Bone Marrow

Spleen

Liver

Lymph Nodes

Thymus Gland

Carry O2 to cells

Remove Carbon Dioxide and Waste

Hormone Transport

Inflammatory/Immune response

Temperature Regulation

Acid-Base Balance

Fluid Electrolyte Balance

Maintaining blood coagulation

Inside of all bones

Spongy long center of bones

Accounts for 4-5%

Primary Function of Bone Marrow

Hematopoesis

Carries out Hematopoiesis

Erythoid

Myeloid

Thrombocytes

Also one source of lymphocytes/macrophages

Ribs, Vertebrae, other flat bones

< 12 LOW

>16 HIGH

increases viscosity (thickens blood)

rupturing or destroying blood cells by liver or spleen through phagocytes

(average life span is 120 days)

What is not recycled is converted to bile and removed by liver.

Largest Lymphatic Organ

Functions as filter system and reservoir for blood sysytem.

Phagocytosis

Five Stages of hemostasis

which maintain steady state with relation to an injured vessel.  They prevent excessive bleeding or clotting.

Hematocrit (Hct)

% of packed cell volume of RBC in total blood volume

Females 38-47%

Men 40-54%

MCV

Size of a single RBC

MCH

Weight of Hgb within a single RBC

MCHC

% of HgB within a RBC

Stomatitis

Cold Intolerance

PICA

Chelosis

Microcytic and Hypochromic

TIBC high

PO liquid : dilute and use straw b/c it can stain teeth. Administer with OJ to help absorption.

IM : Z track

IV: Have Epi on hand and do small test dose

Aplastic Anemia

Bone Marrow Fails and Is Replaced By Fat

MAy be secondary to chemicals or viruses

Parasteshia

Decreased prioprioception

CNS damage

Beefy Red Tongue

Macrocytic

Increased MCV

Can eat cheese with this one

lack of Intrinsic Factor in the gut.

s/s Sore beefy red tongue and diarrhea

Do schilling test

Folic Acid Deficiency

Runs with undernourishment

Macrocytic

ETOH/Drug addictions

Older adults

TPN

Glossitis

Chelosis

Neural Tube Defect in Pregnancy

Dialysis Patients

NO NEUROLOGICAL SYMPTOMS

Green Leafy Veg

Organ Meats

Wheat Germ

Eggs

Asparagus

Kidney Beans

Folic Acid Supplements 0.4 mg- 1 mg per day

Premature destruction of RBS due to Defects, sickle cells, Drugs, Chemicals, Toxin/Venoms (snakes, spiders), Bacterial Infections, Parasitic Infections

Trauma/ Burns

Medical Valve (damages RBC)

Bleeding into joints (immobilize)

Genetic Counseling a Must

Painful! Jaundice

Treat w/ oxygen and IV fluids

Possible Blood transfusion, Folic Acid

Pt.Ed: Early treatment for infections

Group of Inherited Disorders of HgB synthesis where an alpha or beta chain is missing or defective

Decreased HgB production

Fragile RBC's

Microcytic

Bronze Coloring

Bone marrow hyperplasia

Jaundice

May lead to HF

Long Bone FX

Repeated blood transfusions cause deposits of iron in heart liver and pancreas and may lead to  organ failure.

G6PD deficiency is a lack of an enzyme that catalyzes glycolosis which is the method used for cellular energy for RBC.

RBC's are destroyed 7-12 after stressor exposure

Hereditary disease affecting African Americans and Mediterranean Descent

x chromosome= mother to son and males>females

Common stressors:Fava Beans, Sulfa, Aspirin            Vitamin k Derivatives

s/s: Jaundice and HgB in urine

Polycythema

Excess of RBC's 

Primary:Overproduction of RBC w/ unknown cause. Thrombis

Increased viscosity w/ ruddy complexion & painful itching on fingers and toes, enlarged spleen.

Secondary: same as primary w/o enlarged spleen and chronic hypoxia

Relative: Fluid Volume deficit so rehydrate

Treatment of Primary and Secondary 

Polycythema

Smoking cessation

Periodic phlebotomy

PRIMARY Take hyroxurea-suppress bone marrow function

Aspirin a day to control thrombis

Antihistamine for puritis

platelet count < 100,000

Normal is 150,000 to 400,000

usually bleeding of small vessels

Autoimmune disorder where spleen destroys platelets

Females>Males

Lupus inducing

Take immunosuppressant drugs ie Prednisone, Azathioprine, Cyclosporine

Splenectomy and Blood Transfusion

Rare- where thrombi can occlude arterioles and capillaries

petichiae, headaches, seizure, altered LOC

Abnormal response to heparin

Type I reacts directly w/ platelets and removed by phagocytosis

Type II More severe and some people form antibody to heparin.

Treatment d/c heparin

Avoid NSAIDS, Antibiotics (Penicillin and Sulfinamides), Heparin, Thiazide diuretics

THEY DESTROY PLATELETS

Leukemia

Replacement of bone marrow by Immature WBC

Manifestations

Anemia

Bleeding Infection

Infiltration of all organs

Male

Smoking 

Downs Syndrome

BENZENE AND RADIATION

HTLVI virus

Hyperplasia  of Bone Marrow and Spleen manifested as decreased Neutrophils (recurrent severe infections) Decreased platelets, bone infections, Anemia

death is from Infection or hemmorhage

Uncontrolled proliferation of all bone marrow elements

Philadelphia chromosome

Males>females

Early asymptomatic

Aggressive phase=hypermetabolism

Abnormal proliferation of lymphoblasts that are immature and non-functionable lymphocytes.

Most common in children and young adults

Rapid onset

Combo therapy=complete remission in 80-90%

Chemo

Radiation

Bone Marrow Transplant

Stem cell transplant

Malignancies of lymphoid tissue-proliferation of lymphocytes, histocytes,

Can be Hodgkins or Non-Hodgkins

Environmental factors like chemical, herbacide

Age 15-35 and >50   and  M>F

Spreads and has Reed Sternberg cells

Manifestations: commonly painless w/ enlarged nodes. Impaired immune response.

ONE OF MOST CURABLE CANCERS

Affects older adults and M>F

Environmental and genetic factors

GI and CNS involvement

prognosis depends on cell type and grade of differentiation (Low is more curable)

CBC

Chest XRay

CT scan

PET Scan

Biopsy

Total Body Scans

Hemophilia

Manifested by bleeding

Hereditary Disorder of clotting factors

Hemophilia B= Christmas Disease 

Need vit K to activate clotting

Treatment FFP or Synthetic Missing Factor

Hemophilia A (most common)

A/B x linked recessive

C = Male and Female

Von Willebrand Disease

Hereditary Bleeding Disorder

Reduced Factor VIII

M=F

Bleeding is not usually severe

Treatment DDVAP synthetic

DIC

Disseminated Intravascular Coagulation

Bleeding and Clotting Simultaneously until eventually clotting factors are exhausted causing excessive bleeding.

Life threatening: Treat w/ FFP and Heparin

Multiple Myeloma

Radiation or oncogenic virus or Possibly genetic: African Americans

M>F and increases with age

Plasma cells multiply uncontrollably and infiltrate: bone marrow, lymph nodes, spleen, and tissues. Lg amounts of M Protein which damages kidney tubules and leads to pathologic FXPunch outs on bone xrays

S/S Bone pain, hypercalcemia, recurrent infections, M proteins in urine.

Treatment of Multiple Myeloma

NO CURE ONLY TREATMENT

• Chemo
• Management of hypercalcemia- increase fluids to flush out.
• Plasmapheresis to remove protein. Blood drawn out and spun to remove protein.
• Supportive care to prevent fractures