CArdiology

Question 1

Where in the USA is dirofilariasis predominantly found? Which geographic location particularly?

Answer 1

The southeast and mississipi river valley region

Question 2

Outline the main lifecycle stages of dirofilariasis in the dog include timings.

At what stage can signs of HWD be seen?

Answer 2

1. Adults live in the pulmonary artery where they can release microfilaraise into the circulation.
2. Mf moult through L1 to L3 in the mosquito over 8 - 17 days. This is dependent on Wolbachia and temperature.
3. In the dog the L3 larvae go to L4 then S5 in the SQT, adipose or skeletal muscle.
4. S5 enter the circulation before setting up as adults

3 & 4 takes around 6 - 7 months.

HWD can be seen 2 - 3 months post infection when the S5 larvae enter the circulation. (so prior to ability to detect infection)

Question 3

At what time of day and season are heartworm Mf released?

Answer 3

During the evening hours and summer months

Question 4

Which lung lobes are most affected by heartworm proliferation? What is the histologic main mechanism of heartworm disease?

Answer 4

Myointimal proliferatoin of the vasculature is the histologic change. The caudal lung lobes seem to be most affected.

Question 5

What are the main mechanisms contributing to development of PHT in canine heartworm disease.

Answer 5

1. Release of vasoactive substances by heartworms
2. Production of ET-1 by the vasculature
3. Platelet activation
4. Hypoxia

Question 6

What are the main pathophysiologic consequences of canine HWD?

Answer 6

Vascular - resulting in PHT
PTE (often in response to worm death)
Glomerulonephritis (due to immune complex deposition)
Abherrent migration through other tissues
Eosinophilic lung disease

Question 7

How can Mf from D. immitis be distinguished from D. reconditum?
- Number
- Motion
- Shape
- Length

Answer 7

Question 8

What is the diagnostic approach to the detection of heartworm?

Answer 8

1. Perform antigen test
2. If positive then perform modified Knott test to look for Mf
   a) If negagative then start a preventative, doxyclycline and melarsomine after 2 months
   b) If positive then do as above but also clear microfilaraie prior to melarsomine
3. If negative then either this is a true negative but if clinical suspicion remains high then serum should be heat-treated.

Question 9

Which heartworm preventative is licenced for microfilarae?

Answer 9

Imidacloprid and moxidectin

Question 10

What stage of the HW lifecycle is heart worm prevention most targeted at?

Answer 10

Mostly targets L3 - L4 moulting

Question 11

Outline the adulticidal protocol for canine heart worm infection

Answer 11

Question 12

What is caval syndrome?

Answer 12

A syndrome of cardiogenic shock resulting from heavy heartworm burden. Features:
1. Haemoglobinuria is the pathognomonic feature
2. Haeolytic anaemia
3. Cardiac arrythmias

Question 13

What is the treatment of choice for heart-worm associated caval syndrome?

Answer 13

Removal of the worms from the pulmonary artery surgically.

Question 14

What is the main difference between canine and feline heartworm consequences?

Answer 14

Feline heartworm infections are unccomon. Although they can get the more classical HWD like dogs this occurs uncommonly. Usually they get HARD which is characterised by the abscence of female worms.

Question 15

How is feline HARD diagnosed?

Answer 15

By demonstrating antibody in the abscence of antigen. antigen positivity is associated with the presence of adult worms and therefore chronic HWI.

Question 16

What is the most sensitive marker of feline HARD on radiography?

Answer 16

he most sensitive marker is left caudal pulmonary artery greater than 1.6x the ninth rib at the ninth intercostal space on the VD projection (only present in 53% of cases).

Question 17

How is feline HWD treated?

Answer 17

Adulticides are a last resort so use macrocyclic lactones.

Question 18

What are the 5 Ps of ischaemic neuromyopathy?

Answer 18

Pain
Paralysis
Pulselessness
Palor
Poikilothermy

Question 19

Streptokinase
- MoA
- Side effects

How does urokinase differ?

Answer 19

Activates plasmin through binding to plasminogen and production of plasmin activator complex.

Side effects can include antigenic stimulation (as it is derived from streptococci), acute respiratory distress (cats), bleeding and reperfusion injury.

UK has a similar mechanism of action but acts more specifically on fibrin bound plasminogen than free plasminogen. N.b that it is associated with very high mortality rates.

Question 20

Hepatin MoA

Answer 20

Binding and activation of ATIII which inhibits IIa, Xa, IXx and XIIa +/- inhibition of vWF

Question 21

How are drugs like heparins ideally monitored

Answer 21

Measurement of anti-Xa activity.

Question 22

What does this image show?

Answer 22

A peritoneopericardial mesothelial remnant - suggests PPDH

Question 23

What are the most common causes of pericardial effusion?

Answer 23

Neoplasia with HSA being most common

Idiopathic pericarditis

Question 24

How does the predilection of heamangiosarcoma, chemodectoma and mesothelioma differ in pericardial disease?

Answer 24

HSA = RA
Chemodectoma = heart base
Mesothelioma = may not have a mass

Question 25

What is electrical alternans?

Answer 25

Variation in QRS complex height that appears regularly and is sometimes seen with pericardial effusions.

Question 26

What chemotherapy agents can be used in patients with mesothelioma?

Answer 26

Intracavity cisplatin +/- intravenous doxorubicin

Question 27

What is the MST of heart base mass tumours compared to HSA when causing pericardial effusion?

Answer 27

With a heart base mass a subtotal pericardectomy can prolong survival (up to 730 days!) compared to not having surgery (42 days)

Question 28

How does the aitiology of pericardial effusion differ between dogs and cats?

Answer 28

In dogs the vast majority of cases are caused by neoplasia. In cats the majorty are due to CHF, followed by neoplasia. In cats the neoplasia is rarely primary cardiac.

Question 29

What are the 6 factors that can result in oedema formation?

Answer 29

1. Intravascular hydrostatic pressure
2. Extravascular hydrostatic pressure
3. Intravascular oncotic pressure
4. Interstital oncotic pressure
5. Vascular permeability
6. Lymphatic function

Question 30

Outline starlings equation

Answer 30

Q = K[(Pmv − Ppmv) − (pmv − ppmv)], where Q = net transvascular fluid flow, K = membrane permeability, Pmv = hydrostatic pressure in the microvessels, Ppmv = hydrostatic pressure in the perimicrovascular interstitium, pmv = plasma protein osmotic pressure in the circulation, and ppmv = protein osmotic pressure in the perimicrovascular interstitium.

Question 31

Which image here (top or bottom) illustrated bigeminy vs. a couplet?

Answer 31

Question 32

What do the following aspects of the ECG trace illustrate:
a) P-wave
b) PR interval
c) Q
d) R
e) S
f) T

Answer 32

a) Atrial depolarisation
b) Conduction of impulse accross the AV node
c) Ventricular septal depolarisation
d) Left ventricular depolarisation
e) The last bit of LV depolarisation (changes direction as direction of travel is away from lead 2)
f) ventricular repolarisation

Question 33

How to calculate heart rate and instantaneous rate on ECG

Answer 33

Question 34

outline einthovens triangle

Answer 34

Question 35

Mobitz type 1 AVB vs. type 2 AVB

Answer 35

1 = Progressive prolongation of the PR interval - this is not pathologic and an atropine response test is indicated
2 = Set PR inverval with dropped beats - pathologic

Question 36

Difference between RBB and LBB?

Answer 36

Left will be upright QRS in lead II (think about an L)

Question 37

What are the main radiographic features of canine HWD?

Answer 37

1. Prominance of the main pulmonary artery
2. RV hypertrophy
3. Large pulmonary artery and tortous or pruned pulmonary artery