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MCM Exam 2 > Final Review Exam 2 > Flashcards

Final Review Exam 2 Flashcards

1
Q

GTP is used in translation when:

A

An AA is added, when a EF is added, and when the ribosomal complex disasociates.

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2
Q

Termination and STOP codons

A

Ribosome recognized STOP codon, RFs bind to the A site and cleave the polypeptide.

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3
Q

Prokaryotic Elongation Inhibitors mechanisms of action:

A

Tetracycline: bind smal SU and block entry of AA-tRNA.
Chloramphenicol: inhibits peptidyl transferase.
Clindamycin and erythromycin: binds to large SU and blocks translocation of ribosome.
Streptomycin: binds to small SU and interferes with the binding of fmet-tRNA.

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4
Q

Eukaryotic Elongation Inhibitors mechanisms of action:

A

Cyclohexamide: inhibits peptidyl transferase.
Diphtheria toxin: inactivates eEF-2.
Shiga toxin and Ricin: binds to large SU and blocks entry of AA-tRNA.

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5
Q

Secretory pathway signals (4)

A

ER lumen: KDEL
Secretory vesicle: Trp-rich domain.
Lysosome: Mann 6-P
CM: N terminal apolar

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6
Q

Cytoplasmic pathway signals (3)

A

Mitochondria: N term a-helix
Nucleus: Lys Arg rich
Peroxisome: SKL

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7
Q

Mechanism of AD

A

APP breaksdown to amyloid beta peptide (AB). AB forms plaques in brain

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8
Q

Mechanism of PD

A

a-synuclein aggregates to form Lewy bodies. Causes death of dopaminergic neurons in substantia negra.

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9
Q

Mechanism of HD

A

Huntington gene is mutated resulting in CAG repeats, causing poly-Gln. Causes selective death of cells in basal ganglia.

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10
Q

GEF, GTPase and GAP

A

GEF causes ADP –> ATP
GTPase does opposite
GAP stimulates GTPase

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11
Q

Gq pathway

A

GTP –> PLC –> DAG, IP3

IP3 –> Ca 2+ (2nd messenger) –> PKC

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12
Q

Viagra mechanism

A

Inhibits cGMP PDE

Increases cellular cGMP –> smooth muscle relaxation, vasodilation.

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13
Q

NO mechanism

A

Activates guanylate cyclase

GMP –> cGMP (smooth muscle relaxation and vasodilation).

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14
Q

Cholera and Pertussis

A

Cholera: prevents inactivation of Gs (AC always on)
Pertussis: prevents activation of Gi (AC not inhibited).

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15
Q

GRKs

A

Phosphorylate GPCR. Arrestin binds and inactivates GPCR.

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16
Q

Reciprocal and Robertsonian transocations

A

Reciprocal: exchange of material between nonhomologues
Robertsonian: Long arm of 2 chromosomes combined. Short arm lost.

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17
Q

Imprinting

A

Silencing of a gene.
If a gene is “paternally imprinted”, the paternal gene is silenced.
These are reset after meiosis in each generation.

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18
Q

Same genotype but multiple phenotypes:

A

Pleiotropy (PKU)

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19
Q

Multiple genotypes but single phenotype:

A

Ex: CF

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20
Q

Penetrance

A

Frequency a gene manifests itself

Rb

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21
Q

Expressivity

A

Variation in phenotype

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22
Q

E2F drives the expression of which cyclins?

A

A and E (G1 to S)

23
Q

CDK2 function

A

Hyperphosphorylates Rb (making it inactive) and activates E2F.

24
Q

APC/C function

A

Degrade cyclins in progression from metaphase to anaphase. APC/C ubiquinates S and M cyclins targeting them for degredation.

25
Q

CDC20

A

Activates APC/C

26
Q

MDM2

A

Keeps p53 inactive via degredation. p53 gets phosphorylated to become active.

27
Q

p21 function:

A

Main target for p53, but mainly acts on inhibiting CDK2 (to inactivate E2F)

28
Q

Hallmarks of cancer (6)

SEAEIR

A
  1. self-sufficient in growth signals
  2. evading growth suppressors.
  3. activating invasion and metastasis.
  4. enabling replicative immortality.
  5. inducible angiogenesis.
  6. resisting cell death.
29
Q

HPV

A

E6 + p53 —> p53 degredation

E7 + Rb —> displaces E2F, E2F active

30
Q

Taxol
Colchicine
Vinblastine

A

Drugs that affect microtubules
Taxol: binds and stabilized microtubules.
C & V: binds tubulin dimers and prevents polymerization.

31
Q

Phalloidin
Cytochalasin
Latrunculin

A

Drugs that affect actin
Phalloidin: binds and stabilized f-actin
Cytochalasin: caps filaments, preventing polmerization
Latrunculin: binds actin monomers and prevents polymerization

32
Q

Adherens junctions

A

Type: cell-cell
CAM: cadherins
Attachment: actin
Function: shape, tension, signaling

33
Q

Desmosomes

A

Type: cell-cell
CAM: cadherins
Attachment: intermediate filaments
Function: strength

34
Q

Hemidesmosomes

A

Type: cell-matrix
CAM: integrin
Attachment: intermediate filaments
Function: shape, rigidity, signaling

35
Q

Tight junctions

A

Type: cell-cell
CAM: N/A
Attachment: actin
Function: solute flow

36
Q

Gap junctions

A

Type: cell-cell
CAM: N/A
Attachment: adapters to other junctions
Function: communication, small molecule transmission

37
Q

Hereditary hemochromatosis

A

Organ dysfunction due to iron overload.

38
Q

Why is RBC production dependent on folate and cobalamin?

A

They are needed for DNA synthesis in the bone marrow.

39
Q

Deficiency of cobalamin and/or folate can cause?

A

Megaloblastic anemia

40
Q

Pernicious anemia

A

Form of megaloblastic anemia from cobalamin deficiency.

41
Q

Neutrophils

A

Multi-nucleated
Acute inflammation and injury; function in bacterial infections.
Contain 3 granules.
Undergo diapedesis.

42
Q

Eosinophils

A

Bi-nucleated

Parasitic infections, chronic inflammation and allergies.

43
Q

Basophils

A

Hard to see nucleus.

Hypersensitivity and anaphylaxis.

44
Q

Monocytes

A

Heart-shaped nucleus, but large cell.

Becomes macrophage.

45
Q

Lymphocytes

A

Large nucleus.

46
Q

HbS mutation and chromosome

A

b-globin
Glu –> Val
Chromosome 11

47
Q

Pathophysiology of acute splenic sequestration in HbS

A

Sickle cells cause vaso-occlusion.
Elevated reticulocyte count.
Enlarging spleen (asplenia)

48
Q

Acute chest syndrome in HbS

A

Infection (infiltrate on CXR)

Causes infarction.

49
Q

Kids w/ HbS are at risk of what infections? (DMS)

A
  1. Dactylitis
  2. Mycoplasma
  3. Strep pneumoniae
50
Q

ALA synthase requires:

A

Vit B6

51
Q

Porphyrias (4)

A
  1. Acute intermittent: PBG demainase
  2. Congenital erythropoetic: uroporphyrinogen III synthase
  3. PCT: Uroporphyrinogen decarboxylase
  4. Variegate: protoporphyrinogen IX oxidase
52
Q

Pre hepatic Jaundice

A

Increased unconjugated BR.

Eveyrthing else is fine, just overwhelmed.

53
Q

Intra hepatic

A

Impaired uptake, conjugation or secretion of conjugated BR.
Liver is sick (cirrhosis, hepatitis, C-N, Gilbert)
Increased ALT, AST.
Conjugate BR in urine.

54
Q

Post hepatic

A

Cannot excrete BR.
Blockage in live/bile duct.
Pale stool, conjuated BR in urine (causing a dark tint).

MCM Exam 2 (15 decks)

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