Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BOD > What I don't know > Flashcards

What I don't know Flashcards

1
Q

What diseases are inflammasomes related to

A

Atherosclerosis, Gout, Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do Weibel-Palade bodies produce

A

P-selectin only.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Angiogenesis is a feature of pathological states in adults, apart from where?

A

Female reproductive tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fibrosis means what

A

Scar formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Types of ficolins

A

M H L ficolins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which complement factor binds sialic acid residues

A

Factor H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where to T lymphocytes arise

A

They arise in the bone marrow but mature in the thymus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AID induced mutation rate

A

1 per 1000 base pairs per cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Anti rhesus IgG antibodies

A

CAN’T agglutinate RBCs or fix complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MHC class I

A

alpha chain is NON-COVALENTLY linked to beta2-microglobulin. Beta2-microglobulin is NOT transmembrane.

Peptides bind MHC class I and II grooves in an ‘extended conformation’. Slightly longer than peptide lengths than 8-9 or 13-25 respectively can bind if they bend in the middle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MHC polymorphism

A

Alleles differ by many amino acids (1-50). This extensive polymorphism is pathogen driven and unique to MHC molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Anchor residues

A

Anchor residues determine the peptide binding motif of a particular MHC molecule.
Review ‘promiscuous’ and ‘fastidious’ binding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MHC numbers

A 
A particular peptide-MHC complexes are present at roughly 100 per cell.
A cell with 1x10^5 MHC class I molecules of a single allotype can present 1000 different peptides.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Major cause of thymocyte death

A

Lack of positive selection. If fail once, alpha chain can be rearranged - multiple opportunities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Thymus dependent antigens

A

APCs that take up antigen will increase MHC class II synthesis and begin to express the co-stimulatory molecules B7.1 (CD80) and B7.2 (CD86).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Linked recognition

A 
Antigen recognised by TCR on naive T cell must be physically associated with the antigen recognised by naive BCR.
Antigen presented on MHC class II on B cell must be the exact same antigen recognised by naive T cell.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IL-4

A

Causes production of M2 macrophages, TH2 cells, IgE production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Anergy

A

T cells: Lack of signal 2.
B cells: High doses of SOLUBLE antigen. High doses of antigen attached to a cell causes negative selection as part of central tolerance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SLE

A

More common in African and Asian women. Causes a butterfly/wolf rash on the face.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

EAE

A

Induced animal model for MS. Inject mouse with myelin basic protein, Freund’s adjuvant, autoreactive T cells. Mouse gets EAE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Autoimmune diseases more common in each sex

A

Females: Graves, Hashimotos’, SLE
Males: Ankylosing spondylitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atopy

A

Predisposed state for type I hypersensitivity. They have IgE 10-100 times normal level.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ABO antigens

A

Core H antigen
A: Terminal N-acetylgalactosamine
B: Terminal galactose

24
Q

Reactive arthritis

A

Type III hypersensitivity. One main mechanism is mast cell degranulation via FCgammaRIIIb binding.

25
Q

Contact hypersensitivty

A

Cutaneous responses to haptens

26
Q

Abacavir hypersensitivty

A

Type IV hypersensitivity due to people possessing HLA-B57

27
Q

Indirect recognition in acute rejection

A

Cross reactivity with donor MHC and peptide. MHC sharing.
Indirect recognition is slower, but adds an extra issue: isogenic grafts can be rejected if donor is male (XY) and recipient is female (XX).

28
Q

Chronic rejection

A

Type 3 hypersensitivity - IgG to allogeneic MHC molecules.

Kidney damage can cause chronic rejection by a non-immune mechanism.

29
Q

Microtoxicity test

A

To determine HLA matching. Revise P.89.

Cross-matching: To determine if there are pre-formed anti-donor HLA antibodies in the recipient.

30
Q

dsDNA viruses replication

A

Input virus as no nucleic acid polymerase. viral DNA alone is infectious.
Exception: Poxvirus. Replicates in cytoplasm so input virus needs to carry its own DNA dependent RNA polymerase. Viral DNA alone is NOT infectious.

31
Q

Polyprotein processing

A

Mainly used by RNA viruses. Eukaryotic mRNAs are monocistronic - they code for a single polypeptide. So for virsues, that long polypeptide must be cut.

Influenza don’t need so much polyprotein processing as its genome has 8 segments.

Retroviruses (+ve ssRNA) use RNA splicing and ribosomal frameshifting instead. Also need polyprotein processing! (gag-pol needs to be cleaved, gp160 made from env needs to be cleaved to gp120 and gp41)

32
Q

Assembly

A

Helical capsid like TMV: Capsomeres added around nucleic acid.
Icosahedral capsid: Genome inserted into ‘empty’ capsids.

33
Q

Which virus has IRES?

A

Poliovirus. Poxvirus don’t have IRES but also cause host cell shut-off by cleaving 5’caps (both host and viral).

34
Q

OAS + PKR

A

Need to be activated by dsRNA.

PKR, OAS, MX all inhibit protein synthesis, BOTH host and viral.

35
Q

Virus-host co-evolution

A

Poxviruses exploit all strategies to interfere with type I interferons.

36
Q

Hydrophobia

A

Rabies

37
Q

Infectious mononucleosis

A

EBV: In children, asymptommatic. In adults, glandular fever (a.k.a infectious mononucleosis).

VAV: In children less severe, in adults more severe.

HAV: 90% of children, asymptomatic. In adults, acute hepatitis with jaundice.

38
Q

Figure 32 P.118

A

Learn again

39
Q

Measles

A

Cell associated virus with HCMV.
Can become persistent in neurones and cause SSPE.
Physically unstable, antigenically stable, only infects humans, lifelong immunity.

40
Q

Influenza virus morphology

A

Spherical shape in a micrograph, but filamentous morphology in clinical isolates (22nm lipoprotein complexes with HBsAg also filamentous).

Viral glycoproteins (HA and NA) are transported to host cell surface independently of the nucleocapsid. Depending on where glycoproteins are transported to, influenza virus buds from the cell apically or basally, former causes local infection in respiratory tract, latter enters tissue and cause systemic infection.

41
Q

Endogenous retrovirus

A

These are retroviruses integrated into germ line cells. Xenografts can cause them to reactivate.

42
Q

How are new HCV virions made

A

Internal budding into the ER, and release by exocytosis.

43
Q

Other lentiviruses apart from HIV

A

Visna, equine infectious anaemia virus, feline immunodeficiency, simian immunodeficiency.

44
Q

Genome of ALL retroviruses

A

+ve ssRNA, with 5’cap and 3’poly-A tail. Genome is diploid, contains tRNA that primes reverse transcription.

45
Q

HIV provirus structure.

A

Provirus genome contains extra LTR at both ends. Promoter in U3 region of left LTR.
Early in infection, there’s heavy splicing to make regulatory proteins like tat and rev. Later on, there’s less splicing to make structural proteins.

HIV budding does NOT kill the cell. Can bud for a long time.

46
Q

Transposons

A

Has insertion sequences on either end.

They enter the main chromosome or plasmids using their own recombination system.

47
Q

Prevent membrane attack complex formation

A

(1) LPS O-antigen, (2) Capsule

48
Q

Neisseria evading host

A

(1) Attach sialic acid to LPS

(2) Antigenic variation: Antigenically distinct pili genes.

49
Q

Aedes aegypti

A

Spreads dengue fever, chikungunya, Zika, yellow fever viruses.
Anopheles transmits plasmodium.

50
Q

Complement deficiency

A

C1,C2,C4: Immune complex disease
C3: Infection with encapsulated bacteria, especially pyogenic ones
C5-C9: Neisseria infection
Factor D and Factor P (properdin): Neisseria infection
Factor I and Factor H: C3 depletion so infection with encapsulated bacteria
DAF + Protectin (GPI-anchored): Paroxysmal nocturnal haemoglobinuria

51
Q

WATCH OUT FOR SPORES

A

They don’t make toxins. So C.tetani SPORES in anaerobic wounds don’t make toxins.

52
Q

Alpha-toxin

A

Made by C.perfringens AND Staphylococcus aureus. Former degrades membrane phospholipids, latter forms pores.

53
Q

Granulocyte

A

Mast cell, basophil, eosinophil, neutrophil.

54
Q

Neutrophil

A

Most abundant WBC but very short lived.

55
Q

VEGF

A

Macrophage release this to recruit endothelial cells in granulation tissue.

56
Q

Sentinel cells

A

Mast cells, Macrophages, Dendritic cells

BOD (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions