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mental dental > MD PHARMACOLOGY > Flashcards

MD PHARMACOLOGY Flashcards

1
Q

WHAT ORGAN METABOLIZES AMIDES?

EX OF AMIDES

A

LIVER

BLAMP

  • bupivicaine
  • lidocaine
  • ariticaine
  • mepivicaine
  • prilocaine
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2
Q

WHAT METABOLIZES ESTERS?

EX OF ESTERS?

A

Pseudocholinesterase in PLASMA

procaine (not prilocaine)

benzocaine

tetracaine

cocaine

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3
Q

which amide is the safest in children?

lidocaine

bupivicaine

mepivicaine

articaine

pilocaine

A

LIDOCAINE

also has shortest duration of action on the list = inc blood flow = less potent = less lipid soluble

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4
Q

which amide causes least vasodilation?

lidocaine

bupivicaine

mepivicaine

articaine

pilocaine

A

mepivicaine

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5
Q

which amide is NOT safe in children ?

lidocaine

bupivicaine

mepivicaine

articaine

pilocaine

A

BUPIVICAINE ( longest duration)

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6
Q

Which local anesthetic causes METHEMGLOBINEMIA?

prilocaine

lidocaine

mepivicaine

bupivicaine

A

PRILOCAINE

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7
Q

lognest duration ?

lidocaine

bupivicaine

mepivicaine

articaine

pilocaine

A

bupivicaine ( not child safe)

longest duration = highest PKA

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8
Q

which amide has longest duration? **

lidocaine

bupivicaine

mepivicaine

articaine

pilocaine

A

BUPIVICAINE

mepiv: 7.6

lido,prilo,arti 7.8

bupiv: 8.1

higher the potency = longer duration of action = higher lipid solubility

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9
Q

TOPICAL ANESTHETIC IS ESTER OR AMIDE? what is the name of it?

A

ESTER

BENZOCAINE

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10
Q

pharmacodynamics of LA causes what in ion channels?

A

SODIUM CHANNEL BLOCKER

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11
Q

which has the highest pka of LA?

mepivicaine

lidocaine

prilocaine

articaine

bupivicaine

A

mepivicaine: 7.6 ( more rapid onset)

lido, prilo, arti : 7.8

bupiv: 8.1 (longer duration)

lower pka = stronger the acid = faster onset of action

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12
Q

how much liquid in carpule?

A

1.8 mL

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13
Q

2% lidocaine has how many mg of lidocaine per carpule ?

board**

A

2 x 18 mg = 36 mg per carp

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14
Q

3 fxns of vasoconstrictors?

  • effects on numbness?
  • effect on toxicity?
  • effects on hemostasis?
A

prolong numbness

reduce toxicity (flushes out)

promote hemostasis

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15
Q

max epi dose for ASA 1 patient

A

.2 mg

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16
Q

max epi dose for cardiax patient

A

.04 mg

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17
Q

max lido dose without vasoconstrictor

A

4.4 mg/kg

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18
Q

max lido dose of LA with vasoconstrictor

A

7 mg/ kg

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19
Q

PROPER WAY TO DELIVER LA?

A

slow: 1 carpule/ min

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20
Q

length of long needle? **

A

32 mm

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21
Q

length of short needle ? **

A

20 mm

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22
Q

which guage needle has better aspiration?

27

15

25

30

A

30 !!! ( smaller hole)

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23
Q

width of 30, 27, 25 gauge?

A

30- .3mm

27 - .4 mm

25 - .5 mm

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24
Q

how much of the carpule for IA nerve block?

A

3/4

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25
Q

how much carpule of Buccal nerve block?

A

1/4 carpule

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26
Q

where is mental nerve block given and how much of carpule?

A

apices of PM

1/3

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27
Q

which nerve block do you have to apply 3 minute pressure so it works?

A

INCISIVE nerve block

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28
Q

THIS BLOCK HAS HIGHEST HEMATOMA RISK?

A

PSA

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29
Q

HOW DEEP FOR PSA ?

A

16 MM ( HALF LENFTH OF LONG NEEDLE)

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30
Q

THIS IS CALLED THE TRUE ASA BLOCK

A

IO BLOCK

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31
Q

WHICH IS MOST PAINFUL BLOCK?

A

NP

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32
Q

WHAT LA IS BEST FOR LOCAL INFILTRATION?

A

ARTICAINE (SEPTOCAINE) BECAUSE BEST BONE PENETRATION

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33
Q

SULFONAMIDES MECHANISM OF ACTION ??

A

SULFONAMIDES

FOLATE SYNTHESIS INHIBITOR : inhibit incorporation of PABA into folic acid,

sulfadiazine ; sulfamethoxazole

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34
Q

which calss of drugs is a folate synthesis inhibitor?

A

sulfamides

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35
Q

FLUOROQUINOLONES:

mechanism of axn

cidal or static>

examples ?

A

DNA synthesis inhibtor

cidal

ciproflaxocin ; levo_floxacin_

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36
Q

Penicillin:

bactericidal or static?

mechanism of penicillin?

molecular structure?

BOARD *****

A

bactericidal

cell wall synthesis inhibitor

B-Lactam ring

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37
Q

Penicillin is cross allergenic with what?

A

CEPHALOSPORINS (chemically related; allergic to this if allergic to penicillin)

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38
Q

which type of penicillin is taken orally ?

BOARD ***

A

PENICILLIN V

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39
Q

which penicillin is taken by IV sedation ?

BOARD ***

A

PEN G !

IV RHYMES WITH G!!

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40
Q

what is AUGMENTIN?

A

PENICILLIN !!!!

combo of

AMOXICILLIN

+

CLAVULANIC ACID (*b -lactamase- resistant*)

clavulanic acid= stops breakdown of penicillin b-lactam ring !!!

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41
Q

WHICH PENICILLIN BEST AND BROADEST?

augmentin

ampicillin

penicillin V

Methicillin

amoxicillin

A

AMPICILLIN

best and broadest g- spectrum !!!

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42
Q

a patient who is allergic to cepphalosporin should never be given this

A

PENICILLIN ( chemically related)

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43
Q

CEPHALOSPORIN:

cidal or static?

what is the mechanism?

examples

A

bactericidal

cell wall synthesis, B-lactam ( same as penicillin)

Cephalexin, cefuroxin, ceftriaxone, ceftriaxone, cefepime

cephala same as penicillin

anything with CEF or CEPH !!

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44
Q

ANTIBIOTIC WITH BROADEST SPECTRUM**

tetracycline

macrolide

lincosamides

A

tetracycline

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45
Q

TETRACYCLINE:

static or cidal?

mechanism ?

examples ?

A

PROTEIN SYNTHESIS INHIBITOR

(30S ribosomal subunit)

static

tetracycline doxycycline minocycline

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46
Q

TETRACYCLINE DRUGS

A

TETRACYCLINE

DOXYCYCLINE

MINOCYCLINE

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47
Q

MACROLIDES:

static or cidal

mechanism

types

A

STATIC **

Protein Synthesis inhibtor ( 50 S )

Eryhthromycin

Clarithromycin

Azithromycin

MAC LIKED TO THROW MICE

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48
Q

First choice for INFECTIOUS ENDOCARDITIS prophy?

A

amoxicillin 2g ( 1 hr before)

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49
Q

LINCOSAMIDES:

static or cidal ?

mechanism ?

types?

A

STATIC

PROTEIN SYNTH INHIBITOR (50S)

CLINDAMYCIN

LINCOMYCIN

LINK ALSO HIDES MICE

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50
Q

MACROLIDES VS LINCOSAMIDES

static or cidal?

mechanism ?

examples?

A

STATIC

Protein Synthesis inhibtor ( 50 S )

Eryhthromycin

Clarithromycin

Azithromycin

MAC is from AZ; Clari from Eryth

STATIC

PROTEIN SYNTH INHIBITOR (50S)

CLINDAMYCIN

LINCOMYCIN

Linco says LInc rearranged is Clin

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51
Q

WHEN IS AB PROPHYLAXIS NECESSARY IN CARDIOVASCULAR CONDITIONS?

4 reasons

BOARD ***

A
  • prosthetic heart valve
  • history of endocarditis
  • heart transplant with VALVULOPATHY/ VALVE DYSFUNCTION
  • CONGENITAL HEART PROBLEMS
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52
Q

WHEN IS AB PROPHYLAXIS REQUIRED IN COMPROMISED IMMUNITY?

3 reasons

A

ORGAN TRANSPLANT

NEUTROPENIA

CANCER THERAPY

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53
Q

First choice for INFECTIOUS ENDOCARDITIS prophy in children?

antibiotic type?

dosage?

A

amox 50mg/kg 1 hr before

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54
Q

INFECTIOUS ENDOCARDITIS prophy with penicillin alergy ?

A

CLINDAMYCIN 600 mg 1Hr before

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55
Q

RX FOR PROSTHETIC JOINT PROPHYLAXIS and dosage?

clindamycin

amoxicillin

keflex

ampicilin

A

KEFLEX 2G (1 hr before)

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56
Q

mitral valve AB prophy ?

A

none!!

mitral valve prolapse isnt necessary for AB

neither is

cardiac pacemaker

rhematic fever w/out valvular dysfunction

mitral valve prolape w/out valvular regurgitation

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57
Q

This antibiotic causes PSEUDOMONAS COLITIS?

clindamycin

tetracycline

macrolides

lincosamides

A

CLINDAMYCIN

causes GI issues !!!

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58
Q

PSEUDOMONAS COLITIS CAUSED FROM WHAT DRUG?

A

CLINDAMYCIN

inflammation of colon

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59
Q

what type of drug causes SUPERINFECTION?

A

Broad spectrum AB ! (kill good and bad bacteria)

  • TETRACYCLINES ( doxy, mino)

- AMPICILLIN

- augmentin

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60
Q

what AB is associated with APLASTIC ANEMIA?

tetracycline

chloramphenicol

ampicillin

erythromycin

A

CHLORAMPHENICOL

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61
Q

what types of antibiotics cause LIVER DAMAGE? **

erythomycin

chloramphenicol

tetracycline

clindamycin

A

TETRACYCLINE

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62
Q

This antibiotic associated with allergic cholestatic hepatitis ?

clindamycin

chloramphenicol

tetracycline

erythomycin

A

ERYTHOMYCIN ESTOLATE

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63
Q

A patient walks in and is on birth control, what type of medication should you not prescrive for infection?

A

ANTIBIOTICS ( cancel out)

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64
Q

what happens when give bacteriaxidal and bacteriasttic drug?

A

cancel out !

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65
Q

WHERE IS CLINDAMYCIN CONCENTRATED IN THE BODY?

A

BONE

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66
Q

HERE IS TETRACYLINE CONCENTRATED IN THE BODY?

A

GCF (that is why used in perio tmnt)

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67
Q

WHAT DO YOU USE TO TREAT HERPES?

A

ACYCLOVIR / VALCYCLOVIR

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68
Q

what do you use for CANDIDIASIS?

A

FLUCONAZOLE

KETOCONAZOLE

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69
Q

FLUCONAZOLE USED TO TREAT WHAT?

A

CANDIDIASIS

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70
Q

What is the drug that you give to treat candidiasis in trochea form ?

A

CLOTRIMAZOLE !!!

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71
Q

MECHANISM OF ASPIRIN (ASA)

A

COX 1 AND 2 BLOCKER ( irreversible)

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72
Q

MECHANISM OF IBUPROFEN?

A

COX 1 AND 2 BLOCKER (reversible)

aspirin: irrevirsible
ibuprofen: reversible

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73
Q

WHAT NSAID CAUSES GI ISSUES?

ibuprofen

asprin

celebrex

naproxen

A

ASPIRIN

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74
Q

WHAT NSAID CAUSES KIDNEY ISSUES?

aspirin

ibuprofen

celebrex

aleve

A

IBUPROFEN

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75
Q

WHAT IS WORSE COX 2 OR 1

A

COX 2

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76
Q

NSAIDS MECHANISM OF AXN

A

BLOCK COX 1 AND 2

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77
Q

What does each drug effect?

aspirin

ibuprofen

acetaminophen

A

aspirin: GI

Ibuprofen: kidney

Acet: liver

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78
Q

WHAT IS THE DRUG OF COICE FOR CHILD WITH FEVER?

aspirin

acetiminophen

ibuprofen

A

ACETIMINOPHEN

(childrens tylenol)

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79
Q

what disease can develop when a feverish child is givin aspirin?

A

REYES SYNDROME

(encephalopathy; hepatic dysfunction)

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80
Q

wWHAT DRUG IS HEPATOTOXIC

A

ACTAMINOPHEN

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81
Q

flucanazole is used to treat what?

A

candidiasis (anti fungal)

-azole

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82
Q

A PATIENT HAS KINDEY DISEASE, WHAT MED SHOULD HE TAKE ?

A

ACETIMINOPHEN

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83
Q

PATIENT HAS LIVER DISEASE, WHAT MED SHOULD HE TAKE?

tylenol

ibuprofen

aspirin

A

IBUPROFEN

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84
Q

MAXIMUM DOSE OF IBUPROFEN

A

3.2 G/DAY

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85
Q

max dose of acetiminophen ?

A

4g / day

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86
Q

mechanism aspirin as analgesia?

A

INHIBITS COX 1 AND 2

( inhibits PG syntehsis)

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87
Q

HOW DOES ASPIRIN WORK AS AN ANTIPYRETIC ?

A

inhibits PG syntehsis in HYPOTHALMUS

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88
Q

MECHANISM OF HOW ASPIRIN EFFECTS BLEEDING TIME?

A

inhibits TXA2 SYNTHESIS which inhibits PLATELET AGGREGATION

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89
Q

MECHANISM OF ASPIRIN:

ANALGESIC

ANTIPYRETIC

BLEEDING TIME

MOST IMPORTANT SLIIDE !!

A

inhibits Cox 1 (AA) and 2 (PG syntehsis)

inhibits PG syntehsis in Hypothalmus

inhibits thromboxin (A2) synthesis inhibits platelet aggregation

PG = INFLAMMATION

ANTIPYRETIC = TEMPERATURE (hypothalmus)

bleeding time: thomboxane 2 syntehsis

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90
Q

CORTICOSTEROID:

how many rings?

A

4 ring structe

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91
Q

MECHANISM OF STEROIDS?

A

Analgesic

inhibits phospholipas A2 (AA syntehsis) turns to prostoglandis

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92
Q

biggest side effect of taking steroids? ****

A

ADRENAL INSUFFICIENCY

rule of 2, adrenal insufficiency can happen if :

20 mg / 2 weeks/ 2 years ( take 20 mg of cortisone for 2 weeks within 2 years of tmnt)

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93
Q

what receptoirs do narcotics/ opiod affect ?

A

Mu-opioid receptor agonists (in CNS)

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94
Q

which narcotic has controlled release ?

morphine

hydrocodone

oxycodon

codeine

heroin

A

oxycontin / oxycodone

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95
Q

Drug combination of Vicodin?

A

HYDROCODONE + ACETAMINOPHEN

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96
Q

what drugs combine to form percocet?

A

OXYCODONE (stronger) + ACETAMINOPHEN

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97
Q

TYLENOL 2 COMBINATION AND DOSAGE>

A

300 mg ACET + 15 mg codenine

98
Q

TYLEONL 1 COMBO?

A

300 mg ACET + 8mg codeine

99
Q

TYLENOL 3 COMBO?

A

300 mg ACET + 30 mg CODEINE

100
Q

TYLENOL 4 COMBO?

A

300 mg acet + 60 mg codeine

101
Q

TYLENOL 1,2,3,4 COMBO?

A
  • 300 / 8
  • 300/ 15
  • 300/ 30
  • 300 / 60
102
Q

SIDE EFFECTS OF MORPHINE ***

A

Spells out MORPHINE

MIOSIS

OUT OF IT

*** RESPIRATORY DEPRESSION****

PNEUMONIA

HYPOTENSION

INFREQUENCY

NASUSEA

EUPHORIA AND DYSPHORIA (happy and sad)

103
Q

TREAT ADDICTION USING WHAT?

104
Q

sensation before and after nitrous oxide

A

tingling

naseua

105
Q

peripheral neuropathy is caused by what?

A

long term exposure to nitrous oxide

causes weakness, numbness and pain, usually in your hands and feet.

106
Q

minimal alveolar concentration of nitrous oxide?

107
Q

WHAT HAPPENS TO LUNGS WHEN NITROUS OXIDE TURNED OFF

A

DIFFUSION HYPOXIA

108
Q

PHARMACOKINETS STEPS?

A

0 administration

1 absorption

2 distriubtion

3 metabolism

4 elimination

109
Q

HOW IS INSULIN DELIVERED?

oral

sublingual

subcutaneous

IM

IV

A

SUBCUTANEOUS (under skin)

110
Q

how is epi pen delivered?

IM

IV

Subcutaneous

A

IM ( in muscles)

111
Q

how is nitroglycerin delivered?

A

sublingually

112
Q

most common method of drug administration?

IV

IM

Inhalation

Oral

subcutaneous

113
Q

ABSORPTION:

How do drugs get into body?

A

Local Drugs: cross cell membrane (epithelium) through PASSIVE DIFFUSION (must be non-ionized) into bloodstream (endothelium)

Systemic : straight to blood stream

114
Q

WHAT IS BIOAVAILABILITY?

A

fraction of dosage that reaches system

115
Q

PH and PKA of drugs

A

weak acids: pH < PKA

weak bases: pH > pka

acid environment/ acidic drug: NON IONIZED

basic environment/ basic drug: NON IONIZED

non ionized: what we want, moves freely across membrane

116
Q

where does drug have to get in order to be distriburted effectively?

117
Q

DESCRIBE FIRST PASS EFFECT

A

ORAL drugs go through LIVER reduces bioavailability

118
Q

distribution of drugs across 3 bodies of water in the body?

A

40%: intracellular

16%: Interstitiial

4%: Plasma

119
Q

who has more body water. obese or normal?

120
Q

what part of body uses most and least water?

A

most: BRAIN AND MUSCLE
least: ADIPOSE

121
Q

describe phase I and phase II of metabolism of drugs *****

A

drug ->phase I metabolite -> phase II inactive

PHASE I:

fxn: oxidation, reduction, hydrolysis

CYTOCHROME P450

PHASE II:

conjugation ( joining of group): glucouronide, glutathione, glycine

UDP-GLUCOURONOSYTRANSFERASE

122
Q

DESCRIBE ELIMINATION PROCESS OF DRUG

A

PHASE 1: PEE ( polar)

PHASE II: poop (nonpolar)

123
Q

constant amount of drug elinmintated per unit of time is what?

0 order kinetics

1st order kinetics

2nd order kinetics

A

ZERO:

doesnt matter amount drug taken b/c same amount elinated per hr

mg/hr

124
Q

constant fraction of drug elinmintated per unit of time is what?

0 order kinetics

1st order kinetics

2nd order kinetics

A

FIRST ORDER

% of drug per hour thats eliminated

%/hr

125
Q

higher risk of drug accumulation

zero order or first order

A

ZERO ORDER

fraction of drug

126
Q

what is the process called when a drug is inducing liver cytochrome enzyme does what to drug #2?

A

INDUCTION

reduces effect

127
Q

what is it called when drug #1 competes for metabolism or directly inhibits liver cytochrome.

what does this do to drug 2?

A

INHIBITION

increased toxicity !!

128
Q

pharmacokientics vs pharmacodinamics ?

A

kinetics:

absorption / distribution / metabolism / clearance

dynamics:

drug receptor interction

129
Q

almost all drug targets are what ??

A

PROTEINS !!

receptors

ion channels

enxymes carriers

130
Q

a substance which initiates a physiological response when combined with a receptor.

131
Q

full vs partial agonist

A

partial: cant produce 100% of desired effect

Full: can produce 100% of desired effect

132
Q

inhibits normal function of endogenous agonist

A

antagonist

133
Q

competitive vs noncompetitive antagonist?

A

comp: competes for same binding site on receptor

non-comp: binds to differnet binding site and changes morphology which prevents from binding

134
Q

INVERSE AGONIST inhibits what?

define it

A

BASAL ACTIVITY

drug that binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist.

135
Q

TYPE 1 DOSE RESPONSE CURVE:

X axis?

Y acis?

CURVE TYPE?

A

x- dose of drug

y- response/ efficacy of drug

hyperbolic or SIGMOID/ LOG FORM

136
Q

TYPE 1 DOSE RSPONSE CURVEL

what is intrinsic activity?

A

MAXIMAL EFFECT OF DRUG (EMAX) (full agonist )

full agonist: intrinsic of 1

partial agonist 0-1

antagonist = )

137
Q

TYPE 1 DOSE CURVE:

what is efficacy?

A

effect of a drug as a function of bonding

138
Q

TYPE 1 DOSE CURVE:

what is affinity?

A

attractiveness of drug to receptor

LOWER the dissaosication constant (kd) = HIGHER the affinity

139
Q

DIFFERNECE BETWEEN PENEICILLING G AND V ?

***** important !!!

A

PEN G : more sensitive to acid degredation !!!!!

some PEN V preferred

140
Q

WHICH PENICILLIN BROADEST SPECTRUM ??

AMPICILLIN

CARBENICILLIN

METHICILLIN

AUGMENTIN

A

AMPICILLIN (preferred for G-)

141
Q

WHICH PENICILLIN IM OR IV ??

AMPICILLIN

CARBENICILLIN

METHICILLIN

AUGMENTIN

A

AMPICILLIN 2G

142
Q

HOW IS POTENCY MEASURED ?

A

EC50 : affective conventration of drug leading to half its minimal effect

MORE POTENT = LOWER EC50

143
Q

competitivt antagonist shifts agonist curve which way?

144
Q

NONCOMPETITIVE GONIST SHIFTS AGONIST CURVE WHICH WAY?

145
Q

COMPETEITIVE VS NONCPM[ETOTOVE ANTAGONIST AND HOW SHIFTS AGONIST CURVE?

A

competitive: RIGHT
noncomepetitive: DOWN

adding competitive antagonist = drags curve right ( need more drug to produce response)

146
Q

TYPE II DOSE RSPONSE CURVER

X AND Y AXIS?

A

X: DOSE OF DRUG

Y: # OF SUBJECTS RESPONDING TO DRUG (rather than efficacy like type I curve)

147
Q

TYPE II :

ED50 ?

TD 50?

LD 50 ?

A

ED: effective dose; 50% population rseponded effectively (treated)

TD50: toxic dose: 50 % population experienced toxic side effects

LD50: lethal dose; 50% population responded lethally (died)

148
Q

type I vs TYPE 2 DOSE response curves !!! what do they measure?

A

type 1: dose v efficacy of drug

type II: dose vs reponse of patient

149
Q

WHEN TALKING ABOUT DRUGS WHAT IS ADDITIVE EFFECT?

A

combining drugs COMBINES their effect

150
Q

what is an antagonistic drug?

A

combining drugs causes lesser effect than each one alone

151
Q

what is synergistic in drugs?

A

combining drug leads to MORE THAN THE SUM of 2 independelty !!

152
Q

ANS PHARMACOLOGY:

which drugs affect PSNS?

which drugs affect SNS?

IMPORTATNT !!!!!!

A

PSNS: cholinergic

sns: adrenergic

153
Q

SNS VS PSNS HOW THEY AFFECT:

pupils

saliva

HR

airway

digestion

bladder

A

rest and digest (feed and breed) :

constriction

stimulate saliva

dec HR

airway constriction

stimulate digestion

bladder constriction

154
Q

RECEPTORS IN ANS:

IONOTROPIC VS METABOTROPIC

A

ION: ION CHANNELS (once open allows ions to pass thru)

METABOTROPIC: G-PROTEIN COUPLES RECEPTORS ( acitvates 2nd messenger)

155
Q

RECEPTORS IN ANS :

CHOLINERGENIC VS ADRENERGENIC ******

what do they bind ?

A

CHOLINERGENIC: binds acetycholine

  • NICOTONIC : binds nicotine; ionotropic
  • MUSCURANIC: binds muscarine; metabotropic

ADRENERGIC: binds EPI/NE; metabotropic (always)

156
Q

CHOLINERGENIC

2 RECEPTORS?

A

NICOTINIC

MUSCURINIC

157
Q

ADRENERGENIC RECEPTORS

what does it bind?

metabotropic or ionotropic?

A

binds epi/ ne

METABOTROPIC ( g cpuples recetor)

158
Q

RECEPTORS IN THE ANS

159
Q

SNS VS PSNS BY REGION OF SPINAL CORD:

A

PSNS : CRANIO/SACRAL CS

SNS: THORACO/LUMBAR TL

160
Q

SNS VS PSNS BY LEGNTHS OF PRE AND POST GANGLIONIC NERVES

A

PSNS: long pre; short post

SNS: short pre; long post

161
Q

SNS VS PSNS neurotransmitters they use :

A

PSNS: AcH everywehre

SNS: AcH to ganglion NE from nerves; EPi/NE from adrenal gland

162
Q

ANS:

SNS VS PSNS neurotransmitters they use ****

A

PSNS: muscarinic metabotropic

SNS: adrenergenic metabotropic

163
Q

HOW IS THE SYNTHESIS RXN OF ACETYLCHOLINE ?

A

Acetyl CoA + choline= ACETYLCHOLINE

catalyzed by choline acetyltransferase

reversed by acetylcholineesterase

164
Q

WHAT DO THESE MUSCURANIC RECEPTORS AFFECTS?

M1

M2

M3

M4

M5

A

M1, M4, M5: CNS

M2: heart

M3: Smooth muscle

165
Q

MUSCURANIC RECEPTOR

PSNS or SNS?

A

PSNS

rest and digest

166
Q

function oF M2 AND M3 MUSCURANIC RECEPTORS?

A

RMBR, MUSCURANIC IS PSNS = REST AND DIGEST !!!

M2= HEART; BRADYCARDIA

M3= SM; SLUDS / BAM

SLUDS: salivation, lachrymation, urination, defecation, sweating

BAM: brnchoconstriction, ab cramps, miosis ( constritction)

167
Q

M AGONIST AFFECTS WHICH M RECEPTOR?

A

NON-SELECTIVE (SO AFFECTS ALLA SM1-M5)

168
Q

WHAT IS THE ISSUE WITH M AGONISTS >

A

non selective ( works all M receptors)

dont use on:

  • peptic ulcers (gastric acid)
  • asthma/ COPD (bronchconstriction)
  • CHF (dec. cardiac output)
169
Q

M AGONIST USED FOR STUMULATING SALIVA OR EYE DROPS ?

A

PILOCARPINE (constricts pupils)

glaucoma and salivary production

170
Q

what are the 2 DIRECT acting M agonists

A

PILOCARPINE

METHACHOLINE

remember. these are M agonists so they work on PSNS. agonist affet heart, SM , CNS

171
Q

WHAT ARE THE FXN OF INDIRECT ACTING M AGONISTS?

A

INHIBIT ACETYLCHOLINEESTERASE**!

stops breakdown of aCh

172
Q

THIS INDIRECT-ACTING DRUG RESERSIBLY INHIBITS CHOLINESTERASE

A

NEOSTIGMINE

Inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to acetylcholinesterase at sites of cholinergic transmission

173
Q

IRREVERSIBLY INHIBITS CHOLINESESTERASE

A

ORGANOPHOSPHATE INSECTICE

potent and poisonous

174
Q

ORGANOPHOPSHATE INSECTICIDE POISONING CAN BE TREATED WITH ? **

A

PRALIDOXAMINE

175
Q

DIRECT ACTING VS INDIRECT ACTING M AGONIST ***

what they fxn?

drugs in each?

A

DIRECT: activates M receptor; mimics ACH

  • pilocarpine (saliva; constrict)
  • methacholine

INDIRECT: non competitively inhibits cholinesterase

  • neostigmine (reversibly inhibts cholinesterase)
  • organophosphate insecticide (irreversibly inhibits cholinesterase )
176
Q

WHICH DRUG REDUCES SALIVA OR EMERGENCY DRUG TO TREAT BRACHYCARDIA ( CAN ALSO CAUSE TACHYCARDIA)

A

ATROPINE!!!

m antagonist/ antimuscarinic!!! ( opposite of psns)

opposite drug: pilocarpine

177
Q

WHAT IS ATROPINE?

A

m antagonist/ antimuscarinic!!! ( opposite of psns)

OPPOSITE OF PILOCARPINE

178
Q

MECAMYLAMINE

fxn?

what class of drug is it whats it due to receptors?

A

ANTIHYPERTENTSIVE

N ANTAGONIST/ GANGLIONIC BLOCKERS

non polarizing!!

blocks N receptor at allosteric site (site that allows molecules to inhibit or turn on enzyme activity)

179
Q

THIS N ANTAGONIST is a ganglionic blocker that used to treat extreme hypertensive patients.

A

MECAMYLAMINE

180
Q

THIS DRUG IS AN N ANTAGONIST/GANGLIONIC BLOCKER THAT BINDS TO N RECEPTOR BUT CANT BE REMOVED

A

NICOTINE !!!

DEPOLARIZING: binds N receptor and cant be moved

in image: Na+ causes DEPOLARIZATION allows nicotine in and binds to N receptor

181
Q

THIS DRUG IS FOUND IN ARROW POISON:

name?

drug class/ type?

A

TUBOCURARINE

N-_antagonist_/ neuromuscular blocker

non-depolarizing ; blocks N receptor at active site

182
Q

THIS DRUG PREVENTS LARYNGOSPASMS AND SKELETAL MUSCLE RELAXANT

A

SUCCINYLCHOLINE

Depolarizing: binds N receptor but cant be removed

n antagonist/ neuromuscular blocker

183
Q

M RECEPTORS and N RECEPTORS OVERVIEW !!!! ****

IMPORTANT !!!!

A

M AGONIST:

direct acting; activates M receptor (mimics ACh)

PILOCARPINE

METHACOLINE

indirect -acting; non competitbely inhibits acH-esterase

NEOSTIGMINE: reversibly inhibits ach-esterase

ORG PHOSPHATE INSECTICIDE: irreversibly inhibits cholinsterase

M ANTAGONIST/ ANTIMUSCARINIC:

competitive inhibitors; block N receptors compete with ACh

Atropine: dec. saliva/treat bradychard (cause tachy)

_______________________________

N ANTAGONIST: GANG BLOCKERS

non-depolarizing; blocks N receptors at allosteric sites

MECAMYLAMINE: antihypertensive

Depolarizing; binds N receptor but cant be removed

NICOTINE

N ANTAGONIST/NEUROMUSCULAR BLOCK:

non-depolarizing/blocks n recetor at active site

TUBOCURARINE: arrow poison

depolar. binds to N receptor but cant be removed

SUCCINYLCHOLINE: skeletal muscle relax

184
Q

STEPS OF EPINEPHRINE AND NE SYNTHESIS

A

TYROSINE -> L-DOPA -> DOPAMINE -> NE -> EPI

185
Q

CATECHOLAMINES VS MONAMINES ?

A

CATECH : Dopamine, NE, EPI

MONAMINES: catecholamines + serotonin (5-HT) and histamine

186
Q

WHAT ARE THE 4 ADRENERGENIC RECEPTORS AND WHAT PART OF BODY DO THEY AFFECT? **

A

a1: SM (vasculature)
a2: SM

B1: Heart (sa/av node)

B2: SM ( albuterol)

187
Q

which adrenergenic receptors affect the heart?

188
Q

which adrenergic receptors affect SM?

189
Q

what do a-receptors do:

blood pressure

urinary system

pupils

A

VCONSTRICTION

URINARY RETENTION

DILATION (MYDRIASIS)

190
Q

WHAT DOES a -1 vs a-2 receptors do?

A

a-1 :

vasoconstriction

urinary retention

dilation (mydriasis)

a-2:

vconstriction

191
Q

B1 VS B2 RECEPTORS:

A

B1: FIGHT OR FLIGHT (SNS)

  • tachycardia
  • inc HR, electircal conduction, contraction
  • RENIN RELEASE FROM KIDNEYS ( vasocontrictor or dilator)

B2:

  • bronchodilation
  • vasodilation
  • stop peristalsis
192
Q

which receptor causes tachycardia ?

a1 a2 b1 b2

193
Q

which receptor causes dilation (broncho and vaso)?

a1 a2 b1 b2

194
Q

which receptor causes bradychardia?

a1 a2 b1 b2 m1 m2 m3 m4

195
Q

During epinephrine reversal, what happens to effect of epi? what type of medicine used for epi reversal ?

A

Vconstrictor effect of epi converted into vdilator effect with a-blocker then B2 vdilator effect becomes major control

(basically a-blocker cancels out epi a activation effects and only activates B receptors)

196
Q

what blocker to give for epi reversal?

A

a-blocker so that only B receptors active

197
Q

DESCRIBE VASOVAGAL REFLEX and CHEMICAL PLAYS ROLE IN IT

A

ALSO CALLED VASOGAGUL SYNCOPE

NE activates baroreceptors that stimulate vagal reflex to reduce HR, Leads to opp response to what NE usually does

198
Q

WHAT DRUG BLOCKS VASOVAGAL REFLUX (syncope) ?

**

199
Q

IS HUMAN CIRCULATORY SYSTEM OPEN OR CLOSED?

200
Q

in circulatory system formula :

what does the pump in a heart tell you?

what does tubing tell you?

what does fluid tell you

A

pump: CO

Tubing: peripheral resistance (PR)

fluid: blood volume (SV)

201
Q

WHAT IS SYSTOLE?

A

Pressure in arteries when heart contracts

202
Q

what is diastole

A

pressure in arteries when heart relaxes

203
Q

WHAT IS PRELOAD?

A

pressure in ventricles BEFORE contraction

204
Q

what is afterload?

A

pressure in arteries against which ventricles must pump (systole)

205
Q

side effect of Hydrochlorthiazide ?

A

HYPOKELEMIA

need K+ supplement

206
Q

side effect of spironolactone

A

HYPERKALEMIA

207
Q

WHAT TYPE OF DRUG IS HYDROCHLOROTHIAZIDE (HCTZ)

A

DIURETIC DRUG (ANTIHYPERTENSIVE) aka water pills

blocks salt reabsorption it then releases more salt when you pee decreasing BP

208
Q

spironolactone causes what advere reaction?

A

hyperkalemia (K+ sparing drug)

209
Q

what are vasodilation drugs and what do they do?

A

HYDRALAZINE: opens K+ channels cause vdilation

CCB: block Ca+ influx cause vdilation

210
Q

WHAT DOES AN ACE INHIBITOR DO AND WHAT ARE SOME DRUGS? ***

A

BLOCKS ENZYME CONVERTS ANGIOTENSIN I -> ANG II (VASOCONTRICOR)

-IPRIL

211
Q

WHAT DOES AN ARB DO AND EXAMPLES

A

competitive antagonist at angiotenis II receptor

- SARTAN

212
Q

MECHANISM OF ACTION FOR LISINOPRIL

A

ACE INHIBITOR

blocks conversion of angiotensin I -> II

213
Q

LOSARTAN

type of drugmechanism of action

A

this is a ARB !!!

competitive antagonist: BLOCKS ANGIOTENSIN II RECEPTOR

214
Q

WHAT ARE ANTIANGINAL DRUGS FOR? WHAT ARE SOME OF THE DRUGS?

A

FOR INSUFFICENT O2 TO CARDIAC MUSCLE / COMBAT ANGINA

MONA:

  • morphine
  • oxygen
  • nitroglycerin
  • aspirin
215
Q

what type of drugs do you need if heart fails to pump enough blood?

A

Anti-Congestiive Heart failure drugs

216
Q

function and mechanism of ANTI CHF drugs and examples

A

HELP HEART PUMP BLOOD

CARDIAC GLYCOSIDES:

block na/k ATPase to increase ca+ influx and promotie positive inotropy in cardiac cells muscles ONLY

*basically causes induction of na+ which would cause influx of Ca+ that would contract heart *

ACE INHIBITORS:

block angiotensin I to II (potent vasoconstrictor)

DIGOXIN

DIGITALIS

-PRILS

217
Q

WHAT IS DIGOXIN ?

A

ANTI CHF DRUG ( caridac glycoside)

block Na/K AtPase to increased ca+ influx promotes inotropy (contraction)

218
Q

MAIN FUNCTION OF LISINOPRIL?

A

VASODILATOR !!!

block angio 1 -> angio II

angio II is a potent vasoconstrictor

219
Q

what type of drugs do you give for irregular heartbeats?

A

ANTI-ARRYHTMICS

220
Q

MATCH:

Type: 1,2,3,4

na+ blockers for cardiac muscle only

K+ channel blockers

Beta blockers

Ca2+ channel blockers CCB

A

1- Na+ channel blockers

2- beta blockers

3- K+ blockers

4 - Ca3+ channel blockers

221
Q

WHAT IS FUNCTION OF HABBA RECEPTORS?

A

CAUSE CNS TO GET DEPRESSED

222
Q

WHAT ARE DOPAMINE AND SEROTONIC RECEPTORS FCN?

A

CAUSES CNS TP GET EXCITED

223
Q

WHAT TYPE OF DRUGS FOR SCHIZOPHRENICS?

A

ANTIPSYCHOTICS : schizoz cns system overstimulated need inhibitors

1ST GEN: DOPAMINE BLOCKER :

  • haloperidol
  • phenothiazine

2ND GEN: DOPAIMINE AND SEROTONIN BLOCKER

  • clozapine
224
Q

best drug of choice for manic depression ?

225
Q

what are the 3 categories of antidepressants?

what are we trying to increase in antidepressants?

A

increase MONAMINES ( serotonin, dopamine, etc)

  1. SSRI (slective serotonin reuptake inhibitor)
  2. SNRI/TCA (serotonin and NE reuptake inhibtor
  3. MAOI (monamine oxidase inhibtors)

ssri: fluoxetine , citalopram , trazodone
snri: amitriptyline, imipramine

MAOI: phenlzine, tranylcypromine

226
Q

WHAT DOES A PATIENT TAKE FOR ANXIETY OR SEDATION ??

A

ANXYIOLITICS

BENZOS

  • dizaepam (valium)
  • Triazolam
  • chlordiazepoxide

-

BARNITURATES

  • thiopental
227
Q

mechanism of action of benzo ?

issue causes ?

A

inc GABA binding:

  • chloride ion influx
  • CNS depressed

THROMBOPHLEBITIS (blood clots)

228
Q

MECHANISM OF ACTION OF BARBS?

ISSUE WITH BARBS ?

A

SAME MECHANISM AS BZD

RESPIRATORY DEPRESSION

THIOPENTAL : quick onseted short duration of action

229
Q

Barbs are contraindicated in patients with what illness?

A

INTERMITTENT PROPHYRIA

230
Q

MOST IMPOERTANT FACTOR IN EFFECTS OF GENERAL ANESTHTICS ?

A

MORE SOLUBLE = MORE POTENT

231
Q

WHAT IS DENTAL ANESTHESIA THAT IS USED TO PUT PATIENTS TO SLEEP FOR SURGERY ?

A

HALOTHANE ?

232
Q

WHAT IS HALOTHANE AND A COMPLICATION OF IT?

A

EXTREMELY POTENT DENTAL ANESTHESIA

HEPATOXICITY !!!

233
Q

PARKINSONS DISEASE:

cause of it?

what drug we use ?

A

DOPAMINE DEFICIENCY !

  • dopamine cant cross BBB but Levodopa L-dopa can
  • CARBIDOPA blocks dopa decarboxylase allows L-dopa to cross BBB where it is converted to dopamine
234
Q

WHAT DRUG DO PARKINSONS PATIENTS TAKE AND WHAT IS MECHANISM?

A

CARBIDOPA:

blocks DOPA decarboxylase ( causes levodopa to conver to dopamine) allows LDOPA to cross BBB where it is converted to dopamine in brain

235
Q

tardive dyskineasia is aneurological side effect of which class of drugs?

  1. alcohol
  2. tricyclic antidepressants
  3. barbs
    1. phenothiazine antipsychotics
  4. MOAI
A

pheno antipsychotics

involuntary neurological movement disorder caused by the use of dopamine receptor blocking drugs

236
Q

which peniccilin only administered by deep IM injections?

  1. ampicillin
  2. dicloxacillin
  3. pen G
  4. Pen V
237
Q

QUINIDINE USED USED TO TREAT:

hypertension

angina pectoris

CHF

supraventricular tacharryhtmia

A

supraventricular tachyarryhmiia

240
Q

a child developes a disease called REYE SYNDROME from what?

A

ASPIRIN !

(give acetiminophen instead )

241
Q

which receptor does oxycodone, morphine, and codeine effect?

A

Mu-opoid receptors

242
Q

which drug is lethal if combines with MAOI ?

A

MEPERIDINE

mental dental (18 decks)

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