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USMLE Studying > Immunology > Flashcards

Immunology Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the encapsulated bacteria to watch out for in sickle cell or in splenectomy?

A

SHINE SKIS

Strep pneumo

HFlu T1

Neisseria meningitisi

ECOLI

Salmonella

Klebsiella pneumoniae

group B strep

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2
Q

What are things you would see in serum post-splenectomy?

A

Hoewll Joly bdies - nuclear remnants

Target Cells

Loss of sequestration and removal of platelets so thrombocytosis

lymphocytosis

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3
Q

What’s happening in transfusion reactions?

A

When cross checked for abs (indirect coombs test) and pass then NK cells recognize different MCH1 or no MCH1 on surface and kills OR Kills via ADCC - CD16 binds Fc portion of Ig and activates NK cell

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4
Q

What are the 4 mediators for PMNs?

A

LTB4

IL8

C5a

Bacterial products

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5
Q

what are the 3 things that activate mast cells?

A

Trauma

C5a/C3a

IgE Antigen crosslink

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6
Q

What are signs of inflammation and mechanismss?

A

1) Rubor - red and warm
- Hist, PGI2/E2/D2 and BK vasodilate and SM relax arterioles
2) Tumor - swelling
- Leaky post-capillary venules and exudate from tissue damage and Histamine
3) PAin - dolor
- BK and PGe2 sensitize nerve endings
4) FEVER

Macro make IL-1 and TNF to Perivascular Hypothal cells that increase AA –> PGE2 and increase temperature set point

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7
Q

What are bacteria that have catalse? What genetic disease would make yuou really susceptible to these?

A

Chronic Granulomatous Disease - boys w/ no NADPH oxidase and no Nitroblue Tetrazolum color change bc no Respiratory burst

Catalase+ Organisms Need PLACESS

Nocardia

Pseudomonas

Listeria

Aspergillous

Candida

Ecoli

Straph Aureus

Serratia

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8
Q

Complement deficiencies and susceptibilities?

A

HANE - C1 esterase inhibitor - ACE inhib contraindicated

C3 deficiency = Increased risk recurrent pyyogenic suns and resp tract infections and increased T3 hypersensitivity reactions - SLE

C5-C9 deficiencies in MAC complex - NEISSERIEA!!!!!!!

DAF (GPI-anchored protein) deficiency (CD55) - allow MAC onto RBC and get peroxysmal nocturnal hemoglobinuria

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9
Q

Hot T bone steak means what?

A

IL1 - fever

IL2 - T cell actiation

IL3- Bone marrow stimulus

IL4- IgE

IL5 - IgA

IL6 - APR

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10
Q

What enzymes are required for innate immunity killing?

A

NAdPH Oxidase (w/o is Chronic Granulomatous DiseasE)

SOD

MPO

Glutathione Peroxidase/Reuctase and both require Selenium!!!!

G6PD!!

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11
Q

What are examples of bugs w/ Antigenic Variation

A

Bacteria:

  • salmonella - 2 flagella

2- Borrelia Recurrentis - relapsing fever

  • Neisseria Gonorrhea Pilus protein

Viruses - Influenza, HIV, HCV

Parasites - Trynapnosomes

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12
Q

What are bugs that you get passive immunity protection from when you are exposed?

A

To Be Healed Very Rapidly

Tetanus toxin

Botulinum

HBV

Varicella

Rabies virus

After expsore, unvaccinated patients are given abs

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13
Q

What is the only live attenuated vaccine given to HIV+ PAtoents

A

MMR

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14
Q

wHAT ARE SOME examples of Inactivated or Killed vaccines?

A

RIP Always

Rabies

Influenza (injection)

Polio (salk)

hep A

need boosters bc immunity goes away and is only humoral repsonse

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15
Q

What are the 2 types of transfusion reactoins?

A

Febrile non-hemolytic transfucsion rxn - T2 hypersensitivity host abs against donor HLA antigens and WBC - Fever, HA, Chills, Flushing

Acute Hemoltyic Transfusion rxn - T2 hypersensitivity

Intravascular Hemolysis - ABO incompatibility

Extravascular Hemolysis - hist antibody reaction w/ foregn antigen on donor RBC

Fever Hypotensions, Tachypnea, Tachycardia, Flkank pain, hemoglobinuira, and Jaundice

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16
Q

Little boy who can’t walk and has cerebellar problems + Infections + telangiectasia

A

Ataxia Telangiectasia

  • AR mutation leads to defects in ATM gene and failure to repair DNA double strand breaks leading to cell cycle arrest

IgA Deficiency, cerebellar defects, Angiomas,

Increased AFP, decreased IgA, IgG, and IgE and lymphopenia and cerebellar atrophy

RADIOSENSITIVE + Chorea

PIP kinase

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17
Q

INfliximab - drug and reactions

A

Binds TNF alpha used for RA, IBD, Spondylitis, Psoriasis

Infection prone - risk of infections and malignancy

elevated LFTs

other drugs are like andalimumab and certolizumab

Infliximab - Remicabe and Etanercept - enbrel humanized anti-TNF Ig reduce inflamattion and DTH Type 4

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18
Q

1 yr old boy gets recurrent skin infections and gingivitis

Delayed separation of Umbilical cord 10 weeks after birth

What protein is under-expressed?

A

LAD Type 1

No pus formation in infections

CD18 on phagocytes so impaired chemotaxis

AR defect in LFA1 Integrin

19
Q

What is acute serum sickness? When does it occur? What happens?

A

Type 3 hypersensitivity reaction to drugs 5-10 days after admnistration/antigen exposure

commonly to drugs like Infliximab and other Ig and non-human proteins

Vasculitis from tisue deposition of immune complexes w/ small vessel fibrinoid necrosis and PMN infiltration

Fever, ithching rash, arthralgia, LOW C3/C4 levels

20
Q

LAD

A

late separation of umbilical cord, poor wound healing, recurrent infections WITHOUT pus formatin and gingivitis

AR absence of CD18 for formatin of integrins so no migration or chemotaxis from vascular space into tissues

Rolling - selectins

Adhesion - Integrins

Transmigration

21
Q

Difference between CGD and MPO deficiency?

A

MPO deficiency can allow BOTH catalase + and catalase - organisms to surive within phagocytes

vs CGD can kill some organisms that bring in their own H2O2

22
Q

graft vs host disease

A

Liver and BM trasnplant

Allogenic transplant

host is immuno-deficiemt and so the immunocompetemt T cells within donor tissue recognize new, different MCH antigens on host as foreign and attack

Both CD4 and CD8 t cells

Target tissues are skin, liver, GI most affected

Acute within 1 week

23
Q

Chronic renal transplant rejection - what do you see?

A

months (at least 3) to years after transplantation

WORSENING HTN, Increased Cr, Proteinuria w/ normal urine sediemtn

Chronic, indirect immune response against Donor alloantigens

Obliterative Intimal Thickening, Tubular Atrophy, and Interstitial Fibrosis

Obliterative Vascular Fibrosis

24
Q

Vaccines for what with polysacharride conjugated w/ Diptheria Toxoid allow immunity against what infections?

A

STrep Pneumo

Neisseria meningitidis

HFlue

Encapsulated bacteria w/ polysacharide components bound to protein carriers to use as vaccine

Protein carriers change vaccine from T cell independent to T cell dependent antigens

Carrier Proteins - nontoxic diptheria toxioid, neisseria outer membrane protein complex, and tetanus toxoid

25
Q

Whats the defect in Hyper IGm?

A

XLRecessive defect in CD40L on Th cells so can’t induce class switching in B cells

Pyogenic infections and opportinustic and Crypto, CMB, Pneumocystis

Tx IVIG

*LYMPHOID HYPERPLASIA and recurrent sinopulmonary infections

26
Q

Job Syndrome - what’s happening?

A

AD Hyper IgE

Deficiency of Th17 cells due to STAT3 mutation impaired recruitment of PMNs to sites of infection

FATED

Faces coarse, cold noninflamed staphylococcal Abscesses, retained primary Teeth, increased igE, and Dermatologic - excema

high Ige and low IFN gamma

27
Q

Serum elevations of what??? in Anaphhylaxis?

A

Tryptase!!! Mast cell release

+ Histamine

28
Q

XLA - XL (Bruton) Agammaglobulinemia Presentation and other details?

A

defect in BTK tyrosine kinase

NO BE CELL MATURATION

XL Recessive - boys

Presntation - recurrent bacterial and enteroviral infections

  • Extracellular/Encapsulated infectoins - pyogenic (encapsulated) bacteria + GIARDIA bc no neutralizing abs

NO B cells and No Ig

No LN or Tonsils –> no lymphoid follicles or germinal centers (bc no mature b cells or SHH occuring)

No CD19or20

29
Q

EXZEMA, REcurrent Infections and Thrombocytopenia in a little boy/??

A

WISCKOTT ALDRICH!!!!

WAS gene mutation can’t reorganize T cell Actin Cytoskeleton

X chromosome mutation - Xlinked REcessive - males

SCID + Purpura

Smaller/fewer platelets - bruising and HUS and purpura

Increased Encapsulated infections bc no humoral and increased opportunistic pathogens bc no T cell

Infections worsen w/ age

Tx is HLA BM transplantation

30
Q

Only meningitis to cause Petechia?

A

Neisseria - induced small vessel vasculitis (palms and soles)

Tx IV Ceftriaxone

31
Q

What organisms are catalse Positive? Why is that significant?

A

Catalase positive organisms can affect people w/ GCD bc no H2O2 for them to use to make bleach in lysosome and destroy

ASPERGILLOUS

Staph

PSEUDOMONAS

Serratia

Nocardia

32
Q

How is Ataxia telangiectasia inherited? Causes? Presentation?

A

AR ATM gene failure to fix dsDNA breaks leading to cell cycle arrest

Ataxia, cerebellar atrophy, Telangiectasia and IgA deficiency

XRAY and radiosensitive –> Imcreased risk of cancer bc ineffective DNA repair

Increased AFP

33
Q

Inherited Disorders of deficient DNA repair Enzymes:

A

1) Ataxia -telangiectasia - DNA hypersensitivity to ionizing radiation
2) Xeroderma Pigmentosum - DNA hypersens to UV causing premature skin aging and increased risk of cancer - malignant melanoma and SCC
3) Fanconi Anemia - Hypersensitivity of DNA to cross-linking agents
4) Bloom syndrome - generalized chromosomal instability and Increased cancers
5) HNPCC - defect in DNA mismatch repair enzymes - increased colon cancer

34
Q

What are granulomas of TB made of?

A

IFN and IL2 activate macrophages and T cells to wall off tuberulous foci making caseating granulomas

Epitheliod Cells

Langhans multinucleated giant cells

fibrobasts

collagen

35
Q

IL2 function?

drug simulating it and it’s use?

A

IL2 activates NK cells and T cell autocrine growth and differentiation of CD8/4 t cells

IL2 has anti-tumor effects

Aldesleukin = IL2 immunotherapy for metastatic melanoma and RCC

  • tumor regression
36
Q

What is the Dihydrorhodamine Flow Cytometry Test?

A

assesss production of Superoxide radicals by measuring conversion of DHR to rhodamine which turns fluorescent green = can be detected by flow cytometry

cells w/o NADPJ oxidase will have less fluorescence and look like they have no PMNs

CDG!!!! defect in NADPH oxidase

XL recessive

37
Q

Presentation and causes of SCID

A

Severe Viral and Bacterial infections as maternal immunity wanes

Mucocutaneous candidiasis

Persistent Diarrhea

Failure to thrive

NO CD3+ T cells and Hypogammaglobulinemia

Thymic hypoplasia/aplasia

XL = IL-2R gamma chain mutation

AR = ADA deficiency

38
Q

How do NK cells kill? Get activated? what do they express?

A

NK cells are CD16 or CD56

Present in Athymic patients - dont need thymus for maturation

have no antigen-specific activities and do not require exposire to antigen for activation and do no posses antigen memory

activated by IFN gamma and IL-12

Kill cells with decreased or absent MHC Class I like virus and tumor cells

Come from lymphoid stem cells

Cytoplasmic granules w/ Perforins and Granzymes

(holes and apoptosis)

39
Q

Some bacteria have IgA proteases that cleave IgA at hinge region yielding Fab and compromised Fc fragments….they are?

A

Neisseria gonorrhea

Neisseria Meningitis

Strep Pneumo

Hflu

This leads to bacterial adherence to mucosa

40
Q

Patients w/ DiGeorge syndrome would have what changes in their Lymph Nodes?

A

Poor development of Paracortex region bc that’s where T cells hang out - between medulla and follicles

41
Q

2 forms of IgA?

A

Serum form - monomer

Secretory form - Dimer w/ J chain and Secretory component

MOst components made by plasma cell BUT the secretory component is made by epithelial cells and facilitates movement through mucosal membranes and prevents degradation in secretions

Saliva, Mucus, tears, colostrum

42
Q

What immuno deficiency has neuropathies and nystagmus?

A

Chediak higashi

also albuminism from abnormal melanin storage

Defect in PMN phagosome lysosome fusion –> giant lysosomal inclusions

43
Q

Poison ivy is an example of?

A

Contact Dermatitis - Type 4 DTH reaction mediated by T cells and CMi

USMLE Studying (8 decks)

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