Lymphatic Vessels

 transport fluids that have escaped from the blood

vascular system back to the blood
 one-way system; flows only to the heart
 low pressure but pumpless system

Lymph
 excess tissue fluids
 water and small
amounts of proteins
Right Lymphatic Duct – drains
lymph from the right arm and the
right side of the head and thorax

Thoracic Duct – receives lymph

from the rest of the body

Cisterna Chyli – receives lymph

from the digestive organs
 filter lymph
 protect the body by removing foreign
materials such as bacteria and tumor
cells
 concentrated mostly in the axillary,
cervical and inguinal area
 produce and store lymphocytes and
macrophages
 organs that house phagocytic cells and
lymphocytes
SPLEEN
 filters blood of bacteria, viruses and
other debris
 destroys worn out RBCs (Red
Pulp)
 stores lymphocytes (White Pulp)
THYMUS
 a lymphatic mass found low in the
throat overlying the heart
 functions only during youth
 produces thymosin, that programs
certain lymphocytes to carry out
their protective role

BONE MARROW
 produces white blood cells
 Mucosa Associated Lymphatic Tissue -
protects the upper respiratory and digestive
tracts
TONSILS
 small masses of lymphatic tissue
that ring the pharynx
 trap and remove bacteria or other
foreign pathogens that enter the
throat
PEYER’S PATCHES
 found in the wall of the small
intestine
 trap and remove foreign materials in
the intestines
 NON-SPECIFIC DEFENSE SYSTEM
 mechanical barriers that cover the body surfaces
 cells and chemicals of the body that act initially to
ALL invading pathogens
Surface Membrane Barriers
Intact Skin Intact Mucous Membrane
 acidic skin  mucus
secretions  nasal hairs
 sebum  cilia
 keratin  gastric juice
 acid mantle of the vagina
 lacrimal secretions
 saliva
 2nd line of Defense

Inflammatory Response
 second line of defense
 non-specific response triggered whenever body tissues
are injured
 chemotaxis
 five cardinal signs: RUBOR, CALOR, DOLOR,
TUMOR and LIMITATION of JOINT MOVEMENT
 inflammatory chemicals: HISTAMINE & KINNINS

 Phagocytosis- macrophages & leuocytes

SPECIFIC DEFENSE SYSTEM
Immune Response
 third line of defense
 recognizes foreign molecules (antigens) and
acts to inactivate or destroy them
 functions: DEFENSE, HOMEOSTASIS,
SURVEILLANCE
 characteristics:
1. Self or Non-self recognition
2. Antibody production
3. Memory
4. Self Regulation
CELLS of the IMMUNE SYSTEM
Lymphocytes
T Cells
 lymphocytes that mature in the thymus

Helper T cells – commander; detect the infection

and initiates T cell and B cell responses
Cytotoxic T cells – detect and kill infected body
cells
Suppresor T cells – slow or stop the activated T
cell or B cell when infection has been
conquered
B Cells
 lymphocytes that mature in the bone marrow
 precursor of plasma cell specialized to
recognize specific antigens
Plasma Cells – produce antibodies directed
against specific foreign antigens
Memory Cells – enable the body to respond
quickly and efficiently to subsequent infections
from the same antigen
Interferon - nonspecific viricidal protein capable of
inducing a immune response
ANTIBODIES
 a.k.a. Immunoglobulins
 soluble proteins secreted by activated B cells or
plasma cells in response to an antigen
ANTIBODY CLASSES
 IgD – activates B cells
 IgM – found in B cells or plasma; first to increase in
immune response; activates complement; form natural
AB; involved in ABO incompatibility
 IgG – found in plasma; most common AB in the blood;
main antibody of primary and secondary responses;
provides passive immunity to fetus; anti-bac, viral,
anti-toxin AB
 IgA – found in mucosal secretions (tears/saliva);
mucous membranes; colostrum (protects newborn)
 IgE – secreted by plasma cells; triggers release of
histamine; mediates inflammatory and allergic
reactions; binds to mast cells
ANTIBODY
Functions:
 Agglutination – clumping of foreign cells
 Precipitation – formation of insoluble
complex when an antibody binds with a
soluble antigen
 Neutralization – binding of antibodies to
toxins to block its harmful effects
 Lysis – cell rupture
 Opsonization – coating of bacteria by
antibodies to increase susceptibility to
phagocytosis
Complement System
 blood-borne proteins
 activated when an antibody couples with its
antigen
 causes lysis and death
functions:
 defends the body against bacterial infection
 bridges natural and acquired immunity
 disposes the byproducts of inflammation
IMMUNE RESPONSES
stages:
 Recognition – initiating event wherein the
immune system recognizes the antigens as
foreign
 Proliferation – stimulation of the dormant B
and T cells to divide
 Response – either cellular or humoral
 Effector – series of events that results in
total destruction of the foreign material
Humoral Immune Cellular Immune
Response Response
 antibody mediated  Cellular immunity
 provided by B
lymphocytes
 Provided by T-cells
IMMUNE RESPONSES Acquired
Immunity

Naturally Acquired
Acquired Immunity

ACTIVE PASSIVE ACTIVE PASSIVE

Infection; Antibodies Vaccine; Injection of
contact pass from dead or immune
with mother to attenuated serum
pathogen fetus via pathogens
placenta; or
to infant in
her milk
NATURAL ACTIVE
 Pathogens enter body and
cause illness
 AB form in host
 Memory: Yes
 Example: Chickenpox once
ARTIFICIAL ACTIVE
 Vaccine (live or attenuated
org) injected to person
 No illness results but AB
form
 Memory: Yes
 Example: Measles vaccine
and gains immunity
NATURAL PASSIVE ARTIFICIAL PASSIVE

 AB passed directly from  AB injected to person (anti-

mother to child to provide serum) to provide
temporary protection temporary protection or
 Memory: No minimize severity of
 Example: Placental infection
passage during pregnancy  Memory: No
or breastfeeding  Example: Gammaglobulin
if recent exposure to
microbe
 Rejection- complex process involving Type IV
cell-mediated hypersensitivity but can also
involve humoral response

Types:
1. Host vs Graft disease
2. Graft vs Host disease
 Hyperacute- occurs right away

 Acute- occurs in several weeks

 Chronic- months-years
 Allograft (homograft)- same species
 Isograft- tissue transferred between two
genetically identical bodies (twins)
 Autograft- from self
 Xenograft (heterograft)- transferred from a
member of one species to a different species
(pig to man)
-reflection of excessive or aberrant immune
responses
-abnormal, heightened reaction to any type of
stimuli
-usually not on the first exposure
-re-exposure after sensitization in a
predisposed individual
- at times, damaging immune responses to
normally harmless substances
Anaphylactic (Type I) Hypersensitivity
 most severe form
 characterized by edema in many tissues
 immediate reaction beginning within minutes of
exposure to an antigen
 mediated by IgE antibodies
 requires previous exposure to specific antigen
 primary chemical mediators skin, lungs, GIT
 delayed reaction may occur, 24 hours
 local and systemic anaphylaxis
Allergic Reactions

*IgE = allergic
disorders, some
parasitic infections
 trigger mast cells or
basophils to release
chemical mediators
(respiratory and
digestive tract)
 allergic skin
reactions, asthma,
hay fever
 time from exposure to antigen to onset of symptoms:
indicates severity
* faster onset, more severe reaction
 mild
peripheral tingling, sensation of warmth, fullness in mouth
and throat, nasal congestion, periorbital swelling, pruritus,
sneezing, tearing of eyes
*onset of symptoms: w/in first 2 hrs of exposure
 moderate
flushing, warmth, anxiety, itching, * + symptoms of mild rxn
 serious
bronchospasm, edema of airways or larynx, dsypnea,
coughing, wheezing
*onset of symptoms: w/in 1st 2 hrs upon exposure

 severe
- abrupt onset
bronschospasm, laryngeal edema, severe dyspnea, cyanosis,
hypotension, dysphagia, abdominal cramping,
- vomiting, diarrhea, seizures may occur
- cardiac arrest and coma
- strict avoidance of potential allergens
allergic to insect stings
 avoid areas populated by insects
 appropriate clothing
 insect repellents
- epinephrine (Epi-Pen)
- screening for med allergies before administration
drug Hx, skin tests
allergy Hx (contrast agents, foods, insect stings, latex, meds)
- allergic to insect venom: insect immunotherapy
- desensitization: controlled anaphylaxis w/ gradual release of
mediators
- *NO LAPSES in therapy – prevent reappearance of allergic
rxn
- evaluate respiratory and cardiovascular fxns
- cardiac arrest: CPR
- high conc. O2 : during CPR, cyanosis, dyspnea, wheezing
- epinephrine (1:1000, SC, upper arm or thigh ff by continuous
IV)
- antihistamines and corticosteroids: prevent recurrences, tx for
urticaria and angioedema
- IVfluids (NSS), volume expanders, vasopressors: maintain BP
and normal hemodynamic status
- aminophylline and corticosteroids: bronchospasm, Hx of
asthma, COPD
- glucagon : hypotension unresponsive to vasopressors
- close monitoring w/in 1st 12-14 hrs esp pts w/ severe rxns
 allergic reaction to natural rubber proteins (Hevea proteins)
 Not all objects composed of latex have the same ability
to stimulate allergic response

 Health care workers, pts w/ atopic allergies, pts w/

multiple surgeries, people in factory manufacturing
latex products, females, pts. w/ spina bifida, food
handlers, hairdressers, automechanics, police

 *food handlers w/ latex gloves may stimulate allergic

response

 cross reaction to kiwis, bananas, pineapples, passion

fruits, avocados, chestnut
 most frequent source of infection: cutaneous route
 powder to facilitate wearing latex gloves may be
carriers of latex proteins; the particles become airborne
and can be inhaled or settles on skin, mucus
membranes or clothing
 mucosal exposure: latex condoms, catheters, airways,
nipples
 parenteral: Iv lines, hemodialysis equipment
 household items: balloons, feminine hygiene pads,
diapers, diaphragms, wheelchair cushions
Cytotoxic (Type II) Hypersensitivity
 system mistakenly identifies a normal body
constituent as foreign
 binding of either IgG or IgM antibody to a cell-
bound antigen
 activation of the complement cascade
 destruction of the cell to which the antigen is bound
 e.g. Myasthenia gravis,drug-induced immune
hemolytic anemia, Rh-hemolytic disease of the
newborn, incompatibility reactions in blood
transfusions
Immune Complex (Type III) Hypersensitivity
 Antigen-AB complexes are formed
 cleared from circulation by phagocytic action
 deposited in tissues or vascular endothelium
 increased amount of circulating complexes,
presence of vasoactive amines
 increase in vascular permeability, tissue injury
 joints and kidneys
 e.g. SLE, rheumatoid arthritis, serum sickness
Delayed – Type (Type IV) Hypersensitivity
 “cellular hypersensitivity”
 24-72 hours after exposure
 mediated by sensitized T cells and macrophages
 e.g ID injection of tuberculin antigen or PPD
 lymphokines are released -> macrophages  lysozymes  tissue
damage
 edema and fibrin - + tuberculin reaction
 e.g. contact dermatitis – primary exposure results in sensitization
 hapten + proteins/carriers Langerhans cells in skin - itching,
erythema, raised lesions
 Delayed hypersensitivity; transplant rejection
 Chronic inflammatory disease that can affect
virtually any organ system
 Collagen disorder
 AutoAB affects connective tissue
 10 times more frequent in women than men
(androgen protects and estrogen favors SLE
development)
 Pathophysiology:
Abnormal suppressor T-cell functioning>>>
excessive functioning of helper T cells>>>
B-cell hyperactivity
 Autoantibodies combine with corresponding antigen>>>
immune complexes deposited in vascular and tissue
surfaces
 inflammation>>> local tissue injury
 CLINICAL MANIFESTATIONS
 Musculo-skeletal system:
▪ Arthralgia
▪ Arthritis
▪ Joint swelling, tenderness
▪ Pain in movement
▪ Morning stiffness
 CLINICAL MANIFESTATIONS
 Integumentary System
▪ Discoid lupus erythematosus (only the skin)
▪ Butterfly-shaped rashes across the bridge of
nose and cheeks.
▪ Lesions worsen during flares or provoked by
sunlight or artificial UV light.
▪ Photosensitivity
▪ Alopecia
 CLINICAL MANIFESTATIONS
 GI system:
▪ Oral ulcers
▪ Anorexia

 CV system:
▪ Pericarditis
▪ Early atherosclerosis
 CLINICAL MANIFESTATIONS
 Urinary System:
▪ Renal damage
▪ Can lead to hypertension

 CNS:
▪ Neropsychiatric presentation
▪ Depression
▪ Seizure
▪ Peri-neuropathy
Discoid rash
Oral ulcers
Photosensitivity
Arthritis
Malar rash
Immunologic disorder
Neurologic disorder
Renal disorder
Anti-nuclear antibodies
Serositis
Hematologic disorder

* If 4 of these criteria are present at any time during the course

of disease, a diagnosis of SLE can be made with 98%
specificity and 97% sensitivity.
 Diagnostic Findings
 CBC-pancytopenia
 Increased ESR
 (+) ANA
 (+) Anti-DNA
 (+) LE factor
 (+) Anti-Sm: most specific for SLE
 MEDICAL MANAGEMENT
 Intervention directed at controlling increased disease
activity or exacerbations.
 Goals: prevent progressive loss of organ function,
reduce likelihood of acute disease, minimize disease
related disability, and prevent complication from
therapy.
 NSAID
 Corticosteroids
 Antimalarial medications: Hydroxychloroquine
 Immunosuppressive agents
 Plasmapheresis
 NURSING MANAGEMENT
 Common problems: fatigue, impaired skin
integrity, body image disturbance, and knowledge
deficit
 Avoid exposure to sunlight
▪ Sunblock
▪ Long-sleeved clothings
▪ Hats
▪ Sunglasses
 High caloric and CHON diet
 A defect or deficiency in phagocytic cells, B
lymphocytes, T lymphocytes, or the
complement system

Classified either primary or secondary

Cardinal symptoms:

Chronic or recurrent severe infections

Infections caused by unusual organisms

Normal body flora infections

Poor response to treatment of infections

Chronic diarrhea
 Rare
Genetic in origin
Caused by intrinsic defects in the cells of the
immune system
Infants and young children
Symptoms develop early in life after
protection from maternal antibodies decreases
Without treatment children and infants seldom
survive to adulthood
Phagocytic dysfunction

B-cell deficiency

T-cell deficiency

Combined B-cell and T-cell deficiency

Deficiencies of the Complement System

 Clinical manifestations

Bacterial, fungal (Candida), and viral

(Herpes) infections
Recurrent furunculosis, cutaneous abscess,
chronic eczema, bronchitis, pneumonia,
chronic otitis media, and sinusitis
Severe neutropenia = deep and painful
mouth ulcers, gingivitis, stomatitis and
cellulitis
 Hyperimmunoglobulinemia E
Syndrome
Formerly known as Job syndrome
WBC can’t produce inflammatory
response to skin infection
Results in deep-seated cold abscess
2 TYPES:
Lack of differentiation of B-cell
precursors into mature B cells

Lack of differentiation of B cells

into plasma cells
 aka Common Variable Immunodeficiency
(CVID)
most common in adults in either gender often onset at
second decade of life
symptomatic 15-35 y/o
major immunologic features: recurrent pyogenic
infections, inc autoimmune disease, dec level of total
Ig (IgG below 250 mg/dl)
B-cell count usually normal
etiology unknown and multifactorial
ranges from IgA deficiency (lack plasma cell
production) to severe panhypoglobulinemia
 CVID
Lymphoid hyperplasia of small intestine and spleen
Gastric atrophy by biopsy (Pernicious anemia)
Susceptible to encapsulated bacteria infections (H.
influenzae, S. pneumoniae, S. aureus)
Frequent respiratory tract infections = chronic progressive
bronchiectasis and pulmonary failure
MEDICAL MANAGEMENT
Intravenous immunoglobulin (IVIG)
Prophylactic antibiotic not needed unless
chronic respiratory disease is present

Antimicrobial therapy
For respiratory infections to prevent
pneumonia, sinusitis and otitis media

Metronidazole (Flagyl)
10-day course treatment intestinal
infection with G. lamblia
 Thymus gland fails to develop normally
during embryogenesis

Leads to opportunistic infection

Genetic in origin

Because of regulatory role of T-cells in

immune system function, loss of function
leads to some loss of B-Cell activity
 DiGeorge Syndrome
aka Thymic Hypoplasia
▪ results from absence of genes on
chromosome 22
▪ variation of symptoms depends on
amount of affected genetic material
▪ symptoms immediately after birth
 DiGeorge Syndrome
Hypoparathyroidism with resultant hypocalcemia
within 24 hours of life resistant to standard
therapy
Congenital heart disease > CHF
Characteristic facial features
Renal abnormalities
Susceptible to yeast, fungal, protozoan, and viral
infections, severe childhood diseases (chickenpox,
measles, and rubella) may be fatal
 Pneumocystis carinii prophylaxis
Oral calcium supplementation w/ Vit. D or PTH for
hypocalcemia
Thymus graft
Transplantation of fetal thymus, postnatal thymus
Human Leukocyte Antigen – matched bone
marrow
IVIG therapy
Used if antibody deficiency exists
 Ataxia – Telangiectasia
Autosomal recessive disorder
Associated with neurologic, vascular, endocrine,
hepatic and cutaneous abnormalities
Accompanied by progressive cerebellar ataxia,
telangiectasias, recurrent bacterial infection of
sinuses and lungs, and increased incidence of
cancer
 Severe Combined
Immunodeficiency Disease
(SCID)
Early onset of infections
Lymphoid aplasia, thymic dysplasia
Inheritance x-linked, autosomal recessive,
sporadic
Wiskott-Aldrich Syndrome

Variation of SCID compounded by

thrombocytopenia.

Poor prognosis because most affected infants

develop overwhelming fatal infections.
Ataxia – Telangiectasia
Ataxia and telangiectasia in first 4 years of life
Some symptom free for first 10 years, 2nd
decade = chronic lung disease, mental
retardation, neurologic sx, physical disability
Long-term survivors develop progressive
deterioration of immunologic and neurologic
functions
Cause of death = overwhelming infection and
lymphoreticular or epithelial cancer.
 Severe Combined Immunodeficiency Disease
(SCID)
Onset at first 3 months of life
Respiratory infections, pneumonia, thrush, diarrhea
and failure to thrive
Infections often resistant to treatment
Shedding of virus RSV and CMV from respiratory and
GIT is persistent.
Maculopapular and erythematous skin rashes may
occur
Vomiting fever and persistent diaper rash
Ataxia – Telangiectasia
Antimicrobial therapy

Postural drainage and physical therapy for

chronic lung disease

Transplantation of fetal thymus tissue

IVIG administration
 Severe Combined
Immunodeficiency Disease
(SCID)
Stem cell and bone marrow transplantation
Donor is ideally HLA-identical sibling
IVIG replacement
Administration of thymus-derived factors
Thymus gland transplantation
 Prevent transmission of infection

Reverse isolation and aseptic

technique

Monitor patient at all times

 May be primary or secondary

C2 and C3 deficiencies = diminished

resistance
SECONDARY
IMMUNO-
DEFICIENCY
 more common than primary
occur as a result of an underlying disease process or
from the treatment of other disease
common causes: malnutrition, chronic stress, burns,
uremia, DM, certain autoimmune disorders, certain
viruses, exposure to immunotoxic medications and
chemicals
AIDS is the most common
Patients have immunosupression and referred to as
immunocompromised hosts
 A disorder characterized by a profound defect in
cellular & humoral immunity weakening the body’s
ability to fight diseases. Making the patient highly
susceptible to certain opportunistic infections.
 Illnesses which are common complications in
patients with AIDS, it is caused by various
organisms, some of which usually do not cause
disease in persons with normal immune systems.
E
T
I
O
L
O
G
Y
 Primary Infection
It is defined as the period from infection
to the development of antibodies to
HIV.
• Intense Viral replication and widespread
dissemination of HIV throughout the body.
• VIREMIA
– Symptoms: None to Severe flu-like
• Window Period
– HIV antibodies – seen in the sera of infected
individuals – 2 to 3 weeks post infection
(6months at times)
• Antibodies lack ability to inhibit virus.
 Primary Infection
• Neutralizing Antibodies are detected – HIV is established
already
1. High Viral Replication and killing of CD4 T cells
a. High HIV in Blood & Low CD4 T cell count
2. Symptoms: Mononucleosis (Acute Phase)
• Fever
• Enlarged Lymph Nodes
• Rash
• Muscle Aches
• Headaches
 Primary Infection
• Viral Set point occurs (6 weeks after symptoms are
detected / Steady State)
a. Immune System produces antibody molecules to
contain the virus; bind to free HIV particles – removed.
i. CD4 T cells stimulate other immune cells (CD8
lymphocytes)

Normal: CD4T cell count: 800-1200/microliter of blood

Usually lasts 100 days
AIDS: lasts 2 days
 It is defined as a chronic asymptomatic state after
viral set point.
• Rate of viral replication reach a low but steady levels
(at a set point)
– Set Point varies among patients
– Subsequent rate of the disease
– Average 8-10 years before major HIV complication
• Apparent Good Health with few if any symptoms
– CD4 T cells levels remain high – preserve defense
mechanism to other pathogens.
 CD4 T cell levels gradually falls
 Consists of symptomatic conditions in HIV infected
patients that are not classified in category C.
• Condition is due to HIV infection or a defect in
cellular immunity.
• Condition must be considered to have clinical
course or require management complicated by HIV
infection
 Patient developed was treated for category B; has
not developed category C and symptom free > still
belong to category B.
 T cell Levels – below 200/mm3 > AIDS
 T cell Levels – below 100/mm3 > severely impaired
Immune System
• Blood samples are tested for presence of antibodies
to HIV:
• EIA (Enzyme immunoassay) test / ELISA (Enzyme-
linked immunosorbentassay)
– Identifies antibodies specifically against HIV
– (+) for antibodies in blood > Seropositive
– Saliva can be utilized
• Western Blot Assay
– To confirm seropositivity when the EIA is positive
• OraQuick Rapid HIV-1 Antibody Test
– A drop of blood used to test for antibodies
– Fast (20 minutes) and reliable (99.6% accuracy)
• Target Amplification – quantify HIV RNA or DNA levels
– Reverse transcriptase polymerase chain reaction (RT-PCR)
• Detects HIV in high-risk seronegative people before development
of antibodies
• Confirms positive EIA
• Neonate screening
– Nucleic acid sequence based amplification (NASBA)
• To tract the viral load and response to treatment
• Better than CD4 count
• Low Viral Load = longer time to AIDS diagnosis and the
longer the survival rate
• Maximal suppression of viral load
• Restoration/preservation of immunologic function
• Improved quality of life
• Reduction of HIV related morbidity and mortality
• Nucleoside analog reverse transcriptase inhibitors
– Becomes part of the DNA and derail its building
process, the damaged viral DNA can not take control
of the host cell’s DNA
» zidovudine (AZT, Retrovir)
» lamivudine (3TC, Epivir)
» d4t (Zerit, stavudine)
» ddi (Videx)
» ddc (Hivid, zalcitabine)
» abacavir (Ziagen)
• Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
– Attach to the reverse transcriptase enzyme, which
prevents it from converting HIV RNA into HIV DNA
» nevirapine (Viramune)
» delavirdine (Rescriptor)
» efavirenz (Sustiva)
» tenofovir (Viread)
T
R
E
A
T
M
E
N • Protease Inhibitor
T
– Prevents the protease enzyme from cutting HIV viral
O proteins into the viral particles that infect new CD4 T4
F
cells. New copies of HIV are defective and unable to
H infect new host cells.
I
V » nelfinavir (Viracept)
I » ritonavir (Norvir)
N
F » saquinavir (Invirase)
E
C » indinavir (Crixivan)
T » amprenavir (Agenerase)
I
O
N
T
R
E
A
T
M
E
N • Block viral replication within cells by inhibiting
T
either reverse transcriptase or the HIV protease
O
F • Duration of treatment needed to control HIV
H infection is unknown, but may continue for
I
V several years (average of 5-7 years) or for life.
I
N
F
E
C
T
I
O
N
• contains two antiretroviral agents

Highly Active Antiretroviral

Therapies (HAART)
• Two nucleoside reverse transcriptase inhibitors plus a
protease inhibitor
• Non-nucleoside reverse transcriptase inhibitor
• Two protease inhibitors and one other antiretroviral agent
• Opportunistic Infections (OIs)
– Shortness of Breath (SOB)
– Dyspnea
– Cough
– Chest pain
– Fever
 Pneumocystis carinii pneumonia
 Mycobacterium avium complex (MAC)
 TB
 Diarrhea (50-90% of all patients)
 Wasting syndrome- >10% body weight
 Kaposi sarcoma- skin cancer (brownish pink to deep
purple)
 Peripheral neuropathy
 HIV encephalopathy
 Cryptococcus neoformans
 GI Manifestations

• Oral Candidiasis
– Fungal infection – occurs to almost all patients with AIDS
– Characterized by creamy white patches in the oral cavity
– Patients complain of difficult and painful swallowing; and
retro sternal pain
– Untreated > esophagus and stomach
• Ulcerating oral lesions
– Medical Management
• Clotrimazole (Mycelex)
• Nystatin Suspension
• Ketoconazole (Nizoral) or fluconazole (Diflucan) – with
esophageal involvement