• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/74

Click to flip

74 Cards in this Set

  • Front
  • Back
1°: protein
aa sequence (peptide bonds C-N-C, planar, flat, restrictive motion trans configuration)
2°: protein
α-helix (twisted organs: GI, vv) vs. β-pleated sheet (flat stuff: skin, flat bones)
3°: protein
3-D shape, consider hydrophobic/hydrophilic interactions
4°: protein
>/=2 proteins interact (Ex: Hb)
Allosterism:
rate-limiting (slowest) enzymes
Acid Hydrolysis:
dip protein in acid=> denatures (Gln ⇨ Glu, Asn ⇨Asp-)
Gel Electrophoresis:
separates protein based on size and charge
• cation (+) => cathode (-)
Ninhydrin Reaction:
all aa =purple (except Pro =yellow)
Restriction peptidases:
cut on the right
Edmund Degradation:
uses PITC to remove 1 aa at a time (100 aa limit)
Carboxypeptidase
cuts to left of any amino acid on carboxy terminal
Aminopeptidase
N-terminus
• CNBr-Met
Mercaptoethanol
Cys, Met (disulfide bonds)
Elastase
Gly, Ala, Ser (small) - "GAS"
Trypsin
Arg, Lys (basic groups)- ''take a basic Tryp to L4"
Chymotrypsin
Phe, Tyr, Trp (bulky)
α1-AT:
inhibits trypsin from getting loose (b/c he can activate everything)
⇧ESR or CRP
inflammation
Falsely ⇧ESR
anemia
Falsely ⇩ESR
sickle cell anemia, polycythemia
⇧Acute phase reactants (IL-6)
amyloidosis
Amyloidosis: stain and 2 types
stains Congo red, Echo Apple-green birfrinngence
• 1° Amyloidosis
• 2° Amyloidosis
1° Amyloidosis: presentation and what is the complication of increased proteins?
(AD): big organs, ⇧protein causes intracranial hemorrhage
2° Amyloidosis
(chronic disease): Scleroderma, asthma, Wegener's
Amyloid: ESR levels
AA
⇧ESR
Any chronic disease
AB
Brain (Alzheimer's)
AB2
β2 microglobulinemia (renal failure)
AE
Endocrine (medullary CA of thyroid)
AF
Familial (MEN II)
AL
Light chains (multiple myeloma)
Zero-order Kinetics: define and examples
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
Alcohol Limit:
0.08:
0.1:
0.3:
0.4:
0.08: legal limit
0.1: zero-order kinetics
0.3: coma
0.4: "embalming"
1st order Kinetics define and example
- 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
t1/2 formula
= (.693)(Vd) +clearance
Vd formula: what does large Vd mean?
total drug+ plasma concentration
large Vd =>most of drug is sequestered)
Loading dose formula
(desired plasma conc)(Vd)
Maintance dose formula
(desired plasma conc)(clearance)
define Steady-state plasma concentration (Css)? how many half lives does it take?
availability rate = elimination rate, takes 4.5 half lives
Clearance
volume of plasma cleared of drug
Excretion rate formula
(clearance)(plasma conc) - rate of elimination
TI formula, what does a high TI mean? what is this equal to? (2)
toxic dose+ therapeutic dose (high TI => safe drug) = LD50, ED50
Peak level
4 hrs after dose (too high=> decrease dose)
Trough level
2 hrs before dose (too high => give less often)
1) define Potency, when is this lower?
2) define efficacy, when is this lower?
1) amount of drug needed to produce effect (lower w/ comp antagonist)
2) max effect regardless of dose (lower w/ non-competitive antagonist)
Kd
[D] that binds 50% of receptors
EC50
[D] that produces 50% of maximal response
Competitive Inhibition
potency decreases
define Competitive Inhibition, how does it affect Vmax?
fights for active site, no ΔVmax
define Non-competitive Inhibition, what happens to Km and efficacy?
binds a regulatory site, no ΔKm therfore, efficacy decreases
what does Km affect? Vmax?
Km affects potency and Vmax affects efficacy
Km equation
= [S] at 1/2V max
as Km increases, what happens to affinity?
decreases. they are inversely proportional
Collagen is made up of what aa
every 3rd aa is Gly
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?
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
Collagen Requirements: Vitamins, metal, aa
• Glycine (Every 3rd aa is Gly, smallest amino acid)
• Lysine
• Proline
• OH-Proline (requires Vit C)
• OH-Lysine (requires Cu2+)
Collagen Synthesis: describe the steps of collagen synthesis
(Pro-OHase, Lys-OHase ⇨ needs Vit C, Cu)
• PreProCollagen ⇨ ER ⇨
• ProCollagen ⇨ Golgi ⇨
• Tropocollagen ⇨ Plasma ⇨
• Plasma peptidases tighten it up at the site of action
Who makes collagen? what does contracture mean?
Fibroblasts: scars
Myofibroblasts: wound contraction (contracture means it happened too much)
Keloids: another name, pathogenesis
= hamartoma
• Fibroblasts release too much collagen
what collagens are involved in Scleroderma? presentation (2)
• Collagen types I (skin, bone) and type III (aa.)
• Tightened skin, blood vessel problems
what collagens are involved in Ehlers Danlos? presentation?
• Collagen types I (skin, bone) and type III (aa.)
• Hyperstretchable skin "velvety
Marfan's: mode of inheritance, collagens involved, presentation (ie joints, hands, height vs wing span, heart (3), eyes)
(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"
Homocysteinuria: pathogenesis, labs, presentation, heart and eyes, renal.
• LysOHase not inhibited by homocysteine
• Increased Met levels
• Marfanoid features
• Childhood strokes
• Dislocated lens from top ⇨ "always looking down toward "COLA" urine stones"
Kinky Hair Disease: which aa is affected?
• Cu deficiency (Lys-OHase affected)
• Hair looks like copper wire
Scurvy: deficiency, presentation and type of collagen affected
Collagen type III (aa.)
• Vit. C deficiency
• Bleeding gums, hair follicles
Takayasu Arteritis: what collagen is affected?
• Collagen type III (aa.)
• Asian female with very weak pulse = "pulseless aortitis"
collagen disease 3° Syphilis: what collagen is affected?
• collagen type III (aa.)
• Obliterative endarteritis => "tree bark" appearance
Osteogenesis Imperfecta: what collagen is affected?, presentation (3)
• All 4 types of collagen involved; pleiotropy
• Shattered bones, looks like child abuse
• Blue sclera
• Desmoplasia:
• Collagenous reaction surrounding a tumor
how does elastin become elastic? and what happens when elastase breaks bond? what disease has this?
Pro-OHase (no OH-Lysines)
• Desmosine (Lys box) = > (+) repel each other, making it elastic
• Elastase breaks up elastin=> lose recoil => emphysema
Emphysema: define and what are its 4 types
elastin destroyed, loss of recoil
Pan-acinar
Centro-acinar
Distal acinar
Bullous "pneumatocele"
Keratin
Cys⇨ disulfide bonds⇨ tensile strength
Curly hair -> more bonds -> broken down by heat/ chemicals to straighten hair
Pan-acinar emphysema: mode of inheritance, pathogenesis, stain and presentation on a neonate.
(AR): alpha 1-AT deficiency => can't inhibit-elastase, PAS(+), neonatal hepatitis
Centro-acinar emphysema
smoking "comes in through the center"
define Distal acinar: complication
aging(least blood supply) ⇨spontaneous pneumothorax
Bullous "pneumatocele": what bugs causes this and how?
elastase (+) bacteria = pseudo/Staph aureus