Renal phys.pathophys.disease Flashcards
What is SDMA
Symmetric dimethylarginine
byproduct of cellular protien metabolism that is released in to circulation >90% renal excreted
No renal secretion/reabsorbtion
Why might SDMA be better than creatinine for a maker of GFR
Less effected by age, sex, breed and lean body mass.
Less interindividual variability
What is the agent in Lyme disease
Borrelia burgdorferi – gram negative spirochete
Ixodes transmission
How does lyme disease result in PLN
Immune mediate glomerular nephritis with antigen antibody complex
How to tx Lyme nephritis
Stardard PLN therapy
Montior for hyptertension
If biopsy and active immune complex then immunosuppress- Mycophenolate
If not biopsy then need severe progressive disease to treat
What stimulates parathyroid hormone to be released
released by decreased plasma Ca levles
Where does parathyroid hormone act
Bone: Break down and release of phos and Ca
Kidney: activates calcitriol
Nephron: DCT to reabsorb Ca blocks reabsorb of Phos
Where is calcitriol made
Skin (cholecalciferol) –> Liver (calcidiol) –>Kidneys
Where does calcitriol act
Bone: release of Ca
Parathyroid: Neg feedback
GIT: increase Ca and Phos absorbpiton
Neprhon: PCT reabsorption of Ca
What is calcitonin and what does it do
Released for thyroid gland in response to increase in Ca.
Works in the same way as PTH to block Ca release
How does high phosphoruls levels occur in CKD
High phos block calcitriol
Less functional nephrones so less phos is excreted
Trade off hypothesis
What is the pathophys of uroabdomen
Hyperosmolar potassium rich urine accumulates
osmotic pull of extracellular fluid to peritoneal due to concentration gradient of Na and Cl
Does palpation of the bladder rule out uroabdomen
No
What is the diagnostic criteria for creatinine and K for ab fluid: Peripheral
Dogs: Crea > 2:1 K > 1.4: 1
Cats: Crea > 2:1 K > 1.9:1
What is the urethral healing time versus cystotomy healing time
Urethra 3-21 days
Bladder can seal at 45 hrs
Define oliguria, anuria
Realtive Oliguria < 2 ml/kg/day for renal disease
Absolute Oliguria < 1 ml/kg/day
Anuria 0-0.5 ml/kg/day
What is UOP a function of
GFR
Tubular solute reabsorption
Tubular solute excretion
What are the causes of oligioanruia
Decreased renal blood flow
Tubular obstruction casts/cellular debris
Backflow of glomerular filtration into the renal interstitium
Intrarenal RAAS activation
Altered permeability of glomerular filtration barrier
How does mannitol work for oligioanuria
Osmotic diuretic: may also serve as free radical scavenger and flush debris
Only use in normovolemic patients to avoid pulmonary edema
How does furosemide work for oligioanuria
NaK2Cl transporter in the LOH; Decreased renal O2 consumption; less ischemic damage
Concentration within tubular filtrate determines effect why with anuria may not work
How does fenoldopam work for oligioanuria
Post synaptic dopamine receptor agonist
More renal vasodilationa nd naturesis than dopamine
Can lead to systemic hypotension and decrease SVR
Define azotemia
Increase in concentration of nitrogen containing substances in the blood Bun or Creatinine
Markers for other uremic toxins that build up
Define AKI
An increase in creatinine by >/= 0.3 mg/dl from baseline regardless of creatinine (normal range). Severe AKI- abrupt loss of GFR
What are the Iris grades for AKI
1: Crea < 1.6 mg/dl
2: Crea 1.7-2.5 mg/dl
3 Crea 2.6- 5.0 mg/dl
4 Crea 5.1-10.0 mg/dl
5 crea > 10.1 mg/dlFurther classified by non-oliguric, oliguric, and RRT
What is the mechanism of pre-renal azotemia and list broad categories
decrease GFR occuring secondary to hypoperfusion in structually normal kidney
hypovolemia
Poor CO in cardiac dysfunction
Pathologic vasodilatory conditions
What are some characteristics of pre-renal azotemia
Higher BUN: Crea ratio > 20:1
Higher concentration of urine (USG)
Define CKD
Kidney damage that has persisted greater than 3 months. Loss of functional nephrons, other nephrons compensate to increase excretatory load of each nephron
What are the consequences of lost of compensation to the nephron
hypertension Edema hyperphosphatemia metabolic acidosis
Gradual increase in uremic solutes