Ppal99 Dissecting The Usmle 1,2,3 Proteins

Front 1

1°: protein

Back 1

aa sequence (peptide bonds C-N-C, planar, flat, restrictive motion trans configuration)

Front 2

2°: protein

Back 2

α-helix (twisted organs: GI, vv) vs. β-pleated sheet (flat stuff: skin, flat bones)

Front 3

3°: protein

Back 3

3-D shape, consider hydrophobic/hydrophilic interactions

Front 4

4°: protein

Back 4

>/=2 proteins interact (Ex: Hb)

Front 5

Allosterism:

Back 5

rate-limiting (slowest) enzymes

Front 6

Acid Hydrolysis:

Back 6

dip protein in acid=> denatures (Gln ⇨ Glu, Asn ⇨Asp-)

Front 7

Gel Electrophoresis:

Back 7

separates protein based on size and charge
• cation (+) => cathode (-)

Front 8

Ninhydrin Reaction:

Back 8

all aa =purple (except Pro =yellow)

Front 9

Restriction peptidases:

Back 9

cut on the right

Front 10

Edmund Degradation:

Back 10

uses PITC to remove 1 aa at a time (100 aa limit)

Front 11

Carboxypeptidase

Back 11

cuts to left of any amino acid on carboxy terminal

Front 12

Aminopeptidase

Back 12

N-terminus
• CNBr-Met

Front 13

Mercaptoethanol

Back 13

Cys, Met (disulfide bonds)

Front 14

Elastase

Back 14

Gly, Ala, Ser (small) - "GAS"

Front 15

Trypsin

Back 15

Arg, Lys (basic groups)- ''take a basic Tryp to L4"

Front 16

Chymotrypsin

Back 16

Phe, Tyr, Trp (bulky)

Front 17

α1-AT:

Back 17

inhibits trypsin from getting loose (b/c he can activate everything)

Front 18

⇧ESR or CRP

Back 18

inflammation

Front 19

Falsely ⇧ESR

Back 19

anemia

Front 20

Falsely ⇩ESR

Back 20

sickle cell anemia, polycythemia

Front 21

⇧Acute phase reactants (IL-6)

Back 21

amyloidosis

Front 22

Amyloidosis: stain and 2 types

Back 22

stains Congo red, Echo Apple-green birfrinngence
• 1° Amyloidosis
• 2° Amyloidosis

Front 23

1° Amyloidosis: presentation and what is the complication of increased proteins?

Back 23

(AD): big organs, ⇧protein causes intracranial hemorrhage

Front 24

2° Amyloidosis

Back 24

(chronic disease): Scleroderma, asthma, Wegener's

Front 25

Amyloid: ESR levels
AA

Back 25

⇧ESR
Any chronic disease

Front 26

AB

Back 26

Brain (Alzheimer's)

Front 27

AB2

Back 27

β2 microglobulinemia (renal failure)

Front 28

AE

Back 28

Endocrine (medullary CA of thyroid)

Front 29

AF

Back 29

Familial (MEN II)

Front 30

AL

Back 30

Light chains (multiple myeloma)

Front 31

Zero-order Kinetics: define and examples

Back 31

metabolism independent of concentration
Ex: Phenytoin, Chemo drugs
Ex: EtOH (100mg/dL/hr): 1 glass wine, 1 shot whiskey, 2 cans of beer
Ex: high dose asa

Front 32

Alcohol Limit:
0.08:
0.1:
0.3:
0.4:

Back 32

0.08: legal limit
0.1: zero-order kinetics
0.3: coma
0.4: "embalming"

Front 33

1st order Kinetics define and example

Back 33

- constant drug percentage metabolism over time
Ex: 10% of drug (conc=100mgldL) eliminated every 2 hours:
o T=O hrs: [D]=100mgldL
o T=2 hrs: [D]=90 mgldL
o T =4 hrs: [D]=81 mgldL

Front 34

t1/2 formula

Back 34

= (.693)(Vd) +clearance

Front 35

Vd formula: what does large Vd mean?

Back 35

total drug+ plasma concentration
large Vd =>most of drug is sequestered)

Front 36

Loading dose formula

Back 36

(desired plasma conc)(Vd)

Front 37

Maintance dose formula

Back 37

(desired plasma conc)(clearance)

Front 38

define Steady-state plasma concentration (Css)? how many half lives does it take?

Back 38

availability rate = elimination rate, takes 4.5 half lives

Front 39

Clearance

Back 39

volume of plasma cleared of drug

Front 40

Excretion rate formula

Back 40

(clearance)(plasma conc) - rate of elimination

Front 41

TI formula, what does a high TI mean? what is this equal to? (2)

Back 41

toxic dose+ therapeutic dose (high TI => safe drug) = LD50, ED50

Front 42

Peak level

Back 42

4 hrs after dose (too high=> decrease dose)

Front 43

Trough level

Back 43

2 hrs before dose (too high => give less often)

Front 44

1) define Potency, when is this lower?
2) define efficacy, when is this lower?

Back 44

1) amount of drug needed to produce effect (lower w/ comp antagonist)
2) max effect regardless of dose (lower w/ non-competitive antagonist)

Front 45

Kd

Back 45

[D] that binds 50% of receptors

Front 46

EC50

Back 46

[D] that produces 50% of maximal response

Front 47

Competitive Inhibition

Back 47

potency decreases

Front 48

define Competitive Inhibition, how does it affect Vmax?

Back 48

fights for active site, no ΔVmax

Front 49

define Non-competitive Inhibition, what happens to Km and efficacy?

Back 49

binds a regulatory site, no ΔKm therfore, efficacy decreases

Front 50

what does Km affect? Vmax?

Back 50

Km affects potency and Vmax affects efficacy

Front 51

Km equation

Back 51

= [S] at 1/2V max

Front 52

as Km increases, what happens to affinity?

Back 52

decreases. they are inversely proportional

Front 53

Collagen is made up of what aa

Back 53

every 3rd aa is Gly

Front 54

4 types of collagen:
• Type I:
• Type II:
• Type III:
Type IV:
what collagen is affected in faciitis, cellulitis, GN, vasculitis?
what arteries are affected first?

Back 54

4 types of collagen: SCAB
• Type I:Skin,bone
• Type II: Connective tissue (tendons, ligaments cartilage), aqueous humor, blood⇨ fasciitis,cellulitis
• Type III: Arteries (coronary aa. affected first) ⇨ vasculitis
• Type IV: Basement membrane ⇨ GN

Front 55

Collagen Requirements: Vitamins, metal, aa

Back 55

• Glycine (Every 3rd aa is Gly, smallest amino acid)
• Lysine
• Proline
• OH-Proline (requires Vit C)
• OH-Lysine (requires Cu2+)

Front 56

Collagen Synthesis: describe the steps of collagen synthesis

Back 56

(Pro-OHase, Lys-OHase ⇨ needs Vit C, Cu)
• PreProCollagen ⇨ ER ⇨
• ProCollagen ⇨ Golgi ⇨
• Tropocollagen ⇨ Plasma ⇨
• Plasma peptidases tighten it up at the site of action

Front 57

Who makes collagen? what does contracture mean?

Back 57

Fibroblasts: scars
Myofibroblasts: wound contraction (contracture means it happened too much)

Front 58

Keloids: another name, pathogenesis

Back 58

= hamartoma
• Fibroblasts release too much collagen

Front 59

what collagens are involved in Scleroderma? presentation (2)

Back 59

• Collagen types I (skin, bone) and type III (aa.)
• Tightened skin, blood vessel problems

Front 60

what collagens are involved in Ehlers Danlos? presentation?

Back 60

• Collagen types I (skin, bone) and type III (aa.)
• Hyperstretchable skin "velvety

Front 61

Marfan's: mode of inheritance, collagens involved, presentation (ie joints, hands, height vs wing span, heart (3), eyes)

Back 61

(AD): fibrillin problem
• Collagen type II (CT) and type III (aa.)
• Hyperextensible joints, arachnodactyly, wing span longer than height
• Aortic root dilatation, aortic aneurysm, mitral valve prolapse
• Dislocated lens from bottom of eye "always looking up to Mars"

Front 62

Homocysteinuria: pathogenesis, labs, presentation, heart and eyes, renal.

Back 62

• LysOHase not inhibited by homocysteine
• Increased Met levels
• Marfanoid features
• Childhood strokes
• Dislocated lens from top ⇨ "always looking down toward "COLA" urine stones"

Front 63

Kinky Hair Disease: which aa is affected?

Back 63

• Cu deficiency (Lys-OHase affected)
• Hair looks like copper wire

Front 64

Scurvy: deficiency, presentation and type of collagen affected

Back 64

Collagen type III (aa.)
• Vit. C deficiency
• Bleeding gums, hair follicles

Front 65

Takayasu Arteritis: what collagen is affected?

Back 65

• Collagen type III (aa.)
• Asian female with very weak pulse = "pulseless aortitis"

Front 66

collagen disease 3° Syphilis: what collagen is affected?

Back 66

• collagen type III (aa.)
• Obliterative endarteritis => "tree bark" appearance

Front 67

Osteogenesis Imperfecta: what collagen is affected?, presentation (3)

Back 67

• All 4 types of collagen involved; pleiotropy
• Shattered bones, looks like child abuse
• Blue sclera
• Desmoplasia:
• Collagenous reaction surrounding a tumor

Front 68

how does elastin become elastic? and what happens when elastase breaks bond? what disease has this?

Back 68

Pro-OHase (no OH-Lysines)
• Desmosine (Lys box) = > (+) repel each other, making it elastic
• Elastase breaks up elastin=> lose recoil => emphysema

Front 69

Emphysema: define and what are its 4 types

Back 69

elastin destroyed, loss of recoil
Pan-acinar
Centro-acinar
Distal acinar
Bullous "pneumatocele"

Front 70

Keratin

Back 70

Cys⇨ disulfide bonds⇨ tensile strength
Curly hair -> more bonds -> broken down by heat/ chemicals to straighten hair

Front 71

Pan-acinar emphysema: mode of inheritance, pathogenesis, stain and presentation on a neonate.

Back 71

(AR): alpha 1-AT deficiency => can't inhibit-elastase, PAS(+), neonatal hepatitis

Front 72

Centro-acinar emphysema

Back 72

smoking "comes in through the center"

Front 73

define Distal acinar: complication

Back 73

aging(least blood supply) ⇨spontaneous pneumothorax

Front 74

Bullous "pneumatocele": what bugs causes this and how?

Back 74

elastase (+) bacteria = pseudo/Staph aureus