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NU 360 > Ch. 17, 33, 34 > Flashcards

Ch. 17, 33, 34 Flashcards

1
Q

peripheral perfusion

A

total arterial blood flow through the tissues

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2
Q

central perfusion

A

blood that is pumped by the heart

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3
Q

clotting

A

complex, multi-step process by which blood forms a protein-based structure (clot)

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4
Q

bone marrow

A
  • bone forming organ
  • produces most blood cells
  • involved immune responses
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5
Q

name the accessory organs

A

liver
spleen

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6
Q

plasma proteins

A
  • albumin
  • globulins
  • fibrinogens
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7
Q

cells

A
  • RBC (erythrocytes)
  • WBC (leukocytes)
  • platelets
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8
Q

RBCs

A
  • 120 day life span
  • produce Hgb (need iron too)
  • production is triggered by tissue oxygenation (erythropoiesis)
  • growth factor- erythropoietin
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9
Q

RBC medications

A

epoetin alfa
- procrit
- epogen

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10
Q

WBC

A
  • inflammatory response
  • immunity
  • 5000-10000 k
  • higher count: infection
  • lower count: immunocompromised, at risk for infection bc low count of immune defender cells
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11
Q

WBC medication

A
  • filgrastim (neupogen)
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12
Q

platelets

A
  • aggregation
  • stored in spleen
  • 1-2 week life span
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13
Q

blood clotting/hemostasis balances

A

clotting and dissolving factors

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14
Q

blood clotting/hemostasis: 3 sequential processes

A
  • plt aggregation with formation of plt plug
  • blood clotting cascade
  • formation of complete fibrin clot
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15
Q

platelets need to be activated by

A

collagen and other substances (exogenous or themselves)

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16
Q

platelet aggregation

A
  • membranes become sticky
  • NOT clots
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17
Q

clotting factors

A
  • platelet plug
  • clotting factors
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18
Q

fibrinogen activated by

A
  • fibrin by thrombin
    (thrombin activated fibrinogen)
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19
Q

prothrombin activated by

A

prothrombin activated by thrombin

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20
Q

fibrin activated by

A

fibrin activated by clot

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21
Q

anticlotting forces

A

plasminogen –> plasminogen activators/thrombin –> plasmin (activated form of plasminogen) –> digestion –>fibrin clot –> fibrin degradation products

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22
Q

hematologic changes associated with aging

A
  • decrease in blood volume with lower levels of plasma proteins
  • bone marrow produces fewer blood cells
  • total RBC, WBC counts lower
  • lymphocytes are less reactive to antigens, and lose immune function
  • hemoglobin levels fall after middle-age
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23
Q

hematologic diagnostic assessment

A
  • CBC
  • reticulocyte (retic) count - immature rbc have nucleus
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24
Q

hematologic diagnostic assessment in older adults

A
  • plts stay the same
  • hgb decrease (think bc RBC decreases)
  • WBC does not increase as much with infection
  • RBC decreases (think bone marrow suppression)
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25
Q

prothrombin (PT)

A
  • measures how long blood takes to clot
  • clotting factors II, V, VII, X
  • normal PT 11-12.5 secs
  • abnormal values
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26
Q

partial thromboplastin time (PTT)

A
  • assess intrinsic clotting cascade
  • clotting factors II, V, VIII, IX, XI, XII
  • normal = 32-45 secs
  • therapeutic range: 1.5-2x nl
  • abnormal values
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27
Q

INR- international normalized ratio

A
  • client’s PT divided by nl PT value
  • normal range: 0.7-1.8
  • warfarin therapy, want INR to be: 2-3
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28
Q

nursing implications for INR

A
  • monitor based on hospital policy (ie q6h)
  • adjust warfarin rate based on INR
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29
Q

abnormal values of PTT

A

anything outside of 32-45 seconds

  • want abnormal PTT value when on heparin therapy
  • want 1.5-2x the normal to show heparin is being therapeutic
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30
Q

bone marrow aspiration/biopsy: patient preparation

A
  • provide accurate information and emotional support
  • explain procedure
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31
Q

bone marrow aspiration/biopsy: procedure

A
  • iliac crest
  • local anesthesia
  • aspirate bone marrow to test (think testing leukemia to test RBCs)
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32
Q

bone marrow aspiration/biopsy: follow-up care

A
  • teach to inspect the site every 2 hours for 24 hours
  • avoid activity that could result in trauma
  • analgesic (aspirin-free) and ice packs
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33
Q

bone marrow aspiration can be used to identify the presence of

A

Study of the bone marrow can be used to identify the presence of leukemia or other malignancies or to determine the cause of anemia.

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34
Q

acquired immune deficiency syndrome (AIDS)

A
  • Serious worldwide epidemic
  • HIV can progress to AIDS
  • most common immune deficiency disease in the world
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35
Q

most common immune deficiency disease in the world

A

AIDS

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36
Q

HIV is a ___ virus

A

retrovirus that infects human CD4+ T-cells

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37
Q

CD4+ T-Cells direct

A

immune system defenses
- replicate 100 million times a day

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38
Q

CD4+ T-Cells: types

A
  • memory: remember cells that body has been exposed to
  • naive: attack everything

CD4 cells = CD4+ cells = T cells = T lymphocytes (all the same thing, all immune cells that attack invaders)

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39
Q

CD4+ T-Cells: memory cells

A

those programmed to recognize a specific antigen after it has been previously seen

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40
Q

CD4+ T-Cells: naive cells

A

non-specific responders

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41
Q

HIV: need to knows

A
  • spread HIV through bodily fluids: blood, semen, sputum, breastmilk
  • HIV messes around with the way that the CD4 cell functions: the CD4 now hosts a virus factory, which buds and continuously spreads
  • issue with HIV is that the CD4 cells cannot fight infections anymore (immunodeficiency)
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42
Q

HIV life cycle

A
  1. free virus
  2. binding and fusion
  3. infection
  4. reverse transcription
  5. integration
  6. transcription
  7. assembly
  8. budding
  9. immature virus breaks free of the infected cell

take away: multiple steps for the virus to grow and make babies; this is important because the drugs work on specific steps (this is why we use ie 3 drugs to treat)

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43
Q

effects of HIV infection

A
  • CD4+ T-cells become “HIV factory” to make new viral particles daily
  • Gradually, CD4+ T-cell count falls, viral load rises
  • Immune systems weakens
  • Everyone with AIDS has HIV; not everyone with HIV has AIDS
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44
Q

AIDS and HIV relationship

A

everyone with AIDS has HIV; not everyone with HIV has AIDS

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45
Q

CD4+ T-Cell Count: normal

A

800-1000 cell/mm³

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46
Q

CD4+ T-Cell Count: stage 1 HIV

A

> 500 cell/mm³ with confirming blood test

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47
Q

CD4+ T-Cell Count: intermediate stage HIV

A

200 – 499 cell/mm³
- Lower the count – patient at risk for bacterial, fungal, viral, cancers, and opportunistic infections

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48
Q

CD4+ T-Cell Count: AIDS

A

<200 cell/mm³
- Once diagnosis of AIDS, then always have that diagnosis even if CD4+ T-cells count goes over 200.

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49
Q

HIV-II, class 0

A

Patient develops a first positive HIV test result within 6 months after a negative HIV test result. CD4+ T-cell counts are usually in the normal range and no AIDS-defining condition is present.

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50
Q

HIV-III, class 3

A

Patient has a CD4+ T-cell count of less than 200 cells/mm3 (0.2 X 109/L) or a percentage of less than 14%. Any patient, regardless of CD4+ T-cell counts or percentages who has an AIDS-defining illness. AIDS diagnosis.

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51
Q

HIV-II, class 1

A

Patient has a CD4+ T-cell count of greater than 500 cells/mm3 (0.5 X 109/L) or a percentage of 29% or greater. No AIDS-defining illnesses are present.

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52
Q

HIV-II, class 2

A

Patient has a CD4+ T-cell count between 200 and 499 cells/mm3 (0.2 to 0.499 X 109/L) or a percentage between 14% and 28%. No AIDS-defining illnesses are present.

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53
Q

HIV-class unknown

A

Patient has a confirmed HIV infection but no information regarding CD4+ T-cell counts, CD4+ T-cell percentages, and AIDS-defining illnesses is available.

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54
Q

transmission of HIV

A
  • unprotected sexual intercourse with an infected partner
  • vertical transmission: mother to child- in utero, during delivery, breastmilk
  • injection drug use (rare: infected blood products)
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55
Q

highest prevalence of HIV

A
  • Blood and Semen have highest transmission, then vaginal secretions
  • anal sex is the highest risk (more than vaginal): rectal mucosa tears more easily, no natural lubrication, receiving partner at highest risk
  • vaginal sex is 2nd highest risk transmission
  • saliva is the 3rd highest risk transmission
  • Need contact of infected body fluid to mucous membranes or non-intact skin or directly into the bloodstream
  • just because you have sex with an HIV+ person does not mean that you will automatically get HIV
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56
Q

who is at high risk for HIV

A
  • Gender: can be either men or women
  • Sexual act: receiving partner
  • Viral Load: more virus that they have (newly dx, not taking meds) have higher viral load
  • Vulnerable populations: not educated about safe sex, cant afford contraception, IV drug users, incarcerated persons (people that don’t have access to good health care or education), serodiscordant
  • Cultural considerations: certain cultures don’t allow contraception use, anal sex is preferred
  • Elderly considerations: nursing homes have high rates of STI/STDs
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57
Q

safer sex practices to prevent HIV

A
  • A latex or polyurethane condom for genital and anal intercourse
  • A water-based lubricant with a latex condom
  • A condom or latex barrier (dental dam) over the genitals or anus during oral-genital or oral-anal sexual contact
  • Latex gloves for finger or hand contact with the vagina or rectum
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58
Q

HIV: Pre-exposure prophylaxis “PreP”

A

Used for high risk populations (the people that are currently HIV-)
- Men who have sex with men
- Heterosexually active men and women
- Injecting drug users (dirty needles)
- Serodiscordant relationships: HIV+ partner with HIV- partner

“PreP” is a pill that protects you from developing HIV (protects cells from HIV getting in “shield”), must take HIV test to prove negative before starting, then take it very regularly, retest every 6 months; taken for an extended period of time/rest of life
- example: Truvada

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59
Q

HIV: Postexposure prophylaxis “PEP”

A
  • Occupational exposure: nurse gets needle stick
  • Non-occupational exposure
  • Sexual assault

“PEP” is an antiviral medication taken after exposure to HIV; test first, then retest; taken one time for certain regimen; not guaranteed to work but worth taking
- example: cART: combination antiretroviral therapy (cocktail of medication to hit multiple stages of HIV cycle)

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60
Q

health care workers and HIV

A
  • Needle sticks
  • Exposure of non-intact skin or mucous membrane with blood and body fluids
  • STANDARD PRECAUTIONS! (gloves always)
  • PEP (only if source patient is +)
61
Q

HIV testing

A
  • Seroconversion between 3 weeks to 3 months, up to 3 years
  • Testing CD4+ T-cell counts
  • HIV test types: (2 test confirmation)
    -ELISA (blood test)
    -Western blot (blood test)
    -Oral Testing (saliva test)
  • Counseling: Pre and Post-test (life-altering dx, offer support, follow-ups for a plan to proceed)

1st blood test: looking for + or - (- could be really - or we didnt catch it yet; + means you have HIV, but need to look at CD4 count)

62
Q

acute retroviral syndrome

A

Acute/Early Infection:
-Following HIV transmission, approximately 50% of individuals will develop a febrile, flu-like illness

63
Q

acute retroviral syndrome before HIV: s/sx

A
  • febrile
  • Swollen glands
  • Rash
  • Oral ulcers
  • Muscle aches
  • Sore throat
  • Headache
  • Diarrhea
  • N/V
64
Q

suspicion of HIV (key sx)

A

Suspicion of HIV - Recurrent Vaginal Candidiasis (yeast infection) or STI**

65
Q

intermediate disease stage of HIV

A

In general - if untreated, there is an 8-10 year period during which an HIV+ individual undergoes a gradual decline in immune function (CD4 count) and increase in HIV viral load
- Often no symptoms exhibited during the intermediate disease stage

66
Q

advancement of HIV

A

Untreated, the rapid replication of HIV will eventually deplete the immune system in most people to such an extent that the patient will lose critical body defenses and can succumb to infections, AIDS (because CD4 cell count falls) and ultimately death.

67
Q

hallmarks of the advanced stage of HIV

A
  • Opportunistic infections** (think progression to AIDS) or malignancies
  • Rashes (like karposi’s)
  • Diarrhea
  • Recurrent vaginal candidiasis
  • Neuropathy
  • Herpes zoster/shingles (think blistered rash)
  • Cancers (think bc immune system is at very low point)
  • Thrush (oral)
  • Anemia
68
Q

Actual diagnosis of AIDS is made when (hint: CD4+ T-cell)

A

Actual diagnosis of AIDS is made when the CD4+ T-cell count falls below 200 cells/mm³ or when an AIDS-defining condition is diagnosed.

69
Q

stage of HIV: AIDS

A

More likely to see Opportunistic Infections – should always assess for these in HIV+ patients
- Important to teach patients and their families how to prevent infection

70
Q

fungal/protozoal opportunistic infections

A
  • Pneumocystis jiroveci pneumonia (PCP/PJP): most common **only kind of PNA that happens because of no immune system defenses (HIV+ pt only)
  • Toxoplasma encephalitis: cat feces or infected undercooked meats (HIV+ at risk for these infections)
  • Candidiasis: Oral (Thrush) or Vaginal
71
Q

bacterial opportunistic infections

A
  • Mycobacterium avium complex (MAC)
    -Respiratory and GI - systemic
  • Tuberculosis* (biggest problem, TB and HIV- rusty sputum, night sweats, unintended weight loss)
72
Q

parts of the body TB affects (think s/sx)

A

rusty sputum, night sweats, unintended weight loss

73
Q

viral opportunistic infections

A
  • Cytomegalovirus (CMV)
  • Herpes Simplex Virus (HSV): lips hurt
  • Varicella Zoster Virus (VZV)
    -Shingles
74
Q

malignancies- opportunistic infections

A

Karposi’s Scarcoma
- 1-21% of AIDS patients
- Non-painful/non-itchy
- brown plaques over the body
- hallmark sign of AIDS
- you can only get Karposi’s Sarcoma from AIDS

75
Q

AIDS dementia

A
  • a lot of people with AIDS get dementia
  • attacks brain, confusion
  • Supportive Care: around the clock care
  • Diagnosis made by exclusion
  • 70% of people
76
Q

priority patient problems with AIDS

A
  • Potential for infection
  • Inadequate oxygenation
  • Pain
  • Inadequate nutrition
  • Diarrhea
  • Reduced skin integrity
  • Confusion*
  • Reduced self-esteem
  • Potential loss of social contact
  • Comfort/safety priorities*
77
Q

HIV medications- HAART

A
  • antiretrovirals
  • “cocktails”
  • each type of class targets different phases of HIV infection
  • be regular about taking meds
  • lifelong for patients that are HIV+ patients
78
Q

antiretroviral therapy inhibits

A

Antiretrovirals therapy only inhibits viral replication

79
Q

issues with HIV meds

A

*ADHERENCE
- Drug resistance
- Expensive
- Side effects
- Frequency
- Food and Timing Requirements
- Life-long
- PreP: for HIV- patient taking part in risky HIV+ behavior, take PreP as long as they are partaking in the risky behavior

80
Q

anticoagulants “blood thinners”

A
  • Heparin: half-life 1-6 hrs; lab value PTT; thrombin
  • Lovenox (low-molecular-weight-heparin, Xa)
    -Fondaparinux
  • Warfarin/Coumadin: 48-96 hrs peaks; 1 week to clear, PT and INR; inhibit synthesis vit K
81
Q

anticoagulants: how they work

A
  • Interferes with steps in blood clotting
  • Limit or prevent extension of clots and prevents new clots
  • want the levels to be abnormal to indicate that the anticoagulants are working
    -if the level is normal, then we may need to increase the dose of the anticoagulant
82
Q

aPTT is

A

a specialized version of PTT

83
Q

fibrinolytics

A
  • clot busters; the only drug class that break up existing clots
  • priority problem: widespread bleeding
  • Selectively degrade fibrin threads
  • “-ases”
  • Tissue plasminogen activator (t-PA)
  • think neuro changes: start acting funny = brain bleeding
84
Q

novel anticoagulants (DOACs/NOACs)

A
  • Don’t require dose adjustment or monitoring of PT/INR or PTT (no blood monitoring)
  • PO pills, more compliance
  • Indicated for AF, DVT or PE
  • Fast acting
  • 2 types
    -Direct Thrombin Inhibitor
    -Factor XA inhibitor
85
Q

direct thrombin inhibitor (name drug)

A

Dibigitran (pradaxa)
- has reversal agent

86
Q

factor XA inhibitors (name drugs)

A
  • Rivaroxaban (xarelto)
  • Apixiban (eliquis)
87
Q

platelet inhibitors

A
  • Prevents platelets from becoming active or activated platelets from clumping together (prevent clots from growing)
  • Aspirin
  • Clopidogrel

-worry about: allergy, bleeding ulcer

88
Q

anemia

A
  • Reduction in # of RBCs
  • Low amount of Hgb
  • Low amount of HCT (HCT is the ratio of RBC to blood in body, percentage, dehydration = high HCT bc low blood compared to RBC)
89
Q

RBC disorders are secondary to

A
  • Dietary deficiencies
  • Genetic disorders
  • Bone marrow disease
  • Excessive bleeding
90
Q

hypochromic anemia

A

iron or vitamin deficiency

91
Q

pernicious anemia

A

lack of intrinsic factor (lack of Vit B12)
- have megaloblasts, not healthy RBCs
- “pins and needles” sx*
- smooth, glossy tongue; glossitis*
- crappy digestion

92
Q

erythroblastosis fetalis anemia

A

destruction by antibodies

93
Q

secondary anemia

A

bleeding, leukemia, cancer, chronic kidney disease

94
Q

genetic factors anemia

A

sickle cell anemia or spheroidal

95
Q

aplastic anemia

A

malfunctioning bone marrow
- something is hurting the bone marrow and now we are not getting adequate production of RBCs, WBCs, and platelets
- caused by: radiation, chemotherapy, exposure to certain chemicals

96
Q

Anemias Resulting from Increased Destruction of RBCs

A
  • Sickle cell disease
  • Glucose-6-phosphate dehydrogenase deficiency anemia
  • Immunohemolytic anemia
97
Q

Anemias Resulting from Decreased Production of RBCs

A
  • Iron deficiency anemia
  • Pernicious anemia (Vitamin B12 deficiency)
  • Folic acid deficiency
  • Aplastic anemia
98
Q

diet management with anemia: iron rich foods

A
  • chicken
  • liver
  • pork
  • eggs
  • beef
  • broccoli
  • dried beans/green peas
  • spinach
  • potatoes with skin
  • iron fortified cereal
  • raisins
99
Q

s/sx of anemia

A
  • Integumentary: pale: vasoconstriction, blood cells are going to core not periphery
  • Cardiovascular: low BP, increased HR
  • Respiratory: SOB
  • Neurologic
  • clubbing fingers
100
Q

sickle cell incidence and prevalence

A
  • Occur in people of ALL races and ethnicities
  • MOST common among African Americans in the U.S.
  • Occurs in 1 in 500 African Americans
  • About 1 in 13 African Americans are carriers
101
Q

sickle cell disease

A
  • Genetic disorder; 40% total hgb contains abnormal hgb (HbS), normal Hgb is HbA
  • During hypoxemia – hgb becomes sickle-shaped, rigid, clumping together, masses occlude vessels (no blood or oxygen, tissues are dying, terrible pain)
  • die faster, dont last 120 days that normal RBC does
102
Q

sickle cell crisis

A

hypoxemia –> tissue damage –> infarcted areas + organ death

  • 45 year life span
  • crisis is a flare-up of the symptoms/disease
  • a crisis can be caused by: vigorous exercise, cold, illness, smoking (anything that decreases oxygen supply)
103
Q

s/sx of sickle cell

A
  • Pain (chronic*)
  • Jaundice* (abundance of bilirubin, liver cant handle it all, back up of bilirubin causes jaundice: yellow skin, eyes)
  • Cardiovascular
  • Skin changes
  • Musculoskeletal
  • Psychosocial –
    “Chronic, painful, life-limiting genetic disorder.”
104
Q

diagnostics/labs of sickle cell

A
  • HCT is low
  • Retic count high** (many immature RBCs)
  • Total bilirubin high** related to RBC destruction
  • WBC is high** (hypoxia and ischemia lead to chronic inflammation)
  • Electrophoresis (used to find percentage of HbS* baby Hgb)
  • Imaging (organ enlargement, hepatomegaly, splenomegaly), EKG, Echocardiogram
105
Q

sickle cell patient problems

A
  • Pain due to poor tissue perfusion and joint destruction with low oxygen levels
  • Potential for infection, sepsis, multiple organ dysfunction syndrome (MODS), and death (think sickled cells block blood flow to the spleen, increasing risk of infection to spleen; blocked blood flow in general leads to edema of hands and feet- frequent infections)
105
Q

sickle cell interventions

A
  • Analgesics* prioritize pain meds: NO PO/PRN, need morphine, dilodid, PCA pump round the clock; prns for breakthrough only
  • Hydration* (sickle cell makes blood clumpy, want to keep hydrated, fluids by mouth and IVF)
  • Check circulation- need to keep patient warm!*
  • Oxygen*
  • Potential for sepsis
  • Blood Transfusions
  • Patient Education
106
Q

sickle cell outcomes

A
  • Report pain to be maintained at an acceptable level
  • Maintain perfusion and gas exchange to extremities and vital organs
  • Remain free of infection, sepsis, and multiple organ dysfunction syndrome (MODS)
107
Q

leukemia: etiology & genetics

A
  • Genetic and environmental factors
  • Damage to genes that control cell growth
108
Q

risk factors for leukemia

A
  • Ionizing radiation
  • Viral infection
  • Exposure to chemicals and drugs
109
Q

leukemia: incidence and prevalence

A
  • 3-4% of new cases of cancer and all deaths from cancer
  • 61,780 new cases annually in U.S.
110
Q

leukemia is

A
  • Uncontrolled production of immature WBCs in bone marrow; “baby blasts” can’t protect you from infection, don’t let RBC or platelets be made: no room to make bc so many baby blasts
  • Normal blood cells are decreased, platelets are decreased
  • Becomes malignant state – classified by cell types
111
Q

leukemia: malignant cell types

A
  • AML: acute myelogenous leukemia
  • ALL: acute lymphocytic leukemia
  • CML: chronic myelogenous leukemia
  • CLL: chronic lymphocytic leukemia
  • 2% all cancers
112
Q

s/sx of leukemia: ANT

A

Anemia: low hgb
Neutropenia: risk of infection
Thrombocytopenia: bleeding

LOTS of immature WBCs

113
Q

clinical manifestations of leukemia

A
  • Decreased platelet functioning
  • CV: anemia, low BP, high HR, longer cap refill, temperature/fever
  • Resp: SOB, cough, dyspnea, increased RR
  • Skin: bleeding, bruising, petechiae
  • Intestinal changes: mouth sores, poor digestion, poor absorption of nutrients
  • CNS: confusion, AMS
114
Q

dx tests/labs of leukemia

A
  • Hgb, Hct, plts (low because blood is full of baby blasts)
  • Wbc abnormal (super high baby blast)
  • bone marrow aspiration
115
Q

definitive dx of leukemia

A

bone marrow aspiration examination of cells

116
Q

priority nursing interventions for leukemia

A
  • preventing infection
  • washing hands
  • explaining bone marrow aspiration procedure
  • monitor bleeding s/sx
  • monitor s/ transplant rejection
117
Q

leukemia patient problems

A
  • Potential for infection due to reduced Immunity and chemotherapy
  • Potential for injury due to poor clotting from thrombocytopenia and chemotherapy
  • Fatigue due to reduced gas exchange and increased energy demands
118
Q

bone marrow transplantation

A
  • Standard treatment for leukemia
  • Purges present marrow of the leukemic cells
  • After conditioning, new, healthy marrow given to the client toward a cure
  • Sources of stem cells
  • Conditioning regimen
  • Transplantation: if doesnt work, need another transplant
119
Q

transplant rejection

A
  • Hyperacute graft rejection: minutes
  • Acute graft rejection: days or weeks
  • Chronic rejection: months or years
  • Treatment of transplant rejection: need new transplant
  • Maintenance: anti-rejection meds
  • Rescue therapy: only used if rejecting transplant
120
Q

malignant lymphomas

A
  • Abnormal overgrowth of a lymphocyte
  • Solid tumors
  • Hodgkin’s
  • Non-Hodgkin’s
121
Q

Hodgkin’s

A
  • Men, mid-20s
  • Large painless node mainly in neck*
  • fevers
  • Reed-Sternberg cell: seen in blood test
  • treatment: bone marrow transplant, chemotherapy
122
Q

Non-Hodgkin’s

A
  • no Reed Sternburg in blood test
  • found other places beside the neck
  • swollen lymph nodes all over the body
  • scattered tumors all over the body (mostly lower body)
  • metastasis
  • young people/adults
  • treatment: bone marrow transplant, chemotherapy
123
Q

when is AIDS officially diagnosed?

A

<200 CD4+ cells
- if the cell count goes up after dx of AIDS, the patient still has AIDS

124
Q

AIDS and HIV stand for

A

acquired immunodeficiency syndrome

human immunodeficiency virus

125
Q

when is an AIDS+ person most contagious?

A

newly infected (usually asymptomatic or have viral syndrome that seems general)
- viral load is high

126
Q

HIV dx verses AIDS dx

A

HIV is dx based on if it is present in the blood or not

AIDS is dx based on CD4+ T cell count

127
Q

how is AIDS managed?

A
  • not curable
  • we focus on comfort care at this point
128
Q

Glucose-6-phosphate dehydrogenase deficiency anemia

A
  • stimulated by meds, infection, stress
  • faba-beans
129
Q

causes of iron deficiency anemia

A
  • bleeding (think heavy menstruation)
  • diet
  • usually seen in child-bearing age females
130
Q

iron deficiency anemia treatment/teaching

A
  • dietary iron
  • iron supplements: PO drink: use straw, stains teeth; IM injection: Z-track
  • teach patient to increase fiber: it darkens stool, constipates
131
Q

pernicious anemia treatment

A
  • vit B12 shot
  • folate
132
Q

aplastic anemia s/sx

A
  • SOB, tachycardia, fatigue (like other anemias)
  • risk of infection
  • bruising, bleeding, petechiae

“pancytopenia” because decrease of RBC, WBC, and platelets

133
Q

aplastic anemia treatment

A
  • self-limited: has to have chemo or radiation for cancer, but will get better when chemo or radiation is stopped
  • use shields for x-ray, etc.
134
Q

types of transfusions

A
  • packed RBC
  • platelet (does not need ABO compatibility)
  • plasma: FFP (replaces volume)
  • cryoprecipitate
  • granulocyte (white cell)
135
Q

determination of need for blood transfusion

A

lab: hgb/hct: hgb of 7 or less is standard

s/sx
- CV: palpitations
- Resp: breathless
- CNS: pallor, fatigue
- VS
- active bleeding; chronic anemia

136
Q

pre-transfusion RN responsibilities

A
  • verify order
  • test donor’s and recipient’s blood for compatibility
  • examine blood bag for ID
  • check expiration date
  • inspect blood for discoloration, gas bubbles or cloudiness
137
Q

during transfusion, RN responsibilites

A
  • VS
  • 2 RNs or RN/APRN or RN/PA or RN/MD or RN/CRNA to complete checks before administering blood
  • administer blood per protocol
  • begin transfusion slowly and stay with the patient first 15-30 min
  • ask patient to report unusual sensations such as chills, SOB, hives, or itching
138
Q

typical blood transfusion protocol

A
  • maximum is over 4 hours
  • bring saline and IV tubing to room
  • NO meds in same IV line
  • can flush with NS ONLY!
  • blood is it’s own primary line
139
Q

hemolytic transfusion reactions

A
  • RH factor incompatible
  • fever, chills, life-threatening
  • tx: STOP! flush and administer rescue meds
140
Q

allergic transfusion reactions

A
  • up to 24 hours post-transfusion
  • itchy, bronchospasm, anaphylaxis
  • tx: benadryl
  • prevention: pre-medicate with benadryl, use leukocyte-reduced or washed
141
Q

febrile transfusion reactions

A
  • develop after multiple transfusions
  • chills, fever, tachycardia, low BP, high RR
  • prevention: pre-medicate with tylenol
142
Q

circulatory overload transfusion reactions

A
  • infuse over 4 hours
  • careful with cardiac and older patients
  • edema
  • prevention/tx: can give IV lasix in between, before, or after
143
Q

priorities for patient receiving a blood transfusion

A

Use Clinical Judgment to determine how severe the reaction is…. Does it need to be stopped?
If severe:
- Stop Tx!
- Flush with New bag of 0.9% NS with new IV tubing.
- Call RRT/Provider
- Administer rescue medications (dependent on problem) & O2
- Document, Obtain Samples, Save Blood to return to lab

144
Q

ethical and legal considerations with blood transfusions

A
  • consent: need written consent before
  • children: court orders can be used when parents deny
  • emergency cases: implied consent for a trauma
  • religious affiliations
  • Jehovah Witness: no blood products
  • if patient is awake, A&O, and sound mind, they have the right to decline blood transfusions
145
Q

allogenic transplant

A

stem cell transplant from donor

146
Q

autologous transplant

A

stem cell transplant from self

147
Q

Universal blood donor

A

O-

148
Q

Universal blood recipient

A

AB+

NU 360 (12 decks)

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