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a m.d. step 3 - ZIP DECK > XL1 [Rx +] > Flashcards

XL1 [Rx +] Flashcards

1
Q

Albuterol

MOA (2)

A

[β2🟢] > [β1🟢]

agonist

for acute asthma

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2
Q

Albuterol

Indication

A

acute asthma

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3
Q

Salmeterol

Indication (2)

A
  1. chronic asthma
  2. chronic COPD
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4
Q

Salmeterol

MOA (2)

A

[β2🟢] > [β1🟢]

agonist

= chronic asthma / chronic COPD

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5
Q

doButamine

Indication (2)

A
  1. HF
  2. cardiac stress testing
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6
Q

doButamine

MOA (3)

A
  1. [β1🟢] > [β2🟢]
  2. [general α🟢]
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7
Q

Dopamine

MOA (4)

A

{([D1🟢 = D2🟢] >[general β🟢] > [general α🟢*]}

[inotropic & chronotropic (α)] predominates at high doses

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8
Q

Dopamine

Indication (3)

A

1.cardiogenic shock
2.HF
3.unstable bradycardia

{([D1🟢 = D2🟢] >[general β🟢] > [general α🟢]}⼀{HIGH dose → INC (α) effects }

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9
Q

Epinephrine

MOA (2)

A
  1. [(general β🟢{low concentration}]
    >
  2. [general α🟢{HIGH CONCENTRATION}]

“with low effort you’ll get a B….with HIGH EFFORT YOU’LL GET AN A”

✏️Epi is stronger at β2🟢 than NorEpi is at β2🟢

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10
Q

Epinephrine

Indication (6)

A
  1. ANAPHYLAXIS
  2. asthma
  3. angle-open glaucoma
  4. arrest (cardiac arrest)
  5. [a heart block]
  6. [A low bp (shock)]

[(general β🟢 ⬅︎ ⬇︎ Epi ⇪ → general α🟢]

“with low effort you’ll get a B….with HIGH EFFORT YOU’LL GET AN A”

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11
Q

Isoproterenol

MOA (2)

A

[(β1🟢 = β2🟢)]

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12
Q

NorEpinephrine

MOA (3)

A

[(α1🟢 > α2🟢 > β1🟢)]

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13
Q

NorEpinephrine

Indication

A

hypOtension(but note: NE⬇︎renal perfusion)

[(α1🟢 > α2🟢 > β1🟢)]

📝Epi is stronger at β2🟢 than NorEpi is at β2🟢

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14
Q

Isoproterenol

Indication

A

electrophysiologic eval of tachyarrhythmias🛑note: can worsen ischemia!

[(β1🟢 = β2🟢) ]

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15
Q

Phenylephrine

MOA (2)

A

[α1🟢] > [α2🟢]

([α1🟢] vasoconstriction can → [baroreceptor-reflex mediated bradycardia])

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16
Q

Phenylephrine

Indication (3)

A
  1. hypOtension
  2. myDriasis for ocular procedures
  3. rhinitis(PNE is also a decongestant)

[(α1🟢 > α2🟢)]

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17
Q

Amphetamine

MOA (2)

A

Indirect Sympathomimetic via:
1. [NE🔻reuptake inhibitor]
2. releases stored NE🚰

[InDirect Sympathomimetic] –(🔻 [⇪NE catecholamine]

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18
Q

Ephedrine

Indication (3)

A
  1. Nasal Decongestant
  2. urinary incontinence
  3. hypOtension

InDirect Sympathomimetic via [⇪ NE/E catecholamines]

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19
Q

Cocaine

MOA

A

[(NE🔻reuptake inhibitor) InDirect Sympathomimetic]

→ ⇪ adrenergic NE → ⇪ Sympathetic NS

❗️NEVER GIVE β🟥 if cocaine intoxication suspected since this may → unopposed α activation

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21
Q

Ephedrine

MOA

A

[(releases stored NE🚰) InDirect Sympathomimetic]

→ ⇪ adrenergic NE → ⇪ Sympathetic NS

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22
Q

Clonidine

MOA

A

[α2🟢]

sympatholytic

📝DECREASES Peripheral vasoconstriction CENTRALLY (inhibits sympathetics) but will have SOME INC peripheral vasoconstriction by acting directly in the PERIPHERAL BODY also

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23
Q

Clonidine

Indication (3)

A
  1. HTN Urgency
  2. ADHD
  3. Tourette syndrome

[α2🟢 sympathoLytic]

(does not ⬇︎Renal blood flow)

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24
Q

Clonidine

Toxicity (5)

A
  1. CNS depression
  2. [pupillary depression (miosis)]
  3. [cardiac depression (bradycardia)]
  4. [respiratory depression]
  5. vascular depression (hypOtension)

[α2🟢 sympathoLytic] ⼀ “Clonidine makes me depressed”

(does not ⬇︎Renal blood flow)

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25
Q

α-methyldopa

MOA
_________________
Indication

A

[α2🟢 sympathoLytic]
_________________
HTN in pregnancy

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26
Q

α-methyldopa

Toxicity (2)

A

can →
1. [⊕DAT hemolysis]
2. [SLE-like syndrome]

[α2🟢 sympathoLytic]

DAT = [Direct_Coombs AntiHumanglobulin Test]

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27
Q

pheNOxybenzamine

MOA
_________________
Indication

A

iiRREVERSIBLEgeneral α🟥
_________________
[Px for HTN catecholamine crisis] in [Pheochromocytoma resection]

given preop

[(pheNOxybenzamine) = NO reversing ]

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28
Q

phentolamine

MOA
_________________
Indication

A

REVERSIBLEgeneral α🟥
_________________
[Px for HTN catecholamine crisis] in [MAOI pts who eat tyramine containing food]

“OF COURSE THIS TOLL BOOTH TICKET IS REVERSIBLE!”

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29
Q

pheNOxybenzamine and phentolamine

side effects (2)

A
  1. orthostatic hypOtension
  2. reflex tachycardia
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30
Q

[DEPT”-osin “]

MOA

A

α1🟥

🔎{[DEPT“-osin “] = DoxazOSIN \ tErazOSIN \ PrazOSIN \ TamsulOSIN}

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31
Q

[DEPT”-osin “]

Indication(s) (3)

A

[DEPT”-osin “]
1. [BPH Urinary sx (DEPT)]
2. [PTSD (P)]
3. [HTN (DEP)]

α1🟥

🔎{[DEPT“-osin “] = DoxazOSIN \ tErazOSIN \ PrazOSIN \ TamsulOSIN}

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32
Q

Mirtazapine

MOA

A

α2🟥

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33
Q

Mirtazapine

Indication

A

Depression

α2🟥

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34
Q

Mirtazapine

Side Effects (3)

A
  1. sedation
  2. HLD
  3. hunger

α2🟥

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35
Q

[DEPT”-osin “]

Side Effects (3)

DoxazOSIN \ tErazOSIN \ PrazOSIN \ TamsulOSIN

A

[DEPT”-osin “]
1. [1st dose orthostatic hypOtension (DEPT)]
2.[dizziness (DEPT)]
3.[HA (DEPT)]

α1🟥

{[DEPT“-osin “] = DoxazOSIN \ tErazOSIN \ PrazOSIN \ TamsulOSIN}

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36
Q

Receptors are divided into [5 major groups (CADHV)]

Describe the 2 types of Cholinergic receptors

A

▶Nicotinic (autoNomic vs neuroMuscular): ACh Receptors that are Na+/K+ channels
▶Muscarinic (M1,M2,M3,M4/M5): ACh Receptors that are {[G protein coupled R (M1,M2,M3 require 2nd messenger systems [q|i|s])}

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37
Q

function

α1(3)

sympathetic Receptor

A

[Vascular smooth muscle ctn (vasoconstricts)]
[Internal Urethral Sphincter ctn & Intestinal ctn]
[Dilator of pupil (myDriasis)]

“Give me the alpha 1 VID…”

📖Dilates pupil via [contracts pupillary Dilator m (myDriasis)]
🔎ctn = contraction

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38
Q

Receptors are divided into [5 major groups (CADHV)]

Describe the 2 types of Adrenergic receptors

A

▶αlphaadrenergic : Sympathetic NE Receptors (α1, α2 requireq|i|s2nd messenger)
▶βetaadrenergic: Sympathetic NE Receptors (β1, β2 requireq|i|s2nd messenger)

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39
Q

Name the 5 major Receptor groups

A

(CADHV)Receptors
Cholinergic
[Adrenergic SYMPATHETIC]
Dopaminergic
Histaminergic
Vasopressin

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40
Q

function

α2(5)

Receptor

A

⇪ Coagulation (via ⇪ Platelet aggregation)]
_________________
[⬇︎lipolysis (⬇︎fat breakdown)]
⬇︎aqueous humor production
[⬇︎sympathetic (via neg feedback)]
[⬇︎sugar cell entry (via ⬇︎ INSULIN release)]

“…Give her the {αlpha 2 Class}”!

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41
Q

function

β1(4)

sympathetic Receptor

A

⇪ Contractility Heart
⇪ Rate Heart
[⇪Adipocyte lipolysis]
⇪ Kidney RENIN release

“* βeta1 ⇪ CRAK*”

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42
Q

function

β2 (7)

sympathetic Receptor

A

⇪ {[VasoDilates autonomic smooth m] [Tremors somatic skeletal m]}
⇪ Aqueous humor production
[⇪BronchoDilation]
[⇪Uterine Relaxation (tocolysis)]
[⇪ Lipolysis & Liver Glycogenolysis]
⇪ Insulin release
⇪ Ciliary m Relaxation

“…βeta2 ⇪ VABULIC!!”

👓gProtein: (s)

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43
Q

function

M1 (2)

ParaSympathetic Receptor

A
  1. CNS
  2. ENS

“

👓gProtein: (q)
🔎ENS = Enteric Nervous System

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44
Q

function

M2 (2)

ParaSympathetic Receptor

A
  1. ⬇︎HR
  2. ⬇︎Heart Contractility

👓gProtein: (i)

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45
Q

function

M3 (6)

ParaSympathetic Receptor

A
  1. [Gut peristalsis ⇪]
  2. [Accommodation (contracts ciliary m)]
  3. [Miosis (contracts pupillary sphincter m)]
  4. Bladder contraction
  5. [Lung contraction (bronchoconstriction)]
  6. [Exocrine secretion (salivary/lacrimal/gastric acid)]

“M3s took a huge GAMBLE”

👓gProtein: (q)

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46
Q

function

D1

Receptor

A

renal vasoDilation

👓gProtein: (s)

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47
Q

function

D2

Receptor

A

inhibits nerve terminal adenyl cyclase = modulates (especially brain) NTS release

👓gProtein: (i)

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48
Q

function

H2

Receptor

A

⇪ Gastric acid secretion

👓gProtein: (s)

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49
Q

function

H1 (6)

Receptor

A
  1. ⇪ Production of nasal mucus
  2. ⇪ Production bronchial mucus
  3. [⇪ Permeability vascularly → edema]
  4. ⇪ Pruritus
  5. ⇪ Petit breathing (bronchoconstriction)]
  6. ⇪ Pain

👓gProtein: (q)

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50
Q

function

V1

vasopressin Receptor

A

vasoconstriction

👓gProtein: (q)

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51
Q

function

V2

vasopressin Receptor

A

⇪ H2O permeability&reabsorption in renal CD

👓gProtein: (s)

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52
Q

Name the 3 types of opioid receptors

MOA of opioid receptors (4)

A

[morphine|enkephalin |dynorphin opioid Receptors
_________________
{[opens K+ channels] and [closes Ca+ channels]}
→ [⬇︎synaptic transmission]
→ {⬇︎release of [ACh/norEpi/5HT/glutamate/substance-P]}

(TOXICITY → somnolence, miosis, bradypnea, constipation, Addiction )

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53
Q

Butorphanol

MOA (2)

A

[dynorphinopioid🟢] + [morphine (partial) opioid R agonist]

has less respiratory depression than FULL opioid R agonist

note: OD not easily reversed with nalaxone

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54
Q

Tramadol

MOA (3)

A
  1. [very weak opioid🟢]
  2. [5HT🔺reuptake inhibitor]
  3. [NorEpi🔺 reuptake inhibitor]

(TOXICITY → seizure, serotonin syndrome + same as other opioid TOX)

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55
Q

Ethosuximide

MOA

A

[(Thalamic)T-type Ca+ channel Blocker]

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56
Q

Benzodiazepine

MOA

A

⇪ GABAA effect

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57
Q

Phenytoin

MOA

A

Na+ channel inactivation(zero order kinetics)

✏️ IV requires Fosphenytoin

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58
Q

MOA for the [1st line tx of trigeminal neuralgia]

A

Carbamazepine
[⇪ Na+ channel inactivation]

✏️also used for: simple partial/complex partial/GTC

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59
Q

MOA for the anti-epileptic also used to treat bipolar depression (2)

A

Valproic acid
1. [ ⇪ Na+ channel inactivation]
2. [inhibits GABA transaminase → ⇪ GABA concentration]

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60
Q

MOA for anti-epileptic also used to treat peripheral neuropathy (2)

A

GABApentin
1. [inhibits high voltage gated Ca+ channels]
2. GABA analog

(indications: peripheral neruopathy, postherpetic neuralgia, simple szure, complex szure)

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61
Q

MOA for the anti-epileptic also used to prevent Migraine HA (2)

A

Topiramate
1. [Na+ channel blocker] antiepileptic
2. [ ⇪ GABA effect]

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62
Q

Lamotrigine

MOA
_________________
notable precaution?

A

[Na+ channel blocker] antiepileptic
_________________
[(must be titrated slowly) ⼀otherwise possible → Stevens-Johnson syndrome]

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63
Q

Levetiracetam

MOA

A

unknown

(antiepileptic that possibly modulates GABA and glutamate)

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64
Q

TiaGabine

MOA
_________________
Indication (2)

A

[GABA🔻reuptake inhibitor] antiepileptic
_________________
1. simple partial seizure
2. complex partial seizure

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65
Q

VigaBatrin

MOA
_________________
Indication (2)

A

[iiRREVERSIBLYinhibits GABA transaminase ➜ ⇪ GABA ] antiepileptic
_________________
1. simple partial seizure
2. complex partial seizure

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66
Q

Describe cp for Steven Johnson Syndrome (3)
_________________

Which drugs are known to cause Steven Johnson Syndrome? (4)

A

{[malaise and fever] –(rapid)–> [(ocular/oral/genital) erythematous/purpuric macules] → [epidermal necrosis and sloughing]}
_________________
1. [antiepileptics (esp. lamotrigine)]
2. allopurinol
3. sulfa
4. PCN

Steven Johnson has epileptic allergy to sulfa and PCN

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67
Q

What is the difference in MOA between Barbiturates and Benzodiazepines

A

B(A)RB = potentiates GABAA by ⇪ dur(A)tion of [GABA Cl-channel] opening
_________________

B(E)NZO =
1. potentiates GABAA by ⇪ fr(E)quency of [GABA Cl- channel] opening
2. ⬇︎REM sleep
3. ATOM are short acting benzo ➜ addictive!

(ATOM = Alprazolam/Triazolam/Oxazepam/Midazolam)

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68
Q

Nonbenzo hypnotics act as ⬜ and the 3 primary examples are ⬜

A

[(BZ1 GABA subtype) R agonist]; Zolpidem/Zaleplon/esZopiclone

✏️rapid hepatic metabolism = unlike other sedative-hypnotics, day after psychomotor depression with few amnestic effects

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69
Q

In Anesthesia, drugs with high blood/lipid solubility have ⬜ induction and ⬜ potency

A

slow; high

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70
Q

Define M.A.C. in terms of anesthesia

A

Minimal Alveolar Concentration (of anesthesia) required to prevent 50% of subjects from moving after noxious stimuli
..so [potency = 1/MAC]

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71
Q

Name and briefly describe each of the 5 [IV anesthetics]

A

[Barbiturates (Thiopental)] = high lipid solubility = high potency = rapid brain entry = use in short surgical procedures
_________________
[Benzodiazepine (Midazolam)]] = ⭐popular for endoscopy ⼀but may → postop bradypnea (tx = flumazenil)
_________________
[Ketamine/Arylcyclohexylamines] = [NMDA R Blocker PCP analog] → dissociative anesthesia
_________________
Opioids(Morphine|fentanyl)
_________________
PropoFOL = potentiates GABAA = rapid anesthesia induction, ICU sedation

“B. B. King on OPIOIDS PROPOses-FOLgers”

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72
Q

Name and describe the 6 local anesthetics

A

“BLM locally anesthetizes CPT”

“BLM = Amides (will have 2 i)
BupivAcaine
LIdocaine
MepivAcaine
_________________

“CPT” = Esters”
Cocaine
Procaine
Tetracaine

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73
Q

Succinylcholine

MOA

A

[strongACh R agonist] → blocks (by binding tightly to ) [NMJ postsynpatic ACh R] → sustained depolarization → prevents [NMJ action potential] → prevents muscle contraction = paralysis

Toxicity = HYPERKFC

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74
Q

how does reversal of Succinylcholine work? (2)

A

[phase 1 PD] = no antidote
= (🛑[cholinesterase inhibitors] will exacerbate block}
_________________
[phase 2 RD] = (✅give [cholinesterase inhibitors])
=ACh R have repolarized now ⼀but still desensitized

📖
[phase 1 Prolonged Depolarization] =ACh R are bound tight by Sux and undergoing PD = no antidote = (🛑[cholinesterase inhibitors] will exacerbate block}
_________________
[phase 2 Repolarized (but) Desensitized] = ACh R have repolarized now ⼀but still desensitized = (✅give [cholinesterase inhibitors]) →flood and resensitize R with ACh substrate

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75
Q

Succinylcholine

Toxicity (3)

A
  1. [HYPER K+]
  2. [HYPER Fever (MMalignant Hyperthermia)]
  3. [HYPER Ca+]

“HYPERKFC”

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76
Q

There are 2 types of paralytic agents: depolarizing vs nondepolarizing

a: describe MOA for nondepolarizing paralytic drugs
_________________
b. describe reversal process (2)

A

{tubocurarine or [(⼀curium) drugs]} = nondepolarizing competitive inhibitors against ACh for [NMJ postsynaptic ACh R]
_________________
Reversal =
▶give [AChE inhibitors(neostigmine/edrophonium) ] → reverses blockade
▶but (neostigmine) may also cause [acute cholinergic tox (DUMBBELSS)] = co-admin with Atropine

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77
Q

Local Anesthetics

MOA (4)

“BLM locally anesthetizes CPT”

A
  1. [preferentially blocks activated Na+ channels] = targets & blocks rapid firing neurons = inhibits depolarization of highly active (painful) tissue
  2. infected tissue requires ⇪ local anesthesia*
  3. order of loss = PETS (1st Pain → tEmp → Touch → last preSsure) and [myelinated small] > unmyelinated LARGEa]}7
  4. give with epinephreine vasoconstrictor = [enhances local action (by preventing systemic circulation)] +

“BLM locally anesthetizes CPT”

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78
Q

Local Anesthetics

Toxicity (6)

“BLM locally anesthetizes CPT”

A
  1. [CNS ❌]
  2. [CV❌(bupivacaine)]
  3. [arrhythmias(Cocaine)
  4. [methemoglobinemia(benzocaine)]
  5. HTN
  6. hypOtension

✏️(if allergic to [*ester*local anesthetic] give [*amide*local anesthetic])

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79
Q

Dantrolene

MOA
_________________
Indication (2)

A

prevents release of Ca+ from [sk muscle sarcoplasmic reticulum]
_________________
1. [MMalignant Hyperthemia]
2. [Neuroleptic Malignant Syndrome]

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80
Q

Baclofen

MOA
_________________
Indication

A

Inhibits [spinal cord GABAB R] → sk muscle relaxer
_________________
[Muscle spasm(ie acute low back pain)]

muscle relaxer

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81
Q

Cyclobenzaprine

MOA (2)
_________________
Indication

A

[(TCA-cousin✏️) with anticholinergic effect] + [centrally acting sk muscle relaxer]
_________________
[Muscle spasm(ie acute low back pain)]

muscle relaxer

📝Cyclobenzaprine is structurally similar to (and has similar anticholinergic effect) as TCA

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82
Q

(-triptans)

MOA (4)

.

A

⭐[5HT(1B/1D)🟢] →
🔧Inhibits trigeminal n activation
🔧inhibits vasoactive peptide release
🔧induces vasoconstriction

TOX: [Coronary Vasospasm (CTD in CAD/Prinzmetal angina)], paresthesia

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83
Q

Why is Sumatriptan contraindicated in patients with ⬜(2) ?

A

CAD | Prinzmetal angina
_________________
(⼀triptans) cause Coronary Vasospasm

84
Q

sulfa drug allergy ranges from mild to fatal

Name the 8 Sulfa drug groups

A
  1. Sulfonamide abx
  2. Sulfasalazine
  3. Sulfonylurea
  4. Probenacid
  5. Furosemide
  6. Acetazolamide
  7. Celecoxib
  8. Thiazides

“Sulfa Sounding Serious? Popular FACT”

85
Q

Name 3 drugs that in addition to their primary MOA secondarily also are [Muscarinic R Blockers]

A
  1. TCA
  2. [H1🟥]
  3. antipsychotics
86
Q

Which drugs produce [Disulfiram-like reactions]? (5)

A
  1. metronidazole
  2. cephalosporins(select)
  3. griseofulvin
  4. procarbazine
  5. Sulfonylurea1st GEN
87
Q

How should Warfarin be adjusted if a patient starts taking amiodarone?

A

⬇︎Warfarin by 25% (since amiodarone inhibits CYP2C9)

88
Q

Metformin can dangerously cause ⬜

Name Metformin contraindications? -5

________________

how is iodine contrast related to Metformin?

A

lactic acidosis ;

  1. renal failure
  2. liver dysfxn
  3. EtOH abuse
  4. sepsis
  5. CHF (especially if GFR < 30)

________________

[large dose IV iodine contrast] ⇪ lactic acidosis risk … so Metformin IS HELD ON DAY contrast is given ➜ Metformin restarted 2 days later

________________

common SE = GI upset and VB12 malabsorption

89
Q

Pindolol

a. MOA (2)
_________________
b. explain its Indication

A

a. {[general β🟥] but also is <partial [general β🟢]>}!
_________________
b. because <part of general β R are stimulated> → less [“general β🟥 BRADYCARDIC effect “] = give to patients with poor tolerance to [“β🟥 BRADYCARDIC effect” or reduced exercise capacity]

90
Q

What 6 drugs make up the Amphetamine family?

A
  1. Amphetamine
  2. Methamphetamine
  3. Ephedrine
  4. Pseudoephedrine
  5. Methylphenidate
  6. Tyramine 👀

📝Tyramine displaces NE. It is catabolized by MAO. [MAO inhibitors] can → ⇪ Tyramine which may → HTN crisis

91
Q

[general β🟥]

Toxicity (6)

A
  1. Bronchospasm
  2. Bradycardia
  3. CNS depression
  4. CNS insomnia
  5. MASK sx of hypOglycemia
  6. TAG ⇪
92
Q

List the 5 drugs eliminated by COMT
_________________
Which 2 are special? why?

A
  1. doButamine
  2. isoproterenol
  3. NOREPINEPHRINE⭐
  4. epi
  5. DOPAMINE⭐

[⭐= eliminated by COMT and MAO]

“COMT d.i.N.e.D on 5 drugs”

93
Q

a: How does Cell/Tissue Damage lead to Pain/Inflammation/Fever?

a1: Damage induces ⬜ to produce ⬜
a2: ⬜ binds to Cyclooxygenase and is converted into ⬜

a3: ⬜ is then modified by multiple syntheses into
what 3 major compounds?

a4: ⬜ can then go to induce pain/inflammation/fever.

B: What is the rate limiting step for this reaction?

A

1: Damage induces [Phospholipase A2] to produce [Arachidonic Acid]
2: ⭐[Arachidonic Acid] binds to [COX (Cyclooxygenase)] and is converted into [Prostaglandin H2] = RATE LIMITING STEP! ⭐

3: [Prostaglandin H2] is then modified by multiple syntheses into
- [PGi2 Prostacyclin]
- [Prostaglandin E2]
- [TXA2 Thromboxane]

4: [Prostaglandins] can then go to induce pain(via central/peripheral pain sensitization) /inflammation/fever

B: What is the rate limiting step for this reaction?
[Arachidonic Acid] conversation into [PGH2] by Cyclooxygenase

94
Q

describe how COX1 and COX2 are different in terms of tissue expression

A

*📝
-COX1 = HIGH constitutive expression and located ubiquitously⼀in most tissue
-COX2 = low constitutive expression = generally has to be induced (by proinflammatory stimuli)

95
Q

[ASA Aspirin]

MOA (3)

A
  1. IRREVERSIBLE
  2. NON-Competitive
  3. COX inhibitor

📝
-COX1 = HIGH constitutive expression and located ubiquitously⼀in most tissue
-COX2 = low constitutive expression = generally has to be induced (by proinflammatory stimuli)

96
Q

A: What is another name for PGi2?

B: What are its roles? (2)

C: Endothelial cells express COX1 or COXTWO? What are the primary compounds produced from Endothelial cells?

A

A: Prostacyclin!

B:

1) VasoDilates
2) INHIBITS Clotting

C: Endothelial cells express BOTH COX1 and COXTWO!
They primarily produce only {[PGi2 Prostacyclin] and [PGE2]} because Endothelial cells do NOT contain [Thromboxane synthase]

“(PGi2 Prostacyclin) | (PGE2) “

97
Q

Elucidate the steps of Fever Production starting with Tissue Damage

  1. Damaged Tissue produces [⬜ and ⬜ ] which travels to the CNS
  2. [⬜ and ⬜ ] stimulate endothelial cells of the [⬜ blood vessels] to express ⬜ and [⬜ synthase]
  3. ⬜ and ⬜ in the endothelial cells of the [⬜ blood vessel] produce [⬜ ] which goes to stimulate hypOthalamus to INC body temperature
A
  1. Damaged Tissue produces [IL-1 and TNFa] which travels to the CNS
  2. [IL-1 and TNFa] stimulate endothelial cells of the [hypOthalamus blood vessels] to express COXTWO and [PGE synthase]
  3. [COXTWO and PGEsynthase] in the endothelial cells of the [hypOthalamus blood vessel] produce [Prostaglandin E2] which goes to stimulate hypOthalamus to INC body temperature
98
Q

Name the 3 Groups of NSAIDs

A
  1. Aspirin/Salicylates
  2. Traditional Non-Selective NSAIDs (ibuprofen)
  3. Coxibs (COX inhibitors)
99
Q

COX1

A: Physiological Role (4)

B: What compounds do COX1 produce that facilitate these roles?

A

HOUSEKEEPING:
1. Platelet Regulation (monitors blood clotting)

  1. Kidney Function
  2. Cytoprotection of Stomach by regulating Acid/Mucus production & [gastric blood flow]
  3. Maintains Patent Ductus Arteriosus for Fetus and stimulates [Uterine contractions during labor (involves PGF2a) ]

(COX1 is NOT inhibited by Celecoxib)

B: [PGE2/PGi2]

100
Q

COX-TWO

Physiological Role

A

PRO-INFLAMMATORY RESPONSE (Mitogenesis and Signaling)

101
Q

A: Platelets express ONLY _____[COX⬜] but primarily produce ________.

B: What are the roles of the compound produced? (2)

A

A: Platelets express ONLY COX1 but primarily produce [Thromboxane].

B: What are the roles of the compound produced? (2)

1) vasoconstricts
2) promotes clotting

102
Q

A: Why is PGi2 particularly important in Pt with Renal Dz or Heart Failure? (3)

B: Is [ ______-medicated acute renal failure] caused by taking NSAIDs in a diseased state, reversible?

A

A: [Renal Dz and Heart Failure]—> INC Renal VasoCONSTRICTORS. [PGi2] is a vasodilator that will

  • INC Renal Blood flow to prevent Renal ischemia
  • INC GFR
  • INC water and Na+ excretion

B: Is [ HEMODYNAMICALLY-medicated acute renal failure] caused by taking NSAIDs in a diseased state, reversible?

->YES! JUST TAKE THEM OFF OF THE NSAIDS!

103
Q

A: Why is Aspirin READILY absorbed in the stomach and [upper small intestine]?

A

ASA (AcetylSalicylicAcid) is a weak acid and in the acidic environment of the stomach it will be in a [NEUTRAL PROTONATED FORM]—> Allows EASY ABSORPTION!

104
Q

Aspirin Recommended Dosing

  1. Anti-Platelet activity = ⬜ dose
  2. Anti-Pyretic = ⬜ dose
  3. Analgesic = ⬜ dose
  4. Anti-Inflammation= ⬜ dose
A

Aspirin Recommended Dosing

  1. Anti-Platelet activity = [81mg qD]
    _________________
  2. Anti-Pyretic(must cross BBB) = [400mg BID]
    _________________
  3. ]Anti-Pain (Analgesic)] = [400mg BID]
    _________________
  4. [Anti-Puff (anti-Inflammation)= [4,000mg - 6,000mg qD]
105
Q

A: Why is concurrently taking [Salicylates/Aspirin] and Warfarin OR Sulfonylureas contraindicated?

B: Sulfonylurea Toxicity —> ⬜

A

[Salicylates/Aspirin] are 50-90% Protein bound once they enter the serum. This will DISPLACE other very protein bound drugs like WARFARIN OR Sulfonylureas—-> Warfarin/Sulfonylurea Toxicity!

B: Sulfonylurea toxicity —-> hypOglycemia

106
Q

How do you treat Salicylate OVERDOSE and why?

A

Alkalinize the Urine (make urine more basic) —>cause Salicylate to convert into its [DeProtonated CHARGED Form] —> Trap it in the urine—> INC Excretion and prevents renal Absorption

107
Q

A: Ibuprofen has a _____[slow/rapid] onset of ____ min and is _____[better/least] tolerated than Aspirin even though it is just as _____.

B: INDICATIONS (2)

A

Ibuprofen has a RAPID onset of [15-30 min] and is BETTER tolerated than Aspirin even though it is just as potent.

INDICATIONS:

  • Fever
  • Acute Pain
108
Q

A: Naproxen is ___ times more potent than aspirin and has a RAPID onset of ____ min.

B: Naproxen has a serum half life of ___ hours which allows for _____ dosing

C: Naproxen is an extremely ideal _______

A

A: Naproxen is 20 x more potent than aspirin and has a RAPID onset of 60 min.

B: Naproxen has a serum half life of 14 hours which allows for twice/day dosing

C: Naproxen is an extremely ideal Anti-Pyretic

109
Q

INDOMETHACIN

A: Primary Indications (3)

B: Cons

A

A: Indication

1) NSAID Used to promote closure of [Fetal Ductus Arteriosus]
2) 10-40 x more potent than Aspirin at anti-inflammation
3) Inhibits neutrophil mobility

B: Cons
(x) NOT TOLERATED AS WELL AS IBUPROFEN-Toxicity limits usage

110
Q

KETOLORAC

A: Primary Indication

B: What can this NSAID replace?

A

A: Indication:
[Intravenous NSAID] that treats post-surgical pain

B: Can be used as an Opioid Replacement Drug

111
Q

DICLOFENAC

B: What’s the cons of this drug and its class?

A

A: DICLOFENAC= Relatively Selective COXTWO Inhibitor

B: [COXTWO Inhibitors] INC chances of Stroke/Heart Dz!!

112
Q

What are 2 ASPIRIN-Specific Adverse Effects?

A
  1. Reye’s syndrome (occurs in genetic subset of children/teens who take Aspirin during a viral infection) = FATAL degenerative liver dz associated w/encephalitis
  2. INC Risk of Gout
113
Q

A: What is the most common adverse effect reported for [tNSAIDs & (Aspirin/Salicylates) ] ?

B: How do [tNSAIDs & (Aspirin/Salicylates) ] cause Gastric damage? (2)

C: How do you treat [tNSAIDs & (Aspirin/Salicylates) ] induced Gastric damage? (2)

A

B:
1) DIRECTLY damage gastric epithelium from being ion trapped in the compartment sometimes

C: Treatment:
-Misoprostol = PGE1 in a pill [CAN NOT GIVE TO PREGNANT WOMAN SINCE IT INDUCES ABORTION]

-Omeprazole

114
Q

A: [Acute interstitial nephritis and Nephrotic Syndrome]

B: Who does this occur most in/

A

A: RARE but important clinical syndrome associated with IDIOPATHIC Glomerular [inflammatory cell infiltration] / proteinuria and NV. Caused by month exposure to NSAIDs!

-Pt recovers once NSAIDs are discontinued

B: Occur most in Women and Elderly

115
Q

[CHRONIC interstitial nephritis and Analgesic Nephropathy]

A

A: Caused by CHRONIC Daily OVER USE of NSAIDs which leads to Chronic Renal Ischemia—> ESRD

ESRD= End Stage Renal Dz

116
Q

A: What is [NSAID Hypersensitivity]?

B: What are the sx and what is the onset?

A

A: NON-IMMUNE inflammatory attack that occurs when pt takes [Aspirin / tNSAIDs/ COXTWO inhibitors]. Arachidonic acid accumulation–> Leukotriene production–> [airway hypersensitivity rxn]

B: Rapid Severe asthma attack that onsets 30-60 min after intake

117
Q

NSAIDs taken in pregnant women after ____ weeks gestation can cause [Premature Ductus Arteriosus ____] in the fetus

A

NSAIDs taken in pregnant women after 30 weeks gestation can cause [Premature Ductus Arteriosus CLOSURE] in the fetus

118
Q

A: COXTWO inhibitors such as Celecoxib are BEST used for what 3 circumstances?

B: What type of effect does [COXTWO inhibitors] have on Kidneys?

C: Why is Celecoxib NOT a first-choice NSAID?

A

A: COXTWO inhibitors such as Celecoxib are BEST used for

  • [Rheumatoid Arthritis]
  • Osteoarthritis
  • Pt who are at higher risk for GI bleeds

B: [COXTWO inhibitors] have SAME NEPHROTOXICITY as tNSAIDS and [Aspirin/Salicylates] because Kidneys constitutively express COXTWO and need it

C: Celecoxib significantly Increases Stroke/Heart Dz probability and so is NOT a 1st choice NSAID

119
Q

Which 3 Drugs have Dangerous impaired Renal Clearance due to NSAID usage?

A
  1. Lithium
  2. Methotrexate
  3. [Gentamicin-Aminoglycoside]
120
Q

A: Acetaminophen is metabolized into its active metabolite (______) which inhibits ______ AND activates the ______ system—> DEC Fever & Pain

B: Acetaminophen is not a good anti-______ or anti-______ because it does not inhibit ________. This is due to [peripheral ______] that quickly degrade it in the periphery only

C: How does Acetaminophen affect the Kidneys and GI system?

A

A: Acetaminophen is metabolized into its active metabolite (AM404) which inhibits CNS COXTWO AND activates the cannabinoid system—> DEC Fever & Pain

B: Acetaminophen is not a good anti-inflammatory or anti-platelet because it does not inhibit [Peripheral COX1 or COXTWO]. This is due to [peripheral HydroPerOxides] that quickly degrade it

C: How does Acetaminophen affect the Kidneys and GI system?
:-) It safe for both due to inability to act on [Peripheral COX1 and COXTWO]

121
Q

Pralidoxime:

Mechanism of Action

A

Peripheral AchE reactivator

122
Q

Pralidoxime:

Rx

A

Respiratory muscle weakness in organophosphate poisoning

[Tx for organophosphate poisoning/serine gas - reactivation of alkylphosphorylated AChE with Pralidoxime Chloride (2-PAM) ]

123
Q

Baclofen:

Mechanism of Action

A

GABA agonist

Inhibits neurotransmitter
release from skeletal muscle sensory afferent- (by inhibiting calcium influx and therefore reducing the release of excitatory transmitters)

124
Q

General for benzodiazepines
(Diazepam, cloneazepam…)

Mechanism of Action (1):

A

Facilitate GABA mediated pre-synaptic inhibition

125
Q

Rocuronium

MOA

A

[Non-Depolarizing Muscular Nicotinic BLOCKER]

126
Q

Rocuronium

Location of Elimination

A

Liver

127
Q

Vecuronium

MOA

A

[Non-Depolarizing Muscular Nicotinic BLOCKER]

128
Q

Bromocriptine

Mechanism of Action

A

D2 Agonist

129
Q

Selegiline

Mechanism of Action

A

MAO-b inhibitor

130
Q

Methylphenidate

Mechanism of Action

A

Dopamine reuptake inhibitor

131
Q

Mu (OP3)

Locations (6)

A

Brain:

  • cortex (lamina III-IV)
  • Thalamus
  • Striosomes
  • periaqueductal gray

Spinal Cord
- substantial gelatinosa

-Intestinal tract

132
Q

Mu - subtype 1

Function (2)

A
  • Supraspinal analgesia

- physical dependence

133
Q

Mu - subtype 2

Function (5)

A
  • Respiratory depression
  • miosis
  • euphoria
  • reduced GI mobility
  • physical dependence

” Mu2 was a kinda GRUMP “

134
Q

Mu - subtype 3

Function

A

unknown

135
Q

Naloxone

Receptors - antagonist/agonist (3)

A

mu-R: antagonist
Delta-R: antagonist
Kappa-R:antagonist

136
Q

MethaDone

Receptor - Antagonist/agonist (2)

A

mu - agonist
delta- agonist

  • (M)etha(D)one *
137
Q

MethaDone

Side effects

Firm occupancy of opioid receptors by MethaDone ____ (INC/DEC) desire for other opioid intake, because it is producing a _______ but ___ (INC/DEC) effect which attenuates withdrawal manifestations.

A

dependence

Firm occupancy of opioid receptors by MethaDone DEC desire for other opioid intake, because it is producing a LONGER but DEC EFFECT which attenuates withdrawal manifestations.

138
Q

MethaDone

Function

A

Treats Opioid Dependence

139
Q

Tizanidine

Physiological effect:

A

[CENTRAL a2 agonist] that acts on pre and post-synpatic nerves of Spinal Cord —> Inhibition

140
Q

Dantrolene

Physiological Actions

A

Blocks calcium release from SR of skeletal muscle

141
Q

Dantrolene

Indications (5)

A
  • SPASMS 2º to Stroke
  • SPASMS 2º to Spinal Cord Injury
  • Malignant Hyperthermia
  • Cerebral Palsy
  • Multiple Sclerosis
142
Q

Metaclopramide

MOA:

Side effects (2) :

A

MOA: [D2 Blocker] with some [5HT4 agonist]

SE: [Focal dystonia], Akathisia, [Tardive Dystonia after 3 months]

M.SE.FAT

143
Q

Metaclopramide:
Contraindications:

A

Contraindications: long-term rx (3 months

can cause tardive dyskinesia)

144
Q 
Trazadone
MOA (2)
A

[5-HT2A/2C BLOCKER] + SSRI

145
Q 
Trazadone
Indications (2)
A

Anxiety/depression

146
Q

Trazadone

SE

A

Warning of suicidality in young adults at initiation of treatment

147
Q

Trazadone

Contraindicaitons

A

MAO inhibitors

148
Q

Nociceptin receptor
(OP4)
Subtypes

A

ORL1

149
Q

Nociceptin receptor location (7)

A

Brain:

  • Cortex
  • Amygdala
  • hippocampus
  • septal nuclei
  • habenula
  • hypothalamus

Spinal cord

150
Q

Nociceptin function (3)

A
  • anxiety
  • depression
  • appetite
151
Q

Pentazocin

Receptor subtypes and action

A

m-receptor: antagonist
d-receptor: agonist
K-receptor: agonist

152
Q

Pentazocin

Indications

A

Dental extraction

153
Q

Buspirone

Mechanism of Action

A

5-HT1A partial agonist

154
Q

Sumatriptan

Mechanism of Action

A

5-HT1D agonist

155
Q

Sumatriptan

Rx

A

Migraine

156
Q

Sumatriptan

Side Effects

A

Coronary vasoconstriction

157
Q

Risperidone

Mechanism of Action

A

5-HT2A/2C BLOCKER

158
Q

Risperidone

Rx (2)

A
  • Depression

- Psychosis

159
Q

Risperidone

Side Effects (2)

A
  1. Akathisia (also occurs as Metaclopramide SE)

2. Weight Gain

160
Q

Delta (OP1)

Function (3)

A
  • Analgesia
  • Antidepressant effects
  • Physical dependence
161
Q

Kappa (OP2)

Function (5)

A
  • Miosis (and MEPERIDINE uses this receptor)
  • Inhibits ADH release
  • Sedation
  • Spinal Analgesia

-Dysphoria

” [MISS D] loved her some Kappas”

162
Q

Morphine

receptor type

A

Mu

163
Q

Morphine

Indication

A

severe pain

164
Q

Meperidine

Receptor type

A

Kappa receptor

165
Q

Meperidine

Indication

A

Severe pain

166
Q

Meperidine

Side Effects (4)

A
  • Seizure
  • Dysphoria
  • Tremor
  • Respiratory Depression
167
Q

Meperidine

Other Notes (2)

A

1) Also binds: K+ channels, Muscarinic receptors, Dopamine transporter
2) Do not use Naloxone as andtidote

168
Q

Hydrocodone

Receptor types (2)

A

Mu

Delta

169
Q

Hydrocodone

Indication (2)

A
  1. Moderate pain

2. Coughing (anti-tussive)

170
Q

Hydrocodone

Side Effects (3)

A
  • Constipation
  • Respiratory Depression
  • Nausea
171
Q

Codeine

Receptor type

A

Mu receptor

172
Q

Codeine (4)

Indications

A
  • Irritable Bowel Syndrome
  • Narcolepsy
  • Diarrhea
  • Cough

“Why would I need Codeine [IN DC] ? “

173
Q

Codeine

Side Effects (5)

A
  • Euphoria
  • Itching
  • Urinary Retention
  • Depression
  • Constipation
174
Q

Codeine

Other Note

A

Active metabolite is morphine

175
Q

Procaine (HCl)

Potency

A

1

176
Q

Procaine (HCl)

Anesthetic Use

A

Infiltrative Nerve Block: Subarachnoid

177
Q

Cocaine (HCl)

Potency

A

2

178
Q

Cocaine (HCl)

Onset of Analgesia

A

Rapid (1 min)

179
Q

Cocaine (HCl)

Duration of Action

A

Medium (1 hr)

180
Q

Cocaine (HCl)

Anesthetic Use

A

Topical

Easily absorbed through mucous membrane

181
Q

Tetracaine (HCl)

Potency

A

16

182
Q

Tetracaine (HCl)

Onset of Analgesia

A

Slow for Spinal (15 - 20 min)

183
Q

Tetracaine (HCl)

Duration of Action

A

Long (2-5 hr)

184
Q

Tetracaine (HCl)

Anesthetic Use

A

Subarachnoid

185
Q

Benzocaine

Potency

A

(Topical use only)
poorly water soluble
dusting powder/ointment for wounds without concerns for systemic toxicity

186
Q

Lidocaine (HCl)
(Xylocaine)

Potency

A

4

187
Q

Lidocaine (HCl)
(Xylocaine)

Onset of Analgesic

A

Rapid

188
Q

Lidocaine (HCl)
(Xylocaine)

Duration of Action

A

Medium (1.25 hr)

189
Q

Lidocaine (HCl)
(Xylocaine)

Anesthetic Use (4 Locations of Administration)

A 
Infiltrative Nerve Block:
Intravenous-
Epidural
Subarachnoid
Regional
190
Q

Ketamine

MOA

A

[NMDA RECEPTOR BLOCKER]

191
Q

Ketamine

Description of anesthesia

A

Dissociative anesthesia

192
Q

Ketamine

Physiological effects (6)

A

INCREASES in:

  • CMR O2 (Cerebral Metabolic Rate)
  • HR
  • Intra Cranial Pressure (ICP)
  • Cerebral Blood Flow
  • BP
  • BronchoDilation

” Ketamine INC that [C.H.I.C. BP] “

193
Q

A: List the 4 Systemic Effects of Propofol?

B: How is Propofol administered?

A

A:
1) DEC Intracranial Pressure

2) DEC CMRO2 of the brain
3) Vaso/venoDILATES –> Reduces both preload AND Afterload
4) Respiratory Depression

B: Propofol Route of Administration: INTRAVENOUS

194
Q

A: Ketamine is very strongly used as a ___Dilator

B: What does it do to these factors?

  • CMRO2
  • Cerebral blood flow
  • Intracranial Pressure
  • Blood Pressure
  • HR

C: MOA for Ketamine?

D: What are its 2 indications?

A

A: Ketamine is very strongly used as a BRONCHODILATOR

B: What does it do to these factors?

  • CMRO2 = INC
  • Cerebral blood flow = INC
  • Intracranial Pressure = INC
  • Blood Pressure = INC
  • HR = INC

C: MOA for Ketamine?
[NMDA Receptor BLOCKER]

D: ºShort Procedures ºAnesthetic Inducer

195
Q

3 Side Effects of Ketamine

A

1) Bad Dreams
2) Salivation
3) Twitching

196
Q

A: What’s the most dangerous side effect of [Intravenous Thiopental]?

B: Does Thiopental INC or DEC CMRO2?

A

A: Thiopental is a vasoCONSTRICTOR —> LIMB ISCHEMIA!

B: Thiopental still DEC CMRO2 in the brain

197
Q

A: Which IV Anesthetic has the least cardiovascular side effects?

B: What is the primary SIDE EFFECT for this [IV Anesthetic]?

C: This [IV Anesthetic] is a _______ [vasoDilator/vasoCONSTRICTOR] and will ______[INC/DEC] CMRO2

A

A: ETOMIDATE

B: Adrenal Suppression: Pt will not produce [Adrenal NorEpi] and thus be UNABLE TO MAINTAIN THEIR OWN BP

C: This [IV Anesthetic] is a vasoconstrictor and will DEC CMRO2 {like Thiopental}

198
Q

D-Tubocurarine

Duration of Action

A

> 60 min

199
Q

D-Tubocurarine

Mechanism of Action

A

[Non-Depolarizing Muscular Nicotinic Blocker]

200
Q

D-Tubocurarine

Rx

A

Prototype

only used in lethal injection

201
Q

List the 7 Sterile Body Sites and their associated fluids

A

“Pts Should Produce Sterile Blood Upon Probing”

ºPericardium = Pericardial Fluid

ºSubArachnoid Space = CSF

ºPleural Space = Pleural Fluid

ºSynovium = Synovial Fluid

ºBloodstream = Blood

ºUrinary Tract = DIRECT URINE FROM BLADDER

202
Q

Name 4 Dz that BacteriCidals are specifically needed to treat

A

“You can only kill FOME with BacteriCidals”

  1. [Febrile neutropenia]
  2. Osteomyelitis
  3. Meningitis
  4. Endocarditis
203
Q

A: Name the Only 7 [Abx Classes] that are bacteriostatic

B: These all are _______ Inhibitors

A

“Macrolides: Some Of Them Can Limit Growth “

  1. Macrolides
  2. Streptogramins
  3. Oxazolidinones
  4. Tetracyclines
  5. Chloramphenicol
  6. Lincosamides
  7. ## GlycylcyclinesB: These ALL are PROTEIN SYNTHESIS Inhibitors
204
Q

5 Steps for Antimicrobial Selection

A

CEiSM

1st: Confirm presence of actual infection
2nd: Empiric Therapy
3rd: Identify Pathogen
4th: STREAMLINE Abx therapy

5th: Monitor Therapeutic Response
- ——————————————————————————

205
Q

Amphetamine

Indication (3)

A
  1. ADHD
  2. Narcolepsy
  3. Obesity

[⇪ NE ] InDirect Sympathomimetic

a m.d. step 3 - ZIP DECK (6 decks)

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