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Foundations of Medicine > FOM: week 4 > Flashcards

FOM: week 4 Flashcards

1
Q

What are some benefits of personalized medicine?

A
  1. safer drugs – reduction of side effects
  2. increased drug effectiveness
  3. alternative drugs for “standard treatment”
  4. Dosages based on an individual’s genetics - stop overdosing
  5. cost reduction due to effectiveness
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2
Q

What is warfarin used for?

A

Warfarin is used to prevent blood clots from forming or growing larger in blood/blood vessels. Basically it’s a blood thinner.

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3
Q

What are some factors that affect Warfarin usage?

A

Diet: vitamin K intake needs to be lowered
Schedule: needs to be regular/consistent
Ethnicity: decrease dosage in East Asian people
Genetics: variants of vitamin K epoxide reductase (VKORC1) and cytochrome P450 2C9 (CYP2C9) impact warfarin sensitivity – genetic testing!

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4
Q

What is a single nucleotide polymorphism (SNP)?

A

A SNP is a change in one nucleotide to another and is naturally occurring

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5
Q

How are SNPs detected?

A

Deep sequencing, Direct sequencing, and exon trapping

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6
Q

What makes the cytochrome P450 family of enzymes so important?

A

Cytochrome P450s contribute to the metabolism of approximately half of all medications!

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7
Q

What are the two main cytochrome P450s and which on is essential for life?

A

3A4 – essential!

2D6

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8
Q

How do these cytochromes work with each other?

A

3A4 and 2D6 need to be in balance with each other in order to metabolize drugs correctly. In example, codeine.

3A4&raquo_space; 2D6 –> poor metabolism
3A4 ~ 2D6 –> extensive (normal) metabolism
3A4 &laquo_space;2D6 –> ultrarapid metabolism

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9
Q

What is poor metabolism and how is it characterized?

A

Poor metabolism = cannot metabolize enough drug (codeine)

  • Overdose is common due to less functional 2D6 enzyme,
  • 3A4 converts codeine to norcodeine which body cannot use.
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10
Q

What is extensive metabolism?

A

Extensive metabolism = normal drug metabolism

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11
Q

What is ultrarapid metabolism and how is it characterized?

A

Ultrarapid metabolism = drug is metabolized too quickly to receive effective benefit

Less than 10% of pop. has this issue
Constantly need more pain medication; can be mistaken for person addicted to pain killers

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12
Q

What are two ‘medications’ that inhibit codeine metabolism?

A

Quinidine – inhibits 2D6

Grapefruit juice – inhibits 3A4

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13
Q

What is physiology?

A

It is the study of how various parts of the body work together to achieve optimal functional capacity. Primarily involved in maintaining homeostasis. This is a dynamic process.

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14
Q

What are the essential components of a neural/hormonal reflex?

A

signal –> sensory receptor –> afferent portal –> integrating center –> efferent portal –> effector organ(s)

Neural uses nerve impulses and neurons whereas hormonal uses hormones and blood vessels.

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15
Q

Pulmonary circulation and systemic circulation are in _________.

A

series

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16
Q

Systemic organ circulations to each other are arranged in ____________.

A

parallel

This allows for compensation when blood flow needs to go to another system when switching from resting to active state.

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17
Q

What are the equations that describe flow and mean arterial pressure?

A

Q = deltaP/R

MAP = CO x TPR

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18
Q

What influences cardiac output and total peripheral resistance?

A

CO = SV x HR; stroke volume (volume/beat), heart rate (beats/minute)

TPR determined by vasodilation or vasoconstriction of blood vessels and is controlled by sympathetic and parasympathetic nervous systems.

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19
Q

What vascular segment has the greatest effect on TPR?

A

Arterioles due to wall thickness and total cross-sectional area.

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20
Q

How are arterial baroreceptors involved in blood pressure homeostasis?

A

Arterial baroreceptors sense the pressure within the blood vessel due to how much the vessel is stretched. It acts as the sensing receptor in the neural pathway described previously.

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21
Q

What is the pathway to regulate blood pressure physiologically?

A

High BP –>arterial baroreceptor stretched –> sends message via afferent neuron –> Medulla (processed) –> parasympathetic efferent neuron –> vasodilation (lowers BP)

Note: this is the acute response, if becomes chronic the kidneys are involved with ADH –> hypertension

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22
Q

What are the functions of a drug receptor?

A

Recognition (binds drug or endogenous ligand)

Transduction (transfer of information)

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23
Q

What are the general mechanisms of receptor-mediated signal transduction?

A
  1. Alter function of receptor
  2. Generate 2nd messenger (GPCR –> cAMP) which alters cellular function
  3. Activated receptor complex with DNA to change transcription
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24
Q

What are the major attributes of drug receptor-mediated processes?

A
  1. highly compartmentalized
  2. self-limiting
  3. organized into opposing systems
  4. create opportunities for signal amplification
  5. operate through small number of 2nd messenger systems (drug-drug interactions)
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25
Q

What are some non-receptor modes of drug action?

A
  1. interaction with small molecules/ions
  2. agents that act by physiocochemical mechanisms
  3. drugs that target rapidly dividing cells
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26
Q

What is drug occupancy theory?

A

Drug occupancy theory assumes that the effect is proportional to receptor occupancy and that interaction is monovalent (one receptor binds one ligand)

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27
Q

Affinity

A

characterized as 1/Kd and describes the ability of a drug to form a complex with a receptor

increase affinity = decrease in Kd and EC50

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28
Q

Efficacy

A

characterizes the ability of a drug-receptor complex to produce a response

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29
Q

Response

A

function of both the affinity of the drug to receptor and the efficacy of the drug-receptor complex

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30
Q

EC50

A

concentration of a drug that produces 50% of the maximal response and is an estimate of the drug’s Kd

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31
Q

ED50

A

the dose of the drug producing 50% of the maximal response

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32
Q

Potency

A

comparative term used to describe the relative positions of several agonist dose-response curves

lower log drug concentration = higher potency
higher potency does NOT confer drug any inherent benefit

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33
Q

What are some features of a competitive antagonist?

A
  • Interaction with receptor is reversible
  • Agonist dose-response curve shifts right
  • Slope of agonist dose-response curve does NOT change
  • Agonist is capable of producing maximal response, but apparent affinity is reduced
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34
Q

What are some features of a non-competitive antagonist?

A
  • interaction is irreversible – “covalent” bond
  • agonist’s maximal response is reduced
  • agonist affinity for receptor changes little, if at all
  • slope of agonist dose-response curve is reduced
  • apparent number of receptors is reduced
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35
Q

What is physiological antagonism?

A

Physiological antagonism involves interactions between regulatory pathways mediated by different receptors
i.e. insulin vs. cortisol (glucocorticoid)

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36
Q

How does inverse agonism and the concept of spare receptors challenge occupancy theory?

A

Theory: effect is proportional to receptor occupancy, monovalent (1 receptor to 1 ligand)

Inverse agonism: violates monovalent clause
Spare receptor: violates proportional clause

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37
Q

What is a quantal log dose-response curve and what information does it tell us?

A

Quantal log dose-response curve is a frequency distribution curve of the response of a population to a drug; all or nothing response; uses ED50

Provides information on variability in population response and can be used to judge a drug’s potency relative to that of another drug

canNOT be used to determine Kd or maximal efficacy

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38
Q

What is ED50 in regards to quantal dose-response curves?

A

ED50 refers to the toxic effect exhibited by 50% of the population to a specific quantal response.

Amount that harms 50% pf population tested.

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39
Q

What happens if a person is above or below the ED50 mark?

A

If &laquo_space;ED50 – hyperreactive
If&raquo_space; ED50 – hyporeactive

Tolerance is a type of hyporeactivity induced by repeated administration of a drug.

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40
Q

What is a therapeutic index (TI)?

A

It is the ratio of LD50 to ED50 and is a measure of relative safety of a drug

higher ratio = safer drug

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41
Q

What is a certain safety factor (CSF)?

A

It is the ratio of the dose producing death in 1% of the population (LD1) to the dose of drug producing the therapeutic response in 99% of population (ED99).

  • higher ratio = safer drug
    This ratio is better than TI, but is used less frequently due to difficulty obtaining these values.
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42
Q

What is the main driving force of passive diffusion? And what are some other features of this type of transport?

A

Driving force = electrochemical/concentration gradient

  • does not saturate
  • rate movement described by Fick’s Law
  • limited to nonionizable lipid soluble drugs (acids/bases)
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43
Q

What is Fick’s Law anyway?

A

Flux = DAK/deltaX (Cout-Cin)

DAK/deltaX = P; permeability constant
D = diffusion constant
A = surface area of membrane
K = membrane:partition coefficient (measures hydrophobicity)
deltaX = thickness of membrane
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44
Q

What is driving force of filtration? What are some features too?

A

Driving force = hydrostatic or osmotic pressure differences

  • allows for bulk flow of fluids through channel
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45
Q

What is involved in endocytosis?

A
  • involves active bulk flow through membrane invagination
  • nonselective or selective
  • reverse process called exocytosis
46
Q

What is driving force of facilitated diffusion? What are some features?

A

Driving force = movement DOWN a concentration gradient

  • transports large, water-soluble molecules (ions or non-ions)
  • carrier mediated
  • selective and inhibited by closely related chemicals
  • saturates at high [substrate]
47
Q

What is the driving force of active transport? What are some features?

A

Driving force = hydrolysis of ATP, movement UP a concentration gradient

  • primary (ATP hydrolysis), secondary (coupled to another compound’s electrochemical gradient)
  • transports large, water-soluble molecules
  • selective and inhibited by closely related chemicals
  • saturates at high [substrate]
48
Q

Ion trapping involves passage of ions through biological membranes. Explain this phenomenon and what effect pH has on it.

A

Usually acids or bases participate in ion trapping and can be in a neutral state (pass through membrane) or ionic state (retained on one side).

Weak acids going to be trapped in basic environ.
Weak bases going to be trapped in acidic environ.

49
Q

What are ABCs and how do they function?

A

ABC = ATP-binding cassette

Function: use active transport (primary) and move substances OUT of cells

50
Q

What are SLCs and how do they function?

A

SLC= solute carrier

Function: uses facilitated diffusion and active transport (secondary) and may move substances INTO or OUT of cells

ex. serotonin reuptake transporter (SERT), dopamine reuptake transporter (DAT)

51
Q

Why are transporters common drug targets?

A

Transporters are targets because very cell uses them and they are vital to cell survival!

52
Q

What is bioavailability?

A

Bioavailability is determined by the fraction of an administered drug dose that is absorbed into the systemic circulation.

Can be altered by: dissolution rate, particle size, solubility of preparation, disintegration rate.

Better bioavailability = better drug

53
Q

What are the major factors that affect internal distribution of a drug?

A
  1. relative tissue perfusion rates
  2. plasma protein binding
  3. partitioning between plasma and tissues
54
Q

A higher perfusion rate means that equilibrium is reached ________ between tissue and plasma.

A

faster

55
Q

Plasma binding proteins affect distribution how?

A

They bind to drugs and this inhibits drug:

  1. movement across membranes
  2. free concentration, reduces free [drug] which reduces gradient possibilities for passive diffusion
  3. considered pharmacologically inert
  4. cannot be filtered by kidneys

Acidic drugs plasma protein = albumin
Basic drugs plasma protein = a1-acid glycoprotein

56
Q

Partitioning between plasma and tissues is another factor that affects internal distribution of drugs. What are some causes of this partitioning?

A
  • differences in pH (ion trapping)
  • drugs binding to tissue proteins (compete with plasma binding proteins)
  • lipid-water coefficient (hydrophobic drugs may stay in high fat tissue as storage)
57
Q

Volume of distribution (VD)

A

volume in which the drug appears to be distributed, at equilibrium

The VD is the volume of plasma that would be required to contain all of the drug in the body given the measured concentration in plasma.

58
Q

What causes the VD to increase or decrease?

A

Increase: drug goes into tissue
Decrease: drug remains in plasma

58
Q

What are some ways drugs can be terminated?

A
  1. Storage (redistribution)
  2. excretion
  3. biotransformation
59
Q

What are some ways drugs can be terminated?

A
  1. Storage (redistribution)
  2. excretion
  3. biotransformation
60
Q

What are the two phases of drug redistribution (storage)?

A
  1. flow-dependent drug goes rapidly to high perfusion tissues (brain, kidney, liver, etc)
  2. drug distribution goes to tissues with low flow and perfusion rates (fat, bone)
61
Q

What is renal clearance?

A

Renal clearance is the volume of plasma from which that target substance is removed completely by the kidneys per unit time

62
Q

When does renal clearance give a good approximation of GFR?

A

When the substance being measured is neither reabsorbed nor secreted. Substances like: inulin (best) and creatinine (most commonly used) – not true estimate of GFR but close (higher approximation)

63
Q

What are the major mechanisms of excretion accomplished by the kidneys?

A
  • liver secretes drugs/their metabolites into bile
  • conjugation of drugs before secretion
  • may be reabsorbed through enterohepatic circulation
64
Q

There are two major phases of biotransformation. What are some features of each phase?

A

Phase 1:
- Drug has a functional group chemically added or exposed
- Oxidation is the most common chemical reaction
- Metabolite usually becomes more polar and water soluble
- Metabolites are often less active than the parent substance
Phase 2:
- Synthetic conjugation reactions add a large molecule to drug or metabolite
- Glucuronidation is the most common conjugation reaction
- Water solubility is usually increased (more polar) and drug is generally inactivated

65
Q

Biotransformation commonly occurs in _______ perfusion tissues such as ____________.

A

high; liver, kidneys, GI tract, etc.

66
Q

What are the main components of the microsomal drug oxidizing system?

A

The microsomal drug oxidizing system is contained within the SER and houses cytochrome P450s which are responsible for drug oxidation.

67
Q

What are some ways drugs are responsible for drub biotransformation?

A
  • competition between two drugs for one enzyme
  • disulfiram inhibits ALDH
  • iproniazid inhibits monoamine oxidase (MAO)
  • drugs can cause CYP expression – rifampin, alcohol, phenobarbital
68
Q

Draw out pathway of alcohol metabolism including the Microsomal Ethanol Oxidizing System and the disulfiram reactions.

A

Ethanol –>Acetaldehyde –> acetate –> acetyl CoA –> FA synthesis or TCA cycle
Disulfiram: inhibits ALDH and conversion of dopamine to norepinephrine
MEOS – CYP2E1 (more active at higher [EtOH] because has lower Km)

69
Q

What are the primary homeostatic roles in the respiratory system?

A
  • Regulate plasma levels of oxygen and carbon dioxide
  • Regulate plasma pH
  • Protect against inhaled pathogens
  • Provide an adequate surface for gas exchange with the external environment
  • Assure adequate alveolar air movement by alterations in rate and depth of ventilation
  • support vocalization of sound
70
Q

What are the controlled variable of the respiratory system?

A

Oxygen and Carbon Dioxide

71
Q

What is the site of greatest airway resistance?

A

Bronchioles – these are constricted in people with Asthma which decreases the amount of air flow into the lung.

72
Q

tidal volume

A

amount of air inhaled or exhaled in one breath

73
Q

residual volume

A

amount of air remaining in the lungs after maximum

74
Q

expiratory reserve volume

A

amount of air in excess of tidal expiration that can be exhaled with maximum effort

75
Q

inspiratory reserve volume

A

amount of air in excess of tidal inspiration that can be inhaled with maximum effort

76
Q

vital capacity

A

amount of air that can be exhaled with maximum effort after maximum inspiration (IRV + TV + ERV)

77
Q

total lung volume

A

maximum amount of air the lungs can contain (VC + RV)

78
Q

How do peripheral and central chemoreceptors act on regulating pulmonary ventilation?

A

These receptors detect the partial pressure of O2 and CO2 in the blood mainly through pH. When levels decrease a message is sent to the medulla to respirate.

79
Q

What are the primary homeostatic functions of the kidney?

A
  • Regulate extracellular fluid volume and blood pressure
  • Regulate osmolarity
  • Maintain ion balance
  • Regulate pH
    • All above are under homeostatic control
  • Excrete waste – urea
  • Produce hormones – vitamin D (D2 to D3)
80
Q

What are the primary homeostatic roles of GI system?

A
  • Provide a connection with the external environment for ingesting nutrients and eliminating wastes
  • Regulate the secretory and motility processes involved in normal gut function
  • Assure that ingested nutrients are digested to absorbable forms
  • Provide an absorptive surface for nutrients (etc.) uptake
  • Protect against ingested pathogens
81
Q

What are the four basic processes of the digestive system? Which ones are controlled by neural and hormonal processes?

A
  1. digestion - uses enzymes to breakdown nutrients
  2. absorption - molecules transported to blood
  3. secretion - molecules have paracrine, autocrine, and endocrine effects
    • under hormonal control
  4. motility - movement of molecules down tract
    • under neural control (enteric plexus)
82
Q

What do mucous neck cells secrete in the stomach?

A

mucus and bicarbonate

83
Q

What do parietal cells secrete in the stomach?

A

HCl, intrinsic factor

84
Q

What do enterochromaffin-like (ECL) cells secrete in the stomach?

A

histamine

85
Q

What do chief cells secrete in the stomach?

A

pepsin(ogen) and gastric lipase

86
Q

What do D cells secrete in the stomach?

A

somatostatin

87
Q

What do G cells secrete in the stomach?

A

gastrin

88
Q

There are short and long reflexes involving ANS. What are the short and long reflexes?

A

Short: Local stimulus –> sensory receptor –>interneurons –> myenteric/submucosal plexus –> smooth muscle/secretory cells –> muscle contraction/relaxation, exocrine secretion

Long: stimulus –> sensory receptor –> brain –> (para)sympathetic neurons –> myenteric/submucosal plexus –> smooth muscle/secretory cells –> muscle contraction/relaxation, exocrine secretion

89
Q

What are the three influences on gastric parietal cells?

A

Neural: vagus nerve innervation (acetylcholine – via enteric plexus)
Hormonal: gastrin (from G cells)
Paracrine: histamine (from ECL cells)
Somatostatin inhibits H+ secretion from parietal cells (from D cells)

90
Q

Draw the pentose phosphate pathway and denote the pathology expected as well as areas where subtrates divert to other pathways.

A

Key Enzymes: G6PDH (oxidative phase), Transketolase and transaldolase (regenerative phase)

Xylulose 5-phosphate acts as a transcriptional regulator of FA synthesis genes

Many substrates are used in glycolysis

91
Q

Draw the fructose and galactose pathways and how they interact with glycolysis and glycogenogenesis. Also denote the pathologies of this pathway.

A

Deficiencies:

  • Fructokinase – essential fructosuria
  • Aldolase B – hereditary fructose intolerance
  • Galactokinase deficiency
  • Transferase deficiency
  • Epimerase deficiency
92
Q

Zero order kinetics

A

rate is constant and is drug concentration independent

i.e. there is a fixed amount of drug that is absorbed and eliminated per unit of time

93
Q

First order kinetics

A

rate is proportional to the amount of drug concentration

  • follows an exponential decay curve
94
Q

In first order kinetic terms, what does Co mean?

A

Co is the concentration of drug in the body at time zero. It is extrapolated from the straight line generated in the beta-phase of the graph.

95
Q

In regards to first order kinetics, what does Vd mean and how is it calculated?

A 
Vd = volume of distribution of a drug
Vd = X/Co
X = amount of drug administered
Co = concentration of a drug in the body at time zero
96
Q

What is t (1/2)?

A

t(1/2) is the half-life of a drug – how much time it takes for half of the drug to be eliminated from the body

t(1/2) = 0.693/ke = 0.693(Vd/Cl)

Cl = drug clearance

97
Q

What is whole body clearance (Cl)?

A

Whole body clearance is defined as the rate of chemical elimination from the body/Cplasma.

Can be thought of as the volume of plasma that you would have to completely clear of a chemical in a unit of time to account for the observed rate of elimination

Cl= ke(Vd) –> ke = Cl/Vd

98
Q

What is the plateau principle?

A

The plateau principle states that at 4 times the half-life of a drug that >93% of the drug is in tissue.

99
Q

What does Xmax denote?

A

Xmax is the maximum amount of a drug in the body at steady state condition

Xmax = 1.44 (Ki)(t1/2)

100
Q

What is the concentration of a drug at steady state equal to?

A

Css = Ki/Cl

= rate of infusion/clearance

101
Q

What is a maintenance dose and how is it calculated?

A

Maintenance dose is a dose of a drug that will produce the desired therapeutic level at plateau (steady state).

MD = dosing rate (amt/hr) x dosing interval (hr/f)

f = bioavailability

102
Q

What is a loading dose and how it is calculated?

A

A loading dose is a single dose which, administered at the outset, will produce the desired steady-state plasma concentration.

This is used when t1/2 is large since it takes 4 times the half-life to reach steady state concentration which takes a long time!!

Loading dose = Css (Vd)/f

103
Q

What are the key regulatory steps of gluconeogenesis?

A
  1. Phosphoenolpyruvate Carboxylase
  2. Fructose-1,6-bisphosphatase
  3. Glucose-6-phosphatase
104
Q

What are the three ways that carbon can enter gluconeogenesis?

A
  1. glycerol –> G3P and DHAP
  2. alanine (protein) –>pyruvate
  3. lactate –>pyruvate
105
Q

What is the cause of diabetic ketoacidosis?

A
  • abundant amount of glucose in body, unable to use it
  • need energy, so convert acetyl CoA to ketone bodies for fuel (brain, heart, skeletal muscle)
    - enters ketone body synthesis due to reduced amount of oxaloacetate
  • usually ketoacidosis results from hypoglycemia but with diabetics the body feels as though it is hypoglycemic and uses ketone bodies for fuel
106
Q

What causes GSD I?

A

a deficiency in glucose-6-phosphatase (found in glycogenolysis and gluconeogenesis pathways)

  • results in an inability to make glucose thus patients present with hypoglycemia, lactic acidosis (increased lactate in blood), and an enlarged liver (increased glycogen stores)
107
Q

What test is most commonly performed if diabetes mellitus is suspected?

A

Oral glucose tolerance test

108
Q

What are the components of the oral glucose tolerance test?

A
  1. patient must fast overnight

2. patient drinks high glucose drink in clinic and has blood drawn/tested for blood glucose over a certain interval

109
Q

What is an anion gap and what does it indicate?

A

Anion gap is the difference between measured cations minus measured anions and it indicates metabolic homeostasis if normal.

When elevated it indicates metabolic acidosis.
Calculated: AG = [Na] - ([Cl] + [HCO3])

Foundations of Medicine (8 decks)

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