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BYU - Health 619 > Public Health > Flashcards

Public Health Flashcards

1
Q

What is the #1 cause of death in the U.S.?

A

Cardiovascular disease

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2
Q

What is the #2 cause of death in the U.S.?

A

Cancer

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3
Q

What is the #3 cause of death in the U.S.?

A

Unintentional injuries

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4
Q

What is the #4 cause of death in the U.S.?

A

Chronic lower respiratory diseases

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5
Q

What is the #5 cause of death in the U.S.?

A

Stroke

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6
Q

What is the #6 cause of death in the U.S.?

A

Alzheimer’s Disease

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7
Q

What is the #7 cause of death in the U.S.?

A

Diabetes

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8
Q

What is the #8 cause of death in the U.S.?

A

Pneumonia and influenza

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9
Q

What is the #9 cause of death in the U.S.?

A

Nephritis, nephrosis, and nephrotic syndrome

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10
Q

What is the #10 cause of death in the U.S.?

A

Suicide

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11
Q

What is the CEA Winslow definition of public health?

A

The science and art of preventing disease, prolonging life, and promoting physical health and efficiency…
(PrevProlProm)

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12
Q

Name a few of the greatest public health achievements of the 20th and 21st centuries.

A 
Immunizations
Motor-vehicle safety
Workplace safety
Family planning
Fluoridation of drinking water
Infectious disease control
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13
Q

Describe Leavell and Clark’s Levels of Prevention (Primordial, primary, secondary, tertiary, and quaternary).

A

Primordial - Population measures (E.g. legislation)

Primary - Addressing individual risk factors (E.g. proper nutrition)

Secondary - Screenings (E.g. pap smears)

Tertiary - Disease treatment (E.g. a type 1 diabetic receiving insulin administration)

Quaternary - Reducing over-medicalization (E.g. strict opioid administration to prevent unnecessary use)

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14
Q

Define incidence rate.

A

The number of new cases of a disease over a certain period of time

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15
Q

Define prevalence rate.

A

The number of existing cases within a certain window of time

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16
Q

Define social determinants of health.

A

The social determinants of health are the conditions in which people are born, grow, live, work and age. These circumstances are shaped by the distribution of money, power, and resources at global, national and local levels. The social determinants of health are mostly responsible for health inequities - the unfair and avoidable differences in health status seen within and between countries (WHO definition).

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17
Q

What is the difference between absolute and relative poverty?

A

Absolute poverty is defined as living on less than $2 a day and refers to all individuals under this amount globally.

Relative poverty refers to the difference in wealth between an individual and those in their community (E.g. an individual that makes $40,000 per year living near an individual making $200,000 per year is relatively impoverished in comparison).

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18
Q

What is the federal poverty level?

A

The recognized U.S. poverty line.

Examples:
< $12,000 per year for individuals
< $16,500 per year for a family of two
(The amount steadily increases with the size of the family)

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19
Q

What is the absolute poverty level?

A

Living on less than $2 per day (1 billion individuals are in this bracket worldwide)

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20
Q

What is the difference between active and passive immunity?

A

While both are forms of acquired immunity, active immunity refers to immunity in which the individual synthesizes their own antibodies. Passive immunity refers to immunity in which the individual receives pre-synthesized antibodies from an external source.

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21
Q

Give an example of active natural immunity.

A

An individual gets exposed to a pathogenic antigen and begins synthesizing their own antibodies.

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22
Q

Give an example of active artificial immunity.

A

Vaccination

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23
Q

Give an example of passive natural immunity.

A

A mother passing her antibodies (IgA) to her baby through her breast milk

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24
Q

Give an example of passive artificial immunity.

A

Lab-synthesized gammaglobulins being administered (E.g. following a hepatitis needle stick or bite by a rabid dog)

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25
Q

What are live-attenuated vaccinations?

A

Vaccinations in which the pathogen in question has been weakened but not fully killed before being introduced to the patient (E.g. the Sabin polio or MMR vaccine)

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26
Q

What are inactivated (killed) vaccinations?

A

Vaccinations in which the pathogen in question has been killed before being introduced to the patient (E.g. the Salk polio vaccine)

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27
Q

What are component vaccinations?

A

Vaccinations in which the only a component of the pathogen in question is introduced to the patient (E.g. the pertussis portion of the DTaP vaccine)

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28
Q

Define herd immunity.

A

The resistance of a group to a disease due to the overall immunity of the group (A certain percentage of the population must be vaccinated to prevent infectious disease spread. This percentage depends on the disease in question)

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29
Q

Define R0

Pronounced R-naught

A

The number of people one sick individual will infect (On average)

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30
Q

Describe innate immunity.

A

Nonspecific mechanisms that protect the body against disease.

Examples: Skin, hair, mucus, macrophages, neutrophils, lysozyme secretions, stomach acidity, etc.

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31
Q

Describe acquired immunity.

A

Mechanisms that protect the body against specific, previously encountered antigens.

Examples: B-lymphocytes, T-lymphocytes, immunoglobulins

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32
Q

T/F The MMR vaccine causes autism?

A

False

Many large, well-designed studies have found no link between MMR and autism.

Autism usually becomes apparent around the same time MMR is given—no evidence of causality.

Autism probably has multiple components, including genetics (e.g., one study found that if one identical twin had autism, the chance that the second twin had autism was greater than 90%, but with fraternal twins the chance was less than 10%).

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33
Q

T/F Multiple vaccinations can overwhelm an infant’s immune system, so vaccines should be spread out on a long-term schedule.

A

False

Vaccines use only a tiny proportion of a baby’s immune system’s ability to respond; though children receive more vaccines than in the past, today’s vaccines contain fewer antigens (e.g., sugars and proteins) than previous vaccines. Smallpox vaccine alone contained 200 proteins; the 11 currently recommended
routine vaccines contain fewer than 130 immunologic components.

Delaying vaccines increases the time children will be susceptible to diseases. There is no evidence that spreading out the schedule
decreases the risk of adverse reactions.

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34
Q

What is an odds ratio?

A

An odds ratio (OR) is a measure of association between an exposure and an outcome. The OR represents the odds that an outcome will occur given a particular exposure, compared to the odds of the outcome occurring in the absence of that exposure.

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35
Q

What type of study uses an odds ratio to report its conclusions?

A

A case-control study

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36
Q

Define epidemic.

A

An epidemic is a period of time with a higher than expected incidence rate but over a broader geographic region.

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37
Q

Define endemic.

A

The term endemic refers to a region where there is a persistent baseline incidence and prevalence rate.

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38
Q

Define pandemic.

A

A pandemic is an epidemic where the disease is being actively transmitted on multiple continents.

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39
Q

Define outbreak.

A

An outbreak is defined as a higher than expected incidence rate tied to a geographic focal point.

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40
Q

What are some modes of infectious disease transmission?

A 
Airborne
water-borne
fecal-oral 
vector-borne
fomite
perinatal 
food-borne 
animal bites 
sexual transmission
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41
Q

Define incubation period.

A

The time between being infected with a pathogen and showing symptoms (Actively dividing pathogen)

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42
Q

Define latency period.

A

The time between being infected with a pathogen and showing symptoms (Non-actively dividing pathogen)

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43
Q

What is the difference between the latency period and the incubation period?

A

In an incubation period, the pathogen is actively dividing. In a latency period, it is not.

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44
Q

Define infectious dose.

A

The number of a certain type of pathogenic microb needed in order to cause disease in an infected individual.

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45
Q

What is the difference between eradication and elimination?

A

Eradication refers to the complete removal of a disease from the world (E.g. smallpox).

Elimination refers to the complete removal of a disease from a specific geographic region (E.g. polio).

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46
Q

Define pathogen.

A

A microorganism that can cause disease.

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47
Q

Are all infectious diseases widely contagious?

A

No (Think botulism or tetanus). They are infectious but not widely transmissible from person to person.

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48
Q

Describe fomite transmission.

A

Touching surface, object or person

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49
Q

Describe airborne transmission.

A

Respiratory drops in the air (Due to sneezing, coughing, breathing)

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50
Q

Describe vector-borne transmission.

A

Carried by non-host species to host (Typically insects)

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51
Q

Describe fecal-oral transmission.

A

Ingesting microscopic amounts of contaminated fecal matter

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52
Q

What are some other types of modes of transmission?

A 
Water-borne
Perinatal (mother to child) 
Food-borne 
Animal bites (Zoonotic)
Sexual transmission
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53
Q

What are anti-helminthic drugs?

A

Anti-parasitic drugs

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54
Q

What are antibiotic drugs?

A

Drugs that kill bacteria or interfere with bacterial growth

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55
Q

What is a non-pharmacological intervention?

A

Non-drug related treatments.

E.g. hand washing, exercise, isolation of infected individuals

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56
Q

What are the characteristics of a bacteria?

A

Prokaryotic cells that can both be helpful and harmful to humans. They reproduce on their own (Unlike viruses).

Helpful bacteria work as our microbiome and protect us and help us with digestion.

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57
Q

What are the characteristics of a virus?

A

They are not alive. They are protein shells (Capsids made of protomers) that contain genetic material (Single- or double-stranded DNA or RNA) and require a host cell in order to replicate themselves. They hijack the host cell’s enzymes and other machinery.

Viral glycoproteins allow the cell to interact with host cells in order to inject their genetic material or to be completely endocytosed.

More complex viruses sometimes have a lipid coat around their capsid.

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58
Q

What are the characteristics of a parasite?

A

Multicellular (Usually) eukaryotic organisms (Like us). Things like malaria, leishmaniasis, hookworm, guinea worm, etc.

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59
Q

Define dynamics.

A

How we describe infectious disease movements, patterns, and behaviors over time and geography

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60
Q

Define system.

A

Any group of interacting parts that form a whole

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61
Q

Define a complicated system.

A

Has many interacting parts that need to work correctly in a sequence to reach the desired result. However, each step of the process is completely predictable based on the step before it

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62
Q

Define the results of a complex system. Can we easily predict them?

A

No, the results brought about by the interacting parts of a complex system are not directly predictable

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63
Q

Define emergent properties.

A

Behaviors or outputs of a system that arise from two or more interacting components that cannot be explained by either of them on their own

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64
Q

What is an epidemic curve?

A

A graph of the number of cases or incidence rate of cases versus time.

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65
Q

Define propagate.

A

To travel

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66
Q

What is human ecology?

A

How humans interact with and are impacted by their surrounding environment and each other

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67
Q

What is a node?

A

An individual entity in the network, like a person or a hospital

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68
Q

What is an edge (In relation to a node)?

A

What connects two nodes

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69
Q

What is a random network?

A

A lot of people/things randomly connected to each other with no rhyme or reason

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70
Q

What is a scale-free network?

A

A network where some nodes are more highly connected than others

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71
Q

What are network hubs?

A

Nodes that are more connected than others

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72
Q

What is synchronous spread?

A

The timing of an epidemic overlapping in multiple locations

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73
Q

What is (sexual) concurrency?

A

Individuals having multiple partners at the same time

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74
Q

What is compartmental flow?

A

We are essentially coming up with a fake scenario in which people flow from one “compartment” or stage to another

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75
Q

Describe a deterministic model.

A

The model does not worry about random effects, like individual differences in susceptibility. Everyone follows the same rules of probability about what compartment they are in at any given time.

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76
Q

Describe the SIR model.

A

“Susceptible, Infectious, and Recovered.” Each person is either in the S, I or R compartment at any given time. The simplest version of the SIR model doesn’t take into account birth and death.

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77
Q

What is the S in the SIR model?

A

Susceptible individuals (May become sick)

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78
Q

What is the I in the SIR model?

A

Infectious individuals (Are sick and may infect others)

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79
Q

What is the R in the SIR model?

A

Recovered individuals (Are no longer in danger of becoming sick again)

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80
Q

Describe a stochastic model.

A

A model that takes individuality into account. They are very commonly used and based off of the same mathematical principles as deterministic models. They just use more complicated probability formulas describing whether someone will move into the next compartment, and are not deterministic.

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81
Q

What is an agent-based model?

A

Helpful to study diseases that are very difficult to trace through a network to a particular infecting person (like respiratory diseases). They use computer simulations to estimate the behaviors of a real-world city, region or country. The simulations can help predict what emergent properties might occur as an infectious disease travels.

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82
Q

What is R0?

A

The number of infected individuals one person is expected to infect while they are infectious

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83
Q

What is the herd-immunity threshold?

A

The proportion of people that need to be immunized in order to eradicate a disease, or prevent an outbreak (Varies from disease to disease)

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84
Q

What is hysteresis?

A

A change in status. ex. a new emerging disease can cause an epidemic, and if not eliminated, reach a new stable equilibrium where it is now endemic

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85
Q

How do we calculate the number of people that will move from the S compartment to the I compartment?

A

cBSI/n

c = contacts
Beta = P(Infected/contacted)
S = susceptible
I = infected
n = population
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86
Q

How do we calculate the number of people moving from the I compartment to the R compartment?

A

1/DI

D = duration
I = Infectious
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87
Q

What is Rt?

A

Real-time or effective reproduction. Our goal when trying to prevent infectious diseases is to push Rt below 1, so that the epidemic will die out. In essence, you want to “remove” susceptible or infectious individuals from the population faster than the disease spreads. Vaccines do this very effectively

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88
Q

What is the formula for R0?

A

cB/y

c = contact
B = P(Infected/contacted)
y = rate of recovery
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89
Q

What is our R0 goal?

A

R0 < 1 (The disease is not actively propagating)

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90
Q

What is the E in the S(E)IR system?

A

Exposed

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91
Q

What are agent-based models used for?

A

Predictions

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92
Q

Selective mixing is a trend of what kind of network?

A

Sexual networks

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93
Q

<p>Define ecology.</p>

A

<p>The study of factors influencing the abundance and distribution of organisms</p>

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94
Q

<p>Define competition and cooperation.</p>

A

<p>Competition - Driving force of natural selection (Remember viruses damaging each other and competing for resources)

Cooperation - Differing species working together to benefit all species involved (Remember biofilms)</p>

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95
Q

<p>What is a biofilm?</p>

<p>What is quorumsensing?</p>

A

<p>A biofilm is a collection of bacteria cooperating and working together. Biofilms often form on hospital catheters / instruments and are responsible for many nosocomial infections</p>

<p></p>

<p>Quorum sensing is the cell-to-cell communication that regulates the density of bacteria growth so they can share resources.</p>

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96
Q

<p>What is a habitat?</p>

A

<p>The physical area a species inhabits</p>

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97
Q

<p>What is an ecological niche?</p>

A

<p>The habitat + behaviors of a particular species</p>

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98
Q

<p>How many species can occupy the same ecological niche?</p>

A

<p>Only 1.

Either one species will evolve to separate the niches, or one will out-compete the other, resulting in its extinction. </p>

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99
Q

<p>How does climate change affect ecology (Particularly disease dynamics)?</p>

A

<p>1) Warming can cause a shift in timing, where epidemic peak may occur at a different time of year than it did in the past

2) Warming can cause more epidemic “cycles”, meaning that there may be two epidemic peaks in the same year
3) Warming can cause overall epidemic intensity to either increase or decrease, depending on whether the pathogen can well-tolerate the new climate. </p>

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100
Q

<p>What is it mean for a disease to be zoonotic?</p>

A

<p>A zoonotic disease is a disease that has its origins in a species other than humans
(This includes vector-borne diseases as well as direct zoonotic diseases)</p>

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101
Q

<p>What does it mean for a disease to be frequency-dependent?</p>

A

<p>Transmission rates increase with the number of infectious people, but it doesn’t matter how geographically dense they are.

(I.e. STDs and some vector-borne diseases)</p>

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102
Q

<p>What does it mean for a disease to be density-dependent?</p>

A

<p>Transmission rates increase with population density of the host.

(E.g. influenza)</p>

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103
Q

<p>What is it called when an area has everything necessary for disease to spread (Pathogen, climate, resources, etc.), but humans don't inhabit the area?</p>

A

<p>A silent zone</p>

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104
Q

<p>What happens when a large population enters a silent zone?</p>

A

<p>There will be an epidemic</p>

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105
Q

<p>What are the principal modes of transmission? (8)

| PAAWSFFF</p>

A 
<p>Perinatal
Airborne
Animal bites
Water-borne
Sexual
Fecal-oral
Fomite
Food-borne</p>
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106
Q

<p>What is the name of this type of zoonotictransmission cycle?</p>

<p>Human --> Human --> Human</p>

<p></p>

A

<p>Direct human-to-human</p>

<p>(E.g. influenza)</p>

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107
Q

<p>What is the zoonotic transmission cycle in which a disease principally found in animals is passed to a human (Who does not pass it to other humans)?</p>

A

<p>Direct zoonosis</p>

<p>(E.g. rabies)</p>

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108
Q

<p>What is the zoonotic transmission cycle if the disease can only be passed from human to human via an insect or animal?</p>

A

<p>Vector-borne</p>

<p>(E.g. malaria)</p>

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109
Q

<p>If a disease can only be passed to humans from animals via a vector, what is the zoonotic transmission cycle?</p>

A

<p>Vectored zoonosis</p>

<p>(E.g. encephalitis)</p>

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110
Q

<p>(Here's the trickiest one)</p>

<p>If a disease can only be passed to humans from animals via a vector, and then it is transmitted from human to human via a vector, what is the zoonotic transmission cycle?</p>

A

<p>Anthropo-zoonosis</p>

<p>(E.g. yellow fever)</p>

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111
Q

<p>What is a reservoir?</p>

A

<p>A host species for a viral disease that does not usually become seriously ill from the disease</p>

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112
Q

<p>What are some examples of common reservoirs?</p>

A

<p>Bats, mice, and birds</p>

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113
Q

<p>What is the term that describes the transference of a disease from one species to another?</p>

A

<p>A spillover event</p>

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114
Q

<p>How does biodiversity protect us from disease?</p>

A

<p>The greater the number of species in a given area, the fewer interactions humans are likely to have with a particular disease-carrying species (Remember the Lyme disease example). This is called the dilution effect.</p>

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115
Q

<p>What is disease emergence?</p>

A

<p>The process by which a disease gains strength in the general population following a spillover event</p>

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116
Q

<p>Are deer ticks born with Lyme disease?</p>

<p>Where do they typically get it?</p>

A

<p>No.</p>

<p>Usually, they get Lyme disease from theirfirst blood meal(If the meal is infected, as white-footed mice often are).</p>

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117
Q

<p>Describe the life cycle of a tick.</p>

A

<p>Uninfected larva hatch in late Summer --></p>

<p>The feed on a (possibly) infected small animal --></p>

<p>They molt and become nymphs till the end of Winter --></p>

<p>In Spring/Summer/Fall they feed on vertebrates --></p>

<p>Ticks that feed on deer mate and lay eggs</p>

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118
Q

Who is the main international player conducting global surveillance?

A

The WHO

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119
Q

What laws must the WHO operate under in order to conduct global surveillance?

A

The International Health Regulations (IHR)

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120
Q

What is the order of players involved in reporting global surveillance (From local data collection all the way to the WHO)?

A

Field surveillance –>
National focal point (E.g. CDC) –>
Regional contact point (E.g. The Pan-American Health Organization) –>
WHO

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121
Q

What weekly report does the CDC release on surveillance and research activities?

A

Morbidity and Mortality Weekly Report (MMWR)

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122
Q

What are syphilis, smallpox, and AIDS examples of (Regarding data collection in the U.S. around infectious disease control)?

A

These are examples of reportable diseases .

(AIDS, chickenpox, gonorrhea, hepatitis A and B, measles, mumps, rubella, salmonella, shigella, syphilis, and TB

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123
Q

What are some of the fundamental components of surveillance programs?

A

Catchment areas

Case-report forms (CRFs)

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124
Q

What is a catchment area? When should one be designated in forming a surveillance plan?

A

A catchment area is the defined geographic region in which the surveillance will be operated.
The catchment area designation is the first step in the surveillance program design.

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125
Q

What is a case-report form?

A

Data collection tool (Basically a survey) where information on sick -or suspected to be sick- individuals can be recorded.

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126
Q

What are the first three essential steps in planning and running a successful surveillance program? What are some important components of each?

A
  1. System design (Catchment area designation, disease identification protocols, reporting process set up, etc.)
  2. Data collection (CRFs, contact tracing, etc.)
  3. Collation (Data aggregation, standardization, and organization)
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127
Q

What are essential steps four and five in planning and running a successful surveillance program? What are some important components of each?

A
  1. Analysis (Statistical / epidemiological measures)

5. Interpretation (Rates, vulnerable / geographic areas, morbidity / mortality, etc.)

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128
Q

What are the final two essential steps in planning and running a successful surveillance program? What are some important components of each?

A
  1. Dissemination / Communication (Radio, social media, television, health departments, scientific journals, etc.)
  2. Program change (Target vulnerable populations, modify program procedures)
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129
Q

Define syndromic surveillance.

A

Uses non-diagnostic health data (E.g. Google searches or ambulance records) to determine how many people are symptomatic of a disease.

Remember GPHIN from the TED video shown in class. They prevented a SARS epidemic.

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130
Q

What can syndromic surveillance help us catch?

A

Very useful in the detection of emerging diseases, disease outbreaks, or bioterrorist threats.

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131
Q

What is the Emerging Infections Program?

A

CDC catchment zones scattered across the U.S. monitoring antibiotic-resistant bacteria, foodborne outbreaks, influenza, and nosocomial infections.

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132
Q

What is the Active Bacterial Core?

A

An EIP program responsible for collecting data surrounding bacterial disease trends.

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133
Q

How do we prevent epidemics and pandemics?

A

Early detection, early response

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134
Q

<p>Superbug</p>

A

<p>When there are high morbidity and mortality due to a bacteria that has become resistant, it is often referred to as a superbug.</p>

<p></p>

<p>Extra info: Resistance to pharmacotherapy is not only an issue for bacteria, but it can arise in cancer cells, parasites, fungi, and other infections. Bacteria with acquired resistance include TB, S. aureus, Acinetobacter, E. coli, and V. cholera.</p>

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135
Q

<p>Why mechanisms for resistance exist in nature</p>

A

<p>Microscopic organisms have been battling one another for millions of years by producing chemicals that can limit the growth of other organisms. Resistance to these chemicals has evolved in synchronization with them.</p>

<p>Mechanisms for resistance are therefore not new to human populations. They have been in development long before we ever started using antibiotics therapeutically. In fact, a large portion of your microbiome is already resistant to antibiotics you have never been exposed to.</p>

<p>(Example: Penicillinase was discovered in the natural bacterial population in samples that pre-date the use of therapeutic penicillin.)</p>

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136
Q

<p>Horizontal gene transfer</p>

A

<p>When a bacteria takes up DNA from another source, it is called horizontal (or lateral) gene transfer (HGT)</p>

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137
Q

<p>Genetic island/cassette</p>

A

<p>The part of a bacteria’s genome resulting from HGT is called a genomic island, or a genetic cassette.

Genomic islands can confer resistance in the new bacteria. </p>

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138
Q

<p>Vertical gene transfer</p>

A

<p>If a gene is inherited directly from a “parent” bacteria during reproduction, it is called vertical gene transfer (VGT).</p>

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139
Q

<p>Intrinsic resistance</p>

A

<p>In the case of intrinsic resistance, no mutation is necessary to confer resistance.

The bacteria simply overcomes the antibiotic by making more copies of the protein that the antibiotic targets. </p>

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140
Q

<p>Ways in which resistance can develop (change drug target, modify cell walls, metabolize antibiotic, etc.)</p>

A

<p>It is important to note that resistance genes exist in bacteria with or without selection (does not “cost” them anything).</p>

<p></p>

<p>There are many different biological mechanisms by which they work. These include:</p>

<p>1. changing the shape of the antibiotics target protein,</p>

<p>2. developing the ability to metabolize the antibiotic,</p>

<p>3. developing the ability to recognize and actively pump out the antibiotic</p>

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141
Q

<p>Conjugation</p>

A

<p>Transfer of genetic material from bacteria to bacteria through a sex pilus connection</p>

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142
Q

<p>Transduction</p>

A

<p>Transfer of genetic material from bacteria to bacteria via a bacteriophage (Virus that infects bacteria)</p>

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143
Q

<p>Transformation</p>

A

<p>Direct uptake of 'spilled' DNA from outside the bacterial cell into the bacteria</p>

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144
Q

<p>The roles of humans in creating resistance</p>

A

<p>1. Less than ½ of the therapeutic antibiotics in existence are for human use.</p>

<p>2. There is a dramatic overprescription of antibiotics in the U.S. and internationally (Often for viral infections).</p>

<p>3. In agriculture, antibiotics are often used prophylactically because it was thought that they improve weight gain of animals (not to treat or prevent infection).</p>

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145
Q

<p>What can be done to mitigate the problem of antibiotic resistance?</p>

A

<p>Identifying resistant bacteria earlier, and developing new methods for identifying antibiotics or other antimicrobial therapies.</p>

<p></p>

<p>For example, genotyping of strains in clinics to test for resistance is on its way to becoming common practice. Another common strategy is to use combinations of antibiotics, so that the bacteria is not able to acquire resistance. This is a method used often in the treatment of drug-resistant TB.</p>

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146
Q

<p>What is a vector-borne disease?</p>

A

<p>Diseases that are transmitted between hosts by another species</p>

<p></p>

<p>(The vector is typically not infected, but that is not true in cases such as malaria)</p>

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147
Q

<p>What specific ecological challenges do vector-borne diseases produce?</p>

A

<p>How do we eliminate/control the vector without wide-ranging ecological effects?</p>

<p></p>

<p>How will climate change affect vector and host distributions?</p>

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148
Q

<p>What are some methods to prevent vector-borne disease?</p>

A

<p>Indoor residual spraying</p>

<p>Bednets / window screens</p>

<p>Genetic modifications</p>

<p>Larvae extermination</p>

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149
Q

<p>Name four vector-borne diseases.</p>

A

<p>Malaria</p>

<p>Dengue fever</p>

<p>Zika</p>

<p>Chikungunya virus</p>

<p>Etc.</p>

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150
Q

<p>How is the chikungunya virus transmitted?</p>

<p>Where is it found?</p>

<p>What is its incubation period?</p>

<p>What are some associated signs/symptoms?</p>

<p>How is it treated?</p>

A

<p>Mosquito-borne</p>

<p>Central / Southeast Asia and Sub-Saharan Africa</p>

<p>1 - 12 days</p>

<p>Rash, fever, polyarthralgia, vomiting, headache</p>

<p>Anti-inflammatories</p>

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151
Q

<p>How is the Dengue fever virus transmitted?</p>

<p>Where is it found?</p>

<p>What are some associated signs/symptoms?</p>

<p>How is it treated?</p>

A

<p>The <em>Aedes aegypti</em> mosquito</p>

<p>More than 100 countries in both hemispheres</p>

<p>Crushing bone pain (It is often called 'bone break fever'), fever, lethargy, can be hemorrhagic</p>

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152
Q

<p>How is the Zika virus transmitted?</p>

<p>Where is it found?</p>

<p>What are some associated signs/symptoms?</p>

A

<p>The<em>Aedes Agypti</em>mosquito</p>

<p>Microindonesia, Brazil, several other locations</p>

<p>Usually, mild symptoms lasting a few days to a week</p>

<p>Causes microcephaly and Guillan-Barre Syndrome among infants of affected mothers</p>

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153
Q

<p>How long can Zika remain present in semen? How long should a woman wait after her symptoms abate to try to have children?</p>

A

<p>6 months</p>

<p>2 months</p>

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154
Q

<p>Where did HIV come from?</p>

A

<p>It is a zoonotic disease that originated in non-human primates as SIV.</p>

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155
Q

<p>When was HIV first reported in the U.S.?</p>

A

<p>1981</p>

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156
Q

<p>What populations are especially at risk for HIV transmission?</p>

A

<p>Intravenous drug users</p>

<p>Homosexual men (44x higher risk than heterosexual men)</p>

<p>Impoverished women (Especially those that have little sexual control in their relationships)</p>

<p>Prostitutes</p>

<p>Healthcare workers (Due to needle sticks and accidental fluid exchange)</p>

<p></p>

<p>African-Americans, Asian-Americans, and Pacific Islanders also experience higher rates of HIV in the US than is found in other ethnic groups (Likely from a socioeconomic or stigma-related disparity).</p>

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157
Q

<p>What does it mean that HIV is a retrovirus?</p>

A

<p>It means that, upon infection, the virus (RNA) is transcribed (By reverse transcriptase) to DNA and inserted into the host genome after infection. This makes it very hard to treat as it becomes part of our own DNA!</p>

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158
Q

<p>What does it mean that HIV is a lentivirus?</p>

A

<p>It replicates slowly. There can be long incubation and latency periods between infection and symptoms</p>

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159
Q

<p>How does HIV spread?</p>

<p></p>

<p>What is seroconversion?</p>

A

<p>HIV spreads via bodily fluids such as blood, blood products, semen, rectal or vaginal fluids, or breast milk.</p>

<p></p>

<p>Seroconversion is when the immune system first begins producing antibodies against HIV. This usually happens a few weeks after the initial infection.</p>

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160
Q

<p>What type of human cell is preferentially infected by HIV?</p>

<p></p>

<p>What are the initial signs/symptoms of infection?</p>

A

<p>The virus preferentially infects CD4+ Helper T-cells (A type of white blood cell).</p>

<p></p>

<p>Upon initial infection, there are acute symptoms which are typically flu-like.</p>

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161
Q

<p>When has an HIV infection officially advanced to AIDS?</p>

A

<p>When CD4+ Helper T-cell count below 200/ml (normal counts are 500-1500 per ml).</p>

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162
Q

<p>What are some of the rare infections that typify AIDS (Due to decreased host immune response)?</p>

A

<p>- Pneumocystic (fungal) pneumonias</p>

<p>- Pneumonia due to cytomegalovirus, toxoplasmosis, herpes simplex, or gastrointestinal protozoa</p>

<p></p>

<p>- Some patients develop a rare form of cancer called Kaposi’s sarcoma. The cancer is caused by Kaposi sarcoma herpesvirus (KSHV) that inserts its genes into the host (Kaposi’s sarcoma is 20,000 times more common in AIDS patients than in the general public).</p>

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163
Q

<p>What is ART/ARV? Do they fully cure HIV?</p>

A

<p>Antiretroviral Therapy</p>

<p></p>

<p>They do not fully cure the disease; they only keep the viral load down.</p>

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164
Q

<p>What is an HIV superinfection?</p>

A

<p>When an HIV-infected patient on ARV becomes infected with an additional strain of HIV (Double HIV infection).</p>

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165
Q

<p>What is vertical HIV transmission?</p>

A

<p>Transmission from an infected mother to her child.</p>

<p></p>

<p>Transmission can occur in utero, during delivery, or through breastfeeding. Breastfeeding is the most common type of transmission from mother to child.</p>

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166
Q

<p>How is HIV different in children than adults?</p>

A

<p>More recurring opportunistic bacterial and viral infections, (but they are less likely to develop Kaposi’s sarcoma) more rapid disease progression as well</p>

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167
Q

<p>How can vertical HIV transmission be prevented?</p>

A

<p>A special ARV regimen (Highly effective).</p>

<p></p>

<p>The Pediatric AIDS Clinical Trials Group (PACTG) 076 AZT regimen is a series of ARV drugs given in different amounts during pregnancy, delivery and just after birth to prevent transmission of HIV to a child.</p>

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168
Q

<p>What are a few general methods by which to prevent HIV spread?</p>

A

<p>Condomdistribution</p>

<p>Education</p>

<p>Prophylactic ARV treatment (reduces transmission by 60-80%)</p>

<p>Needle exchange programs</p>

<p>Male circumcision</p>

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169
Q

<p>Do all HIV-infected individuals in the U.S. know they are infected?</p>

A

<p>No. About 20% of HIV+ persons in the United States are unaware of their infection. </p>

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170
Q

<p>What is the bacterium responsible for TB infections?</p>

A

<p><em>Mycobacterium tuberculosis</em></p>

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171
Q

<p>What percentage of the world population is infected with latent TB today?</p>

<p></p>

<p>What percentage of those infected with latent TB will become sick with active TB at some point in their lifetimes?</p>

A

<p>33%</p>

<p></p>

<p>10%</p>

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172
Q

<p>How is TB spread?</p>

<p></p>

<p>What body system does it most commonly infect? Can it infect other systems?</p>

A

<p>Respiratory droplets (Airborne transmission)</p>

<p></p>

<p>Respiratory system</p>

<p></p>

<p>Yes, TB can disseminate to organs other than the lungs</p>

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173
Q

<p>What is Milliary TB?</p>

A

<p>Many small areas of local TB spread throughout an organ</p>

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174
Q

<p>What human cell in the respiratory tract is preferentially infected by TB bacterium?</p>

A

<p>Alveolar macrophages</p>

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175
Q

<p>After alveolar macrophages are infected by TB bacterium, what happens?</p>

A

<p>Immune cells surround the area, promote inflammation, and accumulate as dead cells</p>

<p></p>

<p>(This forms nodules called granulomas)</p>

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176
Q

<p>Does the immune system usually manage to wipe out all the TB bacterium on its own?</p>

A

<p>No, the immune system usually only manages to keep the bacterium at bay</p>

<p></p>

<p>(This is called latent TB and is true for 90% of infected individuals)</p>

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177
Q

<p>What is it called when a latent TB becomes active?</p>

A

<p>Reactivation</p>

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178
Q

<p>How is TB diagnosed?</p>

A

<p>The Mantoux Tuberculin test (TB antigen injected under the skin) and chest x-rays</p>

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179
Q

<p>What is a Gohn focus?</p>

A

<p>A TB granuloma large enough to be seen on x-ray</p>

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180
Q

<p>What is it called if a patient presents with a Gohn focus and regional lymph node involvement?</p>

A

<p>This is a Gohn complex</p>

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181
Q

<p>What is the difference between primary vs. secondary TB infection?</p>

A

<p>Primary infection is the initial host encounter with TB bacterium.</p>

<p></p>

<p>A secondary infection refers to EITHER being infected with TB after being cured OR reactivation of latent TB</p>

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182
Q

<p>What are the signs/symptoms of TB infection?</p>

A

<p>Fever, cough, bloody sputum, weakness, and chest pain.</p>

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183
Q

<p>What is the most common cause of death among AIDS patients?</p>

A

<p>TB</p>

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184
Q

<p>How is TB treated?</p>

A

<p>- 2 initial months of chemotherapy (antibiotics) and varying amounts of continuing treatment (No need to memorize drug names, but know it’s a drug cocktail given for months).</p>

<p>- Patients may be asked to take a complex regimen of drugs including:</p>

<p>Isoniazid (an anti-metabolite)</p>

<p>Rifampin (inhibits RNA polymerase)</p>

<p>Ethambutol (inhibits cell wall formation)</p>

<p>Pyrazinamide (converts to an acid and accumulates, killing the cell).</p>

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185
Q

<p>What are our main prevention strategies for TB?</p>

A

<p>Vaccination (18-30% efficacy)</p>

<p>Prophylactic antibiotics</p>

<p>Isolation of infected individuals</p>

<p>DOTS program (Involves much closer patient-physician interaction and follow-up than usual)</p>

186
Q

<p>What is MDR-TB?</p>

<p></p>

<p>Where is it present?</p>

A

<p>Multi-drug resistant TB</p>

<p></p>

<p>In all countries</p>

187
Q

<p>What is XDR-TB?</p>

<p></p>

<p>What is TDR-TB?</p>

A

<p>Extremely-resistant TB</p>

<p></p>

<p>Totally resistant TB</p>

188
Q

<p>What is malaria?</p>

A

<p>A protozoan parasite that exists in many different animals</p>

189
Q

<p>What is the basic evolution of malaria?</p>

A

<p><em>Plasmodium </em><em>malariae</em>--></p>

<p><em>Plasmodium vivax</em>--></p>

<p><em>Plasmodium falciparum</em></p>

190
Q

<p>How has<em>Plasmodium vivax</em>impacted human evolution?</p>

A

<p><em>Plasmodium vivax</em>enters human erythrocytes via the Duffy receptor (An RBC glycoprotein). Being 'Duffy-less' is now a dominant human mutation in most Africans, and so <em>P. </em><em>vivax</em>is more prevalent in Europe and Asia</p>

191
Q

<p>How has<em>Plasmodium falciparum</em>affected human evolution?</p>

A

<p>Hemoglobin disorders confer some immunity to<em>P. falciparum</em>, and so now 1/14 of humans carry genetic mutations related to thalassemia, sickle-cell anemia, ovalocytosis, and other hemoglobin disorders.</p>

192
Q

<p>What are the 3 stages of the malaria lifecycle?</p>

A

<p>Inside the mosquito --> Inside the human liver --> Inside the human bloodstream --></p>

193
Q

<p>What are the signs/symptoms of malaria?</p>

A

<p>Fever, chills, nausea, and sweating</p>

194
Q

<p>What is the average incubation period for malaria?</p>

A

<p>~10 days</p>

195
Q

<p>The malaria types,<em> P. vivax</em>and<em> P. ovale</em> can remain dormant for long periods of time. What does this trait make them?</p>

A

<p>Hypnozoites</p>

196
Q

<p>What are some of the main prevention methods for malaria?</p>

A

<p>Insecticide-treated bed nets</p>

<p>Indoor residual spraying</p>

<p>Prophylactic medication (E.g. Doxycycline and primaquine)</p>

<p>Possible vaccines in the pipeline</p>

197
Q

<p>What are the main anti-malarial drugs?</p>

A

<p>Quinine and artemisinin</p>

<p>(Resistant strains of malaria are developing to both these drugs)</p>

198
Q

Antibiotic

A

A naturally occurring compound that can kill a microbial organism (Usually bacteria or parasites)

199
Q

Antimicrobial

A

Antibiotics as well as synthetic compounds

Multiple mechanisms of action including interfering with the building of cell wall and stopping nucleic acid synthesis

200
Q

Pharmacotherapy

A

Basically drug treatment

Antibiotics are a different form of pharmacotherapy (Treatment) than drugs used to treat chronic diseases, in that they target bacterial receptors/proteins instead of patient’s proteins. This makes each patient’s treatment unique as organisms fight back, hide, etc.

201
Q

Empiric therapy

A

Nonspecific treatment

When a bacterial infection is suspected but isn’t identified yet, a doctor can prescribe a general antibiotic until it is identified. This is called empiric therapy

202
Q

Definitive therapy

A

Specific treatment

Once the bacteria is identified by laboratory tests, they are supposed to describe an antibiotic that is specifically tailored to that pathogen, which is called definitive therapy.

Doctors don’t always transition from empiric to definitive therapy the way they should, which can be a driver of antibiotic resistance.

203
Q

Pharmacodynamics

A

How antibiotics interact with both the bacteria and the patient

Can impact a lot of how effective an antibiotic is going to be. Some antibiotics may inhibit bacterial growth (bacteriostatic), while others kill the organism (bacteriocidal). For example, if the antibiotic interferes with DNA replication it is likely bacteriostatic. If it causes cell lysis, it is bacteriocidal. Usually both are effective, but some infections (like meningitis) require bacteriocidal antibiotics.

204
Q

MIC

A

The minimum amount of antibiotic for inhibiting bacterial growth (If it is bacteriostatic)

205
Q

MBC

A

The minimum amount of antibiotic needed to kill a bacteria (if it is bacteriocidal)

206
Q

Pharmacokinetics

A

Pharmacokinetics is how the patient impacts the concentration of the antibiotic in the body. When an antibiotic is administered, it goes through three stages: absorption, distribution (concentrated differently throughout the body), and metabolism/excretion (most excreted in same form).

How quickly the antibiotic goes through each stage depends on a variety of factors. For example, it matters whether an antibiotic is hydrophobic or hydrophilic, how large the antibiotic is, and how it is administered.

207
Q

Who discovered/popularized penicillin

A

Alexander Fleming formally discovered in 1928

Mold Penicillum notatum on petri dish

Purified by Florey and Chain (British researchers) and disseminated during WWII

208
Q

The process of absorption, distribution, metabolism/excretion of antibiotics, what impacts it and why it matters in conjunction with pharmacodynamics in determining dosage.

A

How quickly the antibiotic goes through each stage depends on a variety of factors. For example, it matters whether an antibiotic is hydrophobic or hydrophilic, how large the antibiotic is, and how it is administered.

209
Q

Side effects of antibiotics

A

Antibiotics can alter microbiome composition and allow for opportunistic pathogen infection.

210
Q

How do beta-lactams work?

A

Beta-lactams are a type of antibiotic (E.g. penicillin and cephalosporin) that have a double-ring structure and work by interfering with the enzyme that constructs bacteria cell walls.

They are effective against many types of bacteria, but not against certain atypical organisms such as MRSA.

211
Q

How does tetracycline work?

A

Tetracyclines are 4 ring structures that work by physically preventing binding of tRNA to the ribosome, thus inhibiting translation and protein synthesis.

212
Q

How do anti-metabolites work?

A

Anti-metabolites function by mimicking something that the bacteria needs to metabolize to survive and starving the bacteria by inhibiting its enzymes.

213
Q

How do vaccines work?

A

They mimic natural infection to ‘trick’ the body into building up an immunity to a specific pathogen.

214
Q

What are antigens?

A

Anything that produces an immune response in the body (Usually the pathogenic components like glycoproteins that act as antigens to our bodies)

215
Q

What are antibodies?

What is another name for antibodies?

A

Proteins produced by our bodies (By B Cells) that will stick to pathogen antigens.
Immunoglobulins.

216
Q

Which is faster, your first or second immune response to a specific pathogen?

A

The second.

The first can take anywhere from a few days to two weeks, but the second often takes less than a day.

217
Q

What is a live-attenuated vaccine?

A

Vaccines that are made with a pathogen that is alive but weakened. The pathogen can still reproduce a little bit, but not cause disease (e.g. the MMR vaccine or the Sabin polio vaccine)

218
Q

What is a killed/inactivated vaccine?

A

An inactivated or killed vaccine is what it sounds like. The pathogen is completely dead, but the antigen still promotes an immune response (E.g. the Salk polio vaccine or the flu vaccine)

219
Q

What is a toxoid vaccine?

A

Vaccines made up of an inactivated toxin that the pathogen normally secretes. Mostly used for bacterial infections (E.g. the DTaP vaccine)

220
Q

What is a subunit vaccine?

A

If only a part of the pathogen is used to make the vaccine, it is referred to as a subunit vaccine (E.g. the Pertussis portion of the DTaP vaccine).

221
Q

What is a gene-based vaccine?

A

Gene-based vaccines use the injection of a small amount of the pathogen’s genetic material rather than an antigen. The person’s cells uptake the genetic material and produce the antigen themselves, promoting an immune response.

222
Q

What are virus-like particles used as vaccines?

A

Virus-like particles are a technology where the capsid or envelope of the virus is made in a laboratory but without any genetic material inside. This way, the antigens can be presented to the immune system intact without any risk of the virus causing infection. The HPV vaccine uses this method.

223
Q

What are a few of the main leukocytes involved in immune responses?

A

T-Cells, B-Cells, and macrophages

224
Q

Describe the two main types of T-Cell.

A

CD4+ - Helper T-Cells that support the other immune cells

CD8+ - Killer T-Cells that kill our own infected cells

225
Q

Describe the two main types of B-Cell.

A

Plasma cells - Produce antibodies

Memory B-Cells - Retain immunogenic memory of past antigens the body has seen

226
Q

What do macrophages do?

A

Ingest foreign materials and enemy cells to present their antigens to T- and B-Cells (They also clean up any debris in the human body).

227
Q

What are vaccine adjuvants?

A

Adjuvants are chemical additives to vaccines that are able to boost immune response through various mechanisms.

These include possibly clumping vaccine particles at the injection site (which recruits more APCs) or directly stimulating immune cells.

228
Q

What is Thimerosol? Why is it controversial?

A

Thimerosol is a preservative (not an adjuvant) containing trace amounts of mercury.

It was used in some vaccines to prolong shelf life. It has been taken out of all vaccines given to children under 6, and is only now included in some multi-dose flu vaccine vials.

It is often discussed as one of the possible reasons for the (disproven) hypothesis that vaccines are associated with autism. Some anti-vaccine literature suggests it was used in the MMR shot, however, it never was. Thimerosol was removed as a precaution and other preservatives were used.

229
Q

What is the only type of adjuvant permitted in the U.S.?

A

Only aluminum-based compounds

230
Q

What is reverse vaccinology?

A

A method of epitope prediction.

In reverse vaccinology, researchers compare the genetic sequences of many different strains of the pathogen, looking for regions of the genome that are always consistent. These are areas that don’t mutate much, likely because the virus needs that very specific protein for survival. When they identify a region, it becomes a good antigen to potentially include in a vaccine.

231
Q

What is an epitope?

A

An epitope is the specific chemical site on an antigen to which an antibody binds.

It can be helpful to try to identify good epitopes for antibody binding in advance, instead of having to try many different antigens (This is very difficult for diseases like HIV which mutate very quickly).

232
Q

How are adjuvants different from preservatives?

A

Adjuvants boost immune responses.

Preservatives prevent contamination (Typically fungal).

233
Q

What is the most common form of vaccine delivery?

What are some other forms?

A

Intramuscular injection (IM)

Oral vaccines (Usually for live vaccines)
Nasal sprays (Usually for live vaccines)
Vaccine patches
234
Q

Why would vaccine patches be more useful than injections?

A

You have far more immune cells right under the surface of your skin (to respond to scratches and cuts) than you do deep in your muscles. So delivering vaccine directly under the skin can increase the number of immune cells exposed, and thus the immune response.

It also lowers the risk of accidental needle-sticks for healthcare providers.

235
Q

How does cocooning work in vaccine delivery?

A

Booster shots are used in some cases to reinforce immunity as immunity can fade over time.

Ex: It is recommended that a DTaP booster be given to all caregivers for newborns and young children.

236
Q

What is the Tdap/DTaP vaccine protective against?

A

Covers Bordatella Pertussis infection (Whooping cough), diphtheria and tetanus

(Toxoid vaccine)

237
Q

What is the MMRV vaccine protective against?

A

Measles, Mumps, Rubella (German measles), Varicella (chicken pox)

(Live-attenuated)

238
Q

What is the pneumococcal vaccine protective against?

A

Pneumococcal disease caused by S. pneumonia

Live-attenuated vaccine

239
Q

What kind of vaccine is the influenza vaccine?

Where is the influenza vaccine mass-produced?

A

A killed vaccine, unless it’s the nasal spray, which is live-attenuated

The vaccine is incubated in chicken eggs (Although we are shifting over to human cell cultures for incubation)

240
Q

What is essentially the most effective vaccine we have?

A

The MMR vaccine

241
Q

How many children still die from measles per day (Today, in our vaccinated world)?

A

250 children

242
Q

Is there controversy today as to whether or not vaccines work?

A

No, it is a settled issue on both sides of the vaccination argument.

243
Q

How many diseases do we try to prevent with vaccines?

A

About 14

244
Q

Will multiple vaccines overwhelm a baby’s immune system?

A

No. Even a baby’s body is rapidly acquiring immunity to all sort of bacteria and viruses all the time. Vaccines only use a tiny portion of the baby’s immune system.

245
Q

How should we approach individuals with fears and concerns about vaccines?

A

Don’t be dismissive or condescending.
Build common ground.
Validate their real, lived experience.

246
Q

We don’t know, but what are likely to be the chief causes behind autism?

A

Genetic and environmental exposures (Maybe environmental effects on the microbiome)

247
Q

What two factors are compared in a two-by-two table?

A

Exposure (Yes or No) and Outcome (Yes or No).

‘Total’ columns are often added to this table.

248
Q

How is a risk ratio calculated?

A

Divide the risk of the outcome in the exposed (a / (a + b)) by the risk of the outcome in the unexposed (c / (c + d)).

(a / (a + b)) / (c / (c + d)) = RR

249
Q

How is a risk difference calculated?

A

Subtracting the risk of the outcome in the unexposed (c / d) from the risk of the outcome in the exposed (a / b).

(a / (a + b)) - (c / (c + d)) = RD

250
Q

What three measures of association can be calculated from a two-by-two table?

A

Risk difference
Risk ratio
Odds ratio

251
Q

What is the difference between calculating a rate and calculating a risk?

A

A rate is an observed number of cases per unit time.

A risk is just a proportion.

252
Q

What is the difference between odds and risk ratios?

A

Odds ratios are more useful for case-control studies and/or rare diseases. This is more useful when we don’t have totals that represent the population (I.e. we’ve matched 500 cases for 500 controls).

Risk ratios are based on the total percentage in the group, and so we need somewhat representative groups to utilize RRs.

Useful link:
https://www.mdedge.com/jfponline/article/65515/relative-risks-and-odds-ratios-whats-difference

253
Q

How is an odds ratio calculated?

A

(a / b) / (c / d)
OR (a / c) / (b / d)
OR (ad) / (bc)

Basically, the odds of your having the outcome if exposed over the odds of your having the outcome if not exposed.

254
Q

Define food security.

A

Lack of knowledge as to where future meals will come from.

255
Q

Define food desert.

A

An area where healthy foods are not available or accessible.

256
Q

What are phytonutrients?

A

Plant-based compounds (Usually non-essential to human diet) with some health benefit

257
Q

What are the major macronutrients?

A

Carbohydrates, proteins, and lipids

258
Q

What is lutein?

A

A phytonutrient - Aids in healthy vision

259
Q

What are indoles?

A

A phytonutrient - May aid in intestinal immune cells

260
Q

What is beta-carotene?

A

A phytonutrient - Aids in vitamin A absorption

261
Q

What is lycopene?

A

A phytonutrient - May help to prevent CVD

262
Q

What is anthocyanin?

A

A phytonutrient - Possible antioxidant

263
Q

What is allicin?

A

A phytonutrient - May aid in intestinal immune cells

264
Q

What is the DASH diet?

A

An antihypertensive diet cetnered around salt-reduction and an increase in fruits and vegetables

265
Q

What is the MIND diet?

A

A combination of the Mediterranean and DASH diets designed to increase cognitive health and functioning

266
Q

What are some examples of Federal programs centered around nutrition?

A

WIC (Women, Infants, and Children)
SNAP (Supplemental Nutrition Assistance Program)
School breakfast program
Farm Bill

267
Q

<p>What is the adult obesity prevalence rate in the U.S. (As of 2014)?</p>

A

<p>36.5%</p>

268
Q

<p>What percentage of the U.S. is overweight or obese (As of 2014)?</p>

A

<p>68.5%</p>

269
Q

<p>What percentage of U.S. children are obese?</p>

A

<p>17%</p>

270
Q

<p>What is the BMI equation?</p>

A

<p>Kilograms / meters2</p>

<p>(Or) lbs. / inches2x 703</p>

271
Q

<p>What is an underweight BMI?</p>

<p>What range is a normal BMI?</p>

<p>What range is an overweight BMI?</p>

A

<p>≤ 18.4</p>

<p>18.5 - 24.9</p>

<p>25 - 29.9</p>

272
Q

<p>What range is an obese class I BMI?</p>

<p>What range is an obese class II BMI?</p>

<p>What is an obese class III BMI?</p>

A

<p>30 - 34.9</p>

<p>35 - 39.9</p>

<p>≥ 40</p>

273
Q

<p>Dothe adult BMI categories work for children?</p>

A

<p>Not quite. Weuse a percentile chart to standardize the BMIs for all the variation in child growth rates.</p>

274
Q

<p>What is an underweight percentile for a child?</p>

<p>What is an overweight percentile?</p>

<p>What is an obese percentile?</p>

A

<p>< 5th percentile</p>

<p>> 85th percentile</p>

<p>> 95th percentile</p>

275
Q

<p>Which states have the highest burden of obesity?</p>

A
276
Q

<p>How does obesity break down by age?</p>

<p>By gender?</p>

<p>By race?</p>

<p></p>

A

<p>Higher rates among the middle-aged and older.</p>

<p>Slightly more women than men</p>

<p>Blacks > Hispanics > Whites > Asians</p>

277
Q

<p>What are some of the complications and common comorbidities of obesity?</p>

A

<p>CVD </p>

<p>Obstructive Sleep Apnea</p>

<p>GERD</p>

<p>GI issues</p>

<p>Cancer</p>

<p>Stroke</p>

<p>Diabetes</p>

<p>Heart failure</p>

<p>Hypertension</p>

<p>Dyslipidemia</p>

<p>Osteoarthritis</p>

<p>Atherosclerosis</p>

<p>Atrial fibrillation</p>

<p>Alzheimer’s Disease</p>

<p>Non-alcoholic fatty liver disease (NAFLD)</p>

<p>Polycystic Ovarian Syndrome (PCOS)</p>

<p>Surgical and anesthetic complications</p>

<p>Psychosocial disorders</p>

<p>etc...</p>

<p></p>

278
Q

<p>How does obesity relate to CVD?</p>

A

<p>1. Increased body mass leads to increased systemic blood pressure. →</p>

<p>Increased BP leads to chronic cardiac overload →</p>

<p>Overload leads to cardiac hypertrophy and strain.</p>

<p><br></br>
2. Lower HDL and higher LDL levels lead to atherosclerotic blood vessels and increased systemic blood pressure.</p>

279
Q

<p>How does obesity relate to diabetes?</p>

A

<p>1. Excess weight and body mass disrupt normal metabolic processes’ ability to regulate blood sugar levels →</p>

<p>Hyperglycemia and diabetes often result.</p>

<p><br></br>
2. Obesity is generally related to excessive and long-term carbohydrate intake, very directly leading to chronic hyperglycemic conditions.</p>

280
Q

<p>How does obesity relate to cancer (Obviously it depends on the typeof cancer)?</p>

A

<p>1. Increased levels of insulin and insulin growth factor (IGF-1) lead to excess growth.</p>

<p></p>

<p>2. Excess adipose tissue increases estrogen levels (Affecting breast and endometrial cancer rates).</p>

<p><br></br>
3. Fat cells are suspected to also affect cancer cell growth regulation in a yet unknown way.</p>

281
Q

<p>What is the difference between visceral and subcutaneous fat? Which is more harmful in excess?</p>

A

<p>Visceral fat is the fat that sits between and compresses the organs of themselves (Usually gives rise to an apple-shaped torso).</p>

<p>Subcutaneous fat is the less harmful fat that sits just below the skin (Usually gives rise to a pear-shaped torso).</p>

282
Q

<p>What are the five factors involved in metabolic syndrome?</p>

<p>How many of the factors must be present to classify an individual as having metabolic syndrome?</p>

A

<p>Blood pressure, triglycerides, HDL cholesterol, plasma glucose, and abdominal obesity.</p>

<p>3/5</p>

283
Q

<p>How can obesity be diagnosed?</p>

A

<p>BMI (Principalmethod)</p>

<p>DEXA scanning</p>

<p>underwater weighing</p>

284
Q

<p>What are the lab values involved with the following five factors of metabolic syndrome?</p>

<p>Blood pressure</p>

<p>Plasma triglycerides</p>

<p>Fasting plasma glucose</p>

<p>Abdominal obesity</p>

<p>HDL cholesterol</p>

A

<p>Blood pressure (High)≥ 130 / 85 mmHg</p>

<p>Plasma triglycerides (High) ≥ 150 mg/dl</p>

<p>Fasting plasma glucose (High) ≥ 100 mg/dl</p>

<p>Abdominal obesity (High) ≥ 35" (women); ≥ 40" (men)</p>

<p>HDL cholesterol (Low) ≤ 40 mg/dl</p>

285
Q

<p>What is the only method of obesity treatment and management that has shown to be consistently effective in morbidly obese populations?</p>

A

<p>Gastric bypass surgery</p>

286
Q

<p>Which cholesterol is associated with positive health benefits?</p>

<p>Which cholesterol is associated with negative health benefits?</p>

A

<p>HDL</p>

<p>LDL and VLDL</p>

287
Q

<p>What are the main types of bariatric surgery used in obesity management?</p>

A

<p>Gastric sleeve bypass</p>

<p>Gastric roux-en-y bypass</p>

<p>Gastric banding</p>

288
Q

<p>What is diabetes mellitus?</p>

A

<p>A condition in which blood sugar is highly elevated.</p>

289
Q

<p>What are the two main types of diabetes mellitus?</p>

<p>Which is more common in the U.S.?</p>

A

<p>Type 1 and type 2</p>

<p>Type 2 (90-95% of cases)</p>

290
Q

<p>Is the pancreas an endocrine or exocrine organ?</p>

A

<p>Both</p>

291
Q

<p>What are the primary endocrine secretions of the pancreas?</p>

<p>What are the clusters of endocrine cells called?</p>

A

<p>Insulin and glucagon secretion</p>

<p>Islets of Langerhans</p>

292
Q

<p>Which pancreatic cells secrete insulin?</p>

<p>Which pancreatic cells secrete glucagon?</p>

A

<p>Beta cells</p>

<p>Alpha cells</p>

293
Q

<p>What are the primary functions of insulin?</p>

A

<p>Decrease blood glucose by:</p>

<p>Increasing glucose transport into adipose and skeletal muscle tissues through GLUT-4 transporters</p>

<p>Increasing glycogenesis</p>

<p>Decreasing gluconeogenesis</p>

<p>Decreasing lipolysis</p>

294
Q

<p>What are the primary functions of glucagon?</p>

A

<p>Increase blood glucose by:</p>

<p>Increasing glycogenolysis (Glycogen breakdown)</p>

<p>Increasing gluconeogenesis (Protein breakdown)</p>

<p>Increasing lipolysis (Fat breakdown)</p>

295
Q

<p>What is the primary dysfunction in T1DM?</p>

A

<p>Insulin deficiency due to autoimmune destruction of pancreatic beta cells</p>

296
Q

<p>What is the primary dysfunction in T2DM?</p>

A

<p>Insulin insensitivity </p>

297
Q

<p>What is a hemoglobin A1c measurement?</p>

<p>What is it used for?</p>

A

<p>A measure of how much glucose has gotten 'stuck' on hemoglobin for the past 120 days (The lifespan of an RBC).</p>

<p>Used as a measure of long-term blood glucose control.</p>

298
Q

<p>What are the normal, pre-diabetic, and diabetic A1c readings?</p>

A

<p>Normal < 5.7%</p>

<p>Pre-Diabetic 5.7 - 6.4%</p>

<p>Diabetic > 6.4%</p>

299
Q

<p>Define hyperglycemia.</p>

A

<p>Elevated blood sugar</p>

300
Q

<p>What is a fasting plasma glucose (FPG) reading?</p>

A

<p>A measurement of an individual's blood glucose levels during a fasting state</p>

301
Q

<p>What are the normal, pre-diabetic, and diabetic FPG readings?</p>

A

<p>Normal < 100 mg/dl</p>

<p>Pre-Diabetic 100 - 125 mg/dl</p>

<p>Diabetic > 125 mg/dl</p>

302
Q

<p>At what age does T1DM usually manifest?</p>

<p>At what age does T2DM usually manifest?</p>

A

<p>Early. Often between 12 and 18 Later in life</p>

<p>Usually after 35 or 40</p>

303
Q

<p>What are the cardinal signs and symptoms of diabetes? (Remember the 3 P's)</p>

A

<p>Polyphagia (Excessive hunger)</p>

<p>Polydipsia (Excessive thirst)</p>

<p>Polyuria (Excessive urine production)</p>

304
Q

<p>Besides the 3 P's, what are some other signs and symptoms of diabetes?</p>

A

<p>There are many systemic effects, including, but not limited to:</p>

<p>Peripheral neuropathy</p>

<p>Diabetic retinopathy</p>

<p>Infection and gangrene</p>

<p>Acanthosis nigricans</p>

<p>Weight loss (Mainly in T1DM)</p>

<p>Renal damage</p>

305
Q

<p>What is the extreme and life-threatening effect of T1DM?</p>

A

<p>Diabetic ketoacidosis (DKA)</p>

306
Q

<p>What is the extreme and life-threatening effect of T2DM?</p>

A

<p>Hyperosmolar Hyperglycemic Non-Ketotic Coma (HHNC)</p>

307
Q

<p>How is T1DM typically treated?</p>

A

<p>Insulin administration and diet adjustment</p>

308
Q

<p>How is T2DM typically treated?</p>

A

<p>Diet and weight loss; oral hypoglycemic medications as needed (E.g. metformin)</p>

309
Q

<p>What is the leading cause of death among individuals with T1DM?</p>

A

<p>Renal failure</p>

310
Q

<p>What is the leading cause of death among individuals with T2DM?</p>

A

<p>Heart failure</p>

311
Q

<p>Where does diabetes mellitus fall in as a leading cause of death in the U.S.?</p>

A

<p>#7</p>

312
Q

<p>What geographic region in the U.S. has the highest prevalence of diabetes mellitus and in what racial group?</p>

A

<p>The Southeastern United States</p>

<p>(The obesity/stroke/diabetes belt)</p>

<p>African-Americans are at increased risk over other racial groups</p>

313
Q

<p>Which type of diabetes mellitus holds a stronger genetic disposition, type 1 or 2?</p>

A

<p>Type 2</p>

314
Q

<p>What factors can greatly increase one's chances of developing T2DM?</p>

A

<p>Obesity, metabolic syndrome, high-sugar and high-fat diet, family history</p>

315
Q

<p>What effect have gastric bypass surgeries been shown to have on obese patients with T2DM?</p>

A

<p>A complete cure of some patients' T2DM (As well as an average of 2/3 excess weight lost)</p>

316
Q

<p>What is diabetic ketoacidosis (DKA)?</p>

A

<p>Usually seen only in T1DM, glucose is unable to make it into the cells, the cells begin to starve, and lipids are broken down at a quick rate for energy production. Lipid breakdown leads to the production of ketone bodies that are acidic to normal blood pH.

Blood pH drops and the individual enters a coma.</p>

317
Q

<p>What are the ketone bodies produced during DKA?</p>

A

<p>Beta-hydroxybutyrate and acetoacetate</p>

318
Q

<p>Define hypoglycemia.</p>

<p></p>

<p>What is a danger of extended periods of hypoglycemia?</p>

A

<p>Low blood sugar (< 70 mg/dl)</p>

<p></p>

<p>Brain damage</p>

319
Q

<p>What are the ABCs of diabetes control (After an individual has already been diagnosed)?</p>

A

<p><strong>A1c</strong> < 7%</p>

<p><strong>Blood pressure</strong> < 130 / 85</p>

<p><strong>Cholesterol </strong></p>

<p>LDL < 100 mg/dl</p>

<p>HDL > 50 mg/dl (Women) > 40 mg/dl (Men)</p>

320
Q

<p>At what BMI should most Americans start being screened for diabetes?</p>

<p>Who else should be screened?</p>

<p></p>

A

<p>BMI ≥ 25 (Overweight)</p>

<p></p>

<p>≥ 45 years of age</p>

<p>Family history of T2DM</p>

<p>History of gestational DM</p>

321
Q

<p>What is the BMI at which members of the Asian population should be screened for diabetes?</p>

A

<p>23</p>

<p>(<em>Screen at 23</em>)</p>

322
Q

<p>What is the technical term for glucose production through the breakdown of fat and protein?</p>

A

<p>Gluconeogenesis (glucose-new-production)</p>

<p>(Promoted by glucagon; inhibited by insulin)</p>

323
Q

<p>What is the technical term for fat breakdown?</p>

A

<p>Lipolysis</p>

<p>(Promoted by glucagon; inhibited by insulin)</p>

324
Q

<p>What is the technical term for glucose breakdown to pyruvate?</p>

A

<p>Glycolysis</p>

<p>(Inhibited by glucagon; promoted by insulin)</p>

325
Q

<p>What is the storage form of glucose?</p>

<p>Where is it found?</p>

A

<p>Glycogen</p>

<p>Liver and skeletal muscle tissue</p>

326
Q

<p>What is the technical term for glycogen synthesis?</p>

A

<p>Glycogenesis</p>

<p>(Inhibited by glucagon; promoted by insulin)</p>

327
Q

<p>What is the technical term for glycogen breakdown (producing glucose)?</p>

A

<p>Glycogenolysis</p>

<p>(Promoted by glucagon; inhibited by insulin)</p>

328
Q

<p>What is primary (essential) hypertension?</p>

<p></p>

<p>For what percentage of HTN cases does it account?</p>

A

<p>An idiopathic form of HTN (cause unknown)</p>

<p></p>

<p>90%</p>

329
Q

<p>What is secondary HTN (responsible for 10% of cases)?</p>

A

<p>HTN due to some underlying disease</p>

330
Q

<p>What is the normal blood pressure classification?</p>

A

<p>< 120 / 80 mmHg</p>

331
Q

<p>What is systolic blood pressure? What is diastolic blood pressure?</p>

A

<p>Systolic BP = BP while the ventricles are contracting - Top number (e.g.<strong>120</strong>/ 80)</p>

<p>Diastolic BP = BP while the ventricles are relaxing- Bottom number (e.g.120​/ <strong>80</strong>)</p>

332
Q

<p>What is the proper classification for an individual with a BP ranging from 120 - 129 / 80 mmHg?</p>

A

<p>Elevated BP</p>

<p></p>

<p>(No longer known as pre-HTN)</p>

333
Q

<p>What is the stage 1 HTN pressure reading?</p>

A

<p>130 to 139 / 80 to 89 mmHg</p>

334
Q

<p>What is the stage 2 HTN pressure reading?</p>

A

<p>≥ 140 / ≥ 90 mmHg</p>

335
Q

<p>At what BP reading is an individual considered to be in a hypertensive crisis (at immediate risk for organ damage)?</p>

A

<p>≥ 180 / ≥ 120 mmHg</p>

336
Q

<p>What are some common complications of HTN?</p>

A

<p>Stroke</p>

<p>Atherosclerosis</p>

<p>Thrombosis</p>

<p>Aneurysm formation</p>

<p>Organ damage</p>

<p>(Not a comprehensive list)</p>

337
Q

<p>What is the DASH diet?</p>

A

<p>An antihypertensive diet focusing on the reduction of salt and lipid intake</p>

338
Q

<p>What lifestyle modifications can be utilized to lower BP?</p>

A

<p>Weight loss</p>

<p>Salt intake reduction</p>

<p>Physical activity increase</p>

<p>Meditation</p>

339
Q

<p>What is the REGARDS study?</p>

A

<p>the REasons for Geographic And Racial Differences in Stroke</p>

340
Q

<p>Define ischemia</p>

A

<p>Lack of oxygen delivery to tissues</p>

341
Q

<p>Define infarct.</p>

A

<p>Cell damage and death due to loss of blood flow</p>

342
Q

<p>What is the definition of a transient ischemic attack?</p>

A

<p>A 'mini-stroke' that results in signs and symptoms that have completely resolved 24 hours after the insult</p>

343
Q

<p>Just as heart attack refers to an acute myocardial infarction, what is the term that can also refer to a cerebral infarction (stroke)?</p>

A

<p>Cerebrovascular attack (CVA)</p>

344
Q

<p>What are the two main types of stroke?</p>

<p>Which is more common?</p>

<p>Which is more deadly?</p>

A

<p>Ischemic (thrombotic; loss of blood supply) and hemorrhagic (rupture leads to blood entering cranial space)</p>

<p></p>

<p>Ischemic is more common (85-90% of cases)</p>

<p>Hemorrhagic is more deadly</p>

345
Q

<p>What is the core zone of a stroke? What is the ischemic penumbra?</p>

A

<p>The core zone refers to the infarcted tissues following complete loss of blood supply</p>

<p></p>

<p>The penumbra refers to the affected area of tissue that is often still viable tissue but will die if perfusion is not reestablished; there is usually some collateral circulation supplying the tissues with some blood flow</p>

346
Q

<p>Define aneurysm.</p>

A

<p>Aweakening or outpouching in the blood vessel wall (a ballooning that is more likely to rupture than surrounding tissue)</p>

347
Q

<p>What are some of the risk factors for stroke?</p>

A

<p>Hypertension (Most important factor)</p>

<p>Metabolic syndrome</p>

<p>Atherosclerosis</p>

<p>Atrial fibrillation</p>

<p>Aneurysms</p>

<p>Race (African-Americans more at risk)</p>

<p>Medical history of thrombotic events</p>

348
Q

<p>What are some of the common signs and symptoms of stroke?</p>

A

<p>Headache, weakness, paralysis, dizziness, vision changes, balance changes, drooping facial features, slurred speech, disorganized speech or thoughts</p>

<p></p>

<p>(Physical signs often unilateral)</p>

349
Q

<p>On which side of the body will a right-sided stroke manifest?</p>

<p></p>

<p>What is the term for this manifestation?</p>

A

<p>The left side (and vice-versa for a left-sided stroke)</p>

<p></p>

<p>Contralateral</p>

350
Q

<p>How can stroke be diagnosed?</p>

A

<p>Clinical presentation, MRI, CT scans, angiography</p>

351
Q

<p>What medication can be given to prevent thrombotic stroke?</p>

<p></p>

<p>What medication can be given to dissolve the clot that is causing thrombotic stroke?</p>

A

<p>Aspirin and/or heparin</p>

<p></p>

<p>TPA (tissue plasminogen activator)</p>

352
Q

<p>Where does stroke fall in the U.S. leading causes of death?</p>

A

<p>#5</p>

353
Q

<p>Where in the U.S. leading causes of death does heart disease fall?</p>

A

<p>CVD is #1 (for the U.S. and the world)</p>

354
Q

<p>Try drawing out the flow of blood through the pulmonary and systemic circuits.</p>

A
355
Q

<p>Define thrombus and embolus</p>

A

<p>Thrombus = <em>stationary </em>blood clot</p>

<p>Embolus = <em>moving </em>blood clot</p>

<p>(or other clumped substance such as bacteria, fat, air, tumors, amniotic fluid, etc.)</p>

356
Q

<p>Describe the difference between ischemia and an infarct</p>

A

<p>Ischemia refers to reduced blood flow to tissues</p>

<p></p>

<p>Infarct refers to tissue necrosis secondary to reduced blood flow</p>

357
Q

<p>Define the following terms:</p>

<p>Atherosclerosis</p>

<p>Angina</p>

<p>Acute Myocardial Infarction</p>

A

<p>Atherosclerosis - Arterial hardening due to fatty plaque buildup</p>

<p></p>

<p>Angina - Chest pain</p>

<p></p>

<p>Acute Myocardial Infarction - Infarction of heart tissue</p>

358
Q

<p>Name the main six coronary arteries discussed in class. What part of the heart does each supply?</p>

A

<p>Right coronary artery</p>

<p>- Acute marginal artery (Anterior right ventricle)</p>

<p>- Posterior descending artery (Posterior right ventricle)</p>

<p></p>

<p>Left main coronary artery</p>

<p>- Left anterior descending (Anterior left ventricle and interventricular septum)</p>

<p>- Lateral and posterior left ventricle</p>

359
Q

<p>Which artery is themost common site of an AMI?</p>

A

<p>The left anterior descendingartery</p>

360
Q

<p>What is the Million Hearts Initiative? Was it successful?</p>

A

<p>This is awesome:</p>

<p></p>

<p>https://millionhearts.hhs.gov/files/MH-meaningful-progress.pdf</p>

361
Q

<p>What are the four behavioral components of Life's Simple Seven?</p>

A

<p>Physical activity</p>

<p>Weight reduction</p>

<p>Diet</p>

<p>Don't smoke</p>

362
Q

<p>What are the three laboratory tests in Life's Simple Seven?</p>

A

<p>Blood pressure</p>

<p>Plasma cholesterol</p>

<p>Plasma glucose</p>

363
Q

<p>Name all seven of the Life's Simple Seven factors.</p>

A

<p>Physical activity</p>

<p>Weight reduction</p>

<p>Diet</p>

<p>Stop smoking</p>

<p>Blood pressure</p>

<p>Plasma cholesterol</p>

<p>Plasma glucose</p>

364
Q

<p>Name the type of proteins that help transport cholesterol in the bloodstream (remember, fat is hydrophobic and must be carried by hydrophilic proteins).</p>

A

<p>Lipoproteins</p>

365
Q

<p>Which type of lipoprotein removes cholesterol from the bloodstream by taking it to the liver? Is this protective or damaging against heart disease?</p>

<p></p>

A

<p><strong>H</strong>igh-density lipoprotein (HDL)</p>

<p>Protective</p>

<p></p>

<p><strong>(H</strong>appy cholesterol)</p>

<p><strong>(H</strong>ealthy cholesterol)</p>

<p>(<strong>H</strong>elpful cholesterol)</p>

366
Q

<p>Which type of lipoprotein is bound to cholesterol and contributes to atherosclerotic plaque buildup by increasing the quantity of cholesterol deposited into atheromas?</p>

A

<p><strong>L</strong>ow-density lipoprotein (LDL)</p>

<p></p>

<p>(<strong>L</strong>ousy cholesterol)</p>

<p>(<strong>L</strong>ame cholesterol)</p>

<p>(<strong>L</strong>oser cholesterol)</p>

367
Q

<p>What is the underlying problem in angina? Are cells necessarily dying at this point?</p>

A

<p>Chest pain caused by ischemia in the heart tissues.</p>

<p>This is not necessarily an infarction and so cells are not always dying at this point.</p>

368
Q

<p>Describe stable (classical) angina.</p>

A

<p>Ischemic chest pain that begins on physical and/or emotional exertion and subsides on rest and/or intake of nitrates</p>

369
Q

<p>Describe unstable (crescendo) angina.</p>

A

<p>Ischemic chest pain that begins at rest and/or exertion and doesnot subside after rest and/or intake of medication.</p>

<p></p>

<p>Often called crescendo angina as it tends to worsen over time.</p>

370
Q

<p>Describe Printzmetal (variant) angina.</p>

A

<p>Ischemic chest pain due to atypical contraction and spasm of the coronary arteries.</p>

<p></p>

<p>Occurs most often in young women</p>

<p></p>

<p>Not related to atherosclerosis</p>

371
Q

<p>Which type of angina pectoris often shows ST-elevation and is most likely to devolve into an AMI?</p>

A

<p>Unstable (crescendo) angina</p>

372
Q

<p>Are there any recreational drugs that can worsen angina or increase the likelihood of acute myocardial infarction?</p>

A

<p>Cocaine (Vasoactive - causes arterial constriction)</p>

<p>(Also nicotine)</p>

373
Q

<p>What are the signs and symptoms of AMI? Differentiate between the two sexes.</p>

A

<p><b>Women:</b>Typically characterized by flu-like symptoms, fatigue, aches, chest tightness or pain, nausea, dyspnea</p>

<p></p>

<p></p>

<p><b>Men:</b>More classically associated symptoms such as crushing chest tightness, pain that radiates into the neck and left arm, and dyspnea</p>

374
Q

<p>How does aspirin prevent AMI?</p>

A

<p>Through decreased production of thromboxane A2(A clotting activator) from arachidonic acid</p>

375
Q

<p>What is the difference between a subendocardial and a transmural AMI?</p>

A

<p>Subendocardial infarction involves only the innermost layer of the heart.</p>

<p>Transmural infarction involves all three layers of the heart (leads to ST-elevation).</p>

376
Q

<p>How is the pathophysiology of heart disease different in women than in men?</p>

<p>How does this difference manifest on angiography (X-ray of the blood vessels)?</p>

A

<p>Men are characterized by macrovascular atherosclerotic plaque buildup (Fat buildup in clumpsin the bigger arteries)</p>

<p>Women are characterized by inflammatory processes which lead to microvascular dysfunction and widespread, even occlusion of the smaller arteries</p>

<p></p>

<p>On angiography, this difference often manifests as women's arteries being clearer than men's (even though there may be similar amounts of plaque buildup overall)</p>

377
Q

<p>What are some mechanisms of heart disease diagnosis?</p>

A

<p>Electrocardiogram (ECG), coronary angiography, stress test, cardiac enzymes present in blood(high-sensitivity C-Reactive protein (hsCRP) specifically in women)</p>

378
Q

<p>What is a common cardiac enzyme often found in the blood during an AMI?</p>

A

<p>Troponin I</p>

379
Q

<p>Name the three layers of an artery or vein.</p>

A

<p>Tunica intima (Endothelium)</p>

<p>Tunica media (Smooth muscle)</p>

<p>Tunica externa (Connective tissue)</p>

380
Q

<p>What is the main risk factor for atherosclerosis?</p>

A

<p>Hypertension</p>

381
Q

<p>Describe the general steps of atherosclerosis.</p>

A

<p>1. The endothelium is damaged</p>

<p>2. Cholesterol is deposited in the ruptured space</p>

<p>3. Macrophages enter the site, die, and become fat-laden foamy macrophages</p>

<p>4. The vessel lumen continues to narrow, pressure increases, and the risk of full occlusion or vessel rupture increase</p>

382
Q

<p>Define dementia.</p>

A

<p>An umbrella term for the effects of diseases resulting in a syndrome of effects including some mix of the following symptomsand behavioral changes:</p>

<p></p>

<p>memory loss, aphasia, agnosia, apraxia, executive function decline.</p>

<p>Also, agitation, mood swings, aggression, depression, sundowning, perseveration, hallucination, apathy, confusion, wandering, etc.</p>

383
Q

<p>Define aphasia.</p>

A

<p>Inability to speak</p>

<p>(a-phrase-ia)</p>

384
Q

<p>Define agnosia.</p>

A

<p>Inability to recognize faces and symbols</p>

<p>(a-nose-ia)</p>

385
Q

<p>Define apraxia.</p>

A

<p>Loss of fine motor skills and ability to perform practical motor tasks (e.g. buttoning shirt, tying shoes, brushing teeth)</p>

<p>(a-practical-ia)</p>

386
Q

<p>What is sundowning?</p>

A

<p>The worsening of dementia symptoms as night falls</p>

387
Q

<p>What is the most common cause of dementia?</p>

A

<p>Alzheimer's Disease (60 - 80% of dementia cases)</p>

388
Q

<p>Where does Alzheimer's Disease fall in the top 10 leading causes of death in the U.S.?</p>

A

<p>#6</p>

389
Q

<p>What are some common risk factors for Alzheimer's Disease development?</p>

A

<p>Age</p>

<p>Gender (women make up 2/3 of cases)</p>

<p>Family history</p>

<p>Social isolation</p>

<p>Low educational attainment</p>

<p>Metabolic syndrome</p>

390
Q

<p>How is Alzheimer's Disease diagnosed (In a definitive manner)?</p>

A

<p>Only by death after autopsy</p>

<p>All other diagnoses made by exclusion</p>

391
Q

<p>What is the usualage of onset for Alzheimer's Disease?</p>

A

<p>65 and older</p>

<p>(Althoughit is important to remember that AD is NOT a part of the normal aging process)</p>

392
Q

<p>What is the age of onset for early-onset Alzheimer's Disease?</p>

A

<p>Younger than 65 years of age</p>

393
Q

<p>What is the main function of the parietal lobe?</p>

A

<p>Sensory interpretation and organization</p>

394
Q

<p>What are the main lobes of the cerebrum?</p>

A

<p>Frontal</p>

<p>Parietal</p>

<p>Temporal</p>

<p>Occipital</p>

395
Q

<p>What is the function of the frontal lobe?</p>

A

<p>Executive function, planning, reasoning, planned motor functions</p>

396
Q

<p>What are the main functions of the temporal lobe?</p>

A

<p>Memory organization, auditory function</p>

397
Q

<p>What is the main function of the occipital lobe?</p>

A

<p>Visual processing</p>

398
Q

<p>What is the gene associated with Alzheimer's Disease (although only a small percentage, ~10% of cases, are associated with it)?</p>

<p></p>

<p>Is there a protective isoform of this gene?</p>

A

<p>APOE-E4 (Apolipoprotein-E4)</p>

<p></p>

<p>Yes, APOE-E2</p>

399
Q

<p>What genes are associated with early-onset Alzheimer's Disease? In families in which early-onset AD is prevalent, what is the hereditary nature of the disease?</p>

A

<p>APP (Amyloid protein precursor)</p>

<p>PSEN1 (Presenilin-1)<br></br>
PSEN2 (Presenilin-2)</p>

<p>Autosomal dominant (50% chance for offspring)</p>

400
Q

<p>What are the two main pathophysiological aspects of Alzheimer's Disease? Which is intracellular (inside the cell)? Which is extracellular (outside the cell)?</p>

A

<p>Beta-amyloid plaques (extracellular)</p>

<p>Tau-protein tangles (intracellular) - also known as neurofibrillary tangles</p>

401
Q

<p>How do we stop or cure Alzheimer's Disease?</p>

A

<p>There is no definitive treatment available yet</p>

402
Q

<p>Although no definitive treatment exists, what are current recommendations around preventing or slowing Alzheimer's Disease development?</p>

A

<p>Reduce metabolic syndrome factors</p>

<p>Learn as much as you can (Cognitive reserve hypothesis)</p>

403
Q

<p>Describe the cognitive reserve hypothesis.</p>

A

<p>The more social interaction, education, and other activities that stimulate the brain, the more protected an individual is against the effects of Alzheimer's Disease.</p>

<p></p>

<p>AKA more brain usage = more neural connections = more of a buffer against neuronal damage or loss</p>

404
Q

<p>Are there any clinical tests that can help in the diagnosis of Alzheimer's Disease and other forms of dementia?</p>

A

<p>Yes, the mini-cognitive test (mini-cog) and the mini-mental-state exam (MMSE)</p>

405
Q

<p>Describe mild, moderate, and severe Alzheimer's Disease.</p>

A

<p>Mild - Person still functions independently; mild cognitive decline; may be noticed by family and friends</p>

<p></p>

<p>Moderate - Longest stage; level of care required; sociobehavioral changes; increased cognitive impairment</p>

<p></p>

<p>Severe - Loss of ability to respond to environment; personality changes; comprehensive care-giving required; loss of awareness and physical abilities</p>

406
Q

<p>What are the common first signs of Alzheimer's Disease?</p>

A

<p>Mild cognitive impairment and loss of short-term memory</p>

<p>(This leads to difficulty in separating AD from the normal cognitive decline associated with the aging process)</p>

407
Q

<p>What is the average length of life for an individual after diagnosis with Alzheimer's Disease?</p>

A

<p>4-8 years (although this number can stretch out to up to 20 years)</p>

408
Q

<p>What is a common cause of death in individuals with Alzheimer's Disease?</p>

A

<p>Pneumonia or other respiratory issues associated with loss of proper swallowing ability</p>

409
Q

<p>What is the second most common type of dementia?</p>

A

<p>Lewy body dementia</p>

<p>Note: In our review, I said vascular dementia was 2nd. There is some debate around this topic, and for the purposes of our class, Lewy body dementia is 2nd MC. However, vascular dementia is commonly cited as 2nd MC and Lewy body as 3rd MC.</p>

410
Q

<p>What is the main dysfunction associated with Lewy body dementia?</p>

A

<p>Abnormal protein deposits (alpha-synuclein) in the brain, somewhat similar to AD</p>

<p></p>

<p>These deposits lead to a deficiency of dopamine and can cause some Parkinsonian symptoms</p>

411
Q

<p>What is the main dysfunction of vascular/multi-infarct dementia?</p>

A

<p>Vascular damage or defects lead to loss of sufficient blood flow to the brain and subsequent brain damage</p>

<p>(Basically, stroke or other vascular insults damage the brain)</p>

412
Q

<p>Describe Creutzfeldt-Jacob Disease.</p>

A

<p>An infectious disease caused by prions (misfolded proteins) that accumulate in the brain and cause neuronal degeneration</p>

413
Q

<p>Describe Multiple Sclerosis.</p>

A

<p>An autoimmune attack on the myelin sheath that leads to scanning speech, incontinence, decreased motor ability, fatigue, nystagmus, etc.</p>

<p></p>

<p>(Remember, <strong>M</strong>ultiple <strong>S</strong>clerosis affects the <strong>M</strong>yelin <strong>S</strong>heath)</p>

414
Q

<p>Describe Parkinson's disease.</p>

A

<p>Not characterized by dementia until the disease has severely progressed</p>

<p>Loss of dopamine-producing region of the brain (substantia nigra pars compacta in basal ganglia)</p>

<p>Characterized by rigidity, tremor, akinesia, shuffling walk</p>

415
Q

<p>Describe Huntington's Disease.</p>

A

<p>A hereditary, autosomal dominant genetic mutation with an onset between 20 and 50 years of age</p>

<p></p>

<p>Characterized by loss of motor inhibition, dementia, and depression</p>

416
Q

<p>Describe the MIND diet.</p>

A

<p>A combination of the DASH (antihypertensive) and Mediterranean diets; it is thought to decrease inflammatory and metabolic processes and thus improve cognitive function</p>

417
Q

<p>What is the most common killer among cancers?</p>

A

<p>Lung cancer</p>

418
Q

<p>What is the most common cancer in women?</p>

A

<p>Breast cancer</p>

419
Q

<p>What is the most common cancer in men?</p>

A

<p>Prostate cancer</p>

420
Q

<p>Do most women diagnosed with breast cancer have a previous family history?</p>

A

<p>No, 85% have no family history of the disease</p>

421
Q

<p>What percentage of breast lumps are non-cancerous?</p>

A

<p>80%</p>

422
Q

<p>What are some of the possible signs and symptoms of breast cancer besides finding a lump?</p>

A

<p>- nipple or another part of breast pulling inwards</p>

<p>- dimpling or puckering</p>

<p>- sudden discharge from a nipple</p>

<p>- itchy, scaly sore or rash on the nipple</p>

<p>- localized pain that doesn't go away</p>

<p>- thickening, redness or darkening of the skin on the breast or underarm area</p>

<p>- "peau d'orange" orange peel effect</p>

<p>- unusual swelling and warmth, or a change in breast size or shape.</p>

423
Q

<p>True/False. Self-breast exams are the gold standard for breast cancer detection.</p>

A

<p>False. They are not even recommended.</p>

424
Q

<p>What percentage of women have dense breasts?</p>

<p>What causes a breast to be considered dense?</p>

<p>In what age group is the breast typically denser?</p>

A

<p>~40%</p>

<p>A larger presence offibroglandular tissue (lactiferouslobules and ducts); as opposed to adipose tissue</p>

<p>Younger women (as their breasts are preparing for lactation)</p>

425
Q

<p>What is the best breast cancer detection tool we have?</p>

A

<p>Mammography (x-ray of the breast)</p>

426
Q

<p>Is it more difficult to detect breast cancer via mammography in a dense or non-dense breast?</p>

<p>Is breast density related to breast size?</p>

A

<p>Dense breast tissue 'shields' the tumor from detection.</p>

<p>No, there is no relation.</p>

427
Q

<p>What are some risk factors for breast cancer?</p>

<p>(Gender? Age? Genetics? Estrogen exposure?)</p>

A

<p>Gender - much more common in females</p>

<p>Age- more common as age increases</p>

<p>Genetics - BRCA1 and BRCA2 (<strong>BR</strong>east <strong>CA</strong>ncer genes) genes</p>

<p>Any increase in estrogen exposure - Nulliparous, no breastfeeding, early menarche, late menopause (Estrogen stimulates breast growth)</p>

428
Q

<p>A woman finds a lump in her breast. What are some possible causes of this lump?</p>

A

<p>A cyst - fluid-filled space</p>

<p>Fat necrosis - usually due to trauma</p>

<p>A benign tumor - fibroadenoma</p>

<p>A malignant tumor (cancer) - adenocarcinomas (much more common) and fibrosarcomas</p>

429
Q

<p>Where is breast cancer more commonly found in the breast (by quadrant)?</p>

<p>Where in the anatomical structures of the breast is it more common (the milk lobes, the ducts, the supporting tissues)?</p>

A

<p>Upper outer quadrant (armpit area)</p>

<p>The ducts</p>

430
Q

<p>Which race is most commonly diagnosed with breast cancer?</p>

<p>Which race most commonly dies of breast cancer?</p>

A

<p>Caucasian women</p>

<p>African-American women</p>

431
Q

<p>When is breast cancer awareness month?</p>

A

<p>October</p>

432
Q

<p>The BRCA 1 gene is associated with which types of cancer?</p>

A

<p>Breast, ovarian, and uterine cancers</p>

433
Q

<p>The BRCA 2 gene is associated with which typeof cancer?</p>

A

<p>Mainly breast cancer</p>

434
Q

<p>What does it mean for a breast cancer to be triple-negative?</p>

<p></p>

<p>Is this a more or less dangerous form of cancer?</p>

A

<p>The breast cancer cells have no receptors for estrogen (E), progesterone (P), or human epidermal growth factor (HER-2)</p>

<p></p>

<p>This type of cancer is not responsive to hormone therapyand thus more dangerous</p>

435
Q

<p>How much earlier can mammogram detect breast cancer than self- or clinical breast examination?</p>

A

<p>2 years</p>

436
Q

<p>Which lymph nodes drain the breast?</p>

A

<p>The axillary lymph nodes</p>

437
Q

<p>What is the name of the first lymph node to drain the fluid surrounding a tumor?</p>

A

<p>The Sentinel node</p>

438
Q

<p>What are the ACS guidelines for mammography?</p>

A

<p>Annual screening for women from 45-54 years of age</p>

<p>Biennialscreening for women ≥ 55 years of age</p>

439
Q

<p>What are the USPSTF recommendations for mammography?</p>

A

<p>Biennial screening after 50 years of age</p>

440
Q

<p>When should a woman begin breast cancer screening earlier than the average recommended guidelines?</p>

A

<p>When she has a higher risk</p>

<p>- Personal or family history</p>

<p>- Genetic susceptibility</p>

<p>- History of chest radiation (e.g. past TB patients)</p>

441
Q

<p>Describe fibrocystic disease in the breast.</p>

<p>What age group does it typically present in?</p>

A

<p>Most frequent breast lesion.</p>

<p>Painful, multiple bilateral masses that worsen in pain and increase in size during premenstrual cycle</p>

<p>Most common in women aged 30-50</p>

442
Q

<p>How can breast cancer be treated?</p>

A

<p>Depends on the extent of the disease growth.</p>

<p></p>

<p>Lymph node dissection</p>

<p>Lumpectomy</p>

<p>Mastectomy</p>

<p>- Simple</p>

<p>- Partial</p>

<p>- Total</p>

<p>- Radical Halsted</p>

<p>- Modified-radical</p>

443
Q
A
444
Q

What are the three main forms of thinking that have negative emotive effects?

A

Human rating
Demands
Catastrophizing

445
Q

What are two fundamental principles of rational emotive behavioral therapy?

A
  1. Work to persuade people to change thinking that upsets them
  2. All emotion, thought, behavior, and perception are intricately connected
446
Q

What is the #10 leading cause of death in the U.S.?

A

Suicide

447
Q

What is the #9 leading cause of death in the U.S.?

A

Kidney diseases (nephritis, nephrosis, nephrotic syndrome)

448
Q

What is the #8 leading cause of death in the U.S.?

A

Influenza and pneumonia

449
Q

What is the #7 leading cause of death in the U.S.?

A

Diabetes mellitus

450
Q

What is the #6 leading cause of death in the U.S.?

A

Alzheimer’s Disease

451
Q

What is the #5 leading cause of death in the U.S.?

A

Stroke

452
Q

What is the #4 leading cause of death in the U.S.?

A

Chronic lower respiratory disease

453
Q

What is the #3 leading cause of death in the U.S.?

A

Unintentional injuries (increasing as a result of the opioid epidemic)

454
Q

What is the #2 leading cause of death in the U.S.?

A

Cancer (Neoplastic disease)

455
Q

What is the #1 leading cause of death in the U.S.?

A

Cardiovascular disease

456
Q

Of deaths due to non-communicable disease in individuals under the age of 70, 82% are in low-, middle-, or high-income countries?

A

82% are in low- and middle-income countries

457
Q

What are the four major upstream risk factors associated with nearly all chronic disease?

A

Diet
Physical activity
Alcohol use
Tobacco use

458
Q

What is the leading cause of cancer death in the U.S.?

A

Lung cancer

459
Q

What is the most common cancer among men?

A

Prostate cancer

460
Q

What is the most common cancer among women?

A

Breast cancer

461
Q

What is the most common dyad of disease in the U.S.?

A

Hypertension and arthritis

462
Q

What is the most common triad of disease in the U.S.?

A

Hypertension, arthritis, and diabetes mellitus

BYU - Health 619 (24 decks)

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