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FunMed Random > EOY1 > Flashcards

EOY1 Flashcards

1
Q

name two types of antibiotics that interfere with DNA replication in bacteria

A
  1. Fluroquinolones: taret topoisomerases in resp. and urinary tract infections
  2. Trimethoprim: target nucleotide synthesis
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2
Q

what is name of disease for failure of healthy bile acid cycle?

what needs to happen for this to occur?

A

only need failure in ONE transporter (ATP8B1 in hepatocytes) cause this disease

progressive familial intrahepatic cholestasis (PFIC)

  • jaundice
  • dark urine
  • pruritis (severe itching)
  • foul smelling fatty stool

failure to thrive

  • nause / vomiting

need liver transplant .

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3
Q

what is klinefelter syndrome caused by? symptoms?

A

Klinefelter syndrome: (47, XXY). Extra X chromosome. Infertile - no sperm produced. Poorly developed secondary sexual characteristics, tall. 1/1000 males

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4
Q

which of the following best describes patau syndrome?

trisomy 21
trisomy 18
trisomy 13
trisomy 11
trisomy 10

A

which of the following best describes patau syndrome?

trisomy 21
trisomy 18
trisomy 13
trisomy 11
trisomy 10

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5
Q

which of the following best describes edwards syndrome?

trisomy 21
trisomy 18
trisomy 13
trisomy 11
trisomy 10

A

which of the following best describes edwards syndrome?
​
trisomy 21
trisomy 18
trisomy 13
trisomy 11
trisomy 10

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6
Q

which of the following best describes Turners syndrome?

45X-
47 XXY
47 XYY
45Y-

A

which of the following best describes Turners syndrome?

45X-
47 XXY
47 XYY
45Y-

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7
Q

describe Turner syndrome?

A

Turner syndrome -(45, X) Loss of X chr: 1/5000 females. 99% lost spon. in preg. short. abscence of menstruation (amenorrhea). congenital heart d: 20%. webbed neck

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8
Q

which of the following best describes Klinefelter syndrome

45X-
47 XXY
47 XYY
45Y-

A

which of the following best describes Klinefelter syndrome
​
45X-
47 XXY
47 XYY
45Y-

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9
Q

what are the risk factors that are increased bc of Barker Hypothesis? what diseases do they lead to?

A
  • increased adipose tissue, increased lipid accumulation in muscles: type 2 diabetes
  • impaired glucose sensing: hyperinsulinemia (means the amount of insulin in your blood is higher than what’s considered normal. )
  • leptin resistance in brain (think always hungry): obesity
  • lipid accumulation in CV system: CVD
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10
Q

where does DNA methlyation occur? (epigenetics)

A
  • on cytosine: to form methyl-5-cytosine
  • specifically on: CPG islands of promoter regions; where cytosine is adjacent to guanine
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11
Q

which of the following is inherited?

histone modification
DNA methylation
micro and small RNAs
chromatin architecture

A

which of the following is inherited?

histone modification
DNA methylation
micro and small RNAs
​chromatin architecture

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12
Q

name enzymes that make histones a) accessible? b) inaccessible

where specifically on the histone does modication occur?

A

a) histone acetylase (HAT): opens DNA to make it accessible

b) Histone deactylase (HDAC) associated with closing DNA to make it inaccessible

/

modifcation: on lysine and serine

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13
Q

name enzymes that make histones a) accessible? b) inaccessible

where specifically on the histone does modication occur?

A

a) histone acetylase (HAT): opens DNA to make it accessible

b) Histone deactylase (HDAC) associated with closing DNA to make it inaccessible

/

modifcation: on lysine and serine

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14
Q

on a chromosome - what are the differnces between the G-light band and G-dark band?

A

G-light: gene rich, GC-rich, early replicating
G-dark: gene poor, AT-rich, late replicating

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15
Q

name and explain two imprinting syndromes?

A

Prader-Willi / Angelman syndrome

both produced by same genetic mutation. but phenotype is different depending if on male / female

Prader-Willi: (autosomal). deletion is on fathers copy of Chr. 15. region: 15q11-q13. excess weight gain. development delays

Angelman syndrome: deletion of maternal copy Chr. 15. happy demeanour, severe mental b

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16
Q

what are the DNA and RNA start and stop codons?

A

RNA: start - AUG. (methionine) stop - UAA, UGA, UAG

DNA: start - ATG. stop - TAA, TGA, TAG

-

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17
Q

what does aminoacyl RNA transfer synthase enzyme do?

A

adds correct amino acids onto the tRNA, via hydrolysis reaction

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18
Q

what is RNA cap made from? which end?

A

5’ end: 7-methly guanoside and triphosphate linkage

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19
Q

what is the name of structure where centromere and mitotic spindle fuse in metaphase?

A

kinetochore

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20
Q

what is the difference between kinetochore and centromere?

A

The main difference between centromere and kinetochore is that centromere is the region where the two sister chromatids are held together after the replication of chromosome where kinetochore is the protein complex on the chromosome where spindle fibers are attached during cell division.15 Mar 2017

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21
Q

Cohesin holds sister chromatids together after DNA replication until which phase, when removal of cohesin leads to separation of sister chromatids?

prophase
metaphase
anaphase
telophase

A

Cohesin holds sister chromatids together after DNA replication until which phase, when removal of cohesin leads to separation of sister chromatids?

prophase
metaphase
anaphase
​telophase

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22
Q

what is A?

cohesin
kinetochore
centromere
chiasmata
condensin

A

what is A?

cohesin
kinetochore
centromere
chiasmata
condensin

23
Q

label 1-4:

1
2
3
4

A

label 1-4:

1: cyclin D
2 cyclin E
3 cyclin A
4 cyclin B

24
Q

when is each cyclin actived?

A
  • G1 checkpoint passed: activates cyclin D (regulates early G1 phase) and cyclin E (regulates early G1 phase and triggers S phase)
  • S checkpoint passed: activates cyclin A (cyclin A acitvates DNA replication in S phase and movement into G2 phase)
  • G2 / M checkpoint passed: activates cyclin B (takes cells into mitosis)
25
Q
A
26
Q

explain how C-myc proto oncogenes cause cancer

A
  • proto-oncogene: c-MYK (~50% of cancers)

- promotion of transcription of cyclin genes (promotes cell cycle progression)

  • c-MYK is correlated with agressive tumour pattern and poor clinical outcome

( - causes increased growth, metabolism, cell adhesion, differentiation and metastasis)

  • seen in: Burkitt lymphoma, breast cancer
27
Q

what are the names for pro [1] and anti [1] apoptopic proteins?

A

Bax: pro-apoptotic protein

Bcl2: anti-apopotic protein

a balance is required for normal apoptosis

28
Q

explain the roles of BRCA1 and BRCA2

A

BRAC1:

  • normally: triggers the activation of the CDK inhibitor: p21WAF-1 and p53, so can control cell cycle
  • also involved in DNA repair
  • mutations lead to genomic instability
  • *BRAC2**:
  • normally facilitates HR
  • BRAC2 deficient cells: cant recruit RAD51 (protein that binds to ssDNA and needed in dsDNA repair
  • mutations: cant repair ss and dsb DNA breaks
29
Q

name 3 gate keeper genese x

A
  1. Bax
  2. p53
  3. Rb
30
Q

what are the 4 stages of gram staining?

A

Gram stain: Crystal violet –> Iodine –> Ethanol –> Safranin

31
Q

name a benign and malignant cancer type from hyperplasia and what causes it?

A

hyperplasia leads to increased growth: can be:

benign - VEGF (vascular endothelial growth factor) - (up regulate the synthesis of blood vessels.): leads t benign prostatic hyperplasia (enlarged prostate). benign growth

malignant - platelet derived growth factor (PGDR) - leads to glioblastoma

32
Q

what do u use to stain:

a) Mycobacteria:
b) fungi:
c) spirochaetes:

A

a) Mycobacteria: Zielh-Nielson stain
b) fungi: Cotton blue stain
c) spirochaetes: darkfield microscopy

33
Q

how does muscarininc acetylcholine receptor work?

A
  • acteylcholine binds to acteylcholine receptor
  • trimeric G-protein activated
  • alpha subunit of trimeric G-protein binds to activated ion channel
34
Q

Q

what is p53 activated by? [3]
what is normal function and how does it work?

A
  • p53 activated by DNA damage, hypoxia or cell injury
  • causes cells with mutations to undergo cycle arrest, allows DNA repair or entry to apopotic pathway
  • p53 activation activates p21 -> inhibits cyclin complexes (prevents cell leaving G1 / entering S-phase
35
Q

what are the three components of CT? [3]

A
  1. collagen fibres
  2. reticular fibres / tissue
  3. elastic tissue
36
Q

which pathways does Ras pathway swtich on

A

AKT & ERK pathways

37
Q

what are the two pathways initated by growth factor binding to cell, that eventually lead to activation of gene expression and transcription factors occur.

A

MAPK & PI3Kinase

38
Q

what are the five categories of proto-oncogenes?

A
  1. **growth factor
  2. growth factor receptor
  3. signal transduction
  4. transcription factor**
    * *5. anti-apoptopic**
39
Q

which cells can produce alpha smooth muscle actin?

A

myofibroblasts

40
Q

where do DNA viruses replicate? [1]
where do RNA viruses replicate? [1]

A

where do DNA viruses replicate? [1] nucleus
where do RNA viruses replicate? [1] cytoplasm

41
Q

what is ECM made of? [3]

A
  1. proteoglycans
  2. collagens
  3. noncollagenous glycoproteins (fibronectin and laminin)
42
Q

what are the 4 types of virus structure? [4]

A

helical
polyhedral
spherical
complex

43
Q

what is the baltimore classifcation for:

  • coronavirus
  • influenza
  • HIV
A
  • coronavirus: (+)ssRNA viruses
  • influenza :(-)ssRNA viruses
  • HIV: ssRNA-RT viruses
44
Q

explain basic process of drinking being a mutagen

A

ethanol:

  • reaction: ethanol –> acetaldeyde
  • acetaldeyde reacts with deoxyguanosine = weak mutagen. further reaction -> stronger mutagen (DNA adduct
45
Q

what are the three main mechanism of gene alterations that activate oncogenes? [3]

A

- point mutations: single base change in DNA (e.g. Ras oncogene)

- chromsomal rearrangements: translocation of chr activates oncogene by using regulatory elements from a highly transcribed gene to drive expression of oncogene

  • gene amplification (e.g HER2)
46
Q

explain the mechanism of how Burkitt lymphoma occurs

explain the mechanism of how lymphoma (other) occurs

A

explain the mechanism of how Burkitt lymphoma occurs
- c-myc: found on chr 8

  • IgH: chromsome 14. has a very strong promoter
  • translocation of region of chr 8 and 14: myc gets translocated near to promoter of IgH
  • results in strong promoter driving the expression of c-myc: Burkitt lymphoma

explain the mechanism of how lymphoma (other) occurs
- BCl-2 gene is on chromosome 18

  • IgH: chromsome 14. has a very strong promoter
  • switches ON bcl-2 gene (anti-apoptotic protein) in active B-lymphocytes (is normally switched off)
  • cells that harbour mutations do not go into apoptosis
  • causes lymphoma
47
Q

explain how 1) smoking and 2) uv can cauese cancer

A

smoking
- (benzopryene (BP) from smoke is oxidised (x2))- results in BPDE (ultimate carcinogen)

  • BPDE forms adduct with guanosine residues in lung epithelial cells
  • occurs often in tumour suppressor genes, such as p53

UV:
- damage in basal cells of melansomes (particularly keratinocytes)

  • p53 implicated
  • formation of cylobutane pyrmindine dimers (CPD) covalent bonds form between 2 adjacent pyrimidines in same DNA strand. VERY STRONG BOND
48
Q

how do you grade and stage tumours?

A
  • *Grading depends on:**
    1. degree of anaplasia (degree of differentiation) -> more undifferentated = lower grade
    2. rate of growth
  • *Stage depends on:**
    1. size of tumour
    2. spread / extent of tumour

TNM: - Tumour (size), Nodes: has it spread to lymph nodes? M: has it mestasistsed

49
Q

what level does thoracic aorta start?
what level does abdominal aorta start?

A

what level does thoracic aorta start? T4
what level does abdominal aorta start? T12

50
Q

what is influenza virus structure like?

what is influenza virus serology like?

A
  • Orthomyxovirus (family)
  • enveloped
  • surface spikes: Hemagglutinin protein (HA) (16 types), Neuraminidae protein (NA) (9 types)
  • SS(-)RNA
  • 8 segmented genes
  • *- serology:**
  • A = humans, animals and birds
  • B = humans only (more chill)
  • C = humans only (more more chill - mild resp. tract infections
51
Q

what is the mutation that causes Hb S to occur?

A

A –> T
glutamic acid –> valine
6th codon, beta globin chain
chromosome 11

52
Q

state the 3 mechanisms of spontaneous mutations [3]

A

1. tautomeric shift (base substitution)

2. depurination
- loss of a purine base (A or G)
- leads to deletion mutation
(can occur in double DNA helix)

  • *3. deamination**
  • removal of the amino (-NH3) group through hydrolysis water
  • leads to substitution reaction

2 & 3 corrected by: polymerase enzymes

53
Q

what is layer of brand new cells at stratum basale?

A

stratum germitativum

FunMed Random (19 decks)

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