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Test 2 NUR231 > All but HIV for Test 2 > Flashcards

All but HIV for Test 2 Flashcards

1
Q

. Patients with hematologic disorders are diagnosed how? What signs and symptoms?

A

Patients have few signs and symptoms. But blood tests show significant abnormalities.

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2
Q

What is Plasma

A

is the fluid portion of blood; it contains various proteins, such as albumin, globulin, fibrinogen, and other factors necessary for clotting, electrolytes, waste and nutrients

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3
Q

What are the three types of cells

A

Erythrocyte, Leukocyte and Thrombocyte

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4
Q

What is hemostasis

A

Blood loss, is prevented by an intricate clotting mechanism that is activated when necessary to seal any leak in the blood vessels. Excessive clotting is equally dangerous, because it can obstruct blood flow to vital tissues. To prevent this, the body has a fibrinolytic mechanism that eventually dissolves clots (thrombi). The balance between these two systems, is called hemostasis

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5
Q

Fibrinolysis

A

Clot dissolution

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6
Q

What does the presence of a large amount of hemoglobin on RBC mean?

A

enables the red cell to perform its principal function, the transport of oxygen between the lungs and tissues.

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7
Q

erythropoietin is produced primarily by what organ?

A

Kidney

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8
Q

normal erythrocyte production needs:

A

requires iron, vitamin B12, folic acid, pyridoxine ( vitamin B6), protein and other factors.

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9
Q

Nutrition: Menstruating women may need up to ____ mg Iron daily, because of blood lost.

A

2

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10
Q

Rate of Iron absorption is based upon:

A

is regulated by the amount of iron already stored in the body and by the rate of erythrocyte production.

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11
Q

Iron is stored as:

A

Ferritin

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12
Q

Iron is lost through

A

Bile, feces, mucosal cells in intestine, blood

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13
Q

Iron deficiency in adults is from : (3) and not: (1)

A

From: Blood loss, GI, menstrual flow

NOT diet

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14
Q

Vitamin B12 and Folic Acid is required for:

A

DNA synthesis

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15
Q

Vitamin B12 and Folic Acid comes into the body which way?

A

Through diet!

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16
Q

Nutrition: Vitamin B12 deficiency could be found in two types of people. What are they

A
  1. Vegetarians, because Vit B12 is from animal origin

2. Partial/ Total gastrectomy ( Because Vit B 12 combines with intrinsic factor in the stomach)

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17
Q

Vitamin B12 and Folic acid deficiency is apparent on the blood work because it shows in the CBC : (1)
And results in : (2)

A
  1. production of abnormally large erythrocytes called megaloblasts
  2. megaloblastic anemia
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18
Q

Two categories of leukocytes. What are they?

A

Granulocytes and lymphocytes

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19
Q

Normal range for leukocytes

A

4000-11000 cells/mm3

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20
Q

Aplastic anemia. What is it? ( 1)

Besides anemia what else occurs? (2)

A

(1) is a rare dz caused by a decrease in or damage to marrow stem cells, damage to the micro environment within the marrow, and replacement with fat.
(2) pancytopenia

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21
Q

Priority Assessment for pt with aplastic anemia ?

Why is it important

A

For infection and bleeding. It’s important because death is usually by hemorrhage or infection

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22
Q

Classic method of determining the cause of Vitamin b12 deficiency is:

A

Schilling test.

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23
Q

Chelation therapy is

A

a process that is used to remove excess iron acquired from chronic transfusion. Iron is bound to a substance, the chelation therapy removes only a small amount of iron with each treamtnet, patients with chronic transfusion requirements ( and iron overload) need to continue chelation therapy as long as the iron overload exists, potentially for the rest of their lives

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24
Q

Megablastic Anemia:

A

caused by deficiencies of vitamin B12 or folic acid, identical bone marrow and peripheral blood changes occur because both vitamins are essential for normal DNA synthesis. In either anemia the RBC that are produced are abnormally lg. are called megaloblastic cells. The erythrocytes are abnormally shaped, and the shapes may vary widely ( poikilocytosis). Because the erythrocytes are very large the MCV is high usually exceeding 110 um3.

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25
Q

Why might it be important to differentiate between folic acid deficiency and Vitamin B12 in megablastic anemia?

A

: Symptoms of folic acid and vitamin B12 deficiencies are similar and the two anemias may coexist. However the neurologic manifestation of Vitamin B12 do not occur with folic acid deficiency and they perisist is vitamin B12 is not replaced.

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26
Q

Hemolytic Anemia:

A

erythrocytes have a shortened lifespan, their number in the circulation is reduced. Fewer RBC result in a decreased available O2, causing hypoxia. Erythropoietin stimulates the bone marrow to compensate by producing new erythrocytes and releasing RBC prematurely as reticulocytes

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27
Q

Sickle Cell Anemia: .

A

is severe hemolytic anemia that results from inheritance of the sickle hemoglobin gene

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28
Q

Sickle Cell Anemia: What does this gene do to the RBC. Why is it a problem?

A

The sickle hemoglobin (HbS) acquires a crystal – like formation when exposed to low oxygen tension. The oxygen in venous blood can be low enough to cause this change, causing the Rbc to become deformed, rigid, and sickle shaped. These long, rigid RBC can adhere to the endothelium of small vessels, and they can reduce blood flow to a specific area of the body

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29
Q

Sickle Cell Anemia: If infarction or ischemia results what symptoms does the patient have?

A

Pain , swelling, fever

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30
Q

Sickle Cell Anemia. True or False. If the deformed RBC is exposed to adequate amounts of oxygen it can revert to normal shape.

A

True. The sickling process takes time, and if the RBC is not too ridgid it can go back too normal.

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31
Q

Sickle Cell Anemia: True or False “Sickling crises” are intermittent.

A

True

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32
Q

Why can the cold aggravate the sickling process?

A

Because vasoconstriction slows the blood flow.

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33
Q

What is the most severe form of Sickle cell disease?

A

Sickle Cell Anemia

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34
Q

Sickle Cell trait referes to:

A

The carrier state for Sickle Cell diseases; it is the most benign type of SC disease, in that less that 50% of the hemoglobin within an erythrocyte is HbS. However if two people with sickle cell train have children, the children may inherit two abnormal genes and will have sickle cell anemia.

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35
Q

When is best to take iron ?

A

Empty stomach

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36
Q

Situations can precipitate a sickle cell crisis. What can a pt. do to prevent or diminish them?

A

Keep warm and maintain hydrAtion

37
Q

In hereditary hemochromatosis what symptoms occur earlier in illness trajectory?

A

weakness, lethargy, arthralgia, wt. loss, loss of libido

38
Q

What is hereditary hemochromatosis.

who is affected more men or women?

A

is a genetic condition in which excess iron is absorbed from the GI tract.

Men, because women lose iron through menses

39
Q

Polycythemia

A

increased volume of RBC

40
Q

What is the most common form of leukemia ?

A

Chronic lymphocytic leukemia

41
Q

CLL chronic lymphocytic leukemia is typically derived from ?

A

A malignant clone of B lymphocytes ( t lymphocytes cll is rare). In contrast to acute forms of leukemia - cells are fully mature.

42
Q

(AML) Uric acid and phosphorus levels make the patient vulnerable to

A

renal stone formation and renal colic, which can progress to acute renal failure.

43
Q

Leukocytosis refers to:

A

an increased level of leukocytes in the circulation

44
Q

(AML) : Aim of induction therapy is to:

A

eradicate the leukemic cells, but this is also accompanied by the eradication of normal types of myeloid cells. Thus the pt. becomes severly neutropenic ( an ANC of 0 is not uncommon.), anemic and thrombocytopenic ( less than 10,000/mm3).

45
Q

CML : Pt with high leukocyte count can be SOB, or slightly confused bc of

A

decreased capillary perfusion to the lungs and brain from leukostasis ( the excessive volume of leukocytes inhibits blood flow through the capillaries)

46
Q

Nursing Management during a transfusion reaction. Priority is:

A

STOP the transfusion. Maintain the IV line with normal saline through new IV tubing, administered at a slow rate. Next assess patient carefully.

47
Q
  1. Natural Immunity
    a. is also called?
    b. when does a person acquire it?
    c. barriers/defenses?
    d. chemical response?
    e. cellular response y/n? what ?
A
  1. Natural Immunity
    a. also called “innate” or “non-specific immunity”
    b. this is the immunity someone is born with
    c. includes physical barriers such as skin, cilia and membranes
    d. includes chemical response such as cytokines, acidic gastric secretions (acid kills bacteria)
    e. includes cellular response such as phagocytes (WBC action)
    f. Inflammatory response is a major function of the natural immune system that is elicited in response to tissue injury or invading organisms. Chemical mediators assist this response by minimizing blood loss, walling off the invading organism, activating phagocytes, and promoting formation or fibrous scar tissue and regeneration of injured tissue.
48
Q

Two types of acquired immunity: active and passive

A

i. Active acquired immunity – immunity developed by the body’s own production of antibodies in response to exposure to an antigen, a pathogen or to a vaccine
ii. Passive acquired immunity – immunity acquired by the transfer of antibody from one individual to another, such as from mother to baby

49
Q

Describe Acquired Immunity

A

a. also called “adaptive” or “specific” immunity
b. immunity that is introduced into someone’s body after they are born and something they didn’t have before
c. examples are vaccines and exposure to disease
d. defends against the disease upon re-exposure to the specific antigen

50
Q

autoimmune disease:

A

immune system’s recognition of one’s own tissues as “foreign” rather than self leading to tissue damage

51
Q

Immune Regulation: Hypersensitivity

A

overactive immune system produces inappropriate or exaggerated responses to specific antigens

52
Q

Response to invasion: humoral immune response

A

i. also called “antibody” response
ii. activation of B-lymphocytes that transform themselves into plasma cells that manufacture antibodies specific to invading antigens that are transported in the bloodstream in an attempt to disable invader

53
Q

Response to invasion: phagocytic immune response

A

proliferation of WBC that ingest foreign/invading particles

54
Q

Response to invasion: cellular immune response

A

i. activation of T-lymphocytes which can turn into specialized cytotoxic (killer) T cells that attack the pathogen

55
Q

Acute Lymphocytic Leukemia: ( ALL) results from :

A

uncontrolled proliferation of immature cells ( lymphoblasts) derived from the lymphoid stem cell.

56
Q

Acute Lymphocytic Leukemia: ( ALL) : is more common in male or females? And what is outcome of response to treatment and remission rates?

A

Young boys. Increased age decreased survival.

57
Q

Chronic Myeloid Leukemia: CML:

A

arises from a mutation in the myeloid stem cell. Normal myeloid cells continue to be produced, but there is a pathologic increase in the production of forms of blast cells. Therefore a wide spectrum of cell types exists within the blood, from blast forms to mature neutrophils.

58
Q

Explain in Chronic Myeloid Leukemia what the BCR-ABL gene is

A

in 90-95% of pt with CML a section of DNA is missing from chromosome 22 and it is translocated to chromosome 9. When these two genes fuse BCR-ABL gene , they produce an abnormal protein ( a tyrosine kinase protein) that causes leukocytes to divide rapidly. This gene is present in virtually all pt with dz.

59
Q

What are the three stages of Chronic Myeloid Leukemia ( CML)

A

Three stages Chronic, transformation ( can be insidious or rapid ; it marks the evolution to the acute form (blast crisis), and accelerated/blast crisis ( tx may resemble induction therapy for acute leukemia, using the same meds. Pt. whose disease evolves into a “lymphoid” blast crisis are more likely to be able to reenter a chronic phase after induction therapy.

60
Q

Medical Management : Medication used for CML ( Chronic Myeloid Leukemia)

A

Oral formulation of a tyrosine kinase inhibitor, imatinib mesylate ( Gleevec), works by blocking signals within the leukemia cells that express the BCR-ABL protein. ( most useful in chronic).

If imatinib does not elicit a molecular remission or when remission is not maintained other tx options may be considered. Might be cured with BMT, PBSCT

61
Q

folate is found in what kinds of foodS? ( 1)

folate deficiencies occurs in people who (2)

A

(1) : green vegetables and liver.

(2) : rarely eat raw vegetables.

62
Q

Liver Dz: most blood coagulation factors are synthesized in the liver except

A

VIII

63
Q

Hepatic dysfunction can result in diminished amt, of factors needed to maintain (2):

A

coagulation and hemostasis.

64
Q

Prolongation of the PT may indicate severe hepatic dysfunction.

A

Unless it is caused by Vitamin K deficiency

65
Q

What kind of patient is deficient in Vitamin K?

A

Malnourished patient

66
Q

Prolonged use of some antibiotics decrease intestinal flora. Why can this become a problem?

A

They produce vit k, depleting vit k stores

67
Q

PHYTONADIONE can : ?

A

correct Vit K deficiency

68
Q

Vitamin K is the antidote for: ?

A

Warfarin Toxicity

69
Q

Protamine Sulfate is the antidote for?

A

Heparin Toxicity

70
Q

Bleeding Disorders:

A

failure of normal hemostatic mechanisms can result in bleeding. This bleeding is commonly provoked by trauma, in certain circumstances it can occur spontaneously.

71
Q

Increase platelet production is called:

A

Thrombopoiesis

72
Q

Sometimes the increased platelet does not result from increased production but from a loss is platelet pooling within the spleen. Describe this:

A

The spleen typically holds about 1/3 of the circulating platelets at one time. If the spleen is absent the platelet reservoir is lost, and an abnormally high number of platelets are sent into circulation. In time the rate of thrombopoiesis slows to reestablish a more normal level.

73
Q

Unless bleeding is severe, bleeding can be stopped how?

A

Local pressure applied.

74
Q

Coagulation Factor defects and Bleeding:

A
  • Does not tend to cause superficial bleeding. Why? Because the primary hemostatic mechanisms are still intact.
  • Bleeding occurs deeper in the body.
  • External bleeding diminishes very slowly when local pressure is applied and it often recurs several hours after pressure is removed.
75
Q

Primary Thrombocythemia / Essential Thrombocythemia is:

A

A stem cell disorder. A marked increase in platelet production occurs with the platelet count consistently greater than 600,000/ mm3. Size abnormal, survival normal. Affects women twice as often as men,

76
Q

Primary Thrombocythemia / Essential Thrombocythemia Clinical Manifestations:

A

Clinical Manifestations: asymptomatic, findings occur during routine CBC. The toxic effects of platelet substances include painful burning, warmth, redness in a localized distal area of the extremities. Headaches are a common neurologic manifestation, transient ischemic attacks, and diplopia. DVT, pulmonary embolism. Spleen may be enlarged. Minor or major hemorrhage may occur.

77
Q

Primary Thrombocythemia / Essential Thrombocythemia : How does Hydroxyurea help?

A

It can lower the platelet count

78
Q

Medications that alter platelet functions are:

A

ALCOHOL, ASPIRIN, NSAID

79
Q

Risk Factors for Primary Thrombocythemia/Essential Thrombocythemia are:

A

risk factors such as HX of peripheral vascular disease, HX of tobacco use, atherosclerosis, prior thrombotic events,

80
Q

Secondary Thrombosis is:

A

Secondary thrombosis: Increased platelet production is the primary mechanism of secondary or reactive thrombocytosis. The platelet count is above normal but in contract to primary thrombocythemia an increase of more than 1 million.mm3 is rare. Platelet fct is normal. The platelet survival time is normal or decreased. Symptoms associated with thrombosis or hemorrhage is rare. Many disorders or conditions can cause a reactive increase in platelets including infection, inflammatory disorders, iron deficiency, acute hemorrhage, splenectomy

81
Q

Secondary Thrombosis aim of tx is:

A

Treat underlying disorder

82
Q

Thrombocytopenia is? And why does it occur?

A

Thrombocytopenia: LOW platelet level. Various factors decreased production, increased destruction, increased consumption.

83
Q

What clinical signs can be seen when platelets are below 20,000mm/3

A

petechiae can appear along with nasal and gingival bleeding, excessive menstrual bleeding, and excessive bleeding after dental apt.

84
Q

What clinical signs can be seen when platelet counts are below 5,000 mm/3

A

Spontaneous, potentially fatal CNS or GI hemorrhage can occur.

85
Q

What is “pseudothrombocytopenia”

A

is “pseudothrombocytopenia” Here platelet aggregate and clump in the presence of ethylenediamine tetra-acetic acid ( EDTA).

86
Q

What is the most common cause of platelet destruction?

A

idiopathic thrombocytopenic purpura. ( ITP)

87
Q

Two forms of Idiopathic Thrombocytopenic Purpura ( ITP) are:

A

Acute and Chronic

88
Q

Acute Idiopathic Thrombocytopenic Purpura

A

Predominantly seen in kids, appears 1-6 weeks after a viral illness. Self-limiting. Remission often occurs spontaneously within 6 months.

89
Q

ITP Clinical manifestations:

A

May have 0 symptoms. Physical manifestations could be easy bruising, heavy menses, petechiae on the trunk or extremitities.

Test 2 NUR231 (2 decks)

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