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basic science > MRC Basic Science/Stats/Epi > Flashcards

MRC Basic Science/Stats/Epi Flashcards

1
Q
  1. ) What is a Case-Control Study? What Level of Evidence?

2. ) What stat is calculated?

A
  1. ) Group of patients compared RETROSPECTIVELY (ie. look at disease and see what risk factors they had) = Level 3
  2. ) Odds Ratio = probability event will occur/probability event will not occur
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2
Q
  1. ) What is a Cohort Study? What Level of Evidence?

2. ) What stat is calculated?

A

1.) Group of patients compared PROSPECTIVELY (ie. look at risk factors 1st and see who gets dz) = Level 2
2.) Relative Risk = risk in exposed/risk in unexposed
(RISK = INCIDENCE!)…only a cohort study can tell you incidence b/c it is going forward in time!
RR = 1: No association
RR > 1: positive association (risk in exposed > risk in unexposed) CANNOT INFER CAUSAL!! - can’t tell!
RR < 1: negative association (risk in exposed < risk in unexposed) CANNOT INFER PROTECTIVE!!
**If 95% CI crosses 1 = NOT SIGNIFICANT

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3
Q

1.) What type of study are:
Case-Control, Cohort, Case Series, and Case Report?
2.) What type of study is a RCT?

A
  1. ) Observational

2. ) Experimental

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4
Q
  1. ) What Level of Evidence is a RCT typically?

2. ) What can downgrade it?

A
  1. ) Level 1
  2. ) Poor f/u (<80%), heterogeneous results, no blinding, concerns about randomization. ANY OF THESE WOULD MAKE IT A LEVEL 2 STUDY!!
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5
Q

What is the difference b/t a systematic review and a meta-analysis?

A

Systematic review just looks at a bunch of studies.

Meta-analysis uses fancy STATS to combine the results!

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6
Q

FDA Phases of Research - what happens in each Phase I-IV?

A

I -> “First in Man” to determine safety
II -> Determine if device/drug is effective (MOST COMMON phase of failure)
III -> Confirm efficacy through large trials
IV -> Postmarketing surveillance

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7
Q

Does QI study require IRB?

A

NO! Not research!!

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8
Q

Name the studies that are Levels 1-5 of evidence?

A

o Level 1 – Randomized controlled trial or Meta-analysis
o Level 2 – Cohort study (PROSPECTIVE)
o Level 3 – Case-control study (RETROSPECTIVE)
o Level 4 – Case series, cross sectional
o Level 5 – Expert opinion

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9
Q

What types of Bias occurs BEFORE a study (3)?

A

o Selection – improper recruitment of subjects with different features
*Prevent this with randomization that is blinded
o Channeling – subjects unequally given treatment based on their features
o Chronology – use of historical controls

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10
Q

What types of Bias occurs DURING a study (5)?

A

o Detection – looking harder at one group than another
o Recall – relying on patients to remember events
o Interviewer – influence the interviewer has on responders
o Performance – procedures not performed in uniform way
o Hawthorne Effect – alteration of behavior of subjects based on knowledge they are being observed

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11
Q

What types of Bias occurs AFTER a study (3)?

A

o Citation – more likely to believe study in top journal
o Publication – positive results more likely to be published
o Conflict of Interest – researcher personal conflicts

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12
Q

What is the difference b/t incidence and prevalence?

A 
Incidence = risk over time (looked at  with cohort studies b/c they are PROSPECTIVE)
Prevalence = proportion of existing cases in the population being looked at - at a single moment (snapshot)
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13
Q

What statistical tests are used to evaluate categorical data? And how do you know which one to use?

A

Chi-squared (most common to use)

Fischer exact -> use for SMALL groups (remember that exact count easier with small group!)

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14
Q

What statistical tests are used to evaluate continuous data? And how do you know which one to use?

A

T-test, ANOVA, Pearson correlation co-efficient, Regression, Mann-Whitney U test.
PARAMETRIC DATA: (bell curve, data normally distributed)
T-test (two groups)
ANOVA (3 or more) “OVA two!
NONPARAMETRIC DATA -> pick Mann-Whitney U test

Determine relationships -> Pearson correlation co-efficient

Predict outcomes from variables -> Regression

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15
Q

What is sensitivity?

How do you calculate sensitivity?

A

Sensitivity = ability of a test to detect dz
TP/TP+FN
SnOUT = negative result rules OUT a diagnosis if you have high sensitivity

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16
Q

What is specificity?

How do you calculate specificity?

A

Specificity = ability to detect health
TN/TN+FP
SpIN = positive result rules IN a diagnosis if you have high specificity

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17
Q

What is PPV?

How do you calculate PPV?

A

How likely you are to have dz w/ a positive result.

TP/TP+FP

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18
Q

What is NPV?

How do you calculate NPV?

A

How likely you are to not have dz w/ a negative result.

TN/TN+FN

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19
Q

What is a Type I error?

A

Alpha error = False positive error
Incorrectly rejected the null hypothesis -> said there was a difference and there IS NOT! (Cried wolf!) MORE DEVASTATING!
Only willing to except this 5% of the time
p < 0.05 is a marker of certainty -> which means the likelihood of the results happening by random chance is 5/100 when no association really exists. *NOTE: A HIGH P-VALUE DOES NOT MEAN IS STATISTICALLY INSIGNIFICANT, IT MEANS THAT THERE IS A HIGH DEGREE OF UNCERTAINTY!!

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20
Q

What is a Type II error?

A

Beta error = False negative
Incorrectly accepted the null hypothesis -> said there was no difference/association and there was - you missed it!
LESS devastating
Willing to accept this 20% of the time.

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21
Q

What is the Power of a study?

A

Probability of finding a significant association if it exists -> ability to find a true positive or true negative.
Calculated by 1-beta = 80% chance of doing a study that finds p < 0.05 if true association exists.

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22
Q

What test gives you detection of publication bias in meta-analysis?

A

Funnel plot

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23
Q
  1. ) What is the equation of Stress?

2. ) What is the equation of Strain?

A
  1. ) Stress = Force/Area

2. ) Strain = change in height/original height

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24
Q

What is the definition of Hooke’s Law?

A

Stress is proportional to strain in the elastic zone of the stress strain curve (initial linear part of curve)

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25
Q

What is the definition of the Yield Point?

A

Point at which when you go past adding more strain there is permanent deformation (move from the elastic/linear part of Stress/Strain curve to the plastic/nonlinear portion

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26
Q

What is Young’s Modulus?

A

The slope in the elastic zone - this is a unique characteristic of each material.
A higher Young’s Modulus can withstand greater force = more stiff.
Remember: Stiffness = slope = Youngs Modulus

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27
Q

The linear/elastic region of the stress/strain curve ends in “X” and the non-linear/plastic region ends in “Y”

A 
X = Yield Point
Y = Ultimate Strength
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28
Q

What is is Ultimate Strength?

A

Maximum stress the material can sustain. The highest point on the graph! (*NOTE: this is not the breaking point….that occurs at a lower stress b/c the material will deform/necking and cross-sectional area will decrease and then the material will fail under less stress)

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29
Q

What is necking?

A

Occurs after the Ultimate Strength - and is the reduction of cross-sectional area of the material, overall decrease stress

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30
Q

What is the breaking point = fracture point?

A

Failure of material that occurs after necking of the material

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31
Q

What is fatigue?

A

Failure of the material below the ultimate strength due to numerous loading cycles

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32
Q

What is the difference b/t stiffness, strength, and toughness of a material?

A
  • Stiffness depends on the elastic properties = ability of an object to resist deformation. Young’s Modulus tells you stiffness (higher means more stiff!) - so higher slope means more stiff on graph and lower slope means more flexible!
  • Strength depends on the plastic properties; highest area on curve occurs in plastic zone = ultimate strength.
  • Toughness is amount of energy a material can absorb before failure = area under the stress/strain curve
33
Q

What is the ductiliy of a material?

How is the represented on the stress/strain curve?

A

Amount of deformation a material undergoes before fracture.
Difference b/t the Yield Point and Fracture/Breaking Point.
Brittle material = small diff
Ductile material = big difference

34
Q

What does viscoelastic mean?

A

Mechanical properties vary with external conditions. Biologic materials are typically viscoelastic

35
Q

What is creep?

A

Deformation with time under a constant load.

Can cause failure under loads significantly below ultimate strength.

36
Q

What is the difference b/t isotropic material and anisotropic material?

A

Isotropic -> behaves the same regardless of force

Anisotropic -> behaves differently depending on force (MOST biomaterials are this!!)

37
Q

Which metal has the MOST bacterial adherence?

The LEAST?

A 
MOST = Titanium alloy
LEAST = Tantalum
38
Q

What additional quality is seen on the Stress/Strain curve of ligaments that is not seen on curves for metals/biomaterialas?

A

Toe region at beginning of curve! In the toe region until the crimped fibers of the ligaments have straightened.

39
Q

What is the equation for stiffness of a:

  1. ) Plate
  2. ) Cylindrical nail
A
  1. ) R^3

2. ) R^4

40
Q

What is Wolff’s Law?

A

Remodeling of bone occurs in response to mechanical stress (this is what happen when the fracture callus remodels)

41
Q
  1. ) What cell lineage do osteoblasts come from and what 3 key transcription factors contribute to their formation (versus other types of cells forming)?
  2. ) What other cells come from this same cell lineage and what factors make these cells form?
  3. ) What cell line are osteoclasts derived from?
A
  1. ) Mesenchymal progenitor cell. Runx2, Osx, Wnt/Beta-catenin
  2. ) Adipocytes: PPAR-gamma; Chondrocytes: Sox
  3. ) Hematopoietic/myeloid progenitor
42
Q
  1. ) What is the function of Sclerostin (SOST)?
  2. ) What effect does PTH have on Sclerostin?
  3. ) What effect does Calcitonin have on Sclerostin?
A

1.) Released by osteocytes and inhibits Wnt pathway/osteoblasts-> inhibits bone formation (part of normal feedback mechanism).
When bone is not loaded -> SOST is released and you get less bone formation! (lack of stress = lack of bone….in accordance with Wolff’s law!)
2.) PTH increases Sclerostin (makes sense b/c PTH is secreted in response to low Ca and thus in line w/ osteoblast inhibition to make sure the Ca isn’t taken up from blood to make bone!)
3.) Calcitonin decreases Sclerostin

43
Q
  1. ) How do osteoclasts bind to bone?

2. ) How is bone resorbed by osteoclast?

A
  1. ) Integrin on the surface of the osteoclast binds to Vibronectin on surface of the bone to create a sealing zone
  2. ) W/in sealing zone Howships lacunae is created and carbonic anhydrase creates an acidic area is created and cathepsin K enzyme digests organic matrix at the ruffled border
44
Q

What 2 molecules produced by Osteoblasts regulate Osteoclasts?

A
  1. ) RANKL - activates osteoclasts

2. ) OPG - binds to RANKL so that it cannot interact with RANK; prevents osteoclast activity

45
Q

What is the role of Calcitonin?

A

Released by the parafollicular (“C”) cells of the thyroid gland.
DIRECTLY BINDS osteoclasts to slow bone resorption -> reducing serum Ca
(opposes the effect of PTH - which is secreted by the Chief cells of the parathyroid gland)

46
Q

What is the role of PTH?

A
  • PTH is secreted by the Chief cells of the parathyroid gland in response to low Serum Ca
  • Sustained PTH makes osteoblasts release RANKL to activate osteoclasts and get bone resorption to help increase Ca in serum. Also causes increased Ca re-absorption in kidneys
  • Pulsed/Intermittent PTH gives net ANABOLIC effect and builds bone! (this is how Teraparatide = 1st 34 AA’s of PTH drug works! Only anabolic osteoporosis drug!)
  • *Also remember that Vit D parallels PTH (“PDH”) and also causes increases in reabsorption of Ca in the kidneys and intestines
47
Q

What collagen type is predominantly found in bone?

A

bONE = Type ONE

48
Q

What is the most abundant noncollagenous matrix protein in bone?
What is another important fact about this protein?

A

Osteocalcin - most specific marker of mature osteoblasts

49
Q

What is the Hueter-Volkmann Law?

A

Compressive force -> inhibit bone growth

Tensile force -> stimulates bone growth

50
Q

What are the 3 main types of bone formation?

A
  1. ) Intramembranous -> flat bones, primary fx healing
  2. ) Enchondral -> long bones, physis, fracture callus (bone laid down on cartilagenous framework - converts a soft callus to hard callus)
  3. ) Appositional -> Periosteal bone enlargement (width)
51
Q

What area of the physis do SH fx occur through?

A

Zone of Provisional Calcification (which is in the Zone of Hypertrophy)

52
Q

What dz effects the reserve zone?

A

Diastrophic dwarfism

53
Q

What dz effects the proliferative zone?

A

Gigantism

Achondroplasia

54
Q

What dz effects the hypertrophic zone?

A

Muccopolysaccharidosis (Morquio, Hurler)
Rickets
(SH fxs!!)

55
Q

In appositional bone growth what group of cells is responsible for this growth of width?

A

Groove of Ranvier = wedge-shaped zone of cells contiguous with the epiphysis at the periphery -> supplies chondrocytes to the periphery

56
Q

What is the Perichondral Ring of La Croix?

A

Involved in appositional growth and is a dense fibrous tissue that supports the physis peripherally
(Picture in my mind like a crown supporting the outside of the physis around the bone!)

57
Q

How do NSAIDs effect fracture healing molecularly?

A

Inhibition of COX-2 by NSAIDS causes repression of Runx2/Osx (which is critical for differentiation of osteoblasts)
(Remember that the 3 main stages of fx healing are -> INFLAMMATION, repair, remodeling)

58
Q

Are the following items Osteoinductive, Osteoconductive, or Osteogenic?

  1. ) Autograft
  2. ) DBM
  3. ) CaPhosph and CaSulfate
  4. ) Allograft
A
  1. ) Autograft - all 3!
  2. ) DBM - osteoinductive and condutive
  3. ) CaPhosph and CaSulfate - osteoinductive and conductive
  4. ) Osteoinductive and osteoconductive
59
Q

When does peak bone mass occur?

A

3rd Decade of life (b/t 16-25 yo)

60
Q

What is the recommended intake of Ca and VitD for adults over 50 yo for osteoporosis prevention?

A

Ca 1200-1500 mg

Vit D 800-1,000 IU

61
Q

What is an XR finding of Rickets?

A

Physeal cupping

62
Q
  1. ) What is the inheritance of Familial Hypophosphatemic Rickets?
  2. ) What lab value helps to differentiate this from Nutritional Rickets?
A
  1. ) X-linked from mutated PHEX gene -> cannot absorb phosphate
  2. ) They will have NORMAL CALCIUM LEVELS!
63
Q
  1. ) What are the 2 types of Vit D dependent rickets?

2. ) How do you tell the difference w/ the labs?

A

1.) Type I -> defect in 1 alpha-hydroxylase so cannot make active Vit D. (Autosomal recessive inheritance). Tx: just give physiologic dose Vit D
Type II -> defect in the receptor for 1,25-Vit D. Tx: give HIGH dose Vit D
2.) Look at Vit D levels. In Type 1 have low 1,25-OH; and Type 2 has HIGH levels!

64
Q

What 5 medications should you be aware that might disrupt the Vit D pathway?

A 
Prednisone
PPI's
Antiepileptics
SSRIs 
Heprin
65
Q

What score gives you the dx of osteoporosis?

What about osteopenia?

A

Osteoporosis: T score < -2.5 (T score to treat!)

Osteopenia T score b/t -1 and -2.5

66
Q

Who should receive osteoporosis treatment?

A
  • Have prior hip or vertebral fx
    OR
    * T score -2.5 or less at femoral neck or vertebrae
    OR
    * Osteopenia (T-score between -1 and -2.5) AND
    * FRAX score suggestive of 10 yr risk of hip fx is 3% or more OR
    * major osteoporosis fx risk 20% or more
67
Q

What is the MoA of Bisphosphonates?

A

Binds to bone surface and gets taken up by osteoclasts -> apoptosis.
Non-Nitrogen containing -> ATP toxic/non-functional analog
Nitrogen containing -> inhibits farnesyl pyrophosphate synthease enzyme which inhibits protein prenylation and GTPase formation needed in cholesterol pathway.

68
Q

What are examples of osteoporosis medications and how do they work?

A
  1. ) Bisphosphonates - bind to bone and are ingested by osteoclasts -> apoptosis.
  2. ) Estrogen based - ie Raloxifene -> reduces osteoclast activity
  3. ) Teriparatide -> activates adenyl cyclase -> pulsed administration has net anabolic effect (CONTRAINDICATED IN PTS w/ Paget’s or previous bone mets due to risk of secondary osteosarcoma)
  4. ) Denusomab -> Ab to RANKL (can be used in osteoporosis, MM, GCT, mets -> remember that the tumor cells secrete cytokines that make osteoblasts secrete more RANKL)
69
Q
  1. ) What is the functional unit of a muscle?

2. ) What is it composed of?

A

1.) Sarcomere
2.) Thick filaments = myosin (longer/thicker word)
Thin filaments = actin
A band = myosin
I band = actin

70
Q

What are the main sources of energy for muscles in:

  1. ) 0-10sec of activity
  2. ) 1-4 min
  3. ) 4+ min
A
  1. ) ATP & CP
  2. ) Glycogen & lactic acid
  3. ) Glycogen & fatty acids
71
Q

When muscle is injured what is the common location of injury and what type of contraction typically causes injury?

A
  1. ) Myotendinous jxn

2. ) Eccentric contraction

72
Q

What is the organization of nerve anatomy?

A

axon (surrounded in myelin), surrounded by endoneurium, grouped together into fascicles which are surrounded by perineurium, surrounded by epineurium

73
Q

What are C type nerve fibers?

A

Pain

74
Q

What is the rate of nerve regeneration?

A

1 mm/day

75
Q

What is the return of function after a nerve injury (ie in what order do things come back?)

A
  1. ) Sympathetic activity
  2. ) Pain
  3. ) Temp
  4. ) Touch
  5. ) Proprioception
  6. ) Motor
76
Q

What must be intact for full nerve recovery after injury?

A

Endoneurium

77
Q

What type of collagen makes up majority of tendons?

A

Type I

78
Q

What are the transitional tissues involved in tendon attachment to bone?

A

Tendon -> Fibrocartilage -> Mineralized Fibrocartilage -> Bone

79
Q

What are the 2 types of ligament attachment to bone?

A
  • Direct: ligament-fibrocartilage-mineralized fibrocartilage-bone
    • Indirect (more common): ligament-mineralized fibrocartilage-periosteum-bone
      • MCL attaches indirectly to bone via Sharpey’s fibers (made of Type I collagen)

basic science (3 decks)

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