Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm 2024 > final exam > Flashcards

final exam Flashcards

1
Q

What is Pharmacokinetics?

A

What the body does to the drug
Ex) Half life after metabolizing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is Phamacodynamics?

A

What a drug does to the body
Ex) Increases heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is a poison?

A

a nonbiological substance that has negative effects on the body.
Ex) lead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is a toxin?

A

biological substance that has negative effects on the body (created from living substances)
Ex) poison mushrooms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a Stereoisomerism?

A

Isomers that differ in spatial arrangement of atoms, rather than order of atomic connectivity
(Optical Isomers or mirror images)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where does orthosteric bonding take place?

A

Binding at the primary active site on the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does allosteric bonding take place?

A

Drug binds to something other than the primary active site (Non-competitive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the relationship between strength and bond specificity?

A

It is inversely proportional.
The stronger the bond, the less specific the bond. The weaker the bond, the more specific the bond.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the pharmacokinetics acronym?

A

ADME
Absorption
Distribution
Metabolism
Excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is EC(50) and E(max) in the Drug Concentration Response Curve?

A

EC(50) is a point on the horizontal axis (Drug Concentration) where you see 50% of drug effects.
E(max) is a point on the curve where you max out the drug effects right before the curve plateaus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is K(d) and B(max) on the Drug Concentration Response Curve?

A

K(d) is a point on the horizontal axis (Drug Concentration) where 50% of the receptors are bound.
B(max) = max receptors bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between K(d) and EC(50)?

A

K(d) is referring to 50% of receptors bound vs EC(50) refers to 50% max effect of drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the relationship between an agonist and an allosteric antagonist?

A

You cannot outcompete an allosteric antagonist (non-competitive antagonist) because it’s not competing for the same receptor site.
If you keep increasing dose of agonist, you will only see a toxic effect - insurmountable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the relationship between an agonist and an allosteric activator?

A

An agonist and and allosteric activator (allosteric agonist) work together to get an increased result. An allosteric activator binds outside out of the active site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is an inverse agonist?

A

Acts as an antagonist; has a greater affinity to R(i) and stabilizes R(i) form.
Can shut down the downstream response.
Drops BELOW the constitutive activity
In practice, we will refer to as antagonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the relationship between K(d) and receptor affinity?

A

The relationship is inverse.
Low K(d) = high drug/receptor affinity; the drug binds well to the receptor.
High K(d) = low drug/receptor affinity; the drug doesn’t bind well to the receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is physiological antagonism?

A

Acts at a different receptor but produces an opposite physiological effect to that of the agonist
Effect: Does not compete with the agonist at the same receptor, but rather opposes its action through a different mechanism.
Example: Epinephrine (which increases heart rate) can act as a physiological antagonist to histamine (which decreases heart rate), even though they act on different receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe a graph in which an agonist is alone, an agonist + competitive antagonist, agonist + allosteric agonist, and an agonist + allosteric inhibitor

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe a graph showing constitutive activity, full agonist, partial agonist, antagonist, and an inverse agonist

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does therapeutic index correlate with drug safety?

A

The larger the therapeutic index the safer the drug is; est. margin of safety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

If pH>pKa

A

favors unprotonated form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

If pH<pKa

A

favors protonated form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If a weak acid is protonated it is…

A

Not charged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If a weak base is protonated it is…

A

charged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In order to cross barriers, a compound will want to be ____

A

uncharged; more lipid soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

If aspirin (weak acid) has pKa = 3.5, what form does it take in the stomach (pH = 1.5)?

A

Protonated, uncharged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

If aspirin (weak acid) has pKa = 3.5, what form does it take in the intestine (pH = 6.5)?

A

Unprotonated, charged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What medication for morning sickness was rejected by the FDA due to it causing Phocomelia?

A

Thalidomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 4 mechanisms of transmembrane signaling?

A
  1. Direct crossing to intercellular receptor (lipid soluble)
  2. Enzymatic action mediated by ligand binding
    a. Tyrosine kinase activated receptors
  3. Ligand gated ion channel
  4. G protein receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What receptors are intracellular?

A

Lipid soluble - uncharged
Gasses - easily diffuses through membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the steps to the GPCR cascade?

A
  1. Drug binds to receptor - activates alpha subunit of G protein (conformation change)
  2. G protein releases GDP and binds GTP
  3. G protein activates effector protein
  4. Secondary messenger cascade or ion conductance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Differentiate between desensitization and resensitization

A
  • When first give agonist, response jumps up, peaks, then declines (muted response with same amount of agonist) - desensitization
  • Stop giving agonist, then wait, then give agonist again → see same response - resensitization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the steps to the desensitization process

A
  1. Drug binds to receptor → promotes receptor interaction with G proteins in cytoplasm (closed → open conformation)
  2. Agonist-activated receptors phosphorylated by G protein-coupled receptor kinase (GPK), preventing receptor interaction with G protein → attracts beta-arestin (B-Arr)
  3. B-Arr receptor complex binds to coated pits, promoting receptor internalization
  4. 2 possibilities:
    Possibility 1 - resensitization (Drug falls off receptor→ phosphatase dephosphorylates receptor and receptor recyles back to cell membrane)
    Possibility 2 → degradation (Can’t get drug off of receptor → lysosome merges with drug/receptor complex → enzymes from lysosome degrade receptor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 2 signal types for ion channels?

A

Ligand and voltage gated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Differentiate ionotropic from metabotropic ligand-gated ion channels

A

Ionotropic - Ligand binding site and channel on same protein
Metabotropic - Ligand activates GPCR, second messenger activity opens channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

First-order elimination

A

Rate of elimination varies with concentration - clearance constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Zero-order elimination

A

Rate of elimination is constant, clearance varies with concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is meant by a high Vd?

A

The higher the Vd, the less amount of drug is in the blood; drug distributed in other areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the difference between elimination and clearance?

A

Elimination changes based on clearance (doesn’t change)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is clearance?

A

Ability of body to eliminate drug in relation to drug concentration in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is volume of distribution?

A

Apparent volume in blood
- How much did we give them vs how much stayed in blood (how much stayed in blood vs how much went to other areas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the main two components of standard drug dosing?

A

Volume of distribution and clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is rational dosing?

A

Goal – to achieve desired beneficial effect with minimal adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe what occurs in zero-order elimination

A

Occurs when the body’s ability to eliminate a drug has reached its maximum capability (i.e., all transporters are being used). As the dose and drug concentration increase, the amount of drug eliminated per hour does not increase, and the fraction of drug removed declines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What order of elimination do most drugs follow?

A

First-order

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the 4 parameters affective passive diffusion?

A

Molecular weight
pKa
lipid solubility
plasma protein binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How many half-lives are usually required for drug to achieve full effects?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the 4 phase I reactions?

A

Oxidation, reduction, dehydrogenation, and hydrolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Cytochrome 450 enzymes are _________

A

oxidases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Cytochrome p450 oxidation occurs in the ________ of the hepatocyte

A

Sarcoplasmic endoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Drugs that increase cytochrome P450 activity

A

induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Drugs that decrease or irreversibly inhibit cytochrome P450 activity

A

inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Cytochrome P450 induction causes a decreased drug effect – IF metabolism ________ drug

A

deactivates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Cytochrome P450 induction causes an increased drug effect – IF metabolism ________ drug

A

activates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Cytochrome P450 inhibition causes an increased drug effect – IF metabolism ________ drug

A

inactivates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Cytochrome P450 inhibition causes a decreased drug effect – IF metabolism ________ drug

A

activates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Define the role of drug efflux transporters.

A

Cell survival mechanism to pump unwanted substances out of the cell. Cell can increase the amount based on exposure over time.
1. Solute carrier (SLC) proteins - Passive transport via gradient
2. ABC gene family - ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Most drug efflux transporters are _______

A

ATP-binding cassette (ABC) transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

3 major drug efflux transporters

A

B, C, G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

List the components of the intact blood-brain barrier.

A

tight gap junctions
ABC transporters
Glial cells- astrocytes, podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Where are neuron cell bodies of the autonomic system located?

A

outside the CNS (ganglia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the subdivisions of the autonomic nervous system?

A

sympathetic, parasympathetic, and enteric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Chain ganglion are present in which NS? parasympathetic or sympathetic?

A

sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Where do sympathetic axons leave the CNS?

A

Thoracolumbar region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

For sympathetic NS, preganglionic fibers are ________, while postganglionic fibers are _________.

A

preganglionic= short
postganglionic= long

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

For parasympathetic NS, preganglionic fibers are ________, while postganglionic fibers are __________

A

Preganglionic= long
postganglionic= short

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Where do parasympathetic axons leave the CNS?

A

Craniosacral regions.

Most from brainstem, bladder and genitals from sacral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Which muscarinic receptors are excitatory?

A

M1, M3, M5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Which muscarinic receptors are inhibitory?

A

M2, M4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What neurotransmitter(s) acts on cholinergic receptors?

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Which alpha receptors are stimulatory and what does it activate?

A

alpha 1, activates Gq protein, activates phospholipase C which activates secondary messengers IP3 and DAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

which alpha receptors are inhibitory and what does it inhibit?

A

alpha 2, inhibits adenylyl cyclase; leads to decreased cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Where is the ganglia located in the sympathetic NS?

A

Close to the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Where is the ganglia located in the parasympathetic NS?

A

In the visceral effector organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the GPCR that alpha 1 activates? Effector?

A

Gq/G11 - activates phospholipase C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the GPCR that alpha 2 activates? Effector?

A

Gi - inhibits adenylate cyclase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the GPCR that beta activates? Effector?

A

Gs - stimulates adenylate cyclase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Where are alpha 1 receptors primarily found?

A

in the smooth muscle cell that surrounds the blood vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What type of receptors are nicotinic receptors?

A

Ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What type of receptors are muscarinic receptors?

A

GPCRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Are Beta receptors inhibitory or stimulatory?

A

All beta receptors are stimulatory - stimulates adenylate cyclase, increasing cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How does the activation of beta receptors work in the heart?

A

NE activates beta receptors - G stimulatory → stimulates adenylyl cyclase → increases cAMP → activates PK-A → more ICF Ca++ (from ECF and from sarcoplasmic reticulum) → contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How does the activation of beta 2 receptors work in the peripheral muscle?

A

NE binds to B2 in periphery → Increases cAMP → inhibit MLCK → no active myosin → relaxation - allows peripheral vessels to dilate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Compare the SNS vs PANS of the SA node and which receptors are present

A

SNS: accelerates SA node - B1 and B2
PANS: decelerates the SA node - M2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Compare the SNS vs PANS of the heart contractility and which receptors are present

A

SNS: increases heart contractility - B1 and B2
PANS: decreases heart contractility - M2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Compare the SNS vs PANS of bronchiolar smooth muscle and which receptors are present

A

SNS: relaxes bronchiolar smooth muscle - B2
PANS: contracts bronchiolar smooth muscle - M3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

The ____ is the gap between the neuron and the cell

A

synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the role of the neuron?

A

Sends AP from neuron cell body to the telodendria (endpoints) capped with synaptic boutons (where neurotransmitters are stored)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

info is coming into neuron through the _____

A

Dendrites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Action potentials are generated in the ________

A

axon hillock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the 6 Neurotransmitter Classes?

A
  1. Esters
  2. Monoamines
  3. Amino Acids
  4. Purines
  5. Peptides
  6. Inorganic gases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Give an example of an ester neurotransmitter

A

Acetylcholine (ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Give an example of a monoamine neurotransmitter

A

NE, Serotonin, Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Give an example of an amino acid neurotransmitter

A

Glutamate, GABA, glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Give an example of a peptide neurotransmitter

A

Substance P, Endorphins - mediate pain and analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Give an example of a purine neurotransmitter

A

Adenosine, ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Give an example of a inorganic gas neurotransmitter

A

Nitric oxide (NO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

NO is different than other neurotransmitters because it is not ______

A

stored - made as needed by nitric oxide synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Which drugs are esters of choline?

A

Ach, Methacholine, Succinylcholine (Sux), Carbachol, and Bethanechol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

List Direct acting adrenergic agonists

A

albuterol
clonidine
dobutamine
dopamine
epinephrine
isoproterenol
norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What drugs are indirect acting adrenergic agonists

A

amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What drug is both direct and indirect acting adrenergic agonist?

A

ephedrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Which adrenergic receptor stimulates the heart?

A

B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Which receptors does epinephrine act on

A

a1, a2, B1, B2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

which receptors does norepinephrine act on?

A

a1, a2, B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

which receptors does isoproterenol act on?

A

B1, B2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

which receptors does dopamine act on?

A

D1-5, higher doses: a1, B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

which receptors does dobutamine act on?

A

B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Beta antagonists result in negative ________ & ________

A

inotropy, chronotropy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Differentiate between direct and indirect-acting cholinoceptor stimulants

A

Direct-acting - agonists of receptors (choline esters and alkaloids)
Indirect-acting - cholinesterase inhibitors, prolonging ACh in the synapse (reversible and irreversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Where are muscarinic receptors found?

A

Nerve, heart and smooth muscle, and glands and endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Where are nicotinic receptors found?

A

Neuromuscular end plate, skeletal muscle, and autonomic ganglion cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the indirect-acting cholinomimetics that we need to know?

A

Alcohols - edrophonium
Carbamates - neostigmine and pyridostigmine
Organophosphates - echothiophate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is edrophonium used for and how long does it last?

A

Myasthenia gravis diagnosis, ileus, and arrhythmias; 5-15 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the mechanism of indirect-acting cholinomimetics?

A

Targets ACh esterase (AChE), preventing the breakdown of ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

How can an organophosphate covalent bond be broken?

A

Need a strong nucleophile - Pralidoxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are the 4 major therapeutic uses of indirect-acting cholinomimetics?

A
  1. Disease of the eye - glaucoma
  2. GI and urinary tracts - ileus
  3. Neuromuscular junction - MG and anesthesia
  4. Atropine overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the symptoms of overdose of direct-acting muscarinic stimulants?

A

SLUDGE-M: Need atropine
Salivation, lacrimation, urination, defecation, GI motility, emesis, myosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the symptoms of overdose of cholinesterase inhibitors?

A

SLUDGE-M - need atropine and pralidoxime (organophosphate poisoning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are the indications for the use of atropine?

A

Blocks the parasympathetic response
- Bradycardia
- Poisonous mushrooms and organophosphate poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the signs and symptoms of atropine overdose?

A

BRAND - blindness, redness, absent bowel sounds, nuts (CNS), dilated pupils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the treatment for atropine overdose?

A

Physostigmine - can produce dangerous CNS effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Differentiate between direct acting and indirect-acting adrenergic agonists

A

Direct agonist - bind to receptors and illicit response
Indirect agonist - Increase amount of catecholamines in synapse; either facilitating removal or preventing reuptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Alpha 1 vs alpha 2 effects

A
  • α1: Gq → phospholipase C → increases IP3 and DAG
    • contracts vascular smooth muscle, prostate contraction, heart - increases force of contraction
  • α2: Gi → decreases cAMP
    • inhibited transmitter release at adrenergic and cholinergic nerve terminals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Compare the effects of beta 1, 2, 3

A

Gs - all increase cAMP
- β1: increases force and rate of contraction (heart) and increases renin release (juxtaglomerular cells)
- β2: promotes smooth muscle relaxation at respiratory, uterine, and vascular smooth muscle
- β3: activates lipolysis in fat cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Describe the mechanism of action for alpha 1 receptors

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Describe what happens in the cardiovascular system after the administration of an alpha-agonist

A
  • Increases vascular resistance/tone
  • HR decreases (indirect effect)
  • BP increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Describe what happens in the cardiovascular system after the administration of a beta-agonist

A
  • Decreases vasculature resistance/tone
  • Increased contractility and HR
  • BP decreases overall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Describe the effects of epinephrine

A
  • Potent vasoconstrictor
    • α receptors
  • Cardiac stimulant (β1)
    • Positive inotropic (force)
    • Positive chronotropic (rate)
  • β2 activation in some vessels
    • Dilation of skeletal muscle vessels
    • Dilation in bronchioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Describe the effects of norepinephrine

A
  • Effects on α and β1
  • Little effect on β2
  • Results
    • Increase in systolic and diastolic
    • Vagal reflexes overcome chronotropic effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Describe the effects of isoproterenol

A
  • Potent β agonist - vasodilator - heart
  • Little effect on α receptors
  • Results
    • Increase cardiac output
    • Fall in Mean arterial pressure
    • Slight decrease or increase in systolic BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Describe the effects of dopamine

A

Triphasic response:
- Low dose: Activates D1 receptors - vasodilation,
decrease in peripheral resistance
- Higher dose: mimics action of epinephrine; β1 receptors in the heart
- Highest dose: activates alpha, increases BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Describe the effects of dobutamine

A
  • β1 selective agonist
  • Cardiac shock, acute heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is angina caused by

A

accumulation of metabolites due to myocardia ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What drug is given for immediate relief of angina?

A

nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what type of angina is also known as Prinzmetal angina or vasospastic?

A

Variant angina
O2 delivery decreased due to coronary vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Which type of angina is classic angina

A

“angina of effort”
O2 requirement increases with activity, but coronary blood flow not enough, leads to O2 debt and ischemia with toxic metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What drugs are good for angina prophylaxis?

A

calcium channel blockers and beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What type of angina is also known as “angina at rest”?

A

Unstable angina
microvascular disease s/t small patelet clots and atherosclerotic plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Which type of angina is an emergency?

A

unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Which type of angina is most rare?

A

variant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is treatment of classic angina?

A

reduction of demand through beta blockers, calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what is treatment of variant angina?

A

primarily calcium channel blockers to prevent , vasodilators/nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

How does NO lead to vasodilation?

A

NO activates guanylyl cyclase, which converts GTP to cGMP. cGMP dephosphorylates Myosin-LC leading to relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What are the good effects from Nitrates and Nitrites?

A

Increased venous capacitance
decreased ventricular preload
decreased heart size
decreased cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What are the bad effects of nitrates and nitrites?

A

Headache (most common), orthostatic hypotension, syncope, reflex tachycardia, hemoglobin interactions (methehemoglobin = low affinity for oxygen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Describe how Ca++ contributes to blood vessel contraction

A
  • Ca++ binds to calmodulin (protein) → activates MLCK → MLC-P interacts with actin to contract
  • cAMP inhibits MLCK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are the different drugs that induce relaxation of vascular tone?

A

Ca++ channel blockers (prevent contraction)
K+ channel blockers (prevent depolarization)
B2 agonists (increase cAMP)
Nitrates (increase cGMP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

How are Beta Blockers used for angina treatment?

A

Not vasodilators - decrease oxygen demand
↓ HR
↓ BP
↓ Contractility
- more B2 receptors in micro-arteries → dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

How do Ca++ channel blockers treat angina?

A
  • L-type channel most dominant in cardiac and smooth muscle
  • Drug binds to depolarized membranes
  • Decreased opening frequency with drug binding
  • relaxation and reduced BP in smooth muscle
  • Heart: ↓ contractility, ↓ SA node pacemaker rate, ↓ AV node conduction velocity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is an example of an irreversible alpha antagonist?

A

Phenoxybenzamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What are the beneficial effects of beta blockers?

A

decrease oxygen demand,

decrease HR, BP and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Calcium channel blockers target

A

L-type calcium channels of vascular smooth muscle and heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Calcium channel blockers in smooth muscle cause

A

relaxation, reduce blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

calcium channel blockers in heart cause

A

decrease contractility, decreased SA node pacemaker rate, decreased AV node conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Which calcium channel blockers are more peripheral vascular selective?

A

Dihydropyridines (nifedipine, amlodipine, and nimodipine.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

which calcium channel blockers are more cardiac selective?

A

verapamil and diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What are toxicities of calcium channel blockers?

A

bradycardia, arrest
AV block
CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What are the 4 types of antihypertensive agents?

A

diuretics: deplete sodium
Sympathoplegics: decrease PVR, reduce CO
Direct vasodilators: relax VSM
Anti-angiotensins: block activity or production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What is the hydraulic equation?

A

BP= CO x PVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Cardiac output is a function of

A

stroke volume, heart rate, venous capacitance (preload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

another word for preload is

A

venous capacitance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Which drugs are CNS sympathoplegics?

A

Methyldopa, clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Which drugs are adrenoceptor antagonists

A

Propanolol, metoprolol, atenolol, prazosin, terazosin, doxazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Propanolol acts on which receptors?

A

B1 and B2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What are the effects of propanolol

A

Lowers BP, prevents reflex tachycardia
Decreases CO
Inhibits renin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Which drugs are alpha 1 blockers?

A

Prazosin, Terazosin, Doxazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What are the effects of alpha 1 blockers?

A

block a1 receptors in arterioles and venules.
dilates both resistance and capacitance vessels

BP is reduced more in upright position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Which drugs are direct vasodilators

A

Minoxidil, hydralazine, sodium nitroprusside, fenoldopam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What is the mechanism of action of minoxidil

A

Opens K+ channels in smooth muscles, stabilizes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What are factors that affect blood pressure?

A

peripheral resistance
vessel elasticity
blood volume
cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Why is methyldopa better than clonidine for pregnant women?

A

Doesn’t cross the placental barrier like clonidine does

used for 2nd and 3rd trimester HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are the 4 mechanisms of action of vasodilators? Give examples of drugs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are the two main ways vasodilators lower BP?

A
  1. Relax smooth muscle of arterioles (all) and veins (nitroprusside and nitrates)
  2. Reduction of PVR and MAP - Elicits compensatory responses; Best when given in conjunction with other hypertensives that combat these mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

Describe the effects of combination therapy of beta blockers and diuretics in lowering blood pressure

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

How does hydralazine lower BP?

A

Dilates arterioles – induces NO production in endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What are the symptoms of hydralazine toxicity?

A
  • HA, nausea, sweating, flushing
  • Worse in slow acetylators (Symptoms resemble SLE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

How does Sodium Nitroprusside lower BP?

A

Relaxes vascular smooth muscle, dilating arterial and venous vessels
- Breaks down in blood to release NO
- Increases intracellular cGMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What are the clinical indications for Sodium Nitroprusside?

A

HT emergencies and Cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What is the upside and downside of Sodium Nitroprusside use?

A

Upside - Rapidly lowers BP; Effects disappear 1-10 min after d/c
Downside - CN accumulation, slowly eliminated by kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

How does Fenoldopam lower BP?

A

Peripheral arteriolar dilator - Agonist of D1 receptors
- dilates renal vascular bed (lowers BP, diuresis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What are the clinical indications for Fenoldopam use?

A

HTN emergencies, post-op HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What are the symptoms associated with Fenoldopam toxicity?

A

Reflex tachycardia, flushing, HA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

How do Ca++ channel blockers lower BP?

A

Dilate peripheral arterioles by inhibiting Ca2+ influx in arterial smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

Which Ca++ channel blockers target the heart vs the periphery?

A
  • Verapamil - more targeted to heart
  • Diltiazem - both heart and periphery
  • Dihydropyridine family - more targeted to periphery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are the types of Inhibitors of Angiotensin?

A

ACE inhibitors (-pril)
Angiotensin competitive inhibitors (angiotensin receptor blockers, ARB) (-artan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

______ is the prototype drug of ACE inhibitors

A

Captopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Renin release in kidney stimulated by what 4 mechanisms?

A
  • Reduced arterial pressure
  • Reduced sodium delivery
  • Increased sodium concentration
  • Sympathetic stimulation (beta receptors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Why is a persistent, non-productive cough a symptom for ACE inhibitors but not ARBs?

A

ARBs have no effect on bradykinin - no cough
ACE inhibitors - inhibit breakdown of bradykinins, which stimulate PG synthesis - excess bradykinin causes non-productive cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Which angiotensin inhibitors do we need to know?

A

ACE inhibitors - Captopril
Angiotensin receptor blockers – Losartan, Valsartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What are the first line drugs for HTN?

A
  • Low dose diuretic
  • Beta blocker
  • CCB
  • Dual therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Define heart failure

A

Heart fails to meet the metabolic demands of tissues - CO inadequate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What is the most common cause of heart failure?

A

Coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Differentiate between systolic and diastolic heart failure

A

Systolic failure – reduced cardiac function
- Acute; heart walls thinned (less effective pumping)
↓ CO, ↓ Ejection fraction

Diastolic failure – reduced cardiac filling (can be peripheral)
- Chronic; heart more stiff/thicker walls (chronic HTN)
- ↓ CO, Normal Ejection fraction
- Does not respond well to positive inotropic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Differentiate between symptoms of right vs left ventricular failure of CHF

A

Right ventricle – peripheral congestion
Left ventricle – pulmonary congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What are the 4 factors of cardiac performance?

A

CO = SV x HR
- Preload
- Afterload
- Contractility
- Heart Rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Heart failure where the normal CO not sufficient for demands of body

A

“High-output” failure (rare)
- Hyperthyroidism
- Beriberi
- Anemia
- Arteriovenous shunts
Responds poorly to inotropic agents – treat underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

In systolic heart failure, CO is ______ and ejection fraction is _______

A

decreased, decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

In diastolic heart failure, CO is ______ and ejection fraction is _______

A

decreased, normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Systolic heart failure responds ______ to positive inotropes

A

well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Diastolic heart failure responds _______ to positive inotropic drugs

A

poorly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Digoxin mechanism of action

A

Directly inhibits Na/K ATPase
maintains normal resting potential, positive inotrope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Digoxin has a ____ therapeutic index

A

narrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What are ways to decrease preload?

A

salt restriction, diuretics, venodilation (Nitroglycerin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

Discuss the normal control of cardiac contractility

A
  1. Trigger Ca++ enters cell
    - depends on number of L type channels, duration of channel opening, and sympathetic stimulation
  2. Binds to channel is SR, release stored Ca++
    - depends on amount stored and amount of trigger Ca++
  3. Frees actin to interact with myosin
  4. Removal of Ca++
    - SR Calcium ATPase
    - Na+/Ca2+ antiporter – sodium gradient
    - Na+/K+ ATPase: removes sodium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What are the EKG changes that occur with digoxin toxicity?

A

tachycardia, fibrillation, arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What effect does hyperkalemia have on digoxin effects?

A
  • Potassium competes with digoxin
  • Excess K+, decreased effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What effect does hypomagnesia have on digoxin effects?

A

Increased risk of digoxin induced arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

How do phosphodiesterase inhibitors help treat HF?

A

Enzymes that inactivate cAMP and cGMP - positive inotropic effects, vasodilation
Increase contractility w/o inhibiting Na+/K+ ATPase (increase/prolong Ca++)
PDE3 specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

The pacemaker of the heart is _______ and is located in the ________

A

SA node, right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

The SA node fires at a rate of

A

75bpm

209
Q

Where is the AV node located

A

junction of the atria and ventricles

210
Q

where is the atrioventricular bundle/bundle of His located

A

in the interventricular septum

211
Q

Where are the purkinje fibers located

A

spread within the muscle of the ventricle walls

212
Q

how fast does the AV node fire

A

40-50bpm

213
Q

In phase 0 of the cardiac AP, which ions are moving, which direction, and through which channels

A

Na+, in, fast VG Na channels

214
Q

In phase 1 of the cardiac AP, which ions are moving, which direction, and through which channels

A

K+ and Cl- moving out through leak channels

215
Q

In phase 2 of the cardiac AP, which ions are moving, which direction, and through which channels

A

Ca++ moving in through L type Ca++ channels

K+ moving out through slow delayed rectifier channels

216
Q

In phase 3 of the cardiac AP, which ions are moving, which direction, and through which channels

A

K+ moving out through slow delayed rectifier channels, rapid delayed rectifier channels and inward rectifier channels

217
Q

Phase 4 of the cardiac AP is the

A

Vrm, resting membrane potential

218
Q

What are the types of disturbances in impulse conduction that result in arrhythmias?

A
  • Block
  • Reentry
219
Q

Describe the reentry block and “circus movement”

A

One impulse “circles around” and re-excites areas more than once

220
Q

What must happen in order for reentry to occur?

A
  • There must be an obstacle (scar tissue)
  • Block must be unidirectional
  • Conduction time must be long enough to reenter same areas after refractory period
221
Q

What are the 4 classes of antiarrhythmic agents?

A

Vaughan-Williams classification:
- Class I – sodium channel blockade
- Class II – sympatholytic (beta blockers)
- Class III – prolong action potential duration (other mechanisms besides sodium channels – K+)
- Class IV – block cardiac calcium channel currents

222
Q

What are the 3 subclasses of Class I antiarrhythmic agents?

A

IA, IB, IC

223
Q

What meds are included in Class IA antiarrhythmic agents? What are the effects on APD and ERP? What are the cardiac effects?

A

Quinidine (Procainimide, Disopyramide)
- Prolong the action potential duration (APD)
- ↑ Effective Refractory Period (ERP)
- Cardiac effects: Depresses pacemaker rate, Lengthens QT interval, Depresses conduction and excitability

224
Q

What meds are included in Class IB antiarrhythmic agents? What are the effects on APD and ERP?

A

Lidocaine
- Shorten the APD
- ↓ ERP

225
Q

What meds are included in Class IC antiarrhythmic agents? What are the effects on APD and ERP?

A

Flecainide
- Minimal effects on APD
- Slow dissociation
- No effect on ERP (But Na+ channels are still blocked)

226
Q

Which drug is the only antiarrhythmic with all 4 Vaughan-Williams’ class effects

A

Amiodarone

227
Q

What is the drug of choice for VT

A

amiodarone

228
Q

What meds are included in Class II antiarrhythmic agents? How do these agents work as antiarrhythmics?

A

Beta blockers - propanolol and esmolol (short acting)
- Antiarrhythmic properties associated with direct membrane effects - Exact antiarrhythmic action unknown
- Suppress ventricular ectopic depolarization
- Prevent infarction and sudden death in patients recovering from acute MI

229
Q

What meds are included in Class III antiarrhythmic agents? How do these agents work as antiarrhythmics?

A

Amiodarone (VT) and dronedarone (A-fib)
Prolong AP usually by:
- Blocking cardiac K+ channels
- Enhancing inward current (Na+ or Ca2+ channels)

230
Q

What meds are included in Class IV antiarrhythmic agents? How do these agents work as antiarrhythmics?

A

Calcium channel blockers - verapamil
- Prolongs AV node conduction
- Slows SA node
- Hypotensive action
- Useful for supraventricular arrhythmias
- Can reduce ventricular rate in atrial fibrillation and flutter

231
Q

What is the treatment for symptomatic bradycardia?

A

1st - atropine
2nd - epi, dopamine

232
Q

What is the treatment for chronic bradycardia?

A

pacemaker

233
Q

What is the treatment for symptomatic heart block?

A

atropine and transcutaneous pacing

234
Q

What is the treatment for chronic heart block?

A

pacemaker

235
Q

What is the treatment for symptomatic SVT?

A

adenosine

236
Q

What is the treatment for chronic SVT?

A

CCBs, beta blockers

237
Q

What is the treatment for symptomatic sinus tachycardia?

A

Adenosine, CCBs, cardioversion

238
Q

What is the treatment for chronic sinus tachycardia?

A

catheter ablation

239
Q

What is the treatment for symptomatic Vtach?

A

amiodarone

240
Q

What is the treatment for chronic Vtach?

A

amiodarone, satolol

(jesus)

241
Q

What is the treatment for symptomatic Afib?

A

diltiazem, verapamil

242
Q

What is the treatment for chronic Afib?

A

beta-blockers, amiodarone

243
Q

What is the treatment for symptomatic Vfib?

A

CPR, defirillation

244
Q

What is the treatment for chronic Vfib?

A

amiodarone, lidocaine, magnesium

245
Q

What are the Proximal Tubule Targets?

A

NaCl and NaHCO3

246
Q

Which drugs target Proximal Tubule Targets?

A

Carbonic anhydrase inhibitors (block NaHCO3 reabsorption)

Caffeine (weakly blocks adenosine receptors in PCT (Na+))

247
Q

The _______ loop of henle is responsible for water reaborption

A

descending

248
Q

The ______ loop of henle is impermeable to water

A

ascending

249
Q

What is the pump that transports NaCl and K in the ascending loop of henle?

A

NKCC2 - sodium, potassium, 2 chloride
- all pumped from urine to thick ascending limb

250
Q

The excess ____ in the urine of the ascending loop of henle drives ____ out of the urine and into the blood

A

K+ (charge gradient)
Mg++ and Ca++

251
Q

What is the MOA of loop diuretics? What is an example?

A

Selectively inhibit NaCl reabsorption in the thick ascending limb (TAL)
- Reduction in NaCl absorption
- Diminish lumen positive potential - Increase secretion (loss) of Mg2+ and Ca2+ in urine

Lasix

252
Q

Carbonic anhydrase inhibitors ___ pH, while loop diuretics and thiazides ___ pH

A

Decrease, increase

253
Q

What diruertics should be avoided in patients with sulfa alergies?

A

Loop diuretics (lasix) and thiazides (HCT)

254
Q

What is the MOA of thiazides?

A
  • Inhibit NaCl transport in DCT
  • Some inhibition of CA activity
  • HCT
255
Q

What is reabsorbed in the distal convoluted tubule? By what?

A

Ca++, by PTH

256
Q

What is the role of the principal cells in the collecting tubule?

A

Builds up (-) charge in lumen
- more Na+ in than K+ out
- drives Cl- out through paracellular route

257
Q

Diuretics upstream result in excess ___ in CT

A

Na+

258
Q

What is the effect of aldosterone at the collecting tubule?

A

Increase Na+ and water reuptake (ENaC) - increasing BP and vol

259
Q

K+ sparing diuretics work by what MOA?

A
  1. Antagonize the effects of aldosterone - spironolactone
  2. Inhibition of sodium flux through ion channels in luminal membrane - amiloride
260
Q

What parts of the nephron are freely permeable to water?

A

PCT and descending loop

261
Q

ADH agonist vs antagonist

A
  • Agonist: Vasopressin
  • Antagonist: Conivaptan
262
Q

ADH (vasopressin) effects at the collecting duct

A
  • Increases water reabsorption
  • Adds preformed AQP2 to apical membrane
  • Increases blood volume
  • Makes more concentrated urine
263
Q

What are the classes of diuretics?

A
  • Carbonic Anhydrase Inhibitors
  • Loop Diuretics
  • Thiazides
  • Potassium Sparing Diuretics
  • Osmotic diuretics
264
Q

Mannitol is an example of what type of diuretic

A

osmotic diuretic

265
Q

Osmotic diuretics are mainly used to

A

reduce ICP
promote removal of renal toxins

266
Q

Toxicity of mannitol includes

A

extracellular volume expansion and dehydration

267
Q

What are the meds given for asthma progression?

A

Mild - SABA
Moderate - ICS or LTRA
- ICS for relief
Severe - oral corticosteroids, anti-IgE antibody

268
Q

What are the 3 classes of short-term relievers in obstructive airway diseases?

A
  1. B2 agonists
  2. Methylxanthines
  3. M3 antagonists
269
Q

Short term relief drugs for Asthma are

A

Bronchodilators:
beta agonists
Antimuscarinics
Methylxanthines

270
Q

Long term controllers for asthma include

A

Anti-inflamatory agents:
steroids
antibodies
slow anti-inflammatory drugs

Leukotriene antagonists:
lipoxygenase inhibitors
Receptor inhibitors

271
Q

What are the mediators in the autocoid group?

A

Histamine, serotonin, prostaglandins, leukotrienes

272
Q

_____ is the mediator of allergic and inflammatory response

A

histamine

273
Q

Where are histamine H2 receptors located?

A

GI, cardiac muscle, mast cells, brain

274
Q

Where are histamine H4 receptors located?

A

eosinophils, neutrophils, CD4 T cells

275
Q

What is the physiologic antagonist of histamine?

A

Epinephrine

276
Q

Differentiate between H1 antagonists, 1st vs 2nd gen

A

1st generation
- Sedative effects
- ANS blocking
- motion sickness, nausea
2nd generation
- Less sedation (↓ CNS distribution, doesn’t cross BBB)

277
Q

What are the 3 components of the triple response of allergy testing?

A

1- Wheal/welt development
2- flare/redness
3- Sensory nerve ending activation/itching

278
Q

Histamine is released in response to what?

A
  1. Allergen binding to IgE on mast cells
  2. Displacement – morphine, tubucurarine
  3. Rupture of mast cells (mechanical)
279
Q

Which histamine receptor causes bronchoconstriction and vasodilation

A

H1

280
Q

Antihistamines are ____ selective inverse agonists

A

H1
diphenhydramine (Benadryl)
most useful for type 1 hypersensitivities

281
Q

1st generation H1 receptor antagonists are used also used for

A

Sedation: resembles antimuscarinic drugs, sleep aids, children may have reverse effects

Antinausea/antiemetic: motion sickness

Antiparkinsonism: suppress extrapyramidal symptoms

Local anesthesia: block sodium channels in excitable membranes

Other: inhibition of mast cell release, negative feedback?

282
Q

H2 receptor antagonists are used for

A

stomach ulcers, acid reflux/GERD. Not as effective as PPIs

283
Q

What is the slow reacting substance of anaphylaxis?

A

leukotrienes

284
Q

Where are leukotrienes liberated from?

A

lung during inflammation

285
Q

Leukotrienes produce (GPCR)

A

Bronchospasm, mucous secretion, microvascular permeability, airway edema

286
Q

Which drugs are leukotriene pathway inhibitors

A

interupt synthesis pathway:

inhibit 5-lipoxygenase = Zileuton

inhibit binding to receptor= Zafirlukast, Montelukast (Singulair)

287
Q

What are the 3 drugs that are 2nd gen H1 antagonists?

A

Claritin, Allegra, Zyrtec

288
Q

Histamine effect on on respiratory system

A

Bronchoconstriction

289
Q

Where is serotonin produced?

A

Raphe nuclei

290
Q

Serotonin effect on CV

A
  • Contraction of vascular SM
    • Exception: skeletal muscle, heart
  • Platelet aggregation
291
Q

Serotonin effect on GI

A
  • Increases tone
  • Facilitates peristalsis
  • Overproduction - diarrhea
292
Q

Serotonin effect on respiratory

A
  • Facilitate ACh release - constriction
  • Hyperventilation
293
Q

Serotonin effect on nervous system

A
  • Melatonin precursor
  • Vomiting reflex
  • Pain and itch (similar to histamine)
  • Chemoreceptor reflex
    • Bradycardia
    • Hypotension
294
Q

Which serotonin receptor is an ion channel?

A

5-HT3
- the other 6 are GPCRs

295
Q

Which serotonin receptors are agonist targets?

A

1A, 1B, 1D

296
Q

Which serotonin receptors are antagonist targets?

A

2A and 3

297
Q

What are the 2 serotonin agonist drugs? Which receptors do they target? What do they treat?

A
  1. Buspirone
    - 5-HT1A agonist (partial)
    - Non-benzodiazapine anxiolytic - no drowsiness
    - GAD, OCD
  2. Sumatriptan
    - 5-HT1D/1B agonist
    - Migraine HA
298
Q

How do triptans treat migraines?

A
  • Bind 5-HT1D/1B in cranial blood vessels
  • Prevent dilation and stretching of pain endings
  • Not prophylactic
299
Q

What are the 3 hyperthermic syndromes? and their treatments?

A
  1. Serotonin syndrome = Sedation (benzo), paralysis, intubation/ventilation
  2. Neuroleptic malignant syndrome= benadryl, cooling, sedation
  3. Malignant hyperthermia= dantrolene, cooling
300
Q

What drugs can cause serotonin syndrome?

A

Antidepressants (SSRIs, SNRIs, MAOIs), opioids, illicit drugs, St. John’s wort, ginseng

301
Q

What drugs can cause neuroleptic malignant syndrome?

A

D2-blocking antipsychotics

302
Q

What drugs can cause malignant hyperthermia?

A

Volatile anesthetics, sux

303
Q

What are the 3 drugs classified as serotonin antagonists? What receptors do they act at? What is their clinical use?

A

Phenoxybenzamine, Cyproheptadine
- 5-HT2
- Carcinoid tumors
- Cold induced urticaria

Ondansetron
- 5-HT3
- Prevent N/V for Surgery and CA chemotherapy

304
Q

What are the 4 major classes of antidepressants?

A
  1. Selective serotonin reuptake inhibitors (SSRIs)
  2. Selective serotonin-NE reuptake inhibitors (SNRIs)
  3. Tricyclic antidepressants (TCAs)
  4. Monoamine oxidase inhibitors (MAOIs)
305
Q

Focal seizure treatment is

A

Lamotrigine, phenytoin, phenobarb, carbamazepine

306
Q

Absence seizure treatment is

A

Ethosuxamide, valproic acid, benzo

307
Q

Treatment for infantile spasms

A

carbamazepine, Vigabatrin

308
Q

treatment for generalized seizures

A

phenytoin, phenobarb, carbamazepine, benzo

309
Q

Which drug can displace phenytoin from albumin binding sites?

A

valporic acid

310
Q

Which drugs compete with phenytoin for albumin binding sites?

A

Carbamazepine, sulfonamides, valporic acid

311
Q

Differentiate between therapeutic, free, toxic, and lethal levels of phenytoin

A
  • Therapeutic: 10-20 mcg/ml
  • Free phenytoin: 1-2.5 mcg/ml
  • Toxic: 30-50 mcg/ml
  • Lethal: >100 mcg/ml
312
Q

What are the toxic effects of phenytoin?

A
  • Nystagmus
  • Loss of extraocular pursuit of movement
  • Diplopia
  • Ataxia
  • Sedation
313
Q

What are the toxic effects of phenytoin with chronic use?

A
  • Gingival hyperplasia
  • Hirsuitism
  • Coarsening of facial features
314
Q

What is the #1 toxic effect of phenobarbital?

A

SEDATION

315
Q

What are the 4 phases of thrombogenesis?

A
  1. Adhesion
  2. Aggregation
  3. Secretion
  4. Cross-linking of adjacent platelets
316
Q

What is the blood vessel involvement in thrombogenesis

A

vasoconstriction, formation of platelet plugs, regulation of coagulation and fibrinolysis

317
Q

What are the 2 parts to platelet adhesion?

A
  • vWF binds to GP 1b receptor
  • collagen binds to GP 1a receptor
318
Q

Describe the coagulation pathway Dr. T wants us to know for final

A
319
Q

____ is the over stimulation of the blood clotting mechanism

A

DIC - Disseminated coagulation

320
Q

What are the 3 results of DIC?

A
  • Generalized blood coagulation
  • Excessive consumption of factors and platelets
  • Leads to spontaneous bleeding
321
Q

What are the 4 causes of DIC?

A
  • Massive tissue injury
  • Malignancy
  • Bacterial sepsis
  • Abruptio placentae
322
Q

How is DIC treated?

A

Plasma transfusions and treat the underlying cause

10-50% mortality

323
Q

What are the 2 major systems of coagulation regulation?

A
  • Fibrin inhibition
  • Fibrinolysis
324
Q

What are the 4 classes of coagulation modifier drugs?

A
  1. anticoagulants
  2. anti-platelets
  3. thrombolytic drugs (fibrinolytic)
  4. hemostatic or antifibrinolytic drugs
325
Q

Indirect thrombin inhibitors

A

Enhances antithrombin activity

-unfractionated heparin (HMW)
dec. thrombin, Xa
HIT, bleeding-treat with protamine

-LMW heparin
dec. Xa

-Fondaparinux
dec. Xa

326
Q

Direct thrombin inhibitors

A

Bind to both active and substrate recognition sites of thrombin:
-Hirudin (from leeches) and lepirudin (recombinant)
-Bivalirudin (angiomax)

Bind only to thrombin active sites:
-argatroban
-melagatran

327
Q

Warfarin MOA, onset, and therapeutic range

A

inhibits Vit K cycling

8-12hr delay in onset

therapeutic range defined by INR

Normal=0.8-1.2
Warfarin target= 2-3

328
Q

How do fibrinolytics work?

A

Catalyze the formation of serine protease plasmin and rapidly lyse thrombi

329
Q

What are the 3 fibrinolytics?

A

Streptokinase
Urokinase
Tissue plasminogen activators (t-PA)

330
Q

What is the recombinant form of Tissue plasminogen activators (t-PA)?

A

Alteplase

331
Q

What do fibrinolytic drugs treat?

A

MI and PE

332
Q

What are the 3 antiplatelet aggregation drugs?

A

aspirin
clopidogrel
abciximab

333
Q

MOA of aspirin

A

Inhibition of TXA2 synthesis, COX-1 Selective

platelet changes shape, granule release, aggregation

334
Q

MOA of clopidogrel

A

Irreversibly inhibit ADP receptor on platelets

335
Q

MOA of Abciximab

A

IIb/IIIa Receptor Blocker - Activation of this receptor complex in the final common pathway

336
Q

What are the 5 drugs used to treat bleeding disorders?

A
  1. Vitamin K
  2. Plasma Fractions
  3. Desmopressin Acetate
  4. Aminocaproic acid
  5. Tranexamic Acid (TXA)
337
Q

Vitamin K confers activity on what?

A
  • Prothrombin
  • Factors VII, IX, and X
338
Q

What is the fibrinolytic inhibitors?

A

Aminocaproic acid

  • inhibit plasminogen → plasmin
339
Q

What are the 2 major types of secretory tissues of the pancreas?

A

Exocrine gland (digestive enzymes)
Endocrine gland (Islets of Langerhans)

340
Q

What are the 2 main pancreatic cell types

A

Alpha and Beta

341
Q

What do the alpha Islets of Langerhans cells secrete?

A

glucagon and proglucagon

342
Q

What do the beta Islets of Langerhans cells secrete?

A

insulin, C-peptide, proinsulin, amylin

343
Q

Insulin receptors are _____

A

RTKs - receptor tyrosine kinases

344
Q

What are the 4 types of diabetes mellitus?

A

Type I - Insulin dependent
Type II - Non-insulin dependent
Type III - Other causes elevated blood glucose (pancreatitis, drug therapy, etc.)
Type IV - Gestational

345
Q

The proform of insulin contains ______ which is _____ before entering the bloodstream

A

C-peptide
cleaved off

346
Q

C-peptide is a measure of how much _____ function a patient has

A

beta cell

347
Q

Describe the effects of inward movement of glucose into pancreatic beta cells via GLUT2 transporters

A

excess glucose converted into ATP via metabolism → higher level of ATP binds to potassium channel - closing the channel → more positive Vrm → calcium channels open up → calcium enters beta cell → calcium triggers vesicle fusion and insulin exocytosis

348
Q

When insulin binds to insulin receptors, what occurs inside the cell?

A

Glucose transporters migrate to cell surface

Increased glycogen formation

Activation of multiple transcription factors

349
Q

What are the 4 types of insulin preparations?

A
  1. Rapid acting
  2. Short acting (regular)
  3. Intermediate acting
  4. Long acting
350
Q

What is the MOA of Biguanides?

A

Reduction in hepatic glucose production
- gluconeogenesis: making glucose from other things

351
Q

What is the MOA of insulin secretagogues?

A

Bind to K+ channel
- Rectifier current
- Binding causes depolarization and additional release of insulin

352
Q

What are the 3 classes of Insulin Secretagogues?

A
  • Sulfonylureas
  • Meglitinide
  • Phenylalanine derivatives
353
Q

What is the MOA Thiazolidinediones (TZDs)?

A
  • Decrease insulin resistance (PPAR mediated)
  • Increase insulin signal transduction
354
Q

What is the MOA of α-glucosidase Inhibitors? What is the medication called?

A

Block digestion of complex carbohydrates - more beneficial for people have primary carbohydrate diet
Acarbose

355
Q

What is the MOA of Bile Acid Sequestrant?

A

Surrounds food, preventing absorption
- Large cation exchange resins – not absorbed
- Bind bile acids – prevent reabsorption

356
Q

What is the MOA of Amylin Analogs?

A

Suppresses glucagon release, decreases circulating glucose

357
Q

What is the MOA of Incretin-based Therapies?

A

Mimicking a substance normally produces by intestines

358
Q

What are the 2 types of Incretin-based Therapies?

A
  • Glucagon-Like Polypeptide-1 (GLP-1) Agonists - Semaglutide
  • Dipeptidyl Peptidase-4 (DPP-4) Antagonists - Sitagliptin
359
Q

What is the MOA of SGLT2 Inhibitors (Gliflozins)?

A

Prevents glucose reabsorption in PCT
- specifically inhibits SGLT2
- increased glucosuria

360
Q

Describe the cycle of atherosclerosis in LDLs

A

LDL entry and enlargement → foam cell formation → cholesterol crystallization in foam cells → apoptosis of foam cells and extracellular lipid deposit → plaque with lipid-rich necrotic core

361
Q

What is the 3 part synthesis of cholesterol in cells

A
  1. Mevalonate from Acetyl-CoA
  2. Conversion of mevalonate to squalene
  3. Cyclication of squalene to cholesterol
362
Q

What are the 4 types of lipoproteins?

A

chylomicrons, VLDLs, LDLs, and HDLs

363
Q

Which type of lipoproteins are formed in the intestine and end up in the liver?

A

Chylomicrons

364
Q

Which type of lipoproteins are secreted by the liver and travel to peripheral tissues?

A

VLDLs

365
Q

Which type of lipoproteins transport cholesterol from the liver to the cells, resulting in deposition in arteries in excess?

A

LDLs

366
Q

Which type of lipoproteins scavenge cholesterol from cells, resulting in decreased levels of atherosclerosis?

A

HDLs

367
Q

Desirable lipoprotein levels

A
368
Q

What are the 6 classes of hyperlipidemia drugs?

A
  1. Statins
  2. Niacin
  3. Fibrates
  4. Binding Resins
  5. Absorption Inhibitors
  6. Monoclonal Antibodies
369
Q

What is the MOA of statins?

A

Structural analogs of HMG-CoA- decrease cellular cholesterol synthesis by inhibiting HMG-CoA reductase

370
Q

What are the effects of statins?

A
  • Mostly reduce LDL
  • Increase LDLR
  • Modest decrease of triglycerides
  • Small increase in HDL
371
Q

What is the toxicity of statins?

A
  • Elevated liver enzymes - Increased with liver damage, patients of Asian descent
  • CK elevations - Muscle pain or weakness
372
Q

What are the effects of niacin?

A
  • Decreases VLDL, LDL - Reduces VLDL secretion from liver
  • Increases HDL
373
Q

What is the toxicity of niacin?

A

1 - Cutaneous vasodilation (flushing)

  • Pruritis, dry skin, rash
  • N, abdominal discomfort (rare)
  • Elevation of liver enzymes
374
Q

What is the name of the medication that is a fibrate?

A

Gemfibrozil (Lopid)

375
Q

What are the effects of fibrates?

A
  • Decrease VLDL
  • Modest decrease in LDL
  • Increase lipolysis in liver - PPAR
376
Q

What are toxicities of fibrates

A

Rare, include:
GI upset
arrhythmias
elevated liver enzymes
potentiation of comadin
myopathy

377
Q

What are the 2 drugs that are bile acid binding resins?

A

Colestipol, cholestyramine

378
Q

What are the side effects of bile acid binding resins?

A
  • Constipation, bloating
  • Steatorrhea (lipid in stool)
379
Q

What is the medication considered an intestinal sterol absorption inhibitor?

A

Ezetimibe (Zetia)

380
Q

What is the MOA of Ezetimibe?

A

Blocks the NPC1L1 transporter that transports cholesterol transport from the lumen into the enterocyte

381
Q

Monoclonal antibodies used to treat hyperlipidemia are called ___________

A

PCSK9 Inhibitors

382
Q

Monoclonal antibodies used to treat hyperlipidemia are called ___________

A

PCSK9 Inhibitors

383
Q

How do PCSK9 inhibitors combined with statins lower LDLs? By how much?

A

Statin therapy upregulates PCSK9
PCSK9 inhibitors allow receptor recycling
65%

384
Q

List the antibiotics that work by inhibiting cell wall synthesis. Describe their MOA

A
  • Penicillin, ampicillin, and amoxicillin
  • Cephalosporins
  • Carbapenems
  • Vancomycin
    ß-lactam ring attaches to the enzymes that cross-link peptidoglycans and prevent cell wall synthesis (Gram +)
385
Q

Which antibiotic is considered the “drug of last resort”? What is it used for?

A

Vancomycin
- Alternative to PCN resistant bacteria (MRSA)

386
Q

Adverse reactions of vancomycin

A

Tissue irritation
Ototoxicity
Nephrotoxicity
“Red neck” syndrome

387
Q

What are the 2 antibiotics that work by disrupting the cell membrane? What is their MOA?

A
  • Polymyxin and Daptomycin
  • Polypeptide antibiotics
  • Act as detergents – bind to phospholipids
  • Best action – Gram (-)
388
Q

List the antibiotics that inhibit protein synthesis. What is their MOA?

A

Tetracycline
Macrolides (Erythromycin, Azithromycin)
Neomycin
- Attack bacterial cells without significantly damaging animal cells - wide spectrum

389
Q

_______ have the widest spectrum of activity of any antibiotics

A

Tetracyclines

390
Q

What is the main side effect of antibiotics that inhibit protein synthesis?

A

GI

391
Q

What are the antibiotics that work by inhibiting nucleic acid synthesis? What is their MOA?

A

Rifamycin family - binds to bacterial RNA polymerase
Fluoroquinolones (Ciprofloxacin) - Inhibit DNA gyrase (bacterial)

392
Q

What are fluoroquinolones used to treat?

A
  • UTI, RTI
  • Bone and joint infections
  • ADR
  • Excellent Gram (-) activity
393
Q

What are the 2 antibiotics that work by inhibiting folic acid synthesis?

A

Sulfonamides, trimethoprim

394
Q

What are the 2 ways antibiotics can function to inhibit folic acid synthesis?

A
  1. Competitive inhibition
  2. Incorporated into important molecules
395
Q

What do folic acid synthesis inhibitors treat?

A

Pneumocystis, toxoplasmosis

396
Q

Viruses are considered ______ instead of organisms

A

infectious particles

397
Q

Define how viruses are considered obligate intracellular parasites

A
  • Cannot multiply unless they invade a specific host cell
  • Must instruct the genetic and metabolic machinery of the host cell to make and release new viruses
398
Q

Instead of being alive or dead, viruses are what?

A

Active or inactive

399
Q

What 2 parts do viruses have that are required to invade and control a host cell?

A
  • External coating (capsid)
  • Core containing nucleic acids
400
Q

A naked virus only consists of a ______

A

nucleocapsid

401
Q

The _______ is usually a modified piece of the host cell membrane

A

Envelope

402
Q

A _______ is the protein shell that surrounds the nucleic acid

A

Capsid

403
Q

Which drug is considered the prototype for antiviral drugs that inhibit viral DNA synthesis?

A

Acyclovir

404
Q

When viruses mistakes acyclovir for dGTP, _______ is irreversible

A

chain termination

405
Q

What does acyclovir look similar to? What is the difference?

A

the normal nucleotide bases - missing hydroxyl group

406
Q

Acyclovir is _______ for pregnant women

A

safe

407
Q

What are the 3 indications for acyclovir therapy?

A

HSV1, HSV2, and VZV infections

408
Q

What is the main drug used to treat HIV?

A

Zidovudine (Azidothymidine, AZT)

409
Q

What is the MOA of Zidovudine (Azidothymidine, AZT)?

A

Inhibitor of reverse transcriptase

410
Q

What is the drug combination therapy called to treat HIV?

A

Highly Active Antiretroviral Therapy (HAART)

411
Q

What is the MOA of lamivudine?

A

Inhibits HBV DNA polymerase and HIV reverse transcriptase

412
Q

HIV targets which cells? and with which spike?

A

T-cells - CD4+

gp120 spike

413
Q

The cell surface antigen that has a role in virus attachment to cells is ________

A

hemagglutinin (H1, H2, H3)

414
Q

The cell surface antigen that has a role in virus penetration to cells is ________

A

neuraminidases (N1, N2)

415
Q

Influenza subtypes are determined by what?

A

cell surface antigens hemagglutinin and neuraminidase

416
Q

Differentiate between Influenza Type A and Type B

A

A - Causes moderate to severe illness; Affects all age groups
B - Milder illness; Primarily has had an impact on adolescents and schoolchildren

417
Q

What are the 3 antivirals used to treat influenza?

A

Oseltamivir phosphate (Tamiflu)
Zanamivir (Relenza)
Baloxivir marboxil (Xofluza)

418
Q

Which antiviral for the treatment of the flu must be taken when exposed?

A

Relenza

419
Q

The hallmark of Parkinsonism is ______

A

Tremor at rest

420
Q

______ is rhythmic movement around a joint

A

tremor

421
Q

______ is muscle jerks in various areas that impair movement and coordination

A

Chorea

422
Q

______ is a type of chorea that includes violent abnormal movements

A

Ballismus

423
Q

______ - slow, writhing/twisting

A

Athetosis

424
Q

______ – abnormal posture

A

Dystonia

425
Q

____ – Single repetitive movements, especially of face

A

Tics

426
Q

Choreathetosis combines which 3 involuntary movements?

A

Chorea, athetosis, and dystonia

427
Q

Which neurotransmitter does the Substantia nigra release to control the thalamus?

A

Dopamine

428
Q

What are the symptoms of Parkinsons?

A

TRAP
- Tremor
- Rigidity
- Akinesia
- Postural instability

  • Cognitive decline
429
Q

What is the pathogenesis of Parkinsons?

A

Dopaminergic neuron degradation
- Nigro-striatal pathway
- Decreased dopamine levels

430
Q

What is the main gene associated with Parkinsons?

A

SNCA - α-Synuclein (neurotransmitter release)

431
Q

What are the 3 main methods of treating Parkinsons?

A
  • Exercise – physical therapy
  • Restore dopamine levels – Levodopa
  • CNS Antimuscarinics – control dopaminergic release
    -Dopamine receptor agonists- Pramipexole, Ropinirole, Rotigotine
    -MAOIs- Selegiline, Rasagiline
    -COMT inhibitors- Tolcapone, Entacapone
    -Apomorphine (for “off” periods, akinesia)
432
Q

What should be avoided in Parkinsons treatment?

A
  1. Dopamine receptor antagonists (antipsychotic agents)
  2. MPTP – destroys dopaminergic neurons - Impurity in some illicit drugs (synthetic opioids)
433
Q

What is the main adverse effect of L-DOPA? What is the treatment?

A

Hallucinations and delusions
Pimavanserin (Nuplazid) – antipsychotic

434
Q

What is the MOA of Pimavanserin (Nuplazid)?

A

Antipsychotic - Inverse agonist at 5-HT2A – Visual cortex

435
Q

What is the onset and symptoms of Huntington’s disease?

A
  • Onset – age 30-40
  • Progressive loss of muscle control, Chorea, Dementia, Death – 15-20 years after onset of symptoms
436
Q

What is the cause of Huntington’s disease?

A
  • GABA reduced in basal ganglia
  • Reduction in Choline acetyltransferase (ChAT)
437
Q

What are the treatments for Huntington’s disease?

A
  • Tetrabenazine - Depletes dopamine
  • Dopamine Receptor Blockers - Haloperidol
  • Genetic counseling, speech therapy, PT/OT
438
Q

What are the 2 pathways of arachidonic acid?

A
  1. Cyclooxygenase pathway - Arachidonic acid (AA) converted to prostaglandin by COX
  2. Lipoxygenase pathway - AA converted to leukotrienes by lipoxygenase
439
Q

Differentiate between COX1 and COX2

A

COX1 - constitutive, wide distribution, homeostatic functions (platelets, GI, renal)
COX2 - expression is stimulus-dependent, facilitates inflammatory response

440
Q

What is the original NSAID?

A

Aspirin

441
Q

Which NSAIDs inhibit COX and lipoxygenase?

A

Indomethacin and Diclofenac

442
Q

Which 2 NSAIDs inhibit COX1 < COX2?

A

Celecoxib and Meloxicam

443
Q

Acetaminophen is used when ___________ effect of NSAIDs isn’t required

A

anti-inflammatory

444
Q

What are the 5 mediators released during chronic inflammation?

A
  • Interleukins
  • GM-CSF
  • TNF
  • Interferons
  • PDGF
    All increase WBCs
445
Q

What are the indications for indomethacin?

A
  • Rheumatism
  • Gout
    Patent ductus arteriosus
446
Q

Differentiate between acute and chronic effects of glucocorticoid use

A

acute - suppresses inflammation, salt and water retention, improved cognitive function, mobilizes energy stores
chronic - immunosuppression, diabetes, depression, HTN

447
Q

glucocorticoid transcription

A
448
Q

what is a DMARD

A

Disease modifying anti-rheumatic drug

Measures:
-reduced inflammation
-Decreased damage to bones and joints

Often given in conjuction with NSAIDs

449
Q

Biologic DMARDs

A

Abatacept, Rituximab, Adalimumab

450
Q

Non-biologic DMARDs

A

Methotrexate, Cyclophosphamide, Cyclosporine

451
Q

Transmission of sensation

A
  • interpret pain in the somatosensory cortex
  • 3 main types of afferent neuron fibers:
    1. A beta - all cutaneous mechanoreceptors, highly myelinated
    2. A delta - sharp pain, initial reflex, highly myelinated
    3. C - slow, burning pain, unmyelinated

Gate Control Theory of Pain

  • “Gates” in spinal cord allow pain signal through
    • Gates can be adjusted - A and C can suppress each other depending on strength of stimulus
    • Increase or decrease pain sensation
452
Q

Noxious chemicals

A
  • Tissue damage – bradykinin
    • Receptors – B1 (inflammatory) and B2 (constitutive)
    • Activate PLA and PLC
  • AA Cascade – COX and LOX
    • Prostaglandins
453
Q

What are the different pain pathways and gate theory?

A
  • spinothalamic - primary pain pathway
  • spinoreticular - emotional pain sensation
  • spinomesencephalic - terminates in periaquaductal grey matter → mu opioid receptors

Gate Control Theory of Pain

  • “Gates” in spinal cord allow pain signal through
    • Gates can be adjusted - A and C can suppress each other depending on strength of stimulus
    • Increase or decrease pain sensation
454
Q

What are the 3 opioid receptor subtypes?

A

μ (mu), δ (delta), and Κ (kappa)

455
Q

What is the medication that is a μ (mu) receptor antagonist?

A

naloxone (Narcan)

456
Q

What are the 2 medications that are μ (mu) receptor partial agonists?

A

codeine, oxycodone

457
Q

What are the 2 medications that are μ (mu) receptor full agonists?

A

morphine, fentanyl

458
Q

Pharmacokinetics of opioids: absorption

A

Well absorbed (IM, SQ, Oral)
- Nasal, patch – avoid first pass effect
- Codeine: low 1st pass metabolism

459
Q

Pharmacokinetics of opioids: distribution

A

Highly perfused tissues – accumulation
- Brain, heart, kidney, liver
- Skeletal muscle – reservoir

460
Q

Pharmacokinetics of opioids: metabolism

A

Varied:
- Morphine – Phase II to active forms (M3G, M6G)
- Esters (heroin) – tissue esterases to morphine
- Other – Phase I (CYP3A4, CYP2D6)

461
Q

Pharmacokinetics of opioids: excretion

A

Mainly in urine

462
Q

What is the MOA of opioids?

A
  1. Bind to receptors in brain and spinal cord
  2. Modulation of pain
  3. Receptor effects
    - Reduce neurotransmitter release (Glutamate, ACh, NE, serotonin, substance P)
    - Hyperpolarize postsynaptic neurons
463
Q

What are the 6 CNS effects of opioids?

A
  • Analgesia – sensory and emotional aspects
  • Euphoria (dysphoria)
  • Sedation
  • Respiratory depression - brainstem
  • Cough suppression
  • Miosis (always – marker)
464
Q

What are the CV effects of opioids?

A
  • Most have no direct effects
  • Bradycardia (CNS)
  • Meperidine (Demerol) - tachycardia
465
Q

What are the GI effects of opioids?

A

Constipation (ENS) – marked, no tolerance

466
Q

List the 7 applications of opioids

A
  1. Analgesia
  2. ACS -MONA
  3. Acute pulmonary edema
  4. Cough
  5. Diarrhea
  6. Shivering
  7. Anesthesia
467
Q

_____ is given for alcohol withdrawal

A

Naltrexone

468
Q

______ is given for opioid drug overdose

A

Naloxone (Narcan)

469
Q

Why should opioids be given sparingly in head injuries?

A

Opioids may enhance respiratory depression (lethal)

470
Q

What are the 3 structural classes of opioids?

A
  • Phenanthrenes
  • Phenylheptylamines
  • Phenylpiperidines
471
Q

What are the 3 Phenanthrenes that are strong opioid agonists?

A
  • Morphine, hydromorphone (Dilaudid)
  • Heroin (diacetylmorphine)
472
Q

What is the Phenylheptylamine that is a strong opioid agonist?

A

Methadone

473
Q

Which opioid is the only opioid that causes tachycardia? How?

A

Meperidine (Demerol) - Antimuscarinic effects (tachycardia)

474
Q

What is the main use for Meperidine (Demerol)?

A

Post-op shivering: k-opioid receptor

475
Q

What are the 3 Phenanthrenes that are moderate opioid agonists?

A
  • Codeine, oxycodone
  • More effective as combinations
    • Oxycodone + acetaminophen = Percocet
    • Oxycodone + Aspirin = Percodan
476
Q

What are the 3 opioid antagonists?

A

Naloxone, naltrexone, naloxegol

477
Q

What are the 5 classes of sedative-hypnotics?

A
  1. Benzodiazepines - Diazepam, Midazolam
  2. Barbituates - Phenobarbital
  3. Sleep aids - Zolpidem (non-benzodiazepine)
  4. Anxiolytics - Buspirone
  5. Ethanol
478
Q

What are the 2 major pathways of metabolism to acetaldehyde?

A

Alcohol dehydrogenase pathway
Microsomal ethanol-oxidizing system (MEOS)

479
Q

What drug inhibits alcohol dehydrogenase

A

Fomepizole

480
Q

What drug inhibits aldehyde dehydrogenase

A

Disulfiram

481
Q

What enzyme breaks down ethanol to acetaldehyde?

A

Alcohol dehydrogenase

482
Q

What enzyme breaks down acetaldehyde to acetate?

A

aldehye dehydrogenase

483
Q

Differentiate alcohol dehydrogenase pathway from Microsomal ethanol-oxidizing system (MEOS)

A

During conversion of ethanol by ADH to acetaldehyde, hydrogen ion is transferred from ethanol to the cofactor nicotinamide adenine dinucleotide (NAD+) to form NADH. A result of continuous alcohol oxidation, it creates an excess of NADH. Excess NADH production contributes to the metabolic disorders that occur with chronic alcoholism (i.e. lactic acidosis and hypoglycemia, both of which are present in acute alcohol poisoning).

484
Q

Which sedative-hypnotics are useful anesthesia adjuncts?

A

Barbituates – thiopental and methohexital
- very lipid-soluble, penetrating brain tissue rapidly
-short duration of action
Benzodiazepines - diazepam, lorazepam, and midazolam
-In combination with other agents
-May contribute to a persistent postanesthetic respiratory depression
-reversible with flumazenil

485
Q

What are the 3 phases of Drug development

A

In vitro -> animal study -> 3-4 human trials

486
Q

Which supplement is claimed to improve memory, immune function, and analgesia?

A

Ginseng

487
Q

What effects does the supplement St. John’s Wort have?

A

antidepressant

488
Q

Which supplement reduces hepatotoxicity?

A

Milk Thistle

489
Q

What effects does the supplement echinacea have?

A

Stimulation of immune system, Anti-inflammatory

490
Q

What effects does the supplement garlic have?

A

HMG CoA Reductase inhibitor

491
Q

What effects does the supplement ginkgo have?

A

improved blood flow, free radical scavenger

492
Q

Which supplement is used for benign prostatic hyperplasia?

A

Saw Palmetto

493
Q

3 tradition treatments for cancer

A

surgery, radiation, CHEMOTHERAPY

494
Q

Differentiate chemotherapy modalities

A

Primary Chemotherapy:
- Primary treatment is chemotherapy
- Advanced disease – goal is to limit spread, improve QOL

Neoadjuvant Chemotherapy:
- Chemotherapy induced to reduce tumor size prior to and after surgery
- Surgery is primary treatment, chemotherapy secondary
- Useful in many GI cancers, breast, lung

Adjuvant Chemotherapy:
- After surgery – reduce incidence and resurgence of tumor
- Both surgery and chemotherapy equally important, possibly radiation
- Goal is disease-free survival (DFS) and overall survival (OS)

495
Q

What are the 4 types of Alkylating Agents

A

Nitrogen Mustards (most common used)= cyclophosphamide, chlorambucil

Nitrosureas= cross BBB

Alkyl Sulfonate

Platinum analogs= cisplatin (testicular cancer), carboplatin

496
Q

What is the primary use of Cisplatin

A

Testicular cancer

497
Q

What is the MOA of methotrexate

A

Inhibits dihydrofolate reductase (DHFR)- interferes with DNA/RNA synthesis

Cytotoxic actions:
-predominant on bone marrow
-ulceration of intestinal mucosa
-Crosses placenta interferes with embryogenesis = fetal malformations and death

Immunosuppressive action
- prevents clonal expansion of B & T lymphocytes

Anti-inflammatory actions:
-interferes with release of inflammatory cytokines

498
Q

Be able to match the name and drug class of the antineoplastic drugs

A

Antimetabolites- 6MP, 5-FU

Plant based- Vincristine, Paclitaxel (Taxol)

Antibiotics- Dactinomycin, Doxorubicin, Bleomycin

Hormonal Agents- Croticosteroids, Tamoxifen, Fulvestrant

Miscellaneous- Imatinib, Trastuzumab, Rituximab

499
Q

Differentiate between the 2 types of host defenses

A

Innate - first and second line of defense
Acquired - third line of defense, B and T cells

500
Q

What 3 components are involved in the first line of defense?

A

Physical barriers, chemical barriers, and genetic components

501
Q

What 4 components are involved in the second line of defense?

A

Phagocytosis, inflammation, fever, antimicrobial proteins

502
Q

What are the components involved in the third line of defense?

A
  • B and T cells
    active - infection
    passive - maternal antibodies
503
Q

What are the 5 immune system cytokines?

A
  1. Interleukins (ILs)
    - signal among leukocytes
  2. Interferons (IFNs)
    -Antiviral proteins that may act as cytokines
  3. Growth factors
    -Proteins that stimulate stem cells to divide
  4. Tumor necrosis factor (TNF)
    -Secreted by macrophages and T cells to kill tumor cells and regulate immune responses and inflammation
  5. Chemokines
    -Chemotactic cytokines that signal leukocytes to move
504
Q

What are the 4 types of hypersensitivity?

A

Types I-IV - ACID
- A – Anaphylaxis, allergies
- C - Cytotoxic
- I – Immune complex
- D - Delayed

505
Q

_________ is the primary immunodeficiency disease lacking a thymus

A

DiGeorge Syndrome: No Thymus (no T cells)

506
Q

_________ is the primary immunodeficiency disease lacking B cells and T cells

A

Severe combined immunodeficiency disorder (SCID)

507
Q

What is an example of a secondary immunodeficiency disease?

A

Acquired Immune Deficiency Syndrome

508
Q

_______ is the immune response against normal, healthy tissue

A

Autoimmune

509
Q

Females are _____ affected than males in autoimmune diseases

A

more

510
Q

_________ are self-antigens that induce immune response

A

Autoantigens

511
Q

_______ are antibodies against autoantigens

A

Autoantibodies

512
Q

Which neuromuscular autoimmunity involves autoantibodies and T-cells against neurons, myelin?

A

MS

513
Q

Which neuromuscular autoimmunity involves destruction of ACh receptors?

A

MG

514
Q

_____ is the autoimmune disease with autoantibodies against DNA

A

SLE - lupus

515
Q

______ is the autoimmune disease of pancreas endocrine cells

A
  • Insulin-dependent Diabetes mellitus
  • Cytotoxic T cells attack beta cells (Insulin)
516
Q

Which category of immunosuppressive agents suppress immune response and mimic naturally occurring adrenal corticosteroids?

A

Glucocorticoids (corticosteroids)

517
Q

Which category of immunosuppressive agents involves inhibiting the activation of the T-cell pathway?

A

Calcineurin Inhibitors

518
Q

Which category of immunosuppressive agents kill rapidly proliferating cells?

A

Cytotoxic Agents

519
Q

Which category of immunosuppressive agents are antibodies directed against cell-surface antigens/receptors?

A

Immunosuppressive Antibodies

520
Q

What are 3 examples of glucocorticoids?

A

Prednisone, hydrocortisone, Dexamethasone

521
Q

What are 2 examples of Calcineurin inhibitors?

A

Calcineurin- necessary for T-cell receptor signaling, activation

Cyclosporine:
-Peptide antibiotic- transplantation, GVHD, other autoimmune disorders
-multiple toxicities: kidney, BP, hyperglycemia, liver, seizures

Tacrolimus:
-macrolide antibiotic
-similar uses, similar toxicities to cyclosporin
-topical-atopic dermatitis and psoriasis

522
Q

What are 3 examples of Cytotoxic Agents?

A

Azothioprine, Cyclophosphamide, Hydroxychloroquine

523
Q

What are the 5 categories of immunosuppressive agents?

A
  1. Glucocorticoids (corticosteroids)
    -suppress immune response, mimic naturally occuring adrenal corticosteroids
    -prednisone, hydrocortisone, dexamethasone
  2. Calcineurin Inhibitors
    -T cell activation pathway
    -cyclosporine, tacrolimus
  3. Cytotoxic Agents
    -kill rapidly proliferating cells
    -Azothioprine, cyclophosphamide, hydroxychloroquine
  4. Immunosuppressive Antibodies
    -antibodies created in lab, directed against cell-surface antigens/receptors
    -Muromonab(CD3), RhoGAM, Adalimumab(TNF-a)
  5. Additional Agents
    -Sirolimus, mycophenylate mofetil, thalidomide derivatives

Pharm 2024 (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions