Applied Cases

Question 1

Case: dog with no other signs except excessive panting/ found to have high BP

What does raised ALKP and ALT show?

Answer 1

ALT is specific because it’s in hepatocytes so if raised there’s liver damage

ALKP is seen in many things e.g. Raises in cushings

Question 2

What is normal systolic BP?

Answer 2

120

But allow 150 in the consult room

Question 3

Why would you get a reduced echogenicity in the liver with high BP

Answer 3

More block flow to liver therefore darker (remember fluid is dark)

Question 4

What anatomical structure sits at the cranial pole of the kidney close to the caudal vena cava

Answer 4

Adrenal gland

Question 5

What does the adrenal gland produce

Answer 5

Mineralocorticoids
Glucocorticoids
Androgens
Catecholamines e.g. Adrenaline

Question 6

Can glucocorticoids effect RAAS?

Answer 6

Yes they have some mineralocorticoid effect
May have CNS effect on cardiac output
Activate vasoactive substances

Question 7

What can you look at too see if normal aldosterone function

Answer 7

NA and K

Question 8

What else could you check in the blood to see what an adrenal tumour is making to result in high BP??

Answer 8

If patient is on preds: can’t measure basal cortisol!

ACTH

Noradrenaline clearance in urine

Question 9

Where in the adrenal glands are catecholamines made??

Answer 9

The medulla

Question 10

In this case (where the tumour has invaded the adrenal gland) why can’t we remove it?

Answer 10

Risk damage to caudal VC

Question 11

What drugs could we use to reduce BP

Answer 11

Direct ones are only used for rapid change and not long term e.g. Nitrates

Alpha antagonists (prazosin)- vasodilation in non essentials

Ca channel blocker (amylodipine)- good as minimal side effects

PDE5 inhibitor - results in CAMP build up with means no cross bridges so stops smooth muscle contraction

Question 12

Why is phenoxybenzamine especially good for this dog?

Answer 12

Because it’s not metabolised in the liver

Because it blocks a1 receptors which is good because he has a high level of circulating catecholamines

Question 13

Case: cyanotic westie with Ascites, loss of appetite, muscle wastage, high HR, jugular vein pulsing, loud systolic heart murmur with point most intensity at 4th intercostal space. History or iodopathic pulmonary fibrosis (crackly westie syndrome)

Which clinical signs are due to IPF?

Answer 13

Cyanoptic as poor gas exchange due to increased interstitial tissue between capillaries and alveoli

If your alveoli are poorly oxygenated you get vasoconstricted vessels to keep perfusion ventilation ratio constant, they do this to divert blood to good alveoli but in this case there is none so you get an increased pulmonary hypertension overall.
Also…
With more interstitial tissue, this is going to be squashing the capillaries also causing a pulmonary hypertension

This increases the right ventricular afterload, so this ventricle will appear thicker due to increased work load. The blood has nowhere to go so it goes backwards.

Question 14

Why have we got hepatosplenomegaly?

Answer 14

Blood can’t go into caudal vena cava as can’t go into right atria

Question 15

Why is there a jugular pulse?

Answer 15

Blood is shooting back into the atria, into the vena cava and into the jugular etc.

Question 16

What does mean electrical axis tell us?

Answer 16

The overall vector of the AP through the heart

Question 17

Why might we have a right axis deviation?

Answer 17

Right hypertrophy

Unexpected conduction pathway

Change in position e.g. Big tumour

Question 18

What’s an ECG most useful for

Answer 18

Heart rate and rhythm

Question 19

What should the end of the trachea be parallel to?

Answer 19

The sternum

Question 20

What drug would you give to solve pulmonary hypertension??

Answer 20

PDE5 inhibitor

Sildenafil

Causes vasodilation

Question 21

How would we treat congestive heart failure

Answer 21

Quadruple therapy

ACE inhibitor: benazepril
Aldosterone inhibitor: spironalactone
(Cardalis is a combo of these)
Diuretics
PDE3 inhibitor: build up of camp, ca increase, inc contractility, inc HR due to faster depolarisation (don't want but mild). Vasodilation. Camp inhibits MLCK and Cgmp activates MLCP

Question 22

Which diuretic would be best

Answer 22

Furosemide - biggest effect with least side effects. If given IV it can also increase contractility

Question 23

Why can horses get AF in a normal heart

How is this different in a dog

Why would a horse be exercise intolerant with AF

Answer 23

Atria are just so big

In a dog, you’d have underlying cardiac disease causing a huge stretched atria

The atria is fluttering and not contracting so EDVV reduced and therefore reduced CO. Also beating faster so less diastolic filling time

Question 24

What is the aim of treatment in the horses case

How would this differ in the dog

Answer 24

We want to reset the heart and allow the SAN to regain control

Dog has structural damage, you’re never going to make it normal again, you can only manage it.

Question 25

Which class would be appropriate for this horse? Which drug specifically? What are the particular considerations with this drug

Answer 25

Class 1a: quinidine: preferentially blocks active Na channels.
Monitor ECG constantly, once into sinus rhythm stop drug. Monitor for signs of colic too.

Question 26

What would you use in the dog?

Answer 26

You need to slow the heart rate/slow conduction through AV node.

Beta blocker: atenolol
Digoxin: mimics vagus nerve, which is parasympathetic

Question 27

What’s another good thing about digoxin- which differs from all other drugs?

Answer 27

It’s a positive ionotrope

Increases Na in cell, so less Ca in cell=theory