Khawla has complication

Diabetic nephropathy
1. What is it?
  1. Damage to the kidneys caused by long standing diabetes. In severe cases it can lead to kidney failure. But not everyone with diabetes has kidney damage.
2. Epidemiology
  1. World wide
    1. The prevalence of diabetes worldwide has extended epidemic magnitudes and is expected to affect more than 350 million people by the year 2035.
  2. UAE
    1. The prevalence rate of MA was considerably high ( 61%) among diabetic patients in the UAE.
3. Signs and symptoms
  1. Worsening blood pressure control
  2. Increased need to urinate
  3. Persistent itching
  4. Swelling of feet, ankles, hands or eyes
  5. Protein in the urine
  6. Less need for insulin or diabetes medicine
  7. Confusion or difficulty concentrating
  8. Nausea and vomiting
  9. Fatigue
  10. Loss of appetite
4. Pathophysiology
  1. Three major histologic changes
    1. First, mesangial expansion is directly induced by hyperglycemia, perhaps via increased matrix production or glycation of matrix proteins.
    2. Second, thickening of the glomerular basement membrane (GBM) occurs.
    3. Third, glomerular sclerosis is caused by intraglomerular hypertension (induced by dilatation of the afferent renal artery or from ischemic injury induced by hyaline narrowing of the vessels supplying the glomeruli). These different histologic patterns appear to have similar prognostic significance.
  2. The key change in diabetic glomerulopathy is augmentation of extracellular matrix.
  3. The severity of diabetic glomerulopathy is estimated by thickness of the peripheral basement membrane and mesangium and matrix expressed
5. Complications
  1. Infections - infection caused by urinary loss of immunoglobulins
  2. Thromboembolism - Loss of clotting factors in the urine
  3. Cardiovascular complications - Hyperlipidemia, increased thrombogenesis, and endothelial dysfunction
  4. Hypovolemic crisis - Severely depressed albumin levels, high dose diuretics, and vomiting.
  5. Anemia
    1. Urinary loss of EPO -> EPO-deficiency anemia
    2. Transferrinuria + increased transferrin catabolism -> hypotranferrinemia
    3. iron-deficiency anemia
  6. Acute renal failure - Fall in GFR
  7. Edema - Increased glomerular permeability and hypoalbuminemia, resulting in decreased plasma oncotic pressure and functional hypovolemia.
  8. Damage to the blood vessels of the retina (diabetic retinopathy)
  9. Hyperkalemia
  10. Hormonal, mineral alterations and intussusceptions
6. Treatment
  1. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs)
  2. Cholesterol-lowering drugs called statins
  3. Medications can often reduce the level of the protein albumin in the urine and improve kidney function
  4. Medications that help manage your calcium phosphate balance are important in maintaining healthy bones.
  5. Kidney dialysis
  6. Transplant.
  7. Symptom management.
7. Diagnosis
  1. Blood tests
  2. Urine tests
  3. Imaging tests.
  4. Renal function testing.
  5. Kidney biopsy.
8. Causes and risk factors
  1. Diabetes, type 1 or 2
  2. High blood sugar (hyperglycemia) that's difficult to control
  3. High blood pressure (hypertension) that's difficult to control
  4. Being a smoker and having diabetes
  5. High blood cholesterol and having diabetes
  6. A family history of diabetes and kidney disease
Kidney
1. Anatomy of the kidney
  1. Location --> retroperitoneal in position and extends from T12 to L3
  2. Surface anatomy
  3. Parts of kidney
2. Histology of kidney
3. Physiology of filtration
  1. What can pass?
    1. The filtration barrier permeable to
      1. Major electrolytes: sodium, chloride, potassium, bicarbonate
      2. Metabolic waste products: urea, creatinine
      3. Metabolites: glucose, amino acids, organic acids (ketone bodies)
      4. Non-natural substances: inulin, PAH (p-aminohippuric acid)
      5. Lower-weight proteins and peptides: insulin, myoglobin
  2. The Starling forces
    1. Glomerular capillary hydrostatic pressure (remains constant because of efferent arteriole constriction)
    2. Glomerular capillary oncotic pressure (dramatically increases along filtration due to increased albumin)
    3. Bowman’s space Hydrostatic pressure (due to the fluid in the lumen)
    4. Bowman’s space oncotic pressure (ZERO) no proteins!
  3. GFR= Kf [(PGC-PBS)-π GC
    1. Kf is filtration coefficient.
    2. It’s the water permeability or hydraulic conductance of the capillary walls
    3. Highest in the glomerular capillaries than anywhere else in the body!
  4. At the beginning of the capillary
  5. At the end of the capillary

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Khawla has complication

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	Erstellt von amna mohd vor fast 7 Jahre