Final stuff lecture 21-30 Flashcards

1
Q

igA

A

-main role - external body surfaces, surface protection of gut, resp and genitourinary tracts

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2
Q

Cytotoxic T cell action

-3 ways of action

A
  • perforin and enzymes
  • hydrolytic enzymes
  • cytokins for apoptosis
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3
Q

Viridian streptococci - lab test

A

Same as strep pneumonia - except

has resistant to optochin sensitivity

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4
Q

3 things that can cause endocardititis

A
  • viridans streptococci - MAinly this!! - peniclin + gentamicin
  • staph aureus - flucoxacillin + gentamicin
  • enterococcus facalis - amoxycillin + gentamicin
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5
Q

Differences between viral, bacterial or protozoa cause of gastroenteritis

A

Bacteiral - may get blood in stool if the bacteria gets into the intestine

  • Colonisation of intestines and the production of toxins
  • clostridium difficle
  • escherichia coli
  • vibrio cholerae
  • Colonisation of intestines invasion of intestinal tissue (may see blood in stool)
  • campylobacter jejuni
  • salmonella
  • escherichia coli
  • toxin produced in food and ingested, no infection - food poisoning (generally short lived, symptoms cleared within 1-2 days)
  • staphylococcus aureus
  • clostridium perfringens

Viral (rota virus, norovirus) - watery dihorrhea

Protozoa - can last for 4-6 weeks

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6
Q

How to diagnose which microbe with gastroenteritis

A
  • Sheeps blood agar - grows most organism (apart from listeria)
  • MAC - e.coli - ferment lactose - goes pink, salmonella, shigella - do not and goes yellow
  • XLD - salmonella and shigella grow
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7
Q

what are the main ones in food?

A

salmonella, campylobacter

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8
Q

Salmonella lab test

A

Gram negative, oxidase negative
-MAC plate - non fermenter - goes yellow

-can grow on XLD agar

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9
Q

Risk factors for pneumonia

A

age less than 2, over 56
chronic lung disease
smoking
immune dysfunction

  • problem with lung innate immune system
  • people are unable to clear the infection
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10
Q

Streptococcus pneumonia

  • where it colonises
  • virulence factors
A

colonises nasopharynx, increase colonisation in winter

Capsule - causes disease
-prevents neutrophil recognition and phagocytosis
-prevents compliment opsonisation
Pili - help to colonise and bind to human cells
-when gets into lungs, it produces a toxin (pneumolysin) and this damages neutrophils and epithelial cells

others

  • choline binding protein on the outside which binds immunoglobulin on epithelial cells and allows entrance into cells
  • Pneumococcal surface protein A helping it bind to epithelial cells and prevents opsonisation

treatment - pencillin IV, macrolides

lab test - same as strept pyogenes but alpha haemolysis

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11
Q

4 clinical features found with pneuomonia

A
  • Increased resp rate
  • crackles when listening to lungs
  • fever/ chills
  • can see on xray - puss in lungs
  • fatigue
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12
Q

5 features of the innate immune system of resp tract that prevent healthy people developing pneumonia

A
  1. ciliated epithelium - removes pathogens from large airways
  2. Mucuous - traps the bacteria, or dust ect. and then can cough it back up so doesnt get into lungs
  3. Lysozyme - has enzymes in it which will kill bacteria
  4. Macrophages in lung - phagocytose material and can get inflammation ocuring
  5. Pamps can be recognised by dendritic cells and then can go on to warn immune system

In mucous can have igA and igE antibodies

  • these serve as a blocking thing and stops bacterial adherence
  • often in resp tissues there are mast cells and these have a high affinity for igE, so are often coated in igE material and antigen/pathogen that associate with these lead to degranulation and releasing molecules that affect blood vessel permeability and are chemotactic for neutrophils and other cells
  • this stops things going in, and also helps the recruitment of non specific mediators through mast cell degranulation
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13
Q

How to diagnose

A

Listen to the lungs - chest expansion for pneumonia decreased, sacs filled with pus, and also can hear crackles

  • if examine someone good enough do not need a chest Xray
  • sputum culture
  • blood culture
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14
Q

Dealing with viral infections

A
  • First thing made is interferon (released by virally infected cells to signal to other cells to induce as state to become less able to be infected by viruses)
  • these up regulate NK activity
  • also then get cytotoxic T cells - to kill these cells infected with viruses
  • then we have the antibodies developing later on and these can prevent re infection and viruses from spreading from cell to cel
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15
Q

peritonitis signs and symptoms

A
Fever
increased heart rate 
Increase resp rate
nausea and vomiting
diffuse abdominal pain that may become localised
rebound tenderness
abdominal wall rigidity 

increase blood leukocytes
fluid accumulation, inflammation

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16
Q

What are the main bacteria when there is peritonitis

  • what lab tests
  • how to treat?
A

Bacteriodetes fragilis (anerobic)
E.coli (mac agar - ferments lactose - pink colonies)
Enterococcus

Metronidazole - b. fragilis
ampicillin - enterococous

17
Q

How body responds to Live attenutated vaccines vs innactivated vaccines

A

Live virus vaccine - cytotoxic t cells, antibodies

  • while viruses or bacteria - (influenza, pertussus)
  • Protein based vaccines (toxoids - tetanus) - T cell dependent
  • Polysacharide based vaccines - t cell independent (s. pneuomniae vaccine)
  • Recombinant vaccines (hep B
18
Q

passive immunity with tetanus who is most likely to get disease

A
  • will nuetralise the toxins, no tprotected agaisnt another attack
  • children - no passive immunity from mother
19
Q

Bordetella pertussis - whooping cough

A
  • gram negative bacillis
  • vaccine preventable
  • highest mortality in first year of life
  • highly contagious, household spread
  • is spread by aerosol droplets and is very infectious
  • catarrhal phase- 1 to 2 weeks - runny nose, conjunctival injection, malaise
  • Paroxysmal phase - short expiratory burst of rapid coughs, then inspiratory gasp and high pitched whoop
  • convalescent phase - weeks- months

Complications
-can get secondary bacterial infections such as pneumonia

Treatment - antibiotics are useful, erythromycin can shorten the corse of illness and also make you less infective later on

vaccine - Now we use an acellular vaccine

  • consists of a number of virulence factors
  • very effective, however need 3 donese and then 2 booster doeses (hard to get people to come back and get booster doses)

-however can get it when you are adults later on

20
Q

Measles

A
  • highly infectious
  • red dots, also can have rash on their inner lip
  • conjunctivities, fever, rash
  • can get secondary infections quite commonly
  • Need two doses

MMR - 15 months, 4 years

21
Q

viral agents that can cause meningitis

A

-herpes simplex, enterovirus

22
Q

conjugate vacine example

A

HiB - haemophilus influezna type b

  • polyscharide added to a carrier protein
  • taken up by b cells
  • carrier protein digests antigen, presents to t helper lcels
  • convertsa t cell independt carb antigen to a t cell depeneidn
  • good immunogeniciity in those less than 2
  • good production of memory cells
  • given at 6 weeks, 3 months, 5 mothsn , 15 months
  • mostly eradicated disease
23
Q

Meninigicocal vaccine

A

also is a recombinant vaccine

24
Q

what does t17 do?

A

mucosal immunity and promote inflammatory processes

25
Q

interferons

A

Interferons - induce transient antiviral state, activate NK activity, upregulate HLA expression (improves cytotoxic T cell killing)

26
Q

what happens to b and t cells when we get increased or decreased igG or igM

A
  • can also depend on levles of igG and igM - high levels of igM can promote B cells, weather high conc of igG tend to diminish b cells
  • igM - want to make more to respond, and when have lots of igG have more memory cells so dont need to make as many
27
Q

Nervous system interacting with Immune system

A

have autonomic nervous system interacting with the endocrine system and immune system

  • get increase body temp, slow wave sleep, promote illness behaviours
  • IL-1 acts on vagus nerve branches and has neurotransmitter activity
28
Q

Nervous system interacting with Immune system

A

have autonomic nervous system interacting with the endocrine system and immune system

  • get increase body temp, slow wave sleep, promote illness behaviours
  • IL-1 acts on vagus nerve branches and has neurotransmitter activity
  • there are sympathetic autonomic nerves inside lymph nodes going into secondary lymphoid organs
  • are in strong influence of T cells
  • norepinephrine communicates with T cells
29
Q

severe combined immunodeficiency

A
  • produces defects in both antibody and cellular immunity
  • causes -genetic
  • widespread effects on immune system

-both low b and t cells

30
Q

hyper igM syndrome

A
  • high levels of igM antibodies but low igG and igA
  • this is because all lymphocytes initially make igM
  • then they switch, but this requires a signal from helper T lymphocytes
  • this occurs when CD40 molecule on the B cell binds its ligand on the T cell
  • patients can have a mutation in the CD40 ligand molecule so cant make the switch
31
Q

selective igA deficiencey

A

lack igA - this is important in mucous membranes lining mouth, airways ect.

32
Q

Complement deficiency syndrome

A

-get infections with certain bacteria such as - neisseria meningitidis, niserria gonorrhoeae

33
Q

Clinical presentations of immunodeficiency

A

type of infection can give a a hint at what immune defect there is.

Extracellular bacteria (e.g streptococci) - igM and igG antibodies, complement, phagocytes

Intraceulluar bacteria (TB) - t cells, macrophages

Viruses (measles) - t cells, igG and igA antivoides, complement, interferon

Parasits - ascaris - t cells, igE, eosinophils, mast cells

Fungi (candidia) - t cells, iga, neutrophils

34
Q

when do you suspect immunodeficiency?

A

-when a patient has recurrent bacterial infections, or infections with unusual organisms

secondary immunodeficinceyc - suspected if patietn is takign steroid, or cytotoxic drugs for other disorders, with known major disease
-lifestyle risk factors for HIV

35
Q

WHAT ANTIBODIES DO !!

A

IGM - blood and lymphatics, effective agglutinator, complement activator, important against blood borne spread infections e.g bacteria

igG - antitoxic antibody, effective barrier against virus infections, protects child when born, bound to phagocytic cells

igA - mucous membranes, fungal infections, gut, respt tract ect.

igD - on outside of antibody, foudn on surface of antigen senstivie naive B cells

igE - trace amounts in blood, binds to mast cells, important for parasitic and allergic reactions

36
Q

Campylobacter and salmonella

A
  • gram negative
  • oxidase positive
  • have a helical shape or curved, not a straight rod - yes
  • growth on hba, no growth on MAC -
  • urease est - negative

salmonella - oxidase negative, growth on lactose fermantion on MAC plate - negative