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Pharmacology > Pharmacology final - ALL > Flashcards

Pharmacology final - ALL Flashcards

1
Q

Parasympathetic receptors and NT?

A

Nicotinic - Muscarinic

Ach - Ach

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2
Q

Sympathetic receptors and NT

A

Nicotinic - Adrenergic

Ach - NE/Epi

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3
Q

Ach synthesized from?

Enzyme?

A

Coline + Acetyl-CoA

Choline-Acetyl transferase

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4
Q

Choline uptake into presynaptic cell inhibitor?

A

Hemicholinum

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5
Q

Inhibitor of Ach exocytosis in presynaptic nerve ending?

A

Botulinum toxin

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6
Q

Major termination of synaptic Ach?

A

Acetylcholine esterase enzyme breaks it down

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7
Q

Reversible indirect acting cholinomimetic drugs?

A

Edrophonium
Physostigmine
Neostigmine

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8
Q

Irreversible indirect acting cholinomimetic drugs?

A

Malathion

Parathone

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9
Q

Function of indirect acting cholinomimetic drugs?

A

Inhibit Ach esterase causing no breakdown of Ach in synapse

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10
Q

Result of:

  1. Presynaptic cholinomimetic stimulation
  2. Direct cholinomimetic stimulation
  3. Indirect cholinomimetic stimulation
A
  1. Increase Ach
  2. Direct receptor binding increasing effect
  3. Prolonging synaptic Ach by inhibiting break down
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11
Q

Presynaptic increase of Ach ?

A

4-aminopyridin - increase Choline uptake
Increased EC calcium
Alpha-Latrotoxin stimulates Ach release in absence of Ca (Widow spider venom)

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12
Q

Difference between Ach and Carbachols?

A

Carbachols have a NH3 instead of a CH3 group

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13
Q

Carbachol T 1/2 and choline esterase resistance?

A

very resistant

long acting

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14
Q

Neostigmine administration?

A

No GI absorption must be given IV

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15
Q

Inhibitor of Ach storage?

A

Vesamicol

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16
Q

Negativ feedback of Ach release?

A

Alpha-2 receptor binding of Ach or NE
Dopamin-2 receptor binding dopamin
Block AP in NMJ by Procaine so no release

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17
Q

AB that may inhibit Ach release?

A

Tetracyclines
Aminoglycosides
Especially in Myasthenia gravis

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18
Q

Myasthenia Gravis?

A

Ab against nicotinic receptors in the NMJ causing no activation

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19
Q

Treatment og Myasthenia Gravis?

A

The -stigmines causing increase Ach in synapse
Neostigmin
Pyridostigmine
physostigmine

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20
Q

Drug used in diagnosis of Myasthenia Gravis?

A

Edrophonium since it is very short acting and can test if the patient has relife when administered
(t1/2 is 15 min)

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21
Q

Anti-Ach esterase that can pass the BBB?

A

Physostigmine

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22
Q

Drug used in Atropin overdose?

A

Physostigmine

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23
Q

SE of Ach-esterase inhibitors?

A 
Just lis what would happen if we have an overstimulation of Ach (parasympathetic)
DUMBELL
Diarrhea 
Urination 
Miosis 
Bradycardia 
Bronchospasms 
Lacrimation 
Salivation
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24
Q

Why can increased Ach lead to flaccid paralysis?

A

Nicotinic overactivation leads to inhibition (Cholinergic toxicity) like insecticide poisoning

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25
Q

significance of anti-muscarinic drugs on the heart?

A

Not really of significance unless bradycardia and AV block

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26
Q

Effect of Atropin in the CNS?

A

DOESE DEPENDENT

  1. antiemetic
  2. antianxiety 1-2mg
  3. Dyskinesia and tremor 10mg
  4. Rage and hallucinations 10mg
  5. Convulsion
  6. Coma death > 150mg
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27
Q

Effect of Ipratropium?

A

Inhaled causing bronchodilation. Not absorbed so only local action

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28
Q

What can you give in the case of severe bradycardia?

A

Atropin - block parasympathetic activation increasing heart rate

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29
Q

How can you acutely reverse a hear block in patients with depressed AV nodal conduction?

A

IV atropin

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30
Q

M3 muscarinic antagonists?

A

Ipratropium

Tiotropium

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31
Q

muscarinic receptor in the CNS and its antagonist?

A

M1

Scopolamide

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32
Q

Procyclidine?

A

Anti-muscarinic agent used in Parkinson: decrease the excitatory activity of cholinergic neurons in the striatum

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33
Q

Cyclopentolate

A

Non-selective anti-muscarinic agent

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34
Q

Solifenacil

A

M3 antagonist used in bladder spasm

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35
Q

administration of epinephrin?

A

IV since it is metabolized in GI

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36
Q

Indication of Epinephrin?

A

Anaphylaxis
Angioneurotic edema
with local anesthesia to increase effect

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37
Q

Location of beta-1 adrenergic receptors?

A

Heart SA AV
Purkinje
Atrial and ventricular muscle
Kidney

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38
Q

Location of Alpha-1 adrenergic receptors?

A

Almost everywhere

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39
Q

Location of alpha-2 adrenergic receptors?

A 
Almost everywhere but this is an inhibitory receptor 
Brain
Body 
Platelets 
Pancreas
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40
Q

Effect of Beta-2 adrenergic receptor on SM?

A

ALWAYS relaxation!! The increase in cAMP inhibits action of MLCK on the

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41
Q

how can you save the kidneys during shock?

A

Low dose dopamin causing vasodilation in the renal artery

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42
Q

selectivity of peripheral dopamin during low and moderate dose?

A

low: D1 in kidney
moderate: B1
high loses B1 sensitivity

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43
Q

Dobutamine

A

B1 selective given in cardiogenic shock together with dopamin to save the kidney

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44
Q

Alpha-1 adrenergic receptors found in?

A

veins and arteries so both contract!

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45
Q

Alpha-1 receptors in the eye leads?

A

Pupillary muscle contraction results in pupillary DILATION (mydriasis)

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46
Q

NE affinity to adrenergic receptors?

A

Alpha > Beta

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47
Q

Epinephrin affinity to adrenergic receptors?

A

Beta&raquo_space; Alpha unless very high doses

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48
Q

Adrenergic receptors in the Bronchi?

A

Beta-2

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49
Q

What’s the function of an alpha-2 antagonist?

A

inhibits NE negative feedback resulting in increased NE release –> goes to heart causing tachycardia

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50
Q

can out body generate new alpha reseptors in an irreversible antagonist is used?

A

yes, it takes 48h

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51
Q

alpha receptor in prostate?

A

alpha-1 A

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52
Q

what is reflex tachycardia

A

If blood pressure decreases, the heart beats faster in an attempt to raise it - reflex tachycardia. Can happen in response to a decrease blood volume or change in blood flow

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53
Q

what is orthostatic hypertension

A

Also known as postural hyertension is a medical condition where a person’s BP increase when standing up or sitting down.

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54
Q

First generation beta blockers are?
Second generation beta blockers are?
Third generation beta blockers are?

A

Non-selective
Beta-1 selective
Selective and non-selective

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55
Q

which beta blocker can cross the BBB and is therefore also used in?

A

Propranolol also used as a migraine prophylaxis

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56
Q

what is the difference between propranolol and pindolol on HR?

A

pindolol is a partial beta agonist and will not decrease heartrate as much as propranolol

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57
Q

drug used in paroxysmal supraventricular tachycardia?

A

esmolol since it i very short acting

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58
Q

are second generation beta blockers always beta-1 selective?

A

they become non-selective in high doses

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59
Q

betablockers used in glaucoma?

A

Timolol + Betaxolol

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60
Q

beta blockers used in stress?

A

Pindolol due to no severe bradycardia

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61
Q

contraindications of beta blockers?

A

AV block
Bradycardia
DM
Asthma

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62
Q

indication of beta blockers?

A 
hypertension 
angina pectoris
supraventricular tachycardias 
CHF 
glaucoma
migraine 
stress
panic disorder 
tremor
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63
Q

beta-adrenergic receptor in the kidney?

A

Beta-1 causing renin release, we can block this in heart failure so no renin, no angiotensin, no aldosterone and no water retention

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64
Q

what can be given in B-blocker toxicity?

A

Glucagon

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65
Q

beta-bloker safe in pregnancy?

A

Labetolol

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66
Q

Dangerous side effect of atracurium

A

in high doses penetrates the BBB causing seizures, also causes histamin release (bronchoconstriction and decreased BP)

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67
Q

why is Cisatracurium a better choice than atracurium?

A

less side effects

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68
Q

Duration of succinylcholine?

A

short: 5-10 min due to degradation by plasma cholinesterase (only small amount reaches NMJ)

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69
Q

When would you use depolarizing vs non-depolarizing muscle relaxants?

A

Depolarizing used in ventilation control and convulsion

Non-depolarizing used in anesthesia

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70
Q

how can succinylcholine cause cardiac arrest?

A

It increases potassium (K) release into blood

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71
Q

how does atracurium cause seizures?

A

it leads to production of LAUDOSINE which is neurotoxic

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72
Q

what’s the 4 things that happen in astma?

A
  1. Bronchial hypersensitivity
  2. Bronchospasms
  3. Increased mucous secretion
  4. Cellular infiltrate causing constriction
  5. Edema
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73
Q

COPD?

A

chronic inflammation of the airways eventually leading to emphysema (bronchial narrowing and hyperinflated alveoli) increase Co2/decreased O2

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74
Q

other drugs used in asthma and COPD?

A
  1. IgE ab (no binding to mast cells so no histamine)
  2. Ca-channel blockers (no depolarization)
  3. K-channel opener (hyperpolarization)
  4. NO donors causing relaxation
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75
Q

steroid in urgent asthma?

A

Methylprednisolone IV

prednisone oral

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76
Q

inhalation asthma corticosteroids?

A

Fluticasone

Budesonide

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77
Q

Name 3 leukotrienes causing inflammation?

A

LTB4 neutrophil chemotaxis

LTC4 and LTD4 bronchoconstriction, hypersecretion and increased reactivity

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78
Q

Drug inhibiting LT pathway?

A

Montelukast 10mg/day

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79
Q

When should cough not be supressed?

A

if productive cough suppressing it leads to mucous plug

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80
Q

opioid and a non-opioid cough suppressor?

A

Opioid: Codeine
Non-opioid: Butamirate
(They give no analgesic effect)

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81
Q

In antitussive agen Codeine does not..:

A

No analgesia
No euphoria
No resp suppression
No addictiveness

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82
Q

what is the function of expectorants?

A

remove mucous from bronchi

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83
Q

taking AB with acetylcystein you have to…

A

take them 2h apart since acetylcystein inhibit function of AB

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84
Q

What is the reason of claudication in peripheral vascular disease?

A

ischemia causes release of adenosine which is toxic to nerve eneding causing pain

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85
Q

Drugs increasing cerebral circulation?

Indication?

A

Vinpocetine
Nicergoline
Brain circulatory disease, Alzheimer and post-stroke

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86
Q

location of migrain center in brain?

A

Dorsal raphe nucleus, Locus coeruleus

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87
Q

cause of migraine?

A

NO induces inflammatory neuropeptide release:
- CGRP
Substance-P
Neurokinin-A

Causing meningeal vasodilation and neurogenic inflammation (sterile)

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88
Q

migraine prophylaxis?

A

propranolol
carbamazepine
verapamil
Galcanzumab

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89
Q

bodies response to decreased CO ?

A

baroreceptors in aorta and carotid senses decreased P av induces NE release which bind to Beta-1 adrenergic receptors

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90
Q

Response of increase NE due to HF on kidney?

A

NE bind Beta-1 adrenergic reseptors in kidney inducing renine release

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91
Q

why is the bodies response to HF not good?

A

increased water retention further increases strain on heart -give diuretics

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92
Q

during which phase of HF should Beta blockers be given?

A

from first to third, not the last phase might cause decompensation. You should rather give beta agonists at this point

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93
Q

what does beta blockers do in the heart?

A 
Decrease contractility 
Decrease conductivity (HR)
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94
Q

effect of ACEI?

A

inhibit angiotensin conversion and increase bradykinin causing vasodilation (ACE norm degrades brady)

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95
Q

K+ sparing diuretic?

A

Spironolacton

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96
Q

Sodium wasting loop diuretics?

A

Furosamide

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97
Q

first steps in AHF

A
  1. evaluate hypotension and determine shock state
  2. oxygen if SpO2 < 90 %
  3. Secure IV access
  4. continue monitoring BP, SpO2. ECG
  5. Patient must sit in a 45 degree position
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98
Q

What is completely contraindicated in AHF?

A

Beta-blockers

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99
Q

why are digoxin and digitoxin good to usen in AHF?

A

they have a positive inotropic effect but negative chronotropic effect

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100
Q

Mechanism of the digitalis drugs

A

Na/k ATPase blockers causing decreased Na/Ca antiporters leading to Ca staying in the cell and contraction

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101
Q

Cardiac glycosides (digoxin and digitoxin) on the CNS?

A

they increase the vagal parasympathetic tone causing decreased atrial conduction hence decrease chronotropy

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102
Q

cardiac glycosides elimination?

A

digitoxin liver

digoxin kidney

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103
Q

relationship between K+ and cardiac glycosides?

A

K+ acts as an antagonist so be carefull if patient is on K+ wasting diuretic it will potentiate the drugs and if the patient is on spironolactone it will inhibit them

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104
Q

Class IA antiarrhythmic drug Quinidine effect on HR?

A

It’s anti-muscarinic meaning it inhibits parasympathetic tone causing increased HR

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105
Q

how can we prevent Quinidine tachycardia?

A

Give Digitalis before Quinidine

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106
Q

Class IA antiarrhythmic drug quinidine on Alpha-adrenergic receptors?

A

It’s an Alpha-blocker causing vasodilation and hypotension

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107
Q

relationship between K+ and Quinidine?

A

K+ potentiates Quinidine

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108
Q

Quinidine vs Digoxin on excretion

A

competes for excretion sites therefor may cause digitalis intoxication due to decreased excretion

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109
Q

Class IA antiarrhythmics: can we use Procainamide chronic?

A

No due to drug induced lupus

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110
Q

Class IA antiarrhythmics: procainamide effect of autonomous nervous system?

A

It serves as a ganglionic blocker causing decreased sympathetic tone hende hypotension

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111
Q

penthyon is an antiarrhythmic drug but also an..

A

Anti-epileptic drug

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112
Q

Class II antiarrhythmic drugs? (4)

PEMS

A

Propranolol
Esmolol - negative chrono and dromo
Metoprolol - sympatomimetic
Sotalol - prolong AP

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113
Q

Class III antiarrhythmics? (2)

A

Amiodarone

Sotalol

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114
Q

Class IV antiarrhythmics?

A

Verapamil

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115
Q

Class IV antiarrhythmics verapamil function?

A

reduce plateau by inhibiting L-type Ca-Channel

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116
Q

Class V antiarrhythmic drug adenosine function?

A

Opens K+ causing hyperpolarization

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117
Q

Mg+ effect as an antiarrhythmic class V?

A

Antagonizes digitalis, used in hypokalemia

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118
Q

Hypertension?

A

> 140/90

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119
Q

causes of secondary HT?

A
  1. renal artery stenosis
  2. primary hyperaldosteronism
  3. aortic corotation
  4. cushings syndrom
  5. pheochromocytoma
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120
Q

4 classes of HT treatment?

A
  1. diuretics
  2. sympatholytic
  3. direct vasodilators
  4. Angiotensin inhibitors
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121
Q

what type of Ca channel is blocked by CCB?

A

L-type

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122
Q

most common SE of CCB?

A

Edema since the effect is greater on areries then veins

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123
Q

CCB with a cardiac action?

A

Verapamil

Diltiazem

124
Q

Why is ACEI good to use in ischemic heart patients?

A

because they dont have an effect on the heart or cause reflex tachycardia (like vasodilators)

125
Q

why is ACEI good to use post MI?

A

inhibits remodeling

126
Q

why is ACEI good to use in diabetic nephropathy?

A

they reduce the efferent arteriole resistance lowering intraglomerular P and thereby reduce proteinuria

127
Q

why should you not give ACEI to renal stenosis patients?

A

Because the HT keep the kidneys going, if you decrease blood flow then you stop renal perfusion

128
Q

effect of ARB?

A

Decreased aldosterone so Na+ loss
K+ retention
vasodilation

129
Q

how long does it take for ARB’s to fully function?

A

6 weeks

130
Q

how much occlution to get stable angina pectoris?

A

> 70%

131
Q

what is the bad Cholesterol and why?

A

LDL because it adheres to the vascular wall causing AS. Oxiation of LDL also causes an inflammatory response

132
Q

why do we want HDL>LDL?

A

HDL removes LDL causing less AS

133
Q

what is elevated in hypercholesteremia?

A

LDL

134
Q

what can cause LDL clearance defect?

A

Apo-B defect

Low LDL receptors

135
Q

Cause of type I hyperlipidemia?

A

Hyperchylomicronemia
Hypertriglyceridemia
Decreased clearance og Chy and VLDL
APO-CII deficiency and Lipoprotein lipase deficiency

136
Q

Cause of type II hyperlipidemia?

A

increased LDL

137
Q

Cause of type III hyperlipidemia?

A

Dys-beta-lipoproteinemia

Accumulation of Beta-VLDL due to defect Apo-E decreasing clearance

138
Q

Cause of type IV hyperlipidemia?

A

Increased TG due to increase VLDL

Very common and due to obesity and insulin restance

139
Q

Why is thiazide a weak diuretic?

A

Because it works at the distal tubule and by this time almost all sodium is already absorbed

140
Q

Spironolactone and eplerenones SE?

A

Gynecomastia
Metabolic acidosis
Hyperkalemia

141
Q

diuretics in cerebral edema?

A

Mannitol

Glycerol

142
Q

H1 receptor in lung and GI causes?

A
  1. Vasodilation
  2. Increased permeability
  3. Edema
  4. SM contraction
143
Q

which non-histamin receptors do histamin also bind to?

A

Cholinergic, seretonin and Alpha-adrenergic receptors giving an agonistic effect

144
Q

main difference between 1st generation and 2nd generation antihistamins?

A

1st generation penetrates the BBB causing sedation and decreased cognitive function

145
Q

which antibiotic should you not give antihistamins with?

A

Macrolides in legionella

146
Q

Where do we have opioid receptors?

A

CNS area related to pain
GI
Adrenal medulla

147
Q

Endogenous opioids?

A

Endorphins
Enkephalins
Dynorphins

148
Q

opioid receptor related to GI motility?

A

Kappa

149
Q

natural opioird?

A

Morphine

Codeine

150
Q

which opioides does not cause addiction?

A

Methadon

codein

151
Q

alcohol with opioids causes?

A

serum peak concentration increases

152
Q

opioid with muscarinic effect?

A

miperidine

153
Q

opioid with NO CNS effect?

A

Loperamide

154
Q

opioid used in withdrawal after addiction

A

Methadone

Buprenorphine

155
Q

spinal analgesia opioid?

A

Nalbuphine

156
Q

General opioid SE

A
  1. Sedation
  2. biliary colic
  3. opioid induced hyperalgesia (increased nociception)
  4. Pseudo-allergy (Mast cell release without IgE)
  5. Constipation
157
Q

management of aspirin overdose?

A

Gastric lavage
activated charcoal
ventilation support
acid base managment

158
Q

when can you give aspirin to children?

A

Kawasaki vasculitis

159
Q

function of anti-gout medications?

A
  1. Decreased LTB4 - decreased migration of leukocytes and granulocytes
  2. decrease purin synthesis - decreased uric acid
  3. Urate oxidase enzyme - removes Uric acid
160
Q

NSAID effect on kidney?

A

Inhibit COX1 causing no PGE which normally dilates renal artery, decreased renal blood flow now activates RAAS causing hypertension.

161
Q

should you take non-selective NSAIDS with aspirin?

A

NO, they compete with aspirin in binding to COX- 1 interfering with aspirins antiplatelet function

162
Q

should you use aspirin in gout?

A

NO, it competes with uric acid in secretion so can further worsen hyperuricemia

163
Q

Antibody nomenclature?

A

UMAB is human
XIMAB is mixed
ZUMAB - non-human but humanized

164
Q

What are the 4 big groups of heart failure medications?

A
  1. Diuretics
  2. ACEI/ARB’s
  3. Direct vasodilators
  4. Sympatolytics
165
Q

what are the two classes of CCB?

A

Dihydropyridines (end with -dipin)

Non-dihydropyridines

166
Q

which class of CCB have the greater effect on SM and which on the heart?

A

Non-dihydropyridines more on the heart

Dihydropyridines more on smooth muscle

167
Q

Most rapid local anesthetic?

A

Articaine

168
Q

Lidocaine SE

A 
hypotension 
vasodilation 
excitation 
arrhythmia 
seizures
169
Q

Cocaine SE

A

hypertension
arrhythmias
seizure
coronary vasospasms

170
Q

Indirect acting sympathomimetics?

A

Ephedrine
Amphetamine
Thymidine

171
Q

Direct Alpha-1 agonist

A

Phenylephrine (direct Alpha-1)

172
Q

ions enhancing or decreasing effect of local anesthetics?

A

IC K increases effect

EC Ca decreases effect

173
Q

Bupivacaine SE

A

CV collapse

CNS toxicity

174
Q

inhaled corticosteroids?

A

Fluticasone

Budesonide

175
Q

cream corticosteroids?

A

fluocinolone

Mometasone

176
Q

drug used to test adrenal function?

A

Metyrapone is used and it blocks cortisol synthesis

177
Q

effect of mineralocorticoid and what is the drug?

A

Fludrocortisone
Increased Na+
Decreased K+ and H+
overall increase in BP and increase in pH

178
Q

three results of increased angiotensin?

A

ADH secretion
Aldosterone secretion
Vasoconstriction

179
Q

fludrocortisone antagonist?

A

Spironolacton

180
Q

locations of androgen synthesis?

A

ovary
male testis
adrenal cortex

181
Q

why give testosterone?

A 
Hypogonadism 
Hormone replacement 
Wasting syndrom for weight gain 
RBC production on some anemias 
Anabolic steroid misuse
182
Q

function of finasteride and bicalutamide?

A

It is an anti-testosteron as it inhibits 5a-reductase conversion of testosteron to DHT in tissue

183
Q

Goserelin and Degarelix function?

A

Goserelin: GnRH Agonist

Degarelix GnRH antagonist

184
Q

Androgen sideeffect?

A

Remember that in males it causes feminization due to feedback mechanism
Hepatocellular carcinoma
Jaundice
Elevated liver enzymes

185
Q

Diuretics with anti-androgen properties?

A

Spironolactone is also a androgen receptor antagonist

186
Q

when would you use and androgen antagonist and which one?

A

precocious puberty use Gosereli bec. of negative feedback

187
Q

what is the function of sildenafil? when can we use it?

A

Phosphodiesterase 5 inhibitor causing no cGMP to GTP so increased cGMP and relaxations - vasodilation.

Used in erectile dysfunction and pulmonary HT

188
Q

why would we give estrogen replacement?

A 
Post-menopausal replacement 
hypogonadism 
contraception 
dysmenorrhea 
uterine bleeding
Acne
189
Q

function of anastrazole?

A

Aromatase inhibitor

190
Q

SERMS functions?

A

Tamoxifen (xbreast, +bone, +endopetrium)
Raloxifene (xbeast, +bones, no endometrium)
Clomiphene ( CNS antagonist causing no neg. feedback increasing FSH and LH)

191
Q

drug having a full antiestrogenic effect in all tissues?

A

Fulvistrant

192
Q

contraindications of estrogen?

A

History of thromboembolism
Estrogen dependent neoplasm
Serve liver disease

193
Q

anti-progesterons?

A

Mifepristone

Ulipristal

194
Q

causes of hypothyroidism?

A 
Hashimoto 
Congenital 
Drug induced 
iodine deficiency 
Malignancy
195
Q

halv life of levothyroxine?

A

7 days

196
Q

what are the thee ways we can treat hyperthyroidism?

A
  1. surgery
  2. Interfere with hormone synthesis
  3. Modify tissue receptors
197
Q

function of propylthiouracil and thiamazole?

A

inhibit TOP causing to hormone synthesis

Also inhibit T4-T3 in tisse

198
Q

when dues anti-thyroid drugs start to work?

A

takes 3 weeks because stored hormones must be used up first

199
Q

when do we use radioactive iodine?

A

hyperthyroidism Ir causes destruction of gland

200
Q

what other drugs should you give in hyperthyroidism?

A

beta blockers

201
Q

GH agonist?

A

somatostatin SC injection

202
Q

GH antagonist?

A

octreotide

203
Q

Prolactin antagonist?

A

Bromcriptine binding to D2 receptor

204
Q

Bromocriptine SE?

A

GI
Postural HT
CNS

205
Q

Desmopressin mechanism?

A

Antidiuretic replacement therapy in the management of central diabetes insipidus
Treatment of nocturia
Used to prepare patients with mild hemophilia or
von-Willebrand disease for elective surgery

206
Q

why is desmopressin used in hemophilia A and VW disease?

A

Stimulate release of VW factor and factor VIII from endothelial cells

207
Q

daily requirement of iodine?

A

150 ug

208
Q

octreotide SE?

A

GI
Steatorrhea
Gallstone
Cardiac Conduction abnormalities

209
Q

rapid acting injected insulin?

A

Glulasin
Aspart
Lisprio

210
Q

injected moderate acting insulin?

A

NPH insulin

Regular insulin

211
Q

Long-acting injected insulin?

A

Detamer

Glargin

212
Q

how long does Glargin insulin last?

A

24h

213
Q

Dietary insulin release?

A

GLP and GIP already in the oral cavity so increase release

214
Q

what is the difference between endo and exogenous insulin distribution concentration?

A

endogenous goes through the portal circulation where 50% is removed, exogenous is 100% what you administer

215
Q

insulin requirements for an average person/day

A

30-80 U/day

216
Q

what are the two types of insulin secretions?

A
  1. Post prandial

2. Basal

217
Q

insulin administration types?

A
  1. Sliding scale (used in very unstable patients at hospital)
  2. Basal + bolus (most used method for IDDM)
218
Q

how does sulfonylureas cause insulin secretion?

A

They bind potassium channels closing them causing depolarization

219
Q

how does meglitinides cause insulin secretion?

A

They bind potassium channels closing them causing depolarization

220
Q

what is very dangerous with meglitinides and sulfonylureas?

A

they cause insulin secretion independentof glucose level and can quickly couse severe hypoglycemia

221
Q

Function of Liraglutide?

A

GLP-1 analogue (glucagon like peptide. It decreases glucagon release and gastric emptying and increases insulin release and satiety

222
Q

Function of vildagliptin?

A

inhibit DPP-4 degrading of GLP-1 causing increased serum level of GLP-1

223
Q

Acarbose function?

A

Inhibit Alpha-cells in Gi causing decreased glucose absorption

224
Q

PTH function?

A

Increase Ca
Decrease Pi
Stimulate kidney to produce calcitriol

225
Q

what is the active form of vitamin D and where is it synthesized?

A

Calcitriol synthesized in the kidney

226
Q

what does vit D do?

A

Increase Ca2+ AND Pi absorption from GI

227
Q

can you give cholecalciferol in vitamin D deficiency if the patient has liver failure or renal failure?

A

No, cholecalciferol mist be turned into calcitriol in the kidney to function

228
Q

estrogen effect on bone?

A

bindes estrogen R on bone inhibiting RANK -L secretion and no activation of osteoclasts

229
Q

DEXA scan t-score for osteoporosis?

A

< -2.5

230
Q

action of bisphosphonates?

A

inhibit mevalonic acid pathway causing OC inhibition

231
Q

SE of zolendronates taken IV?

A

osteonecrosis of the jaw

232
Q

common SE with aspirin?

A

Peptic ulcers

233
Q

Aspirins antiplatelet mechanism?

A

inhibit COX so no PGE and TxA2 so no platelet aggregation and activation

234
Q

antiplatelet drug in acute coronary syndrom and PCI?

administration?

A

Abciximab binding to GP IIb/IIIa receptors

Must be given IV due to very short half-life (30 min)

235
Q

when do we use Clopidogrel, Prasugrel and ticagrelor?

A

Transient ischemic attack
Stroke
Unstable angina
Stent implantation

236
Q

mechanism of heparin?

A

Bind fX and AT-III inhibiting thrombin formation

237
Q

difference between HMWH and LMWH?

A

It’s the tail that bind to AT-III and in LMWH there is a short tail so cannot bind AT-III just fX

238
Q

Heparin tail is made up of?

A

Glycosaminoglycans

239
Q

LMVH?

A

Daltaperin

Fondaparinux ( has no tail)

240
Q

Clotting times normally and with heparin? when is it to long?

A

normal: 30-40s
Heparin: 50-90s
Too long: > 100s

241
Q

Heparin SE?

A

prolonged bleeding
Thrombocytopenia
Osteoporosis

242
Q

clotting time measured if heparin is given?

A

activated Partial Thromboplastin Time (aPTT)

243
Q

what clotting factors are inhibited by warfarin?

A

remember the year 1972

10
9
7
2

244
Q

how do we measure prothrombin time? and what are th values?

A

as standardized INR which should be:
Normal: <1.1
w/warfarin: 2-3

245
Q

Does Protamin work as an antidote for LMWH?

A

No, only UFH

246
Q

Function of filgrastim in anemia?

A

Stimulate G-CSF receptors

Granulocyte colony stimulating factor

247
Q

what can we see an increase of in the blood if iron deficiency anemia?

A

Transferrin in increased in serum and apoferritin which stores iron is decreased

248
Q

chronic iron overload can lead to…

A

hemochromatosis causing damage on the heart, liver and pancreas

249
Q

acute iron overdose can cause…

A 
necrotizing gastritis
abdominal pain 
constipation/diarrhea 
lethargy
dyspnea
250
Q

how is B12 absorbed?

A

binds IF secreted by the stomach and absorbed in ileum

251
Q

anemia caused by B12 deficiency?

A

Megaloblastic anemia

252
Q

where is folic acid absorbed?

A

Proximal Jejunum

253
Q

anemia in folic acid deficiency?

A

megaloblastic anemia

254
Q

what can folate deficiency cause in embryos?

A

neural tube defects

255
Q

What does blood gass partition coefficient meand in regards to inhaled anesthetics?

A

Refers to solubility of the drug

The higher GPC the more soluble

256
Q

What is the relationship between function and solubility of inhaled anesthetics?

A

High solubility = delayed onset

Low solubility = rapid onset

257
Q

what is minimal alveolar concentration (MAC) referred to in inhaled anesthetics?

A

dose of anesthetic causing 50% of patients to become non-responders to pain

258
Q

inhaled anesthetics effect on respiration?

A

respiratory depressors

259
Q

non solubel inhaled anesthetics?

A

N20

260
Q

Soluble anesthetics (several desiliters of ice)

A

Isoflurane
Desflurane
Sevoflurane

261
Q

why does the soluble inhaled anesthetics have a slow onset?

A

they bind blood proteins so we must wait for saturation before they give effect which takes more time then the non-soluble

262
Q

Ultra-short acting anesthesia?

A

Thiopental - surgical anesthesia within 1 min

263
Q

which IV anesthesia should be used in CV patients?

A

etomidate

264
Q

which IV anesthesia produces a dissociative state?

A

Ketamines, they are awake but has amnesia

265
Q

which IV anesthesia must have an antidote due to PO respiratory depression?

A

Midazolam - have Flumazenil ready!!

266
Q

which IV anesthesia should be used in head trauma eith increased IC pressure?

A

Thiopental

267
Q

which IV anesthesia should not be used in asthma patients?

A

Thiopental causes bronchoconstriction due to histamin release

268
Q

dose dependent effect of benzo’s?

A

Low: sedation, anxiolytics
Moderate: hyposis
High: Anesthesia

269
Q

What are the non-Benzo normally used to treat? except one of them..

A

Sleep disorders mostly, except Buspirone which is a serotonin agonist used in general anxiety

270
Q

Ramelteon bindes to which receptor?

A

Melatonin (MT) receptors

271
Q

function of the 5-HT1a receptor?

A

regulates sleep, feeding and anxiety

272
Q

NT causing depression?

A

decrease in the NT serotonin, dopamin and NE

273
Q

Indications for SSRI?

A

Depression to increase seretonine and remove symptomes of depression

274
Q

seretonin syndrom?

A

Muscle rigidity
Hyperthermia
CV instability
Seizures

275
Q

SE of Ramelteon?

A

Testosterone depression and increased prolactine

276
Q

5 fluorouracil specific SE?

A

Cardiotoxicity

Hand foot syndrom

277
Q

5 fluorouracil indication?

A

COLORECTAL first line!!!

breast cancer in combination

278
Q

chemo Cytarabine specific SE?

A

Liver dysfunction

279
Q

Indication for chemo Cytarabine?

A

NON SOLIDS!!
Leukemia (AML, ALL)
Lymphoma (non-Hoskin)

280
Q

Drug interaction between Allopurinol and 6 Mercaptopurine?

A

6 MP is metabolized by xanthine oxidase but this enzyme is inhibited by Allopurinol, which is often given to cancer patients due to high risk of tumor lysis syndrom in order to prevent gout. BE carefull with 6MP dose when allopurinol is also administered

281
Q

6 mercaptopurine indication?

A

Acute lymphoblastic leukemia (ALL)

282
Q

Severe SE of cyclophosphamides?

A
  1. The toxic metabolite Acrolein causing hemorrhagic cystitis
  2. Pulmonary fibrosis
283
Q

difference between barbiturates and benzos?

A

Barbiturates bind GABA receptors even if there is no GABA NT

284
Q

which Benzo’s can you use if liver failure?

drink a LOT

A

Temazepam
Oxazepam
Lorazepam

Can be used due to glucoronidation as metablism not in the liver

285
Q

Why is SNRI and SSRI the first line choice in depression?

A

no cholinergic and adrenergic SE

286
Q

Seizure types in epilepsy?

A

Tonic: freeze
clonic: contract
tonic-clonic freeze then contract
Absence: loose conciseness for some time

287
Q

status epilepticus?

A

seizures > 5 min

288
Q

which enzyme is inhibited by vigabatrin?

A

GABA transaminase

289
Q

cause of Parkinson and symptoms?

A 
Loss of dopamine 
Bradykinesia (slow) 
Hypokinesia (loss of range) 
Dyskinesia (involuntary movement) 
rigidity 
No loss of strength
290
Q

what is a tocolytic agent?

give 4 drugs?

A 
used to delay labor 
Atosiban 
Terbulatine 
Mg 
Ethanol
291
Q

what are the three areas affecting the vomiting center?

A

Vestibular
Pain via GI
Chemoreceptor trigger zone

292
Q

receptor in the vomiting pathway?

A

Muscarinic 1 receptor

293
Q

receptors antagonizing the vomiting center?

A

5-HT 3
D2
M1
NK1

294
Q

How can blocking D2 receptors provide a pro-kinetic effect in the GI?

A

D2 activation inhibit cholinergic response, and by removing this we increase the cholinergic response

295
Q

Irritant and stimulant laxatives?

A

Sennosides (irritates)

Bisacodyl (stimulant)

296
Q

bulkforming laxative?

A

Plant fibers

297
Q

osmotic laxatives?

A

MgSO

Lactulose

298
Q

Lubricant laxatives?

A

Parafin oil

299
Q

definition of constipation?

A

less then 3 stools a week

300
Q

treatment of constipation?

A

Follow this in order:

  1. first change lifestyle
  2. then try osmotic laxatives
  3. if not then use stimulant laxatives
301
Q

Two drugs used in diarrhea?

A

Diphenoxylate
Loperamide
Synthetic opioids binding to u-receptor inhibiting Ach release

302
Q

what is the function of imidazole receptors?

A

I1 is involved in inhibition of the sympathetic nervous system to lower blood pressure without binding to an alpha receptor

303
Q

which of the alpha 1 receptor blocker does not cause reflex tachycardia?

A

Urapidil sice it has CNS effect

304
Q

selective alpha 2 blocker?

A

Mirtazapine used in depression

305
Q

Non-selective B-blockers?

A

Propranolol
Pindolol
Sotalol
Timolol

306
Q

B1 selective B-blockers?

A 
BIEAM 
Bisprolol 
Esmolol 
atenolol 
Metoprolol
307
Q

what the problem with high doese B1 selective b-blockers?

A

they become non-selective

Pharmacology (3 decks)

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