N497 chronic kidney disease

Chronic Renal Disorders

• Encompasses Chronic Kidney Disease, Dialysis, and Kidney Transplants

Chronic Renal Disease Risk Factors

• Chemical or environmental toxin exposure increases risk
• Low birth weight that can lead to reduced nephron endowment and lower renal volume is another risk factor
• Diet high in sodium
• Heart failure and hypertension are risk factors
• Contact sports or trauma raises the risk of renal disease
• The use of certain medications are also risk factors
• A family history of renal disease is a risk factor
• Certain races/ethnicities have increased rates as well, due to other conditions like diabetes mellitus (DM) and Hypertension (HTN).

Chronic Kidney Disease (CKD)

• Involves progressive loss and ongoing deterioration in kidney function
• Characterized by a glomerular filtration rate (GFR) of less than 60 mL/minute for at least 3 months
• Progression is based on the degree of proteinuria
• It is irreversible and leads to uremia or end-stage kidney disease (ESKD)
• Requires dialysis or kidney transplantation to sustain life

Stages of CKD

• A GFR less than 60 for 3 months or longer indicates chronic kidney disease
• Stage 1: Normal or increased GFR (≥ 90 mL/min per 1.73 m2) with kidney damage
• Stage 2: Mildly decreased GFR (60-89 mL/min per 1.73 m2) with kidney damage
• Stage 3: Moderately decreased GFR (30-59 mL/min per 1.73 m2)
• Stage 4: Severely decreased GFR (15-29 mL/min per 1.73 m2)
• Stage 5: Kidney failure (GFR < 15 mL/min per 1.73 m2)

CKD: Pathophysiology

• Diabetic nephropathy involves changes in the glomerular basement membrane and ischemia, leading to glomerulus sclerosis and gradual nephron destruction
• Hypertensive nephrosclerosis is caused by long-standing hypertension and leads to glomerular destruction and tubular atrophy
• Chronic glomerulonephritis is characterized by a bilateral inflammatory process of the glomeruli, leading to ischemia
• Chronic pyelonephritis results from a chronic infection and leads to reflux nephropathy
• Polycystic kidney disease gradually destroys normal renal tissue through the compression of bilateral cysts
• Systemic lupus erythematosus has basement membrane damage by immune complexes, leading to glomerulonephritis

CKD: Associated Labs and Clinical Manifestations

• GFR declines, causing plasma creatinine to increase
• GFR decreases, resulting in increased creatinine and urea levels
• Kidneys lose the ability to regulate sodium and water balance, causing edema and hypertension
• Total body potassium can increase to life-threatening levels, needs to be controlled by dialysis
• With GFR decline, renal phosphate excretion decreases, binding calcium and contributing to hypocalcemia
• Acidosis contributes to a negative calcium balance
• Decreased serum calcium levels stimulate parathyroid hormone secretion
• Increases risk of fractures

CKD: Neurological Manifestations

• Asterixis (tremor of the hand when wrist is extended)
• Ataxia (alteration in gait)
• Coma
• Inability to concentrate or decreased attention span
• Myoclonus
• Paresthesias (tingling, tickling, burning sensations)
• Seizures
• Slurred speech

CKD: Cardiovascular Manifestations

• Cardiac tamponade
• Cardiomyopathy
• Heart failure
• Stroke
• Pericarditis
• Hypertension
• Pericardial effusion
• Peripheral edema
• Dyslipidemia
• Ischemic Heart Disease
• Sudden cardiac death

CKD: Respiratory Manifestations

• Crackles, due to pulmonary edema
• Deep sighing, yawning
• Depressed cough reflex
• Kussmaul's respirations, due to metabolic acidosis
• Pulmonary hypertension
• Pleural effusion, resulting from extra volume
• Shortness of breath, because of pulmonary edema and pulmonary hypertension
• Tachypnea, required to improve gas exchange
• Unpleasant "uremic" breath odor

CKD: Gastrointestinal Manifestations

• Anorexia
• Changes in taste acuity and sensation
• Constipation
• Uremic gastroenteritis
• Nausea
• Vomiting
• GI bleeding
• Diarrhea

CKD: Hematologic Manifestations

• Normochromic-normocytic anemia
• Impaired platelet function
• Decreased platelet numbers and altered vascular endothelium promotes increased bleeding
• Alterations in thrombin and clotting factors contribute to hypercoagulability
• Lethargy
• Dizziness
• Low hematocrit

CKD: Immune System Manifestations

• Suppressed immune system
• Phagocytosis
• Antibody production
• Cell-mediated immune response
• Deficient responses to vaccinations
• Increased risk for infection
• Virus-associated cancers (EBV, HPV, Hep B, and C)
• Malnutrition, metabolic acidosis, and hyperglycemia, all increase immunosuppression

CKD: Clinical Manifestations

• Skin: decreased skin turgor, dry skin, ecchymosis, pruritus, purpura, and yellow-gray pallor
• Urinary: diluted straw-colored appearance, hematuria, oliguria (later), polyuria (early), and proteinuria
• MSK: bone pain, muscle weakness and cramping, and pathological fractures
• Reproductive: decreased fertility and libido, impotence, and infrequent or absent menses

Hemodialysis

• Function is to cleanse blood and get rid of accumulated waste products
• It removes by-products of protein metabolism, such as ammonia, urea, creatinine, and uric acid.
• Removes the body of excess fluids and correct electrolyte levels
• Can't replace hormones

Complications during Hemodialysis

• Disequilibrium syndrome includes removal of urea from blood, cerebral edema, headache, nausea, vomiting, confusion, twitching and convulsions
• Hypotension is related to the rate and amount of fluid removed or antihypertensive medications
• Transfusion reactions
• Dysrhythmias are due to hypotension, fluid overload, or rapid removal of potassium
• Sepsis and Shock
• Psychological problems

Peritoneal Dialysis

• Dialysis where dialysate solution passes from the blood stream, through the peritoneum, and into the dialysate solution.
• The peritoneum acts a natural filter.
• The peritoneal cavity is rich in capillaries allowing access to the blood supply

Complications during Peritoneal Dialysis

• Peritonitis
• Abdominal pain
• Bladder or bowel perforation
• Insufficient outflow
• Leakage around the catheter site
• Blockage of catheter

Kidney Transplants

• A human kidney from a compatible donor is placed into the iliac fossa of a recipient and the anastomosis of its ureter to the bladder of the recipient; most common solid organ transplant
• Is performed for irreversible kidney failure; specific criteria are established for eligibility
• Donors are screened for ABO blood group, tissue-specific antigen and more
• Ideal kidney source for transplant
• The living donor must have two working kidneys, and emotional well-being
• Cadavever donors must meet the institution's criteria of brain death, and not be older than 70 years of age.
• Potential kidney transplant recipients must not have malignant diseases outside of the CNS, general infection or communicable diseases, or have sustained a renal trauma

Rejection of Kidney Transplantation

• Acute rejection is most common and occurs in the first 6 weeks postoperatively
• Potentially reversible with high doses of corticosteroids
• Chronic Rejection occurs slowly, months or years after transplant, and mimics CKD
• Temperature > 37.7 °C is a manifesation
• Interventions include immunosuppressive medications and retransplantation
• 85-95% of kidney transplants are successful after year 1

Pathologies of the GI Tract

• Muscular tube problems with muscle or innervation
• Obstruction of tube is one cause
• Deficient digestion and/or absorption
• Blood vessel irregularities

GI Tract Disorders Causes

• Blood supply abnormalities including upper and lower GIB, or ischemia
• Inflammation causes disorders such as, Esophagitis. Gastritis, Colitis, or Crohn's disease
• Tumors can disturb healthy function
• Region-specific concerns with esophagus, stomach small intestine, large intestine

Disorders with Aging

• Dysphagia, decreased saliva production
• Decreased sense of smell and taste
• Decreased peristalsis, decreased secretion of digestive enzymes
• Decreased liver function, decreased protection of Gl tract

Age-Related Changes in Appetite Hormones

• Ghrelin decreases with age
• Peptide tyrosine-tyrosine (PYY) levels increase with age
• Cholecystokinin (CCK) secretion increases with age
• Insulin production decreases with age
• Leptin levels rise, but evidence is conflicting

Celiac Disease: Gluten-Sensitive Enteropathy

• Autoimmune disease T-cell mediated, caused by gluten ingestion for genetically susceptible people
• Gluten damages the villi epithelium, leading to inability to absorb nutrients
• Glycoproteins in gluten found in wheat (gliadin), rye (secalins), barley (hordeins) lead to inflammation
• Diagnosed often in children but can develop during adulthood
• Is associated with type 1 diabetes, autoimmune thyroid disease, RA, SLE (etc)

Gluten-Sensitive Enteropathy: Pathophysiology

• Undigested gluten triggers immune response in small intestine
• Gluten fragments pass through the enterocytes of the villi of the small intestine accumulating under the enterocytes
• Accumulation of gluten causes enterocytes to send chemical signal to the immune system
• Immune cells attack and damage the enterocytes (tight junctions loosen)
• Damaged enterocytes release an enzyme
• Villi become shortened and flattened, and atrophy

Gluten-Sensitive Enteropathy: Pathophysiology continued

• Fat Soluble Vitamins (K) deficiencies are cause of hypoprothrombinemia
• Iron and Folic Acid result in cheilosis, anemia and smooth, red tongue (glossitis)
• Vitamin B12 absorption is effected with ileal disease

Clinical Manifestations of Gluten-Sensitive Enteropathy

• Diarrhea is an early sign, stools can be greasy, oil filled and foul
• 3-5 days of constant and bowel movements, constipation can occur with other children
• Organic failure to thrive, anemia
• Vomiting and pains occur with infants, short stature with older children

Diagnostic and Treatment of Gluten-Sensitive Enteropathy

• Intestinal, duodenal biopsy shows characteristic changes of inflammation or villous atrophy
• Celiac crisis is an complication of infancy, with gluten intolerance
• Results in Abdominal distension & Explosive watery diarrhea
• Hypoproteinemia because of malabsorption
• Leads to hypotensive shock, metabolic syndromes

Inflammatory Bowel Disease:

• Ulcerative Colitis and Crohn’s Disease
• In ulcerative colitis inflammation is contained to intestinal mucosa [inner lining] of colon from the anus
• Crohn's is involved anywhere of the Gl tract of lower part of small bowel
• increased risk of colon cancer and intestinal cancer for CD

Ulcerative Colitis

• Causes ulcerations in the colonic and rectal mucosa
• Usually begins in rectum and progresses upward

Ulcerative Colitis: Pathophysiology

• Inflammation spreaders, to a wall defect
• Stimulates dendrite to release inflammatory cells and damages epithelial cells

Crohn Disease: Risk Factors

• Age of diagnosis around 30
• Ethnicity with Caucasian and Jewish descent
• Environmental risks with smoking etc

Crohn's Disease: Pathophysiology

• Is initiated in luminal in the GI with impaired epithelium
• clearance of foreign and activates chronic inflammation

Symptoms for Crohn's Disease

• With chronic diarrhea loose stools and pains
• Low abdomianal mass and anaemia
• Growth delays and inflammation of lining

Irritable Bowel Syndrome (IBS)

• Disorder of Gl tract with abdominal pains
• Risk is high being female and history of conditions

Irritable Bowel Syndrome: Pathophysiology

• intestinal contraction changes
• alterations to nerves

Pathophysiology: Symptoms related to Irritable Bowels

Symptoms with abdominal is related to BMs

• Change often
• Mucus build
• Bloating

Irritable Bowel Syndrome

• Recurring discomfort for 3 months
• Changes with BM form/feel

Chronic Pancreatitis

• where the doesn't heal well
• ETOH most common case
• Genetic, tumors and blockades

Chronic Pancreatitis: Pathophysiology

• Non obstruction to pancreatic duct
• Fibrous damage

Chromic Pathophysiology symptoms and treatments

• Bouts of pains
• Elevated serum
• Diet modifications oral enzymes

Viral Hepatitis Review

• Hepatitis can be transmitted in Fecal-Oral / Sexual / Blood
• Acute in hepatitis , or chronic
• Inflammatins and celucal

Chronic Hepatitis: Pathophysiology

• Bodies are inflated with immune responses
• lead to death/cancer

Chronic Hepatitis: Pathophysiology

• Prodomal with Anorexia, N/V
• Symptoms get worse as goes to brain (encephalopathy)

Cirrhosis:

• Irreversible damage from liver damage
• Response creates function decline

Caused from Cirrhosis:

• From Chronic alcoholism
• Bile duct restrictions
• Toxic responses

Cirrhosis: Pathophysiology

• Inflammation leads to cell damage
• Leads to fibrosis
• Can compromise fatty deposits

Biliary Fibrosis:

• is autoimmune response attacking epithelial lining
• bile ducts
• leads to tumors

Esophageal Varices

• Causes from lower flow of blood through the liver
• causes blockages

Cirrhosis: Hepatorenal Syndrome (HRS)

• A complication is liver malfunction
• Decreases blood flow

Common Problems from Cirrhosis

• High surgery risks
• Transplants
• High infections

Obesity:

• Based on BMI of 30kg
• Can be impacted by the genetics and environments

risk to obesity:

• Genetics
• Culture
• Levels of actibitu

Symptoms from Pathophysiology:

• Hormonal imbalances on thyroid

The process of Leptin for bodies:

• Peptide hormones will supresis diet and burn calories