Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y4 SA - urinary & endocrine disease > Approach to PUPD > Flashcards

Approach to PUPD Flashcards

1
Q

Polyuria definition

A
  • > 50ml/kg/day of urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Polydispsia definition

A
  • > 100ml/kg/day intake (dogs)
  • > 50ml/kg/day intake (cats)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of primary polydipsia

A

A difficult thing to prove and often diagnosed as idiopathic.

Altered thirst
- Centrally mediated disease
– Primary e.g. neoplasia
– Secondary e.g. changes to osmolarity or endocrine effects
– Compensating for losses other than urinary e.g. GI, third space.
- Physiological
– Salt toxicity e.g. seawater
– Exercise
– High Environmental temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Broad causes of primary polyuria

A
  • intrinsic renal problem
  • or extrinsic effect on the kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of primary polyuria

A
  • Problems with ADH or its receptors (e.g. no ADH production/release, or reduced ADH sensitivity/response)
  • Osmotic diuresis
  • Medullary solute washout
  • Interstitial tonicity reduction
  • Increased GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is ADH and what does it do?

A

= Anti-diuretic hormone
- increases aquaporin density and increases reabsorption from tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does central diabetes insipidus affect ADH?

A
  • no ADH production (hypothalamus) or release (pituitary)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of reduced ADH sensitivity/response

A
  • Primary Nephrogenic Diabetes Insipidus (rare)
  • Secondary NDI – primarily endocrine/inflammatory but can be other poorly known interactions
    – Hyperadrenocorticism (Cushings)**
    – Hypoadrenocorticism (Addisons)**
    – Hyperthyroidism**
    – Hyperaldosteronism (Conns)
    – Liver Disease
    – Pyelonephritis
    – Pyometra**
    – Hypokalaemia
    – Hypercalcaemia (various causes e.g. hyperPTH, neoplasia)**
    – Erythrocytosis
    – Lepto
    – Acromegaly (Excess GH – 25% of DM cats)
    – Neoplasia – Leiomyosarcoma, Haemangiosarcoma (unknown mechanism)
    – Drugs e.g. steroids**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does osmotic diuresis cause polyuria?

A
  • if urine contains solutes above normal values (e.g. glucose in diabetes mellitus) this ‘draws’ water into the tubules increasing output
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of osmotic diuresis

A

Glucose
- Diabetes Mellitus**
- Primary renal glycosuria
- Fanconi’s syndrome

Sodium
- Post obstructive diuresis (blocked cats – multifactorial, glomerular/renal damage e.g. ADH response is probably also reduced)**
- High salt diet
- Addisons**
- Diuretics**
– Spironolactone
– Furosemide (loop diuretic – also lose potassium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fanconi’s syndrome

A
  • Basenjis, small breed dogs
  • secondary to dodgy jerky ingestion
  • Proximal tubular disease -> reduced resorption of solutes -> loss of glucose, amino acids, bicarb, electrolytes, lactate, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of reduced medullary/interstitial tonicity causing primary polyuria

A
  • Low protein diet
  • Medullary washout (e.g. prolonged PUPD, prolonged aggressive fluid therapy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mixed/unknown causes of primary polyuria

A

Chronic Renal Failure
- Don’t forget, this could be present from youth in congenital defects e.g. renal dysplasia

Acute Kidney Injury
- Phaeochromocytoma (Catecholamine producing tumour of the adrenal gland i.e. adrenaline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diagnostic approach - History and signalment

A
  • Age e.g. congenital in young
  • Breed e.g. Fanconi syndrome in small breeds
  • Species e.g. HyperT4 and CKD in older cats
  • Toxin/drug/medications?
  • Vaccination status – Lepto
  • Diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnostic approach - Clinical Exam

A
  • Body condition – chronic vs acute disease missed by the owners
  • Signs of dehydration – primary polyuria
  • Neurological disease – central lesion
  • Other signs associated with endocrinopathies – e.g. dermatalogical disease (Cushings), or waxing/waning GI disease (addisons)
  • Clinical signs of other body systems e.g. jaundice in hepatopathy, increased GI loss in diarrhoea driving thirst, enlarged abdomen and third space loss.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

USG - key question to ask yourself when interpreting results

A
  • is it appropriate to the patients hydration status?
17
Q

Interpretation of USG >1.030 with normal hydration

A
  • either normal (i.e. the owner is wrong)
  • or primary polydipsia driving intermittent polyuria (not present at time of sampling) e.g. primary polydipsia, variable hypothalamic or pituitary disease e.g. inflammatory/infectious (look for CNS signs) or physiological
18
Q

Interpretation of USG >1.030 with dehydration

A
  • check for glucosuria, consistent with diabetes mellitus, Fanconi’s and renal tubular glycosuria.
19
Q

Interpretation of USG <1.030 with normal hydration

A
  • Consider primary polydipsia again, but consistently present
20
Q

Interpretation of USG <1.030 with dehydration

A
  • Consider primary polyuria and intrinsic renal disease or extrinsic disease
    affecting renal function
21
Q

Interpretation of USG <1.006 (Hyposthenuria)

A
  • Diabetes insipidus, primary polydipsia, hypercalcemia, hyperadrenocorticism
22
Q

What to do when you suspect primary polydipsia

A

History
- Could this just be physiological
- Toxin exposure
- GI losses

Rule out third space loss
– POCUS

Endocrine or osmolarity changes
– Haem and Biochem (polycythaemia, electrolyte disturbances) and consider HyperT4 in cats and liver disease

Central disease
– Neuro assessment +/- MRI

23
Q

What serum osmolality supports primary polydipsia?

A
  • low serum osmolality
24
Q

What to do when you suspect primary polyuria?

A

Dependent on the history; rule out major life threatening disease first e.g.
- pyometra
- addisons
- AKI
- DM progressing to diabetic ketoacidosis
- haemangiosarcoma

Triage
- POCUS, Elecs, BG, UG, U/C/K+

25
Q

What to do if you suspect intrinsic renal disease

A
  • Further urinalysis including UPCR, urine sediment exam (e.g. casts in tubular disease), culture and sensitivity (e.g. pyelonephritis)
  • Biochemistry – Urea, Creatinine, symmetric dimethylarginine (SDMA) (see following slide on azotaemia)
  • Further imaging +/- renal biopsy
26
Q

What to do if you suspect extrinsic disease

A
  • Further urinalysis including urine glucose and C&ST (ascending infections common in diabetes mellitus, HAC and hyperthyroidism)
  • Haematology and biochemistry
  • Ideally ionised calcium for hypercalcaemia
  • Further imaging +/- FNA/Biopsy
  • Physiological assessment e.g. inappropriate hypertension in phaeochromocytoma
27
Q

What is azotaemia?

A
  • elevated urea and creatinine
28
Q

3 causes of azotaemia

A
  1. Pre-renal - fluid loss i.e. haemoconcentration and reduced renal blood flow
  2. Renal - AKI or CRF (intrinsic dz) (2/3rd renal mass lost)
  3. Post-renal – Obstruction or uroabdomen
29
Q

Why does pre-renal azotaemia become renal also?

A
  • reduced renal blood flow -> renal hypoxia
30
Q

Pre-renal azotaemia:
- potential cause?
- what element is likely to be high?
- USG?
- fluid responsive?

A

➢ Addison’s can cause a marked pre-renal azotaemia similar to renal disease.
➢ Phosphorous is likely to be high (GFR dependant)
➢ PUPD may be present depending on the cause, so USG can vary
➢ Rapidly fluid responsive

31
Q

Post-renal azotaemia:
- PUPD?
- care re what?
- investigation?

A

➢ PUPD not really a feature –until after removing the obstruction.
➢ POCUS
➢ DANGEROUS - Hyperkalaemia can develop rapidly

32
Q

Renal azotaemia
- USG
- what element is likely to be high?
- care re what?
- other notes

A

➢ USG will be poorly concentrated (functional loss) but NOT dilute (i.e. hyposthenuric) which indicates
active dilution from the kidneys (proximal tubules and loop of Henle).
➢ Cats can develop glomerular disease without issues of concentration and maintain a normal USG.
➢ Phosphorous is likely to be high (GFR dependant)
– In AKI –Phosphorous increase is marked
– In CKD –Phosphorous increase is more moderate, and consistent with the creatinine elevation
➢ DANGEROUS - Hyperkalaemia can develop in AKI (oliguria or anuria)
➢ Albumin and UPCR–Protein losing nephropathy
➢ Non-regenerative anaemia–CKD (reduced EPO production)

33
Q

Use of water deprivation test

A
  • Differentiates between primary polydipsia, central diabetes insipidus and nephrogenic diabetes insipidus.
34
Q

Water deprivation test - how to

A
  • 3-5 days of gradual water restriction, then complete removal of water until 5% dehydration achieved
    – Vasopressin (DDAVP – ADH analogue) is then administered.
35
Q

Water deprivation test - primary polydipsia result (specific gravity)

A
  • SG improves with just water deprivation
36
Q

Water deprivation test - CDI result (specific gravity)

A
  • SG improves with vasopressin
37
Q

Water deprivation test - NDI result (specific gravity)

A
  • SG never improves
38
Q

Why do you need to be careful with the water deprivation test?

A
  • Fatal amounts of fluid loss in the PU patient is possible
  • close monitoring
  • realistically hospital only
39
Q

Water deprivation test alternative

A
  • trial Vasopressin therapy
  • a response is consistent with CDI
  • can be done in first opinion but vasopressin is expensive

Y4 SA - urinary & endocrine disease (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions