Urology

Up to 65% of filtered sodium and water is reabsorbed in:

the proximal convoluted tubule

Which of the following are used as crude indicators of GFR:

1. BUN

2. Creatinine

3. SDMA

4. All of the above

All of the above.

A 4 y/o MC DSH is presented to you with a 12 hour history of straining to urinate without producing urine. PE reveals a large, turgid bladder. Lab work shows a creatinine of 12 mg/dL. Which of the following is most likely for this patient?

1. Normal, non-azotemic patient

2. Pre-renal azotemia

3. Renal azotemia

4. Post-renal azotemia

Post-renal azotemia

Renal Blood supply starting at renal artery

Renal artery → interlobar arteries → arcuate arteries → interlobular arteries → afferent arterioles → glomerulus → efferent arterioles

What is the functional unit of the kidney?

The Nephron

Functions of the kidney

• Excretion of metabolic waste products

• Regulation of water and electrolyte balance

• Regulation of acid-base balance

• Regulation of erythrocyte production

• Activation of vitamin D

• Secretion, metabolism, and excretion of hormones

List the factors that contribute to GFR

• Forces favoring filtration

  • Glomerular hydrostatic pressure P_G = 60

  • Bowman’s capsule colloid osmotic pressure 𝝿_B = 0

• Forces Opposing Filtration

  • Bowman’s capsule hydrostatic pressure P_B = 18

  • Glomerular capillary colloid osmotic pressure 𝝿_G = 32

  • Net filtration pressure = 60 - 18 - 32 = +10mmHg

Describe RAAS

Decrease in arterial pressure leads to a decrease in glomerular hydrostatic pressure (↓GFR) → decreased NaCl at the macula densa. This triggers the release of rennin, which converts Angiotensinogen to Angiotensin I. ACE then converts Angiotensin I to Angiotensin II.

Effects of Angiotensin II

1. Increased Sympathetic Activity

2. Tubular Na+ Cl- reabsorption and K+ excretion. H2O retention

3. Aldosterone secretion from adrenal cortex (water retention)

4. Arteriolar vasoconstriction. Increase in blood pressure

5. ADH secretion from the pituitary glands = collecting duct H2O absorption

Causes of a low BUN

1. Decreased protein intake or protein anabolism (young animals)

2. Increased excretion of BUN (ex. DM, Cushing’s) = PU/PD

3. Decreased production (ex. Liver disease, urea cycle defect)

Causes of a high BUN

1. Increased protein catabolism (ex. Fever, burns, steroids, starvation, exercise)

2. Increased protein ingestion (ex. GI bleed, high protein diet)

3. Decreased GFR (ex. azotemia)

Causes of low creatinine

1. Decreased muscle mass, cachexia

2. Increased GFR

Causes of high creatinine

1. Normally higher in greyhounds

2. Decreased GFR (azotemia)

Pre-renal azotemia

1. Decreased blood flow to the kidneys

2. Causes

   1. Hypovolemia

   2. Cardiac Disease

   3. Renal vasoconstriction

3. Clinical evidence of dehydration of hypovolemia - UA shows concentrated sample

Renal Azotemia

1. Results from decreased GFR when there is loss of >75% renal mass

2. Causes

   1. Primary renal disease

   2. Secondary injury (ischemia, obstruction, etc.)

3. Generally accompanied by loss of urine concentration ability, electrolyte changes, and signs of clinical illness

Postrenal Azotemia

1. Results from obstruction or rupture of the urinary outflow tracts

2. Causes

   1. Urolithiasis

   2. Bladder rupture

3. Marked hyperkalemia is common, may see evidence of uroabdomen.

How do we use SDMA to determine GFR?

1. Produced by all nucleated cells at a constant rate

2. Excreted primarily by the kidneys, and is not reabsorbed by the renal tubules or influenced by non-renal factors

3. Considered a more sensitive early marker for declining GFR in dogs and cats

Normal USG range for dog and cat

Dog: 1.015-1.045

• Adequate >1.030

Cats: 1.035-1.060

• Adequate >1.040

What is isosthenuria?

Kidney cannot concentrate OR dilute (1.008-1.012)

What is hyposthenuria?

Kidney can dilute but cannot concentrate (<1.008)

Understand pathophysiology mechanisms of AKI in cows/horses

1. Acute Kidney Injury is caused by an abrupt reduction in glomerular filtration rate - leads to azotemia, fluid/electrolyte/acid-base disturbances.

2. Defined as acute increase in serum creatinine of 0.3mg/dl or greater

   1. If sustained → Acute Kidney Failure

Three Major Categories

1. Pre-Renal

2. Renal

3. Post-Renal

Describe vasomotor nephropathy in bovine/equine

1. persistent causes of pre-renal hypoperfusion

   • ischemic tubular injury > necrosis

2. Sepsis/systemic inflammation

   • decreased renal perfusion

   • release of cytokines, vasopressors altering afferent/efferent pressure balance.

3. Thrombotic disorders

Which drugs can cause toxic nephropathy in bovine/equine

1. Aminoglycosides, oxytetracycline

2. NSAIDs

3. Imidocarb

Which pigments can cause toxic nephropathy in cows/horses?

Hemoglobin

Myoglobin

Which plants can cause toxic nephropathy in cows/horses?

Sorghum, oxalate, oak

How do aminoglycosides cause toxic nephropathy?

• Nephrotoxicity associate with high trough levels not high peak

• Proximal tubule intracellular accumulation = cellular death

• Urinalysis: proteinuria, cylindruria, enzymuria, and hematuria

• Renal failure can develop even after drug withdrawal

How do NSAIDs cause toxic nephropathy?

• Inhibition of PGE2 and PGI2 synthesis => inability to regulate renal blood flow

• Medullary crest or papillary necrosis

• Urinalysis: Hematuria (early stage)

• Ultrasound: Renal medullary rim sign

How do oxytetracycline cause toxic nephropathy?

• inhibition of tubular cells oxidative enzymes

  • hydropic degeneration

  • necrosis

• Propylene glycol (vehicle) may decrease renal blood flow

How does salt poisoning cause ARF?

hyperfiltration - leading to increased glomerular pressure

What is the toxic part of oak, that causes ARF in heifers?

Tannic and gallic acids

How does pigweed cause ARF?

Oxalates + calcium ions = insoluble crystals > tubular blockage and necrosis

Pathophysiology of post-renal failure in cows/horses?

Retrograde increase in tubular hydrostatic pressure

Glomerular mesangial cell contraction

vasoconstriction of the afferent arteriole

Leads to: decreased glomerular blood flow, decreased GFR, tubular damage

Renal pelvis enlargement, loss of medullary tissue, hydronephrosis, atrophy.

In horses, what creatinine is defined as azotemia? Bovine?

>1.5 mg/dL horses

>0.9mg/dL bovine

What electrolyte abnormalities do we see in cows with ARF?

Significantly low Chloride

Significantly high Phosphorus

Low Sodium

High Magnesium

What is normal equine/bovine urine production?

15-30ml/kg/day

Describe glomerulonephritis in bovids. Etiology and pathophysiology.

Etiology

• Antigen-antibody complexes deposition in the glomeruli

• specific antibodies against glomerular basement membranes

Associated with infection: Abscesses, mastitis, liver fluke infestation, metritis, BVD

Leads to → increased permeability of the glomerular barrier, severe proteinuria, progressive renal failure, hypoalbuminemia, weight loss, ventral edema.

How do you diagnose glomerulonephritis?

Renal biopsy - hypercellularity of the glomerular tufts (proliferative GN) or thickening of the glomerular barrier (membranous GN)

What is Nephrotic Calf Syndrome?

A type of glomerulonephritis associated with hyperimmune serum administration

• bottle jaw and generalized edema, tricavitary effusion

• Anemia, Azotemia, Hypoalbuminemia

• Enlarged kidney

• Urinalysis: proteinuria, isosthenuria, granular or hyaline casts, RBCs, WBCs

What is pyelonephritis in the bovid?

• Ascending infection from lower urinary tract

• E.coli or Corynebacterium renale

• Acute/Subacute or chronic

Describe the difference between acute/subacute and chronic pyelonephritis in the bovid.

• Acute/subacute

  • Fever > 103.5

  • Anorexia

  • Sudden drop in milk production

  • Colic

  • Urinary Obstruction (blood clots)

  • Stranguria, polyuria, arched stance

  • Hematuria

• Chronic

  • Weight loss

  • Poor hair coat

  • Anorexia

  • Poor milk production

  • Diarrhea

  • Polyuria

  • Anemia

  • Stranguria

What is the pathophysiology of amyloidosis in the bovid?

Extracellular deposition of amyloid in kidney, intestine, liver, adrenal gland, spleen

Pathophysiology -

1. primary = immune-mediated or metabolic storage disease

2. secondary = associated with chronic infections (most commonly systemic AA type amyloid)

What are the clinical findings of amyloidosis in the bovid?

diarrhea, edema, weight loss, enlarged kidneys, hypercoagulation (urinary losses of antithrombin III), nephrotic syndrome

Diagnosis and prognosis of amyloidosis?

Dx: renal biopsy

Prognosis: fatal, no treatments exist

What is enzootic hematuria?

Pathophysiology - progressive noninfectious cystitis with tissue metaplasia of the bladder mucosa

• chronic exposure to non-toxic levels of bracken fern toxins ± bovine papilloma viruses (BPV2)

Clinical signs - severe hematuria, stranguria, and anemia, urethral obstruction from blood clots bladder wall thickening, bladder neoplasm.

Dx: presumptive based on multiple animals affected in same pasture, r/o infectious

Treatment/prognosis - remove bracken fern. Hematuria will resolve if exposure is discontinued before development of bladder tumor

Know pathophysiologic mechanisms of chronic renal failure in horses

•  Progressive loss of renal function

  • Loss of urinary concentrating ability

  • Retention of nitrogenous and other metabolic end products

  • Alterations in electrolyte and acid-base status

  • Dysfunction of several hormone systems

  • Uremia - multiple organ dysfunction

Common causes of acute renal failure in horses

• Infectious causes

  • Pyelonephritis

    • Secondary to lower UTI

    • Stranguria, dysuria, dermatitis

    • Culture, colony count, sensitivity

    • Gram negative bacteria, streptococcus spp.

  • Leptospira interrogans

    • Serovar Pomona

    • Vasculitis and endotheliitis >>> interstitial nephritis

    • Sporadic in adult horses

    • Outbreak of fever and ARF in young horses

    • Clinical signs

      • Fever (anorexia, depression, hematuria)

      • Urine analysis - pyuria w/o bacteriuria

      • Enlarged kidneys on U/S

    • Diagnosis

      • PCR on urine - second voided sample after furosemide

    • Treatment

      • Antibiotics

        • Beta lactams

        • Fluoroquinolones

      • Fluid therapy

    • Prevention

      • Vaccination - killed, whole cell bacterin

    • Prognosis = good

• ARF - acute glomerulopathies

  • Purpura hemorrhagica horses

    • Streptococcus equi equi

    • May cause hematuria and proteinuria but very rarely ARF

  • Actinobacillus equuli foals - bacteremia to kidneys

Common causes of chronic renal failure in horses

• Developmental = renal agenesis, renal hypoplasia, renal dysplasia, and polycystic kidney disease

• Primary glomerular disease = weight loss and pitting edema

• Primary tubulo-interstitial disease = weight loss w/o edema

  • causes

    • Chronic/irreversible nephrotoxic or vasomotor causes

    • Chronic pyelonephritis - most common in mares

    • chronic/intermittent obstruction

    • Renal dysplasia

Mechanisms of incontinence in horses

• Cystitis and chronic urethritis

  • Irritation of stretch receptors in the bladder wall

  • Stimulation of stretch receptors in parasympathetic afferents

  • Stimulation of detrusor contractions

  • Pollakuria

• Ectopic ureter - more common in fillies

• Urethral injury

  • Post obstruction

  • Post foaling mares

• Cystolithiasis

• Bladder paralysis

  • “Lower Motor Neuron” bladder = loss of anal sphincter tone, tail paralysis, perineal hypoalgesia, hindlimb weakness

    • Polyneuritis (cauda equina neuritis)

    • Lumbo-sacral trauma

    • EHV-1 myeloencephalitis

  • Atonic and distended bladder with relaxed urethral muscles, continuous incontinence (vs UMN dysfunction - intermittent)

  • Chronic distension of the bladder -> accumulation of calcium carbonate crystals -> Sabulous urolithiasis/cystitis

    • Stretching of the detrusor muscle, inability to contract

    • Loss of sphincter function

    • Incontinence

Causes of hematuria in horses

• Urolithiasis

• UTI

• Polypoid cystitis

• Urethritis

• Neoplasia

• Idiopathic renal hematuria

• Idiopathic hemorrhagic cystitis

• NSAIDs - induced ulcerative cystitis

• Urethral rents

How do you differentiate psychogenic PU/PD from diabetes insidious in horses?

Measure serum electrolytes esp. Sodium - DI cases may have hypernatremia

• Check ACTH and signs of Cushing’s disease

• Any recent environmental, social changes 

• Water deprivation test - 24 hours or until 5% dehydration or modified water deprivation test (over 5-7 days)

• ADH (40-80 IU/ 500kg) administration (to diagnose central DI)

List common urinary disorders in foals.

• Spurious hypercreatininemia

  • Elevated creatinine at birth associated with placental dysfunction and neonatal encephalopathy but usually no renal injury

  • Azotemia -

    • Creatinine 3.2-8mg/dl

    • BUN increased, but not as much as creatinine

  • Decline 50% in 24 hours, normal 2-3 days with or without fluids

  • Electrolytes usually normal

• AKI/ARF

• Hydroureter syndrome

  • Incomplete obstruction of urine flow causing ARF

  • Signs

    • Hydroureters, hydronephrosis, severe hyponatremia, encephalopathy

  • Etiology unknown but may be related to dysfunction of the ureterovesical valves

  • Treatment frustrating.

• Congenital defects (renal agenesis/dysplasia, polycystic kidney, ectopic ureters)

What are the most common causes of acute renal failure in horses, and what is the management?

• Most common causes:

  • Hemodynamic or nephrotoxic insults

• Management: correction fluid deficits, treatment of the underlying causes

Prognosis of acute renal failure in horses

• High recovery rate in horses ~70% IF:

  • Primary disease quickly treated

  • Toxins removed

  • Horse not oliguric

Clinical findings of tubulo-interstitial CRF in horses? Diagnosis?

• Clinical signs - Weight loss, PU/PD, anorexia, dental tartar, colic, occasionally fever and/or incontinence

• Laboratory findings - minimal proteinuria, normal or increased serum protein, hyponatremia and hypochloremia, occasional hypercalcemia, isosthenuria

• Diagnosis - clinical signs, laboratory findings, ultrasound, biopsy

• Ultrasound - often small kidneys, increased echogenicity, stones sometimes

Sabulous Cystitis in horses

• Causes

• Clinical signs

• Treatment

• Sabulous Cystitis

  • Causes

    • Bladder paralysis

    • Neurologic disease or musculoskeletal problems that prevent the normal posturing for urination

  • Clinical signs: incontinence

    • Affected horses may not present for months to years after onset of the problem

  • Treatment

    • Urine evacuation

    • Bladder lavage (repeated)

    • Bethanechol - parasympathomimetic drug, to stimulate the muscarinic receptors in the detrusor muscle.

Causes of stranguria in foals

• “Dummy bladder”

  • Aspect of neonatal encephalopathy syndrome

• Ruptured bladder

• Urachal abscess

• “Neurogenic bladder” 

• Newborn colts

• Stranguria without obstruction or urinary tract rupture

• Part of neonatal encephalopathy syndrome

• Treatment

  • Indwelling catheter

  • Phenoxybenzamine - 5mg PO q12h

    • (a-adrenergic antagonist used to reduce urethral hypertonus)

Diagnosis and treatment of a ruptured bladder.

• Diagnosis

  • Common in foals, post-partum mare, gelding with urethral obstruction

  • Stranguria, abdominal distention

  • Ultrasound

  • Bloodwork

    • Hyponatremia/chloremia, hyperkalemia

    • Azotemia

  • Peritoneal tap

• Treatment

  • A medical emergency

  • Improve respiratory function

  • correct electrolyte, acid-base abnormalities

    • Hyperkalemia

    • Hyponatremia

      • Acute (<3 days) - do not raise serum [Na+] by >1-2 mEq/L/h

      • Chronic - do NOT raise serum [Na+] by >0.5-1.0 mEq/L/h

  • Peritoneal drain

Which of the following antibiotics is nephrotoxic?

1. fluoroquinolones

2. penicillins/beta-lactams

3. Aminoglycosides

4. Macrolides

Aminoglycosides

You diagnose a patient with AKI whose blood pressure is 220/110 and has several pinpoint retinal hemorrhages. How would you address the patient’s hypertension?

1. reduce the patient’s fluid rate

2. administer amlodipine and monitor blood pressure to optimize dosing to effect

3. administer ace inhibitor alone

4. recheck BP in 24 hours before intervening.

Administer amlodipine and monitor blood pressure to optimize dosing to effect

Which of the following drugs has the added benefit of affecting PPAR-gamma and has dramatically improved proteinuria in our experience at Cornell?

1. Benazepril

2. Telmisartan

3. Losaran

4. Enalapril

Telmisartan

Which of the following is NOT part of the general strategies for the medical management of urolithiasis?

1. Decreasing urine volume

2. increasing the solubility of crystalloids

3. increasing crystallization inhibitors

4. decreasing the concentration of calculogenic crystalloids

Decreasing urine volume (you want to increase urine volume)

You document persistent proteinuria in one of your canine patients. The urine protein:creatinine (UPC) ratio is 8.2 with an inactive sediment. Their USG has recently been as high as 1.032. Which of the following best describes the likely source of proteinuria?

1. pre-renal

2. renal, glomerular

3. renal, tubular

4. post-renal

renal, glomerular

Which of the following would be the most radio-opaque urolith?

1. cystine

2. urate

3. xanthine

4. calcium oxalate

Calcium oxalate

A 6-year-old female spayed Labrador retriever presents for stranguria and hematuria. You determine she has a urinary tract infection and radio-opaque cystic calculi. What diet would you consider to attempt dissolution?

Hill’s s/d

You diagnose a cat with Stage 1 CKD that has significant periodontal disease. In planning a dental procedure, which of the following is the LEAST important consideration to minimize the progression of your patient’s renal disease?

1. monitoring blood pressure and avoiding hypotension under anesthesia

2. avoiding NSAID for post-op pain management

3. minimizing extractions

4. providing appropriate fluid therapy to optimize peri-procedure hydration

minimizing extractions

What is the most common histologic lesion associated with chronic kidney disease in dogs and cats?

1. lymphoma

2. glomerulonephropathy

3. amyloidosis

4. chronic tubulointerstitial nephritis

Chronic tubulointersitial nephritis

A 9-year-old male castrated mixed breed dog presents for annual examination and vaccines. The client reports he is doing well and is very active and went swimming this morning. His PE is unremarkable. You recommend a CBC, Chemistry, and UA to screen for emerging diseases as he ages. His 4Dx is negative. He has a 3+ protein with a USG of 1.028 and no other lab abnormalities. What do you recommend next?

1. start ace inhibitor

2. abdominal and thoracic imaging

3. recheck a first-morning urine sample on a day after minimal activity

4. referral to an internist

recheck a first-morning urine sample on a day after minimal activity (swimming can lead to pre-renal proteinuria)

On average, SDMA blood concentrations are increased with what percentage loss of kidney function?

45%

Decreased cardiac output falls under which etiology of acute kidney injury?

1. intra-renal

2. pre-renal

3. post-renal

pre-renal

Which of the following is NOT a suitable treatment for urethral sphincter mechanism incompetence (USMI)?

1. Prazosin

2. Estriol (incurin)

3. Urethral bulking

4. PPA (Proin)

Prazosin

Patients with ectopic ureters may also present with which of the following conditions:

1. UTI

2. Paramesonephric septal remnant

3. Renal hypoplasia

4. All of the above

All of the above

Treatment options for Detrusor Urethral Dyssynergy (DUD) include:

1. Tamsulosin

2. Prazosin

3. Castration

4. All of the above

All of the above

What are the indications for a nephrectomy?

• Irreparable trauma

• Persistent hydronephrosis

• Renal/perirenal masses

• Persistent infection

• Kidney donor

Postoperative considerations of a nephrectomy?

• Fluids

  • Maintain renal perfusion and prevent clots in urinary tract

• Monitor for azotemia

• Monitor blood pressure

• Avoid renal toxins

  • NSAIDs, Abx, dyes

indications for ureteral surgery

• Ureteral obstructions

  • Calculi (Most common)

  • Stricture

  • Spay ligations

  • Neoplasia (rare - but can crawl up from bladder - TCC)

• Ureteral ectopia necessitating reimplantation (extramural type) or laser ablation (intramural type)

• Kidney transplantation

Normal Ureteral diameter in dogs and cats is:

• 0.4mm cats

• Approx: 3mm in dogs

Surgical intervention of choice for chronic stone formers:

Ureteral stenting!!

Preferred over ureterotomy (creation of a stoma in the ureter) as this is associated with many complications.

What is SUBS and why would you perform this?

Subcutaneous ureteral bypass system

Indications

1. ureteral strictures, calculi, trauma, neoplasia

2. ureteral stent reaction or intolerance.

Most often performed on cats! There is a high SUB calcification rate seen in canine patients, requiring a device exchange. Stents in cats are hard to place, so this was invented.

What is the appropriate procedure for ureteral obstructions in dogs?

ureteral stent

What is the most common cause for ureteral obstruction in dogs and cats?

ureterolithiasis

Indications for ureteral reimplantation in dog

• Ureteral trauma

• Distal ureteral obstruction

• Extramural ectopic ureters

How do you surgically treat an extramural ectopic ureter?

Ureteroneocystostomy

How do you surgically treat an intramural ectopic ureter?

cystoscopic laser treatment

You COULD go a neoureterostomy, but this method is associated with less ureteral trauma and stricture. It is minimally invasive.

Cystotomies are most commonly performed for ______.

the removal of cystic calculi

True/false: antibiotics change culture results in dogs undergoing cystotomy.

false = treat them with antibiotics!!!!

Should you approach the bladder dorsally or ventrally during a cystotomy?

• Ventral cystotomy

  • Veterinarians are nervous about ventral cystotomys due to pressure on the bladder, however this is not something that we see problems with

  • Going ventrally allows you to avoid the ureters

What samples should you collect during a cystolithotomy

• Collect stones for stone analysis and culture

• Collect bladder mucosa for culture

• Do NOT waste client money on a pre-op urine culture

What is the holding layer of the bladder?

submucosa

Healing ability of the bladder? Which suture would you use?

full thickness defects regain 100% of normal tissue strength in 14-21 days.

Use absorbable or delayed absorbable monocryl

Postoperative management after a cystotomy

• Always take postoperative imaging

  • In studies 14-20% of cases had stones left behind

• Intravenous balanced electrolyte solution for 12-24h

• Inform owner that cystotomy offers temporary relief and medical management may be necessary to prevent recurrence

• Hematuria and small blood clots can be expected for 4-5 days postop.

  • UROKINASE produced by the endothelium

Most common bladder cancer in dogs and cats. Treatment?

transitional cell carcinoma.

Treat with a partial cystectomy - be careful of seeding/exfoliating.

check for metastasis first.

Prognosis of dog diagnosed with TCC

• This is a very aggressive neoplasm

• Most dogs die from urethral obstruction

  • Urethral stents

  • Permanent cystotomy catheter

• Surgery alone 3-6 mo median survival

• Chemotherapy

  • Piroxicam 6m median survival

    • COX2 inhibition

    • 70% initial response rate

• Mitoxantrone and piroxicam: 11m median survival.

Cats with FLUTD present with a small/large urinary bladder on PE

SMALL!

FLUTD is usually seen in

1. males or females

2. indoor or outdoor

Males

Indoor

self-limiting disease

What factors contribute to FLUTD?

• Stress/lifestyle

• inflammation

• Crystalluria (stones)

• Diet H2O

• Urethral Plug

• Genetics

• Infection (uncommon)

3 main causes

1. Feline Interstitial (idiopathic) cystitis - FIC: most common

2. Urethral plugs (crystals, cells, mucus, debris)

3. Urolithiasis

True/false: bacterial cystitis is uncommon in cats <10years.

true

What are the indications that FLUTD is caused by bacterial infection?

• Uncommon cause <10years

• Female more likely

• Recent urinary procedures

• Urethral catheterization

• Perineal urethrostomy

• Urolithiasis

• Systemic disease

How do you treat FLUTD?

Multimodal treatment

• Pain, stress, DIET, water intake

• NOT antibiotics! NOT NSAIDs! Steroids…probably not

• Environmental modification/enrichment

• Anxiolytics

  • gabapentin

  • Amitriptyline

  • Fluoxetine

• Analgesics

  • buprenorphine

  • fentanyl

  • gabapentin

• Alpha-1 Antagonist (smooth muscle relaxation)

  • prazosin

  • phenoxybenzamine

Client Education is key

• self limiting but recurrent condition

Acid base and electrolyte derangements caused by urethral obstruction.

1. metabolic acidosis

   • uremic acids

   • Hyperlactatemia caused by hypoperfusions

2. Respiratory acidosis

   • hypoventilation

3. Hyperkalemia

   • decreased renal excretion

   • shifting from IC > EC due to acidosis

   • cardiac implications

4. Hypocalcemia

   • unclear pathophysiology

   • cardiac implications