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GROUP ACTIVITY POWERPOINT  PRESENTATION Abella, Fernie Acielo, Kharen Grace Celoso, Rickel Dasas, Gerald Cris Otayde, Ruffa Tolentino, Santa Rina
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The Nephron ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Death Alkalosis Normal Acidosis Death
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
METABOLIC ACIDOSIS ↓ ↓ Anorexia Nausea and vomiting Abdominal pain Weakness Fatigue General malaise Decreasing level of consciousness Dysrhythmias Bradycardia Warm, flushed face  Hyperventilation acid  production. acid excretion bicarbonate loss chloride pH  HCO 3 PaCO 2 Rate and depth of respirations increase, eliminating additional CO 2 (bicarbonate deficit)- is characterized by low ph (<7.35) and low bicarbonate (<22 mEq/L). It may be caused by excess acid or loss of bicarbonate from the body.. Manifestation Causes ABG Compensatory  Mechanism Definition
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Nursing Management: Nursing Outcomes Nursing Intervention Nursing Management ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
METABOLIC ALKALOSIS Confusion Decreasing level of consciousness Hyperreflexia Tetany Dsyrhythias Hypotension Seizures Respiratory failure bicarbonate excess pH  HCO 3 PaCO 2 Rate and depth of respirations decrease, retaining CO 2 Metabolic alkalosis (bicarbonate excess) is characterized by high ph(>7.45) and high bicarbonate (>26mEq/L).It may be caused by loss of acid or excess bicarbonate in the body. Manifestation Causes ABG Compensatory  Mechanism Definition
Diagnostic Tests: ABG  – pH > 7.45 and bicarbonate > 26 mEq/L; PaCO2 is  >45  mmHg Serum electrolytes  - ↓ potassium-serum (< 3.5 mEq/L)  and  decreased  chloride (< 95 mEq/L). Serum  bicarbonate level is high. Urine pH  -  low (pH 1 to 3) if metabolic acidosis is caused  by  hypokalemia ECG pattern  – show changes similar to hypokalemia. Medical management: Prescribing K ( potassium  salt ) if hypokalemia is present or NaCl solutions to correct volume depletion when extracellular fluid volume has decrease rapidly.
Nursing Management ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Nursing Outcomes Nursing Interventions Nursing Diagnosis
RESPIRATORY ACIDOSIS ACUTE Headache Warm, flushed skin Blurred vision Irritability , altered mental status Decreasing LOC Cardiac arrest. CHRONIC Weakness Dull headache Sleep disturbance with daytime sleepiness Impaired memory Personality changes Retained CO 2  and excess carbonic acid. ↓  pH  HCO 3 PaCO 2 Kidneys conserved bicarbonate to restore carbonic acid: bicarbonate ratio of 1:20 characterized by a pH of < 7.35 and a PaCO2 greater that 45 mmHg. It may be  acute  or  chronic . In chronic respiratory acidosis, the bicarbonate is higher than 26 mEq/L as the kidneys compensate by retaining bicarbonate. Manifestation Causes ABG Compensatory  Mechanism Definition
DIAGNOSTIC EXAM ABG’s show pH less than7.35 and Paco2 of more than mmHg Serum electrolytes may show hypochloremia (chloride level < 98mEq/L) in chronic respiratory acidosis. Pulmonary Function Test may be done to determine if chronic lung diseases is the cause of the respiratory acidosis. MEDICATION: Bronchodilator drugs Antibiotics prescribed to treat respiratory infections IV sodium bicarbonate
Nursing Management: ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Nursing Outcomes Nursing Interventions Nursing Diagnosis
RESPIRATORY ALKALOSIS Dizziness Numbness and tingling around mouth , of hands and feet Palpitations Dyspnea Chest tightness Anxiety/panic Tremors, tetany seizures,  loss of consciousness Loss of CO2 and deficient carbonic acid. pH  ↓  HCO 3 ↓  PaCO 2 Kidneys excrete bicarbonate and conserve Hydrogen ions to restore carbonic acid: bicarbonate ratio Respiratory alkalosis is characterized by a pH greater than 7.45 and Paco2 of less than 35 mmHg. It is always caused by hyperventilation leading to a carbon dioxide deficit. Manifestation Causes ABG Compensatory  Mechanism Definition
DIAGNOSTIC EXAMS ABG’s generally show a pH greater than 7.45 and Paco2 less than 35 mmHg. In chronic hyperventilation, there is a compensatory decrease in serum bicarbonate to less than 22 mEq/ L and the pH may be near normal. MEDICATIONS: sedative or anxiety
Nursing Management: ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Nursing Outcome Nursing Intervention Nursing Diagnosis
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Infection calculi Infection calculi Tubular damage HYDRONEPHROSIS
Assessment: ,[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Increased  aldosterone  secretion Decreased Renal function Salt and water retention Decreased renal function Edema NEPHROTIC SYNDROME Reduced intravascular oncotic pressure Loss of fluid into the interstitial space Reduced plasma volume
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Nursing Diagnosis ,[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Urinary Tract Infection ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infection gain access to bladder SCHEMATIC DIAGRAM Colonized epithelium Evade host defense mechanism Inflammation  Organisms ascends to urethra and bladder ADHERE MUCOSAL SURFACES
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Antigen( group A beta hemolytic streptococcus  Antigen-antibody product Deposition of the  antigens-antibody complex in glomerulus Increased production of epithelial cells lining the glomerulus Leukocyte infiltration of the glomerulus Thickening of the glomerular filtration membrane Scarring and loss of glomerular filtration membrane Decreased glomerular filtrations PATHOPHYSIOLOGY
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Slow, progressive destruction of the glomerolus Cortex layer shrinks to 1-2 mm in thickness Bands of scar tissue distort the remaining cortex Surface of the kidney becomes rough & irregular shape Scarring at the glomeruli & tubules Thickenned branches of the renal artery Severe glomerular change End stage renal disease PATHOPHYSIOLOGY GLOMERULONEPHRITIS CHRONIC
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]

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Group 1 Robb

  • 1. GROUP ACTIVITY POWERPOINT PRESENTATION Abella, Fernie Acielo, Kharen Grace Celoso, Rickel Dasas, Gerald Cris Otayde, Ruffa Tolentino, Santa Rina
  • 2.
  • 3.  
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12. METABOLIC ACIDOSIS ↓ ↓ Anorexia Nausea and vomiting Abdominal pain Weakness Fatigue General malaise Decreasing level of consciousness Dysrhythmias Bradycardia Warm, flushed face Hyperventilation acid production. acid excretion bicarbonate loss chloride pH HCO 3 PaCO 2 Rate and depth of respirations increase, eliminating additional CO 2 (bicarbonate deficit)- is characterized by low ph (<7.35) and low bicarbonate (<22 mEq/L). It may be caused by excess acid or loss of bicarbonate from the body.. Manifestation Causes ABG Compensatory Mechanism Definition
  • 13.
  • 14.
  • 15. METABOLIC ALKALOSIS Confusion Decreasing level of consciousness Hyperreflexia Tetany Dsyrhythias Hypotension Seizures Respiratory failure bicarbonate excess pH HCO 3 PaCO 2 Rate and depth of respirations decrease, retaining CO 2 Metabolic alkalosis (bicarbonate excess) is characterized by high ph(>7.45) and high bicarbonate (>26mEq/L).It may be caused by loss of acid or excess bicarbonate in the body. Manifestation Causes ABG Compensatory Mechanism Definition
  • 16. Diagnostic Tests: ABG – pH > 7.45 and bicarbonate > 26 mEq/L; PaCO2 is >45 mmHg Serum electrolytes - ↓ potassium-serum (< 3.5 mEq/L) and decreased chloride (< 95 mEq/L). Serum bicarbonate level is high. Urine pH - low (pH 1 to 3) if metabolic acidosis is caused by hypokalemia ECG pattern – show changes similar to hypokalemia. Medical management: Prescribing K ( potassium salt ) if hypokalemia is present or NaCl solutions to correct volume depletion when extracellular fluid volume has decrease rapidly.
  • 17.
  • 18. RESPIRATORY ACIDOSIS ACUTE Headache Warm, flushed skin Blurred vision Irritability , altered mental status Decreasing LOC Cardiac arrest. CHRONIC Weakness Dull headache Sleep disturbance with daytime sleepiness Impaired memory Personality changes Retained CO 2 and excess carbonic acid. ↓ pH HCO 3 PaCO 2 Kidneys conserved bicarbonate to restore carbonic acid: bicarbonate ratio of 1:20 characterized by a pH of < 7.35 and a PaCO2 greater that 45 mmHg. It may be acute or chronic . In chronic respiratory acidosis, the bicarbonate is higher than 26 mEq/L as the kidneys compensate by retaining bicarbonate. Manifestation Causes ABG Compensatory Mechanism Definition
  • 19. DIAGNOSTIC EXAM ABG’s show pH less than7.35 and Paco2 of more than mmHg Serum electrolytes may show hypochloremia (chloride level < 98mEq/L) in chronic respiratory acidosis. Pulmonary Function Test may be done to determine if chronic lung diseases is the cause of the respiratory acidosis. MEDICATION: Bronchodilator drugs Antibiotics prescribed to treat respiratory infections IV sodium bicarbonate
  • 20.
  • 21. RESPIRATORY ALKALOSIS Dizziness Numbness and tingling around mouth , of hands and feet Palpitations Dyspnea Chest tightness Anxiety/panic Tremors, tetany seizures, loss of consciousness Loss of CO2 and deficient carbonic acid. pH ↓ HCO 3 ↓ PaCO 2 Kidneys excrete bicarbonate and conserve Hydrogen ions to restore carbonic acid: bicarbonate ratio Respiratory alkalosis is characterized by a pH greater than 7.45 and Paco2 of less than 35 mmHg. It is always caused by hyperventilation leading to a carbon dioxide deficit. Manifestation Causes ABG Compensatory Mechanism Definition
  • 22. DIAGNOSTIC EXAMS ABG’s generally show a pH greater than 7.45 and Paco2 less than 35 mmHg. In chronic hyperventilation, there is a compensatory decrease in serum bicarbonate to less than 22 mEq/ L and the pH may be near normal. MEDICATIONS: sedative or anxiety
  • 23.
  • 24.
  • 25.
  • 26.
  • 27.
  • 28.
  • 29. Increased aldosterone secretion Decreased Renal function Salt and water retention Decreased renal function Edema NEPHROTIC SYNDROME Reduced intravascular oncotic pressure Loss of fluid into the interstitial space Reduced plasma volume
  • 30.
  • 31.
  • 32.
  • 33.
  • 34.
  • 35.
  • 36.
  • 37. Infection gain access to bladder SCHEMATIC DIAGRAM Colonized epithelium Evade host defense mechanism Inflammation Organisms ascends to urethra and bladder ADHERE MUCOSAL SURFACES
  • 38.
  • 39.
  • 40.
  • 41.
  • 42. Antigen( group A beta hemolytic streptococcus Antigen-antibody product Deposition of the antigens-antibody complex in glomerulus Increased production of epithelial cells lining the glomerulus Leukocyte infiltration of the glomerulus Thickening of the glomerular filtration membrane Scarring and loss of glomerular filtration membrane Decreased glomerular filtrations PATHOPHYSIOLOGY
  • 43.
  • 44.
  • 45.
  • 46.
  • 47.
  • 48.
  • 49.
  • 50. Slow, progressive destruction of the glomerolus Cortex layer shrinks to 1-2 mm in thickness Bands of scar tissue distort the remaining cortex Surface of the kidney becomes rough & irregular shape Scarring at the glomeruli & tubules Thickenned branches of the renal artery Severe glomerular change End stage renal disease PATHOPHYSIOLOGY GLOMERULONEPHRITIS CHRONIC
  • 51.
  • 52.
  • 53.
  • 54.
  • 55.

Editor's Notes

  1. Ntibody ci