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4th Year Exams > Urinary > Flashcards

Urinary Flashcards

1
Q

Filling of the bladder is under the control of the ______ nervous system. With the ______ nerve going to ______ the detrusor muscles and ______ the internal urethral sphincter.

A 
sympathetic
hypogastric
relax
constrict
**with help from the pudendal nerve and the external urethral sphincter
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2
Q

Two nerves function as part of the parasympathetic nervous system to allow urination, what are they and what is the function on the bladder?

A

Pelvic contracts bladder wall

Pudendal relaxes external urethral sphincter

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3
Q

Why does polyuria occur with CKD?

A
  1. solute diuresis- all the solutes are presented to the remaining healthy nephrons, they can compensate but eventually overwhelmed
  2. loss of medullary hypertonicity- solutes eventually flood those nephrons and have very high flow rate–>less opportunity to reabsorb solutes–>lack of medullary hypertonicity AND less responsive to ADH
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4
Q

Why does azotemia occur?

A

Anything causing decreased GFR

Pre-renal, renal, or post-renal

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5
Q

What’s the difference between azotemia and uremia?

A

Uremia is when azotemia leads to clinical signs

ex. anorexia, vomiting, diarrhea, ulcerative stomatitis

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6
Q

Which 2 things if present in urine will overestimate USG?

A

Glucose and protein

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7
Q

After bladder rupture, what 4 things will you find on bloodwork?

A

azotemia, hyperphosphatemia, hyperkalemia, hyponatremia

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8
Q

True or false- CKD causes hypokalemia

A

True- but may be masked if concurrent acidosis, which is common in late stage CKD

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9
Q

True or false- AKI causes hypokalemia

A

False- causes hyperkalemia from drop in GFR

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10
Q

Which two pancreatic enzymes may be increased in the blood due to decreased GFR?

A

Amylase and lipase- not very reliable but if present don’t assume pancreatic cause
Amylase <3x URL
Lipase <4x URL

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11
Q

Anemia of renal disease is due to decreased erythropoietin production. What classification of anemia will this be?

A

Non-regenerative

Normocytic, normochromic

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12
Q

Which system in the kidneys is affected by NSAIDs?

A

RAAS

Signal to afferent arteriole is dependent on COX products

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13
Q

If fluid flow through the renal tubules is TOO HIGH, the Macula densa sends a signal to _______ the ______ arteriole, reducing pressure in the Bowman’s capsule.
What about TOO LOW?

A

constrict
afferent
if too low- constricts EFFERENT

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14
Q

True or false- renin is an important enzyme in the RAAS system and is secreted by the afferent arterioles of the kidneys

A

TRUE you’re a genius

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15
Q

What is produced at the end of the RAAS pathway and what is its function?

A

Angiotensin II
preferentially constricts efferent arteriole
Na and water retention by aldosterone and ADH
*all in response to low BP, prostaglandins and NO, or sympathetic stimulation

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16
Q

What is the importance of prostaglandin (PGE2 and PGI2) and NO in relation to the kidneys?

A

Protect afferent arterioles from vasoconstriction by Angiotensin II

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17
Q

What can cause nephrocalcinosis?

A

secondary renal hyperparathyroidism
primary hyperparathyroidism
Vitamin D intoxication
hypercalcemia of malignancy (paraneoplastic syndrome)

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18
Q

What is familial renal disease?

A

aka progressive juvenile nephropathy

animal has shrunken and irregular kidneys within a few months of life

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19
Q

Which pathogen causes pulpy kidney in ruminants?

A

Clostridium perfringens toxin- causes acute tubular necrosis

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20
Q

Which canine disease causes lymphocytic interstitial nephritis?

A

infectious canine hepatitis (adenovirus)

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21
Q

How do you assess size of kidneys in radiographs?

A

Use length of L2 vertebrae and see how many times fits into length of kidney
Dog 2.5-3.5x
Cat 1.9-2.6x (bigger in tom cat)

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22
Q

True or false- you should always be able to visualize ureters on radiographs

A

False- you normally can’t see them but should follow path with your eyes checking for any abnormalities

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23
Q

With any newly documented azotemia, what are the first questions you should ask?

A

Acute or chronic?

Pre-renal, renal, or post-renal?

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24
Q

What would you expect USG to be in a dog with pre-renal azotemia? What about a cat?

A

If pre-renal azotemia, should find very concentrated urine:
>1.030 in dog
>1.035 in cat
*alternatively, if low USG and think renal instead, make sure this was done before IVFT and no concurrent reason for lack of urine concentrating ability

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25
Q

Name two things that cause AKI as a result of interstitial nephritis

A

Pyelonephritis and Leptospirosis

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26
Q

What are some causes of CKD in a cat?

A

Lymphoma, FIP, polycystic kidney disease, amyloidosis, primary glomerular disease, pyelonephritis, toxins, recovery from AKI, obstructive uropathy, chronic tubulointerstitial nephritis (most common)

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27
Q

What are some causes of CKD in a dog?

A

Tubulointerstitial nephritis, primary glomerular disease, familial disease syndromes, also pyelonephritis and recovery from AKI

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28
Q

What is another name for mineral bone disorder?

A

Secondary renal hyperparathyroidism

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29
Q

Dietary management of CKD is very important and has low levels of which important mineral?

A

Phosphate

also reduce protein and important to maintain adequate calories- have to change if they won’t eat the renal diet

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30
Q

What is one food type a CKD patient should not have?

A

home cooked food especially anything with dairy (really high in phosphate)

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31
Q

What is autoregulation in reference to kidneys and why is it important in CKD?

A

Kidney keeps pressure through glomerular capillaries stable over a wide range of systemic BP
This ability to auto regulate is reduced with CKD so nephrons are exposed to high pressures and can damage, exacerbated by systemic hypertension

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32
Q

What is the most important prognostic indicator of CKD?

A

Proteinuria

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33
Q

Angiotensin II has a preferential effect on one type of the arterioles of the kidney. Which one and how does this relate to ACE inhibitors or angiotensin receptor blockers?

A

EFFERENT- these drugs will therefore have more effect on the efferent arteriole (relaxing it and reducing glomerular pressure)

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34
Q

What is a contraindication of using ACEinhibitors or angiotensin receptor blockers in CKD?

A

Cannot use if patient with severe azotemia as can cause AKI- only use these if patient has controlled, mild disease

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35
Q

What are some factors contributing to morbidity of CKD?

A

UTIs, anemia, dehydration (including constipation), hypokalemia, acidosis, systemic hypertension

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36
Q

What is subclinical bacteriuria and why is it important to recognize?

A

Bacteria in urine without clinical signs

No treatment necessary

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37
Q

How do you define sporadic bacterial cystitis

A

Presence of bacteriuria, clinical signs (pollakiuria, hematuria, stranguria, dysuria), < or = 3 episodes/year

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38
Q

What is recurrent bacterial cystitis?

A

> 3 episodes/year or more than 2 in 6 months, always showing clinical signs, may be relapse/persistent or re-infection, important to look for reason for recurrence

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39
Q

What are the common uropathogens?

A 
Fecal flora (E. coli most common isolate) or skin flora
Ascending infections
In most cases caused by a single organisms
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40
Q

What are some risk factors for developing UTI?

A

conditions resulting in dilute urine, catheterization, immunosuppression, female, increased age, anatomical abnormality, incontinence, inability to empty bladder, urolithiasis

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41
Q

What are some clinical signs of pyelonephritis?

A

Pyrexia, renal pain, renomegaly, PU/PD, hematuria, lethargy

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42
Q

When reading a dipstick during urinalysis, which value cannot be trusted in dogs and cats?

A

Leukocytes- inaccurate

Also wouldn’t trust USG or nitrite

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43
Q

What are some empirical antibiotics for sporadic bacterial cystitis and how long is the treatment course?

A

Amoxicillin, amoxiclav, TMPS
3-5 days
Clinical signs should resolve in 48 hours- no follow up culture needed

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44
Q

How do you treat recurrent bacterial cystitis?

A

Need to investigate underlying cause- further diagnostics depend on presentation
Culture and sensitivity for antibiotic choice
short courses (3-5 days) may work for some co-morbidities but others may require longer (7-14 days)
Important to do follow up culture

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45
Q

Describe the difference between calcium oxalate monohydrate and calcium oxalate dihydrate crystals?

A

calcium oxalate dihydrate are square with an X through it, monohydrate are long and thin like a picket-fence

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46
Q

When might you see calcium oxalate monohydrate crystals in urine?

A

ethylene glycol toxicity

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47
Q

When might you see ammonium biurate crystals in urine?

A 
Liver disease (ex. PSS)
Or normally in Dalmatians
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48
Q

True or false- a small amount of bilirubinuria is normal in cats but always pathological in dogs

A

FALSE- it’s the opposite

dogs might have a small amount normally due to renal conjugation of bilirubin

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49
Q

Which kind of crystals are normal to see in horse and rabbit urine?

A

Calcium carbonate

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50
Q

True or false- lipid is normal to see on cat urine sediment analysis and is a result of normal tubular degeneration

A

TRUE

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51
Q

Why do some animals develop alkaline urine with UTI?

A

Urea splitting bacteria produce ammonia+bicarbonate –> very alkaline

52
Q

Why is proteinuria difficult to interpret and what is an alternative test that takes out the ambiguity?

A

Cannot just look at protein value because depends on amount of urine, need to put them in context (more concentrated=higher protein)
urine protein:creatinine ratio takes out the water content issue

53
Q

What is paradoxical incontinence?

A

Patient has a urinary obstruction and cannot urinate normally, bladder becomes over-distended and when they lay down urine leaks out

54
Q

urethral sphincter mechanism incontinence is most commonly acquired in spayed female dogs but what is another way it can occur?

A

may be congenital and may occur with anatomical defects (ex. ectopic ureters)

55
Q

What are the medical options for USMI if animal is not PU/PD and there is no concurrent UTI?

A

Phenylpropanolamine, ephedrine hydrochloride- alpha adrenergic agonists, works on internal urethral sphincter
Estriol- short acting estrogen licensed for USMI in bitches
Testosterone- sometimes used for male dogs with USMI

56
Q

What are some indications for cystotomy?

A

Removing uroliths, incisional/excisional biopsy, ectopic ureter repair

57
Q

When is urethrotomy indicated?

A

Only when uroliths cannot be returned to bladder by retro hydropropulsion

58
Q

The 3 main considerations for dietary management of CKD are phosphorus, protein, and caloric intake. What else may be included as the 4th?

A

May need to supplement potassium

59
Q

What are some benefits of omega-3s in renal disease?

A

reduces inflammation, lowers systemic arterial pressure, alters plasma lipid concentrations, alters blood flow, lower glomerular pressure, may improve appetite

60
Q

What is the most common age group of cats to have FLUTD?

A

<10 years old

61
Q

What are some risk factors for FLUTD?

A

obesity, spayed/neutered, decreased activity, dry cat food, stress, Persians/pedigree, aged 2-6, live with another cat/have conflict with another cat

62
Q

True or false- you should treat a young cat with lower urinary tract signs with empirical antibiotics while waiting for culture and sensitivity

A

False- no justification for antibiotic treatment in cats with lower UT signs unless they culture positive (rare cases, usually older cats)

63
Q

What are some predisposing factors for urolithiasis in ruminants?

A

castrated males, obesity, diet, hard water, dehydration, UTI

64
Q

What is a difference radiographically in uroliths between ruminants and small animals?

A

in ruminants: calcium carbonate and oxalate are visible (radiopaque) but not struvite

65
Q

What is the bacteria involved in pizzle rot?

A

aka ulcerative posthitis/vulvitis
Corynebacterium renale
high protein diets predispose

66
Q

Why are Addisonian patients often confused for AKI patients?

A

Often both present azotemic, hyperkalemic, and isosthenuric

67
Q

How would you classify the azotemia in an Addisonian patient? (ex. pre, renal, post)

A

Pre-renal due to dehydration and hypotension

Possible to have renal as well if renal injury results

68
Q

How could you differentiate an AKI patient from an Addisonian patient if they were both azotemic and hyperkalemic?

A

AKI patients will often be oliguric/anuric

Addisonian patients can still make urine, the hyperkalemia is due to lack of aldosterone not anuria

69
Q

What is the most common stone type of the upper urinary tract?

A

calcium oxalate

70
Q

When is medical management of uroliths appropriate?

A

No obstruction, no contra-indications of diet therapy, urolith composition is amenable to dissolution (struvite, cystine, urate)

71
Q

How do struvite stones develop?

A

UTI in dogs- urease producing bacteria–>ammonia and bicarbonate (usually sterile in cats)
Struvite less soluble in alkaline pH
aka magnesium ammonium phosphate, triple phosphate

72
Q

True or false- medical dissolution of calcium oxalate stones is not possible

A

TRUE

surgery, urohydropropulsion, or benign neglect

73
Q

Will ammonium urate stones show up on radiographs?

A

No- radiolucent

Need contrast

74
Q

What is the treatment for ammonium urate stones?

A

Allopurinol- reduces uric acid

Low purine diet!!

75
Q

Why do cystine stones develop?

A

Congenital renal tubular defect–>excess urine cystine

*Also radiolucent

76
Q

True or false- treatment for emergency hyperkalemia is the same as treatment for acute hypocalcemia

A

True- calcium gluconate and IVFT

77
Q

After removing a urethral obstruction, you may also need muscle relaxants (most cats have urethral spasm). What are the 2 main categories you need to use?

A

Smooth muscle relaxants- alpha adrenergic blockers (phenoxybenzamine, prazosin, tamsulosin)
Skeletal muscle relaxants- dantrolene, diazepam

78
Q

What is the cause of pre-glomerular proteinuria?

A

Overload of small proteins that fit across the barrier - immunoglobulin light chains/hemoglobin/myoglobin
Ex: multiple myeloma producing immunoglobulin light chains

79
Q

What is the cause of post-glomerular proteinuria?

A

lower urinary tract neoplasia, hemorrhage (urine needs to be grossly contaminated with blood to get proteinuria), inflammation/infection

80
Q

Describe the syndrome of protein losing nephropathy

A

severe proteinuria, may result in hypoproteinemia (usually just albumin, not globulin), caused by glomerular disease

81
Q

What should you consider when you have low albumin but normal globulin on bloodwork?

A

Liver failure, PLN, hypoadrenocorticism

82
Q

What should you consider when you have low albumin and globulin on bloodwork?

A

PLE, hemorrhage

83
Q

What will you see with nephrotic syndrome?

A

proteinuria, hypoalbuminemia, hyperlipidemia (cholesterol), edema/ascites
Not always azotemic

84
Q

Which drug class can cause proteinuria?

A

Steroids- can be reversible but may cause scarring

85
Q

Which drugs could you use for patients with glomerular disease to improve gross proteinuria?

A

ACEinhibitors/ARB- reduce glomerular pressure=reduce proteinuria
*may need to add amlodipine if BP stays high

86
Q

What are some other treatments for glomerular disease?

A 
mild-mod protein restriction
omega-3s
sodium restriction
aspirin/clopidogrel
thoracocentesis/abdominocentesis if discomfort from edema/ascites
87
Q

Is immune complex glomerulonephritis more common in dogs or cats?

A

Dogs

88
Q

What are some examples of target organ damage from hypertension?

A

Eye, CNS, CVS, kidney

89
Q

What are some neurological signs associated with hypertension?

A

depression, stupor, seizures, altered mentation, ataxia, head tilt

90
Q

What is the most common form of hypertension in dogs?

A

Secondary due to underlying disease (ex. CKD, AKI, HAC, DM)

91
Q

What is the guideline for BP cuff size and why does it matter?

A

30-40% of limb circumference
if too small- overestimate
if too large- underestimate

92
Q

How would you use Telmisartan for proteinuria vs. for hypertension?

A

Higher dose for hypertension

93
Q

True or false- if a cat has CKD or AKI it is safer to use amlodipine for hypertension rather than telmisartan?

A

True- telmisartan is contraindicated for many stages of CKD and AKI and will also slightly increase creatinine
(but amlodipine doesn’t help proteinuria)

94
Q

What is the method of action of amlodipine for hypertension?

A

calcium channel blocker, arterial vasodilator- preferential afferent arteriolar vasodilator (will decrease glom pressure if systemic BP decreases)

95
Q

What are some drugs used for hypertension in dogs?

A

Telmisartan, Amlodipine, Benazepril (ACEinhibitor)

96
Q

What is different about treating dogs for hypertension compared to cats?

A

Dogs frequently need multi-modal therapy or won’t be effective

97
Q

What is the systolic BP number considered as the point you can diagnose hypertension?

A

> 160 mmHg

98
Q

What causes emphysematous cystitis?

A

Glucosuria –> increased bacterial growth - bacteria split glucose and CO2 gets released (glucose is C6H12O6) –> gas in bladder –> lymphatics absorb gas –> emphysema
Examples of these bacteria = E.coli and Clostridium Perfringens

99
Q

What is the normal urine output for dogs and cats?

A

15-45 ml/kg/day
Cats have lower urine output
Loss through respiration and feces = insensible losses

100
Q

True or false: 99% of what is filtered at the glomerulus gets reabsorbed.

A

TRUE - HELL YEAH BITCH!!!

101
Q

True or false: urea is a reliable indicator of renal disease in ruminants.

A

FALSE - USE CREATININE

Cattle can have severe renal disease with normal BUN

102
Q

If hyposthenuria indicates that the kidney is working well, where is the problem more than likely occurring?

A

COLLECTING DUCT - Diabetes insipidus

103
Q

What are the three components involved in the IRIS staging scheme for CKD?

A

Fasting blood creatinine
Urine protein creatinine ratio
Systemic blood pressure
helps to determine the most appropriate treatment and monitoring of patients with CKD

104
Q

What is the most common “diagnosis” in cats with CKD?

A

Chronic tubulointerstitial nephritis

105
Q

What is the most important hormone in controlling phosphate regulation?

A

FGF-23 - acts in the kidney to try and reduce the reabsorption of phosphate by acting on the NaPO4 transporters in the PCT

106
Q

In addition to diet, how else can we decrease phosphorus in patients with CKD?

A

PHOSPHATE BINDERS - Aluminum hydroxide

107
Q

True or false: renal disease progresses more rapidly in dogs than cats.

A

TRUE :(

108
Q

Which vasopressin receptor is most important in regards to water absorption/CDI?

A

V2!
V2 activates cytoplasmic aquaporin 2 (the molecule that moves from cytoplasm to the luminal membrane on the tubular side of the collecting duct) - allows water to move from the lumen to the interstitium for absorption

109
Q

What is the cause of enzootic hematuria in farm animals?

A

Grazing BRACKEN!

110
Q

What is the pathogenesis of ethylene glycol toxicity?

A

Ingested and absorbed
Oxidized in the liver by alcohol dehydrogenase to toxic metabolites - glycolic acid and oxalate
These are filtered by the glomeruli and directly cause acute tubular necrosis
Calcium oxalate crystals forms –> obstruction and mechanical damage

111
Q

What would a gross kidney with pyelonephritis look like?

A

Renal calyces contain suppurative exudate bordered by a red rim of hemorrhage
commonly seen after calving

112
Q

What would be the gross appearance of a canine kidney with chronic renal disease?

A

The capsular surface would have multifocal white depressions due to fibrosis creating a nodular appearance
Could have pale wedge-shaped area extending into the medulla from ischemia

113
Q

Histologically - what would diseased pancreatic islets look like?

A

Vaculoated Beta cells in the islets (degeneration)

Will see areas of white patches instead of normal pink/purple looking tissue

114
Q

Histologically, what features would an emphysematous bladder have?

A

Thickened bladder wall
Edema and hemorrhage
Multiple round clear spaces
Lymphoplasmacytic inflammation

115
Q

Management of AKI emergencies

A

1) triage to see if the patient is hypovolemic
2) Take bloods (see degree of azotemia)
3) Start IVFT and Furosemide CRI if the patient is oliguric/anuric -> this is important to re-equilibrate electrolytes and establish appropriate blood flow through nephron
4) put a catheter in and strictly monitor urine output
5) Investigate what caused AKI (urinalisys, biochem, hematology, imaging…)
6) specific treatment to correct underlying cause
7) Check electrolytes ever 12h, check PCV/TP to ensure not dehydrated by furosemide, check BP
8) Consider hemodialysis or peritoneal dialysis to re-equilibrate toxins
9) Supportive GIT treatment (nutrition and gastroprotectant, antiemetics)
10) in general, keep alive until nephrons have had a chance to repair
11) If not getting better consider euthanasia
12) if the patient is better and can be taken off fluids you must do urine culture after taking catheter out

116
Q

What’s the most common urinary problem in cattle?

A

Pyelonephritis

117
Q

What is Nephrotic Syndrome? What is the relationship with PLN?

A

Nephrotic Syndrom can be a consequence of PLN (but not every patient develops it).
It’s caused by hypoalbuminemia and patients often present with hypercholesterolemia (hyperlipidaemic) and proteinuria. these patients are not necessarily azotemic
Nephrotic syndrome indicates poorer prognosis

118
Q

Distinguish between PLN and PLE?

A

PLN -> loss of albumin ALONE. globulins don’t get through. Other differentials are hypoAC or liver failure
PLE -> loss of TP. Other differential is hemorrhage

119
Q

You found significant protein in the urine. What is the diagnostic approach?

A
  1. Is the proteinuria significant? Always interpret in light of USG and blood work. hypoalbunemia-> proteinuria IS significant
  2. Measure P:C ratio in the urine
  3. Check cholesterol and albumin in the bloodwork-> is there nephrotic syndrome? Is there just PLN (hypoalbuminemia alone)
  4. Determine whether it’s prerenal (loads of small proteins flood neprhon) renal (due to glomerular or nephron damage) or postrenal (addition of protein after urine formation)
  5. Firstly rule out post renal causes: check for UTI, presence of blood, LUT signs
  6. Then check bloodwork to see any evidence of prerenal causes (hyperglobulinaemia)
  7. Once you think the cause must be renal damage, establish whether glomerular or tubular. If there is only albumin in the urine (hypoalbunemia with normal TP) -> glomerular. If albumin is normal -> tubular damage.
  8. Measure BP, abdominal palpation and fundic exam to quantify the severity of hypoalbuminemia
  9. Investigate the cause of proteinuria.
    Serology/PCR for infectious causes, Joint tap for evidence of immune med disease, biochem/CBC, imaging.. In the end however only glomerular biopsy will help you distinguish between familial glomerulonephritis, amyloidosis, glomerulosclerosis and immune mediated disease
120
Q

T or F: all patients with glomerular disease are azotemic

A

False. But azotemia is a negative prognostic factor for glomerular disease

121
Q

Treatment of proteinuria

A

Depends on the cause.
If proteinuria caused by bacterial infectious disease or immune mediated you have to treat with either AB or steroids.

However, all other causes of glomerular disease (including FIP, familiar disease, amyloidosis..) can only be managed symptomatically.

The aim of treatment is to reduce renal hypertension. Therefore ACEi (benazepril) and ARB (Telmisaltran) can be used to increase efferent arteriole diameter ONLY IF THERE ISNT MARKED AZOTEMIA. Ca channel blockers (amlodipine) can be used to decrease systemic BP -> reduces renal BP. Important to give anti-thrombotic meds as these patients are losing anti-thrombin. Also keep on renal diet like all other kidney patients

122
Q

How do you deal with a blocked cat that presents as an emergency?

A

1) Triage: normally these cats are hypovolemic and bradycardic -> MOST important FIRST thing to do is to give resuscitation fluids (LRS or Hartman’s best) to resolve HYPERKALEMIA
2) Supplement Ca borogluconate -> Ca stabilizes myocardium
3) Also give insulin + dextrose infusion(but must check that they don’t develop hypoglycemia as a result. These will help with long term K management)
4) Opioid analgesia (don’t you even dare giving NSAIDs)
5) If the bladder feels distended do a decompressive cysto
6) The aim is to get the cat stable enough for anesthesia. Once stable, anesthetize and pass a catheter. If you can’t pass it try the retrograde hydropropulsion
7) Put in an indwelling catheter, keep on fluids, keep monitoring until obstruction resolves
8) After resolution expect massive diuresis, so must measure all urine output in a closed system to provide enough fluids. monitor closely (hypokalemia, hypovolemia..)
9) take the indwelling catheter out once azotemia has resolved and once the urine looks normal. Do a C&S test for UTI
10) keep the cat on opioid analgesia, avoid NSAIDs even after sending home. Prescribe a combo of smooth muscle + striated muscle relaxants (diazepam + prazosin)

123
Q

What is currently the main theory to explain FLUTD?

A

lack of cortisol inhibition of sympathetic stimulation to the bladder
urinary tract inflammation–>urethral spasm
alternative is interstitial cystitis
*Rarely cats develop FLUTD as a result of mucous plugs

124
Q

T or F: Hypercalcemia is a common finding in CKD patients

A

T! Not sure why

125
Q

Medical management of functional urethral obstruction in dogs

A

phenoxybenzamine- alpha blocker to relax blood vessels
diazepam
Can be difficult to treat medically - may need to opt for tube cystotomy

4th Year Exams (8 decks)

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