Exam 4: Wed 11/11 blood review Flashcards

1
Q

Function of the Red Blood Cells AKA Erythrocytes (3)

A
  1. Transport hemoglobin - O2 carrier
  2. Transport enormous quantities of CO2 in the form of bicarbonate ion (HCO3−) away from the tissues to the lungs
  3. RBCs responsible for most of the acid-base buffering power of whole blood
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2
Q

True or false: Hemoglobin sucks at trying to be an acid-base buffer

A

False

  • Hemoglobin in the cells is an excellent acid-base buffer
  • True of most proteins
  • Binds H+
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3
Q

What is the concentration of Red Blood Cells in the Blood?

A
  • In normal men, the average # RBCs 5,200,000/m3 & in normal women, it is 4,700,000/m3
  • Persons living at high altitudes have greater numbers of red blood cells
    • Natural, “legal” blood doping
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4
Q

What is the quantity of Hemoglobin in the RBCs?

A
  • Hemoglobin in RBCs =34 grams/100 ml of cells which is the metabolic limit of the cell’s hemoglobin-forming mechanism
  • Whole blood has average of 14-15 grams of hemoglobin/100 ml
  • Lab norms: Hgb male 14-18; Hgb female 12-16
  • Millions Hb or Hgb molecules per RBC
  • Each gram of pure hemoglobin is capable of combining with 1.34 ml of O2

*Hematocrit (% of blood that is RBCs) - normally 40-45%

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5
Q

Where are RBCs produced?

A
  • exclusively in the bone marrow
  • Basically all bones produce red blood cells until a person is 5 years old
  • Marrow of the long bones, except proximal portions of the humerus and tibia, becomes quite fatty; produces no more red blood cells after about age 20 years.
  • Beyond this age, most RBCs continue to be produced in the marrow of the membranous bones, such as the vertebrae, sternum, ribs, and ilia.
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6
Q

Two reasons RBCs # regulated within narrow limits

A
  1. Adequate number of RBCs available to provide sufficient transport of oxygen from the lungs to the tissues
  2. Not too many, so cells do not impede blood flow (would thicken the blood)
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7
Q

What are the causes for a decrease in O2 transported to tissues which in turn increases the rate of red blood cell production?

Dr. T has 4 bullet points listed under this heading

A
  • Hemorrhage
  • Destruction of major portions of the bone marrow
  • High altitudes
  • diseases of the circulation that decrease blood flow through the peripheral vessels & failure of blood oxygen absorption in the lungs
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8
Q

What is Erythropoietin (EPO)?

A

a hormone secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues.

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9
Q

Some things to know about erythropoietin and its role in the regulation of RBC production (4)

A
  • Principal stimulus for red blood cell production in decreased O2 states
  • About 90% of all erythropoietin is formed in the kidneys with rest formed mainly in the liver
  • Norepinephrine, epinephrine and several of the prostaglandins increase erythropoietin production
  • End Stage Renal Disease (kidney failure) patients have only 33-50% RBCs due to only 10% of the normal erythropoietin
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10
Q

3 key roles of leukocytes

A
  1. Immune response: Innate – polymorphonuclear granulocytes & monocytes, Acquired - lymphocytes
  2. Inflammation
  3. Allergic reactions
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11
Q

4 things to note about neutrophils

A
  1. Most numerous of WBCs accounting for 55-70% of WBCs
  2. Phagocytic
  3. First on scene in infection or injury
  4. Short-lived and self-destruct after eating harmful antigens
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12
Q

Two things to note about lymphocytes

A
  1. 30-40% of WBCs
  2. Make up B cells, T cells, and NK cells
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13
Q

Three things to note about monocytes

A
  1. 3-8% of WBCs
  2. Macrophages - phagocytic activity
  3. Secretion of cytokines which stimulates the attraction of other phagocytes
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14
Q

Three things to note about eosinophils

A
  1. 1-6% of WBCs
  2. Release of cytokines, growth factors and other enzymes/factors
  3. Important in parasitic infections & allergic response
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15
Q

Four things to note about Basophils

A
  1. Few in number - 0.01% to 0.3% of WBCs
  2. Secrete the following substances: heparin, histamine, serotonin, kinins, leukotrienes , prostaglandins & Platelet activating factor
  3. Potentiates other vasoactive substances &inflammatory mediators
  4. Assists in regulation of blood clotting
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16
Q

What does plasma do?

A

carries antibodies and nutrients to tissues, removes wastes

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17
Q

Common causes of blood problems/disorders that you may encounter as a PT (4)

A
  1. Use of NSAIDs
  2. Neurological complications from pernicious anemia
  3. Complications of chemotherapy and radiation
  4. Orthopaedic blood disorders are usually either bleeding (hemostasis) or clotting (hypo- or hypercoagulation disorders)
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18
Q

Where are the platelets and coagulation factors in the blood?

A

Plasma

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19
Q

What might we assume if someone has blood issues?

A

They have oxygen issues

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20
Q

Signs and symptoms of hematologic disorder

listed by Dr. T (5)

and I’m adding some from Goodman and Fuller (4)

A
  1. Exaggerated response to minimal exercise (dyspnea, chest pain, palpitations, severe weakness, fatigue)
  2. Neurological symptoms (headache, drowsiness, dizziness, syncope, polyneuropathy)
  3. Skin and fingernail bed changes (cyanosis, clubbing)
  4. Easy bruising
  5. Swelling, pain in joints

Goodman and Fuller

  1. congestion (accumulation of excessive blood w/in vessels in tissues/organ)
  2. edema (lymphedema, pulmonary, ect..)
  3. infarction (heart, brain, kidney, ect..)
  4. shock (weak distal pulse, hypotension, all other signs of shock)
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21
Q

Changes seen in the skin from hematologic disorders and their respective cause (5)

A
  1. Untreated pernicious anemia= light, lemon yellow tint
  2. Severe anemia resulting from acute hemorrhage= white,waxy appearance
  3. Chronic blood loss= gray-green yellow
  4. Leukemia= gray tint
  5. Anemia= pale hands or palmer creases
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22
Q

Changes seen in the nail bed from hematologic disorders and its respective cause

A

Long-standing iron deficiency anemia= brittle and/or convex (rather than concave)

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23
Q

Change seen in the oral mucosa from hematologic disorders and its respective cause

A

Anemia= pale or yellow color

24
Q

Disorders and what not where we may see too few erythrocytes (6)

A
  1. Chronic diseases (cancer, kidney, liver)
  2. Iron deficiency- possibly from chronic GI blood loss due to NSAIDs
  3. Inflammatory (RA or SLE)
  4. Infectious diseases (TB, AIDS)
  5. Neurologic diseases (pernicious anemia)
  6. Neoplastic diseases
25
Q

Why are older people more suseptible to anemia?

A
  • They don’t process iron as well
  • Their diet is typically not rich in iron. May select foods that do not require a lot of chewing. May prefer soups that will aleviate a dry mouth and are easy to prepare.
26
Q

Clinical signs and symptoms for anemia (chapter 5 in Goodman and Snyder)

A
  1. Skin Pallor (palms, nail beds) or yellow-tinged skin (mucosa, conjuctiva)
  2. Fatigue and listlessness
  3. Dyspnea on exertion accompanied by heart palpations and rapid pulse (more severe anemia)
  4. Chest pain with min exertion
  5. Decreased diastolic BP
  6. CNS manifestations (pernicious anemia)
27
Q

CNS manifestation seen in pernicious anemia (6)

A
  1. headache
  2. polyneuropathy
  3. apathy, depression
  4. drowsiness
  5. dizziness, syncope
  6. slow thought processes
28
Q

S/S and possible causes of a hemorrhage

A
  • blood in urine/stool
  • nose bleed
  • had surgical procedure
  • “leaky guts”
29
Q

How does the body cope with blood loss anemia (hemorrhage)?

A
  • Body replaces the fluid portion of the plasma in 1 to 3 days, but this leaves a low concentration of red blood cells
  • If no additional bleeding, RBCs usually returns to normal within 3-6 weeks
30
Q

What is aplastic anemia?

A
  • a disease in which the bone marrow, and the blood stem cells that reside there, are damaged.
  • A rare condition in which the body stops producing enough new blood cells.
31
Q

Causes of aplastic anemia (4)

A
  • Gamma ray radiation can sustain destruction of bone marrow
  • Cancer chemotherapy
  • Excessive x-ray treatment
  • certain industrial chemicals and drugs sensitivities can cause the same effect
32
Q

According to Dr. T why may we as PTs see Megaloblastic Anemia more frequently than our predecessors?

A

The increased frequency of gastroplasty

(stomach stapling)

33
Q

4 points to note about Megaloblastic Anemia

A
  • Atrophy of the stomach mucosa, loss of the entire stomach after surgical total gastrectomy, & intestinal sprue (a syndrome in which intestinal villi atrophy) can lead to megaloblastic anemia
  • RBCs are oversized, have bizarre shapes, and have fragile membranes
  • These cells rupture easily
  • S/S are teh same as other anemias
34
Q

What is the connection between bilirubin, jaundice, and studying hematological disorders?

A
  • Bilirubin is a by-product of metabolized HgB. How HgB eventually becomes bilirubin is a long, complicated process and a certain amount of it in the body is normal.
  • At the liver, bilirubin is not properly metabolized.
  • There are oodles of reasons that jaundice can occur which may vary from too much destruction of RBCs to hepatic diseases or injury.
  • Some types of treatment: Often use of UV light, medications, liver transplant…..
35
Q

What is polycythemia?

A

Too many RBCs

also called erythrocytosis

36
Q

What causes Primary polycythemia?

A

a rare bone marrow neoplasm

37
Q

What causes secondary polycythemia?

A
  • decreased O2 - may be due to living at high altitudes
  • smoking
  • radiation
  • chronic heart/lung disorders
38
Q

Clinical signs and symptoms of polycythemia (17)

A
  • malaise and fatigue
  • SOB
  • Intolerable pruritus (skin itching)
  • headache
  • dizziness
  • irritability
  • blurred vision
  • fainting
  • decreased mental acuity
  • disturbances of sesnation in hands and feet
  • weight loss
  • easy bruising
  • cyanosis (blue hue in skin)
  • clubbing of fingers
  • splenomegaly (enlargement of spleen)
  • gout
  • hypertension
39
Q

What might we monitor with polycythemia?

A
  • watch for ↑ BP and hematocrit levels due to ↑ blood viscosity
  • Viscous blood plugs capillaries
40
Q

Two points on the pathology of Polycythemia Vera (primary polycythemia)

A
  • Caused by lack of proper feedback control which ↓ RBC production, but also ↑ # of RBCs
  • It usually causes excess production of white blood cells and platelets as well

Dr. T also said this was a type of secondary polycythemia, but the book and wikipedia say primary

41
Q

Four points on the pathology of Sickle cell anemia

A
  1. It is a type of Hemolytic Anemia
  2. RBCs contain abnormal hemoglobin S, containing faulty beta chains
  3. When hemoglobin S is exposed to low concentrations of O2 develops a sickle appearance rather than a biconcave disc
  4. RBCs also highly fragile, leading to serious anemia
42
Q

How does a person get Sickle cell anemia?

A
  • Inherited disease – autosomal recessive
  • Both copies of the gene in each cell have mutations
  • Most common inherited blood disorder in the US, 1 in 500 African Americans and 1 in 1,000 Hispanic Americans
43
Q

clinical signs and symptoms of sickle cell anemia

A

There are about 1 billion. Please refer to list in chapter 5 of Goodman Snyder book.

44
Q

2 leukocyte disorders

A
  1. leukocytosis
  2. leukopenia
45
Q

What is lekocytosis and what are some signs and symptoms?

A

↑ neutrophils

S/S include: fever, symptoms of localized or systemic infection, inflammation or tissue trauma

46
Q

What is leukopenia and what are some signs and symptoms?

A

too few leukocytes

S/S: sore throat, cough, high fever/chills, ulcerations, persistent infections, frequent/painful urination

47
Q

What type of disorder is thrombocytosis and what is it?

A
  • Platelet disorder
  • an increased platelet count
  • usually compensatory after surgery, hemorrhage, splenectomy
48
Q

What factors can affect platelet levels and or platelet aggregation (increase and decrease)?

A
  • NSAIDs and anticoagulants- decrease
  • Diet – lecithin (dairy, eggs, salmon, avocado, and legumes) prevents coagulation
  • vitamin K (dark leafy greens) increase levels, promote clots
    • “Vitamin K . . . is often called the blood coagulation vitamin or antihemorrhagic vitamin.” The name is is derived from koagulation, the danish word for coagulation. (Sara’s undergrad nutrition book)
  • Exercise – helps destroy clots
  • Liver disease- affects Vit K so decrease platelet levels
  • radiation- decrease levels
  • chemotherapy- decrease levels
49
Q

A few signs and symptoms of thrombocytosis (3) SET

A
  • Splenomegaly
  • Easy bruising
  • Thrombosis
50
Q

What type of disorder is thrombocytopenia and what is it? And two poorly placed facts

A
  • platelet disorder
  • decreased platelets
  • may be idiopathic in children
  • Valsalva should never happen due to possible rupture
51
Q

Causes of thrombocytopenia (7)

A
  1. Cytotoxic agents (chemotherapy)
  2. Radiation
  3. Aplastic anemia
  4. Bone marrow failure
  5. Metastic carcinoma
  6. Meds: NSAIDs, methotrexate, gold, coumadin
  7. Leukemia
52
Q

Signs and symptoms of thrombocytopenia

A
  • bleeding after minor trauma
  • sponatenous bleeding: petechiae, ecchymoses, purpura spots, epistaxis (nose bleeds)
  • menorrhagia (mega-menstration, like mega)
  • gingival bleeding
  • melena* (black tarry stools)

*glad that’s not my name!

53
Q

What is hemophilia? and a possible form of treatment?

A
  • Bleeding disorder caused by a deficiency in one of two blood clotting factors: factor VIII or factor IX
  • Several different gene abnormalities can cause the disorder
  • People bleed unexpectedly or after minor injuries

Possible Treatment= Transfusions are given to replace missing clotting factors, can be given prophylactically (expensive though)

54
Q

Two forms of hemophilia

A
  1. Hemophilia A, which accounts for about 80% of all cases, is a deficiency in clotting factor VIII
  2. Hemophilia B is a deficiency in clotting factor IX

The bleeding patterns and consequences of these two types of hemophilia are similar

55
Q

Things to watch for and monitor with hemophilia

A
  • Watch for acute hemarthrosis
  • bleeds into muscle, CNS, GI tract
  • Muscle bleeds- Trunk flexion in presence of iliopsoas bleed causes severe pain. If a hip joint bleed; hip rotation causes severe pain.
  • Over time, repeated bleeds will cause fibrotic tissue and contractures
  • Possibility of peripheral nerve lesions from compression
  • Pseudo-tumor or bone erosion with hemarthrosis
56
Q

Who is Grigori Rasputin?

A
  • a Russian peasant, mystical faith healer and a trusted friend to the family of Nicholas II, the last Tsar of Russia
  • He was thought to heal the czar’s son Alexei from his Hemophilia B.
  • One of the ways he may have helped “cure” the boy was by stopping the doctors from contining administration of aspirin (the medicine du jour)
57
Q

Quick reminder of why the spleen is important to blood (3)

A
  • removes old and deformed RBCs
  • produces antibodies
  • removes antibody laden bacteria or cells