306 week 3 - hematologic system

hematologic system

delivers needed substances to tissues, defends against invading microbes and injury, and balances acid/base as it carries CO2

blood components

Plasma, red blood cells, white blood cells, and platelets, 55% Plasma, 45%-Formed Elements

plasma

55% of blood, liquid part, made of - salts, glucose, amino acids, vitamins, urea, proteins, and fats

plasma proteins

made in liver, made of albumin, regulates passage of water and solutes through osmotic pressure, carry molecules for exogenous substances

plasma contains

proteins, antibodies, and clotting factors

erythrocytes

Men = 48% of blood, women = 42%, don't divide like other cells, no nucleus, mitochondria, or ribosomes, life span = 120 days

erythrocytes role in tissue oxygenation

bioconcave shape that allows them to change shape without rupturing (reversible deformity), increased SA allows for more gas diffusion

medullary hematopoiesis

Begins in bone marrow: 1. Stem cells signaled when RBCs are low (low O2), 2. Increased RBC production by converting yellow inactive marrow into red active marrow, 3. More stem cells made, 4. increased differentiation

erythropoiesis

Stem cells in bone marrow differentiate into erythroblast (huge nucleus + many mitchondria), nucleus and other organelles are removed + lots of Hgb made, nearly mature RBC = reticulocyte enters blood, within 24-48 hours it becomes a mature erythrocyte

erythropoietin

hormone made in the kidney, stimulated by hypoxia, tells bone marrow to increase RBC production

normal % of reticulocytes in the blood

1%

nutrition needed to produce new RBCs

Protein, intrinsic factor, vitamin B12, folate, iron

protein - RBC formation

body uses amino acids from protein to produce Hgb

intrinsic factor - RBC formation

secreted by parietal cells in gastric mucosa, facilitates B12 absorption in the ileum

vitamin B12 - RBC formation

DNA/RNA synthesis, stored in liver

folate - RBC formation

DNA/RNA synthesis, absorbed in upper small intestine, stored in liver

iron - RBC formation

necessary for making new RBC's, 67% body iron bound to heme, stored by ferritin and hemosiderin in the macrophage of bone marrow

hemoglobin

2 pairs (4 total) of different polypeptide chains, end of the chains are attached to a heme unit, 4 heme units carry 4 O2 molecules

heme

porphyrin and Iron (Fe) that binds the oxygen

erythrocyte destruction

Macrophages in spleen do most work, spleen = dysfunctional, macrophages (Kupffer cells) in liver take over, heme -> bilirubin, bilirubin removed from blood by liver and converted to bile (released in small intestine)

bone marrow aspiration

looking for cell production, used to diagnose anemia, leukemia, tumors, platelet disorder, lymphocyte production, and iron stores

complete blood count

measures number of RBCs, WBCs, platelets, Hgb, and Hct

MCV

mean corpuscular volume = size of RBC

MCHC

mean corpuscle hemoglobin concentration = concentration of Hgb

MCH

mean cell hemoglobin = weight of Hbg in cell, lots of iron = heavier

elderly effects of RBCs

anemia, increased time to reproduce RBCs, low iron, RBC membrane more fragile, platelets stickier and more prone to blood clots, increased clotting factors

anemia

decreased number of RBCs, decrease quality of Hbg, or decreased Hct

causes of anemia

decreased production of RBCs, blood loss, RBC destruction

general cues of anemia

Tachycardia, hypoxia, dyspnea, dizziness, fatigue, nausea, vomiting, constipation, impaired renal, peripheral vasoconstriction, delayed healing, low grade fever

pernicious anemia RBC type

macrocytic, normochromic

pernicious anemia cause

decreased intrinsic factor and decreased B12 absorption

pernicious anemia pathophysiology

lack of intrinsic factor due to gastric mucosal atrophy or autoimmune destruction of parietal cells or IF itself, lack of IF = no B12 absorption

what can cause gastric mucosal atrophy

gastric bypass, autoimmune diseases, alcoholics, heavy tea drinkers, smokers, bacterial invasion

main cues of pernicious anemia

Paresthesia, beefy red tongue, fatigue

treatment of pernicious anemia

1000 mcg/day B12 IM for 2 wks, then weekly until Hgb is normal, then monthly, assess for neurological problems, prevent injury

folate deficiency RBC type

Macrocytic, normochromic

folate deficiency cause

poor nutrition, alcoholism, malabsorption

folate deficiency pathophysiology

impairs DNA synthesis (doesn't need IF to be absorbed)

folate deficiency cues

fatigue, glossitis, no neurologic symptoms, fissures in corners of mouth and tongue

folate deficiency treatment

oral folic acid

iron deficiency RBC type

microcytic, hypochromic

iron deficiency cause

chronic blood loss, poor intake, pregnancy

iron deficiency pathophysiology

decrease iron stores lead to decrease hemoglobin

iron deficiency cues

pallor, spoon and brittle nails, fatigue/dyspnea, pale palms and conjunctiva, sores at corners of mouth and tongue, brittle hair

iron deficiency treatment

treat underlying cause and replace missing iron with dietary changes or iron supplements

aplastic anemia

pancytopenia due to bone marrow failure from infection or massive hemorrhage, pts are very sick and fatigued

ferrous sulfate moa

absorbed in duodenum/jejunum, replenishes iron stores for HgB synthesis and erythropoiesis

ferrous sulfate drug interactions

Ca, antacids, proton pump inhibitors, H2 blockers, tetracyclines, fluoroquinolones, levothyroxine dec absorption

ferrous sulfate contraindications

hemochromatosis, hemosiderosis, hemolytic anemia, active GI ulcer

ferrous sulfate adverse effects

constipation, dark stool, nausea, stains teeth, abdominal pain

ferrous sulfate pt. teaching

Avoid Ca for two hours after taking, stools may be dark, inc fluid and fiber to prevent constipation, take on empty stomach with vit. C to inc absorption

iron sucrose moa

IV iron supplement taken up by reticuloendothelial system and incorporated into Hgb

iron sucrose drug interactions

don't give with oral iron

iron sucrose contraindications

Use carefully with active infection, asthma, or hist. of drug allergies

iron sucrose adverse effects

hypotension, headache, nausea, infusion rxn, dizziness

iron sucrose pt teaching

teach signs of infusion rxn: dizziness, rash, SOB, or chest discomfort, sit during infusion, follow-up labs after

ferric carboxymaltose moa

Large amounts of stable iron-carbohydrate complex for rapid iron repletion

ferric carboxymaltose drug interactions

avoid concurrent IV iron therapy

ferric carboxymaltose contraindications

Hypersensitivity rxns, hypophosphatemia (low blood phosphate levels)

ferric carboxymaltose adverse effects

hypophosphatemia, hypertension, nausea, flushing, dizziness

ferric carboxymaltose pt. teaching

signs of hypophosphatemia: weakness, bone pain, or fatigue, follow-up labs, injection rxn: report dizziness, flushing, or SOB during infusion

Cyanocobalamin (B12) moa

absorbed with IF in the liver, required for DNA synthesis, neurological function, and RBC maturation, corrects B12 deficiency and megaloblastic anemia

Cyanocobalamin (B12) drug interactions

Metformin, PPIs, H2 blockers, colchicine dec absorption

Cyanocobalamin (B12) contraindications

Hypersensitivity to cobalt or cyanocobalamin, Leber's optic neuropathy, severe hypokalemia risk

cyanocobalamin adverse effects

injection site rxn, hypokalemia, headache

Cyanocobalamin (B12) pt teaching

Report numbness, tingling, gait changes, or vision changes, and maintain scheduled injections

folic acid moa

rapid GI absorption and conversion to active tetrahydrofolate in liver, required for DNA synthesis and RBC production, corrects folate deficiency

before giving folic acid you should

rule out B12 deficiency, folate corrects megaloblastic anemia but not the neurological symptoms of B12 deficiency

folic acid drug interactions

Methotrexate, phenytoin, phenobarbital, and sulfasalazine may alter folate levels, high-dose folic acid may reduce effectiveness of anticonvulsants

folic acid contraindications

Untreated vitamin B12 deficiency (may mask neurologic damage)

folic acid adverse reactions

rare rash or nausea

folic acid pt teaching

Eat folate (leafy greens, beans, fortified cereals)

sickle cell trait

heterozygous, HbS from one parent and normal HbA from other, carrier with rare clinical signs (stress, ex. Under anesthesia, high altitude, COPD)

sickle cell anemia

homozygous, more severe than trait, causes abnormal hemoglobin, resulting in some RBC's assuming a sickle shape during times of stress

sickle cell anemia pathophysiology

HbS not bound to O2 becomes sickle-shaped + stiff + sticky -> vessel occlusion -> organ infarction, ALSO sickle cells have more sensitive membrane = destruction = anemia

causes of sickling

hypoxia, acidosis, dehydration, decrease plasma volume, decrease temperature (vasoconstriction), cells return to normal once stressor is gone

complications of sickle cell anemia - vessel occlusion

blood flow stopped distal to occlusion leading to localized cell death, causes severe pain for abt 4-6 days

common sites of vessel occlusion

abdomen, chest, bone and joints --> infarction to kidneys, lungs, CNS

complications of sickle cell anemia - Splenic damage/sequestration crisis

sluggish blood flow + low O2 = ischemia, inc risk of splenic infarction and infection: strep pneumoniae, Hemophilus influenzae type B, klebsiella

treatment of sickle cell anemia

pain meds + hydroxyurea

NSAID

ibuprofen

NSAID moa

Inhibit COX-1 and 2 enzymes, decreasing prostaglandin synthesis reducing pain, inflammation, and fever

NSAID drug interactions

Anticoagulants, antiplatelets, corticosteroids, SSRIs inc bleeding risk, ACE inhibitors and diuretics may reduce renal function

NSAID contraindications

Active GI bleeding, peptic ulcer disease, severe renal disease, NSAID allergy

NSAID pt. teaching

Take with food, avoid multiple NSAIDs, monitor for black stools, abd. pain, or decreased urine output, maintain hydration

opioid analgesics

fentanyl, morphine, hydromorphone

opioid analgesic - moa

Opioid receptor agonist that inhibits pain transmission in CNS

opioid analgesic - drug interactions

CNS depressants (alcohol, sedatives), benzodiazepines increase respiratory depression risk

opioid analgesic - contraindications

Significant respiratory depression, acute severe asthma, paralytic ileus

opioid analgesic - pt teaching

Avoid alcohol and sedatives, do not drive until effects known, report excessive sedation or breathing difficulty, inc fluid/fiber to prevent constipation

Antimetabolite Disease-Modifying Agent

hydroxyurea

hydroxyurea moa

Increases fetal hemoglobin production and dilutes the formation of abnormal hemoglobin S

hydroxyurea drug interations

Myelosuppressive meds make it less affective, antiretroviral drugs may increase toxicity

hydroxyurea contraindications

Pregnancy, severe bone marrow suppression, significant cytopenias

hydroxyurea pt. teaching

Adherence is critical, regular CBC monitoring, use contraception, report fever/signs of infection immediately

hemostasis

blood clotting, 1. vasoconstriction 2. platelet plug formation 3. blood coagulation

impaired hemostasis

vitamin K deficiency and liver disease

how to treat vitamin K deficiency

give vitamin K and fresh frozen plasma

why does liver disease cause impaired hemostasis

decreased clotting factor and decreased formation of antithrombin

platelets

cell fragments w/o nucleus, constantly circulating in blood