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Doctor of Veterinary Medicine (Work in progress) > Veterinary Medicine - Urinary Tract Diseases > Flashcards

Veterinary Medicine - Urinary Tract Diseases Flashcards

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1
Q

Urine stick - What are 3 unreliable parameters?

A

Nitrates / Nitrites, Leukocytes, USG

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2
Q

Renal patients tend to suffer from Hypotension/Hypertension

A

Hypertension

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3
Q

US-guided kidney biopsy - Main indications

A

Proteinuria, Kidney mass

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4
Q

Kidney biopsy - From what region of the kidney are biopsies usually taken? Why?

A

Renal cortex. As to not damage the Arcuate blood vessels between the cortex and medulla

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5
Q

Low USG - When to suspect inability to concentrate urine? (4)

A

Persistently low USG, Cat with low USG, Concurrent Pu/Pd, Inappropriately low USG in the face of dehydration

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6
Q

Causes for elevated Creatinine

A

Pre-Renal: Dehydration. Renal: AKI, CKD. Post-renal: Bladder rupture, Urinary tract block

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7
Q

Causes for elevated Urea

A

Pre-renal (dehydration), Renal and post-renal causes. GI Bleeding. High protein diet. Catabolic states

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8
Q

Causes for elevated Urea

A

Pre-renal (dehydration), Renal and post-renal causes. GI Bleeding. High protein diet. Catabolic states

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9
Q

AKI - Ethylene Glycol toxicity - What is the antidote? How does it work?

A

4-MP Ethanol. Alcohol dehydrogenase works on Ethylene Glycol and to produce Oxalate. Ethanol acts as a substitute-substrate (Competitive inhibition)

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10
Q

AKI - Ethylene Glycol toxicity - Damage to the kidney is reversible (T/F)

A

False

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11
Q

Why Is AKI usually associated with hypocalcemia?

A

AKI => Decreased GFR (Oliguria/Anuria) => Phosphorus excretion decreases => Phosphorus binds with calcium => Calcium concentration in the blood decreases

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12
Q

AKI - Grapes / Raisins toxicity - Main panel finding associated with this cause for AKI

A

Hypercalcemia

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13
Q

AKI - Ethylene Glycol toxicity - Clinical signs

A

Lethargy, Anorexia, Vomiting, Halitosis, Oliguria / Anuria, CNS signs (e.g. Ataxia, Depression, Stupor)

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14
Q

AKI - What are the characteristics of the ““Recovery stage”” in AKI?

A

Polyuria. Normalization of azotemia and electrolytes

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15
Q

Contraindications for Mannitol? Why?

A

Overhydration / Hypertension. Draws fluids from the extra to the intravascular space through osmotic pressure and can further worsen overhydration / hypertension

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16
Q

AKI - Hyperkalemia - Treatment options

A

Fluids, Dextrose, Insulin, Bicarbonate. *Calcium gluconate - doesn’t treat the hyperkalemia itself but protects the cardiomyocytes from its deleterious effects (e.g. bradycardia, arrhythmias)

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17
Q

AKI Treatment - What is the common acid-base imbalance caused by kidney disease? How to correct it?

A

Metabolic Acidosis. HCO3- to be added to fluids = Body weight X 0.3 X Base-deficit. Can be corrected over a long period of time (e.g. 12-24 hours in CRI) or shorter times (e.g. half the amount over 1-2 hours, the other half over 4-6 hours)

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18
Q

AKI - Explain the mechanisms behind metabolic acidosis in kidney patients

A

Decrease in HCO3- production and reabsorption by the kidney. Decrease in H+ excretion by the kidney

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19
Q

AKI Treatment - Why is the usage of D5W especially important in AKI patients as opposed to other patients?

A

Patients with functioning kidneys can easily regulate increased amounts of electrolytes (e.g. Sodium, Chloride) coming from IV fluids and excrete the surplus in the urine. Kidney patients suffer from decreased to completely halted GFR and therefore are at risk for developing electrolyte imbalances (e.g. Hypernatremia). D5W is comprised of dextrose and free-water not associated with sodium, therefore not burdening the kidneys as much as saline/LRS, and should be added to them to decrease the overall electrolytes intake in oliguric/anuric patients

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20
Q

AKI - What are the general indications/considerations when administering Mannitol? And Furosemide? Explain

A

Mannitol - When dehydration has been corrected and the patient is still oliguric/anuric. Furosemide - When the patient is overhydrated (Furosemide doesn’t increase the fluid volume in the intravascular space like Mannitol does). Also considered a more effective diuretic and used when Mannitol isn’t producing the desired effect.

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21
Q

AKI - General considerations on when to give fluids and when to give diuretics?

A

Fluids (Saline/LRS +/- D5W) - Until dehydration is corrected. After that - give based on the amount of urine production (“in Vs. out”) until the kidneys recover. Diuretics - After correction of dehydration + urine production is insufficient. Also, used to correct overhydration due to fluid therapy

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22
Q

Hypertension - What are the most commonly affected organs?

A

Brain, Eyes, Kidney, Heart

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23
Q

AKI - Hypertension - Treatment options

A

Amlodipine (Usually 1st choice in both dogs and cats in AKI), Hydralazine, Nitroprusside, ACE-i /ARB (secondary drugs, not enough as sole treatment for hypertension due to AKI)

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24
Q

AKI - Prognosis - from the time of initial insult to the kidneys - over what period of time can the kidneys continue to heal (i.e. Creatinine decrease on follow up)

A

3 Months. after that - further decrease in creatinine is unlikely

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25
AKI - Etiology-specific prognosis - Leptospirosis | Pyelonephritis | Ethylene Glycol | Lilly | Grapes, Raisins | Gentamycin | NSAIDS, ACE Inhibitors
Leptospirosis - Good & Reversible. Pyelonephritis - Good. Ethylene Glycol - Not reversible. Lilly - Severe, not reversible. Grapes/Raisins - Good & Reversible. Gentamycin - Potentially reversible. NSAIDs, ACE-i - Reversible
26
CKD - What is the corner stone of treating CKD? How does it help?
Renal-diet. -Contains less protein that is broken down to produce Urea -Less phosphorus -Less sodium -More omega-3 fatty acids
27
AKI Treatment - Describe general overview of AKI treatment and give examples for treatment options
-Treat underlying issue if possible! -Rehydrate if necessary -Promote urine flow - diuretics (Mannitol/Furosemide) -Once euvolemic - In vs. Out -Treat hyperkalemia (Bicarbonate/Dextrose + Insulin || Calcium Gluconate) -Treat hypertension (Amlodipine) -Treat acidosis (Bicarbonate) -Treat GI Symptoms (Anti-Emetics, GI Protectants, Pro-Motile, Appetite stimulant) *Dialysis if possible/indicated/no response to conventional treatment
28
CKD - General treatment - Various pathologies that may have to be addressed in a CKD patient
Treat underlying cause if possible. Fluids if tends to get dehydrated (usually SQ). Renal diet, Anti-emetics, Appetite stimulants. Treat hypertension (first choice: Dogs - ACE-i, Cats - Amlodipine). Treat hyperphosphatemia (Renal diet, Phosphorus binders). Treat Anemia (Blood transfusion, Darbepoetin). Treat acidosis (Bicarbonate). Treat electrolyte imbalances
29
CKD - Clinical signs
Decreased appetite, Weight loss, Vomiting, Nausea, PUPD, Pale mucus membranes, Halitosis
30
CKD - Stage 1 - Creatinine-levels, Lab findings
<1.4 mg/dL (dogs). <1.6 mg/dL (cats). -Low USG -Proteinuria -Underlying kidney pathology that has not caused azotemia yet (e.g. Neoplasia, Polycystic kidney disease)
31
CKD - Stage 2 - Creatinine-levels? Lab findings
1.4-2.8 mg/dL (dogs). 1.6-2.8mg/dL (cats). Aside from azotemia and stage 1 abnormalities - usually no additional lab finding and clinical signs mild to absent
32
CKD - Stage 3 and 4 - Creatinine levels, Lab findings
Stage 3: 2.9 - 5 mg/dL. Stage 4: > 5mg/dL. Anemia, Electrolyte Imbalance, Acidemia
33
CKD - What are the 3 elements of CKD staging
Creatinine levels, Degree of proteinuria (UPC), Blood pressure
34
CKD Treatment - Why is low protein diet important in CKD patients
Leads to decreased urea production and thus decreases the deleterious effects of increased urea: Nausea, Vomiting, GI ulceration, Bleeding tendencies. Also - reduces phosphate load. Reduces acidosis
35
Hyperphosphatemia occurs in AKI/CKD and is treated in AKI/CKD
Occurs in both (usually to a greater degree in AKI due to lack of compensatory mechanisms). Treated only in CKD
36
Explain the calcium and phosphate changes in CKD
Phosphate concentration in the blood increases => Hyperphosphatemia => Phosphate binds to ionized calcium => Hypocalcemia. Hypocalcemia + Hyperphosphatemia => Increase in PTH => Secondary hyperparathyroidism. Through the regulation of PTH - calcium concentrations is kept at normal-low levels and the degree of hyperphosphatemia is lessened.
37
CKD Treatment - Hyperphosphatemia
Renal diet. Phosphate binders (e.g. Aluminum Hydroxide)
38
CKD Treatment - Hypertension
Dogs - ACE-i (First choice), Amlodipine (2nd choice). Cats - Amlodipine (First choice)
39
CKD - Reasons for anemia in CKD patients
Decrease in erythropoietin production. GI Bleeding (Uremia, Hypergastrinemia). RBCs have a shorter half life in the face of uremia. Bone marrow toxicity
40
AKI - Classic clinical signs, lab findings and imaging in Ethylene Glycol toxicity
AKI (Anorexia, Lethargy, Vomiting, Oliguria/Anuria) + CNs signs (Ataxia, Depression, Stupor). Hypocalcemia. Metabolic acidosis. US - Kidneys with "Halo" sign and hyperechoic renal cortex. Calcium-oxalate uroliths
41
Glomerulonephritis - Etiologies
Primary (Idiopathic). Secondary (Extra-renal diseases): -Infections (e.g. Leishmaniasis, Ehrlichiosis, FIV, FeLV) -Systemic Inflammation -Vaccines / Drugs -Neoplasia
42
Glomerulonephritis - 2 Most common glomerular diseases (Be specific in dogs and cats)
Amyloidosis. Glomerulonephritis: Cats - Membranous glomerulopathy. Dogs - Membranoproliferative glomerulonephritis.
43
Renal Amyloidosis - Common dog breed
Shar-Pei
44
Glomerulonephritis - Explain the basic pathogenesis in dogs
Due to a trigger resulting in the activation of the immune system, immune complexes (Antigen + Antibodies) are produced and deposited in the endothelium of the glomerulus -> Causing inflammation and increased permeability -> leading to protein-losing nephropathy
45
Glomerulonephritis - Explain the basic pathogenesis in cats
Antigens are deposited in the basal membrane or in the sub-epithelium of the glomerulus. Does not cause local inflammation like in dogs but compromises the selective properties of the glomerulus -> leading to protein-losing nephropathy
46
Glomerulonephritis - What are the 2 major proteins that are lost and treated for in PLN
Albumin, Anti-Thrombin III
47
Glomerulonephritis - Nephrotic syndrome - 4 main characteristic findings/Clinical signs
Proteinuria, Hypoalbuminemia, Hypercholesterolemia, Ascites/Peripheral Edema/Pleural effusion
48
Explain the diagnostic approach to proteinuria
Are there systemic clinical signs? CBC, Panel, UA + Culture may be indicated right at the beginning. If not: Is it a post renal cause (e.g. Inflammation, Infection, Uroliths, Neoplasia). Also could be due to problems in the genitalia. - UA (Cystocentesis) + Culture +/- US. Is it pre-renal (e.g. Hemoglobin/Myoglobin/Bence-Jones proteins) - CBC + Panel. Is it a transient proteinuria due to another disease process/fever? -Check again in 2-3 weeks. Persistent proteinuria - is it tubular? (e.g. Fanconi syndrome, CKD) - UA, Panel Is it glomerular ?(Glomerulonephritis/Amyloidosis) - UPC, Renal biopsy. If strong suspicion for glomerulonephritis - Search for secondary causes (CBC, Panel, UA + Culture, US, Screening for infectious diseases, X-rays)
49
Glomerulonephritis - UPC upper limit of normal reference range in dogs and cats
Dogs - 0.5. Cats - 0.4
50
Glomerulonephritis - What UPC and Above is Considered Specific to Renal Proteinuria
2 <
51
Glomerulonephritis - Treatment
Treat underlying cause if possible, Low-protein diet, ACE-i / ARB (for anti-proteinuric effects), Anti-coagulatives (e.g. Low-dose Aspirin, Clopidogrel, Rivaroxaban). Immunosuppression
52
Glomerulonephritis - Monitoring and expected results for good prognosis
UPC every 2-4 weeks. Mean decrease of 50% in UPC
53
An animal presents with a chief complaint of urinary incontinence but also urinates normally. What 2 categories of urinary incontinence are relevant for this animal?
Anatomical defects (e.g. Ectopic ureters, Urine pooling, Ureterocele, Pelvic bladder). Decreased urethral tone (e.g. PMSI, Lower motor neuron disease such as Cauda equina syndrome, S1-S1 Trauma)
54
Ectopic ureters - Common signalment. Explain
Young female dogs. Male dogs have a long and narrow urethra which causes the urine to flow back to the bladder, so urinary incontinence due to ectopic ureters in male dogs is usually non-clinical
55
Pelvic bladder - Classic clinical sign. Explain
The dog drips urine while barking. This is caused due to intra-abdominal pressure being exerted only on the cranial pole of the bladder (apex) due to the trigon being abnormally located caudally in the pelvic region.
56
Ectopic ureters - What are common concurrent disease/abnormalities you should look for
PMSI, Dilated ureters, Renal dysplasia
57
When you have an animal with a chief complaint of urinary incontinence and you suspect decreased urethral tone - What is an important neurological test you can perform
Anal sphincter contraction reflex (tests if there is damage to S1-S3 (Pudendal N.)
58
PMSI - Classic signalment
Middle age - to old female dogs - Months to years after castration ,or concurrent with ectopic ureters
59
PMSI - Diagnosis
History & Signalment - Adult female castrated dog with first time Incontinence. Gold Standard - Pressure profilometry
60
PSMI - Treatment options
Phenylpropanol amine (Works 80-90% of cases). DES (Estrogen derivative). Collagen injections to the urethral walls. Occluder (Surgically placed on the urethra)
61
Urinary incontinence - Increased urethral tone ("Overflow bladder") - 2 Main Clinical signs/Physical exam findings
Stranguria, Large, firm bladder
62
Urinary incontinence - Reflex Dyssynergia - What is the category of urinary incontinence it falls under? Common signalment
Increased urethral tone ("Overflow bladder"). Middle age to old, large breed male dogs
63
Increased bladder contractility ("Overreactive bladder") - Common causes
Cystitis, Cystic uroliths, Neoplasia
64
Urolithiasis - What is the only urolith that is more common in female dogs than male dogs? Why?
Struvite. Females tend to have more lower urinary tract infections than males (A predisposing factor for struvite stones)
65
Urolithiasis - Urates - Predisposed breeds? Other causes
Dalmatian, English Bulldog. Congenital/Acquired shunts (Ammonium-biurate)
66
Urolithiasis - What hints/clues we can get from signalment, history and urine stick about the possible identity of certain uroliths (Aside from direct visualization and composition analysis)
Sex (Female tend to suffer from struvite). Medications (e.g. Steroids - Ca-Ox, Allopurinol - Xanthine). Urine pH (e.g. acidic - Ca-Ox, Basic - Struvite). Breeds (e.g. Urates - Dalmatian, English Bulldogs, Cysteine - English bulldogs, Long-haired cats - Ca-Ox). Stone location (Renal/Ureter in a cat - Ca-Ox). Metabolic conditions (e.g. Cushing's diseases/Hyperparathyroidism - Ca-Ox)
67
Urolithiasis - Struvite - Primary/Secondary in Dogs/Cats
Cats - Primary. Dogs - Usually secondary to UTI
68
Urolithiasis - Struvite - Treatment
Complete obstruction - surgical removal. Dissolution (Non-obstructive / Prevention: Acidifying diet, Increase water intake, Treat UTI (C&S recommended)
69
Urolithiasis - Calcium oxalate - Common Causes
Primary, Hypercalcemia, Cushing's disease, Ethylene glycol poisoning
70
Urolithiasis - Calcium-oxalate - Signalment in cats
Long haired cats
71
Urolithiasis - Calcium-oxalate - Treatment
Surgical removal / Laser lithotripsy (No option for dissolution). Prevention: Treat underlying cause if possible (e.g. hypercalcemia), Increase water intake, Alkylating diet , Potassium citrate, Thiazide diuretics , B6
72
Urolithiasis - Urates - Treatment
Primary: Increase water intake, Low purine diet, Allopurinol, Alkylating diet, Secondary: Treat PSS/Liver failure
73
Urolithiasis - Cysteine - Treatment and Prevention
Castration! Very effective. Increase water intake. Low protein diet
74
Urolithiasis - Cysteine - Common breeds
English bulldog, Newfoundland, Dachshund, Basset hounds
75
Lower urinary tract infections (UTI) - More common in young/old cats. Explain possible reason
Old cats. When young - cats produce very concentrated urine which inhibits growth of bacteria. As the kidneys lose nephrons with age (e.g. CKD, which is very common in aging cats) the urine concentrating abilities diminishes, the urine becomes more dilute which allows bacteria to grow.
76
Lower urinary tract infections (UTI) - What are the 2 most important tests in diagnosing UTI
Urinalysis (including sediment), Culture & sensitivity (Gold standard)
77
Chronic (Recurrent) UTI - Possible causes
Anatomical (e.g. Ectopic ureters, Urine pooling, Ureterocele, Recessed vulva, Patent urachus). Uroliths. Neoplasia, Proliferative urethritis, Polypoid urethritis. Endocrine (e.g. DM, Cushing's disease). CKD. Catheterization. Antibiotics (resistant strains)
78
What is the most common lower urinary tract disease in young cats
FIC (Feline Interstitial Cystitis) - 54% of LUTI cases in young cats
79
Feline Interstitial Cystitis (FIC) - Diagnosis
History, Clinical signs. Diagnosis of exclusion. Rule out: UTI, Urolithiasis. Urinalysis + Urine sediment + Culture and sensitivity (Usually sufficient) US, X-rays optional.
80
Feline Interstitial Cystitis (FIC) - Treatment for first episode
Analgesia - Buprenorphine/NSAIDs
81
Feline Interstitial Cystitis (FIC) - Treatment for more recurrent disease
Decrease stress (e.g. removal stressful factors from the environment, Feliway, anti-stress medication). Increase water intake
82
Feline Interstitial Cystitis (FIC) - What is the one proven treatment element
Increase water intake
83
Urethral plugs - Most common composition
Proteinaceous matrix + Struvite
84
Most common cause for urethral obstruction in young cats
Urethral plugs
85
AKI - General prognosis and name 5 factors that further affect it
If the patient is producing an adequate amount of urine - approximatly 50% survival. If the patient is oliguric/anuric - 25% percent survival. Etiology (e.g. Pyelonephritis vs. Ethylene Glycol). Complications (e.g. Multiple organ dysfunction, ARDS, SIRS). Co-morbidities (e.g. Cardiac disease). Facilities and equipment (e.g. availability of dialysis). *Degree of azotemia on arrival not necessarily a negative prognostic indicator or associated with worse outcome
86
Feline Lower Urinary Tract Disease (FLUTD) - When a cat presents with clinical signs of FLUTD - What are your DDs?
FIC, Urethral Plugs, Urolithiasis, Infection (UTI), Stricture, Neoplasia
87
Feline Lower Urinary Tract Disease (FLUTD) - How can you differentiate between FIC (without urethral plugs) and urethral obstruction? (One "Test")
Palpate the Bladder: -Full and distended - Obstruction. -Small - FIC
88
Urinary Obstruction - Why do cats present with Hypocalcemia?
Hyperphosphatemia (in cases of decreased GFR)
89
Urinary Obstruction - Common panel findings
Azotemia, Hyperkalemia, Hyperphosphatemia, Hypocalcemia, Metabolic Acidosis
90
Urinary Obstruction - Main treatment elements (In order)
-Fluids. -Treat Hyperkalemia: Bicarbonate / Dextrose + Insulin / Terbutaline / Calcium Gluconate. -Catheterize and unblock. -Analgesia. Long term: Treat underlying cause (e.g. Uroliths, Urethral plugs)
91
Urinary Obstruction - Fluid therapy management - How do you adjust it on the go? What to monitor?
Give fluids based on ongoing losses. Serial weighings and adjust according to ideal body weight. Recheck and monitor azotemia. Try challenging with less/more fluids and see the response on serial weighings. Look For Signs of Fluid Overload: Monitor Heart for Murmurs/Gallop Auscultate the Lungs for Crackles Nasal Discharge Chemosis
92
Urinary Obstruction - What are some drugs that causes relaxation of the urethra? What drug family are they?
Prazosin, Phenoxybenzamine, Tamsulosin. alpha Adrenergic Antagonists
93
Urinary Obstruction - What is the surgical solution for recurring urethral obstructions?
Perineal Urethrostomy
94
Benign Prostatic hyperplasia - Clinical signs
Stranguria, Hematuria, Tenesmus / Constipation
95
Benign Prostatic hyperplasia - Diagnosis
US, Cytology, Prostate-specific arginine esterase (CPSE)

Doctor of Veterinary Medicine (Work in progress) (17 decks)

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