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
List two electrolyte abnormalities seen in endstage CKD
low iCa Increased K+ Hyperphos- worse outcome in cats the higher it is
What are the factors that lead to anemia in CKD
decreased EPO production
decreased red blood cell life span
Poor nutritionGI blood loss- uremic gastroenteritis
Why may some cats have concentrated urine despite CKD
Glomerular disease termd glomerulotubular imbalance
How do you determine glomerulonephritis vs. tubulointerstitial nephritis
Normoglycemia with glucosuria is due to tubular disease as the PCT reabsorbs almost all the glucose filtered. Both will have protien loss. In glomerular it is the larger protiens, and tubular it is smaller protiens
List 7 medications that may need to be dose adjusted due to
Amakacin, penicillins, cephalsporins, enrofloxacin, gentamicin, TMS, tobramycin
In the osmolality calculation what is the ineffective osmole
Urea (BUN)- high membrane permeability therefore does not alter water distribution.
What is the regulatory response to increase in sodium
osmoreceptors in the hypothalmus sense change in effective osmoles (~1%): Increase water via thirst and increase water reabsorption via ADH
What is the regulatory response to decrease in sodium
Osmoreceptors in the hypothalmus. Decrease water intake, and increase water excretion (absence of ADH)
What occurs with hypovolemia and sodium balance
Hypovolemia can override the hypothalmus function due to the RAAS will have thirst and increased ADH in the face of low Na
What is the difference between osmoregulation and volume reg
Osmoregulation: ratio of solutes and water
Volume regulation: determined by the absolute quantity of solutes and water
Solutes=Na
How does Isotonic Hyponatremia occur and differentials
Error with sampling such as hyperlipidemia or hypoprotienemia
How does hypertonic hyponatremia occur and differentials
increase in osmolality is due to high plasm glucose or high osmole such as mannitol. Water retained in the ECV by osmotic gradient, low Na due to dilution
How does hypovolemic hypotonic hyponatremia occur and what are ddx
Non- osmotic stimulation of ADH (Decrease volume) results in H20 rention and low NaUrine Na < 30 mEq/L: Fluid loss- GI, third space, cutaneousUrine Na > 30 mEq/L: hypoadrenocortism, loop diuretics
How does normovolemic hypotonic hyponatremia occur and what are ddx
Urine Na < 30 mEq/L: Excessive water intesion, hypotonic fluid administrationUrine Na > 30 mEq/L: SIADH, Thiazide diuretics, low T4, antidiuretic drugs
How does hypervolemic hypotonic hyponatremia occur and and what are ddx
inadequate water excretion (urine > 200 mOsm/kg) or decreased extracellular volume despite increased total body water
Urine Na < 30 mEq/L: Heart failure, liver cirrhosis, nephrotic syndrome
Urine Na > 30 mEq/L: Kidney failure
What is the Na adjustment calculation due to glucose elevation
Glu > 400 mg/dl: Na decreases by 2.4 mEq/L for every 100 ml increaseGlu <400 mg/dl: Na decreased by 1.6 mEq/L for every 100 ml increase
Why do chronic Na have less severe signs (what is the brain’
loss of K and Na followed by loss of ogranic solutes such as myonositol and amino acids. Cerebral edema due to hypo osmolality
How do you calculate the Na deficit
mEq = 0.6 x BW x (Na normal - Na patient)
How do you calculate the change in sodium for 1 liter of inf
Change Na/L infusate = ( Na infusate + K infusate - Na patient) / (0.6 x BW) + 1
In hypovolemic hyponatremic patients how do you treat
Use fluid near Pt Na ( w/in 10 mEq/L)Administer desmopression accetate if corrects quickly and need to suppress water excretion
What is osmotic demyelation syndrome
osmotic shrinkage of axons severing there connections with surrounding myelin sheathsCentral pontine and extrapontine demyelination
What are the treatment goals for correcting hyponatremia reg
Increase by < 10 mEq/L in first 24 hrsand < 18 mEq/L in first 48 hrsIf severely neuro- give bolus of 3% hypertonic 1-2 ml/kg over 20 minutes to raise 4-6 mEq/L until signs dissappear- goal is still <10 in first 24 hrs
How does hypernatremia occur
animals can not replace the water loss with water intake
Toxicity- salt ingestion
Hyperaldosterism
How does the neurologic signs of hypernatremia occur
Water moves out of brain cells down concentration gradient. Adapt: increase brain cell osmolality by increasing Na + K uptake by cells then increase in H20 in cellsIntracellular osmolytes also accumulate
How do you treat hypernatremia
Acute < 24 hrs rapidly correct in 24 hoursChronic> 48 hrs, decrease < 10 mEq/L in 24 hrs then < 18 mEq/L in first 48 hrs. Avoid excessively slow correction < 0.25 mEq/L/hr
Define SIADH
Vasopressin release in the abscence of normal osmotic or nonosmotic stimuli
What are the 7 criteria for diagnosis of SIADH
Hyponatremia w/ plasma hypoosmolarity
Inappropriate high urine osmolarlity in the prescence of plasma hypoosmolarity
Normal renal, adrenal, and thyroid function
Prescence of naturesis despite hyponatremia and plasma hypoosmolality
No evidence of hypovolemia
No ascites or edema
Correction of hyponatremia with fluid restriction
Describe the different layers of the glomerular capillary membrane and what determines the movement of molecules through it
Fenestrated endothelium - negative charge
Basement membrane - neg charge, size
Visceral epithelium podocytes - neg charge
Determined by size (< 4 nm) and favors positive charge
What are the determinants of GFR
Starling forces: Main is glomerular hydrostatic pressure
arterial pressure
afferent and efferent arteriole resistance
Explain the effects of vasoconstriction /dilation of the afferent and efferent arterioles on GFR and RBF
Afferent VC Dec RBF and GFR, VD Inc RBF and GFR
Efferent VC Dec RBF and Inc GFR, VD Inc RBF, Dec GFR
Describe how GFR can be measured
by substances that are passively filtered but not absorbed or secreted by tubules
Inulin used to be standard
Creatinine and SDMA
Explain the relationship between GFR and creatinine
Only when in steady state and logarithic, no linear realtionship
At lower amt of plasma creatinine increase greater decrease in GFR. At higher amt same increased less decrease in GFR
Explain concept of renal autoregulation and which mechanisms are implicated
The Kidneys will Maintain GFR with BP between 80-180 mmHg…. lost with GA regardless of BP
Myogenic and tubloglomerular feedback
Where and how is NA reabsorbed
PCT 65% Na/H exchanged, co transport with Glu, aa, phos, organic solutes; gradient AGII, GFR, Norepi
LOH Ascending: 20-30% NaKCl2 co trans; Flow
DCT 5%; NaCl co transport; Flow
CD 5% Na channels; Aldosterone, transport max
Where is Cl reabsorbed
PCT 55%
LOH ascending 30-40%
DCT 5%
CD 5%
Explain how urea gets reabsorbed in the kidney and which factors regulate the reabsorption
Reabsorbed in medullary CD down gradient as increases [] in PCT as water is reabsorbed.
Recycling: Secreted back in tubular lumen in ascending LOH
Total 50% reabsorbed that is filtered
Explain how and where water gets reabsorbed
PCT 65% passive
D LOH 10% Passive
CD 5-24% ADH dependent
Explain the concept of glomerulotubular balance vs. Tubuluglomerular feedback
Glomerular tubular balance: change in GFR leads to an increased oncotic pressure in capillaries which leads to increased re-absorption of solutes
Tubularglomerular feedback: Change in (Na)Cl sensed by macula densa, leads to paracrin of adenosite and PGE2 for the change in afferent and efferent arteriole size
Explain peri-tubular physical forces
Change in peritbular capillary will change tubular reabsorption by chagning the interstitum in the same way
Describe the osmolality through the tubules and the mechanism
PCT: 300 mOsm/kg, No change as solutes and H20 both reabsorbed
Dec LOH 300–> 1200 mOsm/kg, H20 reabsorbed by osmosis as tubular fluid equibilirates with surrounding interstitail fluid in medulla
ASC LOH 1200 –> 300 mOsm/kg, Impermeable to H20, Solues are reabsorped
DCT 100 mOsm/kg Max dilutaion of tubular fluid as continued solute reabsorption
CD 100-1200 mOsm Additional reabsorption of solutes however H20 is based on the presence of ADH
What are the mechanism for urine dilution
Absence of ADH
What are the renal mechanisms for urine concentration
ADH
Hyperosmotic renal medulla (via countercurrent mechanism and urea recycling)
Explain the countercurrent multipliyer
Ascend LOH pumps NaK2CL co transport out of the lumen to intestium changing gradient. The descending then works to balance by H20 leaving, while continued solute pumping.
The descending loop will increase mosm/l and will flow to ascending loop
Multiple times leads to gradient
Explain the vasa rectras role in urine concentration
Progressive equilibration as interstitium. MAINTENANCE only
Descending–> Solutes inter as water leaves
Ascending Solute leave as water enters
Medullary blood flow < 5%… if increase how you get medullary washout as not able to maintain gradient
