Blood Pathology-Anemia- Bickmen Flashcards
1
Q
Normal red blood cells, why are they paler in the center ?
A
Biconcave shape (on both sides)
becasue the cell has very little organelles
2
Q
Complete Blood Count (CBC)
A
essential in determining the nature of a blood disorder
- RBC
- Hemoglobin (more –> reder)
- Heatocrit (ratio of RBC 50%)
3
Q
MCV
A
mean corpuscular volume
(too small)microcytic–> normocytic–>macrocytic (too big)
cytic= size
4
Q
MCHC
A
Mean corpuscular hemoglobin concentration
Hypochromic (lack of hemoglobin)
normochromic
5
Q
anisocytosis
A
size variaiton
6
Q
poikilocytosis
A
shape variation of RBC
7
Q
Anemia
A
“without blood”
a reduction below normal in hemoglobin or RBC #
8
Q
Symptoms of Anemia
A
Pale skin, mucous membranes
Jaundice (if hemolytic)
Breathlessness
Tachycardia
Dizziness
Fatigue
9
Q
anemia causes
A
- Blood loss
- Excessive RBC destruction
- Insufficient RBC production
10
Q
Excessive RBC destruction
A
Extracorpuscular reasons
Intracorpuscular reasons
11
Q
Insufficient RBC production
A
too little material
too few erythroblasts
not enough room
12
Q
Anemia
blood loss
A
cause: trauma resulting in acute blood loss
* after 2-3 days reticulocyte spike (normal 1%)
13
Q
Reticulocytes
A
develop and amture in the red bone marrow and then circulate for about a day in the blood before developin into mature erythroctes
(kidneys release erthropotein to induce the relase of Red bone marrow)
14
Q
Hemolytic Anemias
Signs of destruction
A
Increased bilirubin
Increased LDH (lactate dehydrogenase)
Reduced haptoglobin
Extracorpuscular
15
Q
Hemolytic Anemias
Signs of Production
A
increased reticulocutes
nucleated red cells in blood
Intracorpuscular
16
Q
Erythrocytes Destruction
A
- Life span of RBC is about 120 days
- RBC destroyed by resident macrophages in spleen and liver
17
Q
RBC recyling
A
- Globin (into AA)
- Heme (Iron-containing part)
- Remainder converted to bilirubin
18
Q
Iron used in
A
variousn tissues
- Liver
- spleen
- bone marrow
19
Q
Unconjugated bilirubin
A
- Is toxic
- “Bilirubin+Albumin” (water insoluble)
- Lipid soluble
- Damage cell membranes
20
Q
Bilirubin Eliminaiton
A
- Unconjugated bilirubin is taken up by the liver
- Conjugated via glucuronyl transferase
- conjugated bilirubin is excreted with the bile to the small intestine
21
Q
How is bilirubin eliminated from the body
A
as fecal material
22
Q
what conjugates bilirubin
A
glucuronyl transferse
23
Q
Some bilirubin in the intestine is converted to_____ by _________
A
urobilinogen by intestinal bacteria
24
Q
Urobilinogen can be reabsorbed into the blood where
A
the liver can vurther metabolize it and excrete it as bile
25
small amounts of urobilinogen are excreted from the body to
to the kidneys in the urine
26
Jaundice
Excess biliruben accumulation in the body
* Skin
* nail beds
* whites of the eye --\>yellow
27
jaundice two causes
excess bilirubin produciton
decreased bilirubin excretion
28
Excess bilirubin production
Jaundice
due to RBC destruciton
surpasses livers ability to conjugate
29
Decreased bilirubin excretion
Jaundice
3
1. Reduced hepatic uptake (hepatitis, cirrhosis)
2. Decreased conjugation (hepatitis, cirrhosis, enzyme deficiency)
3. Bile duct obstruction (tumor, stone)
30
Bilirubin very toxic to
brain cells
31
Jaundice treatment
* Treat cause of condition
* Blood transfusion
* Sun
32
Light or clay colored feces and dark urine
Extrahepatic obstructive jaundice
obstruction of bile duct
(outlet for billirubin is urine)
33
Normal to light colored feces and light colored urine
Intrahepatic obstructive jaundice
damaged hepatocytes
(hepatitis, cirosisi)
34
Dark feces and urine
Hemolytic anemia
everything is working but you just have too much
35
Besides color feces and urine what other techniques are used to diagnosis Jaundice
x-ray
ct scan
liver biopsy
(help determine stones, tumor, or cirrosis)
36
A 63-year-old man has been an alcoholic for 30 years. His skin and eyes have a yellowish coloring. He is now most likely suffering from what:
A. Prehepatic jaundice
B. Intrahepatic obstructive jaundice
C. Extrahepatic obstructive jaundice
D. Hemolytic jaundice
B
(urine and feces are both light)
37
Mircoangiopathic Hemolytic Anemia
Extracorpuscular (something is physically damaging the RBC)
* Physical trauma to red cells
* Schistocytes
38
Schistocytes
RBC fragments
39
Microangiopathic Hemolytic Anemia
Causes
Causes
* Artificial heart valve
* Malignancy
* Obstetric complications
* Sepsis
* Trauma
40
Autoimmune Hemolytic Anemia
**Extracorpuscular - Abs attack RBC**
**w**arm
* IgG
* Spleen
* Spherocytes
Cold
* IgM, Complement
* Intravascular hemolysis
* Agglutination
41
Autoimmune Hemplytic Anemia is based on
temp
IgG is more active at higher temps
IgM (C3b) more active at lower temps
(gives rise of where the anemia is happening)
42
Sickle cell anemia
**Intracorpuscular**
* Hemoglobinopathy
* Single aa substitution in β chain (Val for Glut Acid)
* -/+ vs. +/+
* African ethnicity
43
sickles causes
* clog vessels and are fragile
* Infarcted spleen with HbS
44
Thalassemia
**Intracorpiscular Hemolytic Anemia -point mutation**
* Can’t make enough α or β chain
* Hypochromic, microcytic anemia
* Increased RBC synthesis (EPO)
45
Thalassemia
alpha:
beta:
α: SE Asian
β: Mediterranean
46
Thalassemia, clinical manifestations
medullary expanision due to increased erythropoiesis
47
Herditary Spherocytosis
* Many spherocytes (round ball shape)
* Caused by a spectrin defect
* Splenectomy is curative
48
Hereditary Spherocytosis RBCs
form polymers and get entrapped in spleen causing Splenomegaly
49
Howell-Jolly Bodies
Evidence of markedly decreased splenic function
**(intracorpuscular hemolytic anemia)**
excessive RBC destruction
50
G6PD Deficiency
intracorpuscular
* decrease G6PD --\> increase peroxide--\> cell lysi
* ROS exposure kills RBCs
* Devlopment/removal of Heinz bodies
51
G6PDH deficiency causes a loss in
glutathione
52
what happens if there is a loss of glutathione?
build up radical peroxide which damages lipids and dna
53
Heinz bodies
globin denatures, sticks to RBC membrane
forms bite cells
54
what are the symptoms and triggers of Intracorpuscular
* some asymptomatic other episodes
* triggers: drugs or fava beans
55
insufficient RBC produciton
*too little material*
anemia
1. Iron deficiency
2. Chronic disease
3. Megaloblastic
56
Insufficient RBC production
*too few erythroblasts*
anemia
aplastic anemia
57
Insufficient RBC production
*not enought room*
anemia
Myelophthisic anemia
58
Iron deficiency anemia
manifestations
**Mircocytic, hypochromic anemia**
* atrophic glossitis
* koilonychia
59
Iron dieficiency anemia causes
* **Decreased iron intake**
* Poor diet
* Poor absorption
* **Increased iron loss**
* GI bleeding
* Menses
* Hemorrhage
* **Increased iron requirement**--\>Pregnancy
60
Anemia of chronic disease
causes
**Normochromic, normocytic anemia**
Cause:
Distrupted iron metabolism → moree hepcidin in liver
61
Megalblastic Anemia
causes
**Normochromic, macrocytic anemia**
* *reduced B12/folate in the body (need to split the cell)*
* inadequate absorption through insufficient Intrinsic Factor
62
Pernicious anemia
cause
treatment
* decrease RBC synthesis due to low Vitamin B12 in body ( bc low intrinsic factor)
* treatment B12 injections
type of Megablastic anemia
63
Clinical manifestaions of Pernicious Anemia
low levels of B12 in the blood and low uptake of B12 from intestine
disease develops slowly due to large stores of B12 in liver
64
B12 deficiency generally due to lack of intrinsic factor caused by:
* Autoimmune disease of stomach
* GI surgery (e.g., gastric bypass surgery)
* Chronic gastritis
65
Megaloblastic Anemia histological manifestations
large oval shaped RBC
Hypersegmented neutrophils
66
Schilling Test
A clinical test to determine whether a patient has pernicious anemia
(via B12 absorption)
67
Aplastic anemia
causes
Normochromic, normocytic anemia
* Idiopathic
* Drugs/chemicals
* Viruses
* Pregnancy
* Fanconi anemia (DNA damage)
68
Aplastic anemia
histological manifestations
* pancytopenia (deficency of all blood cells)
* Hypoplastic(empty) bone marrow
* bleeding and compromised immune function
69
Myelophthisic Anemia
causes
**Normochromic, Normocytic amenia**
* infilatration of one marrow by tumors or fibrosis
* possible pancytopenia
70
Myelopthisic anemia histology
tear-dropped shaped RBX (dacryocytes)
71
In sickle cell anemia, the globin portion of the molecule is abnormal due to the amino acid valine being substituted for which of the following amino acids?
A.Glutamine
B.Glutamic acid
C.Aspartic acid
D.Glycine
B
72
From the following list select the THREE items associated with the normocytic classification of anemia.
A.Iron deficiency
B.Thalassemias
C.Aplastic anemia
D.Anemia of chronic disease
E.Liver disease
F.Vitamin B12 and folate deficiency
G.Acute and chronic blood loss
C,D,G
a,b(microcytic)
73
The Schilling test may be used to detect:
A.Folate deficiency
B.Aplastic anemia
C.Pernicious anemia
D.Myelophthisic anemia
C
