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Patho 1 (PATH 254) > Mod 1 Respiratory diseases + pharmacology > Flashcards

Mod 1 Respiratory diseases + pharmacology Flashcards

1
Q

What are 2 parasympathetic receptors

A

Nicotinic receptors

Muscarinic receptors

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2
Q

What is a significant trait of Ligand-gated ion channel?

A

They are fast acting/stimulate quickly

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3
Q

Which parasympathetic receptor takes longer to take action/see change?

A

Muscarinic Receptors

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4
Q

-ases ending is usually associated with what?

A

Enzymes -> that breakdown certain things?

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5
Q

What role does Cholinestrate have in the body?

A

Breakdown enzymes, to be specific Acetylcholine

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6
Q

What are the terms used to describe nerve fibres that stimulate or inhibit the sympathetic nervous system?

A

Sympathomimetic - Stimulate

Sympatholytic - inhibit

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7
Q

What nerve fibres stimulate or inhibit the parasympathetic nervous system?

A

Parasympathomimetic - Stimulate/mimic

Parasympatholytic - inhibit/block

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8
Q

Which neurotransmitters/receptors stimulate or inhibit the sympathetic nervous system?

A

Adrengic - stimulate

Antiadrenergic - inhibit

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9
Q

Which neurotransmitter/receptors stimulate or inhibit the parasympathetic nervous system?

A

Cholinergic - stimulate

Anticholinergic - inhibit

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10
Q

Afferent is a sensory nerve signal that carry’s signals…

A

From the periphery to the CNS

(toward the body)

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11
Q

Efferent motor signals carry signals to…

A

From the CNS site to action (away from the body)

Efferent nerve fibres transmit commands from the CNS

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12
Q

What are the 2 exclusive neurotransmitters of the Peripheral Nervous System (PNS)

A

Acetylcholine

Norepinephrine

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13
Q

Acetylcholine is released by…

A

Sympathetic and parasympathetic preganglionic neutrons

Parasympathetic post gangilionic neutrons

Somatic motor neutrons

Sympathetic post ganglion if neurons that innervate sweat glands

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14
Q

Norepinephrine is released by…

A

All post ganglion neurons of the sympathetic nervous system except those innervating sweat glands

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15
Q

Neurophysiology of the PNS: Where does Acetylcholine stimulate nicotinic receptors?

A

On sympathetic and parasympathetic postganglionic neurons at the neuromuscular junction

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16
Q

Neurophysiology of the PNS: Where does Acetylcholine stimulate muscarinic receptors?

A

On sweat glands and on tissue innervated by parasympathetic postganglionic neutrons

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17
Q

Neurophysiology of the PNS: Where does Norepinephrine stimulate Alpha and Beta adrengeric receptors?

A

on tissues innervated by sympathetic postganglionic neutrons

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18
Q

Why do Muscarinic Receptors take longer to see changes?

A

G protein coupled receptors see larger change than ion channels

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19
Q

Which sites are affected/stimulated by Muscarinic receptors?

A

Parasympathetic terminal sites:

-Exocrine glands (i.e exocrine glands, salivary, bronchial mucus glands)

-cardiac muscle

-GI smooth muscle

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20
Q

Why is degradation of acetylcholine important?

A

Prevents unwanted activation of neighbouring neutrons or muscles

ensure proper timing of signalling at the postsynaptic cell.

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21
Q

What are Adrenergic receptors identified as?

A

Alpha and Beta Receptors sympathetic receptors; they’re G-coupled receptors

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22
Q

Where can Alpha 1 receptors be found?

A

Heart
+
Smooth muscles:
-Bronchial smooth muscle
-Vascular smooth muscle
-Intestinal smooth muscle
+
Liver

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23
Q

What are some of the functions of Alpha 1 receptors

A

Contraction of smooth muscle

  • Increased inotrophy (contraction) and excitability of the heart without increasing hr
  • Glycogenolysis and glucenogensis
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24
Q

What action does Alpha 2 receptors have?

A

Inhibitory

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25
Q

what are some common results of Alpha 2 activation?

A

Reduce insulin secretion

Decrease in norepinephrine release

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26
Q

Why do Alpha 2 receptors further inhibits norepinephrine release?

A

Alpha 2 receptors provide a negative feedback control mech

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27
Q

Where are beta 1 receptors located

A

Heart and kidneys

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28
Q

what response can you expect by the release of Beta 1 receptors?

A

Increased chronotropy and inotrophy

Increased AV node conduction velocity

Increased overall heart rate (SA node)

Increased Renin secretion via the kidneys

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29
Q

Where are Beta 2 receptors located?

A

Dilation of bronchial smooth muscle

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30
Q

What is an example of a Beta 2 receptor response?

A

Dilation of bronchial smooth muscle

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31
Q

Where are Beta 3 receptors located?

A

adipose tissue

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32
Q

what do Beta 3 receptors activate?

A

Lypolysis

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33
Q

Therapeutic effect

A

The intended effect of a drug

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34
Q

What does Efficacy reflect about drug use?

A

The ability of a drug to produce a desired effect

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35
Q

What does affinity reflect on about drug use?

A

The tendency of a drug to combine with a matching receptor

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36
Q

Acetylcholine is used primarily for which system?

A

The parasympathetic nervous system
(preganglionic)

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37
Q

Post ganglionic innervates which group?

A

Muscles or sweat glands associated with the sympathetic nervous system.

Usually to help regulate our body.

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38
Q

What does the therapeutic dose refer to?

A

The amount of agent that provides the desired clinical effect

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39
Q

What does bioavailability refer to?

A

The amount of agent that reaches systemic circulation to produce th effect required.

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40
Q

What factors affect bioavailability?

A

Absorption, route of admin, and metabolic

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41
Q

what is a loading dose?

A

an initial dose of agent that may be given at the beginning of a course of treatment

it is followed up by a maintaince dose.

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42
Q

Why do we admin ventolin for heart related issues?

A

It is primarily a Beta 2 agonist, but can still bind with Beta 1 sites at the heart.

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43
Q

Why are loading doses useful?

A

they’re useful for drugs that eliminate from the body slowly (long systematic half-life)

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44
Q

Maintaining dose

A

amount of agent required to keep a desired mean steady state concentration in the tissues

TLDR; Top up

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45
Q

What does half-life refer to?

A

Time necessary to reduce an initial dose by half

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46
Q

What factor effects half-life in relation to dosage?

A

Affected by plasma protein binding, metabolism, and elimination

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47
Q

Median lethal Dose (LD50)

A

does at which 50% of the test animals die

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48
Q

Median effective dose (ED50)

A

Dose at which 50% of the test animals show the desired effect

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49
Q

Therapeutic index (TI)

A

The ratio of (LD50)/(ED50) gives a relative as to the safety of the drug

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50
Q

How do you know how toxic a drug is with the TI ratio?

A

the greater the difference between ED50 and ED50 the safer the drug.

the close to TI is to 0 = more toxic

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51
Q

Agonist vs Antagonist response

A

Agonist: Excite
-full and partial agonists

Antagonist: inhibit or stop.

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52
Q

Define Synergism

A

Occurs when 2 drugs together produce an effect greater than the 2 drugs along could produce

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53
Q

Define potentate

A

1 drug has no affect but can increase the effect of the other drug.

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54
Q

What does tolerance infer about drug use?

A

Progressive decrease in effectiveness over time, requiring increase the drug amount to produce the same effect due to increased metabolism of the drug by the body

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55
Q

Tachyphylaxis

A

Repeated admin of the same dose of a drug results in reduced effect of drug over time

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56
Q

What does hypersensitivity mean in relation to drug use?

A

An allergic or immune-mediated reaction to a drug

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57
Q

What is a Teratogens effect?

A

Drugs that are known to cause birth defects

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58
Q

Carcinogens

A

drugs/substances that produce cancer (or increase) risk of developing cancer

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59
Q

Phases of drug action (slide 9) from “the nervous system”

A
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60
Q

Define pharmacokinetic action?

A

How drugs get to where it needs to be
- i.e absorption or metabolism

(the effect of drug on body)

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61
Q

What is pharmacodynamic action?

A

how a drug produces (or doesn’t) a effect.

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62
Q

What are 4 routes of drug admin?

A

Enteral (tablets, capsules, liquids)

Parenteral (injection)

Inhalation

Transdermal/topical (topical)

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63
Q

What is the purpose of lidocaine?

A

A topical sedative/anesthetic

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64
Q

Installation route: Lean or Navel?

A

Direct admin of an agent via the ETT to obtain a systemic/local effect.

Lean is used when IV/IO access is not an option.
-lidocaine, EPI, Atropine, Narcan

NAVEL: Narcan, atropine, ventolin, EPI, lidocaine.

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65
Q

What is IO access?

A

Typically drilling down to bone when a line can’t be inserted

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66
Q

What are 2 ways neurotransmitters can effect agents?

Edit

A

direct acting: binds directly to a neurotransmitter to produce a excitatory/inhibit response

indirect acting: does not interact with a receptor but with the neurotransmitter instead

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67
Q

Agonist vs Antagonist

A

Agonist: produce a excitatory response (via binding) to a a full or partial effect

Antagonist: inhibit the ability of their targets to be activated (or inactivated)

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68
Q

What does Cholinergic pharmacology reflect about the properties of acetylcholine?

Edit

A

Generally involve the neuromuscular junction (interface between nervous system muscular system), the autonomic nervous system, particularly the parasympathetic system, and the CNS.

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69
Q

Parasympathomimetics are affected by what?

A

Cholinergic agonist or Cholinergic

70
Q

why is Methacholine is used during pulmonary function tests?

A

reflects bronchoconstriction in the lungs to measure the response by irritation response.

TLDR; a diagnostic tool

71
Q

Nicotinic agonist vs Nicotinic antagonist?

A

paralytic response

(insert more later)

72
Q

Parasympatholyics are referred to as?

A

cholinergic antogists = anticholinergic

73
Q

Andrenrgic pharmacology modulate which functions?

A

vital functions, rate and force of contraction, resistance of blood vessels, and release of insulin and the breakdown of fat (sympathetic response)

74
Q

Adregergic pharmacology act on which pathways?

A

mediated by endogenous catecholamines norepinephrine, epinephrine, and dopamine

75
Q

In the ICU, what is the primary PHARMACOLOGICAL way to affect blood pressure?

A

Admin of norepinephrine (bc it is a A1 and A2 agonist)

76
Q

Effect of Adrengeric agents?

A

Act on pathways mediated by endogenous catecholamine: norepinephrine, epinephrine, and dopamine.

They modulate vital functions such as:
-heart contraction (rate and force)
-resistance of blood vessels (and bronchioles)
-release of insulin
-breakdown of fat (sympathetic response)

77
Q

what are Sympathomimetics?

A

Adrenergic agonists:

  • Norepinephrine (a1 & b1) agonist
  • Epinephrine ( (both a1 + a2 and b1 + b2 agonist)
  • phenylephrine (a1 agonist)
  • Dobutamine (b1 agonist)
  • salbutamol (b2 agonist)
78
Q

What are sympatholytics?

A

Adrenergic antagonists

-Doxazosin (a1 antagonist)
- metoprolol (b1 antagonist)

79
Q

What is a function of Alpha 2 receptors ?

needs an edit

A

Alpha 2 acts a negative feedback loop

  • stop the release of norepinephrine
  • activation decreases in BP
80
Q

Define Obstructive Lung Pathology

A

Diseases that reduce a patients ability to exhale fully

  • Characterized by increased airway resistance as a major contributing factor
81
Q

Define Restrictive lung pathology

A

Characterized by a loss of lung volume

Major contributing factor is a decrease in pulmonary compliance

82
Q

What are examples of obstructive lung pathology or factors obstructive process?

A

Excess mucous
Air trapping (dynamic compression)
Tumour
Swelling (such as edema)

83
Q

3 types of obstruction

insert image from slide 6

A

Intraluminal
Extramural
Intramural

84
Q

Intraluminal obstruction

A

Something inside the airway lumen blocking/narrowing airway

i.e foreign bodies or secretions

85
Q

Extramural obstruction

A

external pressures causes airway narrowing

i.e enlarged lump nodes, carcinoma, lymphoma

86
Q

Intramural obstruction

A

Lesions inside the bronchial wall, swelling.

Neoplasm

87
Q

Examples of restrictive pathology or causing factors?

A

Pulmonary fibrosis
pulmonary edema (create fluid or consolidation)
pneumonia

88
Q

Is the compliance and elastance relation inverse or direct?

A

As one increases, the other decreases

89
Q

Can diseases be both obstructive and restrictive characteristics?

A

Yes, think about edemas or swelling.

90
Q

Which of the 3 airway obstruction estiologies cause upper airway obstruction or lower airway obstructions?

A

non-cartilougs airway = lower

cartilaginous airway = upper

91
Q

Lower airway obstruction causes

A

distal airway and also lay weakening (emphysema)

Excessive bronchial secretions (consolidation)

Bronchospasm

all end with a potential airway collapse or potential hypoxemia from blockage

92
Q

4 cardinal signs of upper airway obstruction

A

hot potato voice (muffled)
difficulty in swallowing secretions
dyspnea
strider

strider is the only that may result in immediate obstruction

93
Q

inhalation sound or exhalation that refer to obstruction (lack of air exchange)

A

exhalation = wheezes
inspiration = strider

94
Q

Intrapulmonary conditions leading to decreased compliance (7)

A

-Lung compression

-atelecasis

-consolidation

-calcification (tuberculosis, asbestosis)

-Fibrosis (pneumoconiosis, chronic interstitial lung disease i.e sarcoidosis)

-Bronchogenic tumor (squamous cell carcinoma)

-Cavitation (tuberculosis or lung abscess)

95
Q

Extrapulmonary conditions leading to decreased lung compliance

A

pleural disorders; restriction of lung expansion by something occupying the pleural space

TLDR;something that’s gonna compress the lungs

-chest compression

-obesity

-deformities of spine

-deformities of the chest cage

96
Q

Extrapulmonary conditions of nerves that decrease compliance

A

interference of nerve transmission (or decreased resp. muscle function)
-aka issues with the diaphragm

inability of generate normal resp. pressures
-decreased TLC, increased RV, normal FRC

normal lung/ chest wall compliance
-if you don’t inhale, you can’t exhale it

97
Q

What does Intrapulmonary refer to w/restrictive lung pathology

A

Interstitial disorders (issues w/lung tissue itself)
-results in decrease in compliance of lung tissue

i.e surfactant dysfunction

98
Q

What does extrapulmonary refer to w/restrictive lung pathology

A

Pleural, neuromuscular, or skeletal/thoracic issues

99
Q

Clinical manifestations of obstructive disease

A

-Dyspnea on exertion
-productive cough
-hyper-resonant percussion notes
-wheezing
-Diminished breath + heart sounds
-prolonged expiration

100
Q

Clinical manifestations of restrictive lung disease

A

-Dyspnea on exertion
-non-productive cough
-hypo-resonant or normal percussion notes
-fine bilateral inspiratory crackles
-rapid shallow breathing

101
Q

What does Idiopathic pulmonary fibrosis?

A

sound like if you rub your hair beside your ear or velcro separation

102
Q

Andrenergic agonists vs antagonists effects?

A
103
Q

What is Obstructive lung pathology characterized by?

A

Decreased ability to exhale fully

  • Increased airway resistance is the major contributing factor for obstructive diseases
104
Q

What is restrictive lung pathologies characterized by?

A

loss of lung volume

  • Decreased pulmonary compliance is one major contributing factor in restrictive process
105
Q

Traits of Type 1 respiratory failure?

A

-Hypoxemic failure (not enough O2 in blood)

-PaO2 (arterial) less than 60mmHg @ room air

-most common cause is V/Q mismatch

106
Q

Traits of Type II respiratory failure?

A

-Hypercapnic failure or ventilatory failure (too much CO2)

-PaCO2 greater than or equal to 50mmHg

107
Q

Primary causes of hypoxemia

A

-Diffusion defect
-hypoventilation
-hypoxic environment
-anemia
-CO poisoning
-hemoglobin dysfunction

108
Q

Signs for impending respiratory failure type II?

A

-Demand for CO2 elimination is beginning to reach capacity

-Tachypnea with normal PaCO2 and normal pH

109
Q

Chronic respiratory failure type I

A

progressive lung pathologies that damage the AC interface.

Patients have > 60mmHg @ room air at all times.

110
Q

Describe the complications of Chronic respiratory failure type II

A

Progressive lung pathologies continue to reduce efficient ventilation.

when COPD is involved (or obesity-hypoventilation syndrome) it can prompt a renal response.

-Kidneys retain HCO3 to elevate low blood pH
-renal system takes over when it isn’t efficient, it compensates.

111
Q

Acute on chronic respiratory failure

A

An acute respiratory failure type II superimposed on chronic respiratory failure type II

Patients with chronic hypercapnic respiratory failure are at a significant risk of this condition

112
Q

Late vs early inspiratory crackles?

A

excessive secretions vs atelectasis

113
Q

Idiopathic pulmonary fibrosis (IPF)

A
114
Q

Why can pneumothorax cause cardiac arrest?

A

extra pressure pushing on one side can affect if the heart contracts or not. Blood cannot be pumped properly/effectively

115
Q

fine bilateral inspiratory crackles is indicative of what?

A

atelectasis

116
Q

FEV of a normal person is typically what percentage in comparison to someone with COPD?

A

80% in a healthy person, 30% for someone with COPD

117
Q

Primary causes of hypoxemia

A

(Perfusion w/no ventilation) pulmonary shunt:
ARDS, pneumonia, atelectasis, pulmonary edema

-can cause refractory hypoxemia: when SpO2 is not affected w/oxygen therapy because of shunt. no gas is transferring

Hypoventilation: OD, sedation, PNS conditions (guillain-barre)

V/Q mismatch (unequal distribution of ventilation and perfusion) : COPD, PE,

Decreased inspired O2: high altitude low O2 content, enclosed breathing spaces

118
Q

How do you know that a person is expierecing a chronic . failure rather than a partial compensation from an ABG?

A

larger or lower than normal BE usually indicates that a ABG is chronic rather than acute/partial response

119
Q

what could a Acidosis or alkalosis tell us about a persons breathing?

A

Acidosis = hypoventilation (breathing too slowly)

Alkalosis = hyperventilation (breathing too fast)

120
Q

Acute resp. failure type II vs. Chronic resp. failure type II

A

Acute:
pH decreases by 0.08 for every 10mmHg increase in PaCo2

Chronic:
pH decreases 0.03 for every 10mmHg increase in PaCO2

Acute on chronic falls between those values.

121
Q

For chronic patients with a abnormal ABG (but normal for them), what value do you pay to attention to for change?

A

pH

122
Q

What does the acronym LEAN represent?

A

Drug admin when IV/IO access is not a option for the following drugs:

-Lidocaine
-Epi
-Atropine
-Narcan

emergency drugs to “lean” on

123
Q

Which meds can be administered via endotracheal tube

A

LEAN

124
Q

What action does Lidocaine have?

What is its main use?

A

Action: Suppresses automaticity of ventricular cells, decreasing diastolic depolarization and increasing ventricular fibrillation threshold.

USES: Ventricular arrhythmias, topical/local anesthetic

Extra: Bonus: Produces local anesthesia by reducing sodium permeability of sensory nerves, which blocks impulse generation and conduction.

125
Q

Epinephrine action and use?

A

ACTION: Stimulates alpha- and beta-adrenergic receptors, causing relaxation of cardiac and bronchial smooth muscle and dilation of skeletal muscles.

USE: bronchodilation; anaphylaxis; hypersensitivity reaction; Acute asthma attack; Chronic simple glaucoma

126
Q

Atropine sulfate action and use?

A

ACTION: Inhibits acetylcholine at parasympathetic neuroeffector junction of smooth muscle and cardiac muscle
-blocking sinoatrial (SA) and atrioventricular (AV) nodes to increase impulse conduction and raise heart rate.

USE: Decreases respiratory secretions, treats sinus bradycardia, reverses effects of anticholinesterase medication

127
Q

Naloxone (Narcan) action and use?

A

ACTION: used to treat opioid emergency (overdose)

USE: Opioid induced toxicity; opioid-induced respiratory depression; used in neonates to counteract or treat effects from narcotics given to mother during labor

128
Q

What does the Pharmacology pneumonic “NAVEL” represent?

A

NARCAN, ATROPINE, VENTOLIN, EPI, LIDOCAINE

129
Q

What do receptors at skeletal neuromuscular junctions and what kind of receptors are they?

A

Muscle activation.

cholinergic receptors

130
Q

What do cholinergic receptors in the CNS (brain) do?

A

leads to excitation

131
Q

How many Muscarinic receptors are there?

A

5, m1-m5

132
Q

Where are M2 receptors found?

A

The heart, activation causes bradycardia

133
Q

Where are M3 receptors found?

A

Smooth muscles:
-bronchial and vascular smooth muscle
-mucous glands
-mast cells

134
Q

What do muscarinic 3 (m3) receptors do?

A

-Bronchoconstriction
-increased mucus production
-mast cell degranulation

135
Q

Alpha (⍺) 1 function and location

A

Vasoconstriction.

found in peripheral vascular smooth muscle

136
Q

Alpha (⍺) 2 function and location

A

Vasodilation; activation causes less norepinephrine.

centrally located

137
Q

Beta (𝛃) 1 function and location

A

Increases heart rate and contractility.

found on the heart.

138
Q

Beta (𝛃) function and location

A

Bronchodilation and vasodilation

found on bronchial and vascular smooth muscles

139
Q

Dopaminergic function and location

A

Multiple functions: vasoconstriction, increased HR, CNS excitement

chemically similar to norepi and can activate alpha and beta receptors.

found throughout the body.

140
Q

What are non-depolarizing neuromuscular blockers commonly used as?

A

Muscle relaxants

141
Q

Where are nicotinic receptors found?

A

autonomic ganglia, neuromuscular junctions , and CNS

142
Q

What are cholinergic receptors?

A

Nicotinic

Muscarinic

143
Q

Receptors for the parasympathetic nervous system?

A

Muscarinic and nicotinic

144
Q

Receptors for the sympathetic nervous system?

A

Alpha, beta, and dopaminergic

145
Q

What are neurotransmitters for the parasympathetic nervous system?

A

Acetylcholine at all sites

146
Q

What are neurotransmitters for the sympathetic nervous system?

A

Acetylcholine at ganglionic

Norepinephrine at receptor

147
Q

3 common Neuromuscular blocking agents (NMB) agents?

needs a edit but not wrong

A

NMB = Neuromuscular blocking agents aka muscle relaxants = paralyzing agents

-Cisatracurium (nimbex)
-rocuronium (Zemuron)
-Succinycholine (Anectine) - not a non actually.

148
Q

What are 3 adrenergic receptors?

A

Alpha
Beta
Dopaminergic

149
Q

Adrenergic vs cholinergic receptors?

accuracy needs check

A

Adrenergic = sympathetic
-responds to epi/norepi

Cholinergic = parasympathetic
-responds to acetylcholine

150
Q

What is used to reverse opioid overdose

A

Naloxone (Narcan)
-opioid antagonist
-has a high affinity to opioid receptors preventing their activation

151
Q

Descending order for the pharynx?

A

nasopharynx
oropharynx
hypopharynx

152
Q

What 2 neurotransmitters does the PNS use?

A

Acetylcholine
Norepinephrine

153
Q

What releases norepinephrine?

A

All POSTganglionic neurons of the sympathetic nervous system except those innervating sweat glands

154
Q

Acetylcholine is released by?

A

sympathetic and parasympathetic PREganglionic neurons
-parasympathetic postganglionic neurons
-somatic motor neurons
-sympathetic postganglionic neurons that innervate sweat glands

155
Q

which of the following represent obstructive vs. restrictive disease?

A

A: obstructive
B: restrictive

156
Q

What obstruction is this?

A

Intraluminal obstruction

something inside airway blocking/narrowing it.
(foreign body or excretion)

157
Q

What obstruction is this?

A

Extramural obstruction

External pressure causing narrowing
(enlarged lymph nodes, carcinoma, tumor)

158
Q

What is a neoplasm?

A

basically a tumor like clot or blocking agent

159
Q

What obstruction is this?

A

Intramural obstruction.

Lesions inside bronchial wall
(swelling -> neoplasm)

160
Q

Parasympathetic postganglionic neurons release what neurotransmitters?

A

Acetylcholine

161
Q

sympathetic postganglionic neurons innervate sweat glands that release what neurotransmitter?

A

Acetylcholine

162
Q

Sympathetic and parasympathetic preganglionic neurons release what NT?

A

Acetylcholine

163
Q

All post ganglionic neurons of the sympathetic nervous system release what neurotransmitter?

A

Norepinephrine

(except those that stim sweat glands)

164
Q

Norepinephrine stimulates which adrenergic receptors @ the tissues, and which neurons are innervated?

A

Alpha and Beta

Sympathetic postganglionic neurons are innervated

165
Q

Difference between Nicotinic and muscarinic receptors?

A

Nicotinic has ion channels and is faster

Muscarinic takes longer to see changes
(G protein-coupled receptors)

166
Q

which enzyme breaks down acetylcholine?

A

Cholinesterase

167
Q

Why is the breakdown of acetylcholine important?

A

Prevents unwanted activation of neurons or muscle cells.

AND

Ensures proper timing of signals to postsynpatic cells

168
Q

What are 3 main phases of drug action other than administration?

A
  1. Pharmacokinetic phase: How drugs are absorbed, distributed, metabolized, and excreted by the body. It involves the processes by which drugs are transported throughout the body, how they are metabolized and eliminated, and how long they remain in the body.
  2. Pharmacodynamic phase: How drugs interact with specific receptors and produce their effects. It involves the relationship between drug concentration and response, the onset and duration of drug action, and the mechanism of action of drugs.
  3. Pharmacogenetic phase: How genetic variations influence drug response. It involves the study of genetic polymorphisms that affect drug metabolism and drug-target interactions, which can lead to differences in drug response between individuals.
169
Q

What is drug potentiation

A

Drug potentiation is the increased effect of a drug caused by another drug or substance that does not have an effect on its own.

170
Q

What is drug desensitization

A

Drug desensitization is the process by which a drug loses its effectiveness over time. This can be due to repeated use of the drug, leading to a reduction in the number or sensitivity of the receptors that the drug targets.

171
Q

What is Drug inactivation

A

Drug inactivation is the process by which a drug is rendered inactive or ineffective. This can occur through various mechanisms such as metabolism, excretion, or chemical reactions with other substances.

172
Q

What is Down-regulation

A

Down-regulation is the process by which the number of receptors for a particular drug or substance is reduced. This can occur as a result of prolonged exposure to the drug or substance, leading to a decreased response to the drug.

Patho 1 (PATH 254) (17 decks)

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