Post on 07-Apr-2018
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V. Renal Disorders
A. INFLAMMATORY DISORDERS
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LETS HAVE AREVIEW
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A. INFLAMMATORY DISORDERS
GLOMERULUS----Tuft of capillaries, capillary network in thekidneys; filters the blood that would pass the kidney
BOWMANS CAPSULE--- cuplike structure that covers
the glomerulus;
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Whats our firstdisease?
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis Inflammation of the glomerular capillaries
Complication of streptococcal infection e.g. URTI, middleear infections, strep throat
Occurs 2-3 weeks after the antecedent infection
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
CA- Group A beta hemolytic streptococcus
Caused by trapping of antibodies and antigen complexes in
the kidneys
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1. Post Streptococcal glomerulonephritis
What should I expect
from a person withAGN?
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
1. Edema, generalized-a.k.a anasarca
- As the colloid osmotic pressure of blood drops and sodium is retained
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
2. proteinuria
- Due to increased glomerular permeability
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
3. Cola-colored urine, coffee -colored
- Due to hematuria; protein ad RBC leaked into it
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
4. s/s of anemia
-decreased production of erythropoietin
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
5. Increase in BUN and creatinine level
-
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
6. Flank pain / back pain
-Due to the swelling of kidney tissues thus stretching the capsule
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
7. Hypertension
-due to the increase in renin secretion and decrease in GFR, due to water andsodium retention-----triggered by the decrease in blood flow leading to renin secretion thus HPN
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
8. Urine output decreases
-GFR declines, water and sodiumretention
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1. Post Streptococcal glomerulonephritis
a. Acute Glomerulonephritis
9. Azotemia
-concentration of urea and other nitrogenous wastes in the blood
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a. Acute Glomerulonephritis
What should I do to a
patient with AGN?
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management
a. Acute Glomerulonephritis
1. penicillin
Drug of Choice for strep infection
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management
a. Acute Glomerulonephritis
2. Corticosteroids
To decrease production of antibodies and antigen complexes
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management
a. Acute Glomerulonephritis
3. Glucocorticoids
To reduce inflammation
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management
a. Acute Glomerulonephritis
4. Anti-hypertensive
Reduce blood pressure
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management
a. Acute Glomerulonephritis
5. Sodium restriction, CHON and fluid intake is reduced
Carbs are given to reduce catabolism of protein
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management
a. Acute Glomerulonephritis
6. Monitor intake and output
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a. Acute Glomerulonephritis
We are done with AGN.Lets proceed to the
Chronic form!!!
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1. Post Streptococcal glomerulonephritis
a. Chronic Glomerulonephritis
Due to repeated episodes of acute glomerulonephritis,
hypertensive nephrosclerosis (hardening of renal
arteries), hyperlipidemia
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1. Post Streptococcal glomerulonephritis
a. Chronic Glomerulonephritis
Kidneys are reduced to as little as one fifth their normal size
Cortex layer shrinks to 1-2 mm in thickness or less
Glomeruli and their tubules become sccarred and the branches of
the renal artery are thickened- severe glumerular damage -ESRD
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management
a. Acute Glomerulonephritis
5. Sodium restriction, CHON and fluid intake is reduced
Carbs are given to reduce catabolism of protein
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1. Post Streptococcal glomerulonephritis
What should I expect from aperson with CGN?
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Assessment findings
a. Chronic Glomerulonephritis
1. hyperkalemia
Due to decrease potassium excretion, acidosis, catabolism and excessivepotassium intake from foods and medications
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Assessment findings
a. Chronic Glomerulonephritis
2. anemiaSecondary to decreased erythropoiesis a.k.a
Production of RBC
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Assessment findings
a. Chronic Glomerulonephritis
2. anemiaSecondary to decreased erythropoiesis a.k.a
Production of RBC
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Assessment findings
a. Chronic Glomerulonephritis
3. Hypoalbuminemia with edema-
to protein loss through damaged glomerular membrane
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Assessment findings
a. Chronic Glomerulonephritis
4. Increase serum phosphorous
Due to decrease renal excretion of phosphorous
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Assessment findings
a. Chronic Glomerulonephritis
5. Decreased serum calcium level
Calcium binds to phosphorous to compensate for elevated serum phosphorouslevels
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Assessment findings
a. Chronic Glomerulonephritis
6metabolic acidosis
From decreased acid secretion by the kidney and inability to regeneratebicarbonate
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Assessment findings
a. Chronic Glomerulonephritis
7. Mental status changes
Headache, dizziness, increasing irritability,
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Assessment findings
a. Chronic Glomerulonephritis
8. Digestive disturbancesLoss of weight
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Assessment findings
a. Chronic Glomerulonephritis
9. nocturia
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Assessment findings
a. Chronic Glomerulonephritis
10. Impaired nerve conduction
due to electrolyte abnormalities and uremia
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What are the diagnosticfindings in pts with
Chronic GN?
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Diagnostic Tests
a. Chronic Glomerulonephritis
1. Blood tests
Increased serum urea Increased creatinine Decreased GFR
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Diagnostic Tests
a. Chronic Glomerulonephritis
2. Blood levels
Presence of streptococcal antibodies, Antistreptolysin O exoenzyme
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Diagnostic Tests
a. Chronic Glomerulonephritis
3. urinalysis
Presence of proteinuria Gross hematuria Erythtrocyte
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management
a. Chronic Glomerulonephritis
1. CHON restrictionIf there is renal insufficiency and nitrogen retention
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management
a. Chronic Glomerulonephritis
2. Sodium restriction
For patients with HPN, edema and heart failure
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management
a. Chronic Glomerulonephritis
3. MIO
Plus daily weight monitoring
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management
a. Chronic Glomerulonephritis
4. Dialysis
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management
a. Chronic Glomerulonephritis
5. Diuretic
Treat fluid overload
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What is the next diseasethat we will discuss?
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Nephrotic Syndrome
Primary glomerular disease
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Nephrotic Syndrome
Marked proteinuria
Hypoalbuminemia
Edema
hyperlipidemia
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Nephrotic Syndrome
Marked proteinuria
- Increased protein or albumin in the urin
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Nephrotic Syndrome
hypoalbuminemia
1. Decreased albumin in the blood
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Nephrotic Syndrome
edemaIncreased permeability
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Nephrotic Syndrome
hyperlipidemiaHigh serum cholesterol and low density
lipoprotein
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Nephrotic Syndrome
Hyperlipidemia
Results from
increased hepatic llipoprotein synthesis in response todecreased serum albumin
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Will someone do me a
discussion on the causes
of the disease?
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Causes
2. Nephrotic syndrome
1. Chronic glomerulonephritis2. DM with intercapillary glomerulosclerosis3. Amyloidisis of the kidney ( infiltrated with amyloid, a starch-like
substance
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Causes
2. Nephrotic syndrome
4. Multiple myeloma (malignant, in the bone marrow)5. Systemic lupus erythematosus ( chronic inflammatory disease)6. Renal vein thrombosis- can obstruct blood flow
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Clinical manifestations
2. Nephrotic syndrome
1. Urinalysis
Marked proteinuria Lipiduria and casts (fatty, epithelial hyaline) Frothy urine
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Clinical manifestations
2. Nephrotic syndrome
2. Edema
Soft and pitting Commonly occurs:-- around the eyes (periorbital
edema),----in dependent areas ( sacrum, ankles,
hands)----abdomen (ascites)
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Clinical manifestations
2. Nephrotic syndrome
2. Irritability3. Headachemalaise
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Clinical manifestations
2. Nephrotic syndrome
3. Weight gain and pallor
li i
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complications
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Complication
2. Nephrotic syndrome
1. Skin breakdown Because of impaired arterial flow and capillary exchange
C
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Complication
2. Nephrotic syndrome
2. infection Due to a deficient immune response
C li i
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Complication
2. Nephrotic syndrome
2. thromboembolism Especially in the renal vein
C li i
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Complication
2. Nephrotic syndrome
4. Pulmonary emboli
C li ti
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Complication
2. Nephrotic syndrome
5. ARF
Due to hypovolemia
C li ti
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Complication
2. Nephrotic syndrome
6. Accelerated atherosclerosis
Due to hyperlipidemia
t
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management
t
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management
1. diuretics
Prescribed for severe edema
management
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g
2. Angiotensin- converting enzyme( ACE) inhibitors plus loop diuretics Taken for 4-6 weeks to be effective Ex. Ramipril- decrease CHON loss in the urine
management
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3. Corticosteroids
To decrease the immune response
management
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4. Diet
Low sodium + Liberal potassium- for those who have no hyperkalemia Enhances the Na-K pump mechanism and assists in elimination of sodium to reduce
edema
Low fat low protein Help lower lipidemia
management
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5. glucocorticoids
Prednisone To reduce inflammation Other meds including antineoplastic agents, immuno-suppressants and
cyclosporine
Nursing management
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g g
1. Early stages of nephrosis Similar to AGN
2. If nephrosis Worsens, Similar to Chronic Renal Failure
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Nursing management
3. If receiving corticostroids, instruct about about meds
s/s that should be reported to physician including s/s of
infection
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Nursing management
4. Dietary instructions
Low protein. Low fat low sodium liberal potassium
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The end