MOD 5 Hematologic System Flashcards
Bone Marrow creates
The bone marrow stem cells differentiate into:
Red blood cell (erythrocytes)
White blood cell (leukocytes)
Platelet (thrombocytes)
CBC lab test do what
CBC lab test is a panel of tests that evaluates the red blood cells, white blood cells and platelets
RBC normal value
3.6-5.4
Hematocrit count
37-50%
Hemoglobin count
12-16.5
WBC
5,000-10,000
Neutrophil count
47-63%
Lymphocytes count
24-40%
Platelet count
150,000-400,000
CBC (complete blood count)
Helps diagnose conditions, such as anemia, infection, inflammation, bleeding disorder, or leukemia
Monitor the condition and or effectiveness of treatment after a diagnosis is established
Monitor treatment that is known to affect blood cells, such as chemotherapy or radiation
RBC
red blood cell count, a count of the actually number of RBC’s in a person’s sample of blood
Hematocrit
measures the percentage of a person’s blood that consists of red blood cells
Critically low HCT
<15% leads to heart failure
*Fluid Overload
Low HCT means what
The patient is losing blood (either internally or externally)
Critically high HCT
> 60% leads to blood clotting problems
caused by *dehydration
HCT is affected by what
the person’s fluid status
HCT is used to asses what
a person’s fluid status and how well they are responding to fluid replacement treatment
What test is HCT ordered with
HCT is often ordered with a hemoglobin test (H&H) to verify the accuracy of the HCT if BOTH the Hct and Hgb are decreased = blood loss
Hemoglobin measures what
The *amount of oxygen-carrying protein in the blood. Measured in grams.
Reticulocyte count measures what
The absolute count or percentage of *immature red blood cells in blood (if elevated it means that mature RBCs are depleted and the body is now relying on immature RBC’s
Red Blood cells indices are what
Calculations that provide information on the physical characteristics of the RBC’s (MCV, MCH, MCHC, RDW) RBC indices lab tests are used to determine if a person has anemia
-used to diagnose types of anemia
MCV
mean corpuscular volume (measurement of the average size of RBC’s
MCH
Mean corpuscular hemoglobin (calculation of the average amount of oxygen-carrying hemoglobin inside a red blood cell)
MCHC
Mean corpuscular hemoglobin concentration (calculation fo the average percentage of hemoglobin inside a red cell)
RDW
Red cell distribution width (calculation of the variation in the size of RBCs)
Red Blood cell count is ELEVATED in the following conditions (polycythemia)
Cardiovascular disease
stress
polycythemia
smokers
high altitude
hemoconcentration and dehydration
renal cell carcinoma
Red Blood cell count is DECREASED in the following conditions (anemia)
ANEMIAS
HEMORRHAGE
hemolysis
chronic renal failure
failure of marrow production
Anemia
NOT ENOUGH RBC’s
Clinical manifestations common to ALL anemias
Low hemoglobin and hematocrit levels in addition to reduced RBC’s
Plasma expansion “watery” blood, i.e., less viscous blood. This causes more turbulent blood flow, and “pale” look of blood
Test anemia by
checking inside of person’s mouth for pale colored mucosa and gums
S/S of anemia are a result of what
HYPOXIA (low oxygen levels in blood)
Causes:
Fatigue
tachypnea
tachycardia
pallor
Causes of anemia
blood loss
excessive RBC destruction
Decreased or faulty RBC production
decreased or faulty RBCs
Anemia due to blood loss
gastrointestinal (GI) conditions, upper or lower GI bleeds
NSAID overuse (risk factor; patients with chronic pain)
Excessive menstruation or childbirth complications
Anemia due to excessive RBC destruction
Hemolytic Anemias
RBCs die quicker than the bone marrow can replace them. Causes intrinsic (inherited defective RBCs) or Extrinsic (everything else)
-inherited: sickle cell and thalassemia
-stressors: infections drugs snake or spider venom
-toxins: advanced liver or kidney disease
-autoimmune: antibody-mediated lupus cancer rh fact or drugs.
-Spleen: blood moves more slowly through an enlarged spleen, causing RBCs to become prematurely destroyed before they get through the spleen
Decreased or faulty RBC production
-Nutritional Deficiencies: Iron, Vitamin B-12, and folate are necessary components of RBC production
-Bone marrow and stem cell problems: leukemia and lymphoma are examples. Also, aplastic anemia*
-Sickle cell anemia
Other conditions associated with decreased or faulty RBCs
Advanced kidney disease
-Hypothyroidism: cause lowered iron levels in the blood
-Chronic diseases: inflammation causes production of cytokines that then destroy all blood cells including erythrocytes
Kidney Connection
Erythropoietin (made in kidneys) signals bone marrow to make ore RBCs so if kidneys are damaged erythropoietin is not excreted and RBCs are not made
Erythropoietin injections
Given to patients with severe anemia caused by kidney failure or bone marrow failure
These injections increase RBC production and may eliminate the need for a blood transfusion
Three vitamins/minerals required to produce RBCs
Iron, Vitamin B-12, Folate
Iron deficiencies caused by
lack of iron in diet or blood loss
Examples:
-metabolic demands of pregnancy and breastfeeding
-blood loss through excessive menstruation, childbirth, or blood
-digestive conditions (crohn’s) Or removal of stomach/ small intestines
-medications, excess caffeine
S/S of iron deficiency anemia
“lightheaded”, dizzy, stomatitis, difficulty swallowing, headache, confusion, memory loss
Iron replacement
Mineral supplements/ iron injections; foods - soybeans, lentils and beans, red meat, chicken, fish, fortified foods
Cobalamin
(vitamin B-12) is a necessary vitamin required to make RBCs
Low Vitamin B-12 levels caused by
Dietary: eating little or no meat may cause a lack of B-12
Lack of intrinsic factor: Intrinsic factor (protein excreted by the stomach) is needed for vitamin b12 absorption. if the stomach/upper intestine is damaged or removed, the intrinsic factor is not secreted, so there is no absorption of vit b-12.
a) conditions causing lack of IF are Crohn’s disease, gastric bypass, cancer
b) lifelong b12 replacement injections*
Folate Vit-B-9
Also called folic acid, this key element is an integral part of cell growth, especially RBCs.
Low folate levels are caused by
1- overcooking or eating too few vegetables may cause folate deficiency
2- other: pregnancy, medications, alcohol abuse, intestinal disease
Aplastic Anemia
destruction of bone marrow stem cells. Damaged BM is diagnosed as either aplastic or hypoplastic. causes pancytopenia = ALL blood cells are depressed
Aplastic
meaning that its empty
Hypoplastic
Contains very few blood cells
Aplastic Anemia develops because
of bone marrow damage. the damage may be present at birth or occur after exposure to radiation, chemotherapy, autoimmune disease, toxic chemicals, some drugs, or infection
Viruses linked to aplastic anemia
hepatitis, epstein barr, cytomegalovirus, parovirus B19 and HIV
S/S of Aplastic Anemia
may develop slowly or suddenly
-fatigue and rapid heart rate (due to low RBCs)
-frequent infections (due to low WBCs)
-Bleeding tendencies (due to low platelets) as evidenced by bleeding gums/nose bleeds/ petechiae, easy bruising, heavy, menstrual cycle, G.I. bleeding, etc.
Treatment for Aplastic anemia
Medications, blood transfusions, and stem-cell transplants
Sickle Cell anemia
An autosomal recessive defect of hemoglobin
is the most common inherited blood disorder in the US. Individuals with a single defective gene have sickle cell “trait” while those with 2 defective genes have sickle cell “disease”
treatment options for sickle cell anemia
There are several drug therapies and bone marrow transplants available (with complications of rejection i.e. septicemia or host vs graft disease)
3 types of sickle cell crisis can occur
Vaso-occlusive
Sequestration
aplastic
Vaso-occluisve
Occurs when the SICKLED RED BLOOD cells trigger the formation of blood cloths within circulation. Tissue damage is minor and can resolve within a week DEHYDRATION AND INFECTION are an initiating
cause: Stroke, pulmonary infarction, myocardial infarction, gangrene
Sequestration
When the sickled red blood cells are removed from the general circulation by the spleen the severity depends on the amount o f blood removed and held in the spleen and liver thereby reducing the amount of circulating red blood cells. CAN PRODUCE HYPOVOLEMIA SHOCK.
Aplastic
caused by exhaustion of the bone marrow. Erythropoiesis cannot keep up with the constant need to replace red blood cells. SICKLED RED BLOOD CELLS HAVE A LIFESPAN OF 10-20 DAYS this constant stress on bone marrow stem cells can eventually lead to bone marrow failure
Treatment for sickle cell crisis
Give OXYGEN (to relieve hypoxia)
IV FLUIDS (to treat dehydration and prevent sickle cells sticking together)
PAIN MEDS (patient will develop painful clotting throughout the body and go into shock)
SC crisis
Considered physiological and not psychosocial on NCLEX
ABC priorities sickle cell crisis
Circulation issue
Polycythemia
too many RBC’s
opposite of anemia can cause hyperviscosity or thrombosis
Primary polycythemia
absolute
polycythemia vera is an INHERITED condition affecting primarily Caucasians with European Jewish ancestry. The onset of S/S could occur at any age but usually over 60 years. Mostly men
Secondary polycythemia
Relative
physiologic response to CHRONIC HYPOXIA that triggers the body to make more RBCs for oxygen transport in an effort to get more oxygen to the cells of the body
Cause of polycythemia
Sleep Apnea
COPD
Heart Failure
Pulmonary Disease
High Altitude
EPO (erythropoietin) shots
Sleep apnea and polycythemia
due to either obstructive sleep apnea or central sleep apnea (the brain does not signal the lungs to breathe). Both types result in oxygen deprivation
COPD and polycythemia
Chronic obstructive pulmonary disease (asthma and emphysema) that hamper gas exchange in the lungs
Heart failure and polycythemia
reduces tissue profusion, which create hypoxic tissue even if the blood volume and concentrations are normal. The low oxygenation will trigger an increase in production of RBCs
Pulmonary disease
gas exchange between lungs and vasculature may be impaired. The decrease in O2 exchange will produce hypoxia and trigger an increase in production of RBCs
High altitude
body compensates for lower O2 levels at higher altitudes by making more RBCs to carry oxygen. Takes 6-8 weeks to build up enough erythrocytes
EPO
EX: blood doping by athletes for performance enhancement or who abuse anabolic steroids
S/S of polycythemia
caused by reduced blood flow of viscous blood and clotting- PLETHORA: RUDDY COMPLEXION; FATIGUE; DIZZINESS; HEADACHE. Thick blood increases the workload on the heart and leads to High blood pressure which leads to decreased perfusion to the brain due to sluggish blood flow of thick blood
Treatment for polycythemia
periodic phlebotomy i.e. blood letting to siphon off some excess blood also O2
CPAP
aspirin to prevent blood clotting.
radioactive phosphate also used
Total WBC
5,000-10,000
Neutrophil count
47-63%
Lymphocyte count
24-40%
Associated organs with leukocytes
Bone marrow
thymus
spleens
White blood cell differential
Identifies counts the number of the varioius types of white blood cells present.
neutrophils
lymphocytes
monocytes
eosinophils
basophils
Elevated white blood cell count
leukocytosis
-neutrophils = acute bacterial infection
-lymphocytes = viral infection and or chronic bacterial infection
-eosinophils = allergies or parasitic infection
Decreased white blood cell count caused by:
leukopenia
-steroids (or medications that contain them aka prednisone)
-chemotherapy
-bone marrow failure (aplastic anemia or cancer such as leukemia)
-use of antiseizure medication such as Tegretol
Cancers affecting WBCs
Leukemias
lymphomas
multiple myelomas
Leukemia is cancer of what
cancer of white blood cells
Lymphoma is a cancer of what
Cancer originating in the lymphatic system
Myelomas is a cancer of what
cancer that affects the type of B-cell (that make antibodies)
Leukemia’s main cause is what
malignant growth of lymphocytes leading to overproduction of nonfunctioning white blood cells that grow faster than the functioning cells.
how is leukemia classified?
speed and progression and the type of cells involved
4 main types of leukemia
How fast it progresses:
acute leukemia
chronic leukemia
type of blood cell effected:
lymphocytic leukemia
myelogenous leukemia
Acute leukemia
the abnormal blood cells are immature blood cells (blasts). They can’t carry out their normal functions, and they multiply rapidly, so the disease worsens quickly. Acute leukemia requires aggressive, timely treatment.
Chronic Leukemia
some produce too many cells and some cause too few cells to be produced.
Chronic leukemia involves more mature blood cells.
These blood cells replicate or accumulate more slowly and can function normally for a period of time.
Some forms of chronic leukemia initially produce no early symptoms and can go unnoticed or undiagnosed for years.
Lymphocytic leukemia
This type of leukemia affects the lymphoid cells (lymphocytes) which form lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system.
Myelogenous leukemia
this type of leukemia affects the myeloid cells. Myeloid cells give rise to red blood cells, white blood cells, and platelet-producing cells.
Leukemia S/S
fatigue, low fever, night sweats, weight loss
Specific to leukemia:
lymphadenopathy
anemia, infection, bleeding problems
pallor
Lymphadenopathy
S/S specific to leukemia
swelling lymph nodes. may swell without any other s/s or well in random patterns.
Anemia, infection, bleeding problems
Specific to leukemia
due to bone marrow damage that affects all blood cells
Pallor
specific to leukemia
malignant leukocytes crowding the bone marrow and leading to decreased erythrocyte and thrombocyte production (causing pale skin color)
Lymphomas
Blood cancer that affects the lymphatic system, causes an overproduction of malfunctioning lymphocytes this overload compromises the immune system. Lymphoma can develop in many parts of the body, including lymph nodes, bone marrow, blood, spleen, and other organs
There are two main types of lymphoma
Hodgkin’s and Non-hodgkin’s
Hodgkin’s lymphoma
Cell affected: B-cell lymphocytes, REED-STERNBERG CELLS PRESENT
Age of onset: 20-30 years old (more common in younger) and 60-70 years old
Node involvement: cervical, inguinal, axillary, and retroperitoneal
Extra-nodal involvement: uncommon
Symptoms: PAINLESS SWOLLEN LYMPH NODES, WEIGHT LOSS, BONE MARROW DAMAGE (BLOOD DYSCRASIAS)
Curability: 90%
Treatment: RADIATION THERAPY (localized), CHEMOTHERAPY (generalized), IMMUNOTHERAPY (MAB), BONE MARROW (stem cell) TRANSPLANT
Non-Hodgkin’s Lymphoma
Cell affected: B AND T LYMPHOCYTES
Age of onset: 50 years old (95% are adults)
Node involvement: cervical, axillary, inguinal, femoral
Extra-nodal involvement: common
Symptoms: same as Hodgkin’s plus
pleural effusion, abdominal pain, splenomegaly
Curability: LESS THAN 25%
Treatment: same general treatments as Hodgkin’s disease but specific chemo and drugs are different
multiple myelomas
MM is a cancer that starts in a type B-cell lymphocyte called plasma cells in the bone marrow. These are protein-making cells which normally make all the different kinds of proteins that comprise the antibodies of the immune system.
How are myelomas classified
they are classified by the type of immunoglobulin being attacked
What happens with MM
bone marrow stops making different forms of immunoglobulin and instead starts to produce a single abnormal type of protein referred to as a MONOCLONAL OR M PROTEIN.
Collection of MM cells called plasmacytomas can ERODE THE HARD OUTER SHELL OR CORTEX OF THE BONE that normally surrounds the marrow. causing bone lesions
Bone lesions cause what
pain and PATHOLOGICAL (SPONTANEOUS) FRACTURES of the bones affected by the cancer.
Multiple myeloma signs and symptoms
High calcium levels in the blood (hypercalcemia) due to calcium moving from damaged bone into the blood
Renal failure myeloma nephrosis caused by damage to kidneys by paraproteins that cause hyperviscosity of body fluids a distinctive feature of myeloma.
Tumor markers are M-PROTEINS (found in serum) and BENCE-JONES PROTEIN found in urine
Anemia: BM not functioning and kidney not producing Erythropoietin leads to blood dyscrasias
Bone pain: The first symptom, and pathological fractures (occur spontaneously w/o an injury
Platelets normal range
150,000-400,000
Platelets defined as
also called thrombocytes
they are CELL FRAGMENTS (NOT CELLS) that are vital for normal blood clotting
Associated organs with platelets
LIVER
platelet production is regulated by thrombopoietin
Low platelet count occurs because
The body’s bone marrow doesn’t make enough platelets
the bone marrow makes enough platelets, but the body destroys them or uses them up
the spleen holds on to too many platelets
Platelet count increased in what conditions
Thrombocytosis
-some cancers
-inflammatory conditions
-birth control pills
-recover phase of trauma/surgery
Platelet count is decreased what conditions
Thrombocytopenia
-Medications such as aspirin, ibuprofen, and acetaminophen (damages liver leads to bleeding problems)
-“G” herbs (garlic, ginger, ginkoba, ginseng)
-DIC (disseminated intravascular coagulation)
S/S of bleeding
Hemorrhage- blood leaving the blood vessel (internal or external bleeding)
Menorrhagia- Heavier than normal menstrual bleeding
Epistaxis- bleeding from the nose
Petechiae
Pinpoint hemorrhages of small capillaries in the skin, conjunctiva of the eyes or mucous membranes
Purpura
red or purple discolorations on the skin that do not black on applying pressure
Ecchymosis
blood leaks into tissues under the skin causing bruising
Hematoma
collection of blood usually clotted, in organs, body spaces or under the skin
Causes of thrombocytopenia
idiopathic thrombocytopenia purpura - ITP
Thrombotic thrombocytopenia purpura - TTP
Drug-induced Thrombocytopenia
idiopathic thrombocytopenia purpura - ITP
Autoimmune disorder that causes an IgG antibody to bind with platelets destroying their function. Results in low platelet count and s.s of bleeding
Idiopathic = arising spontaneously or from an obscure or unknown cause
Thrombotic thrombocytopenia purpura - TTP
thought to be caused by widespread endothelial damage that triggers thrombosis (clots) and platelet destruction due to a lack of activity in the ADAMTS13 enzyme ( a type of protein in the blood)
The ADAMTS13 gene controls the enzyme, which is involved in blood clotting not having enough enzyme activity causes overactive blood clotting
S/S of thrombotic thrombocytopenia
Fever, hemolytic anemia renal failure neurological decline
Drug induced thrombocytopenia
a hypersensitivity reaction causes platelet destruction. Heparin can induce a type 3 hypersensitivity reaction that can quickly be resolved after eliminating the drug
S/S of thrombocytopenia
EPISTAXIS
MENORRHAGIA
PURPURA
BLEEDING GUMS
GI BLEEDS
PETECHIAE
Treatment for thrombocytopenia
Immunosuppression treatments
plasmapheresis
ELIMINATE THE CAUSATIVE DRUG
PLATELET INFUSION
Thrombosis caused by
High bp
Low bp
Injured vessel walls
altered blood constituents
High blood pressure (thrombosis)
blood flow leads to clots developing in arteries due to increased turbulence caused by high blood pressure
this turbulent flow of blood causes damage to vessel walls or blood cells. the resulting inflammation then triggers the clotting
Low pressure (thrombosis)
leads to cots in the veins due to lower blood pressure and slower flow of blood in veins as compared in arteries - slow blood clots
Injured vessel walls (thrombosis)
interior of blood vessels can be damaged bu the development of atherosclerotic plaque. DEEP VEIN THROMBI in legs break off to create pulmonary EMBOLI
Altered Blood constituents (thrombosis)
increased viscosity of blood
Thrombocytosis leads to increased abnormal production of platelets (40% of people with unexplained high platelet count have cancer)
Treatment of thrombosis
Anti-coagulant drugs
Thrombolytic drugs
acetaminophen
Anti-coagulant drugs treating thrombosis
reduce the blood cell’s ability to clot. These drugs prevent future clots but have no effect on existing clots
Heparin- injected fast acting and too high of levels causes bleeding problems
Coumadin- oral med- long acting too high of levels causes bleeding tendencies
Aspirin- oral - small does everyday prophylaxis to prevent clotting causes GI bleeding
Thrombolytic drugs (treating thrombosis)
So-called clot busters these drugs break up or dissolve existing blood clots, which are the main cause of both heart attacks and stroke but do not prevent future clots (EX: TPA, streptokinase)
Acetaminophen (treatment thrombosis)
Tylenol - Very damaging to the liver
Overdose accidental or intentional are lethal because the liver dies quickly
without a functioning liver, clotting factors are not available to combine with platelets and blood cannot clot.
Pertinent lab tests for bleeding problems
Bleeding time tests
Blood clot test
Bleeding time tests
PT AND INR (intentional normalized ratio) are used to test patients on coumadin blood thinning medication PTT test patients on heparin blood thinning medication
Blood clot test
D-DIMER. Done to determine the extent of clotting in the body and is done for DVT (deep vein thrombosis) P.E. (pulmonary embolism) and DIC (disseminated intravascular coagulopathy)
Disseminated Intravascular Coagulopathy
DIC is a coagulation disorder that results in both
BLOOD CLOTTING and HEMORRHAGING.
DIC is what
Not a specific illness, rather it is a complication. It is always secondary to an underlying disorder
Definition of DIC
DIC is a serious disruption in the body’s clotting mechanism
OVERPRODUCES MANY SMALL BLOOD CLOTS THROUGHOUT THE BODY DEPLETING THE BODY OF CLOTTING FACTORS AND PLATELETS.
THESE SMALL CLOTS ARE DANGEROUS AND CAN INTERFERE WITH THE BLOOD SUPPLY TO ORAGANS, CAUSING DYSFUNCTION AND FAILURE.
THEN MASSIVE BLEEDING CAN OCCUR DUE TO THE BODY’S LACK OF CLOTTING FACTOR AND PLATELETS. DIC IS LIFE-THREATENING AND NEEDS TO BE TREATED PROMPTLY.
Inflammatory process activation
Coagulation and inflammatory pathways interact in substantial ways. Inflammation gives rise to activation of the clotting cascade and the resultant coagulation stimulates more vigorous inflammatory activity.
triggers of inflammatory process activation
the chemical mediator CYTOKINE is released when the inflammatory response is triggered. CYTOKINE IS IMPLICATED AS A CAUSATIVE AGENT IN DIC.
Triggers to organ failure (DIC)
sepsis and septic shock
obstetrics complication
trauma (especially burns and head injury)
Blood transfusions
some cancers
hematologic disease
DIC basic definition
Increase use of platelets leads to decrease amount of platelets
DIC S/s
related to either the blood clotting or the hemorrhage phase
Note: BLEEDING FROM AT LEAST 3 UNRELATED SITES IS PARTICULARLY SUGGESTIVE OF DIC
Clotting phase of DIC
DVT deep vein thrombosis
Renal Failure clots in the kidneys
Difficulty breathing clots in the lungs
Neurologic changes clots in the brain
numbness clots in the spinal cord
Liver dysfunction clots in the liver
Hemorrhage phase
Blood oozing from an existing IV site
Bleeding gums
GI bleeds
Petechiae/ purpura/ Ecchymosis
Treatment of DIC
Life support (oxygen n, give fluids/IV meds to maintain blood pressure: probably drug-induced coma)
Treat the underlying cause (i.e. give antibiotics if caused by an infection)
Give heparin (to stop the clotting process)
Platelet transfusions (restore lost platelets)
Pertinent Lab tests for DIC
Decreased platelet count (less than 100,000) and abnormal D-DImer
