PPA 524 ER Pharm

What are the 7 causes of DKA?

1.infection

2.physical or emotional trauma, starvation from anorexia

3.medication noncompliance

4.heart attack or stroke

5.pancreatitis

6.pregnancy

7.alcohol or drug abuse, particularly cocaine

For diabetic ketoacidosis , how will the following labs present?

K

pH

pCO2

HCO3

You’ll have to check these every what?

1.potassium FIRST

1.hydrogen ion displaces K+ from intracellular space

2.usually high (normal is 3.5-5.2)

3.can drop precipitously as acidosis is corrected

2.pH

• low (less than 7.35)

3.pCO2

1.usually low

2.rapid, shallow breathing

4.HCO3-

usually low

EVERY HOUR

For DKA how does blood sugar present and what are 3 other labs you want to get?

ublood sugar

• usually over 250mg/dL

• can have euglycemic DKA

• starvation, chronic liver disease, pregnancy, infection, alcohol use, SGLT2 inhibitors

ubeta-hydroxybutyrate (BHB) – ketone body

upositive

umagnesium, phosphate

uanion gap

• ([Na] + [K]) – ([HCO3] + [Cl]), normal 14-18

• [Na] – ([HCO3] + [Cl]), normal 10-14

4 step tx for DKA?

1. BUCKETS of intravenous fluids bc they are dehydrated from osmotic diuresis of hyperglycemia

•NaCl 0.9% (normal saline solution)

–

2. insulin – regular insulin STAT

•bolus

•continuous IV infusion

•

3. potassium

4. other

• at BS of 250mg/dL, D5%NS or D5% 0.45%NS

• lower BS 50-150mg/dL/hr

Tx in general for hypoglycemia?

Sx?

Tx medication 1 with forms?

Med 2 with MOA and AE and protip?

uinsulin, most oral medications for diabetes

usymptoms of hypoglycemia:

• Shakiness or trembling

• Sweating

• Hunger

• Dizziness or lightheadedness

• Anxiety or irritability, confusion, blurred vision

• Fast heartbeat 

utx:  dextrose 50% IV;  glucagon IM, IV, intranasal (IN)

utx:  octreotide (Sandostatin) SQ or IV

MOA:  antagonizes pancreatic insulin release

AE:  diarrhea, abdominal discomfort

pro tip: type 1 DM pts will not respond to it bc they don’t produce insulin

5 immediate considerations for status epilecpticus

1.electrolyte disturbances

2.hypoglycemia

3.drug withdrawal (benzodiazepine, baclofen)

4.AED withdrawal

5.organic neurologic disease

• cerebrovascular accident

• tumors

• head trauma

what is first line for immediate control of status epilepticus?

(3) other types?

MOA

AE

benzodiazepines

MOA:  GABA agonist

AE:  respiratory depression, sedation, amnesia

lorazepam (Ativan)

diazepam (Valium)

midazolam (Versed)

(3) meds for secondary control, immediately following benzodiazepine for status epilepticus? WHICH IS FIRST LINE and dose for adult?

plus

phenobarbital IV

ketamine IV

MOA

AE

for both

• fosphenytoin (Cerebyx) IV/IM or phenytoin IV

• valproic acid IV (Depacon)

• levetiracetam IV (Keppra) (FIRST LINE), give 1 GRAM and likely more later

phenobarbital IV

MOA: GABA potentiation

AE: sedation

ketamine IV

MOA: glutamate and NMDA antagonist

AE: dissociative reaction, hypotension, anxiety

Status Asthmaticus

2 immediate considerations

5 meds

immediate considerations

1. oxygen saturation

2. acid/base status

medications

1. for sure IV fluids

2. for sure albuterol 2.5mg neb q20min x3, then hourly

3. methylprednisolone (Solu-Medrol) 125mg IV x1

4. ipratropium (Atrovent) 0.5mg SAMA neb (NOT PO)

5. magnesium 2gm IVPB over 20min x2

Alcohol withdrawal timing of events:

occurs in first few ___ after stopping, lasts ___; these 5 sx appear ____

________ and _____; most withdrawal episodes, even untreated, stop here

seizures (what type seizures?) in 10-15%

______; rare; mortality is 20%

first few hours after stopping, lasts 3-5 days; tremor, tachycardia, diaphoresis, anxiety, N/V

auditory and visual disturbances; most withdrawal episodes, even untreated, stop here

seizures (generalized tonic-clonic) in 10-15%

delirium tremens; rare; mortality is 20%

Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) Score

(10) sx CIWA measures

range:

what to what is mild?

nausea/vomiting, tremor, sweat, anxiety, activity, tactile disturbance, auditory disturbance, visual disturbance, headache, orientation

range: 0-67

8-10 = mild

Acute tx of alcohol withdrawal

general class with 3 ex. and protip?

(4) vitamins w/ form and duration

protip for the most important vitamin?

(3) other generalish things you need to give?

benzodiazepines

• lorazepam (Ativan) IV or PO

• diazepam (Valium) IV or PO

• chlordiazepoxide (Librium) PO only

• pro tip: could be scheduled with a taper or used PRN based on symptoms

vitamins

1. multivitamin in IV fluids (1 bag of IV fluids per day, the rest are plain) OR oral multivitamin if tolerated

2. thiamin BEFORE GIVE GLUCOSE: 100mg IM or IV or PO daily for 3 days, then 50-100mg orally every day as follow-up

   • WILL GET WERNICKE’S encephalopathy if don’t give thiamin 1st before glucose

   • alcohol abusers should take PO thiamin in general

3. folic acid: 1mg IM or IV or PO daily

4. vitamin K: if prothrombin time/INR elevated and liver is functioning

fluid replacement/electrolytes

• NS

• LR

• D5LR or D5NS (ONLY after thiamin)

magnesium

potassium

what med do you give to stop acute seizures?

NO anti-epileptics unless what?

lorazepam (Ativan) to stop acute seizures

NO anti-epileptic drug (AED) therapy is warranted unless status epilepticus develops

(5) meds for long term tx of alcohol withdrawal and how each works

1. disulfiram (Antabuse) – inhibits aldehyde dehydrogenase; with alcohol, increases serum levels of acetaldehyde

   • this induces vomiting and is same process that occurs when you drink too much

   • it’s a deterrent so that they can get turned off from drinking

2. naltrexone (ReVia) – narcotic antagonist, decreases cravings

3. clonidine (Catapres) - alpha 2 agonist lowers BP via vasodilation to lower HR

4. acamprosate (Campral) – may increase activity of GABA system and decreases activity of glutamate

med for CVA?

MOA

AE

• -hour (up to ___ hour) window from time of ____ to _____

• ____ tests

• _____ criteria

• _____ stabilization

• dose: ______

• ______ – single _____

tissue plasminogen activator (tPA, Activase)

MOA: activates clot dissolution cascade

AE: bruising, bleeding, hemorrhagic conversion

• 3-hour (up to 4.5 hour) window from time of symptom onset to be able to still give the drug uuyfv

• diagnostic tests

• inclusion/exclusion criteria

• vital sign stabilization

• dose: 0.9mg/kg (maximum 90mg), 10% IV bolus over 1 minute then 90% as infusion over 1 hour

• tnk-tPA – single IV bolus

Pulmonary embolism tx?

(3) different options

Then what IF massive PE

DOAC (rivaroxaban, apixaban, dabigatran)

or

IV heparin infusion

or

SQ enoxaparin or dalteparin or fondaparinux

or

IF massive PE + hemodynamic instability: alteplase (tPA) 100mg IV infusion over 2 hours followed by parenteral anticoagulation

Disseminated intravascular coagulopathy (5) part tx?

What is DIC?

1. heparin – prevents consumption of clotting factors

2. activated protein C

3. intravenous fluids

4. fresh frozen plasma

5. packed red cells if anemic

(3) part tx for anaphylaxis?

2 ex. for each except first?

1. epinephrine

• Epi-Pen

2. antihistamine

• diphenhydramine (Benadryl) - H1antagonist

• cimetidine (Tagamet) PO -H1/2 antagonist

3. corticosteroids

• prednisone

• methylprednisolone (Solu-Medrol, Depo-Medrol)

(4) part tx for Gastrointestinal Hemmorrhage?

with an example

1. nothing by mouth = NPO (nil per os) bc need to locate specific bleeding source

2. H2RA - histamine H2-receptor antagonists or H2-blockers. It works by decreasing the amount of acid produced by the stomach.

• famotidine IV (Pepcid)

3. PPI

• pantoprazole IV (Protonix)

4. IV fluids

code blue (ACLS)

give these to tx what?

epinephrine

• ___

atropine

• ___

amiodarone (Cordarone)

• ___

magnesium

• ___

epinephrine - alpha-1 vasoconstrictor, b-1 increases HR,

• vfib, asystole, bradycardia

atropine

• bradycardia

amiodarone (Cordarone)

• vfib, vtach

magnesium

• vfib, vtach, torsades

what are the 5 steps for PRE-op care?

which 2 examples for each one except straightforward ones

1. NPO

2. stopping anti-platelet medications

• aspirin = 5-7 days

• clopidogrel, prasugrel = 5-7 days

• ticagrelor = 3-5 days

3. stopping immunosuppressive medications

4. stopping anticoagulant medications

   • warfarin = 5 days

   • apixaban, rivaroxaban, dabigatran = 2-3 days

5. prophylactic antibiotic

   • most: cefazolin (or clindamycin or vancomycin)

   • GI: cefazolin + metronidazole (or FQ + metronidazole)

Infectious Diseases – Antimicrobial Prophylaxis

choice of agent and dose depends on what 5 things?

1. surgery being performed

2. patient allergies

3. patient weight

4. timing of antibiotic prophylaxis

   • 30-60 minutes prior to cut

5. single dose to 48 hours post-op

what is PONV risk assessment used for?

what are the MOA for the 5 meds?

what are 2 other things you need to give/do?

Used for pre-op care

1. prochlorperazine (Compazine)

MOA: dopamine antagonist

2. metoclopramide (Reglan)

MOA: dopamine antagonist

3. ondansetron (Zofran)

MOA: serotonin antagonist

4. scopolamine (TransdermSCOP)

MOA: anticholinergic patch

AE: dry mouth, confusion

5. midazolam (Versed)

   MOA: GABA agonist

   AE: sedation, amnesia

6. analgesic

7. blood sugar management

MOA of anesthesia – Local Anesthetics

primary differences are what 3 things?

3 uses?

MOA: inhibits initiation and conduction of nerve impulses by blocking sodium channels

• primary differences are onset, duration, and chemical class

uses

1. diagnose

2. treat (pain management)

3. facilitate surgery

3 common local ESTER anesthetics with onset and duration?

Epi typically what?

esters

1. tetracaine (Pontocaine)

• onset: <15min

• duration: 2-3hr

2. procaine (Novocaine)

• onset: 2-5min

• duration: 15-60min

NOTE: epinephrine generally increases duration of action and decreases bleeding)

3 common local AMIDE anesthetics with onset and duration?

what should you do with these 2?

Epi typically what?

amides

1. lidocaine (Xylocaine)

• onset: <2min

• duration: 30-60min

2. bupivacaine (Marcaine)

• onset: 5min

• duration: 2-4hr

COMBINE THESE 2 for longer duration and efficacy

(NOTE: epinephrine generally increases duration of action and decreases bleeding)

what 5 things do you need to do for INTRA-op care?

MOA + AE of the agent?

1. Paralyzing agent (paralyzing agents are needed for surgery bc be fr you want them knocked out for duration)

• MOA: inhibits ACh at skeletal muscle receptor

• AE: respiratory failure, hypotension

2. analgesics

3. sedative

4. amnesia-inducing agent

5. blood sugar management

6 step NAAARB management of POST-op care?

1. nausea and vomiting (PONV – a complication of general anesthesia & analgesia)

2. analgesic(s)

3. antibiotic

4. anticoagulation for DVT prophylaxis

5. blood sugar management (over 80 under 150)

6. restarting most medications held pre-operatively

etomidate (Amidate)

what is it/for?

MOA

AE

if you give this be ready to what?

used for anesthesia

MOA: GABA agonist

AE: adrenal suppression, apnea, myoclonus

be ready to INTUBATE

propofol (Diprivan)

what is it/for?

MOA

AE

if you give this be ready to what?

used for anesthesia

MOA: GABA agonist

AE: hypotension, apnea, hypertriglyceridemia (lipid emulsion), injection site reactions, infusion syndrome

be ready to INTUBATE

ketamine (Ketalar)

what is it/for?

MOA

AE

used for anesthesia

MOA: NMDA antagonist (amnesia, analgesia, anesthetic)

AE: ***dissociative reaction-yemporary***, tachycardia, hypertension or hypotension

2 nondepolarizing paralytic anesthetics with onset and duration?

what does nondepolarizing mean?

need to give what and when with paralytic agents?

remember to what with paralytics?

1. atracurium (Tracrium)

• onset: 2-3min

• duration: 35-45min

2. rocuronium (Zemuron)

• onset: 1 minute

• duration: 45-60 minutes

• nondepolarzing means they won’t twitch before going into sedation

NEED TO GIVE AMNESIA MED (PROPOFOL) BEFORE paralytic agent

INTUBATE pts STAT AFTER GIVE PARALYTIC bc they paralyze diaphragm too

1 depolarizing paralytic anesthetic with onset, duration, and protip?

depolarzing paralytics cause what?

MOA

succinylcholine (Anectine)

• onset: 1min

• duration: 5-10min

• pro tip: avoid in patients with hyperkalemia, skeletal muscle injury

• Depolarization can cause a release of K+ from muscle cells, potentially leading to dangerously high K+ levels, especially in patients with certain condition

• DEPOLARIZING PARALYTICS CAUSE TWITCHING before paralysis sets in

  • Depolarizing muscle relaxants, such as succinylcholine, act as agonists at the nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction.

  • They bind to these receptors, mimicking the action of acetylcholine, a neurotransmitter that normally stimulates muscle contraction.

  • However, unlike acetylcholine, which is rapidly broken down, depolarizing agents remain bound to the receptors for a longer period, causing a sustained depolarization of the muscle membrane.

  • This prolonged depolarization prevents the muscle from responding to further nerve signals, leading to paralysis

sugammadex (Bridion)

MOA

AE

Protip

MOA: complexes with rocuronium and vecuronium; reversal agent

AE: bradycardia, hypotension, afib, AV block, nausea, cardiac arrest, hypersensitivity, Vfib

pro tips: may need repeat doses; given in PACU

what paralytic do you give for for malignant hyperthermia?

what is malignant hyperthermia?

1. dantroline

2. (a rare but serious complication of general anesthetics & succinylcholine)

what is the 2 step Rapid sequence induction of anesthesia (in the field, E.D., or O.R.)?

1. midazolam (Versed) or propofol or etomidate or ketamine

2. succinylcholine or atracurium (Tracrium) or rocuronium (Zemuron) or another NMB

what is PONV?

6 meds for it?

1. prochlorperazine (Compazine)

MOA: dopamine antagonist

2. metoclopramide (Reglan)

MOA: dopamine antagonist

3. ondansetron (Zofran)

MOA: serotonin antagonist

4. scopolamine (TransdermSCOP)

MOA: anticholinergic

5. dexamethasone (Decadron)

MOA: corticosteroid

6. aprepitant PO, fosaprepitant IV (Emend)

MOA: neurokinin antagonist

AE: headache, hypersensitivity,

post-operative nausea and vomiting (a complication of general anesthesia & analgesia)

4 meds for ICU sedation?

dexmedetomidine (Precedex) MOA + AE

1. benzodiazepine (lorazepam, diazepam, midazolam) – frequent administration or continuous infusion to keep patient calm and/or reduce fighting the ventilator

2. propofol (Diprivan) – alternative to benzo. continuous infusion for short-term (up to 3 days), the drug is suspended in oil so it increases their triglycerides, chronic use = HLD

3. dexmedetomidine (Precedex)

• MOA: centrally-acting alpha-2 agonist, reducing NE secretion and producing analgesia

• AE: hypotension, bradycardia, hyperthermia (w/ precedex infusions in OR)

4. delirium/agitation – haloperidol (Haldol)

what should you do in ICU care regarding:

narcotics

NM blockade

environment

narcotic (fentanyl, hydromorphone, morphine)

• frequent administration or continuous infusion to minimize pain and/or reduce fighting the ventilator

neuromuscular blockade

• paralyze patient to prevent fighting the ventilator, must be given with sedation +/- analgesia to prevent panic

environmental conditions

• bright lights, loud noise, overnight interruptions contribute to delirium and agitation

4 vasopressors for ICU care?

receptors for all?

what do they each do?

3 meds for BP?

pressors

1. epinephrine: a1, B1, B2

2. norepinephrine: B1 and a1

3. phenylephrine: a1 (when used alone may cause bradycardia initially)

4. dopamine: B1 and a1

• B1 increases HR

• B2 bronchodilation

• A1 vasoconstriction

blood pressure reduction

1. nitroprusside/nitroglycerin

2. labetalol: injection or continuous infusion

3. nicardipine (Cardene): dihydropyridine CCB (dilates vessels w/o effecting HR)

4 notes about ICU care regarding:

PICC lines

Parenteral nutrition

Infection control

Abx therapy

1. central venous access – PICC lines or central lines

2. parenteral nutrition transitioning to enteral nutrition

3. infection control

• wash hands

• glove and gown

4. aggressive antibiotic therapy – ANY infection that originates in the ICU is considered nosocomial until proven otherwise; must address resistant bacteria (Pseudomonas, MRSA, MRSE, VRE, fungi, etc)

3 things for DVT prophylaxis?

2 things for stress ulcer prophylaxis?

DVT prophylaxis

1. enoxaparin (Lovenox), dalteparin (Fragmin), fondaparinux (Arixtra), heparin

2. TED hose

3. intermittent pneumatic compression devices (IPCD)

stress ulcer prophylaxis

1. H2RA (famotidine IV)

2. PPI (pantoprazole IV)

acid/base management in ICU

pH = x

HCO3- = x

pCO2 = x

6 buffers?

compensation

fast

• increased x

• decreased x

slow

• increased x

• increased x

pH = 7.35-7.45

HCO3- = 22-28

pCO2 = 35-45

buffers

1. albumin & other proteins

2. hemoglobin

3. phosphate

4. bicarbonate

5. trapping of H+ by ammonia (NH3)

6. release of H+ by ammonium (NH4+)

compensation

fast

• increased respiration rate to lower pCO2

• decreased respiration rate to raise pCO2

slow

• increased H+ elimination by kidneys

• increased HCO3- synthesis and/or conservation by kidneys

metabolic acidosis

lab values

cuases

meds that cause (4)

Tx:

sepsis:

ketoacidosis:

hypoperfusion:

meds:

pH = less than 7.35

HCO3- = low (consumption or loss)

pCO2 = normal, then low

• causes: sepsis, ketoacidosis, hypo-perfusion, diarrhea

medications

1. nephrotoxic medications

2. excess normal saline solution

3. propofol (Diprivan)

4. aspirin

Tx:

sepsis: aggressive antibiotic therapy, fluid resuscitation, blood pressure control

ketoacidosis: insulin (if DKA), fluids

hypo-perfusion: fluids, pressor medications (AFTER fluid resuscitation)

medications: discontinue offender, bicarbonate (for aspirin OD); bicarbonate for pH below 7.2

metabolic alkalosis

labs

causes

meds that cause

Tx

pH = greater than 7.45

HCO3- = elevated

pCO2 = normal, then high

• causes: NG suction

• medications: antacids (e.g., calcium carbonate), diuretics

• treatment: H2RA or PPI, sodium chloride infusion, potassium supplementation, carbonic anhydrase inhibitor

respiratory ACIDosis

labs

causes

meds that cause

Tx

pH = less than 7.35

HCO3- = normal, then high

pCO2 = high

causes: respiratory failure

medications

• opioid analgesics

• propofol

treatment: ventilation, B2 agonist, steroids, naloxone (beware of pulmonary edema)

respiratory ALKAlosis

labs

causes

med causes

Tx

pH = greater than 7.45

HCO3- = normal, then low

pCO2 = low

• causes: pain, anxiety, hyperventilation

• medications: aspirin (due to metabolic acidosis)

treatment: analgesic, benzodiazepine

just fyi why don’t paralytics stop the heart?

The short answer is: none! The better answer is: Neuromuscular blocking drugs like atracurium, rocuronium, mivacurium etc act on the neuromuscular junction. They antagonise nicotinic acetylcholine receptors and this cause an inability to pass inputs from nerve to muscle cells (as opposed to suxamethonium which agonises the nictotinic receptors hence people twitch briefly after sux before paralysis sets in).

Cardiac tissues do utilise acetylcholine but they have muscarinic receptors and as such the neuromuscular blockers have no effect. Cardiac tissue also has an intrinsic automaticity which organises cardiac impulses/beating.

It is interesting that when you 'reverse' neuromuscular blockers with neostigmine (an acetylcholineesterase inhibitor) you get more acetylcholine available but not just at the neuromuscular junction, also in cardiac tissue. This means that neostigmine alone would cause a bradycardia (potentially significantly) and so we (almost) always give it with glycopyrrolate which causes a relative tachycardia.