Immunity - Midterm 1 Flashcards

1
Q

What does the term Virulence refer to?

A

The capacity to cause severe disease – how hard is it to treat microorganism, how likely is someone to die from this disease.

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2
Q

Type 1 allergy anaphlactic?

A

-Emergency situation (2 - 3 min to develop)

Difficulty breathing
Wheezing, stridor
↑ heart rate - ↓ blood pressure

*corticosteroids- decrease swelling

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3
Q

T-cell deficiency can be associated with?

A

Viruses (varicella herpes, cytomegalovirus)
o Fungi
o Yeasts (Candida, Histoplasma)
o Atypical microorganisms (Pneumocystis carinii - now known as Pneumocystis jirovecii)

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4
Q

What kind of deficiency is ADA, and what does it result in?

A

Is a combined deficiency (affecting both B + T cells)

-Results in the accumulation of toxic purines

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5
Q

What are the developmental stages of AIDS? What occurs during each phase?

A

Stage 1 – Acute
Occurs about 1 to 2 weeks after initial infection. During this stage, the virus undergoes massive replication. Patients may be asymptomatic or have a flu-like symptoms

2.) Stage 2 – Asymptomatic HIV
During this stage, chronic signs or symptoms are not present. T-cell count may be used to monitor progression of the disease. With the patient’s own resistance and drug therapy, this stage can last for 10 to 12 years or longer. - person feels asymptomatic, but virus is proliferating in lymph nodes

3.) Stage 3 – Symptomatic HIV
This stage has two phases: early and late. When the T-cell count falls below 200 cells per cubic millimeter of blood, it is the late phase. This stage of HIV is defined mainly by the emergence of opportunistic infections and cancers to which the immune system normally helps maintain resistance.

Stage 4 – Advanced HIV
A T-cell count of 50 cells per cubic millimeter or less represents advanced HIV. With the onset of this stage, patients are at the highest risk for opportunistic infections and malignancies - Parasitic, fungal, bacterial, viral infections, and neoplasms

-Treated with “cocktail” (3 or more drugs)

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6
Q

Endotoxins (when are these released) Vs Exotoxins?

A

Exotoxins – secreted toxins - elicit the production of antitoxins - a toxin released by a living bacterial cell into its surroundings.

Endotoxins - also known as pyrogens - cell wall released during cell death– can’t prevent the toxic effects – causes the inflammatory process to be activated

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7
Q

Type 3 hypersensitivity ? (immune complex)

A

-Reaction from antigen-antibody complexes (Not organ specific)

  • Type III antibody binds to antigen in body or in fluid, then complex is deposited onto tissue
  • IgG or IgM bind to antigen – form complexes deposited in various tissues = target tissues and destroys them
  • =arthritis, Lupus, serum sickness
  • 1- 3 weeks
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8
Q

Primary (congenital) immune deficiency Vs Secondary (acquired) immune deficiency?

A

Primary (congenital) immune deficiency – a genetic defect

Secondary (acquired) immune deficiency – caused by another condition (ie. Cancer, aging)

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9
Q

Autoimmunity Vs Alloimmunity?

A

Autoimmunity – disturbance in the immunological tolerance of self-antigens T-cells damages tissues in self

Alloimmunity – immunological reactions to transfusions, transplants, or fetus during pregnancy

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10
Q

Type 4 hypersensitivity? What do the antigens do here?

A

-Delayed response
-Antigen sensitizes cell to release cytokines that activate macrophages, the macrophages remove cells, because of this the reaction is delayed

-Continued exposure to the irritant makes the reaction worse each time the person is exposed

-Reaction occurs 1 - 3 days after exposure

Ex. latex, Nickle, poison ivey

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11
Q

Primary Vs Secondary Immunodeficiency?

A

-Primary – born with it – congenital – defect – part of the immune system is either absent or not functioning properly

-Secondary or acquired deficiencies more common - immune system is compromised due to an environmental factor (HIV, severe burns, chemotherapy, radiation, diabetes, malnutrition)

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12
Q

What is the window period for the AIDS infection to appear as antibodies?

A

4-7wks

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13
Q

What are the normal rates of infection for adults and children?

A

Preschool-age children: 6-12 infections a year

Adults: 2-4 infections a year

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14
Q

Portal of entery?

A

How the disease enters the body
Inhalation – ingestion – bites

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15
Q

What are community and nosocomial infections?

A

Community-acquired – influenza – (Hospital acquired, Health care acquired)

Nosocomial – infection exists in a hospital - central lines, catheters, pneumonia – interchangeable with hospital acquired

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16
Q

What is Type 4 hypersensitivity?

A

-It is mediated by T - cells and don’t involve antibodies - takes days to weeks for oneset to occur

Tc cells – attack and destroy cells directly. Damage happens from cell being destroyed.
o Th1 and Th17 cells – produce cytokines that recruit and activate phagocytic cells (macrophages).

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17
Q

What is serum sickness? What are some symptoms? Potential cause?

A

-Type 3 hypersensitivity

-Immune complexes formed in blood and deposited on tissue this typically affects blood vessels, joints, and kidneys causing damage

Symptoms include:
* Fever
* Enlarged lymph nodes
* Rash
* Pain at sites of inflammation

Can be caused by IV administration of other antigens like medication

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18
Q

Aerobic Vs anaerobic bacteria?

A

Aerobic (survives in oxygen environment) or anaerobic (does not require oxygen) – motile or immotile (can they move or not) – bacteria produces endotoxins and exotoxins that cause cell damage

19
Q

Patients with an immune deficiency may have bouts of?

A

Pneumonia
o Otitis media
o Sinusitis (sinus infections)
o Bronchitis
o Septicemia
o Meningitis
o Infections of opportunistic pathogens (ie. Pneumocystis carinii)

20
Q

What do the terms direct contact, indirect contact, droplet, airborne, while, and vector refer to in regard to immunity and infection?

A

Direct contact: with body lesions, personal contact HIV

Indirect: contaminated object, hands – virus can live on inanimate objects

Droplet: sneeze, cough, talk – mucous, fluid needs to carry the virus - COVID

Airborne: microorganisms attached to dust, inhaled – chicken pox, influenza, anthrax – N95 mask

Vehicle: eat, drink contaminated things (soil, water, food)

Vector: transferred via bites (flea, mosquito)

21
Q

What is Bruton agammaglobulinemia? What does it result in? What does it cause?

A

Blocked development of mature B-cells in bone marrow

▪ Results in no circulating B-cells, but T-cells are fine

Causes repeated bacterial infections

22
Q

Viral infection stages of contamination?

A

Host cell is not killed in the process – continues to make new virus
1 attachment – virus attaches to epithelial cell
2 penetration – cell engulfs the virus
3 uncoating – virus contents released within the cell
4 biosynthesis – RNA enters the nucleus of cell
5 Assembly – new phage particles are assembled
6 Release – new viral particles are made and released

23
Q

What is acquired immunity?

A

2 forms:

1.) Active Immunity:
-Exposing body to an antigen
-Naturally develop antibodies after first exposure (chicken pox)
-Artificially develop antibodies through vaccination

2.) Passive
-Naturally received through mother (breast milk)
-Artificially received through medication transfusion

24
Q

What are Phagocyte Defects? Ex of one

A

Phagocyte: Type of cell within the body capable of engulfing and absorbing bacteria and other small cells and particles.

-Affects the number of phagocytes or their overall function

Ex.Chronic granulomatous disease (GCD)

25
Q

What are the stages for AIDS?

A

Stages
1.)Acute infection
Present with mild, nonspecific symptoms
1-6 weeks

2.) Clinical latency
Virus appears to be latent, but it is active
With treatment can now last decades
Many don’t know they have it as this point

3.) Development of AIDS
Vulnerable to multiple infections
CD4 cells < 200/mm³ (normal 600-1200)
Without treatment - infection to AIDS < 10 yr

26
Q

What do Predominantly Antibody Deficiencies result in? which conditions can they result in?

A

▪ Result in defects of B-cell maturation and function
o T-cell not affected in C-cell deficiencies

Results in one of the following conditions:
▪ Hypogammaglobulinemia – lower levels of circulating immunoglobulin
▪ Agammaglobulinemia – no or nearly no immunoglobulins

27
Q

What is Arthus Reaction? When do these reactions typically start?

A

-Its a type 3 hypersensitivity (Celiac disease is an Arthus reaction Type III hypersensitivity)

*Most people are tolerant of their own antigens, but its unknown what breaks this tolerant state

-Peaks at 6 - 12 hours

▪ Reactions typically happen after injection, ingestion, or inhalation of allergins

▪ Lesions are characterized by:
* Typical inflammatory reaction
* Increased vascular permeability
* Accumulation of neutrophils
* Edema
* Hemorrhage
* Clotting
* Tissue damage

28
Q

What are combined deficiencies disorders? Ex of one?

A

Include the most life-threatening disorder

-Defects that affect the development of both T and B cells

-Most severe is called severe combined immunodeficiencies (SCIDs)

29
Q

What is Selective IgA deficiency? What do they exhibit recurring problems with?

A

-Only IgA is suppressed (most patients are asymptomatic)

Some exhibit recurring problems with:
▪ Sinuses
▪ Pulmonary systems
▪ GI infections
▪ Severe allergies and autoimmune disease

30
Q

What are the 3 most common Primary (Congenital) Immune Deficiencies?

A

*Rare occurrences
*Mutations are sporadic and NOT inherited

o Common variable immune deficiency (Deficiency in IgG, IgM, IgA) affect 34% of those with primary immune deficiency

o Selective Immunoglobin A (IgA) deficiency affect 24%

o IgG subclass deficiency affect 17%

31
Q

Type 2 hypersensitivity?

A

-Responds only to proteins (cytotoxic - causes death of cells)
- 5 -8 hours to develop
-Tissue-specific - reactions against a specific cell or tissue

(Alloimmunity – antigen isn’t the cause of the problem the reaction to the antigen is the problem)

Type II hypersensitivityis an antibody-dependent - specific antibodies bind to antigens, - tissue destruction, inflammation, or dysfunction.

Thrombocytopenia
Transfusion reaction - wrong blood type administered
Hemolytic disease in new born-(mothers blood is incompatible with fetus blood )

32
Q

What is Sepsis/septicemia? What are the sings and symptoms?

A

Septicemia/Sepsis: bacteria in bloodstream (I.e. thru lymph system) causing a generalized infection

Sepsis – severe sepsis – septic shock (endotoxic shock) endotoxic shock – 50% mortality
These bacteria produce endotoxins
cause:
vasodilation
lowers BP
Hypoxia
Cardiovascular shock
Fever, shivering, increased HR, increased RR, sweaty/clammy skin, changes in mental status – need antibiotics

33
Q

What is X-linked SCID?

A

X-linked SCID – defect in important IL receptors needed for lymphocyte maturation (IL-2, IL-4, IL-7)

34
Q

Signs + symptoms of pediatric patients infected with AIDS?

A

Failure to thrive
Not reaching milestones
Nervous system issues – seizures, walking
Frequently sick from childhood illnesses

35
Q

What are Opportunistic infections?

A

Secondary infection – ocurs during or after treatment of another infection – yeast infection (they occur when your immune system is weak and take the “opportunity” to “attack” the system)

36
Q

What kind of deficiency is SCIDs? signs + symptoms?

A

-It’s a combined deficiency

-Few detectable lymphocytes in circulation

o Few detectable lymphocytes in lymphoid organs (spleen, lymph nodes) o Thymus is underdeveloped due to lack of T Cells

o Immunoglobulin levels (usually IgM and IgA) are absent or reduced

o Result in accumulation of toxic metabolites

Lack of both T and B cells, little to no antibody production or cellular immunity

Outcome: Recurrent, life-threatening infections with a variety of microorganisms

37
Q

What is steven Johnson - syndrome?

A

It is a type 4 hypersensitivity that it mediated by T cells, it is felt that is triggered by drugs or an infection – about 3 weeks after exposure entire body, skin and mucus membranes, will develop blisters or rash – over time the top layer of skin dies and is shed – healing takes several days

38
Q

What is Systemic lupus erythematosus (SLE)? What can it cause inflammation of? signs + symptoms?

A

-Type 3 hypersensitivity

-Most common, complex, and serious autoimmune disorder

-It is the production of a wide variety of antibodies against self-antigens such as nucleic acids, histones, ribonucleoprotein

Can cause inflammation in:
▪ Kidneys
▪ Brain
▪ Heart
▪ Spleen
▪ Lung

-Occurs more often in women aged 20-40

Signs:
* Photosensitivity (rash from sunlight)
* Oral or nasopharyngeal ulcers
Facial rash confined to cheeks (malar rash
Nonerosive arthritis of two peripheral joints
* Serositis (pleurisy or pericarditis)

Symptoms:
Arthralgias or arthritis (90%)
Vasculitis and rash (70-80%)
Renal disease (40-50%)
Hematological abnormalities (50%, with anemia being the
most common)
Cardiovascular disease (30-50%

39
Q

Type 1 hypersensitivity clinical manifestations? What does it cause (through what kind of receptors)?

A

-Most common are allergic reactions

Through H1 receptors:
-Contracts bronchial smooth muscles (bronchial constriction)
-Increases vascular permeability (edema)
-Causes vasodilation (increase blood flow)

Clinical manifestations: Mainly through reaction to histamine
-Itching
-anaphylaxis
-Hives

Reactions happen within 1 hour

40
Q

What is Wiskott-Aldrich Syndrome (WAS)? What does it manifest as?

A

-X-linked recessive disorder

-IgM antibody production is greatly depressed and antibody responses against antigens from bacterial walls are deficient

-Ressults from a mutation in the WAS gene that affects actin in the cytoskeleton which is important for platelet function

Manifests as:
▪ Bleeding secondary to thrombocytopenia (low platelet count)
▪ Eczema
▪ Recurrent infections of otitis media, pneumonia, herpes simplex, and cytomegalovirus

41
Q

What is DiGeorge Syndrome a result of? What does it result in? What does it present as?

A

-Results from lack or partial lack of thymus resulting in greatly decreased T-cell numbers

Results in thymic defects and no parathyroid gland (this regulates Ca+ concentration), Low Ca+ causes muscles to become rigid

▪ Cardiac and aortic defects
▪ Abnormal facial features
▪ Thymic aplasia/hypoplasia
▪ Cleft palate
▪ Hypocalcemia /Hypoparathyroidism

Presents as:
▪ Abnormal facial features ▪ Low-set ears
▪ Fish-shaped mouth

42
Q

What is Bare lymphocyte syndrome? What does it prevent? at what age do children typically die?

A

It is an immune deficiency with inability of lymphocytes and macrophages to produce major histocompatibility complex (MHC) class I or class II molecules

o Prevents effective antigen presentation
o Children with this usually die before the age of 5

43
Q

What does the term Susceptibility refer to?

A

how prone the host is to infection

(2 groups of people are more susceptible to COVID-19 Over the age of 60 and those with underlying medical conditions)