Pathophysiology Review

1
Pathophysiology Review
2
Objective 1Cellular Adaptations to
InjuryFigure 3-1, Page 66

• Five Cellular Adaptations to Injury
• Atrophy
• Hypertrophy
• Hyperplasia
• Metaplasia
• Dysplasia

3
Objective 1Cellular Adaptations to
InjuryAtrophy

• Decrease or shrinkage in
• cellular size.
• Physiological/Pathological
• Pathologic
• Decrease in
• Workload
• Pressure
• Use
• Blood supply
• Nutrition
• Hormonal Stimulation
• Nervous Stimulation

4
Objective 1Cellular Adaptations to
InjuryHyperplasia

• Increase in number of cells
• resulting from increased rate of
• cellular division.
• Physiologic
• Compensatory
• Hormonal
• Pathologic

5
Objective 1Cellular Adaptations to
InjuryMetaplasia

• Reversible replacement of one
• mature cell type by another.
• New cells are created because of
• signals generated by cytokines
• (growth factors) in the cells
• environment.

6
Objective 1Cellular Adaptations to
InjuryDysplasia

• Refers to abnormal changes in
• the size, shape, and organization
• of mature cells.
• High and low grade

7
Objective 2Processes responsible for cell
injuryHypoxia/Ischemia

• Hypoxia
• Lack of sufficient oxygen (single most common
  cause of cellular injury)
• Causes of hypoxia
• Ischemia
• Reduced blood supply
• Time is muscle
• Gradual vs. acute blockage

8
Section B Part I ImmunityObjective 2
Describe how the immune response is induced.

• ABO System

9
Objective 2Processes responsible for cell
injuryMechanical Injury

• Cell injury
• Definitions
• Contusion
• Hematoma
• Abrasion
• Laceration

10
Section B Part II InflammationObjective 1
Identify characteristics of the phases of
inflammation

• Resolution
• Restoration of original structure and physiologic
  function
• Repair
• Replacement of destroyed tissue with scar tissue
• Primary Intension
• Wounds that heal under conditions of minimal
  tissue loss
• Secondary Intension
• Longer process, cell injury is more extensive

11
Nursing 280 PathophysiologyExamination
2Module ISection C Alterations in the
Hematologic System

• Presented by
• Ronda M. Overdiek, M.S.N., R.N.

12
Objective 4Describe normal physiological
effects of anemia

• Anemia
• Reduction in the total number of circulating
  erythrocytes
• Decrease in the quality or quantity of hemoglobin
• Causes
• Altered production of erythrocytes
• Blood loss
• Increased erythrocyte destruction
• Combination of all three

13
Progression/Manifestations Of Anemia
14
Classifications of Anemia

• Macrocytic-Normochromic (Megaloblastic)
• Defective DNA synthesis resulting in unusually
  large stem cells in the marrow that mature into
  unusually large erythrocytes in the circulation.
  
• Increase in size, thickness, and volume.
• Deficiencies of Vitamin B12/Folate
• Microcytic-Hypochromic
• Small erythrocytes that contain abnormally
  reduced amounts of hemoglobin
• Iron metabolism disorders, porphyrin/heme
  synthesis, globin synthesis
• Normocytic-Normochromic
• Erythrocytes normal in size and Hgb content but
  insufficient in number

15
Objective 5 Differentiate major anemias by
etiology, signs/symptoms, treatmentPernicious
Anemia

• Macrocytic-Normochromic (Megaloblastic)
• Most common type
• Caused by Vitamin B12 deficiency due to lack of
  enzyme (IF) required for gastric absorption
• Congenital, gastric mucosal atrophy, chronic
  gastritis (autoimmune disorder), environmental
• Signs/Symptoms weakness, fatigue, loss of
  appetite, abdominal pain, weight loss,
  hepatomegaly, splenomegaly, right-sided heart
  failure.
• Treatment Vitamin B12 replacement (high dose)
• NOT CURABLE, untreated can be fatal

16
Iron Deficiency Anemia

• Microcytic-Hypochronic Anemia
• Causes
• Continuous blood loss (ulcers, cirrhosis,
  hemorrhoids, ulcerative colitis, cancer,
  menorrhagia) decreased dietary intake of iron.
• Signs/Symptoms
• Onset s/s gradual, fatigue, weakness, shortness
  of breath, headache, numbness, tingling, memory
  loss, disorientation.
• Evaluation blood tests
• Treatment Identify cause and eliminate, iron
  replacement therapy.

17
Aplastic Anemia

• Normocytic-Normochromic
• Caused by bone marrow hypoplasia / aplasia
  (marrow or erythrocyte stem cells are
  underdeveloped, defective, or absent)
• Acquired/Hereditary
• Chemical exposures (arsenic, benzene), HIV,
  hepatitis, drug effects (amphotericin,
  penicillin, dilantin, aspirin, motrin,
  immunosupressant drugs, etc.
• Signs/Symptoms weakness, fatigue, dyspnea, etc.
• Treatment Treat the underlying disorder, blood
  transfusions.

18
Hemolytic Anemia

• Normocytic-Normochromic
• Premature accelerated destruction of erythrocytes
• Causes Acquired/Hereditary
• Infection, drugs/toxins, liver disease, kidney
  disease or abnormal immune responses
• Signs/Symptoms Jaundice, splenomegaly,
  hepatomegaly.
• Treatment Remove the cause, splenectomy.

19
Sickle Cell

• Abnormal form of hemoglobin
• Stretches the erythrocyte into elongated sickle
  cell shape
• Cause Inherited autosomal recessive
• Signs/Symptoms vascular occlusion, pain, organ
  infarction, fatigue, weakness
• Treatment Supportive care/avoid crisis
• Fever, infection, acidosis, dehydration, exposure
  to cold.
• Blood transfusions
• Genetic Counseling

20
Objective 6 Describe the pathogenesis of
polycythemia.

• Two Classifications of Polycythemia
• Relative Dehydration
• Treatment Hydration
• Absolute Primary/Secondary
• Primary
• Polycythemia Vera (Abnormal proliferation of bone
  marrow stem cells)
• Secondary
• Physiologic response resulting from
  erythropoietin secretion caused by hypoxia
• High altitudes/increased levels of CO2, COPD,
  coronary heart failure
• Familial
• Genetic
• Table 20-5, Page 547

21
Objective 8 Identify Alterations in Leukocytic
Function

• Function is affected if
• Quantitative
• Too many (leukocytosis) or too few white cells
  (leukopenia)
• Bone marrow dysfunction, premature destruction of
  circulating cells, invasion of infectious
  microorganisms.
• Too many granulocytes (granulocytosis) or too few
  (granulocytopenia)

22
Objective 2Processes responsible for cell
injuryHypoxia/Ischemia
Figure 3-5, Page 70
23
Objective 8 Identify Alterations in Leukocytic
Function

• Laboratory Reports
• Shift to the left
• Bands Immature Cells
• Segs Mature Cells
• When bands gtSegs
• Table 20-6 Page 550

24
Objective 8 Identify Alterations in Leukocytic
Function

• Leukemia
• Clonal malignant disorder of the blood and
  blood-forming organs causing an accumulation of
  dysfunctional cells and loss of cell division
  regulation.
• Uncontrolled proliferation of leukocytes
• Overcrowding of bone marrow
• Decreased production/function of normal
  hematopoietic cells
• Acute/Chronic

25
Objective 8 Identify Alterations in Leukocytic
Function

• Acute Leukemia
• Onset abrupt/rapid
• Characterized by undifferentiated/immature cells
  (blast cell)
• Short survival time
• Chronic Leukemia
• Onset is gradual/prolonged clinical course
• Predominant cell is mature but does not function
  normally
• Relatively longer survival time

26
Objective 8 Identify Alterations in Leukocytic
Function

• Leukemia
• Cause is unknown
• Genetic predisposition
• Signs/Symptoms
• Fatigue, bleeding, fever, anorexia, wasting of
  muscle, liver/spleen/lymph node enlargement,
  headache, etc.
• Evaluation blood tests/bone marrow
• Treatment Chemotherapy, blood transfusions,
  antibiotics, antifungals, antivirals.

27
Objective 9 Identify alterations in lymphoid
function.

• Lymphadenopathy
• Enlarged lymph nodes
• Caused by proliferation of lymphocytes and
  monocytes
• Caused by
• Neoplastic disease
• Immunologic/Inflammatory conditions
• Endocrine Disorders
• Lipid storage Diseases

28
Objective 7 Hemostatic DisordersHemorrhagic
Diseases

• Hemophilia
• Genetic X-Linked
• Coagulation Factors affected
• Signs/Symptoms
• Abnormal bleeding/bruising
• Evaluation/Treatment
• Laboratory blood tests
• Blood transfusionseducate patients to be careful

29
Objective 7 Hemostatic DisordersHemorrhagic
Diseases

• Disseminated Intravascular Coagulation (DIC)
• Acquired clinical syndrome occurs because of
  unregulated release of thrombin and subsequent
  fibrin formation and accelerated fibrinolysis.
• Clinical presentation Massive hemorrhage and
  thrombosis to chronic, low-grade condition
• Localized or involve multiple organs
• Clinical conditions that facilitate procoagulant
  activity are
• Arterial hypotension often accompanying shock
• Hypoxemia
• Acidemia
• Stasis of capillary blood flow

30
DIC
31
Objective 7 Hemostatic DisordersHemorrhagic
Diseases DIC

• Signs/Symptoms
• Acute/Chronic
• Hemorrhaging, petechiae, hematomas, etc. Most
  individual with DIC demonstrate bleeding at three
  unrelated sites and any combination may be
  observed.
• Evaluation/Treatment
• Based on clinical observations/laboratory tests
• Eliminate underlying pathology, restore
  hemostasis, maintain organ function

32
Objective 3Describe defects of autosomal
chromosomes

• Trisomy 21 (Downs Syndrome)
• Common cause is nondisjunction
• Phenotypes
• Mental retardation, broad flat face, short
  stature, short hands with a crease across the
  middle, large, wrinkled tongue.

33
Objective 4Describe defects of sex chromosomes

• Turners Syndrome
• Presence of a single X chromosome and no
  homologous X or Y chromosome. Total 45
• Phenotype
• Short stature, female genitalia, webbed neck,
  shieldlike chest, sterile.
• Incidence 15,000 births

34
Objective 4Describe defects of sex chromosomes

• Klinefelter Syndrome
• Combination of XXY
• Sex chromosome trisomic
• Phenotype
• Testicular atrophy, lanky build, mentally
  retarded, sterile, breast development, etc.

35
Objective 3Describe tumor development

• Metastasis
• The spread of tumor cells from a primary site of
  origin to a distant site
• Life threatening characteristic
• Sequential Steps of Metastasis
• Direct or continuous extension of local invasion
  of tumor cells into surrounding tissue
• Penetration into lymphatics, blood vessels, or
  body cavities
• Release into lymph or blood
• Transport to secondary sites
• Entry and growth in secondary sites

36
Objective 2Correlate pathophysiology and
clinical manifestations of altered water movement.

• Edema
• Accumulation of fluid within the interstitial
  spaces
• Localized Limited to site of trauma or localized
  within particular organ system
• Generalized Uniform distribution of fluid
• Increases the distance required for
  nutrients/waste products to move between
  capillaries and tissues.
• Third spacing or Fluid Overload

37
Objective 2Correlate pathophysiology and
clinical manifestations of altered water
movement.Edema
Figure 4-3 Page 109
38
Objective 2Correlate pathophysiology and
clinical manifestations of altered water
movement.Dehydration

• Dehydration
• Term used to describe a water deficit
• Can be used to describe both sodium and water
  loss
• Causes
• Increased renal clearance of free water as a
  result of impaired tubular function or inability
  to concentrate the urine
• Signs/Symptoms
• Thirst, dry skin and mucous membranes, elevated
  temperature, weight loss, concentrated urine,
  poor skin turgor, s/s hypovolemia (tachycardia,
  weak pulse, postural hypotension). Laboratory
  Elevated hematocrit (polycythemia),
  hypernatremia.
• Treatment Rehydrate

39
Objective 3 Describe relationship of sodium,
chloride, and water balance.

• Hypertonic Alterations
• Osmolality of ECF is above normal
• Causes
• Deficit of ECF water
• Causes ICF dehydration
• Increase in sodium (hypernatremia)
• Serum sodium levels exceed 147 mEq/L
• Causes hyperosmolality
• Caused by inappropriate administration of
  hypertonic saline solutions (sodium bicarbonate),
  oversecretion of aldosterone. Can be associated
  w/respiratory infections, fever, polyuria,
  profuse sweating, diarrhea, insufficient water
  intake.
• S/S thirst, fever, dry mucous membranes,
  restlessness. CNS muscle twitching and
  hyperreflexia, convulsions.

40
Objective 3 Describe relationship of sodium,
chloride, and water balance.

• Hypotonic Alterations
• Osmolality of ECF is less than normal
• Causes Sodium deficit (hyponatremia) or water
  excess leading to edema.
• Decrease in Sodium (Hyponatremia)
• Serum sodium concentrations falls below 135 mEq/L
• Cause movement of water into cells
• Causes Vomiting, diarrhea, GI suctioning, burns,
  diuretics, IV administration of free water (D5W)
• S/S Lethargy, confusion, apprehension, depressed
  reflexes, seizures, coma.
• Water Excess
• Compulsive water drinking, renal disease,
  congestive heart failure.
• SIADH (Syndrome of inappropriate secretion of
  ADH) Decreased renal excretion of water
• Fear, pain, acute infection, brain trauma,
  surgery, pharmacological interventions.

41
Potassium DeficiencyHypokalemia

• Serum potassium levels fall below 3.5 mEq/L.
• Causes
• Reduced intake (elderly individuals, alcoholics,
  anorexia nervosa), increased entry into cells
  (alkalosis), increased losses of body potassium
  (diarrhea, intestinal drainage tubes, laxative
  abuse).
• S/S Skeletal muscle weakness, cardiac
  dysrhythmias (delays ventricular repolarization),
  loss of smooth muscle tone (intestinal
  distension, anorexia, nausea, vomiting).

42
Potassium ExcessHyperkalemia

• Elevation of ECF above 5.5 mEq/L
• Caused by
• Increased intake, shift from cells to ECF
  (acidosis, insulin deficiency, cell hypoxia), or
  decreased renal excretion (renal failure).
• Signs/Symptoms
• Restlessness, intestinal cramping, diarrhea,
  muscle weakness, paralysis. Decreased cardiac
  conduction/more rapid repolarization of heart
  muscle, cardiac arrest.

43
Calcium DeficiencyHypocalcemia

• Deficits in calcium
• Inadequate intestinal absorption, deposition of
  ionized calcium into bone or soft tissue, blood
  transfusions, decreases in PTH (parathyroid
  hormone) and vitamin D.
• Signs/Symptoms
• Confusion, hyperreflexia, convulsions, tetany,
  w/continuous severe muscle spasms that can
  interfere with breathing and cause death.
  Prolonged ventricular depolarization and
  decreased cardiac contractility, intestinal
  cramping.

44
Calcium ExcessHypercalcemia

• Causes
• Hyperparathyroidism, cancers, vitamin D excess,
  tumors that produce PTH.
• Signs/Symptoms
• Fatigue, weakness, lethargy, anorexia, nausea,
  constipation. Kidney stones develop, ECG
  changes.

45
Phosphate DeficiencyHypophosphatemia

• Common Cause
• Intestinal malabsorption and increased renal
  excretion
• Signs/Symptoms
• Reduced capacity for oxygen transport by red
  blood cells
• Disturbed energy metabolism (ATP)
• Leukocyte/platelet dysfunctions-infection/blood
  clotting impairment, confusion, numbness, coma,
  convulsions.

46
Phosphate ExcessHyperphosphatemia

• Causes
• Cell destruction associated w/treatment of
  metastatic tumors with chemotherapy, long term
  use of phosphate-containing enemas or laxatives,
  hyperparathyroidism.
• High levels of phosphate lower calcium levels so
  watch for signs of hypocalcemia
• Signs/Symptoms
• Same as for hypocalcemia, soft tissue
  calcification in lungs, kidneys, joints

47
Objective 1Describe the normal regulations of
acid/base

• Carbonic Acid-Bicarbonate Buffering
• Operates in the lung and the kidney
• Major Extracellular Buffer
• Lungs
• Decreases the amount of carbonic acid by blowing
  off carbon dioxide and leaving water
• Kidneys
• Reabsorb bicarbonate or regenerate new
  bicarbonate from carbon dioxide and water

48
Blood Gas Components

• PaO2
• Partial pressure of oxygen (O2) dissolved in
  plasma
• 3-5 of total O2 content of arterial blood
• Reflect diffusion of O2 from alveoli into blood
• Normal 90-100 mmHg
• Abnormal lt60 mmHg Hypoxemia

49
Blood Gas ComponentsPractice PaO2

• 68
• 58
• 42
• 100
• 70

50
Blood Gas ComponentSaO2

• SaO2
• Degree to which hemoglobin molecules are
  saturated with O2
• Normal Greater than or equal to 95
• Abnormal Less than 90 Hypoxemia

51
Blood Gas ComponentsPractice SaO2

• 68
  60
• 58
  38
• 42
  50
• 100
  99
• 70
  75

52
Blood Gas ComponentsAcid/Base Imbalances

• pH
• Measure of H
• Normal 7.35-7.45
• Abnormal
• Less than 7.35 Acidemia/Acidosis
• Greater than 7.45 Alkalemia/Alkalosis
• DOES NOT TELL THE ORIGIN OF THE IMBALANCE

53
Objective 2Identify alterations in acid-base
balance

• Acidosis
• Systemic increase in H
• Alkalosis
• Systemic decrease in H
• Respiratory/Metabolic
• CO2 H2O H2CO2
  HCO3- H
• (Regulated by lung) (Regulated by
  kidney)

54
Blood Gas ComponentsPractice pH

• 7.38 68
  60
• 7.50 58
  38
• 7.20 42
  50
• 7.34 100
  99
• 7.60 70
  75

55
Respiratory ComponentPaCO2 (Ventilation)

• PaCO2
• Partial pressure of carbon dioxide (CO2)
  dissolved in plasma
• 5 percent of total CO2 content of arterial blood
• Measure of carbonic acid
• Direct reflection of alveolar ventilation
• Normal 35-45 mmHg
• Abnormal
• lt 35 mmHg Hyperventilation (Alkalosis)
• gt 45 mmHg Hypoventilation (Acidosis)

56
Objective 3Describe major categories of
acid/base imbalance and their clinical
manifestations

• Respiratory Acidosis
• Decrease in alveolar ventilation
  (hypoventilation) in relation to the metabolic
  production of carbon dioxide and an increase in
  carbonic acid.
• PaCO2 level gt 45 mm Hg
• Causes respiratory depression/muscle paralysis,
  pulmonary edema, pneumonia, asthma, anything
  causing decrease in ability to ventilate.
• Signs/Symptoms
• Breathlessness, restlessness, apprehension
  followed by lethargy disorientation, muscle
  twitching, tremors, convulsions,and coma.
• Treatment Increase alveolar ventilation/correct
  cause

57
Objective 3Describe major categories of
acid/base imbalance and their clinical
manifestations

• Respiratory Alkalosis
• Alveolar hyperventilation and excessive reduction
  in plasma carbon dioxide levels.
• PaCO2 levels lt35 mm Hg
• Signs/Symptoms
• Dizziness, confusion, tingling of extremities,
  convulsions, coma, cerebral vasoconstriction.
• Causes
• Hypoxemia, CHF, overdose, hysteria, cirrhosis,
  improper use of mechanical ventilation.
• Treatment Decrease alveolar ventilation/correct
  cause

58
Blood Gas ComponentsPractice PaCO2

• 7.38 68 40
  60
• 7.50 58 28
  38
• 7.20 42 80
  50
• 7.34 100 48
  99
• 7.60 70 22
  75

59
Metabolic ComponentHCO3-

• Bicarbonate (HCO3-)
• Measure of metabolic base
• Regulated by kidneys
• Normal 22-28 mEq/L
• Abnormal
• Less than 22 mEq/L metabolic acidosis
• Greater than 28 mEq/L metabolic alkalosis

60
Objective 3Describe major categories of
acid/base imbalance and their clinical
manifestations

• Metabolic Acidosis
• Noncarbonic acids increase or bicarbonate is lost
  from extracellular fluid
• Signs/Symptoms Changes in function of
  neurologic, respiratory, gastrointestinal, and
  cardiovascular systems. Headache, lethargy, coma,
  Kussmaul respirations, anorexia, nausea,
  vomiting, diarrhea, death.
• Treatment Correct cause if necessary administer
  bicarbonate

61
Objective 3Describe major categories of
acid/base imbalance and their clinical
manifestations

• Metabolic Alkalosis
• Loss of metabolic acids occurs, bicarbonate
  increases
• Causes loss of chloride (vomiting, GI suction)
  hyperaldosteronism, diuretics
• Signs/Symptoms
• Weakness, muscle cramps, hyperactive reflexes,
  tetany, depressed respirations, confusion,
  convulsions.
• Treatment
• Administer chloride/correct cause

62
Blood Gas ComponentsPractice HCO3-

• 7.38 68 24 0
  60
• 7.50 58 35 5
  38
• 7.20 42 18 -4
  50
• 7.34 100 21 -3
  99
• 7.60 70 32 4
  75

63
Objective 2Identify alterations in acid-base
balance

• Compensation occurs in levels
• Absent or Uncompensated
• Only primary problem exists
• pH abnormal
• Partial Compensation
• Primary and Secondary problem exists
• pH abnormal
• Complete Compensation
• Primary and secondary problems exist
• pH normal
• Correction
• Occurs when primary and secondary problems
  return to normal and pH is normal.

64
Complete Compensation

• Two factors
• 1. pH is normal
• 2. Primary and secondary problems exist
• (Metabolic/Respiratory abnormal)
• Compensated Respiratory Acidosis
• Compensated Metabolic Alkalosis
• Normal pH
• pCO2 ( ) Acidotic HCO3- ( ) Alkalotic

65
Complete Compensation

• Compensated Metabolic Acidosis
• Compensated Respiratory Alkalosis
• Normal pH
• PaCO2 ( ) Alkalosis
• HCO3- ( ) Acidosis
• Remember To determine which one came first, you
  need to know the patients history.

66
Blood Gas ComponentsComplete Compensation
Practice

• 7.40 68 52 30
  60
• 7.45 58 30 19
  38
• 7.37 42 80 34
  50
• 7.43 100 18 12
  99
• 7.35 70 40 24
  75

67
Partial CompensationAlkalosis

• Respiratory and Metabolic Alkalosis
• pH Alkalotic (not compensated fully)
• Respiratory
• PaCO2 ( ) Alkalosis
• HCO3- ( ) Acidosis
• Metabolic
• PaCO2 ( ) Acidosis
• HCO3- ( ) Alkalosis

68
Partial CompensationAcidosis

• Respiratory and Metabolic Acidosis
• pH is Acidotic (not fully compensated)
• Respiratory
• PaCO2 ( ) Acidosis
• HCO3- ( ) Alkalosis
• Metabolic
• PaCO2 ( ) Alkalosis
• HCO3- ( ) Acidosis

69
Blood Gas ComponentsPartial Compensation
Practice

• 7.30 68 30 20
  60
• 7.50 58 28 18
  38
• 7.20 42 80 31
  50
• 6.80 35 108 35
  30
• 7.60 70 70 32
  75

70
SummaryBlood Gas Interpretation

• 1. Oxygenation
• Look at PaO2 lt60 mmHg Hypoxemia
• Look at SaO2 lt90 Hypoxemia
• 2. pH (1) normal pt is normal or
• completely compensated (primary
  and secondary problems exist)
• (2) gt7.45 alkalosis
• (3) lt7.35 acidosis

71
SummaryBlood Gas Interpretation

• 3. Ventilation (Respiratory Component)
• PaCO2 lt 35 mmHgrespiratory alkalosis
• If pH is alkalotic, respiratory alkalosis is
  primary problem
• PaCO2 gt 45 mmHgrespiratory acidosis
• If pH is acidotic, respiratory acidosis is
  primary problem

72
SummaryBlood Gas Interpretation

• 4. Metabolic (kidneys)
• HCO3- lt 22 mEq/L metabolic acidosis
• If pH is acidotic, metabolic acidosis is primary
  problem
• HCO3- gt 28 mEq/L metabolic alkalosis
• If pH is alkalotic, metabolic alkalosis is
  primary problem

73
SummaryBlood Gas Interpretation

• 5. Look for compensation
• 1. No compensation pH abnormal, only primary
  problem exists
• 2. Partial compensation pH is abnormal and
  primary and secondary problems exist
• 3. Complete compensation pH is normal and both
  primary and secondary problems exist

74
Renal Blood Flow

• Kidneys receive
• 1000-1200 ml of blood per minute (20-25 of
  cardiac output)
• 55 is Plasma (600-700 ml/min) Renal Plasma Flow
  (RPF)
• 20 of RPF (120-140 ml/min) filtered and enters
  Bowmans capsule
• 80 of RPF (480-660 ml/min) continues to the
  efferent arteriole and into the peritubular
  capillaries
• Filtration of Plasma Glomerular
  Filtration
• Unit Time Rate or (GFR)

75
Objective 4Identify tests of renal function.

• Measuring Creatinine.
• Plasma/urine
• A natural substance produced by muscle and
  released into the blood at a relatively constant
  rate
• It is freely filtered in the glomerulus
• Amount filtered is approximately equal to the
  amount excreted
• Creatinine levels are equivalent to the GFR
• Disorders of kidney function prevent maximum
  excretion of creatinine

76
Objective 4Identify tests of renal function.

• Creatinine clearance and GFR
• Specific measurement of kidney function,
  primarily GFR
• Can be used to evaluate renal function in
  patients with wasting and to monitor the
  progression of renal disease
• 12-24 hour specimen collection (refrigerated)
• Decreased levels in impaired kidney function,
  renal disease, glomerulonephritis,
  pyelonephritis, nephrotic syndrome, acute tubular
  dysfunction, interstitial nephritis.

77
Objective 4Identify tests of renal function.

• Plasma Creatinine Concentration
• The amount filtered is approximately equal to the
  amount excreted so
• When GFR declines, plasma creatinine increases
  proportionally
• When GFR increases, plasma creatinine decreases
  proportionally
• Most useful for chronic renal disease because it
  takes 7-10 days for the plasma creatinine level
  to stabilize when GFR declines.

78
Objective 4Identify tests of renal function.

• Blood Urea Nitrogen (BUN)
• Normal range 10-20 mg/dl of blood
• Reflects glomerular filtration and urine
  concentrating capacity
• Urea is filtered in the glomerulus
• BUN levels increase as GFR drops
• Urea is reabsorbed by the blood through the
  permeable tubules
• BUN rises in states of dehydration and
  acute/chronic renal failure when passage of fluid
  through the tubules is slowed.

79
Objective 4Identify tests of renal function.

• Urinalysis (U/A)
• Color
• Turbidity
• Protein
• pH
• Specific Gravity
• Sediment
• Glucose
• Ketones
• Bilirubin
• Hemoglobin
• Leukocyte

80
Objective 4Identify renal terms

• Dysuria Painful urination
• Anuria Absence of urination
• Hematuria pink or red colored urine, blood in
  urine
• Oliguria decreased urine output
• Polyuria excessive excretion of urine
• Frequency urination in short intervals w/o
  increase in daily volume of UOP due to reduced
  bladder capacity or cystitis.
• Urgency the sudden, compelling desire to urinate
• Micturate urinate

81
Objective 4Identify tests of renal function

• Intake Output (I O)
• Blood Pressure

82
Objective 4Identify renal terms

• Dysuria Painful urination
• Anuria Absence of urination
• Hematuria pink or red colored urine, blood in
  urine
• Oliguria decreased urine output
• Polyuria excessive excretion of urine
• Frequency urination in short intervals w/o
  increase in daily volume of UOP due to reduced
  bladder capacity or cystitis.
• Urgency the sudden, compelling desire to urinate
• Micturate urinate

83
Objective 4Identify renal terms

• Renal Insufficiency
• Decline in renal function to about 25 of normal,
  levels of serum Creatinine/BUN are slightly
  elevated
• Renal Failure
• Significant loss of renal function.
• End Stage Renal Failure (ESRF)
• lt10 of renal function remains
• Uremia
• Syndrome of renal failure and includes elevated
  BUN/Creatinine levels w/fatigue, anorexia,
  nausea, vomiting, pruritus, neurologic changes.
• Azotemia
• Increased serum urea levels and often increased
  creatinine levels as well.
• Caused by renal failure or insufficiency

84
Objective 5Differentiate the various types of
renal failure Acute

• Acute
• Abrupt reduction in renal function
• Signs/Symptoms
• Oliguria OR normal OR polyuria, BUN/Creatinine
  are elevated
• Most types are reversible if diagnosed and
  treated early
• Causes
• Severe hypotension, vascular obstruction, severe
  glomerular disease, radiocontrast media
• Classifications
• Prerenal, Intrarenal, Postrenal

85
Objective 5Differentiate the various types of
renal failure Acute

• Prerenal
• Most common cause of ARF
• Caused by impaired renal blood flow
• GFR decreases because of decrease in filtration
  pressure
• Caused by
• Renal vasoconstriction, hypotension, hypovolemia,
  hemorrhage, or inadequate cardiac output
• Can Cause
• Acute tubular necrosis (ATN) or acute cortical
  necrosis.

86
Objective 5Differentiate the various types of
renal failure Acute

• Intrarenal
• Caused by ATN, cortical necrosis, acute
  glomerulonephritis, vascular disease (malignant
  hypertension, disseminated intravascular
  coagulation, renal vasculitis) or interstitial
  disease (drug allergy).

87
Objective 5Differentiate the various types of
renal failure Acute

• Postrenal
• Is a rare condition
• Occurs w/urinary tract obstruction that affects
  the kidneys bilaterally.
• Signs/symptoms
• Several hours of anuria w/flank pain followed by
  polyuria

88
Objective 5Differentiate the various types of
renal failure Acute

• Clinical Manifestations
• Three phases
• Oliguria, diuresis, recovery
• Return to normal may take 3-12 months
• 30 of patients do not have a full recovery
• Assessment
• K Mg , Na Ca , BUN,
  Creatinine
• Specific Gravity, UOP
• Edema present

89
Objective 5Differentiate the various types of
renal failure Acute

• Treatment
• Correct the cause, promote regeneration
  function, and prevent complications
• Prerenal fluid replacement/stimulation of output
• Intrarenal Hemodialysis. Save life until
  kidney function returns, correct fluid
  electrolyte problems, treat infections, maintain
  nutrition
• Postrenal Alleviate obstruction

90
Objective 5Differentiate the various types of
renal failure Chronic

• Chronic
• Progressive, irreversible loss of renal function
• Etiology
• Glomerulonephritis, diabetes, hypertension
• Signs/Symptoms
• Kidneys reduce in size, decrease GFR,
  hypertension, CHF, decrease in vitamin D
  absorption resulting in decrease in calcium
  which causes bone fractures, decrease in
  erythropoietin which causes anemia, CNS
  disturbances
• End Stage Renal Disease Uremic Syndrome
• Treatment Restrict fluids and sodium/potassium
  intake, give Epogen, dialysis, kidney transplant,
  treat congestive heart failure and hypertension.

91
Objective 6Identify the pathophysiology and
clinical manifestations of urinary tract
obstructionKidney Stones

• Kidney stones
• Masses of crystals, proteins, or other substances
  that cause obstruction
• Most common stone type is calcium oxalate or
  phosphate, struvite, and uric acid.
• Formation
• Supersaturation of one or more salts in the urine
• Precipitation of the salts from a liquid to a
  solid state
• Growth through crystallization

92
Objective 6Identify the pathophysiology and
clinical manifestations of urinary tract
obstructionKidney Stones

• Signs/Symptoms
• Renal colic-moderate to severe pain, urgency,
  frequency, incontinence.
• Evaluation
• History Physical, radiology examinations,
  urinalysis, ultrasound.
• Treatment Increase intake, dietary
  interventions, pain control, extracorporeal
  ultrasonic or laser lithotripsy (high frequency
  sound waves to fragment stones), surgery.

93
Objective 7Identify the pathophysiology and
clinical manifestations of urinary tract
infections.

• UTI
• An inflammation of the urinary epithelium in
  response to colonization with a pathogen (most
  common is bacterial w/E-coli accounting for 80
  of all uncomplicated infections.)
• Cystitis Inflammation of the bladder causing
  urinary frequency, dysuria, urgency, and/or lower
  abdominal, lower back, or suprapubic pain.
• Resistance to UTI
• Urinary pH, osmolarity, glucose content, urea,
  presence of glycoproteins.

94
Objective 7Identify the pathophysiology and
clinical manifestations of urinary tract
infections.

• Urethra has a periurethral mucus-secreting glands
  that surround the distal two-thirds of the
  urethra. Mucus traps bacteria.
• Length of urethra and secretions from the
  prostate and accessory periurethral glands
  protect against infection.

95
Objective 7Identify the pathophysiology and
clinical manifestations of urinary tract
infections.

• UTI (Cystitis)
• Evaluation
• History and physical examination includes queries
  about risk factors s/s such as pain, odor,
  hematuria, vital signs, temperature, U/A,
  culture.
• Treatment
• Antimicrobial therapy, pain medication.

96
Objective 7Identify the pathophysiology and
clinical manifestations of urinary tract
infections.

• Pyelonephritis
• An infection of the renal pelvis and
  interstitium.
• Causes include kidney stones, reflux, pregnancy,
  neurogenic bladder, instrumentation, female
  sexual trauma.
• Pathophysiology Can be spread by ascending
  microorganisms along the ureters or blood borne
  pathogens. Inflammation affecting the pelvis,
  calyces, medulla.
• Signs/Symptoms Fever, chills, flank or groin
  pain, frequency, dysuria.
• Evaluation Urine culture, U/A, clinical s/s,
  radiologic evaluation.
• Treatment Antibiotic therapy, pain management

97
Objective 8Describe glomerulonephritis
including etiology, pathophysiology, and clinical
manifestations.

• Glomerulonephritis
• Inflammation of the glomerulus
• Glomerular disease is the most common cause of
  chronic and end-stage renal failure.
• Etiology (Varied)
• Immunological causes (most common), drugs,
  toxins, vascular disorders, and systemic diseases
• Types
• Acute, rapidly progressive, chronic.

98
Objective 8Describe glomerulonephritis
including etiology, pathophysiology, and clinical
manifestations.

• Clinical Manifestations
• Urine
• Hematuria w/red blood cell casts
• Proteinuria exceeding 3-5 g/day (associated
  w/nephrotic syndrome)
• Decrease in UOP/decrease in GFR
• Evaluation
• Defined by progressive development of clinical
  manifestations and laboratory findings.
• Abnormal U/A w/ proteinuria, RBC's, WBCs, and
  casts. Microscopic evaluation from renal biopsy
  shows specific determination of renal injury and
  type of pathologic condition.
• Treatment
• Treating the primary disease, preventing or
  minimizing immune responses, symptomatic
  treatment for edema, hypertension, infections
  (antibiotics), corticosteroids (decrease
  inflammatory response).

99
Objective 9Describe nephrotic syndrome
including etiology, pathophysiology, and clinical
manifestations.

• Nephrotic Syndrome
• Excretion of 3.5 g or more of protein/day,
  hypoproteinemia, edema.
• Characteristic of glomerular injury
• Etiology
• Any condition causing increase in glomerular
  membrane permeability glomerulonephritis,
  diabetes, infectious process, toxins, drugs,
  malignancies.
• Pathophysiology
• Plasma proteins (albumin, immunoglobulins) cross
  the injured glomerular filtration membrane.
  Basement membrane of the glomerulus looses
  negative charge. Hypoalbuminemia ensues. Loss of
  albumin stimulates lipoprotein synthesis by the
  liver and hyperlipidemia.

100
Objective 9Describe nephrotic syndrome
including etiology, pathophysiology, and clinical
manifestations.

• Signs/Symptoms
• Proteinuria, edema, hyperlipidemia, lipiduria,
  loss of vitamin D leading to hypocalcemia.
• Evaluation
• Protein level in urine is gt 3.5 g. Serum albumin
  decreases, and cholesterol, phospholipids, and
  triglycerides increase. Pathologic condition is
  identified by biopsy.
• Treatment
• Diet (normal protein, low fat, salt restriction),
  treat cause if known, diuretics, steroids,
  albumin IV. Monitor closely for hypovolemia,
  hypokalemia or hyperkalemia secondary to renal
  insufficiency.

101
SIADH

• Syndrome of inappropriate ADH secretion (SIADH)
• Posterior pituitary disorder-rare
• High levels of ADH without normal stimuli
• Associated with cancers
• Post pituitary surgery
• Psychiatric disease and various drugs

102
SIADH

• Pathophysiology
• Enhanced renal water retention
• Increases in total body water
• Hyponatremia, hypoosmolarity, and urine that is
  inappropriately concentrated
• Clinical Manifestations
• Serum hypoosmolality and hyponatremia
• Urine hyperosmolarity
• Urine sodium excretion that matches sodium intake
• Normal adrenal and thyroid function
• Absence of conditions that can alter volume
  status

103
SIADH

• Sodium levels decrease from 140 to 130 mEq/L
• Thirst, impaired taste, anorexia, dyspnea on
  exertion, fatigue and dulled sensorium
• Sodium levels decrease from 130 to 120 mEq/L
• Severe gastrointestinal symptoms (nausea,
  vomiting, and abdominal cramps
• Serum sodium levels below 115 mEq/L
• Confusion, lethargy, muscle twitching, and
  convulsions
• Peripheral edema
• Treatment
• Correction of hyponatremia

104
Diabetes Insipidus

• Related to an insufficiency of ADH
• Types
• 1. neurogenic or central form
• Caused by absence of ADH
• 2. nephrogenic form
• Caused by inadequate response of renal tubules to
  ADH
• 3. psychogenic form
• Caused by extremely large volumes of fluid intake

105
Diabetes Insipidus

• Pathophysiology
• Alteration in ability to concentrate urine
  related to chronic polyuria with washout of
  medullary concentration gradient
• Insufficient ADH secretion causes immediate
  excretion of large volumes of dilute urine
• Nephrogenic diabetes insipidus
• ADH levels are normal or high but the collecting
  ducts do not increase their permeability to water
• Diabetes insipidus usually has an acute onset

106
Diabetes Insipidus

• Clinical Manifestations
• Polyuria, nocturia, continuous thirst,
  polydipsia, low urine specific gravity, low urine
  osmolality and high-normal plasma osmolality
• May develop large bladder capacity and
  hydronephrosis
• Evaluation and Treatment
• Water deprivation testing
• ADH replacement, oral hydration

107
Hypopituitarism

• Pathophysiology
• Absence of selective pituitary hormones causing
  dysfunction or complete failure
• Infarction
• Pituitary gland is extremely vascular, even more
  so in pregnancy
• After tissue necrosis, edema occurs
• Intravascular coagulation from excessive fibrin
• Sheehan syndrome

108
Hypopituitarism

• Clinical manifestations
• Panhypopituitarism
• All hormones are absent
• May affect growth in children (dwarfism),
  postpartum women cannot lactate
• ACTH deficiency leading to cortisol insufficiency
• Nausea, vomiting, anorexia, fatigue, and weakness
• Hypoglycemia (increased insulin sensitivity),
  decreased gluconeogenesis (hypocortisolsim)
• Limits aldosterone secretion

109
Hypopituitarism

• Thyroid-stimulating hormone (TSH) deficiency
• Cold intolerance, skin dryness, mild myxedema,
  lethargy, decreased metabolic rate
• Follicle-stimulating hormone (FSH) and
  luteinizing hormone (LH) deficiencies in women
• Amenorrhea, atrophic vagina, uterus, and breasts
• In men decreased body hair, diminished libido

110
Hypopituitarism

• Evaluation and treatment
• Diagnostic tests and individuals signs and
  symptoms
• Correct underlying disorder
• Thyroid and cortisol replacement therapy
• Sex steroid replacement therapy

111
Hyperpituitarismprimary adenoma

• Pathophysiology
• Pituitary ademonas usually benign, slow-growing
  tumors, cause unknown
• Expansion of the adenoma may impinge on the
  nerves, optic chiasma
• Secretes hormone of cell type from which it
  arose, without regard to feedback systems

112
Hyperpituitarismprimary adenoma

• Clinical Manifestations
• Related to tumor size and hormone secretion
• Headache, fatigue, neck pain or stiffness,
  seizures
• Visual changes , temporary blindness
• Hyposecretion of pituitary hormones may result
• Evaluation and Treatment
• Diagnosis involves physical and lab values
• Goal of treatment to control hormone secretion,
  surgery, and radiation therapy

113
Graves Disease

• The result of stimulation of the thyroid with
  antibodies against the TSH receptor
• Antibodies stimulate thyroid cells to produce
  high concentrations of TH
• Symptoms
• Diffuse thyroid enlargement (goiter),
  tachycardia, palpitations, nervousness,
  depression, tremor, lid lag, increase systolic
  blood pressure, ocular changes

114
Hypothyroidism

• Deficient production of TH
• Primary congenital defects or loss of thyroid
  tissue after treatment of hyperthyroidism,
  defective hormone synthesis
• Secondary pituitary or hypothalamic failure

115
Hypothyroidism

• Clinical Manifestations
• Lowers energy metabolism and heat production (low
  basal metabolic rate, cold intolerance, lethargy,
  tiredness and lowered body temperature, goiter,
  elevated TSH
• Characteristic sign of long-standing or severe
  hypothyoidism is myxedema (nonpitting, boggy
  edema thick, slurred speech and hoarseness
• Page 483-484 Table 18-2

116
Hypothyroidism

• Evaluation and Treatment
• Decreased levels of T3 and T4, increased TSH
• Hormone replacement therapy is treatment of choice

117
Primary Hypothyroidism

• Acute thyroiditis
• Bacterial infection
• Subacute thyroiditis
• Nonbacterial inflammation of thyroid gland
• Painless thyroiditis
• Course similar to subacute thyroiditis
• Postpartum thyroiditis
• 95 spontaneously recover
• Autoimmune thyroiditis
• Hashimoto disease, chronic lymphocytic
  thyroiditis
• Destruction of thyroid tissue by thyroid
  antibodies and infiltration of lymphocytes

118
Congential Hypothyroidism

• Thyroid tissue is absent or born with hereditary
  defects in TH synthesis
• TH is essential for embryonic growth
• Mental retardation
• symptoms
• High birth weight, hypothermia, delay in passing
  meconium, and neonatal jaundice
• Treatment
• Administration of thyroxine
• Skeletal growth stunted if not detected at birth,
  dwarfism, cretinism

119
Hyperthyroidism

• A form of thyrotoxicosis
• Excess amounts of thyroid hormone
• Causes
• Graves disease, toxic multi nodular goiter,
  thyroid cancer and increased TSH secretion
• Clinical Manifestations
• Metabolic rate increases (menstrual changes,
  weight loss w/increased appetite, excessive
  sweating and flushing, tachycardia, loud heart
  sounds, restlessness, fatigue, insomnia), heat
  intolerance, increased tissue sensitivity to
  sympathetic stimulation, goiter is usually
  present
• Page 481 Table 18-1

120
Hyperthyroidism

• Evaluation and Treatment
• Elevated T4 and T3, decreased TS
• Control excessive TH production, secretion, or
  action (drug therapy, radioactive iodine therapy,
  surgery)

121
Alterations of Adrenal Function

• Cushings syndrome hypercortisolism caused by
  hyperfunction of adrenal cortex
• Cushings disease refers to pituitary dependent
  hypercortisolism (pituitary adenoma), increased
  ACTH secretion
• Clinical Manifestations
• Weight gain, trunk, face, and buffalo hump,
  glucose intolerance, polyuria, scalp hair
  thinning, easy bruising, hyperpigmentation,
  elevated blood pressure, suppression of the
  immune system with increased risk of infection

122
Cushings

• Evaluation and Treatment
• Treatment is specific for cause
• Need to determine if hypercortisolism is from
  pituitary, adrenal or ectopic cause
• Includes medication, radiation, and surgery

123
Addison Disease

• Caused by autoimmune mechanisms that destroy
  adrenal cortical cells
• Occurs in adults 30-60 year olds, women
• Characterized by elevated serum ACTH levels with
  inadequate corticosteroid and mineralocorticoid
  synthesis
• Clinical Manifestations
• Weakness, fatigue, anorexia, nausea, vomiting,
  hypoglycemia, mental confusion,
  hyperpigmentation, vitiligo Page 501 Table 18-9

124
Addison Disease

• Evaluation and Treatment
• Treatment involves glucocorticoid and possibly
  mineralocorticoid replacement therapy, combined
  with dietary modifications
• Lifetime daily glucocorticoid replacement,
  increasing dose with acute stressors.
• Diet should include 150 mEq sodium/day
• Correct all underlying disorders

125
Hyperparathyroidism

• Usually the result of an adenoma producing excess
  amounts of parathyroid hormone
• Hypercalcemia (bone resorption), metabolic
  acidosis, formation of calcium stones in the
  kidney
• Diagnosed by exclusion, at least a 6-month
  history of symptoms associated with hypercalcemia
• Treat by lowering calcium levels, diuretics (to
  excrete excess calcium), surgical removal

126
Hypoparathyroidism

• Low PTH levels, most common cause is damage to
  parathyroid glands during thyroid surgery
• Impaired resorption of calcium from bones
• Hyperphosphatemia, hypomagnesemia
• Symptoms of hypocalcemia (dry skin, loss of body
  and scalp hair, horizontal ridges on nails,
  muscle spasms, hyperreflexia
• Treatment with vitamin D an