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Unit 3 HDC > HDC LGS > Flashcards

HDC LGS Flashcards

1
Q

Distinguish between Immunogen and Toleragen and their immune responses

A

Immunogen - something you want the body to repsond to and lead to inflammation
Toleragen - something you don’t want to activate an immune response

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2
Q

What is the failure of tolerance to self?

A

Autoimmunity

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3
Q

Explain the pathogenesis of Autoimmune polyglandular syndrome (APS-1)/ APECED

A

AIRE gene mutation - Finn-major R257X mutation - nonsense mutation that results in premature stop codon and nonfuncational AIRE –> reduced expression of peripheral tissue antigens in the thymus –> defective elimination of self-reactive T cells –> T cells leave thymus and react with peripheral antigesn that weren’t properly presented

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4
Q

Clinical features: generalized tonic-clonic seizures, recurrent oral ulcerations, dental problems, delayed growth, prolonged diarrhea, proptosis, pigmentation of lips and tongue, fingersnails yellow and mottled

A

Parahypothyroidism due to Autoimmune polyglandular syndrome (APS-1)/ APECED

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5
Q

Explain the pathogenesis for Immune-dysregulation polyendocrinopathy, enteropathy, X-linked (IPEX)

A

FOXP3 mutation –> deficiency of T regulatory lymphocytes

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6
Q

Clinical features: child with consanguinous parents, diarrhea, malnutrition, failure to thrive, hx of Celiac disease, failed to response to gluten free diet.

Height and weight < 5th percentile, hepatomegaly, eczematous dermatitis on trunk and extremities

Labs: increased liver enzymes (AST/ALT), increased glucose, anemia

Treg lymphocytes at 0.03% of all CD4+ T cells (normal = 4.4%)

A

Immune-dysregulation polyendocrinopathy, enteropathy, X-linked (IPEX) disorder

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7
Q

How does the development of Central T cell tolerance differ from Central B cell tolerance?

A

T cell Central Tolerance - T cells undergo negative selection –> Medullary thymic cells present AIRE proteins (self-antigens) to T cells –> T cells with abnormal affinity undergo apoptosis (small percent become Tregs), T cells with normal affinity go on to become naive T cells

B cell Central Tolerance - Mature B cells presented with self-antigen in bone marrow –> Receptor editing - reexpression of RAG, resume light chain recombination of VJD, express new Ig light chain

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8
Q

How does the development of Peripheral T cell tolerance differ from Peripheral B cell tolerance?

A

Peripheral T cell tolerance - mature T cell recognizes self-antigen –> Treg induces suppression of T cell

Peripheral B cell tolerance - mature B cell recognizes self-antigen –> deletion (apoptosis) or anergy (functionally unresponsive)

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9
Q

What are some mechanisms by why infection may promote development of autoimmunity?

A

increase of PAMPS & DAMPS, or self-antigen mimicry

Activation of tissue APCs –> self-reactive lymphocytes bind and activate –> self-reactive lymphocytes present self-antigen to B cells –> formation of antibodies –> increase of inflammatory cytokines

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10
Q

Explain how a genetic deficiency of complement proteins (C1q or C4) may lead to autoimmunity in the context of self-tolerance failure

A

Deficiencies in complement proteins –> no clearance of necrotic debri –> sustained exposure of debri to immune system –> allows opportunity for autoreactive lymphocytes to engage with antigens

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11
Q

Describe the clinical manifestations of Sjogren syndrome.

A

Fatigue, arthralgia
Dry eyes - “feels like dirt/sand in eyes”
Dry skin
Dry mouth - may have difficulty swallowing, poor dentition

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12
Q

Explain the pathogenesis of Sjorgen Syndrome and the laboratory tests used to confirm it

A

Autoreactive lymphocytes triggered by infection –> local cell death –> release of tissue self-antigens –> Increased activation of autoimmunity –> lymphocytic infiltration –> destruction of salivary and lacrimal glands

Non-specific tests: ANA, RF, ESR/CRP, Anti-Sm
Specific: Anti-Ro, Anti-La

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13
Q

A patient diagnosed with Sjogren syndrome turns out to be pregnant. What are the possible complications?

A

Fetal fibrosis of the heart

Maternal Ro IgG antibodies cross placenta –> IgG inhibits physiologic clearance and binds to macrophages –> secretion of TGF-B and TNF and hypoxia induce myofibroblast formation of the heart

Unsure how much detail of this we need to know

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14
Q

You and a friend are skiing in Colorado when you see their hands with well demarcated areas of lightening color, loss of vasular color to digits, and cyanosis.

What is the likely syndrome and what is it typically caused by?

A

Raynaud’s phenomenon - vasoplastic response to cold weather –> decreased blood flow to extremities –> ischemia

Can be idiopathic, but commonly associated with underlying diseases, medications or hyperviscocity

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15
Q

Outline CREST syndrome

A

Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerofactyly, Telangiectasia

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16
Q

Systemic Sclerosis is a response from which three interrelated processes

A

Autoimmune response, vascular damage, collagen deposition

Autoimmunity - CD4+ T cells respond to unidentified antigen
Vascular damage - repeated yccles of endothelial injury follows by platelet aggregation –> release of factors that trigger endothelial proliferation
Collagen deposition - fibrosis

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17
Q

How do you distinguish Systemic Sclerosis from other autoimmune disorders?

A

Striking cutaneous changes

Diffuse SS - initial widespread skin involvement with rapid progress, early visceral involvement
Limited SS - mild skin involvement, late involvement of viscera, CREST syndrome

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18
Q

Why is it important to always rule out GAS when a viral or bacterial infection is suspected?

A

Group A Strep can cause Rheumatic Fever

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19
Q

Outline the sequence of events in a typical Type I hypersensitivity reaction

A

Initial exposure - Allergen (Ag) recognized by APC –> APC binds to Ag –> APC binds MHC II receptor to CD4+ TCR and displays Ag –> T cell activation –> T cell binds to activated B cell receptor –> CD40L bind to CD40 for costimulation –> IL4 and IL13 released for IgM change to IgE antibodies –> FcE receptor of IgE antibodies bind to mast cell/basophils –> sensitized mast cell/basophils –> Fab portion open for future Ag binding

Re-exposure - Ag binds Fab portion of IgE antibody on sensitized mast cell/basophil –> crosslinking of IgE antibodies –> degranulation of mast cell –> histamine release –> bronchoconstriction, vasodilation, vascular permeability –> fluid leak into superficial dermis causing wheals and flares (urticaria)

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20
Q

Food, medication, and insect sting allergies are what type of hypersensitivity

A

Type I

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21
Q

Outline the pathophysiology of a Type II hypersensitivity

A

Antigen bind to cell-surface molecule –> antibody binds to antigen through Fab portion –> cell targeted as pathogen –> 4 different paths:

  1. Complement binds to Fc region of antibody –> MAC complex activation –> MAC breaks down cell wall –> cell lysis –> cell destroyed
  2. Complement binds to Fc region of antibody –> C3b actiation –> recruits phagocytic cells –> opsonization –> cell destroyed
  3. Complement binds to Fc portion of antibody –> C5a activation –> stimulation of neutrophil chemotaxis –> neutrophils release peroxidase –> cell destroyed
  4. Antibody binds to receptor on NK cell –> NK releases enzymes –> antibody-dependent cell mediated cytotoxicity (ADCC) –> cell destroyed
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22
Q

What are some diseases that can be caused by Type II Hypersensitivity?

A

From RBC destruction:
Autoimmune hemolytic anemia, ITP, Acute hemolytic transfusion reaction, erythroblastosis fetalis

From inflammatory mediators:
Good pasture syndrome - targeting type IV collagen in lungs and kidneys
Rheumatic fever, Hyperacute transplant rejection

From issues with receptor binding:
Myasthenia Gravis - IgG antibodies binding to Ach receptors
Graves disease - IgG antibodies bind to and overstimulate TSH receptors on thyroid follicle causing overproduction of thyroid hormone

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23
Q

Discuss how a Type III hypersensitivity can cause tissue injury and disease

A

Ag free floating in blood –> IgG antibody binding –> formation of Ag/Antibodies complexes –> deposited into endothelium, tissues, joints, kidneys –> extreme complement activation –> large amounts of C3a, C4a, C5a released –> vascular permeability, neutrophil chemotaxis –> edema, lysosomal destruction of tissue

Diseases:
Polyartheritis nodosa - deposition in vasculature
Post-strep golmerulonephritis - deposition in kidneys
Systemic Lupus - deposition in kidneys
IgA nephropahty
Hypersensitivity pnueumonitis - deposition in lungs

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24
Q

What is Serum Sickness and what type of hypersensitivity is it?

A

Creating antibodies to an antitoxin or antivenom upon initial exposure –> re-exposure to antitoxin or antivenom –> systemic immune complex formation

Type III

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25
Q

List examples of disease caused by T cells and differentiate the CD4+ ones from CD8+ ones

A

Type IV hypersensitivity reactions -
CD4+
Initial exposure of Ag through epithelial cells –> Ag binds to protein –> APC presents Ag to naïve T cell –> CD4+ T cell binding MHC II –> release of IL-12 –> stimulation of Th1 differentiation –> Th1 release of IL-2 and IFN-y –> not as big a reaction
Re-exposure –> pre-formed T cells (memory response) –> increased release of IFN-y by Th1 –> macrophage activation –> larger inflammatory response
Disease: Allergic Dermatitis

CD8+
APC presents Ag on MHC I –> CD8+ T cell activation and proliferation –> CD+ T cells target cells expressing Ag –> release perforins and granzymes –> cell lysis –> cause of most inflammation and tissue damage on re-exposure
Diseases:
Multiple Sclerosis - CD8+ T cells target oligodendrocytes
IBD - targeting pancreatic cells
T1DM - targeting pancreatic cells
Hashimoto Thyroiditis - targeting thyroid tissue –> hypothyroidism

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26
Q

How do you distinguish between Type II and Type III hypersensitivies?

A

What is the primary target?
Is the antibody/antigen complex targeting a specific tissue, or is there just a predisposition for deposition?

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27
Q

What is the immediate treatment for anaphylaxis and it’s MOA?

A

Epinephrine injected into lateral thigh

Agonist for adrenergic alpha receptors –> causes vasoconstriction
Agonist of adrenergic beta receptors of the lungs –> bronchodilation

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28
Q

What is the criteria for anaphyalxis?

A
  1. Skin reaction + respiratory involvement or hypotension
  2. Any two organ systems involved
  3. Hypotension alone is exposure to allergen is known
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29
Q

A patient presents to urgent care three days after starting TMP-SMX for a UTI. They have an widespread erythematous rash you believe to be exanthematous drug eruption. What is the likely cause?

A

Delayed hypersensitivity reaction due to the Sulfa in TMP-SMX

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30
Q

Why should patients always be tapered off of long-term glucocorticoids?

A

To reduce risk of adrenal insufficiency

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31
Q

What is the MOA of glucocorticoids?

A

Anti-inflammatory - decreases proinflammatory gene transcription and inhibit PLA2
Immunosuppressive - cytotoxic to leukocytes

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32
Q

What is the MOA of antihistamines?

A

Inverse agonist - competes with active site and gets the opposite effect

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33
Q

What is the biggest difference between the first and second generation of antihistamines?

Which generation should be given to children?

A

First generation crosses the BBB –> can lead to sedative effect (Benadryl)

Second generation

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34
Q

A patient presents to the clinic with fever, bullae and peeling skin over < 30% of their body. They have a positive Nkolski sign and mentioned they recently switched their seizure medication.

What is the likely cause and how do you treat it?

A

Likely cause: Type IV hypersensitivity to drugs
SATAN drugs most common
Sulfa, Allopurinol,Tetracyclines, Anticonvulsants, NSAIDS

Treat with: infeciton contraol, skin grafting, pain management, steroids

Disease is Steven Johnson Syndrome

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35
Q

What are the classic clinical findings of seasonal allergies, and what type of hypersensitivity are they?

A

Mildly erythemetous conjunctiva
Boddy pale to bluish nasal turbinates
Postnasal drainage
Mild tenderness of frontal and maxillary sinuses

Type I hypersensitivity

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36
Q

What type of medication do you avoid giving to someone with Karposi Sarcoma?

A

Corticosteroids - increases the replcation of the virus

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37
Q

What are some of the PREP and PEP access issues?

A

Cost barriers
Provider Reluctance (lack of training, time restraints)
HIV stigma
Legal challenges

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38
Q

Drug interactions with amphotericin B

A

Chemotherapy drugs, vancomycin, aminoglycosides
Anti-HTN drugs (lowers BP)

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39
Q

Adverse effects of amphotericin B

A

Acute: Rigors syndrome, electrolyte abnormalities, hypotension
Seizures if given intrathecally

Delayed: Nephrotoxicity

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40
Q

Which fungi forms a spherule with endospores?

A

Coccidioides immitis

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41
Q

Label the fungi for each geographic location

A

Orange - coccidioimycosis
Blue - Histoplasmosis
Green - blastomycosis

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42
Q

Which fungi is often associated with bat/bird droppings?

A

Histoplasma Capsulatum

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43
Q

What class of medications can cause hepatotoxicity due to its interactions with CP450?

A

Azoles

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44
Q

What medication is typically used for aspergillis and candidiasis, and what’s the MOA?

A

Echinocandins - blocks B-1,3-glucan synthase –> stops formation of B-1,3-glucan –> prevents cell wall formation

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45
Q

What fungi is the exception to the “mold in the cold, yeast in the heat” rule?

A

Candida - yeast at 25, mold at 37

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46
Q

Which disease has a characteristic rash described as “Sea of Red with Islands of White”?

A

Dengue fever

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47
Q

What is the case definition of Dengue fever?

A

2 or more in febrile person who traveled to or lives in endemic area:
N/V
Rash
Aches/pains
positive tourniquet test
leukopenia

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48
Q

What is the case definition of severe Dengue?

A

Any of the following symptoms:
Severe plasma leakage –> shock or fluid accumulation
Severe bleeding
Severe organ impairment
impaired consciousness
heart impairment

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49
Q

Explain the difference between Jungle, Urban and Intermediate transmission styles for Yellow fever

A

Jungle: mosquito –> primate –> mosquito –> primate
Urban: human –> mosquito –> human –> mosquito
Intermediate: human –> mosquito –> primate –> mosquito

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50
Q

What are the four Zika transmission routes?

A
  1. Mosquito to human
  2. Human to mosquito
  3. Mother to baby in utero
  4. Sexual transmission
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51
Q

What a mosquito infected with West Nile bites a human or other mammal, what are they called?

A

Dead end hosts - cannot be passed on to other mosquitos

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52
Q

What is the most significant variable that determines the severity of a parasitic infection?

A

Parasite burden

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53
Q

Outline the different forms of the life cycle of the malaria species

A

Ring (thin rings inside RBC) –> Trophozoite (variable shape) –> Schizont (cell filled with replicants, mini parasites) –> Gametocyte

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54
Q

Which malarial parasite replicates in young RBC?

A

P. vivax

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55
Q

Which malarial parasite replicates in old RBC?

A

P. malariae

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56
Q

Which malarial parasites causes the RBC to become enlarged?

A

P. ovale

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57
Q

How does Cloroquine treat malaria?

A

Induces breakdown of heme –> parasite needs heme to form hemazoan

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58
Q

How does Ato-Pro treat malaria?

A

Ato - disrupts electron transport in plasmodium
Pro - dihydrofolate reductase inhibitor

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59
Q

What medication is contraindicated for G6P deficient patients and why?

A

Primaquine/tafenoquine
Pts can’t neutralize free radicals

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60
Q

Small eye, larger than RBC = T. [ ]

A

Brucei

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61
Q

Large eye, smaller than RBC = T. [ ]

A

cruzi

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62
Q

What are the treatments for West African Trypanosomiasis

A

Early - Pentamidine
Late - Eflomithine

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63
Q

What are the treatments for East African Trypanosomiasis

A

Early - Suramin
Late - Melarsoprol

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64
Q

What disease is it common not to have acute symptoms?

A

Chagas (T. cruzi - American Trypanosomiasis)

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65
Q

What is Romana sign and what disease is it associated with?

A

Elastic edema of the upper and lower eyelids, chmosis of th econjunctiva, and enlargement of the ipsilateral lymph nodes

Pathogneumonic for T. cruzi

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66
Q

What type of hypersensitivity reaction is Romana sign?

A

Type II - antibody and antigen - lysis of cells holding the organism

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67
Q

What parasite only replicated in cells of infected tissues?

A

T. cruzi

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68
Q

What parasite shows tetrad figures in RBC?

A

Babesia

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69
Q

Name the hosts, vectors and reservoirs of Babesia

A

Primary reservoir - field mouse
Vector - Ixodes tick
Host - human
Incompetent host - Deer - host of where tick grows

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70
Q

How do you calculate sensitivity and specificity?

A

Sensitivity = A/(A+C)
Specificity = D/(B+D)

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71
Q

How do you calculate PPV and NPV?

A

PPV = A/(A+B)
NPV = D/((C+D)

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72
Q

How do you calculate Case Fatality Rate?

A

(Death/cases) * 100

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73
Q

How do you calculate Attack Rate?

A

(cases/number of people exposed) * 100

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74
Q

What does normal staph flora release to rid bad staph from the body? How does it work?

A

Lysostaphin

Degrades the crossbridge of the cell wall

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75
Q

Explain the difference between simple stain and negative stain

A

Simple stain - stains bacteria with basic dye
Negative stain - stains background with acidic dye

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76
Q

What is the Schaeffer-Fulton method?

A

Endospore stain

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77
Q

Differentiate between selective, differential and enriched media

A

Selective - testing for specific properties
Differential - determining which bacteria can/can’t do something
Enriched - enriching media to help specific bacteria grow

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78
Q

What antibiotic interferes with CP450 enzymes, and thus can’t be used with medication that need CP450 metabolism?

A

Macrolides - Erythromycin and Clarythromycin

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79
Q

What is the role of the innate immune response to the pathogen?

A

Recognize PAMPs and recruit phagocytic cells

First line of defense against pathogens

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80
Q

High nitrate levels in a dipstick urinalysis is indicative of

A

gram negative bacteria

81
Q

PTX3 is detected in concentrations very early in innate immunity because

A

it’s released by epithelial cells as soon as they are in contact with the pathogen

82
Q

Where are TLRs located?

A

On the surface of the cell and within endosomes

83
Q

In mild COVID19, what roles do TLR3/7 play? What roles do TLR2/4 play?

A

TLR 3/7 are antiviral and release Type I/III IFN - covid virus supresses TLR 7

TLR 2/4 are proinflammatory and release IL6, IL8, TNFa

84
Q

Whats a major difference from mild COVID that leads to severe COVID?

A

Mild - rapid IFN response

Severe - Delayed or poor IFN response –> increase of viral replication and auto-IFN antibodies

85
Q

What are the roles of NK cells?

A
  1. Killing of virus infected cells - binding activating receptor to activating ligand
  2. Killing of phagocytosed microbes - macrophage releases IL12 onto NK cells –> NK cell realeases IFN-y onto macrophage
86
Q

Explain how the inhibitory receptor of an NK cell works?

How does it work with viral infected cells?

A

When NK cell binds to normal cell –> normal cell expresses MHC I self peptide complex –> NK cell binds and recognizes self peptide –> not activated

With viral infected cells –> virus inhibits MHC I expression –> NK cell doesn’t detect MHC I receptor –> NK cell activated –> kills cell

87
Q

Where are NOD, Mannose, and DNA/RNA receptors found?

A

NOD - cytosol
Mannone - plasma membrane
DNA/RNA - cytosol

88
Q

Which complement pathway is activated by antibodies?

A

Classical

89
Q

Which complement pathway is activated by the microbial cell surface?

A

Alternative

90
Q

What are the role of C3a and C3b in the complement pathway?

A

C3a - inflammation
C3b - opsonization and phagozytosis

91
Q

What pathogen bind factor H to its surface and induces C3bBb dissociation?

What does this lead to?

A

Borrelia Burgdorferi - Lyme disease

No C3bBb of the alternative pathway –> no formation of C5 convertase –> no MAC complex

92
Q

What are the components of innate immunity?

A

Epithelial barriers, Mast cells, phagocytes, dendritic cells, complement, NK cells

93
Q

What are the components of adaptive immunity?

A

T cells, B cells, antibodies

94
Q

What is the action of T helper cells?

A

IL12 stimualtes Th1 helper - releases IFN-y –> macrophage activation against intracellular pathogens –> plays role in chronic inflammation, granuloma formation

IL4 stimualtes Th2 helper - releases IL4, IL5, IL13 –> eosinophil and mast cell activation –> plays role in allergic reactions

Th17 - releases IL17, IL22 - neutrophil recruitment and activation against extracellular bacteria/fungi –> plays role in autoimmunity

Tfh - release IL21, IFN-y, IL4 –> B cell activation leading to antibody production - plays role in autoimmunity

95
Q

Explain Cytotoxic T cells activation

A

Nucleated cells present Ag via MHC I –> CD8+ cells bind to MHC I and recognizes intracellualr pathogen –> CD8+ T cell releases perforin and granzyme B –> perforation of cell membrane –> cell death

96
Q

What is the role of Tregs and how are they

A

TGF-B stimulates Tregs - effective against autoimmunity - releases TGF-B, IL10 - decreased immune response

97
Q

What mechanism provides the most diversity to Ig and TCR?

A

Junctional diversity - addition or removal of nucleotide base pairs after VDJ recombination

98
Q

What is the role of PD-1 expression by CD4+ T cells?

A

PD-1 is a regulatory molecule –> has suppressive effect on CD4+ –> diminsihed adaptive immune response

99
Q

Discuss the significance of higher concentratops of IL-6 and TNF-a in blood panel

A

IL6 and TNF-a levels indicate acute phase reactants

100
Q

Discuss the significance of decreased HLA-DR4 expression by monocytes

A

HLA-DR4 encodes for MHC II receptors –> less receptors –> less CD4+ activity –> decreased adaptive immune response

101
Q

Explain the roles of the following surface molecules:
TCR
CD4
CD8
CD3
CD28
CTLA-4
PD-1
LFA-1

A

TCR - antigen recognizition of any MHC-peptide
CD4 - signal transduction of APC
CD8 - signal transduction of all nucleated cells
CD3 - initial stimulation
CD28 - costimulation of APC B7 - cytokine production
CTLA-4 - regulatory protein w/ higher affinity for B7 - target for cancer therapeutics
PD-1 - negative regulation of APC, tissue cell or tumor cell PD-L1 - inhibits initial stimulation
LFA-1 - adhesion to APC or endothelium ICAM-1

102
Q

What activates expression of B7 on MHC-II cells?

A

PAMPs

103
Q

Explain the role that CD4+ and CD8+ T cells play in the adative immune response to viral infections

A

Virus inside endosome in cell –> CD4+ recognition of MHC-II –> release of IFN-y –> disruption of translation of viral protein

Viral microbe in cytosol –> CD8+ recognition of MHC-I –> release of perforins and granzymes –> perforins facilitate entry of granzymes into cytosol –> granzymes activate apoptosis –> cell death

104
Q

Explain the process of T cell maturation

A

RAG (Recombinase Activating Gene) creates precursor T cell –> Adds CD4/8/3 (double positive stage) –> positive selection –> negative selection –> naive T cell

105
Q

Explain the process of T cell Positive selection

A

Thymic epithelial cells present either MHC-I or MHC-II to double positive T cells –> weak binding of one or the other leads to CD4+ or CD8+, no binding or too strong binding leads to apoptosis

106
Q

Explain the process of T cell negative selection

A

Positively selected T cells transported to thymic medulla –> medullary thymic cells present self-antigen (AIRE protein) –> if T cell binds it undergoes apoptosis, cells that don’t bind become naive mature cells

107
Q

What HLAs encode for MHC-I receptors? MHC-II receptors?

A

MHC-I - HLA-A/B/C
(MHC-1 = 1 letter)

MHC-II - HLA-DP/DQ/DR
(MHC-2 = 2 letters)

108
Q

What is the purpose of the costimulatory signal B7/CD28

A

Activates T cell –> proliferation, cytokine production and release

109
Q

What section of the antibody contains light chain?

A

Fab portion - antigen binding

110
Q

What part of the antibody changes to determine the isotope?

A

Heavy chains

111
Q

What is the site of complement binding? Site of phagocyte binding?

A

Complement - CH2
Phagocyte - CH3

112
Q

Differentiate the role of naive B cells, activated B cells, memory B cells, and plasma cells

A

Naive B cells - B cell that hasn’t come into contact with antigen - only IgM/IgD

Activated B cells - B cell that has come interacted with antigen, ingone class switching, and can proliferate/differentiate

Memory B cells - B cells that have been produced by activated B cells can contain antibodies for specific antigens

Plasma cells - produce and release antibodies for specific antigen

113
Q

Distinguish T cell independent activation from T cell dependent activation

A

T cell dependent:
Antigen presentation on B cell MHC-II binds to T cell –> Th cell activates B cell –> isotype switching –> B cell proliferation and differentiation to memory/plasma cells
Two signals required: B7/CD28 - stimualtion of t cell cytokine production; CD40/CD40L - Isotype class switching

T cell independent:
B cell antibodies bind to peptide –> B cell Ig receptors crosslink –> intracellular signalling –> B cell activation –> maturation to plasma cells –> generation of IgM antibodies but no class switching or memory B cells formed

114
Q

```

Describe the varied functions of the Ig subclasses

A

IgG - neutralization of microbes, opsotionzation fo antigens, activation of classical pathway, antibody dependent cellular cytotoxicity, neonatal immunity, feedback inhibition of B cell activation

IgM - activation of classical pathway

IgA - mucosal immunity, neutralization of microbes

IgE - eosinophil and mast cell mediated defense against helminths (response to allergens)

115
Q

Discuss the antibody response to bacteria on initial and subsequent exposure

A

Initial - IgM formation and eventually IgG
Subsequent - More rapid neutralizing effect of IgG expression of antibodies

116
Q

Discuss the role IgG plays in facilitating phagocytosis of microbes

A

Neutralization of microbes/toxins
Opsonization and phagocytosis
Antibody-dependent cellular cytotoxicity
Complement activation –> lysis of microbes, phagocytosis of microbes with C3b receptor, inflammation

117
Q

What is B cell inhibition?

A

IgG turns down B cell response after infection

T dependent B cell activation –> formation of B cells that secrete IgG –> IgG binds to pathogen and fomrs complex –> Fc receptors on B cell bind to IgG/pathogen complex –> B cell turned off

118
Q

Define variolation

A

practice of taking a lancet to a ripe pistule of an infected person and introducing the infectious material to a non-infected person

119
Q

Why was small pox able to be eradicated?

A

Humans were the only host, no animal reservior
Only one serotype = only one vaccine needed
No carrier state = disease is shown fast and pt can be quarantined to prevent spread

120
Q

What are the sources of passive immunity?

A

Blood tranfusions
Homologous human antibody (IgG) - PEP for hep a, measles
Homologous human hyperimmune globulin (specific antibodies) - PEP for hep B, rabies, tetanus, varicella
Hereologous hyperimmune serum (from animals) - antitoxin, antivenom

121
Q

What are the live, nonattentuated vaccines?

A

Adenovirus

122
Q

What are the live, attenuated vaccines?

A

VZV, MMR, Influenza, rotavirus, BCG (TB), Dengue, Ebola, Yellow fever, Typhoid, Herpes zoster

123
Q

What are the inactive, whole cell vaccines?

A

Hep A, Rabies, Influenza (IM), Pertussis

124
Q

What are the inactive, Fractional vaccines and the types?

A

Subunit: HepB, Influenza (IM), Pertussis, HPV, HZ, Anthrax, Pneumococcus, Meningococcus, SARS-CoV-2

Toxoid: diphtheria, tetanus

Conjugate: HiB, Pneumococcus, Miningococcus, Malaria

Nucleic Acid: SARS-CoV-2

125
Q

How are the different types of fractional vaccines made?

A

Subunit - using a protein from the virus
Toxoid - using a toxin from the virus
Conjugate - using a protein connected to a toxoid
Nucleic Acid - using viral dna/rna

126
Q

Which vaccines induce a humoral response only?

A

Live attenuated bacteria - Pertussis, BCG
Killed viruses - Hep A, polio, rabies
Recombinant protein subunit vaccines - HPV, Hep B
Modified protein vaccines - Tetanus toxoid, diphtheria toxoid

127
Q

Which vaccines induce a T cell mediated and antibody response?

A

Live attenuated viruses - MMR, Rabies, influenza A
Conjugate vaccines - HiB, strep pneumoniae
mRNA vaccines - SRAS-CoV-2
Hybrid viral vaccines - SARS-CoV-2, Ebola
DNA vaccines

128
Q

Justify the use of the following ingredients in vaccines:
Preservatives
Adjuvants
Stabilizers
Cell culture materials
Inactivating ingredients
Antibiotics

A

Preservatives - help prevent contamination
Adjuvants - help stimulate stronger immune response
Stabilizers - help vaccines maintain potency during transport and storage
Cell culture materials - vaccines are grown in cultures and hard to eliminate
Inactivating ingredients - used to kill the vaccine or inactivate toxins
Antibiotics - helps with prevention of contamination

129
Q

All DNA viruses are double stranded except

A

Parvovirus

130
Q

What is the difference between negative and positive sense RNA

A

negative sense RNA must come with extra components to be able to be transcribed into positive sense and hist host machinery

131
Q

Nonenveloped, dsDNA viruses

A

Adenoviruses - common cold, meningitis
Papillomaviruses - warts, cervical cancer

132
Q

Enveloped, dsDNA viruses

A

Smallpox
Herpesviruses
Hep B

133
Q

Noneveloped, ssDNA viruses

A

Parvoviruses

134
Q

dsRNA viruses

A

Reoviruses

135
Q

nonenveloped, +ssRNA viruses

A

Polio, Hep A, Common cold
Gastroenteritis

136
Q

enveloped, +ssRNA viruses

A

Togaviruses
Flaviviruses
Coraonaviruses
Retroviruses

137
Q

enveloped, -ssRNA viruses

A

Filorviruses
Orthomyxoviruses
Paramyxoviruses
Rhabdoviruses

138
Q

What vaccines are given at birth?

A

HepB, RSV

139
Q

What vaccines are given at 2m, 4m, 6m?

A

Rotavirus, DTaP, HiB, Pneumococcal conjugate, Inactivated polio

140
Q

When are the MMR, Varicella, and Hep A vaccines given?

A

1 year, earlier for at risk groups

141
Q

By 13, what vaccines should be completed?

A

RSV
HepB
Rotavirus
DTaP
HiB
Pneumococcal conjugate
Influenza
COVID
MMR
Varicella
HepA
1st dose of Tdap, HPV, Meningococcal

142
Q

How would you differentiate between AML and CML on a CBC w/ differential?

A

CML would show more differentiated WBCs - higher neutrophils/eosinophils/basophils/monocytes, or metalyelocytes/myelocytes

AML would should a left shift of immature cells - less differentiated, more blasts

143
Q

What would you see on a PBS in the case of CML?

A

adbundant mature leukocytes - nothing more immature than myelocytes

144
Q

What would you see on a PBS with AML?

A

Blasts
AURE rods

145
Q

What is the pathogenesis of CML?

A

t(9:22) BCR-ABL
BCR-ABL fusion –> ABL is a kinase, BCR keeps signaling turned on –> proliferation and survival of pluripotent hemopoietic stem cell w/ preferential differentiation into neutrophils

146
Q

What are the three phases of CML?

A

Chronic phase - often no symptoms, most of life spent in this phase - leukocytosis of all granulocytes –> possible splenomegaly (N/V, fullness), thrombocytosis; < 10% blasts

Accelerated phase - more proliferation leads to more mutations earlier on –> neutrophil differentiation becomes progressively impaired - more blasts cells (10-19%) decrease space in bone marrow –> anemia, thrombocytopenia; high basophils –> increase histamine –> pruritis

Blast crisis - high mortality - transition to AML - >20% blast cells - anemia, thrombocytopenia, leukocytopenia, increased blasts –> infections; leukostasis, TLS

147
Q

What is the treatment for CML?

A

Tyrosine kinase inhibitors

148
Q

What is the etiology of Essential Thrombocytosis that is absent in CML?

A

JAK2 mutation

149
Q

Explain the natural history of Primary Myelofibrosis

A

Early on looks similar to others - same pathogenesis - high platelet count, high WBC

Later on - bone marrow replaced with scar tissue - pancytopenia

150
Q

What is the definitive test used to determine AML?

A

Bone marrow aspirate confirming 20% or more blasts (w/ or w/out AURE rods) present

151
Q

What role can flow cytometry play for determining myeloid neoplasms?

A

Can tell us the difference between acute and chronic by the markers on the cell surface
CD34 on immature stem cells, CD63 on mature myeloids
Determine if T-ALL (CD2-8) or B-ALL (CD10)
Determine if B-ALL (CD10) or B-CLL (CD5)

152
Q

What is the pathogeneis of Acute Promyelocytic Myelocytic Leukemia?

A

t(15:17) - disfunctional retinoic acid receptors
AMP-RAR

153
Q

What is the treatment for APML?

A

ATRA - All Trans Retinoic Acid Receptors
dysfunctional retinoic acid receptors –> poor differentiation –> stuck in intermediate phase/stuck at blasts –> ATRA allows for maturation –> short term allows cells to mature to neutrophils

154
Q

What is the most significant risk of APML?

A

Disseminated Intravascular Coagulation
High cell turnover –> granule release –> myleoperoxidase –> spontaneous coagulation
Tissue factor release –> coag cascade –> DIC
No platelets –> prolonged bleeding

155
Q

What immunochemistry can differentiate between AML and ALL?

A

myloperoxidase (+) - AML
Tdt (+) - ALL

156
Q

What is the treatment for AML?

A

Chemotherapy
Stages: Induction –> Consolidation –> Maintainence

Meds: Cytarabine, Ida/Daunarubicin

157
Q

What are the three common genetic disorders that lead to ALL?

A

Down Syndrome
t(12:21) - most common - seen more in children
t(9:22) - seen more in adults

158
Q

What is the relationship between Human T Lymphotrophic Virus infection and ALL?

A

While other ALL is primarily B cell lines being effected, HTLV ALL only effects T cells

159
Q

Hepatosplenomegaly and meningeal Leukemia are complications of

A

ALL

160
Q

What are the complications are specific to T-ALL?

A

Thymic enlargement:
Compression of the trachea - dypsnea, stridor
Compression of the esophagus - dysphagia
Compression of the SVC - SVC syndrome - enlargement of head/neck/UE veins, cyanosis

161
Q

Splenomegaly in CML is caused by

A

Deposition of leukocytes
Extramedullary hematopoiesis - Luekocytosis can cause the spleen to start producing RBC to help the bone marrow

162
Q

What can CLL turn into if lymphocytes begin to deposit in the lymph nodes and create a tumor?

A

Diffuse Large B-cell Lymphoma

(Richter Transformation)

163
Q

What is Evans Syndrome?

A

In CLL when plasma cells are over proliferating and not maturing correctly, they can release autoantibodies that attack the RBC and platelets.

The ensuing Autoimmune Hemolytic Anemia + Immune Thrombocytopenic Purpura = Evans Syndrome

164
Q

Smudge cells on a PBS are indicative of which disease?

A

Chronic Lymphocytic Leukemia

165
Q

How do you classify CLL?

A

RAI Classification

RAI 0 - Lymphocytosis
RAI 1 - RAI 0 + LAN
RAI 2 - RAI 1 + Hepatosplenomegaly
RAI 3 - RAI 2 + Anemia (not AIHA)
RAI 4 - RAI 3 + Thrombocytopenia (not ITP)

166
Q

What is the treatment for CLL classes?

A

Asymptomatic RAI 0, 1, 2 - no treatment, observation only

Symptomatic RAI 1, 2 - chemotherapy

RAI 3, 4 - chemotherapy

167
Q

Which types of non-Hodgkin’s Lymphoma occur due to decreased cell apoptosis?

Are they slow or aggressive?

A

Follicular Cell (14:18) BCL2
Marginal Zone lymphoma - BCL10

Slow

Both lymphomas that happen after Centroblast maturation

168
Q

What types of non-Hodgkin’s lymphoma occur due to increased cell proliferation?

Are they slow or aggressive?

A

Mantle cell (11:14) Cyclin D
Burkitt’s Lymphoma (8:14) c-myc
Diffuse Large B cell - BCL6

Aggressive

169
Q

What is the pathogenesis of Follicular lymphoma?

A

t(14:18)
Increased expression of BLC2 - inhibits apoptosis

170
Q

What is the pathogenesis of Marginal Zone Lymphoma?

A

Increased expression of BCL10 –> increased NK-kB –> decreased apoptosis

171
Q

What is the pathogenesis of Mantle cell lymphoma?

A

t(11:14)
Increases expression of Cyclin-D –> pushes cells into S phase –> increases cell proliferation

172
Q

Mutations of the Centroblast can cause what types of cancers, and how are they different?

A

Burkitt’s Lymphoma - t(8:14) - increased c-myc expression –> massive cellular proliferation
– triggered by EBV/HIV

Diffuse large B cell lymphoma - increased expression of BCL6 on chromosome 3 –> increased cell proliferation
– most common type of NHL
High association with EBV/HIV

173
Q

What is a key clinical feature that differentiates Hodgkin’s from Non-Hodgkin’s lymphoma?

A

Hodgkin’s Lymphoma has continguous LAD
NHL is noncontiguous LAD

174
Q

Alcohol-induced Lymphadenopathy pain is associated with

A

Hodgkin’s Lymphoma

175
Q

Explain how Marginal Zone Lymphoma can be caused by chronic infection

A

Chronic infections such as H. pylori, Hashimoto, Sjogren’s - chronic inflammation can lead to mutation and increased expression of BCL10 gene

176
Q

Explain why patients with NHL present with hypercalcemia

A

Large deposits in the kidneys can stimulate expression of 1-a-hydroxylase enzyme –> increases Vit D –> increases calcium absorption

177
Q

What is the treatment for NHL?

A

R-CHOP
Rituximab (only for CD20+ B cells) - complement mediated lysis of B cells - eliminate mature B cells

Cyclophosphamide
Hydroxydaunarubicin
Onvolin (Vincristine)
Prednisone (Steroids)

178
Q

What type of hypersensitivity reaction is Steven Johnson Syndrome?

A

Type IV delayed hypersensitivity

179
Q

What type of hypersensitivty reaction are season allergies?

A

Type I

180
Q

What is a positive Nkolski sign?

A

Sloughing of the epidermis - seen in Steven Johnson Syndrome as a result of reaction to medication

181
Q

Describe Good Pasture Syndrome

A

Glomerulanephritis as a result of type II hypersensitivity - antibodies specific for glomerular basement membrane of the kidney

182
Q

Describe Sjogren syndrome

A

Chronic disease resulting from Ig mediated destruction of lacrimal and salivary glands - can be triggered by viral infection

183
Q

Describe Systemic Sclerosis

A

Three interrelated processes:
Autoimmunity - CD4+ T cells response to unidentified antigen
Vascular damage - repeated cycles of endothelial injury follwoed by platelet aggregation lead to release of factors that trigger proliferation and fibrosis
Fibrosis

184
Q

Why is Rituximab associated with an increased risk of death by infection?

A

Elimination of all B cells leave opportunity for serious infection without having an immune response to fight back

185
Q

Describe CART therapy used in Diffuse Large B cell Lymphoma

A

Chimeric Antigen Receptor Therapy

Newly bioengineered protein that enables T cell to engage malignancy without costimulation with CD28
Small chain receptor is directed at CD19

186
Q

What antibodies titers are seen in Sjogren syndrome?

A

SS-A, SS-B, Anti-Ro, Anti-La

187
Q

ANA testing determines what

A

ANtibodies directed at nuclear antigens - just identifies autoimmune antibodies

188
Q

Rheumatic fever caused by Strep is considered what type of hypersensitivity

A

Type II

189
Q

What HIV medication is contraindicated for HLA-B5701 positive patients?

A

Abacavir

190
Q

What HIV medication can result in lipodystrophy?

A

Indinavir - protease inhibitor

191
Q

What is the primary receptor for EBV?

A

CD21 on B cells (C3d complement receptor)

192
Q

What are the three potential outcomes of EBV?

A
  1. Replcate in B cells or epithelial cells permissive for EBV replication and produce and spread virus
  2. Cause latent infection of memory B cells in presence of competent T cells
  3. Stimulate grown and immortalize B cells
193
Q

What are the three key clincal presentation of EBV and relate to pathophysiology

A

Pharyngitis - virus adheres to epithelium, , atypical Downey cells reactive to antigen

LAD - signs that antigen is being filtered through lymph nodes –> T cells become activated –> fight between B and T cells in small space –> swelling

Malaise - Physically draining process until EBV force dinto latency –> length of time depends on immune system

194
Q

What bugs grow on chocolate agar?

A

Moraxella catarrhalis
HiB
Tularemia

195
Q

What ILs do macrophages secrete?

A

IL1, IL6, IL8, IL12 (NK cell activation), TNF-a

196
Q

What ILs do Th1 cells secrete?

A

IL2 - growth of T cells
IL3 - eosinophil survival
IFN-y - macrophage recruitment, NK activaiton

197
Q

What ILs do Th2 cells secrete?

A

IL2
IL3
IL4 - enhances class switching to IgG and IgE
IL5 - stimualtes eosinophil growth/differentiation
IL6
IL10
IL13

198
Q
A

Unit 3 HDC (8 decks)

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