Brainscape's Knowledge GenomeTM

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


See full index

Fall 2024 > Pharm Final > Flashcards

Pharm Final Flashcards

1
Q

Define pharmacology/medical pharmacology

A

Study of the effects of drugs in the body

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

Define toxicology

A

Undesirable effects of chemicals on living systems, from individual cells to humans to complex ecosystems

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

What are the different types of drug groups?

A

Agonists, partial agonist, antagonist, inverse agonists, agonist mimics

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

Define pharmacodynamics

A

The effects of the drug on the body

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

Define pharmacogenomics

A

Looking at genetic profile to determine how you will respond to drug

The primary reason patients respond differently to the same drug

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

Define pharmacokinetics

A

Effects of the body on the drug (half-life, can it cross barriers, ADME, etc)

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

Drugs can either be an ______ or an ______

A

agonist; antagonist

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

Define agonist

A

Binding to specific site elicits a conformational change in the protein that is bound which activates the receptor, producing the same, or similar, effect to that of a native ligand

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

Define antagonist

A

Competitive in nature to agonists and they bind to a specific receptor before an agonist can, inhibiting the response to the amount of normal constituent activity

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

Define receptor

A

A large protein, usually on the cell surface, that can bind to drugs or endogenous ligands

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

Define endogenous

A

Produced inside the organism or cell

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

Define Exogenous

A

Growing or originating from outside the organism

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

Define poisons

A

Non-biological substances (arsenic or lead)

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

Define toxins

A

Biological substances from living organisms (mushrooms)

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

Define partial agonist

A

Like agonists in binding sites but can act like antagonists if in the presence of an agonist because it only produces a partial response and prevents the agonist from binding.

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

Define inverse agonist

A

Favor the inactive receptors which effectively makes them stronger forms of an antagonist because they lower the constitutive form of the receptor

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

Define stereoisomerism

A

Same chemical formula, but doesn’t behave the same in the body

Optical isomers (D:L; R:S) - applies to more than half the body

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

Define physiologic antagonist

A

two different drugs bind to different receptors and have opposite effects

Ex: epi binding to beta receptors and increasing HR, while acetylcholine binds to muscarinic receptors and decreases HR

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

Differentiate between competitive inhibitor and allosteric inhibitor

A

Competitive inhibitor: a drug that binds to the same active site as the agonist, competing for that binding site
Allosteric inhibitor: binds to a different site on the receptor, preventing the agonist from binding and eliciting a response, even at high agonist concentrations (can’t be surmounted)

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

What 4 things make up pharmacokinetics?

A

Absorption, distribution, metabolism, elimination

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

How does the Henderson-Hasselbach equation apply in pharm?

A

In practice, pKa is pH at which ionized and un-
ionized concentrations are equal

If pH < pKa; favors protonated form
If pH > pKa; favors unprotonated form

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

How do you solve for the therapeutic ratio?

A

TD50 / ED50

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

What is a dose-response curve?

A

A graph illustrating different pharmacologic potencies and different maximal efficacies

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

What is the goal of rational dosing?

A

To achieve desired beneficial effect
with minimal adverse effects

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

Bond strength is indirectly proportional to ____

A

Specificity

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

Flux is directly proportional to _______

A

Concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Kd is indirectly proportional to ________

A

Drug binding affinity

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

Drug safety is directly proportional to the _______

A

Therapeutic index (TI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Volume of distribution (Vd) is directly proportional to the _____

A

Concentration of a drug outside of the systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Define volume of distribution

A

The space available in the body to contain the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define clearance

A

The ability of the body to eliminate the drug

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

Define rate of elimination

A

The rate at which the drug is eliminate from the body

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

Define half-life

A

The time it takes for the drug concentration to decrease by 50%

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

Define steady-state dosing, maintenance, and loading dose

A

Steady state: administering just enough to replace how much the body is eliminating per hr

Maintenance: maintain steady state of a drug by giving enough to replace eliminated drug

Loading dose: used when needing to reach steady state quickly

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

What are the parameters affecting 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
36
Q

What are the 4 basic mechanisms of transmembrane signaling?

A
  1. Direct crossing to intercellular receptor (lipid
    soluble)
  2. Enzymatic action mediated by ligand binding (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
37
Q

Explain ligand-gated ion channels

A

Ligand gates ion channels open in response to the binding of a specific ligand

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

Explain GPCR structure

A

Receptor:
Seven transmembrane spanning domains, with an extracellular ligand-binding site (amino terminal) and an intracellular G protein-binding site (carboxy terminal). Several downstream effects possible

G-Proteins
- Trimeric: alpha, beta, gamma
- GDP (inactive) → GTP (active)

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

How many families/genes do drug efflux transporters have?

A

Seven families (A-G), over 50 genes

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

Define allosteric

A

The drug binds to a different site on the receptor (away from the active site)

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

Define orthosteric

A

The drug binds directly the the active site

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

Differentiate how a full agonist, partial agonist, antagonist, and inverse agonist would look on a graph

A
  • Full agonist has the max response
  • Partial agonist is slightly above constitutive activity, but below full agonist
  • Antagonist is equal to constitutive activity
  • Inverse agonist is below constitutive activity
    See page 6 of review for reference
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is permeation? What are the 4 different types?

A

Ways to get the drug from outside the body to the inside of the body where it will eventually work

  • Aqeuous
  • Lipid
  • Endo/exocytosis
  • Special carriers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is aqueous diffusion?

A

Water soluble drugs can cross membranes

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

What is lipid diffusion?

A

Lipid soluble drugs can cross membranes (steroid nuclei drugs)

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

What are special carriers?

A

Something that will bind to a large molecule, bring it into the cell and oftentimes may stay in the cell or then pushed outside of the cell

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

What is endocytosis?

A

Membrane engulfs drug, brings it in and spits it out the other side; usually due to clathrin coated pits in receptors that bind that drug and bring it in

This is an important mechanism for very large drugs to get across impermeable membranes

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

What is exocytosis?

A

Merging of the vesicle with the membrane

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

What are examples of aqueous components in aqueous diffusion?

A

Blood, ECF, ICF

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

What are things that can’t cross the membrane through aqueous diffusion?

A

Highly charge molecules: Will interact with the cell surface and won’t be able to cross the cell membrane

Bound to large proteins (carriers): can’t cross the barrier while bound to large proteins

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

Potency is measured by ____

A

EC50 (effective concentration fr 50% of the maximum effect)

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

A drug with a lower EC50 is considered more _____

A

Potent

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

List the components of the blood-brain barrier

A

Vascular endothelium with tight junctions, astrocytes, pericytes

These constrict the entry of most drugs in the brain

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

Describe drug biotransformation

A

Chemical modifications that a drug undergoes in the body, typically to make it more water-soluble and easier to excrete

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

Some metabolites become ____ after biotransformation

A

Active

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

Major phase 1 metabolic reactions include (4) _____ and are primarily catalyzed by _____

A

Oxidation, reduction, dehydrogenation, hydrolysis

Cytochrome P450

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

If a drug induces a metabolic enzyme it will ______ the metabolism and clearance of other drugs that are substrates of that enzyme

A

Increase

This potentially reduces efficacy

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

If a drug inhibits a metabolic enzyme, it will ______ the metabolism and clearance of other drugs that are substrates of that enzyme

A

Decrease

This potentially increases toxicity

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

What can induction of a metabolic enzyme do?

A

Enhance synthesis, inhibit degradation

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

What can inhibition of a metabolic enzyme do?

A
  • Decrease or irreversible inhibit P450
  • Competitive inhibition by co-administering drugs metabolized by the same P450
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are potential results of induction of p450?

A
  • Decreased drug effect: if metabolism deactivates the drug
  • Increased drug effect: if metabolism activates the drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Define agonist mimic

A

Doesn’t bind to the active site, but can still elicit a response as if they did (cocaine, meth)

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

Differentiate between competitive and non-competitive antagonist

A

Competitive: bind and inhibit agonist response; can be countered by increasing amounts of agonist (surmountable)

Non-competitive: irreversible and insurmountable

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

What is an example of an organic compound?

A

Carbohydrate, lipid, protein, nucleic acids

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

What is an example of an inorganic compound?

A

Lithium, iron, hydrogen, oxygen

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

What are the receptor interactions?

A

Appropriate size, electrical charge, shape, composition

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

What is Bmax?

A

The maximum number of receptors available for the drug to bind to

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

What is EMax?

A

The maximum response or effect that can be achieved by the drug

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

What is Kd?

A

Drug concentration at which 50% of the receptors are occupied

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

What is TD50?

A

The point where we see 50% of toxic side effects

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

What is important about a dose-response curve in regards to therapeutic index?

A

The distance in between the ED50 line and LD50 line is the therapeutic index

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

An agonist + a noncompetitive antagonist will _______ the agonist effect

A

Decrease

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

On a dose-response curve, the higher the response, the _____ efficacious a drug is

A

More

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

Define target concentration

A

The desired concentration of the drug in the body to achieve the desired effect

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

Define bioavailability

A

The fraction of the administered dose that reaches the systemic circulation

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

A high volume of distribution (Vd) means the drug is distributed to the tissues ___________

A

Outside of the blood

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

A high clearance means the drug is eliminated from the body _________

A

More rapidly

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

Differentiate between first order and zero order elimination

A

First order: clearance is constant, rate of elimination varies with concentration
Zero order: rate of elimination is constant, clearance varies with concentration

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

First-order elimination

A

Occurs with most drugs

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

Zero-order elimination

A

Occurs when the body’s ability to eliminate a drug has reached it’s maximum capability

As the dose and drug concentration increase, the amount eliminated per hr does not

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

What is a racemic mixture?

A

Refers to a combination of optical isomers

Remember R-ketamine and S-ketamine, where S-ketamine is four times more potent than R-ketamine but has increased risk of dissociative effects and hallucinations.

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

What are the 4 main causes of drug variation?

A

Genetic factors
Physiologic factors (age, sex)
Environmental factors (diet, smoking)
Pharmacokinetic factors (ADME)

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

Describe the cell signaling process

A
  1. signaling molecules (drug, endogenous ligand) binds to the receptor
  2. the receptor undergoes a confirmational change
  3. activation of signal transduction proteins (G proteins, kinases)
  4. Generation of second messengers
  5. Activation effector proteins that elicit the cellular response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Phosphorylation cascade

A

Inactive Protein is activated by a drug or endogenous ligand → Kinase 1 (active) → Kinase 2 (active) possibly 2 or more kinases→ Kinase 3 (active) possibly more than the previous number of activated kinases→ Eventually reaches effector protein (active response)

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

Describe RTK structure

A

Extracellular ligand-binding domain, a single transmembrane domain, and an intracellular tyrosine kinase domain.

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

What is an example of a ligand gated ion channel?

A

Nicotinic ACh receptor; the receptor opens when ACh binds to it

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

Process of a ligand gated ion channel

A
  1. The signal molecule binds to the receptor
  2. Surrounding ions go through the channel and elicit a response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Explain the mechanism of GPCR signaling

A
  1. Ligand binds to the GPCR, causing a conformational change.
  2. The conformational change activates the associated G protein.
  3. The activated G protein dissociates into its α and βγ subunits.
  4. The Gα subunit releases its bond to GDP and binds with GTP which then activates an effector protein (e.g., adenylyl cyclase).
  5. The effector protein generates second messengers (e.g., cAMP, IP3).
  6. The second messengers initiate downstream signaling cascades.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What do second messengers do?

A

Amplify and propagate the signal initiated by the first messenger (drug, ligand)

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

What is desensitization?

A

The process where the cell reduces its responsiveness to a stimulus overtime

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

What is a voltage gated ion channel?

A

Ion channels that open and close in response to changes in the membrane potential

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

Define the generic pathway of CYP450 metabolism

A

The generic pathway of CYP450 metabolism involves the drug binding to the enzyme, followed by a series of oxidation and reduction reactions followed by dehydrogenation, and then release of the metabolite via hydrolysis.

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

Define the role of drug efflux transporters

A

They actively pump drugs out of cells, reducing intracellular drug concentrations. This can contribute to drug resistance.

Ex: ATP-binding cassette (ABC)

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

What are the major drug efflux transporters?

A

ABCB1: broadest substrate specificity; wide distribution and are critical to maintenance of the blood brain barrier
ABCC: antineoplastics
ABCG2: breast cancer resistance protein; also an efflux transporter of folate

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

What is the difference in inotropic and metabotropic ion channels?

A
  • Ionotropic ion channels directly allow the passage of ions across the membrane.
  • Metabotropic ion channels indirectly regulate ion movement through second messenger signaling. (E.g. GPCR activates cAMP which opens an ion channel)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are common examples of second messengers

A

cAMP
IP3 (Inositol triphosphate)
Diacylglycerol
Calcium
cGMP

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

Describe the structure of a neuron

A

A cell with a nucleus with dendrites (fingers on the outside), connected to an axon. At the end of the axon, there is a telodendria (looks like little fingers at the end). Telondendria are also known as synaptic boutons

Refer page 24 in the review

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

Neurons send action potentials/signals from the __________ to the _________

A

Neuron cell body
Telondendria

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

Where are neurotransmitters stored?

A

Telodendria

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

Where does the information coming into the neuron come in?

A

Dendrites

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

Describe the neuron process:

A
  • Once information is in dendrites it can send a “go” or “stop” signal to nucleus of neuron to either activate or suppress activation of neuron
  • Decision in cell body can activate the axon hillock and this will generate action potential
  • Action potential can go faster if myelin sheath is present; this is known as saltatory conduction.
  • Action potential will reach the telodendria (capped with synaptic boutons)
  • Synaptic boutons release neurotransmitter into the synapse and the neurotransmitter binds to receptors on the postsynaptic cell
  • Neurotransmitters are stored in synaptic terminal/boutons but they are actually made in the neuron itself
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is a synapse?

A

Gap between the neuron and the cell

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

What are the types of synapses?

A

Chemical: release neurotransmitters into the synapse (ACh, GABA)
Electrical: pass electrical current from one cell to the other through gap junctions (commonly in the heart)

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

What are the 6 main classes of neurotransmitters?

A
  • Esters (ACh): cholinergic
  • Monoamines (norepinephrine, serotonin, dopamine, many catecholamines): adrenergic
  • Amino acids (glutamate, GABA)
  • Purines (adenosine, ATP)
  • Peptides (substance P, endorphins)
  • Inorganic gases (Nitric oxide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Why are inorganic gasses considered a neurotransmitter?

A

It is released by effector cell and has effect on postsynaptic cell

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

Afferent is going ____ the CNS; Efferent is going _____ from CNS

A

Towards
Away

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

What are the efferent divisions?

A

Somatic nervous system: controls skeletal muscle; conscious control
Autonomic nervous system: includes parasympathetic and sympathetic; no conscious control over

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

The autonomic nervous system is seperated into:

A

Parasympathetic, sympathetic, and enteric

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

Neuron cell body clusters in the CNS are called _____

A

Nuclei

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

Neuron cell body clusters in the PNS are called ________

A

ganglia

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

Describe the sympathetic nervous system

A

Known for fight or flight (increasing HR, bronchiole dilation, shunt blood to skeletal muscles and away from GI)

Affects a lot of our CV system. Widespread impact, reaches organs and tissues

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

Describe the parasympathetic nervous system

A

Rest and digest system

This brings you back down to normal. It conserves energy and shunts blood to GI and endocrine system. Innervates only specific visceral structures, effects are shorter lived

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

The gut has its own nervous system called

A

Enteric nervous system: associated with causing “gut feelings”

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

Where do the fibers origin in the sympathetic nervous system?

A

Thoracolumbar region of the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Where do the fibers origin in the parasympathetic nervous system?

A

Brain and sacral spinal card

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

What is the length of fibers in the sympathetic nervous system?

A

short preganglionic and long postganglionic

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

What is the length of fibers in the parasympathetic nervous system?

A

Long preganglionic and short postganglionic

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

Where is the location of the ganglia in the sympathetic nervous system?

A

Close to the spinal cord

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

Where is the location of the ganglia in the parasympathetic nervous system?

A

In the visceral effector organs

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

What is the difference in receptors in the SNS and PNS?

A

SNS: beta and alpha receptors - GPCR
PNS: muscarinic (GPCR) and nicotinic receptors (ion channel)

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

How does the alpha and beta receptor work in the SNS?

A

SA node is primary node that sets the pace for the heart – if we release norepinephrine or epinephrine, it binds to beta 1 and 2 receptors and increases heart rate and heart contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Where does the PNS primarily work through?

A

Vagus nerve: PNS stimulation is not constant, it returns to homeostasis and shuts off

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

Define sympathomimetics

A

drugs that mimic the sympathetic nervous system (mimic fight or flight)

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

Define cholinomimetic (aka parasympathomimetics)

A

drugs that mimic acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Define parasympatholytics (aka antimuscarinics/parasympathoplegic)

A

Drugs that block parasympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Define sympatholytics/Sympathoplegic (alpha or beta blockers/sympathoplegic)

A

drugs that block sympathetic nervous system response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

List the ANS receptors

A

Cholinergic (receptors that bind to and are activated by ACh)
Adrenergic (respond to norepinephrine and epi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are the adrenergic receptors divided into?

A

Alpha 1/Alpha2
Beta 1-3
Dopamine (1-5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What does alpha 1 do?

A

activates Gq → GDP to GTP → activates phospholipase C → activates IP3 and DAG (second messengers)

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

What does alpha 2 do?

A

activates Gi → inhibits adenylyl cyclase → inhibits cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What does beta 1-3 do?

A

activates Gs → stimulates adenylyl cyclase → produce cAMP

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

What does IP3 do after it’s activated?

A

Goes to sarcoplasmic reticulum where calcium is produced in the cell (binds to calcium channels) → Calcium is mobilized into the cell → activates protein kinase → MLCK activated → interacts with actin to contract the muscle cell

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

What does DAG do after it’s activated?

A

activates protein kinase C: this is something that inhibits myosin light-chain phosphatase → MLCK doesn’t get stripped up the phosphate

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

When you think of beta 1, think of the _____

A

heart

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

What is the pathway for beta 1 (and beta 2)?

A

GDP to GTP → stimulates adenyl cyclase → ATP to cAMP → activates protein kinase A → (2 effects) 1. More calcium gets in from the outside 2. Protein kinase A is going to stimulate calcium release from sarcoplasmic reticulum

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

In the heart, beta 2 = ______. In the periphery, beta 2 = _________

A

Contraction
Relaxation

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

How does beta 2 work in the periphery?

A

Increases in cAMP → inhibit myosin light-chain kinase (MLCK is going to phosphorylate myosin and make it so that it can interact with actin in a form of contraction.) → relaxation

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

What are the cholinergic receptors divided into?

A

Nicotinic and muscarinic (1-5)

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

Which muscarinic receptors are stimulatory?

A

1, 3, 5

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

What will the muscarinic Gq activate?

A

Gq activates phospholipase activation. → increase IP3 and DAG

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

Which muscarinic receptors are inhibitory?

A

2 and 4

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

What does muscarinic Gi inhibit?

A

Adenylyl cyclase

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

Where can our cholinergic nicotine receptors be?

A

Ganglionic, skeletal muscle, neuronal CNS

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

What is different about nicotinic receptors vs muscarinic receptors?

A

Muscarinic receptors are GPCRs, nicotinic are ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Where are the muscarinic receptor subtypes found?

A

Pacing centers of the heart
Smooth muscle
Nerves
Glands
Endothelium

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

Where are our dopamine receptors?

A

Most are in the brain, but there are some in the CV system and smooth muscle in the kidney

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

Effects of alpha 1 (sympathetic)

A

Smooth blood vessels: contract
GI Sphincter smooth muscle: contract
Kidney/urinary sphincter: contract
Liver: glycogenolysis

reference page 29

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Effects of alpha 2 (sympathetic)

A

GI tract wall smooth muscle: relax

reference pg 29

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

Effects of beta 1 (sympathetic)

A

SA node: accelerates
Contractility: increases
Kidney: renin release

reference pg 29

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

Effects of beta 2 (sympathetic)

A

SA node: accelerates
Contractility: increases
Skeletal blood vessels: relax
Bronchiolar smooth muscle: relax
GI tract wall smooth muscle: relax
Bladder: relax
Liver: glycogenolysis

reference pg 29

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

Effects of M2 (parasympathetic)

A

SA node: decelerates
Contractility: decreases

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

Effects of M3 (parasympathetic)

A

Smooth blood vessels: relax
Bronchiolar smooth muscle: contract
GI wall smooth muscle: contract
GI spinchter smooth muscle: relax
GI secretions: increase
Bladder: contract
Urinary spinchter: relax

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

What is the autonomic feedback loop?

A
  1. Baroreceptors sense increased pressure and send it to the vasomotor center
  2. If MAP is high, it will send to PNS and decrease CO and HR
  3. If MAP is too low, it will send to SNS → sends norepi which binds to beta 1 to increase CO; norepi will also bind to alpha to increase BP
  4. If MAP is low, SNS will also increase HR, contractility, and venous tone; so works on chronotropic and inotropic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is the hormonal feedback loop?

A
  1. MAP low → kidney sees this (juxtaglomerular apparatus) → release renin → changes angiotensinogen to angiotensin (1,2) → aldosterone → constrict blood vessels, take up more water, produce less urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What are the direct acting adrenergic agonists?

A

Albuterol
Clonidine
Dobutamine
Dopamine
Epi
Isoproterenol
Norepi

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

What are the indirect acting adrenergic agonists?

A

Amphetamines

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

What is a direct and indirect acting adrenergic agonist?

A

Ephedrine

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

What organ system to beta receptors determine direct effects?

A

Heart

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

What does stimulation of beta receptors in the heart do?

A

Increased CO
Decreased peripheral resistance

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

How do you solve for CO?

A

SV (70ml/beat) X HR (75 beat/min) = CO (ml/min)

This would equal 5250 ml/min

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

What are examples of catecholamines?

A

Epi
Norepi
Isoproterenol
Dopamine
Dobutamine

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

What receptors does epi work on?

A

Alpha 1 & 2, Beta 1 & 2

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

What is the structure of a catecholamine?

A

Catechol group and amine group

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

What receptors does norepinephrine work on?

A

Alpha 1 & 2, Beta 1

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

What receptors does isoproterenol work on?

A

Beta 1 & 2

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

What receptors does dopamine work on?

A

D 1-5; higher doses alpha 1 and beta 1

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

What receptor does dobutamine work on?

A

Beta 1

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

When would you use an adrenoceptor antagonist as treatment?

A

HTN related to phenochromocytoma

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

What are examples of reversible adrenoceptor antagonist drugs?

A

Phentolamine, tolazoline, prazosin, labetalol, propanolol, metoprolol, atenolol, terazoin, doxazosin

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

What is an example of an irreversible adrenoceptor antagonist? Why is it irreversible?

A

Phenoxybenzamine

It forms a covalent bond; requires new receptors

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

What do beta antagonists do in the heart?

A

Negative inotropic
Negative chronotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What do beta antagonists do in the blood vessels?

A

Opposes B2 mediated vasodilation
Acute: increased peripheral resistance
Chronic: decreased peripheral resistance (mechanism unclear)

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

What are examples of beta antagonist drugs?

A

Propanolol
Metoprolol
Atenolol
Esmolol

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

Where does propranolol work?

A

Beta 1 and 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Where does metoprolol and atenolol work?

A

Mainly B1 selectivity

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

What 2 diseases is it safer to use metoprolol or atenolol when picking a beta blocker?

A

COPD, diabetes

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

Esmolol is _________ acting

A

ultra short

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

What are cholinomimetics (direct acting) mode of action?

A
  • Bind to and active M or N receptors
  • Esters of choline, alkaloids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What are cholinomimetics (indirect acting) mode of action?

A

Inhibit hydrolysis of ACh
- inhibit action of acetylcholinesterase
- prolongs effects of ACh released at junction

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

What are cholinomimetic effects on the eye?

A
  • muscarinic agonists: miosis
  • increase intracocular drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What are cholinomimetic effects on the CV system?

A
  • reduction in peripheral vascular resistance
  • vasodilation (reduction in BP; reflex tachycardia)

In large doses, can cause bradycardia

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

What are examples of indirect acting cholinomimetics?

A

Simple alcohols
- quaternary ammonium group (ex: edrophonium)
Carbonic acid esters of alcohols
- quaternary or tertiary ammonium group (ex: carbamates and neostigmine)
Organic derivatives of phosphoric acid
- Ex: organophosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What are the major therapeutic uses of indirect cholinomimetics?

A

Disease of the eye
GI and urinary tracts
Neuromuscular junction (myasthenia gravis)
- autoimmune against ACh receptor
Atropine OD

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

S/S of organophosphate exposure? What is the treatment?

A

SLUDGE-M
Tx: atropine, pralidoxime

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

What is edrophonium used for?

A

Diagnostic test for MG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What does SLUDGE-M stand for?

A

Salivation
Lacrimation
Urination
Defecation
GI motility
Emesis
Miosis (constriction of the pupil)

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

S/S of muscarinic excess? What can cause this, and what is the treatment?

A

SLUDGE-M
Caused by poisonous mushrooms
Tx: atropine

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

S/S of atropine OD? What can cause this, and what is the treatment?

A

BRAND
Caused by belladona
Tx: physostigmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What does BRAND stand for?

A

Blind, red, absent bowel sounds, nuts, dry

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

What type of receptors are all adrenergic receptors?

A

GPCR

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

In angina classification, what is the difference in stable, unstable, and variant?

A

Stable: angina of effort (classic)
Unstable: acute coronary syndrome
Variant: Prinzmetal, angina inversa

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

What are the causes of stable, unstable, and variant angina?

A

Stable: plaque
Unstable: plaque
Variant: hyperreactive vessels

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

What are the precipitating factors of stable, unstable, and variant angina?

A

Stable: exercise, stress
Unstable: resting
Variant: resting/vasospasm

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

Stable angina is ______ and may be relieved by ______

A

Brief
Rest

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

Unstable angina is an __________

A

Emergency

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

Variant angina is considered ______ with only _______ of anginas being this type

A

Rare
2%

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

What are NO, nitrates, nitrites actions on vascular smooth muscle?

A

Activate GC, increase cGMP: relaxation

Good: increase venous capacitance, decrease ventricular preload, decrease heart size, decrease CO

Bad: orthostatic hypotension, syncope, HA, reflex tachycardia

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

What are beta-2 agonists actions on vascular smooth muscle?

A

GPCR, cAMP, relaxation (mainly respiratory)

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

What are beta blockers actions on vascular smooth muscle?

A

Decrease demand (HR)

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

What are calcium channel blockers actions on vascular smooth muscle?

A

Less total calcium: relaxation

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

What is sildenafil actions on vascular smooth muscle?

A

Block PDE5, increase cGMP: relaxation

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

Describe the pathway of blood vessel contraction in periphery

A

Involves an influx of calcium
1. Calcium is released from SR and binds to calmodulin
2. Calcium calmodulin activates MLCK (MLCK is responsible for adding phosphate group to myosin light chain)
3. Phosphorylated myosin can interact with actin, causing contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

Pathway of relaxation in the periphery

A
  1. Beta 2 agonists increase cAMP production
  2. cAMP deactivates MLCK
  3. Increase in cGMP will dephosphorylate MLCK (cGMP can be increased by NO)
  4. This will cause relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What is the other way that relaxation in the periphery can occur (in terms of guanylyl cyclase)?

A
  1. NO activates guanylyl cyclase
  2. GC turns GTP into cCMP
  3. gCMP desphosphorylates MLCK, causing relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What type of drug is sildenafil, and what is its MOA?

A

PDE inhibitor
Inhibits breakdown of cAMP and cGMP by blocking phosphodiesterase

Postive inotropic effects

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

What type of channels do calcium channel blockers work on?

A

L-type in the vascular smooth muscle and heart

Relaxation:
- some effects on GI, GU, uterine

Long lasting smooth muscle relaxation, reduce BP

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

What do CCB do in the heart?

A

Decrease contractility
Decrease SA node pacemaker rate
Decrease AV node conduction velocity

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

When it comes to selectivity, what are the two main types of CCB and what is their focus? sorry I know this is worded weird

A

Dihydropyridines: more peripheral vasculature
Verapamil and Diltiazem: more cardiac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

What is the toxicity associated with CCB?

A

Serious cardiac suppression (rare)
Bradycardia
AV block
CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

Small facts about beta blockers

A
  • not vasodilators
  • used in angina of effort and silent (ambulatory) ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

Beneficial effects of beta blockers

A

Decrease oxygen demand
- decrease HR
- decrease BP
- decrease contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

What are the 4 anatomical control sites that antihypertensives work on?

A
  • diuretics: deplete sodium
  • sympathoplegics: decrease PVR and CO
  • direct vasodilators: relax vascular smooth muscle
  • anti-angiotensins: block activity or production

Antihypertensives can act on 1 or more of these

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
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
214
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
215
Q

What drugs are CNS sympathoplegics?

A

methyldopa
clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

What do CNS sympathoplegics do? (clonidine and methyldopa)

A

Primary antihypertensive activity due to alpha agonist activity in the brainstem; decreases sympathetic stimulation

Bind more tightly to alpha 2 than alpha 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

Propanolol MOA and what does it do?

A

Antagonizes beta 1 and 2 receptors

Lowers BP, decreases CO, inhibits renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

What is propanolol toxicity associated with?

A

Beta blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

What are the alpha 1 adrenoceptor antagonist? How do they work?

A

Prazosin, terazosin, doxazosin

Block alpha 1 at arterioles and venues
Dilates both resistance and capacitance vessels

BP is more reduced in upright position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

Vasodilators example

A

Minoxidil
Hydralazine
Sodium nitroprusside
Fenoldopam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

What is minoxidil MOA?

A

Opens K+ channels in smooth muscle
- stabilized potential, less likely to contract

Dilates arteries and arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

What is hydralazine MOA?

A

Dilates arterioles (NO production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

What is the toxicity associated with hydralazine?

A

HA, nausea, sweating, flushing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

What is sodium nitroprusside used for?

A

HT emergencies, cardiac failure
Dilates arterial and venous vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

MOA of sodium nitroprusside

A

Relaxes vascular smooth muscle
- breaks won in blood to release NO
- increases intracellular cGMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

What is fenolopam used for?

A

HTN emergencies, post op HTN
Peripheral arteriolar dilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

MOA of fenoldopam

A

Agonist of D1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

What does D1 and D5 work on?

A

Brain, effector tissues, smooth muscle of the renal vascular bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

What does D2 work on?

A

Brain, effector tissues, smooth muscle, presynaptic nerve terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

What does D3 work on?

A

Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

What does D4 work on?

A

Brain, CV system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

What do ACE inhibitors do?

A

Block ACE, which is what converts angiotensin 1 to angiotensin 2

This causes decreased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

What do ARBS do?

A

Block angiotensin II so it can’t convert to aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

What does aldosterone do?

A

Increased sodium and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

Definition of heart failure

A

When the heart fails to meet the metabolic demands of the tissues or not pumping properly (inadequate CO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

Causes of HF

A

Most common: CAD
Chronic BP
Uncontrolled hyperthyroidism
Graves disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

How does CAD cause HF?

A

Coronary artery disease → angina→ MI (death of cardiac myocytes→ cannot proliferate→ scar tissue replaces them making heart pump ineffectively) → scarring/remodeling→ heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

What are the two types of HF?

A

Systolic: reduced cardiac function
Diastolic: reduced cardiac filling (peripheral), cardiac hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

Describe systolic HF

A

Heart is not pumping due to thin heart muscle walls

Decreased CO and EF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

Describe diastolic HF

A

Heart muscle is too thick, so it’s pumping effectively but unable to pump as much blood because there isn’t room

Decreased CO with normal EF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

What is congestive heart failure?

A

Increased left ventricle pressure at end diastole
Results in increased pulmonary pressure (pulmonary edema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

Pathway of normal cardiac contractility

A
  1. Trigger calcium enters cell
  2. binds to channel in SR, release stored calcium
  3. Frees actin to interact with myosin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

What are the 4 factors in cardiac performance?

A

Preload
Afterload
Contractility
HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

Define preload

A

Measure of stretch, not volume
If there is increased blood volume or venous tone, this will increase preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

Define after load

A

Force that the heart has to pump against

Essentially is our BP: the higher the BP, the higher the after load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

Define contractility

A

Contraction of myocytes (inotropy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

MOA of digoxin

A

Inhibits Na/K ATPase pump to maintain normal resting potential

Positive inotrope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

What is the EC50 and TC50 of digoxin?

A

EC50: 1 ng/ml
TC50: 2 ng/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

What are the effects of digoxin on other organs?

A

Affects all excitable tissues d/t inhibition of Na/K pump
- Smooth muscle
- CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

What is an example of PDE inhibitor?

A

Milrinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

What is the crescent shaped node in the right atrium?

A

SA node / pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

What is the rate of contraction at the SA node?

A

75 beats/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

What is the node at the junction of the aria and ventricles?

A

AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

What is the bundle at the interventricular septum? Another name for this?

A

Atrioventricular bundle
Bundle of His

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
255
Q

What are the fibers within the muscle of the ventricular walls?

A

Purkinje

256
Q

What are the phases of a cardiac action potential?

A

Phase 4 (straight horizontal line)
Phase 0 (straight vertical line)
Phase 1 (peak at the top)
Phase 2 (horizontal line at the top of the graph)
Phase 3 (downward slanted line)
Phase 4 (straight horizontal line)

reference pg 73

257
Q

Explain phase 4 in cardiac action potential

A

-96 mv
K+ channels close, membrane potential is at resting

258
Q

Explain phase 0 in a cardiac action potential

A

Fast Na+ channels open, Na+ goes into cell

259
Q

Explain phase 1 of cardiac action potential

A

K+ and Cl- go out of cell
Per Schmidt, K+ inward rectifying channels close

260
Q

Explain phase 2 of cardiac action potential

A

Ca+ comes into the cell
K+ goes out of the cell

261
Q

Explain phase 3 of cardiac action potential

A

K+ continues to leave, returning cell to resting membrane potential into phase 4

262
Q

What is an example of a disturbance of impulse conduction?

A

Heart block/reentry

263
Q

In order for reentry to occur: (3)

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
264
Q

What are the 4 classes of antiarrhythmic agents?

A

Class I: sodium channel blockade
Class II: sympatholytic (alpha and beta adrenergic inhibition)
Class III: prolong action potential duration (other mechanisms besides sodium channels; K+)
Class IV: block cardiac calcium channel currents (CCB)

265
Q

What are the divisions of class I antiarrhythmics?

A

A
B
C

266
Q

Describe class 1A of antiarrhythmics

A

Drug: Quinidine
APD/ERP: lengthens
Dissociation: Intermediate
State Affinity: Activated

267
Q

Describe class 1B of antiarrhythmics

A

Drug: Lidocaine
APD/ERP: shortens
Dissociation: Fast
State Affinity: inactivated, some activated

268
Q

Describe class 1C of antiarrhythmics

A

Drug: flecainide
APD/ERP: no effect
Dissociation: slow
State Affinity: inactivated

269
Q

What is the only anti arrhythmic with all 4 class effects?

A

Amiodarone

270
Q

What is the drug of choice for VT?

A

Amiodarone

271
Q

What are the initial, symptomatic, and chronic treatments of bradycardia?

A

Initial: Underlying cause, d/c drugs
Symptomatic: 1st: atropine; 2nd: epi, dopamine
Chronic: pacemaker

272
Q

What are the initial, symptomatic, and chronic treatments of a heart block?

A

Initial: 1st degree - not usually treated (asymptomatic)
Symptomatic: atropine; transcutaneous pacing
Chronic: pacemaker

273
Q

What are the initial, symptomatic, and chronic treatments of SVT?

A

Initial: assess cause, r/o atrial flutter
Symptomatic: adenosine
Chronic: CCB, beta blockers

274
Q

What are the initial, symptomatic, and chronic treatments of sinus tach?

A

Initial: assess cause, r/o wide complex
Symptomatic: adenosine, CCB, cardioversion
Chronic: catheter abrasion; ICD

275
Q

What are the symptomatic and chronic treatments of VT (wide complex)?

A

Symptomatic: amiodarone, lidocaine, magnesium (torsades)
Chronic: amiodarone, satolol

276
Q

What are the symptomatic and chronic treatments of afib?

A

Symptomatic: diltiazem, verapamil
Chronic: beta blockers, amiodarone

277
Q

What are the symptomatic and chronic treatments of vfib?

A

Symptomatic: CPR, defib, epi, vasopressin
Chronic: amio, lido, mag

278
Q

What are the 5 classes of diuretics?

A

Carbonic anhydrase inhibitors
Loop diuretics
Thiazides
Potassium sparing diuretics
Agents that alter water excretion

279
Q

Where do carbonic anhydrase inhibitors work?

A

Proximal tubule

280
Q

Explain what goes on the proximal tubule (brief)

A

NHE3 starts cycle
- countercurrent exchange
- H+ binds to barcyrbonate to form carbonic acid
Carbonic anhydrase
- conversion of carbonic acid into water and CO2

See pg 80 for picture

281
Q

Where do loop diuretics work?

A

Loop of henle

282
Q

Explain what goes on the loop of henle (descending/ascending) *brief

A

Descending
- water reabsorption (hypertonic medullary interstitium)
Ascending
- impermeable to water
- active transport of NaCl via NKCC2
- K+ excess, diffusion, causes charge in lumen
- charge difference drives out cations

see pg 81

283
Q

Where do you have passive diffusion of water?

A

Descending loop of henle

284
Q

Where do you have active transport of NaCl?

A

Ascending loop of henle

285
Q

Where in the tubule is impermeable to water?

A

Ascending loop of henle

286
Q

What can the urinary concentration get up to?

A

1200

287
Q

T/F: Loop diuretic have no development of acidosis

A

True

288
Q

Loop diuretics are the most ______ diuretics

A

Efficacious

289
Q

What are examples of loop diuretics?

A

Furosemide
Ethacrynic acid

290
Q

MOA of loop diuretics

A

Inhibit NKCC2 pump
- selectively inhibit NaCL reabsorption in the thick ascending loop

291
Q

Where do thiazides work?

A

Distal convoluted tubule

292
Q

DCT has a _____ amount of sodium reabsorption

A

low

293
Q

In the DCT, there is active ______ reabsorption done by ______

A

Calcium
PTH

294
Q

MOA of thiazides

A

Block NCC
- inhibit NaCl transporter
- some inhibition of CA activity

295
Q

What is the thiazide prototype?

A

hydrochlorothiazide

296
Q

What types of cells are present in the collecting tubule?

A

Principal cells

297
Q

Explain principal cells

A

Sites for water, Na+, and K+ transport
No cotransporter atypically, only cation channels
Builds a (-) charge in lumen

298
Q

Why do the principal cells build a negative charge in the lumen

A
  • More Na+ in than K+ out
  • Drives Cl- out through the paracellular route

see pg86

299
Q

Diuretics upstream result in excess ______ in the CT

A

Sodium

300
Q

Some diuretics block NaCl, which causes _____ to leave via _______ route

A

Chloride
Paracellular

301
Q

Some diuretics block NaHCo3, which means _____ can’t leave through ______ route, and drives _______ depletion

A

HCO3
Paracellular
Potassium

see pg 87 for picture

302
Q

What hormones are working at the CT?

A

Aldosterone
ADH

303
Q

What does aldosterone do at the CT?

A

Increase Na+ and water reuptake (ENaC)
Increase blood volume

304
Q

What diuretics are responsible for blocking aldosterone receptors? Example?

A

Potassium sparing diuretics
Spironolactone

305
Q

What does ADH do at the CT?

A
  • Increases water reabsorption
  • Adds preformed AQP2 to apical membrane
  • Increases blood volume
  • Makes more concentrated urine
306
Q

What is an antagonist to ADH?

A

Conivaptan

307
Q

What is an example of osmotic diuretics and what is it used for primarily?

A

Mannitol
Reduce ICP (promote removal of renal toxins)

308
Q

What is mannitol associated toxicity?

A
  • Extracellular volume expansion
  • Rapidly distributed to extracellular compartments

Dehydration
- excessive use without water replacement

309
Q

See pg 93 for picture related to allergy

A

I had no idea how to put a flashcard over this lmao

310
Q

What are the 4 histamine receptors in humans? What type of receptor are they?

A

H1, H2, H3, H4
GPCR

311
Q

What is H1 responsible for?

A

bronchoconstriction
vasodilation

312
Q

Antihistamines are what type of drug?
Example?

A

H1 selective inverse agonist
Diphenhydramine (most useful for type I hypersensitivity)

313
Q

What are common histamine effects?

A

Nervous system
- Stimulates pain/itching
CV
- lower BP (vasodilation)
- increase HR (reflex tachy)
Sectretory
- stomach: secretes hydrochloric acid (H2)
Lungs
- bronchoconstriction
GI Smooth muscle
- contraction (peristalsis)

314
Q

What is the “wheal and flare”?

A

Microcirculation smooth muscle
Capillary endothelium
Sensory nerve endings

“triple response”

315
Q

What can h1 receptor antagonists be used for?

A

Sedation
- resembles antimuscarinic
- sleep aids
- children may have reverse effects
Antinausea/antiemetic
- motion sickness
Antiparkinsonism
- suppress extrapyramidal symptoms
Local anesthesia
- block Na+ channels in excitable membranes
Other
- inhibition of mast cell release

316
Q

H2 receptor agonists are not as _______ as PPIs

A

effective

317
Q

There is heavy OTC use in ______

A

H2 receptor antagonists

318
Q

What is another mediator that is liberated from the lung during inflammation? What type of receptor?

A

Leukotrienes
GPCR

319
Q

Leukotrienes are a ____ reacting substance of anaphylaxis

A

Slow

320
Q

What do leukotrienes produce?

A
  • bronchospasm
  • mucous secretion
  • microvascular permeability
  • airway edema
321
Q

What are the 3 types of drugs used in asthma?

A

Bronchodilators
Anti-inflammatory
Leukotriene antagonists

322
Q

What 3 classes are in bronchodilators?

A

Beta agonist
Antimuscarinics
Methylxanthines

323
Q

What 3 classes are in anti-inflammatory agents?

A

Steroids
Slow anti-inflammatory drugs
Antibodies

324
Q

What 2 classes are in leukotriene antagonists?

A

Lipoxygenase inhibitors
Receptor inhibitors

325
Q

What is a toxic effect of sympathomimetics?

A

Skeletal muscle tremor

326
Q

What drugs are included in sympathomimetics?

A

Epi (arrythmogenic)
Isoproterenol (arrythmogenic, increased mortality)
Terbutaline
Formoterol
Salmeterol

327
Q

What are the safer options out of the list of sympathomimetics?

A

Terbutaline
Formoterol
Salmeterol

Beta2 selective, long acting (lipid soluble)

328
Q

List the administration routes for sympathomimetics

A

Epi: SQ, Inh (320 mcg) - 60-90 min effect
Isoproterenol: Inh (80-120 mcg) - 60-90 min effect
Terbutaline: Inh, IV
Formoterol: Inh
Salmeterol: Inh

329
Q

What are examples of methylxanthines?

A

Theophylline, theobromine, caffeine

330
Q

Methylxanthines MOA

A

Several proposed, none established
- inhibits PDE
- inhibits adenosine receptors
- anti-inflammatory action

331
Q

Pharmacodynamics of Methylxanthines

A

Bronchodilation
CNS stimulation

332
Q

What is the clinical use of muscarinic antagonist?

A
  • effective bronchodilators: block contraction of airway smooth muscle, mucus secretion
  • parasympathetic blockage
333
Q

What are examples of muscarinic antagonists?

A

Atropine: parenteral
Ipratropium bromide: COPD
Tiotropium (24 hr): COPD

334
Q

MOA of leukotriene pathway inhibitors & examples

A

Inhibit synthesis pathway
- inhibit 5 lipoxygenase (ex: zileuton)
- inhibit binding to the receptor (ex: zafirlukast, montelukast)

335
Q

What type of drug is omalizumab (Xolair)?

A

Anti-IgE monoclonal antibody

336
Q

MOA of Xolair

A

Targets portion of IgE that binds to mast cells
- does not activate IgE already on mast cells
- does not provoke degranulation

337
Q

Xolair lessens ________ severity, and decreases ______ requirement and _________

A

asthma
corticosteroid
hospitalizations

338
Q

List serotonin effects on the body

A

Nervous system
- melatonin precursor
- vomiting reflex
- pain and itch (similar to histamine)
- chemoreceptor reflex (bradycardia, hypotension)

Respiratory
- facilitate ACh release: constriction
- hyperventilation

Gi
- overproduction (diarrhea)

CV:
- contraction of vascular SM (exception: smooth muscle/heart)
- platelet aggregation

339
Q

What are the serotonin receptors for this class? (1st gen)

A

5-HT 1A
5-HT 1D/1B
5-HT 2
5-HT 3

340
Q

Explain 5-HT1A receptor, give an example, and uses

A

Agonist
Example: buspirone
Uses: anxiolytic (GAD, OCD)

341
Q

Explain 5-HT 1D/1B receptor, give an example, and uses

A

Agonist
Ex: triptans
Uses: Migraine HA

342
Q

What is toxicity associated with triptans?

A

Recurrence of migraine
Serotonin syndrome (triptans + SSRI, MAOI)

343
Q

Explain 5-HT 2 receptor, give an example, and uses

A

Antagonist
Ex: phenoxybenzamine
Uses: carcinoid tumors, cyproheptadine (cold induced urticaria)

344
Q

Explain 5-HT 3 receptor, give an example, and uses

A

Antagonist
Ex: ondansetron
Uses: anti-emetic

345
Q

List the 3 main types of hyperthermic syndromes

A

Serotonin syndrome
Neuroleptic syndrome
Malignant hyperthermia

346
Q

List common precipitating drugs, clinical presentation, and treatment for serotonin syndrome

A

Drugs:
SSRI, MAOI, St Johns wort, triptans, tramadol
Presentation:
HTN, tremor, hyperthermia, hyperactive bowel, coma
Tx:
Sedation (benzes), intubation, 5-H2 blocker

347
Q

List common precipitating drugs, clinical presentation, and treatment for neuroleptic malignant syndrome

A

Drugs:
D-2 blocking antipsychotics
Presentation:
HTN, hyperthermia, acute severe Parkinsonism
Tx:
Diphenhydramine, cooling, benzos if needed

348
Q

List common precipitating drugs, clinical presentation, and treatment for malignant hyperthermia

A

Drugs:
volatile anesthetics, succs
Presentation:
hyperthermia, HTN, tachycardia, muscle rigidity
Tx:
Dantrolene, cooling

349
Q

What are the 3 main classes of antidepressants?

A

SSRI (SNRI)
TCA
MAOI

350
Q

All antidepressants carry a black box warning for increased ___________

A

Suicidal tendencies

351
Q

What is the MOA of SSRI/SNRI & examples

A

Inhibit SERT
- Prozac, zoloft
Inhibit SERT and NET
- pristique, Cymbalta

352
Q

MOA of TCAs and example

A

Inhibit SERT, NET, and anticholinergic
- Elavil

353
Q

What are the two main classes of seizures and divisions underneath those?

A

Focal
- simple partial
- complex partial
- partial seizures secondarily generalized

Generalized
- tonic-clonic (grand mal)
- absence (petit mal)
- tonic
- atonic
- clonic and myoclonic
- infantile spasms

354
Q

What is the emergency treatment for all seizure types?

A

Benzos

355
Q

What is the drug of choice for focal seizures?

A

Lamotrigine

356
Q

What drugs can be used for all focal seizures + generalized tonic clonic?

A

Phenytoin, phenobarbital, carbamazine

357
Q

What is the drug of choice for absence seizures?

A

Ethosuxamide

358
Q

What drugs can be used for all generalized seizures, except tonic clonic and infantile?

A

Valproic acid

359
Q

What is the drug of choice for infantile spasms?

A

Vigabatrin

360
Q

What is the toxicity associated with carbamazepine (tegretol)

A

diplopia, ataxia, GI, drowsiness

361
Q

What is the toxicity associated with phenobarbital?

A

Sedation, hepatic enzyme inducer

362
Q

What is the toxicity associated with ethosuximide?

A

GI, lethargy, hiccup, euphoria

363
Q

Ethosuximide is only available as _______

A

syrup

364
Q

What is the toxicity associated with valproic acid?

A

Hepato, GI, sedation, fine tremor, drug displacement

365
Q

What are the plasma levels for phenytoin?

A

Therapeutic:
10-20 mcg/ml

Free phenytoin:
1-2.5 mcg/ml

Toxic:
30-50 mcg/ml

Lethal:
>100 mcg/ml

366
Q

What is the toxicity associated with phenytoin?

A

drug displacement

367
Q

Why would you prefer to use a 2nd gen H1 receptor antagonist than a 1st gen?

A

More systemic effects, less CNS (does not cross BBB)

368
Q

What does thrombogensis do in the blood vessels?

A
  • vasconstriction
  • formation of platelet plugs
  • regulation of coagulation and fibrinolysis
369
Q

What are the 4 phases of platelets?

A
  1. Adhesion
  2. Aggregation
  3. Secretion
  4. Cross-linking of adjacent platelets
370
Q

Platelet aggregation pathway

A
  1. Damage exposes collagen and von willebrand factor
  2. Collagen binds to platelets specifically at the glycoprotein 1-A receptor.
    - Von willebrand factor binds to platelets at the glycoprotein 1-B receptor.
  3. adenosine(ADP), thromboxane A-2, and serotonin(5 HT) is released
  4. Serotonin causes vasoconstriction of smooth muscle on vessels and it binds to serotonin receptors on other platelets which activates those platelets.
  5. ADP and thromboxane A2 also bind to additional receptors on other platelets that are going to activate more platelets
  6. Once the second platelet is activated it degranulates and releases additional ADP, thromboxane A2 and 5 HT.

It’s a positive feedback mechanism where multiple platelets are going to join together to be cross linked into this network

371
Q

Common pathway steps

A
  1. Factor 10 is activated.
  2. Factor 10 activates the inactive form of thrombin (aka prothrombin) to its active form called thrombin.
  3. Thrombin increases the release of more thrombin, it activates platelets, and it converts the inactive form of fibrinogen into the active form of fibrin.
  4. Fibrin helps platelets aggregate together and it forms a mesh network to trap platelets.
372
Q

Steps in the intrinsic pathway

A
  • Damage to the surface activates factor XII(12)
  • XII activates factor XI(11)
  • XI activates factor IX(9)
  • IX + VIII(8) activates factor X(10)

this starts the common pathway

373
Q

What is the result of DIC?

A

Generalized blood coagulation
Consumption of factors and platelets
Spontaneous bleeding

374
Q

Cause of DIC

A

Massive tissue injury
Malignancy
Bacterial sepsis
Abruptio Placentae

375
Q

Treatment of DIC

A

Plasma transfusions
Underlying cause
10%-50% mortality

376
Q

Pathway for fibrinolysis

A

Plasminogen → plasmin (active form) → breaks down fibrin into FSP and fibrinogen into degradation products
○ tPA activates plasminogen into plasmin (active form)
○ Urokinase and streptokinase also do this ^^

377
Q

What can we use to keep a clot from breaking down (fibrinolytic inhibitor)? how does it work?

A

Aminocaproic acid
transischemic acid (TXA)

inhibits the breakdown of plasminogen to plasmin

378
Q

What are examples of fibrinolytics?

A

Tissue plasminogen activator (t-PA)
Urokinase
Streptokinase

379
Q

What protects clots of lysis?

A

Aminocaproic acid

380
Q

What does indirect thrombin inhibitors do? What are examples of each?

A

Enhances antithrombin activity
- unfractionated heparin (HMW)
- LMW heparin
- fondaparinux

381
Q

What does HMW do?

A

Decreased thrombin and factor Xa

382
Q

What adverse effects can come from HMW? How do you treat?

A

HIT, bleeding
Protamine sulfate

383
Q

What does LMW do?

A

Decrease factor Xa

384
Q

What does fondaparinux do?

A

Decrease factor Xa

385
Q

What does direct thrombin inhibitors do? Give examples of each

A

Either
Bind to active and sublate recognition sites of thrombin
- Hirudin (from leeches; lepirudin is recombinant)
- Bivalirudin (Angiomax)
Bind only to thrombin active sites
- argatroban
- melagatran

386
Q

What does hirudin target?

A

Thrombin in clot

387
Q

MOA of warfarin

A

Inhibits vit. K cycling

388
Q

What is the onset of action of warfarin?

A

8-12 hour delay

389
Q

The therapeutic range of warfarin is defined by _____. The goal is to reduced _______ activity by _____ of normal

A

INR
Prothrombin
25%

390
Q

Normal INR
INR target for warfarin

A

0.8-1.2
2-3

391
Q

How does t-PA work?

A

Preferentially activates plasminogen that is bound to fibrin

392
Q

What is streptokinase synthesized by?

A

Streptococci

393
Q

What is urokinase synthesized by? How does it work?

A

Kidneys
Lyses the thrombus from within

394
Q

What are the different types of platelet inhibition? Examples?

A

Inhibition TXA2 synthesis : ASA
Blocking ADP : Plavix and ticlid
- reduce platelet aggregation
Blocking GP2&3 : Abiciximab

395
Q

What are different platelet changes that can be seen?

A

Shape
Granule release
Aggregation

396
Q

Vitamin K is ____ soluble

A

Fat

397
Q

Where do you get vitamin K from?

A

Leafy green vegetables
Gut bacteria

398
Q

Vitamin K confers activity on:

A

Prothrombin
Factors VII, IX, X

399
Q

Vitamin K has a _______ effect

A

delayed

400
Q

Vitamin K is necessary for ____________

A

efficient blood coagulation

401
Q

MOA of aminocaproic acid

A

Completely inhibits plasminogen activation

402
Q

Uses for aminocaproic acid

A
  • adjunctive hemophilia therapy
  • bleeding from fibrinolytic therapy
  • intracranial aneurysms
  • post surgical bleeding
403
Q

What are the two major types of secretory issues in the pancreas?

A

Exocrine
Endocrine

404
Q

What does the exocrine gland do?

A

Releases digestive enzymes into the duodenum to help with protein and carb digestion

405
Q

Where is the endocrine gland? What does it consist of?

A

Smallest portion of the pancreas, in locations called pancreatic islets

Islet of langerhans

406
Q

What does the islet of langerhans consist of? What do these cells release?

A

Alpha cells: release glucagon and proglucagon
beta cells: release of insulin, proinsulin, C peptide, and amylin
delta cell: releases somatostatin

407
Q

What is the approximate percent of islet mass of alpha and beta cell?

A

Alpha: 20%
Beta: 75%

408
Q

What is diabetes mellitus? What are the 4 types?

A

Elevated blood glucose
Type I: insulin dependent
Type II: non-insulin dependent
Type III: other causes (pancreatitis, drug therapy, etc)
Type IV: gestational

409
Q

Function of beta cells

A

Proform
Activated in granules

410
Q

C peptide has ________ function

A

no known

411
Q

Insulin secretion pathway

A

When BG is high, we will get a large influx of glucose through Glut 2 transporters into the beta cell.

That glucose is metabolized via glycolysis to produce ATP

High levels of ATP bind to the potassium channels on the cell surface (inward rectifying K+ channel that maintains the normal membrane polarization).

ATP closes the potassium channels, depolarizing the membrane making us more positive.

This causes VG- CA++ channels to open
Ca++ rushes into cell and increased Ca++ levels bind to the vesicle complex that contains the stored insulin

The vesicle then fuses with the cell membrane and releases insulin into the blood

412
Q

What type of receptor is insulin?

A

Tyrosine kinase

413
Q

What are the effects of an insulin receptor?

A
  • Membrane translocation of GLUT
  • Increased glycogen formation
  • Activation of multiple transcription factors
414
Q

What are the 4 types of insulin preparations?

A

Rapid acting
Short acting
Intermediate acting
Long acting

415
Q

Rapid acting insulin examples

A

lispro
aspart
glulisine

416
Q

Short acting insulin examples

A

novolin
humulin

417
Q

Intermediate acting insulin examples

A

NPH, isophane

418
Q

Long acting insulin examples

A

glargine
detemir

419
Q

8 classes of oral anti diabetic agents

A

Biguanides
Insulin secretagogues
Thiazolidinediones
Alpha-glucosidase inhibitor
Incretin-based therapies
Amylin analogs
Bile acid sequestrant
SGLT2 inhibitors

420
Q

MOA of biguanides and example

A

Block glucose formation in the liver
Metformin

421
Q

MOA of insulin secretagogues and example

A

K+ channel
Sulfonylureas

422
Q

MOA of thiazolidinediones

A

PPAR mediated increase in insulin signal

423
Q

Other classes in incretin-based therapies

A

GLP1 agonist
DPP4 antagonist

424
Q

MOA of amylin analogs

A

suppress glucagon release

425
Q

MOA of SGLT2 inhibitors and example

A

Prevent glucose absorption in PCT
Gliflozins

426
Q

Plaque formation is _________

A

inflammatory

427
Q

What is the cholesterol 3 part synthesis in cells?

A
  • mevalonate from acetyl-coa
  • conversion of mevalonate to squalene
  • cyclization of squalene to cholesterol
428
Q

Atherogenesis pathway

A
  • excess LDL gets sequestered underneath the intima of the artery
  • WBC come in
  • differentiate into macrophages (proinflammatory)
  • Swallow up LDL
  • proinflammatory-> releases things to oxidase LDL
    -now oxidized LDL enters blood stream and antibodies are formed against it.
  • Macrophage itself can’t break down cholesterol so macrophages build up. Called foam cells
  • crystallization of the cholesterol inside of the foam cell makes them rupture

INFLAMMATION= positive feed back
when they all die it forms a calcified plaque

429
Q

4 types of lipoproteins

A

Chlomicrons
VLDL
LDL
HDL

430
Q

Where are chylomicrons formed? What do they do? Where are they degraded?

A

Formed in the intestine (dietary)
Carry triglycerides and cholesterol
Degraded by liver

431
Q

Where is VLDL secreted? What is is converted to?

A

Secreted by liver, travel to peripheral tissues
Converted to LDL

432
Q

What does LDL do? What happens in excess?

A

Transporter
Excess gets stuck in arteries

433
Q

What does HDL do? Decreased levels are associated with what?

A

Scavenger of cholesterol from cells
Atherosclerosis

434
Q

Normal total cholesterol

A

<200

435
Q

Normal LDL

A

<130

436
Q

Normal HDL (men and women)

A

> 40
50

437
Q

Normal triglycerides

A

<120

438
Q

Drug classes for lowering cholesterol

A

Statins (HMG-CoA reductase inhibitors)
Niacin
Fibrates
Binding resins
Absorption inhibitors
PCSK9 inhibitors

439
Q

MOA of statins

A

Structural analogs of HMG-CoA reductase
Decrease cellular cholesterol synthesis
Increase LDLR
- scavenge LDL from blood
- major effect on liver
Modest decrease in triglycerides
Small increase in HDL

440
Q

Dosing and uses in statins

A

Dose range from 10-80 mg
Absorption enhanced by food - at night
Restricted use in children, pregnant, lactating

441
Q

Statin toxicity

A

Elevated liver enzymes
- increased with liver damage, pts of Asian descent
CK elevations
- muscle pain or weakness

442
Q

What does niacin do? Dosing?

A

Decreases VLDL, LDL
- reduces VLDL secretion from liver
Increases HDL
Incorporated into NAD
Cutaneous vasodilation

Dosing 2-6 g daily

443
Q

What do fibrates do?

A

Decrease VLDL, modest decrease in LDL
Increase lipolysis in liver

444
Q

Toxicity in fibrates

A

Rare
GI upset
Arrhythmias
Elevated liver enzymes
Potentiation of coumarin
Myopathy

445
Q

What do bile acid binding resins do? Dosing?

A

Isolated increases in LDL
Large cation exchange resins (not absorbed)
Bind bile acids - prevent reabsorption
Primary hypercholesterolemia
May increase VLDL
Granular preparations

Dosing: 5 g/day; up to 30 g/day

446
Q

Absorption inhibitor MOA

A

block NPC1L1 transporter from transporting cholesterol from the bile acid into the body

447
Q

Example of absorption inhibitor

A

Ezetimibe

448
Q

PCSK9 pathway and example

A

PCSK9 binds to LDL-r. Goes into clatherin coated pit. Receptor is now marked for destruction by the lysosome.
This leads to a decrease in LDL-r

less cholesterol being taken in d/t limited receptors=more in bloodstream

statin increase PCSK9

Example: Evolocumab

449
Q

MAB- PCSK 9 inhibitors are never given

A

alone, always with a statin
Lowers LDL by 65% if given with statin

450
Q

side effects of MAB- PCSK 9 inhibitor

A

Risk of hypocholesterolemia

451
Q

General properties of antimicrobial agents

A

Selective toxicity
Spectrum of activity
Modes of action
Side effects
Resistance of microorganisms

452
Q

5 modes of action of antibiotics

A

Inhibition of cell wall synthesis
Disruption of cell membrane function
Inhibition of protein synthesis
Inhibition of nucleic acid synthesis
Action as antimetabolites

453
Q

Examples of cell wall inhibition antibiotic drugs

A

Penicillin, bacitracin, cephalosporin, vancomycin

454
Q

Examples of disruption of cell membrane antibiotics

A

Polymyxin

455
Q

Examples of protein synthesis inhibitor antibiotics

A

Tetracycline
Erythromycin
Streptomycin
Chlormphenicol

456
Q

Examples if nucleic acid inhibitors antibiotics

A

Rifamycin (transcription, mRNA synthesis)
Quinolones (DNA replication, inhibit DNA gyrase)
Metronidazole

457
Q

Examples of antimetabolite antibiotics

A

Sulfonilamide
Trimethoprim

458
Q

What is the structure of penicillin and cephalosporin? What type of bacteria?

A

Beta lactam ring
Gram (+) cocci; anaerobes

459
Q

Adverse reactions of penicillins

A

Hypersensitivity
- most common drug allergy
- can cross react with similar abx
Allergic reactions
- anaphylactic shock (0.05%)
- skin rash (<1%)
- oral lesions
- hemolytic anemia
- interstitial nephritis

460
Q

Cephalosporins are _______ to b-lactamase

A

More resistant

461
Q

Cephalsporins are a ________ spectrum

A

broader

462
Q

Uses for cephalosporins

A

UTI, Staph
Alternative to PCN (less allergy)

463
Q

Vancomycin is resistant to _________

A

b-lactamase

464
Q

Vancomycin is known as the drug of _______

A

last resort

465
Q

Vancomycin is an alternative to _________ and can be used for _______

A

PCN resistant bacteria
MRSA

466
Q

Vancomycin toxicity

A

10% adverse reactions
Irritating to tissues
Chills/fever
Ototoxicity
Nephrotoxicity
“red neck syndrome”

467
Q

Polymyxins act as _________ and bind to ________

A

detergents
phospholipids

468
Q

Polymyxins are especially effective against _________ which have an ______ membrane

A

Gram (-) bacteria
outer

469
Q

Tetracyclines are __________

A

bacteriostatic

470
Q

Pharmacokinetics of tetracyclines

A

readily absorbed
widely distributed

471
Q

Tetracyclines have the _____ spectrum of activity of any abx

A

widest

472
Q

Tetracyclines destroy the normal _________ and often produce severe _______

A

Intestinal microbiota
GI disorders/bone deposition disorders

473
Q

What is the prototype drug of macrolides? Where does it come from?

A

Erythromycin
Streptomycin Erythreus

474
Q

What are semi-synthetic derivatives of macrolides?

A

Clarithromycin (biaxin)
Azithromycin (Zithromax)

475
Q

What spectrum do macrolides work on?

A

(+), (-), atypicals

476
Q

Quinolones have excellent ______ activity and good _______ activity

A

gram (-)
gram (+)

477
Q

Types of quinolones and uses

A

Cipro
levoquin
floxin

Uses: UTI, RTI, bone/join infections, ADR

478
Q

Antimetabolites are structurally similar to ______ and work on _______

A

PABA
synthesis of folic acid

479
Q

Antimetabolite toxicity

A

Allergenic
May precipitate in urine
Hematopoetic disturbances

480
Q

Uses of antimetabolites and examples

A

Pneumocystis, toxoplasmosis
- in conjunction with trimethoprim
- bactrim, septra

481
Q

Unique properties of viruses

A

Infectious particles
- rather than organisms
Active or inactive
- rather than alive or dead
Obligate intracellular parasites
- 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

482
Q

Components of viruses (some may or may not have all)

A

Capsid: protein coating of outer shell
Envelope
Naked virsus
Spikes

483
Q

Uses for antivirals

A

HSV
Cytomegalovirus
Varicella zoster
Hepatitis B/C
Influenza
HIV
RSV
Covid

484
Q

Acyclovir MOA

A

missing OH group
herpes can’t tell difference and mistakes it for DGTP and results in chain termination. This blocks nucleic acid synthesis

485
Q

Antiretroviral nucleoside/nucleotide analogs

A

Zidovudine (Azidothymidine, AZT)
- combined with other virals in highly active antiretroviral therapy (HAART)
- inhibitor of reverse transcriptase
Lamivudine

486
Q

Lamivudine MOA

A

Inhibits HBV DNA polymerase and HIV reverse transcriptase

487
Q

Antivirals used to treat influenza

A

Tamiflu
Relenza: powder (used for prevention if exposed)
Xofluza

488
Q

Types of flu are separated by:

A

Type A and Type B
Hemaglutinin
Neuroaminidase

489
Q

Define tremor

A

Rhythmic movement around joint

490
Q

Define chorea

A

Muscle jerks in various areas

491
Q

Define ballismus

A

WILD, violent abnormal movements
*subtype of chorea

492
Q

Define athetosis

A

Slow, writhing and twisting movement

493
Q

Define dystonia

A

Non-movement related abnormal posture

494
Q

Define tics

A

Single, repetitive movements, especially with the face

495
Q

Define choreathetosis

A

Chorea + athetosis
Intermittent, regular jerking movements and regularized flowing/twisting movements

496
Q

Dopamine pathway (indirect)

A

Not enough dopamine → use indirect pathway → stimulates basal ganglia using glutamate → stimulates thalamus → stimulates motor cortex → causes Parkinson’s tremors → lose direct pathway → lose fine motor control

497
Q

Dopamine pathway (direct)

A

Dopamine comes from the pars compacts in the sustantia nigra → striatum → GABA and substance P inhibit the basal ganglia → inhibits the thalamus → inhibits motor cortex

498
Q

Parkinsons presentation:

A

TRAP (tremor, rigidity, akinesia, postural instability)
Cognitive decline

499
Q

Patho of Parkinsons

A

Most common genetic predisposition: alpha synuclein gene (SNCA)
- SNCA produces the alpha synuclein protein which controls neurotransmitter release in dopaminergic neurons and the neurons that turn on or off the dopaminergic neurons.
Alpha synuclein
- Found in CNS neurons - specifically in substantia nigra
- Found in Lewy bodies - concentrations of alpha synuclein that conglomerates together

500
Q

Treatments of Parkinsons

A

Exercise (physical therapy)
Restore dopamine levels
Avoid:
- dopamine receptor antagonists (antipsychotics)
- MPTP: destroys dopaminergic neurons

501
Q

What are drugs can we give to restore dopamine levels?

A

Levodopa
Dopamine receptor agonist: pramipexole, ropinirole, rotigotine
MAOI: selegiline, rasagiline
COMTi: tolcapone, entacapone
CNS antimuscarinics: control dopaminergic release
Apomorphine: for “off periods”, akinesia (ex: amantadine)

502
Q

What are the considerations of levodopa? Side effects?

A

Only 1%-3% can cross BBB, use with crabidopa
S/S: n/v, depression, hallucination (use primavanserin), dyskinesia, on/off periods

503
Q

What causes Huntington’s?

A

GABA is reduced at the basal ganglia
Reduction in choline acetyltransferase (ChAT)
Excess dopamine

504
Q

Treatments of Huntingtons

A

Tetrabenzine
- depletes dopamine
Dopamine receptor blockers
- haloperidol
- Genetic counseling, ST/PT/OT

505
Q

What is the cell damage pathway to arachidonic acid?

A

cell damage
releases eicosanoids (signaling molecule) to release membrane phospholipids

phospholipase uses those to create arachidonic acid.
AA can do the cox or Lox pathway

506
Q

See pg 166 for arachidonic acid pathway

A

LOX/COX

507
Q

cox1 vs cox2

A

cox1-constitutive, widespread, converts aa into pg and txa2
“housekeeping” does homeostatic functions so generally don’t want to inhibit

Cox2- stimulus (cytokines) dependent. Facilitates inflammatory response so inhibiting is beneficial.

508
Q

pros and cons to cox 2 specific drugs

A

pros:
* no impact on plt aggregation
* no GI effects
* no impact on COX 1
- good for arthritis

cons:
* debilitating side effects
* sulfonamide so allergy risk
* black box warning for adverse CV events

509
Q

Does aspirin favor cox 1 or 2? What is the clinical use?

A

Cox 1
Clinical use:
- widely used, not for severe pain (1200-1500 mg TID)
- rheumatoid arthrities, fever
- clot prevention (81-325 mg/day)

510
Q

Aspirin platelet effect

A

aspirin binds to serine molecule and prevents aa from getting into the cell
which blocks COX which blocks TXa2 which prevents plt. aggregation and it forms and irreversible block.

plts that are circulating for 8-10 days will be impacted as well as all the plts being produced

This is why you have to stop asa several days before surgery.

511
Q

List other NSAIDS for this class and if they favor cox 1 or 2

A

Celecoxib: Cox2
Ibuprofen: Cox1 = Cox2
Indomethacin: Cox and Lox
Acetaminophen (not an NSAID, but it was on the table, possible cox2)

512
Q

List use, adverse effects, and other considerations for celecoxib

A

Use: arthritis
Adverse: CV BB warning

Other: it is a sulfonamide, so high allergy alert

513
Q

List use, adverse effects, and other considerations for ibuprofen

A

Use: pain, inflammation
Adverse: NSAIDS, agranulocytosis, aplastic anemia

Less GI upset than ASA

514
Q

List use, adverse effects, and other considerations for indomethacin

A

Use: arthritis, gout, PDA
Adverse: GI (1/3 pts)

515
Q

List use for acetaminophen

A

Use: pain, fever

516
Q

Acute effect of glucocorticoids

A

Suppress inflammation
Mobilize energy stores
Improve cognitive function
Salt and water retention

517
Q

Chronic effect of glucocorticoid

A

Immunosuppression
Diabetes, obesity, muscle wasting
Depression
HTN

518
Q

List examples of drug classes that use glucocortiocid transcription

A

Annexin-1 (lipocortin-1)
- suppresses phospolipase A2
- inhibit leukocyte response
Secretary leukoprotease inhibitor
IL-10: immunosuppressive enzyme
InH-NFkB

519
Q

List drug examples of glucocorticoid and route of admin

A

Hydrocortisone, prednisone, dexamethasone

Route: topical, oral, parenteral, injected, inhaled

520
Q

What are DMARDS? What are they used for?

A

Disease modifying anti-rheumatic drugs
- reduced inflammation
- decreased damage to bones and joints

521
Q

DMARDS are often given in conjunction with ______

A

NSAIDS

522
Q

Non-biologic DMARDS

A

methotrexate, cyclophosphamide, cyclosporine

523
Q

Biologic DMARDS

A

Abatacept (Orencia), rituximab (Rituxan), adaimumab (humira)

524
Q

What are A beta fibers for?

A

nNon-noxious mechanical stimuli

525
Q

What are A delta fibers for?

A

Noxious heat, mechanical stimuli (sharp pain, produces initial reflex response)

526
Q

What are C fibers for?

A

Noxious chemical, heat, and mechanical stimuli (slow, burning pain)

527
Q

Pathway for sensation (brief)

A

Primary afferent neurons (A beta, delta, C fibers) → dorsal root ganglion → spinal cord (3 different paths) → thalamus

528
Q

What are the 3 main pain pathways?

A

Spinothalamic: primary pain
Spinoreticular: emotional sense of pain
Spinomesencephalic: gate theory of pain, ends in periqueductal gray matter

529
Q

What does tissue damage release? What receptors?

A

Bradykinin
B1 (inflammatory)
B2 (constitutive)

530
Q

What does the AA pathway produce?

A

COX/LOX pathway
Prostaglandins

531
Q

Noxious chemicals work on ______ channel action potentials

A

sodium

532
Q

Affective sensation

A

pain in processes in CNS and we want to do something about it

Brain picks 1 of the 3 pain pathways

533
Q

Almost every opioid is going to target the ____ receptor

A

Mu

534
Q

Gate theory of pain

A

A fibers can sometimes shut down C fibers since they are technically faster

Why we “rub” an area we just hurt to help control pain

“Gates” in spinal cord allow pain signal through but they can be adjusted to increase or decrease pain sensation
Pain pathway

Small fibers (C) – readily transmit pain through gate
Large fibers (A) – can suppress pain signaling (close gates)

535
Q

Different opioid classifications

A

Agonists
Partial agonists
Antagonists

536
Q

Receptor specificity in opioids

A

Mu
- full agonist: morphine/fentanyl
- partial agonist: codeine, oxycodone
antagonist: narcan
Delta
Kappa

537
Q

Pharmacokinetics of opioids

A

A: well absorbed (IM, SQ, Oral)
D: Highly perfused tissues - accumulation
M:
*morphine: phase II to active forms (M3G, M6G)
*esters (heroin): tissues esterases to morphine
* other: phase I (CYP3A4, CYP2D6)
E: mainly in urine

538
Q

Pharmacodynamics of opioids

A

MOA:
* bind to receptors in brain and spinal cord
* modulation of pain
*receptor effects
- reduced neurotransmitter release
- hyper polarize postsynaptic neurons

539
Q

What neurotransmitters are reduced by opioids?

A

glutamate, ACh, NE, serotonin, substance P

540
Q

CNS effects of opioids

A

Analgesia: sensory/emotional aspects
Euphoria: dysphoria
Sedation
Resp. depression: brainstem
Cough suppression
Miosis (always, used as a marker)
Increased muscle tone: trunk
N/V
Hyperthermia (mu) or hypothermia (kappa)

541
Q

Analgesia is used in ___ and ____ pain; it is not as effect in _____ and ______

A

severe/constant
sharp/intermittent

542
Q

In terminal illness, analgesia is used in a ____ interval and with ______ release

A

FIxed
Sustained

543
Q

When analgesia is used in obstetrics, it’s important to use __________

A

Fetal monitoring

544
Q

Other uses for analgesia:

A

Pulmonary edema
Cough
Diarrhea
Shivering
Anesthesia
*preop (anxiety) or post (pain)
*periop: anesthetic (fentanyl)
*epidural

545
Q

Minimal or no degree of tolerance that develops with opioids

A

Miosis
Constipation
Convulsions
Antagonist actions

546
Q

Moderate degree of tolerance to opioids

A

Bradycardia

547
Q

High degree of tolerance with opioids

A

Analgesia
Euphoria/dysphoria
Mental clouding
Sedation
Respiratory Depression
Antidiuresis
N/V
Cough suppression

548
Q

Cautions with opioids

A

Drug OD
- use narcan
Head injuries
- opioids may enhance resp. depression (lethal)
Impaired pulm. function
Pregnancy
- fetal dependence

549
Q

What are the classes within strong agonist opioids?

A

Phenanthrenes
Phenylheptylamines
Phenylpiperidine

550
Q

Phenanthrenes (strong agonist) drugs

A

Morphine
Dilaudid
Heroin

551
Q

Phenylheptylamines drug and uses

A

Methadone

Uses: chronic pain (morphine intolerance)
opioid abuse

552
Q

Phenylpiperidine (strong agonist) drugs

A

Fentanyl: different analogs and routes
Meperidine (demerol)

553
Q

Demerol uses and side effects

A

Post op shivering (K-opioid receptor)

side effects:
Antimuscarinic effects (tachycardia)
(-) inotrope
Seizures

554
Q

List the classes within moderate agonists of opioids

A

Phenantheres
Phenylpiperidines

555
Q

Phenanthrenes (moderate agonist) drugs

A

Codeine
Oxycodone

these are more effective in combinations

556
Q

Percocet is a combination of

A

Oxycodone + acetaminophen

557
Q

Percodan is a combination of

A

Oxycodone + aspirin

558
Q

Phenylpiperidine (moderate agonist) drugs and uses

A

Loperamide (imodium) : diarrhea

low incidence of abuse

559
Q

Opioid antagonist are a derivative of _______. Examples are___

A

morphine

Naloxone
Naltrexone
Naloxegol

560
Q

Opioid antagonists complete and dramatically reverse opioid effects in _______. ______ has a short duration and some opioid effects may return

A

1-3 minutes
Naloxone

561
Q

Opioid antagonist have _____ effect in the absence of an ______

A

Little
Agonist

562
Q

5 classifications of sedative-hypnotics and examples

A

Benzos
- diazepam, midazolam
Barbiturates
- phenobarbital
Ethanol and chloral hydrate
Sleep aids
- zolpidem, ramelteon (addition potential)
Anxiolytics
- Buspirone

563
Q

Clinical uses for sedative-hypnotics

A

Relief of anxiety
Insomnia
Sedation and amnesia before/during medical procedures
Treatment of epilepsy/seziures
Component of balanced anesthesia
Control of ethanol or other sedative-hypnotic withdrawal states
Muscle relaxation in neuromuscular disorders
Diagnostic aids for treatment in psychiatry

564
Q

Describe the Alcohol dehydrogenase pathway (AD)

A

Ethanol is broken down by alcohol dehydrogenase (ADH) into acetaldehyde.

If we are drinking at moderate levels, acetaldehyde is broken down by aldehyde dehydrogenase → then produced into acetate → acetate can be broken down into lipids/glucose or it can be breathed out

Alcohol dehydrogenase and Acetaldehyde both utilizes NAD (nicotinamide adenine dinucleotide) → NAD is converted into NADH → NADH goes through electron transport chain to make ATP/energy

565
Q

what drug can inhibit alcohol dehydrogenase?

What is the result of this?

A

Fomepizole

increases our ethanol levels

566
Q

Acetaldehyde is a toxic compound that produces what symptoms?

A

headaches, N/V

Associate acetaldehyde with hangover symptoms

567
Q

Disulfiram (antabuse) MOA

Who is a target for this drug and why?

A

inhibits aldehyde dehydrogenase that converts acetaldehyde into acetate (so you’ll have more acetaldehyde in the body)

This can be given to chronic alcoholics. Within minutes of drinking alcohol, they have these hangover symptoms
The goal is to make them feel bad so they stop drinking

568
Q

Describe the Microsomal ethanol-oxidizing system (MEOS) pathway

A

This pathway produces NADPH as a byproduct, instead of NAD/NADH
These individuals get less calories from alcohol. They tend to be thinner as well (this is because they aren’t having the conversion of NAD → ATP → calories)
This pathway still produces acetaldehyde

569
Q

Which pathway is going to increase in activity with people who have chronic alcohol use?

A

MEOS

570
Q

What are the treatment options for alcohol withdrawal syndrome and alcohol-use disorders?

A

Detoxification: Taper sedative to benzodiazepines
Alcohol counseling

Meds:
Naltrexone
Acamprosate
Disulfiram

571
Q

How does Naltrexone work?

A

Long acting opioid antagonist
Patients must be opioid free before initiating because it could cause acute withdrawal syndrome from opioids

572
Q

How does Acamprosate work?

A

Deals with the desire for alcohol
GABA channels in CNS decrease over time → patient has withdrawals and does not have normal brain function → acamprosate increases GABA activity
Adjunct therapy, not effective alone

573
Q

Anesthesia can be separated into ____ and _______

A

Barbituates
Benzos

574
Q

Barbituates examples & pharmacokinetics

A

Thiopental and methohexital

Very lipid soluble; penetrating brain tissue rapidly
Short duration of action

575
Q

Benzo examples and reversal agent

A

Diazepam
Lorazepam
Midazolam

Flumazenil

576
Q

Benzos may contribute to a persistent _________

A

Postanethetic respiratory depression

577
Q

Describe the process from discovering a drug till it gets on the market.

A

A. In vitro studies-done on the cell to find a lead compound
B. apply for a patent
C. animal testing
D. investigational new drug has to be approved
E. clinical testing in 3 phases
1. is it safe pharmacokinetics 20-100 broke college students healthy
2. does it work on patients? double blind sick people100-200
3. does it work on pts. with the disease? 1000-6000
F. Marketing
4. post marketing surveillance

578
Q

List herbal supplements

A

Echinacea
Garlic
Ginkgo biloba
St Johns Wort
Ginseng
Milk thistle
Saw Palmetto
Co Q10
Glucosamine
Melatonin

579
Q

Echinacea claims and possible issues

A

Immune function, inflammation

Issue: GI upset

580
Q

Garlic claims and possible issues

A

Lower cholesterol, coagulation, cancer, anti-bacterial

Issue: odor (breath, body), coagulation

581
Q

Ginkgo claims

A

Increased blood flow, memory, dementia

582
Q

St Johns wort claims and possible issues

A

Depression

Issue: Induce CYP

583
Q

Ginseng claims

A

Memory, immunity, analgesia

584
Q

Milk thistle claims

A

Hepatotoxicity

585
Q

Saw Palmetto Claims

A

BPH

586
Q

Co Q10 claims

A

Blood pressure, MI

587
Q

Glucosamine claims

A

Joint health

588
Q

Melatonin claims

A

Depression, jet lag

589
Q

Traditional treatments of neoplasia

A

Surgery, radiation, chemo

590
Q

Define Primary, Adjuvant, and Neoadjuvant Chemotherapy

A

Primary: chemo is primary treament; no surgery or radiation
Neoadjuvant: chemo is used to reduce tumor size prior to and after surgery
Adjuvant: chemo after surgery; reduces resurgence of tumor

591
Q

Toxicity of chemo

A

attacks rapidly dividing cells
- N/V
- bone marrow depression
- alopecia
-abortion
- fetal death
- teratogenicity
- carcinogenicity
- immunosuppression

592
Q

Differentiate the different cell types of cancers

A

Carcinoma
* epithelial origin; highly replicative; skin, GI tract
Sarcoma
* connective tissue or muscle; slow growing
Leukemia
* “liquid”; cancer of the immune cells in the blood
Lymphoma
* “solid” cancer of the immune cells in lymph nodes

593
Q

Alkylating agents are the ____ and ______ diverse class

A

largest
most

594
Q

Groups of alkylating agents

A

Nitrogen Mustards (cyclophosamide, chlorambucil)
Nitrosoureas (can cross BBB)
Alkyl Sulfonate
Platinum Analogs (cisplatin, carboplatin)

595
Q

MOA of cisplatin

A

enters cell

forms highly reactive platinum complexes

cross links

dna damage

inhibits cell proliferation

596
Q

Cisplatin is ____ bound to plasma proteins and concentrates in the ____

A

Highly
kidney, intestine, testes

597
Q

Cisplatin _____ penetrates the BBB and is slowly excreted in the _____

A

Poorly
Urine

598
Q

Uses of cisplatin

A

Testicular cancer (85%-95% curative)
Ovarian cancer
Other solid tumors (lung, esophagus, gastric)

599
Q

MOA of methotrexate?

A

dihydrofolate reductase- interferes with DNA and RNA synthesis

600
Q

What are the different actions of methotrexate?

A

Cytotoxic actions
Immunosuppressive actions
Anti-inflammatory actions

601
Q

How does methotrexate have cytotoxic actions?

A
  • predominant in bone marrow
  • ulceration of intestinal mucosa
  • crosses placenta, interferes with embryogenesis (fetal death)
602
Q

How does methotrexate have immunosuppressive actions?

A

Prevents clonal expansion of B and T lymphocytes

603
Q

How does methotrexate have anti-inflammatory actions

A

Interferes with release of inflammatory cytokines

604
Q

Other antineoplastic drugs
Just know name and class

A

Antimetabolites: 6-MP, 5-FU
Plant based: Vincristine, paclitaxel
Antibiotics: dactinomycin, doxorubicin, bleomycin
Hormonal agents: corticosteroids, tamoxifen, fluvestrant
Miscellaneous: imatinib, trastuzumab, rituximab

605
Q

Explain defense mechanisms of the host

A
  1. Host defenses split into innate and acquired
  2. Innate is split into the first and second of defense
  3. The first line of defense includes physical barriers, chemical barriers, genetic components to keep microbes from penetrating sterile body compartments
  4. The second line of defense includes phagocytosis, inflammation, fever, antimicrobial proteins that comes into play when agents make it past the surface defenses
  5. The acquired defense includes the 3rd line of defense
  6. The 3rd line of defense includes active (infection) and passive (maternal antibodies), which combines into B and T cells

see pg 197 for reference

606
Q

Immune system cytokines

A
  • Interleukins (signal among leukocytes)
  • Interferons (antiviral proteins that may act as cytokines)
  • Growth factors (proteins that simulate stem cells to divide)
  • Tumor necrosis factor (secreted by macrophages and T cells to kill tumor cells and regulate immune responses)
    -Chemokines (chemotactic cytokines that signal leukocytes to move
607
Q

Immune response picture see pg 199

A
  1. Hyposensitives are split into primary immunodeficiency and secondary immunodeficiency
  2. Primary immunodeficiency is split in type I and type II
  3. Type 1 is immediate (hay fever, anaphylaxis)
  4. Type II is antibody mediated (blood type incompatibilities)
  5. Secondary immunodeficiency is split into type III and type IV
  6. Type III is immune complex (rheumatoid arthritis, serum sickness)
  7. Type IV is cell mediated, cytotoxic (contact dermatitis, graft rejection)
608
Q

Immunodeficiency is split into ____ and ____ , which means _____ and ______

A

Primary (born with)
Secondary (acquired)

609
Q

Primary immunodeficiency includes:

A

DiGeorge Syndrome: No thymus (no T cells)
Agammaglobinemia: No B cells (no antibodies)
Severe combined immunodeficiency disorder (SCID): no B or T cells

610
Q

Secondary immunodeficiency inclues

A

Acquired immune deficiency syndrome

611
Q

Hypersensitive is the _______ of the immune system to innocuous stimuli (AKA as _____)

A

overreaction
allergy

612
Q

4 types of hypersensitivity

A

A: anaphylaxis, allergy
C: cytotoxic
I: Immune complex
D: delayed

613
Q

Define autoimmunity

A

Immune response against normal, healthy tissue

614
Q

Who is more affected by autoimmunity, male or females?

A

Females

615
Q

What is SLE?

A

Autoantibodies against DNA

616
Q

What is MS?

A

Autoantibodies and T cells against neurons and myelin

617
Q

What is MG?

A

Destruction of ACh receptors

618
Q

Autoimmune disease of thyroid

A

Hashimoto’s
Grave’s

619
Q

Autoimmune disease of adrenals

A

Addison’s disease (hypocortisolism)

620
Q

Autoimmune disease of the pancreas

A

Insulin-dependent diabetes
Cytotoxic T cells attack beta cells (insulin)

621
Q

What are the 5 immunosuppressive agents?

A

Glucocorticoids
*Suppress immune response, mimic naturally occurring adrenal corticosteroids
Calcineurin inhibitors
* T cell activation pathway
Cytotoxic agents
*Kill rapidly proliferating cells
Immunosuporresive antibodies
* antibodies created in the lab, directing against cell surface antigens
Additional Agents

622
Q

Glucocorticoids interfere with cell cycle of _______

A

Activated B & T cells

623
Q

Glucocorticoids decrease ______ cells in spleen and lymph nodes

A

lymphoid

624
Q

Glucocorticoids are used for:

A

Adrenal insufficiency
Suppression of allergy and inflammatory reactions
Asthma
Transplantation

625
Q

Side effects of glucocorticoids

A

Immunodeficiency, exogenous Cushing’s syndrome

626
Q

Examples of calcineurin inhibitors

A

Cyclosporine
Tacrolimus

627
Q

What are cyclosporine (calcineurin inhibitor) used for and what are the toxicities?

A

Uses:
transplantation, GVHD, other autoimmune disorders

Toxicities:
Kidney, BO, hyperglycemia, liver, seziures

628
Q

Tacrolimus can be used topical for

A

Atopic dermatitis and psoriasis

*Similar uses and toxicities to cyclosporin

629
Q

What are examples of cytoxic agents? MOA?

A

Azathioprine

MOA:
-Antimetabolite targeting proliferating cells (immunosuppressive, anti-cancer)
-Metabolized by xanthine oxidase to mercaptopurine
- Interferes with purine metabolism

Cyclophosphamide
MOA: acylating agent
- destroys proliferating lympoid/cancer cells
- potent in autoimmune disorders in smaller doses

630
Q

What is azathioprine used for and side effects?

A

Uses: graft rejection, lupus, Crohn’s, MS
Side effect: leukcytopenia caused by bone marrow suppression

631
Q

Immunosuppressive antibody examples

A

Muromonab, RhoGAM, Adalimumab

632
Q

Additional examples of immunosuppressive agents

A

Sirolimus
Mycophenylate
Mofetil
Thalidomide derivatives

633
Q

Most commonly used alkylating agent

A

Cyclophosphamide

634
Q

Monoclonal antibody used as treatment for RH- mothers who give birth to RH+ babies

A

RhoGAM

635
Q

Describe desensitization

A

Beta arrestin binds to the OH groups attached to the end of the carboxyl terminal on the 7TM protein and blocks further activity from occurring.

The protein gets “eaten” by the cell via a clathrin pit.

opt 1. drug breaks off of receptor: G-protein gets moved back to the cell surface to be reused.

opt.2 Lysosome merges with the ligand and the lysosome degrades the entire drug&receptor

Fall 2024 (86 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions