Gastrointestinal tract health care ppt free

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1. Nursing care of Patients with Genitourinary disorders By kinfemicheal Melaku ( C .N, BSC N, MSC in AHN) E-mail: [email protected]

2. LEARNING OBJECTIVES On completion of this chapter, the learner will be able to: Describe the structure and function of the renal and urinary systems. Explain the role of the kidneys in regulating fluid and electrolyte balance, acid–base balance, and blood pressure. Describe genitourinary system disorders (GUSDs). Explain causes of genitourinary system disorders. Identify clinical manifestations of GUSDs. Discuss management methods of GUSDs.

3. GLOSSARY A ldosterone: H ormone synthesized and released by the adrenal cortex; causes the kidneys to reabsorb sodium A ntidiuretic hormone (ADH): H ormone secreted by the posterior pituitary gland; causes the kidneys to reabsorb more water; also called vasopressin A nuria: Decreased urine output of less than 50 mL in 24 hours

4. GLOSSARY … Creatinine : Endogenous waste product of muscle energy metabolism Diuresis : Increased urine volume Frequency : Voiding more frequently than every 3 hours. Glomerular filtration rate (GFR): Amount of plasma filtered through the glomeruli per unit of time Nocturia : Awakening at night to urinate

5. GLOSSARY … Oliguria : U rine output less than 0.5 mL/kg/ hr Pyuria : White blood cells in the urine R enal clearance: A bility of the kidneys to clear solutes from the plasma S pecific gravity : Expression of the degree of concentration of the urine U rea nitrogen : End product of protein metabolism

6. Introduction Function of the renal and urinary systems is essential to life. The primary purpose of the renal and urinary systems is to maintain the body’s state of homeostasis by carefully regulating fluid and electrolytes, removing wastes, and providing other functions. Dysfunction of the kidneys and lower urinary tract is common and may occur at any age and with varying degrees of severity. Assessment of upper and lower urinary tract function is part of every health examination and requires that the nurse have an understanding of the anatomy and physiology of the urinary system as well as the effects of changes in the system on other physiologic functions.

7. Fluid and electrolyte imbalances 1/16/2024 7

8. FLUID VOLUME DISTURBANCES Hypovolemia or fluid volume deficit (FVD) FVD, or hypovolemia , occurs when loss of ECF volume exceeds the intake of fluid. It occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids; thus, the ratio of serum electrolytes to water remains the same. FVD should not be confused with dehydration, which refers to loss of water alone, with increased serum sodium levels. 1/16/2024 8

9. Pathophysiology FVD results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake. FVD can also develop with a prolonged period of inadequate intake. 1/16/2024 9

10. Pathophysiology… Causes of FVD include: Abnormal fluid losses, such as those resulting from vomiting, diarrhea, GI suctioning, and sweating; D ecreased intake, as in nausea or lack of access to fluids; and Third-space fluid shifts, or the movement of fluid from the vascular system to other body spaces (e.g., with edema formation in burns, ascites with liver dysfunction). 1/16/2024 10

11. Clinical Manifestations Acute wt loss, Decrease skin turgor, Concentrated urine, Prolonged capillary filling time, Decreased BP, Dizziness, Delirium Increased PR, Muscle cramps, Sunken eyes Cold extremities More than one longitudinal furrows on tongue 1/16/2024 11

12. Assessment and Diagnostic Findings Hx and P/E Normal BUN to serum creatinine concentration ratio is 10:1. A volume-depleted patient has a BUN elevated out of proportion to the serum creatinine (ratio greater than 20:1). The hematocrit level is greater than normal. Urine specific gravity is increased. 1/16/2024 12

13. Medical Management I f fluid losses are acute or severe, the IV route is required. Isotonic electrolyte solutions (e.g., lactated Ringer solution, 0.9% sodium chloride) are frequently the first-line choice to treat the hypotensive patient with FVD because they expand plasma volume. As soon as the patient becomes normotensive, a hypotonic electrolyte solution (e.g., 0.45% sodium chloride) is often used to provide both electrolytes and water for renal excretion of metabolic wastes. 1/16/2024 13

14. Medical Management … Accurate and frequent assessments of I&O, weight, vital signs, central venous pressure, level of consciousness, breath sounds, and skin color are monitored to determine when therapy should be slowed to avoid volume overload. If the patient with severe FVD is not excreting enough urine and is therefore oliguric , the primary provider needs to determine whether the depressed renal function is caused by reduced renal blood flow secondary to FVD ( prerenal azotemia) or, more seriously, by acute tubular necrosis from prolonged FVD. 1/16/2024 14

15. Medical Management … The test used in this situation is referred to as a fluid challenge test . During a fluid challenge test, volumes of fluid are given at specific rates and intervals while the patient’s hemodynamic response to this treatment is monitored (i.e., vital signs, breath sounds, orientation status, central venous pressure, urine output). The response by a patient with FVD but normal renal function is increased urine output and an increase in blood pressure and central venous pressure . 1/16/2024 15

16. Nursing Management To assess for FVD, the nurse monitors and measures fluid I&O at least every 8 hours, and sometimes hourly. Once FVD has developed, the kidneys attempt to conserve body fluids, leading to a urine output of less than 1 mL/kg/h in an adult. Vital signs are closely monitored. In a volume-depleted patient, the urine specific gravity should be greater than 1.020, indicating healthy renal conservation of fluid. 16

17. Hypervolemia Fluid volume excess(FVE) caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF. It is most often secondary to an increase in the total-body sodium content. Because there is isotonic retention of body substances, the serum sodium concentration remains essentially normal. 1/16/2024 17

18. Pathophysiology FVE may be related to simple fluid overload or diminished function of the homeostatic mechanisms responsible for regulating fluid balance. Contributing factors can include heart failure, kidney injury, and cirrhosis of the liver . Another contributing factor is consumption of excessive amounts of table or other sodium salts. Excessive administration of sodium-containing fluids in a patient with impaired regulatory mechanisms may predispose him or her to a serious FVE as well. 1/16/2024 18

19. Clinical manifestations Clinical manifestations of FVE result from expansion of the ECF and may include: Peripheral edema and ascites , D istended neck veins, C rackles (abnormal lung sounds), Acute W t gain, ↑BP and RR, ↑UOP, B ounding pulse and cough, ↓ Hct & Hgb , ↓ U rine sodium and specific gravity 1/16/2024 19

20. Assessment and Diagnostic Findings Laboratory data useful in diagnosing FVE include BUN and hematocrit levels. In FVE, both of these values may be decreased because of plasma dilution, low protein intake, and anemia . The urine sodium level is increased if the kidneys are attempting to excrete excess volume. A chest x-ray may reveal pulmonary congestion. 1/16/2024 20

21. Medical Management Management of FVE is directed at the causes, and if related to excessive administration of sodium-containing fluids, discontinuing the infusion may be all that is needed. Symptomatic treatment consists of administering diuretics and restricting fluids and sodium. 1/16/2024 21

22. Nutritional Therapy Treatment of FVE usually involves dietary restriction of sodium chloride. Lemon juice, onions, and garlic are excellent substitute flavorings, although some patients prefer salt substitutes ( eg . ammonium chloride). Depending on its source, water may contain as little as 1 mg or more than 1500 mg of sodium per quart. 1/16/2024 22

23. Nutritional Therapy… Patients may need to use distilled water if the local water supply is very high in sodium. Bottled water can have a sodium content that ranges from 0 to 1200 mg/L; therefore, if sodium is restricted, the label must be carefully examined for sodium content before purchasing and drinking bottled water. 1/16/2024 23

24. Nursing Management To assess for FVE, the nurse measures I&O at regular intervals to identify excessive fluid retention. The patient is weighed daily, and rapid weight gain is noted. An acute weight gain of 1 kg is equivalent to a gain of approximately 1 L of fluid. 1/16/2024 24

25. Nursing Management… Breath sounds are assessed at regular intervals in at-risk patients, particularly if parenteral fluids are being given. Pitting edema is assessed by pressing a finger into the affected part, creating a pit or indentation that is evaluated on a scale of 1+ (minimal) to 4+ (severe). 1/16/2024 25

26. ELECTROLYTE IMBALANCES Disturbances in electrolyte balances are common in clinical practice and may need to be corrected based on history, physical examination findings, and laboratory values (with comparison to previous values). 1/16/2024 26

27. Sodium Imbalances Sodium (Na+) is the most abundant electrolyte in the ECF; its concentration ranges from 135 to 145 mEq /L (135 to 145 mmol /L), and it is the primary determinant of ECF volume and osmolality . The two most common sodium imbalances are sodium deficit and sodium excess. 1/16/2024 27

28. Sodium Deficit ( Hyponatremia ) Hyponatremia refers to a serum sodium level that is less than 135 mEq /L. Hyponatremia can present as an acute or chronic form. Acute hyponatremia is commonly the result of a fluid overload in a surgical patient. Chronic hyponatremia is seen more frequently in patients outside the hospital setting, has a longer duration, and has less serious neurological sequelae . 1/16/2024 28

29. Pathophysiology Hyponatremia primarily occurs due to an imbalance of water rather than sodium . The urine sodium value assists in differentiating renal from nonrenal causes of hyponatremia . Low urine sodium occurs as the kidney retains sodium to compensate for nonrenal fluid loss (i.e., vomiting, diarrhea). 1/16/2024 29

30. Pathophysiology… High urine sodium concentration is associated with renal salt wasting ( i.e. diuretic use). In dilutional hyponatremia , the ECF volume is increased without any edema. 1/16/2024 30

31. Clinical Manifestations Poor skin turgor, dry mucosa, headache , decreased saliva production, orthostatic fall in blood pressure , nausea, vomiting, and abdominal cramping occur. Neurologic changes, including altered mental status, status epilepticus , and coma, 1/16/2024 31

32. Clinical Manifestations… As the extracellular sodium level decreases, the cellular fluid becomes relatively more concentrated and pulls water into the cells . In general, patients with an acute decrease in serum sodium levels have more cerebral edema and higher mortality rates than do those with more slowly developing hyponatremia . 1/16/2024 32

33. Chronic decreases in sodium, developing over 48 hours or more, can occur in status epilepticus and other neurologic conditions. Features of hyponatremia associated with sodium loss and water gain include anorexia , muscle cramps , and a feeling of exhaustion . 1/16/2024 33

34. Clinical Manifestations… When the serum sodium level decreases to less than 115 mEq /L (115 mmol /L), signs of increasing intracranial pressure, such as lethargy, confusion, muscle twitching, focal weakness, hemiparesis, papilledema, seizures, and death, may occur. 1/16/2024 34

35. Assessment and Diagnostic Findings Hx taking P/E with a focused neurologic examination In Lab. investigations; serum sodium level is less than 135 mEq /L, Serum osmolality is also decreased, T he urinary sodium content is less than 20 mEq /L and the Sg is low (1.002 to 1.004 ) in the case of hyponatremia is due primarily to sodium loss but if the hyponatremia is due to syndrome of inappropriate secretion of antidiuretic hormone(SIADH) the urinary sodium content is greater than 20 mEq /L, and the urine Sg is usually greater than 1.012. 1/16/2024 35

36. Medical Management The key to treating hyponatremia is an assessment that focuses on the clinical symptoms of the patient and signs of hyponatremia (including laboratory values ). As a general rule, treating the underlying condition is essential. 1/16/2024 36

37. Medical Management… Sodium Replacement The most common treatment for hyponatremia is careful administration of sodium by mouth, nasogastric tube, or a parenteral route. For patients who can eat and drink, sodium is easily replaced, because sodium is consumed abundantly in a normal diet. For those who cannot consume sodium, lactated Ringer solution or isotonic saline ( 0.9% sodium chloride ) solution may be prescribed. 37

38. Medical Management… Serum sodium must not be increased by more than 12 mEq /L in 24 hours to avoid neurologic damage due to demyelination (exceeding 140 mEq /L or presence of hypoxia or anoxia .). The usual daily sodium requirement in adults is approximately 100 mEq . 1/16/2024 38

39. Medical Management… The SIADH, the administration of hypertonic saline solution (2 %, 3%, 5%, 7%, and 23% NaCl ) alone cannot change the plasma sodium concentration in whom water restriction is difficult, lithium can antagonize the osmotic effect of ADH on the medullary collecting tubule. 39

40. Water Restriction In patients with normal or excess fluid volume, hyponatremia is usually treated effectively by restricting fluid . However, if neurologic symptoms are severe (e.g., seizures, delirium, coma), or in patients with traumatic brain injury, it may be necessary to administer small volumes of a hypertonic sodium solution with the goal of alleviating cerebral edema . 40

41. Water Restriction… Incorrect use of these fluids is extremely dangerous, because 1 L of 3% NaCl solution contains 513 mEq of Na . The recommendation for hypertonic saline administration in patients with craniocerebral trauma is 3% saline between 0.10 and 1.0 mL/kg/hr. 1/16/2024 41

42. Medical Management … Pharmacologic Therapy IV conivaptan hydrochloride ( Vaprisol ) use is limited to the treatment of hospitalized patients . It may be a useful therapy for those patients with moderate to severe symptomatic hyponatremia but is contraindicated in patients with seizures, delirium, or coma, which warrants the use of hypertonic saline . 1/16/2024 42

43. Nursing Management The nurse monitors I&O as well as daily body weight . Hx taking Hyponatremia is a frequently overlooked cause of confusion in older patients, who are at increased risk because of decreased renal function and subsequent inability to excrete excess fluids. Administration of prescribed and OTC medications that cause sodium loss or water retention is the predisposing factor. 1/16/2024 43

44. Nursing Management… The nurse be alert for GI manifestations such as anorexia, nausea, vomiting, and abdominal cramping and for central nervous system changes, such as lethargy, confusion, muscle twitching , and seizures . Because diuretics promote sodium loss, the patient taking lithium is instructed not to use diuretics without close medical supervision . For all patients on lithium therapy, normal salt and oral fluid intake (2.5 L/day) should be encouraged and a sodium restricted diet should be avoided. 44

45. Sodium Excess (Hypernatremia) Hypernatremia is a serum sodium level higher than 145 mEq /L. It can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium . It can occur in patients with normal fluid volume or in those with FVD or FVE . With a 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. This is both an extracellular and an intracellular FVD. 45

46. Pathophysiology A common cause of hypernatremia is fluid deprivation in patients who cannot respond to thirst . Most often affected are very old, very young, and cognitively impaired patients . Administration of hypertonic enteral feedings without adequate water supplements leads to hypernatremia. In addition, diabetes insipidus can lead to hypernatremia if the patient does not experience or cannot respond to thirst, or if fluids are excessively restricted . IV administration of hypertonic saline or excessive use of sodium bicarbonate also causes hypernatremia. 46

47. Clinical Manifestations Cellular DHN and a more concentrated ECF. Thirst ↓ U rine sodium ↑ PR, BP, T⁰, serum sodium and urine Sg . Swollen dry tongue and sticky mucous membranes, Hallucinations, L ethargy, R estlessness, I rritability, S imple partial or tonic- clonic seizures, Pulmonary edema, Twitching, N &V, anorexia 1/16/2024 47

48. Assessment and Diagnostic Findings The serum sodium level exceeds 145 mEq /L The serum osmolality exceeds 300 mOsm /kg (300 mmol /L ). The urine specific gravity and urine osmolality are increased as the kidneys attempt to conserve water. 1/16/2024 48

49. Medical Management Rx of hypernatremia consists of a gradual lowering of the serum sodium level by the infusion of a hypotonic electrolyte solution (e.g., 0.3% sodium chloride) or an isotonic nonsaline solution (e.g., dextrose 5% in water [D5W ]). Hypotonic sodium solution is thought to be safer than D5W because it allows a gradual reduction in the serum sodium level, thereby decreasing the risk of cerebral edema . 49

50. Medical Management… As a general rule, the serum sodium level is reduced at a rate no faster than 0.5 to 1 mEq /L/h to allow sufficient time for readjustment through diffusion across fluid compartments. 1/16/2024 50

51. Nursing Management To prevent hypernatremia by: Providing oral fluids at regular intervals, enteral feedings or by the parenteral route If enteral feedings are used, sufficient water should be given to keep the serum sodium and BUN within normal limits. For patients with diabetes insipidus , adequate water intake must be ensured. 1/16/2024 51

52. Potassium Imbalances Potassium (K+) is the major intracellular electrolyte; in fact, 98% of the body’s potassium is inside the cells. The remaining 2% is in the ECF and is important in neuromuscular function. Potassium influences both skeletal and cardiac muscle activity . Under the influence of the sodium–potassium pump, potassium is constantly moving in and out of cells. 1/16/2024 52

53. Potassium Imbalances… The normal serum K+ concentration ranges from 3.5 to 5 mEq /L (3.5 to 5 mmol /L), and even minor variations are significant . Potassium imbalances are commonly associated with various diseases, injuries, medications (e.g., NSAIDs and ACE inhibitors), and acid–base imbalances. 1/16/2024 53

54. Potassium Imbalances… To maintain potassium balance, the renal system must function, because 80% of the potassium excreted daily leaves the body by way of the kidneys; the other 20% is lost through the bowel and in sweat . Aldosterone also increases the excretion of potassium by the kidney. Because the kidneys do not conserve potassium as well as they conserve sodium, potassium may still be lost in urine in the presence of a potassium deficit. 1/16/2024 54

55. Potassium Deficit (Hypokalemia) S erum potassium level below 3.5 mEq /L usually indicates a deficit in total potassium stores. However , it may occur in patients with normal potassium stores: When alkalosis (high blood pH) is present, a temporary shift of serum potassium into the cells occurs. 1/16/2024 55

56. Pathophysiology K+ losing diuretics, such as the thiazides and loop diuretics , can induce hypokalemia. Other medications that can lead to hypokalemia include corticosteroids, sodium penicillin, and amphotericin B. Vomiting and gastric suction frequently lead to hypokalemia. Potassium deficit occurs frequently with diarrhea, which may contain as much potassium as 30 mEq /L. 1/16/2024 56

57. Pathophysiology … Hyperaldosteronism increases renal potassium wasting and can lead to severe potassium depletion. P atients with persistent insulin hypersecretion may experience hypokalemia, which is often the case in patients receiving high carbohydrate ( eg . glucose 40%) parenteral nutrition. Magnesium depletion causes renal potassium loss and must be corrected first; otherwise, urine loss of potassium will continue . 1/16/2024 57

58. Clinical Manifestations Severe hypokalemia can cause death through cardiac or respiratory arrest . Clinical signs develop when the potassium level decreases to less than 3 mEq /L. Polyuria, Nocturia Excessive thirst Glucose intolerance 1/16/2024 58

59. Clinical Manifestations… Fatigue, Anorexia, N&V Muscle weakness, Polyuria, ↓ Bowel motility, Ventricular fibrillation, Paresthesias , Leg cramps, ↓ BP Abd . Distention, Hypoactive reflexes, ECG disturbances 1/16/2024 59

60. Assessment and Diagnostic Findings Hx taking ECG exam: An elevated U wave is specific to hypokalemia . Urine test Urinary potassium excretion exceeding 20 mEq /day with hypokalemia suggests that renal potassium loss is the cause . 1/16/2024 60

61. Medical Management Oral potassium supplements K+ loss must be corrected daily; administration of 40 to 80 mEq /day of K+ is adequate in the adult if there are no abnormal losses of K+. Encourage foods high in potassium include most fruits and vegetables, legumes, whole grains, milk, and meat IV potassium replacement therapy (commonly KCl ) with severe hypokalemia (e.g., serum level of 2 mEq /L). 1/16/2024 61

62. Nursing Management Administering Intravenous Potassium Potassium should be given only after adequate urine output has been established. A decrease in urine volume to less than 20 mL per hour for 2 consecutive hours is an indication to stop the potassium infusion and notify the primary provider. Potassium is primarily excreted by the kidneys; when oliguria occurs, potassium administration can cause the serum potassium concentration to rise dangerously . 1/16/2024 62

63. Nursing Management… Administration of IV potassium is done with extreme caution using an infusion pump with the patient monitored by continuous ECG . Caution must be used when selecting a premixed solution of IV fluid containing KCl , as the concentrations range from 10 to 40 mEq /100 mL. Renal function should be monitored through BUN and creatinine levels and urine output if the patient is receiving potassium replacement. During replacement therapy, the patient is monitored for signs of worsening hypokalemia as well as hyperkalemia. 63

64. Potassium Excess (Hyperkalemia ) Serum K+ level > 5 mEq /L [5 mmol /L] seldom occurs in patients with normal renal function. In older adults, there is an increased risk of hyperkalemia due to decreases in renin and aldosterone as well as an increased number of comorbid cardiac conditions . It is usually more dangerous than hypokalemia because cardiac arrest is more frequently associated with high serum potassium levels. 1/16/2024 64

65. Pathophysiology Major causes of hyperkalemia are: D ecreased renal excretion of K+, R apid administration of K+, and M ovement of K+ from the ICF compartment to the ECF compartment . Patients with hypoaldosteronism or Addison disease are at risk for hyperkalemia because deficient adrenal hormones lead to Na+ loss and K+ retention. 1/16/2024 65

66. Pathophysiology … The ff medications are probable contributing factors for > 60% of hyperkalemia episodes: KCl , H eparin , ACE inhibitors , NSAIDs , B eta blockers, C yclosporine, P otassium-sparing diuretics. 1/16/2024 66

67. Pathophysiology … An elevated ECF potassium level should be anticipated when extensive tissue trauma has occurred, as in burns, crushing injuries, or severe infections. Similarly , it can occur with lysis of malignant cells after chemotherapy . Pseudohyperkalemia A false hyperkalemia has several causes, including: the improper collection or transport of a blood sample, a traumatic venipuncture, and use of a tight tourniquet around an exercising extremity while drawing a blood sample, 1/16/2024 67

68. Pathophysiology … WBC count exceeding 200,000/mm3 and thrombocytosis (platelet count exceeding 1 million/mm3 ); drawing blood above a site where potassium is infusing; Lack of awareness of these causes of pseudohyperkalemia can lead to aggressive treatment of a nonexistent hyperkalemia, resulting in serious lowering of serum potassium levels. Therefore , measurements of grossly elevated levels in the absence of clinical manifestations (e.g., normal ECG) should be verified by retesting. 1/16/2024 68

69. Clinical Manifestations The most important consequence of hyperkalemia is its effect on the myocardium . Muscle weakness, T achycardia followed by bradycardia , D ysrhythmias, F laccid paralysis, I ntestinal colic, C ramps, A bdominal distention, Irritability, A nxiety. ECG: tall tented T waves, prolonged PR interval and QRS duration, absent P wave. 1/16/2024 69

70. Assessment and Diagnostic Findings Serum potassium levels and ECG changes are crucial to the diagnosis of hyperkalemia. Arterial blood gas analysis may reveal both a metabolic and a respiratory acidosis. Correcting the acidosis helps correct the hyperkalemia. 1/16/2024 70

71. Medical Management In nonacute situations, restriction of dietary potassium and potassium containing medications may correct the imbalance . Administration, either orally or by retention enema, of cat-ion exchange resins may be necessary. 1/16/2024 71

72. Medical Management… Emergency Pharmacologic Therapy If serum potassium levels are dangerously elevated, it may be necessary to administer IV calcium gluconate . Within minutes after administration, calcium antagonizes the action of hyperkalemia on the heart but does not reduce the serum potassium concentration. Monitoring the BP is essential to detect hypotension, which may result from the rapid IV administration of calcium gluconate . 1/16/2024 72

73. Medical Management … The ECG should be continuously monitored during administration; the appearance of bradycardia is an indication to stop the infusion . Beta-2 agonists, such as albuterol (Proventil, Ventolin ), are highly effective in decreasing potassium; however, their use remains controversial because they can cause tachycardia and chest discomfort (may be used in the absence of ischemic cardiac disease). 1/16/2024 73

74. Nursing Management The nurse monitors I&O and observes for signs of muscle weakness and dysrhythmias . When measuring vital signs, an apical pulse should be taken . The presence of paresthesias and GI symptoms such as nausea and intestinal colic are noted. Serum potassium levels, as well as BUN, creatinine , glucose, and ABG values, are monitored for patients at risk for developing hyperkalemia. 1/16/2024 74

75. Nursing Management… Preventing Hyperkalemia Potassium-rich foods to be avoided include many fruits and vegetables, legumes, whole-grain breads, lean meat, milk, eggs, coffee, tea, and cocoa. Conversely , foods with minimal potassium content include butter, margarine, cranberry juice or sauce, ginger ale, gumdrops or jellybeans, hard candy, root beer, sugar, and honey. Labels of cola beverages must be checked carefully because some are high in potassium and some are not . 75

76. Calcium Imbalances More than 99% of the body’s calcium ( Ca ++) is located in the skeletal system; it is a major component of bones and teeth . Calcium plays a major role in transmitting nerve impulses and helps regulate muscle contraction and relaxation, including cardiac muscle . The normal total serum calcium level is 8.6 to 10.2 mg/ dL (2.2 to 2.6 mmol /L ). 1/16/2024 76

77. Calcium Imbalances… Calcium exists in plasma in three forms: ionized, bound, and complex . Calcium is absorbed from foods in the presence of normal gastric acidity and vitamin D . It is excreted primarily in the feces, with the remainder excreted in the urine. The serum calcium level is controlled by PTH and calcitonin. 1/16/2024 77

78. Calcium Deficit (Hypocalcaemia) S erum calcium value lower than 8.6 mg/ dL occurs in a variety of clinical situations. A patient may have a total-body calcium deficit (as in osteoporosis) but a normal serum calcium level . Older adults and those with disabilities, who spend an increased amount of time in bed , have an increased risk of hypocalcemia , because bed rest increases bone resorption . 1/16/2024 78

79. Pathophysiology Several factors can cause hypocalcemia , including primary hypoparathyroidism and surgical hypoparathyroidism (more common). Transient hypocalcemia can occur with massive administration of citrated blood (i.e., massive hemorrhage and shock), because citrate can combine with ionized calcium and temporarily remove it from the circulation. Hypocalcemia is common in pancreatitis. Hypocalcemia is common in patients with kidney injury. 1/16/2024 79

80. Pathophysiology … Other causes of hypocalcemia include: I nadequate vitamin D consumption, Magnesium deficiency, Medullary thyroid carcinoma , Low serum albumin levels , Alkalosis , and alcohol abuse. Medications predisposing to hypocalcemia include: Aluminum-containing antacids, Aminoglycosides , Caffeine , Cisplatin , Corticosteroids , Mithramycin , P hosphates , I soniazid , Loop diuretics, and P roton pump inhibitors 1/16/2024 80

81. Clinical Manifestations Tetany (spasms of the hands, feet and larynx), the most characteristic manifestation of hypocalcemia and hypomagnesemia . Chvostek sign consists of twitching of facial muscles located anterior to the earlobe, just below the zygomatic arch, is tapped . Trousseau sign can be elicited by inflating a blood pressure cuff on the upper arm to about 20 mm Hg above systolic pressure; within 2 to 5 minutes, carpal spasm will occur as ischemia of the ulnar nerve develops. 1/16/2024 81

82. Clinical Manifestations … Numbness, T ingling of fingers, toes, and circumoral region Seizures, Carpopedal spasms, Hyperactive deep tendon reflexes, Irritability, Bronchospasm, Anxiety, Impaired clotting time, ↓ Prothrombin , Diarrhea, ↓ BP, ECG: prolonged QT interval and lengthened ST ↓ Mg++ 82

83. Assessment and Diagnostic Findings When evaluating serum calcium levels, the serum albumin level and the arterial pH must also be considered. Because abnormalities in serum albumin levels may affect interpretation of the serum calcium level. For every decrease in serum albumin of 1 g/ dL below 4 g/ dL , the total serum calcium level is underestimated by approximately 0.8 mg/ dL . Quick Calculation Method Measured total serum Ca ++ level (mg/dl) + 0.8*(4- measured albumin level [g/ dL ]) = corrected total Ca ++ concentration (mg/dl) 1/16/2024 83

84. Assessment and Diagnostic Findings… Example : A patient’s reported serum albumin level is 2.5 g/ dL ; the reported serum calcium level is 10.5 mg/ dL . First, 4 g/ dL – 2.5 g/ dL = 1.5 g/ dL . Next, the following ratio is calculated : 0.8mg/dl →1g/ dL X → 1.5g/ dL = 1.2mg/dl calcium Finally 1.2 mg/ dL + 10.5 mg/ dL = 11.7 mg/ dL of corrected total serum calcium level. 84

85. Assessment and Diagnostic Findings… When the arterial pH increases (alkalosis), more calcium becomes bound to protein . As a result, the ionized portion decreases. Magnesium and phosphorus levels need to be assessed to identify possible causes of decreased calcium. 1/16/2024 85

86. Medical Management Emergency Pharmacologic Therapy Acute symptomatic hypocalcemia is life threatening and requires prompt treatment with IV administration of a calcium salt includes calcium gluconate and calcium chloride . calcium gluconate is more preferable. IV administration of calcium is particularly dangerous in patients receiving digitalis-derived medications (can cause digitalis toxicity). 1/16/2024 86

87. Medical Management … The IV site must be observed often for any evidence of infiltration because of the risk of extravasation and resultant cellulitis or necrosis. A 0.9% NaCl solution should not be used with calcium because it increases renal calcium loss . Solutions containing phosphates or bicarbonate should not be used with calcium because they cause precipitation when calcium is added . 1/16/2024 87

88. Medical Management … Calcium replacement can cause postural hypotension; therefore, the patient is kept in bed during IV infusion, and BP is monitored. Nutritional Therapy Vitamin D therapy may be instituted to increase calcium absorption from the GI tract. Aluminum hydroxide, calcium acetate, or calcium carbonate antacids may be prescribed to decrease elevated phosphorus levels before treating hypocalcemia in the patient with chronic kidney disease. 88

89. Medical Management … Increasing the dietary intake of calcium to at least 1000 to 1500 mg/day in the adult is recommended. Calcium supplements must be given in divided doses of no higher than 500 mg to promote calcium absorption. Calcium-containing foods include milk products; green, leafy vegetables; canned salmon; canned sardines; and fresh oysters . Hypomagnesemia can also cause tetany ; if the tetany responds to IV calcium, then a low magnesium level is considered as a possible cause in chronic kidney injury. 89

90. Nursing Management The nurse: To initiate seizure precautions if hypocalcemia is severe . Monitors the status of the airway closely, because laryngeal stridor can occur . Educate the patient about foods that are rich in calcium . Advise the patient to consider calcium supplements if sufficient calcium is not consumed in the diet. Moderate cigarette smoking increases urinary calcium excretion . Cautioned the patient to avoid the overuse of laxatives and antacids that contain phosphorus, because their use decreases calcium absorption. 90

91. Calcium Excess ( Hypercalcemia ) Hypercalcemia (serum calcium value >10.2 mg/ dL ) is a dangerous imbalance when severe; in fact, hypercalcemic crisis has a mortality rate as high as 50% if not treated promptly . 1/16/2024 91

92. Pathophysiology The most common causes of hypercalcemia are malignancies and hyperparathyroidism. Calcifications of soft tissue occur when the calcium–phosphorus product (serum calcium × serum phosphorus) exceeds 70 mg/ dL . Most cases of hypercalcemia secondary to immobility occur after severe or multiple fractures or spinal cord injury . 1/16/2024 92

93. Pathophysiology… Thiazide diuretics can cause a slight elevation in serum calcium levels because they potentiate the action of PTH on the kidneys, reducing urinary calcium excretion . Vitamin A and D intoxication, as well as chronic lithium use and theophylline toxicity, can cause calcium excess. Calcium levels are inversely related to phosphorus levels . Calcium enhances the inotropic effect of digitalis; therefore, hypercalcemia aggravates digitalis toxicity . 1/16/2024 93

94. Clinical Manifestations The more severe symptoms tend to appear when the serum calcium level is approximately 16 mg/ dL (4 mmol /L) or higher . Hypercalcemic crisis refers to an acute rise in the serum calcium level to 17 mg/ dL (4.3 mmol /L) or higher . Severe thirst and polyuria are often present. 1/16/2024 94

95. Clinical Manifestations… Muscle weakness, I ntractable nausea, Abdominal cramps, S evere constipation, D iarrhea , P eptic ulcer symptoms, and bone pain . Lethargy, confusion , and coma may also occur. This condition is dangerous and may result in cardiac arrest. 1/16/2024 95

96. Assessment and Diagnostic Findings The double-antibody PTH test may be used to differentiate between primary hyperparathyroidism and malignancy as a cause of hypercalcemia ECG examination X-rays may reveal bone changes if the patient has hypercalcemia secondary to a malignancy, bone cavitations , or urinary calculi. 1/16/2024 96

97. Medical Management Treating the underlying cause (e.g., chemotherapy for a malignancy, partial parathyroidectomy for hyperparathyroidism) is essential . Pharmacologic Therapy Mobilizing the patient, and restricting dietary calcium intake . IV administration of 0.9 % NaCl solution temporarily dilutes the serum calcium level and increases urinary calcium excretion by inhibiting tubular reabsorption of calcium. 1/16/2024 97

98. Medical Management … Administering IV phosphate can cause a reciprocal drop in serum calcium . Furosemide is often used in conjunction with administration of a saline solution; in addition to causing diuresis, furosemide increases calcium excretion . Calcitonin can be used to lower the serum calcium level. 1/16/2024 98

99. Medical Management … Calcitonin is given by IM injection rather than SC, because patients with hypercalcemia have poor perfusion of subcutaneous tissue. For patients with cancer, treatment is directed at controlling the condition by surgery, chemotherapy, or radiation therapy . Corticosteroids may be used Mithramycin , a cytotoxic antibiotic, inhibits bone resorption and thus lowers the serum calcium level. 1/16/2024 99

100. Nursing Management Increasing patient mobility and encouraging fluids can help prevent hypercalcemia . Hospitalized patients at risk should be encouraged to ambulate as soon as possible . Fluids containing sodium should be given unless contraindicated, because sodium assists with calcium excretion . Patients are encouraged to drink 2.8 to 3.8 L of fluid daily . Adequate fiber in the diet is encouraged to offset the tendency for constipation The cardiac rate and rhythm are monitored for any abnormalities . 1/16/2024 100

101. Magnesium Imbalances Magnesium (Mg++) is an abundant intracellular cation . It acts as an activator for many intracellular enzyme systems and plays a role in both carbohydrate and protein metabolism . The normal serum magnesium level is 1.3 to 2.3 mg/ dL . Approximately one third of serum magnesium is bound to protein; the remaining two thirds exist as free cations —the active component (Mg ++). Magnesium balance is important in neuromuscular function . 1/16/2024 101

102. Phosphorus Imbalances Phosphorus (HPO4–) is a critical constituent of all body tissues. It is essential to the function of muscle and red blood cells; the formation of ATP and of 2,3-diphosphoglycerate, which facilitates the release of oxygen from hemoglobin; and the maintenance of acid–base balance, as well as the nervous system and the intermediary metabolism of carbohydrate, protein, and fat. It provides structural support to bones and teeth. Phosphorus is the primary anion of the ICF . The normal serum phosphorus level is 2.5 to 4.5 mg/ dL in adults. 102

103. Chloride Imbalances Chloride ( Cl −), the major anion of the ECF, is found more in interstitial and lymph fluid compartments than in blood . Sodium and chloride make up the largest electrolyte composition of the ECF and assist in determining osmotic pressure. The excretion and reabsorption of chloride ions takes place mostly in the kidneys. The normal serum chloride level is 97 to 107 mEq /L. Inside the cell, the chloride level is 4 mEq /L. 103

104. Assignment Parenteral fluid therapy and managing systemic and local complications (group1 & 2, 3&4, 5&6) . Do based on the group and submit. Magnesium Imbalances Phosphorus Imbalances R eading assignment Chloride Imbalances 1/16/2024 104

105. Acid-Base balance 1/16/2024 105

106. ACID – BASE BALABCE Acid–base disturbances are commonly encountered in clinical practice. Plasma pH is an indicator of hydrogen ion (H+) concentration. Homeostatic mechanisms keep pH within a normal range (7.35–7.45 ). - These mechanisms consist of buffer systems, the kidneys, and the lungs. 1/16/2024 106

107. ACID – BASE BALABCE … The H+ concentration is extremely important: The greater the concentration, the more acidic the solution and the lower the pH. The lower the H+concentration , the more alkaline the solution and the higher the pH. 1/16/2024 107

108. ACID – BASE BALABCE … Buffer systems Buffer systems prevent major changes in the pH of body fluids by removing or releasing H +. Hydrogen ions are buffered by both intracellular and extracellular buffers . The body’s major extracellular buffer system is the bicarbonate–carbonic acid buffer system. Assessed when ABG are measured . 1/16/2024 108

109. ACID – BASE BALABCE … Normally, there are 20 parts of bicarbonate (HCO3−) to 1 part of carbonic acid (H2CO3 ). It is the ratio of HCO3− to H2CO3 that is important in maintaining pH. If either bicarbonate or carbonic acid is increased or decreased so that the 20:1 ratio is no longer maintained, acid– base imbalance results . CO2 is a potential acid; when dissolved in water, it becomes carbonic acid (CO2 + H2O = H2CO3 ). Therefore , when CO2 is ↑ ed , the carbonic acid content is also ↑ ed , and vice versa. 109

110. Intracellular buffers include proteins , organic and inorganic phosphates , and hemoglobin. The kidneys: Regulate the HCO3 − level in the ECF; they can regenerate HCO3 − ions as well as reabsorb them from the renal tubular cells . In respiratory acidosis and most cases of metabolic acidosis , the kidneys excrete H+ and conserve HCO3 − ions to help restore balance . In respiratory and metabolic alkalosis , the kidneys retain H+ and excrete bicarbonate ions to help restore balance. The kidneys obviously cannot compensate for the metabolic acidosis created by kidney injury . Renal compensation for imbalances is relatively slow . 110

111. The lungs: Control the CO2 and thus the carbonic acid content of the ECF. They do so by adjusting ventilation in response to the amount of CO2 in the blood. A rise in the partial pressure of CO2 in arterial blood (PaCO2) is a powerful stimulant to respiration . Of course, the partial pressure of oxygen in arterial blood (PaO2) also influences respiration. I ts effect is not as marked as that produced by the PaCO2. 111

112. In metabolic acidosis, the respiratory rate increases, causing greater elimination of CO2 (to reduce the acid load ). In metabolic alkalosis, the respiratory rate decreases, causing CO2 to be retained (to increase the acid load ) 1/16/2024 112

113. Cont`d 1/16/2024 113

114. Blood Gas Analysis 1/16/2024 114 Parameter Arterial blood Mixed Venous blood PH 7.35 – 7.45 7.32 – 7.42 PaCO 2 35-45 mmHg 38-52mmHg HCO3 - 22-26 mEq /L 19-25mEq/L PaO 2 80 -100 mmHg 24-48 mEq /L O₂ saturation( SaO ₂ %) >94% 65 – 75% Base excess/deficit ±2 mEq /L ±5mEq/L

115. Metabolic Acidosis (Base Bicarbonate Deficit) Metabolic acidosis is a common clinical disturbance. C haracterized by: A low pH (increased H+ concentration) and A low plasma bicarbonate concentration . Causes :- Excessive accumulation of acid, diarrhea, the use of diuretics; early renal insufficiency; excessive administration of chloride; and the administration of parenteral nutrition without bicarbonate (e.g ., lactate). 1/16/2024 115

116. Clinical Manifestations Headache, C onfusion , D rowsiness, Increased RR and depth, N ausea , and vomiting, P eripheral vasodilation, D ecreased BP, C old and clammy skin, D ysrhythmias , and Shock. Chronic metabolic acidosis is usually seen with chronic kidney disease . May be tetany . 1/16/2024 116

117. Assessment and Diagnostic Findings ABG measurements Expected blood gas changes include a low bicarbonate level (less than 22 mEq /L) and a low pH (less than 7.35). The cardinal feature of metabolic acidosis is a decrease in the serum bicarbonate level. Hyperkalemia may accompany metabolic acidosis as a result of the shift of potassium out of the cells. Later , as the acidosis is corrected, potassium moves back into the cells and hypokalemia may occur. Hyperventilation decreases the CO2 level as a compensatory action. 1/16/2024 117

118. Medical Management If the problem results from excessive intake of chloride, treatment is aimed at eliminating the source of the chloride. When necessary, bicarbonate is given. The serum potassium level is monitored closely, and hypokalemia is corrected as acidosis is reversed . In chronic metabolic acidosis, low serum calcium levels are treated before the chronic metabolic acidosis is treated to avoid tetany . Treatment modalities may also include hemodialysis or peritoneal dialysis. 1/16/2024 118

119. Metabolic Alkalosis ( Base Bicarbonate Excess ) Metabolic alkalosis is a clinical disturbance characterized by a high pH (decreased H+ concentration) and a high plasma bicarbonate concentration. 1/16/2024 119

120. Pathophysiology A common cause is vomiting or gastric suction with loss of hydrogen and chloride ions . Other causes includes: Pyloric stenosis. Diuretics that promotes excretion of potassium. Excessive alkali ingestion. Chronic metabolic alkalosis can occur due to: Villous adenoma , external drainage of gastric fluids , significant potassium depletion, cystic fibrosis, and the chronic ingestion of milk and calcium carbonate 1/16/2024 120

121. Clinical Manifestations Tingling of the fingers and toes, Dizziness, Hypertonic muscles Symptoms of hypocalcemia Respirations are depressed as a compensatory action by the lungs. Atrial tachycardia may occur . Decreased motility and paralytic ileus may also be evident . 1/16/2024 121

122. Assessment and Diagnostic Findings pH greater than 7.45 Serum bicarbonate concentration > 26 mEq /L. The PaCO2 increases as the lungs attempt to compensate for the excess bicarbonate by retaining CO2. Urine chloride levels may help identify the cause of metabolic alkalosis if the patient’s history provides inadequate information . 1/16/2024 122

123. Medical Management Monitor carefully I&O of the pt`s Restore normal fluid volume by administering sodium chloride fluids. In patients with hypokalemia, potassium is given as KCl to replace both K+ and Cl − losses. H2 receptor antagonists, such as cimetidine, reduce the production of gastric hydrogen chloride ( HCl ), 1/16/2024 123

124. Respiratory Acidosis ( Carbonic Acid Excess) Respiratory acidosis is a clinical disorder in which the pH is < 7.35 and The PaCO2 is > 45 mm Hg. A compensatory increase in the plasma HCO3 occurs. It may be either acute or chronic . A decrease in PaO2 1/16/2024 124

125. Pathophysiology Acute respiratory acidosis occurs in emergency situations, such as acute pulmonary edema, aspiration of a foreign object, atelectasis, pneumothorax, and overdose of sedatives . I n nonemergent situations, such as sleep apnea, severe pneumonia, and acute respiratory distress syndrome. Respiratory acidosis can also occur in diseases that impair respiratory muscles, such as muscular dystrophy, multiple sclerosis, myasthenia gravis. Mechanical ventilation may be associated with hypercapnia . 1/16/2024 125

126. Clinical Manifestations ↑PR and RR, ↑BP Mental cloudiness or confusion, and A feeling of fullness in the head, or A decrease in the level of consciousness . An elevated PaCO2 , > 60 mm Hg, causes cerebrovascular vasodilation and increased cerebral blood flow . Ventricular fibrillation may be the first sign of respiratory acidosis in anesthetized patients. 1/16/2024 126

127. Clinical Manifestations… Chronic respiratory acidosis occurs with pulmonary diseases such as chronic emphysema and bronchitis, obstructive sleep apnea, and obesity. If the PaCO2 increases rapidly, cerebral vasodilation will increase the intracranial pressure, and cyanosis and tachypnea will develop. 1/16/2024 127

128. Assessment and Diagnostic Findings ABG analysis reveals a pH less than 7.35, A PaCO2 greater than 42 mm Hg, A variation in the bicarbonate level. Monitoring of serum electrolyte levels , Chest x-ray for determining any respiratory disease, and A drug screen if an overdose is suspected. An ECG examination. 1/16/2024 128

129. Medical Management Treatment is directed at improving ventilation; exact measures vary with the cause of inadequate ventilation Pharmacologic agents are used as indicated. For example, bronchodilators help reduce bronchial spasm, antibiotics are used for respiratory infections, and thrombolytics or anticoagulants are used for pulmonary emboli 1/16/2024 129

130. Medical Management … Pulmonary hygiene measures are initiated. Adequate hydration (2 to 3 L/day). Mechanical ventilation, used appropriately, may improve pulmonary ventilation. Elevated PaCO2 must be decreased slowly. Placing the patient in a semi-Fowler position facilitates expansion of the chest wall . Treatment of both chronic and acute respiratory acidosis is the same. 1/16/2024 130

131. Respiratory Alkalosis ( Carbonic Acid Deficit) Respiratory alkalosis is a clinical condition in which the arterial pH is greater than 7.45 and the PaCO2 is less than 35 mm Hg. As with respiratory acidosis, acute and chronic conditions can occur. 1/16/2024 131

132. Pathophysiology Respiratory alkalosis is always caused by hyperventilation. Causes include extreme anxiety, hypoxemia, early phase of salicylate intoxication, gram-negative bacteremia, and inappropriate ventilator settings. Chronic respiratory alkalosis results from chronic hypocapnia , and decreased serum bicarbonate levels are the consequence . Chronic hepatic insufficiency and cerebral tumors are predisposing factors. 1/16/2024 132

133. Clinical Manifestations Lightheadedness due to vasoconstriction and decreased cerebral blood flow, Inability to concentrate , Numbness and tingling from decreased calcium ionization, Tinnitus , and sometimes loss of consciousness . Cardiac effects of respiratory alkalosis include tachycardia and ventricular and atrial dysrhythmias . 1/16/2024 133

134. Assessment and Diagnostic Findings Analysis of ABG assists in the Dx of respiratory alkalosis. In the acute state, the pH is elevated above normal as a result of a low PaCO2 and a normal bicarbonate level. Evaluation of serum electrolytes: Expected:- Decreased in Potassium, calcium and phosphate. A toxicology screen Diagnostic evaluation and plan of care are the same as for acute and chronic respiratory alkalosis. 1/16/2024 134

135. Medical Management Treatment depends on the underlying cause of respiratory alkalosis. If the cause is anxiety, the patient is instructed to breathe more slowly to allow CO2 to accumulate or to breathe into a closed system (such as a paper bag ). An antianxiety agent may be required to relieve hyperventilation in very anxious patients. Treatment of other causes of respiratory alkalosis is directed at correcting the underlying problem. 1/16/2024 135

136. Mixed Acid–Base Disorders Patients can simultaneously experience two or more independent acid– base disorders . A normal pH in the presence of changes in the PaCO2 and plasma HCO3− concentration immediately suggests a mixed disorder. An example of a mixed disorder is the simultaneous occurrence of metabolic acidosis and respiratory acidosis during respiratory and cardiac arrest. The only mixed disorder that cannot occur is a mixed respiratory acidosis and alkalosis, because it is impossible to have alveolar hypoventilation and hyperventilation at the same time . 136

137. Table of Acid–Base Disorders and Compensation Acid base imbalance Primary Disturbance Respiratory compensation and predicted response Renal compensation and predicted response Metabolic acidosis ↓PH and HCO3 ↑ventilation and ↓PCO2 ↑H⁺ excretion and ↑HCO₃¯ reabsorption if no renal disease Metabolic alkalosis ↑PH and HCO₃¯ ↓ventilation and ↑PCO2 ↓H⁺ excretion and ↓HCO₃¯ reabsorption if no renal disease Respiratory acidosis ↓PH and ↑PCO2 None ↑H⁺ excretion and ↑HCO₃¯ reabsorption Respiratory alkalosis ↑PH and ↓PCO2 None ↓H⁺ excretion and ↓HCO₃¯ reabsorption 1/16/2024 137

138. Exercises 1. P H = 7.48 PaCO2 = 32 mm Hg HCO3 − = 24 mEq /L 2. PH = 7.48 PaCO2 = 40 mm Hg HCO3− = 30 mEq /L 3. PH = 7.1 PaCO2 = 50 mm Hg HCO3− = 24 mEq /L 4. PH = 7.1 PaCO2 = 44 mm Hg HCO3− = 18 mEq /L 5. PH= 7.15 PaCO2= 55mmHg HCO3− = 25mEq/L 6. PH= 7.4 PaCO2= 55mmHg HCO3− = 33mEq/L 7. PH= 7.37 PaCO2= 58mmHg HCO3− = 12mEq/L 1/16/2024 138

139. Anatomic and Physiologic Overview Anatomy of the Kidney and Urinary Systems The kidney and urinary systems include the: kidneys, u reters, bladder, and urethra .

140. K idneys Located retroperitoneally (behind and outside the peritoneal cavity) on the posterior wall of the abdomen—from the 12th thoracic vertebra to the 3rd lumbar vertebra in the adult. The average adult kidney weighs approximately 113 to 170 g and is 10 to 12 cm long, 6 cm wide, and 2.5 cm thick. The right kidney is slightly lower than the left due to the location of the liver. An adrenal gland lies on top of each kidney. The kidneys and adrenals are independent in function, blood supply, and innervation.

141. Kidneys … The kidney consists of two distinct regions The renal parenchyma The renal pelvis. The renal parenchyma is divided into T he cortex and T he medulla The cortex contains Glomeruli P roximal and distal tubules Cortical collecting ducts and their adjacent peritubular capillaries. 141

142. Kidneys … The renal pelvis is the beginning of the collecting system and is composed of structures that are designed to collect and transport urine. Once the urine leaves the renal pelvis, the composition or amount of urine does not change. The cortex contains the nephron which is responsible for urine formation .

143. Kidneys … Blood Supply to the Kidneys The hilum is the concave portion of the kidney through which the renal artery enters and the ureters and renal vein exit. The kidneys receive 20% to 25% of the total cardiac output, which means that all of the body’s blood circulates through the kidneys approximately 12 times per hour.

144. Kidneys … The renal artery (arising from the abdominal aorta) divides into smaller and smaller vessels, eventually forming the afferent arterioles . Each afferent arteriole branches to form a glomerulus, which is the tuft of capillaries forming part of the nephron through which filtration occurs. Blood leaves the glomerulus through the efferent arteriole and flows back to the inferior vena cava through a network of capillaries and veins.

145. Nephrons Each kidney has 1 million nephrons and are responsible for the formation of filtrate that will become urine. The large number of nephrons allows for adequate renal function even if the opposite kidney is damaged or becomes nonfunctional. If the total number of functioning nephrons is less than 20% of normal, renal replacement therapy needs to be considered. The length of the tubular component of the nephron is directly related to its ability to concentrate urine.

146. Nephrons are made up of two basic components: the glomerulus and the attached tubule . The glomerular membrane is composed of three filtering layers: the capillary endothelium, the basement membrane, and the epithelium . This membrane normally allows filtration of fluid and small molecules yet limits passage of larger molecules, such as blood cells and albumin. Renin is a hormone directly involved in the control of arterial blood pressure; it is essential for proper functioning of the glomerulus

147. Ureters, Bladder, and Urethra The urine formed in the nephrons flows through the renal calyces and then into the ureters. These narrow tubes, each 24 to 30 cm long. The lining of the ureters is made up of transitional cell epithelium called urothelium . The urothelium prevents reabsorption of urine . The movement of urine from each renal pelvis through the ureter into the bladder is facilitated by peristaltic contraction of the smooth muscles in the ureter wall .

148. Ureters, Bladder, and Urethra … Each ureter has three narrow areas that are prone to obstruction by renal calculi (kidney stones) or stricture. These three areas include the ureteropelvic junction, the ureteral segment near the sacroiliac junction, and the ureterovesical junction . Obstruction of the ureteropelvic junction is the most serious because of its close proximity to the kidney and the risk of associated kidney dysfunction.

149. Ureters, Bladder, and Urethra … The urinary bladder is a distensible muscular sac located just behind the pubic bone. The usual capacity of the adult bladder is 400 to 500 mL, but it can distend to hold a larger volume. The bladder is characterized by its central, hollow area, called the vesicle , which has two inlets (the ureters) and one outlet (the urethra ). The bladder has internal urethral and external urinary sphincters.

150. Functions of the Kidney Urine formation Excretion of waste products Regulation of electrolytes Regulation of acid–base balance Control of water balance Control of blood pressure Renal clearance Regulation of red blood cell production Synthesis of vitamin D to active form Secretion of prostaglandins

151. Function of the Kidney and Urinary Systems Urine Formation The healthy human body is composed of approximately 60% water. Water balance is regulated by the kidneys and results in the formation of urine. Urine is formed in the nephrons through a complex three-step process : glomerular filtration , tubular reabsorption, and tubular secretion

152. Cont`d The various substances normally filtered by the glomerulus, reabsorbed by the tubules, and excreted in the urine include sodium, chloride, bicarbonate, potassium, glucose, urea, creatinine , and uric acid . Amino acids and glucose are usually filtered at the level of the glomerulus and reabsorbed so that neither is excreted in the urine. Normally , glucose does not appear in the urine .

153. Glomerular Filtration The normal blood flow through the kidneys is between 1000 and 1300 mL/min. Under normal conditions, about 20% of the blood passing through the glomeruli is filtered into the nephron, amounting to about 180 L/day of filtrate. As blood enters the glomerulus from the afferent arteriole, filtration depends on adequate blood flow that maintains a consistent pressure through the glomerulus called hydrostatic pressure.

154. Tubular Reabsorption and Tubular Secretion The second and third steps of urine formation occur in the renal tubules. In tubular reabsorption, a substance moves from the filtrate back into the peritubular capillaries or vasa recta. In tubular secretion, a substance moves from the peritubular capillaries into tubular filtrate. Of the 180 L of filtrate that the kidneys produce each day, 99% is reabsorbed into the bloodstream, resulting in the formation of 1 to 2 L of urine each day. Tubular secretion helps with the elimination of potassium, hydrogen ions, ammonia, uric acid, some drugs, and other waste products.

155. Osmolarity and Osmolality Osmolarity refers to the ratio of solute to water. As little as a 1% to 2% change in the serum osmolarity can cause a conscious desire to drink and conservation of water by the kidneys. Osmolality is the most accurate measurement of the kidney’s ability to dilute and concentrate urine. It measures the number of solute particles in a kilogram of water. Serum and urine osmolality are measured simultaneously to assess the body’s fluid status. In healthy adults, serum osmolality is 280 to 300 mOsm /kg , and normal urine osmolality is 200 to 800 mOsm /kg . For a 24-hour urine sample, the normal value is 300 to 900 mOsm /kg.

156. Antidiuretic hormone (ADH ) Secreted in response to changes in osmolality of the blood. With decreased water intake, blood osmolality tends to increase, stimulating ADH release. ADH then acts on the kidney, increasing reabsorption of water and thereby returning the osmolality of the blood to normal. With excess water intake, the secretion of ADH by the pituitary is suppressed; therefore, less water is reabsorbed by the kidney tubule, leading to diuresis (increased urine volume). A dilute urine with a fixed specific gravity (about 1.010) or fixed osmolality (about 300 mOsm /L) indicates an inability to concentrate and dilute the urine, which is a common early sign of kidney disease.

157. Specific gravity Specific gravity( sg ) is a measurement of the kidney’s ability to concentrate urine . It compares the wt of urine to wt of distilled H20 w/c has sg of 1.000. Normal urine sg is 1.010 to 1.025 Urine sg depends largely on hydration When fluid intake decreases, sg normally increases. With high fluid intake , sg decreases.

158. Regulation of Water Excretion A person normally ingests about 1300 mL of oral liquids and 1000 mL of water in food per day. Of the fluid ingested, approximately 900 mL is lost through the skin and lungs (called insensible loss), 50 mL through sweat, and 200 mL through feces . Daily weight measurements are a reliable means of determining overall fluid status. 0.5kg equals approximately 500 mL, so a weight change of as little as 0.5kg could suggest an overall fluid gain or loss of 500 mL.

159. Regulation of Electrolyte Excretion When the kidneys are functioning normally, the volume of electrolytes excreted per day is equal to the amount ingested. The regulation of sodium volume excreted depends on aldosterone, a hormone synthesized and released by the adrenal cortex. With increased aldosterone in the blood, less sodium is excreted in the urine, because aldosterone fosters renal reabsorption of sodium.

160. Regulation of Electrolyte Excretion … Release of aldosterone from the adrenal cortex is largely under the control of angiotensin II. This complex system is activated when pressure in the renal arterioles falls below normal levels, as occurs with shock, dehydration, or decreased sodium chloride delivery to the tubules . Activation of this system increases the retention of water and expansion of the intravascular fluid volume, thereby maintaining enough pressure within the glomerulus to ensure adequate filtration.

161. Regulation of Acid–Base Balance The normal serum pH is about 7.35 to 7.45 and must be maintained within this narrow range for optimal physiologic function. The kidney performs major functions to assist in this balance. One function is to reabsorb and return to the body’s circulation any bicarbonate from the urinary filtrate; other functions are to excrete or reabsorb acid, synthesize ammonia, and excrete ammonium chloride.

162. Regulation of Acid–Base Balance… A person with normal kidney function excretes about 70 mEq of acid each day . The kidney is able to excrete some of this acid directly into the urine until the urine pH reaches 4.5, which is 1000 times more acidic than blood.

163. Autoregulation of Blood Pressure Regulation of blood pressure is an important function of the kidney. Specialized vessels of the kidney, called the vasa recta, constantly monitor blood pressure as blood begins its passage into the kidney. When the vasa recta detect a decrease in blood pressure, specialized juxtaglomerular cells secrete the hormone renin . Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II—the most powerful vasoconstrictor known; angiotensin II causes the blood pressure to increase.

164. Autoregulation of Blood Pressure… The adrenal cortex secretes aldosterone in response to stimulation by the pituitary gland, which occurs in response to poor perfusion or increasing serum osmolality. The result is an increase in blood pressure. When the vasa recta recognize the increase in blood pressure, renin secretion stops. Failure of this feedback mechanism is one of the primary causes of hypertension.

165. The regulation of sodium volume excreted depends on aldosterone, (RAAS)

166. Urine Storage The sensation of bladder fullness is transmitted to the central nervous system when the bladder has reached about 150 to 200 mL in adults , and an initial desire to void occurs. A marked sense of fullness and discomfort with a strong desire to void usually occurs when the bladder reaches its functional capacity of 400 to 500 mL of urine . Under normal circumstances with average fluid intake of approximately 1 to 2 L/day , the bladder should be able to store urine for periods of 2 to 4 hours at a time during the day.

167. Bladder Emptying Micturition normally occurs approximately 8 times in a 24-hour period . Any obstruction of the bladder outlet, such as in advanced benign prostatic hyperplasia (BPH), results in a high voiding pressure . High voiding pressures make it more difficult to start urine flow and maintain it . Normally, residual urine amounts to no more than 50 mL in the middle-aged adult and less than 50 to 100 mL in the older adult.

168. Gerontologic Considerations Upper and lower urinary tract function changes with age. The GFR decreases, starting between 35 and 40 years of age, and a yearly decline of about 1 mL/min continues thereafter. Older adults are more susceptible to acute and chronic kidney injury due to the structural and functional changes in the kidney. Examples include sclerosis of the glomerulus and renal vasculature, decreased blood flow, decreased GFR, altered tubular function, and acid–base imbalance.

169. Gerontologic Considerations… Older women often have incomplete emptying of the bladder and urinary stasis, which may result in urinary tract infection or increasing bladder pressure, leading to overflow incontinence, hydronephrosis , pyelonephritis, or chronic kidney disease. Urologic symptoms can mimic disorders such as appendicitis, peptic ulcer disease, and cholecystitis , which can make diagnosis difficult in older adults due to decreased neurologic innervation

170. Assessment Health history It is also important to review risk factors Childhood diseases: “strep throat” impetigo, Nephrotic syndrome Advanced age Instrumentation of urinary tract, cystoscopy, Catheterization Immobilization Occupational Recreational 173

171. Health hx… Family hx (b/c Persons with a family history of urinary tract problems are at increased risk for renal disorders.) M any persons with a history of systemic lupus erythematosus ( SLE ) develop lupus nephritis 174

172. When Obtaining The Health History, The Nurse Should Inquire : The patient’s chief concern The location, character, and duration of pain History of urinary tract infections Fever or chills Previous renal or urinary diagnostic tests Dysuria Urinary incontinence 175

173. Cont’d Hesitancy- straining, or pain during or after urination Hematuria or change in color or volume of urine Nocturia and its date of onset Renal calculi (kidney stones) Female patients: C/S deliveries; use of forceps ; vaginal infection; contraceptive practices, STI Habits: use of tobacco, alcohol, or recreational drugs Use of medication Gastrointestinal Symptoms 176

174. Physical Examination Direct palpation of the kidneys may help determine their size and mobility. Palpation of the kidneys is generally difficult. Renal dysfunction may produce tenderness over the CV angle The abdomen is auscultated to assess for bruits ( indicate renal artery stenosis/aortic aneurysm). The bladder should be percussed after the patient voids to check for residual urine. The sound changes from tympanic to dull when percussing over the bladder 177

175. Physical Examination… 178

176. Diagnostic Evaluation Urinalysis ( Normal urine pH is 4.5 to 8.0; a value of < this reveals acidic urine pH and vise-versa) and urine culture X-ray films Renal function tests Renal concentration tests Creatinine clearance Serum creatinine Blood urea nitrogen levels Imaging modalities Kidney, ureter, and bladder studies General ultrasonography Bladder ultrasonography Computed tomography and MRI 179

177. Dx…Cont’d Renal Concentration Tests Specific Gravity(1.010–1.025) Urine Osmolality( 300–900 mosm/Kg/24h ) Blood Urea Nitrogen/BUN/ 7–18 mg/dL Patients over age 60 years: 8–20 mg/dL Creatinine clearance Measures effectiveness of renal function. Creatinine is end product of muscle energy metabolism. In normal function, level of creatinine remains constant Normal range 0.6–1.2 mg/dL (50–110 μ mol /L) 180

178. URINARY TRACT DISORDER Expectations:- Identify factors contributing to urinary tract infections . Compare and contrast pyelonephritis, glomerulonephritis , and the nephrotic syndrome Describe causes of acute and chronic renal failure Describe management strategies for renal calculi/stone Describe interstitial cystitis and its physical & psychological effects on the patient 181

179. Urinary tract infections(UTIs ) Caused by Pathogenic Microorganisms Classified as t he Upper or Lower UTIs Lower UTIs include:- bacterial cystitis ( inflammation of the urinary bladder ) bacterial prostatitis (inflammation of prostate gland) bacterial urethritis (inflammation of urethra ). There can be acute or chronic non bacterial causes of inflammation in any of these areas ( misdiagnosed ) 182

180. Urinary tract infection(UTIs) Upper UTIs are much less common and include: Acute/Chronic Pyelonephritis (Inflammation of Renal Pelvis ) Interstitial Nephritis (Inflammation of Kidney) Renal Abscesses . 183

181. Cystitis It is inflammation of urinary bladder Bladder is sterile Several mechanisms maintain the sterility such as:- The physical barrier of the urethra Urine flow Ureterovesical junction competence Various antibacterial enzymes and antibodies, Anti-adherent effects mediated by the mucosal cells 184

182. Cystitis Cont’d… Risk factors Inability or failure to empty the bladder completely Obstructed urinary flow Immunosuppression Instrumentation Contributing conditions( DM/pregnancy /gout/neurologic disorders Escherichia coli are the most common MO causing UTI. Females are more affected than men. 185

183. Cystitis Cont’d… Clinical manifestations Burning on urination Frequency Urgency Nocturia Incontinence Suprapubic or pelvic pain Hematuria and back pain 186

184. Diagnosis Physical examination Urine analysis , what it reveals? Urine culture Medical Management Pharmacotherapy Cephalosporin Co- trimoxazole Ampicilline/ Amoxacillin Gentamicine Quinolones 187

185. Cystitis Cont’d… Diet management Encourage fluid intake Avoid urinary tract irritants e.g. Coffee, tea, alcohol 188

186. Urethritis Inflammation of the urethra Caused By Microorganisms Trauma hypersensitivity to chemicals /vaginal deodorants, spermicidal jellies Signs and symptoms Dysuria, frequency, urgency, and bladder spasms Urethral discharge may be noted 189

187. Diagnosis Based on patient signs and symptoms, urinalysis and urethral smear Medical treatment- Similar with cystitis Antimicrobials Cephalosporin Co- trimoxazole Ampicilline/ Amoxacillin Gentamicine Quinolones 190

188. Pyelonephritis Inflammation of the renal pelvis Acute pyelonephritis most often caused by ascending bacterial infection , but it may be blood-borne Chronic pyelonephritis often the result of reflux of urine from inadequate closure of the ureterovesical junction during voiding 191

189. Acute Pyelonephritis Causes: ascending infection - vesicoureteral reflux into the renal pelvis and papillae; E. coli, Proteus, Enterobacter. hematogenous seeding - due to septicemia or endocarditis; Staphlococcus and E. coli. 192

190. Acute Pyelonephritis… Common in patients with: incompetent ureteral valves. diabetes. immunocompromise . Dx Patchy suppurative inflammation, tubular necrosis, neutrophilic casts. Abscesses and papillitis more common in diabetics. C/M Flank pain, fever, dysuria, pyuria and bacteriuria, GI upset 193

191. Chronic Pyelonephritis Chronic tubulointerstitial inflammation with renal scarring . Important cause of end-stage renal disease ( ESRD ). Two forms: reflux-associated : common, congenital vesicourteral reflux or intrarenal reflux. Obstructive : posterior urethral valves, ureteral calculi or abnormalities. 194

192. Chronic Pyelonephritis... Characteristic morphologic features are seen on gross examination: irregular scarring. corticomedullary scar overlying a dilated, blunted, or deformed calyx . most in upper and lower poles consistent with the frequency of reflux in these sites. 195

193. Chronic Pyelonephritis…. Signs and symptoms Chronic pyelonephritis Bladder irritation Chronic fatigue, and slight aching over one or both kidneys GI upset Skin changes (Itching, discoloration) 196

194. Dx of pyelonephritis Hx and P/E Lab →WBC, ESR, BUN, U/A Imaging testes→ x-ray, ultrasound… Medical treatment Antibiotics - depend on U/A value Urinary tract antiseptics Analgesics Drink excess of fluid Intravenous fluids may be ordered if N/V Dietary salt and protein restriction for patient with chronic disease 197

195. Nephritis (acute glomerulonephritis) It is the inflammation of glomeruli Etiology/pathophysiology Previous infection with β -hemolytic streptococcus (2-3 weeks prior) Preexisting multisystem diseases e.g DM, HPN, systemic inflammations Clinical manifestations Edema of the face Anorexia Azotemia Proteinuria Dyspnea with exertion Hematuria Oliguria ; dysuria 198

196. Cont’d… Dx Hx P/E Lab investigation CBC ESR (male= < 10 mm/h, female = <6mm/h) BUN, creatinine Imaging tests Electron microscopy and Immunofluorescent analysis Kidney biopsy 199

197. Cont’d … Complications Hypertensive encephalopathy Heart failure P ulmonary edema . ESKD

198. Cont’d… Medical management/ Pharmacological management Antibiotics - If residual streptococcal infection is suspected, penicillin is the agent of choice Corticosteroids Diuretics Controlling proteinuria Antihypertensives Supportive management Diet Protein restrictions when renal insufficiency and elevated BUN develop . Sodium restrictions when the patient has hypertension, edema, and heart failure. 201

199. Cont’d… Nursing interventions Increase carbohydrates I&O is carefully measured and recorded . Fluids are given based on the patient’s fluid losses and daily body weight. Diuresis Patient education about the disease process, explanations of laboratory and other diagnostic tests, and preparation for safe and effective self-care at home .

200. Nephritis (chronic glomerulonephritis ) May be due to: R epeated episodes of AGN Hyperlipidemia Hypertensive nephrosclerosis Slow, progressive destruction of glomeruli Commonly caused by other chronic illnesses Diabetes mellitus Systemic lupus erythematous (SLE) 203

201. Cont’d…. Clinical manifestations Headaches Loss of weight and strength Increasing irritabilit y Nocturia Hypertension As chronic GN progresses , S/S of CKD may develop . Visual and digestive disturbances yellow-gray pigmentation of the skin periorbital and peripheral edema . Weight gain Cardiomegaly Anemia 204

202. Cont’d…. Dx Hx P/E Urinalysis Renal function test Blood chemistry Chest x-rays ECG CT scan and MRI Medical management/nursing interventions Same as acute glomerulonephritis Renal dialysis Kidney transplant 205

203. Nephrotic Syndrome A condition of increased glomerular permeability Is not a specific glomerular disease Is a syndrome with a cluster of findings that include: Marked increase in proteinuria (especially albumin) > 3.0 to 3.5 g per 24 hour urine Hypoalbuminemia Edema High serum cholesterol and LDL (hyperlipidemia ). Hypercoagulability - due to loss of antithrombin III 206

204. Hematuria Oliguria Azotemia Hypertension Nephritic syndrome Massive proteinuria Hypoalbuminemia Edema Hyperlipidemia/- uria Nephrotic syndrome 207

205. 208

206. 209

207. 210

208. Nephrotic Syndrome…. Caused by: Chronic glomerulonephritis, Diabetes mellitus with glomerulosclerosis, Amyloidosis (deposit of amyloid /non nitrognous food in organs) Lupus, multiple myeloma and renal vein thrombosis 211

209. Summary… 212

210. Clinical features Proteinuria & hypoalbuminemia Edema - common sites in the early stage (face, peri -orbital areas & scrotum). Hyperlipidemia May due to  hepatic lipoprotein synthesis & ↓clearance May accelerate atherosclerosis & progression of renal d/se. Hyper coagulability  due to loss of antithrombin III Peripheral venous or arterial thrombosis Renal vein thrombosis Pulmonary embolism 213

211. Clinical features … Other complications Anemia - due to transferrin loss (a globulin in blood plasma that carries iron) Hypocalcemia - due to excretion of cholecalciferol (a fat-soluble vitamin which prevents skin/bones) Increased susceptibility to infection - as result of urinary loss & increased catabolism of immuniglobulin and loss of complements. 214

212. Dx Hx P/E Urine analysis – protein, micro organism. Lipid…. Imaging testes – to reveal other problems Renal biopsy to determine specific cause 215

213. Treatment of nephrotic syndrome High protein diet Bed rest  promotes rest & decrease protein catabolism Limit sodium intake Diuretics in moderate dose Adrenocorticosteroids (e.g. prednisone) Immunosuppressive agent e.g , Azathioprine, Mycophenolate, Cyclosporine ACEIs can decrease proteinuria e.g Captopril, Enalapril Cholesterol lowering agents Heparin to reduce coagulability 216

214. Complications of N ephrotic S yndrome Massive proteinuria Hypoalbuminemia Edema Lipiduria Hyperlipidemia Increased coagulation Renal insufficiency 217

215. Renal Failure 218

216. Renal Failure or Kidney Failure (Renal Insufficiency) Describes a medical condition in which the kidneys fail to adequately filter toxins and waste products Described as a decrease in the GFR . Biochemically, RF is typically detected by an elevated serum creatinine level . The two forms are 1 . acute (acute kidney injury) 2 . chronic (chronic kidney disease) 219

217. A) Acute Renal failure Sudden drop in GFR Can develop in a previously healthy person Last from a few days to several weeks Risk Factors Diabetes Hypertension Chronic glomerulonephritis Heart disease (heart failure) Advanced age Sepsis 220

218. Causes of ARF The following categories better explain how ARF develops.  Prerenal ARF : caused due to perfusion impairment Intrarenal ARF : caused due to damage of kidney Post renal ARF : caused due to Urine flow obstruction 221

219. Contributing Factors for ARF Development Prerenal Causes : Hypotension Hypovolemia(Shock) Decreased cardiac output Dehydration Diabetes Intrarenal Causes: Nephrotoxic episodes Infection Hemolytic blood transfusion reactions Glomerular diseases (systemic lupus, glomerulonephritits ) 222

220. Cont… Postrenal Causes: Benign prostatic hypertrophy Prostate cancer Ovarian cancer Obstruction of a urinary catheter Renal calculi Bladder/pelvic neoplasms, Urethral strictures , Spinal disease Medications w/c Cause ARF: Contrast media e.g barium swallowing Diuretics (Furosemide) Heavy metals (Hg, Au & Pb ) Ibuprofen ( NSAID ) Organic chemicals or solvents e,g benzin , easters Nephrotoxic antibiotics ACE Inhibitors 223

221. Pathophysiology of ARF Changes in the renal hemodynamic , nephron structure/function and cellular metabolism are the pathophysiologic changes that are seen with acute renal failure. Phases of Acute Renal Failure There are four clinical phases of ARF:- Onset Phase Oliguria/ Anuric Phase Diuretic Phase Recovery Phase 224

222. Onset Phase Is characterized by: Renal flow at 20% of normal Oxygenation to the tissue at 20% of normal Urine output at 30 ml (or less) per hour Urine sodium excretion greater than 40 mEq /L. Oliguria with urinary output less than 400ml/24h R ising potassium, BUN, Creatinine n ot responsive to fluid challenges. 225

223. Cont’d… Oliguric/ Anuric Phase : Is characterized by Further damage to the renal tubular wall and membranes. Great reduction in the glomerular filtration rate (GFR) Increased blood BUN/ Creatinine level Electrolyte abnormalities ( hyperkalemia, hyperphosphatemia and hypocalcaemia ) Metabolic acidosis Oliguria < 400 ml/24 Hrs , the normal is 1.5L/24Hrs 226

224. Cont’d Diuretic Phase :- is characterized by: Increase in glomerular filtration rate (GFR) Urine output as high as 2-4 L/day (N=1.5L/Hrs) Renal cells that cannot concentrate urine Recovery Phase : Is characterized by Edema decreases The renal tubules begin to function adequately Fluid and electrolyte balance are restored At this point the GFR has usually returned to 70% to 80% of normal . 227

225. Consequences Uremic Syndrome: Azotemia : accumulation of nitrogenous metabolites in the blood Uremia: azotemia plus the clinical signs and symptoms of weakness, ill feeling, n/v/d, itching ( pruritis ) Ca, Na deposition) , muscle cramps, hiccups, twitching, emotional irritability,  mental capacity. Hiccups : b reathe spasmodically, and make a sound Proteinuria Hyperkalemia (secondary to  clearance; nephropathy can cause deficiency in or resistance to aldosterone 228

226. Sodium : sodium retention resulting in fluid retention, HTN, edema, CHF. Some patients experience loss of high amounts of sodium: salt losing enteropathy . Hyperphosphatemia Acid-base balance:  uric acid secretion and bicarbonate production  metabolic acidosis Blood volume changes Oliguric phase : very little urinary output – blood pressure rises sharply Can  pulmonary edema Diuretic phase : large losses of fluids and electrolytes Urine output as high as 2-4 L/day (N=1.5L/Hrs) Recovery phase : (hopefully) – everything normalizes. 229 Consequences…

227. Signs and Symptoms Decreased urine output Urine may be pink or reddish in color Edema (face, arms, legs, feet, eyes) Flank pain/pelvic pain Poor appetite (nausea, vomiting) Bitter or metallic taste in mouth Dry itchy skin Easy bruising, fatigue Seizures, shortness of breath , arrhythmias Sudden weight gain 230

228. Diagnosing Acute Renal Failure Confirmatory Lab Values for Acute Renal Failure Lab Test Prerenal Value Intrarenal Value Urine Specific Gravity Greater than 1.020 1.010 to 1.020 BUN/Creatinine ratio Greater than 20:1 10-20:1 Urine Osmolality Greater than 500 mOsm/kg 300-500 mOsm/kg Urine Sodium 10 mEq/L or less 20 mEq/L or more Urine Sediment (urinalysis) Hyaline casts Granular casts Fractional excretion of sodium percent (FENa) Less than 1% Greater than 1 % N= BUN / Creatinine ratio is 10 – 20 to 1 231

229. Cont… Imaging Studies/Procedures/Tests Creatinine Clearance Test Ultrasound Renal Biopsy 232

230. Collaborative mgt for ARF Primary goals of treatment. Identifying and treating the cause. Maintaining volume homeostasis Correcting biochemical abnormalities The management includes Maintaining adequate intravascular volume Maintaining blood pressure Discontinuing all nephrotoxic medications ( NSAIDs, Gentamycin ) Eliminating exposure to any other nephrotoxins 233

231. Cont… Correcting acidosis (sodium bicarbonate for severe acidosis) Correcting hemolytic abnormalities (blood transfusion required) Correcting all electrolyte abnormalities (Hyperkalemia common) Strict monitoring on intake and output /daily weight (Hydration) Serious monitoring of labs (BUN/Creatinine/Osmolality [urine/blood] Diet and fluid restrictions/replacement(in a state of oliguria/polyuria) 234

232. Rx cont’d… Pharmacologic Rx IV glucose & insulin as an emergency and temporary measure to treat hyperkalmia that is released due to break down of proteins. Na HCo3 to treat acidosis Dialysis if there is excess serum urea, creatinine , hyper kalemia , pericarditis , neuropathy, encephalopathy Diet mag’t Restrict food & fluids containing potassium and phospherous (e.g. banana, coffee) during oliguric phase With held protein during oliguric phase but increase during recovery. 235

233. B ) Chronic kidney disease CKD/CRF Chronic kidney disease occurs when one suffers from gradual and usually permanent loss of kidney function This happens gradually (months to years). With loss of kidney function, there is an accumulation of water, waste, and toxic substances, 236

234. Stages of Chronic Kidney Disease Stage Description GFR* mL /min/1.73m 2 1 Slight kidney damage with normal or increased filtration More than 90 2 Mild decrease in kidney function 60-89 3 Moderate decrease in kidney function 30-59 4 Severe decrease in kidney function 15-29 5 End-stage kidney disease or CKD Less than 15 (or dialysis) *GFR is glomerular filtration rate, a measure of the kidney's function. Normal rage 100-130 ml/min * 237

235. Causes Major causes are diabetes and high blood pressure. Glomerulonephritis. Polycystic kidney disease. Use of analgesics such as acetaminophen (Tylenol) and ibuprofen Hardening of the arteries ( Nephroscloosis )=HTN Obstruction of the flow of urine by stones, an enlarged prostate Other causes HIV infection, sickle cell disease, heroin abuse, amyloidosis , kidney stones, chronic kidney infections, and certain cancers. 238

236. C/ Ms CKD Nocturia Swelling of the legs and puffiness around the eyes (fluid retention); High blood pressure ; Fatigue and weakness Loss of appetite, nausea&vomiting ; Itching , easy bruising, and pale skin (from anemia); Shortness of breath( sob ) Headaches, numbness in extremities ( p. Neuropathy ) Disturbed sleep, altered mental status / encephalopathy , restless legs syndrome 239

237. CRF summary of C/m…. Electrolyte disturbance Hyponatremia Hyper kalemia Acidosis Hypocalcemia Endocrine disturbances Renal osteodystrophy  due to change in ca , p & parathyroid hormone imbalance Osteomalacia  due to  1, 25 dihydroxycholecalciferol Decrease libido, impotence, amenorrhea 240

238. CRF summary of C/m…. Metabolic disturbances Hyper uricemia Neuromuscular Peripheral neuropathy Fatigue, head ache & insomnia CVs disturbance HPN pericarditis Dermatological disturbances Pruritus(intense itching)  due to ca /p imbalance Ecchymosis  because uremia leads to bleeding 241

239. CRF summary of C/m…. Gastro intestinal Anorexia, nausea and vomiting Peptic ulcer GI bleeding Haematologic disturbances Anemia ( normocytic) - due to decreased erythropoietin production by the kidney Increased susceptibility to infection Chest pain due to pericarditis (inflammation around the heart); Bleeding (due to poor blood clotting); Bone pain and fractures; and Decreased sexual interest and erectile dysfunction. 242

240. Symptoms of Chronic Kidney Disease….. 243

241. Diagnostic studies Urine Tests Urinalysis: Twenty-four hour urine tests: Estimated GFR ( eGFR ). Blood Tests Creatinine and urea (BUN) in the blood: Electrolyte levels and acid-base balance: Blood cell counts Other tests Ultrasound: Biopsy , X-ray 244

242. Collaborative mgt for CRF I. Diet management : dietary guidelines recommend that: Protein restriction: Decreasing protein intake. Salt restriction: Limit to 2.4 grams a day Fluid intake: Limit excessive water intake Potassium restriction: Decrease K+ intake. Phosphorus restriction: Decreasing p3+intake. Calcium supplement along with synthetic vit.D to minimize symptoms of renal osteodystrophy . Antihypertensive H+ - blockers  to minimize peptic ulceration & bleeding Dialysis Renal transplantation

243. Cont… Advise the patient & family about the need to Control of blood pressure and/or diabetes; Stop smoking Lose excess weight. Avoid nephrotoxic drugs. III . Drug Treatment There is no cure for chronic kidney disease. The four goals of therapy are to: Slow the progression of disease; Treat underlying causes and contributing factors; Treat complications of disease Replace lost kidney function 246

244. Cont… Strategies for slowing progression and treating conditions underlying chronic kidney disease include the following :- Control of blood glucose Control of high blood pressure Diet management Treatment of the following complications like: Fluid retention Anemia Bone disease Acidosis 247

245. Renal Replacement Therapies In end-stage kidney disease, kidney functions can be replaced only by dialysis or by kidney transplantation . The planning for dialysis and transplantation is usually started in Stage 4 of chronic kidney disease. 248

246. Chronic Kidney Disease Prognosis There is no cure for chronic kidney disease. People undergoing dialysis have an overall five year survival rate of 32%. Recipients of a kidney transplant from a living related donor have a two year survival rate greater than 90%. Recipients of a kidney from a donor who has died have a two year survival rate of 88%. 249

247. UROLITHIASIS Stones (calculi) in the urinary tract Stones are formed due to increase urinary concentration of : Calcium oxalate Calcium phosphate Uric acid 250

248. Etiology Contributing factors: Infection Urinary stasis Immobility High serum calcium High urine calcium Dehydration Medications 251

249. Medications that are known to cause stones Antacids Acetazolamide Vitamin D Laxatives High doses of aspirin 252

250. Epidemiology Occurs predominantly in the third to fifth decades of life Affects men more than women Pathogenesis Stones formed due to: Increase urinary concentration crystalloids Deficiency of substances that normally prevent crystallization in the urine (citrate, magnesium ) 253

251. Types of stones Uric acid stones May be seen in patients with gout Cystine stones Patients with a rare inherited defect in renal absorption of cystine 254

252. Characteristic of stones Most stones contain calcium or magnesium in combination with phosphorus or oxalate. Most stones are radiopaque and can be detected by x-ray studies 255

253. Clinical Manifestations Stones in the renal pelvis (nephrolithiasis) Intense, deep ache in the costovertebral region Hematuria Pyuria Pain originating in the renal area radiates Toward the bladder in the female Toward the testes in the male 256

254. Episode of renal colic Tenderness over the costovertebral area Nausea and vomiting Diarrhea and abdominal discomfort 257

255. 258

256. Stones in the ureter (ureteral obstruction) Ureteral colic Acute, excruciating, colicky, wavelike pain, radiating down to the thigh and to the genitalia Desire to void, but little urine is passed, and it usually contains blood 259

257. 260

258. Diagnostic Findings History Dietary and medication histories Family history of renal stones Imaging X-ray Ultrasonography Intravenous urography, or retrograde pyelography 261

259. Laboratory Blood chemistries 24 hr urine test for measurement of calcium, uric acid, creatinine, sodium 262

260. Medical Management Goals To determine the stone type To prevent nephron destruction To control infection To relieve any obstruction To eradicate the stone 263

261. Opioid analgesics for pain High fluid intake For Calcium Stones Advised to restrict calcium in their diet High fluid intake Dietary restriction of protein and sodium High protein diet increased urinary excretion of calcium High sodium intake increase the amount of calcium in the urine 264

262. For uric acid stones Low - purine diet Allopurinol Reduce serum uric acid levels Reduce urinary uric acid excretion For cystine stones Low -protein diet Penicillamine Reduce the amount of cystine in the urine 265

263. Stone Removal Methods Ureteroscopic Extracorporeal shock wave lithotripsy (ESWL) Electrohydraulic lithotripsy Endourologic Chemolysis Surgical 266