Heart Valves and Heart Failure, Exams of Nursing

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NR 507: MIDTERM REVIEW

Hematology

Hematopoiesis: -process of blood cell production

-Constant throughout life to replace RBCs that grow old and die, are killed by disease, or are lost through bleeding

-Occurs in liver and spleen of fetus

-Occurs in bone marrow after birth

-2 stages: 1. Proliferation (mitotic division)

2. Maturation (differentiation)

-Bone marrow: red (hematopoietic/active) & yellow (fatty/inactive)

Hematopoietic stem cells (HSCs)- all blood cells are created from HSCs

-signaled to undergo differentiation (by cytokines and chemokines, growth factors) to form RBC, WBC, & platelets

 Lymphoid: T cell (T-lymphocyte) & B cell (B-lymphocyte)

 Myeloid: Monocyte & Granulocytes (WBCs)

 Erythrocyte (RBC)

 Megakaryocyte (Platelets)

Mesenchymal stem cells-develop into osteoclasts, fibroblasts, & adipocytes

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Erythropoietin: -hormone that stimulates erythrocyte production

Hemoglobin: oxygen carrying protein of the erythrocyte

-hemoglobin packed blood cells pick up oxygen in the lungs and exchange it for carbon dioxide in the tissues

-composed of 2 pairs of polypeptide chains (globins) & 4 colorful iron complexes (hemes)

-can carry up to 4 molecules of oxygen

Oxyheoglobin- binding of oxygen to Fe in heme molecule, RED

Deoxyhemoglobin- reduced hemoglobin, after it releases the oxygen to the tissues, BLUE

Risk factors and causes for developing any type of anemia:

-blood loss (acute or chronic)

-impaired erythrocyte production

-increased erythrocyte destruction

-a combination of these factors

Iron Deficiency Anemia- Microcytic-Hypochromic Anemia

-most common nutritional disorder

-occurs when iron stores are depleted reduced hemoglobin synthesis

-more common in toddlers, adolescent girls and, women of childbearing age

• causes:

 Dietary deficiency

 Impaired absorption

 Increased requirement

Sickle Cell Anemia-Normocytic-normochromic/Hemolytic

-inherited autosomal recessive disorder

-presence of atypical hemoglobin-Hemoglobin S

-amino acid change on the beta-globin chain (glutamine replaced for valine)-distort erythrocytes into sickle shape= cannot properly carry O2.

-vaso-occlusive crisis (pain), aplastic crisis (anemia), sequestration crisis (blood pooling in spleen), hyperhemolytic crisis ( accelerated RBC destruction)

• Stress, hypoxia, anxiety, fever, cold, dehydration = lower O2 binding
• ↑ risk of CVA, splenic damage, or kidney damage. Most people with sickle cell will become asplenic by adulthood.

Hemolytic Anemia-

-premature destruction of erythrocytes

-majority occur within phagocyctes in lymphoid tissue

-congenital (sickle cell or thalassemia) acquired (transfusion reaction, infection, autoimmune)

-causes elevated erythropoietin to induce accelerated production of erythrocytes and in increase in the products of hemoglobin catabolism

-transfusion with incorrect blood type: intravascular hemolysis by activation of complement system; extravascular hemolysis by phagocytosis of antibody-coated erythrocytes in spleen

Pernicious Anemia-Macrocytic

-vitamin B deficiency

-Autoimmune gastritis-impaired intrinsic factor (transporter needed for vitamin B absorption)

smallest of conducting airways

-3 layers:

1. Epilthelial layer- (inner layer) mucous containing goblet cells, ciliated cells
2. Connective tissue layer- lamina propia- cartilage, WBCs
3. Smooth muscle layer- outer layer to constrict and dilate

-Bronchioles branch out from the bronchi and connect to the alveoli.

-Controlled by the ANS (autonomic nervous system).

o Parasympathetic stimulation- mediated via vagus nerve

 Releases neurotransmitter acetylcholine-binds to cholingeric receptors leading to bronchial constriction (decreased air flow)

 Dominates to limit exposure to external substances (protection mechanism)

o Sympathetic stimulation- stimulation of neurotransmitter epinephrine- binds to beta-2 adrenergic receptors  leading to bronchial dilation (increased air flow)

Asthma-

chronic inflammatory disorder of the bronchial mucosa

-causes bronchial hyper-responsiveness, constriction of airways, and variable airflow obstruction that is reversible

Pathophysiology : Antigen enters bronchial airway binds to sensitized mast cells and cover with IgEtriggers mast cell degranulation and release of inflammatory mediators’ histamines, bradykinins, prostaglandins, platelet- activating factors, prostaglandins, leukotrienes, interleukin. smooth muscle constriction, mucus secretion, and vasodilation  mucosal edema and migration of more WBCs to site  dendritic cells also present Ag to Th2 cells  causing interleukin release to produce more IgE to coat mast cells and facilitate Ag binding. Interleukin also activates eosinophils release of chemicals designed to rid the area of Ag, but instead damage surrounding airway tissue activated neutrophils amplify this damaging effect. Long term damage can lead to permanent airway remodeling.

o chest constriction

o expiratory wheezing

o dyspnea

o nonproductive coughing

o prolonged expiration

o tachycardia

o tachypnea

• severe attacks:

o use of accessory muscles of respiration

o wheezing during both inspiration and expiration

o pulsus paradoxus- decrease in SBP during inspiration >10mmHg

Alveolar hyperinflation with asthma

-airway obstruction increases airflow resistance and decreases flow rates.

-impaired expiration causes air trapping, hyperinflation distal to obstruction, and increased WOB.

• continued air trapping increases intrapleural pressure and alveolar gas pressuresdecreased alveolar perfusion

-hyperventilation is triggered in response to increased lung volume and obstruction (early hypoxemia without CO 2 retention and respiratory alkalosis)

-with progressive obstruction of expiratory airflow, airtrapping becomes more severe  lungs and thorax hyperexanded, disadvantage to respiratory musclesdecrease in tidal volume and increase in CO 2 retentionrespiratory acidosis (triggering respiratory failure)

Anticholinergic drugs and the treatment for asthma

Chronic bronchitis and related acid/base disturbances,

-narrowed airwaysobstructionventilation-perfusion mismatch with hypoxemia

-Hypercapnia develops as air trapping worsens and the work of breathing increases

-reduced tidal volumes, hypoventilationrespiratory acidosis

Polycythemia vera

-Marked hypoxemia (e.g. chronic bronchitis) leads to polycythemia (overproduction of erythrocytes) and cyanosis.

-PV is a chronic neoplastic, nonmalignant condition characterized by overproduction of red blood cells (frequently with increased levels of white blood cells [leukocytosis] and platelets [thrombocytosis]) and splenomegaly.

-Erythrocytosis is the essential component of PV. Clonal proliferation of erythroid progenitors occurs in the bone marrow independent of erythropoietin, although the cells express a normal erythropoietin receptor

Cardiac

<clip_image002.png>Blood flow between heart and lungs

-The superior & inferior vena cava carry systemic

DEOXYgenated blood to the right atrium.

-The tricuspid valve opens to allow blood flow into the

right ventricle.

to the left atrium.

-The bicuspid valve opens to allow blood flow into the

left ventricle.

The aortic semilunar valve opens to allow blood flow into the

aorta,a large blood vessel that divides to form the brachiocephalic,

left common carotid, and subclavian arteries that will further

branch to carry blood to the rest of the body.

Cardiac cycle:

1. Atrial systole, atria contract blood pushes through open tricuspid and mitral valves into ventricles. Semilunar vavles are closed
2. Beginning of ventricular systole, ventricles contract, increased pressure in ventricles. Tricuspid and mitral valves close, (1st^ heart sound)
3. As pressure rises, semilunar valves open when ventricular pressure>atrial pressure blood pushed into aorta and pulmonary arteries
4. Beginning of ventricular diastole, pressure in relaxing ventricles drop below that in the arteries and semilunar valves close (2nd^ heart sound)
5. As pressure falls, blood flows from veins into relaxed atria. Tricuspid and mitral valves open when pressure in ventricle falls below atrial pressure

Heart Valves

-One-way blood flow through the heart is ensured by the four heart valves

- Atrioventricular valves

-mitral (left AV valve) and tricuspid (right AV valve)