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Leah URO > Week 6 > Flashcards

Week 6 Flashcards

1
Q

How do we lose fluid?

A

Urine

Faeces/diarrhoea

Vomit

Blood loss

Third space loss (body cavities)

Inflammatory exudate

Insensible losses
- e.g. sweating & breathing (fluid lost but only to a small degree)

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2
Q

What are the 3 major compartments within the body where fluid is stored

A
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3
Q

Define dehydration and give an example

A
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4
Q

Define hypovolaemia and give an example

A
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5
Q

What are the signs of hypovolaemia

A
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6
Q

What are the signs of dehydration

A
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7
Q

Define shock

A
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8
Q

What are the 4 types of shock

A
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9
Q

Label the types of shock

A
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10
Q

How can we recognise the 4 types of shock

A
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11
Q

Gives some signs of fluid loss, clinical signs and reason in cattle

A
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12
Q

Gives some signs of fluid loss, clinical signs and reason in dog/cat

A
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13
Q

What are the types of fluids

A

Crystalloids
- isotonic, hypertonic & hypotonic

Colloids

Transfusion products

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14
Q

Describe isotonic fluids

A

Used for fluid resuscitation

for both hypovolaemia & dehydration

they equilibrate across membranes rapidly to restore both intravascular & extravascular spaces

effect on intravascular volume expansion can be shirt lived

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15
Q

Give examples of isotonic fluids

A

Hartmann’s:
- contains sodium, chloride, potassium, calcium, lactate +- magnesium
- useful in most patients
- esp. metabolic acidosis

sodium Chloride (saline):
- 0.9% sodium chloride only
- less balanced in terms of electrolytes & quite acidifying

Dextrose solutions (D5W):
- 5% glucose in 0.18% saline
- dangerous fluid type because glucose is rapidly metabolised leaving 0.18% sodium chloride which is basically water & thus hypotonic
- dont use, if you need glucose supplementation add glucose to saline or Hartmanns

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16
Q

Give examples of hypertonic fluids

A

Saline in various strengths (usually 7.2%)
- draws fluid into intravascular space (only use IV)
- fluid drawn from interstitial space so dont use in dehydrated patients
- works rapidly (useful for hypovolaemic shock)
- low volumes required so useful for large animals
- draws fluid from brain so useful in head trauma
- sodium can be dangerous so only use 1/2x per 24h & always follow with isotonic fluids

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17
Q

Give examples of hypotonic fluids

A

usually saline (0.45% NaCl)
- rarely used
- main use would be hypernatraemia (high sodium in blood) to dilute it
- be careful how quickly you reduce hypernatraemia
* sodium balances across BBB
* if you drop Na quickly –> osmotic gradient into brain –> flood brain causing cerebral oedema

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18
Q

Describe colloid fluids

A

controversial

contain macromolecules which mimic albumin (protein) in blood to provide oncotic pressure

should provide constant buff to intravascular volume by helping retain fluid

but has been shown to increase risk of death & acute kidney injury in dogs

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19
Q

Describe transfusion products

A
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20
Q

What are the routes for fluid administration

A

intravenous
- rapid & continuous
* useful for dehydration & hypovolaemia

Intraossesous
- almost as fast as IV but difficult to place & complications (rare) can be severe
- isotonic fluids only

Subcutaneous
- reliant on good subcutaneous blood supply to redistribute fluid so only for mild dehydration

Oral
- relies on functioning GIT
- often used in LA
- can be combined with nutrition via feeding tubes
- use isotonic
- too much water is bas

Rectal
- effective in horses
- only for dehydration & not in diarrhoea

Intraperitoneal
- reliant on good peritoneal blood supply
- can be painful
- rarely used

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21
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A
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22
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23
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24
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25
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26
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27
Q
A
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28
Q

How do you calculate rate of fluid administration

A
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29
Q

How can you reduce risk of a reaction when using transfusion products

A
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30
Q

How can you check if fluid is working (5 parameters and change you expect to see)

A
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31
Q

What are signs of fluid overload

A
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32
Q
  1. What is the problem?
  2. Hypovolaemic or dehydrated?
  3. Which fluid type?
  4. Rate?
A
  1. Diarrhoea –> fluid loss +- metabolic acidosis
  2. dehydrated
  3. Hartmanns
  4. picture
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33
Q

What are some common pitfalls of fluid therapy

A
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34
Q
A
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35
Q

Describe normal gross appearance of urine and what the following (abnormal) can indicate:
- dark colour
- red
- brown/green
- brown
- orange/blue
- cloudiness
- fishy odour
- sweet odour

A
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36
Q

What can glucose in urine indicate

A
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37
Q

What can bilirubin in urine indicate

A
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38
Q

What can ketones in urine indicate

A
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39
Q

What can blood in urine indicate

A
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40
Q

What can proteins in urine indicate

A
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41
Q

What are normal USG ranges in dog, cattle, horse, cats

A
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42
Q

What USG in dogs is hyposthenuric, isosthenuric and hypersthenuric

A
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43
Q

What cells in urine sediment exam are normal in small numbers

A

erythrocytes
leukocytes
epithelial cells

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44
Q

Name the structures found in urine sediment

A
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45
Q

What is this

A

Struvite

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46
Q

What is this

A

Struvite

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47
Q

What is this

A

Calcium oxalate dihydrate

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48
Q

What is this

A
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49
Q

What is this

A

Struvite

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50
Q

What is this

A

Calcium carbonate (equine)

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51
Q

What is this

A

Cystine crystals (canine)

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52
Q

What is this

A

Cast (red blood cell)

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53
Q

What is this

A

Red & white blood cells

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54
Q

What is urolithiasis

A

stony secretions in bladder or urinary tract

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55
Q

Where in urinary tract are blockages with uroliths most common in male sheep?

A

sigmoid flexure
glans penis
neck of bladder
vermiforme appendage

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56
Q

Is obstructive urolithiasis more or less common in female sheep then male sheep?

A

More common in males due to longer & narrower urethra

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57
Q

Why does obstruction with uroliths cause lethargy, penis flexing & fever (pyrexia)

A

lethargy due to pain

penis flexing because animal is trying to pass urine

fever due to inflammation

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58
Q

What are the potential causes of urolithiasis if not successfully treated

A

bladder rupture

toxin build up

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59
Q

How can you confirm diagnosis of urolithiasis

A

ultrasound

blood test
- urea, creatinine & potassium

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60
Q

How can you treat urolithiasis in rams

A

catheterisation & then surgery

or change diet

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61
Q

In what form do aquatic organisms excrete nitrogenous waste

A

ammonia

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62
Q

In what form do reptiles/birds excrete nitrogenous waste

A

uric acid

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63
Q

Describe features of uric acid

A

Made in liver

Highly insoluble:
- water conservation
- storage in eggs

Tubular secretion via reptilian-type nephrons

Excretion is independent of:
- urine flow rate
- tubular water reabsorption
- hydration state

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64
Q

Describe gout & its causes in birds & reptiles

A

Hyperuricemia (excess uric acid) => precipitates out of blood into organs and joints => gout (visceral and articular)

Causes:
- renal disease
- high dietary protein - too many AAs => more uric acid
- dehydration - urates produced can’t be flushed => renal gout
- nephrotoxic drugs - damages renal tubules

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65
Q

What are urates

A

Precipitate:
- uric acid
- protein
- Na+ (carnivorous)
- K+ (herbivorous)

Enters cloaca and mixes with faecal material

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66
Q

Why are birds and reptiles able to excrete urates even when dehydrated?

A

Uric acid crystals precipitate => no osmotic pressure so does not draw water out with it

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67
Q

Why is urinalysis useless in birds and reptiles?

A

Due to mixing of urine, urate and faecal material

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68
Q

How does the renal portal system in exotics protect against ischemic necrosis of the kidney?

A

Blood from tail/caudal body travels to the heart via the kidney
Portal system ensures blood flow to tubules (does not supply glomerulus)

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69
Q

Describe the clinical implications of the renal portal system in exotics

A

Drug pharmacokinetics:
- if drugs injected into caudal region, goes to kidneys first => damage or excretion

Caudal mesenteric vein:
- contributes to renal portal system
- disease of GIT => kidneys
- toxins from gut

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70
Q

Label the different fish nephrons

what structure is missing from all 3?

A

Loop of henle missing

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71
Q

Label the reptile nephron

A
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72
Q

describe avian nephrons

A

70-90% Reptile type nephrons:
- no LoH
- Cortex only

10-30% Mammalian type nephrons:
- LoH
- cortex -> medulla

Limited urine concentration

73
Q

Describe the avian response to dehydration

A

Aginine vasotocin (avian ADH)
- stimulated by increased plasma osmolarity
- constricts afferent arteriole (renal portal system maintains perfusion)
-controls tubular water permeability

Urine can be retropulsed from the urodeum into the colon and caecum for sodium-linked water reabsorption

74
Q

Describe sodium linked water reabsorption in avian/reptilian colon & caecum

A

Active transport of Na out of colon
Cl ions follow Na
Water follows via osmosis

75
Q

Describe reptile response to dehydration

A

Arginine vasotocin => afferent arteriole constriction and increased tubular water permeability

Reverse peristalsis of urine from urodeum => rectum/colon

High tolerance for severe dehydration

76
Q

Describe post-renal urine modification in exotics

A

Cloaca, colon, bladder:
- ions
- water
- protein
- Na+, K+
- urates

Voided urine not reflective of renal function

77
Q

Why can kidney disease cause paralysis in avian species

A

Kidneys closely associated with lumbar and sacral plexus
- spinal nerves run through kidney parenchyma

Kidney disease => renomegaly => pressure on nerve plexi => paralysis or lameness

78
Q

Describe anatomy of avian kidneys

A

Paired
Retroperitoneal
Large

79
Q

Describe lizard renal anatomy

A

Caudal aspect of kidneys fused in many species

Only some species have a bladder

80
Q

Describe snake renal anatomy

A

Right kidney cranial to left

No bladder - urine stored in distal colon or flared ends of ureters

81
Q

Describe chelonian renal anatomy

A

Kidneys in caudal coelom

Bladder = single central structure +- paired accessory bladders

Bladder osmotically permeable
- important for hibernation (hydrate them before hibernation to fill bladder)

No pelvis, pyramids, cortex or medulla

Fewer nephrons than mammals

Lower GFR
- less blood flow allows them to conserve water

Poorly developed glomeruli

No LoH (can’t concentrate urine)

82
Q

Describe sexual segment in some male squamates

A

Cells between distal tubule and collecting duct

Cells change in breeding season:
- cuboidal => columnar
- increase in size
- large eosinophilic
granules secreted into lumen

83
Q

Describe salt glands of some avian & reptile species

A

Modified nasal/lacrimal/salivary glands

Excretion of salt without water loss

Excreted by burrowing, sneezing, tongue protrusion

Dries to white powder (can be confused as fungal infection)

High salt exposure => hyperplasia/hypertrophy

84
Q

Describe fish renal anatomy

A

Single kidney

Length of coelom

Cranial division:
- endocrine
- haematopoietic

Caudal division:
- filtration (nephrons)

No LoH => hypo-osmotic urine

85
Q

Describe fish osmoregulation & nitrogenous waste

A

Water movement by osmosis across skin and gills

Nitrogenous waste (ammonia) excreted by gills, some in urine

86
Q

Describe freshwater fish osmoregulation

A

Ion loss/water gain across gills and skin

Kidney excretes water - high GFR

Gills:
- NaCl active uptake
- excrete ammonia

Dietary intake NaCl

Produce large amounts of very dilute urine

More & larger glomeruli

87
Q

Describe saltwater fish osmoregulation

A

Lose water across gills and skin

Drink seawater to replace

Gills:
- excrete NaCl
- excrete ammonia

Kidneys:
- small or no glomeruli
- remove excess divalent ions (Mg2+)

88
Q
A
89
Q

Describe amphibian renal anatomy

A

Renal portal veins:
- blood from hindlimbs => kidney => heart

Caecilians (legless, wormlike lizards):
- one kidney
- full length coelom

Caudates (salamanders, newts) and anurans (frogs, toads):
- paired kidneys
- posterior kidneys
- retroperitoneal

90
Q

Describe amphibian cloacal bladder

A

Outpouching of cloacal wall

No direct connection with excretory ducts

Urine seeps into cloaca and is forced into bladder for urine storage

Cloacal opening is closed by sphincter muscle

91
Q

Describe osmoregulation of aquatic amphibians

A

Skin water permeable - prone to evaporative water losses

Kidney must excrete excess water

Excrete ammonia through gills/skin

92
Q

Describe osmoregulation of terrestrial amphibians

A

Water conservation important

Evaporative losses

Urinary bladders stores water (aquaporins control movement)

Decreased GFR with reduced water

Most excrete urea

93
Q

Describe the clinical relevance of aquatic species osmoregulation

A

Skin is important for fluid balance and respiration:
- disease/damage can be catastrophic for health
- no surgical scrubbing (destroys mucous coating)
- sensitive to environmental contaminants
- minimise handling
- can administer fluids and meds by putting them in water
- water quality very important

94
Q

What is the issue here

A

Articular gout = uric acid deposits in synovial capsules and tendon sheath of joints

95
Q

Describe the murexide test

A

Used to confirm gout

Joint aspirate mixed with nitric acid and dried

Ammonia added

If turns mauve = uric acid present = gout

96
Q

What causes increased & decreased uric acid production in reptiles

A
97
Q

What does pink shell lesions suggest in aquatic chelonian species?

A

septicaemias

98
Q

How can you prevent septicaemia in aquatic chelonian species

A

Keep enclosure clean

Clean water thoroughly

Test water quality regularly

Remove things that could cause injury

Ensure correct temps

Balanced diet

Reduce stress

99
Q

What clinical pathological markers can be used to assess renal function?

A

GFR

Blood conc of:
- urea
- creatinine
- Phosphorous
- SDMA
- potassium

FGF-23

Urinalysis:
- USG
- Fractional clearance
- Proteinuria

100
Q

What does renal clearance depend on

A
101
Q

How dod you calculate clearance

A
102
Q

When does clearance = GFR

A

If the substance is:
- filtered
- not reabsorbed
- not secreted (non-toxic, not plasma protein bound)

103
Q

Why is creatinine a better marker to use for assessing renal function than urea

A
104
Q

Why is it important to get a baseline creatinine level for each animal when using it to assess GFR

A

A small change in creatinine (still within normal range) can be present with a large change in GFR

105
Q

What does proteinuria suggest?

A

issue with filtration in glomerulus

106
Q

What are the causes of pre-renal, renal & post renal proteinuria

A

Pre renal - overload of proteins e.g., glucosuria in hyperglycaemia

Renal (glomerular) - damaged glomeruli

Renal (tubular) - unable to resorb normal amounts of filtered protein

Post renal - inflammatory, haeorrhagic conditions e.g. urinary tract inflammation

107
Q

How is cystatin C used to assess renal function

A

Measured in blood - estimate of GFR

Measured in urine - should be completely resorbed in tubules, presence suggests tubular dysfunction/damage

108
Q

What is fractional clearance

A

the clearance of a substance (X) compared to creatinine that is neither absorbed or secreted

Example:
Volume depletion => sodium retained => fractional clearance falls

Tubular disease => sodium lost => fractional clearance rises

109
Q

How is USG used to determine if there is problem with concentrating ability?

A

Needs correlation with hydration state and/or azotaemia

110
Q

What is azotaemia and indicator of in an animal with healthy renal function?

A

poor renal perfusion

111
Q

What is azotaemia an indicator of in an animal with typical renal perfusion?

A

insufficient nephrons

112
Q

Why is hyposthenuria an ADH problem & not a renal failure problem

A

Kidney is functioning to produce dilute urine

ADH is not working to concentrate it in distal convoluted tubules and collecting duct

113
Q

What are the types of urinary casts (cylinduria)

A

Hyaline - protein

Cellular - RBC/WBC/epithelial
- suggests disease process in tubules

Granular - fine/coarse
- implies longer stasis

Waxy - end product of degeneration
- suggests long period of stasis

114
Q

What is the outcome of acute kidney insufficiency?

A

hyperkalaemia

115
Q

What is the outcome of chronic kidney insufficiency

A

Progressive as functional nephrons decrease:
inappropriate USG => azotaemia => hyperphosphataemia, acidosis

116
Q

Are these pre-renal or renal insufficiencies

A
117
Q

What is the difference between renal disease & failure

A

Failure - when compensatory mechanisms of diseased kidneys are no longer able to maintain the functions of the kidney

Disease needs to be severe to cause failure

118
Q

What is uraemia

A

severe clinical syndrome caused by accumulation of nitrogenous waste products

119
Q

What are the 3 levels of acute kidney injury

A

Pre-renal
- poor perfusion to kidneys

Renal (poor prognosis):
- acute toxicities
- kidney pathology

Post-renal:
- obstruction of urinary tract
- Leak/rupture

120
Q

What is the outcome of acute kidney injury

A

Azotaemia
Hyperkalaemia
Acidosis

121
Q

What are the clinical findings of acute kidney injury

A

Rapid and progressive
VERY sick (poor prognosis)
Can be reversible in some cases

Lethargy
Depression
Anorexia
Vomiting
Dehydration
No urine (anuria) or little urine (oliguria
Large painful bladder and kidneys

122
Q

Describe chronic kidney disease

A

Common (esp. in cats)

prolonged loss of renal tissue

Progressive - chronic interstitial nephritis

Irreversible

Clinical signs aren’t apparent until significant loss of functioning renal tissue

prognosis variable (depends on stage of kidney disease)

123
Q

What are the clinical signs of chronic kidney disease

A

PU/PD (first to appear)

Vomiting

Anorexia

Weight loss

Lethargy

Small knobbly knees

non-regenerative Anaemia

Poor haircoat

Oral lesions

Pale mucous membranes

Dehydration

Osteodystrophy
- in young dogs with CKD
- kidneys unable to maintain Ca levels so get Ca from bone

Ascites or oedema
- protein loss in urine –> not enough protein to maintain oncotic pressure in blood –> fluid leaks out

Poor platelet function

124
Q

How can you differentiate between CKD & AKI?

A

CKD has history of PU/PD

Small kidneys in CKD, swollen in AKI

Non-regenerative anaemia in CKD

Parathyroid glands large in CKD

Hyperkalaemia in AKI

Poor haircoat and skin in CKD

125
Q

Why does CKD cause PU/PD?

A

Progressive nephron loss => declining GFR

Compensatory rise in functional nephron reserve GFR => hyperfiltration

Cannot reabsorb water due to increased GFR => polyuria

126
Q

Describe secondary renal hyperparathyroidism due to renal failure

A

Low iCa due to renal failure:
- phosphate is retained and binds iCa
- urinary losses of iCa
- lower dietary intake of calcium due to inappetance
- less absorption from gut (compromised calcitriol)
=> increased PTH to compensate for iCa loss
=> increased FGF-23 to reduce phosphate levels

127
Q

What is the treatment for renal hyperphosphataemia?

A

Diet with reduced phosphate

Oral phosphate binders

Oral calcitriol therapy

128
Q

Define micturition

A
129
Q

How is retrograde flow of urine prevented

A
130
Q

What muscles control the release of urine + describe them

A

Detrusor muscle:
- around bladder
- smooth muscle
- parasympathetic and sympathetic
- sensitive to stretch

Internal urethral sphincter:
- thickening of bladder musculature
- smooth muscle
- sympathetic supply

External urethral sphincter:
- striated muscle
- voluntary control via somatic NS

131
Q

Label the muscles of the bladder

A
132
Q

describe the somatic motor supply involved in micturition

A

Innervates external urethral sphincter

Pudendal nerve from S1-2

Contracts to retain urine

Voluntary

Control comes from cerebral cortex

133
Q

Describe the parasympathetic supply involved in micturition

A

Pelvic plexus (S1-3 outflow) innervates detrusor muscle

ACh = neurotransmitter

Contracts muscle => squeezes and empties bladder

Control comes from pons & cerebellum

134
Q

Describe the sympathetic supply involved in micturition

A

L1-4 outflow

Norepinephrine =
neurotransmitter

Control comes from pons & cerebellum

Detrusor muscle:
- relaxes muscle to allow bladder to fill
- inhibitory action
- beta receptor

Internal urethral sphincter:
- contracts sphincter to retain urine
- excitatory action
- alpha receptor

135
Q

describe the detrusor reflex

A

Increased vesicular pressure from bladder
filling achieves threshold => detrusor muscle contracts

Contraction against urethral sphincter tone

Positive feedback mechanism
- once started usually continued until bladder emptied

136
Q

Describe the micturition reflex

A

Combination of detrusor reflex with inhibition of sympathetic and voluntary motor supply to bladder and urethra

137
Q

Describe autonomic bladders

A

No voluntary control of urination

Reflex pathways intact so bladder empties spontaneously

138
Q

Describe voluntary control of bladder

A

Suppression of autonomic reflexes

If bladder overfilled, intact bladder will empty automatically

139
Q

what drugs are used for animals with weak bladder that cannot hold urine?

A

Alpha-sympathomimetic drugs:
- Increases internal urethral sphincter tone

140
Q

What is the effect of skeletal muscle relaxant on micturition

A

Decreases external urethral sphincter tone

141
Q

Describe the effects of parasympathomimetic drugs on micturition

A

Increased detrusor tone

142
Q

Define incontinence

A

the lack of voluntary control of excretory functions

143
Q

What clinical syndromes are disorders of micturition

A

Inappropriate voiding

Inadequate voiding with urine overflow => dribbling

Increased urination frequency

Reduced bladder capacity

Incomplete voiding

144
Q

Define dysuria, stranguria, pollakuria, nocturia & enuresis

A
145
Q

Describe the clinical examination for disorders of micturition

A

History of voiding

Bladder size - palpation

Urethral sphincter tone - squeeze bladder to check
for leakage

Integrity of detrusor/micturition reflex - squeeze bladder
to stimulate urination

Perineal reflex - check for ‘winking’ around perineal region to check sacral nerve function

Full neurological assessment

146
Q

What is the result of an upper motor neurone lesion vs lower motor neurone lesion

A
147
Q

Where are lower motor neurone lesions of the bladder and what are the results?

A

Sacral spinal segment damage
Pelvic plexus

Absent voluntary micturition
Atonic bladder
Atonic urethral sphincters
Absent detrusor reflex
Concurrent reduced perineal reflex and anal tone
Bladder flaccid and easily expressed

148
Q

Where are upper motor neurone lesions of the bladder and what are the results?

A

High spinal cord
brain dysfunction

Absent voluntary micturition
Increased urethral tone
High volume urinary retention
Development of automatic bladder - no voluntary control

149
Q

What are some anatomical (non-neurological) disorders causing incontinence

A

Ectopic ureter:
- Congenital malformation
- ureters enter directly into urethra
- continuous dribbling
- can get 1 ectopic ureter & 1 normal (dribbling + normal urination)

Acquired abnormalities of lower urinary tract:
- neoplasia
- calculi (bladder stones block urethra)
- Trauma

150
Q

Describe the clinical findings and treatment of calculi/bladder stones blocking the urethra

A

Large bladder
does not release urine when squeezed

Need to relieve pressure via cystocentesis or catheter

151
Q

Describe the effect of trauma on the lower urinary tract

A

Cannot urinate

Urine goes into abdomen

Bladder will be normal size

Will not be trying to urinate

Fluid in abdomen => very ill

152
Q

Describe disorders of bladder function

A

Functional outflow obstruction:
- reflex dyssynergia
- Initiation of detrusor reflex with reflex contraction of urethral sphincter
- tries to urinate but cannot

Sphincter mechanism incompetence

Secondary detrusor muscle atony:
- stretch related injury => loss of contractility

Urge incontinence:
- micturition reflex at low volume
- bladder mucosa irritation

153
Q

Describe sphincter mechanism incontinence

A

Normal micturition reflex but sphincter too loose in between micturition reflexes => urine leaks when there is increased abdominal pressure e.g., when excited

154
Q

Describe signalment of sphincter mechanism incontinence

A

More common in female due to short urethra

More common in large/giant breeds

More common in spayed female (hormonal changes)

155
Q

Describe treatment strategies for sphincter mechanism incontinence

A

alpha adrenergic agonists (e.g., phenylpropanolamine)

Oestrogens

Surgery - culposuspension:
- band around bladder and pulled up into abdomen stretches urethra
- urethra stretched => increased tone and decreased diameter

156
Q

How does tail stretch injuries in cats cause bladder atony?

A

Sacral nerves stretch and pulled out of spinal cord (avulsion) => lost function

157
Q

What is bovine pyelonephritis?

A

Inflammation of renal pelvis from an ascending bacterial UTI

Most common in adults weeks/months post-partum

158
Q

What is a pyometra and how/when do they usually develop?

A

Uterus filled with bacteria and pus, often during oestrus when cervix is more open and bacteria can enter and cause infection

159
Q

What are the clinical signs of bovine pyelonephritis?

A

bloodstained or cloudy urine
Acute colic
Fluctuating temp
Drop in milk yield
Left kidney enlargement

160
Q

Why does dehydration increase risk of gout in captive birds and reptiles?

A

Uric acid excretion is independent of GFR

Uric acid still produced and secreted even though GFR is low due to dehydration

But uric acid cannot be flushed out => uric acidaemia (uric acid build up in blood) => precipitates in tissues and joints = gout

161
Q

How do you prevent dehydration in captive birds and reptiles causing gout?

A

Adequate supply of drinking water

Bath +/- misting

Adequate humidity

Appropriate diet (not too high in protein)

Measures to prevent renal disease e.g., good hygiene and biosecurity

162
Q

What adaptation do reptiles in hot and dry environments have to conserve water?

A

Fewer nephrons

Lower GFR

Excretion of uric acid instead of urea:
- Urea is high insoluble
- Comparatively lower volume of water is needed for excretion

Dramatic reduction/cease glomerular filtration in times of stress/water scarcity

Salt gland for excess Na/K secretion

Cloacal/colonic reabsorption of water

163
Q

What diet would you recommend feeding pet tortoises

A
164
Q

Name some pros & cons of different tortoise husbandry setups:
- outside all year round
- inside in a vivarium all year round
- inside on a tortoise table

A
165
Q

What 3 things must you tell tortoise owners to do in month leading up to hibernation?

A
166
Q

It is recommended that a tortoise has a vet consult prior to hibernation. when should this be and what is assessed?

A
167
Q

What 3 things should a tortoise owner monitor throughout hibernation? and what changes to these things mean they would need to be woken up?

A
168
Q

How long should tortoises hibernate for

A

6-12 weeks

169
Q

After hibernating how long does it normally take for tortoises to eat, urinate & defecate?

A
170
Q

What is Reptoboost and why might it be given to a tortoise that seems weak after hibernation

A
171
Q
A
172
Q

What diet would you recommend for pet rabbits

A
173
Q

What type of uroliths do rabbits tend to get and why?

A
174
Q

What are 5 common risk factors of urolith formation in rabbits

A
175
Q

What are common clinical signs of uroliths in rabbits

A

enlarged/painful bladder

solides in bladder palpable

blood in bladder/urine

176
Q

Why is cystocentesis risky in rabbits?

A

they have large intestines so high risk of peritonitis

177
Q

What are the common causes of PU/PD and why do they cause it?

A

Kidney disease - poor filtering so cannot reabsorb much

Diabetes insipidus - resistance to ADH or reduced ADH secretion

Diabetes mellitus - more glucose in filtrate so water stays in filtrate

Cushings -inhibition of ADH

Addisons - low aldosterone needed for RAAS - loss of conc gradient in medulla

Hypercalcaemia - association with decreased inner medullary tissue solute content

178
Q

Describe process of osmotic diuresis

A
179
Q

Why are UTIs common in dogs with diabetes mellitus?

A

Urine is more dilute => allows more bacterial growth as chemicals have been diluted

Urine contains sugars which attracts bacteria and help facilitate bacteria growth

Leah URO (8 decks)

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