XL1 [Rx +] Flashcards
1
Q
Albuterol
MOA (2)
A
[β2🟢] > [β1🟢]
agonist
for acute asthma
2
Q
Albuterol
Indication
A
acute asthma
3
Q
Salmeterol
Indication (2)
A
- chronic asthma
- chronic COPD
4
Q
Salmeterol
MOA (2)
A
[β2🟢] > [β1🟢]
agonist
= chronic asthma / chronic COPD
5
Q
doButamine
Indication (2)
A
- HF
- cardiac stress testing
6
Q
doButamine
MOA (3)
A
- [β1🟢] > [β2🟢]
- [general α🟢]
7
Q
Dopamine
MOA (4)
A
{([D1🟢 = D2🟢] >[general β🟢] > [general α🟢*]}
[inotropic & chronotropic (α)] predominates at high doses
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 }
9
Q
Epinephrine
MOA (2)
A
- [(general β🟢{low concentration}]
> - [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🟢
10
Q
Epinephrine
Indication (6)
A
- ANAPHYLAXIS
- asthma
- angle-open glaucoma
- arrest (cardiac arrest)
- [a heart block]
- [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”
11
Q
Isoproterenol
MOA (2)
A
[(β1🟢 = β2🟢)]
12
Q
NorEpinephrine
MOA (3)
A
[(α1🟢 > α2🟢 > β1🟢)]
13
Q
NorEpinephrine
Indication
A
hypOtension(but note: NE⬇︎renal perfusion)
[(α1🟢 > α2🟢 > β1🟢)]
📝Epi is stronger at β2🟢 than NorEpi is at β2🟢
14
Q
Isoproterenol
Indication
A
electrophysiologic eval of tachyarrhythmias🛑note: can worsen ischemia!
[(β1🟢 = β2🟢) ]
15
Q
Phenylephrine
MOA (2)
A
[α1🟢] > [α2🟢]
([α1🟢] vasoconstriction can → [baroreceptor-reflex mediated bradycardia])
16
Q
Phenylephrine
Indication (3)
A
- hypOtension
- myDriasis for ocular procedures
- rhinitis(PNE is also a decongestant)
[(α1🟢 > α2🟢)]
17
Q
Amphetamine
MOA (2)
A
Indirect Sympathomimetic via:
1. [NE🔻reuptake inhibitor]
2. releases stored NE🚰
[InDirect Sympathomimetic] –(🔻 [⇪NE catecholamine]
18
Q
Ephedrine
Indication (3)
A
- Nasal Decongestant
- urinary incontinence
- hypOtension
InDirect Sympathomimetic via [⇪ NE/E catecholamines]
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
21
Q
Ephedrine
MOA
A
[(releases stored NE🚰) InDirect Sympathomimetic]
→ ⇪ adrenergic NE → ⇪ Sympathetic NS
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
23
Q
Clonidine
Indication (3)
A
- HTN Urgency
- ADHD
- Tourette syndrome
[α2🟢 sympathoLytic]
(does not ⬇︎Renal blood flow)
24
Q
Clonidine
Toxicity (5)
A
- CNS depression
- [pupillary depression (miosis)]
- [cardiac depression (bradycardia)]
- [respiratory depression]
- vascular depression (hypOtension)
[α2🟢 sympathoLytic] ⼀ “Clonidine makes me depressed”
(does not ⬇︎Renal blood flow)
25
Q
α-methyldopa
MOA
_________________
Indication
A
[α2🟢 sympathoLytic]
_________________
HTN in pregnancy
26
# **α-methyldopa**
Toxicity (2)
can →
1. [⊕DAT hemolysis]
2. [SLE-like syndrome]
| [α2🟢 *sympathoLytic*]
## Footnote
DAT = [Direct_Coombs AntiHumanglobulin Test]
27
# **pheNOxybenzamine**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication
*iiRREVERSIBLE*general α🟥
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Px for HTN catecholamine crisis] in [Pheochromocytoma resection]
| given preop
## Footnote
[*(phe**NO**xybenzamine) = **NO** reversing* ]
28
# **phentolamine**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication
*REVERSIBLE*general α🟥
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Px for HTN catecholamine crisis] in [MAOI pts who eat tyramine containing food]
| *"OF COURSE THIS TOLL BOOTH TICKET IS REVERSIBLE!"*
29
# **pheNOxybenzamine and phentolamine**
side effects (2)
1. orthostatic hypOtension
2. reflex tachycardia
30
# [DEPT"***-osin*** "]
MOA
α1🟥
## Footnote
🔎{[**DEPT**"***-osin*** "] = **D**oxazOSIN \ t**E**razOSIN \ **P**razOSIN \ **T**amsulOSIN}
31
# [DEPT"***-osin*** "]
Indication(s) (3)
[DEPT"***-osin*** "]
1. [BPH Urinary sx (**DEPT**)]
2. [PTSD (**P**)]
3. [HTN (**DEP**)]
| α1🟥
## Footnote
🔎{[**DEPT**"***-osin*** "] = **D**oxazOSIN \ t**E**razOSIN \ **P**razOSIN \ **T**amsulOSIN}
32
# **Mirtazapine**
MOA
α2🟥
33
# **Mirtazapine**
Indication
Depression
| α2🟥
34
# **Mirtazapine**
Side Effects (3)
1. sedation
2. HLD
3. hunger
| α2🟥
35
# [DEPT"***-osin*** "]
Side Effects (3)
| **D**oxazOSIN \ t**E**razOSIN \ **P**razOSIN \ **T**amsulOSIN
[DEPT"***-osin*** "]
1. [1st dose orthostatic hypOtension (**DEPT**)]
2.[dizziness (**DEPT**)]
3.[HA (**DEPT**)]
| α1🟥
## Footnote
{[**DEPT**"***-osin*** "] = **D**oxazOSIN \ t**E**razOSIN \ **P**razOSIN \ **T**amsulOSIN}
36
# Receptors are divided into [5 major groups (**CADHV**)]
Describe the 2 types of **C**holinergic receptors
▶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])*}
37
# function
α1(3)
| *sympathetic* Receptor
[**V**ascular smooth muscle ctn *(vasoconstricts)*]
[**I**nternal Urethral Sphincter ctn & Intestinal ctn]
[**D**ilator of pupil *(myDriasis)*]
| "*Give me the alpha 1 **VID***..."
## Footnote
📖**D**ilates pupil via [contracts pupillary Dilator m (myDriasis)]
*🔎ctn = contraction*
38
# Receptors are divided into [5 major groups (**CADHV**)]
Describe the 2 types of **A**drenergic receptors
▶αlpha*adrenergic* : Sympathetic *NE* Receptors (α1, α2 requireq|i|s2nd messenger)
▶βeta*adrenergic*: Sympathetic *NE* Receptors (β1, β2 requireq|i|s2nd messenger)
39
Name the 5 major Receptor groups
(**CADHV**)*Receptors*
**C**holinergic
[**A**drenergic SYMPATHETIC]
**D**opaminergic
**H**istaminergic
**V**asopressin
40
# function
α2(5)
| Receptor
⇪ **C**oagulation *(via ⇪ Platelet aggregation)*]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[⬇︎**l**ipolysis *(⬇︎fat breakdown)*]
⬇︎**a**queous humor production
[⬇︎**s**ympathetic *(via neg feedback)*]
[⬇︎**s**ugar cell entry *(via ⬇︎ INSULIN release)*]
| "*...Give her the {αlpha 2 **Class**}*"!
41
# function
β1(4)
| *sympathetic* Receptor
⇪ **C**ontractility Heart
⇪ **R**ate Heart
[⇪**A**dipocyte lipolysis]
⇪ **K**idney RENIN release
| "* βeta1 ⇪ **CRAK***"
42
# function
**β2** (7)
| *sympathetic* Receptor
⇪ {[**V**asoDilates autonomic smooth m] [Tremors somatic skeletal m]}
⇪ **A**queous humor production
[⇪**B**ronchoDilation]
[⇪**U**terine Relaxation (tocolysis)]
[⇪ **L**ipolysis & Liver Glycogenolysis]
⇪ **I**nsulin release
⇪ **C**iliary m Relaxation
| "*...βeta2 ⇪ **VABULIC**!!*"
## Footnote
*👓gProtein: (s)*
43
# function
**M1** (2)
| *ParaSympathetic* Receptor
1. CNS
2. ENS
| "
## Footnote
*👓gProtein: (q)*
*🔎ENS = Enteric Nervous System*
44
# function
**M2** (2)
| *ParaSympathetic* Receptor
1. ⬇︎HR
2. ⬇︎Heart Contractility
## Footnote
*👓gProtein: (i)*
45
# function
**M3** (6)
| *ParaSympathetic* Receptor
1. [**G**ut peristalsis ⇪]
2. [**A**ccommodation (contracts ciliary m)]
3. [**M**iosis (contracts pupillary sphincter m)]
4. **B**ladder contraction
5. [**L**ung contraction (bronchoconstriction)]
6. [**E**xocrine secretion (salivary/lacrimal/gastric acid)]
| "*M3s took a huge **GAMBLE***"
## Footnote
*👓gProtein: (q)*
46
# function
D1
| Receptor
renal vasoDilation
## Footnote
*👓gProtein: (s)*
47
# function
D2
| Receptor
inhibits nerve terminal adenyl cyclase = modulates (especially brain) NTS release
## Footnote
*👓gProtein: (i)*
48
# function
H2
| Receptor
⇪ Gastric acid secretion
## Footnote
*👓gProtein: (s)*
49
# function
**H1** (6)
| Receptor
1. ⇪ **P**roduction of nasal mucus
2. ⇪ **P**roduction bronchial mucus
3. [⇪ **P**ermeability vascularly → edema]
4. ⇪ **P**ruritus
5. ⇪ **P**etit breathing (bronchoconstriction)]
6. ⇪ **P**ain
## Footnote
*👓gProtein: (q)*
50
# function
V1
| *vasopressin* Receptor
vaso**constriction**
## Footnote
*👓gProtein: (q)*
51
# function
V2
| *vasopressin* Receptor
⇪ H2O permeability&reabsorption in renal CD
## Footnote
*👓gProtein: (s)*
52
# Name the 3 types of opioid receptors
MOA of opioid receptors (4)
[*morphine|enkephalin |dynorphin* opioid Receptors
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
{[opens K+ channels] and [closes Ca+ channels]}
→ [⬇︎synaptic transmission]
→ {⬇︎release of [ACh/norEpi/5HT/glutamate/substance-P]}
## Footnote
(*TOXICITY → somnolence, miosis, bradypnea, constipation, Addiction* )
53
# **Butorphanol**
MOA (2)
[*dynorphin*opioid🟢] + [*morphine* *(partial*) opioid R agonist]
| *has less respiratory depression than FULL opioid R agonist*
## Footnote
note: OD not easily reversed with nalaxone
54
# **Tramadol**
MOA (3)
1. [**very weak** opioid🟢]
2. [5HT🔺reuptake inhibitor]
3. [NorEpi🔺 reuptake inhibitor]
## Footnote
*(TOXICITY → seizure, serotonin syndrome + same as other opioid TOX)*
55
# **Ethosuximide**
MOA
[(Thalamic)T-type Ca+ channel Blocker]
56
# **Benzodiazepine**
MOA
⇪ GABAA effect
57
# **Phenytoin**
MOA
Na+ channel inactivation(zero order kinetics)
## Footnote
✏️ IV requires *Fos*phenytoin
58
MOA for the [1st line tx of trigeminal neuralgia]
**Carbamazepine**
[⇪ Na+ channel inactivation]
## Footnote
✏️also used for: *simple partial/complex partial/GTC*
59
MOA for the anti-epileptic also used to treat bipolar depression (2)
**Valproic acid**
1. [ ⇪ Na+ channel inactivation]
2. [inhibits GABA transaminase → ⇪ GABA concentration]
60
MOA for anti-epileptic also used to treat peripheral neuropathy (2)
**GABApentin**
1. [inhibits high voltage gated Ca+ channels]
2. GABA analog
## Footnote
*(indications: peripheral neruopathy, postherpetic neuralgia, simple szure, complex szure)*
61
MOA for the anti-epileptic also used to prevent Migraine HA (2)
**Topiramate**
1. [Na+ channel blocker] antiepileptic
2. [ ⇪ GABA effect]
62
# **Lamotrigine**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
notable precaution?
[Na+ channel blocker] antiepileptic
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[*(must be titrated slowly)* ⼀otherwise possible → Stevens-Johnson syndrome]
63
# **Levetiracetam**
MOA
unknown
| *(antiepileptic that possibly modulates GABA and glutamate)*
64
# **TiaGabine**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication (2)
[GABA🔻reuptake inhibitor] antiepileptic
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. simple partial seizure
2. complex partial seizure
65
# **VigaBatrin**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication (2)
[iiRREVERSIBLYinhibits GABA transaminase ➜ ⇪ GABA ] antiepileptic
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. simple partial seizure
2. complex partial seizure
66
Describe cp for Steven Johnson Syndrome (3)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Which drugs are known to cause Steven Johnson Syndrome? (4)
{[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** **all**ergy to **sulfa** and **PCN**
67
What is the difference in MOA between Barbiturates and Benzodiazepines
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!
## Footnote
(*ATOM* = Alprazolam/Triazolam/Oxazepam/Midazolam)
68
Nonbenzo hypnotics act as ⬜ and the 3 primary examples are ⬜
[(BZ1 GABA subtype) R agonist]; Zolpidem/Zaleplon/esZopiclone
## Footnote
✏️rapid hepatic metabolism = unlike other sedative-hypnotics, day after psychomotor depression with few amnestic effects
69
In Anesthesia, drugs with high blood/lipid solubility have ⬜ induction and ⬜ potency
slow; high
70
Define M.A.C. in terms of anesthesia
Minimal Alveolar Concentration (of anesthesia) required to prevent 50% of subjects from moving after noxious stimuli
..so [potency = 1/MAC]
71
Name and briefly describe each of the 5 [IV anesthetics]
**[B**arbiturates (Thiopental)] = high lipid solubility = high potency = rapid brain entry = use in short surgical procedures
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**[B**enzodiazepine (Midazolam)]] = ⭐popular for endoscopy ⼀but may → postop bradypnea (tx = flumazenil)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**[K**etamine/Arylcyclohexylamines] = [NMDA R Blocker PCP analog] → dissociative anesthesia
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**Opioids**(Morphine|fentanyl)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
**PropoFOL** = potentiates GABAA = rapid anesthesia induction, ICU sedation
## Footnote
*"**B. B. K**ing on **OPIOIDS PROPO**ses-**FOL**gers"*
72
Name and describe the 6 local anesthetics
| *"**BLM** locally anesthetizes **CPT**"*
## Footnote
*"**BLM** = Amides (will have 2 i)*
**B**upivAcaine
**L**Idocaine
**M**epivAcaine
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
"***CPT**" = Esters*"
**C**ocaine
**P**rocaine
**T**etracaine
73
# **Succinylcholine**
MOA
[*strong*ACh R agonist] → blocks (by binding tightly to ) [**NMJ** postsynpatic ACh R] → sustained depolarization → prevents [**NMJ** action potential] → prevents muscle contraction = paralysis
## Footnote
Toxicity = HYPER**KFC**
74
how does reversal of **Succinylcholine** work? (2)
[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
## Footnote
📖
[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
75
# **Succinylcholine**
Toxicity (3)
1. [HYPER **K+**]
2. [HYPER **F**ever *(MMalignant Hyperthermia)*]
3. [HYPER **Ca+**]
| *"HYPER**KFC**"*
76
# There are 2 types of paralytic agents: depolarizing vs nondepolarizing
a: describe MOA for nondepolarizing paralytic drugs
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
b. describe reversal process (2)
{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
77
# **Local Anesthetics**
MOA (4)
| *"**BLM** locally anesthetizes **CPT**"*
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 **P**ain → t**E**mp → **T**ouch → last pre**S**sure) and [myelinated small] > unmyelinated LARGEa]}7
4. give with epinephreine vasoconstrictor = [enhances local action (by preventing systemic circulation)] +
| *"**BLM** locally anesthetizes **CPT**"*
78
# **Local Anesthetics**
Toxicity (6)
| *"**BLM** locally anesthetizes **CPT**"*
1. [CNS ❌]
2. [CV❌*(bupivacaine)*]
3. [arrhythmias*(Cocaine)*
4. [methemoglobinemia*(benzocaine)*]
5. HTN
6. hypOtension
## Footnote
✏️*(if allergic to [*ester*local anesthetic] give [*amide*local anesthetic])*
79
# **Dantrolene**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication (2)
prevents release of Ca+ from [sk muscle sarcoplasmic reticulum]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
1. [MMalignant Hyperthemia]
2. [Neuroleptic Malignant Syndrome]
80
# **Baclofen**
MOA
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication
***Inhibits* [spinal cord GABAB** R] → sk muscle relaxer
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Muscle spasm*(ie acute low back pain)*]
| *muscle relaxer*
81
# **Cyclobenzaprine**
MOA (2)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Indication
[(TCA-*cousin*✏️) with anticholinergic effect] + [centrally acting sk muscle relaxer]
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
[Muscle spasm*(ie acute low back pain)*]
| *muscle relaxer*
## Footnote
*📝Cyclobenzaprine is structurally similar to (and has similar anticholinergic effect) as TCA*
82
# (-***triptans***)
MOA (4)
| .
⭐[5HT(1B/1D)🟢] →
🔧Inhibits trigeminal n activation
🔧inhibits vasoactive peptide release
🔧induces vasoconstriction
## Footnote
*TOX: [Coronary Vasospasm (CTD in CAD/Prinzmetal angina)], paresthesia*
83
Why is Sumatriptan contraindicated in patients with ⬜*(2)* ?
CAD | Prinzmetal angina
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
(*⼀triptans*) cause Coronary Vasospasm
84
# *sulfa drug allergy ranges from mild to fatal*
Name the 8 *Sulfa* drug groups
1. Sulfonamide abx
2. Sulfasalazine
3. Sulfonylurea
4. Probenacid
5. Furosemide
6. Acetazolamide
7. Celecoxib
8. Thiazides
| "**S**ulfa **S**ounding **S**erious? **P**opular **FACT**"
85
Name 3 drugs that *in addition to their primary MOA* secondarily also are [Muscarinic R Blockers]
1. TCA
2. [H1🟥]
3. antipsychotics
86
Which drugs produce [Disulfiram-like reactions]? (5)
1. metronidazole
2. cephalosporins(select)
3. griseofulvin
4. procarbazine
5. Sulfonylurea1st GEN
87
How should Warfarin be adjusted if a patient starts taking amiodarone?
⬇︎Warfarin by 25% (since amiodarone inhibits CYP2C9)
88
*Metformin can dangerously cause ⬜*
Name Metformin contraindications? -5
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
how is iodine contrast related to Metformin?
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
# **Pindolol**
a. MOA (2)
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
b. explain its Indication
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
What 6 drugs make up the Amphetamine family?
1. Amphetamine
2. Methamphetamine
3. Ephedrine
4. Pseudoephedrine
5. Methylphenidate
6. Tyramine 👀
## Footnote
*📝Tyramine displaces NE. It is catabolized by MAO. [MAO inhibitors] can → ⇪ Tyramine which may → HTN crisis*
91
# [**general β🟥**]
Toxicity (6)
1. Bronchospasm
2. Bradycardia
3. CNS depression
4. CNS insomnia
5. MASK sx of hypOglycemia
6. TAG ⇪
92
List the 5 drugs eliminated by COMT
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
Which 2 are special? why?
1. doButamine
2. isoproterenol
3. **NOREPINEPHRINE⭐**
4. epi
5. **DOPAMINE⭐**
| [⭐= eliminated by COMT *and* MAO]
## Footnote
*"COMT d.i.N.e.D on 5 drugs"*
93
***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.
## Footnote
***B: What is the rate limiting step for this reaction?***
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
## Footnote
B: What is the rate limiting step for this reaction?
[Arachidonic Acid] conversation into [PGH2] by Cyclooxygenase
94
describe how COX1 and COX2 are different in terms of tissue expression
*📝
-COX1 = HIGH constitutive expression and located ubiquitously⼀in most tissue
-COX2 = low constitutive expression = generally has to be induced (by proinflammatory stimuli)
95
# [**ASA Aspirin**]
MOA (3)
1. IRREVERSIBLE
2. NON-Competitive
3. COX inhibitor
## Footnote
*📝
-COX1 = HIGH constitutive expression and located ubiquitously⼀in most tissue
-COX2 = low constitutive expression = generally has to be induced (by proinflammatory stimuli)*
96
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: 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
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
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
Name the 3 Groups of NSAIDs
1. Aspirin/Salicylates
2. Traditional Non-Selective NSAIDs (ibuprofen)
3. Coxibs (COX inhibitors)
99
COX1
A: Physiological Role (4)
B: What compounds do COX1 produce that facilitate these roles?
HOUSEKEEPING:
1. Platelet Regulation (monitors blood clotting)
2. Kidney Function
3. Cytoprotection of Stomach by regulating Acid/Mucus production & [gastric blood flow]
4. Maintains Patent Ductus Arteriosus for Fetus and stimulates [Uterine contractions during labor (involves PGF2a) ]
(COX1 is NOT inhibited by Celecoxib)
B: [PGE2/PGi2]
100
COX-TWO
Physiological Role
PRO-INFLAMMATORY RESPONSE (Mitogenesis and Signaling)
101
A: Platelets express ONLY _____[COX⬜] but primarily produce ________.
B: What are the roles of the compound produced? (2)
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
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: [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
A: Why is Aspirin READILY absorbed in the stomach and [upper small intestine]?
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
Aspirin Recommended Dosing
1. Anti-Platelet activity = ⬜ dose
2. Anti-Pyretic = ⬜ dose
3. Analgesic = ⬜ dose
3. Anti-Inflammation= ⬜ dose
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
A: Why is concurrently taking [Salicylates/Aspirin] and Warfarin OR Sulfonylureas contraindicated?
B: Sulfonylurea Toxicity ---> ⬜
[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
How do you treat Salicylate OVERDOSE and why?
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
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)
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
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: 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
INDOMETHACIN
A: Primary Indications (3)
B: Cons
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
KETOLORAC
A: Primary Indication
B: What can this NSAID replace?
A: Indication:
[Intravenous NSAID] that treats post-surgical pain
B: Can be used as an Opioid Replacement Drug
111
DICLOFENAC
B: What's the cons of this drug and its class?
A: DICLOFENAC= Relatively Selective COXTWO Inhibitor
B: [COXTWO Inhibitors] INC chances of Stroke/Heart Dz!!
112
What are 2 ASPIRIN-Specific Adverse Effects?
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
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: GI Toxicity: Gastric/Duodenal Ulcers & Bleeding
--------------------------------------------------------------------------------
B:
1) DIRECTLY damage gastric epithelium from being ion trapped in the compartment sometimes
2) Inhibit constitutively expressed COX1 ---> DEC [PGE2/PGi2] ---> DEC gastric cytoprotection
--------------------------------------------------------------------------------
C: Treatment:
-Misoprostol = PGE1 in a pill [CAN NOT GIVE TO PREGNANT WOMAN SINCE IT INDUCES ABORTION]
-Omeprazole
114
A: [Acute interstitial nephritis and Nephrotic Syndrome]
B: Who does this occur most in/
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
[CHRONIC interstitial nephritis and Analgesic Nephropathy]
A: Caused by CHRONIC Daily OVER USE of NSAIDs which leads to Chronic Renal Ischemia---> ESRD
ESRD= End Stage Renal Dz
116
A: What is [NSAID Hypersensitivity]?
B: What are the sx and what is the onset?
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
NSAIDs taken in pregnant women after ____ weeks gestation can cause [Premature Ductus Arteriosus ____] in the fetus
NSAIDs taken in pregnant women after 30 weeks gestation can cause [Premature Ductus Arteriosus CLOSURE] in the fetus
118
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: 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
Which 3 Drugs have Dangerous impaired Renal Clearance due to NSAID usage?
1. Lithium
2. Methotrexate
3. [Gentamicin-Aminoglycoside]
120
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: 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
Pralidoxime:
Mechanism of Action
Peripheral AchE reactivator
122
Pralidoxime:
Rx
Respiratory muscle weakness in organophosphate poisoning
[Tx for organophosphate poisoning/serine gas - reactivation of alkylphosphorylated AChE with Pralidoxime Chloride (2-PAM) ]
123
Baclofen:
Mechanism of Action
GABA agonist
Inhibits neurotransmitter
release from skeletal muscle sensory afferent- (by inhibiting calcium influx and therefore reducing the release of excitatory transmitters)
124
General for benzodiazepines
(Diazepam, cloneazepam...)
Mechanism of Action (1):
Facilitate GABA mediated pre-synaptic inhibition
125
Rocuronium
MOA
[Non-Depolarizing Muscular Nicotinic BLOCKER]
126
Rocuronium
Location of Elimination
Liver
127
Vecuronium
MOA
[Non-Depolarizing Muscular Nicotinic BLOCKER]
128
Bromocriptine
Mechanism of Action
D2 Agonist
129
Selegiline
Mechanism of Action
MAO-b inhibitor
130
Methylphenidate
Mechanism of Action
Dopamine reuptake inhibitor
131
Mu (OP3)
Locations (6)
Brain:
- cortex (lamina III-IV)
- Thalamus
- Striosomes
- periaqueductal gray
Spinal Cord
- substantial gelatinosa
-Intestinal tract
132
Mu - subtype 1
Function (2)
- Supraspinal analgesia
| - physical dependence
133
Mu - subtype 2
Function (5)
- Respiratory depression
- miosis
- euphoria
- reduced GI mobility
- physical dependence
" Mu2 was a kinda GRUMP "
134
Mu - subtype 3
Function
unknown
135
Naloxone
Receptors - antagonist/agonist (3)
mu-R: antagonist
Delta-R: antagonist
Kappa-R:antagonist
136
MethaDone
Receptor - Antagonist/agonist (2)
mu - agonist
delta- agonist
* (M)etha(D)one *
137
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.
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
MethaDone
Function
Treats Opioid Dependence
139
Tizanidine
Physiological effect:
[CENTRAL a2 agonist] that acts on pre and post-synpatic nerves of Spinal Cord ---> Inhibition
140
Dantrolene
| Physiological Actions
Blocks calcium release from SR of skeletal muscle
141
Dantrolene
| Indications (5)
- SPASMS 2º to Stroke
- SPASMS 2º to Spinal Cord Injury
- Malignant Hyperthermia
- Cerebral Palsy
- Multiple Sclerosis
142
Metaclopramide
MOA:
Side effects (2) :
MOA: [D2 Blocker] with some [5HT4 agonist]
SE: [Focal dystonia], Akathisia, [Tardive Dystonia after 3 months]
M.SE.FAT
143
Metaclopramide:
Contraindications:
Contraindications: long-term rx (3 months
| can cause tardive dyskinesia)
144
```
Trazadone
MOA (2)
```
[5-HT2A/2C BLOCKER] + SSRI
145
```
Trazadone
Indications (2)
```
Anxiety/depression
146
Trazadone
SE
Warning of suicidality in young adults at initiation of treatment
147
Trazadone
Contraindicaitons
MAO inhibitors
148
Nociceptin receptor
(OP4)
Subtypes
ORL1
149
Nociceptin receptor location (7)
Brain:
- Cortex
- Amygdala
- hippocampus
- septal nuclei
- habenula
- hypothalamus
Spinal cord
150
Nociceptin function (3)
- anxiety
- depression
- appetite
151
Pentazocin
Receptor subtypes and action
m-receptor: antagonist
d-receptor: agonist
K-receptor: agonist
152
Pentazocin
| Indications
Dental extraction
153
Buspirone
Mechanism of Action
5-HT1A partial agonist
154
Sumatriptan
Mechanism of Action
5-HT1D agonist
155
Sumatriptan
Rx
Migraine
156
Sumatriptan
Side Effects
Coronary vasoconstriction
157
Risperidone
Mechanism of Action
5-HT2A/2C BLOCKER
158
Risperidone
Rx (2)
- Depression
| - Psychosis
159
Risperidone
Side Effects (2)
1. Akathisia (also occurs as Metaclopramide SE)
| 2. Weight Gain
160
Delta (OP1)
Function (3)
- Analgesia
- Antidepressant effects
- Physical dependence
161
Kappa (OP2)
Function (5)
- Miosis (and MEPERIDINE uses this receptor)
- Inhibits ADH release
- Sedation
- Spinal Analgesia
-Dysphoria
" [MISS D] loved her some Kappas"
162
Morphine
receptor type
Mu
163
Morphine
Indication
severe pain
164
Meperidine
Receptor type
Kappa receptor
165
Meperidine
Indication
Severe pain
166
Meperidine
Side Effects (4)
- Seizure
- Dysphoria
- Tremor
- Respiratory Depression
167
Meperidine
Other Notes (2)
1) Also binds: K+ channels, Muscarinic receptors, Dopamine transporter
2) Do not use Naloxone as andtidote
168
Hydrocodone
Receptor types (2)
Mu
| Delta
169
Hydrocodone
Indication (2)
1. Moderate pain
| 2. Coughing (anti-tussive)
170
Hydrocodone
Side Effects (3)
- Constipation
- Respiratory Depression
- Nausea
171
Codeine
Receptor type
Mu receptor
172
Codeine (4)
Indications
- Irritable Bowel Syndrome
- Narcolepsy
- Diarrhea
- Cough
"Why would I need Codeine [IN DC] ? "
173
Codeine
Side Effects (5)
- Euphoria
- Itching
- Urinary Retention
- Depression
- Constipation
174
Codeine
Other Note
Active metabolite is morphine
175
Procaine (HCl)
Potency
1
176
Procaine (HCl)
Anesthetic Use
Infiltrative Nerve Block: Subarachnoid
177
Cocaine (HCl)
Potency
2
178
Cocaine (HCl)
Onset of Analgesia
Rapid (1 min)
179
Cocaine (HCl)
Duration of Action
Medium (1 hr)
180
Cocaine (HCl)
Anesthetic Use
Topical
Easily absorbed through mucous membrane
181
Tetracaine (HCl)
Potency
16
182
Tetracaine (HCl)
Onset of Analgesia
Slow for Spinal (15 - 20 min)
183
Tetracaine (HCl)
Duration of Action
Long (2-5 hr)
184
Tetracaine (HCl)
Anesthetic Use
Subarachnoid
185
Benzocaine
Potency
(Topical use only)
poorly water soluble
dusting powder/ointment for wounds without concerns for systemic toxicity
186
Lidocaine (HCl)
(Xylocaine)
Potency
4
187
Lidocaine (HCl)
(Xylocaine)
Onset of Analgesic
Rapid
188
Lidocaine (HCl)
(Xylocaine)
Duration of Action
Medium (1.25 hr)
189
Lidocaine (HCl)
(Xylocaine)
Anesthetic Use (4 Locations of Administration)
```
Infiltrative Nerve Block:
Intravenous-
Epidural
Subarachnoid
Regional
```
190
Ketamine
MOA
[NMDA RECEPTOR BLOCKER]
191
Ketamine
Description of anesthesia
Dissociative anesthesia
192
Ketamine
Physiological effects (6)
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
A: List the 4 Systemic Effects of Propofol?
B: How is Propofol administered?
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
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: 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
3 Side Effects of Ketamine
1) Bad Dreams
2) Salivation
3) Twitching
196
A: What's the most dangerous side effect of [Intravenous Thiopental]?
B: Does Thiopental INC or DEC CMRO2?
A: Thiopental is a vasoCONSTRICTOR ---> LIMB ISCHEMIA!
B: Thiopental still DEC CMRO2 in the brain
197
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: 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
D-Tubocurarine
Duration of Action
>60 min
199
D-Tubocurarine
Mechanism of Action
[Non-Depolarizing Muscular Nicotinic Blocker]
200
D-Tubocurarine
Rx
Prototype
| only used in lethal injection
201
List the 7 Sterile Body Sites and their associated fluids
"**P**ts **S**hould **P**roduce **S**terile **B**lood **U**pon **P**robing"
ºPericardium = Pericardial Fluid
ºSubArachnoid Space = CSF
ºPleural Space = Pleural Fluid
ºSynovium = Synovial Fluid
ºBloodstream = Blood
ºUrinary Tract = DIRECT URINE FROM BLADDER
ºPeritoneum = Peritoneal Fluid
-----------------------------------------------------------------------------
202
Name 4 Dz that Bacteri**Cidals** are specifically needed to treat
"You can only kill **FOME** with Bacteri**Cidals**"
1. [Febrile neutropenia]
2. Osteomyelitis
3. Meningitis
4. Endocarditis
203
A: Name the Only 7 [Abx Classes] that are bacteriostatic
B: These all are _______ Inhibitors
"**M**acrolides: **S**ome **O**f **T**hem **C**an **L**imit **G**rowth "
1. Macrolides
2. Streptogramins
3. Oxazolidinones
4. Tetracyclines
5. Chloramphenicol
6. Lincosamides
7. Glycylcyclines
------------------------------------------------------------------------------
B: These ALL are PROTEIN SYNTHESIS Inhibitors
204
5 Steps for Antimicrobial Selection
**CEiSM**
1st: Confirm presence of actual infection
2nd: Empiric Therapy
3rd: Identify Pathogen
4th: STREAMLINE Abx therapy
5th: Monitor Therapeutic Response
- ------------------------------------------------------------------------------
205
# **Amphetamine**
Indication (3)
1. ADHD
2. Narcolepsy
3. Obesity
| [⇪ NE ] InDirect Sympathomimetic
