Module 17 Week 1 Flashcards

1
Q

(Diagnostic Imaging of the Urinary System)

Why is a plain radiograph limited for imaging the urniary tract?

A
  • Soft tissue & fluid same opacity
  • Cannot distinguish between urinary fluid or renal parenchyma
  • kidney and bladder may not be clearly visible esp R kidney
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2
Q

What are radiographic contrast studies used for?

A

Performed when ultrasound is unavailable
Helps assess specific structures

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3
Q

What structures can be assessed with contrast studies?

A

Intrapelvic structures
Urethral rupture
Bladder rupture

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4
Q

What are the types of contrast media?

A

Negative contrast: Air, CO₂
Positive contrast: Iodine-based contrast medium

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5
Q

What must be done before a contrast study?

A

Take plain radiographic images
Perform an enema (if remembered)

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6
Q

What is Intravenous Urography (IVU)?

A

A contrast study to visualise the kidneys and ureters
Uses an iodine-based contrast medium

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7
Q

How is contrast administered in IVU?

A

Injected intravenously into the cephalic vein

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8
Q

What does IVU demonstrate?

A

Highlights the kidneys and ureters on radiographs

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9
Q

What kind of contrast does a positive contrast cystogram use?

A

Iodine contrast medium

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10
Q

How do you perform a positive contrast cystogram and what does it allow you to assess?

A

Catheter into the bladder allowing you to assess bladder position and if there are any ruptures.

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11
Q

What contrast does a negative contrast cystogram use?

A

Air/Co2

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12
Q

What does a negative contrast cystogram allow you to assess?

A

bladder position and wall thickness

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13
Q

What contrast types does a double contrast cystogram use?

A

1-5ml contrast then air

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14
Q

What does a double contrast cystogram assess?

A

Position, luminal content and wall thickness

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15
Q

Who is a retrograde urethrogram performed on?

A

Males only

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16
Q

Where is the catheter placed in a retrograde urethrogram?

A

Distal urethra

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17
Q

hat structures does a retrograde urethrogram demonstrate?

A

The urethra
The prostate (if abnormal)

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18
Q

How is a retrograde urethrogram performed?

A

A catheter is placed in the distal urethra
Contrast medium is injected
X-rays are taken to visualise the urethra

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19
Q

Who is a retrograde vaginourethrogram performed on?

A

females only

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20
Q

Where is the catheter places in a retrograde vaginourethrogram

A

Through the vulva

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21
Q

What structures does a retrograde vaginourethrogram demonstrate

A

vestibule
vagina
urethra

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22
Q

How is a retrograde vaginourethrogram performed?

A

A catheter is inserted through the vulva
contrast medium is injected
x-rays are taken to visualise

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23
Q

Where should you fan the US probe when doing an renal US to view long axis?

A

Fanny from laterally to medially to see the entire organ

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24
Q

Where should you fan the US probe when doing an renal US to view short axis?

A

Fan through to ensure you scan the entire organ

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25
Q

How might you scan to view right kidney?

A

It can be more difficukt to image so can scan between ribs

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26
Q

Compare cat kindeys to dogs lol

A

Cats be having more mobile kidneys so variable positions
They have a more rounded outline

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27
Q

What should you assess when doing a renal assessment an what compnents of the kidney should you identify?

A

Assess: Location, Size, Shape and Margins
Components: Cortex, Medulla, Corticomedullary junction, Pelvis and (ureter)

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28
Q

What is Echogenicity

A

The ability to bounce an echo

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29
Q

What is echotexture?

A

the visualized internal composition or pattern of echoes within an individual structure

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30
Q

If there is diffuse parenchymal chnages what is on you DDx?

A
  • Acute renal disease / failure
  • Chronic renal disease
  • Renal dysplasia
  • Chronic endstage kidney
  • Neoplasia eg lymphoma
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31
Q

If there is pelvic dilation/hydronephrosis what is your DDx

A
  • Obstruction
  • Pyelonephritis
  • Neoplasia
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32
Q

Describe what you would see on ultrasound of a patient with acute renal disease?

A

rounded, hazy kidney

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33
Q

What conditions are associated with reduced corticomedullary definition (hypertonicity)?

A

Nephritis
Tubular necrosis
Acute renal failure

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34
Q

What might you see in a case of ethylene glycol toxicity?

A

Hyperechic cortex +/- corticomedullary rim sign

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35
Q

What changes can be seen with chronic renal disease?

A
  • Often bilateral
  • Heterogenous cortices
  • Reduced cortico-medullary definition
  • indentations suggest old infarcts
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36
Q

What chanages can be seen with renal dysplasia?

A
  • Loss of corticomedullary definition
  • Distorted outline / abnormal shape
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37
Q

What is pelvic dilation or hydronephrosis best seen with?

A

Short axis

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38
Q

What are key features of ureteral obstruction on imaging?

A

Pelvis retains a normal shape
Ureter visible up to the point of obstruction

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39
Q

What should you check for when assessing ureteral obstruction?

A

Bladder neck
Other kidney

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40
Q

What are the internal causes of ureteral obstruction?

A

Pyelonephritis
Neoplasia

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41
Q

How does neoplasia affect the renal pelvis?

A

Causes irregular or abnormal shape of the pelvis
Leads to disrupted architecture

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42
Q

What are focal renal changes?

A
  • Neoplasia
  • Calculi
  • Cysts
  • Abscesses
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43
Q

What do calculi look like on US?

A

Hyperchoic with shadowing

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44
Q

Where are calculi located?

A

Calyces/pelvis

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45
Q

How do cysts on kidneys appear? where are they located?

A

anechoic/cloudy and located anywhere?

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46
Q

Why might cysts occur in the kidney?

A
  • Congenital
  • Associated with chronic inflammation
  • Polycystic kidney disease (PKD)
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47
Q

T/F renal abcesses are hard to Dx from cysts?

A

True

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48
Q

What should the thickness be of the echogenic wall of the bladder?

A

1-2mm

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49
Q

what are the two components of the echogenic bladder wall?

A
  • serosal layer hyperchoic line
  • mucosal layer
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50
Q

If there are changes to the bladder wall what is your DDx?

A
  • Cystitis
  • Mass - neoplasia or inflammatory polys
  • Rupture
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51
Q

If the content of the bladder are abnormal what could be th causes?

A
  • Calculi
  • Blood clots
  • Cell debris
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52
Q

What wall chanages is seen with cystitis?

A

Increase in wall thickness eitheri uniform or focally.

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53
Q

What are the two types of inflammatory polyps?

A

sessile (flat) or penunculated (with a stalk)

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54
Q

Withe a rupture in the bladder what do we see on US?

A

Free fluid and wall thickened or unchanged and extravasation of contrast.

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55
Q

Which types of urinary calculi are radio-opaque?

A
  • Struvite
  • Oxalate
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56
Q

Which types of urinary calculi are radiolucent?

A
  • Cystine
  • Urate

Mnemonic: “I can’t C U” (Cystine & Urate can’t be seen on radiographs)

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57
Q

What ultrasound feature is often seen with calculi?

A

Acoustic shadowing

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58
Q

How do urinary calculi behave in the bladder?

A
  • Variable size and shape
  • Mobile – They move and settle with gravity
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59
Q

What does radiography provide when assessing urinary calculi?

A
  • An overview of urinary stones
  • Helps check the urethra
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60
Q

Which parts of the urethra should be checked for calculi?

A
  • Perineal urethra
  • Os penis
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61
Q

Which stones are not visible on radiographs?

A

Urate & Cystine – Cannot be seen

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62
Q

What can cause gas in the bladder?

A

Latrogenic (e.g., introduced during catheterisation)
Emphysematous cystitis

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63
Q

How does emphysematous cystitis appear on imaging?

A

Small bubbles that adhere to the bladder wall

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64
Q

What could suspened contents be in the baldder?

A

Concentrated urine
Cell debris
Haemorrhage
Mucous

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65
Q

What must be done before performing a prostatic ultrasound?

A

Ensure the bladder is full

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66
Q

Why is a full bladder necessary for prostatic ultrasound?

A

It serves as a landmark
Helps move the prostate into the abdomen

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67
Q

What is the shape of the prostate on ultrasound?

A

Bilobed

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68
Q

How does the echogenicity of the prostate compare to other organs?

A

Similar to the spleen

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69
Q

What structures can be visualised in a prostatic ultrasound?

A

Capsule of the prostate

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70
Q

What should be noted about the prostate in castrated animals?

A

The prostate will be smaller

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71
Q

What should be assessed during a prostatic ultrasound?

A

Location
Size
Shape
Margins
Echogenicity
Echotexture

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72
Q

What are the parenchymal changes that can affect the prostate?

A

Benign prostatic hyperplasia
Prostatitis
Neoplasia

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73
Q

What fluid-filled lesions can be identified in the prostate?

A

Cysts
Abscess
Para-prostatic cyst

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74
Q

What is benign prostatic hyperplasia most common in?

A

Entire male dogs

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75
Q

How does a benign prostatic hyperplasia appear on US

A

Hyperechoic

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76
Q

How does Acute inflammation of the prostate present on US?

A

Hypoechoic

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77
Q

How is chronic inflammation of the prostate present in the US?

A

Hyperchoice and mottled

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78
Q

How does the prostate appear on US when neoplasia is involved?

A

Mottled
Mineralisation
Locally invasive

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79
Q

Where can prostate neoplasia mestastasis too?

A

lungs

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80
Q

What is prostatic cysts a commone finding with?

A

BPH

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81
Q

Do prostatic abscesses have distinct or indistinct margins?

A

indistinct

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82
Q

What do bladder abscess contents appear like on US?

A

Cloudy with a surrounding reaction

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83
Q

(Approach to Azotaemia and Acute Kidney Injury in Small Animals)

what is the main rolde of the kidneys?

A

To maintain the volume and balanced composition of the ECF.

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84
Q

What are the other functions of the kidneys?

A
  • Filtration of blood & excretion of metabolic waste
  • Acid-base balance
  • Water/volume regulation
  • Electrolyte & mineral homeostasis
  • Blood pressure regulation
  • Erythropoietin release- involved in creation of RBCs
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85
Q

What is the clinical Presentations of Kidney Disease

A

PUPD (Polyuria/Polydipsia)
Inappetence/Weight Loss
Depression/Lethargy
GI Signs (Vomiting/Nausea/Diarrhoea)
Ascites/Subcutaneous Oedema
Haematuria
Pain
Abdominal Mass

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86
Q

What is Azotaemia?

A

Abnormal increase in non-protein nitrogenous wastes in the blood

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87
Q

What does azotaemia suggest?

A

Suggests failure of filtration & excretion of metabolic waste.

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88
Q

Does Azotaemia Always Mean Kidney Disease?

A

No! Kidney disease ≠ azotaemia

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89
Q

What are the Types of Azotaemia?

A

Pre-Renal Azotaemia – Decreased blood flow to kidneys (e.g. dehydration, shock)

Renal Azotaemia – Intrinsic kidney disease, nephron damage

Post-Renal Azotaemia – Urinary obstruction, bladder rupture

90
Q

Hoow is urea made?

A

Urea is made in the liver from ammonia via the urea cycle.

91
Q

How is ammonia made

A

Ammonia is mostly made during degradation of amino acids

92
Q

What Factors Affect Urea Secretion?

A
  • Age
  • Liver function
  • Dietary protein content (including GI bleeding)
  • Endogenous protein catabolism
  • Hydration
93
Q

What Factors Affect Urea Excretion?

A
  • Renal function
  • Lower urinary tract function
94
Q

What is creatinine?

A

Creatinine is a waste product that comes from the breakdown of muscle.

95
Q

What is the rate of production of creatinine?

A

It is produced at a constant rate which is determined by muscle mass and is then filtered in the glomerulus.

96
Q

Serum concentration of creatinine is decreased with what?

A

Reduced muscle mass

97
Q

Serum concentration of creatinine is increased with what?

A
  • Reduced renal clearance
  • Urine excretion failure (eg. urinary tract rupture)
98
Q

What is the GFR?

A

Flow rate of filtered fluid through the kidneys

99
Q

What reduces the GFR?

A
  • Decreased renal perfusion
  • Decreased renal function
  • Obstruction of urine flow
100
Q

Why are meaasurements of urea and creatinine used as inidrect markers for GFR?

A

cheap and easy tests

101
Q

Describe how clinical signs work with azotaemia?

A
  • Not all azotaemic patients have clinical signs
  • Severity of clinical signs not directly proportional to magnitude of increase
  • Rate of accumulation has an effect on severity of signs
102
Q

What is the clinical symptoms of uraemia?

A
  • inappetance
  • Depression
  • Vomiting/nausea
  • Halitosis
  • oral ulceration/stomatitis
  • Diarrhoea
103
Q

T/F All uraemic patients are azotaemic but not all azotaemic patients are uraemic

104
Q

what are your differentials for pre-renal axotemia?

A
  • Hypovolaemia
  • Hypotension
  • Aortic/renal thromboembolism
105
Q

what are your differentials for renal axotemia?

A
  • Nephron damage
  • Nephron loss
106
Q

What are your differentials for post-renal axotemia?

A
  • Ureterolith
  • Urethrolith
  • Bladder rupture
107
Q

If on history you have a animal thats not drinking and has increased losses (vom or diarrhoea) what kind of axotaemia do you potentially have?

108
Q

If your patients had dysuria or stranguria what kind of azotemia might you have?

A

Post-renal

109
Q

If on history your patient they are failing to pass urine, is post-renal the only option for diagnosis?

A

No could be a faulure to produce urine rather than not peeing at all so renal too

110
Q

If the bladder is huge and there is localised subcutaneous fluid around perineum or ventral abdomen, what type of azotaemia is most likely?

A

Post-renal

111
Q

If there is free peritoneal fluid (urine) what kind of azoteamia is it most likely to be?

A

Post-renal

112
Q

When should urine concentration be assessed?

A

Before fluid therapy

113
Q

What does hypersthenuric (very concentrated) urine suggest?

A

Pre-renal azotaemia

114
Q

Can pre-renal azotaemia have dilute urine?

A

Yes! If due to:

Diuretics
Steroids
Hypoadrenocorticism

115
Q

What urinalysis finding suggests renal azotaemia?

A

Active sediment with tubular casts

116
Q

What urinalysis finding suggests renal or post-renal azotaemia?

A

Haematuria

117
Q

Whats the urine specific gravity 1.00 to 1.007 called?

A

hyposthenuria

118
Q

Whats the urine specific gravity 1.008 to 1.012 called?

A

isosthnuria

119
Q

Whats the urine specific gravity 1.013 to 1.055 called?

A

hypersthenuria

120
Q

If you found a dehydrated to have hyposthenuric, isothenuric or minimla concentrated urine what would this suggest?

A

Problem with renal

121
Q

What is renal disease?

A

Damage or functional impairment of kidneys with varying severity

122
Q

What is renal insufficiency?

A

Functional impairment not severe enough to cause axotaemia but sufficient to cause loss of renal reserve

123
Q

What is renal failure?

A

Functional impairment severe enough to cause azoteamia and urine concentrating ability is usually impaired

124
Q

What is acute kidney injury?

A

It is a sudden and often reversible reduction of the elimination and metabolic function of the kidneys

125
Q

Why are kidneys at such a high risk to being damaged?

A
  • High blood floe
  • Toxins may be secreted/reabsorbed by tubular cells
  • Potential concentrating effects of toxins in urine
  • Play a role in biotransformation of drugs/toxins
126
Q

What things can lead to reduced renal perfusion and, ultimately, acute kidney injury?

A
  • Dehydration
  • Hypovolaemia
  • Decreased cardiac output
  • Hypotension
  • Shock
127
Q

What nephrotoxic drugs can cause acute renal injury?

A
  • NSAIDs
  • Aminoglycosides
  • Doxorubicin
  • Cisplatin
128
Q

What infections can cause acute renal injury?

A
  • Leptospirosis*
  • Borreliosis (Lyme disease)
129
Q

What toxins can cause acute renal injury?

A
  • Lilies (cats)
  • Grapes/raisins (dogs)
  • Ethylene glycol (anti-freeze)
130
Q

Describe the initiation phase of acute renal injury?

A

Something damages part of some of the nephron leading to dysfunction

131
Q

Describe the extension phase of acute renal injury?

A

Ischemia, hypoxia, inflammation & cellular injury result in cell death & further nephron damage.

132
Q

Describe the maintenance phase of acute renal injury?

A

Ongoing cell death occurs with cell recovery and early repair

133
Q

Describe the recovery phase of acute renal injury?

A

Gradually reversible renal lesions are repaired & viable nephrons hypertrophy

134
Q

What can you find on clinical examination of patient with acute renal injury?

A
  • Often dehydrated
  • May have uraemic ulcers
  • halitosis
  • Usually normal to large kidneys and could be painful
  • There should also be urine produaction
135
Q

How should you diagnose acute kideny injury?

A
  • Collect blood and urine before fluid therapy
  • Identify azotaemia
  • rule out post-renal causes by history and clinical exam
  • identify reduced urine conc ability via urinalysis
  • differentiate acute from chronic kidney disease
136
Q

How would you differentiate acute from chronic kindey dosease? and why?

A
  • history, clinicale xamination, lab findings
  • It affects treatment and short to long-term prognosis
137
Q

What are other typical clinopathological abnormalities see with acute kidney injury?

A
  • Initial hyperkalaemia
  • Initially normal phosphate then hyperphosphataemia
  • Total calcium may be high, low or normal but if marked high consider hypercalcaemia as cause
  • PCV may be increases due to dehydration
138
Q

What is anuria?

A

No urine production

139
Q

What is oliguria?

A

output less thatn 0.25ml/kg/hr

140
Q

What is polyuria?

A

more than 2ml/kg/hr

141
Q

What is normal urine output?

A

1-2ml/kg/hr

142
Q

What are the general principles for treating acute kidney injury?

A
  • Remove the inciting cause
  • Restore renal perfusion
  • Monitor urine output and consider drugs to increase urine output
  • Monitor electrolytes, acid-base balance, hydration status
  • Treat uraemic complications & provide nutrition
  • Investigate underlying causes
143
Q

(Approach to and Management of chronic kidney disease in Small Animals)

What is chronic kindey disease?

A

It is a loss of functional renal tissue due to prolonged process. It is usually progessive and irreversible

144
Q

Is chronic renal failure a end-stage process?

A

Yes obvs die

145
Q

Why is CKD important?

A
  • Prevalence of 1-3% in cats, 0.5-1.5% in dogs
  • Affects animals of all ages
  • Incurable diseases
  • Treatment can modify disease progression
  • Prolonged survival is common (especially in cats)
146
Q

What are the degenrative causes of CKD?

A
  • Chronic interstitial nephritis
  • Renal infarcts
147
Q

what are the developmental causes of CKD?

A
  • Familial renal dysplasia
  • Polycystic kidney disease
148
Q

What are the metabolic causes of CKD?

A

Hypercalcaemia

149
Q

What are the neoplastic causes of CKD?

A
  • Renal lymphoma
  • Renal carcinoma
150
Q

What are the iatrogenic causes of CKD?

A

Vitamin D supplememtaion
Nephrotoxic drugs

151
Q

What are idiopathic causes of CKD?

A

renal amyloidosis
primary glomerulopathies

152
Q

What are immune-mediated causes of CKD?

A

Immune-complex mediated glomerulonephritis

153
Q

what are the infectious causes of CKD?

A

pyelonephritis
borreliosis

154
Q

What could CKD be a sequel too?

A

Urinary obstruction or acute renal failure

155
Q

Descrine the pathophysiology of CKD?

A

CKD leads to nephron damage and kidneys have limited ways to respond. Nephrons cannot regen or replicate as nephrons are lost, remaining nephrons have to filter more blood leading to glomerular hypertension and hyper filtaration.

156
Q

What can prolonged nephron injury lead to?

A
  • infiltration of inflammatory cells
  • profibrotic cytokine production
  • Hypoxia leading to further injury
157
Q

If number of fephrons falls below a third of normal amount what happens?

A

The urine concenrating ability becomes impaired

158
Q

If number of nephrons falls below a quarter of normal amount what happens?

A

azotaemia develops

159
Q

What are consequences of CKD?

A
  • Azotaemia and uraemia – due to reduced GFR
  • PUPD – due to tubular damage & fewer nephrons
  • Hyperphosphataemia
  • Increased PTH (renal secondary hyperparathyroidism)
  • Hypokalaemia
  • Anaemia
  • Haemorrhage
  • Hypertension
  • Proteinuria
  • Metabolic acidosis
160
Q

What is hyperphosphatemia?

A

Phosphate excreted vua filtration through glomeruli

161
Q

What is Hyperphosphatemia

A

Hyperphosphatemia is a condition in which you have too much phosphate in your blood

162
Q

How is hyperphosphataemia a consequence of CKD?

A

Phosphate excreted via filtration through glomeruli and due to reduced Glomeruli filtration rate with CKD phospahte retained in blood.

163
Q

What are the effects of Hyperphosphatemia?

A

unlikely to directly cause clinical signs but it does drive secondary hyperparathyroidism which leads to disease progression and reduced survival

164
Q

What are the neuro effects of hyperparathyroidism?

A

Neurological: Likely uraemic toxin leading to depression

165
Q

What are the skeletal effects of HYperparathyroidism

A

Skeletal: Can lead to osteopenia, tooth loosening, pathological fractures

166
Q

What are the renal effects of Hyperparathyroidism

A

Renal: Causes renal cell tubular damage

167
Q

What are the causes of hypokalaemia in CKD?

A

Reduced intake, reduced renal potassium reabsorption, renal tubular acidosis.

168
Q

What are the clinical signs of hypokalaemia in CKD?

A

Neuromuscular weakness (ventroflexion of neck), arrhythmias, metabolic acidosis, anorexia, weight loss.

169
Q

What is hypokalaemic nephropathy?

A

A condition where low potassium levels promote PU/PD and worsen kidney function in CKD patients.

170
Q

What type of anaemia is seen in CKD?

A

Non-regenerative, normocytic, normochromic anaemia.

171
Q

What are the causes of anaemia in CKD?

A

Erythropoietin deficiency, reduced RBC lifespan, nutritional abnormalities, chronic GI haemorrhage, iron deficiency.

172
Q

What are the effects of anaemia in CKD?

A

Lethargy, inappetence, possible disease progression due to renal hypoxia.

173
Q

What are common causes of haemorrhage in CKD?

A

Ocular haemorrhage, GI haemorrhage secondary to ulceration.

174
Q

Why does hypertension occur in CKD?

A

Impaired sodium excretion, activation of the renin-angiotensin-aldosterone system (RAAS).

175
Q

What organs can be damaged by hypertension in CKD?

A

Kidneys, eyes, brain, cardiovascular system.

176
Q

Why does proteinuria occur in CKD?

A

Increased glomerular capillary pressure and fewer tubules to reabsorb protein.

177
Q

Why is proteinuria concerning in CKD?

A

It contributes to CKD progression and is a risk factor for mortality.

178
Q

What causes metabolic acidosis in CKD?

A

Reduced excretion of H+ ions, retention of phosphate and organic acids, increased loss of chloride (vomiting).

179
Q

Why is CKD a progressive disease?

A

Ongoing triggers, systemic and glomerular hypertension, mineral imbalances, proteinuria, renal fibrosis, inflammation.

180
Q

What are important targets for CKD treatment?

A

Hypertension, phosphate control, proteinuria reduction, reducing inflammation and fibrosis.

181
Q

What are common clinical signs of CKD?

A

PUPD, weight loss, depression, dehydration, haematuria, oedema, acute blindness, fractures.

182
Q

What findings are seen on clinical examination of CKD patients?

A

Dehydration, poor body condition, small kidneys, pale MM, hypertensive retinopathy, fractures.

183
Q

What laboratory findings indicate CKD?

A

Azotaemia, reduced GFR, low urine specific gravity, hyperphosphataemia, hypokalaemia, anaemia.

184
Q

What urine-specific gravity suggests CKD in dogs and cats?

A

Dogs: 1.008-1.020, Cats: 1.008-1.030

185
Q

Why is proteinuria monitored in CKD?

A

It increases risk of mortality and contributes to renal injury.

186
Q

What imaging methods help diagnose CKD?

A

Ultrasonography (small kidneys, renal lymphoma), Radiography (mineralization, uroliths)

187
Q

Why is blood pressure measurement important in CKD?

A

Hypertension can cause kidney damage and target organ damage.

188
Q

What are the main treatment goals for CKD?

A

Treat underlying causes, improve quality of life, slow disease progression.

189
Q

How is hypertension managed in CKD?

A

ACE inhibitors (dogs), Amlodipine (cats), ARBs, moderate salt restriction.

190
Q

How is dehydration managed in CKD?

A

IV fluids (short-term), oral fluids, subcutaneous fluids, feeding tube if needed.

191
Q

What medications help control nausea in CKD?

A

Maropitant, metoclopramide, ondansetron, H2 antagonists, proton pump inhibitors.

192
Q

What are treatment options for anaemia in CKD?

A

Erythropoietin therapy (rHuEPO or darbepoietin-α), iron supplementation, treating underlying causes

193
Q

Why is phosphate restriction important in CKD?

A

Prevents secondary hyperparathyroidism and slows disease progression.

194
Q

What are common phosphate binders used in CKD?

A

Aluminium hydroxide, calcium carbonate, Ipakitine, Pronefra

195
Q

How do ACE inhibitors benefit CKD patients?

A

Reduce glomerular pressure, proteinuria, sodium retention, and renal fibrosis.

196
Q

What is Telmisartan used for in CKD?

A

Reduces proteinuria and treats hypertension in cats

197
Q

Why are renal diets beneficial in CKD?

A

Reduce uraemic crises, prolong survival, improve quality of life.

198
Q

What nutrients are controlled in renal diets?

A

Phosphate, protein, sodium, potassium, omega-3, antioxidants, B vitamins.

199
Q

How should a diet change be introduced for CKD patients?

A

Gradually over 3-4 weeks, not during uraemic crisis or hospitalization.

200
Q

Why is long-term monitoring important in CKD?

A

To track disease progression, manage complications, and adjust treatments.

201
Q

How often should CKD patients be monitored?

A

Depends on severity, but regular check-ups are essential.

202
Q

What is ‘acute on chronic’ kidney disease?

A

An acute worsening of CKD due to another illness, dehydration, UTI, or obstruction.

203
Q

What is the typical prognosis for CKD?

A

Dogs: months to a few years; Cats: often ~2 years, depending on treatment and stage.

204
Q

How would a patient present who has a kidney disease?

A
  • PUPD
  • Inappetence/weightloss
  • Depression
  • GI signs like vom/naus/diarrhoea
  • ascites/subcut oedema
  • haematuria
  • pain
  • abdominal mass
205
Q

what is proteinuria?

A

It is an increase in the amount of protein in the urine

206
Q

What are physiological/transient causes of protienuria?

A

Strenuous excercise, seizure, fever and stress

207
Q

What are pre-renal causes of proteinuria?

A

Abnormal concentration of protein presented to kidney

208
Q

What are renal causes of proteinuria?

A

Defective renal function or inflammation of renal tissue

209
Q

What are post-renal causesof proteinuria?

A

Inflammation in the ureter, bladder, urethra or prostate

210
Q

What are the presenting signs of proteinuria?

A
  • none and have to detect on dipstick
  • Could be signs of underlying disease such as neoplasia , infection or renal failure
  • Could be signs kdure to low serum levels so weight loss, lethargy, poor appetite, ascites and pitting oedema
211
Q

What protein is a dipstick more senstive than others?

212
Q

Why might a dipstick give a false positive result for proteinuria?

A

If urine is alkaline or contaminated

213
Q

How would you identify pre-renal causes of proteinuria?

A

Haem and biochem that bitch

214
Q

How would you identify physiological causes of proteinuria?

A

Via history and clinical examination

214
Q

Why might a dipstick give a false negative result for proteinuria?

A

If the urine is acidic or bence jones proteinuria

215
Q

How would you identify post-renal causes of proteinuria?

A

History, clinical exam, urinalysis and imaging

216
Q

How would you identify a renal or post-renal inflammation as the cause of proteinuria?

A

Examine urine sediment for inflammatory cells and perform urine culture and sensitivity

217
Q

Why should you quantify proteinuria?

A
  • To evaluate severity of renal lesions
  • assess disease prgression
  • assess response to treatment
218
Q

How should you quantify proteinuria?

A

24hr urine protein measurement is gold standard but difficult so like okay whatev so urine protein:creatinine ratio da fuck

219
Q

What can renal inflammation cauas einterms of protein?

A

Cause protein to leak into filtrate