in fundus/body
- secrete gastric acid in response to: Ach, gastrin, histamine
-
acetylcholine (in stomach)
directly stimulates H+ ion generation by binding to parietal cell muscarinic receptors --> activation of H-K ATPase secretion of stomach acid
-
gastrin
- directly stimulates H+ ion generation by binding to parietal cell receptors --> activation of H-K ATPase secretion of stomach acid
- also stimulates histamine release from ECL cells
-
Histamine
binds to H2 receptor on parietal cell to activate cell --> activation of H-K ATP ase --> secretion of stomach acid
-
gastric acid production
comformational change of pump --> inc acid secretion
-
peptic ulcer disease
- ulcer in stomach lining r/t inc acid/pepsin secretion and impaired mucosal cytoprotection
- causes: NSAID, H pylori, smoking, EtOH, stress
-
h pylori
- spiral bacteria
- once infected, remain colonized until treated
- releases toxins/proteases/phospholipase enzymes --> inflammation
- -impair mucosal integrity
-
h pylori treatment
- 1 acid suppressive (usually PPI)+ 2 antibiotics X 7/14 days
- -no stomach absorption, need something w/ activity in stomach
-
GERD triggers
- chocolate/mint/def/fat/carbs/EtOH: dec LES tone
- acid/caffeince: inc gastric acid
- fat: delay gastric emptying
- tobacco: dec LES tone and inc acid
- anticholinergics, theophyline, CCB, meperidine: dec tone
-
GERD treatment
- PPI: dec acid by ~100%, improve esophageal healing- good for chronic
- H2B: improve esophageal healing
- Antacid*: inc LES tone and pH
- Sucralfate/misoprostol
- metoclopramide/betanechol: inc LES tone, prokinetic
-
chronic use of laxatives
can --> dependency --> fluid/lyte imbalance, steatorrhea, osteomalacia, vit/mineral dificiencyes
-
tartazine sensitivity
- yelow dye
- incidence greater in pt with ASA allergies
- --> excess bowel activity, cramping, flatulence, bloating, perianal irritation
-
-
bowel prep
polyethylene glycol
-
neurotransmitter storage
in vesicles at axon terminal
-
neurotransmitter release
- triggered by arrival of action potential at axon terminal
- then can: bind to post synaptic cell, be taken back up, or broken down by enzymes in synapse
-
acetylcholine
- PNS: activates skeletal muscle
- CNS: arousal, reward, sensory perception, sustaining attention
-
-
dopamine
reward, reinforcement, motivation, motor function
-
norepi
sleep, arousal, pain, food intake, emotions, mood, temp, CV function
-
serotonin
sleep/arousal, pain, food intake, emotions, mood, temp, CV fcn
-
GABA
- inhibitory
- alerts ion specific channels using hyperpolarization
- --> sedation, muscle relaxation, CV/resp, spinal reflexes, pain perception
-
glutamate
- excitatory
- 2 receptors: NMDA, AMPA
-
schizophrenia
too much serotonin and/or dopamine
-
Parkinsonianism
- EPS from antipsychotics
- bradykinesia, rigid, tremors: usually responsive to anticholinergics like benadryl/benzotropin
-
dyskinesia
- EPS from antipsychotics
- spasms of muscle groups
-
Akathisia
- EPS from antipsychotics
- somatic restlessness, inability to stay still/calm
-
tardive dyskinesia
- EPS from antipsychotics
- constantly chewing gum
- only diagnosed after 6 mos of being on med
- not acute, but can be irreversible
-
neuroleptic malignant syndrome
- serious complication of typical antipsychotics, more common w/ high potency
- agitation, confusion, fever, tachy, labile BP, sweating, changing LOC
- treat w/ Dopa Agonist
-
sedative
- moderates excitement and physical activity
- depress consciousness
- retain ability to respond purposely to external stimuli
-
hypnotic
induce and maintain sleep
-
sedative-hypnotic
depress CNS function
-
anticonvulsants for BPD
- valproic acid
- lamotrigine
- carbamezapine
-
epilepsy management
- silence neurons generating abnormal discharge
- inhibit spread of discharge through CNS
- inhibit voltage gated na/ca channels
- antagonize glutamate/enhance GABA
-
ezogabine
- newer antiepileptic, fewer SE
- activated voltage gated K channels
-
vigabatrin
- newer antiepileptic, fewer SE
- prevents gaba inactivation
-
rifunamide
- newer antiepileptic, fewer SE
- Na Channel blocker
-
lacosamide
- newer antiepileptic, fewer SE
- Na Channel blockers
-
parkinsons
- destruction of the group of cells (substantia nigra) that make dopamine --> bradykinesia
- imbalance b/w dopa and Ach --> too much GABA
-
wearing off
- gradual loss of effect of levodopa/carbidopa:
- can add dopamine agonist or COMT inhibitor
- or increase dose/frequency
-
on-off
- acute loss of effect of levodopa/darbidopa
- add MAO-B inhibit, COMT inhibitor, dopamine agonist
- limit dietary protein
- changing dose wont help
-
parkinson's tx
- 1st line: sinimet, dopa agonist, COMT inhibitor alone or in compo
- 2nd line: dopa releaser, MAO-B, anticholinergic
-
somatic pain
- from skin, bone, muscle, joint, CT
- localized
- dull, throbbing, aching, nagging, stabbing
-
visceral pain
- internal organs
- diffuse
- gnawing, cramping, aching
-
neuropathic pain
- injury to peripheral nerves
- sharp, burning, shooting
- management: antidepressants, anticonvulsants- try to solve underlying issue
similar to visceral, but w/ subtle differences
-
AB nociceptors
- light touch, vibration, movement of hairs
- fast
-
C nociceptors
- heat, warmth, mechanical stimuli, chemicals
- slow
-
nociceptor/pain response signal transduction
- in dorsal horn
- stimulation of receptor -->na/ca influx --> membrane depolarization --> voltage gated na threshold --> action potential --> release of NT
-
inhibitory neurotransmitters in dorsal horn
- stop transmission of pain signal
- opioid peptides
- NE
- Serotonin
- Glycine
- Gaba
-
sites of action of pain meds
- brain: alpha agonists, opioids --> highest addiction potential
- dorsal horn: opioids, alpha agonists, local --> most action here
- peripheral nerve: local
- site of trauma: local, anti inflammatory
- action is more direct post dorsal horn
-
mu receptors
respiratory depression, euphoria, bradycardia, pruritis, miosis, n/v, inhibit gut motility, dependence
-
delta receptors
antidepressant, dependence
-
kappa receptors
sedation, psychomimetic, dysphoria, diuresis
-
sigma receptors
dysphoria, delirium, hallucinations
-
opiate
- naturally occuring
- ie morphine, codeine
-
opioids
- all hepatically metabolized
- agonists, partial agonists, antagonists
- only nubain, butorphanol, buprenophine, pentazocine are not full agonists
-
heroin
- 3x morphine r/t lipid solubility
- metabolized to morphine
-
chine white
- 1000X morphine
- metabolites accumulate during chronic use
-
tolerance
- PK: ability to metabolize/excrete increases over time
- PD: change in drug-receptor interaction
- -dec number of receptors, confirmational change, signal transduction pathway change
- Learned: pt alters behavior to hide effects
-
psychological dependence
drug affects reward system of brain
-
physical dependence
- abrupt cessation of agent --> withdrawal
- can develop after a few weeks
- dependant on physical, emotional, social, psychological factors
- 3 factors: tolerance, withrawal, giving up other things
-
addiction
physical dependance plus abuse or drug seeking behavior
(but can be drug seeking and not dependent it no withdrawl)
-
cox-2
pathologic prostoglandins: vasdilate, inflammation, inhibit PLT
-
cox-1
physiologic prostoglandins: GI mucosa, platelet aggregation, vasoconstrict
-
COX inhibitors
- non anti-inflammatory: only APAP
- anti inflammatory: NSAID
-
1st gen NSAID
inhibit cox 1 and cox 2
-
2nd gen NSAID
only inhibit cox 2
-
acetylcysteine
mucomyst: substitutes for glutathione in the rxn that converts toxic metabolite to non toxic form
-
APAP metabolism
- major pathway --> non toxic metabolite
- minor pathway --> toxic metabolite, then converted to non-toxic by glutathione.
- -Minor pathway(P45) induced by ETOH
- -EtOH/APAP OD deplete glutathione
-
reye's
- life threatening disorder in PEDS recovering from virus, higher risk from ASA
- vomiting, lethargy, elevated liver enzymes, progressing to coma
-
low risk NSAID
low dose ibuprofen, naproxen
-
mod risk NSAID
- mod-high dose of ibuprofen, naproxen
- diclofenac
-
high risk NSAID
- ASA
- indomethacin
- ketorolac
- piroxicam
-
renal sparing NSAID
- sulindac
- nabumetone
- celecoxib
-
adjunctive pain therapy: TCA
amitryptyline, nortriptyline
- neuropathy
- also help w/ depression/insomnia of chronic pain
-
adjunctive pain therapy: dual NE/ser reuptake inhibitors
venlaflexine, duloxetine
neuropathic pain, fibromyalgia
-
adjunctive pain therapy: anticonvulsants
- gabapentin: post op
- pregablin: more bioavailable than gabapentin, euphoria in some pts
- cabamazepine: FDA trigeminal neuralgia
- lamotrogine: phantom limb, MS, stroke
-
adjunctive pain therapy: clonidine
- very limited use
- --> postural hypotension
-
monitored anesthesia care
- low dose so pt remain responsive and breathe on their own.
- used during minor surgery
-
general anesthesia
- deep state of sleep
- no sensory perception
- lose consciousness
- no recall
- immobile
- need assisted ventilation
-
malignant hyperthermia
- inc skeletal muscle oxidative
- metabolism → overwhelms body's ability to regulate temp
-
heroin
- close structural analog to morphine
- more hydrophobic --> crosses BBB --> sharper high
-
cocaine/amphetamines
- potentiate dopaminergic, adrenergic, serotinergic neurotransmission
- fast high b/c dumps quickly, but long time for serotonin to go back in --> long high then downer
-
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