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Foundations of Medicine > FOM Week 3 > Flashcards

FOM Week 3 Flashcards

1
Q

Explain the Effects of Buspirone and Erythromyosin When Taken Together

A

Both of the drugs get metabolized by the same enzyme, CYP3A4, in the liver. These two act as competitive inhibitors to each other thus slowing down the metabolism of them and causing side effects

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2
Q

Pharmocodynamic Interactions

A

The capability of one drug to affect another drugs response directly
Can be beneficial or harmful

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3
Q

What is the main form of lipids in our diet

A

Even carbon triglycerols

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4
Q

Two Essential FAs of Human Diet

A

Omega 3 and Omega 6

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5
Q

Where are lipids stored in the body

A

White adipose tissue

Liver

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6
Q

Where in the cell does beta oxidation occur

A

The matrix of mitochondria

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7
Q

What is the activating step of beta oxidation

A

The fatty acid gets converted into fatty acyl CoA
This turns ATP into AMP
Occurs in the cytosol of cell

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8
Q

How does fatty acyl CoA cross the inner membrane of mitochondria

A

It uses the Carnitine Transport Protein

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9
Q

Explain how malonyl CoA regulates beta oxidation

A

Malonyl CoA is produced by glucose metabolism in lipogenesis. This inhibits the carnitine transferase so no FAs are metabolized
When you are using glucose to make lipids there is no need to metabolize FA (occurs after consuming lots of sugar)

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10
Q

Explain what happens when you eat lots of fatty acids

A

Acyl CoA inhibits lipogenesis of from glucose occuring

If you just consumed lots of lipids, you dont want to be making them

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11
Q

Explain the oxidation of even saturated FAs

A

1) Activate them by turning them to acyl CoA
2) Oxidize and create FADH2
3) Hydrolyze
4) Oxidize to create NADH
5) Cleave using CoASH to create acetyl CoA and a 2C shorter acyl CoA

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12
Q

Explain the difference of beta oxidation in unsaturated fatty acids

A

Since there is already a double bond present you skip the first oxidizing step so no FADH2 is created

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13
Q

Explain the difference of beta oxidation in uneven fatty acids

A

Proponiol CoA is formed instead of acetyl CoA and then converted into succinyl CoA

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14
Q

Ketonegenesis vs Ketogenolysis

A

Occurs in the liver
Occurs in the muscle and brain during starvation
Byproduct is acetone which leads to ketoacidosis

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15
Q

Cartilage consists of

A

Chondrocytes

Matrix (ground substance + fibers)

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16
Q

How does cartilage get nutrition and oxygen

A

Through diffusion

It lacks blood vessels

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17
Q

Characteristics of Bone

A

It has a hard compact outside
It has a soft spongy inside
On the inside there are lots of neurons and vessels
It is constantly being remodeled

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18
Q

Diaphysis vs Metaphysis vs Epiphysis

A

Diaphysis is the long shaft bone
Metaphysis is near the edge of the bone
Epiphysis is the edge of the bone where it rounds

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19
Q

Types of Cells in the Bone

A

Osteoprogenitor cells- create osteoblasts
Osteoblasts- synthesis collagen type 1 and alkaline phosphotase
Osteoctyes- Osteoblasts that are surrounded by calcium
Osteoclasts- giant multinucleated cells derived from monocytes that have a ruffled border. They secrete acid to resorb bone

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20
Q

Osteiod

A

Only type 1 collagen and proteoglycans

They are unmatured and uncalcified

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21
Q

ARF Cycle

A 
They cycle bone goes through once it gets damaged
Activation
Resorbtion
Reversal
Formation
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22
Q

Effects of PTH

A

It works to increase Ca in the blood
Binds to osteoblasts which will then secrete RANK-L. This will then bind to RANK on the osteoclasts and activate them which results in calcium being released

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23
Q

Denosumab and Osteoprotegerin

A

They both bind to RANK-L to prevent osteoclasts from binding to it and therefore prevent its activation

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24
Q

Biphosphonates

A

Used to treat osteoperosis

Work by causing the osteoclasts to undergo apoptosis

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25
Q

3 Types of Cartilage

A

Hyaline- smooth and made up of collagen type 2. Found in the bone
Elastic- has elastic fibers that make it not smooth. Made up of collagen type 2 and found in ear and larynx
Fibrocartilage- made up of collagen type 1 and 2. Found in the vertebrae disks

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26
Q

Where does substrate from the TCA cycle come from

A

Acetyl CoA from glycolytic pyruvate
Acetly CoA from beta oxidation
Succinyl CoA from beta oxidation
Amino acid catabolism

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27
Q

How does pyruvate get into the mitochondria

A

It freely passes the outer membrane but gets into the matrix from a carboxylic acid transporter in the inner membrane

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28
Q

Ways to Generate Oxaloacetate if None is Present

A

PEP
Pyruvate
Malate can all be used to make oxaloacete
TCA will not occur unless oxaloacetate is present

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29
Q

Function of Thiamine

A

Cleaves C-C bonds

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30
Q

Function of Riboflavin

A

Involved in redox rxns of FAD

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31
Q

Function of Niacin

A

Involved in redox rxns of NAD

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32
Q

Products of the TCA Cycle

A

CO2

NADH and FADH2 for the ETC

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33
Q

Explain How Cytosol NADH Enter Matix

A

Malate aspartate shuttle–> NADH

Glycerophosphate shuttle–> FADH2

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34
Q

Effects of Azide and CO on ETC

A

They bind to heme group and prevent oxygen from getting to tissues. Since oxygen is the final electron acceptor the ETC would stop and this would cause a build up of lactate

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35
Q

Delta G Naught vs Delta G

A

G naught is when the rxn is in equilibrium (G=0)

G is a snapshot of the rxn and must be negative for a rxn to occur

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36
Q

Importance of Free Energy Being a State Function

A

This means it is independent of its path
Because of this we can use free energy to do work such as couple with unfavorable rxns and make them occur
How enzymes work

37
Q

Creatine Kinase and Phosphocreatine

A

They serve as a buffer system in the muscle

38
Q

Explain How Mutated Proteins Affect G Naught

A

Mutations in proteins generally change the equilibrium of the folded state
Mutated proteins have a higher G Naught which means the reaction is less favorable

39
Q

Useful Ways Our Body Uses ROS

A

Signaling
Immunity
Energy Production

40
Q

Explain How NO Effects Vessels

A

NO is produced by NO synthase and binds to guanyl cyclase in the smooth muscle causing them to relax which serves as a vasodilator

41
Q

Nitroglycerin vs Viagra

A

Nitrogylcerin causes more NO to be produced

Viagra makes the NO signal last longer

42
Q

ROS In ETC

A

1-4% of electrons leak off and can bind with O2 to form superoxides
Is thought to serve as a signal to tell cell the current metabolic state

43
Q

Ways to Prevent ROS Formation in ETC

A

Add more ADP
Slow down the TCA
Produce uncoupler proteins

44
Q

How do metals affect ROS

A

Metals serve as a catalyst to forming ROS

H2O2 can bind to metals to form very toxic ROS

45
Q

Ways ROS can attack our cells

A

They can cause mutations in DNA
They can cross link amino acids making them not able to be degraded
The can decrease the amount of unsaturated FAs in the membrane and thus depleting fluidity

46
Q

Enzymatic Ways to Control ROS

A

They are located all throughout the cell
Dismutase takes superoxide and converts it to H202
Catalase then take H2O2 and converts it to oxygen and water

47
Q

Non Enzymatic Ways to Control ROS

A

These are vitamins that accept the electrons and by doing so they become radical species
They are just more stable because of resonance
Some will also bind to metals to prevent less radicals from forming

48
Q

Importance of Physical Exam

A

The MH interview allows you to get an idea of the diagnoses. The physical exam is a way to confirm it

49
Q 
"Normal" Vital Signs for:
Heart Rate
Respiratory Rate
Blood Pressure
Temp
A

60-100. Anything below is bradycardia. Anything above is tachycardia
12-20 respirations per minutes
120/80
36-38 degrees celcius

50
Q

Which parts go under each of the SOAP categories

A

S- All of patient interview
O- Physical exam and vitals
A- Assessment of everything. What you think it is
P- Plan. What you are going to do to treat it

51
Q

4 Reasons Why Documentation is Important

A

Billing
Legal record
Memory Aid
Communication with other professionals

52
Q

2x2 Table

A

Exposure is on the Top

Disease is on the right side

53
Q

What measures can we establish in cohort study

A

Cumulative incidence, incidence rate, hazard, risk ratio, relative risk, absolute risk

54
Q

What measures can we establish in a case study

A

Odds ratio

55
Q

Odds Ratio Formula

A

AD/BC
If it equals 1 there is no correlation
If it is greater than 1, exposure is a risk factor
If it is less than 1, exposure is a protective factor

56
Q

Risk Ratio Formula

A

(A/A+C) / (B/B+D) or Risk in exposed/Risk in unexposed

57
Q

Relative Risk Difference

A

1 - Risk Ratio (If protective)
Risk Ratio - 1 (If risk factor)
Normally used if exposure is a protective faster
Converts it into numbers that patient will get

58
Q

Absolute Risk Increase

A

If exposure is protective: Risk in unexposed - Risk in exposed
If exposure is harmful: Risk in exposed - Risk in unexposed
*It will always be a positive number

59
Q

Number Needed to Treat

A

1/ARR

You want this number to be low

60
Q

Number Needed to Harm

A

1/Absolute Risk Increase

You want this number to be high

61
Q

Attributable Risk

A

Risk in Exposed - Risk in Unexposed

Same as Absolute Risk Increase

62
Q

Population Attributable Risk

A

Risk in Population - Risk in Unexposed

63
Q

Tertiary Prevention

A

The disease has been ongoing

We are working to prevent it from getting worse

64
Q

Secondary Prevention

A

The disease is relatively new

We catch it at the right time to prevent real damage

65
Q

Primary Prevention

A

Preventing disease from happening in first place

66
Q

Which region in KS has worst health outcomes

A

SouthEast

Wyandotte

67
Q

Where are the largest % of hispanics in KS

A

SouthWest

This also has the lowest number of PCP

68
Q 
What filament do each motor protein bind to and which direction do each go:
Myosin 1
Myosin 2
Kinesin
Dynein
A

Actin and moves towards plus end
Actin and moves towards plus end
MT and moves towards plus end (periphery)
MT and moves towards minus end (body)

69
Q

Gliding

A

When the motor proteins are anchored to a membrane or something. They can be used to move the filaments themselves to different parts of cell

70
Q

Lamellipodium

A

The front part of the cell that has actin extending which causes the cell to move forward in its direction

71
Q

Explain the Importance of Focal Adhesions in Cell Movement

A

Focal adhesions hold the cell down to the substrate
In order for the cell to move, the FA in the back have to get disassembled and then reform in the front
This is done by the assembly/disassembly of MT

72
Q

Matrix MetalloProteases

A

They are proteins that degrade the BM and connective tissue. Very important in melanoma becoming invasive

73
Q

TIMP-2

A

Required for MMP 1 to be active
Inhibits MMP 2
An example of moonlighting

74
Q

How Touch Influences Cilia Movement

A

Cilia cells have mechanoreceptors that open upon touch. This causes an influx of Ca which makes the cilia move more rapid. The calcium also spreads to other cells via gap junctions

75
Q

What tissues use glycolysis

A

All tissues but most occurs in the brain

76
Q

Where does glucose come from

A

Diet (glucose/fructose/galactose)
Glycogen Storage in liver
Gluconeogenesis from amino acids

77
Q

Explain the Steps in Glycolysis

A

1) Phosphorylate glucose to activate it
2) 2 rxns that attempt to make it symmetrical
3) 2 rxns that cleave and isomerize
4) 2 rxns that harness energy
5) 3 rxns that isomerize into pyruvate

78
Q

What cofactors are used in glycolysis

A

ATP
NAD
Mg
K

79
Q

What pathway products are produced by glycolysis

A

NADH
2 ATP
2 Pyruvate

80
Q

What happens if no O2 is present

A

The ETC stops and thus no NAD+ is regenerated
This causes a back up in all the processes that require NAD+ (glycolysis/beta oxidation)
In order to regenerate NAD+ anaerobic respiration occurs

81
Q

How is glycolsis and gluconeogenesis regulate

A

By enzyme inhibitors and free energy

Rxns that have a very low G are considered regulatory steps because they are irreversible (HK, PFK, PK)

82
Q

Inhibitors and Activators of PFK

A

Inhibited by ATP and Citrate

Activated by AMP and F-2,6P

83
Q

Inhibitors and Activators of FBPase

A

Inhibited by AMP and F-2,6P

Activated by ATP and Citrate

84
Q

Goal of the Geriatric Comprehensive Assessment

A

To maintain function and well being

Focuses on quality of life rather than quantity

85
Q

10 Parts to the Geriatric Assessment

A 
AGING GAMES
Audio/Visual
Gait/Movement/Falling
Insomnia
Nutrition
GI
GU
ADL
Mood/Memory
Environment
Sexuality
86
Q

DETERMINE for Nutritional Assessmenet

A 
Disease
Eating Poorly
Tooth Loss
Economic Hardship
Reduction in Social Contact
Medicines
Involuntary Weight Loss
Need for Assistance
Elderly
87
Q

Activities of Daily Living

A 
DEATH
Dressing
Eating
Ambulating
Toileting
Hygeine
88
Q

Instrumental Activities of Daily Living

A 
The first to go in dementia patients
SHAFFT
Shopping
Housework
Accounting
Food Prep
Transportation
Telephone

Foundations of Medicine (5 decks)

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