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Board Review 2020 > Renal phys.pathophys.disease > Flashcards

Renal phys.pathophys.disease Flashcards

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1
Q

What is SDMA

A

Symmetric dimethylarginine
byproduct of cellular protien metabolism that is released in to circulation >90% renal excreted
No renal secretion/reabsorbtion

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2
Q

Why might SDMA be better than creatinine for a maker of GFR

A

Less effected by age, sex, breed and lean body mass.

Less interindividual variability

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3
Q

What is the agent in Lyme disease

A

Borrelia burgdorferi – gram negative spirochete

Ixodes transmission

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4
Q

How does lyme disease result in PLN

A

Immune mediate glomerular nephritis with antigen antibody complex

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5
Q

How to tx Lyme nephritis

A

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

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6
Q

What stimulates parathyroid hormone to be released

A

released by decreased plasma Ca levles

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7
Q

Where does parathyroid hormone act

A

Bone: Break down and release of phos and Ca
Kidney: activates calcitriol
Nephron: DCT to reabsorb Ca blocks reabsorb of Phos

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8
Q

Where is calcitriol made

A

Skin (cholecalciferol) –> Liver (calcidiol) –>Kidneys

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9
Q

Where does calcitriol act

A

Bone: release of Ca
Parathyroid: Neg feedback
GIT: increase Ca and Phos absorbpiton
Neprhon: PCT reabsorption of Ca

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10
Q

What is calcitonin and what does it do

A

Released for thyroid gland in response to increase in Ca.

Works in the same way as PTH to block Ca release

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11
Q

How does high phosphoruls levels occur in CKD

A

High phos block calcitriol
Less functional nephrones so less phos is excreted
Trade off hypothesis

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12
Q

What is the pathophys of uroabdomen

A

Hyperosmolar potassium rich urine accumulates

osmotic pull of extracellular fluid to peritoneal due to concentration gradient of Na and Cl

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13
Q

Does palpation of the bladder rule out uroabdomen

A

No

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14
Q

What is the diagnostic criteria for creatinine and K for ab fluid: Peripheral

A

Dogs: Crea > 2:1 K > 1.4: 1
Cats: Crea > 2:1 K > 1.9:1

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15
Q

What is the urethral healing time versus cystotomy healing time

A

Urethra 3-21 days

Bladder can seal at 45 hrs

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16
Q

Define oliguria, anuria

A

Realtive Oliguria < 2 ml/kg/day for renal disease
Absolute Oliguria < 1 ml/kg/day
Anuria 0-0.5 ml/kg/day

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17
Q

What is UOP a function of

A

GFR
Tubular solute reabsorption
Tubular solute excretion

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18
Q

What are the causes of oligioanruia

A

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

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19
Q

How does mannitol work for oligioanuria

A

Osmotic diuretic: may also serve as free radical scavenger and flush debris
Only use in normovolemic patients to avoid pulmonary edema

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20
Q

How does furosemide work for oligioanuria

A

NaK2Cl transporter in the LOH; Decreased renal O2 consumption; less ischemic damage
Concentration within tubular filtrate determines effect why with anuria may not work

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21
Q

How does fenoldopam work for oligioanuria

A

Post synaptic dopamine receptor agonist
More renal vasodilationa nd naturesis than dopamine
Can lead to systemic hypotension and decrease SVR

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22
Q

Define azotemia

A

Increase in concentration of nitrogen containing substances in the blood Bun or Creatinine
Markers for other uremic toxins that build up

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23
Q

Define AKI

A

An increase in creatinine by >/= 0.3 mg/dl from baseline regardless of creatinine (normal range). Severe AKI- abrupt loss of GFR

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24
Q

What are the Iris grades for AKI

A

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

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25
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
26
What are some characteristics of pre-renal azotemia
Higher BUN: Crea ratio > 20:1 | Higher concentration of urine (USG)
27
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
28
What are the consequences of lost of compensation to the nephron
hypertension Edema hyperphosphatemia metabolic acidosis Gradual increase in uremic solutes
29
List two electrolyte abnormalities seen in endstage CKD
low iCa Increased K+ Hyperphos- worse outcome in cats the higher it is
30
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
31
Why may some cats have concentrated urine despite CKD
Glomerular disease termd glomerulotubular imbalance
32
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
33
List 7 medications that may need to be dose adjusted due to
Amakacin, penicillins, cephalsporins, enrofloxacin, gentamicin, TMS, tobramycin
34
In the osmolality calculation what is the ineffective osmole
Urea (BUN)- high membrane permeability therefore does not alter water distribution.
35
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
36
What is the regulatory response to decrease in sodium
Osmoreceptors in the hypothalmus. Decrease water intake, and increase water excretion (absence of ADH)
37
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
38
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
39
How does Isotonic Hyponatremia occur and differentials
Error with sampling such as hyperlipidemia or hypoprotienemia
40
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
41
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
42
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
43
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
44
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
45
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
46
How do you calculate the Na deficit
mEq = 0.6 x BW x (Na normal - Na patient)
47
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
48
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
49
What is osmotic demyelation syndrome
osmotic shrinkage of axons severing there connections with surrounding myelin sheathsCentral pontine and extrapontine demyelination
50
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
51
How does hypernatremia occur
animals can not replace the water loss with water intake Toxicity- salt ingestion Hyperaldosterism
52
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
53
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
54
Define SIADH
Vasopressin release in the abscence of normal osmotic or nonosmotic stimuli
55
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
56
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
57
What are the determinants of GFR
Starling forces: Main is glomerular hydrostatic pressure arterial pressure afferent and efferent arteriole resistance
58
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
59
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
60
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
61
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
62
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
63
Where is Cl reabsorbed
PCT 55% LOH ascending 30-40% DCT 5% CD 5%
64
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
65
Explain how and where water gets reabsorbed
PCT 65% passive D LOH 10% Passive CD 5-24% ADH dependent
66
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
67
Explain peri-tubular physical forces
Change in peritbular capillary will change tubular reabsorption by chagning the interstitum in the same way
68
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
69
What are the mechanism for urine dilution
Absence of ADH
70
What are the renal mechanisms for urine concentration
ADH | Hyperosmotic renal medulla (via countercurrent mechanism and urea recycling)
71
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
72
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

Board Review 2020 (37 decks)

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