• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/35

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

35 Cards in this Set

  • Front
  • Back
Identify the relative abundance of major plasma components and blood cell types in healthy adults.
-Plasma

1. Water (92%), Proteins (7%),


2. Proteins-Albumin (58%), Globulins (37%), Fibrinogen (4%)


3. 1%-electrolytes, nutrients, respiratory gases, waste products

Formed Elements (42%)

1. RBCs (erythrocytes), Platelets, WBCs (leukocytes-monocyte, lymphocyte), thrombocytes (platelets)


2. Eosinophil, Basophil, Neutrophil (Granulocytes-polymorphnuclear leukocytes)


3. Agranulocytes (mononuclear leukocytes)-natural killer cell, matrure b cell, helper t cell, suppressor t cell, monocytes>macrophages

Serum

plasma without fibrinogen and other clotting factors

Plasma Ion Concentrations (Cation/Anion)

1. Cat-ECF- (NA), ICF (K)


2. An-ECF (CL), ICF (HPO4/Proteins)

Major determinants of plasma osmolality


-directly proportional to the osmotic pressure

NA, CL, HCO, blood urea nitrogen (BUN), and glucose

The molality of plasma is slightly higher than interstitial fluid because the plasma contains proteins (primarily albumin) cannot cross the capillary membrane.

This leads to the force driving water into the vasculature (osmotic pressure).

Colloid Osmotic pressure/Oncotic Pressure

Oncotic pressure produced by plasma proteins. When hydrostatic pressure is above oncotic pressure, filtration goes out arterial end. When oncotic pressure exceeds hydrostatic pressure it's reabsorbed on venous end.

Albumin

1. Responsible for 70-80% colloid osmotic pressure


2. Makes up 58% of plasma protein


3. Important transporter (free fatty acids, calcium, cooper, steroid hormones, bilirubin



Loss of Albumin

1. Decrease in oncotic pressure


2. leads to less reabsorption (edema)

Gamma globulins

Immunoglobulins (antibodies)

Transferrin

Free iron is toxic, binds, transports to bone marrow> erythrocytes

Haptoglobin

1. Binds free hemoglobin that can enter the plasma after the lysis of erythrocytes (hemolysis)


2. Taken up by endocytosis in liver macrophages and broken down and recycled

Major site of hematopoiesis

Bone Marrow

Hematopoiesis

Formation of all blood cell types, replaced by stem cells (rise to all leukocytes, erythrocytes, and platelets)

1. Thrombocytic


2. Erythroid


3. Granulocytic


4. Moncytic


5. Lymphoid Lineage

1. Platelets


2. Erythrocytes


3. Eosinophils, Basophils, Neutrophils


4. Monocytes>Macrophages


5. NK cell, T cell, B cell >plasma cells


-dendritic (mono/lympho)

Erythrocytes

1. Increase surface to volume ration- enhances gas exchange


2. Easily and reversibly deformable-biconcave


3. very tiny to pass through organs

Hemoglobin A

1. In adults! 95% intracellular protein, functions to carrry O2 to tissues and CO2 to the lungs


2. Acid-Base buffer-histidine residues in globin accept H as blood becomes acidic

Erythropoiesis


a) anemia


b) polycythemia

formation of RBCS


highly regulated


a) too few erythrocytes


b) too many erythrocytes

Bone Marrow

1. Hematopoietic


2. Erythroid progenitors (erythropoietin-EPO)


3. Erythroblasts (hemoglobin accumulation, nuclear condensation, decreased cell size, loss of nucleus)

Blood Stream

1. Immature erythrocytes (reticulocytes)


-24-48 hrs, have mitochondria/ribsomes, but lose them to become mature


-incr % of reticulocytes>incr erythopoiesis


-normal up to 2.5%


2. Mature erythrocytes

Erthropoietin is produced by the

kidneys-senses decrease in O2 levels

Factors that decrease O2 delivery in kidney


(negative feedback)

1. low blood volume


2. low erythrocyte numbers (anemic)


3. low f(x)nal hemoglobin (CO2/genetics)


4. poor blood flow (trauma)


5. pulmonary disease

hematocrit

percent of the total volume of RBCs per total volume. viscosity

Abnormally high

1. Polycythemia (elevated RBCs)


2. Diseases that reduce blood oxygen levels


3. dehydration (rbc reduced in plasma volume)

Abnormally low

1. Anemia


2. bone marrow, nutrients, hemolysis, bleeding, overhydration

MCV (Mean Corpuscular Volume)

Single RBC volume

MCH (Mean Corpuscular hemoglobin)

Hgb amount in average RBC (picograms)

MCHC (Mean corpuscular hemoglobin concentration)

Average Hgb concentration (g/dL) in a given volume f RBCs

90 % of old damaged erythrocytes


10% lyse in circulation

1. removed by phagocytosis by liver and spleen macrophages (extravascular hemolysis)


2. intravascular hemolysis

Extravascular Hemolysis (erythrocyte gets broken down to globin>amino acids and Heme


1. Billerverdin


2. Fe via transferrin

1. Billirubin (liver)-bile-intestine>kidney (urobilinogen)


2. Ferritin via Fe to bone marrow>new cell

Haptoglobin

bound to hemoglobin is delivered to splenic and liver macrophages to allow for recycling of iron from heme and amino acids from globin chains

hemolytic anemia

a decrease in RBCs due to an elevation in premature RBC destruction


-increased extravascular/intravascular hemolysis


-rbc membrane defects, immune disorders, infections, drugs

Lab results hemolytic anemia

1. elevated plasma LDH (enzyme in RBC)


2. decreased plasma haptoglobin


3. free hemoglobin in blood (hemoglobinemia/urine (hemoglobiuria)


3. increased, blood plasma bilurubin, urobulunogen, reticulocytes

Morphology


Etiology

1. Size (micro>norm>macrocytic)-macro (decr dna synthesis)


2. Hemoglobin content (hypo/hyperchromic)


3. hemolytic anemia, aplastic anemia

Platelets (thrombocytes)

1. Key players in hemostasis (bleeding stop)


2. Nucleus free fragments of megakaryocytes


3. Destroyed in liver and spleen by phagocytosis


4. Activated when glycoproteins surface bind collagen and sites of injury


5. involves shape changes and secretion of factors for blood clot formation