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immunology Flashcards

1
Q

homeostasis

A

what our bodies aim to maintain

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2
Q

what homeostasis involves

A

continuous motion, adaptation, and change by the body in response to environmental factors to maintain itself in a stable state

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3
Q

scientific definition of homeostasis

A

the tendency of biological systems to maintain relatively constant conditions in the internal environment while continuously interacting with and adjusting to changes originating within or outside the system

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4
Q

for most body systems, homeostatic mechanisms exist to

A

maintain and restore stability to body functions

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5
Q

for most systems, when a disordered physiological process occurs that causes, results from, or is associated with a disease or injury

A

the various systems of the body will act to maintain or return the body to homeostasis

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6
Q

homeostatic imbalance

A

inability to maintain homeostasis

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7
Q

homeostatic imbalance can occur as result of

A

illness or injury

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8
Q

homeostatic imbalance may lead to

A

disease or death

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9
Q

example of diseases that result from homeostatic imbalance

A 
diabetes
dehydration
hypoglycemia
hyperglycemia
gout
hypothermia
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10
Q

homeostasis and aging

A

body’s mechanisms to maintain homeostasis may weaken with age and lead to an unstable internal environment

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11
Q

subjective data

A

what the person says about themselves during history taking

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12
Q

objective data

A

what you as the healthcare professional determines during the physical examination

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13
Q

analyzing data

A

breaking down the data to examine and better understand
identifying issues, strengths, weaknesses
developing potential nursing diagnoses

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14
Q

pathology

A

the nature of the disease and its causes, processes, development, and consequences

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15
Q

physiology

A

describes mechanisms operating within an organism; the functions and activities of organs, tissues, and cells, and accompanying symptoms/occurrences/presentations

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16
Q

pathophysiology

A

the study of the physical and biological abnormalities occurring within the body as a result of the disease

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17
Q

immune system

A

our body’s defense system

protection from foreign organisms

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18
Q

protective response to injury or infection presents as

A 
inflammation 
warmth
redness
swelling
pain
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19
Q

all immune system cells arise from

A

the bone marrow

immune cells travel to other parts of the body

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20
Q

two categories of immunity

A 
innate = the immune system we are born with 
adaptive = the immune system that targets specific threats to the body
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21
Q

innate immunity

A
  • First line of defense
  • Rapid response
  • Not specific to particular pathogen
  • No memory
  • No long-lasting immunity
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22
Q

main components of innate immunity

A

Skin, mucous membranes, GI tract, Respiratory tract, nasopharynx, cilia, eyelashes, body hair
•Phagocytic cells – dendritic cells, eosinophil granulocytes, neutrophils, monocytes, macrophages, Natural killer (NK) cells
•Inflammatory process cells – endothelial cells, fibroblasts, thrombocytes, keratinocytes

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23
Q

lab tests for immune system functioning

A

c-reactive protein (increased levels can indicate inflammation or bacterial infection, marker for inflammation)
immunoglobulin (measures levels of different types of immunoglobulins/antibodies)
white blood cell count

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24
Q

components of white blood cells

A 
neutrophils 
lymphocytes
monocytes
eosinophils 
basophils
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25
Q

neutrophils

A

most common type of white blood cell

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26
Q

lymphocytes

A

two main types of lymphocytes: B cells and T cells

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27
Q

monocytes

A

foreign material, removes dead cells, and boost the body’s immune response

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28
Q

eosinophils

A

fight infection, inflammation, and allergic reactions

defend the body against parasites and bacteria

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29
Q

basophils

A

release enzymes to help control allergic reactions and asthma attacks

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30
Q

adaptive immunity

A

specific immune response stimulated by invading pathogen

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31
Q

t cells

A

originate in thymus
viral infection protection
helper cells (Th), cytotoxic cells (Tc), suppressor/regulatory cells

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32
Q

b cells

A 
originate in bone marrow 
produce antibodies (immunoglobulins) and develop into memory cells
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33
Q

antigen

A

any substance that combines with lymphocyte to trigger immune response

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34
Q

antibody

A

protein that binds to antigen on invading pathogen to eliminate pathogen

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35
Q

how invaders are eliminated (opsonization)

A

marking “invader” for ingestion and elimination by phagocytosis
“gluing” invader/bacteria to neutrophils and macrophages to facilitate phagocytosis

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36
Q

how invaders are eliminated (phagocytosis)

A

cell uses is plasma membrane to engulf the “invader” which is then digested

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37
Q

apoptosis

A
  • Physiological process of cell death
  • Regulates immune response by inducing timely death of T and B cells to prevent prolonged response that can cause problems for the body
  • Eliminates immune cells that target self-antigens to prevent attack on self
  • Used by certain immune system cells to destroy target cells
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38
Q

five primary classes of antibodies

A 
IgG
IgM
IgA
IgD
IgE
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39
Q

IgG antibodies

A

major type (~75%) in plasma
prominent in memory response to antigens already encountered
crosses placenta from mother to fetus

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40
Q

IgA antibodies

A

prominent in secretions and significant in first-line defense

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41
Q

IgM antibodies

A

main antibody synthesized by B cells in primary/initial antibody response

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42
Q

IgE antibodies

A

significant in allergic responses and worm infestations

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43
Q

IgD antibodies

A

significant in primary/initial response to new pathogens

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44
Q

immune response activation

A

immune system activated when a foreign organism/molecule/vaccine is recognized by circulating phagocytic cells (such as macrophages or dendritic cells) that capture and break it down, presenting antigens to B cell lymphocytes
•B cell produces specific antibody against specific antigen to eliminate foreign pathogen

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45
Q

immune response regulation

A

regulatory T cells control immune response by suppressing activity to prevent damage to self
•Regulatory T cells factor in preventing autoimmune responses and anaphylaxis

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46
Q

immune system resolution

A

immune response resolves when foreign antigen eliminated

•T and B cells have differentiated into memory cells for this specific pathogen pending future invasion

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47
Q

adaptive immunity naturally acquired

A 
active = antigens enter the body naturally; body induces antibodies and specialized lymphocytes 
passive = antibodies pass from mother to fetus via placenta or to infant via the mother's milk
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48
Q

adaptive immunity artificially acquired

A 
active = antigens are introduced in vaccines; body produces antibodies and specialized lymphocytes 
passive = preformed antibodies in immune serum are introduced by injection
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49
Q

pediatric differences with immunity

A

Newborns have some antibody protection from mother for first few months
Newborns are susceptible to infections as immune system is immature and developing
Newborns have low immunoglobulin concentrations
Newborns have less responsive Natural Killer cells
Newborns have immature monocytes and macrophages

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50
Q

older adult differences with immunity (immunosenescence)

A

immune system function declines with age
Increased susceptibility to infectious diseases and cancer:Macrophages destroy bacteria and cancer cells more slowly
T cells respond less quickly to antigens
Poorer response to vaccinations: Binding affinity of antibody to antigen decreased
Older adults may have an increase in autoimmune responses as immune system less able to distinguish self from nonself

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51
Q

general signs and symptoms of infection

A 
•Fever 
•Chills and sweats
•Change in cough or a new cough
•Sore throat
•Shortness of breath
•Nasal congestion 
stiff neck 
burning or pain with urination 
redness, soreness, or swelling 
diarrhea
vomiting
new onset of pain
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52
Q

4 phases of clinical process of infection

A

incubation period
prodromal stage
invasion period
convalescence

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53
Q

factors that influence the capacity of a pathogen to cause disease

A 
communicability 
immunogenicity
infectivity 
mechanism of action 
pathogenicity 
portal of entry 
toxigenicity 
virulence
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54
Q

incubation period

A

initial contact with infectious pathogen to the presentation of first symptoms
pathogen multiplying at portal of entry
ranges from 2-30 days depending on host resistance, virulence, and distance from entry to target organ

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55
Q

prodromal stage

A

first presentation of symptoms
1-5 days
non-specific symptoms such as malaise, fever, muscle aches

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56
Q

invasion stage

A

presentation of more specific prominent symptoms

pathogen multiplying and establishing in target organ

57
Q

convalescent stage

A

recovery
pathogen eliminated by immune system cells
memory cells developed

58
Q

epidemic

A

new cases of a disease exceed the normal occurrence during a given period of time
•An increase, often sudden, in the number of cases of a disease above what is normally expected in that population in that area
•Outbreak refers to epidemic for a limited geographic area; localized

59
Q

endemic

A

the steady presence of a disease in a defined geographic area or population
•The baseline of the disease in a community

60
Q

pandemic

A

when disease spread affects a large number of populations worldwide

61
Q

bacteria

A
  • One-celled
  • Multiply by simple division
  • Cause respiratory infections such as otitis media, tonsillitis, pneumonia, bronchitis, sinusitis, pharyngitis, whooping cough
  • Treat with antibiotics
62
Q

viruses

A

some of the smallest organisms known
•Invade cell, take over cell’s machinery, and force cell to reproduce virus
•Cause most respiratory infections such as influenza, the common cold/rhinovirus, some pneumonias and bronchiolitis/respiratory syncytial virus
•Treat with antiviral

63
Q

viruses can only replicate

A

inside the cell of the host invaded

no ability to metabolize on own

64
Q

basic structure of virus

A

consists of nucleic acid protected by a protein shell, the capsid
some may have additional envelope of fat

65
Q

viruses are classified by

A

format of nucleic acid in the virion (ribonucleic acid [RNA] or deoxyribonucleic acid [DNA])
Single stranded (ss) or double stranded (ds)
Presence of the reverse transcriptase (RT) enzyme Present in retrovirusesUsed to make complementary DNA from RNA (reverse of usual normal process of making RNA from DNA)

66
Q

pathologies of the immune system result from

A

increased or decreased white blood cells or immune system cells

67
Q

increased white blood cells

A

expected when fighting an infection

overactivity- hypersensitivity (can result in autoimmunity and allergies)

68
Q

decreased white blood cells

A

immunodeficient- predisposition to infections
secondary to decreased production- bone marrow problem or congenital disease
secondary to loss- infection of white blood cells

69
Q

human immunodeficiency virus (HIV)

A

caused by infection with HIV1 or HIV2 which are retroviruses in the retroviridae family lentivirus genus

70
Q

HIV produces

A

cellular immune deficiency characterized by the depletion of helper T lymphocytes (cd4 cells)
the loss of cd4 cells results in the development of opportunistic infections and neoplastic processes

71
Q

virus pathway

A

Virus attaches to target cell
Penetrates the host cell membrane
Viral RNA is transcribed into the host cell DNA (reverse transcription)
Viral genetic material is integrated into the host cell chromosome
Production of new viral components and assembly of new virions
Virions exit from host cell and maturation occurs

72
Q

HIV pathogenesis

A

Decrease in number of CD4 + Th cells due to infection and destruction by HIV
Glycoprotein gp120 on HIV facilitates entry into cell
HIV infected cells shed gp120 to induce apoptotic cell death of uninfected T lymphocytes, altering immune system response and impeding clearance of HIV
HIV infected CD 4 +Th cells fuse leading to formation of multinucleated cell (syncytium)
With fusion there is death of the uninfected cell

73
Q

characteristics of HIV

A

Can kill host in a short period of time (relatively rare)
Can be completely eliminated from body Or can enter a state of latency
Retrovirus with ability to convert own RNA to DNA with the aid of an enzyme (reverse transcriptase)
Retroviruses are very fragile – easily inactivated by mild detergent, gentle heating, drying or moderately high or low pH
Transitions from acute to chronic infection with persistent replication – HIV unique among viruses
Two primary types of HIV: HIV 1 (most common) and HIV 2 (less virulent; lower viral loads and slower decrease of CD4)

74
Q

three stages of HIV

A

acute seroconversion/acute HIV infection
clinical latency/asymptomatic or chronic HIV infection
acquired immunodeficiency syndrome (AIDS)

75
Q

acute seroconversion/acute HIV infection

A 
2-4 weeks post HIV infection 
flu like symptoms such as fever, malaise, generalized rash
HIV multiplies and destroys cd4 cells
body producing HIV antibodies
HIV level (viral load) high
risk of HIV transmission high
76
Q

clinical latency/asymptomatic or chronic HIV infection

A

generalized lymphadenopathy common
may have no symptoms
HIV multiplies at low levels

77
Q

acquire immunodeficiency syndrome (AIDS)

A 
most severe phase of HIV infection 
HIV level (viral load) high 
risk of transmission high 
cd4 cells low 
risk of opportunistic infections high 
prognosis approximately 3 years
78
Q

clinical manifestations of HIV

A

Patients may manifest one of several different conditions:
Serologically negative (no detectable antibodies)
Serologically positive (positive for antibodies against HIV )
Early stages of HIV disease
Early stages of AIDS illness
Early symptoms are nonspecific to HIV and include fatigue, fever, muscle aches, and headaches (flu like symptoms)
Early stages of HIV are asymptomatic and may last as long as 10 years in untreated people, during which viral load increases and numbers of CD4+ cells progressively decrease

79
Q

over time (8-15 years) chronic infection by HIV causes

A

a depletion in function cd4 T helper cells leading to compromised immune system

80
Q

HIV stimulates systemic immune activation

A

accelerates decline in overall immune competence - increase in dysfunction of T cells and inflammation

81
Q

what percentage of cd4 cells are lost in the early stages of an acute HIV infection

A

80%

82
Q

HIV infection leads to increased gut permeability

A

GI tract major site of HIV replication

83
Q

transmission of HIV

A 
blood transfusion 
condomless sex
needle sharing 
mother to child 
accidental exposure
84
Q

HIV can directly damage the

A

brain (causes cognitive impairment)
gonads (causes hypogonadism)
kidney (causes renal insufficiency)
heart (causes cardiomyopathy)

85
Q

range of HIV manifestations

A

asymptomatic to AIDS

86
Q

AIDS is defined by

A

serious opportunistic infections or cancers or a cd4 count of <200/mcL

87
Q

how can HIV be diagnosed

A

antibody, nucleic acid, or antigen testing

88
Q

nucleic acid tests

A

check blood for presence of the virus’ RNA

determine how much virus is present (viral load)

89
Q

antibody and antigen tests

A

test for presence of HIV antibodies and antigens

HIV produces antigen p24 (before body starts producing antibodies to HIV)

90
Q

antibody tests

A

test for HIV antibodies
venous blood for better detection
can use oral fluid or finger prick blood (later detection)

91
Q

opportunistic fungal infections

A 
Oropharyngeal candidiasis
Candida esophagitis
Vulvovaginal candidiasis
Cryptococcus- meningitis/ pneumonia
Pneumocystisis jiroveci pneumonia (PJP)
92
Q

opportunistic protozoal infections

A

Cryptosporidium
Toxoplasmosis
Isosporiasis

93
Q

opportunistic bacterial infections

A 
Mycobacterium avium complex (MAC)
Tuberculosis
Pneumonia
Bacillary angiomatosis
Listeria monocytogenes
Pelvic inflammatory disease
Salmonellosis
94
Q

opportunistic viral infections

A 
Cytomegalovirus (CMV)
Herpes simplex
Herpes zoster
Oral hair leukoplakia (EBV)
Progressive multifocal leukoencephalopathy (PML)
Castleman’s disease
95
Q

opportunistic cancers

A

Karposi’s sarcoma
Invasive cervical cancer
Lymphoma

96
Q

other opportunistic infections

A

Cellulitis
Osteomyelitis
Endocarditis

97
Q

clinical manifestations of AIDS

A

Fatigue
Unexplained weight loss: greater than 10%
Fever
Lymphadenopathy
Skin or mucous membrane lesions: purplish-red nodules
Cough
Persistent diarrhea
Tongue/mouth “thrush”
Perianal vesicular and ulcerative lesions of herpes simplex infection
AIDS related cancer-Kaposi’s sarcoma
Cytomegalovirus retinitis

98
Q

common signs of AIDS in pediatrics

A

Oral candidiasis
Bacterial infections
Failure to thrive
Lymphadenopathy

99
Q

how neonates get AIDS

A

transmission may be placental
contact with maternal blood at birth
postnatal exposure to parent who is exposed (eg. breastfeeding)

100
Q

systemic lupus erythematosus

A

when the immune system attacks the body’s own tissues and organs
systemic autoimmune disease
chronic, inflammatory, connective tissue disease of unknown origin

101
Q

lupus involves

A

many organs and body systems including skin, joints, kidneys, lungs, CNS, hematopoietic system

102
Q

lupus is characterized by

A

remission and exacerbations

103
Q

lupus ranges from

A

a mil episodic disorder to rapidly fatal disease process

104
Q

3 major classifications of lupus

A

discoid lupus erythematosus (affects skin only), systemic lupus erythematosus (affects one or more organs), and drug-induced.

105
Q

suspected triggers of lupus

A

exposure to ultraviolet lights
estrogen
pregnancy infections
medications

106
Q

autoantibodies

A

antibodies that react to the client’s own tissues

107
Q

autoantibody production results from

A

hyperreactivity of B cells because of disordered T cell function

108
Q

drugs that can cause drug induced lupus

A

Procainamide (used to treat heart arrhythmia)
Hydralazine (used to treat hypertension)
Quinidine (used to treat heart arrhythmia and malaria)

109
Q

pathophysiology characteristics of lupus

A

Large variety of autoantibodies are produced
Autoimmune reaction is targeted at components of the cell nucleus
Production of pathogenic autoantibodies by T and B cells which attack own tissues and organs
Immune complexes containing antibodies against DNA deposit in the membranes of the:
Kidneys
Heart
Brain
Joints
Skin
Results in multiorgan inflammation: Joints, skin, kidneys, blood cells, brain, heart, lungs, GI

110
Q

clinical manifestations of lupus

A 
arthralgia or arthritis 
vasculitis and rash 
renal disease
hematological abnormalities 
cardiovascular disease 
photophobia 
fever 
weight loss 
excessive fatigue
111
Q

involved body systems with lupus

A 
Dermatological 
Musculoskeletal
Cardiopulmonary 
Renal Disease
Nervous System
Hematological
112
Q

lupus nephritis

A

Inflammatory complication
Complexes of autoantibodies and complement accumulate in the glomerulus, causing cell proliferation, inflammation, and injury
Clinical manifestations include:
Proteinuria, edema and signs of nephrotic syndrome (hypoalbuminemia, hypolipidemia, lipiduria, decreased vitamin D levels, hypothyroidism)
Disease progression may be silent or may progress to end-stage kidney failure

113
Q

nervous system manifestations of lupus

A

Generalized or focal seizures
Cognitive dysfunction (disordered thought processes, disorientation, memory deficits, and psychiatric symptoms such as severe depression and psychosis)
Stroke or aseptic meningitis
Headaches

114
Q

hematological manifestations of lupus

A

Anemia
Mild leukopenia
Thrombocytopenia
Increased or decreased coagulopathy

115
Q

does a patient have increased or decreased coagulopathy with antiphospholipid antibody syndrome?

A

increased

116
Q

integumentary and lupus

A 
Alopecia
Dry, scaly scalp
Keratojunctivitis
Malar butterfly rash
Palmar or discoid erythema
Urticaria
Periungal erythema
Purpura, Petechiae
Leg Ulcers
117
Q

diagnosing lupus

A

Fulfillment of at least four criteria–
with at least one clinical criterion AND one immunologic criterion
OR 2) Lupus nephritis as the sole clinical criterion in the presence of ANA
or anti-dsDNA antibodies.

118
Q

SOAP BRAIN MD for lupus

A 
serositis 
oral ulcers
arthritis 
photosensitivity 
blood 
renal 
ANA
immunologic 
neurologic 
malar rash 
discoid rash
119
Q

specific labs to assess for lupus

A

Antibody titers (i.e. anti-DNA, anti-Sm, ANA)
Anti-Sm = anti-Smith antibodies have high specificity for SLE
LE cell preparation
Serum complement levels
Urinalysis
Positive LE preparation, anti-DNA antibody or antibody to Sm nuclear antigen
Proteinuria or cellular casts
Hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia
Antinuclear antibodies
*Specific tests to address system clinical manifestations

120
Q

signs and symptoms of rheumatoid arthritis

A

Inflammation and swelling of joint synovium with subsequent destruction of articular structures.
Systemic inflammation of any other organ systems, leading to associated comorbidities such as cardiovascular disease, pleural effusions, etc. (which can increase morbidity and mortality)
Pain, fatigue, and disability—decrease quality of life

121
Q

the synovitis, swelling, and joint damage that characterize active RA are

A

the end results of complex autoimmune and inflammatory processes that involve components of both the innate and adaptive immune systems.

122
Q

pathophysiology for RA

A

The “trigger” causes the body to create autoantibodies that aim for joint linings
Autoantibodies include rheumatoid factor (RF) and anti-cyclic citrullinate peptide antibody (anti-CCP).
Autoantibodies bind with their target antigens in blood and synovial membranes, forming immune complexes [antibody-antigen complexes] such as RF binds with IgG forming an immune complex.
Immune complexes deposited in synovial membrane attract white blood cells (ie. granulocytes) and activate inflammatory process
T cells activated to secrete inflammatory cytokines [including tumour necrosis factor alpha (TNF-α), Interleukin (IL)-1, IL-6, IL-8, transforming growth factor beta (TGF-β), fibroblast growth factor (FGF) and platelet-derived growth factor (PDGF)]
Cytokines stimulate immune and inflammatory response. Impaired clearance of immune complexes leads to sustained inflammatory response.
Now activated, B and T lymphocytes increase production of rheumatoid factors and enzymes that, in turn, increase and continue the inflammatory response.
Synovial membrane is damaged by the inflammatory and immune process.
Inflammation then spreads and involves synovial blood vessels (become occluded).
As blood flow decreases, metabolic needs increase, and hypoxia and metabolic acidosis occur.
Acidosis stimulates synovial cells to release hydrolytic enzymes into surrounding tissues
Inflammation causes coagulation, and deposits of fibrin on the synovial membrane, in the intracellular matrix, and the synovial fluid.
Fibrin develops into granulation tissue (pannus) over denuded areas of the synovial membrane.
Neutrophils are attracted to the site
Proteolytic enzymes are released
Thickening of synovial lining occurs and cartilage is damaged
Chronic inflammation causes hypertrophied synovial membrane which invades cartilage, ligaments, tendons and joint capsule

123
Q

lab tests for RA

A 
Rheumatoid factor (RF)
Cyclic Citrullinated Peptide (CCP)
Erythrocyte Sedimentation Rate (ESR)
C-Reactive Protein (CRP)
Antinuclear Antibody (ANA)

None of these tests can singularly conclude that a patient has rheumatoid arthritis
The combined results from all, alongside a number of other criteria including physical symptoms and genetics, are used to reach a rheumatoid arthritis diagnosis.

124
Q

clinical manifestations of RA

A

onset = usually gradual, may be abrupt
course = generally progressive, characterized by remission and exacerbations
pain and stiffness = predominant on arising lasting > 1 hour, also occurs after prolonged inactivity
affected joints = appear red, hot, swollen, “boggy” and tender to palpation, decreased range of motion, weakness
systemic manifestations = fatigue, weakness, anorexia, weight loss, fever, rheumatoid nodules, anemia

125
Q

deformities of chronic advanced RA

A

swan neck deformity
boutonniere deformity
ulnar deformity
hallux valgus

126
Q

swan neck deformity

A

flexion of the distal interphalangeal and metacarpophalangeal joints, hyperextension of proximal interphalangeal joint

127
Q

boutonniere deformity

A

avulsion of extensor hood of the proximal interphalangeal joint

128
Q

ulnar deformity

A

ulnar deviation of the fingers at the metacarpophalangeal joint

129
Q

hallux valgus

A

displaced toes, lateral angulation

130
Q

rheumatoid nodules

A

Subcutaneous nodes
Firm, non-tender
Often found on fingers and elbows

131
Q

sjorgen’s syndrome

A

Decreased lacrimal and salivary gland secretion

Decreased tearing and photosensitivity

132
Q

felty’s syndrome

A

Inflammatory eye disorders

Splenomegaly, lymphadenopathy, pulmonary disease, blood dyscrasias (i.e. anemia)

133
Q

complications of RA

A 
Joint destruction
Flexion contractures
Hand deformities- difficulty grasping
Nodular myositis
Cataracts- loss of vision
Nodules on vocal chords
Carpal tunnel syndrome
Cardiac complications
134
Q

signs and symptoms of juvenile idiopathic arthritis (JIA)

A

Arthritis present for at least 6 weeks before diagnosis (mandatory for diagnosis of JIA)
Either insidious or abrupt disease onset, often with morning stiffness or gelling phenomenon and arthralgia during the day
Complaints of joint pain or abnormal joint use
History of school absences or limited ability to participate in physical education classes
Spiking fevers occurring once or twice each day at about the same time of day
Evanescent rash on the trunk and extremities
Psoriasis or more subtle dermatologic manifestations

135
Q

JIA differs from RA

A

Large joints are most commonly affected
Chronic uveitis
Serum tests may be negative for rheumatoid factor, if rheumatoid factors are positive the child will have a worse prognosis
Subluxation and ankyloses may occur in the cervical spine if disease progresses
JIA that continues through adolescence can have severe effects on growth and adult morbidity

136
Q

pediatric severe combined immunodeficiency (SCID)

A

Severe combined immunodeficiency, SCID, is a rare genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in differing clinical presentations.
Life-threatening syndrome of recurrent infections, diarrhea, dermatitis, and failure to thrive
Most patients present before age 3 months; With no intervention, SCID leads to severe infection and death by age 2 years

137
Q

SCID results from and causes changes in

A

Results from mutations in at least 13 different genes
Causes changes in lymphocyte development and function which blocks differentiation and proliferation of T cells and sometimes, B and NK cells

138
Q

pathophysiology of SCID

A

X-linked recessive that affects more males than females
Combined deficiency that affects both T and B cells with little to no antibody production
Few detectable lymphocytes in the circulation and secondary lymphoid organs

139
Q

clinical manifestations of SCID

A

Susceptibility to infections occurs most commonly in the first month of life
Suffers from chronic infections and fails to completely recover from infections
FTT is a consequence of persistent illnesses

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