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HSC 411 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

For most cancers, the stage is based on 3 main factors:

A
  1. Tumor size and invasion
  2. Lymph node involvement
  3. Metastasis
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2
Q

TNM System:

A

T (1-4) - size and invasiveness of primary tumor.

N (0-3) - lymph node involvement

M (0-1) - tumor metastasis
—M0 = no evidence of metastasis

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3
Q

Grading:

A

Tumor grading is a system used to classify cancer cells in terms of how abnormal they look under a microscope and how quickly the tumor is likely to grow and spread. Look at cell characteristics.

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4
Q

After biopsy, tissue is examined for:

A
  1. Degree of Differentiation
  2. Extent of pleomorphism
  3. Frequency of mitosis/mitotic figures (growth fraction)
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5
Q

Grade (numbers)

A

G1: well-differentiated (low grade)
G2: moderately differentiated (intermediate grade)
G3: poorly differentiated (high grade)
G4: undifferentiated/anaplastic (high grade)

*grading systems are different for each type of cancer

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6
Q

Goals of cancer treatment fall into three categories:

A
  1. Curative (tries to completely irradiate)
  2. Controlling (tries to slow progression)
  3. Palliative (not aimed at a cure, tries to reducing suffering; pain management)
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7
Q

Cancer Treatments (listed)

A 
Surgery
Radiation therapy
Chemotherapy
Immunotherapy
Bone marrow and stem cell transplants 
Gene Therapy 
Antiangiogenesis therapy
Combination therapy
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8
Q

Surgery (cancer treatment)

A

removal of tumor - try for clean (negative) margins of resection

(take out whole area around with normal cells so there is a margin on normal cells around the tumor)

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9
Q

Radiation Therapy (cancer treatment)

A

ionizing radiation

localized beams of radiation directed toward tumor site

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10
Q

Chemotherapy (cancer treatment)

A

Anti-neoplastic chemicals. Tends to lose effect with time. Some tumors are resistant.

(works systemically - targets all labile cells, cells dividing at a high rate)

side effects: hair loss, nausea, fatigue, etc.

Interferes with mitosis of bone marrow
-bone marrow suppressed so it affects RBCs, WBCs, and platelets

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11
Q

Immunotherapy

A

attempts to use immune system to fight tumor

  • interferon or interleukin 2 (IL2)
  • monoclonal antibodies - block signals, mark for destruction
  • vaccines - prophylactic (prevent virus = prevent cancer, for example, HPV) and therapeutic (teaches immune system to go and attack cancer by pulling cancer cells out and developing the vaccine and inserting it back in)
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12
Q

Bone Marrow and Stem Cell Transplants (cancer treatment)

A

Use other people’s marrow and/or stem cells to help cure certain diseases

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13
Q

Gene Therapy (cancer treatment)

A

Alteration of one’s genetic material to fight or prevent disease
(replace mutated genes to cure cancer)
(modify virus and insert to replace mutated DNA)

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14
Q

Antiangiogenesis Therapy (cancer treatment)

A

Target VEGF pathway

blocks VEGF receptors so blood vessels aren’t growing in tumors

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15
Q

Combination Therapy

A

Use of two or more therapies. Surgery and/or radiation first, followed by chemotherapy.
(most common/likely)

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16
Q

Prostate (Background Information

A
  • Prostate gland is an encapsulated gland that secretes additional fluids into the seminal fluid
  • It lies between the urinary bladder and the superior surface of the UG diaphragm
  • The prostate gland can be broken down into various lobes; some of which are the anterior, posterior, and median lobes (which have clinical significance)
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17
Q

Anterior Lobe (prostate gland)

A

Fibrous and normally non-pathological in nature

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18
Q

Median Lobe (prostate gland)

A

Is famous for benign prostatic hyperplasia (NOT CANCER)

The lobe may undergo hyperplasia resulting in obstruction of the urethra and the visceral neck of the urinary bladder. (enlarges upward and closes in on urethra, squeezing off urethra)

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19
Q

Benign Prostatic Hyperplasia (BPH) - Signs and Symptoms

A

Urinary frequency, dysuria (difficult urination), and infection due to retention (cannot completely empty the bladder)

This condition begins at about 45 years of age, and occurs in 80% of all men by 80 years of age

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20
Q

BPH - Treatment

A

Take meds to shrink

Less than 10% require TURP

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21
Q

Posterior Lobe (prostate gland)

A

Most predisposed to malignant transformation (carcinoma of the prostate)

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22
Q

Prostate Cancer Statistics

A

Most common cancer in males (1 in 6 men)

Second most common cause of cancer-related deaths in males

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23
Q

Prostate Cancer Etiology

A

Poorly understood, but genetics and testosterone play a role

Risk factors include age (>70, rare before age 65), race (black people have higher risk), and heredity (dad/brother with cancer = 2x risk)

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24
Q

Prostate Cancer Pathology

A

85% originate in posterior lobe
Metastasizes through lymphatic vessels into adjacent structures: rectum, bladder, pelvic structures, vertebral column, liver, others.
Most often slow growing

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25
Q

Prostate Cancer Diagnosis

A

Medical History
Rectal (digital) exam
Confirmed by biopsy
PSA - positive test indicates potential problems and further testing is needed (can have false positives - 2/3 who have elevated PSAs do not have cancer)

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26
Q

Prostate Cancer Treatment

A

Surgery
Radiation (can use permanent seeds)
Watchful Waiting (keep an eye on it and make decisions based on how fast it is growing)

  • It is usually treated with a combination of radiation and hormone therapy with some type of surgery to remove the cancerous tissue.
  • Depends on age of patient and characteristics of the tumor (grade of tumor)
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27
Q

Prostate Cancer Prognosis/Staging

A

Depends on detection stage of tumor growth

  • T1 = not palpable - detected by biopsy
  • T2 = tumor palpable (10 year survival rates as high as 80%)
  • T3 = invasion outside capsule
  • T4 = indications of metastasis (10 year survival rates from 50-0% depending on specific case)

*In general, the earlier you catch it, the better the survival rate

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28
Q

Prostate Cancer Screening

A

Offer men 50 or older get digital rectal exam (DRE) and PSA test/year.

  • Make an informed decision about screening
  • Stop screening at 75
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29
Q

Prostate Cancer (general overview)

A

Very common
Most often slow growing
PSA results are questionable
Treatment has many side effects

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30
Q

Cervical Cancer

A

A highly preventable type of cancer (highly treatable)

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31
Q

Incidence of cervical cancer is declining due to:

A

Early detection and now, prevention

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32
Q

Cervical Cancer Etiology

A

Considered a STD.
Virtually all are caused by infection with Human Papilloma Virus (HPV) passed through skin to skin contact

asymptomatic

In 90% of cases, the immune system clears HPV within two years

Low risk HPV results in genital warts

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33
Q

HPV Infection

A

Mainly asymptomatic

In 90% of cases, the immune system clears HPV within two years

Low risk HPV results in genital warts

Types 16 and 18 (high risk HPV) cause 70% of all cervical cancers

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34
Q

Cervical Cancer Risk Factors

A

Sexual intercourse at early age (higher risk because of likelihood of more partners)
Multiple sex partners
Smoking

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35
Q

Cervical Cancer Signs and Symptoms

A

Asymptomatic, vaginal bleeding, pain during intercourse, metastatic signs and symptoms depending on site

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36
Q

Cervical Cancer Pathogenesis

A

A squamous cell carcinoma-

  • Exocervix
  • Endocervix
  • Transformation zone
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37
Q

Exocervix

A

Projects into superior vagina and is covered with stratified squamous epithelium

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38
Q

Endocervix

A

Portion towards uterine body and is lined with columnar epithelium

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39
Q

Transformation Zone (cervix)

A

Where two epithelia meet. Site of most cervical carcinomas

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40
Q

Stages of Cervical Intraepithelial Neoplasia (CIN)

A

PRE-CANCEROUS
CIN 1 = mild dysplasia. Low grade lesion
CIN 2 = Moderate dysplasia. High-grade lesion
CIN 3 = Severe dysplasia in >2/3 of cells; carcinoma in situ (CIS)

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41
Q

Stages of Cervical Carcinoma and Prognosis

A

Stage 0 = CIS
-5 year survival up to 100%

Stage 1 = tumor confined to cervix
-5 year survival ~85%

Stage 2 = Invasion to adjacent structures; not reaching pelvic wall or middle third of vagina.
-5 year survival ~75%

Stage 3 = Invasion to lower 1/3 of vagina or wall of pelvis.
-5 year survival ~35%

Stage 4 = Extension to bladder or rectum or structures beyond pelvis
-5 year survival ~10%

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42
Q

Cervical Cancer Diagnosis/Screening

A

Pap smear detects dysplastic cells in exo- and endocervix

HPV testing

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43
Q

Cervical Cancer Treatment (listed)

A

Depends on progression of pathology

Cone Biopsy/Leep Procedure
Hysterectomy
Pelvic Exenteration

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44
Q

Cone Biopsy/Leep Procedure

A

Used to examine a portion of both exo- and endocervical tissue

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45
Q

Hysterectomy

A

Removal of uterus

Used in cases of advanced cancer

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46
Q

Pelvic Exenteration

A

Removal of all pelvic viscera

Last resort to reduce tumor burden

-Can include radiation along with surgery

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47
Q

Cervical Cancer Prevention

A
  1. Avoid HPV (and detect)
    - Gardasil - protects against high and low risk; for boys and girls from age 9-26
    - Lifestyle - ABC’s
  2. Prevent precancerous from becoming cancerous - EARLY DETECTION!
    - pap smear at age 21
    - pap and HPV testing at age 30
    - >65 can stop

1/2 of all cervical cancers are diagnosed in women who have never been screened (US)

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48
Q

Breast Cancer

A

70% of cases occur in women over age 50

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49
Q

Etiology (Breast cancer)

A

Idiopathic
Specific Genetic Link: BRCA-1 and BRCA-2 genes
-80% chance of developing cancer in their lifetime

Human epidermal growth factor receptor-2 (HER-2/neu) amplified in up to 30% of breast CA which indicates an aggressive tumor

p53 mutations

Other:

  • family history of breast cancer
  • radiation exposure
  • premenopausal women over age 45
  • obesity
  • early onset menses/late menopause
  • never pregnant
  • first pregnancy after age 35
  • high fat diet
  • endometrial or ovarian cancer
  • alcohol use
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50
Q

Breast Cancer Classification

A

Classified by tissue of origin and location of the lesion

Lobular CA is within the lobes

Ductal CA is within the ducts = MOST COMMON FORM

Inflammatory CA (rare) grows rapidly and causes overlying skin to become edematous, inflammed, and indurated

Also classified as invasive vs non-invasive

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51
Q

Invasive Breast CA

A

Breaks through the duct walls and encroaches on other breast tissue

90% of breast cancer

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52
Q

Non-invasive Breast CA

A

Remains confined to ducts

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53
Q

Signs and Symptoms (Breast Cancer)

A

Thickening of the breast tissue, painless lump or mass
Nipple retraction or discharge, skin changes, redness
Growth rates vary - may take up to 8 years for lump to become palpable
Can spread via lymphatic or bloodstream to lungs and other breast

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54
Q

Diagnosis (Breast Cancer)

A

Breast self exam
Mammography can detect lumps too small to palpate
Fine needle aspiration or biopsy
Hormonal receptor assay (estrogen dependent?)
Ultrasound: fluid or solid?
Chest X-rays for Mets
Scans of bones, brain, liver, etc.

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55
Q

Breast Cancer Stages

A

Stage 1 = T1N0M0
Stage 2 = A. T2N0M0, B. T1N1M0
Stage 3 = A. T3N2M0, B. T1N3M0
Stage 4 = T3N3M1

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56
Q

Breast Cancer Treatment (listed)

A 
Lumpectomy 
Partial mastectomy
Total mastectomy
Modified radial mastectomy
Hormonal Therapy
Herceptin
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57
Q

Lumpectomy

A

For small well defined lesions. Followed by radiation.

58
Q

Partial Mastectomy

A

Remove tumor and region of normal tissue. Followed by chemo or radiation

59
Q

Total Mastectomy

A

Removal of entire breast. Followed by chemo or radiation

60
Q

Modified Radial Mastectomy

A

Removal of entire breast, lymph nodes, lining of chest wall muscles. Chemo and radiation follows.

61
Q

Hormonal Therapy

A

Lowers levels of estrogen (tamoxifen)

62
Q

Herceptin

A

Antibody that selectively binds to the HER-2 oncogene. Inhibits proliferation of tumor cells that overexpress HER-2

63
Q

Hemodynamic disorders arise from:

A

disruptions in normal blood flow

64
Q

Hemostasis

A

Normal hemostatic mechanism to maintain the fluidity of the blood in the vascular system and yet allow the rapid formation of a solid plug to close a vessel defect.

Clotting at an appropriate site

Involves fibrin formation when we have the threat of blood loss

65
Q

Thrombus

A

Solid mass of platelets, cells, and fibrin formed within an intact vessel.

Clotting at an inappropriate site.

66
Q

Thrombus Morphology - Arterial

A

Granular and friable mass
Attached to endothelium
Lines of Zahn - striations (layers)
-formed during flow

“White Thrombus”
(lots of fibrin, few RBCs)

67
Q

Thrombus Morphology - Venous

A

Dark red, long, may form cast
Loosely attached to endothelium
Due to stasis

“Red Thrombus”

Post-mortem clot - blood stops flowing, forms “jelly” like clot

68
Q

Embolus

A

Abnormal mass moving in the blood stream

69
Q

Embolism

A

Sudden occlusion of an embolus

May be solid, liquid, or gas

Most common will be thromboemboli

70
Q

Factors that Predispose Thrombosis

A

Virchow’s Triangle:

  1. Endothelial damage (vessel)
  2. Stasis or turbulence of flow/disturbance in flow
  3. Hypercoagulation (blood)
71
Q

Endothelial Damage

A

Disruption in the endothelium leads to exposure of subendothelial collagen
(blood (platelets) stick to collagen)

More common in arteries than in veins

-Hemodynamic Stress, atherosclerosis, trauma

Endothelial Damage can occur in the veins due to inflammation, iatrogenic (caused by medical intervention), or trauma

72
Q

Hemodynamic Stress (endothelial damage)

A

Wear and tear

Flow of blood stressing and causing endothelium to tear

Hypertension damages endothelium and exposes collagen

73
Q

Athersclerosis (endothelial damage)

A

Vascular disease

Deposition of fatty plaque (under endothelium) thickens wall

Blood doesn’t flow smoothly and can damage endothelium more

74
Q

Trauma (endothelial damage)

A

Physical injury

ex) crushing type injury, smoking, bacteria

75
Q

Disruption in Normal Flow

A

The two most common are turbulence of flow and stasis of flow

Bifurcations: splitting/branching
Plaque (atherosclerosis)
Aneurysms (bulging wall of blood vessel - worried about it rupturing)

76
Q

Atrial Fibrillation

A

Arrhythmia leading to stasis

blood not flowing effectively - can lead to thrombus formation - thrombus can move

77
Q

Stasis

A

Sluggish flow allows for clotting factors to accumulate and increases blood contact with endothelium

78
Q

Mural Thrombus

A

Thrombi can form over an infarcted region on the ventricular wall

79
Q

Saddle Thrombus

A

Straddles the bifurcation of pulmonary trunk

80
Q

Venous Thrombosis/Thrombophlebitis/DVT favored by:

A

Virchow’s Triad - p501

  • post op recovery, bed rest, CHF
  • trauma, IV drug use
  • travel
  • pregnancy

Small can be asymptomatic
Large can cause edema, pain, cyanosis, ischemia

81
Q

DVT Complication

A

Pulmonary Embolism (PE)

Massive PE can cause cardiovascular collapse (CV) and/or pulmonary collapse

A significant cause of mortality

82
Q

Treatment and Prevention of DVT

A

Early ambulation
Pneumatic compression
Anticoagulants/thromboembolytics - like heparin
Vena cava filter (not common)

83
Q

Hypercoagulability States

A 
Birth control pills
Pregnancy
Cancer
Liver disease
Genetic Defect

A general rule: In arteries, thrombi can form in areas of injury or turbulent flow. In veins, thrombi form in areas of stasis.

84
Q

Sequela of Thrombosis

A
  1. Resolution/Dissolution
  2. Infarction
  3. Embolus
  4. Aneurysm
85
Q

Resolution/Dissolution (Sequela of Thrombosis)

A

Rapid shrinkage or complete lysis

-via natural anticoagulants, i.e. plasmin (dissolves fibrin)

86
Q

Infarction

A

Region of necrosis caused by ischemia. A thrombus can either narrow or occlude the lumen of a vessel leading to ischemia/infarction

Examples: MI or CVA, renal artery, mesenteric artery, leg

87
Q

Occlusion of the coronary arteries

A

Myocardial Infarction (MI)

88
Q

Occlusion of the cerebral arteries

A

Cerebral Vascular Accident (CVA) - stroke

89
Q

Infarction Outcome Depends On:

A
  1. Tolerance to Hypoxia
  2. Tissue Vasculature
    - –Anastomoses (connections) allow for an alternate route (ex: Circle of Willis)
  3. Rate of Occlusion
    - –Slow occlusion allows for collateral circulation to develop
  4. Occlusion Duration
    - –length of ischemia (advertisement: D2B time 55 minutes and decreasing)
90
Q

Embolism

A

The sudden occlusion of a traveling mass (embolus)

91
Q

Sites of Origin and Probable Embolism Site

A

Systemic - brian, kidneys, liver, intestines, basically anywhere

Venous - end up in LUNGS

92
Q

Aneurysm

A

Localized dilation of a blood vessel

Most common in the aorta (because of high pressure)

93
Q

Types of Aneurysms (listed)

A

Berry
Fusiform
Dissecting

94
Q

Berry Aneurysm

A

Small spherical dilation usually found in Circle of Willis

lots of turbulence, more of a tendency to clot

95
Q

Fusiform

A

Entire circumference of vessel

dilation of entire vessel; common in aorta, especially abdominal aorta

96
Q

Dissecting

A

(pseudoaneurysm)
Layers of the vessel wall separate and fill with blood

(walls separate and blood flows between; chisel on vessel wall; common in aorta due to high pressure)

Can sometimes lead to ruptured aorta and blood flows into pericardial sac which leads to cardiac tamponade

97
Q

Cardiac Tamponade

A

Blood filled pericardial sac and compresses heart -> cardiac arrest

98
Q

Pathogenesis/Etiology (Aneurysm)

A

Congenital Defect (born with it - not common)
Trauma (crushing injuries, car accident, weakening of vessel walls, etc.)
Infection (bacteria, for example, syphilis used to do this)
Atherosclerosis - most common

99
Q

Signs and Symptoms (aneurysm)

A

Asymptomatic (most often)

100
Q

Sequela and Hemodynamic Effects (aneurysm)

A

Thrombus
Compression
Rupture

101
Q

Treatment of Aneurysms

A

Grafts (takes the pressure off the aneurysm)
Endovascular Coiling (put in coil to fill in aneurysm)
Clipping (cut it off)
Meds to Prevent Enlargement
Watchful Waiting

102
Q

Signs and Symptoms of Blood Disease

A 
Fatigue (RBC)
Pallor (RBC)
Infection (WBC)
Tachycardia (RBC)
Hyperphea/Dysphea - increase respiration rate/trouble breathing (RBC)
Angina (RBC, platelets)
Cyanosis (RBC)
Petechia - tiny red spots (platelets)
Purpura - purple-ish bruises (platelets)
Ecchymoses - large bruises (platelets)
Shortness of Breath (RBC)
Bruising (platelets)
Jaundice (RBC)
103
Q

Erythrocyte Disorders

A

Result when numbers are either excessive or inadequate - a balance must exist between production and destruction

104
Q

Erythropoiesis

A

Production of RBC’s (formed in red bone marrow - myeloid tissue)

Hemocytoblasts differentiate into erythrocytes under the influence of the hormone EPO (erythropoietin) released from the liver or kidneys

Abundance of reticulocytes = red bone marrow working hard

105
Q

Reticulocytes

A

Immature Red Blood Cells

106
Q

RBC Destruction

A

RBC’s live 120 days before becoming fragile and inflexible. They are destroyed in the liver and spleen

107
Q

Fate of RBC Components

A

Heme-

  • Fe+ - keep in body
  • Pigment - get ride of (if backs up = jaundice)

Globin-
-Amino Acids (recycled - kept in body)

108
Q

Polycythemia

A

Elevated number of RBC’s

109
Q

Primary Polycythemia

A

Increase in RBC’s due to hyperactivity of the myeloid tissue

  • Example: Polycythemia Vera - idiopathic, (genetic mutation?)
  • Signs and symptoms include: hyper viscosity, sluggish flow, and thrombosis
110
Q

Secondary Polycythemia

A

Increase in RBC’s due to an increase in demand for oxygen

  • Examples: smokers (decrease oxygen, so EP increases), altitude (kidneys don’t receive enough oxygen so kicks up EPO)
  • Due to artificial or natural increase in EPO (EPO dependent)
111
Q

Anemia

A

Lower than normal oxygen capacity of the blood

Condition, not a disease, of RBC or hemoglobin deficiency

112
Q

Etiology (anemia)

A
  1. <Hb (do not have hemoglobin)
113
Q

Categories of Anemia

A
  1. Deficiencies
  2. Problems with the bone marrow
  3. Hemolytic
114
Q

Anemia - Fe deficiency

A
  1. Hemorrhagic due to chronic blood loss
    - menorrhagia, ulcers, CA
  2. Insufficient dietary intake
  3. Pregnancy

May see hypochromic cells (pale RBC’s) or microcytic cells (smaller than normal RBC’s)

115
Q

Anemia - Vitamin B12 Deficiency

A

Due to inadequate diet (nutritional) or inability to absorb vitamin B12

May see macrocytic/megablastic (really big) or normochromic (normal color)

116
Q

Problems with Bone Marrow

A

Aplastic - due to defect in the red bone marrow resulting in a decrease in stem cell population, due to radiation, chemicals, toxins, chemotherapy, or idiopathic. Or autoimmune.

Results in pancytopenia - all formed elements decreased (biggest concern = opportunistic infections)

Best Treatment = bone marrow transport

117
Q

Pernicious Anemia

A

Lack of gastric intrinsic factor for absorption
“deadly”

(cannot absorb Vitamin B12 from body)

Treatment - Vitamin B12 injections to bypass gastric

118
Q

Hemolytic

A

Rapid destruction of RBC’s due to genetic defect, immune destruction, or mechanical forces
(mechanical forces - generally someone on heart/lung machine or constant pounding on foot = destroyed RBC. Example = army marching and runners)

Two Examples:

  1. Sickle Cell Anemia
  2. Erythroblastosis Fetalis
119
Q

Sickle Cell Anemia

A

Inherited Disorder = defective hemoglobin (Hb)

Incidence

  • 50,000 black Americans affected
  • 1 in 12 are carriers in US
  • 1 in 3 are carriers in Africa
120
Q

Sickle Cell Anemia Description

A

A single amino acid substitution results in deformed hemoglobin causing the RBC to sickle when deoxygenated. The deformed RBC obstructs blood flow in microcirculation causing occlusion and tissue hypoxia.

121
Q

Sickle Cell Anemia Etiology

A

Genetic - Autosomal Recessive Gene Disorder

122
Q

Sickle Cell and Malaria

A

If a person is heterozygous for sickle cell (sickle cell trait) they are protected from malaria and they do not have severe symptoms of sickle cell anemia. Thus this genetic mutation has been favored (a case of balancing selection).

(mutation that was selected)

123
Q

Signs and Symptoms (Sickle Cell Anemia)

A

Sickle Cell Crisis

124
Q

Sickle Cell Crisis Induced by:

A

Exertion (RBC’s live 20 days), Illness, hypoxia, acidosis, dehydration.

People have severe anemia pain (from vessel obstruction) organ damage, and hyperbilirubinemia (too much bilirubin in blood)

(will have infarctions because of cells sticking)

125
Q

Sickle Cell Anemia Treatment

A

No cure unless bone marrow transplant works.

Prevent vasocclusive crisis - hydroxyurea and EPO’s, bone marrow transplant

126
Q

Sickle Cell Anemia Prognosis

A

50% survive until 50

127
Q

Erythroblastosis Fetalis

A

Another type of hemolytic anemia

If mother who is Rh- but sensitized (has anti-Rh antibody) becomes pregnant with Rh+ baby = agglutination
(Never opposite)

128
Q

Erythroblastosis Fetalis Prevention

A

RhoGAM - binds with fetal antigens in mom before antibodies can be produced

(prevents sensitization)

129
Q

Leukocytosis

A

Over 10,000 WBC’s present indicates infection

130
Q

Leukopenia

A

White cell depletion
Usually involves neutrophils
(Normal count is 4-7,200)

Fewer than 1,800 means increased risk of opportunistic infections

131
Q

Leukemia

A

Primary malignant tumors of the leukocyte precursors in the marrow
Do not produce tumor masses

Disseminated CA (released in blood and cells travel throughout the body)

132
Q

General Pathogenesis and Signs and Symptoms of Leukemia

A

Rapid proliferation of non-functional WBC’s

  • spill into blood
  • infiltrate organs

Signs and Symptoms

  • fatigue (anemia; WBC’s take up space)
  • infection (WBC’s not functioning)
  • bleeding (decrease in platelets)
  • pain (infiltrating organs; bone marrow very active and expanding; necrosis of bone
133
Q

Stem Cell Harvest

A
  1. Extract directly from bone
  2. Extract from blood-peripheral blood stem cell harvest
    - Give G-CSF (granulocyte - colony stimulating factor)
    - -causes bone marrow to become active and release in blood
134
Q

Types of Bone Marrow Transplants

A
  1. Allogenic - 1 patient and 1 donor match MHCs/HLAs
    - two people, may have rejection
    - best chance for a cure IF there is a good match
  2. Autologous - patient and donor are same = no rejection
    - cleans out bone marrow and injects healthy cells back into blood
135
Q

Albumins

A

Plasma Protein
Made by liver

Function: maintain osmotic pressure in blood (“sucking” fluid toward blood vessel)

136
Q

Hypoalbuminemia

A

“not enough albumin in blood”

= ascites

137
Q

Ascites

A

Abnormal accumulation of fluid in the abdominal cavity

Seen in: starvation, cirrhosis, kidney

138
Q

Platelets Function

A

Repair slightly damaged blood vessels and initiate the clotting reaction

139
Q

Thrombocytopenia

A

Decreased number of circulating platelets
For symptoms to occur = 10,000-20,000/mL

(Normal Range = 150,000-400,000/mL of blood)

Number must be REALLY low for symptoms

140
Q

Etiology of Thrombocytopenia

A
  1. Decreased production
    - -In malignancy (ex leukemia) normal marrow cells are replaced with malignant cells impairing platelet synthesis
    - -suppression of bone marrow activity (radiation, meds)
    - -aplastic anemia (defective bone marrow)
  2. Increased pooling in the spleen
  3. Decreased survival/lifespan of platelets.
    –can result from an autoimmune response following a viral illness, certain medications, or be idiopathic
    (most are idiopathic)
141
Q

Splenomegaly

A

Enlarged spleen

Up to 80% of platelets may be contained in the spleen
1/3 platelets held in spleen normally

142
Q

Idiopathic Thrombocytopenia Purpura

A

Auto Ab formation against platelets = petechiae and purpura

(most often occurs after viral infection)
(most often in kids <5 years old)

Goes away on its own - no treatment needed - no sequela

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