Term
|
Definition
1. Initiation: immediately following insult to kidney, when pathologic damage is initiated.
2. Extension: Ischemia, hypoxia, inflammation, cellular injury continue, leading to apoptosis/necrosis. Clinical and lab abnormalities may/may not be present.
3. Maintenance: azotemia and/or uremia: may persist for weeks.
4. Recovery (or death??) |
|
|
Term
| How is oliguria defined? Anuria? |
|
Definition
Oliguria: <10ml urine output per pound body weight per day.
Anuria: <2ml urine output per pound body weight per day. |
|
|
Term
| What are the most common causes of AKI? |
|
Definition
Nephrotoxicity
Infection
Ischemia |
|
|
Term
| Is decreased renal blood flow or cellular damage more of a factor in AKI? |
|
Definition
| Both. Ischemia leads to loss of ATP, and when Na+K+ ATP-ase activity is lost, intracellular concentration gradients change and cells can swell (causing tubular obstruction) or burst. Also, loss of ATP leads to cytoskeleton changes, loss of microvilli, etc. |
|
|
Term
| Does inflammation play a role in AKI? |
|
Definition
| Yes. Neutrophils migrate into interstitium, changing vascular permeability. Neutrophils may plug capillaries. They release proteases and cytokines, exaggerating imflammatory response. |
|
|
Term
| What are possible sequelae of acute oliguric renal failure? |
|
Definition
Water retention and expansion of ECF can result in heart failure, hypertension, and/or pulmonary edema (esp. if there's a positive sodium balance too). Hyperkalemia is another major threat. Acidosis is another...and can aggravate the hyperkalemia. Hyperphosphatemia is another threat - causes decrease in free calcium and symptoms of hypocalcemia.
ALI and neuro symptoms can occur with AKI. |
|
|
Term
| What are common non-specific signs of uremia? |
|
Definition
-Anorexia (and nausea, vomiting, diarrhea)
-Lethargy, weight loss
-Depression
-Hypothermia |
|
|
Term
| Common signs of chronic renal failure: |
|
Definition
Anemia (nonregenerative)
Weight loss
Hypertension (can lead to seizures, ventricular hypertrophy, retinal detachment)
Pulmonary edema/tachypnea
Skeletal abnormalities due to secondary hyperparathyroidism |
|
|
Term
| What is the self-perpetuation hypothesis? |
|
Definition
| Chronic renal failure is often irreversible even if inciting cause is removed: this is because in undergoing hypertrophy to "take up the slack," remaining nephrons succumb to resulting glomerular hypertension -> glomerular sclerosis/fibrosis. |
|
|
Term
| 5 differences between acute and chronic kidneys? |
|
Definition
1. AKI: swollen, painful kidneys; CKD: small, firm, irregular kidneys
2. AKI: normal body wt; CKD: weight loss
3. AKI: minimal signs of uremia; CKD: many signs of uremia
4. AKI: hyperkalemia; CKD: normo- or hypokalemia.
5. AKI: anemia unlikely; CKD: nonregenerative anemia due to decreased renal erythropoietin production. |
|
|
Term
| What's the basis for weight loss in CKD? |
|
Definition
-Anorexia due to emetic effect of uremic toxins leads to inadequate dietary intake
-Uremia results in catabolism of muscle |
|
|
Term
| What is the basis for hematemesis in CKD? |
|
Definition
More common in dogs.
Uremic toxins trigger medullary emetic chemoreceptors.
Increased gastrin (due to decreased filtration by kidneys) stimulates gastric acid secretion in stomach; can cause damage to gastric mucosa. Also decreased platelet function can lead to GI hemorrhage. |
|
|
Term
| Why does polyuria (and polydipsia) occur in CKD? |
|
Definition
1. Increased SNGFR results in increased solute load per surviving nephron ->solute diuresis
2. Disruption of medullary "architecture" (tubular damage) ->loss of countercurrent concentration gradient.
3. Impaired renal response to ADH due to tubular cell damage.
Polydipsia is in response to polyuria. |
|
|
Term
| What is hypokalemia polymyopathy? |
|
Definition
In occasional cats with CKD.
Surviving nephrons increase K+ secretion (in exchange for Na+) to avoid hyperkalemia. In combination with decreased dietary intake (anorexia), this can result in hypokalemia. Generalized muscle weakness, manifesting as cervical ventroflexion and stilted gait. |
|
|
