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USMLE 1 > Biochemistry- Celular > Flashcards

Biochemistry- Celular Flashcards

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USMLE® Step 1 flashcards
1
Q

Cell cycle phases

A 
M phase (shortest phase of cell cycle) includes mitosis (prophase, prometaphase, metaphase, anaphase, telophase) and cytokinesis. 
G1 and G0 are of variable duration.
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2
Q

Cyclins

A

Regulatory proteins that control cell cycle

events; phase specific; activate CDKs.

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3
Q

Tumor suppressors

A

p53 induces p21, which inhibits CDKs

Rb inhibition of G1-S progression

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4
Q

Cyclin-CDK complexes

A

Phosphorylate other proteins to coordinate

cell cycle progression

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5
Q

CELL TYPES (according to cell cycle)

A

Permanent (remain G0)
Stable (quiscent) (enter to G1 from G0)
Labile (Never G0, dived rapidly)

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6
Q

Rough endoplasmic

reticulum

A

Site of synthesis of secretory (exported) proteins.
Nissl bodies (RER in neurons)
Free ribosomes

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7
Q

Smooth endoplasmic

reticulum

A

Site of steroid synthesis and detoxification of

drugs and poisons

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8
Q

I-cell disease (inclusion cell disease/mucolipidosis type II)

A

inherited lysosomal storage disorder; defect in N-acetylglucosaminyl-1-phosphotransferas.

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9
Q

clinical features of I-cell disease

A

Coarse facial features, clouded corneas, restricted joint movement, and high plasma levels of lysosomal enzymes. Often fatal in childhood

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10
Q

N-acetylglucosaminyl-1-phosphotransferase 􀁰

A

Golgi to phosphorylate mannose residues on glycoproteins, proteins are to lysosomes.

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11
Q

Vesicular trafficking proteins

A

“Two (COPII) steps forward (anterograde); one
(COPI) step back (retrograde).”
Clathrin: trans-Golgi 􀁰 lysosomes; plasma
membrane 􀁰 endosomes

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12
Q

Peroxisome

A

Catabolism of very-long-chain fatty acids (through

β-oxidation), branched-chain fatty acids, amino acids, and ethanol.

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13
Q

Peroxisomal disorders

A

Zellweger syndrome

Refsum disease

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14
Q

Refsum disease

A

scaly skin, ataxia, cataracts/night blindness, shortening of 4th toe, epiphyseal dysplasia.

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15
Q

Zellweger syndrome

A

hypotonia, seizures, hepatomegaly, early death

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16
Q

Proteasome

A

degrades damaged or ubiquitin-tagged proteins.

17
Q

Microfilaments

A

Actin, microvilli

18
Q

Intermediate

filaments

A

Vimentin, desmin, cytokeratin, lamins, glial

fibrillary acid proteins (GFAP), neurofilaments.

19
Q

Microtubules

A

Cilia, flagella, mitotic spindle, axonal trafficking,

centrioles

20
Q

Drugs that act on microtubules (Microtubules

Get Constructed Very Poorly)

A 
􀂃 Mebendazole (antihelminthic)
􀂃 Griseofulvin (antifungal)
􀂃 Colchicine (antigout)
􀂃 Vincristine/Vvinblastine (anticancer)
􀂃 Paclitaxel (anticancer)
21
Q

Immunohistochemical stains for intermediate filaments

A 
Vimentin (mesenchymal tissue)
Desmin (muscle)
Cytokeratin (epithelial cells)
GFAP (neuroglia)
Neurofilaments (neuron)
22
Q

Cilia structure

A
  • 9 doublet + 2 singlet arrangement
  • Basal body 9 microtubule triplets
  • Axonemal dynein—ATPase that links peripheral
    9 doublet
23
Q

Kartagener syndrome

A

1° ciliary dyskinesia:

  • disminution fertility due to immotile sperm and dysfunctional fallopian tube cilia.
  • bronchiectasis, recurrent sinusitis, chronic ear infections
  • Conductive hearing loss
  • Situs inversus
24
Q

Sodium-potassium

pump

A

3Na+ go out of the cell (pump phosphorylated) and 2K+ come into the cell (pump dephosphorylated)

25
Q

Ouabain

Cardiac glycosides

A
  • inhibits by binding to K+ site.

- directly inhibit the Na+-K+ ATPase

26
Q

Types of collagen

A

Be (So Totally) Cool, Read Books.
I: Bone, Skin, Tendon (osteogenesis imperfecta I)
II: Cartialge
III: Reticuline (vascular ehlers-danlos)
IV: Basement membrane (alport, goodpasteur)

27
Q

Osteogenesis imperfecta

A 
autosomal dominant COL1A1 o COL1A2
Patients can’t BITE:
Bones = multiple fractures
I (eye) = blue sclerae
Teeth = dental imperfections
Ear = hearing loss
28
Q

Ehlers Danlos

A
  • 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.
29
Q

Menkes disease

A
  • X-linked recessive
  • impaired copper absorption and transport due to defective Menkes protein (ATP7A).
  • brittle, “kinky” hair, growth retardation, and hypotonia.
30
Q

Marfan syndrome

A
  • autosomal dominant
  • affecting skeleton, heart, and eyes.
  • FBN1 gene mutation on chromosome 15 results in defective fibrillin

USMLE 1 (73 decks)

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