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Certifying Examination > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Which are the general causes of peripheral edema?

A
  • Increased hydrostatic pressure:
    —- Increase plasma volume (CHF, renal disease, arteriovenous fistulas)
    —- Venous obstruction
  • Decreased oncotic pressure
  • Increased permeability
  • Impaired lymphatic drainage:
    —- Primary/congenital
    —- Secondary: obstruction/destruction (inflammatory, infectious, neoplasia, surgery, trauma)
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2
Q

Which is the cause of myxedema?

A

Increase capillary leakage of proteins + reduction in lymphatic uptake

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3
Q

Which are the main causes of peripheral edema?

A

Vasculitis (40%) > venous/lymphatic obstruction (20%) > hypoalbuminemia (18%) > CHF-r (5%)

Localized (70%) (obstruction > vasculitis) > generalized (30%) (hypoalbuminemia)

CHFr is more typical to produce abdominal/pleural/pericardial effusion

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4
Q

Which is the mechanism of a vasovagal syncope?

A

Sudden autonomic nervous system failure, with a withdrawal of sympathetic tone and abrupt increase in vagal tone –> hypotension due to bradicardia + vasodilation

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5
Q

What is Bezold Jarisch reflex?

A

When a patient has a structural disease such as aortic stenosis or obstrive HCM, it exacerbates high left ventricular pressures –> stimulate ventricular pressure receptors (perceived as hypertension) –> vasovagal reflex

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6
Q

Which is the best biochemistry marker to distinguish between syncope and TCC seizure?

A

Phosphorus (P <0.97 100% E but 50% S of TCC seizure)

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7
Q

What variables determine the turbulence of blood?

A
  • Blood velocity: + velocity, + turbulent
  • Vessel diameter: + diameter, + turbulent
  • Viscosity: - viscosity, + turbulent
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8
Q

Which are main causes of D-hyperlactatemia?

A
  • Bacterial overgrowth
  • EPI
  • Diabetes mellitus
  • Propylenglicol intoxication
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9
Q

Which factors affect/no affect to lactate concentration?

A
  • No affect: venous/arterial sample
  • Affect: exercise, food, stress, seixures, age
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10
Q

Which electrolytic disorder can be a marker of furosemide resistance and refractory tt?

A

Hypochloremia

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11
Q

How is the Laplace law?

A

Tension = P x (r/2h)

  • Eccentric hypertrophy: secondary to volume overload
  • Concentric hypertrophy: secondary to pressure overload
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12
Q

Which are the objectives of spironolactone administration in CHF?

A
  • Diuretic effect (but low)
  • Block of aldosterone detrimental effects on the vasculature (vasoconstriction) and cardiac remodeling
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13
Q

Which are the reasons torasemide have a decreased likelihood of patients to become refractory?

A

Diuretic effect + antialdosterone effect

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14
Q

Which are the most frequent areas of arterial thromboembolism?

A
  • Iliac bifurcation
  • Right subclavian artery
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15
Q

Which are the most common causes of arterial thrombus in dogs?

A

PLN (30%) > neoplasia > corticosteroids > endocrine > inf

In contrast to cats:
**Chronic course
**No cardiac cases!
**25% don’t reach a definitive diagnosis

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16
Q

Which are the effects of antiplaquetar agents in a thromboembolism?

A
  • To prevent platelet aggregation and increasing the thrombus
  • Inhibit production of thromboxane and serotonine, both of wich act reducing blood flow –> increase blood flow and collaterals.
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17
Q

Which is the most difference between unfractionated heparin and low molecular weight heparin?

A

LMWH have the same mechanism of action, but a reduced factor II inhibition –> whereas heparin can be monitored with PTT and TEG, LMWH have to be monitored with antiXa factor.

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18
Q

What is a NET?

A

Neutrophil extracellular traps: DNA, histones and proteins from activated neutrophils that are liberated to the extracellular –> componnet of innate immune response + prothroombotic.

Blood NETs TAE > no TAE –> can be a marker of TAE risk (specially citH3 more than cfDNA)

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19
Q

Which are the most common congenital diseases in dogs and cats?

A
  • Dogs: PDA > SAS and AS > PS
  • Cats: VSD > PDA > TVD > MVD > AV septal defect > AS
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20
Q

Which breed is predisposed to trichuspid dysplasia?

A

Labrador Retriever

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21
Q

Which breed is predisposed to mitral dysplasia?

A

Bull Terrier

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22
Q

Which are the most common clinical signs associated to degenerative valvular disease?

A
  • Mitral valve disease: respiratory signs (dyspnea +/- cough). As a compensatory mechanism there is a eccentric hypertrophy of the ventricle and an increase in contractibility –> stroke volume no reduced –> no weakness/exercise intolerance. However, in cases where the stroke volume is reduced (because with time, contractibility is reduced), also weakness and exercise intolerance.
  • Tricuspid valve disease: in general there is not important signs, but if it goes together with pulmonary hypertension, more signs.
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23
Q

How is the progression of radiographic changes?

A

A heart chamber enlargement has a slow phase of steadily progressing MMVD until about 6-12 months before the onset of CHF, when the rate of change of enalrgement is fast.

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24
Q

Which new markers of CHF exist in dogs?

A
  • TMAO, L carnitine and choline: increased in CHF
  • Heart Fatty Acid Binding Protein: increased in CHF
  • Lymphos subtypes: increased CD8 and reduced CD4
  • NLR and MLR: increased in CHF
  • Galectin 3: increased in CHF
  • Cystatin C (renal marker): increased in patients with less survival
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25
Q

Which antitussigens can be considered in a MMVD?

A
  • Cough supressants:
    —- Butorphanol
    —- Hydrocodone
    —- Dextrometorphane
  • To improve the low respiratory tract stability:
    —- Bronchodilators
    —- Steroids
    —- Methylxantines (teophylline, aminopylline)
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26
Q

Which is the prevalence of concomitant LRTD and MMVD?

A

75%

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27
Q

Which is the etiopathogenesis of infective endocarditis?

A

Bacteremia and immunosupression/endothelial damage –> the toxics produced by the bacteria + inflammatory reaction leads to degeneration of the valve. Also production of immunecomplexes and thromboembolism.

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28
Q

Whics is the characteristic of Bartonella and Staph aureus infection in a endocarditis?

A

They are able to be internalized within endothelial cells and remain undiscovered by immune system.

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29
Q

Which are the most common clinical signs in endocarditis?

A
  • Fever (50-90%) <– can present without fever (aortic involvement / Bartonella)
  • Murmur (70%) <– 26% can present without murmur
  • Lameness (35%)
  • CHF (50%)

**gram negatives tends to course with acute/peracute disease, whereas gram positive have a more chronic course.

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30
Q

Which are the most common infectious agents cultured in endocarditis?

A

Staphylococcus, Streptococcus, E Coli, Pseudomonas, Corynebacterium, Erysepelotrix, Bartonella.
**study 2023 UK: Staph, Pasteurella, E Coli. No Bartonella.

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31
Q

Which are the Duke criteria?

A
  • Major: culture positive (2 or more), new valculr insuficiency, compatible echocardio
  • Minor: fever, >15kg, SAS, immunocomplexes disease, positive culture (less than 2), thromboembolic disease, high Bartonella serology
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32
Q

Which are the antibiotic of choice for endocarditis treatment?

A

Beta lactamic or imipenem + amikacina or enrofloxacine –> 6w

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33
Q

Which is the prognosis of endocarditis?

A

Poor (68% survival)

  • Bad prognosis markers: gram negative or Bartonella infection, aortic involvement, thromboembolic disease,
  • Favorable prognosis: gram positive infection, mitral involvement
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34
Q

Which are the most common analytical abnormalities found in a PPDH?

A
  • Increased ALT (dog)
  • Increased calcium (cat)
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35
Q

Which is the pathophiology of acute and chronic pericardial effusion?

A
  • Acute: reduced diastolic volume right atrium –> reduced diastolic volume right ventricle –> reduced ejection volume right ventricle –> reduced venous return left atrium –> reduced ventricle filling –> hypotension
  • Chronic: right CHF
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36
Q

Which is the pathophiosiology of pulsus paradoxicus?

A

In normal conditions, during inspiration there is a decrease in the intratoracic pressure –> blood flows preferentially into the low pressure vena cava, pulmonary veins, right atrium and right ventricle. It increases the right ventricular stroke volume during inspiration. In contrast, it reduces the preload of the left heart and the left ventricular stroke volume.

This process is more exxagerated in the presence of pericardial effusion (ventricular interdependence): expansion of the ventricles is limited by the presence of effusion, and any increase in the volume of one ventricle can only occur in expenses of the other –> a greater right ventricular filling during inspiration pushes the interventricular septum leftward, reducing the left ventricular chamber size and the left ventricular filling.

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37
Q

Which are the main infectious agents causing infective pericarditis?

A

Streptococcus, Pasteurella, Bacteroides, Coccidioides, Actinomyces

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38
Q

Which is the relevance of troponin in a pericardial effusion?

A

The concentration in dogs with pericardial effusion is greater than dogs with no effusion, and HSA is greater than other causes of pericardial effusion.

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39
Q

Which is the treatment of choice for infective pericarditis?

A

Subtotal pericardiectomy + chest tube drainage + systemic ab (6m)

40
Q

Which are the most differences among pericardial effusion in dogs and cats?

A
  • In cats rarely cause cardiac tamponade
  • In cats most common cause is secondary to CHF
  • In cats tumors are the second most common cause, being chemodectoma and rhabdomiosarcoma the most common
41
Q

Which are the diagnostic criterias to diagnose a B2 MMVD?

A
  • Heart murmur
  • AI:Ao > 1.6
  • Diastolic diameter LV > 1.7
  • VHS > 10.5
42
Q

Which is the furosemide dose that indicate that the disease is evoluting to stage D?

A

8mg/kg/d

43
Q

Which is the most affected cardiac chamber in a DCM?

A

Generally affects to left chambers, but both can be affected.

44
Q

Which breeds can be affected by a juvenil DCM (<1y)

A

Portuguese Water Dog and Toy Manchester Terrier

45
Q

Which is the best biomarker for a DCM?

A

BNP, for both occult and overt stages, but further studies are required. Troponins are also increased in the overt stage.

46
Q

Which is the possible etiology of DCM in every breed?

A
  • Cocker: taurine deficit
  • Dalmata: low protein diet (–> only left side affected)
  • Doberman: genetic (mutation in PDK4 and TTN) (–> arrythmias are detected at diagnosis and use to be the cause of signs)
  • Great Dane: genetic (–> atrial fibrilation tend to be detected before the onset of CHF)
  • Irish Wolfhound: genetic (–> atrial fibrillation tend to be detected before the onset of CHF)
  • Portuguese Water dOg/Manhcester Terrier: juvenile form

All the heritable diseases are autosomal recessive but Doberman are autosomal dominant and Great Dane X-linked

47
Q

Which are the antiarrythmic drugs used in DCM?

A
  • Atrial arrythmias/atrial fibrillation: diltiazem/digoxine/beta blockers/amiodarone/procainamide
  • Ventricular arrythmias: beta blockers/mexiletine/amiodarone/procainamide
48
Q

Which are the Holter criteria to diagnose a ARVC?

A
  • > 100VPCs
  • Periods of couplets, triplets or ventricular tachycardia
49
Q

Which are the indications for treatment in a ARV?

A
  • > 1000 VPCs
  • Episodes of TQV or R on T phenomenon
  • Homozigots for striatin mutation
  • Presence of clinical signs
50
Q

Which are the characteristics of HCM in dogs?

A
  • Most affected breeds: Pointer, ShiTzu, Terriers
  • 80% systolic murmurs
  • Most common signs: exercise intollerance and syncopes, but most diagnosis are due to murmur detection
  • Symmetrical > asymmetrical. No detection of focal forms.
  • Low risk of sudden death or CHF
51
Q

Which are the most common infectious agents causing myiocarditis?

A
  • Trypanosoma cruzi
  • Leishmania, Toxoplasma, Neospora
  • Parvovirus
  • West Nyle virus
  • Blastomyces
52
Q

Which is the classification of feline HCM?

A
  • Diffuse (2/3):
    —- Symmetric (Maine Coon)
    —- Asymmetric (+ common):
    ——– IVS (+ common)
    ——– LVFW
  • Focal (1/3):
    —- Basal (Chartreaux, Persian)
    —- Apical
53
Q

Which breeds are more and less afected by HCM?

A

More: Maine Coon, Chartreaux, Persian, Sphynx, Ragdoll
- In Maine Coon and Ragdoll: mutation MyBPC3 (autosomal dominant)

Less: Abyssinian, Oriental, Siamese

54
Q

Which is the patophysiology of feline HCM?

A
  1. Myofibrils dysorganization + interstitial fibrosis
  2. Increase myocardic mass
    2.1 Reduced LV diameter –> dyastolic disfunction –> LA enlargement –> TAE + CHF
    2.2. Obstruction coronary arteries + Calcium derrangement –> systolic disfunction
  3. +/- LVOTO +/- tachyarrythmias
55
Q

Which markers can be associated with HCM?

A
  • High insulin
  • High IGF1
  • Inflammatory markers / APP
  • High SDMA
  • Low vitamine D
56
Q

Which types of RCM exist?

A
  • Myocardial
  • Endomyocardial
    —- Scar connecting the IVS and LVFW (+ common)
    —- Diffuse (- common)
57
Q

Why cats are more susceptible to taurine deficiency?

A
  • Cats can synthetize a limited amount of taurine from cysteine due to low tissue concentrations of cysteine-sulfinic acid decarboxylase
  • Cats exclusively use taurine for bile acid conjugation
58
Q

Which are the main differences between ARVC in dogs and cats?

A
  • Dogs: the clinical signs on presentation use to be related to arrythmias, and very rare develop CHF. When CHD develops, it is of left side.
  • Cats: the clinical signs on presentation use to be related to CHF, and less frequent arrythmias. The CHF is from right side.
59
Q

Which are causes of feline secondary cardiomyopathy?

A
  • HCM: systemic hypertension, hypersomatotropism, lymphoma, hypertiroidism, corticoids induced, secondary to aortic/pulmonary stenosis
  • DCM: taurine deficiency, doxorubicin toxicoses
60
Q

Which is the NT-proBNP S and E in a cat?

A

100 and 70.8%, resepctively –> realiable discriminates normal cats from cats with cardiomiopathy

61
Q

Which is the recommended treatment for subclinical cardiac diseases phases? (MMVD, canine CM and feline CM)

A
  • MMVD:
    —- Pimobendan
  • Canine DCM:
    —- Pimobendan
    —- ACEI
  • Feline CM: not as clear as in dogs what is better
    —- Calcium blockers or ACEI except in cases with LVOTO where this drugs are contraindicated and atenolol is recommended (but not very clear which is it effect)
    —- Antiplatelet drugs (but not very clear effect in phase B)
62
Q

Which are the two lymphatic trunks?

A
  • Throacic duct: drains most of the body to the brachycephalic vein and left subclavian vein
  • Right lymphatic duct: drain the right side of the head and neck and EAD to the right subclavian and internal jugular
63
Q

Which is the cause of venous varicosis in dogs and cats?

A

It is a rare disorder and it use to go associated with arteriovenous fistula or vein obstruction

64
Q

Which breeds are predisposed to primary lymphedema?

A

Bulldog, Poodle, Sheetland, L Retriever.

Autosomal dominant

65
Q

Why neurons are very susceptible to hypoxia?

A

Because they cannot generate ATP anaerobically –> very dependent of oxigen

66
Q

Which type of shock are there?

A
  • Hypovolemic
  • Distributive
  • Cardiogenic
  • Obstructive (decreased venous return): GVD, pneumotorax, pericardic effusion
  • Metabollic
  • Hypoxic
67
Q

Which is the distribution of fluid in the body?

A
  • Solids: 40%
  • Fluid: 60%
    —- Intracelular: 60%
    —- Extracellular: 40%
    ——– Interstitial: 75%
    ——– Intravenous: 25%
68
Q

Which are the main functions of glycocalix?

A
  • Regulator of vascular permeability
  • Protect endothelial from blood flood damage
  • Regulator of NO production
  • Retain intravascular protective enzymes
  • Avoid loss of coagulation inhibitors
  • Modulator of inflammatory response
69
Q

Which are the differential criterias in synthetic colloids?

A
  • Concentration
  • Molecular weight: + MW, +t1/2
  • Molar substitution: modification of the original substance by the addition of hydroxyethil groups. +MS, +t1/2
  • C2:C6 ratio: site where substitution occurs on the initial glucose molecule. +ratio, + t1/2
70
Q

Which are the main effects of hemoglobin based oxygen carriers?

A
  • Oncotic pressure
  • Vasoconstrition (scavenges NO)
  • Hemoglobin source
71
Q

Which are the dehydration levels?

A
  • <5%: no specific abnormalities in the physical exam but there is a history of fluid losses
  • 7%: enophtalmia, dry mucous membranes, mild/moderate decreased skin turgor
  • 10%: enophtalmia, dry mjucous membranes, weak peripheral pulses, depression, marked decreased skin turgor
  • > 12%: stupor, coma, death
72
Q

Which are the target endpoints of ressuscitation?

A
  • Restoration of vital signs
  • Nornalization of abnormal mentation
  • PAS >80, PAM>65
  • Normal serum lactate
  • Urinary outout > 1
  • SpO2 >93%
  • Central venous pressure > 5
73
Q

Which is the effect of respiratory disorders in sinusal arrythmia?

A

A respiratory disease can make more pronounced a respiratory arrythmia, except if it is due to cardiogenic edema, when respiratory arrythmia is not detected due to sympathetic tone.

74
Q

Which is the objective HR in a atrial fibrillation treatment?
Which are the prognostic indicators?

A
  • HR <125bpm
    Young dogs (or congenital diseases), large atrium (high natriuretic peptide), collapses and hypotension and high PCR associated to more sudden death risk.
75
Q

Which is the percentage of dogs with situational hypertension?

A

40%

76
Q

Which proportion of cats have persistent HTS and transitory HTS?

A
  • Persistent: 15%
  • Transitory: 5%
    –> 1/5 of cats with HTS will have transitory HTS –> because there is not any distinguishing marker, it is important to monitor and control.
77
Q

In which type of HAC is more common to find HTS?

A

Adrenal dependent hyperadrenocorticism

78
Q

Which are the effects of HTS on heart?

A
  • Development of left ventricle concentric hypertrophy –> diastolic dysfunction
  • Reduced coronary blood flow reserve –> systolic dysfunction
  • Cardiac electrical instability
79
Q

Which is the effect of HTS on kidney?

A

Can induce a hypertensive nephrosclerosis, characterized by glomerulosclerosis, medial thickening of the arteriolar wall and initimal fibrosis

80
Q

Which is the effect of HTS on nervous system?

A
  • Acute: vasogenic edema
  • Chronic: vascular remodelation –> hypoperfusion and stroke

(affecting specially cerebrum white matter, but can also affect the spinal cord (C2-C3 segment more common)).

81
Q

Which is the prevalence of neurologic signs in HTS cats?

A

55% of cats with HTS have neuro signs (50% were visit reason, and 50% the visit reason was different).
More common signs: ataxia, seizures, mental abnormalities.
93% of cats with neuro signs have abnormalities in funduscopic exam.

82
Q

Which is the PAS target ot HTS treatment?

A

140-150mmHg

83
Q

Which are the amlodipine characteristics?

A
  • Action mechanism: calcium channel blocker + aldosterone secretion blocker –> afferent arteriole vasodilation
  • Hight t1/2 –> once daily
  • Slow onset (peak at 4-6h, better to evauate 12h postpill)
  • Hepatic metabolism
84
Q

Which is the objective in the treatment of a hypertensive emergency?

A
  • First hour: to reduce 10% PAS value
  • Next hours: to reduce additional 15% PAS value until normotensive

Risk of rapid pressure lowering –> compensatory SNs activation

85
Q

Which are the characteristics of a hypertensive emergency?

A
  • Clinical signs: seizures > blindness > mental status alteration
  • Most common cause: AKI
  • Mortality 53%
86
Q

Which is the action mechanism of fenoldopam?

A

Dopamine agonist (parasimpaticomimetic) –> vasodilation + Na excretion

87
Q

Which are the most common drugs used in a hypertensive emergency?

A
  • IV:
    —- Fenoldopam: dopamine agonism
    —- Nitroprusside: vasodilator
    —- Hydralazine; vasodilator
    —- Labetolol: beta blocker
    —- Phentolamine: alpha adrenergic antagonism
  • PO:
    —- Hydralazine
    —- Amlodipine: calcium channel blocker + inhibitor secretion aldosterone
88
Q

Which are the alternative pathways of ACE?

A
  • Chymase: production of AT1,12 and ATII –> vasoconstriction
  • ACE2: production of AT1,7 and AT1,9: vasodilation + natriuresis
89
Q

Which is the main interes regarding the alternative pathways of ACE?

A

Alternative pathways scape from ACEi –> in those cases where an ACEi is added, it would be interesting to add also a MRA, specially in those cases with polimorphism of ACE (cases where more alternative pathway occur)

90
Q

Which are the causes of systemic hypotension?

A

Blood pressure = blood flow (CO) x resistance = stroke volume x HR x resistance
Stroke volume depends of preload, afterload and contractibility

  • Reduced preload:
    —- Hypovolemia: blood loss, GI losses, PU, hypoadrenocorticism, effusions, burns, heatstroke
    —- Reduced venous return: pericardial disease, pneumothorax/pleural effusion/diaphragmatic hernia, GVD
  • Reduced vascular tone: sepsis, SIRS, anaphylaxis, drug-induced, neurogenic, severe hypoxemia
  • Decreased cardiac function: estructural diseases (cardiomiopathies, valvular diseases), conductibility diseases (bradyarrythmias, tachyarrythmias), electrolit disorder

**per recordar: mateixes causes bàsiques de shock: hipovolemic i obstructiu (= reduced preload), distributiu (reduced vascular tone) i cardiogenic (decreased cardiac function)

91
Q

Which is the prevalence of structural disease in assymptomatic cats with heart murmur?

A

66% (but tends to be mild disease)
(males and murmur > 3 more possibility to be a structural disease)

92
Q

Which are the cardiac structural causes of hyperkinetic pulses?

A
  • DAP
  • Aortic insufficiency
    (in contrast, aortic stenosis cause a hypokinetic pulse)
93
Q

Which are the factors affecting pulse?

A

Pulse = ejection vo / compliance

94
Q

How affect heart rate on pulse?

A

High HR produce a low stroke volume (there is not enough time to empty all blood) –> weak pulse
—- Exceptions: when there is vasodilation due to fever/anemia: hyperkinetic pulse

In contrast, with low HR there is enough time to empty all blood –> hard pulse

95
Q

Which are the classes of anthyarritmics?

A
  • Class 1: Na channel blockers
    —- Ia: procainamida
    —- Ib: lidocaine
  • Class 2: beta blockers
    —- atenolol
    —- esmolol
    —- propanolol
    —- sotalol
  • Class 3: K channel blockers
    —- amiodarona
    —- sotalol
  • Class 4: Ca channel blockers
    —- Diltiazem
    —- Amlodipino
  • Class 5: other
    —- Digoxine
96
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Certifying Examination (10 decks)

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