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Medicine > Biochemistry - Part 1 > Flashcards

Biochemistry - Part 1 Flashcards

1
Q

What is the role of the Rough ER?

A

Protein synthesis and N-linked glycosilation

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2
Q

What is the role of the smooth ER?

A

Lipid synthesis and glucose-6-phosphatase synthesis

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3
Q

In vesicular trafficking to cis-golgi, what kind of transport is required and what enzyme helps with this process?

A

Anterograde transport and COP II

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4
Q

What is the enzyme used to vesicular trafficking to the ER via endocytosis? What type of transport is used?

A

COP I; Retrograde transport

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5
Q

What organelle is responsible for post translational modifications?

A

The Golgi Apparatus

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6
Q

What are the post translational modifications done by the golgi?

A

1.) Modifies N-Oligosaccharides of Asn
2.)adds O-Oligosaccharides of Ser/Thr
3.) Sulfation of Tyr
4.) Addition of Mannose-6-phosphate for proteins destined for lysosome

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7
Q

What is the general jist of I-cell disease?

A

Its the failure to phosphorylate mannose residues leading to inclusions

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8
Q

What Are the two processes from the trans-golgi?

A

1.) Secretory vesicle to cell membrane to exocytosis
2.) Clathrin-mediated transport to the late endosome to eventually the lysosome

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9
Q

Via endocytosis, Clathrin-mediated endocytosis can go one of which two ways?

A

1.) Goes to the trans-golgi for retrograde transport to ER (COP I-mediated)
2.) Goes to lysosome for degredation

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10
Q

The _____ endosome helps breakdown products before transport to the lysosome

A

Late

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11
Q

What does Clathrin do?

A

Helps transport molecules

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12
Q

____-golgi is the proximal side

A

Cis

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13
Q

_____-golgi is the more distal (lateral) side

A

Trans

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14
Q

The golgi normally adds what enzyme needed to proteins destined for the lysosome?

A

mannose-6-phosphate

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15
Q

I I-cell disease, what amino acid is the defect in?

A

N-Acetylglucosamine-1-phosphotransferase

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16
Q

The defect in N-Acetylclycosamine-1-phosphotransferase causes what kind of failure?

A

Failure of the golgi to phosphorylate mannose, which is used by lysosomes as a digestive enzyme

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17
Q

If mannose is not phosporylized, what happens to the digestive enzyme? What does this failure cause?

A

Causes digestive enzymes not to be tagged for lyosome to be transported extracellularly which then causes an increased buildup of cell debris in lysosomes (Inclusion bodies)

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18
Q

What type of inheritance is I-cell disease?

A

Autosomal recessive

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19
Q

What is the presentation of I-Cell disease?

A

1.) In young children, developmental delay/failure to thrive
2.) Coarse facial features, corneal cloudening causing blindness
3.) Skeletal deformities/decreased mobility, kyphoscoliosis, claw hand deformity
4.) Hepatomegaly, gingival hyperplasia

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20
Q

What ar ehte diagnostic findings for finding out if a patient has I-cell disease?

A

1.) Decrease N-Acetylglucosamine-1-phosphotransferase enzyme activity
2.) Elevated serum lysosomal enzymes, normal urinalysis
3.) Inclusion bodies and vacuoles in peripheral blood smeres

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21
Q

How is the N-ac.gl.-1-phsphtrsnfrase activity tested? (prenatal and postnatal)

A

Prenatal: Amniotic fluid/Chorionic villi
Post natal: WBC’s

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22
Q

What is the management of I-cell disease?

A

No cure, symptomatic treatment and nutritional support, physical therapy

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23
Q

What are the complications of I-cell disease?

A

CHF, pneumonia, otitis media, atlantoaxial instability

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24
Q

What is a differential diagnosis of I-cell disease?

A

Mucopolysaccharidoses (Hurler/Hunter syndrome)

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25
Q

Mucopolysaccharidoses has increased urinary _________

A

glycosaminoglycans

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26
Q

What kind of disease is I-cell disease?

A

A lysosomal storage disease

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27
Q

A signal sequence particle is an string of ________ amino acids on proteins destined for the ________

A

hydrophobic; endoplasmic reticulum

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28
Q

What is the signal sequence used for?

A

Used for export or membrane integration

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29
Q

Signal sequences attract _____ ______ particles and binds to it, effectively halting what process?

A

Signal recognition particles; stopping translation

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30
Q

Anti-SRP antibody positive is associated with what pathologies?

A

Polymyositis and dermatomyositis

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31
Q

A positive anti-Jo test can is the primary diagnostic target for what pathology?

A

myositis

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32
Q

What are the presentations of positive Anti-SRP?

A

Elevated muscle enzymes, symmetrical proximal muscle weakness

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33
Q

Is there cutaneous involvement in polymyositis?

A

No

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34
Q

What are the presentations of dermatomyositis?

A

Heliotrope eyelid rash and gottran papules

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35
Q

What are the steps of making a new protein? (SRP and translocon) (First step through fifth step)

A

-First: SRP brings nascent protein complex to ER membrane and binds to SRP receptor
-Second: Ribosome passed to translocon channel where SRP detaches
-Third: Signal sequence opens translocon and binds, translocation continues, and threads through as a large loop
-Fourth: Protein is complete, Signal sequence gets degraded by signal peptidase and translocon closes
-Fifth: Protein is released into ER lumen and escorted to golgi for vesicular trafficking

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36
Q

Transmembrane proteins are made how?

A

By changing location of SRP or adding stop sequences

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37
Q

What happens if there is a failure of the signal recognition protein?

A

Cystolic buildup of proteins

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38
Q

What is the role of a peroxisome?

A

Degrades fatty acids, amino acids, and uric acid

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39
Q

When a peroxisome degrades uric acid, what does it generate?

A

Peroxide

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40
Q

What is the role of Lysosomes?

A

They degrade endocytosed materials and cell debris

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41
Q

What is the role of proteasomes?

A

Degrade ubiquitinated proteins

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42
Q

Fatty acids that are >22 carbons are too ______ to enter the mitochondria

A

large

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43
Q

In Very long chain fatty acid beta oxidation, how many carbons are cleaved per cycle?

A

2 carbons

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44
Q

When a very-long-chain fatty acid (VLCFA) undergoes beta oxidation, what does it now become?

A

a medium-chained fatty acid

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45
Q

How does the uric acid become peroxide?

A

There is an electron transfer to O2 which creates the H2O2

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46
Q

What neutralizes catalase?
-Example?

A

Catalase positive bacteria (e.g. Staphylococci)

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47
Q

Catalase positive bacteria causes increased ________

A

pathogenicity

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48
Q

Catalase reaction degrades _______ or uses in detox reactions which protects the cell from _______ damage

A

peroxide; Oxidative

49
Q

Adrenoleukodystrophy is a ________ mutation

A

ABCD1

50
Q

If there is a ABCD1 mutation, this causes decreased _______ import leading to decreased ________ which causes increased levels of __________

A

Very long chain fatty acids; beta oxidation; VLCFA

51
Q

Adrenoleukodystrophy causes what pathophys for these organs:
-Adrenal glands
-White matter

A

Adrenal insufficiency; Cognitive impairment, neonatal seizures, and hearing loss

52
Q

Branched-chain fatty acid alpha oxidation mostly happens in what two organs?
-How many carbons are cleaved?

A

Brain and liver
-Cleaves 1 carbon

53
Q

What is the substrate in Branched chain fatty acid alpha oxidation?

A

Phytanic acid

54
Q

What is the disease of disorder of peroxisome alpha oxidation?

A

Refsum disease

55
Q

What does disorder of peroxisome alpha oxidation cause increased levels of?

A

Phytanic acid

56
Q

What are the presentations of Refsum disease?

A

Causes ascending polyneuropathy, scaly skin, cataracts, shortening of fourth toe, and epiphyseal dysplasia

57
Q

What does the peroxisome synthesize?

A

cholesterol, bile salts, ethanol, amino acids, and plasmalogens

58
Q

What plasmalogen is primarily produced by the peroxisome?

A

Phospholipids in myelin

59
Q

When there is a PEX mutation causing decreased peroxisome biosynthesis, what disease is this associated with?

A

Zellweger syndrome

60
Q

What mutation is associated with Zellweger syndrome?

A

PEX mutation

61
Q

How does Zellweger syndrome effect peroxisomes?

A

It decreases their biosynthesis

62
Q

What is the overall cellular effect of Zellweger syndrome?

A

Decreased synthetic function and VLCFA oxidation

63
Q

What is the presentation of Zellweger syndrome?

A

Hypotonia, siezures, and hepatomegaly

64
Q

All diseases of peroxisome pathology are apart of the ________ spectrum.
-Are they all different?

A

Zellweger spectrum
-Not all different, just different severities

65
Q

What specific proteins are degraded by proteasomes?

A

Ubiquinated proteins

66
Q

The proteasome degrades things such as?

A

Misfolded proteins, cell cycle regulation, and anti-apoptotic molecules

67
Q

Ubiquitin is a _____ protein tag added to proteins destined for the ________
-Is this initiated by ATP?

A

regulator; Proteasome
-Yes

68
Q

What cascade adds Ubiquitin (Ub) to lysine residues?

A

Conjugation

69
Q

What are the three steps in conjugation of Ub?

A

Activation, conjugation, and ligation

70
Q

What happens during E1 phase of conjugation cascade and how many of what kind of enzyme?
-What is this step known as?

A

Transfers Ub to E2 using one E1 enzyme
-Activation

71
Q

What happens during E2 phase of the conjugation cascade and how many of what enzyme(s) are used?
-What is this step known as?

A

Presents Ub to E3 by several enzymes of E2 and E3
- Conjugation

72
Q

What happens during E3 phase of conjugation cascade and how many of what enzyme(s) are used?
-What is this step known as?

A

Facilitation of Ub attachment to target through many specific enzymes
-Ligation

73
Q

The conjugation cascade ________, creating a Ub ____ formerly known as?

A

repeats; Ub chain; formerly known as a poly-Ub chain

74
Q

is Mono-Ubiquination degradative?

A

No

75
Q

How to proteosomes cleave peptide bonds?

A

Via ATP hydrolysis

76
Q

What reverses Ubiquitination?

A

Deubiquitylating enzymes (DUBs)

77
Q

Proteosome:
-Shape?
-What kind of complex?
-Located where?

A
  • 26S barrel shaped
  • Catalytic enzyme complex
  • in nucleus and cytoplasm
78
Q

When regulatory particles bind with the proteosome, what happens next?

A

The poly-Ub chain is cleaved, denaturing of target protein, and feeding to proteolytic core

79
Q

What are two disorders of Lewy bodies?

A

Parkinsons and lewy body dementia

80
Q

Decreased Ub-proteosome activity causes?

A

Neurodegeneration

81
Q

What are the two causes of Disorders of Lewy bodies?

A

Decreased Ub-Proteosome activity and decreased parkin activity (E3) or elevated DUB activity

82
Q

What occurs if there is decreased parkin (E3) activity or increased DUBs activity?

A

Causes elevated alpha syniclein protein resulting in lewis bodies

83
Q

What do lewis bodies look like under the microscope?

A

Brown spots

84
Q

If lewy bodies were deposited in these areas, what presentations will they have:
1.) BrainStem
2.) Substantia Nigra
3.) Cortex

A

1.) Constipation, depression, fluctuating blood pressure
2.) Motor symptoms (resting tremor, bradykinesia)
3.) Decreased memory and executive function

85
Q

The substantia Nigra is apart of the _____ ______

A

Basal Ganglia

86
Q

What is bradykinesia?

A

Slow or delayed movement or difficulty initiating movement

87
Q

What two enzymes proceed a cell into M phase?

A

Cyclin B and CDK1

88
Q

What process follows exit of M phase in cell cycle regulation?

A

Ubiquitin-mediated proteolysis of Cyclin B

89
Q

What is the ending prefix of proteosome inhibitors?

A

ends in -Zomib

90
Q

what is the effect of proteosome inhibitors?

A

Inhibition of proteolyic subunit causing cell degradation

91
Q

Proteosome inhibitors are perscribed for management of _____ _____ and __________

A

Multiple myeloma and mantle cell carcinoma

92
Q

What do proteosome inhibitors do for the G2-M phase of cell cycle?

A

Arrests G2-M and causes induction of apoptosis

93
Q

the accumulation of misfolded proteins are more frequent in ______ cells

A

cancer

94
Q

What is the cytoskeleton overview? Whats it made of and its function?

A

Cytosolic filament network for transport, stability, movement, and cell division

95
Q

What is the function, structure, and accessory proteins of Actin?

A

Function: Muscle contraction, cytokinesis, and cell migration
Structure: Double Helix
Acc. Proteins: Myosin

96
Q

What is the function, structure, and accessory proteins of Intermediate Filaments?

A

Function: Stability
Structure: Varies
Acc. Protein: Plectin

97
Q

What is the function, structure, and accessory proteins of Microtubules?

A

Function: Movement and cell division
Structure: Cylindrical
Acc. Proteins: Kinesin and Dynein

98
Q

Dynein utilizes what grade of transport?

A

Retrograde (+ to - end of microtubule)

99
Q

Kinesin utilizes what grade of transport?

A

Anterograde ( - to + end of microtubule)

100
Q

What pathologies utilize retrograde transport?

A

Clostridium tetani, herpes simplex, polio, and rabies

101
Q

What is the mechanism of action of microtubule inhibitors?

A

They decrease Microtubule polymerization or increase their stability

102
Q

What microtubule medications can cause neuropathy?

A

Vincristine and taxanes

103
Q

What are the names of some microtubule inhibitors?

A

Mebendazole, griseofulvin, colchicine, taxanes, and vinca alkaloids

104
Q

What are the mechanism of action of Mebendazole, griseofulvin, colchicine and Vinca alkaloids?

A

they inhibit microtubule polymerization

105
Q

What is the mechanism of action of taxanes?

A

They increase stability of microtubules by preventing depolymerization

106
Q

What syndrome also inhibits microtubule polymerization?
-What type of genotype is this disease?

A

Chediac higashi syndrome
-Autosomal recessive

107
Q

What is the pathophysiology of primary ciliary dyskinesia?

A

Defect in dynein causing absent or dysmotile cilia, leading to dysfunctional ciliated epithelia; Causes developmental abnormalities causing thoracoabdominal laterality

108
Q

What is the presentation with primary ciliated dyskinesia?

A

Chronic productive cough. bronchiectasis, recurrent otisis, sinusitis, nasal polyps; Infertility, dextrocardia

109
Q

What is the classical sign associated with primary ciliary dyskinesia?

A

Dextrocardia

110
Q

What is the presentation of Kartagener syndrome?

A

Situs inversus (Including dextrocardia), recurrent sinusitis, bronchiectasis

111
Q

Whats the management of Kartagener syndrome?

A

No cure, maintain airway health

112
Q

The sodium potassium pump utilizes what form of transport?

A

Active transport

113
Q

In the Na/P pump, there is ______ Na out in exchange for ______ K+ into the cell

A

3 Na for 2 K+

114
Q

in the Na/K pump, Cytoplasmic Na+ binds causing ATP ______ which then causes conformational change and ______

A

Phosphorylates; release of Sodium

115
Q

In the Na/K pump, K+ binds causing ______ which then leads to comformational change back to original

A

Dephosphorylation

116
Q

What is the use of insulin in the sodium potassium pump?
-What does it manage?

A

Insulin phosphorylates Na/K pump, increasing pump activity, shifting potassium into the cells and causes a decrease of serum K
-Manages hyperkalemia

117
Q

The sodium potassium pump creates a ______ gradient

A

Concentration

118
Q

Calcium in cardiacmyocytes controls _________

A

Inotropy (contraction strength)

119
Q

Cardiac glycosides mechanism of action?

A

Directly inhibit Na/K pump

Medicine (10 decks)

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