Non-malignant hematology disorders

what is a “shift left”

shift to younger cells

what is the only type pf fluid you can administer with blood

normal saline

what defines hypoproliferatvie anemias

• defect in production of RBCs. 

  • caused by iron, B12, or folate deficiency, decreased erythropoeitn production, cancer 

what defines hemolytic anemias

• excess destruction of RBCs

  • caused by altered erythropoiesis or other causes such as hypersplenism, drug induced or autoimmune processes, mechanical heart valves, ABO incompatibility  

risk factors for anemias 

• blood loss -acute or chronic 

  • chronic example GI bleeds 

• hemolysis 

• dietary intake/metabolism 

  • vegatarians and vegans 

• bone marrow suppression

• age

s/s of mild anemia

• yellowing eyes

• pale, cold, or yellowing skin

• SOB

• weakness, fatigue, dizziness 

• changed stool color 

• heart palpitations and rapid HR

• spleen enlargement 

s/s of severe anemia

• fainting

• chest pain

• angina 

• heart attack

s/s of anemia are depndant on

• severity 

• onset

• duration 

• metabolic requirements 

• concurrent problems 

Hg for female adults

12-16

Hg for male afults

14-17

Hg decreases when in life

after middle age

critical Hg value 

less than 7

HCT % in female adults

36-48%

HCT % in adult males

42-52%

a high RDW indicates

large variation in RBC size

normolytic means

normal MCV and MCH

macrolytic means

high MCV and MCH

microlytic means 

low MCV and MCH

types of anemias that are hypoproliferatvie

• Iron deficiency anemia

• Anemia in renal disease

  • kidneys produce erythropoietin 

• Anemia of inflammation

• Aplastic anemia

• Megaloblastic Anemia:

  • folic acid, Vitamin B₁₂ deficiency

what are some conditions that may cause malabsorbtion of iron (leading to iron deficieny anemia)

celiac disease, gastric pypass, etc 

s/s of iron deficieny anemia

• brittle nails 

• red, smooth tongue 

• angular cheleitis 

  • sores on corners of mouth

  • sores on tongue 

• SOB, fatigue on exertion 

• tachycardia and palpitations 

• dizziness or syncop upon standing or with exertion 

• pallor with pale nail beds and mucous membranes

diagnostics for iron deficiency anemia

• iron studies, ferritin, RBC, H/H, C/T scan, colonoscopy 

oral iron supplements require

acidic environment and absorbtion (dont work if youre taking a bunch of antacids or have malabsorbtion)

cons of IM/IV iron supplements

skin stainng, allergic reactions

iron supplements pt education

• can make stool black/dark green

• take with vitamin c to increase absorption

• avoid antacids, and calcium bc they will decrease absorption

what are some foods high in iron

Meat and Seafood: 

• Red meat (beef, lamb, pork)

• Poultry (chicken, turkey)

• Fish (oysters, shellfish, tuna)

• Liver

Plant-Based Foods: 

• Legumes (beans, lentils, chickpeas)

• Dark leafy green vegetables (spinach, kale, collard greens)

• Nuts and seeds (cashews, almonds, pumpkin seeds)

• Whole grains (brown rice, quinoa, oats)

Other Sources: 

• Molasses

• Iron-fortified cereals

• Tofu

nursing considerations for epoetin alfa

• moniot for increase BP

• mnotr Hgb and Hct twice a week 

• monitor for a cardiovascular event if Hgb increases too rapidly (greater than 1g/dL in 2 weeks)

  • too many RBC make blood thicker and stickier 

pt education for epotein alfa 

• reinforce the importance of having Hgb and and HCT evaluated on a twice-per-week basis until targeted levels are reached 

epotein alfa does what 

increase production of RBC

Low levels of folic acid can cause

red blood cells that are larger than normal -> also means there are fewer RBC’s if they are bigger. These red blood cells don’t live as long as normal red blood cells.

megaloblastic anemia etiology 

• Dietary deficiency: Leafy greens, citrus

  • GI tract absorption issues (Celiac)

• Drug cause malabsorption: Dilantin, ETOH

• Hemodialysis

pernicacious anemia is caused by deficency in

B12

megaloblastic anemia is caused by deficincy in

folic acid

vitamin B12 is needed to

convert folic acid from its inactive form to its active form. All cells rely on folic acid for DNA production. 

b12 deficincy can be caused by

• Impaired DNA synthesis or lack of 

• IF (intrinsic factor)

  • IF secreted by gastric mucosa is required for B12 absorption

• Etiology

  • gastric mucosa atrophy, autoimmune, gastrectomy, Chron’s, ileum resection, long term H2 blocker usage 

s/s of pernicacious anemia

• tissue hypoxia 

• sore/cracked/red tongue, anorexia, NV

• neuromuscular weakness, paresthesias, ataxia, cognitive issues

pernicious anemia diagnostic tests

• RBC abnormal (macrolytic)

• gastroscopy

• schilling test (radioactive B12, 24hr urine. tests if pt is absorbing B12)

• serum B12 levels

aplastic anemia

• Associated with decrease in all blood components (RBC, WBC, platelets)

what can lead to aplastic anemia 

• exposure to chemicals 

• chemotherapy 

• radiation/exposure 

• infections 

aplastic anemia treatment

• immunosuppressants 

• blood products transfusion

  • neupogen (WBC stimulator) 

  • platelets, PRBC

best diagnostic for aplastic anemia

bone marrow biopsy best** but can also use CBC

types of anemias that are hemolytic

• Sickle cell disease

• Thalassemia

• Glucose-6-phosphate dehydrogenase deficiency

• Immune hemolytic anemia

• Hereditary hemochromatosis

Thalassemia

inherited blood disorder in which the body makes an abnormal form or inadequate amount of hemoglobin. Results in large numbers of red blood cells being destroyed, which leads to anemia.

what is sickle cell anemia 

red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body cuasing pain and possibly organ damage

sickle cell anemia is most common in people from which descent

Africa

being a sickle cell carrier (not the disease but carry trait) makes you resistant to malaria

sickle cell anemia is triggered by

low oxegyn levels , cold temp, stress, exercise

signs and symptoms of sickle cell anemia

• anemia

• pain***

• fever, swelling, tenderness, hypertension

• organ damage

• infection d/t spleen dysfncton

sickle cell anemia interventions

• IV fluids 

  • dilutes blood volume to help flush sticky sickle cells out 

• hydroxyurea**

  • maintenance drug that makes RBCs less sticky and prevents sickling to some degree 

• transfusion

• oxygen**

  • cant leave on for too long bc kidneys will produce less erythropoietin 

• pain manage

  • morphine 

  • NSAIDS (ibuprofin)

  • dextrose 5% bc sickle cell has less ability to decrease sodium or something 

cure for sickle cell anemia

only cure is bone marroe and stem cell transplants but this is risky and rarely available 

polycythemia

increased volume of RBC’s

Primary polycythemia (Polycythemia Vera)

neoplastic – genetic mutation

secondary polycythemia

• Excessive production of erythropoietin from reduced amounts of oxygen, COPD, non-pathologic conditions or neoplasms

s/s of polycythemia

• HTN

• blood clots, DVT, stroke, venous stasiss 

• ruddy face and palms

interventions for polycythemia 

• phlembotomoy 

• low dose ASA 

• relieve hypoxia- O2

medical management of polycythemia

• treatment not needed if condition is mild 

• treat underlying cause 

• prevent complications

nursing management for bleeding disorders

limit injury, assess for bleeding, bleeding precautions

what are some types of bleeding disorders

• Secondary thrombocytosis

• Thrombocytopenia

• Immune thrombocytopenic purpura (ITP)

• Platelet defects

• Hemophilia

• von Willebrand disease

• Acquired Coagulation Disorders

what are some acquired coualuation disorders

• Liver disease

• Vitamin K deficiency

• Complications of anticoagulant therapy (HIT)

• Disseminated intravascular coagulation (DIC)

with bleeding disorders, what piece of information is important in determining how you treat it 

where in the clotting cascade is abnormal 

hemophilia and von wilebrand are both

hereditary genetic illnesses that impair the body’s ability to control bleeding

hemophilia is defined by a deficinecy in

clotting proteins such as Factor VIII (Hemophilia A), Factor IX (Hemophilia B)

hemophilia labs (PLT, PTT, PT) will look like 

PLT = normal, PTT prolonged, PT normal

von willebrand is defined by a lack of

Von Willebrand factor (vWD)

a clotting protein that is required for platelet clumping

von willebrand labs (PLT, PTT, PT) will look like 

PLT = normal, PTT prolonged, PT normal

thrombocytopenia

• Decreased platelets < 150K

Platelets < 50K =

prolonged bleeding

Platelets < 20 K =

spontaneous bleeding

s/s of thrombocytopenia

• petechiae 

• purpura 

• ecchymoeses 

• hemorahge

diagnostics of thrombocytopenia

• PLT count 

• bone marrow biopsy 

treatment and care of thrombocytopenia

• treat etiology 

• platelet transfuisons 

• avoid all injections 

• patient education 

• splenectomy 

  • macrophages sequester and destroy platelets 

  • ⅓ platelets are in the spleen

thrombocytopenia can be caused by

• Decreased production 

  •  Inherited 

  •  Acquired

• Increased destruction 

  • ITP – Immune thrombocytopenic purpura

    • Antiplatelet antibodies

  • TTP –Thrombotic TP

  • DIC 

  • HIT

thrombocythemia

bone marrow diseases causes PLT CT Over 400K

too many platelets!!!

dangers of thrombocythemia 

increased risk of thrombosis 

Disseminated Intravascular Coagulation (DIC)

• hemostasis out of control and it can also lead to bleeding 

Accelerated clotting → Loss of clotting factors → Hemorrhage

• Severity is variable; may be life threatening!

DIC triggers

sepsis, trauma, shock, cancer, abruptio placentae, toxins, and allergic reactions

describe altered hemostatis mechanism in DIC

• causes massive clotting in microcirculation. as clotting factors are consumed, bleeding occcurs. symptoms are related to tissue ischemia and bleeding 

DIC treatment

• treat underlying cause, correct tissue ischemia, replace fluids, maintain BP, replace coagulation factors and place them on heparin or LMWH

Heparin Induced Thrombocytopenia (HIT)

• Antibodies develop against heparin which activate platelets

• Drop in platelet count

• Development of thrombosis

• 20% mortality rate

HIT risk factors

surgery and females

treatment for HIT

• STOP HEPARIN

  • other anticoagulants: argatroban