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FoCM > Week 4 > Flashcards

Week 4 Flashcards

1
Q

Enterococcus faecalis

A

Gram positive Cocci
Normal flora in gut
Highly resistant, including vancomycin

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2
Q

Gram Positive Cocci

A

Strep. pyogenes (group A)
Strep. pneumoniae
Strep. viridans (normal flora)

Staph. aureus
Staph epidermidis (normal flora)

Group B beta-hemolytic strep: Strep. agalactiae

Enterococcus faecalis

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3
Q

Central tolerance

A

Deletion of self reactive clones of lymphocytes - negative selection

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4
Q

Peripheral tolerance

A

Lymphocyte interacts with antigen –> no subsequent response

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5
Q

Clonal anergy

A

T cell recognize self antigen but no Co-stimulatory signal

Functional unresponsiveness

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6
Q

Regulatory T cells

A

FoxP3, CD25 - markers for regulatory T-cells

Inhibit T cell activation
Inhibit T cell effector functions

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7
Q

Activation induced cell death

A

Apoptosis induced by apoptotic proteins

Death ligands

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8
Q

Receptor editing (B-cell)

A

New light chain rearrangement replacing original VL chain in B cell

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9
Q

Molecular mimicry

A

Normal foreign antigen response cross reacts with self antigen

(Rheumatic fever)

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10
Q

Celiac disease HLA typing

A

95% DQ2
DQ8

Used for diagnostic exclusion

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11
Q

Multiple Sclerosis

A

Autoimmune response against myelin sheath –> demyelination

Animal model: EAE
Transfer disease to healthy animal –> recipient gets disease

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12
Q

Insulin dependent diabetes mellitus

A

Insulitis in islet cells

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13
Q

Rheumatoid factor

A

Autoantibodies against Fc portion of IgG

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14
Q

X-linked agammaglobulinemia

Bruton’s

A

Defect in btk gene, disrupted B cell development

Pro –> pre blocked

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15
Q

Selective IgA deficiency

A

Deficiency in IgA

Anaphylactoid rxn to blood transfusion

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16
Q

Hyper IgM immunodeficiency

A

Lack of CD40L (t cell help)

Elevated IgM and low/no class switching to other Ig’s

X-linked

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17
Q

CVID - Common variable immunodeficiency

A

Immunoglobulin deficiency

B cell and Ig deficiency

Wide variety

Recurrent infection
Lymphoproliferative diseases
Autoimmune cytopenias

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18
Q

DiGeorge syndrome

A

Thymic aplasia:

Thymus doesn’t form –> low T cell count

Hypocalcemia, congenital heart defects

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19
Q

Gamma chain deficiency

A

SCID: Common gamma chain that is subunit of cytokine receptors (IL-2, 4, 7, 9, 15)

T cell and NK cell deficiency

B cell intact (but T cell count affects B cell activation)

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20
Q

Adenosine deaminase deficiency

A

SCID: Severe absence of T cell function

Accumulation of toxic product that kills T cells

T, B, and NK deficiency

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21
Q

Bare lymphocyte syndrome (II)

A

SCID: Lack of MHC class II expression (transcription factor defect)

No CD4+ cells –> B cells affected

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22
Q

Tcell receptor Excision Circles

A

Circular genome that is lost during T cell gene rearrangement - should have large amount as child while making T cells

Screen for TREC to diagnose immunodeficiencies

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23
Q

PAMPS

A

Pathogen associated molecular patterns

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24
Q

DAMPS

A

Danger associated molecular patterns

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25
Q

PRR

A

Pattern recognition receptors

Cell surface & Intracellular

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26
Q

Familial Mediterranean Fever

A

Autosomal recessive

Fever and localized inflammation (skin, serosal membranes, joints)
- Neutrophil infiltration

Day-weeks

Typically resolve, risk of amyloidosis

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27
Q

FMF Genetics

A

MEFV: Encodes pyrin

4 functional domains

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28
Q

PYRIN domain

A

Domain shared by multiple proteins involved in inflammation and apoptosis

Member of intracellular PRR family
- Sense microbial products –> pro-IL-1beta to active form (NALP3)

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29
Q

NALP3 associated autoinflammatory syndromes

A

Mutation in NACHT domain of NALP3 = 3 autoinflammatory syndromes

Autosomal dominant

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30
Q

Familial Cold (Urticaria) Autoinflammatory syndrome

A

Urticaria 30min after cold exposure: IL-1 development

Fever, chill, malaise, joint stiffness, sweating, thirst

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31
Q

Muckle-Wells syndrome

A

Short episodes
Temp change as trigger
Urticaria-like rash: aching

Sensory neural Hearing loss

Higher risk of amyloidosis (25% in N.America)

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32
Q

Neonatal onset multisystem inflammatory disease

A

NOMID

Early onset (infancy)

Rash at birth

  • non pruritic urticaria
  • neutrophilic infiltrate

CNS disease

  • non infectious meningitis
  • Low IQ

Sensory anomalies
-Deafness, optic nerve atrophy

Arthropathy

  • Arthritis during flares
  • Bone enlargement
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33
Q

Anakinra

A

IL-1 blocker

Binds to IL-1R blocking IL-1a and IL-1B

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34
Q

Canakinumab

A

Neutralizes IL-1B

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35
Q

Rilonacept

A

Neutralizes IL-1B and IL-1a

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36
Q

Gout

A

Recurrent attacks of acute inflammatory arthritis (accumulation of uric acid)

Uric acid crystals are DAMPS and result in IL-1 buildup

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37
Q

Chronic Recurrent Multifocal Osteomyelitis

A

CRMO

Recurrent lytic bone lesions with swelling and pain

Fevers, inflammation can spread to tissues

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38
Q

CRMO treatment

A

NSAIDs
Steroids
TNF-inhibiting agents

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39
Q

TNF receptor associated periodic syndrome

A

TRAPS: Autosomal dominant

Long duration of inflammation and fever

Migratory erythematous rash
Myalgias
Conjunctivitis, periorbital swelling

TNF binds –> initiate inflammatory response –> receptors don’t shed and inflammatory response continues

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40
Q

TRAPS treatment

A

Etanercept: TNF receptor analog

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41
Q

PFAPA

A

Common in children

Regular occurring fevers, early age of onset

Cyclic

Aphthous stomatitis, lymphadenitis, pharyngitis

Normal growth and development

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42
Q

Cyclic Neutropenia

A

Inherited form caused by ELA2 gene mutation

21 day cycle

ANC

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43
Q

Severe inflammatory diseases: Cyclic/non cyclic

Resolve/do not resolve by puberty

A

Non cyclic

Do not resolve by puberty

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44
Q

Omenn syndrome

A

2 weeks-3 months

Many symptoms: Erythroderma, alopecia, diarrhea, lymphadenopathy, opportunistic infections

Normal IgG
High IgE
Low IgA, IgM

Maternal T cells remain, expand and GVHD

RAG disorder

BMT therapy

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45
Q

Allergic Rhinoconjunctivitis epidemiology

A

20million americans

10% children, 10-30% adolescents/teens

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46
Q

Quick relief medications for asthma

A

Bronchodilator: Albuterol, xopenex, maxair

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47
Q

Long acting bronchodilators

A

Salmeterol, formoterol

12hr bronchodilation but no anti inflammatory effect

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48
Q

Anti inflammatory medications for asthma

A

Oral corticosteroids, inhaled corticosteroids, leukotriene blockers

Decrease airway inflammation - long term use results in improved disease control

49
Q

Telodendria

A

Branching at end of axon

50
Q

Epineurium

A

Death connective tissue surrounding nerve

51
Q

Perineurium

A

Surrounds bundle of nerve fibers

52
Q

Endoneurium

A

Loose connective tissue, surrounds individual nerve fibers

53
Q

Function of multipolar neurons

A

Motor

54
Q

Function of bipolar neurons

A

Special sensory

55
Q

Function of unipolar neurons

A

Sensory system

56
Q

4 functions of glial cells

A
  1. Surround neurons and hold them in place
  2. Supply nutrients and oxygen
  3. Insulate one neuron from the other
  4. Destroy and remove dead neurons
57
Q

Oligodendrocyte

A

Form myelin sheath in CNS

58
Q

Astrocytes

A

Induce blood brain barrier phenotype

Maintain chemical environment for generation of nerve impulses

Scaffolding

Scar formation

59
Q

Microglia

A

Phagocytes of CNS

Microglial nodule when virus infects

60
Q

Ependymal cells

A

Cuboidal to columnar cells arranged in single layer that possess microvilli and cilia

Line the ventricles of the brain and central canal of the spinal cord.

61
Q

Sympathetic opthalmia

A

Ag sequestration in eye –> damage leads to released Ag –> Tgcells activated and attack antigen in both eyes

62
Q

IFN-gamma and autoimmune diseases

A

IFN-gamma induces MHC class II molecules to be presented —> MHC II may present sequestered AG which can induce a response

63
Q

Goodpasture’s syndrome

A

Type II hypersensitivity

Abs bind to type IV collagen on basement membranes of kidney and lung

64
Q

Classic neurotransmitters

A

Contained in small vesicles, located in active zone

65
Q

Dense core vesicles

A

Contain neuropeptides

Located further back from active zone

66
Q

Synapsins

A

Vesicle associated proteins

Tether vesicle to cytoskeleton

67
Q

Docking complex

A

Voltage gated Ca channel and additional proteins

68
Q

Vesicle storage and release

A

Vesicles sequestered in storage compartment and releasable compartment

Ca influx moves storage vesicles to release zone, with help of Rab3A

69
Q

Fusion pore

A

Similar to gap junction, opening associated with electrical signal

Much faster response

70
Q

Synaptic vesicle recycling

A

Vesicles release neurotransmitters –> Fused membrane coated in dynamin and clatharin –> taken to early endosome and recycled

71
Q

Ionotropic receptor

A

Ligand gated receptor

Direct receptor channel coupling

72
Q

Metabotropic Receptor

A

G protein mediated receptor channel coupling

Second messenger mediated receptor/channel coupling

73
Q

End plate potential

A

EPP: evoked in muscle cell and triggers PSAP and muscle contraction

Super threshold for muscle contraction, safety factor

150-200 quanta released

74
Q

MEPP

A

Miniature end plate potential

Constantly happening, spontaneous release of ACh

Many MEPPS can result in AP

75
Q

Myasthenia gravis mechanisms

A
  1. Bind to ACh receptor and block binding and receptor activation
  2. Promote endocytosis of ACh –> AChR degradation
  3. Destroy Postsynaptic surface, less AChR’s
76
Q

Lambert-Eaton Myasthenic syndrome

A

Presynaptic disease

Reduction of Voltage gated calcium channels (Immune attack)

Weakness improves with activity

Treat with aminopyridines

77
Q

Clostridial neurotoxins

A

Botulinum toxin A: Botox

Botulinum toxin B: Myobloc
- weaken nerve muscle 4-6months

Bind and cleave SNAP 25 (docking zone protein)

78
Q

Clostridium tetani

A

Passes retrograde along nerve fibers

Inhibits inhibitory neurons that control spinal motor neurons and brainstem excitability

Attacks synaptobrevin

79
Q

Wired transmission

A

Direct connection between pre and post synaptic neurons

80
Q

Volume transmission

A

Release site of neurotransmitter is some distance from target cell

Slower onset, longer effect

81
Q

CNS cessation of neurotransmitters

A

Diffusion

Re-uptake into glial cells and synaptic terminal

82
Q

Retrograde neurotransmitter

A

Messenger that goes from post synaptic cell to presynaptic cell and induces further neurotransmitter release

83
Q

LTP requirement

A

Protein synthesis

84
Q

Pre-synaptic inhibition

A

Inhibitory neuron contacts the terminal of a second presynaptic neuron

Released NT by inhibitory neuron depresses calcium current –> reduces NT release by presynaptic cell

85
Q

Presynaptic facilitation

A

Facilitating neuron enhances release of NT by other presynaptic neuron

86
Q

Squamous metaplasia: Smokers

A

Ciliated columnar –> stratified squamous

87
Q

Desmoplasia

A

Way connective tissue respond to neoplasms

Collagenous stroma laid down by desmoplastic fibroblasts

88
Q

Nicotine

A

AChR agonist

89
Q

Physostigmine

A

AChE inhibitor

90
Q

D-tubocurarine

A

Competitive inhibitor of AChR

91
Q

Tetrodotoxin, Saxitoxin

A

Blocks Voltage gated Sodium channels

92
Q

Conotoxin

A

Blocks Voltage gated calcium channels

93
Q

Succinylcholine

A

AChR agonist

Inactivates end plate sodium channels, desensitization of AChR

94
Q

Organophosphate compounds

A

Irreversible inhibition of AChE

95
Q

4 mechanisms of Calcium level regulation in nerve terminal

A
  1. Binding to proteins (calmodulin)
  2. Na symport channel
  3. Active transport out
  4. Sequestration
96
Q

EPSP

A

Fast - ionotropic receptors that pass NA and K

Inward current = depolarization of postsynaptic membrane

Magnitude proportional to amount of NT released

97
Q

IPSP

A

Fast - ionotropic GABA and Glycine receptors

Increase Cl- conductance into cell (hypoerpolarization)

Or increased K permeability = hyperpolarization

98
Q

ATP depletion

A

Reduced Oxygen - ischemic damage

Mitochondrial damage

Failure of Na/K pump

Disruption of translational machinery

Shift to anaerobic glycolysis –> decrease in pH

99
Q

Elevated cytosolic Ca2+

A

External: failure of Ca pump
Internal: release from mitochondria/ER

Enzyme activation
Disruption of mitochondria membrane potential

100
Q

Oxidative stress

A

Reactive oxygen species: Superoxide, H2O2, hydroxyl radical

ROS scavengers: Vit C and E
Enzymes - superoxide dismutase, catalase, glutathione peroxidase

101
Q

Loss of membrane integrity

A

ATP depletion
Increased Ca
Increased protease activity

102
Q

Protein misfolding

A

Unfolded protein response activated

Unresolved = apoptosis

103
Q

Genotoxic stress

A

p53 transcription factor activation

Cell cycle arrest

Apoptosis

104
Q

Necrosis

A

Damage exceeds repair capacity

Cells swell, leaky membranes, nuclear changes

Due to energy failure

105
Q

Coagulative necrosis

A

Injury causes protein denaturing - infarct

106
Q

Liquefactive necrosis

A

Hydrolytic enzyme release

Focal infections, brain infarcts

107
Q

Caseous necrosis

A

Focal infection and immune response

TB, histo

Granuloma

108
Q

Fat necrosis

A

Focal destruction of fat

Acute pancreatitis

109
Q

Gangrenous necrosis

A

Dry: ischemia, distal limb
Wet: Superimposed bacterial infection
GasL Deadly form, anaerobic bacterial infection

110
Q

Apoptosis

A

Intrinsic: Injury to mitochondria induced

Extrinsic: Growth factor trigger

111
Q

Necroptosis

A

Hybrid of necrosis and apoptosis

TNFR ligation

112
Q

Pyroptosis

A

Self destruct
Capase-1
Pro-inflammatory signals released

113
Q

Neonatal diabetes mutations

A

Kir6.2

SUR1

114
Q

Kir6.2 mutation

A

Decrease ability of ATP to bind to K-ATP channel

No insulin release

115
Q

SUR1 mutation

A

Increase Mg2+ and ADP to bind

Stops ATP binding

116
Q

Myotonia Congenita

A

Defect in Cl- conductance, slow repolarization after AP –> chance for repeated AP’s and thus constitutive muscle contractions

117
Q

Bladder metaplasia

A

Transitional –> Squamous

Stones

118
Q

Esophagus metaplasia

A

Squamous –> Columnar

Reflux

119
Q

Dysplasia

A

Pre-neoplastic change

Cellular atypia: Aberrant mutation, enlarged nuclei, nuclear hyperchromasia

FoCM (6 decks)

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