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Patho > Chapter 13 > Flashcards

Chapter 13 Flashcards

1
Q

2 types of hemoglobin

A

adult (HbA)- adults and children > 6 months

fetal (HbF)- 3-9 months in fetus

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2
Q

Adult hemoglobin (HbA)

A

2 alpha chains
2 beta chains
adults and children > 6 months old

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3
Q

Fetal Hemoglobin

A

2 alpha chains
2 GAMMA chains
have ^ O2 affinity, takes from mom
predominant 3-9 months gestation

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4
Q

how many molecules of O2 can be carried by one hemoglobin?

A

4

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5
Q

How much hemoglobin we make, depends on how much ___ we have

A

iron

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6
Q

65% of iron can be found in the ___

A

hemoglobin (circulating)

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7
Q

15-30% of iron can be found stored in the ___

A

liver
&
reticuloendothelial cells of BONE MARROW

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8
Q

“where RBC’s go to die”

A

spleen

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9
Q

what happens when a RBC is destroyed in the spleen?

A

the iron from the hemoglobin is released into the circulation and returned to the bone marrow, liver or other tissues

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10
Q

iron is typically derived from ___ and absorbed in the ___ .

A 
meat
small intestine (duodenum)
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11
Q

an incomplete, non function protein that turns into transferin when iron gets absorbed into duodenum.

A

Apotransferin

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12
Q

refers to the production of RBC

A

Erythropoeitin

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13
Q

erythropoesis is stimulated by?

A

low O2

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14
Q

Erythropoeitin is made where and stimulated into action where?

A

kidney

Bone marrow- stimulated stem cells to create hemocytoblasts –> proerythroblasts

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15
Q

RBC’s last about ____

A

120 days

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16
Q

why do RBC’s only last a short amount of time? (2)

A
  1. metabolic activity decreased with age (creates weakened cell membranes)
  2. eventually, RBC’s break as they squeeze through spleen capillaries (don’t have strong cell membrane)
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17
Q

If old and Damaged, RBC’s get phagocytized by cells from the:

A

liver, spleen, bone marrow, lymph nodes

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18
Q

when RBCs are destroyed, the heme…

A

gets converted into bilirubin (bile pigment)

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19
Q

when rbc’s die, ____ takes the___to the liver where its stored as Ferin.

A

transferin, iron

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20
Q

Bilirubin is removed from the blood as ____ or _____.

A

conjucated bilirubin
or
unconjucated bilirubin

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21
Q

_____ attaches to glucocorinide which makes it soluble in plasma and can be excreted in bile.

A

Conjugated bilirubin

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22
Q

___ is plasma insoluble. and free floats in the blood causing a yellow pigment to the skin called ___

A

unconjugated bilirubin

jaundice

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23
Q

free hemoglobin in the blood is called:

A

hemoglobinemia

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24
Q

too much hemoglobin being excreted in the urine is called ___

A

hemoglobinuria

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25
Q

defined at the abnormally low # of circulating RBC’s or hemoglobin

A

Anemia

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26
Q

manifestations of anemia depend on:

A
  • severity
  • rapidity of its development
  • underlying pathological mechanisms
  • persons age and health status
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27
Q

symptoms of anemia:

A

pallor- skin, mucous membranes, conjuctivate, nail beds

tachycardia &Palpitations- heart compensating for low O2

28
Q

premature death of RBC’s in bone marrow is called:

A

Hematopoiesis

29
Q

RBC count and hemoglobin provide info on:
while
RBC size, shape and color provide info on:

A

Severity of anemia

Cause of anemia

30
Q

Blood loss anemia can be: ___ or ___

A

acute or chronic

31
Q

acute blood loss affects:
while
chronic blood loss affects:

A

Intravascular volume: create cardiovascular shock or collapse

DOESN’T affect blood volume: leads to iron deficiency with depleted stores (GI bleed, menstrual)

32
Q

Disease characterized by premature destruction of RBC’s in blood circulation

A

hemolytic anemia

33
Q

hemolytic anemia triggers:

A

^ in Erythropoeiten production which creates an ^ # of reticulocytes floating in the blood.

34
Q

hemolytic anemia is characterized into two categories:

A
  1. Intrinsic- hereditary, something is wrong with inside of RBC
  2. Extrinsic- acquired factors like immune dysfunction, mechanical trauma, infections.
35
Q

In hemolytic anemia, the hemoglobin binds to __ and ___ to be carried back to liver.

A

haptoglobin
and
albumin

36
Q

RBC’s are made in the ___ and destroyed in the ___

A

bone marrow, spleen

37
Q

3 main causes of anemia:

A

1- blood loss
2- Hemolysis
3- Impaired RBC production

38
Q

Common types of anemia (3)

A

1- Iron deficiency- no hemoglobin present (pale cells)
2. Megaloblastic- DNA errors so cell gets too big
3- Sickle cell- gene mutation that causes change in structure ( collapse when O2 is not bound to them)

39
Q

3 common types of Hemolytic Anemia

A

1- membrane disorders (hereditary spherocytosis, acquired hemolytic newborn disease)

    • Hemoglobinopathies- sick cell, thalassemia (treat by taking spleen out)
    • G6PD deficiency
40
Q

Sickle Cell Anemia

A

inherited disorder where abnormal hemoglobin (HbS) leads to chronic hemolytic anemia, pain, and organ failure

41
Q

HbS gene-

A

transmitted by recessive inheritance. (heterozygote with 1 HbS gene) OR sickle cell disease (homozygous 2 HbS)

42
Q

HbS gene is caused by

A

mutation in B chain hemoglobin molecule

43
Q

2 major consequences or RBC sickling

A

1- Chronic Hemolytic Anemia- bc of sick structure, RBC’s only live for about 20 days

2.- Blood Vessel Occlusion- disrupts blood flow causing ischemia and pain.

44
Q

Factors associated with sickling and vessel occlusion:

A
  1. Dehydration- ^ hemoglobin concentration, attributes to polymerization and resultant sickling
  2. Acidosis- reduces affinity of hemoglobin to O2= more deoxygenated hemoglobin= sickling
  3. Hypoxia
45
Q

Symptoms of Sickle Cell Anemia
(1-2. caused by sickled cell death)
(3-5 caused by sickled cells blocking capillaries)

A
  1. Hyperbilirubinemia- breakdown of hemoglobin –> jaundice
  2. Pigment gallstones
  3. Prone to Infections- low blood flow, O2, congestion causes Asplenia
  4. Vaso-occlusive pain crisis
  5. Acute Chest Syndrome
46
Q

Vaso-occlusive pain crisis

Acute Chest Syndrome

A
  • common in abdomen, chest, bones, and joint. caused by ischemia to those areas.
- atypical pneumonia resulting from pulmonary infarction.
#1 cause of death in persons with sickle cell.
 * shortness of breath, fever, chest pain, cough.
47
Q

If your spleen is affected due to sickle cell, you are more common to get ___

A

infections.

more susceptible to certain bacterias, especially babies and kids!

48
Q

Sickle Cell Treatment (kids)

A
  1. Penicillin, updated vaccinations, specific pneumococcal vaccine
  2. Hydroxyuria- drug that inhibits DNA synthesis and can help prevent some complications
49
Q

Treatment for intense cases of sickle cell:

A
  1. bone marrow transplant
    (at risk for graft vs. host disease) bone marrow attacks the persons body bc they don’t have the same cell surface molecules that they’re used to.
50
Q

Hemolytic Anemia- Hemoglobinopathies

A
  • sickle cell disease & thalassemia

Thalassemia (different synthesis of 1 of the 2 chains)- deficiency of hemoglobin bc of this.
beta- more serious (Mediterranean)
alpha- less serious

51
Q

microsystic

hypocromic

A

small size

pale or low color

52
Q

Thalassemia (alpha)

A
  • defective gene for alpha chain synthesis
  • 1-4 defective genes
  • Affects both fetal and adult Hb
  • In fetus: gamma4 Hb may form
  • In adult: beta4 Hb may form
  • uneven hemoglobin synthesis
53
Q

Thalassemia (beta)

A

*more severe form- transfusion dependent. have to have transfusions or you cant carry O2.

  • > 100 defective gene mutations
  • Affects only adult Hb
  • Alpha4 Hb may form
54
Q

too much of alpha chain causes insoluble aggregation of RBC’s. this is called:

A

Heinz Bodies

55
Q

Hemolytic Anemia- G6PD deficiency

A
  • defective glucose 6 dihydrodrinase.
  • Defect in pathway that makes G6PD. which makes blood cells more susceptible to oxidative damage.
  • Causes damage to plasma membrane of cells- they burst!
  • Genetic disorder that is common in Males (X linked)
  • No treatment for it- DON’T TAKE Oxidative Drugs
56
Q

Anemias from Deficient RBC Production

A
  1. iron Deficiency Anemia
  2. Megaloblastic Anemia
  3. Aplastic Anemia
  4. Chronic Disease Anemias
57
Q

Iron Deficiency Anemia

A

Cause: blood loss(GI bleed, peptic ulcer) or deficient diet

  • low hemoglobin and hematocrit
  • low serum iron and ferritin
  • Hypochromic and microcytic erythrocytes
  • Poikilocytosis (irregular shape)
  • Anisocytosis (irregular size)
58
Q

Iron Deficiency Anemia Symptoms;

A

tired, out of breath, rapid HR, changes in color (waxy/pale), hair and nails are brittle, PIKA or neurological issues

59
Q

Megaloblastic Anemia

A

also called Pernicious Anemia
Causes: lack of Vitamin B12 and Folic Acid
- Impaired DNA synthesis –> enlarged RBC’s
- Erythrocytes are large, often with oval shape

60
Q

Vitamin B12

A

Needed for DNA synthesis and normal RBC maturation and division.

  • absorbed from animal poteins in mucosal lining of stomach.
  • when cells in stomach are damaged and can’t absorb B12: Atrophic Gastritis
61
Q

Folic Acid

A

Needed for DNA synthesis and maturation of RBC. the Cells get too big to be absorbed through GI tract.
* most common dietary deficiency

  • Causes: celiac disease, antipileptic disease.
62
Q

which type of deficiency is caused by pernicious anemia?

A

Vitamin B12

63
Q

Relative Polycythemia-

Absolute Polcythemia-

A
  • loss of plasma volume (dehydration)
  • increased RBC mass ( ^ in # of RBC’s)
    • Primary- Neoplastic- everything is increased red, white, hemoglobin
    • Secondary- ^ erythropoietin. (living at high altitudes, smoking, lung conditions)
64
Q

Age-Related Changes in Neonate RBC’s

A
  • red cells vary during first week, then drop (normal)
  • HbF turns to HbA transition (around 6 months- alpha gamma to alpha beta switch)
  • Anemia of prematurity- premi babies don’t have a lot of RBC’s to begin with. need to increase over time.
65
Q

Hyperbilirubinemia in Neonate

A
  • common cause of jaundice in neonate
  • risk of Kernicterus
  • Treatment with UV light- excites bilirubin turning it into a water soluble molecule to be removed.
66
Q

Kernicterus

A
  • untreated bilirubin leads to this in neonates*
  • unconjugated bilirubin is fat soluble not water. It crosses the blood/brain barrier and accumulates in brain cells causing brain damage.
  • lethargic, don’t feed well, behavior changes.
    _ leads to seizures, death, or long term brain damage.
67
Q

Hemolytic Disorders of the Newborn

A
  • Erythroblastosis Fetalis-
    • Rh+ babies born to Rh- mothers.
    • Immune response to invader of 2nd baby only
  • causes hemolysis or agglutination of babies RBC’s.

Patho (18 decks)

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