GOUT UPDATE AHMED YEHIA 2024, case based approach with application of the lat...
Immunology
1. Disturbances
in
Inflammatory
and
Immunologic Process
Ma. Tosca Cybil A. Torres, RN
2. Objectives:
At the end of varied teaching and learning activities, the students should be able
to:
1. Define related terms:
2. Recall briefly the components and functions of the immune system and the
immune response
3. Use assessment parameters appropriate for determining status of clients’
immune system
4. Identify abnormal findings that may indicate impairment in immune function.
5. State the purpose and nature of specific diagnostic procedures
Given a situation:
1. Formulate appropriate nursing diagnosis given a set of cues.
2. Use the nursing process as a framework to provide individualized care to
clients with altered immune response.
Given an actual client in the hospital or community the students should:
1. State the nature, purpose and significance of immunization.
2. Observe the universal precautions when caring for immunocompromised
client.
3. Integrate the Dominican teachings on compassion for humanity and
demonstrate caring attitude towards the clients.
3. Definition of terms:
• Immune system- group of cells, molecules, and
organs that act together to defend the body against
foreign invaders that may cause disease such as
bacteria, viruses or fungi.
• Immunology- the study of our protection from
foreign macromolecules or invading microorganisms
and our responses to them.
• Immunity- ability to resist damage from foreign
substances.
• Antigen – any molecules that trigger an immune
response; a protein that stimulates an immune
reaction, causing the production of antibodies.
• Antibodies- proteins that fight infections; a globulin
produced by B cells as a defense mechanism against
foreign materials.
4. Definition of terms:
• Epidemiology – study of how disease is produced, and
its distribution in a given population.
• Pathogens – microorganisms or proteinaceous
substances capable of producing disease.
• Virulence – Ability to cause diseases
• Nosocomial infections – acquired in a health care setting
• Immunocompetent – client whose immune system is
able to identify antigens and effectively destroy or
remove them.
• Immunocompromised - client whose immune system is
unable to effectively destroy or remove antigens
• Mast cells- tissue cells that resemble a peripheral blood
basophil and that contains granules with chemical
mediators.
5. Functions of the immune system:
• Defend and protect the body from infection by
bacteria, viruses, fungi and parasites.
• Removing and destroying damaged or dead
cells.
• Identifying and destroying malignant
cells, thereby preventing their further
development into tumors.
7. Immune response
• Recognition of self and non-self
• Antigens
• Antibody mediated response (humoral) – produced
by B lymphocytes
• Cell-mediated response – produced by T
lymphocytes.
2 Major Classes of T cells
– Effector Cells
• Cytotoxic cells (killer T cells)
– Regulator Cells
• Helper T cells (Majority)- amplify activity of killer T cells
• Suppressor T cells
8. Immune System Components
1. Leukocytes
1. Engulf and destroy
pathogens (bacteria)
2. Suppress inflammation
3. Fight parasitic infections
4. Produce antibodies and
provide immunity
a. Granulocytes- immediate
response to cell injury
• Neutrophils- phagocytic,
first cell to site of cell
injury
• Eosinophils-
hypersensitivity reaction
• Basophil-inflammatory
response
b. Agranulocytes- fight
infection
• Monocytes – phagocytosis
• Lymphocytes- production of
immunoglobulins
9. Immunoglobulin Characteristics And Functions
Percentage
Class Characteristics and Functions
of Total
IgG 75% in blood, lymph, and intestines
Found
Active against bacteria, its toxins and viruses
Enhances phagocytosis, crosses placenta and is active in a
second response
IgA 10-15% Saliva, tears,
bronchial, GI, prostatic and vaginal secretions
Provides local protection on exposed mucous membrane surfaces
and potent antiviral activity
Prevents absorption of antigens from food, and protects
against respiratory, GI, and GU infections
IgM 5-10% decrease during stress
Levels
Found in blood and lymph
First antibody produced with primary immune response
High concentrations early in infection, decrease within about a
week
IgD <1% function, found in blood and lymph
Unknown
on mast cells and basophils
Found
IgE <0.1% Involved in immediate hypersensitivity response
11. Nonspecific inflammatory response
- mechanical barriers that cover the body surfaces and to cells and
chemicals that act on the initial battlefronts to protect the body
from invading pathogens
• surface membrane barrier- the first line of defense of the body is
an intact skin and mucous membranes
• Chemical barriers- acidic gastric juices, enzymes in tears and saliva,
sebaceous and sweat secretions
• Biologic response modifiers- interferon, a viricidal substance,
counters viruses and activates other components of the immune
system
• Natural killer (NK) cells- lymphocytes responsible for immune
surveillance and host resistance to infection
• Inflammation
– Three stages of inflammatory response:
• Vascular response characterized by vasodilation and increased permeability of
blood.
• Cellular response and phagocytosis
• Tissue repair
12. Three stages of inflammatory response:
1. Vascular response characterized by vasodilation and increased
permeability of blood.
– Major chemical mediators:
1. Histamine – vasodilation and increased capillary permeability, producing
tissue redness, warmth and edema.
2. Kinins
3. Prostaglandins
Fluid exudate- fluid that escape from the site of injury
Serous - mild
Sanguineous/serosanguineous- moderate to severe
Fibrinous
Purulent exudate – severe or chronic
2. Cellular response and phagocytosis
3. Tissue repair
13. Specific Immune Response
- A type of immunity effective against specific harmful
agents entering the body
Types:
a. Inborn immunity- inherited immunity of
species, races , and individuals to certain diseases
b. Acquired immunity- immunity that develops as an
individual encounters specific harmful agents.
a. Natural- activated by afffected individual
a. Active- contact with the disease
b. Passive- placenta, breastmilk
b. Artificial – activated by vaccine
a. active- vaccine: killed, attenuated, toxoid
b. passive- immune serum
14. Assessment of the Immune System
• Biographic data
• Focused interview - Sensitive in nature
– Health Perception-Health management
• Perception of general health
• Recent illness or changes in health status
• Past illness/hospitalizations
– BT? Organ transplant? Tissue transplant?
– Transfusion reaction?
• Allergies
• Immunization status
• Screening tests.
• Occupation
• Current medication
• Recreational drug use.
15. Assessment of the Immune System 2
• Focused interview
– Nutritional-Metabolic
• Usual diet
• Recent weight change
• Skin lesion, rashes, impaired healing
– Activity-exercise
• Client’s exercise tolerance and any complaints of
excessive unusual fatigue or weakness.
• Frequent sore throats or upper respiratory illness
• Swollen glands in the neck axilla or groin
• Easy bruising or excessive bleeding from injuries or
gums
16. Assessment of the Immune System 3
• Focused interview
– Role-Relationship & Sexuality-Reproductive
• Living situation including s.o
• Sexual relations and practices
• Number of sexual partners and their gender.
• Specific risk behaviors e.g. anal intercourse
• Barrier protection used
– Value belief
17. Physical Assessment
• General appearance
– Height, weight, ease of movement, evident stiffness, v/s
• Skin
• Head and neck
• Eyes and ears
• Respiratory system
• CV system
• GI System
• Urinary system
• Nervous system
• Musculoskeletal system
18. Acute Inflammation
• Short term reaction
• Last <1-2 weeks
Chronic Inflammation
Slower in onset
Occurs over months or years
19. CAUSES of Inflammation
• Mechanical Injuries
• Physical damage e.g. burns
• Chemical injury from toxins or poisons
• Microorganisms
• Extremes of heat and cold
• Immunologic response e.g. hypersensitivity
reaction
• Ischemia damage such as stroke or MI
20. CARDINAL SIGNS OF INFLAMMATION
• Erythema
• Local heat
• Swelling
• Pain
• Loss of function
SYSTEMIC MANIFESTATIONS
• T->38C or <36C
• P->90/min
• R->20/min
• WBC- >12,000/mm3
• Enlarged lymph nodes
• Loss of Appetite
• Fatigue
21. Factors that may impair healing
Factors Effect
Malnutrition
Protein deficient Prolongs inflammation and impairs healing
process
Carbohydrates and Impairs metabolic process; proteins are
kilocalorie deficient used for energy rather than healing
Vitamin deficits
Vit. A Limits epithelialization and capillary
formation
B-complex Inhibits enzymatic reaction that contributes
to wound healing
Vit. C Impairs collagen synthesis
Tissue Hypoxia Associated with an increase risk of infection
and impaired healing
Impaired blood supply Inadequate delivery of Oxygen and
nutrients
22. Pharmacology
• Acetaminophen (Tylenol) – reduces fever and pain
– has no anti-inflammatory effect.
• Anti-inflammatory Meds
3 GROUPS
– Salicylates
– NSAID ex. Diclofenac Na (Voltaren), Ibuprofen (Advil),
Indomethacin (Indocin), Ketorolac Tromethamine (Toradol)
– for pain management only, Naproxen (Naprosyn)
– Corticosteroids
23. Chain of Infection
1
6 Etiologic
Susceptible Agent
host (microorganism)
5
2
Portal of Entry
Reservoir
to
(Source)
susceptible host
4 3
Method of Portal of exit
transmission from reservoir
24. Pathogens
• Bacteria
– Aerobic
– Anaerobic
• Viruses - intracellular parasite capable of reproducing outside
of a living cell.
• Mycoplasma – similar to bacteria and have no cell wall –
resistant to antibiotics that inhibit cell wall synthesis
• Rickettsiae & Chlamydia- rigid cell wall; with some feature of
both bacteria and viruses.
– Chlamydia- transmitted by direct contact
– Rickettsiae- infect cells of arthropods and are transmitted by these
vectors.
• Fungi- self-limited, affecting the skin and subcutaneous tissue.
• Parasites
25. Reservoir
• -where the pathogen lives and multiplies
– Endogenous
– Exogenous
• Mode of Transmission
– Direct contact
– Indirect contact
• Vector
– Droplet or airborne transmission
26. Host Factors
Factors that enable a host to resist infections:
• Physical barriers
• Hostile environment created by stomach acid
secretions, urine & vaginal secretions.
• Antimicrobial factors e.g. saliva, tears
• Respiratory defenses
• Specific and nonspecific immune responses to
pathogenic invasion.
• Age
• Nutrition
27. Portal of Entry
• Respiratory Tract
• GI Tract
• Genitourinary Tract
• Skin and mucous membrane
• Bloodstream
28. Stages of Infectious Process
• Incubation period – period begins with active
replication but with no symptoms
• Prodromal stage – Symptoms first appear
• Acute phase – proliferation and dissemination of
pathogens
• Convalescent stage- containment of infection and
pathogens are eliminated
• Resolution – total elimination of pathogens without
residual manifestation
Nosocomial infection
– Infection acquired in a health care setting.
– Typically manifest after 48 hrs.
– UTI most common type
29. Gerontologic Consideration
• Cardiovascular changes
• Respiratory system changes
• Loss of muscle tone
• Gastrointestinal system changes
• Skin and subcutaneous changes
• Slowed or impaired healing process.
FACTORS THAT MAY CONTRIBUTE TO INCREASED RISK FOR
INFECTIOUS DISEASE:
• Decreased activity level
• Poor nutrition
• Chronic disease
• Hospitalization
• Presence of invasive device
30. Standard precautions
• Blood
• All body fluids, secretions, excretions,
• Non-intact skin
• Mucous membranes
Essential elements:
• Use barrier protection
• Prevent inadvertent percutaneous exposure, dispose
of needles
• Immediate and thorough hand washing
31. Pharmacology
• Check for:
– History of hypersensitivity.
– Age and childbearing status of the client.
– Renal function
– Hepatic function
– Site of infection
• Classification of antimicrobial preparations:
– Bacteriostatic
– Bactericidal
32. Five Basic Mechanisms of antimicrobial agents:
• Impairing cell wall synthesis, leading to lysis
and cell destruction.
• Protein synthesis inhibition, impairing
microbial function
• Altering the permeability of the cell
membrane, causing intracellular contents to
leak.
• Inhibiting the synthesis of nucleic acids
• Inhibiting other specific biochemical pathways
of the organism.
35. Hypersensitivity Reaction
• Altered immune response to an antigen that results in
harm to the client
CLASSIFICATIONS
• Immediate
– Type I (anaphylactic )reactions- mediated by IgE
antibody, which promotes the release of histamine and
other reactive mediators
– Type II (cytotoxic) reactions – mediated by IgM and IgG
antibodies, which attach to cells and cause cell lysis
– Type III (immune complex) reactions- (rheumatoid
arthritis) mediated by antigen-antibody complexes that
deposit in the lining of blood vessels or on tissue surfaces
• Delayed response
– Type IV (delayed hypersensitivity) reactions (transplant
rejection) are mediated by lymphokines released from
sensitized T lymphocytes
36. Chemical Mediators of Immediate
Hypersensitivity reactions
• Histamine
• Leukotrienes- potent bronchoconstrictor,
cause increased venous permeability
• Prostaglandins- potent vasodilators and
potent bronchoconstrictors
• Cytokines- control and/or regulate
immunologic functions
• Platelet-activating Factor- causes platelet
aggregation
38. Asthma
• Intermittent and reversible airflow obstruction affecting
only the airways, not the alveoli.
Occurs in two ways:
1. Inflammation
2. Airway hyperresponsiveness
Inflammation Triggered by:
Specific allergens
Non-allergenic – cold air, dry air, microorganisms
Airway hyperresponsiveness may be:
Exercise
Upper respiratory illness
39. • Histamine is generated by
white blood cells called
basophil or mast cells,
and is released in allergic
reactions. In this false-
color electron micrograph
of a mast cell, histamine
can be seen as red
granules on the yellow
cell cytoplasm.
40. Causes of Asthma
• The dust mite is a microscopic
arthropod that lives in human homes,
where it feeds on the dust produced by
human and animal skin.
• People with pollen allergies may be
helped by staying indoors during the
midday and afternoon—the times when
pollen concentrations are highest.
• Pollution
• pet hair or cigarette smoke
• perfume, hairspray, cosmetics, and
household
• Intense emotion, such as crying,
shouting, or laughing
Classic symptoms:
• wheezing, coughing, and shortness of
breath.
41. Pathophysiology of Asthma
Stimulus
Chemical mediator release
Bronchospasm Inflammatory cell activation
Edema Increased mucus
Epithelial damage
production
Increased airway resistance,
obstruction and airflow limitation
Acute asthma attack
42. Diagnostic Test
• Skin Testing
– Epicutaneous
– Intradermal
• Radioallergosorbent Test (RAST)
TREATMENT MODALITIES:
Immunotherapy (desensitization)
- indicated for allergic rhinitis and asthma
43. Anaphylaxis
Response that occurs in highly sensitive persons
following injection of specific antigen
ETIOLOGY:
Immunotherapy
Stinging insects
Skin Testing
Medications
Food
Exercise
Latex
45. Severe Reaction of Anaphylaxis
• Air hunger
• Stridor
• Wheezing
• Barking cough
• Anaphylactic shock
IMMEDIATE TREATMENT!!:
46. Assessment
• ABC
• VS, Degree of respiratory distress
• History of onset of symptoms and of
exposure to allergen
DIAGNOSIS:
1. Impaired breathing pattern
2. Decreased cardiac output
3. Anxiety
47. Nursing Interventions
• Restore effective breathing
• Increase cardiac output
• Reduce anxiety
• Patient education and home maintenance
50. Urticaria and angioedema
• a skin rash, usually occurring as an allergic
reaction, that is marked by itching and small
pale or red swellings
ETIOLOGY:
Ingested substance
Infections
Insects
51. SS & DX EVALUATION
• Raised red edematous wheals
• Intense pruritus
• Diffused swelling
Dx Evaluation
1. Labs
2. Challenge testing to determine physical
cause
52. FOOD ALLERGIES
Common Food Allergens:
• Cow’s milk, eggs, shellfish, peanuts, soybeans and
wheat.
Dx Tests:
1. Skin testing
2. RAST
3. Oral challenge
4. Elimination Diet
NSG Diagnosis?
53. TYPE II CYTOTOXIC HYPERSENSITIVITY
• Hemolytic transfusion reaction to blood of an incompatible type.
Antigen attached
To foreign cell or tissue
Plasma cells produce IgG
Or IgM antibodies w/c
Binds to antigens
Binding stimulates
Complement activation
Cell lysis Phagocytes Killer T cell activation
54. Serologic testing
• BT
• Cross matching (compatibility Test)
• Direct Coomb’s Test
• Indirect Coomb’s Test
SCREENING FOR INFECTIOUS DISEASE
- Routine lab test
- Specific condition screened for:
- Hepatitis
- HIV (*antibodies not produced at least 6 weeks)
- Cytomegalovirus
- Syphilis
- Bacteria
- Malaria
55. Coombs test
The two Coombs tests are:
• Direct Coombs test (also
known as direct
antiglobulin test or DAT). -
used to detect if antibodies
factors have bound to RBC
surface antigens in vivo
• Indirect Coombs test (also
known as indirect
antiglobulin test or IAT). is
used to detect in-vitro
antibody-antigen reactions
56. Administration of Whole Blood And Blood
Components
• Whole Blood
– Acute, massive blood loss of
greater than 1,000 mL
• Packed RBC
– Restoration or maintenance
of adequate organ
oxygenation with minimal
expansion of blood volume.
– 90-120 min/unit
• Platelets concentrates
– 5.5 x 1010 platelets and
plasma (50-400 mL)
57. Administration of Whole Blood And Blood Components
• Assignment: Other Blood components for
administration.
– Platelets Concentrates
– Plasma (Fresh or Fresh Frozen)
– Cryoprecipitate
– Fractioned Plasma Products
58. Blood transfusions can be grouped into
two main types depending on their source:
• Homologous transfusions, or transfusions using the stored
blood of others.
• Autologous transfusions, or transfusions using one's own
stored blood.
• A unit (up to 500 ml) of blood
• administered over 4 hours, depending on blood pack.
• In patients at risk of congestive heart failure, many doctors
administer furosemide to prevent fluid overload.
Acetaminophen and/or an antihistamine such as
diphenhydramine are sometimes given before the transfusion
to prevent a transfusion reaction.
59. Complications and risks
• For the donor
– quot;passing outquot;
– Bruise at the needle site — 23 percent
– Sore arm — 10 percent
– Hematoma at needle site — 2 percent
– Sensory changes in the arm used for donation (eg, burning
pain, numbness, tingling) — 1 percent
– Fatigue — 8 percent
– Nausea and vomiting — 1 percent
60. For the recipient
• Transfusion reaction
• bacterial infection and sepsis
• viral infection
• volume overload, iron overload (with multiple
red blood cell transfusions)
• anaphylactic reactions
• acute hemolytic reactions (most commonly
due to the administration of mismatched
blood types).
61. Objections to blood transfusion
• may arise for personal, medical, or religious
reasons
– Jehovah's Witnesses
63. ACUTE
• May occur the transfusion or within minutes to hours
after infusion.
• Reactions include allergic, febrile, septic and
hemolytic rxns, air embolism and circulatory
overload.
DELAYED
May occur from days to years after the transfusion.
Reactions include delayed hemolytic reactions, iron
overload (hemosiderosis), infectious diseases.
64. Immediate Adverse Effects of Transfusion
Febrile Reactions
Cause: Fever and chills during transfusion are thought to be
caused by recipient antibodies reacting with white cell
antigens or white cell fragments in the blood product or due
to cytokines which accumulate in the blood product during
storage.
• Fever occurs more commonly with platelet transfusion (10-
30%) than red cell transfusion (1-2%).
• Fever may be the initial symptom in a more serious reaction
such as bacterial contamination or haemolytic reaction.
Management: Symptomatic, paracetamol
Investigation: If the fever is accompanied by significant changes
in blood pressure or other signs and symptoms, the
transfusion should be ceased and investigated
65. Urticarial (Allergic) Reactions
Cause: caused by foreign plasma proteins. On rare
occasions they may be associated with laryngeal
oedema and bronchospasm.
Management: If urticaria occurs in isolation (without
fever and other signs), slow the rate or temporarily
stop transfusion. If symptoms are bothersome,
consider administering an antihistamine before
restarting the transfusion. If associated with other
symptoms, cease the transfusion and proceed with
investigation.
Investigation: It is also usually possible to restart the
transfusion. Such a decision should be made after
assessment by the treating doctor.
66. Severe Allergic (Anaphylactic) Reactions
• Anaphylactic and anaphylactoid reactions have signs of
cardiovascular instability including
hypotension, tachycardia, loss of consciousness, cardiac
arrhythmia, shock and cardiac arrest. Sometimes respiratory
involvement with dyspnoea and stridor are prominent.
• Cause: In some cases patients with IgA deficiency who have
anti-IgA antibodies can have these reactions.
• Management: Immediately stop transfusion, supportive care
including airway management may be required. Adrenaline
may be indicated. Usually given as 1:1000 solution, 0.01mg/kg
s.c./i.m. or slow i.v.
• Investigation: IgA levels and anti-IgA antibodies.
• Prevention: Patients with anti-IgA antibodies require special
blood products such as washed red blood cells and plasma
products prepared from IgA deficient donors. Manage further
transfusion in consultation with the haematologist-on-call.
67. Acute Haemolytic Reactions
• Cause: caused by transfusion of ABO incompatible blood, eg group A, B or
AB red cells to a group O patient.
• Most haemolytic reactions are the result of human error such as the
transfusion of properly labelled blood to the wrong patient, or improper
identification of pretransfusion blood samples.
• Non-immune haemolysis of RBCs in the blood container or during
administration can occur due to physical disruption (temperature changes,
non-isotonic fluid)
• Symptoms: Chills, fever, pain (along IV line, back, chest), hypotension, dark
urine, uncontrolled bleeding due to DIC (Disseminated intravascular
coagulation).
• Management: Immediately stop transfusion. Notify hospital blood bank
urgently (another patient may also have been given the wrong blood!).
These patients usually require ICU support and therapy includes vigorous
treatment of hypotension and maintenance of renal blood flow.
• Prevention: Proper identification of the patient from sample collection
through to blood administration, proper labelling of samples and products
is essential. Prevention of non-immune haemolysis requires adherence to
proper handling, storage and administration of blood products.
68. Bacterial Contamination
• Cause: Bacteria may be introduced into the pack at the time of
blood collection from sources such as donor skin, donor
bacteraemia or equipment used during blood collection or
processing. Bacteria may multiply during storage.
• Platelets are more frequently implicated than red cells.
• Symptoms: Very high fever, rigors, profound hypotension, nausea
and/or diarrhoea.
• Management: Immediately stop the transfusion and notify the
hospital blood bank. After initial supportive care, blood cultures
should be taken and broad-spectrum antimicrobials commenced.
Laboratory investigation will include culture of the blood pack.
• Prevention: Inspect blood products prior to transfusion. Some but
not all bacterially contaminated products can be recognised (clots,
clumps, or abnormal colour). Maintaining appropriate cold storage
of red cells in a monitored blood bank refrigerator is important.
Transfusions should not proceed beyond the recommended
infusion time (4 hours).
69. Transfusion-Related Acute Lung Injury
• Transfusion Related acute Lung Injury (TRALI) is a clinical
diagnosis of exclusion characterised by acute respiratory
distress and bilaterally symmetrical pulmonary edema with
hypoxemia developing within 2 to 8 hours after a transfusion.
A CXR shows interstitial or alveolar infiltrates when no
cardiogenic or other cause of pulmonary oedema exists.
• Cause: Pulmonary vascular effects are thought to occur
secondary to cytokines in the transfused product or from
interaction between patient white cell antigens and donor
antibodies (or vice versa).
• Management: Symptomatic support for respiratory distress
includes oxygen administration and may require intubation
and mechanical ventilation. Symptoms generally resolve over
24-48 hours.
70. Volume Overload
• Cause: Patients with cardiopulmonary disease and
infants are at risk of volume overload especially
during rapid transfusion.
• Management: Stop the transfusion, administer
oxygen and diuretics as required.
• Prevention: Avoid unnecessary fluids and use
appropriate infusion rates.
71. Hypothermia
• Cause: Rapid infusion of large volumes of stored
blood contributes to hypothermia. Infants are
particularly at risk during exchange or massive
transfusion.
• Prevention and Management: Appropriately
maintained blood warmers should be used during
massive or exchange transfusion. Additional
measures include warming of other intravenous
fluids and the use of devices to maintain patient
body temperature.
72. Immediate adverse effects of transfusion and their management
Category 1: Mild Reactions
Symptom/s
Signs Possible Immediate Management
Cause
Urticaria Pruritus Allergic Assess patient
/rash (itching) An antihistamine may be
required
Transfusion may be restarted if
no other signs/symptoms are
present
If signs/symptoms worsen treat
as Category 2.
73. Category 2: Moderately severe reactions
Immediate
Signs Symptoms Possible cause
Management
Allergic moderately- Stop transfusion
Flushing Anxiety
severe) and maintain
Urticaria Pruritus IV line with
Febrile non-haemolytic
Rigors NSaline
transfusion reaction:-
Palpitations
Fever antibodies to white Contact Medical
Mild cells or platelets Officer
Restlessness
dyspnea antibodies to proteins Patient may require
Tachycardia
including IgA antihistamine
Headache and/or
possible contamination
paracetamol
with pyrogens and /or
Further
bacteria
investigation
and
management
according to
clinical
features
74. Category 3: Life threatening reactions
Immediate
Signs Symptoms Possible cause
Management
Stop transfusion
Anxiety Acute
Rigors
maintain IV line with
intravascular
Chest pain
Fever NSaline
haemolysis
Pain at infusion Manage immediate
Restlessness (wrong blood)
site needs:
Bacterial
Hypotension fluid for hypotension
Respiratory
contamination oxygen
distress
Tachycardia adrenaline for
and septic anaphylaxis
Loin/back pain shock
Dark Urine diuretic for fluid
Headache overload
Fluid overload
Unexplained
Dyspnea Anaphylaxis
bleeding (DIC) Further management
Transfusion according to likely
related acute cause
lung injury
(TRALI)
75. Delayed and Long Term Averse Effects of Transfusion
Delayed Haemolysis
• Cause: Patients may develop antibodies to red cell antigens.
Antibodies can occur naturally, or may arise as a consequence
of previous transfusion or pregnancy. A delayed haemolytic
reaction occurs when a patient develops an antibody directed
against an antigen on transfused red cells. The antibody may
cause shortened red cell survival, with clinical features of
fever, jaundice and lower than expected haemoglobin
following transfusion. Most delayed haemolytic reactions
produce few symptoms and may go unrecognised, however
there are reports of serious consequences in critically ill
patients.
• Prevention: An antibody screen is performed as part of pre-
transfusion testing. When an antibody is detected, it is
identified and appropriate antigen negative blood is provided.
Sometimes antibodies fall below detectable limits and may
not be detected by pretransfusion testing.
76. Drug Category
Diuretics -- These agents are used to increase renal blood flow and preserve
urinary output in hemolytic transfusion reactions. They also may be used in
transfusion-related volume overload
• Furosemide (Lasix)
Vasopressors -- These agents are used to increase renal blood flow and preserve
urinary output in hemolytic transfusion reactions. In severe allergic reactions,
epinephrine is used for its inotropic properties and ability to maintain
perfusion of vital organs.
Dopamine (Intropin)
. Lower doses stimulate mainly dopaminergic receptors that produce renal and
mesenteric vasodilation. Cardiac stimulation and renal vasodilation produced
by higher doses
Epinephrine (Adrenalin, Epinal, Epifrin)
increased peripheral vascular resistance, hypertension, cardiac activity
Antihistamines – Used to treat minor allergic reactions and anaphylaxis.
Diphenhydramine (Benadryl, Benylin, Bydramine
77. • Corticosteroids - These agents have limited benefit in
the initial acute treatment of rapidly deteriorating
anaphylactic patient. However, they may benefit
patients with persistent bronchospasm or
hypotension. Onset of action is approximately 4-6 h
following its administration.
• Methylprednisolone (Solu-Medrol)
78. IMPAIRED IMMUNE RESPONSE
Acquired Immunodeficiency Syndrome (AIDS),
“AIDS: Your Problem, Control With Condoms.”
• human viral disease that
ravages the immune
system, undermining the
body’s ability to defend
itself from infection and
disease.
• Caused by the human
immunodeficiency virus
(HIV), AIDS leaves an
infected person vulnerable
to opportunistic infections.
79. Human Immunodeficiency Virus
• The human
immunodeficiency virus
(HIV), which causes
acquired immunodeficiency
syndrome (AIDS), principally
attacks CD4 T-cells, a vital
part of the human immune
system.
80. • Like all viruses, human immunodeficiency
virus (HIV) is comprised of only genetic
material, a few proteins, and a protective
envelope.
• Its genetic material, carried by single-stranded
RNA molecules, contains all the information
necessary to make more viruses.
• HIV can not reproduce itself outside of a
cell, but when HIV invades a living cell, it turns
the cell into a factory for making more HIV.
81. Three ways that HIV infections spread:
• sexual intercourse with an infected person,
• contact with contaminated blood, and
• transmission from an infected mother to her
child before or during birth or through
breastfeeding.
82. • Left to right, Candy,
Robert, Randy, and
Richard Ray leave
Memorial Elementary
School in Arcadia,
Florida, on August 24,
1987. It was the boys’
first day at school after
having been barred
because they were
infected with HIV.
83. Signs and symptoms
• Within one to three weeks after infection with HIV,
• flu-like symptoms,
– such as fever
– sore throat, headache, skin rash, tender lymph nodes, and
a vague feeling of discomfort.
– During this phase, known as acute retroviral syndrome,
HIV reproduces rapidly in the blood.
– extensive weight loss and fatigue (wasting syndrome),
periodic fever, recurring diarrhea, and thrush, a fungal
mouth infection.
– early symptom of HIV infection in women is a recurring
vaginal yeast infection
84. Diagnostic Evaluation
• Enzyme-Linked
ImmunoSorbent
Assay, or ELISA, is a
biochemical technique
used to detect the
presence of an antibody
or an antigen in a
sample
A 96-well microtiter plate might be used for
ELISA
85. Western Blot test
• can detect lower levels of HIV antibodies. In this test a blood
sample is applied to a paper strip containing HIV proteins. If
HIV antibodies are present in the blood, they bind to the HIV
proteins, producing a color change on the paper.
• Orasure
• Uses saliva rather than blood with result available in about 3
days
• Calypte HIV-1 Urine EIA
89. Supportive Care
• Treatment of reversible illness
• Nutritional support
• Palliation of pain
• Treatment to relieve symptoms
• Antidepressant
90. STANDARD OF CARE
• Universal precautions
• Protect confidentiality
• Education on prevention of HIV transmission
• Develop adherence strategy in taking antiviral drugs
• Educate about HIV symptoms and management
91. Nursing Diagnoses
• Fear
• Risk for infection
• Altered nutrition less than body requirements
• Altered oral mucous membrane
• Diarrhea
• Altered thought process
• Hyperthermia Altered breathing pattern
92. Sjogren's syndrome
- an autoimmune disorder in which immune
cells attack and destroy the exocrine glands
that produce tears and saliva.
- defined by its two most common symptoms —
dry eyes and a dry mouth.
93. Causes
• heredity
• hormones
• viral or bacterial infection
• white blood cells called lymphocytes target,
attack and damage moisture-producing glands
• also damage other organs, including lungs,
kidneys and liver.
94. Signs and symptoms
• Dry eyes
• Dry mouth
• Dental cavities
• Fatigue
• Fatigue
• Fever
• Enlarged parotid glands
• Difficulty swallowing or chewing
• Change in sense of taste
• Hoarseness
• Oral yeast infections, such as candidiasis
• Irritation and mild bleeding in your nose
• Skin rashes or dry skin
• Vaginal dryness
• Dry cough that doesn't produce sputum
• Joint pain, swelling and stiffness
96. Less common complications include:
• Inflammation of organs such as your lungs, kidneys or liver.
• Heart problems for babies born to mothers with Sjogren's
syndrome.
• Cancer of the lymph nodes (lymphoma). A small percentage
of people with Sjogren's syndrome develop lymphoma.
Symptoms include swelling of the salivary glands, fatigue,
weight loss and night sweats.
• Peripheral nervous system disorders. Peripheral
neuropathies are common
– legs may be especially affected
– may experience symptoms of numbness, tingling and burning. The
cranial nerves — such as those relating to the eyes (optic nerve) or
face (trigeminal nerve) — can be affected and may cause visual
problems or facial pain.
97. Risk factors
• Having a rheumatic disease.
• Being female. Women are nine times as likely as men
are to have Sjogren's syndrome.
• Being a certain age. Sjogren's syndrome is usually
diagnosed in people older than 40.
• Having a family history of Sjogren's. Sjogren's
syndrome sometimes runs in families.
98. Screening and diagnosis
• Blood tests can be done to determine if a patient has high levels of antibodies that are
indicative of the condition, such as anti-nuclear antibody (ANA) and rheumatoid
factor (because SS frequently occurs secondary to rheumatoid arthritis), which are
associated with autoimmune disease
• Tear test. measure the dryness of the eyes with a Schirmer tear test, in which a small
piece of filter paper is placed under the lower eyelid to measure your tears. In another
version of the Schirmer test, a cotton swab is used to stimulate the tear reflex in the
nose. A medical eye doctor (ophthalmologist) may also examine the eyes with a slit-
lamp after placing a drop of liquid containing a dye in the eye. The dye stains areas of
the cornea that have been damaged by the dryness.
• Imaging. special X-ray called a sialogram. It detects dye that is injected into the parotid
glands. The dye is injected through the opening of a small duct in the mouth. This
procedure reveals the flow of saliva into the mouth.
• may also perform a parotid gland flow test to determine the amount of saliva that is
produce over time. Another imaging test is a salivary scintigraphy, which measures
salivary gland function.
• Biopsy. lip biopsy to detect the presence of clusters of inflammatory cells. For this test,
a small sliver of tissue is removed from salivary glands located in your lip and examined
under a microscope.
• Slit-lamp exam. use magnifying equipment to determine how dry your eye is and
whether the outside of your eye is inflamed.
99. Medications
• Nonsteroidal anti-inflammatory drugs (NSAIDs). This group
of medications, which includes aspirin, helps relieve both pain
and inflammation. The doctor may recommend these
medications if there is painful or swollen joints. Side effects
may include indigestion and stomach bleeding. Therefore,
always take NSAIDs with food.
• Corticosteroids. These medications reduce inflammation and
may slow joint damage. In the short term, corticosteroids can
make the patient feel dramatically better. But when used for
many months or years, they may become less effective and
also cause serious side effects. Side effects may include easy
bruising, thinning of your bones, cataracts, weight gain, a
round face, diabetes and high blood pressure.
• Immunosuppressants. These medications, such as
cyclophosphamide (Cytoxan), methotrexate (Rheumatrex),
mycophenolate (CellCept) and azathioprine (Imuran),
suppress the immune system. The doctor may prescribe them
for you if problems with the lungs, kidneys, blood vessels or
nervous system develops.
100. Meds continued
• Pilocarpine (Salagen). The doctor may prescribe pilocarpine if there is dry-
mouth symptoms caused by Sjogren's syndrome. It's not an option if the
patient has poorly controlled asthma, inflammation of the iris (acute
iritis), glaucoma or significant cardiovascular disease, or if pregnant or
breast-feeding. Pilocarpine may cause increased sweating and headaches.
• Cevimeline (Evoxac). This prescription medication also is used to relieve
symptoms of a dry mouth. The medication works by causing certain
mouth glands to produce more saliva. Common side effects may include
excessive sweating, nausea, and a runny or stuffy nose. Less common side
effects, may include difficulty breathing, fast heartbeat and itching.
• Cyclosporine. The ophthalmologist may recommend you use eyedrops
containing cyclosporine (Restasis) to treat symptoms of Sjogren's
syndrome that affect the eyes.
101. Surgery
Sealing of the tear ducts that drain tears from
the eyes (punctal occlusion). Collagen or
silicone plugs are inserted into the ducts for a
temporary closure. Collagen plugs eventually
dissolve, but silicone plugs will keep ducts
sealed until they fall out or are removed.
Doctor may use a laser to permanently seal
your ducts
103. Lupus: Prevalence
1 in 700 (ages 15 -64) women have lupus
1 in 250 are African American Women
Asian and Native Americans = ↑ incidence
Usually affects women between 15 to 40
In this age group 1:200 will develop lupus
Usual onset is during childbearing age
Possible hormonal link
8 – 10 times more prevalent in women
104. Types of Lupus
• SLE – Systemic
– Chronic, progressive, inflammatory connective
tissue disorder that causes organ failure;
potentially fatal with a 5-year survival rate of 85%
• Drug Induced Lupus
– Procainimide
– Hydralazine
– INH
• DLE – Discoid
– Affects only the skin
105. Pathophysiology of Lupus
• Autoimmune: Exact Mechanism Unknown
– Viruses
– Environmental chemicals
– Genetic
• Antibodies “attack” healthy tissue
• Causes inflammation to the organ or to the
vessels supplying blood to the organ
– Deprives organs of arterial blood supply
106. Prognosis
• Potentially fatal disorder
• Increase in survival rate in last 20 years
• Now… 85% of clients survive at least 5 years
– Leading cause of death are related to infection
108. Diagnostic Criteria
• Must have four of the following eleven
symptoms or findings:
Malar rash Discoid lupus
Mouth sores Photosensitivity
Arthritis Neurologic disorder
+proteinuria Hematologic disorder
+ ANA
Immunologic Disorder
Thrombocytopenia, severe anemia, and leukopenia
109. Signs and Symptoms of Lupus
• Skin:
– Dry, scaly, raised rash on face
– Appears to be in butterfly
pattern—the “Bite of the
Wolf.”
– Individual round lesions
• Hair
– Hair loss
– Change in texture
110. Signs and Symptoms of Lupus
Musculoskeletal
Joints are affected causing painful mobility
(Polyarthritis in 90% of SLE patients).
Joint inflammation
Avascular necrosis – after 5 years of diagnosis
Muscle atrophy (results from autoimmune
complex invasion—leading to Myositis).
Muscle pain
111. Sign and Symptoms of Lupus
• Renal
– Lupus nephritis
• Changes in the glomeruli
– Decreased urinary output
– Proteinuria
– Hematuria
– Fluid retention
– Leading cause of death
– 50% of all lupus pts have
this
112. Signs and Symptoms of Lupus
• Respiratory
– Pleural effusions
• Results in restrictive and obstructive
changes
–Dyspnea
–Hypoventilation
113. Signs and Symptoms of Lupus
• Cardiac
Pericarditis Raynaud’s Disease
• Tachycardia Lack of circulation
• Pain to hands and feet
• Myocardial ischemia
Chest Pain
Cardiac Dysrrhythmias
114. Signs and Symptoms of Lupus
• Neurological
–Psychoses
–Paresis
–Seizures
–Headaches
–Strokes
–Peripheral neuropathies
115. Signs and Symptoms of Lupus
• GI Tract • Psychosocial
– Abdominal pain – Dealing with illness
• Mesenteric arteritis – Fear of death chronic
• Pancreatitis – Lack of socialization
• Ulcers – Body image changes
• Liver enlargement • Rash
• Spleenomegaly • Medication related
• Sexual Dysfunction • Systemic
– Pain – Fever
– Fatigue/weakness – Generalized weakness
– Self esteem – Fatigue
– Decreased desire – Anorexia
– Weight loss
116. Treatment
• Medications: • Skin protection
– Topical steroids for – Avoid sunlight
lesions – Mild soaps
– Plaquenil – Cosmetic cover-ups
(hydroxychloroquine) - Daily inspection
Can damage retina
– Steroids
• Hair loss
– Immunosuppressives
– Mild shampoo
– Anticoagulants if needed
– No chemicals
117. Nursing management
1. Administer medications which may include NSAIDS and
salicylates
2. Maintain skin integrity
3. Perform CV, neurologic and musculoskeletal assessment
4. Provide meticulous mouth care
5. Arrange for dietary consult- soft easily tolerated foods
6. Apply warm packs
7. Collaborate with the PT department
8. Provide client and family teaching
• encourage protection from the sun and UV light exposure
• avoid people with contagious problems