Inflammatory, Wound, and Immune process Flashcards

1
Q

What do erythrocytes (RBCs) do?

A

Transport O2 and CO2
- Hemoglobin= Iron + protein
- Oxyhemoglobin= O2 + iron
Helps maintain acid base balance (CO2=O2).

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2
Q

What is erythropoeisis?

A

Stimulated by hypoxia, and controlled by erythropoietin.

It stimulates the creation of RBC.

Its also influenced by nutrient availability.

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3
Q

How do you assess the hemotological system?

A

For things like anemia, sickle cell, etc.
1) Health history
2) Subjective data:
- Demographic data
- Current/past individual and familial history (bleeding, hemophilia)
- Medication/herbs/supplements
- Surgical history (heart valve replacement, gastric bypass)
- Other treatments (previous blood transfusions), anemia
3) Objective data:
- Physical examination (pallor, decreased pulse ox)
- Systems aseessment (Skin, lymphnodes, spleen, and liver)

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4
Q

What is pancytopenia?

A

Suppression of all blood cells.

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5
Q

What is a peripheral smear?

A

A blood test that gives you information about the number and shape of blood cells.

The morphology of blood cells.

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6
Q

Who is the universal donor?

A

O negative!!!

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7
Q

What are some diagnostic lab studies for the hemotological system?

A

RBC:
- Total RBC count (not this alone)
- Hgb/Hct
- RBC indices
- Erythrocyte sedimentation rate (ESR/Sed rate)
Most common ESR tells you about the inflammatory process

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8
Q

What test determines Rh status?

A

Coombs test

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9
Q

What is a summary of iron metabolism? What are the steps from ingestion to RBC?

A

1) Ingestion from diet or suppliment
2) Transported via (serum) transferrin were its put into RBC or stored.
3a) Storage (bone marrow, liver, spleen, macrophages) via ferritin and hemosiderin.
3b) RBC via hemoglobin
4) Recycling via macrophages in liver and spleen

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10
Q

What are the laboratory diagnostic studies used to find iron deficient anemia?

A

Tests for iron metabolism are:
- Serum iron
- Total iron binding capacity (TIBC)
- Serum ferritin
- Transferrin saturation

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11
Q

What are the radiologic and biopsy diagnostic studies used to find iron deficient anemia?

A

Radiologic:
- Computed tomography (CT)
- Magnetic resonance imaging (MRI)

Biopsies:
- Bone marrow examination (RBC iron)
- Lymph node biopsy

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12
Q

What are molecular cytogenetics and gene analysis techniques we can do with the biopsies in iron deficient anemia?

A

From bone and lymph tissue samples:
- Florescent in situ hybridization (FISH)
- Spectral karyotyping (SKY)
lets us know if there a hereditary component to it.

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13
Q

What is anemia?

A

A deficiency in the:
- Number of erythrocytes (RBCs)
- Quantity of hemoglobin
- Volume of packed RBCs (hematocrit)

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14
Q

What are the three different characteristic cell types of anemia?

A

Normocytic (normal)
Microcytic (small)
Macrocytic (large)

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15
Q

What are the 6 most common types of anemias? Example of each?

A

1) Hypochromic- iron or vitamin deficiency
Caused by malabsorption and blood loss.

2) Pernicious- lack of intrinsic factor
B12 deficiency in stomach that effects the intrinsic factor. Large RBC

3) Erythroblastosis fetalis- destruction by the antibodies

4) Secondary- bleeding, leukemia, cancer or CKD

5) Genetic factors- sickle cell anemia or spheroidal

6) Aplastic- malfunctioning bone marrow
Not making enough RBC

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16
Q

What clinical manifestations are you going to see with anemia?

A

*Hgb/hct will be low.

*Hematocrit under 8 will be a POTENTIAL blood transfusion. Under 6 is likely blood transfusion.

*Pallor (Due to low hgb and blood flow to the skin)

*Jaundice (Due to concentration of serum bilirubin)

*Pruritus itching (Due to increased serum and skin bile salt concentrations)

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17
Q

What should you assess prior to drawing labs for hematocrit?

A

Patients hydration status.
If they are overloaded, the blood will be thinner leading to a false low reading.
If they are dehydrated, the blood will be thicker, leading to a false high reading.

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18
Q

Trick to determining proper hematocrit range via the hemoglobin level?

A

Hematocrit percentage should be 3X the hemoglobin level.

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19
Q

What are three alterations in erythropoesis that may decrease RBC production?

A

1) Decreased hemoglobin synthesis
2) Defective DNA synthesis in RBCs
3) Diminished availability of erythrocyte precursors.

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20
Q

What is Procrit?

A

It is synthetic erythropoeitin, which increases hct and hgb. Used to treat anemia associated with renal failure and chemotherapy.

Watch for hypertension, headache, nausea.

Other names are redicrit, mercera (not for cancer patients)

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21
Q

What is leukemia?

A

A group of malignant disorders affecting the blood and blood forming tissues such as bone marrow, lymph system, and spleen.

Number of adults affected are 10 times that of children patients.

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22
Q

What are the two different classifications of leukemia based on cell maturity and nature of disease onset?

A

1) Acute which comes from the clonal proliferation of immature hematopoetic cells.

2) Chronic which effects come from mature forms of white blood cells and the onset in more gradual.

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23
Q

What are the classifications of leukemia based on the type of white blood cell?

A

1) Acute lymphocytic leukemia (ALL)
2) Acute myelogenous leukemia (AML)
3) Chronic myelogenous leukemia (CML)
4) Chronic lymphocytic leukemia (CLL)

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24
Q

Acronym for remembering symptoms of leukemia?

A

A- Amemia= low Hgb
N- Neutropenia= Risk of Infection
T- Thrombocytopenia= Bleeding

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25
Q

What is the eitology and pathophysiology of thrombocytopenia?

A

Reduction of platelets.
Resuls in abnormal hemostasis.
-Prolonged or spontaneous bleeding
Primarily and acquired disorder.
- Commonly from ingesting certain herbs or drugs.

26
Q

What herbs can be used as a blood thinner?

A

Garlic
Ginko biloba

27
Q

What pain/fever relievers cause bleeding?

A

Tylenol (acetametophan) does not make you bleed more

Asprin and NSAID, like ibuprophen (other ‘fen’s) and naproxen do.

28
Q

What are some acquired causes of thrombocytopenia?

A

Immune thrombocytopenia purpura (ITP)
Thrombotic thrombocytopenia purpura (TTP)
Heparin-induced thrombocytopenia (HIT)

29
Q

What is von Willibrands disease? What are the clinical manifestations and complications?

A

Von willibrand disease, is a related disorder involving the deficiency of von Willibrands coagulation factor (Factor VIII)

Clinical manifestations:
-Bleeding (may be life threatening).
-Slow, persistant, and prolonged bleeding.
-Delayed bleeding after minor injuries.
-Uncontrollable hemorrhage after dental extraction or irritation with toothbrush.
-Epitaxis
-GI bleed from ulcers and gastritis

30
Q

How would you go about diagnosing Hemophilia/ Von Willibrands?

A

1) Observing the clinical manifestations such as:
-Hematuria
-Ecchymosis and sub-q hematomas
-Compartment syndrome
-Neurologic signs
-Hemarthrosis

2) Diagnostic studies are:
Factor deficiency within intrinsic system (factor VIII, IX, XI, XII, vWF)

31
Q

How would we go about fixing hemophilia and von willebrand?

A

3) Interpersonal care:
-Treatment of complications
-Replacement therapy (of that factor)
-Preventative care (prevention of bleeding)

32
Q

What is lymphoma?

A

1) A malignant neoplasm originating in the bone marrow and lymphatic structures. Metastasizes to non-nodal sites.
-Results in the proliferation of lymphocytes.

2) Fifth most common type of cancer in the united states.

3) Two major types:
- Hodgkin’s Lymphoma- More prevalent in patient 15 to 19 years old.
- Non-Hodgkin’s Lymphoma- More prevalent in children younger than 14 years of age.

33
Q

Explain what hodgkins disease (Hodgkins lymphoma) is?

A

Neoplastic disease origionating in the lymphoid system. Makes up about 10% of all lymphomas.

Starts in a single location than spreads to adjacent lymphatics.

Often metastasizes to the spleen, liver, bone marrow, lungs, and other tissues.

Classified by histologic type.

34
Q

What is the eitology of Hodgkins Lymphoma?

A

1) Bimodal age-specific incidence:
-15 to 30 years of age
-Greater than 55 years of age

2) About 8260 new cases each year.

3) Long-term survival exceeds 80% for all stages.

5) Cause remains unknown but there are key factors:
-Infection with Epstein-Barr virus (EBV)
-Genetic predisposition
-Exposure to occupational toxins

6) Incidence increase in those with HIV.

35
Q

Clinical manifestations of Hodgkin’s Lymphoma?

A

Clinical manifestations: Typically have a gradual onset…
1) Enlargement of cervical, axillary, or inguinal lymphnodes.
2) Second most common place is the mediastinal node mass.
3) Nodes are movable and non tender.
4) Not painful unless nodes exert pressure on adjacent nerves.

Patient may notice:
- weightloss
- fatigue and weakness
- fever and chills
- tachycardia
- night sweats
Advanced cases:
- hepatomegally
- splenomegally
- anemia
- Other physical signs vary, depending on disease location…
RULE OUT TB

36
Q

How do we treat/manage hodgkins disease?

A

Irradiation
Chemotherapy (alone or with radiation)
Prognosis
Nursing considerations
-prepare for diagnostic procedure
-prevent side effects if possible; prepare and treat side effects
-child and family support

37
Q

Explain the stages of Hodgkins lymphoma.

A

Stage 1-Goes to the individual site
Stage 2-Spreads to adjacent sites
Stage 3-More spreading, and liver and spleen enlargement
Stage 4-lung involvement

38
Q

What is the eitology of Non-hodgkin’s lymphoma?

A

Approx. 60% of pediatric lymphomas are NHLs

Clinical appearance:
-Disease is typically diffuse rather than nodular.
-Cell type is undifferentiated or poorly differentiated.
-Dissemination occurs early, often, and rapidly.
-Mediastinal involvement and invasion of meninges.

39
Q

Explain Non hodgkin’s lymphoma management.

A

Diagnostic evaluation is similar to that of hodgkins disease with the exception ot the cancer is more diffuse than hodgkins lymphoma.

Irradiation
Chemotherapy (alone or with radiation)
Prognosis
Nursing considerations
-prepare for diagnostic procedure
-prevent side effects if possible; prepare and treat side effects
-child and family support

40
Q

What is the inflammatory process and its purpose?

A

Its the sequential response to cell injury.
-It neutralizes and dilutes inflammatory agent.
-Removes necrotic materials.
-Establishes an environment suitable for healing and repair.

INFLAMMATION IS ALWAYS PRESENT WITH INFECTION, BUT INFECTION ISN’T ALWAYS PRESENT WITH INFLAMMATION

41
Q

What are the catagories of inflammatory response?

A

Inflammatory response can be divided into:
1) Vascular response- releases histamine; opens vessels up to allow WBC to move in.

2) Cellular response- Sends out neurophils in phases, than monocytes (5 hours later) they’re the clean up crew and last about 3-7 days.

3) Formation of exudate- sometimes just harmless serum, other times it can become fiberous adhesions that solidifies the wound to everything. Sometimes its purulent…this is infection, absess, and boils. Not to be confused with sebaceous cyst (dead skin cells). There also hemorrhagic blisters and can become infectious.

4) Healing- Comes in primary, secondary, and tertiary. Can also be classified as Stage 1 (intact red, non blanchable), Stage 2 (opening in the skin), Stage 3, Stage 4.

SEE IMMUNE CELL HANDOUT FOR RUNDOWN OF DIFFERENT WBCS.

SEE ALSO: Vascular and cellular response to injury pathophsiology map.

42
Q

What are “bands”

A

Immature neutrophils. They also get sent out in mass during an invasion. They cant do the job but are ‘clogging up the works’.

Having these bands of neutrophils are called a “shifting to the left”

43
Q

Explain what happens during the Vascular response stage of the inflammatory process.

A

1) After cell injury, arterioles in the area briefly undergo transient vasoconstriction.

2) After release of histamines and other chemicals by the injured cells, vessels dilate, resulting in hyperemia.

44
Q

Explain what happens during the Cellular response stage of the inflammatory process.

A

1) The first to the site are neutrophils and they arrive at the site of injury in around 6-12 hours. They are released from the bone marrow. They phagocytize bacteria, other foreign material, and damaged cells.
They have a short lifespan of 24-48 hours.

2) Monocytes are the second type of phagocytic cells to migrate to site of injury from circulating blood. Attracted to the site by chemotactic factors and they arrive within 3 to 7 days after the onset of inflammation.

Monocytes:
On entering tissue spaces, monocytes transform into macrophages and assist in phagocytosis of inflammatory debris. Macrophages have a long lifespan and can multiply.

Macrophage:
Important in cleaning the area before healing can occur. May stay in damaged tissue for weeks. Cells may fuse to form a multineucleated giant cell.

3) Lymphocytes arrive later at the site and their primary role involves:
- Cell-mediated immunity (Cell-mediated immunityorcellular immunityis an immune response that does not involveantibodies)
- Humoral immunity (Humoral immunityis an antibody-mediatedresponse that occurs when foreign material - antigens - are detected in the body)
They are major medicators of the inflammatory response.

*Pus is the exudate composed of dead neutrophils, digested bacteria, and other cell debris.

45
Q

What are the two stages of inflammation?

A

*Bacterial infection of 2 weeks or less is considered ACUTE inflammation and presents with:
-Pain
-Redness
-Swelling
-Heat
-Loss of function

*Bacterial infection of longer than 2 weeks or more is considered CHRONIC inflammation and presents with no symptoms.

Persistant onslaught of bacteria= exaggerated host inflammatory response.

46
Q

What is the complement system and what are its major functions?

A

The complement system is the major medicator of the inflammatory response. Its the enzyme cascade (C1-C9) consisting of pathways to mediate inflammation and destroy invading pathogens.

Major functions of the complement system:
-Enhances phagocytosis
-Increased vascular permiability
-Chemotaxis
-Cellular lysis

C8 and C9, the final components of the complement system, pierce the cell surface, causing rupture of the cell membrane and lysis.

47
Q

What is the clinical manifestations of local response to inflammation? What can we do to treat it?

A

Local response to inflammation is:
- Redness
- Heat
- Pain
- Swelling
- Loss of function

Treatment is:
Rest
Ice
Compression
Elevation

48
Q

What are some clinical manifestations of the inflammatory response?

A

Systemic response:
-Increased WBC count with shift to the left
-Malaise
-Nausea and anorexia
-Increased pulse and respiratory rate
-Fever: Onset is triggered by release of cytokines. Cytokines cause fever by initiating metabolic changes in temperature regulating center in hypothalamus. Epinephrine released from the adrenal medulla increasing metabolic rate.

Systemic response to inflammation:
- The causes of systemic response are pooprly understood. Probably due to complement activation and the release of cytokines.
-Some cytokines are IL-1,IL-6, and tumor necrosis factor.

49
Q

What happens in the healing stage of the inflammatory response?

A

Final phase of the inflammation process is healing.
Two major components:
-Regeneration of tissue
-Repair of that tissue. More common than regeneration and more complex and happens by primary, secondary, and tertiary.

*Primary intention includes three phases:
1) Initial phase: lasts 3-5 days. Edges of insicion are aligned. Blood fills the incision area, which forms a matrix for WBC migration. Acute inflammatory reaction occurs
2) Granulation phase: Fibroblasts migrate to the site and secrete collagen. Wound is pink and vascular. Surface epithelium begins to regenerate.
3) Maturation phase and scar contraction: Begins 7 days after injury and continues for several months to years. Fibroblasts disappear as wound becomes stronger. Mature scar forms (can be interrupted by excess cell formation).

*Secondary intention is wounds that occure with trauma, ulceration, and infections that have large amount of exudate and wide, irregular wound margins with extensive tissue loss. Edges cannot be appoximated. Results in more debris, cells, and exudate.

*Tertiary intention is a delayed intention due to delayed suturing of the wound. Occures when a contaminated wound is left open and sutured closed after the infection is controlled. (Cat bites and dog bites)

50
Q

What are some complications of healing?

A

Dehiscence- can happen due to stress/strain on wound, infection, inflammation (becomes friable, or fragile and shreds open)

Hypertrophic scarring- excess cells building up, looks very similar to keloid. More common in whites than blacks, deeper.

Keloid scar-less common, and more superficial. This is more comon in blacks than whites.

51
Q

Three functions of the immune response?

A

Defense
Homeostasis (cell balance)
Surveillance

52
Q

What are the types and subtypes of immunity?

A

1) Innate which is present at birth and is first-line defense against pathogens.

2) Acquired or developed immunity:
-Active: response to actual attack OR vaccination; Lasts longest.
-Passive: Protected from pathogen by immunity gained from someone else like mom to baby or serum injection; Doesnt last as long due to lack of memory cells.

53
Q

What are antigens and antibodies?

A

1) Antigens are substances the body recognizes as foreign that illicit a response. Does not always have to start out as pathogens, can be lipoproteins, glycoproteins etc. and get pissed and turn on you!! The body can actually create these AND your body can become tolerant of them and ignore them…fuckin. crazy.

2) Antibodies are immune globulins produced by lymphocytes in response to antigens.

54
Q

What are our organs of immunity?

A

Tonsils
Thymus gland
Bronchial-associated lymphoid tissue
Lymphnodes
Spleen (major organ of immune response)
Gut-associated lymphoid tissue
Bone marrow (Where all WBC are made)
Lymphnodes
Genital-associated lymphoid tissue

55
Q

What are the various lymphoid organs?

A

Central (primary) lymphoid organs:
1) Thymus gland: Shrinks with age and is involved with the differentiation and maturation of T lymphocytes.
2) Bone marrow: Produces red blood cells, white blood cells, and platelets. They migrate all over.

Peripheral lymphoid organs:
1) Lymph nodes
2) Tonsils
3) Spleen
4) Lymphoid tissues associated with the gut, genitals, bronchi, and skin.

56
Q

Humoral vs. Cell-mediated immunity.

A

Humoral immunity and cell-mediated immunity are two types of anadaptive immune responsethat enable the human body to defend itself in a targeted way against harmful agents such as bacteria, viruses and toxins. Whilst there is some overlap between these arms of the immune response - both rely on the functions of lymphoid cells - there are also some important differences.

Humoral immunityis an antibody-mediated response that occurs when foreign material -antigens- are detected in the body. This foreign material typically includes extracellular invaders such as bacteria. This mechanism is primarily driven byB cell lymphocytes, a type of immune cell that produces antibodies after the detection of a specific antigen. *Antibodies produced by plasma cells (differentiated B lymphocytes) Primary immune response is evident 4-8 day s after initial exposure to antigen.

Unlike humoral immunity,cell-mediated immunitydoes not depend on antibodies for its adaptive immune functions. Cell-mediated immunity is primarily driven by mature T cells, macrophages, and the release of cytokines in response to an antigen.

57
Q

What are the cells of the immune response and what are their roles?

A

*Mononuclear phagocytes: Initiates the immune response
1) Include monocytes in the blood and macrophages found throughout the body.
2) Capture, process, and present antigens to lymphocytes to initiate an immune response.
3) Capture antigens by phagocytosis

*Lymphocytes:
1) Produced in bone marrow
2) Eventually migrate to peripheral organs
3) Differentiate into B and T lymphocytes
-T cytotoxic cells- they attack the antigen.=> memory cells
-T helper cells- help produce cytokines
-Natural killer cells (large lymphocytes) recognizing and killing viruses, tumor cells, and transplanted grafts.

*Cytokines:
1) Soluble factors secreted by the WBCs and a variety of other cells in the body.
2) Acts as messengers among cell types
3) Instructs other cells to alter their proliferation, differentiation, secretion or activity.
4) Currently at least 100 different cytokines
5) Have a beneficial role in hematopoeis and immune function.
6) Can have detrimental effects:
-Chronic inflammation
-Autoimmune diseases
-Sepsis

58
Q

What are different types of cytokines?

A

Interleukins
Interferons (common ones, used in cancers)
Tumor necrosis factor
Colony-stimulating factor
Erythropoietin

A-Interferon and B-interferon:
- Inhibit viral replication
- Activate NK cells and macrophages
- Antiproliferative effects on tumor cells
y-Interferon: (used with MS)
-Activates macrophages, neutrophils, and NK cells
-Promotes B-cell maturation
-Inhibits viral replication

59
Q

What are the 5 classes of immune globulins and their specific characteristics?

A

IgG- Secondary exposer responder. When a person is exposed to an antigen for a second time, the response is faster (1 to 3 days) and lasts longer. Main product of secondary response is IgG rather than IgM. Largest component of total immunoglobulin in body. Can cross placenta and plasma etc. Memory cells account for more rapid prodcution of IgG.

IgA- Found in body secretions such as saliva and tears, breast milk and colostrum, lines mucus membranes.

IgM- Largest immunoglobulin. Also found in the plasma. Rsponsible for primary immune response. This forms antibodies in the ABO blood cell proteins.

IgD- Found in the plasma. Its on the lymphocytes surface. Assists in differentiation of B cells.

IgE- found also in the plasma. Also in interstitial fluid. Responsible for allergic reactions.

IgM (1st to react) AND IgG (2nd to react) are the predominant primary immunoglobulins in primary response to antigens. In subsequent exposure, IgG will be first to respond and it will be more rapid, and severe. IgM willstay the same.

60
Q

What are some of the effect of aging on the immune system?

A

Higher incidences of tumors
Greater suseptibility to infection
Increased autoantibodies (antibodies made against our own body)
Lower cell-medicated immunity
Thymic involution