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PATHOPHYSIOLOGY > U3 > Flashcards

U3 Flashcards

1
Q

RBC’S

A

RBCs: is a count of the actual number of red blood cells in a specified sample size of blood. Normal Value: 3.6 – 5.4

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2
Q

HCT

A

Hematocrit (Hct): % of erythrocytes in whole blood. Normal Value: 37 – 50 %
~ Total volume of erythrocytes compared to total volume of blood in tube = hematocrit
~ A low Hct means patient is losing blood (either internally or externally)
~Can be Affected by the person’s fluid status (⬆ Hct caused
by dehydration; ⬇ Hct caused by fluid overload).
~Critical Low - 60% → blood clotting problems

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3
Q

HgB

A

Hemoglobin (Hgb): Binds O2 for transport. Normal Value: 12 – 16.5
~ Takes up to 1/3 the surface space of an erythrocyte
~ Measured in grams

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4
Q

RETICULOCYTE COUNT

A

Reticulocyte Count: Immature RBCs – If elevated this
indicates that mature RBCs are depleted for some reason.

is a measurement of the absolute count or percentage of immature red blood cells in blood (if this number is high, it means that the adult or mature RBCs are depleted and the body is now relying on immature RBC

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5
Q

ANEMIAS

3 MAIN GROUPS

A

Anemias . (NOT ENOUGH RBC’s)
There are more than 400 types of anemia, which are divided into three groups: Anemia caused by blood loss. Anemia caused by decreased or faulty red blood cell production. Anemia caused by destruction of red blood cells.

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6
Q

RBC fx

A

transport oxygen throughout the body (which is why one of the symptoms of anemia is shortness of breath)

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7
Q

RBC COUNT

A

s a count of the actual number of red blood cells in a person’s sample of blood.

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8
Q

HEMOGLOBIN TEST

A

measures the amount of the oxygen-carrying protein in the blood.

12-16.5

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9
Q

HEMATOCRIT TEST

A

Hematocrit measures the percentage of a person’s blood that consists of red blood cells.

should be 37-50%

  • 15% is critical
  • 60% is critical
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10
Q

RBC INDICES

A

Red blood cell indices are calculations that provide information on the physical characteristics of the RBCs.

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11
Q

WBC COUNT

A

White blood cell (WBC) count is a count of the total number of white blood cells in a person’s sample of blood.

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12
Q

WBC DIFFERENTIAL

A

White blood cell differential may or may not be included as part of the panel of tests. It identifies and counts the number of the various types of white blood cells present. The five types include neutrophils, lymphocytes, monocytes, eosinophils, and basophils. The percentages of each type of WBC can give a clue about what the body is fighting. (see White Blood Cells below)

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13
Q

PLATELET COUNT

A

The platelet count is the number of platelets in a person’s sample of blood.

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14
Q

S/S OF RBC DYSFUNCTION ARE RELATED TO HYPOXIA

A

S/S of RBC dysfunction are related to hypoxia

  1. Fatigue
  2. Tachypnea
  3. Tachycardia
  4. Pallor (can look in the mouth)
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15
Q

CAUSES OF ANEMIA

ANEMIA DUE TO BLOOD LOSS

A

Gastrointestinal (GI) Conditions - upper or lower GI bleeds

NSAID over use (so patients with chronic pain are at risk for anemia)

Excessive menstruation

childbirth complications

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16
Q

CAUSES OF ANEMIA

ANEMIA DUE TO DECREASED TO FAULTY RBC PRODUCTION

A

Anemia due to Decreased or Faulty RBC Production
Nutritional Deficiencies: (Folate, Vitamin B-12, and Iron are necessary components of RBC production)
Sickle Cell Anemia (NOTE: this anemia also falls into Category #3 below): Discussed more on pg.
Bone marrow & Stem cell problems: Leukemia and lymphoma are examples.

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17
Q

CAUSES OF ANEMIA

ANEMIA DUE TO EXCESSIVE RBC DESTRUCTION

A

Anemia due to Excessive RBC destruction - “Hemolytic Anemia” – RBCs die quicker than the bone marrow can
replace them. Causes can be “Intrinsic” (inherited defective RBCs) or “Extrinsic” (everything else).

Inherited – sickle cell & thalassemia
Stressors – RBCs destroyed by infections, drugs, snake or spider venom, etc.
Toxins – advanced liver or kidney disease
Autoimmune – Lupus can affect Bone Marrow
Spleen – in enlarged spleen blood moves more slowly thru, causing RBCs to become prematurely destroyed before they get through the splee

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18
Q

CAUSES OF ANEMIA

OTHER CONDITIONS ASSOCIATED WITH DECREASED OR FAULTY RBC

A

Other conditions associated with decreased or faulty RBCs
Advanced kidney disease - See KIDNEY CONNECTION below*
Hypothyroidism - causes lowered iron levels in the blood
Chronic diseases – INFLAMMATION causes production of cytokines that then destroy all blood cells including erythrocytes. EXAMPLES: cancer, infection, autoimmune disorders (i.e., lupus or rheumatoid arthritis).

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19
Q

CAUSES OF ANEMIA

A

Anemia due to blood loss

Anemia due to decreased or faulty RBC production

Anemia due to excessive RBC destruction

Other conditions associated with decreased or faulty RBC

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20
Q

Etrythropoietin

A

KIDNEY CONNECTION: Erythropoietin (made in kidneys) signals bone marrow to make more
RBCs, so if kidneys are damaged, erythropoietin is not excreted and RBCs are not mad

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21
Q

TYPES OF VITAMIN DEFICIENCY ANEMIA

A

FOLATE B-9
B-12
Fe

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22
Q

SICKLE CELL ANEMIA

A

Sickle cell anemia: An autosomal recessive defect of hemoglobin. Individuals with the single defective gene have sickle cell “trait” while those with 2 defective genes have sickle cell disease. Predominant in those of African decent. Diagnosed at birth with Newborn screens or through amniocentesis. There are several drug therapies and bone marrow transplants available (with complications of rejection i.e. septicemia or Host vs Graft disease)

1 IN 2000 IN CAUCASIONS

1 IN 350 BIRTHS

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23
Q

3 TYPES OF SICKLE CELL CRISIS CAN OCCUR

A

Vaso-occlusive – occurs when the sickled red blood cells trigger the formation of blood clots with in the circulation. Tissue damage is minor and can resolve within a week. Dehydration and infection is an initiating cause. More serious results can include- Stroke, Pulmonary infarction, Myocardial infarction, Gangrene.

Sequestration – When the sickled red blood cells are removed from the general circulation by the spleen. The severity depends on the amount of blood removed and held in the spleen and liver thereby reducing the amount of circulating red blood cells. Can produce hypovolemic shock.

Aplastic – Caused by exhaustion of the bone marrow. Erythropoiesis cannot keep up with the constant need to replace red blood cells. Sickled red blood cells have a lifespan of 10-20 days. This constant stress on bone marrow stems cells can eventually lead to bone marrow failure.

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24
Q

5 EXCEPTIONS TO ASSESSING IF PAIN AN IMMEDIATE THREAT

A

SICKLE CELL CRISIS

CHEST PAIN-

MYOCARDIAL INFARCTION
BURNS

LIMB SPARING COMPARTMENTAL SYNDROME

RENAL PAIN

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25
Q

Polycythemia

Primary (Absolute)

A

Primary (Absolute) – autosomal inheritance. Caucasian with European Jewish ancestry are more at risk .

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26
Q

Polycythemia

Secondary

A

Secondary (Relative) - physiologic response to chronic hypoxia that triggers the body to make more RBCs for oxygen transport in an effort to get more oxygen to the cells of the body.

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27
Q

Polycythemia
Secondary
causes

A

Sleep Apnea – Due to either Obstructive Sleep Apnea (airway “collapses” during sleep → blockage of air and snoring) or Central Sleep Apnea (the brain does not signal the lungs to breathe). Both types result in oxygen deprivation.
COPD – (Chronic Obstructive Pulmonary Diseases such as asthma and emphysema that hamper gas exchange in the lungs.
Heart failure – reduces tissue profusion, which create hypoxic tissue even if the blood volume and concentrations are normal. The low oxygenation will trigger an increase in production of RBCs.
Pulmonary disease – gas exchange between lungs and vasculature may be impaired. The decrease in O2 exchange will produce hypoxia and trigger an increase in production of RBCs.
High Altitude – body compensates for lower O2 levels at higher altitudes by making more RBCs to carry oxygen. Takes 6-8 weeks to build up enough erythrocytes.

28
Q

Polycythemia

s/s

A

Signs & symptoms: caused by reduced blood flow - Plethora: ruddy complexion; Fatigue; Dizziness; Headache

29
Q

Polycythemia

Treatment

A

Treatment: regular blood removal of erythrocytes to decrease the concentration. Radioactive phosphate also used.

30
Q

Pernicious Anemia

A

(*) Pernicious Anemia: Caused when Vitamin B12 is not absorbed by the body. B12 is a necessary component of RBC production. B12 does not survive in the stomach unless it is bound to Intrinsic Factor (IF). IF is a protein excreted by the stomach. In cases where portions of the stomach are removed (i.e., gastric by-pass surgery or removal of stomach cancer) then the stomach does not make the IF and B12 cannot be absorbed by the body which then leads to anemia.

B-12 DEFICIENT
ABSENT GASTRIC INTRINSIC FACTOR
ANGLO SAXONA AND SCANDINAVIAN

31
Q

MACROCYTIC-NORMOCHROMIC ANEMIAS

A

PERNICIOUS ANEMIA

FOLATE ANEMIA

32
Q

Pernicious Anemia

S/S

A
  1. Vitamin B-12 deficiency
  2. Absent gastric Intrinsic
    Factor(*)

HIGH RISK GROUP:
Anglo-Saxon
Scandinavian

S/S:
abdominal pain
sore tongue
anorexia, weight loss
peripheral neuropathy 
tingling / numbness
33
Q

FOLATE ANEMIA

A

dietary deficiency

HIGH RISK GROUP:
Alcoholics
Malnutrition
Pregnancy

Symptoms:
abdominal pain
sore tongue
anorexia, weight loss

34
Q

Microcytic-Hypochromic Anemias

A

IRON DEFICIENCY

AND

SIDEROBLASTIC
THALASSEMIA

35
Q

Normocytic-Normochromic Anemias

A

APLASTIC ANEMIA
POST-HEMORRHAGE
HEMOLYTIC

36
Q

LEUKEMIA

A

Leukemia = Malignant development of leukocytes. Over proliferation of nonfunctioning white blood cells in the bone marrow that grows faster than the functioning cells. Eventually the leukemia cells crowd out all the functioning blood cells in the bone marrow which leads to the various s/s of leukemia (anemia, infections and bleeding problems).

37
Q

LEUKEMIA IS CLASSIFIED

A

Leukemia is classified - by its speed of progression and the type of cells involved. There are 4 main types of leukemia, based on whether they are acute or chronic, and myeloid or lymphocytic: Acute myeloid (or myelogenous) leukemia (AML) Chronic myeloid (or myelogenous) leukemia (CML) Acute lymphocytic (or lymphoblastic) leukemia (ALL), and Chronic lymphocytic leukemia (CLL).

38
Q

ACUTE LEUKEMIA

A

Acute leukemia. In acute leukemia, the abnormal blood cells are immature blood cells (blasts). They can’t carry out their normal functions, and they multiply rapidly, so the disease worsens quickly. Acute leukemia requires aggressive, timely treatment.

39
Q

CHRONIC LEUKEMIA

A

Chronic leukemia. There are many types of chronic leukemias. Some produce too many cells and some cause too few cells to be produced. Chronic leukemia involves more mature blood cells. These blood cells replicate or accumulate more slowly and can function normally for a period of time. Some forms of chronic leukemia initially produce no early symptoms and can go unnoticed or undiagnosed for years.

40
Q

LYMPHOCYTIC LEUKEMIA

A

Lymphocytic leukemia. This type of leukemia affects the lymphoid cells (lymphocytes), which form lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system.

41
Q

MYELOGENOUS LEUKEMIA

A

Myelogenous leukemia. This type of leukemia affects the myeloid cells. Myeloid cells give rise to red blood cells, white blood cells and platelet-producing cells.

42
Q

LEUKEMIA S/S

A

Lymphadenopathy - Swelling lymph nodes. May swell without any other s/s or swell in random patterns.
Anemia, Infection, Bleeding problems (due to bone marrow damage that affects all blood cells)
Pallor – malignant leukocytes crowding the bone marrow and leading to decreased erythrocyte and thrombocyte production (causing a pale skin color).

43
Q

MULTIPLE MYELOMA

A

Multiple Myeloma –cancer that starts in a type of B-Cell Lymphocyte called plasma cells in the bone marrow. These are protein-making cells which normally make all of the different kinds of proteins that comprise the antibodies [immunoglobulins] of the immune system. In multiple myeloma, the bone marrow cells stop making different forms of protein in response to the immune system’s needs and instead starts to produce a single abnormal type of protein referred to as a “monoclonal” or M protein. Multiple myeloma plasma cell populations accumulate and these collections of cells called plasmacytomas can erode the hard outer shell or cortex of the bone that normally surrounds the marrow.

44
Q

Pathological [spontaneous] fracture

A

weakened bones show thinning of the bone such as is seen in nonmalignant osteoporosis or what appear to be punched out or lytic bone lesions. These lesions may cause pain and even breaks or pathological [spontaneous] fractures of the bones affected by the cancer. [NOTE: Myeloma is NOT leukemia]. MM could result in the following:

Skeletal tumors  -  OR  -
Soft tissue tumors
Malignant plasma cells form solid tumors in the soft tissue.
More common in men than women.
Develops after 40 years of age
45
Q

MULTIPLE MYELOMA

S/S

A

Bone pain and pathological fractures [occur spontaneously w/o an injury].

Hypercalcemia (⬆ serum calcium levels) from calcium moving from the bone into the blood.

Tumor markers - “M-proteins” (found in serum) and “Bence-Jones protein” (found in urine)

Myeloma nephrosis caused by damage to kidneys by paraproteins (that cause hyperviscosity of body fluids) – a distinctive feature of Myeloma.

Usual s/s of bone marrow damage (blood dyscrasias)

46
Q

LYMPHOMAS

A

Lymphomas - blood cancer that affects the lymphatic system causing an overproduction of malfunctioning lymphocytes. This overload compromises the immune system. Lymphoma can develop in many parts of the body, including lymph nodes, bone marrow, blood, spleen and other organs. See Pg. 253.

47
Q

HODGKINS LYMPHOMA

A

B-Cell lymphocytes, Reed-Sternberg Cells present
20-30 yo (more common in younger population) and 60-70 yo
Cervical, inguinal, axillary and
Retroperitoneal
Uncommon

Painless swollen lymph nodes
Fever and night sweats
Generalized weakness
Weight loss
Bone Marrow damage (blood dyscrasias)
Approximately 90%
Radiation therapy - localized
Chemotherapy – generalized
Immunotherapy (MAB drugs)
Bone marrow [stem cell] transplant
48
Q

Non-Hodgkin’s Lymphoma

A 
B  and T - lymphocytes
> 50 years old (95% are adults)
cervical, axillary inguinal and femoral
        Common
same as Hodgkin’s disease PLUS:
Pleural effusion
Abdominal pain
Splenomegaly

Less than 25%
same as Hodgkin’s disease

49
Q

S/S OF BLEEDING

A

Hemorrhage – Blood leaving the blood vessel (internal or external bleeding)
Menorrhagia –Heavier than normal menstrual bleeding
Epistaxis – Bleeding from the nose
5. Purpura - red or purple discolorations on the skin that do not blanch on applying pressure
4. Petechiae – pinpoint hemorrhages of small capillaries in the skin, conjunctiva of the eyes, or mucous membranes.
6. Ecchymosis – Blood leaks into tissues under the skin causing bruising
7. Hematoma - Collection of blood, usually clotted, in organs, body spaces or under the skin.

50
Q

CAUSES OF THROMBOCYTOPENIA

A

Altered Coagulation - Thrombocytopenia (platelet count

51
Q

S/S OF THROMBOCYTOPENIA

AND

TREATMENT

A

Signs & symptoms of Thrombocytopenia:

Epistaxis 
Menorrhagia
Bleeding gums
Purpura
Petechiae
GI Bleeds

Treatment: Immunosuppression Treatments (Treatment for TTP)
Plasmapheresis* (Treatment for TTP)
Eliminate the causative drug
Platelet infusion

52
Q

Disseminated Intravascular Coagulopathy (DIC)

A

DIC is a coagulation disorder that results in both massive blood clotting (thrombi) and hemorrhage. DIC is not itself a specific illness; rather, it is a complication or an effect of the progression of other illnesses. It is always secondary to an underlying disorder and is associated with a number of clinical conditions, generally involving activation of systemic inflammation.

Definition - DIC is a serious disruption in the body’s clotting mechanism. Normally, the body forms a blood clot in reaction to an injury. With DIC, the body overproduces many small blood clots throughout the body, depleting the body of clotting factors and platelets. These small clots are dangerous and can interfere with the blood supply to organs, causing dysfunction and failure. Then, massive bleeding can occur due to the body’s lack of clotting factor and platelets. DIC is life-threatening and needs to be treated promptly.  * Cytokine is implicated as a causative agent in DIC.
53
Q

(MICROCYTIC-HYPOCHROMIC)

IRON DEFICIENCY

A

chronic blood loss
dietary deficiency

HIGH RISK GROUPS:
menstruating &
child birth
malnutrition

S/S:
stomatitis, difficulty swallowing, headache, confusion, memory loss, “lightheaded”, dizzy

54
Q

NORMOCYTIC-NORMOCHROMIC ANEMIA:

APLASTIC ANEMIA

A

destruction of bone marrow stem cells

RISK GROUP:
Anyone (Environmental toxins, chemo or radiation, toxic drugs)

S/S:
Infection
bleeding

55
Q

NORMOCYTIC-NORMOCHROMIC

POST-HEMORRAGE

A

POST-HEMORRHAGE
Sudden blood loss

HIGH RISK GROUPS:
surgery
trauma

S/S:
shock
metabolic acidosis

56
Q

Normocytic-Normochromic

HEMOLYTIC

A

HEMOLYTIC (*)

premature destruction of mature erythrocytes (erythrocyte fails to remain intact for standard 90-120 days)

RISK GROUP: ANYONE

S/S: SPLENOMEGALY & JAUNDICE

57
Q

Normocytic-Normochromic

CHRONIC INFLAMMATION

A

Chronic inflammation
bacterial toxins, cytokines from activated macrophages and lymphocytes
immunodeficient diseases

HIGH RISK GROUPS:
autoimmune diseases
neoplasms

58
Q

Normocytic-Normochromic

SICKLE CELL ANEMIA

A

SICKLE CELL ANEMIA (**)
genetic (malformation of hemoglobin in RBCs)

HIGH RISK GROUP:
African heritage

S/S:
hepatomegaly
splenomegaly
localized thrombosis
Sickle Cell Crisis

*MORE INFO: (**) Sickle cell anemia: An autosomal recessive defect of hemoglobin. Individuals with the single defective gene have sickle cell “trait” while those with 2 defective genes have sickle cell disease. Predominant in those of African decent. Diagnosed at birth with Newborn screens or through amniocentesis. There are several drug therapies and bone marrow transplants available (with complications of rejection i.e. septicemia or Host vs Graft disease)

59
Q

HEMOLYTIC DISEASE OF NEWBORNS (ERYTHROBLASTOSIS FATALIS)

A

Rh- Factor - mom carrying Rh+ fetus. 1st baby is ok but mother’s immune system will form immune response the Rh+. The mother’s antibodies will attack the 2nd fetus’s red blood cells. Can lead to miscarriage or infant being born with severe anemia. Treatment: Woman is given a RhoGam shot after first baby is born.

60
Q

IDIOPATHIC THROMBOCYTOPENIA PURPURA (ITP)

A

Idiopathic Thrombocytopenia Purpura ITP : Autoimmune disorder that causes an IgG antibody to bind with platelets, destroying their function. Results in low platelet count and s/s of bleeding. [Definition of IDIOPATHIC: arising spontaneously or from an obscure or unknown cause].

61
Q

DRUG INDUCED THROMBOCYTOPENIA

A

Drug Induced: A hypersensitivity reaction causes platelet destruction. Heparin can induce a Type III Hypersensitivity reaction that can quickly be resolved after eliminating drug.

62
Q

THROMBOSIS

A

THROMBOSIS: Formation of blood clots. Clotting can occur in the arteries or veins. (More common in veins due to lower blood pressure and slower flow of blood in veins as compared to arteries).

63
Q

3 RISKS OF BLOOD CLOT FORMATION

A

Abnormal blood flow – increased turbulence as caused by high blood pressure. More common in arterial system. Damage to vessel walls or blood cells trigger intrinsic clotting cascade.

Injured vessel walls – Interior of blood vessels can be damaged by the development of atherosclerotic plaque (can lead to the development of strokes or heart attack.); Deep Vein Thrombi in legs break off to create Pulmonary Emboli.

Altered blood constituents – Increased viscosity of blood [Dehydration can increase risk of clot formation]. Thrombocytosis → increased/abnormal production of platelets (may be a marker for cancer since 40% of people with unexplained high platelet count have cancer).

64
Q

TREATMENT FOR THROMBOSIS

A

nti-coagulant drugs- Thin the blood to prevent future clots but no effect on existing clots. (examples: Heparin, Coumadin, Aspirin).

Thrombolytic drugs- Breaks up or dissolves existing blood clots, which are the main cause of both heart attacks and stroke but do not prevent future clots.

65
Q

DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)

A

DIC is a serious disruption in the body’s clotting mechanism. Normally, the body forms a blood clot in reaction to an injury. With DIC, the body overproduces many small blood clots throughout the body, depleting the body of clotting factors and platelets. These small clots are dangerous and can interfere with the blood supply to organs, causing dysfunction and failure. Then, massive bleeding can occur due to the body’s lack of clotting factor and platelets. DIC is life-threatening and needs to be treated promptly.

**Cytokine is implicated as a causative agent in DIC.

66
Q

DIC S/S

A

DIC - Signs & symptoms are related to either the blood clotting or the hemorrhage phase [Note: Bleeding from at least 3 unrelated sites is particularly suggestive of DIC.]

PATHOPHYSIOLOGY (10 decks)

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