DL: Thyroid 2 Cases

Question 1

Would you expect to see wt loss with HAC?

Answer 1

NO contraindicated so v suspicion of HAC if appetite decreased
- unless pancreatitis or massive pituitary tumour compressing satiety centre concurrently

Question 2

When would you discount a murmur as unimportant?

Answer 2

No tachycardia, pulses strong, CRT normal

Question 3

What is the most likely cause of a systolic AV vlave murmur in a dog

Answer 3

Insufficiency - Mitral valve degeneration most likely (endocardioasis)

Question 4

What is HAC?

Answer 4

inability to suppress cortisol production normally

Question 5

How can a case be decided to be ‘sick’ enough to invalidate dex suppression test?

Answer 5

Inapetant good makrer - but decided case by case

- difficult to decide

Question 6

What does glucosuria, proteinuria and haemturia indicate with a suspected HAC patient ? Is this to be expected?

Answer 6

No indicates not a straightforward HAC

• likely DM
• likely 2* UTI (^ risk recurrence and tx more difficult with DM and HAC)

Question 7

What shold be considered when DM dx in an entire bitch?

Answer 7

• diestrus induced DM poss -> owners willing to spay? Otherwise will be very hard to control

Question 8

What effects may be seen on repro system with HAC?

Answer 8

Dysmennorhhorea

Question 9

Tx HAC and DM concurrently?

Answer 9

• Trilostane
• Insulin
• Spaying

Question 10

Interpret ACTH stim and LDDST results:

• 100->350
• 0: 38 (50-75)
• 4:

Answer 10

HAC - likely pituitary dependant

Question 11

Why may ALT and ALP rise at different rates?

Answer 11

> ALT should stay intracellular
- so ^ suggests cell necrosis and damage
ALP intracellular but secreted extracellularly
- GC stimulates production (so HAC can also stmi)
- cell swelling/change in microenvironment can also stim (so DM will ^ slightly d/t fatty cells, though not this much)

Question 12

What endocrine disorders can cause 2* hepatomegaly?

Answer 12

(pathogenesis = infiltration, fluid engorgement or accumulation) 
> HAC
- lipid and glycogen accumulation 
> DM 
- lipid accumulation

Question 13

How does hypothyroidism affect PCV ? What potential ddx does not cause this?

Answer 13

causes a non-regenerative anaemia

> HAC does not cause this

Question 14

How can haemorrhage and destruction of RBC be distinguished as causes of ^ loss -> anaemia? How else may anaemia occour?

Answer 14

• may also be d/t v production (non-specific marrow suppression likely d/t chronic dz)
• with haemorrhage TP also likely to be low cf. destruction where TP will be normal (unless bleeding into a body cavity where protein can be resorbed)

Question 15

What is a stress leucogram? When would you expect to see this and when would you expect not to seeit?

Answer 15

> ^ GC levels so expect to see with HAC, and to NOT see with hypoadrenocorticism (as cannot make GCs)

• neutrophilia/monocytosis
• lymphopenia
• eosinopenia

Question 16

What level of hyperglycaemia is likely to cuase glucosuria?

Answer 16

10-12mmol/l threshold

Question 17

When should amylase levels be ignored?

Answer 17

Anything below 2-3x upper limit

Question 18

When may cholesterol be raised?

Answer 18

• lymphoid malignancy s/t ^ cell turneover (cell membrane lipid released)

Question 19

Would you expect splenomegaly with hypothyroidism?

Answer 19

NO

Question 20

When may basal total T4 be decreased?

Answer 20

WITH ANY ILLNESS

• euthyroid sick syndrome
• so this test may not be particularly useful

Question 21

Causes of splenomegaly and hepatomegaly concurrently. How may these be dx?

Answer 21

• accumulation (fat, amyloid etc. unlikely spleen)
• congestion (expect other signs of heart failure/caudal VC compression)
• infiltration ( neoplasia - haemangiosarc/lymphosarc)
  > FNA liver