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:)) Flashcards

1
Q

where is type 4 collagen found?

A

* basal membrane *

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2
Q

where do u find reticular connective tissue?

role?

A
  • found at boundary of connective tissue and epithelium
  • supporting stroma for highly cellular organs (like liver).
    function: wound healing and scar tissue.
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3
Q

what do u stain to see elastic fibres

A

orcein

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4
Q

what is ECM made of?

A
  1. proteoglycans
  2. collagens
  3. noncollagenous glycoproteins (fibronectin and laminin)
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5
Q

what is special about myofibroblast - what do they do?

A

myofibroblasts:

(- appear similar to fibriblasts)

  • express alpha smooth muscle actin.
  • differ from smooth muscle cells bc lack external basal lamina
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6
Q

where are mast cells not found? where found tho

A
  • NOT found in: brain and spinal cord ( remember this!!)
  • found in: CT of skin and mucous (and other places too)
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7
Q

what is the name of the thick layer of dense irregular connective tissue in the skin?
what is the layer find above this?

A
  • *above:** papillary
  • *thick =** reticular layer
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8
Q

where are viral replication sites for viruses?

which type go where?

A
  • *cytoplasm**: most RNA viruses
  • *nucleus**: most DNA viruses

(some do both e.g. retroviruses)

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9
Q

what are the subunits of viral capsids called?

A

capsomere: usually associate with, or are found close to, the virion nucleic acid.

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10
Q

what are normal 4 strucutres of viruses?

name a virus that is an exceptions to the normal 4 structural categories of viruses?

A

exception: pox virus

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11
Q

what is the baltimore classification system?

A

dsDNA viruses
ssDNA viruses
dsRNA viruses
(+)ssRNA viruses
(-)ssRNA viruses
ssRNA-RT viruses
dsDNA-RT viruses

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12
Q

what type of virus (from baltimore classification) is:

  • coronavirus
  • influenza
  • HIV?
A
  • coronavirus: (+)ssRNA viruses
  • influenza:(-)ssRNA viruses
  • HIV: ssRNA-RT viruses
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13
Q

explain how oral and oespophageal cancers are caused by excess alchohol intake

A
  • *ethanol:**
  • reaction: ethanol –> acetaldeyde
  • acetaldeyde reacts with deoxyguanosine = weak mutagen. further reaction -> stronger mutagen (DNA adduct)
  • *UV**
  • p53 implicated
  • formation of cylobutane pyrmindine dimers (CPD) covalent bonds form between 2 adjacent pyrimidines in same DNA strand. VERY STRONG BOND
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14
Q

what is the mutation that occurs in ras gene to make it mutagenic?

A
  • single nucleotide exchange GGC TO GTC in bladder cancers (glycine -> valine)
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15
Q

which cancers does XPA gene increase chance of?

A

a) Non-melanoma (basal cell and squamous cell) skin cancer at UV exposed sites

    • patients with XPA mutation have 10, 000 x increased risk*
    • median age onset 9 years (c.f. 60 in general pop)*

b) cutaneous melanoma (melanocytes)

    • patients with XPA mutation have 2000x increased risk*
    • median age: 22 years (c.f. 30 years)*
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16
Q
  1. what are the three main mechanism of gene alterations that activate oncogenes?
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)

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17
Q

where is c-myc normally encoded?

where is IgH normally encoded?

explain cancer that occurs when the above translocate

A
  • c-myc: found on chr 8
  • on chromsome 14, there is a gene that codes of IgH - 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 myc: Burkitt lymphoma
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18
Q

what is a cause of lymphoma?

A
  • strong promoter of IgH on chromosome 14 translocates to chromsome 18
  • 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
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19
Q

describe how DNA methylation can lead to tumour suppression (epigenetics) in promoter region

A
  • methylation moves from lysine 4 of the histone 3 (H3) (normal function) to lysine 9 of H3
  • leads to transcriptional repression & loss of tumour suppressor gene expression
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20
Q

what type of gene is hudsons two hit hypothesis about?

A

tumour supressor genes

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21
Q

how does DNA damage occur by formation of DNA adducts in lung cancer?

how does DNA damage occur by UV radation ? and where

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
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22
Q

what does HPV cause?

A

HPV: cervical cancer

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23
Q

how do cancer cells become insensitive to anti growth signals?

A

Insensitivity to anti-growth signals:

There are genes that normally express growth suppressing signals e.g. TP53 and RB involved in the cell cycle, but can be mutated in cancer

Therefore there are no longer gatekeeping mechanisms to keep cell cycle progression in check.

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24
Q

what do cancer cells express to maintain telomere length?

A

So, in normal cells, when the telomeres are short enough, it looses its protective ability and the cell is triggered into apoptosis.

In cancer cells, telomerase (not normally expressed in healthy cells) is expressed which counters the erosion to telomeres and therefore removes a barrier to proliferation and the cell will achieve immortality.

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25
Q

which gene encodes for sustained angiogenesis in cancer cells?

A

Controlled by a signalling molecule - VEGF.

This function is normally “turned off” unless needed (e.g. wound healing) but in cancer cells is is permanently “switched on”.

Allows more nutrients to be delivered to tumour for growth.

26
Q

h-ras (and mutated k-ras) is an example of what type of protein?

how work?

A

SIGNAL-TRANSDUCTION PROTEINS:

RAS if active, it SENDS GROWTH PROMOTING SIGNALS TO THE NUCLEUS

KRAS is continuously active

↓

Signals for cell division

↓

Continuous proliferation

27
Q

ovexpression in the following causes what cancers:

VEGF
PDGF
TGFα

A

VEGF = BPH (benign prostate hyerplasia)

PDGF = Glioblastoma

TGFα = Oesophageal cancer

28
Q

what does pRB do in normal cell? when causes cancer?

A

PREVENTS PROGRESSION FROM G1 TO S BY INHIBITION OF S-PHASE GENES EXPRESSION

cause cancer when:

Phosphorylated Rb -> E2F is released -> Transcription and gene expression ->Progression from G1 to S phase

29
Q

which immunuglobulin is made first in an immune response? which one is it followed by?

A

IgM: primary immune response

30
Q

what are the two hypothesis for the generation of cancer stems cells?

A
  1. cancer stem cell model
  2. clonal evo model
31
Q

epithelial tumours are derived from which germ layers?

connective tissue tumours are derived from which germ layers?

bone tumours are derived from which germ layers?

nervous tumours are derived from which germ layers?

A
  • epithelial tumours dervied from: ectoderm, endoderm and mesoderm
  • connective tissue tumours dervied from: mesoderm
  • bone tumours dervied from: mesoderm
  • nervous tissue tumours dervied from: ectoderm
32
Q

where do u find stratified squamous cells?

where do u find simple cuboidal and simple columnar ?

important!!

A

stratified squamous: covering and lining epithelia - lining of skin / lining of internal organs / forms lining of ducts and body cavities (nasal cavity, larynx, lung, cervix and skin)

simple cuboidal / columnar: glandular epithelia - thyroid, adrenal and sweat glands. glands in breast and prostate (lung, colon, breast, pancreas, stomach, prostate))

33
Q

how do u know if a tumour is benign?

A

-oma !

34
Q

what are the charcateristics of cancer cells? (4)

A
  • immortal
  • high cell division
  • ischemic necrosis in middle of tumour -> centre of tumour lacks food / O2 so cells die
  • shedding or loss of tumour cells
  • Grade 1 -> Grade 3 cancer: cells become less differentiated / undifferentiated
35
Q

what are keratin pearls and what do they show?

A
  • when invading tumour cells retain ability to synthesis keratin - keratin becomes trapped inside the tumour: keratin pearls
  • demonstrates still fairly differentiated
36
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

37
Q

what are paraneoplastic syndromes?

A
  • paraneoplastic syndromes: clinical syndromes not caused by direct invasion or metastasis of tumour which accompany malignant disease. non-metastatic manifestation of malignant disease
  • associated with malignancies in: lung, breast, gynaecologica and haemotoligcal tumours
  • arise from tumour secretion of hormones, peptides, cytokines -> interfere with normal metabolic pathways of hormones peptides
38
Q

which organs are the primary lymphoid organs?

which are secondary lymphoid organs?

A

thymus and bone marrow - where cells are made

spleen, lymph nodes and lymphatic vessels

39
Q

how does a bacterial superinfection occur?

A

viral resp tract infections followed by bacterial superinfection:

  • mucociliary escalator (moves mucous out of lungs to be expelled by coughing) damaged
  • viral infection OR inflammation can damaeg mucociliary escalator
  • mucous not expelled
  • followed by bacterial superinfection
40
Q

how u diagnose resp. tract infections? (2)

what is a ct value / high or low ct value?

A

PCR - using a nasal pharyngeal swab:

  • nucleic acids from virus is picked by virus panel -> recognise the viruses
  • (can also check for bacterial panel to d/c if pneumonia is bacterial)
  • *- ct value: no. of rounds of replication required to ID virus on swab**
  • high ct value: need lots of rounds of replication (low virus no.)
  • *- low ct value:** need few rounds to detect to virus
41
Q

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)
42
Q

Q

describe the genome of influenza / how this influences transmission?
what is transmission cycle like?

A

A

genome: segmented - many different parts are expressed on individual nucleic acid pieces: if two viruses infecting the same cell -> pieces swap around (reassortment) and get new varients

  • *point mutations**
  • single point mutations only genome - change antigen
  • most meaningful mutations occur in HA1 protein
  • *antigenic shifts:**
  • mixing of genomes: genetic reassortment between circulating human and animal strains. creates novel H/N combinations
  • accounts for emergence of new strains of virus
  • *- only in type A**
43
Q

what are Vaso vasorum?

A

(blood vessels of blood vessels: blood carried from inner part of BV to outer par) and autonomics

44
Q

when does thoracic aorta start? become abdominal aorta?

A

starts: T4
ends: T12 - becomes abdominal aorta

45
Q

what does the short / lesser saphenous vein flow into/

A

popliteal vein

46
Q

how does excess fluid get back into the veinous system?

A

lymphatic system drains back into the right and left venous angle: junction where subclavian vein and internal jugular vein meet

47
Q

what stimulates cutaneous vasoconstriction when its cold?

A

sympathetic NS: noradrenaline on alpha adrenoreceptors

48
Q

what is an arteriovenous anastomoses?

A

BV that provide a route for blood to bypass from the arterioles directly to venules, bypassing capillaries

  • found in hands, feet, nose, ears and lip skins
49
Q

what happens at the stem cells in stratum basale?

A

stratum germitativum: new keritonocytes form from the stem cells found in stratum basale by mitotic division

50
Q

what’s found in the keratinocytes of stratum granulosum?

A
  • k with keratohyalin granules: cystine and histidine protein granules, which are precurosrs of fillagrin, which aggregates the keratin filaments
51
Q

what are the langerhan cells? derived from? role?

how do u stain them?

A
  • derived from: bone marrow
  • function: interact with keratinocytes through E-cadherins. grab antigens when they see one -> then travel to lymph node to present the antigen and then t-lympocyte activate
  • stain: protein marker S100
52
Q

basal cells of epidermis cells are attached to what?

what do adherens and desmosomes, tight junctions and gap junctions do in epidermis basal lamina?

A
  • basal cells adhere to ECM rich basement membrane: consists of Laminin 332, Collagen IV and Collagen VII)
  • adherens and desmosomes: attach cells extra- and intracellularly, mech support and integrity of epi
  • tight junctions: seal up intercellular space - prevent bacteria passing through
  • gap junctions: communication, nutrients
53
Q

what is cell structure like of eccrine sweat glands?

A

stratified cuboidal

54
Q

what do the different skin receptors detect?

A
  • *1. meissner’s corpsucles:** respond to fine touch and pressure & low vibration frequency. encapsulated nerve endings (axon surroundered by schwann cells)
  • *2. pacinian corpuscles:** look like onions. myelinated nerve ending in the centre. deep in dermis. sensitive to vibration and pressure
  • *3. ruffini endings:** deeper in base of epidermis - detect skin stretch, joint activity and warmth. finger position and movemen
55
Q

what is the change that occurs in Hb S?

A

Single base mutation of Adenine to Thymine. Produces a substitution of valine for glutamic acid at the sixth codon of the beta-globin chain. Hb gene found on chromosome 11

56
Q

which is the most common deletetion in CF?

A

most common mutation: phenylalanine 508 deletion (deletion of CTT: frameshift mutation = less stable protein)

57
Q

what are someo of the different mechanisms of spontaneous mutations?

A

1. tautomeric shift (base substitution)

2. depurination

3. deamination

58
Q

what is depurination mutation?
what is a deamination mutation?

what are most deamination and depurination errors corrected by?

A

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

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

corrected by: polymerase enzymes

59
Q

how does UV radiation cause indirect mutations?
what is the effect of DNA damage by UV radiation to melanocytes?

A
  • *indirect:** ionizing radiation creates free radicals that damage DNA by reacting with it
  • *melanocytess:** pyrimindine dimers -> formed when cyclobutane rings occur between adjacent, same strand pyrimidines in DNA
60
Q

how do H. pylori and HPV cause cancer?

A

Helicobacter pylori: causes stomach cancer. 50% of pop. is infected. causes mutation rate of stomach cells to increase by 2-8% higher spontanous rate. also get epigenetic changes. DNA repair loss

Human papilloma virus: common sexually transmitted virus. viral DNA incorporated into host. produces protein called E6. E6 binds to p53 (tumour supressor) and directs p53 for degradation. disables normal DNA damage repair processes

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