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MCM - Final > MCM Review > Flashcards

MCM Review Flashcards

1
Q

What is the only source of pluripotent stem cells?

A

Cells of the inner cell mass

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2
Q

What is the problem in methemoglobin?

A

Iron is in its ferric state (Fe3+) and will not bind oxygen

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3
Q

Differentiate direct vs indirect methemoglobin

A

Direct –> genetically linked

Indirect –> oxidation by other compounds

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4
Q

What kind of shift does methemoglobin cause?

A

Left shift of oxygen curve

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5
Q

What kind of shift does anemia induce?

A

Anemia causes a right shift of the oxygen curve (decreased affinity

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6
Q

A patient has a blood oxygen content of 17.25 mL/dL and a hemoglobin concentration of 15.1 g/dL. The patient’s oxygen saturation is best described as which of the following?
A. Normal oxygen saturation (97-99%)
B. Decreased oxygen saturation (<97%)
C. Maximum oxygen saturation (100%)

A

B Decreased oxygen saturation (<97%)

1.34 mLO2/1gHb x 15.1g/dL

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7
Q

How many mL of oxygen are there per gram of hemoglobin?

A

1.34 mL O2/1 gHb

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8
Q

What clinical situations could indicate a left shift of oxygen to blood?

A

Polycythemia

Methemoglobemnia

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9
Q

What is primary polycythemia (Vera)

A

⬇️ EPO

Extra RBCs

⬆️ blood volume x2

⬆️ viscosity

normal CO

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10
Q

Why are silent mutations not harmful?

A

First two letters of codon often the same, but the third is able to be 3 separate codons so the same amino acid product is still possible

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11
Q

What mutations of DNA can be significantly detrimental?

A

Nonsense and frameshift mutations

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12
Q

What causes Sickle cell anemia?

A

Single base substitution of Glu for a Val (hydrophobic, neutral)

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13
Q

What common energy expenditure is constant for all three steps of mRNA translation?

A

All three steps utilize GTP

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14
Q

What are the prokaryotic elongation inhibitors?

A

Tetracycline –> binds 30S, blocks tRNA entry

Chloramphenicol –> inhibits peptidyl transferase

Clindamycin/erythromycin –> binds 50s, blocks ribosomal translocation

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15
Q

What are the eukaryotic elongation inhibitors?

A

Cycloheximide –> inhibits peptidyl transferase

Diptheria Toxin –> inactivates GTP-eEF2

Shiga Toxin/Ricin –> binds 60s, blocks tRNA entry

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16
Q

What is the role of puromycin?

A

A eukaryotic elongation inhibitor that shares a similar structure to tyrosyl-tRNA

Enters A site and causes premature stop

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17
Q

What do initiation factors attached to small ribosomal subunit do?

What do initiation factors attached to met-tRNA do?

A

Small ribosomal subunit –> promotes binding of codon and anticodon of tRNA

IF attached to met-tRNA –> hydrolyzes GTP to provide energy for formation of initiation complex

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18
Q

Where are proteins destined that are made in the cytoplasmic pathway?

A

Cytoplasm

Mitochondria

Nucleus

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19
Q

What is the nuclear translocation signal?

A

KKKRK (tryptophan rich signal)

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20
Q

What is the mitochondrial translocation signal

A

An N-terminal hydrophobic α- helix peptide

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21
Q

What residues does O-glycosylation target?

A

Ser and Threonine

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22
Q

What does N-guyscosylation target?

A

Asn and Gln

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23
Q

What residues does phosphorylation target?

A

Ser, Tyr, Asp, Thr, His

Hydroxyls (OH)

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24
Q

What residue does disulfide bonding target?

A

Cystine residues

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25
Q

What may happen if a diabetic has an over-abundance of glycosylation?

A

Cataract formation in the eye

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26
Q

What happens in Alzheimer’s Disease?

A

A mutated gene that produces amyloid precursor protein (APP) formation of neurotic plaques

Supplementation with lys may

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27
Q

What happens in Mad Cow disease?

A

Introduction of prions (misfolded proteins) that induce the same formation in their counterparts

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28
Q

What happens in Huntington’s Disease?

A

Protein aggregations in the brain CAG repeats = polyglutamine (polyQ) tract

The abnormal Huntington protein (mHTT) forms intramolecular hydrogen bonds and aggregates

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29
Q

What happens in Parkinson’s disease?

A

Mutated α-synuclein results in aggregates that form Lewy bodies

Function form is an α-helix while the febrile form is β-sheet

Results in neuronal death of the midbrain and a lack of available dopamine

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30
Q

Describe endocrine signaling?

A

Long distance Signaling - hormone

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31
Q

Describe paracrine signaling?

A

Signal diffused to neighboring cell - NMJ

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32
Q

Describe autocrine signaling?

A

Signaling cell is the targeting cell

33
Q

Where do hydrophobic signal target?

A

The nucleus

34
Q

Where do small polar hydrophilic signals target?

A

An EC receptor that utilizes secondary messengers

35
Q

What are some sensory input for GPCRs?

A

Photons, ions, amino acids

36
Q

An active GPCR switches out ________ for ______ via ________

A

GDP, GTP, GEF

37
Q

What is the role of Gαs?

A

Stimulates production of cAMP via adenylate cyclase ultimately activating PkA

38
Q

What is the role of Gαi

A

Inactivates adenylate cyclase = no PKA

39
Q

What is the role of Gαq

A

Activates PLC (phospholipase C) causing the cleavage of PIP2 –> IP3 & DAG (ca2+ also)

40
Q

What is the role of G protein receptor kinases? What is the end goal?

A

End goal - to desensitize the G protein

GRK phosphorylates GPCRs to which Arrestin can bind (3rd IC loop) and inhibit

41
Q

What’s happening in cholera?

A

Gαs is constantly active. The resulting cAMP keeps Cl- channels constantly open

42
Q

What’s happening in Pertussis?

A

Gαi is inhibited, excessive cAMP produced via adenylate cyclase

Dried out airways

43
Q

What pathways are activated by RTK signaling?

A

Ras - dependent

Ras - independent

44
Q

What blotting technique allows for visualizing of protein?

A

Western blot

45
Q

What blotting technique visualizes DNA?

A

Southern blotting

46
Q

What blotting technique visualizes RNA?

A

Northern blot

47
Q

What is the problem with the heat-stable DNA polymerase used in PCR?

A

It has no proofreading capability an is described as a “dirty” method

48
Q

What is RFLP used for?

A

Forensics

49
Q

What is VNTR (variable number of tandem repeats)

A

Diagnostics of disease (Huntington’s)

50
Q

What is one use of recombinant gene technology?

A

Insulin production (better than wild type)

51
Q

What is the use of ELISA?

A

Practical use –> HIV ag

52
Q

What’s the difference between indirect and sandwich ELISA?

A

Indirect –> Target is Ag

Sandwich –> target is Ab

53
Q

What is the only version of totipotency?

A

Zygote

54
Q

What are the examples of pluripotency?

A
  1. ) ICM of a blastocyst

2. ) iPS

55
Q

What can be associated with embryonic stem cells?

A

Teratomas, cancer, unrestricted growth

56
Q

What growth factors produce an adipocyte?

A

Retinoic acid + insulin + thyroid hormone

57
Q

What growth factors produce a neuron?

A

Retinoic acid

58
Q

What potency is cord blood?

A

Multipotent

59
Q

What potency are fetal stem cells?

A

Multipotent

60
Q

What potency are hematopoietic stems cells?

A

Multipotent

61
Q

What change in potency does iPS induce?

A

Taking a somatic multipotent cell and changing into a pluripotent cell

62
Q

What are 5 important growth factors needed to induce iPS?

A

Oct 3/4, Sox-2, Myc (n-Myc and c-Myc), Nanog, FoxD3

63
Q

Does urobilinogen have color?

A

No, it’s translucent

64
Q

Discern PKU from Cystic Fibrosis

A

Multiple genotype, one phenotype - Cystic Fibrosis

One genotype, multiple phenotypes - PKU

65
Q

What does chemotaxis use to change

A

Monomeric G protein –> pip3 –> Ras –> ARP –> Rho

66
Q

What is the consequence of an intra-hepatic jaundice

A

Build-up in the blood of conjugated and unconjugated billirubin

Increase in ALT and AST

67
Q

What’s the consequence of post-hepatic jaundice

A

Elevated blood levels of conjugated billirubin

68
Q

Break down of heme, what is the first enzyme to act on heme? (Rate-limiting step before the liver)

A

Heme oxygenase

69
Q

What type of signaling is Talin and FAK?

A

Talin (in –> out)

FAK (out –> in)

70
Q

What is a good thing to know about FAK?

A

It’s a drug target

71
Q

What happens in secondary polycythemia?

A

Abnormal CO

⬆️ EPO

⬆️ RBCS

72
Q

What changes in Physiologic polycythemia?

A

Normal CO

⬆️ RBCs

⬆️ EPO

73
Q

What does activation of the RAS-dependent pathway lead to?

A

Gene transcription (increased glucokinase transcription)

74
Q

What does the activation of the RAS-independent pathway lead to?

A

Alteration of protein and enzyme activity - GLUT 4 sequestering activation of glycogen synthase

75
Q

What are important growth factors found in pluripotent cells?

A

Cripto and GDF-3

76
Q

What two diseases are related to intra-hepatic jaundice?

A

Criggler-Najjar syndrome

Gilbert syndrome

77
Q

What are all the cyclin-Cdks and what phases do they operate in?

A

Cyclin - D | D | E | A | A | B
Cdks - 6 | 4 | 4 | 2 | 2 | 1
Phase -G1|G1| S | S |G2|G2

78
Q

Discern Prader Willi Syndrome from Angelman Syndrome

A

Prader Willi - paternal chromosome deletion (maternal silenced)

Angelman Syndrome - maternal chromosome deletion (paternal silenced)

MCM - Final (6 decks)

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