Applied Cases Flashcards
Case: dog with no other signs except excessive panting/ found to have high BP
What does raised ALKP and ALT show?
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
What is normal systolic BP?
120
But allow 150 in the consult room
Why would you get a reduced echogenicity in the liver with high BP
More block flow to liver therefore darker (remember fluid is dark)
What anatomical structure sits at the cranial pole of the kidney close to the caudal vena cava
Adrenal gland
What does the adrenal gland produce
Mineralocorticoids
Glucocorticoids
Androgens
Catecholamines e.g. Adrenaline
Can glucocorticoids effect RAAS?
Yes they have some mineralocorticoid effect
May have CNS effect on cardiac output
Activate vasoactive substances
What can you look at too see if normal aldosterone function
NA and K
What else could you check in the blood to see what an adrenal tumour is making to result in high BP??
If patient is on preds: can’t measure basal cortisol!
ACTH
Noradrenaline clearance in urine
Where in the adrenal glands are catecholamines made??
The medulla
In this case (where the tumour has invaded the adrenal gland) why can’t we remove it?
Risk damage to caudal VC
What drugs could we use to reduce BP
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
Why is phenoxybenzamine especially good for this dog?
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
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?
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.
Why have we got hepatosplenomegaly?
Blood can’t go into caudal vena cava as can’t go into right atria
Why is there a jugular pulse?
Blood is shooting back into the atria, into the vena cava and into the jugular etc.
What does mean electrical axis tell us?
The overall vector of the AP through the heart
Why might we have a right axis deviation?
Right hypertrophy
Unexpected conduction pathway
Change in position e.g. Big tumour
What’s an ECG most useful for
Heart rate and rhythm
What should the end of the trachea be parallel to?
The sternum
What drug would you give to solve pulmonary hypertension??
PDE5 inhibitor
Sildenafil
Causes vasodilation
How would we treat congestive heart failure
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
Which diuretic would be best
Furosemide - biggest effect with least side effects. If given IV it can also increase contractility
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
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
What is the aim of treatment in the horses case
How would this differ in the dog
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.
Which class would be appropriate for this horse? Which drug specifically? What are the particular considerations with this drug
Class 1a: quinidine: preferentially blocks active Na channels.
Monitor ECG constantly, once into sinus rhythm stop drug. Monitor for signs of colic too.
What would you use in the dog?
You need to slow the heart rate/slow conduction through AV node.
Beta blocker: atenolol
Digoxin: mimics vagus nerve, which is parasympathetic
What’s another good thing about digoxin- which differs from all other drugs?
It’s a positive ionotrope
Increases Na in cell, so less Ca in cell=theory
