Pathophysiology Ch. 12 & 13

Front 1

Blood volume 55% ____________.

Back 1

Plasma

Front 2

Blood volume 45% ____________.

Back 2

Cells and elements.

Front 3

Hematocrit:

Back 3

Viscosity of blood
Made up of Erythrocytes and Leukocytes
Males have higher values due to increased muscle mass and O2 demand
Elevation indicates dehydration or excessive RBC production

Front 4

Clear fluid remaining after solutes except for fibrinogen removed:

Back 4

Plasma

Front 5

Fluid remaining after cells and fibrinogen have been removed:

Back 5

Serum

Front 6

immature RBC:

Back 6

Reticulocytes

Front 7

Hormone released by the kidneys when oxygen levels are low. Stimulates proerythroblasts from stem cells in the bone marrow:

Back 7

Erythropoieten (EPO)

Front 8

Hemoglobin:
___________ gives red color.
___________ is colorless protein.

Back 8

Heme gives red color
Globulin is colorless protein

Front 9

On RBCs, C02 carried mostly as:

Back 9

a bicarbonate ion

Front 10

RBC breakdown; What happens to Iron and by products of RBCs?

Back 10

Iron can be reabsorbed and stored in the liver as ferritin.
Balance of the heme is converted to bilirubin and transferred to the liver.

Front 11

What are the two types of Bilirubin?

Back 11

Conjugated (Direct) and Unconjugated (Indirect).

Front 12

Describe Conjugated (Direct) Bilirubin:

Back 12

Excreted in bile
Water-soluable

Front 13

Describe Unconjucated (Indirect) Bilirubin:

Back 13

Transported bound to serum albumin
Normally it is conjugated in the liver w/ glucuronic acid to make it water-soluable but it remains as plasma soluable when not conjugated

Front 14

Describe the hemolysis process and jaundice:

Back 14

Destruction of RBCs can cause jaundice
Due to too many cells in circulation, liver cannot conjugate all of them fast enough and they return to circulation unconjugated (see page 283 –Porth)
Can lead to jaundice of the eye and skin and potential neurological damage from excess bilirubin the brain
Bili lights in infants help congugate bilirubin and excrete in the bile

Front 15

Excessive destruction of RBCs through hemolysis:

Back 15

Hemolytic Anemia

Front 16

Blood Clotting...
Hemostasis requires three steps

Back 16

-Immediate response of vasoconstriction and/or vasospasms. Helps platelet plug form by decreasing blood flow.
-Thrombocytes (platelets) form to make platelet plug and adhere to the tissue if the vessel is small.
-Clot formation is created in larger vessels required a more complex process (see next slide).
ASA(aspirin) prevents cohesion of thrombocytes and other tissues, increases bleeding risk.

Front 17

Hemostasis has these two pathways:

Back 17

Intrinsic & Extrinsic Pathways.
Intrinsic Pathway: activated by endothelial injury of a blood vessel.
Extrinsic pathway: activated by tissue and platelet injury.

Front 18

What does heparin do? Pathway?

Back 18

Heparin blocks prothrombin from becoming thrombin (Extrinsic).

Front 19

What does Coumadin do? Pathway?

Back 19

Coumadin blocks sequence of prothrombin and Vitamin K synthesis (Intrinsic)

Front 20

What does Streptokinase do?

Back 20

Streptokinase (tPA) and ASA blocks at end of sequence, no clot is formed

tPA works best on clots that are recently formed

Front 21

What test determines if antibodies are present in the mother during the pregnancy for Rho?

Back 21

Coombs test.

Front 22

Symptoms of Transfusion Rx:

Back 22

Hypertension and Tachycardia
Headache
Fever and chills
Chest pain
Abdominal Pain
Warmth in blood vessel
Flushed face

Front 23

An increase in WBC.
Often elevated with bacterial infections and inflammation.

Back 23

Leukocytosis

Front 24

What is a CBC?

Back 24

WBC
RBC
Platelets
RBC indices:
MCV
MCH
MCHC
RDW

Differential must be selected, not an automatic of a CBC

Front 25

MCV - Mean Corpuscular Volume

Back 25

Measures the size of RBCs &
the volume of a single cell occupied by oxygen:

Distinguishes whether anemia is present, what type it is, and what the cause of anemia might be:

Front 26

MCV is not an accurate marker of:

Back 26

Not an acute marker of blood loss, may be normal with acute blood loss

Front 27

What is an accurate marker of acute blood loss?

Back 27

Hgb/Hct is an accurate marker of acute blood loss

Front 28

What are the value ranges for MCV?

Back 28

Microcytic anemia<80 fL
Normocytic anemia 80-100 fL
Macrocytic anemia>100 fL
fL unit = femtoliter

Front 29

MCHC - Mean Corpuscular Hemoglobin Concentration:

Back 29

Measures how tight the Hgb is packed into the RBC (32-38%)
The smaller the cell, the higher the concentration
Decreased- Thalassemmia

Front 30

MCH - Mean Corpuscular Hemoglobin:
Normal values?

Back 30

(27-34pg/dl)
Measures the amount of Iron in cell:
Hypochromatic (lack of color) – IDA, Thalassemia, or chronic blood loss
Normochromic – Acute blood loss, renal or bone marrow failure, or hypometabolic states
Hyperchromic – Alcoholism, B12, Folic Acid deficiency or Estrogen administration

Front 31

Reticulocyte count

Back 31

Immature blood cells, released within 48 hrs of stimulation to marrow – erythropoesis
Normal Values (.5-1.5%)
Part of RBC evaluation, but not part of a routine CBC

Front 32

Reticulocyte count helps determine:

Back 32

Helps determine adequate bone marrow function/response

Front 33

Anemia is defined as:
Caused by:

Back 33

a low Hgb.

Reduced production by the bone marrow
Reduced stimulation by kidneys
Both
Excessive blood loss or destruction

Front 34

With anemia, compensation occurs:

Back 34

Compensation occurs with increased HR and peripheral vasoconstriction.

Front 35

Signs and symptoms of low Hgb include:

Back 35

Chest pain, ischemia, CHF
Dyspnea
Fatigue
Pallor
Stomatitis, Chelitis, Ulcers

Front 36

Types of anemia:

Back 36

Microcytic – MCV <80 -TICS
Thalassemia
Iron Deficiency
Chronic Disease

Macrocytic – MCV >100 -FLABS
Folic Acid Deficiency
Liver Disease
Alcoholism
B12 Deficiency

Hemolytic –Normal MCV value with slight increase in reticulocytes
Premature destruction of RBC
Increase in erythropoiesis

Front 37

MCV measures:

Back 37

whether there is enough reticulocytes (bone marrow function)

Front 38

Microcytic Anemia (TICS):

Back 38

Thalassemia

Hereditary Disorder, Genetic defect of one of the alleles to chromosome 16

A reduction in synthesis of either alpha or beta globin chains chains leading to a reduction in the production of Hgb A (Normal concentration is 97%).

A reduction in both chains often leads to death before age 5

Skeletal abnormalities, FTT, liver failure, pallor and fatigue present

Greek and Italian descent -Beta

Front 39

Describe Hemoglobin changes at birth:

Back 39

At Birth – Hgb F (fetal) is approx 70% of volume- reflects a higher oxygen affinity and promotes oxygen across the placenta
Changes quickly to Hgb (A) within 8-10 weeks
Within 6-12 months, all Hgb F is Hgb A
With sickle cell, the Hgb F has been changed to Hgb S
Electrophoresis testing to determine Hgb Sub types (A, F, S, etc)

Front 40

What are the two types of Thalassemia:

Back 40

Major and minor

Front 41

Describe Thalassemia major:

Back 41

Major

Marked growth failure, often seen by 6-9 months

Severely jaundiced, delayed developmental milestones
Prone to infections, organ failure, thrombocytic events, bone fractures

Transfusions frequent, early death

Hgb F level is 40-60-%

Front 42

Describe Thalassemia minor:

Back 42

Minor

No expression of severe traits

May often c/o fatigue, pallor or other non-specific complaints

Normal Ferritin and RDW levels* (diagnostic for Thalassemia vs. normal anemia. Iron would be low with normal anemia)

Low MCV (<80)*

 RBC count normal-high (>5)

Hgb F level <10% but >3%

Basophilic stippling on peripheral smear

Front 43

Describe Iron-Deficiency Anemia:
Definition?

Back 43

Definition
MCV <80

Low Hgb (<12 women and <13 men)
Iron is needed for RBC Synthesis
Gives shape and size to allow O2 molecules to adhere to surface

Most common nutritional deficiency worldwide

Incidence is higher in Hispanic and African American living in United States (19-22%)

Front 44

Clinical Presentation of IDA:

Back 44

Children - diet poor and rapid growth demands, appear weak, pale bulbar conjunctivae, skin

Adults- bleeding from the GI tract, mal-absorption syndromes, heavy menses, Cancer (hypermetabolic state) pregnancy, celiac disease

Onset - slow, allows for compensation to occur

Elderly often have slow, insidious onset, may look like “typical aging” like fatigue and mental slowness, symptoms of CHF, dizziness

Front 45

Complete Blood Count (CBC) indicating IDA:

Back 45

RBC -low
Hgb -low
Hct -low
MCV – low
MCHC - low
RDW –increased due to increased variation of cell shapes from the lack of iron

Front 46

What other diagnostic tests are there for IDA?

Back 46

Ferritin levels.
Lower reflecting the need for more Fe in the circulation and bone marrow
Reflects stored iron in the liver

Front 47

lead toxicity (heme synthesis impairment from damage to bone marrow from lead):

Back 47

Basophilic stippling. Test: Peripheral Smear

Front 48

pale center of cells (lack iron which gives cell vibrant red color)

Back 48

Hypochromatic Test: Peripheral Smear

Front 49

Erythrocytes indices:

Back 49

microcytic or macrocytic Test: Peripheral Smear

Front 50

varying sizes of cells with lack of iron (indicated by the increased RDW values):

Back 50

Anisocytosis Test: Peripheral Smear

Front 51

varying shapes of cells with lack of iron:

Back 51

Poikilocytosis Test: Peripheral Smear

Front 52

Target cells:

Back 52

Sickle cell, Thalassemia minor, Liver disease Test: Peripheral Smear

Front 53

Caused by impaired DNA synthesis that creates enlarged red cells due to impaired cell division & maturation:

Back 53

Megaloblastic Anemias

Front 54

Test for Megaloblastic Anemias? Value?

Back 54

MCV >100fL

Front 55

Causes of Megaloblastic Anemias? Acronym?

Back 55

FLAB
Folic acid deficiency
Liver Disease
Alcoholism
B12 Deficiency

Front 56

Pernicious anemia:

Back 56

Deficit of B12 in diet or absorption

Front 57

Pernicious anemia RBCs:

Back 57

Large, immature erythrocytes

Front 58

Pernicious anemia processes secondary deseases:

Back 58

Loss of B12 absorption from diet in GI tract due to intrinsic factor insufficiency in the lower ileum (bind together to allow absorption)
Loss of stomach acid delays protein breakdown and may also lead to IDA from poor absorption of iron

Front 59

Pernicious anemia RBC shape, lifespan, and affect on nerves?

Back 59

Oval shape instead of biconcave
Lifespan is a few weeks instead of a few months
Leads to a lower erythrocyte count (RBC)
Demyelination of nerves from lack of B12
Leads to loss of nerve conduction and impulses
Autoimmune, genetics and infectious causes as well
T cells and macrophages attack myelin sheath and cause destruction and inflammation
Irreversible condition
Sensory first, motor function last

Front 60

Other causes of Pernicious anemia:

Back 60

ack of protein, animal products
Vegetarians prone to B12 deficiency
Mal-absorption in diet
Increased with age, alcoholics with chronic gastritis
PPI meds blocking absorption and decreased stomach acid
Gastric bypass
Symptoms include
Large, tender glossy tongue (glossitis)
Loss of sensation, discrimination impairment (can’t discriminate between hot vs. cold, sharp vs. dull, etc.)
Tingling and burning sensation chronic to distal regions
B12 level below 200ng/dl (normal >400)
Blood smear with large, hypersegmented cells

Front 61

Symptoms of Sickle cell disease:

Back 61

Severe anemia
Jaundice
Spleenomegaly due to congestion in young children
Asplenic in adults due to fibrotic changes and atrophy
Skin infections, ulcers due to infarctions
Occlusions in hands and feet –swelling in young children
CHF (congestive heart failure)
Frequent infections due to lower immune response, asplenic condition that delays healing and filtering of blood

Front 62

Sickle cell Crisis:

Back 62

Can cause multiple infarctions at the same time
Painful due to ischemic pain
Vessel occlusion increases platelet activation & increases the risk of blood clots
Common areas include
Lungs
Heart
Spleen
Brain
Gallbladder
Kidneys
Bone

Front 63

Sicke Cell disease involves mutations in:

Back 63

Mutation in beta chains of hemoglobin
When hemoglobin is deoxygenated, beta chains link together Forming long protein rods that make the cell “sickle”

Front 64

Primary Polycythemia Vera...

Serum erythropoietin level?
Spleen?
Bone marrow?

Back 64

is low.

Spleen and liver are congested, enlarged
Bone marrow is hypercellular