Urinary Emergencies Flashcards
What structures make up the lower urinary tract?
(Bladder, urethra, +/- caudal ureters)
(T/F) If an animal has a urinary obstruction and a UTI, it is possible the UTI caused the obstruction.
(F, UTI is more likely to be a secondary issue)
What are some common diseases that cause urinary obstruction?
(Idiopathic cystitis, urolithiasis, and lower urinary neoplasia)
What are some common diseases that cause non-obstructive lower urinary disease?
(Idiopathic cystitis, urolithiasis, lower urinary neoplasia, and UTIs)
UTIs are very uncommon in cats when compared to sterile cystitis unless…..
(They have a comorbidity)
(T/F) Urinary obstructions are a life threatening emergency.
(T, they’ll die within a few days)
Both obstructive and non-obstructive lower urinary tract diseases are associated with pollakiuria, stranguria, dysuria, inappropriate urination, hematuria, and/or pyuria; how can you use clinical signs to tell them apart?
(Obstructive urinary tract dzs are more likely to have systemic dz (and will get worse the longer the obstruction goes untreated); this finding is not expected with non-obstructive urinary tract dzs)
When a patient is arriving for what you suspect is lower urinary tract disease based on the owner’s complaints, what is the first question you want to answer that will determine the order of your next steps?
(Whether the animal is obstructed or not)
What is the most useful diagnostic test for a UTI?
(Urine culture, sample should be obtained via cystocentesis)
What is the purpose of radiographs in a lower urinary tract dz case?
(To look for urolithiasis (radio opaque stones are the more common stones seen so that’s useful))
What can you use ultrasound to look for in a lower urinary tract dz case?
(Look for radiolucent uroliths, masses, clots, free fluid, and dilated ureters or kidneys)
Hypervolemia/hypovolemia (choose), hyperkalemia/hypokalemia (choose) and signs of shock (hypothermia, weak pulses, etc.) are common findings with obstructive urinary tract dz.
(Hypovolemia and hyperkalemia)
Why is heart rate not a reliable marker for clinical status in potentially urinary obstruction patients?
(Bc hyperkalemia could be masking tachycardia)
What procedures/treatments are involved in the stabilization of a patient with a urinary obstruction?
(IV catheter placement, fluid therapy, hyperkalemia therapy, pain management/sedation, and unblocking)
Why is LRS better for the kidneys?
(It is balanced which means lower in chloride which can be not optimal for injured kidneys)
What is the purpose of administering calcium gluconate to an urinary obstruction patient with hyperkalemia?
(Stabilize the electrical activity in the heart by restoring the difference between the resting and threshold potentials)
(T/F) Calcium gluconate is used to lower the concentration of potassium in the blood of a hyperkalemic patient.
(F, calcium gluconate has no effect on potassium concentration)
What are some drugs that can be administered to drive potassium into cells in hyperkalemic patients?
(Insulin and dextrose (dextrose can be used alone), bicarbonate, and methylxanthine bronchodilators (terbutaline, aminophylline, and albuterol))
Besides driving potassium into cells, how else can you treat hyperkalemia in a urinary obstruction patient?
(Increase potassium excretion → unblock and give fluids)
Why are opioids, benzodiazepines, and NMDA receptor antagonists some of the pain medications of choice for urinary obstruction patients?
(They are cardiovascular sparing drugs which is important for obstruction patients)
(T/F) The unblocking procedure for urinary obstructions should be sterile.
(T)
What is the normal output of urine in small animal patients?
(1-2 ml/kg/hr, usually obstruction patients have kidney injury so will be polyuric and will need to be monitored for that and return to normal and need to make sure matching losses with fluids)
The ideal length of time to leave a u-cath in for inflammation cases is unknown but ideally it would be after what is attained?
(Normal urine output is attained)
(T/F) It is incredibly rare, like close to 0%, for a male cat with idiopathic cystitis to have a concurrent UTI.
(T)
(T/F) Idiopathic cystitis does not equal blocked.
(T)
What is the treatment for feline idiopathic cystitis?
(Time (and providing comfort via pain meds, anti-anxiety meds))
What types of stones should be considered in young, toy-breed dogs?
(Urate stones resulting from PSS)
When is dissolution of stones not a viable option for treatment of urolithiasis?
(When an animal is blocked)
What blood work values can be compared to abdominal effusion to aid in diagnosing a uroabdomen?
(Creatinine and/or potassium (if abdominal effusion potassium is 40% higher = uroabdomen, if abdominal effusion creatinine is 2x = uroabdomen))
(T/F) BUN is not a marker that should be used for diagnosing a uroabdomen.
(T)
What diagnostic tool will help you to determine if a bladder injury that is causing a uroabdomen can be managed medically versus needing surgery?
(Contrast radiography)
(T/F) Azotemia is an elevated BUN and/or creatinine.
(T)
What are the common causes of prerenal azotemia and how are you sure it is prerenal?
(Causes are dehydration and/or hypovolemia, urine should be concentrated appropriately)
Pair the following patient descriptors with acute versus chronic azotemia:
- Feeling sick with mild to moderate azotemia
- Anemic
- Good MCS
- Small, irregular kidneys
- Not anemic
- Stable with moderate to severe azotemia
- Painful and/or enlarged kidneys
- Poor MCS
- Feeling sick with mild to moderate azotemia (Acute)
- Anemic (Chronic)
- Good MCS (Acute)
- Small, irregular kidneys (Chronic)
- Not anemic (Acute)
- Stable with moderate to severe azotemia (Chronic)
- Painful and/or enlarged kidneys (Acute)
- Poor MCS (Chronic)
You have a small urine sample from what you suspect is a patient with an acute kidney injury that can only be used for two of the following tests, which would you choose?
- Culture
- UPC
- UA
- USG
(Culture and USG, complete UA is great but USG and culture are top priority)
(T/F) There is such a thing as too much fluids in an acute kidney injury case.
(T, bc the kidneys will have to get rid of the extra water you are giving the patient, that’s making them work overtime while already injured = further injury)
If there is no underlying cause of an acute kidney injury, what is the treatment?
(Supportive care and time = maintain hydration but do not overhydrate, treat hypertension as/if it occurs, monitor urine output, manage pain and nausea with meds, and provide nutritional support)
Providing maintenance fluids to an AKI patient that is anorexic/hyporexic may vary depending on what?
(The degree of polyuria or oliguria the patient has, more fluids are need for polyuria, less fluids are needed for oliguria)
(T/F) In an AKI patient, though they may not have any PE changes that indicate dehydration, you can assume they are ~5% dehydrated.
(T → most patients that are presented for acute onset of azotemia have some degree of prerenal component)
You have an AKI patient that is now showing signs of fluid overload but that is still only producing 0.5 ml of urine every 2 hours, is a diuretic an appropriate treatment for treatment of the fluid overload?
(Yes, diuretics in AKI patients may lead to worse outcomes if given to a patient that is NOT fluid overloaded, but they are an appropriate and advisable choice in a fluid overloaded patient who will not be able to urinate fast enough to fix it d/t oliguria)
What are the two administration options for supplemental at home fluids in CKD patients?
(Subq fluids or esophagostomy tube)
What are the pros and cons of at home subq fluids for tx of dehydration in CKD patients?
(Pros → easy, inexpensive initially; cons → excess salt (have to use an isotonic fluids for subq fluids), patient tolerance, and client abilities)
What are the pros and cons of at home fluids given via an esophagostomy tube?
(Pros → more physiologic (no extra salt, can literally use tap water), can adm meds easier, improved patient tolerance, and ease of administration; cons → requires general anesthesia, increased up-front cost, potential complications (stoma infection, dislodgement of tube, esophageal stricture))
Why are phosphorus binders included in treatment of CKD patients?
(Phosphorus clearing is dependent on GFR which is decreased with CKD, CKD patients will have high phosphorus and that contributes to nausea/discomfort and can worsen kidney function, phosphorus binders ameliorate that)
(T/F) Dietary changes to a prescriptions renal diet should be recommended to every CKD patient and that change may slow progression of CKD and extend life-expectancy.
(T)
