Y6S2 - Internal Medicine (CKD + Pancreatitis)

A detailed illustration depicting the anatomy of the kidneys and pancreas in cats and dogs, showing labeled structures and conditions related to CKD and pancreatitis, with a professional and educational tone.

Chronic Kidney Disease and Pancreatitis Quiz

Test your knowledge on the essential aspects of Chronic Kidney Disease (CKD) and pancreatitis in veterinary medicine. This comprehensive quiz encompasses various factors, including diagnostic markers, abnormalities, and the prevalence of diseases in cats.

57 engaging questions.
Deep dive into CKD stages, diagnosis, and management.
Explore the complexities of feline pancreatitis.

57 Questions14 MinutesCreated by LearningVet123

Chronic Kidney Disease

Which of the following abnormalities are found in CKD?

Reduction in glomerular filtration rate, loss of normal glomerular function, abnormalities in renal structure, loss of normal glomerular function

Azotemia, progressive increases in serum creatinine or SDMA over time, persistent proteinuria of renal origin, loss of urine concentrating ability

Hyperstenuria, azotemia, proteinuria

Hyperstenia is wrong

BUT Hyposthenuria (kidney can dilute the urine but is unable to concentrate) would be right.

CKD can be manifest as abnormalities in 1/+ of the kidney's functions or structure:

1) Abnormalities in renal function (↓ in glomerular filtration rate)

Azotemia (nitrogenous products accumulation in blood => normally excreted by kidney)
Progressive ↑ in serum creat/SDMA over time (may occur within reference intervals)

2) Abnormalities in renal function (loss of normal glomerular function)

Persistent proteinuria of renal origin

3) Abnormalities in renal function (loss of normal tubular functions)

Loss of urine concentrating ability => inappropriate urine specific gravity (after nonrenal causes exclusion for polyuria and polydispia)
- In ∅ of azotemia, urine specific gravity <1.035 (cat)
- Dogs: urine specific gravity <1.030 = not uncommon in healthy, so less reliable as an early indicator of renal pathology.
Inappropriate tubular loss of potassium, bicarbonate, glucose or amino acids

4) Abnormalities in renal structure

Renal cysts
Uroliths
Neoplasia

Hyperstenia is wrong

BUT Hyposthenuria (kidney can dilute the urine but is unable to concentrate) would be right.

CKD can be manifest as abnormalities in 1/+ of the kidney's functions or structure:

1) Abnormalities in renal function (↓ in glomerular filtration rate)

Azotemia (nitrogenous products accumulation in blood => normally excreted by kidney)
Progressive ↑ in serum creat/SDMA over time (may occur within reference intervals)

2) Abnormalities in renal function (loss of normal glomerular function)

Persistent proteinuria of renal origin

3) Abnormalities in renal function (loss of normal tubular functions)

Loss of urine concentrating ability => inappropriate urine specific gravity (after nonrenal causes exclusion for polyuria and polydispia)
- In ∅ of azotemia, urine specific gravity <1.035 (cat)
- Dogs: urine specific gravity <1.030 = not uncommon in healthy, so less reliable as an early indicator of renal pathology.
Inappropriate tubular loss of potassium, bicarbonate, glucose or amino acids

4) Abnormalities in renal structure

Renal cysts
Uroliths
Neoplasia

The ideal blood maker for diagnosing CKD should be:

Produced at a stable rate that is unaffected by age and disease status

Freely filtered at the glomerulus, not reabsorbed nor secreted into the tubule

Not metabolised or excreted from the body by any non-renal route of elimination

Metabolised or excreted from the body by any non-renal route of elimination

Selectively filtered at the glomerulus, not reabsorbed nor secreted into the tubule

A surrogate marker present in the blood that indicates the functioning renal mass is extremely useful in staging CKD. The ideal marker is:

Produced at a stable rate that is unaffected by age and disease status
Freely filtered at the glomerulus, not reabsorbed nor secreted into the tubule such that its rate of excretion in urine is dependent on glomerular filtration rate
Not metabolised or excreted from the body by any non-renal route of elimination

Any surrogate marker of GFR will have an exponential relationship between its blood concentration and GFR (since elimination that is dependent on GFR will follow first order kinetics, I.e. A constant proportion or percentage of the marker will be eliminated per unit of time). This means that changes in blood concentrations of any surrogate marker of GFR will be small in the early stages of CKD.

A surrogate marker present in the blood that indicates the functioning renal mass is extremely useful in staging CKD. The ideal marker is:

Produced at a stable rate that is unaffected by age and disease status
Freely filtered at the glomerulus, not reabsorbed nor secreted into the tubule such that its rate of excretion in urine is dependent on glomerular filtration rate
Not metabolised or excreted from the body by any non-renal route of elimination

Current creatinine reference intervals for healthy dogs and cats are influenced by the:

Individual variation in GFR, muscle mass

Different methodologies used by labs, muscle mass, consumption of meat-based diets

Presence of urolits, cystitis

Many of the current creatinine reference intervals for healthy dogs and cats are sufficiently wide that they include patients with mild to moderate kidney disease.

Some of this variation in 'normal' creatinine values between healthy dogs and cats is related to:

Variation in GFR (so will be true for any surrogate marker)
Other sources of variation relates to muscle mass that accounts for significant differences between breeds of dog for example.
Different methodologies are used by diagnostic laboratories to measure creatinine some of which measure non-creatinine chromogens. There is currently no standardisation of blood creatinine measurements across veterinary diagnostic laboratories
Consumption of meat-based diets will lead to absorption of creatinine post-prandially thus it is important that blood samples for measurement of creatinine are collected following a period of fasting (ideally 12h)

Determining a patient's "individual" normal creatinine concentration => more appropriate than using population based reference interval + facilitate earlier detection of reducing renal function than single measurements of blood creatinine allow

Many of the current creatinine reference intervals for healthy dogs and cats are sufficiently wide that they include patients with mild to moderate kidney disease.

Some of this variation in 'normal' creatinine values between healthy dogs and cats is related to:

Variation in GFR (so will be true for any surrogate marker)
Other sources of variation relates to muscle mass that accounts for significant differences between breeds of dog for example.
Different methodologies are used by diagnostic laboratories to measure creatinine some of which measure non-creatinine chromogens. There is currently no standardisation of blood creatinine measurements across veterinary diagnostic laboratories
Consumption of meat-based diets will lead to absorption of creatinine post-prandially thus it is important that blood samples for measurement of creatinine are collected following a period of fasting (ideally 12h)

To classify a patient in CKD stage 1, you should have at least 3 of the following signs:

Abnormal size or shape of kidneys on palpation, confirmed by diagnostic imaging
Persistent renal proteinuria
Increasing blood creatinine and/or SDMA concentration

True

False

For a patient to be classified in Stage 1, at least 1 of those abnormalities should be diagnosis:

Inadequate urinary concentrating ability in the absence of an identifiable extra-renal cause
Persistent renal proteinuria
Abnormal size or shape of the kidneys on palpation, confirmed by diagnostic imaging
Abnormal kidney biopsy findings
Increasing blood creatinine and/or SDMA concentrations (even if they remaining within the laboratory reference range) on serial sampling in an adequately hydrated patient

For a patient to be classified in Stage 1, at least 1 of those abnormalities should be diagnosis:

Inadequate urinary concentrating ability in the absence of an identifiable extra-renal cause
Persistent renal proteinuria
Abnormal size or shape of the kidneys on palpation, confirmed by diagnostic imaging
Abnormal kidney biopsy findings
Increasing blood creatinine and/or SDMA concentrations (even if they remaining within the laboratory reference range) on serial sampling in an adequately hydrated patient

IRIS CKD Stage 2 means

Reference interval blood creatinine values and SDMA concentration of >17 µg/dl

Creatinine values over 2 mg/dl and SDMA concentration of >17 µg/dl

Reference interval blood creatinine values and SDMA concentration of >14 µg/dl

Reference interval blood creatinine values and SDMA concentration between 12 and 14 µg/dl

None of the above

NOT SURE ABOUT THE ANSWER

IRIS CKD Stage 2 has a proportion of dogs and cats that have within reference interval blood creatinine values.

These patients will be diagnosed to have CKD based on the criteria for Stage 1 including a persistent blood SDMA concentration of >17 μg/dl, again reflecting the evidence that elevated blood SDMA often occurs earlier than elevated blood creatinine concentrations in early stage CKD patient.

The blood creatinine range that will place a dog in IRIS CKD Stage 2 has been widened in the revised IRIS Staging system to mirror the upper limit of the range used for the cat (2.7 mg/dl or 249 μmol/l).

This decision has been taken because the spectrum of presentations of dogs seen in IRIS CKD Stage 3 was very broad. Dogs with sCr in the lower part of the IRIS CKD Stage 3 stage often had few to no clinical signs and were more appropriately managed according to the Stage 2 recommendations.

NOT SURE ABOUT THE ANSWER

IRIS CKD Stage 2 has a proportion of dogs and cats that have within reference interval blood creatinine values.

Substaging CKD may be done by using:

Presence of proteinuria

Blood pressure

Secondary organ damage (cardiac failure, brain, ocular)

None of the above

ANSWER C IS UNCLEAR

Following staging, the IRIS Board recommends that dogs and cats be substaged whenever possible based on two other important factors:

the quantity of protein excreted in urine
systemic arterial blood pressure

Evaluation of these 2 variables is recommended because proteinuria and systemic arterial hypertension can occur separately or together at any stage of CKD.

Substaging on proteinuria =>good evidence that it is a prognostic indicator in dogs and cats with CKD.

For substaging on proteinuria:

Proteinuria must be of renal origin:
- pre-renal + post-renal causes have to be ruled out first
Persistent proteinuria = more likely to be significant (≠ transient proteinuria)
- Substaging ideally = persistence of proteinuria demonstrated in 3/+ urine samples collected over at least a 2-week period

Substage classification is based on the urine protein to creatinine ratio (UP/C, determined using mass units):

Non-proteinuric
Borderline proteinuric
Proteinuric

For dogs and cats being proteinuric or borderline proteinuric => significance of finding depends on the concurrent stage of CKD.

Proteinuric substage = more significant in general at Stage 3 than at Stage 1; because filtered protein load presented to tubules reduces as functioning nephron mass declines => a given level of proteinuria attains higher significance as GFR declines

Substaging on systemic arterial blood pressure

Kidney disease can affect blood pressure regulation leading to inappropriately high blood pressure. High blood pressure can be damaging to the kidneys and can also damage other target organs such as heart (left ventricular hypertrophy), eye (hyphema, hypertensive retinopathy) and brain (dullness, lethargy, seizures) leading to extra-renal signs and morbidity.

The IRIS group therefore recommends that arterial blood pressure should be measured in all dogs and cats with CKD.

Blood pressure substaging = based on measured arterial pressure and whether extra-renal target-organ damage is present/threatens.

As with proteinuria, documentation of persistence = based on multiple sequential blood pressure measurements
If extra-renal target-organ damage is already present, demonstration of persistence = not necessary + treatment should begin immediately
If no evidence of extra-renal target-organ damage is recognized, the recommended follow-up depends on blood pressure stage and associated perceived risk of development of such changes

ANSWER C IS UNCLEAR

Following staging, the IRIS Board recommends that dogs and cats be substaged whenever possible based on two other important factors:

the quantity of protein excreted in urine
systemic arterial blood pressure

Evaluation of these 2 variables is recommended because proteinuria and systemic arterial hypertension can occur separately or together at any stage of CKD.

Substaging on proteinuria =>good evidence that it is a prognostic indicator in dogs and cats with CKD.

For substaging on proteinuria:

Proteinuria must be of renal origin:
- pre-renal + post-renal causes have to be ruled out first
Persistent proteinuria = more likely to be significant (≠ transient proteinuria)
- Substaging ideally = persistence of proteinuria demonstrated in 3/+ urine samples collected over at least a 2-week period

Substage classification is based on the urine protein to creatinine ratio (UP/C, determined using mass units):

Non-proteinuric
Borderline proteinuric
Proteinuric

For dogs and cats being proteinuric or borderline proteinuric => significance of finding depends on the concurrent stage of CKD.

Proteinuric substage = more significant in general at Stage 3 than at Stage 1; because filtered protein load presented to tubules reduces as functioning nephron mass declines => a given level of proteinuria attains higher significance as GFR declines

Substaging on systemic arterial blood pressure

The IRIS group therefore recommends that arterial blood pressure should be measured in all dogs and cats with CKD.

Blood pressure substaging = based on measured arterial pressure and whether extra-renal target-organ damage is present/threatens.

As with proteinuria, documentation of persistence = based on multiple sequential blood pressure measurements
If extra-renal target-organ damage is already present, demonstration of persistence = not necessary + treatment should begin immediately
If no evidence of extra-renal target-organ damage is recognized, the recommended follow-up depends on blood pressure stage and associated perceived risk of development of such changes

Pancreatitis in Cats

115 cats undergoing necropsy at the University of California Davis, the overall histopathologic prevalence of pancreatitis was 66.1%, with/

10% of the apparently healthy cats had evidence of pancreatitis.

35% of the apparently healthy cats had evidence of pancreatitis.

30% of the apparently healthy cats had evidence of pancreatitis.

45% of the apparently healthy cats had evidence of pancreatitis.

In a study of 115 cats undergoing necropsy at the University of California Davis, the overall histopathologic prevalence of pancreatitis was 66.1%, with 50.4% of cats having evidence of chronic pancreatitis alone, 6.1% having evidence of acute pancreatitis alone, and 9.6% having evidence of both acute and chronic pancreatitis. Also, 45% of the apparently healthy cats had evidence of pancreatitis.

Which statements about pancreatitis in cats are TRUE?

Acute pancreatitis = inflammation that is completely reversible after removal of the inciting cause

Chronic pancreatitis = irreversible histopathologic changes.

The differences between acute and chronic pancreatitis are mainly clinical

Acute pancreatitis = inflammation that is completely reversible after removal of the inciting cause

Chronic pancreatitis = irreversible histopathologic changes

The differences between acute and chronic pancreatitis are mainly histopathologic, and not necessarily clinical.

It may be impossible clinically to distinguish an exacerbation of chronic pancreatitis from an episode of acute pancreatitis.

Acute pancreatitis = inflammation that is completely reversible after removal of the inciting cause

Chronic pancreatitis = irreversible histopathologic changes

The differences between acute and chronic pancreatitis are mainly histopathologic, and not necessarily clinical.

It may be impossible clinically to distinguish an exacerbation of chronic pancreatitis from an episode of acute pancreatitis.

Which statements about pancreatitis in cats are TRUE?

Pancreatitis has a sex and breed predisposition

Certain parasites and viruses represent rare causes of pancreatitis

Trauma after a road accident or a fall is a cause for pancreatitis

None of the above

NO age, sex, or breed predisposition

Body condition score, dietary indiscretion, or drug history = no association in cats.

ETIOLOGY:

Infections
Parasites
- Toxoplasma gondii , Eurytrema procyonis, Amphimerus pseudofelineus
Viruses
- Coronavirus, parvovirus, herpesvirus, calicivirus
Intraoperative manipulations, pancreatic biopsy
Neoplasia
Autoimmune pancreatitis (AIP)
Idiopatic

NO age, sex, or breed predisposition

Body condition score, dietary indiscretion, or drug history = no association in cats.

ETIOLOGY:

Infections
Parasites
- Toxoplasma gondii , Eurytrema procyonis, Amphimerus pseudofelineus
Viruses
- Coronavirus, parvovirus, herpesvirus, calicivirus
Intraoperative manipulations, pancreatic biopsy
Neoplasia
Autoimmune pancreatitis (AIP)
Idiopatic

According to the consensus, what are the incidences for the following clinical signs in Cat pancreatitis? (Check the table on the following slide for answer)

	Incidence (%)
Dehydratation
Diarrhea
Dyspnea
Icterus
Lethargy
Pain (abdominal)
Vomitting

During an ultrasonography, an acute pancreatitis will present:

Pancreatic enlargement, a hyperechoic surrounding mesentery, and focal abdominal effusion

Hyperechoic or mixed echoic pancreas, a dilated common bile duct, enlarged pancreas, and irregular pancreatic margins.

Sensitivity for diagnosing ranges from 11 to 67%

None of the above

Diagnostic imaging in pancreatitis in cats:

Radiography
Ultrasonography
- Acute pancreatitis = pancreatic enlargement, hyperechoic surrounding mesentery, focal abdominal effusion
- Duodenum can be distended/corrugated. The sensitivity of these findings for diagnosing acute pancreatitis in cats has = range between 11% and 67%, and is severity dependent and operator dependent
- Chronic pancreatitis = hyperechoic or mixed echoic pancreas, dilated common bile duct, enlarged pancreas, and irregular pancreatic margins
Advanced imaging modalities

Diagnostic imaging in pancreatitis in cats:

Radiography
Ultrasonography
- Acute pancreatitis = pancreatic enlargement, hyperechoic surrounding mesentery, focal abdominal effusion
- Duodenum can be distended/corrugated. The sensitivity of these findings for diagnosing acute pancreatitis in cats has = range between 11% and 67%, and is severity dependent and operator dependent
- Chronic pancreatitis = hyperechoic or mixed echoic pancreas, dilated common bile duct, enlarged pancreas, and irregular pancreatic margins
Advanced imaging modalities

In pancreatitis, erythrocyte mass (eg, red blood cell number, hematocrit or packed cell volume) may be:

Increased

Decreased

Erythrocyte mass (eg, red blood cell number, hematocrit or packed cell volume) may be increased secondary to dehydration from fluid loss as a result of decreased intake, vomiting, diarrhea, or some combination of these.

In pancreatitis, Hepatic enzyme activities (eg, alanine amino transferase [ALT], aspartate transaminase [AST]) and total bilirubin concentrations may be:

Increased

Decreased

Hepatic enzyme activities (eg, alanine amino transferase [ALT], aspartate transaminase [AST]) and total bilirubin concentrations may be increased because of concurrent inflammation of the biliary tree, extrahepatic biliary obstruction, hepatic lipidosis, or some combination of these.

In pancreatitis, Serum creatinine, blood urea nitrogen (BUN), and symmetric dimethylarginine (SDMA) concentrations may be;

Increased

Decreased

Serum creatinine, blood urea nitrogen (BUN), and symmetric dimethylarginine (SDMA) concentrations may be increased as a result of dehydration.

In severe pancreatitis, we can observe: hypocoagulability, azotemia, low urine specific gravity, hypoglycemia and hyperglycemia

True

False

In severe cases, evidence for hypocoagulability with disseminated intra vascular coagulation may be present, as evidenced by prolonged clotting times, often occurring concurrently with thrombocytopenia and increased fibrin degradation products (FDPs), D Dimers, or both.

In severe acute pancreatitis, azotemia and low urine specific gravity may result from acute kidney injury, secondary to hypoxemia, impaired renal microcirculation, or hypovolemia. Azotemia has been linked to progression of the disease.

Hypoglycemia and hyperglycemia can be seen with acute necrotizing and suppurative pancreatitis, and hypoglycemia has been associated with poor outcome.

An ideal biomarker for pancreatitis would be one that is:

Synthesized only by acinar cells

Not cleared immediately from the vascular space

None of the above

An ideal biomarker for pancreatitis would be one that is synthesized only by acinar cells and not cleared immediately from the vascular space.

Pancreatic lipase fulfills these criteria, but to be useful as a biomarker, the molecule must be measured using an assay specific for pancreatic lipase, which can be problematic.

An ideal biomarker for pancreatitis would be one that is synthesized only by acinar cells and not cleared immediately from the vascular space.

Pancreatic lipase fulfills these criteria, but to be useful as a biomarker, the molecule must be measured using an assay specific for pancreatic lipase, which can be problematic.

Which statements about serum pancreatic lipase immunoreactivity (fPLI) are true?

Measurement of fPLI is highly specific for the measurement of pancreatic lipase

Sensitivity is higher for severe cases than for mild cases

Sensitive for the diagnosis of pancreatitis

None of the above

Measurement of fPLI is highly specific for the measurement of pancreatic lipase and also is sensitive for the diagnosis of pancreatitis. Sensitivity is higher for severe cases than for mild cases.

Additional laboratory test for pancreatitis

Amylasis

Thyroid Stimulating Hormone

Hemoglobin A1C

Trypsin like immunoreactivity

Historically, increases in serum amylase activity have been associated with acute pancreatitis in some cats. However, because of both, poor diagnostic sensitivity and lack of tissue specificity, enzymatic activity of amylase has minimal utility as a biomarker for pancreatitis in cats.

Trypsin-like immunoreactivity (TLI) measures trypsinogen, trypsin, and likely some trypsin that has been bound by protease inhibitors and is measured using a species-specific immunoassay. Studies indicate variable results in cats with pancreatitis, with sensitivity ranging from 30-86%.

In cytology: poorly cellular, because of the presence of fibrosis, which occasionally forms or more mass like lesions. Mesenchymal cells, including reactive fibroblasts, typically exfoliate poorly. Variable numbers of mixed inflammatory cells often are present, including lymphocytes and plasma cells with occasional neutrophils, indicates:

Acute pancreatitis

Chronic pancreatitis

In cytology: highly cellular inflammatory cells, predominantly neutrophils, that show variable degrees of degeneration with fewer foamy macrophages on a background of amorphous, necrotic debris, which occasionally contains refractile crystalline material, indicates:

Acute pancreatitis

Chronic pancreatitis

Cytology

Acute pancreatitis: pancreatic aspirates often are highly cellular inflammatory cells, predominantly neutrophils, that show variable degrees of degeneration with fewer foamy macrophages on a background of amorphous, necrotic debris, which occasionally contains refractile crystalline material

Chronic pancreatitis: poorly cellular, because of the presence of fibrosis, which occasionally forms or more mass like lesions. Mesenchymal cells, including reactive fibroblasts, typically exfoliate poorly. Variable numbers of mixed inflammatory cells often are present, including lymphocytes and plasma cells with occasional neutrophils

Cytology

In cats with acute pancreatitis, mortality ranges from:

6-32%

43-75%

9-41%

22-26%

The mortality rate in cats with acute pancreatitis ranges from 9% to 41%.

Cats with mild to moderate acute pancreatitis generally have a good prognosis with appropriate management.

Cats with severe acute pancreatitis, especially when complications or comorbidities are present, have a guarded to grave prognosis.

Low plasma ionized calcium concentrations in cats with acute pancreatitis = poor outcome.

Hypoglycemia and azotemia = poor prognostic indicators.

The mortality rate in cats with acute pancreatitis ranges from 9% to 41%.

Cats with mild to moderate acute pancreatitis generally have a good prognosis with appropriate management.

Cats with severe acute pancreatitis, especially when complications or comorbidities are present, have a guarded to grave prognosis.

Low plasma ionized calcium concentrations in cats with acute pancreatitis = poor outcome.

Hypoglycemia and azotemia = poor prognostic indicators.

Management goals for acute pancreatitis are focused on:

Treatment of inciting causes, control of blood glucose concentration, nutritional support, and pain management

Fluid therapy, pain management, control of vomiting and apparent nausea, and nutritional support.

Fluid therapy, treatment of inciting causes, control of blood glucose concentration, control of vomitting and apparent nausea

Pain management, fluid therapy, and control of hypertension

Management goals for acute pancreatitis are focused on fluid therapy, pain management, control of vomiting and apparent nausea, and nutritional support.

In pancreatitis, anti inflammatory and immunosuppressive therapy:

Should not be used

Should only be used in cats that are not hyperglycemic

At immunosuppressive dosages of prednisolone

Although some panel members felt that prednisolone should only be used in cats that are not hyperglycemic and only at anti inflammatory dosages (0.5-1.0 mg/kg PO q24h on a tapering schedule), other panel members felt that immunosuppressive dosages of prednisolone (2.0 mg/kg q12h for 5 days and then 1.0 mg/kg q12h for 6 weeks with a decreasing dosing schedule after that time) with close monitoring (clinical reevaluation and measurement of fPLI after 2-3 weeks) could have a beneficial effect.

If hyperglycemia develops, or is pre-existing, some panel members recommend the use of cyclosporine (5 mg/kg q24h for 6 weeks) with close monitoring (clinical re-evaluation and measurement fPLI after 2 3 weeks).

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