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DUSON Spring '18 > Patho Exam 1 > Flashcards

Patho Exam 1 Flashcards

1
Q

Pharmacokinetics (4)

A

Effect of the body on drugs

Absorption
Distribution
Metabolism
Excretion

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2
Q

Weak acid is a….

A

….proton donator

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3
Q

Weak base is a….

A

….proton acceptor

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4
Q

Ionization is…

A

…when an acid or base becomes a charged particle. Can no longer cross membranes!

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5
Q

Two forms of drug administration (broad)

A

Enteral, Parenteral

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6
Q

Enteral forms of administration (3)

A

Oral
Rectal (erratic absorption)
Sublingual/buccal (bypasses first pass effect)

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7
Q

Parenteral forms of administration (6)

A 
IV
IM
Sub-q
Transdermal
Inhalation
Other (topical)
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8
Q

1st pass effect

A

Oral drugs! Decrease the amount available to the body.

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9
Q

Bioavailability

A

Fraction of the dose that reaches systemic circulation. With IV = 100%

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10
Q

Distribution issues (3)

A

Blood brain barrier
Placenta
Breastmilk

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11
Q

Plasma protein binding

A

Plasma in the blood (albumin) binds to the drug, rendering it inactive. Reversible. Affected by nutritional status, plasma protein levels.

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12
Q

Elimination is affected by….

A

….renal/hepatic function, medications, genetics, age

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13
Q

Metabolism one word definition

A

Biotransformation!

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14
Q

Where does metabolism occur?

A

Liver, GI tract, lungs, skin, kidneys. Via enzymes.

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15
Q

What is a pro-drug?

A

A drug that is inactive until it undergoes metabolism to an active form

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16
Q

What is a metabolite?

A

The product of biotransformation

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17
Q

Renal Excretion (3)

A
  1. Glomerular Filtration - drugs go from blood to urine
  2. Passive tubular reabsorption - lipophilic things go back in to the body, while ions/polar compounds stay in the urine
  3. Active secretion - active transport systems remove organic acids and bases
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18
Q

Schedules of drugs

A
  1. Schedule 1 is fun (aka illegal, only recreational), schedule 5 is lowest likelihood for abuse.
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19
Q

Steps of new drug development

A

Pre-Clinical (on animals, studying toxicology, PK, pharmacology)

IND (Investigational New Drug application)

Clinical (Phase 1-3)

NDA (New Drug Application)

Marketing (Phase 4, post-marketing surveillance for low incidence adverse effects)

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20
Q

Clinical Phases 1-3 of new drug development

A

Phase 1: on healthy individuals, testing PK, safety, dose. n=20-80

Phase 2: testing effects and safety. n=100-300

Phase 3: testing safety/effectiveness. Rigorous design, randomized double blind trials, placebo effects. n=100-3000

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21
Q

Pharmacodynamics is….

A

…the study of the drug on the body

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22
Q

Pharmacologic effects (2)

A

Therapeutic

Toxic

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23
Q

Factors of drug response (3)

A

Administration: med errors, pt adherence

Pharmacokinetics: absorption, distribution, metabolism, excretion

Pharmacodynamics: drug-receptor interaction, pt functional state, placebo effects

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24
Q

Types of receptors (4)

A

Cell membrane embedded
Ligand-gated ion channels
G-protein coupled
Transcription factors

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25
Agonist drug
Activates receptors! (Like endogenous ligand)
26
Affinity is....
....the strength of the attraction between a drug and a receptor
27
Intrinsic activity is....
....the ability of a drug to activate a receptor upon binding
28
Antagonist drug
Blocks receptor activation! Produces pharmacological effects by blocking endogenous ligands (or agonist drugs) from binding. No intrinsic activity
29
Antagonists are either....or....
Competitive - overcome by increased agonists Noncompetitive - irreversible. Less common, long duration, rely on body's natural process of breaking down old receptors and making new ones
30
Partial agonists
Agonists with only moderate intrinsic activity. Maximum effect is lower than a full agonist
31
Drugs that work without a receptor (3)
Antacid Osmotic laxative Chelating agents/resins
32
Efficacy
Maximal response produced by a drug.
33
Potency
Dose of a drug required for a given response. (20 mg of hydrocortisone = 5 mg prednisone)
34
ED50
Does at which 50% of individuals demonstrate the designated response. Median effective dose
35
Therapeutic index =
TD50/ED50 Measure of drug safety, ideally wide
36
Side effect
Nearly unavoidable secondary drug effects
37
Toxicity
Adverse drug reaction caused by excessive dosing. All drugs have toxicity!
38
Types of toxicity (5)
``` Mutagenicity Carcinogenicity Teratogenicity Hypersensitivity (allergic rxn) QT prolongation ```
39
Drug combination effects (4)
Additive (just add) Synergistic (more than additive) Antagonistic (less than individual) Potentiation (drugs enhance each other - way bigger together!)
40
Continuous exposure to an antagonist can result in....
...the cell becoming hypersensitive
41
Continuous exposure to an agonist can result in....
...the cell becoming less responsive, desensitized
42
Tolerance (3)
Pharmacodynamic - long term use of a drug. Requires higher doses (heroin, morphine) Metabolic - accelerated drug metabolism, requires higher doses to increase concentrations Tachyphylaxis - short term reduction in drug responsiveness
43
What is stress?
State in which homeostasis is threatened - actual or perceived (physical, mental)
44
What is a stressor?
Anything that throws or has the potential to throw the body out of homeostasis
45
What is stress response?
Stereotypic, innate response that has evolved to coordinate homeostasis and protect an organism during acute stress. Good, protective.
46
What happens when they hypothalamus senses a stressful stimulus?
It releases CRH
47
What happens after CRH is released?
It activates; 1. Adrenal medulla/sympathetic nervous system, which secrete catecholamines (Epi, NE) 2. Anterior pituitary, which secretes adrenocorticotropic hormone. The adrenal cortex then secretes glucocorticoids (cortisol, aldosterone)
48
What responses do catecholamines trigger in the body?
Increase heart rate, dilate lungs, constrict perfusion, increase BP, decrease peristalsis, increase glucose levels. Arousal, attention, vigilance
49
What does aldosterone do in the body in response to stress?
Retains sodium and H2O to increase BP
50
What does cortisol do in the body in response to stress? (3)
1. Metabolism: gluconeogenesis, increase appetite (leads to stress eating, obesity, diabetes) 2. Inflammation/infection: initially immune system is enhanced, then suppressed. (leads to weakened immune system, more missed days of work) 3. Supports work of catecholamines (Epi, NE)
51
3 phases of general adaptation (stress response)
1. Alarm 2. Resistance 3. Exhaustion
52
Resistance phase of general adaptation
1. Mobilize resources to manage the stressor (growth, repair) 2. Funciton at a new baseline, body adapts (COPD)
53
Exhaustion phase of general adaptation
Body can no longer get back to homeostasis. Energy stores are depleted, at a state of no return. Leads to chronic health issues like htn, diabetes, heart disease, obesity.
54
Long term behavioral and somatic consequences of stress....
Behavioral - anxiety, depression, poor sleep | Somatic - fatigue, obesity, poor health/healing, growth suppression, frequent infections, diabetes.
55
Populations at a higher risk for stress
Single parents, recent immigrants, students, minorities, poc.
56
Adaptation is...
...a biopsychosocial process of changing/adjusting in response to new/altered circumstances
57
Coping is...
...behavioral adaptation
58
ACEs
Adverse Childhood Experiences. Dose-Dependent, the # experienced as a child increases the risk of negative health outcomes. Abuse, neglect, household dysfunction.
59
Types of neurons (3)
Sensory (carry impulses form peripheral sensory receptors to the CNS) Interneuron (carry impulses from neuron to neuron) Motor (carry impulses from CNS to an effector)
60
Process of neurotransmitter release
1. Action potential arrives at axon terminal 2. Voltage-gated CA2+ channels open 3. Ca2+ enters the presynaptic neuron 4. Ca2+ signals to neurotransmitter vesicles 5. Vesicles move to membrane and dock 6. Neurotransmitters released via exocytosis 7. Neurotransmitters bind to receptors 8. Signal initiated in post-synaptic cell

DUSON Spring '18 (7 decks)

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