1/33
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No study sessions yet.
Where are antibodies made from?
The spleen
Blood Overview
Blood Volume (4-6 L)
Blood Components: 45%
RBC
WBC
Platelets
Plasma: 55%
Water
Proteins
Enzymes
Antibodies
Clotting factors
pH of Blood
7.35 - 7.45
Red Blood Cells (RBC): AKA Erythrocyte
Transports O2 on Hgb
Formation depends on:
Stem cells
Bone marrow
Iron
B12
Folic acid
Protein
B6
Copper
Reticulocytes: Immature RBC
RBC Cycle
Stimulus: Reduced O2 carrying capacity
Kidney releases Erythropoietin
Developing erythrocytes in red bone marrow
Increased O2 carrying capacity
Relieves stimulus
Anticoagulants
Interfere with steps in blood clotting
Limit or prevent extension of clots
Prevent new clots
Plate inhibitors
Prevent platelets from becoming active & clumping together
Clot Busters
Thrombolytics: Breaks down proteins (fibrins) that form clots
Fibrinolytics: Selectively degrade fibrin threads in a formed blood clot
Diagnostic Assessment
Tests of Cell Number & Function
CBC
Peripheral Blood Smear
We as nurses do not look at this
Coagulation studies:
PT
INR
aPTT
Anti-Za Assay
Coomb’s test
Serum ferritin, transferrin, & total iron binding capacity (TIBC)
Diagnostic Assessment Cont.
Radiographic Exams
Bone marrow aspiration & biopsy
Patient prep
Procedure
Follow up care
Bleeding
Bruising
Infection Pain
Anemia
Common causes of anemia:
Decreased RBC production
Increased RBC destruction
Chronic RBC loss
Sx similar for all types:
Tachycardia at rest
Fatigue
What are the two types of Blood Loss Anemia?
Acute Blood Loss Anemia & Chronic Blood Loss Anemia
Acute Blood Loss Anemia
Hemorrhage
Trauma, surgery, GI bleed
Symptomatic if is more than 500mL
Chronic Blood Loss
Body compensates with gradual loss, bone marrow responds
Adults
Women
Treatment For Blood Loss
Treat underlying cause
Blood products
Iron supplements, diet
Erythropoietin (Epogen, Procrit)
Hemolytic Anemia
The body is producing ENOUGH RBC, but something is DESTROYING them
Abnormal breakdown of RBC
Most common cause:
G6PD Enzyme Deficiency
G6PD maintains the integrity of RBC
Causes RBC to be fragile
Inherited
Fever
Drugs/chemicals
S/S:
Pallor & Jaundice
Tx:
Stop offending agent
Hydration
Flushes the cellular debris through the kidneys
Transfusion (Severe cases)
Immunohemolytic Anemia or Autoimmune Hemolytic Anemia
Body attacks their own RBC
Exposure of erythrocyte to antibodies
May occur with other autoimmune disorders
Autoimmune Hemolytic Anemia Treatment
Depends on Sx severity
Steroids (Must taper)
Helps stop the body from attacking its own RBC
Immunosuppressant:
Cytoxan (More toxic)
Imuran (Less effective)
Splenectomy
Removes the site of destruction
Plasma exchange therapy
Transfusion
Severe cases but cross-matching can be challenging
Iron Deficiency Anemia
Most common worldwide
Definitive Dx by bone marrow aspiration
Iron Deficiency Anemia Etiology
Bleeding (GI, Menstrual)
Malabsorption
Inadequate iron intake/ absorption
Chronic alcoholism
Partial gastrectomy
Pregnancy
Adolescence
Infection
Iron Deficiency Anemia Sx/Manifestations
Chronic Bleeding
Alterations in the tongue
Brittle nails
Cheilosis
Cracks on the sides of the mouth
Pica
Unusual craving
Fatigue
Exercise intolerance
Tachycardia
Iron Deficiency Anemia Tx
Treat underlying cause
Preventative Education
Nutrition Counseling
Iron Supplements
IV
PO
Vitamin B12 Deficiency: Pernicious Anemia
Failure to absorb B12
Lack of Intrinsic Factor
Intrinsic factor is what allows it to absorb B12
Clinical Manifestations of Vit. B12 Deficiency
Pallor, Slight Jaundice
Sore beefy red tongue
Diarrhea
Neurologic S/S (B12 needed for nerve function)
Paresthesia
Proprioception
Balance difficulty
Cognitive dysfunction
Vit. B12 Deficiency Anemia Tx
If true Vit. B12 deficiency:
Increase PO dietary intake of B12 enriched foods
If Vit. B12 Pernicious Anemia:
Vit. B12 injections
Folic Acid Deficiency Anemia
Common Causes:
Malabsorption
Crohn’s Disease
Chemotherapy
Celiac Sprue (Celiac Disease)
Chronic Alcohol Abuse
Increased need:
Pregnancy
Rapid growth
Chronic Malnourishment:
Elderly
Alcoholics
Folic Acid Deficiency Anemia Clinical Manifestations
Pallor, SOB, Fatigue
Red smooth beefy tongue
Cheilosis
Diarrhea
No neurologic symptoms
Folic Acid Deficiency Anemia Tx
Folic Acid Supplement
Increase intake of green leafy vegetables, fruits, meats, & cereals
Aplastic Anemia
Pathology:
Bone marrow fails to produce blood cells (RBC, WBC, or Platelets):
Pancytopenia
Dec. RBCS
Dec. WBC
Dec. Platelets
Stem cells injured:
# of stem cells decreased
Aplastic Anemia Diagnosis
CBC
Bone Marrow Biopsy
Very few to no cells, often replaced with fat)
Aplastic Anemia Treatment
Blood transfusions
Avoid offending agent
Immunosuppressive therapy
Splenectomy (Controversial)
Stem cell Transplant
Cost
Availability
Complications
Polycythemia
Primarily a cancer in the blood
Increase number of RBC’s (Above normal)
Inc. in RBC, WBC, & platelets
Congestion like traffic (Stagnant)
Leads to clotting
Blood is hyperviscous
Inc. Hematocrit (55% in males, 50% in females)
Not like dehydration (Related to overproduction of RBC)
Polycythemia Vera (PV)
Excessive production of Erythropoietin
Increases in RBCs, WBC, & platelets
Polycythemia Vera (PV) Treatment
Repeat Phlebotomy (2-5 time per week)
First line
Draws blood
Prevents clotting
Pheresis
Withdrawal of whole blood & removal of RBCs
Inc. Hydration
Flushes out the kidneys
Flushes the cellular debris
Usually paired with phlebotomy
Prevent clot formation
Think about bleeding
Polycythemia Vera (PV) Clinical Manifestations
Looks like someone not getting perfused
Skin & mucous membranes have a plethoric appearance
Purplish or cyanotic
Intense itching
Dec. perfusion
Dilated vessels
Superficial veins visibly distended
Appearance similar to fluid overload
Hypertension
Inc. risk of blood clots
Rapid turnover
Immature cells banging into each other & breaking down
Inc. cell debris
Inc. Potassium