Slitt cirrhosis/APAP
a patient comes in with suspicion of APAP OD in the past 2 hours. you decide to give them AC in the meantime while you obtain levels. the levels come back showing an APAP level of 400. it is now 8 hours post-ingestion. Could you still give NAC since you already gave AC?
what would the treatment approach be if the patient had come in over 24 hrs since OD?
Pt is still eligible for NAC due to APAP levels (see nomogram)
you want to start NAC if the levels will not be back before 8 hours since ingestion (in this case- just in time)
if the patient comes in >24 hrs since ingestion, start NAC ASAP and get levels of ALT and AST
how can you increase the potency and lipophilicity of a barbiturate?
longer alkyl side chain
replace O with S (shorter acting as well)
match the drug with the mechanism; insulin, beta2 agonists, digoxin
inhibits the Na+/K+ ATPase
unregulated the K+ transport through Na/K ATPase in tissues
causes insulin secretion from pancreatic beta cells AND activates Na/K ATPase
1. digoxin inhibits this: not a good choice!
2. insulin
3. beta 2 agonists; has 2 MOAs!
explain the steps of the cytokine storm for sepsis (broad explanation)
- dysregulation of blood vessel integrity
- incr. endothelial permeability
- disrupted barrier integrity
- albumin and blood protein lead into the interstitial space causing edema
at low doses nitrates will affect preload or after load?
normal doses; preload
higher doses; after load
mostly dilation of the veins, incr. dose for arteriole
what does CCB mostly work on?
- arterioles
which two drugs cause splanchnic vasoconstriction?
- cephalosporins
- terlipressin
- octreotide
- lactulose
- terlipressin: v1= vasoconstriction, v2= water reabsorption via aquaporin 2 channels
- octreotide; decr. splanchnic blood flow, inhibit vasodilatory peptides in the gut
How does Vanco. inhibit peptidoglycan cross linking?
how does beta lactase inhibit?
mimic ^^^
what infections do you use Vanco. PO for??
T/F; giving calcium carbonate for Hyperkalemia will help to decrease potassium levels in the cell and will be the only treatment needed
False, buys time
- increases action potential threshold to try to limit AP
what drug is used to combat hypotension in septic shock and usually used with norepinephrine.
vasopressin
- v1; vasoconstriction
- v2; increase blood volume through antidiuretic effects on kidney
what drug class if fenoldopam?
an increase in what pressure occurs with this drug?
D1 agonist; renal vasodilator
incr. ocular pressure
reflex tachycardia
which Beta blocker also has alpha 1-antagonist action?
what do you not want to use this one in?
carvedilol
don't use in decompensated cirrhosis or ascites
decreases renal perfusion, increases peripheral vasodilation and causes hypotension
what abx. is associated with ototoxity and kidney tubular necrosis?
gentamicin
which V2 agonist promotes hypotension
Conivaptan (v2+v1); effects V1 which works on the blood vessels
v2; renal
a patient is on sildenafil for their PH, can you add riociguat to their regimen?
no, do not use these 2 together
riociguat is also teratogenic and you also need to increase the dose in smokers
which BB used in HTN emergency is a selective B1 blocker?
what effects will this have on the CO and HR
esmolol
decr. CO, HR
okay in airway dz's
C/I in heart blocks, HF, bradycardia
what CYP metabolizes APAP to NAPQI (toxic)?
how does NAC reduce toxicity?
CYP2E1
NAC forms glutathione which acts as a sponge on the NAPQI to then form cysteine and mercapturic acid conjugates
what is the SAR of local anesthetics
aromatic ring
amide or ester linker; para substituted ester= ^activity
tertiary amine
explain ARP, ERP, and RRP?
ARP; cannot fire AP
ERP; small but incomplete depolarizations can occur
RRP; very strong stimuli can initiate a propagating AP
what are the 5 classifications of PH
which are most treatments for?
1. pulmonary arterial HTN
2. PH due to left heart dz
3. lung dz/hypoxia
4. PH due to pulmonary artery obstructions
5. PH with unclear or multifactorial causes
how do Na channel blockers work to reduce AP
- decr. or slow current
- incr. duration of AP
- incr. time the channel is inactivated
effects related to binding speed
a patient with history of RSI comes into the ER and you draw up their ALT, AST, and APAP levels.
they come back as 64, and 12 respectively. Do you need to treat this?
Yes, give NAC for 12 hours or until clinical and lab. improvement (no APAP, liver function is close to normal)
T/F a pt is experiencing red man syndrome from an IV Vanco. infusion. Since this is considered an allergic run, you need to stop the infusion and switch the drug class?
False
- slow rate of infusion
what are the drugs of choice for a PVC in a pt with no SHD
BB, non-DHP CCB
what drug when combined with tadalafil, do you have to increase the dose of the tadalafil due to interactions?
what is the ideal triple therapy for PH
bosentan
Selexipag +ERA+/- PDE5i
how do K+ channel blockers work to limit APs
- strong effects on slower HR
- slow opening of K+ during AP
- limit reentry arrhthymias (incr. AP duration)