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Step 1 review cards > Biochemistry: Cellular > Flashcards

Biochemistry: Cellular Flashcards

1
Q

What are the phases of cell growth?

A

G0 phase = arrest phase

G1 phase = growth/proliferation phase
- this is where tumor suppressor genes help checkpoint cells and prevent cancer normally

S phase = DNA synthesis phase

G2 phase = preparation for mitosis

M phase = mitosis occurs

  • “IPPMAT”
  • interphase
  • prophase
  • prometaphase
  • metaphase
  • anaphase
  • telophase

Cytokinesis phase

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2
Q

What cells have the most Rough endoplasmic reticulum?

A

Mucus secreting goblet cells

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3
Q

What cells have the most Smooth endoplasmic reticulum

A

Hepatocytes and adrenal cortex cells

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4
Q

I-cell disease

A

A, autosomal recessive, mucolipidosis type 2 disorder

Causes failure of the golgi to phosphorylate mannose residues on glycoproteins, which causes dysfunctional proteins to be secreted extracellular instead of sent to lysosomes for breakdown.

Symptoms:

  • course facial features
  • gingival hyperplasia
  • cataracts
  • restricted joint movements and ROM
  • claw hand
  • increased kyphosis and scoliosis

is often fatal in adolescence years

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5
Q

What are signal recognition particles (SRPs)?

A

Cytosolic ribonucleoproteins that aid in trafficking polypeptide complexes from cytosol to the RER to be packaged out.

If absent = accumulation of proteins in the cytosol

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6
Q

What are the types of vesicular trafficking proteins?

A

COP1: Golgi -> ER (retrograde delivery)

COP2: ER -> golgi (anterograde delivery)

“ two steps forward, one step back”

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7
Q

What is clathrin?

A

A vesicular trafficking protein that marks defective proteins in golgi -> lysosomes

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8
Q

Zellweger syndrome

A

Autosomal recessive disorder that disables peroxisome biogenesis via mutated PEX genes
- normal function, just little numbers

Symptoms:

  • chronic seizures
  • hepatomegaly
  • early death
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9
Q

Refsum disease

A

Autosomal recessive disorder which prevents a-oxidation in peroxisomes.

  • there is a normal number of them, just disabled function
  • causes build up of pristanic acid

Symptoms:

  • scaly skin
  • ataxia
  • cataracts
  • shortening of 4th toe

Treatment:
- plasmapheresis

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10
Q

Adrenoleukodystrophy

A

X-linked recessive disorder which prevents B-oxidation of peroxisomes due to mutations in the ABCD1 gene

  • normal numbers, just dysfunctional
  • causes build up of VLCFA in adrenal glands, white matter and testes
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11
Q

What os the function of proteasomes?

A

Protein complexes that degrade damaged or ubiquinated proteins

there are some linked to dysfunctional proteasomes and Parkinson’s disease

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12
Q

Types of cellular filaments

A

Microfilaments:

  • includes actin and microvilli
  • function is to aid in muscle contraction and cytokinesis during anaphase

Intermediate filaments

  • includes desmin, lamina, glial cells, I mention and GFAP proteins
  • function is to maintain cell structure

Microtubules

  • includes cillia, flagella, mitotic spindles and centrioles
  • function is cell division and movement
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13
Q

Microtubules and molecular motor proteins

A

Microtubules

  • composed of a/b- tubulin w/ 2 GTP bound per dimer.
  • also aid in slow axoplasmic transport of materials in neurons

Molecular motor proteins

  • used as carrier proteins to transport cellular cargo toward ends of microtubules
  • includes dynein and kinesin proteins
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14
Q

Dynein vs kinesin functions

A

Dynein = retrograde transport to microtubule (moves (+) charge -> (-) charge)

Kinesin = anterograde transport to microtubule (moves (-) charge -> (+) charge)

  • positive end is towards the periphery, negative end is towards the nucleus*

“REaDY to AttacK”

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15
Q

What are some examples of microorganisms that use dynein to infect neuronal cell bodies?

A

Clostridium tetani

Herpes

Poliovirus

Rabies virus

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16
Q

What are common medications that affect microtubule production?

A

Mebendazole (antihelminthic)

Griseofluvin (antifungal)

Colchicine (antigout)

Vincristine/blastine (anticancer)

Paclitaxel (anticancer)

17
Q

Kartagener syndrome

Primary ciliary dyskinesia

A

Autosomal recessive disorder which causes Immobile cilia due to defective dynein production
- diagnosed via testing for nasal nitric oxide levels (will be low)

Symptoms:

  • increased sterility
  • increased chance of ectopic pregnancy
  • (+/-) bronchiectasis
  • (+/-) recurrent sinusitis
  • (+/-) chronic ear infections
  • conductive hearing loss
  • sinus inversus
  • no cure*
18
Q

What cardiac glycosides directly inhibit NA/K pumps?

A

Ouabain
- binds directly to the K site

Digoxin/digitoxin

  • binds to the ATPase protein directly
  • also used in heart fill auer since by blocking NA/K pump, indirectly blocks Na/Ca pump and keeps Calcium levels high in cardiac tissue = increased contractility
19
Q

For every 1 ATP used in NA/K pump, how many molecules of NA and K are moved?

A

3 and 2 respectively

20
Q

Types of collagen

A

Type 1:

  • most common type
  • found in bone, skin, tendons, fascia, cornea
  • seen in late wound repairs
    • defects in type 1 collagen = osteogenesis imperfecta type 1

Type 2:
- found in cartilage, vitreous body and nucleus purposes of spinal cord

Type 3:

  • found in skin, blood vessels, uterus, fetal tissue
  • is seen in early wound repair
    • defects in type 3 = vascular Ehlers-Danlos syndrome

Type 4:

  • least common
  • found in basement membrane and lens
    • defect is secondary to Alport and goodpasture syndromes
21
Q

What is the most common AA found in all collagen types?

A

Glycine

22
Q

Steps of collagen synthesis

A

1) synthesis
- translation of collagen a-chains - > glycine-X-Y peptides
( X-Y = combination of proline or lysine residues)

2) Hydroxylation
- hydroxylation of proline and lysine residues
- * requires vitamin C, hence scurvy limits this step

3) glycosylation
- glycosylation of hydroxylysine residues and forms procollagen via hydrogen and disulfide bonds.
- forms triple helix structure
- * osteogenesis imperfecta limits this step

4) Exocytosis
- exocytosis of procollagen into extracellular spaces

5) proteolytic processing
- cleavage of disulfide -rich terminals of procollagen -> tropocollagen
- this occurs in extracellular matrix

6) cross-linking
- covalent founding of lysine- hydroxylysine residues in staggered tropocollagen molecules
- forms mature collagen fibrils
- *uses the copper enzyme Lysyl oxidase to do this step (menkes disease affects this enzyme)

23
Q

Osteogenesis imperfecta

A 
Autosomal dominant (most common form type 1) disorder that causes mutated COLIA1/2 genes and ends up producing defective type 1 collagen 
- produces defective type 1 collagen due to inability to properly form triple helix structure in glycosylation

Symptoms: “patients cant BITE”
Bones: multiple fractures
Iye: blue sclera
Teeth: dental imperfections due to dentin loss
Ear: conductive hearing loss due to middle ear bone osteoporosis

  • often is mistaken for child abuse

Treatment: Not curable
- calcium and bisphosphonates

24
Q

Ehlers Danlos syndrome

A

Autosomal dominant or recessive (recessive is worse) disorder that causes faulty type 3 collagen production (reticulin)

Symptoms:

  • hyperextendable skin (2)
  • hypermobile joints (1/2)
  • in ability to clot properly (3)
  • increased risk of berry and aortic aneurysms (3)
  • increased risk of joint dislocations (1/2)
  • increased chances of muscle and tendon ruptures (3)

Types:

1) hypermobility: most common type and shows joint instability as the most prominent feature
2) classical type: defective type 5 collagen due to gene mutations in COL5A1/2
3) vascular type: most deadly. Defective type 3 collagen due to gene mutations on COL3A1.

25
Q

Menkes disease

A

X-linked recessive disorder that produces impaired copper absorption and transport due to mutations in ATP7A gene
- low copper levels decrease Lysyl oxidase activity and prevent maturation fo collagen fibrils

Symptoms:

  • brittle “kinky” hair
  • growth retardation
  • hypotonia of muscles
  • increased risk of cerebral aneurysms
26
Q

Elastin

A

Subtype of collagen found in skin/lungs/arteries/vocal cords/ligamenta flava

Rich in nonhydroxylated proline, glycine and lysine residues
- normal collagen is hydroxylated

Is broken down by elastase enzymes

  • this is countered by a-antitrypsin proteins until needed
    • a-antitrypsin deficency syndrome affects this and can cause COPD
27
Q

Marfan syndrome

A

Autosomal dominant disorder that poor dudes a gene mutation in FBN1 on chromosome 15.
- results in defective fibrilin (glycoprotein that shealths elastin molecules and keeps them from overstretching)

Symptoms:

  • tall with really long extremities
  • pectus carinatum (can be excavatum also but usually isnt)
  • hypermobile joints
  • arachnodactyly (really long fingers and toes)
  • *increased chances of aortic aneurysms/ruptures (leading cause of death)
  • increases chances of MVP and subluxation of lenses.

Step 1 review cards (24 decks)

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