CArdiology Flashcards

1
Q

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

A

The southeast and mississipi river valley region

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2
Q

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

At what stage can signs of HWD be seen?

A
  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)

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3
Q

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

A

During the evening hours and summer months

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4
Q

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

A

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

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5
Q

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

A
  1. Release of vasoactive substances by heartworms
  2. Production of ET-1 by the vasculature
  3. Platelet activation
  4. Hypoxia
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6
Q

What are the main pathophysiologic consequences of canine HWD?

A

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

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7
Q

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

A
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8
Q

What is the diagnostic approach to the detection of heartworm?

A
  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.
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9
Q

What are the main radiographic features of canine HWD?

A
  1. Prominance of the main pulmonary artery
  2. RV hypertrophy
  3. Large pulmonary artery and tortous or pruned pulmonary artery
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9
Q

Which heartworm preventative is licenced for microfilarae?

A

Imidacloprid and moxidectin

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10
Q

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

A

Mostly targets L3 - L4 moulting

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11
Q

Outline the adulticidal protocol for canine heart worm infection

A
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12
Q

What is caval syndrome?

A

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

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13
Q

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

A

Removal of the worms from the pulmonary artery surgically.

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14
Q

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

A

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.

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15
Q

How is feline HARD diagnosed?

A

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

16
Q

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

A

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).

17
Q

How is feline HWD treated?

A

Adulticides are a last resort so use macrocyclic lactones.

18
Q

What are the 5 Ps of ischaemic neuromyopathy?

A

Pain
Paralysis
Pulselessness
Palor
Poikilothermy

19
Q

Streptokinase
- MoA
- Side effects

How does urokinase differ?

A

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.

20
Q

Hepatin MoA

A

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

21
Q

How are drugs like heparins ideally monitored

A

Measurement of anti-Xa activity.

22
Q

What does this image show?

A

A peritoneopericardial mesothelial remnant - suggests PPDH

23
Q

What are the most common causes of pericardial effusion?

A

Neoplasia with HSA being most common

Idiopathic pericarditis

24
Q

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

A

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

25
Q

What is electrical alternans?

A

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

26
Q

What chemotherapy agents can be used in patients with mesothelioma?

A

Intracavity cisplatin +/- intravenous doxorubicin

27
Q

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

A

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

28
Q

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

A

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.

29
Q

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

A
  1. Intravascular hydrostatic pressure
  2. Extravascular hydrostatic pressure
  3. Intravascular oncotic pressure
  4. Interstital oncotic pressure
  5. Vascular permeability
  6. Lymphatic function
30
Q

Outline starlings equation

A

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.

31
Q

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

A
32
Q

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

A

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

33
Q

How to calculate heart rate and instantaneous rate on ECG

A
34
Q

outline einthovens triangle

A
35
Q

Mobitz type 1 AVB vs. type 2 AVB

A

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

36
Q

Difference between RBB and LBB?

A

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