Podcasts about polyuria

OutlineChapter 14- Hypovolemic States- Etiology - True volume depletion occurs when fluid is lost from from the extracellular fluid at a rate exceeding intake - Can come the GI tract - Lungs - Urine - Sequestration in the body in a “third space” that is not in equilibrium with the extracellular fluid. - When losses occur two responses ameliorate them - Our intake of Na and fluid is way above basal needs - This is not the case with anorexia or vomiting - The kidney responds by minimizing further urinary losses - This adaptive response is why diuretics do not cause progressive volume depletion - Initial volume loss stimulates RAAS, and possibly other compensatory mechanisms, resulting increased proximal and collecting tubule Na reabsorption. - This balances the diuretic effect resulting in a new steady state in 1-2weeks - New steady state means Na in = Na out - GI Losses - Stomach, pancreas, GB, and intestines secretes 3-6 liters a day. - Almost all is reabsorbed with only loss of 100-200 ml in stool a day - Volume depletion can result from surgical drainage or failure of reabsorption - Acid base disturbances with GI losses - Stomach losses cause metabolic alkalosis - Intestinal, pancreatic and biliary secretions are alkalotic so losing them causes metabolic acidosis - Fistulas, laxative abuse, diarrhea, ostomies, tube drainage - High content of potassium so associated with hypokalemia - [This is a mistake for stomach losses] - Bleeding from the GI tract can also cause volume depletion - No electrolyte disorders from this unless lactic acidosis - Renal losses - 130-180 liters filtered every day - 98-99% reabsorbed - Urine output of 1-2 liters - A small 1-2% decrease in reabsorption can lead to 2-4 liter increase in Na and Water excretion - 4 liters of urine output is the goal of therapeutic diuresis which means a reduction of fluid reabsorption of only 2% - Diuretics - Osmotic diuretics - Severe hyperglycemia can contribute to a fluid deficit of 8-10 Iiters - CKD with GFR < 25 are poor Na conservers - Obligate sodium losses of 10 to 40 mEq/day - Normal people can reduce obligate Na losses down to 5 mEq/day - Usually not a problem because most people eat way more than 10-40 mEq of Na a day. - Salt wasting nephropathies - Water losses of 2 liters a day - 100 mEq of Na a day - Tubular and interstitial diseases - Medullary cystic kidney - Mechanism - Increased urea can be an osmotic diuretic - Damage to tubular epithelium can make it aldo resistant - Inability to shut off natriuretic hormone (ANP?) - The decreased nephro number means they need to be able to decrease sodium reabsorption per nephron. This may not be able to be shut down acutely. - Experiment, salt wasters can stay in balance if sodium intake is slowly decreased. (Think weeks) - Talks about post obstruction diuresis - Says it is usually appropriate rather than inappropriate physiology. - Usually catch up solute and water clearance after releasing obstruction - Recommends 50-75/hr of half normal saline - Talks briefly about DI - Skin and respiratory losses - 700-1000 ml of water lost daily by evaporation, insensible losses (not sweat) - Can rise to 1-2 liters per hour in dry hot climate - 30-50 mEq/L Na - Thirst is primary compensation for this - Sweat sodium losses can result in hypovolemia - Burns and exudative skin losses changes the nature of fluid losses resulting in fluid losses more similar to plasma with a variable amount of protein - Bronchorrhea - Sequestration into a third space - Volume Deficiency produced by the loss of interstitial and intravascular fluid into a third space that is not in equilibrium with the extracellular fluid. - Hip fracture 1500-2000 into tissues adjacent to fxr - Intestinal obstruction, severe pancreatitis, crush injury, bleeding, peritonitis, obstruction of a major venous system - Difference between 3rd space and cirrhosis ascities - Rate of accumulation, if the rate is slow enough there is time for renal sodium and water compensation to maintain balance. - So cirrhotics get edema from salt retension and do not act as hypovolemia - Hemodynamic response to volume depletion - Initial volume deficit reduced venous return to heart - Detected by cardiopulmonary receptors in atria and pulmonary veins leading to sympathetic vasoconstriction in skin and skeletal muscle. - More marked depletion will result in decreased cardiac output and decrease in BP - This drop in BP is now detected by carotid and aortic arch baroreceptors resulting in splanchnic and renal circulation vasoconstriction - This maintains cardiac and cerebral circulation - Returns BP toward normal - Increase in BP due to increased venous return - Increased cardiac contractility and heart rate - Increased vascular resistance - Sympathetic tone - Renin leading to Ang2 - These can compensate for 500 ml of blood loss (10%) - Unless there is autonomic dysfunction - With 16-25% loss this will not compensate for BP when patient upright - Postural dizziness - Symptoms - Three sets of symptoms can occur in hypovolemic patients - Those related to the manner in which the fluid loss occurs - Vomiting - Diarrhea - Polyuria - Those due to volume depletion - Those due to the electrode and acid base disorders that can accompany volume depletion - The symptoms of volume depletion are primarily related to the decrease in tissue perfusion - Early symptoms - Lassitude - Fatiguability - Thirst - Muscle cramps - Postural dizziness - As it gets more severe - Abdominal pain - Chest pain - Lethargy - Confusion - Symptomatic hypovolemia is most common with isosmotic Na and water depletion - In contrast pure water loss, causes hypernatremia, which results in movement of water from the intracellular compartment to the extracellular compartment, so that 2/3s of volume loss comes from the intracellular compartment, which minimizes the decrease in perfusion - Electrolyte disorders and symptoms - Muscle weakness from hypokalemia - Polyuria/poly dips is from hyperglycemia and hypokalemia - Lethargy, confusion, Seizures, coma from hyponatremia, hypernatremia, hyperglycemia - Extreme salt craving is unique to adrenal insufficiency - Eating salt off hands ref 18 - Evaluation of the hypovolemic patient - Know that if the losses are insensible then the sodium should rise - Volume depletion refers to extracellular volume depletion of any cause, while dehydration refers to the presence of hypernatremia due to pure water loss. Such patients are also hypovolemic. - Physical exam is insensitive and nonspecific - Finding most sensitive and specific finding for bleeding is postural changes in blood pressure - I don't find this very specific at all! - Recommends laboratory confirmation regardless of physical exam - Skin and mucous membranes - Should return too shape quickly - Elastic property is called Turgur - Not reliable is patients older than 55 to 60 - Dry axilla - Dry mucus membranes - Dark skin in Addison's disease Frim increased ACTH - Arterial BP - As volume goes down so does arterial BP - Marked fluid loss leads to quiet korotkoff signs - Interpret BP in terms of the patients “normal BP” - Venous pressure - Best done by looking at the JVP - Right atrial and left atrial pressure - LV EDP is RAP + 5 mmHg - Be careful if valvular disease, right heart failure, cor pulmonare, - Figure 14-2 - Shock - 30% blood loss - Lab Data - Urine Na concentration - Should be less than 25 mmol/L, can go as low as 1 mmol/L - Metabolic alkalosis can throw this off - Look to the urine chloride - Figure 14-3 - Renal artery stenosis can throw this off - FENa - Mentions that it doesn't work so well at high GFR - Urine osmolality - Indicates ADH - Volume depletion often associated with urine osm > 450 - Impaired by - Renal disease - Osmotic diuretic - Diuretics - DI - Mentions that severe volume depletion and hypokalemia impairs urea retension in renal medulla - Points out that isotonic urine does not rule out hypovolemia - Mentions specific gravity - BUN and Cr concentration - Normal ratio is 10:1 - Volume depletion this goes to 20:1 - Serum Na - Talks about diarrhea - Difference between secretory diarrhea which is isotonic and just causes hypovolemia - And osmotic which results in a lower electrolyte content and development of hypernatremia - Talks about hyperglycemia - Also can cause the sodium to rise from the low electrolyte content of the urine - But the pseudohyponatraemia can protect against this - Plasma potassium - Treatment - Both oral and IV treatment can be used for volume replacement - The goal of therapy are to restore normovolemia - And to correct associated acid-base and electrolyte disorders - Oral Therapy - Usually can be accomplished with increased water and dietary sodium - May use salt tablets - Glucose often added to resuscitation fluids - Provides calories - Promotes intestinal Na reabsorption since there is coupled Na and Glucose similar to that seen in the proximal tubule - Rice based solutions provide more calories and amino acids which also promote sodium reabsorption - 80g/L of glucose with rice vs 20 g/L with glucose alone - IV therapy - Dextrose solutions - Physiologically equivalent to water - For correcting hypernatremia - For covering insensible losses - Watch for hyperglycemia - Footnote warns against giving sterile water - Saline solutions - Most hypovolemic patients have a water and a sodium deficit - Isotonic saline has a Na concentration of 154, similar to that of plasma see page 000 - Half-isotonic saline is equivalent to 550 ml of isotonic saline and 500 of free water. Is that a typo? - 3% is a liter of hypertonic saline and 359 extra mEq of Na - Dextrose in saline solutions - Give a small amount of calories, otherwise useless - Alkalinizing solutions - 7.5% NaHCO3 in 50 ml ampules 44 mEq of Na and 44 mEq of HCO3 - Treat metabolic acidosis or hyperkalemia - Why 44 mEq and not 50? - Do not give with calcium will form insoluble CaCO3 - Polyionic solutions - Ringers contains physiologic K and Ca - Lactated Ringers adds 28 mEq of lactate - Spreads myth of LR in lactic acidosis - Potassium chloride - Available as 2 mEq/mL - Do not give as a bolus as it can cause fatal hyperkalemia - Plasma volume expanders - Albumin, polygelastins, hetastarch are restricted to vascular space - 25% albumin can pull fluid into the vascular space - 25% albumin is an albumin concentration of 25 g/dL compare to physiologic 4 g/dL - Says it pulls in several times its own volume - 5% albumin is like giving plasma - Blood - Which fluid? - Look at osmolality, give hypotonic fluids to people with high osmolality - Must include all electrolytes - Example of adding 77 mEw of K to 0.45 NS and making it isotonic - DI can be replaced with dextrose solutions, pure water deficit - Case 14-3 - Diarrhea with metabolic acidosis - He chooses 0.25 NS with 44 mEq of NaCl and 44 NaHCO3 - Talks about blood and trauma - Some studies advocate delaying saline until penetrating trauma is corrected APR about to. Keep BP low to prevent bleeding. Worry about diluting coagulation factors - Only do this if the OR is quickly available - Volume deficit - Provides formula for water deficit and sodium deficit - Do not work for isotonic losses - Provides a table to adjust fluid loss based on changes in Hgb or HCTZ - Says difficult to estimate it from lab findings and calculations - Follow serial exams - Serial urine Na - Rate of replacement - Goal is not to give fluid but to induce a positive balance - Suggests 50-100 ml/hr over what is coming out of the body - Urine - Insensibles 30-50 - Diarrhea - Tubes - Hypovolemic shock - Due to bleeding - Sequesting in third space - Why shock? - Progressive volume depletion leads to - Increased sympathetic NS - Increased Ang 2 - Initially this maintains BP, cerebral and coronary circulation - But this can decrease splanchnic, renal and mucocutaneous perfusion - This leads to lactic acicosis - This can result in intracellular contents moving into circulation or translocation of gut bacteria - Early therapy to prevent irreversible shock - In dogs need to treat with in 2 hours - In humans may need more than 4 hours - Irreversible shock associated with pooling of blood in capillaries - Vasomotor paralysis - Hyperpolarization of vascular smooth muscle as depletion of ATP allows K to flowing out from K channels opening. Ca flows out too leading to vasodilation - Glyburide is an K-ATP channel inhibitor (?) caused increased vasoconstriction and BP - Pluggin of capillaries by neutrophils - Cerebral ischemia - Increased NO generation - Which Fluids? - Think of what is lost and replace that. - Bleeding think blood - Raise the hct but not above 35 - Acellular blood substitutes, looked bad at the time of this writing - Di aspirin cross linked hemoglobin had increased 2 and 28 day mortality vs saline - Colloids sound great but they fail in RCTs - SAFE - FEAST - Points out that saline replaces the interstitial losses why do we think those losses are unimportant - Pulmonary circulation issue - Pulmonary circulation is more leaky so oncotic pressure less effective there - Talks about the lungs be naturally protected from pulmonary edema - Rate of fluid - 1-2 liters in first hour - Suggests CVP or capillary wedge pressure during resuscitation - No refs in the rate of fluid administration section - Lactic acidosis - Points out that HCO can impair lactate utilization - Also states that arterial pH does not point out what is happening at the tissue level. Suggests mixed-venous sample.ReferencesJCI - Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia and a nice review of this topic: Altered Prostaglandin Signaling as a Cause of Thiazide-Induced HyponatremiaThe electrolyte concentration of human gastric secretion. https://physoc.onlinelibrary.wiley.com/doi/10.1113/expphysiol.1960.sp001428A classic by Danovitch and Bricker: Reversibility of the “Salt-Losing” Tendency of Chronic Renal Failure | NEJMOsmotic Diuresis Due to Retained Urea after Release of Obstructive Uropathy | NEJMIs This Patient Hypovolemic? | Cardiology | JAMAAnd by the same author, a textbook: Steven McGee. 5th edition. Evidence-Based Physical Diagnosis Elsevier Philadelphia 2022. ISBN-13: 978-0323754835The clinical course and pathophysiological investigation of adolescent gestational diabetes insipidus: a case report | BMC Endocrine DisordersSensitivity and specificity of clinical signs for assessment of dehydration in endurance athletes | British Journal of Sports MedicineDiagnostic performance of serum blood urea nitrogen to creatinine ratio for distinguishing prerenal from intrinsic acute kidney injury in the emergency department | BMC NephrologyThe meaning of the blood urea nitrogen/creatinine ratio in acute kidney injury - PMCLanguage guiding therapy: the case for dehydration vs volume depletion https://www.acpjournals.org/doi/10.7326/0003-4819-127-9-199711010-00020?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmedValidation of a noninvasive monitor to continuously trend individual responses to hypovolemiaReferences for Anna's voice of God on Third Spacing : Shires Paper from 1964 (The ‘third space' – fact or fiction? )References for melanie's VOG:1. Appraising the Preclinical Evidence of the Role of the Renin-Angiotensin-Aldosterone System in Antenatal Programming of Maternal and Offspring Cardiovascular Health Across the Life Course: Moving the Field Forward: A Scientific Statement From the American Heart Association2. excellent review of RAAS in pregnancy: The enigma of continual plasma volume expansion in pregnancy: critical role of the renin-angiotensin-aldosterone systemhttps://journals-physiology-org.ezp-prod1.hul.harvard.edu/doi/full/10.1152/ajprenal.00129.20163. 10.1172/JCI107462- classic study in JCI of AngII responsiveness during pregnancy4. William's Obstetrics 26th edition!5. Feto-maternal osmotic balance at term. A prospective observational study

Chris Lattner, the co-founder of Tinder, discusses his experience with polyuria, a rare condition in which excess sweat causes a large volume of urine.

Today's Episode Dr. Suzanne Boyle reviews the case of a 20 year old female suffering from polyuria, polydipsia, and nocturia. About Dr. Raj Dr Raj is a quadruple board certified physician and associate professor at the University of Southern California. He was a co-host on the TNT series Chasing the Cure with Ann Curry, a regular on the TV Show The Doctors for the past 7 seasons and has a weekly medical segment on ABC news Los Angeles. More from Dr. Raj www.BeyondThePearls.net The Dr. Raj Podcast Dr. Raj on Twitter Dr. Raj on Instagram Want more board review content? Crush Step 1 Step 2 Secrets Physiology by Physeo Step 1 Success Stories The InsideTheBoards Study Smarter Podcast The InsideTheBoards Podcast Study on the go for free! Download the Audio QBank by InsideTheBoards for free on iOS or Android. If you want to upgrade, you can save money on a premium subscription by customizing your plan until your test date on our website! Produced by Ars Longa Media To learn more about us and this podcast, visit arslonga.media. You can leave feedback or suggestions at arslonga.media/contact or by emailing info@arslonga.media. Produced by: Christopher Breitigan Executive Producer: Patrick C. Beeman, MD Legal Stuff InsideTheBoards is not affiliated with the NBME, USMLE, COMLEX, or any professional licensing body. InsideTheBoards and its partners fully adhere to the policies on irregular conduct outlined by the aforementioned credentialing bodies. The information presented in this podcast is intended for educational purposes only and should not be construed as professional or medical advice. Learn more about your ad choices. Visit megaphone.fm/adchoices

In this Vet Candy Mini, we talk about the clinical symptom of polyuria from causes and clinical presentation to treatments and continuous care. This show is hosted by board certified veterinary criticalist, Dr Carey Hemmelgarn. This program is brought to you by Merck Animal Health. • What is #polyuria• Clinical presentation of polyuric patients• HowContinue reading "Polyuria"

We try to explain these conditions, from the introduction of the disease to the method of examination and diagnosis and finally treatment.

 Lindsey presents a case of polyuria to Dan, Jack, and Sharmin Hypernatremia schema  Polyuria schema  Download CPSolvers App here Patreon website

Welcome to the WellMedic podcast. In this podcast series. I will focus on going through several MRCGP AKT scenarios that will focus on the application of your knowledge. Each episode will cover a clinical topic taken from within the MRCPG curriculum guide. In this AKT podcast episode, we will cover the differential diagnosis of polyuria. The key is to focus on the application of your knowledge, but also some of the finer details covered within the relevant guidelines. WellMedic.co.uk hosts this MRCGP AKT podcast. WellMedic is a platform that focuses on the wellbeing of doctors across the UK. As a founder of WellMedic, I have developed online courses to help GP trainees PASS the MRCGP AKT.

Stay tuned for the answer

Episode Description Dr. Rencic presents a clinical unknown on Virtual Morning Report to CPSolvers, Rabih and Reza. Download CPSolvers App here Patreon website Schema 1  Schema 2  Whiteboard Want to test your learning? Take our Episode Quiz here.

Lauren and JJ work up weight loss and behavioral changes in a feline patient. This episode includes an overview of the diagnosis and treatment of feline hyperthyroidism. Sources: 1. 2016 AAFP Guidelines for the Management of Feline Hyperthyroidism, Harney, H. C. et al. May 3, 2016. https://catvets.com/guidelines/practice-guidelines/feline-hyperthyroidism 2. Hyperthyroidism in Animals. Peterson, M. E. Merck Veterinary Manual. July 2019. https://www.merckvetmanual.com/endocrine-system/the-thyroid-gland/hyperthyroidism-in-animals 3. Diagnosis and management of feline hyperthyroidism: current perspectives. Vaske, H. et al. Veterinary Medicine: Research and Reports. March 2014. https://www.dovepress.com/diagnosis-and-management-of-feline-hyperthyroidism-current-perspective-peer-reviewed-fulltext-article-VMRR

Dr. Madeline McCrary and Dr. Bob Centor present a clinical unknown to Dr. Joel Topf. Schema #1 Schema #2 Download CPSolvers App here Patreon website Dr. Joel Topf Joel Topf went to medical school at Wayne state University School of Medicine and did Med-Peds at Indiana University. He completed an adult fellowship in nephrology at… Read More »Episode 73: Clinical unknown with Dr. Joel Topf – Polyuria

Main message of this interview centered on Health Goals with Amara 2020. A program I Started on Facebook this year. I was invited by an On Air Personality from GO Uni Radio 106.9fm, Enugu, Nigeria; via a reply I left on his comment in my Facebook post on 31st January 2020. We discussed the first three Goals which are Oral Care, Skin Care in relation to use of antiseptics and disinfectants, and finally we dealt on "people being aware of incorrect health teaching" in this case, who talked on definition of diabetes, and it's major signs(Polydispia, Polyphagia, and Polyuria), hypertension, it's causes and risk factors. If you are new here kindly subscribe to channel, you can follow me on Facebook @Amara Uzodigwe. Don't forget to leave a voice message for me, if you find this podcast interesting. Here is the link to send a voice message to me: anchor.fm/Amara-Uzodigwe/message --- Send in a voice message: https://anchor.fm/amara-uzodigwe/message

Viiden viikon kuluttua sairastumisesta potilas oli jälleen hyvävointinen, mutta runsasvirtsaisuus jatkui edelleen.

Session 21 Today, we’ve got some interesting case of a 14-year-old male with some malaise and abdominal pain. Once again, we're joined by Dr. Karen Shackelford of BoardVitals. Check out the resources they have to offer. Use the promo code BOARDROUNDS to save 15% off upon purchasing a QBank. Also, they have an Ask a Clinician feature where clicking a button gives you access to a physician who will help you through specific questions or content. This feature comes with their 3-month and 6-month plan. This podcast is part of the Meded Media network where we help premeds and medical students as they journey towards becoming great physicians. [02:15] Question of the Week A 14-year-old male is evaluated for malaise and abdominal pain. He reports passing dark urine this morning. His past medical history is significant for Streptococcal pharyngitis ten days ago, for which he received Amoxicillin. Today, his vital signs are within normal limits, except for an elevated blood pressure of 145/95 mmHg. Examination reveals spatial edema with pronounced periorbital swelling. He has 1+ pedal edema bilaterally. Abdominal exam reveals mild, diffuse tenderness without rebound or guarding. Laboratory studies are unremarkable except for a serum creatinine of 2 mg/dL. What is the common finding associated with the patient's condition? (A) Hypovolemia (B) Polyuria (C) Red blood cell cast (D) Hypokalemia [03:30] Thought Process Behind the Answers The correct answer here is C. Basically, the patient has glomerulonephritis. This is characterized by red blood cell casts that are almost pathognomonic for glomerulonephritis. Poststreptococcal glomerulonephritis is not common but also not unusual. The history of streptococcal pharyngitis should lead to that conclusion. Other symptoms of glomerulonephritis include white blood cell casts, hematuria, and proteinuria. But for this question, you have to hone in on the glomerulonephritis. Other findings in the urine sediment include granular casts. Dysmorphic red blood cells are strongly associated with glomerulonephritis and proteinuria. This is clinically manifested by a slow and progressive rise in serum creatinine and fluid hypertension, peripheral or periorbital edema, and sometimes, hypercoagulability. Rhabdomyolysis may come to mind but it wasn't really an option among the choices. This could happen on the boards. There might be systemic manifestations of some underlying disease process associated with glomerulonephritis. There's a group of immunologically triggered disorders that result primarily or characterized by glomerular inflammation. It can also manifest the proliferation of glomerular tissues that damage that basement membrane, mesangium, or the capillary endothelium. [07:15] Understanding the Other Answer Choices Glomerulonephritis is associated with hypervolemia. In this case, you have the proteinuria. But with the edema, you should immediately be able to figure out that it wasn't associated with hypovolemia. The patient had pedal edema and periorbital edema. It is also important to mention that there are three primary mechanisms of glomerular inflammation. And what distinguishes a nephrotic syndrome from glomerulonephritis is the inflammation as a mechanism of damaging the glomerular apparatus. This might come in the boards that the mechanisms are either immune complex deposition as in this case. Anti-glomerular basement disease is associated with Wegener's granulomatosis, eosinophilic granulomatosis with polyangiitis, or microscopic polyangiitis. The other mechanism is the antineutrophil cytoplasmic autoantibody (ANCA) or small vessel vasculitis. It causes damage to the glomerular filtration barrier. This results in the leakage of plasma proteins and inflammatory cells into the renal tubule. Patients may even have pulmonary edema in some cases. The hypertension results from retaining salt and water. The patient has a rising creatinine and so hyperkalemia is more likely to happen. So this is an easy one to rule out. Polyuria is associated with diabetes and causes diabetic ketoacidosis. This isn't that uncommon. Further laboratory testing is needed to determine the ideology. Typically on post-streptococcal glomerulonephritis, it is self-limited. A fair amount doesn't progress to renal failure. But testing is needed to determine the ideology on other cases whether it's long-lasting or the significant decline in glomerular filtration rate. There is usually a raise in serum complement levels, anti-neutrophilic cytoplasmic autoantibodies, antiglomerular basement membrane autoantibodies, antinuclear antibodies, anti-double stranded DNA. The treatment is just supported in these cases or treatment of the underlying disorder if there is one that you can determine from these other tests. Links: Meded Media BoardVitals

Is you dog or cat drinking or urinating more than normal? Find out why this might be happening and how to deal with it. --- Support this podcast: https://anchor.fm/dr-don-k-shreves/support

Silver Marten Rabbit Hello Listener! Thank you for listening.  If you would like to support the podcast, and keep the lights on, you can support us whenever you use Amazon through the link below: It will not cost you anything extra, and I can not see who purchased what. Or you can become a Fluffle Supporter by donating through Patreon.com at the link below: Patreon/Hare of the Rabbit What's this Patreon? Patreon is an established online platform that allows fans to provide regular financial support to creators. Patreon was created by a musician who needed a easy way for fans to support his band. What do you need? Please support Hare of the Rabbit Podcast financially by becoming a Patron. Patrons agree to a regular contribution, starting at $1 per episode. Patreon.com takes a token amount as a small processing fee, but most of your money will go directly towards supporting the Hare of the Rabbit Podcast. You can change or stop your payments at any time. You can also support by donating through PayPal.com at the link below: Hare of the Rabbit PayPal Thank you for your support, Jeff Hittinger. The Silver Marten is a breed of domestic rabbit. Although they are raised to compete in pet shows and agricultural shows, they are also regarded as "loveable and charming" pets. Few can deny that Silver Marten is one of the most striking of rabbit colors. The top color of the rabbit is a dark rich self variety that provides high contrast with silver-white markings underneath. Known for cute expressions, unique coloring and charming personality, the Silver Marten breed of rabbit has been a favorite for nearly a century! Silver Marten is both the name of a breed and a color. The breed came first, and then was used to introduce the color as a variety in a number of other breeds, such as the Netherland Dwarf, Jersey Wooly, and most recently, Mini Rex. This has occurred a number of times: the Lilac, American Sable, Standard Chinchilla, and Chocolate Havana are all examples of breeds that began with a new color mutation, and then lent their genes to produce a new variety in already-accepted rabbit breeds. Description The Silver Marten is a medium-sized rabbit that weighs between 6.5 and 8.5 lbs. when fully grown. They are hardy and have fur that is described as soft "with a beautiful polished look to it". While more timid than some larger breeds of rabbit, they are still considered an excellent pet. The Silver Marten is playful, enjoys romping around, and likes playthings it can toss around its cage. The Silver Marten’s glossy fly-back coat is soft, featuring a shiny dark coat on top and a silver on the bottom. The Silver Marten Rabbit is one of the smallest breeds to have a commercial body type, weighing anywhere from 6.5-9 lbs once it is fully grown. Unlike some breeds in this category, the Silver Marten has small ears that stand vertically on its head. The Silver Marten’s eyes are alert and bright, and should compliment their variety – the darker shades having dark brown eyes and the diluted shades having blue-gray eyes. The body of the Silver Marten is firm without being bulky and should be well rounded from the shoulders and up over the hips, having an almost half-moon appearance when properly posed. Their hips are well-developed and should not pinch in at the table. They often have a muscular look that makes them seem larger than what they actually are. History The Silver Marten breed of rabbit was originally a naturally-occurring mutation in the coats of Chinchilla-colored rabbits. The Silver Marten rabbit is a domestic breed of rabbit which was developed in the United States. Some say these strangely-marked little black rabbits occurred early on, while others say it was the cross-breeding of Black and Tan bloodlines that created the Silver Marten. These genes later manifested as black "sports" described as "strange little black rabbits" as well as similar silver rabbits among standard Chinchilla rabbit litters. According to the Silver Marten Club, these mis-marked Chinchillas occurred on their own, but that the Black and Tan was later introduced, in an attempt to improve the clarity of color and markings on these bunnies. This seems a logical explanation, particularly when one sees the similarity between the Silver Marten and Black and Tan markings. It was in 1924 that the Silver Marten rabbit was finally given his name and, by 1927, they had developed a working standard for the black and chocolate Silver Marten. In 1927, a working standard for black and chocolate varieties was established by the American Rabbit Breeders' Association and the first Silver Marten Club was chartered. A blue variety of this breed was accepted in 1933. The sable variety, the last to be approved, was accepted in 1993. Coat The Silver Marten’s glossy fly-back coat is arguably one of the most beautiful, having a soft, shiny dark coat on top and a silver on the bottom. Despite having this gorgeous coat, Silver Martens do not require much maintenance to keep it in looking its best. Bi-weekly grooming with a slicker brush or damp hands should keep it looking its best. During molting season, simply increase grooming frequency to once a week. Colors When it comes to Silver Marten Rabbit, the ARBA accepts a top color of black, blue, chocolate or sable (a sephia-type hue). Markings consist of a white chin, belly, underside-of-tail, inside of ears, eye circles and nostril markings. Silver Martens should also have some “silvering” or white ticking up the lower sides of the rabbit, edging the belly marking. This is simply a result of the Marten marking pattern, and not to be confused with true silvering found in the Silver or Silver Fox breeds. The pattern of the Silver Marten rabbit has similarity with the Tan rabbit breed, but the only difference is that the Silver Marten rabbit has the Chinchilla gene instead of the normal full color. That means the yellow factor in the Tan rabbits is changed to white; the difference between tan and marten is the same as the difference between chestnut and chinchilla. Varieties Black Silver Marten is the most popular variety of the breed. Specimens should be jet black color, its fur being black as far down the hair as possible, with contrasting silver markings that are shape and defined. A Black Silver Marten should have dark brown eyes and an underside of dark slate blue. Blue Silver Marten is the second most popular breed. Their color should be an even dark "blue" everywhere. Their eyes should be bluish gray. Sharp markings in the blue variety are often slower to fully develop than in the Black Silver Marten. Chocolate Silver Martens should be a rich, dark brown color "like semi-sweet rather than milk chocolate candy" and brown eyes. Their bellies are the same color but lighter, with pigment only at the tips of the fur. Breeders say that their fur has a tendency to fade over time, especially if given much sunlight. Sable Silver Martens, the last variety of the breed to be approved, are the least common. They should be medium sepia brown "on the saddle, shading evenly down the sides to a lighter color". The rabbit's ears, face, tail, outside of the feet, and lower legs should be very dark sepia brown, nearly black, that provides a distinct contrast to the color of the body. Correctly colored sables must be a silvery color at birth, but as they age they take on a blotchy appearance. The coat typically darkens throughout the rabbit's lifetime, each successive molt reducing the contrast with the points. Silver Marten rabbits can also be found in lilac – a light dove gray – but the color is not registerable at this point in time. Silver Marten are a compatible breed for introducing color into Dwarf Rabbit bloodlines. Care Requirements Like any other breed of rabbit, Silver Martens require a diet consisting of at least 70 percent hay. The rest of its diet is made up a healthy balance of pellets, leafy greens, fruits, and vegetables. Be aware of what kind of leafy greens you feed your rabbit, as some (such as iceberg lettuce) contain little vitamins or nutrients and, on the contrary, may contain laudanum, which can be harmful in large quantities. Some vegetables are harmful to rabbits and other fruits contain too much sugar to be considered healthy . This rabbit can either live indoors or out, depending on what it is being bred for and year-round weather conditions. Because this breed is used for show, meat and fur purposes, outdoor enclosures need to be protected from the elements and other predators, and are usually made of either wood or wire. Both indoor and outdoor rabbit enclosures need to have a solid bottom in order to place bedding, which should be spot-cleaned everyday and completely replaced at the end of every week. Enclosures need to be large enough for your rabbit to stretch out to its full length, plus have some space to hop around and explore. Health The Silver Marten Rabbit is usually used for show purposes, but it can also be an excellent pet if it is well socialized. While this breed of rabbit is not susceptible to digestive issues such as Wool Block, care has to be taken in order for it to live a long, healthy life. Two problems that are most common in outdoor rabbits are ear mites and flystrike. Flystrike occurs from soiled fur, usually during the summer. Flies lay their eggs in soiled fur and the larvae eat the rabbit. Flystrike is extremely painful, and symptoms include lack of appetite, fewer droppings in your bunny’s cage and sudden jumping/thrashing in pain. If you suspect flystrike, immediately take your rabbit to a veterinarian to get treated. If your rabbit’s diet does not consist of 70 percent hay, its incisors could begin to grow into its face/jaw. This is a painful condition and can only be corrected by a veterinarian, who can shave down the teeth. A simple change in your rabbit’s diet should keep its teeth naturally worn down. Temperament/Behavior The Silver Marten is known for being a charming little clown and terribly curious. They can, however, be a bit on the skittish side and startle easily – for this reason, one may look for a calmer breed if they are looking for a first bunny for a younger child. They are a delightful companion for older children and adults though, and their markings give them a cute appearance that few can deny. Rabbits are harder to litter train than other animals such as cats, dogs and birds, however it is possible with lots of patience, perseverance, and plenty of treats. Many rabbit owners will have a few boxes scattered across their home so their rabbit can easily access the litter box. Training them may take a few days to a few months. Be sure to provide your rabbit with a few bunny-safe toys. Rabbits have different personalities and can be picky with toys. Some rabbits are content with cardboard or a discarded piece of wood, while others require elaborate toys that provide mental stimulation. It is your responsibility to make sure your pet is healthy and happy – you’ll just have to figure out what kind of toy your rabbit prefers! Silver Marten rabbits, like most other breeds, are notorious chewers. If you are intending to have a bunny as a house pet, be forewarned that you will definitely have to “bunny-proof” your house. This means getting down on the floor and looking at anything and everything that could possibly chewed. Some examples of tasty treats, that bunnies love (and that will have you pulling your hair out about) include wood furniture legs, electrical cords, stereo/DVD/computer wiring, or important papers. Fortunately, products like Bitter Apple are available to help discourage chewing, but the best discouragement is keeping things out of reach. Kits (young rabbits) should be exposed to new people, animals and experiences early on so they are not as easily spooked when adults. This is especially important to the Silver Marten, which can be slightly more timid as adults if it is not socialized properly or for long enough. Socialized Silver Martens are marvelous pets for seniors, singles, couples and even families with children, provided they understand how to properly handle and play with a pet. Rabbits need to be treated with care and lots of love to ensure they live a long, healthy, happy life. Special Notes The average lifespan of Silver Marten rabbits is between 5 and 8 years. But they can live longer if properly cared and if kept in pairs. The Marten is listed as critical on the American Livestock Breeds Conservancy Conservation Priority List. http://www.petguide.com/breeds/rabbit/silver-marten-rabbit/ http://rabbitbreeders.us/silver-marten-rabbits http://www.roysfarm.com/silver-marten-rabbit/ http://animal-world.com/encyclo/critters/rabbits/smarten.php https://madhatterrabbits.com/2012/10/01/silver-marten/ http://www.raisingrabbitsformeat.com/silver-marten-rabbits/ RABBIT AND BIG MAN-EATER Big Man-eater (Atipa-tcoba) came to a village. He killed all of the people there and ate them. He we s going to another village when he met Rabbit. Rabbit said, "All of the people of that village have runaway." Now Big Man-eater and Rabbit both stood on one side of the trail and defecated. Big Man-eater's excrement consisted of bones of the people he had eaten. Rabbit's excrement was green grass. Afterwards they struck up a friendship and started on together. They started along another trail and made a camp. That night when they lay down near each other and Big Man-eater had fallen asleep Rabbit picked up ashes and threw them over him. He picked up some more ashes and put them on his own body. Big Man-eater did not know who did it. When Big Man-eater awoke Rabbit threw a few over himself. Then they moved their camp to another place. While Big. Man-eater was asleep Rabbit made a fire around him. He burned a neighboring dead tree through and pushed it down upon his companion's body. Big Man-eater kicked it away and woke up. He had suffered no harm. To escape suspicion Rabbit laid small pieces of the tree over his own body. He jumped up and down as if in pain. He had thrown only a few on himself. Big Man-eater threw them off in the same manner. Next day the two went on and jumped back and forth over a creek with bluffs on each side. Rabbit said to Big Man-eater, "Let us jump across it four times." Rabbit jumped across four times first and then Big Man-eater jumped across four times. "Let us jump again," said Rabbit. Big Man-eater carried a bag and Rabbit said, "Let me hold it," so Big Man-eater gave it to him. Then Big Man-eater jumped. When he tried to jump across he fell down in the water. It ran on with him out to sea. Rabbit, however, went back to his place. http://www.sacred-texts.com/nam/se/mtsi/mtsi191.htm Excess Urine and Excess Thirst in Rabbits Polyuria and Polydipsia in Rabbits Polyuria is defined as greater than normal urine production, and polydipsia as greater than normal water consumption. The average normal water intake for rabbits is 50-150 mL/kg body weight daily. This is the general expectation of water consumption, since rabbits that are fed large amounts of water-containing foods, such as leafy vegetables, will drink less water than those that are on a dry diet of hay and pellets. Normal urine production is generally expected to be between 120-130 mL/kg body weight per day. The balance between urine production and thirst are controlled by interactions between the kidneys, pituitary gland, and the hypothalamus center in the brain. Excess thirst usually occurs as a result of excess urination, as the body responds to the loss of fluid and attempts to to maintain hydration. The rabbit’s plasma fluids become highly concentrated, and this activates the thirst mechanisms. Occasionally, excess urine occurs as the result of excess thirst. In this situation, blood plasma becomes very diluted because of the excessive water intake, stimulating the center that causes frequent urination. This condition mainly affects the kidney and the heart system. Symptoms and Types Excessive thirst – drinking much more than normal Excessive and frequent urination, possibly with occasional urinary incontinence Causes Renal (kidney) failure Hepatic (liver) failure Drugs Diabetes Large quantities of sodium chloride Behavioral problems, etc. Diagnosis There are several possible causes for polyuria and polydipsia, so your veterinarian will most likely use differential diagnosis to find the underlying cause. This process is guided by deeper inspection of the apparent outward symptoms, ruling out each of the more common causes until the correct disorder is settled upon and can be treated appropriately. A complete blood profile will be conducted, including a chemical blood profile, a complete blood count, and a urinalysis. Visual diagnostics will include ultrasonography and X-ray imaging of the abdominal region. Your veterinarian will be looking for some of the more obvious and common causes, like crystals (stones) in the urine and/or urinary tract, bacterial infection, and pus cells in the urine, indicative of an immune reaction to an infection in the urinary organs. Treatment It is imperative to continue providing water until the mechanism of the disease and the cause of it are clear and the appropriate medications can be prescribed. Encourage plenty of oral fluid intake by offering your rabbit fresh water, wetting leafy vegetables, or flavoring water with vegetable juice. Offer a large selection of fresh, moistened greens such as cilantro, romaine lettuce, parsley, carrot tops, dandelion greens, spinach, collard greens, and good-quality timothy and grass hay instead of alfalfa hay. If your rabbit cannot or will not ingest enough food and water on its own to recover, you will need to maintain fluid levels and hydration by stomach tube feeding of water and nutrients. If kidney stones were found to be the underlying cause of the polyuria, your veterinarian will instruct you to decrease calcium sources, at least until the problem is resolved. Dehydration can rapidly become life threatening. To make sure that your rabbit is sufficiently hydrated, you will need to commit to frequent monitoring of urine output and water intake throughout the day https://www.petmd.com/rabbit/conditions/urinary/c_rb_polyuria_polydipsia?page=2 Word of the week is Pencil © Copyrighted

OBJECTIVES: The objective of this retrospective study was to investigate the actual incidence of postobstructive diuresis after relief of urethral obstruction in cats, as well as to identify changes in blood and urine parameters that might be associated with postobstructive diuresis (POD), and to assess the impact of fluid therapy. METHODS: The medical records of 57 male cats with urethral obstruction that were treated with an indwelling urinary catheter were retrospectively analysed. Absolute urine output in ml/kg/h every 4 h and the incidence of cats with polyuria (urine volume >2 ml/kg/h) at any time point over a 48 h period after the re-establishment of urine flow were investigated. In addition, postobstructive diuresis in relation to fluid therapy (PODFR) was defined as urine output greater than the administered amount of intravenous fluids on at least two subsequent time points. Polyuria and PODFR were investigated for their association with blood and urine laboratory parameters. RESULTS: After 4 h, 74.1% (40/54) of the cats had polyuria, with a urine output of >2 ml/kg/h. Metabolic acidosis was present in 46.2% of the cats. Venous blood pH and bicarbonate were inversely correlated with urine output in ml/kg/h after 4 h. The overall incidence of POD within 48 h of catheterisation was 87.7%. There was a significant correlation between intravenous fluid rate at time point x and urine output at time point x + 1 at all the time points except for the fluid rate at time point 0 and the urine output after 4 h. PODFR was seen in 21/57 cats (36.8%). CONCLUSIONS AND RELEVANCE: POD is a frequent finding in cats treated for urethral obstruction, and can be very pronounced. Further studies are required to determine whether or not a change in venous blood pH actually interferes with renal concentration ability. The discrepancy between the frequency of cats with polyuria and PODFR (87.7% vs 36.8%) in the present study indicates that administered intravenous fluid therapy might be the driving force for the high incidence of polyuria in some cats with naturally occurring obstructive feline lower urinary tract disease.

Polyuria/polydipsia (PU/PD) is a common presenting complaint in small animal practice; a number of different disease states can disrupt normal physiology resulting in this problem. In this episode I discuss PU/PD with Dr Rosanne Jepson who is a Lecturer in Internal Medicine at the QMHA. Some of the things we discuss include what we mean by polyuria and polydipsia, background pathophysiology that can lead to this problem, and a rational approach to the PU/PD patient. Find out more about CPD from the RVC featuring Rosanne here If you have any comments or suggestions, please get in touch (email sjasani@rvc.ac.uk; tweet @RoyalVetCollege using #saclinpod; or use the RVC's Facebook page). Also please rate the podcasts in iTunes.

Polyuria/polydipsia (PU/PD) is a common presenting complaint in small animal practice; a number of different disease states can disrupt normal physiology resulting in this problem. In this episode I discuss PU/PD with Dr Rosanne Jepson who is a Lecturer in Internal Medicine at the QMHA. Some of the things we discuss include what we mean by polyuria and polydipsia, background pathophysiology that can lead to this problem, and a rational approach to the PU/PD patient. Find out more about CPD from the RVC featuring Rosanne here If you have any comments or suggestions, please get in touch (email sjasani@rvc.ac.uk; tweet @RoyalVetCollege using #saclinpod; or use the RVC's Facebook page). Also please rate the podcasts in iTunes.