Pathophysiology Exam #2 Flashcards

1
Q

What percentage of body weight does blood make up?

A

8%

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2
Q

What percentage of blood does the plasma make up?

A

55%

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3
Q

What percentage of blood does the formed elements make up?

A

45%

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4
Q

Most of the plasma is formed of ____?

A

Water, 91%

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5
Q

Proteins make up what percentage of plasma?

A

7%

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6
Q

What is the main contributor to the protein of the blood?

A

Albumin

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7
Q

Other solutes such as gases, ions, nutrients and waste make up what percentage of plasma?

A

2%

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8
Q

When we measure the “formed elements” in the blood we are measuring its?

A

hematocrit

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9
Q

Most of the formed elements are made up of these ____?

A

RBCs

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10
Q

What is the normal range of RBCs in the blood?

A

4.2 - 6.2 million/cubic millmeter(or microliter[microl])

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11
Q

What are the two main functions of RBCs?

A

Transport oxygen to the tissues via iron molecules
Transport carbon dioxide to lungs to be exhaled(CO2 is partially dissolved in the cytoplasm of RBCs and partially bound with hemoglobin

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12
Q

Oxygen binds with the ___ portion of hemoglobin, while carbon dioxide binds with the ___ portion of hemoglobin.

A
  • heme

- globin

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13
Q

Red Blood Cells contains this enzyme that is responsible for?

A

-carbonic anhydrase(metabolizes the reaction of CO2 and Water)
-a weak acid that allows for carbon dioxide to be transported in the cytoplasm of RBCs
CO2 + H2O H2CO3 H+ HCO3-

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14
Q

How does hemoglobin serve as a powerful acid-base buffer to regulate the pH of body fluids?

A

By binding to excess H+ ions if there is an increase in them….if there is a deficit of H+ ions then Hgb will release H+ increasing the concentration of them in body fluids

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15
Q

When carbonic anhydrase is present with CO2 and water, what will be formed?

A
  • Carbonic acid(H2CO3)

- carbonic acid can be formed of water/CO2 without carbonic anhydrase, but it happens much slower

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16
Q

Carbonic anhydrase increases the reaction between CO2 and Water about _____ times.

A

5000

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17
Q

Carbonic acid is a weak acid that disassociates weakly…forming what?

A
  • H+

- HCO3-

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18
Q

CO2 + H2O H2CO3 H+ HCO3-

These elements can go either way either left to right or right to left. What is different when H+ and HCO2 become carbonic acid as opposed with CO2+H2) becomes carbonic acid?

A

H+ and HCO2 do not need carbonic anhydrase to form carbonic acid

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19
Q

CO2 + H2O H2CO3 H+ HCO3-

What determines which way the reaction takes place?

A

The number of reactants on each side. For example…if CO2 increases it is going to combine with water with CA and become H2CO3….if HCO2 increases it drives the reaction the other way.

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20
Q

What is the all important Acid Base formula?

A

CO2 + H2O H2CO3 H+ HCO3-

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21
Q

What is the normal RBC in men?

A

5,200,000/mm^3(or microl)

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22
Q

What is the normal RBC in women?

A

4,700,000/mm^3(or microl)

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23
Q

What are two factors why there is a higher RBC in men than women?

A
  • men have higher testosterone which stimulates RBC

- women have menses

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24
Q

What is the normal percentage of the formed elements(Hct.) part of the total blood volume?

A

38 - 52%

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25
Q

What is the normal hemoglobin?

A

12 -18 gm/dl

1 dl = 100 ml

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26
Q

Each GRAM of hemoglobin can bind to and transport how many mls of oxygen?

A

1.34 ml

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27
Q

RBCs are produced in different places during our lifetime, where are RBCs produced during the prenatal period(3)?

A
  • liver
  • spleen
  • lymph nodes
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28
Q

RBCs are produced in different places during our lifetime, where are RBCs produced from birth until about 5 years old?

A

shifts to all bone morrow

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29
Q

RBCs are produced in different places during our lifetime, where are RBCs produced after 20 years of age(5)?

A
Primarily in the bone marrow of the :
-vertebrae
-sternum
-ilium
with some being produced in the:
-proximal humerus and the tibia
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30
Q

What is the definition of erythropoiesis?

A

production of RBCs

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31
Q

What is the common ancestor shared by all the formed elements of the blood(RBC/WBC/Platelets)?

A

bone morrow stem cell(pleura potential hematopoietic stem cell)

-has the potential to be any of the formed elements of the blood

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32
Q

After the bone morrow stem cell, what is the first cell located in the RBC lineage?

A

Pro-erythroblast

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33
Q

The pro-erythroblast goes through 3 stages called ___, ____, ____ where the ___ is extruded before forming a ___?

A
  • early erythroblast, intermediate erythroblast and late erythroblast
  • nucleus
  • reticulocyte
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34
Q

What is the significance of the nucleus being extruded from the erythroblast?

A
  • mature RBC do not have a nucleus which means they cannot produce(they have a single life span)
  • mature RBC do not have mitochondria, so they cannot participate in aerobic metabolism(cannot produce ATP through aerobic means)
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35
Q

What is the life span of RBC?

A

~120 days

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36
Q

How do RBC get ATP?

A

through glycolysis—>pyruvic acid(net yield of ATP=net of 2)

-They produce ATP through Glycolysis (conversion of
G-6-P > pyruvic acid > net of 2 ATP

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37
Q

What happens when a reticulocyte transforms into a mature RBC?

A
  • It shrinks
  • Hemoglobin concentration will increase (the amount of hemoglobin will NOT increase just the %, because the cell shrunk)
  • the concentration of Hgb increases
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38
Q

If there is an increase reticulocyte count, what does that indicate(2)?

A
  • Normal response to hemorrhage
  • Pharmacological treatment of anemia that works
  • Because reticulocytes are larger than mature RBCs, they are prone to hemolyze (they have harder time traveling in capillaries)
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39
Q

T or F: RBCs are biconcave discs.

A
  • True
  • They have to be a certain size and a certain shape, and pliable
  • They have need to squeeze through capillaries
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40
Q

Describe Erythropoietin (EPO).

A
  • Principal factor that stimulates bone marrow RBC production in the regulation of RBC production
  • 90% produced by peritubular epithelial cells of kidneys
  • Produced in response to HYPOXIA of the cells that secrete EPO

*NOT specifically RBC count or hemoglobin conc. or hematocrit; however, these conditions may cause HYPOXIA, which will then increase EPO secretion**

  • EPO stimulates proerythroblasts and causes them to proceed through further stages of development more rapidly:
  • increases rate at which reticulocytes move from bone marrow to circulating blood
  • percentage circulating retics will increase initially
  • mature RBC count, hgb, and hct will increase

-As RBCs increase, and hypoxia decreases, negative feedback will decrease amount of EPO secretion

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41
Q

What stimulates the production and secretion of EPO?

A

-Hypoxia of the peritubular epithelial cells of the kidneys

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42
Q

List the steps in order of Erythropoietin secretion.

A
  1. Decreased blood O2 (Hypoxia)
  2. Hypoxia of the peritubular epithelial cells of kidneys
  3. Secretion of EPO
  4. Increased EPO in blood
  5. EPO stimulates bone marrow (proerythroblasts)
  6. Increased RBC production
  7. Mature RBC
  8. Increased blood oxygen
  9. Negative feedback to kidneys…stop secretion of EPO
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43
Q

Maturation Factors for RBCs: What is the significance of vitamin B-12 (cobalamin) and what is the outcome of insufficient B-12?

A
  • Essential for RBC DNA synthesis and normal RBC maturation
  • Insufficient B-12: RBC maturation failure and abnormally large RBCs (megaloblasts or macrocytes) which leads to
  • Megaloblastic Anemia or Macrocytic Anemia or Pernicious Anemia which causes *Abnormal O2 transport and easy hemolysis
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44
Q

What are the causes of Vitamin B-12 deficiency and anemia?

A
  • Inadequate dietary intake of B-12 (uninformed vegetarians)
  • Atrophy of gastric mucosa and inadequate intrinsic factor secretion
  • Gastric bypass or gastric reduction operations
  • Small bowel resection, esp. of ileum
  • Malabsorption syndromes of small bowel
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45
Q

Maturation Factors for RBCs: What is the significance of folic Acid (folate)?

A

-Essential for RBC DNA synthesis and normal RBC maturation

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46
Q

How do you differentiate from folic acid and vitamin B-12 deficient anemias?

A

-Draw Vit B-12 and folic acid blood levels

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47
Q

Describe a Hemoglobin molecule.

A
  • Composed of a heme portion and a globin portion
  • Each has 4 globins, alpha-1, a-2, beta-1, b-2 (polypeptide chains, amino acid sequences)
  • Each has 4 heme (center of it is Fe)
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48
Q

What attaches to globin?

A

-CO2

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49
Q

What attaches to the Fe portion of the heme?

A

-O2

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50
Q

Describe the hemoglobin O2 transport system.

A

-HGB combines with O2 at the Alveolar-Capillary level and releases the O2 at Capillary-Tissue level!!!!

**The iron in hemoglobin combines loosely and reversibly with O2. The iron remains in the Fe++ (ferrous) form. It is not oxidized to Fe+++ (ferric) by O2. Oxidation to ferric is irreversible, so the hemoglobin/iron could not release the O2 to cells

EACH FE++ CAN COMBINE WITH ONE O2 MOLECULE (O2). SINCE A HGB MOLECULE CONTAINS FOUR FE++, EACH HGB MOLECULE CAN COMBINE WITH 4 MOLECULES OF OXYGEN (O2)/8 ATOMS OF OXYGEN

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51
Q

What is it called when ferrous (Fe++) is oxidized to ferric?

A

Methemoglbin (MetHb)

-About 1-3% of iron is in ferric (Fe+++) form normally

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52
Q

List the drugs that cause MetHb.

A
  • Prilocaine: generates O-toluidine which oxidizes hemoglobin
  • Lidocaine: Large amount needed (about 600 mg)
  • BENZOCAINE: Hurricaine spray, Cetacaine…BIGGEST CULPRIT
  • Nitroglycerine, Na nitroprusside: (prolonged administration or hepatic/renal failure)
  • Phenytoin —>Dilantin
  • Sulfonamides
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53
Q

What are the clinical clues for MetHb and how is it diagnosed?

A
  • Low SpO2 in the setting of a normal arterial PO2 (pO2 is just the amount of O2 dissolved in the blood)
  • “chocolate, dark-red, brownish to blue” colored arterial blood
  • Brown urine

Diagnosis:

  • Direct measurement of MetHb by co-oximetry
  • Clinical cyanosis in the presence of normal arterial PaO2
  • Pulse oximetry?? (pulse ox does not pick up/measure methb)…will read 85%
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54
Q

What is the Treatment of MetHb?

A
  • Asymptomatic w/MetHb level 20%:
  • Methylene blue (1st line Tx) 1-2 mg/kg IV over 5 min
  • Blood transfusion
  • Hyperbaric Oxygen
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55
Q

How does methylene blue work in treating MetHb?

A

-It converts ferric form back into the ferrous form of iron

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56
Q

How many liters of blood does the average 21 yo, 70 kg male have?

A
  • 6 liters
  • One liter = 1 million muL
  • About 5 million RBC/muL of blood
  • each RBC has about 300 million hemoglobin molecules
  • 4 O2 molecules/hemoglobin molecule
  • Thus, about 36 septillion O2 molecules per person
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57
Q

What does HbA1c stand for? What is Glycosylation?

A

A = Adult *Adult Hemoglobin

1c = portion/subunit of hemoglobin, that over time will combine with glucose
*when glucose attaches to the 1c portion of hemoglobin, it is called glycosylation

-Average a person’s blood glucose over a certain period of time based on the amount of glycosylation of the hgb and A1c

**If someone’s A1c is 6, it means that their bld glucose averaged 120 mg/dL

*Most predictive of last 2-4 weeks of someone’s bld glucose

**Normal = keep A1c under 6

58
Q

Describe Iron Absorption and Loss from GI tract: where is iron mostly absorbed from? Once absorbed it binds with _____, which is a protein synthesized in the liver.

A
  • Iron is poorly absorbed
  • Rate of absorption depends on blood levels of iron (inverse relationship: if bld level of iron low, rate of absorption increases…if bld level of iron is high, rate of absorption decreases)
  • Even if rate of absorption is faster, it is still VERY poorly absorbed
  • If someone loses 1 ml of blood a day on a continuous basis over several days, he is losing more iron in the blood than he is able to absorb thru the GI tract
  • Iron mostly absorbed from the duodenum, with some from jejunum
  • Once absorbed, it will bind with transferrin (protein synthesized in the liver)
  • Transferrin can release iron, and then it becomes FREE iron
  • Free iron can be stored in storage sites, such as:
  • liver
  • spleen

-Free iron binds with another protein synthesized in the liver = Ferritin

59
Q

What is Transferrin?

A
  • Protein synthesized in the liver
  • Transport form of iron…iron binds with it in order to travel to different places in the body
  • Most readily pool of iron to be used for erythropoiesis
60
Q

What is Ferritin?

A
  • Protein synthesized in the liver

- Storage form of iron once it is released by Transferrin.

61
Q

What happens when blood levels of iron decrease? Increase?

A
  • Ferritin releases iron to be moved back into the blood, increase iron blood levels
  • If iron in blood is high levels, it can be bound with ferritin to be stored
62
Q

What happens if Ferritin becomes saturated? What could be a cause of Hemosiderosis?

A
  • Iron then becomes bound as Hemosiderin
  • Almost an irreversible process once this occurs(once it becomes Hemosiderin it is almost impossible to convert back?
  • Hemosiderosis: significant amount of hemosiderin
  • Causes:
  • blood transfusion
63
Q

Describe the process at end of RBC life.

A
  • Last an average of 120 days
  • At cell death, they are broken down, phagocytosed by macrophages
  • Heme portion of hgb has iron > so free iron is then released back into the iron pool of the blood stream
  • Heme portion is converted into bilirubin

RBC death > macrophage phagocytose RBC > hemoglobin broken down into heme and globin > globin made up of amino acids, returned to body to be used again to synthesize proteins > heme portion releases iron, free iron can be used however body needs it > then heme converted first to biliverdin > then bilirubin, free unconjugated form> circulates to the liver, liver conjugates it > conjugated bilirubin is excreted with the bile into the GI tract > excreted: some absorbed from GI tract into blood stream, and then excreted to urine…some stay in GI tract

64
Q

If on a lab report the total bilirubin is elevated, what is a cause of an increase in FREE unconjugated bilirubin?

A
  • ->LIVER FAILURE

- Increase hemolysis of RBCs faster than liver can conjugate them—>-Macrocytic anemia, vit B12/folic acid deficiency

65
Q

If on a lab report the total bilirubin is elevated,what can cause an increase in Conjugated bilirubin?

A
  • Usually an obstruction process in:
  • liver
  • gall bladder
  • bile duct

-Liver can conjugate bilirubin, but it can’t be excreted into the GI tract to be excreted from body

66
Q

Describe the transport of Oxygen….how much is dissolved in the plasma of arterial blood as opposed to how much combines with Fe++ on the hgb on RBCs? How does a decrease in RBC/Hgb affect oxygen transport

A
  • About 2 to 3% of O2 is dissolved in the plasma of arterial blood:
  • This is the component from which PaO2 is measured for ABGs
  • this may or may not represent amount of O2 transported to cells and released to cells
  • About 97-98% combines with Fe++ on hemoglobin in RBCs:
  • decreased RBC count and decreased hgb will decrease O2 transport
  • abnormalities of RBC O2 transport will decrease O2 transport
  • many other factors affect amount of O2 transported and released to cells
67
Q

What is the PO2 and PCO2 at the arterial side of capillary/alveolar interface in the capillary and alveolus?

A

Both are same!!
PO2 = 104
PCO2 = 40

They have equilibrated by this time, from venous to arterial side of capillary

68
Q

After the pulmonary veins leave the lungs, but before it gets to the LA, what is the PO2 and PCO2 levels?

A
PO2 = 95
PCO2 = 40
  • PO2 drops due to bronchial circulation
  • Once circulation gets to heart, it might drop a little further due to Thebesian veins
69
Q

Describe the Oxyhemoglobin Dissociation Curve. When is the affinity of hgb for oxygen high? When is the affinity of hgb for oxygen low?

A

-Depicts the relationship between pO2 and saturation of hgb with O2 or affinity of hgb for O2

  • High pO2:
  • Affinity of hgb for O2 is high
  • Ex: pulmonary capillaries—>to pick up oxygen
  • Low pO2:
  • Affinity of hgb for O2 is low
  • ex: tissue capillaries—>to release oxygen
70
Q

What is a normal oxyhemoglobin dissociation curve with a PO2 of 40 (in tissue at rest) or PO2 of 104 (in lungs)?

A

Tissue: (venous PO2 of 40)O2 saturation of 75%
Lungs: (arterial PO2 of 104)98%

**So, normal venous SpO2 is 60-80%*

71
Q

What is P50? What is the significance in reference to shifts in the Oxyhemoglobin curve?

A
  • The partial pressure of oxygen when the O2 sat is 50%
  • So, if the SpO2 is 50%, the PO2 should be 27-28 mmHg
  • Another way to see if patients have a shift to right or left on dissociation curve
  • if PO2 is less than 27, then the curve is shifted to the left
  • if PO2 is greater than 28, then the curve is shifted to the right
72
Q

How much Oxygen is released to the tissues during exercise?

A

-about 73%

73
Q

Describe the oxyhemoglobin shift down and to the right and causes for the shift.

A

-Decreased affinity of Hgb for O2—>less oxygen will be picked up at the alveolar/capillary interface and more oxygen will be released at the tissue/capillary interface

  • For a given PO2, %O2 saturation is less than expected
  • Causes:
  • acidosis (decreased pH)
  • increase CO2
  • increase temperature
  • increase 2,3-DPG (glycolysis in RBCs)
74
Q

Describe the oxyhemoglobin shift up and to the left and causes for the shift.

A

-Increased affinity of Hgb for O2—->more oxygen will be picked up a the alveolar/capillary interface and less oxygen will be released at the tissue/capillary interface

  • For a given PO2, %O2 saturation is higher than expected
  • Causes:
  • alkalosis (increase pH)
  • decrease CO2
  • decrease temperature
  • decrease 2,3-DPG
  • methemoglobinemia
75
Q

The administration of opioids shifts the oxyhemoglobin dissociation curve in which direction? Why?

A
  • Right
  • RR decreases
  • CO2 increases
76
Q

Describe the Bohr Effect.

A
  • NORMAL PHYSIOLOGIC shifting of the oxyhemoglobin dissociation curve
  • HOW CO2 AFFECTS TRANSPORT OF O2
  • Alveolar-capillary interface: CO2 diffuses out of the capillary > blood becomes more alkaline > 3% shift to the left > FAVORS O2 AFFINITY FOR HEMOGLOBIN
  • Capillary-Cell interface: Co2 diffuses into the blood > blood becomes more acidic > 3% shift to the right > FAVORS O2 RELEASE TO CELLS
77
Q

Describe the Haldane Effect.

A
  • HOW O2 AFFECTS TRANSPORT OF CO2
  • Alveolar-capillary interface: O2 diffuses into the blood (RBCs) > displaces CO2 from Hgb > CO2 CAN BE EXHALED FROM LUNGS
  • Capillary-cellular interface: O2 diffuses into cells > frees up Hgb for CO2 binding > ALLOWS FOR CO2 TRANSPORT
78
Q

T or F: The Bohr and Haldane effects are occurring simultaneously.

A

True

79
Q

Describe the transport of CO2 in venous blood.

A

-Two phases

Phase 1:

  • OCCURS AT CAPILLARY-TISSUE INTERFACE
    1. body cell produces CO2 from aerobic metabolism
    2. CO2 builds up, diffuses from cell to the interstitium and then into the capillary (about 5% of CO2 dissolves in plasma as free CO2)
    3. 95% of CO2 enters the RBC
    4. Small amt. of CO2 in RBC dissolves in intracellular water
    5. 30% of CO2 binds with hgb to produce CARBAMINO HGB
    6a. 65% REACTS WITH WATER TO FORM CARBONIC ACID:

CO2 + H2O > (CA: carbonic anhydrase) > H2CO3 (carbonic acid)

6b. carbonic acid dissociates to form bicarbonate (HCO3-) and Hydrogen ions (H+)

H2CO3 > HCO3- + H+

6c. H+ is carried on hemoglobin (H.Hgb)
6d. As HCO3- concentration increases, some of it diffuses into plasma and chloride diffuses from plasma into RBC (chloride shift): to maintain neutrality (PHASE 1 OF THE CHLORIDE SHIFT or HAMBURGER SHIFT)

Phase 2:

  • OCCURS AT CAPILLARY-ALVEOLAR INTERFACE
    1. Free CO2 diffuses into alveoli and exhaled (the 5% that was diffused in the plasma)
    2a. O2 is moving from the alveoli into the capillary, and O2 will displace CO2 from Hgb (Haldane effect)
    2b. The released 30%(CARBAMINO HGB) of CO2 diffuses into the alveoli to be exhaled:

O2 + Hgb.CO2 > CO2 + Hgb.O2 > CO2 30%

3a. Oxygen combines with hemoglobin, displacing H+:

H.Hgb + O2 > H+ + Hgb.O2 > H+ + HCO3-

3b. HCO3- and H+ recombine to form carbonic acid which separates into CO2 and H2O—>water vapor + CO2 being exhaled
3c. As HCO3- decreases, HCO3- moves into the RBC from the plasma while chloride shifts from the RBC back into the plasma—>known as Phase 2 of the chloride shift(Hamburger shift)
3d. CO2 and water diffuse from the RBC through the plasma into the alveoli to be exhaled

80
Q

T or F: How is most CO2 transported in the blood?

A

Via Bicarbonate

81
Q

In Red Blood Cells, what happens at the same time that the nucleus is extruded from the nucleus and at what point in the maturation of the RBC does this happen?

A
  • RBC enters the circulation

- this happens as the late erythroblast is becoming a reticulocyte

82
Q

What are the characteristic of reticulocytes?

A
  • immature RBC

- they are larger than mature RBC

83
Q

Vitamin B-12 is known as the ____ factor why?

A
  • Extrinsic factor (vitamin B-12 itself…has to be ingested)
  • Must bind with intrinsic factor secreted by gastric parietal cells
84
Q

Where must vitamin B-12 bind with intrinsic factor?

A

-Vitamin B-12 bound with intrinsic factor is absorbed from intact small bowel, specifically ileum

85
Q

What is the result of insufficient folic acid?

A
  • Insufficient folic acid: RBC maturation failure and abnormally large RBCs (megaloblasts or macrocytes)
  • Megaloblastic anemia or Macrocytic anemia
  • Abnormal oxygen transport and easy hemolysis
86
Q

What are causes of inadequate Folic acid?

A

-Causes of folic acid deficiency and anemia: Usually inadequate dietary intake

87
Q

Macrocytes caused by inadequate levels of vitamin B-12 and folic acid lead to(2)?

A
  • abnormal oxygen transport

- hemolysis

88
Q

The iron in hemoglobin combines ___ and ___ with oxygen. It remains in the ___ form. This is important why?

A
  • loosely
  • reversibly
  • Ferrous(Fe++)
  • if it was oxidized to the ferric(Fe+++) form it would be irreversible and the oxygen could not be released to the tissues.
89
Q

How many molecules can a single molecule of hemoglobin carry?

A

A single molecule of hemoglobin has 4 molecules of iron. Each iron molecule can carry 1 molecule of oxygen so a single molecule of hemoglobin can carry 4 molecules of oxygen.

90
Q

If a patient has Methemoglobin anemia, what will their pulse ox probably be reading?

A

85%

91
Q

A HgbA1c of 6 is equal to a blood glucose average of?

A

120

92
Q

The diffusion of O2 and CO2 between the alveoli and the capillary beds is based upon?

A

pressure gradient

93
Q

What does a decrease in venous SPO2 mean?

A

increase uptake of oxygen to the tissues probably related to sepsis

94
Q

How much oxygen is released to the tissues during rest?

A

Oxygen released to tissue at rest: 23%

95
Q

Would it be better to have a right shift of the Oxyhemoglobin curve or a left shift and why?

A
  • Right shift

- cause at least what you picked up could be released to the tissues.

96
Q

What is the normal Hematocrit value in men?

A

40-52%

97
Q

What is the normal Hematocrit value in women?

A

38-47%

98
Q

What is the normal Hemoglobin value in men?

A

13-18 g/dl

99
Q

What is the normal Hemoglobin value in women?

A

12-16 g/dl

100
Q

What is the normal RBC value in men?

A

4.6-6.2 x10/microl

101
Q

What is the normal RBC value in women?

A

4.2-5.4 x 10/microl

102
Q

What is Mean corpuscular volume(MCV) and what is the normal value in men and women?

A
  • average volume or size of the RBC

- 80-98 fl

103
Q

What is Mean corpuscular hemoglobin(MCH) and what is the normal value in men and women?

A
  • average amount of Hgb in RBC

- 26-32 pg

104
Q

What is the Mean corpuscular hemoglobin concentration(MCHC) and what is the normal value in men and women?

A
  • the percent of RBC composed of Hgb

- 32-36%

105
Q

If the MCV decreases, but the MCH stays the same what does the MCHC do?

A

increases

106
Q

What is Red cell distribution width(RDW) and what is the normal value in men and women?

A
  • the variability of size of RBCs
  • 11.6-14.6% variation between RBCs

VARIATION DUE TO DIFFERENT STAGES OF MATURATION—>RETIC CELLS ARE LARGER

107
Q

What is the normal Reticulocyte count in men and women?

A

0.5-2.5%

108
Q

What is the significance of the Total iron binding capacity, and what can we learn from this?

A
  • TIBC is a calculated theoretical #
  • if the transferrin were 100% saturated with iron…how much iron would be present
  • 250-450 mcg/dl

remember transferrin is the transport form of iron

109
Q

What is the significance of Serum ferritin and what can we learn from this?

A
  • Ferritin is the storage form of iron(an acute phase protein)
  • during trauma/inflammation/infection/immunity—> serum ferritin levels increase
  • 20-300 ng/ml
110
Q

How do you distinguish between high serum ferritin and sickness due to it being an acute phase protein?

A

look at C reactive protein—>an inflammatory protein

111
Q

What is the significance of Percentage transferrin saturation?

A

-~30% of transferrin is saturated with iron

112
Q

If a RBC is too large it is called a ___ meaning _____ which is significant for?

A
  • macrocyte(macrocytosis)
  • MCV > 100 fl
  • Megaloblastic/macrocytic anemai
113
Q

If a RBC is too small it is called a ___ meaning _____ which is significant for?

A
  • Microcyte(Microcytosis)
  • MCV<80 fl
  • Iron deficiency anemia, Anemia of chronic disease
114
Q

What is Hypochromia and what is its significance?

A
  • decrease in the color of the RBC secondary to low Hgb which is what gives the RBC its color
  • -MCH < 26 pg/MCHC<27%
  • Decreased cell hemoglobin
115
Q

What is Poikilocytosis and what is its significance?

A
  • variability of RBC shape

- Sickle cell disease, Leukemias, Hemolysis

116
Q

What is Anisocytosis and what is its significance?

A
  • Variability of RBC size

- Reticulocytosis, Abnormal bone marrow production of RBCs

117
Q

What is Spherocytosis and what is its significance?

A
  • MCHC high, loss of biconcave shape

- Hereditary

118
Q

What is Schistocytosis and what is its significance?

A
  • Cell fragments in the circulation

- Trauma to the RBCs, Hemolysis

119
Q

What is Acanthrocytosis and what is its significance?

A
  • Irregularly speculated RBC surface(“mickey mouse cells”)

- Liver disease, Abnormal RBC membrane

120
Q

What is Normocytic?

A

Normal RBC size

121
Q

What is Normochromic?

A

Normal RBC hemoglobin content

122
Q

What is the precursor cell to a monocyte and erythrocytes?

A

A stem cell

-hematopoietic stem cell

123
Q

What is the maximum amount of oxygen that can be transported on each hemoglobin molecule and how many atoms of oxygen.

A
  • 4 molecules of oxygen

- 8 atoms of oxygen

124
Q

Whats the maximum amount of oxygen each gram of hemoglobin can transport?

A

-1.34 ml

125
Q

In a patient with a pH of 7.3…would that be a right shift or a left shift to the oxyhemoglobin curve?
Does this cause an increase or decrease in the affinity of hemoglobin for oxygen?

A
  • Right

- decrease

126
Q

What type of anemia is susceptible in a patient that has had 75% of their Ileum resected?

A

Vitamin B-12 Anemia

127
Q

When oxygen combines with hemoglobin does it bind with the heme or the global portion? C02?

A
  • heme—>iron portion

- globin

128
Q

In a trauma patient with elevated serum ferritin levels is this an accurate portrayal of their iron stores?

A

probably not because ferritin is an acute phase protein

129
Q

In carbon dioxide transport, how much is dissolved in the plasma?

A

5%—>the other 95% enters into the RBC

130
Q

The majority of CO2 is transported in venous blood as?

A

HCO3-

131
Q

What are the causes and treatments of Methemoglobin anemia?

A
  • prilocaine, lidocaine,benzocaine, nitroglycerine, nipride, phenytoin, sulfonamides
  • Asymptomatic w/ MetHb < 20%—>d/c offending agent
  • Symptomatic w/ MetHb > 20%—>Methylene blue, blood transfusion, hyperbaric oxygen
132
Q

What is a low SvO2 indicative of?

A

Sepsis—>increase uptake of oxygen to the tissues/increase metabolic demand

133
Q
In Pernicious Anemia(B12 deficiency anemia) what would you expect the laboratory values to be:
Hgb
Hct
Reticulocyte %
MCV(mean corpuscular volume)
Plasma Iron
TIBC
Serum Ferritin
Serum B12
Folate
Bilirubin
A
Hgb--->low
HCT--->low
Retic--->low
MCV--->high
Plasma Iron--->high
TIBC--->normal
Serum Ferritin--->High
Serum B12--->low
Folate--->normal
Bilirubin--->Slightly high
134
Q
In Folate Deficiency Anemia what would you expect the laboratory values to be:
Hgb
Hct
Reticulocyte %
MCV(mean corpuscular volume)
Plasma Iron
TIBC
Serum Ferritin
Serum B12
Folate
Bilirubin
A
Hgb--->low
HCT--->low
Retic--->low
MCV--->high
Plasma Iron--->high
TIBC--->normal
Serum Ferritin--->normal
Serum B12--->normal
Folate--->low
Bilirubin--->Slightly high
135
Q
In Iron Deficiency Anemia what would you expect the laboratory values to be:
Hgb
Hct
Reticulocyte %
MCV(mean corpuscular volume)
Plasma Iron
TIBC
Serum Ferritin
Serum B12
Folate
Bilirubin
A
Hgb--->low
HCT--->low
Retic--->normal or slightly high or low????
MCV--->low
Plasma Iron--->low
TIBC--->high
Serum Ferritin--->low
Serum B12--->normal
Folate--->normal
Bilirubin--->normal
136
Q
In Posthemorrhagic Anemia what would you expect the laboratory values to be:
Hgb
Hct
Reticulocyte %
MCV(mean corpuscular volume)
Plasma Iron
TIBC
Serum Ferritin
Serum B12
Folate
Bilirubin
A
Hgb--->low
HCT--->low
Retic--->high
MCV--->normal
Plasma Iron--->normal
TIBC--->normal
Serum Ferritin--->normal
Serum B12--->normal
Folate--->normal
Bilirubin--->normal
137
Q
In Hemolytic Anemia what would you expect the laboratory values to be:
Hgb
Hct
Reticulocyte %
MCV(mean corpuscular volume)
Plasma Iron
TIBC
Serum Ferritin
Serum B12
Folate
Bilirubin
A
Hgb--->low
HCT--->low
Retic--->high
MCV--->normal or high
Plasma Iron--->normal or high
TIBC--->normal
Serum Ferritin--->normal
Serum B12--->normal
Folate--->normal
Bilirubin--->high or slightly high
138
Q

What is the PaO2/PCO2 of the venous blood located on the capillary side of the alveolar/capillary interface?

A

PaO2=40

PCO2=45

139
Q

What is the PaO2/PCO2 of the alveolar side of the alveolar/capillary interface before the gases diffuse into the venous blood located in the capillaries?

A

PaO2-104
PCO2=40

Based on the pressure gradient of oxygen/carbon dioxide the gases will move from one side of then interface to the other

140
Q

What is the PaO2/PCO2 of the arterial blood located on the capillary side of the alveolar/capillary interface?

A

PaO2=104
PCO2=40

the gases have equilibrated so its the same on the alveolar side as well as the capillary side

141
Q

Once the arterial blood is ejected from the LV, it travels to the tissues to supply them with oxygen….what is the PaO2/PCO2 in the capillaries, in the interstitial fluid and in the tissues?

A

Capillaries:
PaO2=95
PCO2=40

Interstitial Fluid:
PaO2=40
PCO2=45

Tissues:
PaO2=20
PCO2=45

*Based on partial pressure gradient O2 will move from capillary, to the interstitial and then to the cell providing that tissue/cell with O2 and nutrients.