* losses from excessive sweating, vomiting and diarrhea * Uses of certain diuretic drugs combined with low-salt diets * Hormonal balances: insufficient aldosterone, adrenal insufficiency, excess ADH secretion * Early chronic renal failure * Excessive water intake
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Effects of hyponatremia
* Impaired nerve conduction and result in fluid imbalances in the compartments: fatigue, muscle cramps, abdominal discomfort or cramps with nausea and vomiting * Decreased osmotic pressure in the extracellular compartment: hypovolemia, decreased blood pressure
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Hyperkalemia
Excessive potassium levels in the extracellular fluids
* greater than 5
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Causes of hyperkalemia
* Renal failure * Deficit of aldosterone * Use of “potassium sparing” diuretic drugs: prevent potassium from being excreted in a adequate amounts * Leakage of intracellular potassium into the extracellular fluids * Displacement of potassium from cells by prolonged or severe acidosis
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Effects of hyperkalemia
* Cardiac dysrhythmias that could progress to cardiac arrest * Muscle weakness; could progress to paralysis * Fatigue, nausea * Parethesias: fingers, nose, face * Oliguria
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Hypokalemia
insufficient potassium levels in the extracellular fluids
* less than 3.5
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Causes of hypokalemia
* Diuresis associated with certain diuretic drugs * Presence of excessive aldosterone or glucocorticoids * Decreased dietary intake * Treatment of diabetic ketoacidosis with insulin
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Effects of hypokalemia
* Cardiac dysrhythmias * Impaired neuromuscular function and muscles less responsive to stimuli: fatigue and muscle weakness in the legs; twitch, leg cramps * Paresthesia: abnormal touch sensations such as “pins and needles” * Anorexia, nausea * Slow shallow respirations
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Acidosis
excess hydrogen ions; decrease in serum pH
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Respiratory acidosis
increase in carbon dioxide levels due to respiratory problems
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Causes of respiratory acidosis
* Acute respiratory problems such as Pneumonia, chest injuries, use of opiates, airway obstruction (aspiration or asthma) * COPD: chronic respiratory acidosis is common * Decompensated respiratory acidosis: severe impairment; when a chronic problem develops an additional infection
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Metabolic acidosis
a decrease in serum bicarbonate
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Causes of metabolic acidosis
* Shock * Excessive loss of bicarbonate: diarrhea, loss of bicarbonate in intestinal secretions * Increased utilization of serum bicarbonate to buffer increased acids * Renal disease or failure: decreased secretion of acids and decreased production of bicarbonate
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Acidosis Effects
impaired nervous function- headache, lethargy, weakness, confusion, coma and death
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Acidosis Compensation
deep rapid breathing secretion of urine with a low pH
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Alkalosis
deficit of hydrogen ions, increase in serum pH
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Respiratory alkalosis
decrease in carbon levels due to respiratory problems
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Causes of respiratory alkalosis
Hyperventilation: anxiety, aspirin overdose
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Metabolic alkalosis
increase in serum bicarbonate; loss of hydrogen ions through the kidneys or gastrointestinal tract
1. sensory stimuli move along competing pathways 2. brain produces outgoing transmissions through reticular system 3. brain release opiate-like chemicals: endorphins block substances at the synapse, natural opiate receptors are through brain
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First line of defense:
nonspecific or general mechanism such as skin or mucous membrane
* blocks the entry of bacteria
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Second line of defense
innate immune system mechanism
* non-specific process of phagocytosis, inflammation, interferons
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Third line of defense
specific mechanism in the body: stimulate the production of antibodies, synthesized t-lymphocytes
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Leukotrienes
Group of lipids derived from mast cells and basophils
* cause contraction of bronchiolar smooth muscle and have a role in development of inflammation * causes coughing
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Acute inflammation
self-limiting
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Chronic inflammation
persists for week to months
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Local effects of inflammation
* erythema and warming * edema * pain * loss of function * exudate
a latent form of the bacterium with a coating that is highly resistant to heat and other adverse conditions
* can survive long periods in spore state and remain latent in the body until more favorable conditions
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Prions
protein like agents that are transmitted by consumption of contaminated tissues
* infectious agent of Cruetzfeldt-Jakob disease
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Cellulitis Patho
infection of the dermis and subcutaneous tissues arising from a secondary injury (boils or ulcers)
* usually from Strep Aures
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Cellulitis manifestations
* reddened area * edematous * pain * red streaks running along the lymph vessels proximal to the infected area may develop
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Hypoxia
severe reduced oxygen to tissues
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IgG
most common in blood
* this is because it is the first antigen produced when they body starts to fight off an infection
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IgM
first to increase in immune response
* activates complement * involved in ABO incompatibility reactions
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T cells
cell mediated immunity; WBC
* mature in thymus
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B cells
Hemoral immunity
* mature in bone marrow * activated cells becomes and antibody producing plasma cell becomes and antibody-producing plasma cell or a b memory cell
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Memory cells
Remember antigen and quickly stimulate immune response on reexposure
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Leukocytosis
elevated WBC
* associated with inflammation or infection
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Leukopenia
decreased levels of WBC
* associated with viral infections, radiation, chemotherapy
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Hematocrit
percent by volume of cellular elements in blood
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Reticulocyte count
assessment of bone marrow function
* RBC maturation and count * determines if red bone marrow makes enough RBC at appropriate time
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Iron-deficiency anemia
insufficient iron impairs hemoglobin synthesis; microcytic (small cells) and hypochromic (less color) RBC, result of low hemoglobin concentration in cells
* Etiology: dietary intake, duodenal absorption, sever liver disease, infections, and cancer
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Pernicious Anemia
lack of absorption of vitamin B12 because of lack of intrinsic factor secreted by gastric mucosa
* most common is malabsorption (gastrectomy), dietary insufficiency is rare
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Pernicious Anemia manifestations
* tongue enlarged, red, sore, and shiny (because of lack of bloodflow) * digestive discomfort * Paresthesia (tingling or burning) * ataxia (loss of coordination)
* anemia * leukopenia * thrombocytopenia * petechiae: flat, red, pinpoint hemorrhages on the skin
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Sickle Cell Anemia
inherited characteristics leads to the abnormal hemoglobin S (Hbs); one amino acid in the pair of beta globin chains has been framed to normal glutamic acid to valine;
* causes hemolysis and obstruction of small vessels * shape causes clogged * any stress on the body can be a factor * genetic condition, occurs in homozygous recessive, autosomal, incomplete dominance * blood test to detect gene
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Hemophilia
type A is deficit or abnormality of clotting factor VIII and it the most common inherited disorder, transmitted as an X-linked recessive trait
* type b is factor XI * type C is a milder form * Manifestations: prolonged or severe hemorrhage; persistent oozing blood after minor injuries; spontaneous hemorrhage of joints; hematuria
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Conduction Pathway
* Sinoatrial node (SA): pace maker, sinus rhythem * Atrioaventriclar node (AV node): located on in floor of the right atrium * AV bundle (bundle of His): right and left branches * Purkinje fibers: terminal fibers
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Electrocardiogram
* P wave: depolarization of atria * QRS wave: Depolarization of ventricles * T wave: repolarization of ventricles
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Angina pectoris
occurs when there is a deficit of oxygen to the heart muscle
* oxygen or blood supply impairment; when the heart is working harder than usual and needs more oxygen * types: classic or extertional, variant, unstable
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Variant Angina
vasospasm occurs at rest
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Unstable
prolonged pain at rest
* may precede MI * results in a break down of atheroma
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Myocardial Infarction (MI)
occurs when coronary artery is totally obstructed leading to prolonged ischemia or infarction of the heart wall
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Myocardial Infarction Causes
atherosclerosis with attached thrombus
* thrombus builds up to obstruct the artery, vasospasm (small percentage) may occur in the presence of atheroma leading to total obstruction, part of thrombus breaks away forming and embolus that is then lodged into a smaller branch
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MI Complications
* Sudden death * Cardiogenic shock * Congestive heart failure * Rupture of necrotic heart tissue/cardiac tamponade * Thromboembolism causing cerebrovascular accident (CVA; with left ventricular MI)
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MI treatment
* Reduce cardiac demand * Oxygen therapy * Analgesics * Anticoagulants * Thrombolytic agents may be use * Tissue plasminogen activator
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Congestive Heart Failure
occurs when heart is unable to pump sufficient blood to meet the metabolic needs of another conduction
* usually occurs as a complication of another condition, infarction, valve defect * Left and right sided
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Left sided CHF causes
* infarction of left ventricle * aortic valve stenosis * hypertension * hyperthyroidism
o Increased work for the heart causing left sided CHF
o Damage to cerebral arteries causing stroke
o Damage to arterial walls leading to atherosclerosis
o Damage to retinal blood vessels causing blindness (eyes)
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Tidal volume
amount of air entering lungs with each normal breath
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Residual volume
amount of air remaining in the lungs after forced expiration
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Inspiratory Reserve
maximal amount of air that can be inhaled in excess of normal quiet inspiration
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Expiratory reserve
maximal volume of air expired following a passive expiration
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Vital capacity
maximal volume of air expired following a passive expiration
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Total lung capacity
total volume of air in the lungs after maximal inspiration
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COPD
Group of chronic respiratory disorders
* Causes irreversible and progressive damage to lungs; Debilitating conditions that may affect individual’s ability to work; May lead to the development of cor pulmonale; Respiratory failure may occur
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Emphysema
destruction of alveolar walls and septae
* leads to large permanently inflated alveolar air spaces * loss of elasticity * little sputum, some infections and late Cor pulmonale * Break down of alveolar wall results in: loss of surface area for gas exchange, loss of pulmonary capillaries * Etiology: smoking, genetics
increased mucous glands and secretion, inflammation, obstruction, infection, chronic coughing for 3 months or longer in 2 years
* large amounts of sputum * Etiology: smoking, air pollution * cough dyspnea: early constant cough, dyspnea
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Chronic Bronchitis manifestations
* constant productive cough * tachypnea * shortness of breath * blue bloater * hyperventilation * cyanosis in lips, mucous membranes, nail beds
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Pulmonary Edema
fluid collecting in the alveoli and interstitial area; reduces the amount of oxygen diffusing into the blood and interferes with lung expansion
* May develop when: inflammation is present in the lungs, increasing capillary permeability, plasma protein levels are low, decreasing plasma osmotic pressure; pulmonary hypertension develops
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Pulmonary Edema causes
* left sided heart failure * hypoproteinemia (due to kidney or liver disease) * inhalation of toxic gases * association with tumors * blocked lymphatic drainage due to fibrosis or tumors * obstructive sleep apnea