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DDT > Trigger 4 > Flashcards

Trigger 4 Flashcards

1
Q

What is Sepsis

A

Rare but serious complications after infection
Blood poisoning
Body attacks itself

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2
Q

Where is IL-1B produced and what does it lead to?

A

Made by macropahges and monocytes

leads to fever, inflammation and pain

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3
Q

Where is IFNy produced and what does it lead to?

A

secreted by lymphocytes

activates macrophages and many other functions

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4
Q

Where is Il-6 produced and what does it lead to?

A

made by T cells and macrophages

lead to fever and acute phase proteins response

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5
Q

Where is TNF-a produced and what does it lead to?

A

secreted by monocytes and others
activates macrophages and endothelium
actiavtes NFk-B
causes fever pain and inflammation

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6
Q

What is systematic inflammatory response

A

serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a subset of cytokine storm, in which there is abnormal regulation of various cytokines.

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7
Q

Where is renin released from and what does it stimulate

A

released from the kidneys

stimulates formation of angiotensin

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8
Q

How is renin released (stimulated)

A

Reduction in arterial pressure –> release renin fomr JG cells
B-1 adrenoceptor responds to systematic nerve stimulation by releasing renin
Mucula densa, sense decrese in Na and Cl in the tubular fluid and stimulate the JG

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9
Q

Describe the RASS system

A

Renin released from kidney, travel in blood to liver
Activates angiotensinogen to angiotensin I
Travel to lungs
ACE cleaves angitensin I to angotensin II
- Travels to the brain, release on ADH
- Travels to adrenal gland, release aldosterone
both act on the kidney

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10
Q

Effect of aldosterone on the kidney

A

increase Na+ absorption

increase water reaborption

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11
Q

Effect of ADH on the kindey

A

Causes aquaporin in the collecting duct

increase water reabsorption

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12
Q

outline the steps of the JAK/STAT pathway

A

Cytokine binds to receptor and the dimerise
dimerisation attracts cytosolic JAK
JAK phosphorylates receptor on TYR residue
STAT recruited via STAT SH2 domain binding to receptor phophoryrosine groups
STAT phosphorylated by JAK
STAT dimer translocates to the nucleus
STAT dimer binds to DNA and activates gene expression

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13
Q

what are the biological effects of ROS

A

react with enzyme sites and stimulate pathways
MAP kinase, PI3 kinase and Jak pathway stimulated by cytokines
ROS may induce receptor clustering
activate nuclear receptors - NFk-B, HIF
Biological consequens - prliferation, apoptosis, cell adhesion, inflammation

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14
Q

Descibe the NFk-B signalling pathway

A

ligand binds to TLR4 - TNFα, IL-1β, ROS, Cocaine, Viral and Bacterial antigens e.g. LPS
Confomational change, PTK binding, Kinase cascade
Cause phosphorylation and actiavtion of IKK (IkB Kinase)
IKK phosphorylates IkB, which is an inhibitor of NFk-B
IkB-P marked for ubinqunation and protesomal degradation
NFk-B translocates to oxidse active cite of Cys
gene transcritpion - prodcution of cytokines
ROS produced, positve feedback

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15
Q

What are PAMPs

A

Pathogen assocaited molecular patterns
Allow the innate immune system to recognize the pathogen
Specific to each micro-organism
Expressed by dendritic cells, macrophages,

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16
Q

What are PRRs

A 
Recognize PAMPs
The PRR are divided in four families:
- Toll-like receptors (TLR)
- Nucleotide oligomerisation receptors (NLR)
- C-type lectin receptors (CLR)
- RIG-1 like receptors (RLR)
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17
Q

What are DRRs/Alarmins

A

released by stressed cells undergoing necrosis that act as endogenous danger signals to promote and exacerbate the inflammatory response.
Initiate a non-infectious inflammatory response.

18
Q

What genes does the NFk-B pathway code for

A

iNOS to generate NO
Cytokines
Adhesion molecules
Important in pro and anti-apoptotic gene regulation

19
Q

What is meningitis

A

inflammation of the meninges and subarachnoid space. It may result from infections, other disorders, or reactions to drugs.

20
Q

Normal chemical and visual levls of the CSF

A 
Appearance: Clear 
Opening pressure: 10-20 cm H 2 O 
WBC count: 0-5 cells/µL (< 2 polymorphonucleocytes [PMN]); normal cell counts do not rule out meningitis or any other pathology 
Glucose level: >60% of serum glucose 
Protein level: < 45 mg/dL
21
Q

Meningitis - streptocouus pneumonia

A

Dipoloid shape
positive gram
70% of acutue bacerial meningitis
Vaccine - pneumoncoccal conjugate vaccine

22
Q

meningitsis - Haemophilus influenza

A

rods or coccobacilli shape
negative gram
eliminated due to vaccine

23
Q

Chemical and visual levls of the CSF for bacterial menigitis

A

Appearance: Clear, cloudy, or purulent
Opening pressure: Elevated (>25 cm H 2 O)
WBC count: >100 cells/µL (>90% PMN); partially treated cases may have as low as 1 WBC/µL
Glucose level: Low (< 40% of serum glucose)
Protein level: Elevated (>50 mg/dL)

24
Q

Chemical and visual levls of the CSF for viral menigitis

A

Appearance: Clear
Opening pressure: Normal or elevated
WBC count: 10-1000 cells/µL (lymph but PMN early)
Glucose level: >60% serum glucose (may be low in HSV infection)
Protein level: Elevated (>50 mg/dL)

25
Q

live vaccines

A

contain a version of the living microbe that has been weakened in the lab so it can’t cause disease.

26
Q

inactive vaccine

A

contains killed disease-causing microbe with chemicals, heat, or radiation

27
Q

Congulated vaccine

A

many harmful bacteria possesses an outer coating of polysaccharides, which disguise a bacterium’s antigens so that the immature immune systems of infants and younger children can’t recognize or respond to them.

28
Q

Subunit vaccine

A

include only the antigens that best stimulate the immune system.

29
Q

Toxoid vaccine

A

used when a bacterial toxin is the main cause of illness.

detoxified bacterial toxin

30
Q

DNA vaccines

A

are experimental vaccines similar to recombinant vector vaccines
DNA injceted into cells so cells machinery synthesis antigens which are expressed on cell surface

31
Q

Describe the pre clinical stages of vaccine production

A

Often lasts 10-15 years
Exploratory phases (2-4 years) identifying natural or synthetic antigens that might help prevent or treat a disease
Pre-clinical stage (1-2yrs) - use tissue-culture or cell-culture systems and animal testing to assess the safety of vaccine and its immunogenicity, or ability to provoke an immune response.
IND application - A sponsor, submits an application for an Investigational New Drug (IND) to the U.S. Food and Drug Administration. Describes the manufacturing and testing processes, summarizes the laboratory reports, and describes the proposed study. The FDA has 30 days to approve the application

32
Q

Describe phase I of a clincical trail

A 
Small study 20 - 100volunteers 
last serval motnhs to a year 
testing 
- dose (gradullay increase)
- side effects 
- body reaction 
- process in body
33
Q

Describe phase II of a clincical trail

A

testing safety, efficacy and side effects
several hundred participants
6 months - 3 years
often randomaised and double blinded
Phase IIa - small number to show safety and efficacy
Phase IIb - establish dose and overal efficacy
- establish inital benefit to risk ratio

34
Q

Describe phase III of a clincical trail

A

test efficacy and adverse reactions
300 - 3000 volunteers who have the condition
1 - 3 years
randomaised and double blind trail
Phase IIIa - evidence of efficacy, saftey and side effects
Phase IIIb - after drug has been submitted for marketing approval, compare to current treatments and use in additional populations

35
Q

what is the arachidonic acid pathway

A

inflamation mediated by unsaturated factty acids
production of prostaglandins
tissue specific pathway

36
Q

describe the arachidonic acid pathway

A

Cell damage, platelets, fribroblast
Trigger phosolipase A2, phosphorylated
Cuts phosolipids, produces prescusour - Arachidonate
Cox enzymes cut it and produces precusors - cyclo endoperoxides, e.g PGG2 –> PGH2
make tissue specific

37
Q

decribe the role of COX enzyme

A

Cox enzymes cut arachidonate and produces precusors - cyclo endoperoxides
COX1 - expressed at all times
COX2 - only induced in certain inflammation pathways

38
Q

encisanoids/prostanoids produced in Platelets

A

precusors male thromboaxin

key molecule in platelet adhersion

39
Q

encisanoids/prostanoids produced in vascular endothelium

A

prostacyclan
vasdilation and Gas signalling
produce PGD2 (vasodilator) and PGF2a (vasoconttictor) in smooth muscle

40
Q

encisanoids/prostanoids produced in Leukocytes

A

Leukotrines

key molescule in chemotaxin and bronchoconstriction

41
Q

What do NSAIDS do

A

Block Cox enzymes

inhibts gastric acid secretion and promotes mucus secretion

DDT (10 decks)

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