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NBME Final- Biochem + genetics/NBME exams Comprehensive questions with complete verified solutions)/ update

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NBME Final- Biochem + genetics/NBME exams Comprehensive questions with complete verified solutions)/ update

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  • October 17, 2024
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  • 2024/2025
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  • Questions & answers

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  • nbme final biochem geneticsnbme exams

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10/17/24, 8:02 AM NBME Final- Biochem + genetics/NBME exams Comprehensive questions with complete verified solutions)/2024-2025 updat…




NBME Final- Biochem + genetics/NBME exams
Comprehensive questions with complete
verified solutions)/2024-2025 update


Terms in this set (205)


Na+-K+ ATPase is located in the plasma
membrane with ATP site on cytosolic side.
For each ATP consumed, 3Na+ go out of the
cell (pump phosphorylated) and 2K+ come into
the cell (pump dephosphorylated).
Sodium-potassium
pump
Ouabain inhibits by binding to K+ site.
Cardiac glycosides (digoxin and digitoxin)
directly inhibit the Na+-K+ ATPase, which
leads to indirect inhibition of Na+/Ca2+
exchange > ^ [Ca2+]i > ^ cardiac contractility

Most common (90%)—Bone (made by
osteoblasts), Skin, Tendon, dentin, fascia,
cornea, late wound repair.
Type I Collagen
Type I: bone.
decreased production in osteogenesis imperfecta
type I.

Cartilage (including hyaline), vitreous body,
Type II Collagen nucleus pulposus.
Type II: cartwolage.

Reticulin—skin, blood vessels, uterus, fetal
tissue, granulation tissue.
Type III Collagen
Type III: deficient in the uncommon, vascular
type of Ehlers-Danlos syndrome (ThreE D).




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Basement membrane, basal lamina, lens. Type IV:
under the floor (basement membrane).
Type IV Collagen
Defective in Alport syndrome; targeted by
autoantibodies in Goodpasture syndrome.

translation of collagen α chains
(preprocollagen)—usually Gly-X-Y (X and Y
are proline or lysine). Glycine content best
reflects collagen synthesis (collagen is 1⁄3
Composition of collagen
glycine).
hydroxylation of specific
proline and lysine residues. Requires vitamin
C; deficiency > scurvy.

Genetic bone disorder (brittle bone
disease) caused by a variety of gene defects
(most commonly COL1A1 and COL1A2).
Most common form is autosomal dominant
with ^ production of otherwise normal type I
collagen. Manifestations can include:
-Multiple fractures with minimal
trauma A B ; may occur during the birth
Osteogenesis
process
imperfecta
- Blue sclerae due to the translucent
connective tissue over choroidal veins
-Hearing loss (abnormal ossicles)
- Some forms have tooth abnormalities,
including opalescent teeth that wear easily
due to lack of dentin (dentinogenesis
imperfecta)
May be confused with child abuse.




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, 10/17/24, 8:02 AM NBME Final- Biochem + genetics/NBME exams Comprehensive questions with complete verified solutions)/2024-2025 updat…

Faulty collagen synthesis causing
hyperextensible skin, tendency to bleed (easy
bruising), and hypermobile joints.
Multiple types. Inheritance and severity vary.
Can be autosomal dominant or recessive. May
be associated with joint dislocation, berry and
Ehlers Danlos aortic aneurysms, organ rupture.
Hypermobility type ( joint instability): most
common type.
Classical type ( joint and skin symptoms): caused
by a mutation in type V collagen.
Vascular type (vascular and organ rupture):
deficient type III collagen.

Stretchy protein within skin, lungs, large
arteries, elastic ligaments, vocal cords,
ligamenta flava (connect vertebrae > relaxed
and stretched conformations).
Rich in nonhydroxylated proline, glycine, and
Elastin lysine residues.
Tropoelastin with fibrillin scaffolding.
Cross-linking takes place extracellularly and
gives elastin its elastic properties.
Broken down by elastase, which is normally
inhibited by α1-antitrypsin.

caused by a defect in
Marfan Syndrome fibrillin, a glycoprotein that forms a sheath
around elastin.

SNoW DRoP:
Mnemonic for Blotting Southern = DNA
Procedures Northern = RNA
Western = Protein




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