Exam 4: Hematologic Flashcards
1
Q
structure of hemoglobin
A
o each hgb molecule is composed of two pairs of polypeptide chains (the globins)
- 2 alpha
- 2 beta
**within every chain there is a heme chain, where it binds to iron ion
o four colorful complexes of iron plus protoporphyrin (the hemes)
responsible for blood’s ruby-red color and oxygen-carrying capacity
2
Q
what is oxyhemoglobin
A
Hgb picks up oxygen in the lungs and binds it to the iron ions
3
Q
what is deoxyhemoglobin
A
delivers oxygen to body tissues, becoming darker red
4
Q
how many O2 molecules are carried for every hgb?
A
four
5
Q
RBC structure: HbA
A
o 2 alpha, 2 beta chains
o Major adult Hgb
o About 97%
* most common
6
Q
RBC structure: HbA2
A
o We don’t know significance of having HbA2
o 2 alpha, 2 delta chains
o Minor adult Hgb
o About 2-3%
7
Q
RBC structure: HbF
A
o Major fetal Hgb: The majority of Hgb when we’re born, completely replaced by HgbA by six months of life
o Increased affinity to O2
o 2 alpha, 2 gamma chains
8
Q
RBC structure: Hgb S
A
o Quality dysfunction of beta (sickle trait/disease)
o Adult hgb -> HbF turns into HbS after 6months of age
9
Q
what happens to hgb after death?
A
o After 120 days, macrophages degrade erythrocyte
o Globin (the protein part of Hgb- the alpha/beta) is broken down into amino acids sent back to bone marrow ->alpha and beta chains are removed by kidneys
o Iron in heme portion is;
->stored in liver or spleen, as ferritin OR
-> returned to red bone marrow
o Non-iron portion of heme is degraded to biliverdin bilirubin -> liver ->secreted as bile -> excreted in feces and urine
10
Q
normal values: RBC
A
4.5-6
11
Q
normal value: Hgb
A
o >13 in men, >12 in women
o The measurement of mass hgb
12
Q
normal values: Hct
A
o 40-50 in men, 35-45 in women, USUALLY 3X HGB AMT
o Physical amount of space that the hgb occupies as a percentage of the whole that red cells occupy
13
Q
normal values: Mean Corpuscular Volume (MCV)
A
o 80-100 fl
o measurement of the average volume of an RBC
[tells you if RBC size is small, normal, or large- each one of these have diff kind of anemias]
o Used as a guide NOT to diagnose- should not be used to rule in or out a specific course of anemia!!
This is why—just because you have microcytic anemia, doesn’t mean you don’t have macrocytic.
14
Q
COLOR: Mean Corpuscular Hgb (MCH)
A
o 27-31
o Measurement for the amount of hgb per RBC
LOW means- pallor
15
Q
COLOR: Mean Corpuscular Hgb Concentration (MCHC)
A
o 32-36
o Measurement of hgb concentration per RBC
Deficient in iron, therefore will be pallor looking
hypochromic anemia most commonly seen in iron deficient anemia
16
Q
SIZE: RBC Distribution Width (RDW)
A
o An index of variation in RBC size and shape
Normally RBC size will differ by 11.5-15%
>15% = indicates cells differing in size – smaller or larger – when compared with older cells
* Indicates an evolving microcytic or macrocytic anemia!
17
Q
where is reticulocytes found and what is it?
A
o Found in the bone marrow, it is the final precursor to the formation of RBC
o The last immature form of RBC
18
Q
how long does reticulocytes stay in bone marrow?
A
o Leaves bone marrow after 3 days, enters bloodstream
19
Q
what happens to reticulocytes after 1 day in circulation?
A
they lose their ribosomal network and become mature RBC/erythrocytes
* In order to be able to carry O2 throughout the body
20
Q
is retic count a part of a CBC?
A
no. need to order separate.
21
Q
what is normal retic count?
A
Normal (0.5-2%)
22
Q
low retic count
A
LOW (<0.5%) -> think UNDERPRODUCTION and there is a component with production of RBC that is missing
** the bone marrow is not producing enough**
23
Q
high retic count
A
HIGH (>2%) think destruction/hemolysis or active bleeding is occurring
24
Q
why is ferritin also called acute phase reactant?
A
if theres an infection going on–>ferritin will increase, doesnt necessarily mean theres an iron deficiency
25
underproduction anemia: Microcytic
o MCV low (<80) – cells are smaller
o Low retic count – think underproduction
26
what are possible causes of microcytic anemia? (5)
Iron deficiency
inflammation (anemia of chronic disease)
Thalassemia
Sideroblastic- marrow produces ringed sideroblasts rather than healthy RBC’s secondary to genetic disorder vs myelodysplastic syndrome
Lead exposure
27
underproduction anemia: macrocytic
o “underproduction anemia”
o MCV high (>100) – cells are bigger
o Low retic count
o High MCH weight
28
what are the two groups of macrocytic anemia?
o Two groups-
Megaloblastic (abnormal shape of RBC, usually bigger in shape, and typically anemia of impaired DNA synthesis)
Nonmegaloblastic
29
what conditions will you see Megaloblastic in? (3)
Will see it in-
o B12 deficiency
o Folic acid deficiency
o antimetabolite drugs (methotrexate or zidovudine)
30
what conditions will you see Nonmegaloblastic in? (5)
* Will see it in-
o ETOH
o liver disease
o MDS
o Hypothyroidism – you check a TSH
o Meds- anti seizure, chemo drugs
31
what deficiency is macrocytic anemia typically present in?
typically in someone with vitamin B12 deficiency
32
underproduction anemia: normocytic
o “underproduction anemia”
o normal-sized red blood cells, but you have a low number of them
o MCV normal (80-100)
o Low retic count
33
underproduction anemia: normocytic possible causes
Inflammation
Malignancy
RBC aplasia secondary to;
* aplastic anemia
* suppression by parovirus B19
* medications
Hospitalized patient
* Dilutional from IVF in a small period of time
* Iatrogenic secondary to phlebotomy
Post hemorrhagic anemia is a normocytic-normochromic anemia (NNA) caused by acute blood loss
34
Anemia of Inflammation- Normocytic (6)
Elevated ferritin
* d/t iron isn’t an issue
normal or reduced TIBC
normal peripheral smear
NO classical presentation
Most common anemia in a hospitalized patient!
Acute or chronic immune activation
* Any disease or infectious state
35
Anemia of Inflammation- Normocytic possible causes
* Cytokine-induced leads to changes iron homeostasis
o [Cytokines-interferons, interleukins, tumor necrosis factor]
o Impaired proliferation and differential of erythroid progenitor cells
o Blunted erythropoietin response
o Increased erythrophagocytosis
* CKD/ESRD
o Lack erythropoietin and have marked inflammation- pts received EPO (these patients will be put on EPO 3x a week b/c their kidney cells arent producing EPO)
* Autoimmune diseases
o SLE, RA, vasculitis, sarcoidosis, and inflammatory bowel disease.
* Acute/chronic infections
* Cancer—with multiple cytopenia’s
o [think bone marrow infiltration secondary to leukemia, lymphoma, multiple myeloma, MDS, aplastic anemia]
* Endocrine diseases
* Liver disease
Treatment- TREAT THE UNDERLYING CHRONIC DISEASE
36
what are Macrocytic (megaloblastic) anemia
o are characterized by abnormally large erythroid precursors (megaloblasts) in the marrow that mature into large erythrocytes (macrocytes)
o cells are challenged to make DNA
however, RNA production proceeds normally.
o The cells have slow-maturing nuclei but have normal maturing cytoplasm.
o Therefore, megaloblastic erythroid precursors grow large before the larger nuclei become mature enough to signal division
causing the cell to be larger than normal
37
what are microcytic anemia
Characterized by abnormally small erythrocytes that contain unusually reduced amounts of hemoglobin.
The most common nutritional disorder of microcytic-hypochromic anemia—iron deficiency anemia
* Most common cause of anemia worldwide ^^
* Top two causes— Blood loss from GI or menstrual
* Other causes— Inadequate intake of meats (rare), Malabsorption with patients who have had gastrectomy, bariatric surgery procedures, celiac disease, IBS
o In smear they look small, fewer, and pallor
38
what is the most common cause of anemia worldwide?
iron deficiency microcytic anemia
39
the definition of anemia
- decreased in circulating RBC in the body, as reflected by a reduction in hgb, hct, and/or RBCs
o Hgb <14 males, <12 women
o Low oxygen capacity
There is not enough hgb available to carry the O2
o Anemia is NOT a disease; it is a condition.
YOU TREAT THE DISEASE that is causing the anemia!!!
40
what are the causes of anemia? (3)
Acute or chronic blood loss
Underproduction of RBCs by the bone marrow
Increased destruction of RBCs, “hemolysis”
41
definition for iron deficiency anemia
Microcytic anemia- underproduction!
A condition of too little iron in the body
Iron stores are depleted, and reduce hemoglobin synthesis
Develops slowly through three overlapping stages;
* stage I – body's iron stores are depleted. Erythropoiesis proceeds normally, with the hemoglobin content of erythrocytes remaining normal.
* stage II – iron transportation to bone marrow is diminished, resulting in iron-deficient erythropoiesis.
* stage III – begins when the small hemoglobin-deficient cells enter the circulation to replace the normal aged erythrocytes that have been removed from the circulation.
o The manifestations of IDA appear in stage III when there is depletion of iron stores and diminished hemoglobin production.
42
what are the three overlapping stages of iron deficiency anemia?
* stage I – body's iron stores are depleted. Erythropoiesis proceeds normally, with the hemoglobin content of erythrocytes remaining normal.
* stage II – iron transportation to bone marrow is diminished, resulting in iron-deficient erythropoiesis.
* stage III – begins when the small hemoglobin-deficient cells enter the circulation to replace the normal aged erythrocytes that have been removed from the circulation.
o The manifestations of IDA appear in stage III when there is depletion of iron stores and diminished hemoglobin production.
43
etiology of iron deficiency anemia
MOST COMMON CAUSE OF ANEMIA WORLDWIDE
* Top two causes— Blood loss from GI or menstrual
* Other causes— Inadequate intake of meats (rare), Malabsorption with patients who have had gastrectomy, bariatric surgery procedures, celiac disease, IBS
* increased requirement of iron
* medications that cause GI bleeding, eating disorders; PICA
44
iron deficiency risk factors (3)
Pregnancy with continuous blood loss in labor
Menorrhagia
H.pylori infections
45
lab findings: microcytic anemia: iron deficiency
Early-normal CBC, mild with Hgb 9-12
Low MCH, new cells are smaller and paler (hypochromic)
Low ferritin
* best measure of iron stores,
* also an acute phase reactant
o [with iron deficiency ferritin is low, it is also acute phase reactant- meaning when you have acute inflammation, it will INCREASE; so even though you have elevated ferritin levels, it could still mean you have iron deficiency anemia ALL ABOUT THE CLINICAL PICTURE]
Low reticulocyte count
* bone marrow doesn’t have enough iron to make red cells
High total iron binding capacity
* Not enough iron to bind to, but has a lot of capacity for it
Low serum iron <30
Poikilocytosis
* found on blood smear with abnormally shaped erythrocytes
Transferrin saturation < 16% (serum iron x 100/ TIBC)
Bone marrow biopsy with absence of iron stores (Gold Standard!!)
46
what is the gold standard at diagnosing anemia?
bone marrow biopsy
47
physical exam: iron deficiency anemia
-Fatigue
-irritable
-pagophagia (ice craving)
-pica
-koilonychia (thinning, flattening and then spooning of nail bed)
-hair loss
-glossitis
-stomatitis
-gastritis
-restless leg syndrome (often first sign)
48
what can too much blood transfusion lead to?
iron overload
49
definition: B12 deficiency
Anemia or nervous system injury from lower than normal amounts of vitamin B12
Megaloblastic anemia (macrocytic)
50
pathophysiology for B12 deficiency
B12 is a substrate required for RBC production
Dietary B12 is protein bound and released by peptic digestion of stomach (ileum)
B12 intrinsic factor binds to receptors in ileum where B12 is absorbed
* IF is an important factor in the gut, helps absorb
B12 important for DNA synthesis with folate
Decreased B12 can lead to demyelination of finer neurons with lead to neuro symptoms
* Can lead to irreversible damage but can be reversed if caught early enough
* [if your patient presents with neuro ss, think of vB12 deficiency this is because neuro ss can be at time irreversible]
Takes years to develop because liver has extensive stores of vB12
* B12 levels can be falsely low in folate deficiency, pregnancy, and use of oral contraception
* Levels can be falsely normal in myeloproliferative disorders, liver disease, and bacterial overgrowth syndromes
51
common causes: macrocytic anemia: B12 deficiency
B12 malabsorption from food:
* When B12 isn’t released from food proteins because of impaired acid peptic digestion
o Atrophic gastritis (chronic H pylori infections), gastric surgery, long term acid suppressing meds
o Meds:
PPI (diminish breakdown of B12 from food source)
* Always check a vB12, since are at risk!
metformin/neomycin… (decreases absorption of vB12)
o Malabsorption in terminal ileum secondary to resection, bypass, or Chron’s disease
Lack of intrinsic factor
* Secondary to gastrectomy
* pernicious anemia – type of megaloblastic anemia and is caused by vB12 deficiency, often associated with chronic atrophic (autoimmune) gastritis
o impairs the production of IF
o pernicious= highly injurious or destructive and reflects the fact that this condition was once fatal
o uncommon before 30, usually after 50
o 25% of patients have a fam hx of pernicious anemia and 10% have autoimmune thyroid disease
You test for the antibody, if it is + then they have pernicious anemia
Dietary deficiency
* Rare, unless they are true vegans or malnourished
* Since animal food is the primary natural source of B12, including milk, cheese, eggs, meat.
52
physical exam: B12 deficiency (3)
- Paresthesia/peripheral neuropathies,
- ataxia
- cognitive impairment
53
lab findings for B12 deficiency
Low reticulocyte count
Elevated MCV- macrocytic
Low B12
* less than 200-likely deficient
* 200-300 equivocal
* >300- likely ok (no pernicious anemia)
Intrinsic factor antibody
* + in pernicious anemia
Increased methylmalonic acid (MMA)*
* B12 helps convert methylmalonyl CoA to succinyl CoA
o in B12 deficiency methylmalonyl CoA converts to MMA instead
* Without B12, you will have increase in byproduct MMA which is a big indication for B12 deficiency
Increased homocysteine
* amino acid formed from the conversion of methionine to cysteine
* not as specific/sensitive as MMA test
* will also be elevated in folate deficiency and hypothyroidism
May have associated thrombocytopenia and neutropenia
Smear
* macro-ovalocytes, Howell jolly bodies, nucleated RBCs, hyper segmented neutrophils
Schilling’s test
* Checks B12 absorption but not common test, rarely used
54
complications/consequences for macrocytic anemia: B12 deficiency
Neurocognitive disorders
Encephalopathy
Myelopathy
Peripheral and optic neuropathy
Alzheimer disease
For Pernicious Anemia increased risk for gastric carcinoma. Untreated PA is fatal, usually because of HF
55
which anemia is common for alcoholics?
macrocytic anemia--folic deficiency
56
definiton: macrocytic anemia: folate deficiency
Deficiency in folic acid, results in a megaloblastic anemia (macrocytic)
Folate is an essential vitamin for RNA and DNA synthesis within the maturing erythrocyte
57
risk factors for folate deficiency anemia
Alcoholics – not having enough
Pregnant woman – needing more
Patients taking Medications that are antagonist to folic acid
58
causes of folate deficiency anemia
Most common cause of macrocytic anemia
Inadequate dietary intake
* especially in alcoholic patients
body stores only 4-5 months
absorption occurs in jejunum
* malabsorption is rare except in short bowel syndrome or bacterial overgrowth syndrome
increased demand in pregnancy, chronic hemolysis, leukemia
meds (methotrexate, phenytoin, sulfasalazine)
alcohol
* folate gets depleted with alcohol
59
physical exam: folate deficiency (8)
- diarrhea
- HA
- loss of appetite
- weight loss
- fatigue
- SOB
- dizziness
- pallor
60
lab findings: folate deficiency anemia (5)
Low retic count (because the ingredient to make folic acid isnt there to make reticulocytes)
elevated MCV and MCH
thrombocytopenia and neutropenia +
elevated homocysteine
* this one is MORE sensitive for folate deficiency
low RBC folate
61
Microcytic (iron deficiency)
Most common cause of anemia worldwide and usually from GI bleed or menses
Low ferritin and high TIBC
62
Normocytic anemia (of chronic disease)
Most common anemia of hospitalized pt
Cause of acute or chronic inflammation
Elevated ferritin, normal or reduced TIBC, normal smear
63
Macrocytic anemia (B12 and folic acid deficiency)-what are the caused by and what are the additional testings?
B12 deficiency is usually from poor absorption and will have neurological symptoms
Folic acid deficiency is usually caused by poor intake or pregnancy
Additional testing: IF antibody (pernicious anemia), MMA, and homocysteine
64
definition: sickle cell anemia
Disorder that causes RBC to become misshapen or break down
Identified at birth
* 6 months when HbS replaces fetal Hg
Confirmed by hgb electrophoresis*, CBC, retic count, and smear
* used to detect abnormal and variant Hgb like HbS
65
pathophysiology of sickle cell anemia
Caused by autosomal recessive single gene defect in beta chain of HbA, which results in sickle cell HbS
Crescent shaped/sickle cell Hgb can obstruct small blood capillaries causing painful crises, damage major organs and increase vulnerability to infections
* Replacement of both beta Hgb subunits with HbS is diagnostic for sickle cell anemia (genotype SS)
o Most severe
o Need both genes in order for it to be sickle cell
* Presence of 1 normal beta hgb subunit and 1 HbA is sickle cell trait (genotype AS)
o Child inherits HBS from one parent and normal HbA from the other
o Carrier state, not the actual disorder
66
lab studies: sickle cell anemia
Presence of nucleated RBC’s sickle shaped cells, and Howell-jolly bodies on smear
* Nucleated RBC will also falsely elevate WBC count if not corrected because sickled cells are read as WBCs
Normal iron studies
Elevated retic count
high MCV
elevated unconjugated bili
elevated LDH
low haptoglobin
67
types of crisis: sickle cell anemia (4)
Vaso-occlusive crises (pain)
Aplastic crisis
Sequestration crisis
Hyperhemolytic crisis
* Association with certain drugs/infections
68
concerns/complications: sickle cell anemia
Aplastic crisis is associated with fever, more profound anemia, and hemolysis and parovirus B19 is often the cause
Avascular necrosis of joints
Retinopathy, cholelithiasis, splenic sequestration and auto-splenectomy, liver disease from iron overload
* iron is being spat back into blood with the sickling
Acute chest syndrome (ARDS), pulm HTN, reactive airways
Type 4 renal tubular acidosis, proteinuria
Priapism
Ischemic/hemorrhagic stroke
INFECTION, a significant cause of mobidity/mortality
69
definition: hemolytic/hereditary: thalassemia
blood disorder involving less than normal amounts of an oxygen-carrying protein
diagnosed at a young age
inherited autosomal recessive disorder that causes an impaired synthesis of one of the two chains, alpha/beta
70
pathophysiology: thalassemia
Red cells are microcytic due to defective production of either alpha or beta globin chain
Resulting imbalance in globin subunit production leads to damage of the RBC membrane, resulting in ineffective erythropoiesis and hemolysis
71
pathophysiology for Alpha-thalassemia
Patho:
* Most common
* Common in Asian (68%), African (30%), and Mediterranean (5-10%)
* 4 genes will determine synthesis of alpha chain
o any variation of 4 alpha
* ¼ abnormal: silent carrier-
o usually asymptomatic, clinically normal
* 2/4: alpha thalassemia minor (trait)-
o mild microcytic anemia
* ¾: alpha thalassemia intermedia (HbH disease)-
o chronic anemia, pallor, hepatosplenomegaly, frontal and maxilla body overgrowth, pathologic fractures, pigmented gallstones (full of unconjugated bili), iron overload
* 4/4: alpha thalassemia major hydrops fetalis-
o associated with stillbirth or death shortly after birth
o causes congestive HF intrauterine
** A thalassemia is an inherited blood disorder. It causes the body to make less hemoglobin than normal. There are 4 different types of alpha thalassemia. This condition causes mild to severe anemia, based on the type of alpha thalassemia that is inherited.
an inherited blood disorder in which the body doesn't make as much alpha globin
72
lab findings: Alpha-thalassemia
* Smear with hypochromia, microcytic, target cells, red cell fragments, basophilic stippling
* Normal or increased RBC count
* Normal or increased iron and iron stores
* Hgb can be as low as 3-6
73
patho:o Beta- thalassemia
* Genetic syndrome of ineffective erythropoiesis caused by mutations of the beta-globin gene and no production of the beta chain, which leads to absent HgbA
o This leads to excess alpha-chains
* Found in Mediterranean, African, Indian, and Asian ancestry
74
Beta thalassemia minor (trait)
o only one gene defective leading to about 50% decrease in beta-chain synthesis
o usually asymptomatic, mild microcytic anemia
75
Beta thalassemia Intermedia
o about 90% HgbA with increased HgbA2 (alpha, delta, and gamma chains) and Hgb F
similar presentation as major but as a toddler or child with milder symptoms
o Associated with anemia, hepatosplenomegaly and body disease
*two of the genes are affected*
76
* Beta thalassemia Major (Cooly’s anemia)-
o usually asymptomatic at birth, due to presence of fetal HbF but symptomatic at 6 months with decline of HgbF
o Deficient beta chains leads to excess alpha chains not able to form tetramers, leads to ineffective erythropoiesis, erythroid hyperplasia and extramedullary hematopoiesis
frontal bossing and maxillary overgrowth
o Hepatosplenomegaly, severe hemolytic anemia (jaundice, dyspnea, pallor), osteopenia and stunted growth, iron overload, pigmented gallstones
77
lab findings: beta thalassemia
* Low Hgb/HCT
* low MCV
* normal/elevated retic count
* increased RBC
* Smear will show;
o microcytic red cells, tear drops, microspherocytes, target cells, many nucleated red cells
* Major will show;
o minimal to no HbA,
o elevated HbF and HbA2
* Normal iron studies
78
DESTRUCTION/HEMOLYTIC TYPE OF ANEMIAS
o No classic presentation
o anemia with elevated retic count
o Two types of Hemolytic Anemia intrinsic and extrinsic
79
destruction/hemolytic anemia: intrinsic/heredity etiology
* Enzyme defects such as pyruvate kinase or glucose-6 phosphate dehydrogenase (G6PD) deficiency
* Hemoglobinopathies like sickle cell anemia and Thalassemia
* RBC membrane abnormalities, such as spherocytosis
80
destruction/hemolytic anemia: extrinsic/etiology
an acute process or medication causing this
* Autoimmune hemolytic anemia
* Disseminated Intravascular Coagulation (DIC)
o Concomitant thrombocytopenia and coagulopathy
prolonged PT, decreased fibrinogen, elevated D-dimer, decreased factors V, VIII, X, XIII
o Can find purpura and/or petechiae from thrombocytopenia
* Thrombotic Thrombocytopenic Purpura (TTP)
o Concomitant thrombocytopenia, renal insufficiency, neurological symptoms
* Hemolytic Uremic Syndrome (HUS)
o Concomitant thrombocytopenia, renal insufficiency, neurological symptoms
* Paroxysmal nocturnal hemoglobinuria
* Hypersplensim
* Traumatic (something is injuring the RBC)
o Impact
o Macrovascular shearing secondary to prosthetic valve (literally cutting those RBCs-->the cells are lysing and being shattered which is causing the anemia)
o Microvascular (the irritation to the lining of the vessels-from medication, acute process, or a new cancer dx) (DIC, TTP, HUS)
* Toxins- snake venom and aniline dyes
81
patho: DESTRUCTION/HEMOLYTIC TYPE OF ANEMIAS
During hemolysis, RBC products are released into the circulation and their presence can be measures to support the dx of hemolysis
82
lab findings: DESTRUCTION/HEMOLYTIC TYPE OF ANEMIAS (6)
Elevated Lactate dehydrogenase (LDH):
* enzyme found in RBCs (also the muscle, brain, liver, and kidneys
* Released with cell damage., it is a byproduct released from lysis of RBC
* Also elevated in liver disease and other disease process (pancreatitis, CHF, malignancy, skeletal muscle disease, medications )
Elevated reticulocyte count: RBC are being destroyed in the circulation, the body will compensate and the bone marrow will try to generate more RBC and the reticulocyte is the immature RBC)
Low Haptoglobin
* acute phase reactant protein made by the liver.
* Primary function is to preserve iron by irreversibly binding free hemoglobin from lysed RBCs.
o With increased LDH, 90% specific for hemolysis--- haptoglobin production is exhausted from responding to the lysed RBCs
Elevated Indirect Bilirubin
* measure of unconjugated bilirubin.
* Heme breakdown into unconjugated/indirect bilirubin.
o In liver, unconjugated/indirect bilirubin conjugates to glucuronic acid to form conjugated/direct bilirubin and excreted via biliary system to small intestines and out with feces.
* Overwhelmed liver unable to conjugate and can lead to jaundice.
Positive Direct Coombs/Direct Antiglobulin Test (DAT)
* detects IgG/IgM antibody on the surface of the RBC, found in autoimmune hemolytic anemia
o aid in the processing and removal of immune complexes
Positive schistocytes on peripheral smear
* Fragmented RBCs found in traumatic hemolysis
* Destruction can occur in the spleen, liver or small blood vessels
o i.e. small vessel thrombosis in DIC, TTP, HUS
83
define Hematopoiesis
the production of blood cells
84
define erythropoiesis and where does it occur
the production of erythrocytes (RBC)
occurs mostly in the bone marrow in flat bones of pelvis, vertebrae, cranium/mandible, sternum, ribs, and proximal portions of the humerus and femur.
85
what are the requirements for RBC production
Amino Acids, copper, cobalt, Vitamin B (2,3,6,12), folate, Iron, and Vitamin E
When there isn’t enough of any one of these, we start running into problems with anemia
86
pathophysiology: RBC production
Production of RBC is stimulated by the hormone erythropoietin
* hormone secreted by the kidneys, when decreased oxygen is detected either from;
o decreased oxygen content in the blood
o decreased blood flow
o decreased hemoglobin
i.e. sepsis, dehydration, acute blood loss
When EPO stimulates the production of erythrocytes iron is released from storage (mostly from bone marrow, liver, and spleen), binds to transferrin, carried to the red marrow where it attaches to erythrocyte precursors
87
Relate hemoglobin and hematocrit values
* Hemoglobin: g/dL whole blood, measurement of mass Hgb
o Normal range= >13 in men >12 in women
* Hematocrit: % whole blood with intact RBCs, physical amount of space that the hgb occupies as a percentage of the whole that red cells occupy
o Normal range: 40-50 in men, 35-45 in women
o Usually 3x the hgb count
88
describe thrombocytopenia
Thrombocytopenia: a condition in which there is a lower than normal number of platelets in the blood
o Normal platelet count : 150,000-450,000
89
clinical manifestations of thrombocytopenia
o Easy or excessive bleeding (purpura)
o Superficial bleeding into the skin that appears as a rash of pinpoint sized reddish-purple spots (petechiae), usually on the lower legs
o Prolonged bleeding from cuts
o Blood in urine or stools
o Bleeding from your gums or nose
o Unusually heavy menstrual flows
o Fatigue
o Enlarged spleen
90
define Poikilocytosis and for which anemia is it found in
a term that refers to the presence of abnormally shaped red blood cells
o It is found on blood smear with abnormally shaped erythrocytes for microcytic anemia-iron deficiency
91
define Schistocytes
are red blood cell fragments; the presence of this suggest red blood cell injury from the endothelium
o In destruction/hemolytic anemias- positive schistocytes are found on a peripheral smear
o Fragmented RBCs found in traumatic hemolysis
o Used in diagnosis of DIC, TTP, HUS
