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Renal Diseases

Renal Diseases. AH 120. The Nephron: The Functional Unit of the Kidney. Hypertension Systolic BP > 140 mmhg and/or Diastolic BP > 90 mmhg. Mechanism is similar to what happens in CHF Decreased pressure sensed by JG cells activates the renin-angiotensin-aldosterone mechanism

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Renal Diseases

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  1. Renal Diseases AH 120

  2. The Nephron: The Functional Unit of the Kidney

  3. HypertensionSystolic BP > 140 mmhg and/or Diastolic BP > 90 mmhg • Mechanism is similar to what happens in CHF • Decreased pressure sensed by JG cells activates the renin-angiotensin-aldosterone mechanism • Atherosclerosis is the probable cause of the J-G cells not sensing proper pressure in renal blood flow • Treated by diet, exercise, and drugs • “ACE” inhibitors, Calcium channel blockers, Beta blockers, diuretics

  4. Pyelonephritis: Inflammation of the renal pelvis and interstitial tissue of the kidney

  5. Etiology Bacterial infection that often spreads retrograde from the bladder (cystitis) Common agents: E-Coli, Strep, and Staph

  6. Pathology • Intense inflammation causes abscesses to from in renal pelvis and interstitial tissue • If severe enough, the kidneys may fail • Can be acute or chronic • Fibrosis will be present if chronic Acute Chronic

  7. Signs & Symptoms • Fever • Flank Pain • U.A. shows pyuria and bacteriuria • Urinary signs: frequency, urgency, and burning

  8. Treatment • Antibiotics • If severe enough to cause renal failure, then renal dialysis is indicated

  9. Glomerulonephritis Inflammation of the glomerulus caused by a reaction to immune complexes and complement It can be acute or chronic

  10. Etiology Usually caused by a strep infection Strep throat Strep skin lesion

  11. Pathology • Immune complexes and compliment damage glomerular membrane and cause it to become more permeable • WBCs, RBCs , and plasma proteins pass into Bowman’s capsule

  12. Signs & Symptoms • Initial strep infection • Urinary signs: • Hematuria, proteinuria, dark urine, & decreased output • Facial and ankle edema • Due to hypoproteinemia and sodium and fluid retention • Hypertension • Possible renal failure

  13. Treatment • Supportive treatment if acute • If chronic, patient may eventually need dialysis and/or transplant

  14. Renal Failure Failure of the kidney to adequately remove waste products and maintain fluid and electrolytes. It can be an acute or chronic process

  15. Etiology • Damage due to disease processes, e.g., pyelonephritis , glomerulonephritis, etc • Reduced renal blood flow (shock) • Burns, trauma, dehydration • Toxins • CCL4, Hg, ethylene glycol

  16. Signs & Symptoms • Lab Findings: • Decreased urine output • Increased BUN, uric acid, creatinine, and ammonia • Decreased pH • Abnormal electrolyte levels • Anemia (if chronic) due to decreased erythropoietin

  17. Treatment Hemodialysis (for acute or chronic failure)

  18. Treatment (cont.) Transplant

  19. Pulmonary Diseases May involve the airways and/or the alveoli

  20. Pulmonary Disease Is Classified By the Effect on Pulmonary Function

  21. Restrictive Pulmonary Disease • Decreased volumes during PFT • Lesion is in the alveolar portion of the lung or the chest wall • Primarily occurs during inspiration

  22. Obstructive Pulmonary Disease • Decreased flow rates during PFT • Lesion is usually in the airways • Primarily occurs during exhalation

  23. Obstructive Diseases Caused By Airway Inflammation

  24. Airway Inflammation Causes Obstruction because of the following three things: • Mucosal edema • Bronchospasm • Increased production of thick mucus • These three things encroach on the airway lumen making it harder for air to flow through the airways • Harder to get oxygen in and harder to get carbon dioxide out

  25. Airway Inflammation Treatment • Re-establish airway patency • Drugs to reduce mucosal edema and bronchospasm • Oral or systemic hydration to keep viscosity of mucus normal • Oxygen PRN • Mechanical ventilation PRN

  26. Examples of Airway Inflammatory Diseases

  27. The Common Cold Usually viral in origin

  28. Croup and Epiglottitis Croup • Usually affects very young and is a result of a viral infection • Involves larynx, trachea, and both main stem bronchi and develops rapidly Epiglottitis • Affects mostly older children and is caused by H.Flu

  29. Acute Bronchitis(Chest Cold) • Inflammation in the trachea, main stem and segmental bronchi • Usually a complication of a viral infection

  30. Asthma Transient inflammation of the airways

  31. ETIOLOGY(“Triggers”) • Allergy • Infection • Stress/emotion • Noxious fumes • Cold air • Exercise

  32. Pathology • “Trigger” mechanism causes mast cells on airways to degranulate and release histamine • Mast cells often degranulate if IgE antibody and antigen (allergen) attach to it or if parasympathetic stimulation exceeds sympathetic stimulation • Histamine causes inflammatory reaction in airways • Mucosal edema, bronchospasm, increased production of thick mucus

  33. Signs and Symptoms During attack: Respiratory distress • Dyspnea • Tachypnea • Wheezing • Cough (may or may not be productive) • Cyanosis in severe attack In between attacks, patients are relatively symptom free!

  34. Treatment(During Attack) Inhaled drugs that stimulate the sympathetic nervous system • Relieves bronchospasm • May also be given systemically • Albuterol (Proventil) and other similar drugs If hospitalization required: • Oxygen therapy; possibly mechanical ventilation • Systemic steroids (for anti-inflammatory effect)

  35. Prevention • Avoidance of triggers • Inhaled steroids • Budesonide, fluticasone • NSAIDS • Cromolyn sodium, nedocromil sodium, • Zafirlukast, montelukast • Immuno-therapy

  36. Chronic Bronchitis Productive cough for at least three months of the year during a two year period

  37. Etiology Chronic Irritation • Cigarette smoking • Pollution • Noxious fumes • Chronic/recurrent infection

  38. Pathology • Metaplastic change: ciliated, columnar epithelium becomes squamous and non-ciliated • Hyperplasia/hypertrophy of goblet cells • Weakened, fibrotic airways that collapse easily

  39. Emphysema Hyperinflation of alveoli with destruction of alveolar septa, pulmonary capillary bed, and elastic tissue in alveolar wall

  40. Etiology • Cigarette smoking • Alpha-1 anti-trypsin deficiency • Usually a genetic defect

  41. Pathology • Proteolytic enzymes are activated in the lung due to either substance found in cigarette smoke or due to lack of alpha-1 anti-trypsin • Proteolytic enzymes cause: • Destruction of alveolar septa • Destruction of pulmonary capillary bed • Destruction of elastic tissue in alveolar walls

  42. Result is many alveoli coalesce to form large, hyperinflated alveoli that inflate easily but do not return to their normal volume during exhalation. Because of destruction of the pulmonary capillary bed, there is less surface area for gas exchange.

  43. Normal Emphysema

  44. Chest X-Ray “Barrel” chest Increased retro-sternal airspace

  45. COPD: Chronic Obstructive Pulmonary DiseaseA mixture of emphysema and chronic bronchitis

  46. Emphysema Dominant: Pink Puffer • Works hard enough to maintain acceptable levels of O2 and CO2 • Good color • Appears S.O.B most of time • Minimal sputum • Emaciated appearance • Heart failure occurs late

  47. Chronic Bronchitis Dominant: Blue Bloater • Does not work as hard so has poor color and does not appear to be as S.O.B. as the pink puffer • Lots of sputum production • Minimal weight loss • Heart failure occurs early

  48. COPDComplication: Cor Pulmonale Heart failure due to lung disease

  49. Due to hyperinflated alveoli compressing pulmonary capillaries and there not being as many capillaries, pulmonary hypertension develops • This increases the work on the right heart which eventually hypertrophies and then starts to fail

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