Chronic Kidney Disease (CKD) Flashcards
define CKD
progressive declining renal failure
Why is it difficult to identify the underlying cause?
initial renal insult is often long past by the time clinical signs develop and CKD can be diagnosed
What microscopic changes occurs as a result of chronic inflammation?
- widespread interstitial fibrosis as result of irreversible damage to glomeruli and tubules
- nephrons can’t be replaced in a mature kidney, so the kidney repairs the lost tissue by developing fibrotic tissue
- kidney is smaller than normal
- capsule is pale
- fibrotic tissue retracts and causes pitting on the kidney’s surface
List effects of progressive CKD
uremia
toxin retention
systemic hypertension
late in Dz –> dementia, weakness, stupor, seizures
Def. uremia
a clinical state describing the effects of the retained toxins and other substances that the kidney is supposed to be eliminating from the body
How does uremia present clinically?
as PU/PD
- impairment of renal tubule’s ability to concentrate urine leads to a loss of water into the urine because the tubules can’t reabsorb the water
- PD is compensatory
Toxin retention:
- irritates ______________
- stimulates ______________
- irritation of mucosal lining of GI
- stimulation of chemoreceptor trigger zone of brain leading to nausea and V/D
What happens when gastrin is retained? How does it manifest?
increases secretion of acid into stomach leading to irritation and gastric or duodenal ulcers; can also mainifest as stomatitis and oral ulceration
Why is systemic hypertension caused?
- electrolyte imbalance
- sodium and water retention increases blood pressure (hypertension)
- hypertension contributes to progression of renal dysfunction, retinal hemorrhage and detachment, and neurologic signs
CKD CBC alterations and pathophysiologic reason why you see this specific alteration
mild to moderate nonregenerative anima because kidneys aren’t able to produce erythropoietin which in turn means RBC production is decreased
CKD Serum Chem alterations
- Azotemia w/ isosthenuria
- elevated urea and creatinine
- hyperphophatemia (phosphorus isn’t excreted properly)
- hypokalemia (loss of potassium)
CKD UA alterations
- isosthenuria due to lac of concentrating ability of renal tubules
- proteinuria due to increased loss of protein in urine
Goal of CKD nursing strategies
Hint: Not asking for Tx, but rather what the general goal of Tx is for these patients
- minimize uremia via dietary management and fluid support
- eliminate or minimize vomiting, anorexia, hypokalmeia, hyperphosphatemia, anemia, and hypertension
List therapeutic CKD strategies
Hint: This is a list of Tx that can be used for CKD patients; 9 in total if you get them all right
- dietary management
- fluid therapy
- H2 blockers
- antiemetics
- oral potassium
- oral phosphate binding meds
- meds for hypertension
- blood transfusion
- human erythropoietin
What dietary adjustments can be made for CKD?
- decrease phosphorus content –> decreases phosphorus retention
- decrease protein content –> urea is a metabolite of protein degradation, so you don’t want to make more of something the kidney’s can’t properly excrete; decreases azotemia as a result
- decrease sodium –> minimizes sodium retention and thus hypertension
- increase potassium –> to make up for potassium losses
- calorie dense so pet doesn’t have to eat as much