Chapter 13 Flashcards
(67 cards)
1
Q
2 types of hemoglobin
A
adult (HbA)- adults and children > 6 months
fetal (HbF)- 3-9 months in fetus
2
Q
Adult hemoglobin (HbA)
A
2 alpha chains
2 beta chains
adults and children > 6 months old
3
Q
Fetal Hemoglobin
A
2 alpha chains
2 GAMMA chains
have ^ O2 affinity, takes from mom
predominant 3-9 months gestation
4
Q
how many molecules of O2 can be carried by one hemoglobin?
A
4
5
Q
How much hemoglobin we make, depends on how much ___ we have
A
iron
6
Q
65% of iron can be found in the ___
A
hemoglobin (circulating)
7
Q
15-30% of iron can be found stored in the ___
A
liver
&
reticuloendothelial cells of BONE MARROW
8
Q
“where RBC’s go to die”
A
spleen
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
10
Q
iron is typically derived from ___ and absorbed in the ___ .
A
meat small intestine (duodenum)
11
Q
an incomplete, non function protein that turns into transferin when iron gets absorbed into duodenum.
A
Apotransferin
12
Q
refers to the production of RBC
A
Erythropoeitin
13
Q
erythropoesis is stimulated by?
A
low O2
14
Q
Erythropoeitin is made where and stimulated into action where?
A
kidney
Bone marrow- stimulated stem cells to create hemocytoblasts –> proerythroblasts
15
Q
RBC’s last about ____
A
120 days
16
Q
why do RBC’s only last a short amount of time? (2)
A
- metabolic activity decreased with age (creates weakened cell membranes)
- eventually, RBC’s break as they squeeze through spleen capillaries (don’t have strong cell membrane)
17
Q
If old and Damaged, RBC’s get phagocytized by cells from the:
A
liver, spleen, bone marrow, lymph nodes
18
Q
when RBCs are destroyed, the heme…
A
gets converted into bilirubin (bile pigment)
19
Q
when rbc’s die, ____ takes the___to the liver where its stored as Ferin.
A
transferin, iron
20
Q
Bilirubin is removed from the blood as ____ or _____.
A
conjucated bilirubin
or
unconjucated bilirubin
21
Q
_____ attaches to glucocorinide which makes it soluble in plasma and can be excreted in bile.
A
Conjugated bilirubin
22
Q
___ is plasma insoluble. and free floats in the blood causing a yellow pigment to the skin called ___
A
unconjugated bilirubin
jaundice
23
Q
free hemoglobin in the blood is called:
A
hemoglobinemia
24
Q
too much hemoglobin being excreted in the urine is called ___
A
hemoglobinuria
25
defined at the abnormally low # of circulating RBC's or hemoglobin
Anemia
26
manifestations of anemia depend on:
- severity
- rapidity of its development
- underlying pathological mechanisms
- persons age and health status
27
symptoms of anemia:
pallor- skin, mucous membranes, conjuctivate, nail beds
| tachycardia &Palpitations- heart compensating for low O2
28
premature death of RBC's in bone marrow is called:
Hematopoiesis
29
RBC count and hemoglobin provide info on:
while
RBC size, shape and color provide info on:
Severity of anemia
| Cause of anemia
30
Blood loss anemia can be: ___ or ___
acute or chronic
31
acute blood loss affects:
while
chronic blood loss affects:
Intravascular volume: create cardiovascular shock or collapse
DOESN'T affect blood volume: leads to iron deficiency with depleted stores (GI bleed, menstrual)
32
Disease characterized by premature destruction of RBC's in blood circulation
hemolytic anemia
33
hemolytic anemia triggers:
^ in Erythropoeiten production which creates an ^ # of reticulocytes floating in the blood.
34
hemolytic anemia is characterized into two categories:
1. Intrinsic- hereditary, something is wrong with inside of RBC
2. Extrinsic- acquired factors like immune dysfunction, mechanical trauma, infections.
35
In hemolytic anemia, the hemoglobin binds to __ and ___ to be carried back to liver.
haptoglobin
and
albumin
36
RBC's are made in the ___ and destroyed in the ___
bone marrow, spleen
37
3 main causes of anemia:
1- blood loss
2- Hemolysis
3- Impaired RBC production
38
Common types of anemia (3)
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
3 common types of Hemolytic Anemia
1- membrane disorders (hereditary spherocytosis, acquired hemolytic newborn disease)
2. - Hemoglobinopathies- sick cell, thalassemia (treat by taking spleen out)
3. - G6PD deficiency
40
Sickle Cell Anemia
inherited disorder where abnormal hemoglobin (HbS) leads to chronic hemolytic anemia, pain, and organ failure
41
HbS gene-
transmitted by recessive inheritance. (heterozygote with 1 HbS gene) OR sickle cell disease (homozygous 2 HbS)
42
HbS gene is caused by
mutation in B chain hemoglobin molecule
43
2 major consequences or RBC sickling
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
Factors associated with sickling and vessel occlusion:
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
Symptoms of Sickle Cell Anemia
(1-2. caused by sickled cell death)
(3-5 caused by sickled cells blocking capillaries)
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
Vaso-occlusive pain crisis
| Acute Chest Syndrome
- 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
If your spleen is affected due to sickle cell, you are more common to get ___
infections.
| more susceptible to certain bacterias, especially babies and kids!
48
Sickle Cell Treatment (kids)
1. Penicillin, updated vaccinations, specific pneumococcal vaccine
2. Hydroxyuria- drug that inhibits DNA synthesis and can help prevent some complications
49
Treatment for intense cases of sickle cell:
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
Hemolytic Anemia- Hemoglobinopathies
* 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
microsystic
| hypocromic
small size
| pale or low color
52
Thalassemia (alpha)
- 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
Thalassemia (beta)
*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
too much of alpha chain causes insoluble aggregation of RBC's. this is called:
Heinz Bodies
55
Hemolytic Anemia- G6PD deficiency
- 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
Anemias from Deficient RBC Production
1. iron Deficiency Anemia
2. Megaloblastic Anemia
3. Aplastic Anemia
4. Chronic Disease Anemias
57
Iron Deficiency Anemia
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
Iron Deficiency Anemia Symptoms;
tired, out of breath, rapid HR, changes in color (waxy/pale), hair and nails are brittle, PIKA or neurological issues
59
Megaloblastic Anemia
*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
Vitamin B12
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
Folic Acid
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
which type of deficiency is caused by pernicious anemia?
Vitamin B12
63
Relative Polycythemia-
| Absolute Polcythemia-
- 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
Age-Related Changes in Neonate RBC's
* 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
Hyperbilirubinemia in Neonate
- 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
Kernicterus
* 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
Hemolytic Disorders of the Newborn
* Erythroblastosis Fetalis-
- Rh+ babies born to Rh- mothers.
- Immune response to invader of 2nd baby only
* causes hemolysis or agglutination of babies RBC's.
