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Knowledge Test > Integrity - Immunity > Flashcards

Integrity - Immunity Flashcards

1
Q

Where is the microbiome

A

stomach, dji, colon

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2
Q

what constitutes the microbiome

A

firmicutes and bacteroidetes (breakdown carbohydrates in gut -fermentation- , in obesity there is a higher number of firmicutes and lower number of bacteriodetes)

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3
Q

changes in gut microbiome in life

A

antibiotic use in pregnancy, mother’s diet, hospital, length of gestation, mode of delivery, environment, formula or breast, solid food

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4
Q

breast milk

A

contains oligosaccharides (HMO), babies can’t digest but B . infantis can by releasing SCFAs which also help promote anti-inflammatory molecules and sialic acid for brain development

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5
Q

what is the function of the microbiome

A

energy biogenesis, protection from pathogens, immune system education, brain function, bile salt metabolism, vitamin production, drug metabilism

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6
Q

energy biogenesis

A

resistant starch breakdown by microbiome to SCFAs (fermentation). SCFAs are anti-inflammatory and anti-tumor properties and stimulate protein YY (PYY) whihc induces satiety

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7
Q

microbiome protection from pathogenic bacteria

A

niche competition and nutrient depletion from invading bacteria, SCFAs inhbit virulence gene expression and lower pH to below optimal growth. Microbiota produce bacteriocins that directly kill salmonella, listeria, clostridium

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8
Q

gut-brain axis

A

stomal nerve connections in central, autonomic and enteral nervous system contriubuts to GI disease and brain disease

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9
Q

bile acid metabolism

A

bile acids produced from metabolism of cholesterol involved in emulsification of fat. Microbiota produce secondary bile acids that activate cell surface and nuclear hormone receptors whch cause gut inflammation,

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10
Q

altered microbiome diseases

A

obesity, T2 diabetes mellitus, IBD, colon cancer, asthma

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11
Q

Probiotics

A

Little evidence of benefit exceot for T2 diabetes where it can lower cholesterol and fasting blood glucose

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12
Q

IBD

A

t cell. diarrhoea (blood,mucus), tummy pain

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13
Q

ulcerative colitis

A

affects colon, chron’s affects mouth to anus. treatment -immunosuppression, aminosalicylic acid, glucocoritcoids. andominal pain, diarrhoea, weight loss. ]fewer firmicutes and clostridium, more enterobacteriocace including e.coi

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14
Q

colon cancer

A

More common in lower SES, blood in stool, aged 50 fit test - colonoscopy. Rfs = obesity, insulin resistance, red and processed meat, in microbiome - fermentation of diet derived proteins to phenols, indole, n-nitroso compounds, secondary bile acids, ammonia. protective = fibre and excercise. In microbiome - scfas

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15
Q

helicobacter (H). pylori

A

attaches to gastric mucosa, has enzyme urease which breaks down urea to produce ammonia which neutralises gastic acidity, most common bacterial infection in humans. disrupts gastric mucus layer leading to exposure of mucosa to acidic environment which promotes inflammatory immune response. Causes chronic gastritis which can lead to peptic ulceration, increases risk of stomach cancer

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16
Q

peptic ulcer disease

A

often asymptomatic but can cause bleeding leading to anemia. upper abdominal pain, indigestion, heart burn, can perforate and lead to severe pain. investiagations = urea breath test with carbon 14 urea to detect CO2 in breath, stool anitgen test, endoscopy, biopsy. treatment: proton pump inhibitor (lansoprazole @prazole) which suppress acid secretion. antibiotics 7 day course of amoxicillin and clarithromycin or metronidazole.

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17
Q

clostridioles difficile

A

causes antibiotic associated colitis. prevention antibiotic stewardhip esp ciprofloxacin (resp and utis), clindamycin (lung, female reproductive tract), cephalosporins (septicaemia, pneumonia, meningitis, ). treat with metronidazole or rancomycin. can be treated with foecal microbiota trasnplantation (FMT) if disease is recurrent

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18
Q

Primary, opportunistic, commensal, obligate, zoonotic, saphrophytlm

A

primary - cause harm e.g e.coli
opportunistic - only in right circumstances
commensal - live in harmony but can be pathogenic by accident
obligate - depend on disease for transmission e.g tb
zoonotic- transmitted to animals via direct vector or contact with animal products
saphrophytic - environmental, water or soil

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19
Q

how do pathogens enter, spread, and exit the body

A

enter :mouth, eyes, nose, urogenital openings, wounds, bites

spread: blood, lymph, nerves (HIV,rabies), cerebrospinal fluid
exit: respiratory, urogenital secretions

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20
Q

pathogenisis

A

exposure, adhesion (colonisation), invasion, infection

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21
Q

how do pathogens evade detection

A

concealement of antigens, intracellular persistance, concealment by taking host mmebranes or molecules

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22
Q

people who are more susceptible to infectino

A

diabetes, chronic renal disease, chronic liver disease, COPD, malignancy, immunosuppression (primary -congenital, iatrogenic - chemotherapy,transplants, acquired - HIV)`

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23
Q

straphylococcus aureus

A

produces coagulase which clots plasma.colonises in anterior nares, axilla, throat, GI tract. gram + ve round, spreads through direct contact with person or object, particles. Skin infection common (cellulitis), blood (catheter), lung (pneumonia). Antibiotics

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24
Q

E.coli

A

commonest cause of UTI, ingestion of undercooked foods, water, person to person. Can cause scepticiemia

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25
Q

Sepsis and septicemia

A

septicemia = blood infection as a result of UTI,pneumonia,kidney infections commonly s.aureus.
sepsis is an extreme response to infection and a complication of septicemia. Signs : high HR, low BP, fever, shiver, feels cold, SOB, confusion, extreme pain, clammy, sweaty. Can lead to tissue damage, organ failure and death. In septic shock BP drops to dangerous levels

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26
Q

neisseria meningitidis

A

encapsulated gram -ve, 2nd most comomn cause of meningitis after s.pnuemoniae. colonises nasopharynx (GD1 ganglioside receptors), school children and young adults, person - person. PUBLIC HEALTH. pauparic non-blanching rash

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27
Q

streptococcus pneumoniae

A

colonises nasopharynx, throat and lobar lungs. sees PAMPs and recruits neutrophils to attempt phagocytosis which releases toxins and fluid accumulates

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28
Q

infection

A

invasion, multiplication, and establishment of one or more pathogens in the body

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29
Q

pathogenicity

A

ability of an organism to inflict damage on the host

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30
Q

virulence

A

relative ability of a pathogen organism to cause disease

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31
Q

colonisation

A

no harm carrier of pathogen

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32
Q

innante immune system

A

physical: anatomical barriers, mechanical, microbial colonisation
chemical: acid, antimicrobial peptides (kill bacteria by attacking membranes or interfering with cell functions), cytokines (recruit WBCs to infected area),inflammation eliciting mediators promote vasodilation, bronchoconstriction
cellular: neutrophils (very effective against bacteria, release cytotoxic chemicals, pus), eosinophils (effective for antibody-antigen complexes, release antihistamines, effective against parasites), NKCs ( recognise infected cells due to lack of MHC)

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33
Q

Haemophilus influenzae

A

upper-airway, capsulated strain gives meningitis in kids, pneumonia, epiclotitis. Vaccine Hib B

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34
Q

genome

A

complete set of genetic information provides all info required for organism to funciton. kept in nucelus of eukaryoyes

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35
Q

dna winding

A

double helix wound around histone protein complex making a nucleosome

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36
Q

nucleoside

A

base and sugar, adenosine, guanosine, cytidine, thymodine, uridine

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37
Q

nucleotide

A

base and sugar (joined 5’ to 3’ by phosphodiesterase linkage) and phosphate, linked covalently

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38
Q

base

A

pyrimidines (cytosine, thymine), purines (adenine, guanine) . a + t, c+ g. adenine, guanine, cytosine, thymine, uracil

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39
Q

two dna strands held together by

A

hydrogen bonds

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40
Q

chromatin

A

beads on a string

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41
Q

dna replication

A

semi-conservative, strands must be seperated before (DNA helicase) replication, initiator proteins recognise replication origins and open helax locally. DNA synthesis happens biderectionally at replication forks . DNA polymerase adds new stuff to 3’ direction so new strand is synthesised in 5’ to 3’. the energy rwequired comes from hydrolysis of dNTPs high energy phosphate bond. leading strands synthesised continuosly, lagging discontinuosly joined by DNA ligase. (okzaki fragments)

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42
Q

Short commings of DNA polymerase

A

can’t start synthesis without RNA polymerase aka primase making an RNA primer first. lagging needs continous primer.

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43
Q

xerodema pigmentosa

A

affected individuals can’t repair thymine dimers

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44
Q

mitichondrial DNA

A

circular, genome is not enveloped, not packaged into chromatum, inheritence is strictly maternal

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45
Q

Nuclear dna

A

linear, genome is eneloped, packaged in chromatum, equal inheritance

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46
Q

1 gene codes for

A

1 protein

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47
Q

Dna to protein

A

dna makes rna makes protein, transcription, translation

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48
Q

RNA synthesis

A

done by RNA polymerase but TPA/G/U/C (activated precursors ) used instead of primer

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49
Q

promoters and enhancers

A

promotors found on 5’ end of genee
enhancer 3i end - increae transcription and can act over long distances . Transcription factors bind to promoters and enhancers and increase or decrease gene expression. MyOD = muscle specific transcription factor

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50
Q

site of transcription and translation

A

transcription occurs in nucleus, translation occurs in cytosol

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51
Q

5UTR 3 UTR

A

found before and after translated mrna section respectively

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52
Q

before rna can leave the nucleus it must undergo

A

slicing, capping (guaninet methyl group on 5’ end), polyadenylation (3# end of MRNA)

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53
Q

mRNA ,tRNA, rRNA,

A 
mrna = encodes proteins. trna = adaptor molecules between mrna and aminoacid
rrna= componenet of ribosome
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54
Q

PCR

A

dna replication used for genotyping. 1. separate strands with heat 2. cool to anneal primers 3. dna synthesis

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55
Q

codon

A

nucleotides read in groups of 3

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56
Q

start and stop codons

A

start = AUG. stop = UAA, UAG, UGA

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57
Q

redundancy

A

many amino acids are coded for by more than one codon

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58
Q

ribosome subunits

A 
large = catalyses formation of peptide bonds that covalently link amino acids
small = matchers trnas to mrna codons
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59
Q

translation

A
  1. charged rna binds to vacant a site - basepairing with mrna codon determines which trna binds
  2. new peptide bond formed between p and a sites
  3. shifts to p and e sites
  4. ribosome with vacant a site
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60
Q

analagous networks

A

regulate selective gene expression

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61
Q

tryptophan

A

if low genes are ON

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62
Q

TFIID

A

general transcription factor which binds to TATA and controls position where all protein coding genes start (but not end )

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63
Q

How is memory of differentiation passed on

A

+ve feedback loop

64
Q

DNA methylation

A

gene repression as transcription factors cannot bind

65
Q

haematopoesis

A

blood cell differentiaion all from multipotent haemopoietic stem cell in bone marrow. GATA-1 transcription factor commits cells to lineage that will make RBCs

66
Q

Stromal cell signals

A

regulate stem cell differentiation , contact between stem cell and stromal cell maintains stemness. division causes loss of contact between daughter cell and stromal

67
Q

CSFs

A

released by endothelial cells, fibroblasts, and macrophages in response to tissue infection and act on precursor cells in bone marrow to promote production of neutrophils and macrophages

68
Q

mitogens

A

stimulate cell division by triggering wave of G1/S - cdk activity that relieves intracellulart -ve controls blocking cell cycle

69
Q

growth factors

A

extracellular signals proteins that promote cell growth. oestrogen for breast cancer, blocked by Tamoxifen

70
Q

WNT pathway

A

WNT is produced by paneth cells and recieved by stem cells, it inhibits APC (apc degrated B-catenum) so b-catnim translocates to nuceleus which drives proliferation and stem cell state. Paneth cells tell neighbours to become stem cells

71
Q

FAD

A

genetic predisposition to colorectal cancer

72
Q

immune complement

A

system of soluble proteins serum proteins that activate each other

73
Q

cytokines

A

immune messenger hormones

74
Q

chemokines

A

cytokines specialised in making cells move

75
Q

antibodies

A

secreted molecules which bind to pathogens

76
Q

types of immune cell

A

innate: macrophages, dendritic, neutrophils, eosinophils, basophils, mast cells
adaptive: t cells, b cells ,lymphocytes
leukocytes: wbs innate and adaptive

77
Q

where are immune cells made

A

bone marrow and thymus , b cells mature in bone marrow , t cells in thymus

78
Q

primary lymphoid organs

A

where immune cells are made (bone marrow and thymus )

79
Q

secondary lymphoid organs

A

where immune responses are initiated, lymph nodes, spleen

80
Q

IFNa IFNb

A

released by virally infected cells

81
Q

danger

A

signals indicating there is harm to the body and or infectious agents are present. DAMPS released from damaged cells and PAMPS released by infectious agents, both recognised by PRR

82
Q

Adaptive immune response activation

A

danger and non-self

83
Q

apoptosis

A

programmed cell death, caspases activated, non-inflammatory, membrane remains intact, energy dependant, individual cells

84
Q

necrosis

A

cell swelling, loss of integrity, groups of cells, no energy required.
coagulative - hypoxia secondary to ischaemia
liquefactive - cell protein wet gangrene
caseous - end result of granulomatous formation (Tb)
gangrenous dry, fat - degradation of fat tissue to chalky

85
Q

pathogens lead to the activation of complement (C1-C9) by one of the 3 pathways

A

classical - C1q binds only if antibodies present for specific antigen (IgM , IgG)
mannose-binding lectin- mannose not present on cells
alternative - C3 spontaneously activates and binds to nearby membranes host cells have control proteins to prevent activation, bacterial cells don’t

86
Q

complement lysis

A

membrane attack complex forms in membrane of bacteria, barrel like structure formed from C6-C9, water rushes in and bacteria swells and bursts

87
Q

opsonisation`

A

label for phagocytosis

88
Q

macrophages

A

good at killing if activated (activated by cytokines especially IFN - y), tissue healing, clearence of dead cells . in skeletal muscle cloak trivial damage to reduce inflammation, splenic clear old and damaged RBCs

89
Q

dendritic

A

poor at killing, initiate adaptive immune responses and take messages to T cells

90
Q

neutrophils

A

killers . NETosis trap pathogens in a net and kills them . neutrophils get into circulation via extraversion rolling along endothelium, diapedisis is it exiting

91
Q

phagocytosis

A

phagocyte detects pathogen and engulfs it forming phagosome, lysosome containing toxic products fuses with phagosome to make phagolysosome

92
Q

B and t cell receptors

A

BcRs recognise antigens in harmful form
TcRs need an antigen broken down into peptides presented to it on an MHC. contain variable regions coded by variable, diversity, joining gene segments. Somatic recombination randomly selects

93
Q

healthy immune system

A

sleep, active skeletal muscle (major source of myokines which support immunity and regulate inflammation)

94
Q

obesity

A

stressed adipocytes release danger signals (pro-inflammatory adipokines (IL1b, TNF) which cause insulin resistance, inappropriate chronic inflammation accelerates cardiovascular and chronic diseases

95
Q

IL-10 and TGF b

A

minimise immune response

96
Q

liable, stable, permanent

A

liable cells divide in homeostasis, stable dont but can in response to injury, permanent never

97
Q

scar formation

A

fibroblast migration and proliferation, extracellular matrix deposition, tissue remodelling

98
Q

inflammations

A

red, pain, swelling, warm. loss of function

99
Q

DAMPs and PAMPs

A

recognised by PRR (inflammation) which releases inflammatory cytokines IL1b and chemokines

100
Q

Things that attract neutrophils

A

coagulation products, complemetns C5a,C8a, IL-8,

101
Q

hyperalgesia

A

pain sensitisation

102
Q

allodynia

A

pain to innocuos stimuli

103
Q

resolution of inflammation

A

IL10, IGF1,TGFb

104
Q

naive, effector, memory T and B cells

A 
naive = never been activated 
effector = activated 
memory = stored
105
Q

B - cells

A

antibody producing cells bind to pathogens and kills them/ mark them for phagocytosis

106
Q

CD8+ CTL

A

kills mutated/infected self cells

107
Q

CD4+ Th

A

organise immune responses and produce different cytokines that can differentiate into Th1, Th2, Th17, Treg

108
Q

polygeny

A

multiple independant genes for each MHC type(MHC seen as non self in transplant reject)

109
Q

polymorphisms

A

multiple variants of each gene within a population

110
Q

MHC

A

Class I - only CD8+ CTLs bind, presents only endogenous antigens (Self)
Class II - only CD4+ Th bind on specialised antigen presenting ADC cells (dendritic) presents only exogenous antigens

111
Q

T cell selection

A

in thymus , ability to bind to MHC - allows survivial (+ve selection)
binds stongly- death (-ve selection)

112
Q

outcomes of chronic inflammation

A

focal scarring - protects. widespread - destroys and can lead to cancer

113
Q

Differentiation, priming, tolerance, trained innate immunity `

A

differentiation (like square root) - maturation with long term changes in function and morphology
priming (wave that keeps going up) - failure of transcription to fully return to baseline after challenge
tolerance - big n small n, failure to reactivate after second challenge
trained innate immunity - small n big n, enhanced response to 2nd challenge after return to baseline

114
Q

ulcer

A

eats away

115
Q

abscess

A

puss surrounded by granulation

116
Q

granulomas

A

organised clusters of mature activated marophages in response to persistant stimulus

117
Q

Antibody Imunoglobulin

A

Ig MADEG

118
Q

Fc receptors

A

receptors for antibodies on phagocyte surface

119
Q

ADCC

A

antibody dependant cell cytotoxicity

120
Q

anti-worm allergy respons

A

mast cells and basophils

121
Q

anaphylactic shock

A

systematic mast cell degranulation

122
Q

naive b cells

A

express IgM and G can be activated to express Ig A and E

123
Q

IgA

A

dimeric, (Fca) found in mucosa, gut and lung, good for neutralising intestinal pathogens and ensuring they’re flushed out, poor at activating complement opsonising ADCC

124
Q

IgG

A

monomeric (Fcy) activation depends on subclass but can oppsonise, neutralise, activate complement ADCC

125
Q

IgE

A

monomeric, (FcE) action depends on subclass can opsonise, neutralise and activate complement ADCC

126
Q

IgM

A

multimer, (FcM) great for trapping neutralising antigen, good at activating complmemnt, bad at ADCC

127
Q

Signal 3 on CD4+ Th

A

Th1 - IFN y - intracellular bacterias and viruses - autoimmunity , IBD
Th2 - IL4 - parasitic worm - allergy
Th 17 - IL17 - extracellular bacteria and fungi - autoimmunity, IBD
Treg - IL10 - suppress immune response

128
Q

Linked recognition

A

CD4 + th only provide help to b cells that recognise same antigen as them

129
Q

what signals for macrophages

A

NK, ILC1,macrophages - —– IFNy —— Th1

130
Q

what signals for eosinophils, basophils, mast cells

A

ILC-2 —— IL5, ILiB —–
eosinophils, basophils, mast cells
Th2 —- IL5, IL3 ——

131
Q

what signals for neutrophils

A

ILC3 —- IL17, IL21

Th 17 — IL 17, IL 22

132
Q

Autoimmunity in T1 diabetes

A

CTL kills islet b cells

133
Q

Which figure is nearer skin thickness 1mm or 100 microns ?

A

100 microns

134
Q

which is more cellualr compartment epidermis or dermis, and which is thicker?

A

More cellular = epidermis

thicker = dermis

135
Q

is melanin soley located within melanocytes

A

No melanin is synthesised in melanocytes but is then passed into the surrounding keratinocytes

136
Q

name the extracellualr components/ molecules of the dermis `

A

collagen, elastin, proteoglycans

137
Q

what cells synthesise collagen

A

fibroblasts

138
Q

mast cells are related to what other cell type

A

basophils

139
Q

what is the predominant cell type of skin appendages

A

keratinocytes

140
Q

when does UVR induced erthyema peak?

A

8-24 hours

141
Q

The UVR induced erythema is due to vasodilation of the blood vessels situated where in the skin?

A

Dermis - none in epidermis

142
Q

if no erythema is present no DNA damage has occures

A

false, damage occurs at any level of irradiation and at levels too low to produce visible erythema

143
Q

what is more likely to induce erythema 320 nm or 390?

A

320 nm longer wavelengths produce less damage

144
Q

what is the mode of inheritence of xeroderma pigmentosum

A

autosomal recessive

145
Q

what causes freckles?

A

focal over production of melanin

146
Q

what is more protective constitutive or facultative?

A

constitutive

147
Q

what type of pigmentation is tanning

A

facultative

148
Q

vitiligo is characterised by

A

aread of hypopigmentation

149
Q

if the ration of eumelanin to phenomelann is low

A

red hair

150
Q

why is melanin synthesised in melanocytes

A

melanin production emits free radicals, by keeping the production compartmentalised away from the rest of the cell, it reduces damage to other cell componenets

151
Q

melanocytes communicate with keratinocytes

A

many keratinocytes per one melanocyte

152
Q

albisinim is inherited

A

autosomal recessively

153
Q

What is the nature of primers used in DNA polymerase chain reaction?

A

Pair of oligonucleotide DNA strands

154
Q

age and immunity

A

As we age we lose NK cell function and this allows viral activation.

155
Q

allergy

A

IgE on mast cells respond to the allergen and cause the cell to degranulate and initiating local inflammation.

Knowledge Test (6 decks)

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