Fluid and Electrolytes Review PDF
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This document provides a review of fluid and electrolytes, including amounts, composition, and regulation of body fluids. It also covers laboratory tests and the role of organs in homeostasis. This information would generally be useful for medical students learning about human physiology.
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**MEDSURG** **\ FLUID AND ELECTROLYTES\ \ AMOUNT AND COMPOSITION OF BODY FLUIDS** Approximately 60% of a typical adult's weight consists of fluids (Water and Electrolytes). Body fluid is located in two fluid compartment: **INTRCELLULAR & EXTRACELLULAR SPACE.** The ECF compartment is further divid...
**MEDSURG** **\ FLUID AND ELECTROLYTES\ \ AMOUNT AND COMPOSITION OF BODY FLUIDS** Approximately 60% of a typical adult's weight consists of fluids (Water and Electrolytes). Body fluid is located in two fluid compartment: **INTRCELLULAR & EXTRACELLULAR SPACE.** The ECF compartment is further divided into three; intravascular, interstitial, and transcellular fluid spaces: - **INTRAVASCULAR SPACE** -- plasma, the effective circulating volume. Approximately 3L of the average 6L of blood volume in adults is made up of plasma. The remaining 3L is made up of erythrocytes, leukocytes, and thrombocytes. - **INTERSTITIAL SPACE** -- contains the fluid that surrounds the cells. 11-12L in an adult. - **TRANSCELLULAR SPACE** -- smallest division of the ECF compartment and contains approximately 1L. **TRANSPORT OF BODY FLUIDS** Body fluid normally moves between the two major compartments or spaces in an effort to maintain equilibrium between the spaces. **Third-space fluid shifting** -- Loss of ECF into a space that does not contribute to equilibrium between the ICF and the ECF. **ELECTROLYTES -** are active chemicals. The major **cations** in body fluid are sodium, potassium, calcium, magnesium, and hydrogen ions. Major **anions** are chloride, bicarbonate, phosphate, sulfate, and proteinate ions. Normal movement of fluids throughout the capillary wall into the tissues depends on hydrostatic pressure at both the arterial and the venous ends of the vessel and the osmotic pressure exerted by the protein of plasma. ----------------- ------------------- **ELECTROLYTE** **NORMAL VALUE** Sodium 135 -- 145 mEq/L Potassium 3.5 -- 5.0 mEq/L Chloride 98 -- 106 mEq/L Calcium 8.5 -- 10.5 mEq/L Magnesium 1.8 -- 3.0 mEq/L Phosphorus 2.5 -- 4.5 mEq/L Bicarbonate 24 -- 31 mEq/L ----------------- ------------------- **REGULATION OF BOD FLUID COMPARTMENTS** **OSMOSIS and OSMOLALITY -** When two different solutions are separated by a membrane that is impermeable to the dissolved substance, fluid shifts through the membrane from the region of low solute concentration to the region of high solute concentration until the solutions are equal concentrations. **TONICITY -** Is the ability of all solutes to cause an osmotic driving force that promotes water movement from one compartment to another. **Three other terms associated with osmosis.** - **OSMOTIC PRESSURE** -- amount of hydrostatic pressure needed to stop the flow of water by osmosis. - **ONCOTIC PRESSURE** -- pressure exerted by proteins. - **OSMOTIC DIURESIS** -- increase urine output cause by excretion of substance. **REGULATION OF BOD FLUID COMPARTMENTS** **DIFFUSION -** Is the natural tendency of a substance to move from an area of higher concentration to lower concentration. **FILTRATION -** Hydrostatic pressure in the capillaries filter fluid out of the intravascular compartment into the interstitial fluid. The kidneys filter 180L of plasma per day. **SODIUM-POTASSIUM PUMP -** Sodium concentration is greater in ECF than the ICF, sodium tends to enter the cell by diffusion. Conversely, the high intracellular potassium concentration is maintained by pumping potassium into the cell. In definition these movement is called **active transport.** **SYSTEMIC ROUTES OF GAINS AND LOSSES** - **KIDNEYS** - Usual daily urine volume is 1-2L. 1ml of urine per kg of body weight per hour(IN ALL AGE GROUP) - **SKIN** - Sensible perspiration refers to visible water and electroltye loss through sweating. - **LUNGS** - Normally eliminates water vapor at a rate of approximately 300ml every day. - **GASTROINTESTINAL TRACT** - Usual loss is 100 -- 200 mL daily. **LABORATORY TESTS** **OSMOLALITY -** Concentration of fluid that affects the movement of water between fluid compartments by osmosis. Measure the solute concentration per kilogram in blood and urine. **OSMOLARITY** - Concentration of solutions (mOsm/L). **URINE-SPECIFIC GRAVITY** - kidney's ability to excrete water. Normal lab range 1.010 -- 1.025. **BLOOD UREA NITROGEN** - Made of urea, which is an end product of the metabolism of protein by the liver. Normal BUN is 10 -- 20mg/dL **CREATININE** - End product of muscle metabolism. Normal lab range 0.7 to 1.4mg/dL. **HEMATOCRIT** - Measure the volume percentage of RBCs, in whole blood and normally rnages from 42 -- 52% in men and 35% - 47% in women. **Homeostatic Mechanism -** the body is equipped with remarkable homeostatic mechanisms to keep the composition and volume of the body fluid within normal range. **ORGANS INVOLVED IN HOMEOSTASIS** **KIDNEY** - Regulate fluid and electrolyte balance. They act both autonomously and in response to bloodborne messengers, such as aldosterone and antidiuretic hormone. - Regulate ECF volume - Regulate normal electrolyte levels in the ECF - Regulate pH of the ECF - Excretion of metabolic wastes and toxins. **Head and Blood Vessels** - Pumping actions circulate blood through the kidneys under sufficient pressure for urine formation **Lungs** - Removes 300ml of water daily. **Pituitary Gland** - ADH maintain the osmotic pressure of the cells. **Adrenal Gland** - Aldosterone has a profound effect on fluid balance. **Parathyroid Gland** - Regulate calcium and phosphate balance. **Renin-Angiotensin-Aldosterone System** - Aldosterone is a volume regulator and is also released as serum potassium increases, sodium decreases. **Antidiuretic Hormone** - ADH and the thirst mechanism role is to maintain sodium concentration and oral intake of fluids the release of ADH increase reabsorption of water and decreases urine output. **Natriuretic Peptides** - Is a hormone affecting fluid and cardiovascular function through the excretion of sodium and direct vasodilation. **TOPIC 2: INTRAVENOUS FLUIDS** **PARENTERAL FLUID THERAPY -** When no other route of administration sis available, fluids are given by IV, outpatient diagnostic, surgical settings, and even homes to replace fluids, administer medications, and provide nutrients. **PURPOSE** - Provide water, electrolytes, and nutrients to meet daily requirements - Replace water and correct electrolyte deficits - Administer medications and blood products **TOPIC 3: ELECTROLYTE IMBALANCES** **2.1 Type of IV Solutions** **IV Solutions** - Solutions are often categorized as isotonic, hypotonic, or hypertonic, according to whether their total osmolality is same as, less than, or greater than that of blood. **ISOTONIC -** Fluids that are classified to have a total osmolality close to the ECF and do not cause cells to shrink or swell. - Normal Saline (0.9% Sodium Chloride) - only IV solution that is compatible with BT. **HYPOTONIC -** Lower osmolarity than the extracellular space. Water moves from extracellular space to intracellular space. To replace cellular fluid, provide free water to kidneys for excretion of body wastes, treatment for hypernatremia and prevent dehydration, and causes cells to swell. **HYPERTONIC -** Higher osmolarity than the extracellular space. Water moves out from intracellular space into the extracellular space. Causing the cell to shrink. **2.2 Managing Systemic Complications** **Systemic Complications** **FLUID VOLUME OVERLOAD -** Causes the blood pressure and central venous pressure to increase. **S/Sx** - Crackles - Distended neck veins - Edema - RAPID weight gain - Dyspnea **AIR EMBOLISM -** Most often associated with cannulation of central veins and directly related to the size of the embolus and the rate of entry. Air central veins right ventricle lodges against the pulmonary valve blood flow obstruction. **S/Sx** - Palpitations, dyspnea, wheezing, cyanosis, weak rapid pulse, altered mental status. **INFECTION -** Pyogenic substances in either the infusion solution or IV administration set can cause infection. **S/Sx** - Abrupt temperature elevation, headache, tachycardia, tachypnea, nausea and vomiting, chills, general body malaise. **3.1 SODIUM IMBALANCES** **HYPONATREMIA** - Serum sodium level loss. It can occur during extreme temperatures, because of excessive fluid intake before exercise or prolonged exercise that results in a decrease in serum sodium. **PATHOPHYSIOLOGY** - Imbalance of water rather than sodium. Low urine sodium occurs as the kidney retains sodium to compensate for nonrenal fluid loss. High urine sodium concentration is associated with renal salt wasting. - A deficiency of aldosterone, as occurs in adrenal insufficiency, also predisposes to sodium deficiency and use of certain medications. **CAUSES** - Diarrhea - Sodium Diet Deficiency - IV Fluid Overload - Diuretics - SIADH - Addison - Vomiting - Excessive Physical Exertion **CLINICAL MANIFESTATIONS** - Loss of appetite - Orthostatic Hypotension - Shallow Respiration - Muscle Spasm - Seizure/Stupor - Abdominal Cramps - Lethargic **MEDICAL MANAGEMENT** - Sodium Replacement - IV Fluids - AVP Receptor Antagonists - Treat hyponatremia by stimulating free water excretion. - Incorporation of Sodium Chloride **Nursing MANAGEMENT** - Monitor I&O - Weigh client daily - Increase Sodium intake/diet - Restrict/Decrease oral fluid intake **HYPERNATREMIA** - Serum sodium level that are high, caused by a gain of sodium in excess of water of by a loss of water more than sodium. With water loss, the patient loses more water than sodium; as a result, the serum sodium concentration increases, and the increased concentration pulls fluid out of the cell. **PATHOPHYSIOLOGY** - Common cause is fluid deprivation in patients who cannot respond to thirst. Hypertonic enteral feedings without adequate water supplements leads to hypernatremia, as does watery diarrhea and greatly increased insensible water loss. **CAUSES** - Cushing's - Hypertonic Solutions - Diabetes Insipidus - Burns - Increase Intake of Na+ **CLINICAL MANIFESTATIONS** - FATIGUE - RESTLESS, AGITATED - INCREASED REFLEXES - EXTREME THIRST - DECREASED URINE OUTPUT, DRY MOUTH/SKIN **MEDICAL MANAGEMENT** - IV fluids - Diuretics - Synthetic ADH medication - if D.I. is the main cause. **Nursing MANAGEMENT** - Monitor I&O - Restrict Sodium Intake - Monitor Neurological Behavior **3.2 POTASSIUM IMBALANCES** **HYPOKALEMIA -** Usually indicates a deficit in total potassium stores. **PATHOPHYSIOLOGY** - potassium-losing diuretics, diarrhea, Vomiting, Gastric suctioning, hyperaldosteronism, insulin therapy, poor nutrition, hypokalemia **DIAGNOSTIC FINDINGS** - Electrocardiogram - Arterial Blood Gas - Blood Chemistry **CLINICAL MANIFESTATIONS** **"Everything will be low & slow"** - Muscle - GI Tract - Heart - Lungs - Blood Pressure **MEDICAL MANAGEMENT** - Potassium IV Supplement AVOID!!! - IV BOLUS!!! GO FOR!!! - INFUSION PUMP!!! - Potassium Oral Supplement - Potassium Citrate **Nursing MANAGEMENT** - DIET: Foods rich in potassium - Monitor ECG - Hold Diuretics - Hold Digoxin **HYPERKALEMIA -** Seldom occurs in patients with normal renal function. In older adults, there is an increased risk for hyperkalemia due to decreases in renin and aldosterone. **PATHOPHYSIOLOGY -** Decreased renal excretion of potassium, rapid administration of potassium, untreated kidney injury, hypoaldosteronism HyperKALemia **DIAGNOSTIC FINDINGS** - Electrocardiogram - Arterial Blood Gas - Blood Chemistry **CLINICAL MANIFESTATIONS** - Muscle Weakness - Low urine output - Respiratory Arrest - Poor Cardiac Contraction - Early Muscle cramping/twitching - Abnormal EKG **MEDICAL MANAGEMENT** - Obtain ECG - Administration of cation exchange resins (e.g., sodium polystyrene sulfonate) - Administration of IV Calcium Gluconate - Administration of IV Sodium Bicarbonate - Regular Insulin and a Hypertonic Dextrose Solution - Loop Diuretics **Nursing MANAGEMENT** - DIET: Restrict Potassium - Monitor ECG - Monitor Vital Signs - Monitor and Observe muscle weakness and dysrhythmias - Monitor Serum-Potassium levels **3.3 CALCIUM IMBALANCES** **HYPOCALCEMIA -** Occurs in a variety of clinical situations. A patient may have a total-body calcium deficit but a normal serum calcium level. Older adults and those with disabilities, who spend and increased amount of time in bed, have an increased risk for hypocalcemia. **PATHOPHYSIOLOGY** - Hypoparathyroidism/surgery of the thyroid, massive administration of citrated blood, pancreatitis, kidney injury, unhealthy lifestyle hypocalcemia. **DIAGNOSTIC FINDINGS** - Arterial Blood Gas - Blood Chemistry **CLINICAL MANIFESTATIONS** - Tail Sign - Trousseau Sign - Mental Status Changes - Hyperactive bowel sounds - Dry brittle hair, nails, and bones. - Seizures/Tetany **MEDICAL MANAGEMENT** - Parenteral Calcium Chloride - Calcium Salt - If with hyperphosphatemia - Aluminum Hydroxide **NURSING MANAGEMENT** GO FOR!!! - DIET - Increase Vitamin D - Milk - Salmon, Sardines, Oysters - Turn Patient's head to side if seizure occurs! Avoid!!! - Smoking and Alcoholic Beverages - Laxatives **HYPERCALCEMIA** - Excessive amount of calcium levels in the blood and is a dangerous imbalance when severe. **CAUSES** - Increased Ca+ intake - Hyperparathyroidism - Glucocorticoids - Hyperthyroidism - Poor Calcium Excretion - Addison\'s disease - Lithium Toxicity **DIAGNOSTIC FINDINGS** Blood Chemistry ECG Double-Antibody PTH test X-rays Urinalysis **CLINICAL MANIFESTATIONS** - Weak muscles - ECG changes - Absent - Tendon Reflex - Minded - Bowel Motility - Kidney Calculi Formation **MEDICAL MANAGEMENT** - Administer - Calcium Reabsorption Inhibitors - Bisphosphonates\' - Prostaglandin Synthesis Inhibitors - Dialysis **NURSING MANAGEMENT** GO FOR!!! - DIET - Increase oral fluid intake - Decrease Calcium Rich Food - Turn Patient\'s head to side if seizure occurs! Avoid!!! **Strenuous Activity** **Thiazides** **Calcium Supplements** **3.4 MAGNESIUM IMBALANCES** **HYPOMAGNESEMIA -** Refers to a below-normal serum magnesium concentration. **PATHOPHYSIOLOGY -** Suctioning, diarrhea, intestinal fistulas, inflammatory bowel disease, alcohol consumption, diabetic ketoacidosis, hypomagnesemia. **DIAGNOSTIC FINDINGS** Blood Chemistry **CLINICAL MANIFESTATIONS** - Tachycardia - EKG changes - Twist of tips - Rapid shallow breathing - Diarrhea - Mental Status Changes - Insomnia **MEDICAL MANAGEMENT** - Magnesium Salt - IV MAGNESIUM SULFATE NURSING MANAGEMENT GO FOR!!! - DIET - Increase magnesium intake Monitor - Deep tendon reflexes - ECG - Put patient into seizure precaution **HYPERMAGNESEMIA -** Serum magnesium high level, a rare electrolyte abnormality because kidneys efficiently excrete magnesium. **PATHOPHYSIOLOGY** - Kidney injury slight elevation of serum magnesium. - Untreated Diabetic Ketoacidosis catabolism release of magnesium. - Excessive use of magnesium-based antacid decrease GI motility increase serum magnesium levels. **DIAGNOSTIC FINDINGS** Blood Chemistry ECG findings **CLINICAL MANIFESTATIONS** - CNS Depression - Respiratory Depression - Muscle Weakness - Hypotension - Absent DTR **MEDICAL MANAGEMENT** - Loop Diuretic - Sodium Chloride - IV Lactated Ringers - IV Calcium Gluconate - Hemodialysis **NURSING MANAGEMENT** Monitor - Vital Signs - Deep tendon reflexes - Level of Consciousness AVOID!!! - Magnesium containing meds to compromised renal function. - Magnesium Rich Foods **TOPIC 4 ACID-BASE IMBALANCES** - **ACID-BASE IMBALANCE** - Are commonly encountered in clinical practice, especially in critical care units. It important to identify acid-base imbalance to determine the underlying cause of the disorder and determining appropriate treatment. - **PLASMA pH** - Indicator of hydrogen ion concentration and measures the acidity of alkalinity of the blood. These mechanism consist of buffer systems, the kidneys, and the lungs. - **Buffer system** - prevent major changes in the pH of body fluids by removing or releasing hydrogen ion; they can act quickly to prevent excessive changes in hydrogen ion concentration; which is assess when *ARTERIAL BLOOD GASES are measured.* **4.1 METABOLIC ACIDOSIS** **Metabolic Acidosis** - Common clinical disturbance characterized by low pH and a low plasma bicarbonate concentration. **PATHOPHYSIOLOGY** - Result in direct loss of bicarbonate. **CAUSES** - Diarrhea, lower intestinal fistulas, ureterostomies, and the use of diuretics. **ASSESSMENT AND DIAGNOSTIC FINDINGS** - Arterial Blood Gas measurements low pH (7.35) and low bicarbonate (22mEq/L) - Blood Chemistry hyperkalemia. - ECG **CLINICAL MANIFESTATIONS** - Headache - Confusion - Drowsiness - Tachypnea **MEDICAL MANAGEMENT** Treatment is directed at correcting the met abolic acidosis. When necessary, bicarbonate is given; however, the administration of sodium bicarbonate during cardiac arrest can result in paradoxical intracellular acidosis. **4.2 METABOLIC ALKALOSIS** Metabolic Alkalosis - A clinical disturbance characterized by a high pH and a high plasm bicarbonate concentration. It can be produced by a gain of bicarbonate or a loss of Hydrogen Ions. **CAUSES** - Vomiting, NG Tube Suctioning, pyloric stenosis, use of thiazides, and hypokalemia. **ASSESSMENT AND DIAGNOSTIC FINDINGS** - Arterial Blood Gas measurements pH greater than 7.45 and serum - bicarbonate concentration greater than 26mEq/L. - Blood Chemistry hypokalemia. **CLINICAL MANIFESTATIONS** - Dizziness - Respiratory Depression **MEDICAL MANAGEMENT** - Treatment is aimed at correcting the underlying acid-base disorder. Because of volume depletion from GI loss, the patient\'s I&O must be monitored. - Sufficient chloride excretion of excess bicarb. - H2 receptor antagonists decrease HCL. **4.3 RESPIRATORY ACIDOSIS** **Respiratory Acidosis** - A clinical disorder in which the pH is less than 7.35 and the PaCO2 is greater than 45mmHg. **CAUSES -** pulmonary edema, foreign object aspiration, atelectasis, and overdose of sedatives, sleep apnea Inadequate excretion of CO2 with inadequate ventilation. **ASSESSMENT AND DIAGNOSTIC FINDINGS** - Arterial Blood Gas measurements pH less than 7.35 and PaCO2 greater than 45mmHg. - Chest X-ray identify respiratory disease. - Drug Screening **CLINICAL MANIFESTATIONS** - Mental cloudiness - Feeling of fullness in the head - Decreased LOC **MEDICAL MANAGEMENT** - Improve Ventilation - Bronchodilators - If with respiratory infections Antibiotics. - If with pulmonary embolism thrombolytics - Increase oral fluid intake moisten mucous promote expectorate. - Semi-fowlers Position. **4.4 RESPIRATORY ALKALOSIS** **Respiratory Alkalosis** - A clinical disorder in which the pH is greater than 7.45 and the PaCO2 is less than 35mmHg. **CAUSES** - Hyperventilation **ASSESSMENT AND DIAGNOSTIC FINDINGS** - Arterial Blood Gas measurements - Toxicology Screenr/o salicylate intoxication. **MEDICAL MANAGEMENT** - Treatment of Underlying Cause - Anxiety breathe slow paper bag Antianxiety Agents may be required.\ \ \ **ELIMINATION DISORDER** **01 ANATOMY AND PHYSIOLOGY** **INTRODUCTION** The urinary system include the kidneys, ureters, bladder, and urethra. Urine is formed by the kidney and flows through the other structures to be eliminated from the body. **KIDNEYS** - A pair of bean-shaped, brownish-red structure located retroperitoneally on the posterior wall of the abdomen. The kidneys and surrounding fat are suspended from the abdominal wall by renal fascia made of connective tissue which holds the kidney in place. **Renal Capsule** - fibrous connective tissue, blood vessels, and lymphatics that surrounds each kidney. **Renal Parenchyma** - **Medulla** - inner portion of the kidney that contains the loop of henle, vasa recta, and the collecting ducts from both the juxtamedullary nephrons. - **Renal Pelvis** - beginning of the collecting system and is composed of structures that are designed to collect and transport urine. - **Cortex** - it contains nephrons. - **BLOOD SUPPLY** - hilum is the concave portion of the kidney through which the renal artery enters and the ureters and renal vein exit. Kidneys receive 20-25% of the toal cardiac output, which means that all of the body\'s blood circulates through the kidneys approximately 12 times per hour. - **RENAL ARTERY**- divides into smaller adn smaller vessels, forming the afferent arterioles that branches to form glomerulus farming part of the nephron - filtration occurs - blood leaves the glomerulus and flows back to the inferior vena cava. - **NEPHRONS** - Each kidney has 1M nephrons located within the renal parenchyma and are responsible for the formation of filtrate that will become urine. There are **2 types of nephrons;** ** Cortical Nephrons** ** Juxtamedullary Nephrons -** are distinguished by long loops of Henle and are surrounded by a long capillary loos called vasa recta. Nephrons are made up of two basic components: filtering element and the attached tubule. **Bowman\'s Capsule** - part of nephron that forms a cuplike sack surrounding the glomerulus representing the beginning of the urinary space and is contiguos with the proximal convoluted tubule of the nephron and helps the glomerulus to filter blood. **URETERS, BLADDER, AND URETHRA** - The urine formed in the nephrons flows through the renal calyces and then into the ureters, which are long fibromuscular tubes that connect each kidney to the bladder. **UROTHELIUM** - lining of ureters made of transitional cells epithelium, prevents reabsorption of urine. - The urinary bladder is a distensible muscular sac located just behind the pubic bone with a total capacity of 400-500ml. **Urethrovesical junction** provide downward movement of urine.. - The bladder neck contains bundles of involuntary smooth muscle that form a portion of the urethral sphincter known as the internal sphincter hold urine exit from urinary bladder to urethra. External urinary sphincter maintains continence. **FUNCTIONS** - **URINE FORMATION** -Urine is formed in the nephrons through a complex three-step process: glomerular filtration, tubular reabsorption, and tubular secretion, Excreted through urine include sodium, chloride, bicarbonate, potassium, glucose, urea, creatinine, and uric acid. Within the tubule, some of these substances are selectively reabsorbed into the blood. Amino acids and glucose are usually filtered at the level of glomerulus and reabsorbed so that neither is excreted in the urine. Protein molecules also are not usually found in the urine. - **GLOMERULAR FILTRATION** -normal blood flow is between 1000 to 1300ml/min to be filtered. 20% of blood passing through the glomeruli is filtered into the nephron, amounting to about 180 L/day. - **ANTIDIURETIC HORMONE** - \"**vasopressin**\" a hormone is released in response to changes in osmolality of the blood. Increasing reabsorption of water and thereby returning the osmolality of the blood to normal. - **Water Excretion -** an important function of kidney is the regulation of the amount of water excretion, intake from fluid ingested and the water from food per day. - **Regulation of Electrolyte Excretion** -regulation of sodium volume excreted depends on aldosterone. - **Regulation of Acid-Base Balance** - the kidney performs a major functions to assist in the balance. One function is to reabsorb and retum to the body\'s circulation any bicarbonate form the urinary filtrate. - **Autoregulation of Blood Pressure** - vasa recta monitor blood pressure, renin is secreted by specialized juxtaglomerular cells in response with low blood pressure. - **Renal Clearance** - ability of the kidneys to clear solutes from the plasma. - **RED BLOOD CELL PRODUCTION** -Releases erythropoietin in response to decrease in the oxygen tension in renal blood flow. - **Vitamin D Synthesis** -responsible for the final conversion of inactive vitamin D to its active form for maintaining normal calcium balance in the body. - **Excretion of Waste Products** - creatinine, phosphates, and sulfates, Uric acid and drug metabolites are excreted through urine. - **Urine Storage -** the bladder is the reservoir of urine. **02 DIAGNOSTIC TESTS** **HEALTH HISTORY** Obtaining a urologic health history requires excellent communication skills. When obtaining health hx, the nurse should inquire about the following: - Chief complaint, onset - Location, character, and duration of pain, factors that precipitate pain and those that relieve it - Hx of UTI, including past treatment - Fever/Chills - Hx of Surgical procedure or use of indwelling urinary catheters. - **DYSURIA**- painful urination - **HEMATURIA**- blood in urine - Use of tobacco, alcohol, or recreational drugs - History of taking OTC medications. **COMMON S/SX +** **PAIN**-Usually caused by distention of urinary tract as a result of obstructed urine flow or inflammation and swelling of tissues. **CHANGES IN VOIDING** - Average person voids 1-2L in 24hrs, although this amount varies depending on fluid intake, sweating, environmental temperature, vomiting, or diarrhea. **DIAGNOSTIC TESTS** - **URINALYSIS and URINE CULTURE** -urinalysis provides important clinical information about kidney function and helps diagnose other diseases such as diabetes. Urine culture determines whether bacteria are present in the urine, as well as their strains and concentration. - **URINE-SPECIFIC GRAVITY**-expression of the degree of concentration of the urine that measures the density of a solution compared to the density of water. - **OSMOLALITY**-most accurate measurement of the kidney\'s ability to dilute and concentrate urine. In healthy adults, serum osmolality is 280 to 300 mOsm/kg and normal urine osmolality is 200-800 mOsm/kg. - **BLOOD UREA NITROGEN & SERUM CREATININE (MOST ACCURATE) -** creatinine is the end product of muscle energy metabolism and BUN is the end product of protein metabolism. Both are needed to be excreted via urination. - **BLADDER ULTRASONOGRAPHY** - noninvasive method of measuring urine volume in the bladder. The device automatically calculates and displays urin volume. - **COMPUTED TOMOGRAPHY and MAGNETIC RESONANCE IMAGING**- CT and MRI are noninvasive techniques that provide excellent cross-sectional views of the anatomical structure of the kidney and urinary tract. - **BIOPSY**-used to help diagnose and evaluate the extent of kidney disease. **03 URINARY TRACT** **INTRODUCTION** UTIs are caused by pathogenic microorganisms in the urinary tract. Generally classified as infections involving the upper and lower urinary tract and further classified as uncomplicated or complicated. **03.1 UPPER URINARY TRACT INFECTION** **INTRODUCTION** **Pyelonephritis** is a bacterial infection of the renal pelvis, tubules, and interstitial tissue of one or both kidneys. Causes involve either the upward spread of bacteria from the bladder or spread from systemic sources reaching the kidney via the bloodstream. Pathogenic bacteria from a bladder infection can ascend into the kidney, resulting in pyelonephritis. An incompetent ureterovesical valve or obstruction occurring in the urinary tract increases the susceptibility of the kidneys to infection. **PYELONEPHRITIS - Pyelonephritis can be acute or chronic.** **Acute Pyelonephritis** - usually leads to enlargement of the kidneys with interstitial infiltrations of inflammatory cells. Abscess may be noted on or within the renal capsule and at the corticomedullary junction atrophy and destroy tubules. **Chronic Pyelonephritis -** scarred kidneys, contracted, and not functioning Chronic kidney disease need for renal replacement therapies. **ACUTE PYELONEPHRITIS** **CLINICAL MANIFESTATIONS** Chills Fever Leukocytosis Bacteriuria Pyuria Flank Pain Body Malaise Dysuria **DIAGNOSTICS** **ULTASOUND OR CT** - locate obstruction **RADIONUCLIDE IMAGING with GALLIUM CITRATE and INDIUM**-111-LABELED WBCS useful to identify sites of infection that may not be visualized on CT scan or UTZ **URINE CULTURE SENSITIVITY** - Determine the causative organism **MANAGEMENT** Client with Acute Uncomplicated Pyelonephritis are most often treated on an outpatient basis if they are not exhibiting acute symptoms of SEPSIS and DEHYDRATION. 2-week course antibiotic agents is commonly prescribed for outpatient. Commonly Prescribed antimicrobial agents are: ► Cephalosporin ► Penicillin ► Fluoroquinolone ►Trimethoprim-Sulfamethoxazole Combination ►Urinary Analgesic Agent **NURSING MANAGEMENT** The client may require hospitalization or may be treated as an outpatient. ►Hospitalization Measure 180 and record (if not contraindicated, increase oral fluid intake up to 3-4L/day) Promote bedrest Prevent further infection Educate client for treatment compliance Do Perineal Hygiene **03.1 LOWER URINARY TRACT INFECTION** **INTRODUCTION** Several mechanism maintain the sterility of the bladder, and any abnormalities or dysfunctions of the mechanisms are contributing risk factors for lower UTIs. **PATHOPHYSIOLOGY** Bacteria enters to the bladder attach to and colonize the epithelium of the urinary tract evade host defense mechanisms, and initiate inflammation infection occur. Many UTIs result from fecal organisms ascending from the perineum to the urethra and the bladder and then adhering to the mucosal surfaces. **BACTERIAL INVASION** - The bladder can clear large numbers of bacteria through Glycosaminoglycan (GAG) attracts water molecules, forming a water barrier that serves as a defensive layer between the bladder and the urine. - The normal flora of the vagina and urethral area also interfere with adherence of E. Coli. - IgA also provide barrier to bacteria. ✓ **CLINICAL MANIFESTATIONS** Uncomplicated Pyuria Polyuria Nocturia Suprapubic or Pelvic Pain Hematuria Burning like pain **CLINICAL MANIFESTATIONS** - Complicated - often caused by a broader spectrum of organism. Manifestation can range from asymptomatic bacteriuria to gram-negative sepsis with shock. **DIAGNOSTICS** Urine Culture Urine Analysis Multiple-test Dipstick Tests for STIs CT Scan/Ultrasound Testing for WBCs **MANAGEMENT -** Management of UTIs typically involves pharmacologic therapy and patient education. Pharmacological Therapy Antibacterial Agents **NURSING MANAGEMENT -** Nursing care of the patient with lower UTI focuses on treating the underlying infection and preventing its recurrence. Cranberry Juice Relieving Pain Drink liberal amount of fluids Avoid Caffeinated Beverages Encourage Frequent Voiding Promote Bedrest **04 ACUTE KIDNEY DISEASE** **INTRODUCTION** Is a rapid loss of renal function due to damage to the kidneys. Depending on the duration and severity of AKI. Treatment is aimed at replacing renal function temporarily to minimize potentially lethal complications and reduce potential causes of increased kidney injury with the goal of minimizing long-term loss of renal function. **PATHOPHYSIOLOGY -** Some factors may be reversible if identified and treated promptly, before kidney function is impaired. HYPOVOLEMIA, HYPOTENSION, REDUCE CARDIAC OUTPUT AND HEART FAILURE, AND OBSTRUCCTION REDUCE BLOOD FLOW TO THE KINDEY KINDEY IMPAIREMENT. **CATEGORIES** The major categories of AKI are: PRERENAL INTRARENAL POSTRENAL **PRERENAL -** Is the result of impaired blood flow that leads to hypoperfusion of the kidney commonly caused by volume depletion and renal stenosis, ultimately leading to decreases in the GFR **INTRARENAL -** Result of actual parenchymal damage to the glomeruli or kidney tubules, in which there is damage to the kidney tubules, the most common type of intrinsic AKI. Characteristics are intratubular obstruction, tubular back-leak, vasoconstriction, and changes in glomerular permeability. **POSTARENAL -** Usually results grom obstruction distal to the kidney by conditions such as renal calculi, strictures, blood clots, benign prostatic hypertrophy, and malignancies. Pressure rises in the kidney tubules, and eventually the GFR decreases. **CAUSES** **PRERENAL** - Cardiac Issues (Myocardial Infarction, heart failure) - Burns - Hemorrhage - Dehydration - Renal Stenosis **INTRARENAL** Actual Parenchyma Damage Acute Tubular Necrosis Vasoconstriction Changes in glomerular permeability. **POSTRENAL** - Results from obstruction distal to the kidney by conditions: - Renal Calculi - Strictures - Blood clots - BPH - Malignancy **PHASES OF AKI** There are four phases of AKI: Initiation, Oliguria, Diuresis, and Recovery. **Initiation**-begins with the initial insult and ends when oliguria develops **Oliguria**-accompanied by an increase in the serum concentration of substances usually excreted by the kidneys. Uremic symptoms first appear and life-threatening conditions such as hyperkalemia develops. **Diuresis**-Gradual increase in UO GFR has started to recover. **Recovery** - improvement of renal function and may take 312 months. **✓CLINICAL MANIFESTATION** Almost every system of the body is affected with failure of the normal renal regulatory mechanism. Lethargic Dehydration CNS changes Hematuria Oliguria **DIAGNOSTICS** Assessment of the patient with AKI includes evaluation for changes in the urine, evaluate kidney contour, and a variety of laboratory tests. U/A Low GFR Ultrasonography/Renal Sonogram/MRI show evidence of anatomic changes Serum BUN and Creatinine Progressive Metabolic Acidosis Serum Electrolytes Phsophate may increase, calcium may be low. **MEDICAL MANAGEMENT** The kidneys have a remarkable ability to recover from insult. Objectives are to restore normal chemical balance and prevent complications until repair and restoration of renal function. - **TREAT THE UNDERLYING CAUSE** (Prerenal, Intrarenal, Postrenal) - **Dialysis** - **IV FLUIDS/BLOOD TRANSFUSION** - **If Hyperkalemia occur** administer SODIUM POLYSTYRENE SULFONATE, IV DEXTROSE - Phosphate Binding Agents prevent continuing rise in serum phosphate. **NURSING MANAGEMENT** The nurse has an important role in caring for the patient with AKI. Monitor for complication and participate in fluid and electrolyte imbalance treatment (I&O, Daily weights) Reduce Metabolic Rate Promoting bedrest Promoting Skin Care **04.1 CHRONIC KIDNEY DISEASE** **INTRODUCTION** When a patient has sustained enough kidney damage to require renal replacement therapy on a permanent basis. Also referred to as ESKD. **PATHOPHYSIOLOGY** - Renal Function declines accumulation of toxic waste in the blood Uremia (adversely affects every system in the body) - The rate of decline in renal function and progression of ESKD is related to the underlying disorder. Progress is rapid in patients who excrete significant amounts of protein and have elevated blood pressure. ✓ **CLINICAL MANIFESTATION** Because every body system is affected, patient exhibit several signs and symptoms depends in the part of the degree of renal impairment. It is generally thought that the accumulation of uremic waste products is the probable cause. **Cardiovascular** Distended Neck Veins Hyperkalemia Hypertension Pericardial Effusion Pitting Edema **Neurologic** Asterixis CNS changes Seizures Weakness **GI** Ammonia odor to breath Anorexia Constipation or Diarrhea **Pulmonary** Crackles Pleuritic Chest Pain Shortness of Breath **HEMATOLOGIC** Anemia Thrombocytopenia Musculoskeletal Bone Fractures Loss of muscle strength Muscle Cramps **DIAGNOSTICS** Urinalysis - decreased GFR Serum Electrolytes elevated Na+, K+, Phosphorus, and low Ca+ Blood Chemistry High BUN & Creatinine, Low Hgb & Hct, ABGs Metabolic Acidosis **MEDICAL MANAGEMENT** **GOAL** - maintain kidney function and homeostasis for as long as possible. Dialysis Pharmacologic Therapy Calcium & Phosphorus Binders Antihypertensive and Cardiovascular Agents Anticonvulsant Agents Ertythropoietin **NURSING MANAGEMENT** Requires astute nursing care to avoid the complications of reduced renal function. ► Monitor I&O ► Promote proper nutritional intake within limits ► Collaborative Care to HDU ► Promote bedrest with proper positioning **GASTROINTESTINAL DISORDERS** I. **Inflammatory Bowel Disease** **INTRODUCTION** - I. **II Crohn\'s Disease** **INTRODUCTION** - **RISK/PRECIPITATING FACTORS** - - - - **CLINICAL DIAGNOSTIC TESTS** - - - - **MEDICAL MANAGEMENT** **Pharmacological Treatment** - - - **Surgical Treatment** - **NURSING MANAGEMENT** - - - - - **Surgical Treatment** - - Monitor Color (REPORT DISCOLORATION) I. **II Ulcerative Colitis** **INTRODUCTION** - **RISK/PRECIPITATING FACTORS** - - - - **CLINICAL DIAGNOSTIC TESTS** - - - **MEDICAL MANAGEMENT** **Pharmacological Treatment** - - - **Surgical Treatment** - **NURSING MANAGEMENT** - - - - - **Surgical Treatment** - - - II. **Appendicitis** **INTRODUCTION** - **Pathophysiology** - Inflammatory process → increased intraluminal pressure → edema obstruction of orifice → ischemia → bacterial overgrowth → perforation. **CLINICAL DIAGNOSTIC TESTS** - - **Clinical Manifestations** **M.R. P.R.O.F** has appendicitis - - - - - - **MEDICAL MANAGEMENT** **Surgical Treatment** - **NURSING MANAGEMENT** **PREOPERATIVE NSG CARE** - - - **POSTOPERATIVE NSG CARE** - - III. **PANCREATITIS** **INTRODUCTION** - **Pathophysiology** These enzymes enter the bile duct, where they are activated and, together with bile, reflux occurs into the pancreatic duct → Proteolytic Enzyme (Trypsin) → Self-digestion → Pancreatitis. **RISK/PRECIPITATING FACTORS** - - - **CLINICAL DIAGNOSTIC TESTS** - - - - - **Clinical Manifestations** - - - - - - - **MEDICAL MANAGEMENT** **Pharmacological Treatment** - - - Avoid MEPERIDINE → CNS irritability and Seizures. **NURSING MANAGEMENT** - - - I. **Cholecystitis** **INTRODUCTION -** Inflammation of the gallbladder - Calculous cholecystitis → gallbladder stone obstructs bile out flow → bile remains → chemical reaction → edema occur → compressed blood vessels in the gallbladder. **RISK/PRECIPITATING FACTORS** - o Female o Forty o Fat - o Fertile - o Cholelithiasis **CLINICAL DIAGNOSTIC TESTS** - **Cholescintigraphy** → use of radioactive agent is administered intravenously. - **Ultrasonography** → detect calculi in the gallbladder. - Oral Cholecystography **Clinical Manifestations** - RUQ Pain - (+) Murphy\'s Sig - (+) BOA\'s Sign - Very Dark colored urine and clay colored Stool **MEDICAL MANAGEMENT** **Surgical Procedure** Cholecystectomy/Laparoscopic Cholecystectomy Jackson Pratt Drain **Pharmacological Treatment** **Ursodeoxycholic Acid** - Dissolve Small stone **Lithotripsy** - Dissolve Larger stone **NURSING MANAGEMENT** Pain management (Preop &Postop) Breathing Exercise Promote Biliary Drainage Low fat high carbohydrates **HIV - AIDS** **HUMAN IMMUNODEFICIENCY VIRUS** Definition of terms: - **Immunodeficiency**- results from a loss of function, partial or total of one or ,one components of the immune system. - **Primary immunodeficiency**- involves basic developmental failure somewhere in the system - **Secondary immunodeficiency**- loss of the immune system due to specific causes at anytime during the lifespan. **What is AIDS?** A -- Aquired I -- Immune D- Deficiency S- Syndrome **Global Epidemiology** - 39.5 million people living with HIV/AIDS in 2006 \- 4.3 million newly infected with HIV (more than half are younger than 25) \- 2.9 million people died from AIDS - More than 25 million people have died from AIDS since 1981 - Africa has over 12 million AIDS orphans **Philippines **is a low-**HIV-prevalence** country, with less than 0.1 percent of the adult population estimated to be **HIV**-positive. As of April 2015, the Department of Health (DOH) **AIDS **Registry in the **Philippines **reported 24,936 cumulative cases. **Risk Factors** - **Transmission**: through bodily fluids from an infected person. Three Conditions: 1\. Virus Must be Present 2\. There must be a high enough concentration of the virus in the infected person 3\. There must be a way for the virus to enter the bloodstream Through Blood, Semen, Vaginal Fluid, or Breast milk **Transmission** - Possible Sources of Transmission: \- Blood products/ transfusions \- Mother to child - Pregnancy, birth, and breastfeeding - Contaminated needles \- Injection drug use, tattoos, piercings, acupuncture - Sexual contact \- Unprotected sex \- Unwashed sexual devices \- Greater risk with other STI due to breaks in skin \- Greater risk with increased number of partners **Risk Factors** - NOT transmitted through \- Casual contact (shaking hands) \- Hugging \- Kissing \- Sweat \- Tears \- Donating Blood \- Swimming Pools \- Toilet seats \- Telephones \- Sharing bed linens, towels, eating utensils, or food \- Insect bites **Societal Risk Factors** - Many determinants of health! - These, in turn, become consequences of an epidemic - Societal factors that contribute to the epidemic: \- People in conflict \- Poverty \- Stigma and Denial \- Cultural factors \- Role of Women **Prevention: Practice SAFER sex** - Nurses must be comfortable discussing their clients' sexual activites \- **Assess**: number of partners, protection being used, and whether it is being used properly \- **Ask** everyone! Don't assume! \- **Educate**: know STI status of sexual partners, HIV/AIDS and other STI testing, use of latex condoms, dental dams, latex gloves, water-based lubricants **Prevention: Clean Needles** - Risk reduction - Nurse can : \- Direct client to addiction services \- Direct client to needle exchange program if quitting is not an option at this time \- Alcohol kills HIV \- Educate! Sharing needles with friends is just as risky as sharing with strangers **Prevention: Screening** - Many STI's are tested with gyne exams, but HIV requires a blood test - HIV antibody test **Prevention: Education** - Many myths and misconceptions ie: \- HIV doesn't exist within this community \- HIV only affects sex-trade workers, homosexuals and injection drug users \- If you get HIV you will show symptoms \- Having sex with a virgin will cure you of HIV - Nurses play a large role in providing the facts! **Prevention: Policy** - Society contributes to HIV transmission! \- Empowering women \- Promoting Justice \- Addressing Poverty \- Providing Education \- Addressing Stigma **What exactly is HIV?** - Human Immunodeficiency Virus- a retrovirus belonging to the family of lentiviruses. - Uses their RNA and host DNA to make viral DNA - Uses CD4+ cell to replicate itself and destroying CD4+ - Two types: HIV-1 + HIV-2 - Leads to Acquired Immunodeficiency Syndrome Survival of retrovirus: - Survives 15 days at room temperature But it is inactivated: - Over 60C - 2% glutaraldehyde - Autoclaving - Disinfectants **Overview of Pathophysiology** - HIV destroys body's immune system by selectively attacking T-4 Lymphocytes, also macrophages & B cells - HIV indirectly affects CNS by neurotoxins produced by the infected macrophages - As CD4+ count ¯, body becomes more susceptible to opportunistic infections **Stages of HIV disease** - Based on "clinical history, physical examination, laboratory evidence of immune dysfunction, signs and symptoms, and infections and malignancies" (Smeltzer & Bare, 2004, 1559) - 3 categories: A, B, C **Clinical Category A** - This category is asymptomatic. - The virus reaches a "set point" level after about 6 months. - The "set point" generally determines rate of disease progression. - In general, 8-10 years can pass before HIV-related complications occur. - Why asymptomatic? CD4 levels are high enough to fight off other pathogens (\>500 CD4+ T-lymphocytes/mm\^3) **Clinical Category B** - CD4 cell level starts dropping (200-499 CD4+ T-lymphocytes/mm\^3). - This category consists of conditions that are not covered under category C. The conditions must: \- Be due to HIV infection \- Require management that is complicated by HIV infection - Some of the conditions under this category include: \- Candidiasis (oropharyngeal or vulvovaginal) \- Cervical carcinoma in situ \- Fever (38.5 C), or diarrhea \> 1 month duration \- Herpes zoster (shingles) \- Pelvic inflammatory disease \- Peripheral neuropathy **Clinical Category C** - When CD4 T-cell levels drop below 200 CD4+ T-lymphocytes/mm\^3, the client is said to have AIDS. Below 100, the immune system is significantly impaired. - Once a client is classified as having category C infection, s/he remains in this category. - Some conditions in this category include: \- Candidiasis (bronchi, trachea, lungs, or esophagus) \- Cervical cancer, invasive \- HIV-related encephalopathy \- Kaposi's sarcoma \- Pneumocystis carinii pneumonia \- Toxoplasmosis of brain \- Wasting syndrome due to HIV **Failure of antibodies:** 1. The virus is hidden safely inside host cells in the lymphoid tissue 2. There appear to be a frequent slight mutations in the viral envelope. 3. Progressive destruction of t helper cells and macrophages. **Opportunistic Infections (OI's)** - Infections that occur because of the client's compromised immune system- do not occur in people with normal immune systems. **Pneumocystis carinii Pneumonia (PCP)** - Most common OI which leads to a diagnosis of AIDS. - Without prophylaxis, 80% of all HIV-infected clients will develop PCP. - S&S: nonproductive cough, fever, chills, SOB, dyspnea, chest pain. - Untreated, it causes respiratory failure. **Mycobacterium avium complex (MAC)** - MAC is a group of bacilli that usually causes respiratory infection. - May also be found in the GI tract, lymph nodes, and bone marrow. **Tuberculosis (TB)** - TB tends to occur early in HIV infection. - If it occurs late in HIV infection, there may be no response to a tuberculin skin test. (This is called anergy, which happens due to the immune system that can no longer respond to the TB antigen.) **Oral Candidiasis** - This is a fungal infection that occurs in nearly all patients with AIDS. - It commonly precedes other OI's. - Untreated, it progresses to the esophagus and stomach. **Wasting Syndrome** - Characterized by \>10% weight loss and chronic diarrhea for more than 30 days OR chronic weakness and intermittent or chronic fever. - Wasting syndrome can not be managed by nutritional support alone. **Kaposi's Sarcoma (KS)** - Most common malignancy in HIV infection. - Involves the blood and lymphatic vessels. - AIDS related KS has a more variable and aggressive course than classic KS. - It may be characterized by skin lesions, or multiple organ system involvement. - Diagnosis comes from biopsy of suspicious lesions. **B-Cell Lymphomas** - Second most common malignancy in HIV-infected clients. - Often occurs in the brain, bone marrow and GI tract. - Chemotherapy is not as effective in HIV-related lymphomas. **HIV Encephalopathy** - Formerly referred to as AIDS dementia complex. - Clinical syndrome consisting of a progressive decline in cognitive, behavioral, and motor function. - HIV has been found in the CSF of patients with this syndrome. **S&S of HIV Encephalopathy** - Early stage: memory loss, difficulty concentrating, headache, confusion, psychomotor slowing, apathy, ataxia. - Later stage: Global cognitive impairments, delay in verbal responses, hyperreflexia, psychosis, hallucinations, tremor, incontinence, seizures, mutism, death. **AIDS Phase** - CD4 count \