MEDSURG II- EXAM 1

what is anemia (a deficiency in what 3 things)

For decr. RBC production what 3 things can cause this

When u have blood loss what are examples of acute vs. chronic blood loss

when u have incr. RBC destruction it is called what are what are some examples that can cause this

• what is aquired vs. hereditary

T/F Anemia is not usually the disease itself — it is a sign that something else is going on in the body. (underlying problem→ anemia)

what are the 3 morphology of RBC (appearance → size and color)

• what are the causes for each morphology

Give examples of acute blood loss that causes anemia

Give examples of chronic blood loss that causes anemia

symptoms vary depending on the what

what can acute Gi trigger and due to what

pts with massive blood loss are predisposed to what

Anemia is deficiency in number of erthocytes (RBCs), quantity/quality of Hgb, and volume of packed RBCs (hematocrit)

decr. RBC production:

1. deficient nutrients (i.e eating disorder)

   1. iron (decr. hgb synthesis), cobalamin (vit B12), and folic acid (vit B9) → both vit are defective DNA synthesis

2. decr. erythropoietin (vital protein hormone that stimulates the bone marrow to produce erythrocytes)

   1. iron is transported to bone marrow to make RBCs (Hgb) and the liver stores the iron

3. decr. iron availability

Blood loss:

• chronic: gastric

  • bleeding duodenal ulcer

  • colorectal cancer

  • liver dx (produces clotting factors)

    • pts with elevated liver enzymes will bleed

• Acute: blood vessel rupture

  • acute trauma

  • ruptured aortic aneurysm

  • GI bleeding

Incr. RBC destruction:

• hemolysis

  • sickle cell disease

  • meds (methyldopa (aldomet))

  • incompatible blood

  • trauma (cardiopulmonary bypass)

• Acquired (extrinsic): cancer or Disseminated intravascular coagulation

• Hereditary (intrinsic): sickle cell dx

TRUE EX:

• kidney dx → EPO

• iron deficiency → Hgb/Hgt

• cobalamin defi → vit B12

• folic acid defi → B9

• chemotherapty → damages bone marrow where RBC is made

• blood loss → GI bleed etc

RBC morphology

1. normocytic and normochromic → norm size and color

   1. acute blood loss, hemolysis, CKD, sickle cell anemia

2. microcytic and hypochromic → smaller and less color

   1. iron defi anemia thalassemia, vit B6 defi

3. macrocytic (megaloblastic) and normochromic

   1. colabamin (vit B12) defi, folic acid defi, and liver dx

Acute blood loss:

• sudden hemorrage

• perforated ulcer

• esophageal varices (veins of esophagus get to big w/ lots of pressure and when they burst u have hella blood loss)

Chronic blood loss:

• bleeding ulcer

• hemorrhoids

• menstrual

symptoms vary depending on the AMOUNT OF BLOOD LOSS
acute GI bleed can trigger an ACUTE MI due to LOW CARDIAC OUTPUT and the POTENTIAL for MYOCARDIAL ISCHEMIA

pts with massive blood loss are predisposed to HYPOVOLEMIC SHOCK

what is the most common nutritional disorder in the world

iron defi anemia can be caused by what 3 things

what is thalassemia

t/f thalassemia is NOT heredity

what is thalassemia minor vs thalassemia major and HIGHLIGHT the diff

what is the most common cause a person to have cobalamin (B12) defi and other causes

it may take several months for manifestations to develop but what are they for B12 defi

how do u treat b12 defi → b12 helps with mature of RBC and nerves

what are the causes of folic acid b9 defi → helps with devlopment of RBC

what may pt experience due to b9 defi

how do we tx b9 defi

how do ppl with chronic dx like cancer, autoimmune disorder, and CKD become anemic

• be specific only for ckd

whats some of the diagnostic tests that you will complete for anemia

• when blood loss is sudden what has not had a change to incr which leads to reflect what

what would the diagnostic findings look like for anemia

iron defi anemia

cause for iron defi anemia:

1. inadequate dietary intake

2. malabsoprtion

3. chronic blood loss (menses→ period, ulcer, cancer)

thalassemia: a group of dx involving inadequte production of normal hgb

FALSE it is hereditary

thalassemia minor:

• mild to mod anemia

• mild splenomegaly

• bronzed color of the skin

• and bone marrow hyperplasia

thalassemia major

• severe anemia

• symptoms develop in childhood by 2 yrs old and can cause growth developmental deficits

• pale jaundice

• pronounced splenomegaly

B12 defi:

• most common cause is pernicious anemia, the problem isn't necessarily that the person isn't eating B12. They lack intrinsic factor, so they can't properly absorb B12.

• other causes:

  • Gi surgery (gastrectomy, gastic bypass)

  • chron’s dx, ileitis, or celiac dx

  • alcoholsim

  • long time use of H2 histamines receptor blockers and PPI (protonix)

• Manifestations:

  • sore, red, beefy, and shiny tongue

  • anorexia, n/v

  • weakness, paresthesia of ft and hands

  • ataxia (balance off), muscle weakness

  • confusion

• TX: w/ IV vit B12 or intranasal cyanocobalamin

B9 defi:

• causes:

  • dietary defi

  • incr. demand (prego)

  • malabsorption syndromes

  • hemodialysis → pt goes through artificial kidney and removes b9

  • alcoholism

  • drugs interfering w/ absorption or use of folic acid

• pts may experience stomatitis (inside) , cheilosis (lips/corners) (inflammation and dryness of lips), dysphagia, flatulence, and diarrhea

• TX: w/ replacement therapy

chronic dx cause anemia by under production of rbc and mild shortening of rbc survival

• for CKD specifically → the primary cause of anemia is decr. EPO production

diagnostic tests for anemia:

• CBC

• reticulocyte count

• peripheral blood smear: morphology

• when blood volume loss is sudden, plasma volume has not yet had a chance to incr (order a series)

  • initial blood loss is igb not hct doesnt go down takes a couple of days

  • so initial lab values may not reflect anemia

• after 2-3 days RBC, Hgb and , HCT levels are low and reflect actual blood loss

diagnostic findings for anemia:

• decr. rbc, hgb, hct

• possible decr. in serum iron, ferritin, folate, b12, or EPO levels

• + heme-positive stool → certain age group for colon cancer

what are the manifestations for anemia → symptoms very depending on severity and cause

what levels are often use to determine severity of anemia

how would u assess an anemic pt subjectively and objectively

what are some of nursing diagnoses for anemia

what are some overall goals for pt with anemia

what are some nursing interventions for anemia

What is sickle cell disease (SCD)?

• how is it usually identified

Which organs can SCD affect?

what is some curative tx for SCD

what causes SCD → rbc to sickle

How do normal RBCs differ from sickled RBCs?

What are the types of SCD

Which studies diagnose or evaluate SCD

Manifestations:

• fatigue

• heart palpitations/conjunctival pallor

• dyspnea on exertion (DOE) or SOB

• pallor or jaundice

Hgb levels are often use to determine severity of anemia

assess an anemic pt subjectively and objectively

SUB:

• interview pt

• important health info

  • past medical hx, meds, surgery/other tx, and dietary hx

• functional health patterns

  • signs and symptoms of blood loss

Object:

• head to toe assessment

  • skin, resp, cardio, GI, neuro, GU (hemturia or myoglobin)

• Diagnostic findings

nursing diagnoses for anemia:

• fatigue

• activity intolerance

• impaired gas exchange

• risk for bleeding

• impaired nutritonal stutus

• ineffective tissue perfusion

• chronic pain

• dizziness

• tachycardia

• headache

Anemia Planning:

• overall goals

  • normal activities of daily living w/o fatigue or SOB

  • adequate nutrition

  • managing constipation

  • fall prevention

  • pt education

  • monitor VS and O2

  • lab values (hgb and hct) return to norm

  • manage fatigue

nursing interventions for anemia

• alternate rest and activity

• prioritize activities

  • accommodate energy levels

  • maximize 02 supply for vital functions

• aid to minimize risk of injury from falls

• monitor cardioresp. response

• nutritional consult

• blood transfusion

SCD: A group of inherited, autosomal-recessive disorders involving an abnormal form of hemoglobin in red blood cells.

• It is usually identified during routine newborn screening.

organs affected by SCD: The lungs, kidneys, brain, retina/eyes, bones

Tx: bone marrow transplant, gene therapy

cause of SCD:

• abnormal hgb (Hgb S) causes the RBC to stiffen and elongate

  • The valine replacing glutamic acid is simply the genetic change that creates the abnormal Hgb S

  • this causes the RBC to stiffen and elongate taking a sickle shape in response to low 02

Normal RBCs are compact and flexible, so they squeeze through small capillaries. Sickled RBCs are stiff and angular and can become trapped in small capillaries.

Types of SCD:

1. Sickle cell anemia (the most severe form)

2. sickle cell-thalassemia

3. Sickle cell hemoglobin C disease

4. Sickle cell trait

   1. the person carries one abnormal gene and is generally asymptomatic; disease occurs when abnormal genes are inherited from both parents

SCD diagnostic studies:

• Peripheral blood smear

• hemoglobin electrophoresis: a blood test that tells you what TYPES of hemoglobin a person has.

• skeletal x-rays

• MRI

• Doppler studies→ ultrasound to see how blood is flowing

• chest x-ray

What is the major pathophysiologic event in SCD → sickling episodes

• What can trigger a sickling episode?

Is sickling reversible

what is vaso occlusion

• How does sickling cause vaso-occlusion and tissue injury

How does SCD cause anemia

What are the two clinical hallmarks of SCD

What is a sickle cell crisis

• What happens during a severe vasoocclusive crisis

• what is a possible life threatening crisis due to vasoocclusive crisis

What are the 4 main goals during a sickle cell crisis

What are common clinical manifestations of SCD

• are pts with scd always symptomatic

LOOK AT SLIDE 28 4 SYMPTOMS FOR ALL SYSTEMS OF THE BODY WHEN HAVING SCD

for scd there are 2 complications:

• Why is infection especially dangerous in SCD

• What is acute chest syndrome

What are the overall care priorities for SCD

What nursing interventions are used for SCD or crisis

sickling ep: A sickling episode triggered by low oxygen tension in the blood.

• Infection (the most common precipitating factor)

• dehydration

• acidosis/increased hydrogen ion concentration

• increased plasma osmolality

• decreased plasma volume

• low body temperature

At first, yes. Early sickling can reverse with reoxygenation. Repeated or prolonged sickling causes permanent membrane damage and rigid cells

vaso occlusion: blockage of blood vessels by rigid, sickle-shaped red blood cells

• Rigid crescent-shaped RBCs cannot pass easily through capillaries. They obstruct blood flow, causing hypoxia and chronic tissue injury. Hypoxia deoxygenates more RBCs, which causes more sickling

SCD causes anemia by the spleen removes and hemolyzes circulating sickled RBCs, shortening their life span and causing anemia

2 clinical hallmarks of SCD

1. vaso-occlusive phenomena

2. hemolysis

sickle cell crisis: A severe, painful, acute worsening of RBC sickling that causes a vaso-occlusive crisis

• Severe capillary hypoxia changes membrane permeability, leading to plasma loss, hemoconcentration, thrombi, and further circulatory stagnation

• Shock is a possible life-threatening consequence and may require life support

4 main goals of SCD:

1. Improve oxygenation

2. provide hydration

3. prevent complications

4. manage pain

clinical manifestations of SCD:'

• The patient may be asymptomatic between sickling episodes

• pain from tissue hypoxia/damage

• pale mucous membranes

• jaundice from hemolysis

• gallstones (cholelithiasis)

scd complications:

1. Infection is a major cause of illness and death

   1. Sickled cells damage the spleen and impair its immune function

   2. Severe infection can also trigger an aplastic crisis (temporary, severe drop in rbc production by the bone marrow)

   3. Pneumococcal pneumonia is an important risk

2. acute chest syndrome:

   1. A serious lung complication involving pneumonia, tissue infarction, or fat embolism

   2. characterized by fever, chest pain, cough, new lung infiltrates, and dyspnea and can lead to multiple serious complications

overall care priorities for SCD:

• Prevent sequelae (abnormalities) from sickle cell

• relieve manifestations of complications

• minimize end-organ damage

• continuously assess for and promptly treat serious complication

Nursing Interventions for SCD:

• Give oxygen to treat hypoxia and control sickling

• administer IV fluids

• manage pain

• treat infections

• administer folic acid

• provide patient/caregiver education

• support for living with a chronic illness

What is polycythemia

Why can polycythemia impair circulation

What is primary polycythemia (polycythemia vera)

• what is low/norm

• what can occur due to this

What is secondary polycythemia

• what are the 2 types of secondary and give ex

What causes the clinical manifestations of polycythemia

What causes the clinical manifestations and complications of polycythemia

Which diagnostic studies are used for polycythemia

What diagnostic findings support polycythemia

What are the management goals for polycythemia

• How is polycythemia managed

polycythemia: Production and presence of an increased number of RBC → blood gets thick

polycythemia impair circulation by the increased RBC mass makes blood abnormally thick (hyperviscosity) and increases blood volume (hypervolemia), slowing or obstructing circulation

primary polycythemia: bone marrow disorder with increased production of RBCs and often WBCs and platelets

• EPO is low or normal

• splenomegaly/hepatomegaly can occur

secondary polycythemia: An increase in RBCs caused by increased EPO

• hypoxia-driven: low 02 stimulates the kidnesy production to make EPO

  • high altitude

  • cardiopulmonary dx

  • defective 02 transport

• hypoxia-independent: 02 is norm but something is causing your kidneys to make more EPO

  • renal cysts or tumors

  • extrarenal tumors

Causes for polycythemia:

• Hypervolemia and hyperviscosity

Manifestations and complications for polycythemia

• HTN from fluid/volume overload

• chest pain

• headache

• dizziness

• intermittent claudication (pain or cramping, often in the buttock/leg with activity),

• thrombosis such as pulmonary embolism or stroke.

Diagnostic studies for polycythemia:

• CBC

• bone marrow aspiration

• bone marrow biopsy

• mutation/other marker

diagnostic findings for polycythemia:

• High Hgb, Hct, and RBC mass

• hypercellular bone marrow with increased RBCs, WBCs, and platelets

• JAK2 V617F or JAK2 exon 12 mutation

• low EPO

• high WBC count with basophilia and neutrophilia

• high platelet count with platelet dysfunction

• high uric acid and cobalamin levels

management goals for polycythemia:

• Reduce blood volume, blood viscosity, bone marrow activity

  • Phlebotomy, commonly about 500 mL every 2-3 months to reduce Hct

  • adequate fluids

  • low-dose aspirin

  • allopurinol to lower uric acid

  • myelosuppressive agents such as hydroxyurea, busulfan (Myleran), or chlorambucil (Leukeran)

    • stops production of blood cells in bone marrow

What is thrombocytopenia

• results in what

• how is it primarily acquired

What are major causes/types of thrombocytopenia

What is ITP

• how does it usually present as

  • in children/adults

  • tx

What is TTP

• occurs primarily with who

• why is TTP a medical emergency

What is HIT and when does it develop

• What is the 3 major danger of HIT

What are the skin findings of thrombocytopenia

What other manifestations can thrombocytopenia cause

What platelet count is abnormal, and what coagulation studies may be checked for diagnostic

What is the focus of interprofessional care for thrombocytopenia

What subjective data should the nurse collect

What objective findings should the nurse assess

What nursing diagnoses apply to thrombocytopenia

What are the overall goals for thrombocytopenia → Planning

What nursing interventions are important for thrombocytopenia

thrombocytopenia: A platelet count below 150,000/microliter

• results in abnormal hemostasis and can lead to prolonged or spontaneous bleeding

• mainly acquired and commonly related to ingestion of certain drug

causes/types of thrombocytopenia:

• Inherited disorders

• acquired disorders

  • immune thrombocytopenic purpura (ITP)

  • thrombotic thrombocytopenic purpura (TTP)

  • heparin-induced thrombocytopenia (HIT)

ITP: an autoimmune disorder in which circulating platelets are abnormally destroyed

• most common acquired thrombocytopenia

• presents acutely in children and chronically in adults

• tx with multiple therapies

TTP: enhanced platelet aggregation and formation of microthrombi

• occurs primarily in healthy adults

• It may be autoimmune or caused by drug toxicity

• uncommon syndrome

• It is a medical emergency because clotting and bleeding occur simultaneously

HIT: Thrombocytopenia associated with heparin, usually developing 5-10 days after therapy begins, with a platelet drop greater than 50%

• Venous thromboembolism is the major problem

• arterial thrombosis can also occur

• DVT/VTE and pulmonary embolism commonly result

skin findings of thrombocytopenia:

• Petechiae are tiny 1-2 mm microhemorrhages

• Purpura are larger bruise-like areas made of many petechiae

• Ecchymoses are larger hemorrhagic lesions, usually greater than 1-2 cm

Other manifestations:

• Patients may be asymptomatic, but mucosal or skin bleeding is most common

• Hemorrhage may be slow/insidious or acute

• internal bleeding may cause weakness

• fainting

• dizziness

• tachycardia

• abdominal pain

• hypotension

• Cerebral hemorrhage may be fatal

diagnostic for thrombocytopenia:

• Platelets below 150,000/microliter are low

• Associated tests include activated clotting time (ACT)

• prothrombin time (PT)

• activated partial thromboplastin time (aPTT) → if on heparin

interprofessional care for thrombocytopenia:

• Identify and remove or treat the cause

• Avoid aspirin and other drugs that impair platelet function or production

• Platelet transfusion may be needed when the count is below 10,000/microliter or the patient is actively bleeding

• Use fall precautions and caution with invasive procedures

Nursing Assessment

• Sub:

  • Past health history

  • medications

  • functional health patterns → especially bleeding symptoms and safety risk

• Object:

  • Fever

  • lethargy

  • visible bleeding

  • splenomegaly

  • abdominal distention

  • skin/mucosal lesions

  • vital signs

  • lab data

nursing diagnoses to thrombocytopenia:

• Risk for bleeding

• impaired skin integrity

• activity intolerance

• anxiety/fear

• risk for infection

• deficient fluid volume from bleeding

• altered body image → skin lesions

• risk for falls

Planning/overall goals:

• Prevent bleeding

• monitor for bleeding

• educate safety precautions

• maintain vascular integrity

• safely manage home care to prevent complications for incr. risk of bleeding

Nursing Interventions:

• Closely monitor platelets

• coagulation studies, Hgb, and Hct

• avoid IM injections

• limit IV sticks

• correct coagulopathy before surgery

• prevent/control hemorrhage

• administer platelet transfusions as ordered

What is leukopenia

What is granulocytopenia

What is neutropenia

How is absolute neutrophil count (ANC) calculated

What is the main function of neutrophils

What can cause neutropenia

What infections occur with neutropenia → manifestations

Which diagnostic studies evaluate neutropenia

What are the main management priorities for neutropenia

• What do hematopoietic growth factors do?

• How should the nurse protect a neutropenic patient from infection

What food-safety measures are used for neutropenia

What cultures may be obtained from a neutropenic patient

What teaching is important for neutropenia?

What is hemophilia?

What is von Willebrand disease

What bleeding pattern is common in hemophilia/von Willebrand disease

What clinical manifestations can occur

Why is compartment syndrome dangerous

How are these disorders diagnosed?

How are hemophilia and von Willebrand disease managed

leukopenia: A reduction in the total WBC count

granulocytopenia: A deficiency of granulocytes: neutrophils, eosinophils, and basophils

neutropenia: A reduction in neutrophils. ANC below 1,000 cells/microliter as neutropenia

absolute neutrophil count (ANC) calculated: Multiply the total WBC count by the percentage of neutrophils

• helps determine infection risk

main function of neutrophils: They phagocytose and destroy pathogenic microbes. A low neutrophil count indicates increased infection risk

cause neutropenia:

• Autoimmune disorders

• drugs/chemotherapy

• hematologic disorders

• infections

• hemodialysis

• cobalamin or folic acid deficiencies

• sepsis → worst for cancer pts cause their immune system is trash

Manifestations:

• Serious systemic bacterial, fungal, and viral infections are common

• The patient's own normally nonpathogenic flora can cause life-threatening infection because immune defenses are weak

Diagnostic studies:

• A WBC count with differential, peripheral WBC count

• bone marrow aspiration/biopsy

main management priorities:

1. Determine the cause

2. begin antibiotics promptly

3. identify the organism when infection develops

4. give hematopoietic growth factors prophylactically after chemotherapy

   1. They are proteins that regulate production and differentiation of blood cells in bone marrow

5. use protective practices to prevent infection → IMPORTANT

   1. Ensure everyone performs hand hygiene before, during, and after care

   2. assess for infection

   3. screen visitors

   4. obtain ordered cultures

   5. give antibiotics/growth factors

   6. manage fever

   7. provide daily skin care and frequent oral hygiene

food-safety measures are used for neutropenia:

• Wash fruits and vegetables well, keep hot foods hot and cold foods cold, and avoid undercooked eggs and meats to reduce exposure to foodborne bacteria

cultures for neutropenia pt:

• Sputum, throat, skin lesions, wounds, urine, and feces as indicated

Teaching for neutropenia: Teach hand hygiene, skin and oral care, ways to avoid infection, signs and symptoms of infection, and what to do if symptoms occur

hemophilia: an inherited bleeding disorder where the blood has trouble clotting → missing clotting factors

• the two major types are hemophilia A and hemophilia B

von Willebrand disease: a bleeding disorder where von Willebrand factor (vWF → made in liver) is missing or doesn't work correctly → helps platelet stick to damage nerves

in common w/ both dx: Slow, persistent, prolonged, or delayed bleeding after minor injury. Bleeding can become life-threatening’

manifestations:

• Uncontrollable bleeding after dental extraction or toothbrush irritation

• epistaxis → nosebleed

• GI bleeding from ulcers/gastritis

• hematuria with possible renal failure

• ecchymoses

• subcutaneous hematomas

• compartment syndrome → too much pressure builds up inside a muscle area → blood can't get in → tissue doesn't get oxygen → it is a limb-threatening emergency

• neurologic signs

• hemarthrosis → bleeding into a joint space, most commonly affecting the knee

Diagnostic studies:

• They do blood tests to figure out WHICH clotting factor is missing or not working

  • factors VIII, IX, XI, XII, or von Willebrand factor

Interprofessional care:

• Prevent injury/bleeding

• give the missing factor or other replacement therapy

• treat complications promptly

What is DIC → disseminated intravascular coagulation

• Why does DIC cause both clotting and bleeding

What disorders can trigger DIC

What are general manifestations of DIC

What thrombosis signs may occur by organ system?

What hemorrhage signs may occur by organ system?

What should the nurse monitor in a patient at risk for DIC? → nursing management

• What is the priority treatment for DIC

What blood components and approximate volumes were listed for a blood transfusion

for the administration procedure

• What is required for blood transfusion consent

• What IV equipment is required for blood administration

• Which solution is compatible with blood

• How is the tubing prepared

• When are vital signs taken for a transfusion

• What safety checks are performed before administering blood

• What should the nurse do during the beginning of the transfusion

• What findings suggest a transfusion reaction

What should the nurse do if a transfusion reaction is suspected?

DIC: the body starts making WAY too many tiny blood clots everywhere

• Widespread microthrombi (tiny blood clots) form → platelets + clotting factors (things needed to clot) get consumed/used up → fibrinolysis (body breaks down clots) occurs → fibrin degradation products/FDPs (leftover pieces of broken clots) ↑ → not enough clotting supplies left → uncontrolled bleeding.

trigger DIC: this starts the way too much clots being produced

• Cancer

• autoimmune disease

• septic shock/septicemia

• trauma

• hemolytic processes

• obstetric conditions

• shock

• major tissue damage

Manifestations of DIC:

• Pallor

• petechiae

• purpura

• oozing blood

• hematomas

• occult bleeding

• tachypnea

• hemoptysis

• tachycardia

• hypotension

• upper/lower GI bleeding

• abdominal distention

• bloody stools

• hematuria

• neurologic changes

• and bone/joint pain

thrombosis signs may occur by organ system:

• Neurologic: delirium/coma.

• Skin: ischemia/gangrene

• Renal: oliguria/azotemia

• Pulmonary: ARDS

• GI: paralytic ileus

• Cardiovascular: ECG changes and venous distention

hemorrhage signs may occur by organ system:

• Neurologic: intracerebral bleeding

• Skin: petechiae/ecchymoses

• Renal: hematuria

• Pulmonary: dyspnea/hemoptysis

• GI/mucosal: massive bleeding, epistaxis, and gingival bleeding

DIC nursing management:

• Monitor risk factors for early detection

• assess for external bleeding

  • petechiae and oozing IV sites

• assess for internal bleeding

  • elevated heart rate

  • changing level of consciousness

  • increasing abdominal girth

  • abdominal pain

• TX: treat symptoms and underlying causes

Components for a blood transfusion:

• Whole blood about 500 mL

• packed RBCs about 300 mL

• fresh frozen plasma about 250 mL

• platelets about 25-50 mL

• Cryoprecipitate may also be used for selected clotting-factor deficiencies

Administration procedure

• blood consent:

  • The provider explains risks and benefits, the nurse witnesses the patient's signature, and the patient has the right to refuse

• IV equipment:

  • A 20-gauge IV or larger and blood tubing with a 170-260 micron filter

• Solution:

  • 0.9% NS only. Do not add medications or other additives to the same tubing as blood

• Tube prepared:

  • Prime the blood tubing with normal saline only

• VS:

  • Record baseline vital signs before starting

  • repeat them 15 minutes after starting

  • recheck whenever a reaction is suspected

  • obtain final vital signs when the transfusion is complete

• safety check:

  • When picking up the product, compare it with the order

  • At the bedside, two RNs verify the patient identity against the labeled component, including blood type and expiration date

• Beginning of transfusion:

  • Stay with the patient during the first 15 minutes or first 50 mL, when serious transfusion reactions are most likely to appear

• transfusion reaction:

  • Fever

  • hives

  • abdominal/chest/flank pain

  • tachycardia

  • dyspnea

  • tachypnea

  • hypotension

Transfusion reaction management:

• Stop the blood immediately

• assess the patient and check vital signs

• notify the provider

• disconnect the blood and run a new bag of normal saline through new tubing as directed

• draw blood for serologic testing → to see what went wrong with bag

• send a urine specimen to the laboratory

• do not restart the transfusion

What is bronchiectasis

• what are the hallmark characteristics

• What causes the bronchi to become permanently dilated?

• What cycle occurs in bronchiectasis?

What pathologic changes are seen in bronchiectasis?

What sputum finding is characteristic of bronchiectasis

What are the clinical manifestations of bronchiectasis

• Why can bronchiectasis cause hemoptysis

What are the complications of bronchiectasis?

What is the gold-standard diagnostic test for bronchiectasis?

• What other studies are used for bronchiectasis?

• Which organisms commonly infect patients with bronchiectasis?

What are the nursing priorities for bronchiectasis? → nursing management

What common nursing problems occur with bronchiectasis?

What should the nurse teach a patient with bronchiectasis?

bronchiectasis: permanent widening and damage of the bronchi (large airways), causing mucus to build up

• hallmark characteristics: Permanent, abnormal dilation of medium-sized bronchi

• results from Chronic inflammation destroys the elastic and muscular structures that support the bronchial wall

• cycle is Inflammation causes airway damage and remodeling. Poor secretion clearance allows mucus, pus, and infection to remain, which creates more inflammation and damage. Accumulated neutrophils make the cycle worse

pathologic changes:

• Chronic lung infection → damages the airway walls → airways become stretched/widened (dilated) → thick mucus + pus (purulent/mucopurulent secretions) collect inside → mucus gets trapped → more infections.

Sputum: Production of thick, tenacious, purulent sputum

Manifestation:

• Thick purulent sputum

• recurrent infections

• hemoptysis

  • Abnormal connections (anastomoses) may form between lung blood vessels. Chronic injury may also cause new bronchial blood vessels (neovascularization). These fragile vessels can bleed.

• pleuritic chest pain

• dyspnea

• wheezing

• weight loss

• anemia

Complications:

• Pulmonary hypertension

• chronic inflammation

• hypoxemia,

• colonization by multidrug-resistant organisms

• neovascularization

• hemoptysis

Diagnostic studies:

• CT is golden standard

• Chest x-ray

• spirometry → revelas an obstructive pattern

• sputum cultures → confirm presence of infection

  • Haemophilus influenzae, Staphylococcus aureus, and Pseudomonas aeruginosa

• CBC

• alpha-1 antitrypsin (AAT) level → measures concentration of alpha-1 antitrypsin protein in the blood

nursing management:

• Maintain stable vital signs and a patent airway

• monitor for expectoration of large amounts of blood

• support as much functional independence as possible

Nursing problems when managing:

• Impaired respiratory function and activity intolerance.

Pt teaching:

• Stop smoking

• drink about 2-3 L of fluid daily if not contraindicated

• recognize increased work of breathing

• contact the healthcare provider for fever, dyspnea/SOB, or hemoptysis