Uremic Syndrome Flashcards

1
Q

What is uremia?

A

Symptomatic renal failure in which there is multiple organ dysfxn and biochemical abnormalities. Need transplant or dialysis

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2
Q

What is chronic kidney disease?

A

Slowly progressive decline in GFR. Usually asymptomatic until GFR <20-25ml/min

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3
Q

Effect of uremia on the GI system

A
  • Loss of appetite (eat less protein)
  • Altered taste, metallic due to ammonia in saliva
  • Mouth ulcers due to mucosal irritation from ammonia
  • Uremic fetor: bacterial conversion of urea to ammonium in oral cavity
  • Esophagitis and motility problems-alteration in peristalsis
  • GI bleeding: superficial mucosal abnormalities, angiodysplasia of the GI tract, peptic ulcer
  • Diverticular disease and constipation
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4
Q

CKD Anemia

A

One of the main laboratory manifestations of renal failure

  • usually normochromic normocytic
  • Low reticulocyte count for degree of anemia (hypoproliferative)
  • Normal bone marrow
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5
Q

When does hematocrit start to fall in most pts with CRF?

A

When creatinine clearance reaches 30-35ml/min

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6
Q

Primary causes of anemia ni CKD?

A
  1. Decreased production of EPO
  2. Shortened erythrocyte life span
  3. Inhibitors of erythropoiesis accumulating in uremia
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7
Q

Consequences of anemia in CKD?

A
  • Progressive reduction in activity and energy level and of exercise tolerance
  • LV dilation and diastolic dysfxn
  • Increased hospitalizations
  • Deterioration of cognitive fxn
  • Intractable itching (elevated phos)
  • Impairment of sexual fxn
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8
Q

Aggravating causes of anemia in CKD?

A
  1. Factors hampering EPO production/effect
    - B12/folic acid/iron def
    - Blood loss (GI: inflammation, Dialysis related)
    - Bone marrow fibrosis due to hyperparathy
    - Reticuloendothelial blockade from infections, cancer and inflammatory states
    - Myelofibrosis or aluminum accumulation
  2. Disease causing both anemia and renal failure
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9
Q

Treatment of anemia in CKD?

A
  • Blood transfusion
  • Iron therapy (key, must be repleted for EPO to work)
  • Recombinant human EPO
  • Darbepoetin alfa
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10
Q

Describe the hematopoietic system in CKD

A
  • Bleeding tendency, prolonged bleeding time
  • Platelets: main determinant of altered bleeding in uremia (platelet aggregation dysfxn)
  • Dialysis of uremic serum appears to remove “some compound” that causes the binding defect (not much is lost here)
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11
Q

Why is there increased bleeding in CKD?

A
  • Inc NO inhibits platelet fxn
  • Inc cAMP due to elevated PTH
  • Abn fxn of vascular endothelial wall
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12
Q

Treatment for uremic bleeding disorders

A
  • EPO
  • DDAVP (stimulates von willebrand factor and increases platelet glycoprotein expression)–>tachyphylaxis
  • Conjugated estrogens
  • Transfusions of cryoprecipitate
  • Dialysis to remove “toxins”
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13
Q

Risk factors unique to CKD that inc risk of CVD

A
  • Anemia
  • Increased homocysteine
  • Thrombogenic factors
  • Obesity
  • intake of Ca (leads to deposition in arteries)
  • Hyperparathyroidism
  • Uremic toxins
  • inflammatory state
  • Less aggressively treated with beta blockers and statins
  • Accelerated arterial calcification, endothelial dysfxn, art stiffness, prothrombotic factors, abn apolipoprotein levels
  • Increased TGs and LDL with dec in HDL
  • Increased APO1
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14
Q

Sexual dysfxn in CKD

A

happens

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15
Q

Pregnancy in CKD

A

Rare and dangerous, depends on degree of functional impairment (note return in fertility 1-2mo after transplant)

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16
Q

Dangers with pregnancy in ppl with CKD

A
  • Preeclampsia
  • Fetal growth retardation
  • Prematurity
  • Low birth weight
  • Congenital anomalies
17
Q

CKD and mineral/bone disorder

A
  • Vit D def (kidney activates)
  • No reabs of phosphorus
  • Leads to decrease in calcium, elevated phosphorus, low activated vit D and high PTH and elevated FGF-23
  • Causes abnormalities of bone turnover, mineralization, volume, linear growth and strength
  • Vascular and soft tissue calcification (precipitates as calcium phosphate)
18
Q

FGF-23

A
  • Produced by osteocytes and osteoblasts
  • Acts upon kidney to cause phosphaturia
  • Decreases the production of vit D by suppressing 1 alpha hydroxylase leading to hyperparathy
19
Q

Clinical signs and symptoms of secondary hyperparathy

A
  • Bone pain
  • Spontaneous fractures
  • Periarthritis/arthritis
  • Spontaneous tendon rupture
  • Muscle weakness/myopathy
  • Skeletal deformities
  • Growth retardation
20
Q

Mineral and bone disease treatment

A
  • Correct vit D def
  • Diminish intestinal phosphate abs by low phosphate diet and phosph binders
  • Treat elevated PTH