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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
Q

Agonist drug

A

Activates receptors! (Like endogenous ligand)

26
Q

Affinity is….

A

….the strength of the attraction between a drug and a receptor

27
Q

Intrinsic activity is….

A

….the ability of a drug to activate a receptor upon binding

28
Q

Antagonist drug

A

Blocks receptor activation! Produces pharmacological effects by blocking endogenous ligands (or agonist drugs) from binding. No intrinsic activity

29
Q

Antagonists are either….or….

A

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
Q

Partial agonists

A

Agonists with only moderate intrinsic activity. Maximum effect is lower than a full agonist

31
Q

Drugs that work without a receptor (3)

A

Antacid
Osmotic laxative
Chelating agents/resins

32
Q

Efficacy

A

Maximal response produced by a drug.

33
Q

Potency

A

Dose of a drug required for a given response. (20 mg of hydrocortisone = 5 mg prednisone)

34
Q

ED50

A

Does at which 50% of individuals demonstrate the designated response. Median effective dose

35
Q

Therapeutic index =

A

TD50/ED50

Measure of drug safety, ideally wide

36
Q

Side effect

A

Nearly unavoidable secondary drug effects

37
Q

Toxicity

A

Adverse drug reaction caused by excessive dosing. All drugs have toxicity!

38
Q

Types of toxicity (5)

A 
Mutagenicity
Carcinogenicity
Teratogenicity
Hypersensitivity (allergic rxn)
QT prolongation
39
Q

Drug combination effects (4)

A

Additive (just add)
Synergistic (more than additive)
Antagonistic (less than individual)
Potentiation (drugs enhance each other - way bigger together!)

40
Q

Continuous exposure to an antagonist can result in….

A

…the cell becoming hypersensitive

41
Q

Continuous exposure to an agonist can result in….

A

…the cell becoming less responsive, desensitized

42
Q

Tolerance (3)

A

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
Q

What is stress?

A

State in which homeostasis is threatened - actual or perceived (physical, mental)

44
Q

What is a stressor?

A

Anything that throws or has the potential to throw the body out of homeostasis

45
Q

What is stress response?

A

Stereotypic, innate response that has evolved to coordinate homeostasis and protect an organism during acute stress. Good, protective.

46
Q

What happens when they hypothalamus senses a stressful stimulus?

A

It releases CRH

47
Q

What happens after CRH is released?

A

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
Q

What responses do catecholamines trigger in the body?

A

Increase heart rate, dilate lungs, constrict perfusion, increase BP, decrease peristalsis, increase glucose levels.

Arousal, attention, vigilance

49
Q

What does aldosterone do in the body in response to stress?

A

Retains sodium and H2O to increase BP

50
Q

What does cortisol do in the body in response to stress? (3)

A
  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
Q

3 phases of general adaptation (stress response)

A
  1. Alarm
  2. Resistance
  3. Exhaustion
52
Q

Resistance phase of general adaptation

A
  1. Mobilize resources to manage the stressor (growth, repair)
  2. Funciton at a new baseline, body adapts (COPD)
53
Q

Exhaustion phase of general adaptation

A

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
Q

Long term behavioral and somatic consequences of stress….

A

Behavioral - anxiety, depression, poor sleep

Somatic - fatigue, obesity, poor health/healing, growth suppression, frequent infections, diabetes.

55
Q

Populations at a higher risk for stress

A

Single parents, recent immigrants, students, minorities, poc.

56
Q

Adaptation is…

A

…a biopsychosocial process of changing/adjusting in response to new/altered circumstances

57
Q

Coping is…

A

…behavioral adaptation

58
Q

ACEs

A

Adverse Childhood Experiences. Dose-Dependent, the # experienced as a child increases the risk of negative health outcomes. Abuse, neglect, household dysfunction.

59
Q

Types of neurons (3)

A

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
Q

Process of neurotransmitter release

A
  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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