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PATHO Exam 2 > Alterations Of Hematological Function > Flashcards

Alterations Of Hematological Function Flashcards

1
Q

Anemia

A

Abnormal decrease in RBCs and/or hemoglobin concentration reducing the ability of blood to carry adequate amounts of oxygen to tissues

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2
Q

Lab evaluation of anemia - Hemoglobin (Hgb or Hb)

A

Average amt of hemoglobin in a given volume of blood (g/dL)

Clinically, anemia is usually defined by a hemoglobin less than 14 g/dL in males, less than 12 g/dL in females

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3
Q

Lab evaluation of anemia - Hematocrit (HTC)

A

Percentage of a given volume of blood that is comprised of RBCs

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4
Q

Classification of anemia by cause - inadequate erythopoiesis

A

Erythropoiesis - production of RBCs in bone marrow.

Doesn’t produce enough blood in bone marrow

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5
Q

Classification of anemia by cause - loss of RBCs from the circulation (hemorrhage)

A

Blood transfusions can prevent some anemia

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6
Q

Classification of anemia by cause - Shortened RBC life span within the circulation (hemolysis)

A

RBCs are dying sooner than normal

RBCs live 120 days

Cells are lysing prematurely

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7
Q

Classification of anemia by cause - dilutional anemia

A

Not a true anemia.

Extra water or plasma that dilutes the RBCs or hemoglobin

Fluid overload

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8
Q

Classification of anemia by cell morphology - cell size - macrocytic

A

Larger than normal

Misshapen

Vitamin b12 and folic deficiency

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9
Q

Classification of anemia by cell morphology - cell size - normocytic

A

Lost a liter or two of RBCs, but cells remain normal

A cute hemorrhaging

Some RBCs may be lysed

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10
Q

Classification of anemaia by cell morphology - cell size - microcytic

A

Low iron

Low hemoglobin

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11
Q

Laboratory evaluation of rbc size

A

Mean cell volume (MCV) - average volume of the RBCs

Gives number of all RBCs and tells if its below, normal or high numbers

measured in (fL) “quadrillionth”

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12
Q

Hemoglobin content - normochromic

A

Chromic - color

Normal amt of hemoglobin would keep them normally red

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13
Q

Hemoglobin content - hypochromic

A

Pale on the inside of cells

Not as much hemoglobin

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14
Q

Laboratory evaluation of hemoglobin content

A

Mean cell hemoglobin (MCH)

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15
Q

CNS & musculoskeletal manifestations

A

Caused by decreased o2 delivery to CNS and skeletal muscles

  • Fatigue and weakness
  • Irritability and confusion
  • Parasthesias (numbness and tingling)
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16
Q

Skin and mucus membrane manifestations

A

Pallor - pale skin, races w darker skin look inside of mucus membranes

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17
Q

Cardia manifestations

A

Caused by decreased o2 delivery to cardiac muscle

Chest pain

Heart failure

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18
Q

Pulmonary

A

Caused by hypoxia stimulation of respiratory centers in brain stem

Increased rate and depth of respirations

Dyspnea (shortness of breath) - when ruled out all other respiratory problems

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19
Q

Gastrointestinal

A

Caused by decreased o2 delivery to the digestive tract

Abdominal pain; nausea/vomiting

Decreased bowel activity

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20
Q

Iron deficiency anemia (IDA)

A

Epidemiology

Most frequently diagnosed anemia in US/worldwide

Incidence higher in females (4-6%) than males (4%)

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21
Q

Iron physiology - dietary sources

A

Meat, seafood, leafy greens, nuts and seeds, dried fruit, fortified grains/cereals

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22
Q

Iron physiology - absorption

A

In duodenum; iron absorption increased by vit C

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23
Q

Iron physiology - storage

A

Stored as ferritin in liver and bone marrow

up to 6 months of iron storage

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24
Q

Causes of IDA - chronic bleeding

A

Bleeding from gastrointestinal tract - peptic ulcer disease; gastric or colon cancer. *# 1 cause of IDA

Bleeding from urinary tract (hematuria)

Menstruation in women

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25
Q

Causes of IDA - inadequate dietary iron

Populations at risk

A

Vegetarians: unless diet includes iron-rich food or supplements

Pregnant women: increased demands on maternal iron stores

Infants fed cow’s milk: iron is in breast milk and infant formula, NOT cow’s milk

Young children: increased nutrient demand w growth, limited diet

Adolescents: growth spurts, poor diet, beginning of female menstruation

Elderly: decreased meat intake, decreased iron absorption

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26
Q

Causes of IDA - malabsorption of iron

A

Inflammatory bowl diseases (Chrons disease)

Duodenal ulcers

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27
Q

Patho and lab evaluation if IDA

A

Gradual depletion of iron stores in liver and bone marrow - decrease in plasma ferritin levels

Iron deficient erythropoiesis begins and small, Hgb-deficient RBCs enter circulation - decrease in the MVC of RBCs and decrease in hemoglobin and HCT - development of microcytic hypochromic anemia

Negative feedback to bone marrow results in decreased erythropoiesis - manifested eventually a low rbc count

Low plasma iron -> decreased production of RBCs

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28
Q

Vitamin b12 deficiency anemia

A

Vitamin b12 anemia has historically been known as “pernicious anemia”. This means destructive

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29
Q

Vit b12 physiology - dietary sources

A

Meat (especially liver and shellfish) eggs, dairy products

30
Q

Vit b12 physiology - absorption

A

Requires intrinsic factor secreted by the parietal cells in the gastric lining

Vit b12 and intrinsic factor complex is absorbed in the lieum (distal small intestine)

31
Q

Vit b12 physiology - storage

A

Liver is normally able to store up to 3-6 years of vit b12

32
Q

Causes - inadequate intake of vit b12

A

Pop at risk: strict vegans who do not consume meat, egg or dairy

33
Q

Increased demand for vit b12

A

Pregnancy - expansion of blood volume increases the demand for all nutrients necessary in erythropoiesis

34
Q

Malabsorption of b12

A

Autoimmune antibodies to gastric parietal cells or intrinsic factor (autoimmune form of chronic gastritis)

Congenital (genetic) deficiency of intrinsic factor

Gastrectomy

Disorders of distal ileum (chrons disease)

Surgical resection (removal) of the ileum

35
Q

Role of b12 and folate in erythropoiesis

A

Both vits are co-enzymes necessary for DNA synthesis in developing red blood cell

36
Q

Patho and lab evaluation of vit b12

A

Vit b12 deficiency (manifested by low plasma b12 levels) results in a decrease in the rate of cell division of developing RBCs combined w normal growth rate

37
Q

Schilling test for vit b12 absorption

A

Oral ingestion of radioactive b12 and injection of vit b12, followed by a 24-hr urine collection

38
Q

Vit b12 deficiency results in the following

A
  1. Decrease in number of rbcs produced by bone marrow (low Hgb and Hct)
  2. Production of unusually large stem cells that mature into unusually large erythrocytes (elevated mean cell volume (MCV))
39
Q

Patho of vit b12 deficiency - macrocytes

A

Thin, flimsy plasma membranes, rupture prematurely in micro circulation of spleen and liver (further reduces rbc count, Hgb and Hct, and presents w hemolysis)

40
Q

Severe vit b12 deficiency

A

Results in myelin degeneration

Loss of neurons in the spinal cord

Peripheral nerve degeneration

41
Q

Folate deficiency anemia physiology

A

Dietary sources: leafy greens, broccoli, lemons, bananas, melons, nuts, oranges, navy beans, yeast, grains, liver

Folate stores: 2-4 months in liver

42
Q

Causes of folate deficiency - inadequate dietary folate or low body stores of folate *affected pops

A

Alcoholics: alcohol interferes w folate metabolism, depletes folate stores

Chronically malnourished

Elderly

43
Q

Causes of folate deficiency - increased demand for folate

A

Pregnant women - can lead to neural tube defects

Children undergoing growth spurts

44
Q

Causes for folate deficiency - malabsorption

A

Chronic malabsorption disorders (chrons disease)

45
Q

Patho and lab evaluation of folate deficiency

A

Folate deficiency (low plasma folate levels) results in a decrease in the rate of cell division of developing rbcs combined with normal rate of growth

Same patho and consequences as vit b12 except for neurological effects

46
Q

Hemolytic anemia

A

Premature accelerated destruction of otherwise normal erythrocytes

47
Q

Causes of hemolytic anemia

A

Genetic defects leading to malformation of the hemoglobin or defects in rbc metabolism

Autoimmunity - immune-mediated hemolysis (idiopathic origin)

Infection (malaria, Epstein Barr virus, clostridium, mycoplasma)

Toxic/chemical injury (arsenic, lead, etc)

Many other causes including wide array of meds

48
Q

Patho of immune mediated hemolysis

A

Binding of antibodies and complement proteins to the rbc membrane (opsonization

Opsonized rbcs are phagocytosis by macrophages as they migrate through the narrow capillaries in the spleen

Following hemolysis, excessive amts of hgb are released from rbcs and broken down by the macrophage - unconjugated bilirubin is released into the plasma

49
Q

Lab evaluation and clinical manifestations of hemolytic anemia

A

Low hgb and hct

Elevated unconjugated bilirubin and jaundice

Elevated lactate dehydrogenase (LDH) - enzyme; in every cell; when a cell lysis it produces ldh;

Elevated reticulocyte count as bone marrow tries to compensate for the loss of rbcs

50
Q

Sickle cell disease (sickle cell anemia)

A

Occurs in persons originating in equatorial regions (west and central africa, Middle East, Mediterranean, parts of India)

In US disease is most coming in African Americans (1/400 to 1/500 live births)

51
Q

Cause of sickle cell anemia

A

Inherited autosomal recessive disorder - single gene (single base-pair) defects (aa)

Sickle cell trait: carrier, rarely has clinical manifestations, provides immunity against malaria

52
Q

Pathophysiology of sickle cell anemia

A

Presence of abnormal Hgb S (instead of normal HgbA)

HgbS reacts to hypoxemia and dehydration (also low pH and body temp)

Rbc takes on a rigid, sickle shape; normal flexibility of the rbc is lost

Suckling is reversible at first, but after repeated episodes the cells are irreversibly sickled

Suckling occurs in punctuated “sickle cell crises”

53
Q

Consequences of rbc suckling

A

Sickled rbcs lyse, leading to hemolytic anemia

Sickled cells aggregate in the capillaries and obstruct blood flow (vasoocclusion crisis)

Pooling of sickled rbcs in spleen and liver (sequestration crisis)

54
Q

Aplastic anemia

A

Bone marrow failure associated w reduction of rbcs, WBC, and platelets

55
Q

Causes of aplastic anemia - genetic disorder

A

20% of cases

56
Q

Causes of aplastic anemia - acquired disorders; seen in adulthood

A

80% of cases

Autoimmune disease that targets bone marrow stem cells (50% of acquired cases)

Environmental exposure

  • industrial and agricultural chems ( insecticides, fungicides, cci4, benzene)
  • ionizing radiation (total body)
  • infections (viral hepatitis, hiv, tb, cmv)
57
Q

Pathophysiology of aplastic anemia

A

Reduction in number or absence of bone marrow stem cells or stem cell abnormalities

Inadequate production in rbcs, WBC, platelets

58
Q

Clinical consequences and laboratory evaluation of aplastic anemia

A

Severe pancytopenia

Anemia (low Hgb/Hct)

Leukopenia (low white blood cell count)

Thrombocytopenia (low platelet count)

59
Q

Hemostasis

A

Formation of a stable clot is dependent on platelet function and formation of fibrin

60
Q

Platelets

A

Small cell fragments that arise from specialized stem cells (megakaryocytes) in the bone marrow

Platelets have a 10 day life span

When activated by endothelial injury, platelets aggregate to form a platelet plug

61
Q

Overview of clotting system

A

Activated by injury to endothelial cells

Intrinsic/extrinsic pathway -> factor X -> factor Xa -> prothrombin -> thrombin -> fibrinogen -> fibrin

End product fibrin forms a mesh work of fibers to stabilize to blood clot

62
Q

Hemophilia A (bleeding disorder)

A

Deficiency of clotting factor VIII

63
Q

Hemophilia B

A

Deficiency of clotting factor IX

64
Q

Hemophilia C

A

Deficiency of clotting factor XI

65
Q

Cause of hemophilia A

A

X-linked recessive disorder (X’Y)

Primarily affects males (1/5000)

Females are carriers

66
Q

Patho of hemophilia A

A

Factor VIII deficiency prevents completion of intrinsic pathway of clotting cascade

Increased risk of bleeding

  • mild (6-50% clotting capability); bleeding with severe trauma or surgery
  • moderate (1-5% clotting capability); bleeding w trauma
  • severe (<1% clotting capability); at risk for spontaneous bleeding
67
Q

Clinical consequences of hemophilia A

A

Prolonged bleeding times

Ecchymoses/hematoma formation

Hemarthroses - bleeding in synovial joints

Chronic anemia requiring transfusions

68
Q

Immune thrombotic thrombocytopenia (ITP)

Bleeding disorder

A

Immune mediated platelet consumption

69
Q

Pathophysiology of ITP

A

Antibodies (IgG) produced in response to viral infection leads to cross-sensitization of antibodies to circulating platelets with IgG binding to platelets

Virus -> plasma cells produce antibodies against virus -> antibodies cross-react with and bind to platelets

Enhanced phagocytosis of platelets by WBC in spleen

Results in severe thrombocytopenia

70
Q

Polycythemia Vera (clotting disorder)

A

Caused by overproduction of erythrocytes (rbcs) by the bone marrow, unknown cause

Leads to increased blood coaguability and blood clotting (thrombotic) events such as deep vein thrombosis, stroke, heart attack

71
Q

Disseminated intravascular coagulation (clotting disorder)

A

DIC is a pathological process triggered y the systemic activation of the clotting cascade with the resulting consumption of clotting factors and platelets which leads to generalized bleeding

72
Q

Patho of DIC

A

Cycle of clotting, fibrinolysis, bleeding

Endothelial injury activated platelets and the clotting system

Small clots begin to appear in microcirulation and interfere with blood flow causing tissue and organ ischemia

Inappropriate and excessive clotting depletes available clotting factors and platelets, leads to bleeding

PATHO Exam 2 (9 decks)

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