Chronic Nephropathy Diabetic Glomerulonephritis Chronic Pyelonephritis
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Pathophysiology of Chronic Renal Failure
Diabetic Chronic Chronic Glomerulonephritis Nephropathy Pyelonephritis
Intracellular Glucose
Polycystic Kidney Dse.
HPN
Multiple Bilateral Cysts Non-modifiable Risk Factors: Age Gender Heredity
Repeated Inflammation Supports the formation of abnormal glycoprotein in the basement membrane of Ischaemia, Nephron loss, glomerulus Shrinkage of Kidney
Modifiable Risk Factors: Diet Sedentary Lifestyle Nephrotoxins
Damage to Nephrons 50% damage
Production of large variety of auto antibodies against normal body components such as nucleic acids, RBC, platelet, and WBC SLE antibodies react with their corresponding antigen
Renal blood vessels & nephrons are compressed & obstructed & functional tse. are destroyed
Renal Reserve
Glomerulosclerosis impairs the filtering fxn. of the glomerulus thus protein lost in urine
Long Standing HPN leads to further arteriosclerosis
As cysts fill, enlarge & multiply, kidneys also enlarge
Renal Blood
Stage
Systemic Lupus Erythematosus
Forms Immune Complexes
Renal Parenchyma atrophies & become fibrotic & scarred
GFR 50% Normal BUN, Creatinine
Deposited in the connective tse. such as blood volume & kidneys
More than 75% damage Renal Insufficiency
Stage
GFR 20-50% BUN, Creatinine
Trigger an inflammatory response and damage the kidney
As nephrons are destroyed, the remaining nephrons undergo changes to compensate for those Remaining nephrons must filter more solute particles from the Hypertrophy of remaining nephrons Nephrons cannot tolerate the work Further damage of nephrons 80-90% damage Renal Failure Stage
GFR 10-20% Sharp BUN,
Impaired kidney function & Uremia Nitrogenous Na HHCO3 &KH2O Erythropoietin retention retention retention waste production production impairs in kidney platelets Hyperkalemia Urine Metabolic Bleeding GI Blood Output Anemia stress Acidosis tendencies +
+
Oliguria Malfunction Lungs GI of Compensates RAAS bleeding Kussmaul’s Respiration Heart Edema Anorexia Failure Nausea Vomiting Fatigue Gastroenteritis Weakness Peptic Ulcer Pallor Pulmonary Edema Peripheral Edema
Mg retention +
Vit. D activation
Hypermagnesemia
Phosphate retention
Continuous decline in renal fxn. > 90% kidney
Hyperphosphatemi
Reduction in renal capillaries Scarring of Glomeruli Atrophy & Fibrosis of
Ca+ absorption Blood loss during hemodialysis
Hypocalcemia
Stage Parathyroid overworks (Hyperparathyroidism)
Loss of appetite
PTH secretion Ca+ resorption from bone + Ca absorption from GI tract Renal Osteodysthrophy Osteomalacia Osteoporosis Bone tenderness Bone pain Muscle Weakness
End Stage Renal Dse. (ESRD) Continuous Multisystem Affectation
Toxins irritate pericardial sac Pericarditi Cardiac Tamponade
GFR less than 10%
Toxins impair WBCs, humoral & cell mediated immunity; Fever is suppressed; Phagocyte becomes defective
Immune System Decline
Salivary urea breakdown
Deposit of urea on skin
Uremic Fetor
Uremic Frost Yellowish hue
Irritation of Phrenic Hiccups
Toxins affect the nerve fibers Atrophy & Demyalination Peripheral Neuropath Restless Leg Syndrome
Risk for Superinfection
Toxins causes CNS affectation
Retentio n of
Uremic Encephalopathy
Cells become resistant to insulin
Reduction in alertness & awareness Changes in mentation Difficulty of concentrating Fatigue Insomnia Psychiatric symptoms
Erratic blood glucose level Because of glucose intracellularly, liver produces tryglycerides & HDL
Death Atherosclerosis
Thrombus & Embolus Formation
By: Jonnel Montoya Musngi BSN 4-B
Diabetic Chronic Chronic Glomerulonephritis Nephropathy Pyelonephritis
Intracellular Glucose
Polycystic Kidney Dse.
HPN
Multiple Bilateral Cysts Non-modifiable Risk Factors: Age Gender Heredity
Repeated Inflammation Supports the formation of abnormal glycoprotein in the basement membrane of Ischaemia, Nephron loss, glomerulus Shrinkage of Kidney
Modifiable Risk Factors: Diet Sedentary Lifestyle Nephrotoxins
Damage to Nephrons 50% damage
Production of large variety of auto antibodies against normal body components such as nucleic acids, RBC, platelet, and WBC SLE antibodies react with their corresponding antigen
Renal blood vessels & nephrons are compressed & obstructed & functional tse. are destroyed
Renal Reserve
Glomerulosclerosis impairs the filtering fxn. of the glomerulus thus protein lost in urine
Long Standing HPN leads to further arteriosclerosis
As cysts fill, enlarge & multiply, kidneys also enlarge
Renal Blood
Stage
Systemic Lupus Erythematosus
Forms Immune Complexes
Renal Parenchyma atrophies & become fibrotic & scarred
GFR 50% Normal BUN, Creatinine
Deposited in the connective tse. such as blood volume & kidneys
More than 75% damage Renal Insufficiency
Stage
GFR 20-50% BUN, Creatinine
Trigger an inflammatory response and damage the kidney
As nephrons are destroyed, the remaining nephrons undergo changes to compensate for those Remaining nephrons must filter more solute particles from the Hypertrophy of remaining nephrons Nephrons cannot tolerate the work Further damage of nephrons 80-90% damage Renal Failure Stage
GFR 10-20% Sharp BUN,
Impaired kidney function & Uremia Nitrogenous Na HHCO3 &KH2O Erythropoietin retention retention retention waste production production impairs in kidney platelets Hyperkalemia Urine Metabolic Bleeding GI Blood Output Anemia stress Acidosis tendencies +
+
Oliguria Malfunction Lungs GI of Compensates RAAS bleeding Kussmaul’s Respiration Heart Edema Anorexia Failure Nausea Vomiting Fatigue Gastroenteritis Weakness Peptic Ulcer Pallor Pulmonary Edema Peripheral Edema
Mg retention +
Vit. D activation
Hypermagnesemia
Phosphate retention
Continuous decline in renal fxn. > 90% kidney
Hyperphosphatemi
Reduction in renal capillaries Scarring of Glomeruli Atrophy & Fibrosis of
Ca+ absorption Blood loss during hemodialysis
Hypocalcemia
Stage Parathyroid overworks (Hyperparathyroidism)
Loss of appetite
PTH secretion Ca+ resorption from bone + Ca absorption from GI tract Renal Osteodysthrophy Osteomalacia Osteoporosis Bone tenderness Bone pain Muscle Weakness
End Stage Renal Dse. (ESRD) Continuous Multisystem Affectation
Toxins irritate pericardial sac Pericarditi Cardiac Tamponade
GFR less than 10%
Toxins impair WBCs, humoral & cell mediated immunity; Fever is suppressed; Phagocyte becomes defective
Immune System Decline
Salivary urea breakdown
Deposit of urea on skin
Uremic Fetor
Uremic Frost Yellowish hue
Irritation of Phrenic Hiccups
Toxins affect the nerve fibers Atrophy & Demyalination Peripheral Neuropath Restless Leg Syndrome
Risk for Superinfection
Toxins causes CNS affectation
Retentio n of
Uremic Encephalopathy
Cells become resistant to insulin
Reduction in alertness & awareness Changes in mentation Difficulty of concentrating Fatigue Insomnia Psychiatric symptoms
Erratic blood glucose level Because of glucose intracellularly, liver produces tryglycerides & HDL
Death Atherosclerosis
Thrombus & Embolus Formation
By: Jonnel Montoya Musngi BSN 4-B
