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RUSVM SAM II Fall 2017 > Exam 1: Nephrology/Urology & Dermatology > Flashcards

Exam 1: Nephrology/Urology & Dermatology Flashcards

1
Q

Which of the following tests on a dipstick are reliable?

Leukocytes, protein, pH, SG, blood, urobilinogen, glucose, ketones

A

Protein, pH, blood, glucose, ketones are reliable.

Ignore results from leukocytes, SG & urobilinogen

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2
Q

What is renal failure?

A

Clinical syndrome that occurs when kidneys are no longer able to maintain regulatory function, excretory function and endocrine function.

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3
Q

What percentage of nephrons must be nonfunctional before renal failure occurs?

A

75%

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4
Q

What is renal disease and how does it differ from renal failure?

A

The presence of morphological or functional lesions in one or both kidneys regardless of extent.

Renal failure relies on extent (75% nephron loss). Renal disease may or may not result in azotemia, decreased USG, etc.

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5
Q

What is uremia?

A

The constellation of clinical signs and biochemical abnormalities associated with critical loss of functional nephrons resulting in extra-renal manifestations of renal failure such as uremic gastropathy, hyperparathyroidism, etc.

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6
Q

What other abnormalities (biochemistry) may occur with uremia?

A

Azotemia, hypoalbuminemia, hypercholesterolemia, metabolic acidosis, hypocalcemia, hyperparathyroidism, hyperkalemia.

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7
Q

What is the gold standard for determination of GFR?

A

Renal scintigraphy

Usually only found in university settings

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8
Q

What are the accurate methods of determining GFR?

A

Renal scintigraphy, iohexal clearance, inulin clearance, creantinine clearance.

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9
Q

What are the indirect methods used to determine GFR?

A

Serum urea levels, serum creatinine levels, Cystatin C, SDMA

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10
Q

What extra-renal factors may influence serum [urea]?

A 
species/age
liver function (synthesized in the liver)
Dietary protein content (high protein diet = higher BUN)
Endogenous protein catabolism (same as high protein diet)
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11
Q

What are the limitations in using serum [urea] to evaluate GFR?

A 
Urea is reabsorbed in the tubules (falsely decreases GFR)
High protein diet (protein --> ammonia --> urea)
GIT bleeding (similar as high protein diet)
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12
Q

What are the limitations in used serum [creatinine] to evaluate GFR?

A

Will not show elevated values until GFR has decreased to 25%.

Dependent on muscle mass:
Implies lower GFR in heavily muscled animals - higher serum [creatinine]
Implies higher GFR in poorly muscled animals such as geriatric and/or cachexic patients - lower serum [creatinine]

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13
Q

What biochemistry changes can be seen in blood work when 40% of GFR has occurred?

A

SDMA increase

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14
Q

What is the gold standard for determining urine concentration? What’s most often used in practice and what are it’s limitations?

A

Gold standard is osmolality.

Most often used is urine specific gravity.

USG is influenced by the number and size of particles (e.g. glucosuria falsely increases concentration)

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15
Q

What are the ranges for minimally concentrated USG?

A

1.013-1.030

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16
Q

What are the ranges for inadequately concentrated urine?

A

1.013<1.022

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17
Q

Reference range for normal USG in dogs?

A

> 1.030

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18
Q

Reference range for normal USG in cats?

A

> 1.035

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19
Q

What are the ddx’s for hyposthenuric urine?

A

Diabetes insipidus, psychogenic polydypsia

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20
Q

When performing a water deprivation test, at what point would you expect maximal stimulation of ADH release?

A

after 5% loss of body weight

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21
Q

What is fractional excretion and how is it used when evaluating kidney function?

A

Fractional excretion measures electrolytes in the urine compared with creatinine to evaluate for renal tubular dysfunction.

If the kidneys are functioning properly, there shouldn’t be >1% Na+ lost in the urine. If the FE <1%, there may be prerenal disease present.

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22
Q

What changes occur as urine sits at room temperature before the sediment is run?

A

Growth of crystals

Disintegration of casts and cells

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23
Q

What may cause a false positive on a urine protein creatinine ratio and how might you avoid this false positive?

A

Lower urinary tract disease

Run a sediment to r/o UTI prior to UPC.

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24
Q

Urine sample is red. What could cause that? How would you determine which is the culprit?

A

Red discoloration in the urine may be caused by RBCs, hemoglobin or myoglobin.

Centrifuge the sample: if a red pellet forms at the bottom, RBCs were the cause.
If the supernatant is still discolored red: look at the patient’s centrifuged blood sample. Myoglobin doesn’t accumulate in the blood stream so if the serum/plasma is discolored, it’s hemoglobin. Alternatively, run a CK: muscle damage = myoglobin

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25
Q

Hematuria is

A

presence of intact RBCs in the urine

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26
Q

Pseudohematuria is

A

Reddish or brownish color without the presence of intact RBCs (hemoglobin, myoglobin, chemicals)

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27
Q

What is the normal urine output for dogs and cats?

A

1 mL/kg/hr

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28
Q

Renal Carcinoma:

More common in: dogs or cats?

Unilateral or bilateral?

Early clinical signs?

Paraneoplastic syndrome?

A

Occurs dogs > cats

Unilateral > Bilateral

Very few early c/s’s (d/t reserve capacity - healthy kidney picks up the slack)

Paraneoplastic syndrome results from disruptions in normal endocrine function of the affected kidney: polycythemia (from EPO and/or renal hypoxia), hypertrophic osteopathy (abnormal Ca+/Phos- metabolism). May also cause neurological signs.

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29
Q

What’s the treatment and prognosis for renal carcinoma?

A

Nephrectomy (after ensuring the remaining kidney is functioning adequately).

Mean survival time after tx = 16 months (dogs)

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30
Q

What diagnostics can be performed if renal neoplasia is suspected?

A

Ultrasound & U/S-guided FNA

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31
Q

Renal lymphoma:

More common in dog or cat?

Unilateral or bilateral?

Clinical presentation?

A

Cats > dogs

Bilateral > unilateral

Presents with: renomegaly, weight loss, inappetance, PU/PD, renal azotemia. Often systemic at the time of diagnosis so there may be other signs of lymphoma such as mediastinal mass, neuro signs from mets, and lymphadenopathy).

Has a tendency to spread to the CNS

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32
Q

Treatment and prognosis of renal lymphoma?

A

Multi-agent chemotherapy

~60% go into complete remission (cats)
MST = 91 days with treatment

If azotemia doesn’t improve with chemotherapy = poorer prognosis b/c indicative of larger portion of those kidneys have been destroyed.

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33
Q

What are the DDx’s for renomegaly?

A

Neoplasia: carcinoma vs. lymphoma vs. sarcoma vs. nephroblastoma vs. metastatic mass (e.g. hemangiosarcoma)

Renal inflammation: acute nephrosis, acute pyelonephritis, FIP, leptospirosis

Amyloidosis

Hydronephrosis

Polycystic kidney disease

Portosystemic shunts

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34
Q

Polycystic kidney disease.

More common in ___.

Results in ___.

Caused by ___.

A

More common in cats > dogs.

Results in renal failure from pressure necrosis of nephrons.

Caused by an autosomal dominant defect in PKD-1 gene in persian cats OR an inherited condition > in Bull terriers, cairn terriers and Westies.

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35
Q

DDx’s for renal pain.

A

Pyelonephritis, renal calculi, acute nephrosis, hydronephrosis (early), renal trauma, abscesses, neoplasia (rare)

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36
Q

What are pre-renal causes of AKI?

A

Hypoperfusion to the kidneys: cardiac disease, hypovolemia, hypotension, PGE inhibition (from NSAIDs).

Hypoxia

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37
Q

In what way can post-renal causes of acute renal injury result in diabetes insipidus?

A

Pressure on the collecting tubules will damage the aquaporin channels resulting in nephrogenic DI.

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38
Q

What are the four phases of acute renal failure and what distinguishes them?

A

Initial phase - Usually an ischemic event triggers it. No clinical signs, decreased urine output or increase in creat.

Extension Phase - continued hypoxia and inflammation. Na:K pumps become damaged which results in cellular swelling, Ca accumulates in the cells which eventually leads to tubular cell death.

Maintenance phase - damage is done, you’re now waiting to see if it will improve.

Recovery phase - PU and extreme Na+ loss. takes weeks to months to recover.

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39
Q

What’s the significance of reduced central venous pressure?

A

Indicative of hypovolemia. CV system is pulling as much blood from the veins as possible.

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40
Q

In what way are calcium channel blockers renoprotective?

A

They prevent the intracellular hypercalcemia which results in cell death.

E.g. Amlodipine

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41
Q

In what way are (selective) Dopamine-2 agonists renoprotective?

A

They cause vasodilation.

Be mindful of dose - there are dose-dependent effects

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42
Q

In what way are (selective) Dopamine-1 agonists renoprotective?

A

They prevent vasoconstriction.

E.g. Fenoldopam

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43
Q

In what way are EPO analogs renoprotective?

A

They increase [RBC] which increases O2 delivery to tissues (including kidneys)

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44
Q

What systolic BP should be maintained to ensure adequate perfusion to the kidneys?

A

> /= 80 mm Hg

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45
Q

What parameters can be monitored to evaluate renal perfusion?

A

BP, central venous pressure, PCV/SpO2/PaO2 (hypoxic?), ECG (hyperkalemia-induced bradyarrhythmias)

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46
Q

How can acute kidney injury and acute renal failure be diagnosed?

A

Reduced urine output

Renal tubular epithelial cell casts in urine sediment.

Azotemia

Fractional Excretion >1% Na+.

Renal tubular biomarkers relative to creatinine (GGT: creat, NAG: creat). These biomarkers enter the filtrate through areas of the nephron where RTE cells have died; they do not enter through the glomerulus.

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47
Q

Shock fluid dose for a dog: ___.

A

60-90 mL/kg/hr

administer in 25% of shock dose every 15 minutes and reassess hydration before administering another dose.

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48
Q

Shock fluid dose for a cat: ___.

A

45 mL/kg/hr

administer in 25% of shock dose every 15 minutes and reassess hydration before administering another dose.

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49
Q

How do you determine fluid dose to correct patient dehydration?

A

% Dehydration * BW (kg) = Fluid dose (L).

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50
Q

What needs to be factored in when choosing a maintenance fluid rate? What about if the patient is dehydrated?

A

Insensible losses (respiration and sweating) = 22 mL/kg/day

Sensible losses (urine output) = (usually) 44 mL/kg/day monitor your patient’s urine output to determine

Ongoing losses (vomiting, diarrhea, etc - estimate)

Dehydrated patient rate = {% dehydration * BW (kg)} = L to be administered over the course of 6-12 hours

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51
Q

What is oliguria?

A

Reduce urine output (<0.5 mL/kg/hr)

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52
Q

What treatments for oliguric patients are supported by evidence based medicine?

A

NONE

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53
Q

What treatments can be used for oliguric patients?

A

Fluid therapy!! Mannitol, furosemide, dopamine, calcium channel blockers

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54
Q

How does that administration of mannitol aid in the treatment of ARF? When would it be contraindicated?

A

Osmotic diuretic = increases circulatory volume which flushes tubules., decreases cell swelling and cellular aggregation, scavenges free radicals, blunts the influx of calcium intracellularly.

This treatment is contraindicated in patients that are anuric and/or dehydrated.

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55
Q

How does that administration of furosemide aid in the treatment of ARF? When would it be contraindicated?

A

Loop diuretic - it decreases the Na-K ATPase pump which reduces the oxygen requirements.

It increases urine production without increasing GFR

Contraindicated in dehydration, lethargy, tachycardia, ototoxicity.

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56
Q

What is used in the treatment of ethylene glycol toxicosis?

A

4-methylpyrazole > ethanol

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57
Q

What is used in the treatment of NSAID toxicosis?

A

Misoprostal (PGE-analog)

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58
Q

What is used in the treatment of leptospirosis?

A

Penicillin in the beginning; doxycycline once the animal is producing adequate amounts of urine; amlodipine (calcium-channel blocker) causes pre-glomerular vasodilation and prevents Ca from moving intracellularly

59
Q

What’s used in the treatment of pyelonephritis?

A

Antibiotics based on C&S results.

Fluoroquinolones vs. TMS 4-6 weeks.

60
Q

What is used in the treatment of aminoglycoside toxicity?

A

Ticarcillin IV - it binds with gentamicin

61
Q

What is used in the treatment of TMS toxicity?

A

Urinary alkalinization

62
Q

What is used in the treatment of hyperkalemia?

A

Insulin or dextrose (drives K+ into the cells)

Calcium gluconate (cardioprotective to help prevent hyperkalemia associated bradyarrhythmias)

Bicarbonate in cases of metabolic acidosis (H+ is exchanged for K+ in cells)

63
Q

What is used in the treatment of hypertension in ARF patients?

A

Amlodipine (calcium channel blocker) and hydralazine (arterial vasodilator).

**ACE inhibitors should be avoided in these patients d/t their arterial vasoconstrictive effects*

64
Q

What changes in abdominal palpation would you expect in acute renal disease vs. chronic renal failure?

A

In acute disease, the kidneys feel enlarged d/t cell swelling.

In chronic disease, nephrons die and are replaced by fibrosis leaving kidneys smaller than normal.

65
Q

What are the causes of CKD?

A

Degenerative: chronic interstitial nephritis, renal infarcts.

Developmental: familial renal dysplasia, polycystic kidney disease

Auto-immune

Metabolic: hypercalcemia

Neoplasia: renal carcinoma, renal lymphoma, mets

Infectious: pyelonephritis, Borreliosis, Leptospirosis.
Iatrogenic: Vitamin D supplementation, nephrotoxic drugs
Idiopathic
Immune-mediated: immune-complex mediated glomerulonephritis

66
Q

Why is CKD progressive?

A

Once CKD develops secondary processes are activated that contribute to renal damage: systemic and glomerular hypertension, mineral imbalances, proteinuria, renal fibrosis.

67
Q

What GI signs are associated with chronic renal disease and what is the pathophysiology behind them?

A

Vomiting: uremic toxins accumulate and stimulate the chemoreceptor zone triggering vomiting.

Uremic gastritis: excessive acid production in the stomach d/t reduced rate of excretion of gastrin (stimulates acid production).

Melena: result from uremic gastritis.

68
Q

Pathophysiology of hyperphosphatemia in CKD. Why is hyperphosphatemia an issue?

A

Phosphate enters via the diet and is excreted via the kidneys. Reduced excretion = accumulation.

Hyperphosphatemia stimulates renal secondary hyperparathyroidism: high phos = release of PTH = dissolution of Ca+ from bones and increased absorption of Ca+ from diet.

69
Q

Why does anemia occur in CKD?

A

EPO deficiency

Reduced lifespan of RBCs d/t increased waste products in the blood.

PTH (from renal secondary hyperparathyroidism) suppresses bone marrow

Anemia of chronic disease

GI hemorrhage (uremic gastritis)

70
Q

What treatments can be used in the case of proteinuria? Why bother treating proteinuria?

A

ACE inhibitors (benazapril): cause efferent arteriolar vasodilation which decreases pressure in the glomerulus and results in less protein loss via the urine.

The prevention of proteinuria is renoprotective

71
Q

What parameters must be evaluated when CKD is suspected?

A

Creatinine, proteinuria, BP

These, together, will allow for staging and prognosis.

72
Q

What treatments can be used to combat anorexia in CKD patients?

A

Cyproheptidine (cats only)

Mirtazapine (dogs and cats)

Esophagostomy tube

73
Q

What treatments can be used in hyperphosphatemic patients with CKD?

A

IV fluids

Restrict phos intake (low phos diet)

Intestinal phosphate binders (aluminum hydroxide, calcium carbonate)

74
Q

What are some of the qualities of commercial renal diets that make them a good choice for CKD patients?

A

Phosphate restricted

Sodium restricted

High energy (many are anorexic and have a hard time taking in adequate nutrients which puts them into a catabolic state and leads to poor body condition)

Increased soluble fiber (decreases fecal transit time so gut flora have less time to ferment the feces and form ammonia).

Increased B vitamins

Neutralizing effect on acid-base balance (most patients suffer metabolic acidosis in later stages)

Omega-3 supplemented (reduces inflammation)

75
Q

At which IRIS stage should CKD patients be switched to renal diets?

A

Cats - IRIS stage 2

Dogs - IRIS stage 3

Other indications that may merit starting these diets earlier are hyperphosphatemic patients

76
Q

At what point is EPO therapy warranted in CKD patients?

A

When PCV < 20%

77
Q

What treatment is used in treating hypertension in dogs? Cat?

A

Benazepril (ACE-inhibitor) is the first choice treatment in dogs.

Amlodipine (calcium channel blockers) are the first choice in cats

If one doesn’t work on it’s own, add the other one.

78
Q

What benefits do ACE inhibitors offer patients with CKD?

A

Mild anti-hypertensive effect.

Reduces proteinuria

79
Q

What is Telmisartan and what is it used for?

A

Angiotensin receptor blocker.

Used to reduce proteinuria associated with CKD in cats.

80
Q

Which parameters are important for long-term monitoring of patients with CKD?

A

BUN/Creat/Phos

UPC

PCV

Electrolytes

PCV

Systolic BP

Ophthalmic exam

Kidney palpation

81
Q

What are the hallmarks of CKD?

A

azotemia and inappropriately dilute urine

82
Q

What are physiological causes of proteinuria?

A

strenuous exercise, seizures, fever, stress

83
Q

What are pre-renal causes of proteinuria?

A

Abnormal concentrations of proteins being presented to the kidneys (such as in multiple myeloma - bence jones proteins)

84
Q

What are the renal causes of proteinuria?

A

Defective renal function or inflammation of renal tissue (glomerular or tubular)

85
Q

What are the post-renal causes of proteinuria?

A

inflammation in the lower urinary tract (ureter, bladder, urethra) or prostate.

86
Q

Under what circumstances might you get a false positive result for proteinuria on a dipstick? False negative?

A

False positives: alkaline urine and contamination of the sample

False negative: acidic urine and Bence Jones proteins (too small for dipstick to detect.

87
Q

What is the relationship between proteinuria found on a dipstick and USG?

A

The more dilute the urine, the more likely the dipstick is accurate.

88
Q

What does the exact UPC result tell you with regards to proteinuria?

A

Lower UPC is usually d/t tubular disease (caused by the RTE inability to reabsorb proteins from the filtrate).

High UPC (>2) is usually d/t glomerular disease (caused by increased glomerular permeability)

89
Q

What is glomerulonephritis and what are its potential causes?

A

Groups of conditions where immune-complexes are deposited in the glomeruli.

Caused by chronic antigenic stimulation & idiopathic.

90
Q

Amyloidosis occurs most often in ____.

A

Shar-pei, Beagle, Abyssinian & Siamese

91
Q

What is nephrotic syndrome and what are its features?

A

Kidneys disease characterized by edema and loss of protein from the plasma into the urine due to increased glomerular permeability.

Abdominal and pleural effusion, SQ pitting edema, acute onset blindness (hypertensive retinopathy), thromboembolic disease (from hypercoagulable state), proteinuria, hypoalbuminemia, hypercholesterolemia

92
Q

In what circumstances would a kidney biopsy be contraindicated?

A

Presence of coagulopathies

IRIS stage 4 (results won’t change the tx or tx goals)

93
Q

What tests should be performed from a renal biopsy sample in order to provide an accurate diagnosis?

A

Light microscopy, electron microscopy, immunofluorescent antibody staining

94
Q

In cases where proteinuria has been confirmed to originate from a glomerulonephropathy and the owner does not want to pursue renal biopsy, what treatment course can you try?

A

Immunosuppressive therapy 8-12 week trial

Mycophenolate mofetil first choice

Other options include: cyclosporin, chlorambucin, azathioprine, cyclophosphamide.

Glucocorticoids can also be used, but have a much higher likelihood of long-term adverse effects.

95
Q

What treatments can be used in protein-losing nephropathy to address proteinuria?

A

ACE inhibitors, Renal diets

96
Q

How to ACE inhibitors decrease proteinuria? Exam question likely

A
  • Decreases efferent glomerular arteriolar resistance
  • Reduces loss of glomerular heparan sulphate
  • Decreases the size of glomerular endothelial pores
  • Improves lipoprotein metabolis
  • Slows mesangial cell growth and proliferation
  • Inhibits bradykinin degradation (bradykinin is an inflammatory mediator that causes vasodilation)
97
Q

How can hypercoagulability be addressed in patients with PLN?

A

Aspirin (low doses) or Clopidogrel (“Plavix”)

98
Q

When is draining effusions and/or treating patients with diuretics indicated in patients with PLN?

A

ONLY if they’re having trouble breathing.

99
Q

What is the most significant cause of renal disease and acute uremia in cats?

A

ureteral obstruction

100
Q

What is the clinical presentation of acute unilateral ureteral obstruction?

A

Often clinically silent. May see abdominal pain, erratic or elusive behavior, hematuria.

101
Q

What is the clinical presentation of acute bilateral ureteral obstruction?

A

Bilaterally enlarged & painful kidneys, severe & progressive azotemia, oliguria or anuria

102
Q

What is “Big Kidney-Little Kidney” Syndome?

A

Occurs when there is a ureteral obstruction in a cat with a previous unilateral ureteral obstruction on the contralateral side. Obstructed kidney is enlarged and painful, the contralateral kidney is small/fibrotic/irregularly shaped. Patient will have progressive & severe azotemia and variable urine production.

103
Q

Bilateral chronic kidney disease with concomitant ureteral obstruction prognosis?

A

Most guarded of all ureteral obstruction scenarios because the patient’s capacity to recover is already severely compromised by kidney disease.

104
Q

What can be used to diagnose ureteral obstruction?

A

Radiography (low sensitivity, best for radiodense stones like calcium oxalates)

Ultrasound - hydronephrosis and dilatation of the proximal ureter

Antegrade pyelography - contrast media injected into the renal pelvis

CT with contrast

105
Q

What is used in the medical management of ureteral obstruction?

A

Mannitol (if oliguric), prazosin and amitryptilline (ureteral relaxants), pain management.

106
Q

What’s the standard of care treatment for ureteral obstruction?

A

Ureteral stent

  • Retrograde placement in dogs
  • Antegrade placement in cats
107
Q

What treatment options are there if the owner is unable to afford hospitalization of their cat with a urethral obstruction?

A

Therapeutic cystocentesis, no indwelling catheter and administer anti-spasmotics (prazosin / phenoxybenzamine). Low stress environment!

108
Q

In what circumstances would the placement of a urethral stent be appropriate?

A

Urethral tumor or stricture

109
Q

What are potential consequences of urethral rupture?

A

Stricture

Urethrocutaneous fistula

110
Q

What are the parts of the lower urinary tract?

A

bladder, urethra, prostate

111
Q

What is the treatment for an uncomplicated urinary tract infection?

A

Amoxicillin, cephalosporins or TMS x 10-14 days.

+/- culture

112
Q

Reinfection (definition)

A

You find a new bacteria in culture performed 7 days after the last treatment of antimicrobials

113
Q

Superinfection

A

You find a new bacteria in culture performed 7 days after starting antimicrobials

114
Q

Relapse

A

You find the same organism 7 days after you dicontinue treatment

115
Q

What are possible reasons for relapse UTI’s to occur?

A

Inappropriate drug, dose, frequency, duration.

Pyelonephritis

Nidus of infection

116
Q

What’s a persistent urachus and what are it’s implications with regard to patient health?

A

Urachus is the remnant of the connection between the umbilical vein and the bladder. If it does not regress as it is supposed to after birth, it serves as a nidus for infection because it’s not regularly emptied like the rest of the bladder contents.

117
Q

What is the approach for recurrent UTIs?

A

Culture and sensitivity (required) - ideally before tx, 7 days into tx and 7 days after last tx.

Determine the cause if possible - imaging, underlying diseases?

Antimicrobials should be continued for 4-6 weeks - ensure compliance

Prophylactic therapy (last resort)

118
Q

What is prophylactic therapy used for recurrent UTI patients?

A

(After infection has been erradicated)

Choose a drug that concentrates in the urinary tract. Administer 3-50% the original dose and administer it at night.

Patient will require regular (q 30 days) culture and sensitivity while on tx.

119
Q

What are the most common types of urinary crystals?

A

Calcium oxalates

120
Q

Crystalluria always results in urolithiasis. (T/F)

A

False - crystalluria does not mean urine has been supersaturated

121
Q

Describe urohydropulsion

A

Using the urinary tract to expel uroliths from the bladder. This is accomplished by placing a urinary cathether, filling the bladder and propping the patient up (so that stones may settle in the area of the urethral opening. Then, while compressing the bladder, the catheter is removed and stones are (hopefully) expelled with the urine. THIS CAN ONLY BE DONE WITH FEMALE DOGS

122
Q

Describe lithotripsy

A

A procedure in which sound waves are used to break up uroliths small enough that they may be expelled with the urine. This can be accomplished via endoscopy or via extracorporal techniques.

123
Q

What breeds are predisposed to developing struvite / magnesium ammonium phosphate hexahydrate crystals?

A

Miniature schnauzers, lhasa apso, shih tzu, cocker spaniels and bichon frise

124
Q

What is the relationship between struvite uroliths and UTIs?

A

If the UTI is caused by a urease-producing bacteria, the ammonia content in the urine increases which increases the likelihood of the urine becoming supersaturated and thus crystal formation.

125
Q

Struvite uroliths usually form in ___ pH.

A

Alkaline

126
Q

What are the characteristics of struvite uroliths?

A

big, smooth, radiodense (but less so than CaOx)

127
Q

Struvite, AKA: ___.

A

Magnesium ammonium phosphate hexahydrate

128
Q

What is the treatment of choice for struvite uroliths?

A

Diet change to acidify the urine to dissolve the stones. This can be done with Hills S/D x 3 months. After the stones are dissolved, the patient should be switched to Hills C/D or Royal Canin S/O for maintenance to prevent reformation.

129
Q

Which breeds are predisposed to developing calcium oxalate uroliths?

A

Miniature schnauzer, lhasa apso, shih tzu, mini poodle, yorkshire terrier, bichon frise

130
Q

Calcium oxalate uroliths form in ____.

A

Acidic urine

131
Q

How might hyperparathyroidism result in the formation of calcium oxalate stones?

A

HyperPTH = hypercalcemia = hypercaliciuria

Any condition that results in an increase in serum calcium has the added risk of developing calcium oxalate stones

132
Q

What are the characteristics of calcium oxalate stones?

A

Spiny, rarely cause obstruction, very radiodense.

133
Q

What is the treatment of choice for calcium oxalate stones?

A

Removal: surgical v. lithotripsy v. cystoscopy

these stones cannot be dissolved with diet changes

134
Q

What are some long term therapies that can be implemented to prevent the reformation of calcium oxalate uroliths?

A

Diet changes: Hills U/D (has potassium citrate)

Increase water consumption (canned food vs. soaked dry food)

Thiazide diuretics - flush water through

Potassium citrate

Avoid vitamin C (will acidify urine) and vitamin D (will increase calciuria)

135
Q

What breeds are predisposed to ammonium urate & xanthine uroliths?

A

Dalmations, bulldogs, Black russian terriers

136
Q

What type of crystal is commonly found in patients with porto-systemic shunts?

A

Ammonium urate

137
Q

How are ammonium urate uroliths diagnosed?

A

ultrasound - they are radiolucent and cannot be seen on radiographs

138
Q

What are the potential treatments for urate uroliths?

A

Dietary dissolution: U/D (low purine content), alkalinize urine (potassium citrate, sodium bicarb)

Xanthine oxidate inhibitors - Dalmations only d/t genetic cause decrease uric acid production

139
Q

What breeds are predisposed to developing cystine uroliths?

A

Cattle dogs, Dachshunds, Newfoundlands, Bulldogs

140
Q

What’s the pathophysiology behind the formation of cystine uroliths?

A

Tubular carrier protein that usually reabsorbs cystine from the filtrate in the renal tubules is defective.

141
Q

Describe the innervation of the bladder and urethra with regards to urine storage and release.

A

Pudendal n - supplies acetylcholilne to the external urethra sphincter (conscious control of voiding)

Pelvic n - parasympathetic innervation. Releases acetylcholine to contract the detrusor muscle during micturition.

Hypogastric n - sympathetic innervation. Norepinephrine is released to relax the detrusor muscle (storing urine) and contract the internal urethral sphincter (storing urine)

142
Q

How is feline lower urinary tract disease diagnosed?

A

Diagnosis of exclusion:

Imaging (rads and U/S) to r/o urolithiasis, urinalysis and culture, cystoscopy

143
Q

How is feline interstitial cystitis diagnosed?

A

Cystoscopy (gold standard)

144
Q

What is the treatment for FLUTD?

A

Environment - reduce stress, litter boxes, water sources, activity/playing

Diet: canned > dry

Pheromones

Analgesics (opioids)

RUSVM SAM II Fall 2017 (1 decks)

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