Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Systemic Pathology > Cardio Pathology > Flashcards

Cardio Pathology Flashcards

1
Q

Describe the cardiac skeleton

A

Four fibrous rings, fibrous triangle, and fibrous or membranous part of the septum that supports all the cardiac mm and valves at the heart base

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the cardiac skeleton material differ between species?

A
  • Dense fibrous CT - pigs and cats
  • Fibrocartilage - dogs
  • Hyaline cartilage - horses
  • Bone (os cordis) - large ruminants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When does most coronary arterial blood flow occur?

A

During diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common cause of dysrhythmias?

A

Injury to atrial or ventricular myocytes, resulting in independent repeated depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is another name for the epicardium?

A

The visceral pericardium or visceral layer of the serous pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What substance can be found contained within atrial myocytes?

A

Atrial natriuretic factor - this is released on dilation/stretching of the atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cardiac myocytes lack plasticity, meaning they have a limited ability to respond to what?

A

Physiologic stress, such as atrophy, hypertrophy, degeneration, necrosis or fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What three things are required for the development of hypertrophy?

A

Time, a healthy myocardium and adequate nutrition and oxygenation of myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe cardiac syncope

A
  • Acute cardiac failure
    • leads to arrhythmias, massive necrosis, and extreme changes in BP/HR
  • C/S - collapse, loss of consciousness, DEATH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between forward and backward failure with CHF?

A
  • Forward: decr flow to periph tissues
  • Backward: accumulation behind the failing chamber
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the cycle of cardiac decompensation

A
  • Hypoxia —> Renin release (RAAS) from kidneys —> stim aldosterone release from adrenal cortex —> Na and H2O retention —> incr plasma volume —> edema
  • Edema —> stim erythropoiesis (EPO) —> polycythemia —> incr blood viscosity

Result: failing heart must pump a greater volume of thicker fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What two things can lead to cardiac hypertrophy?

A

Chronic pressure overload and chronic volume overload (also leads to ventricular dilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What things might cause physiologic cardiac hypertrophy?

A
  • It’s a reversible response to exercise or pregnancy, without any deleterious effect
  • initiated by thyroid hormone, insulin, insulin growth factor 1 and GH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the difference between preload and afterload?

A
  • Preload- the end diastolic volume that stretches the ventricle to its greatest dimensions
  • Afterload - pressure that the chamber of the heart must generate to eject blood out of the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe concentric cardiac hypertrophy

A
  • An incr in mass of the ventricle w/o accompanying incr in end-diastolic volume, often w/ decr in ventricular lumen
  • caused by increased afterloads (systolic loads)
    • e.g. aortic/pulmonic stenosis, PDA, cats with hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the gross changes seen with concentric cardiac hypertrophy?

A

Incr thickness of wall of affected chamber, marked incr in size of papillary mm and trabeculae carnae, and right side —> incr size of moderator band

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe eccentric cardiac hypertrophy

A
  • An incr in myocardial mass accompanied by incr end-diastolic volume (dilated chamber)
    • b/c of dilation, thickness of involved ventricular wall is usually no more than normal
  • caused by an incr in diastolic load (incr preload)
    • e.g. AV or semilunar valvular insufficiencies, arteriovenous shunts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the gross pathological changes seen with eccentric cardiac hypertrophy and dilation

A

Heart tends to be globose —> even though mass is incr, the wall is usually thin, papillary mm may also be attenuated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the best indicator of dilation of the atria?

A

Subendocardial fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are two reasons the heart can fail?

A

Because of impaired pump function and/or because of increased cardiac work demands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is congestive heart failure?

A
  • Chronic loss of pumping ability –> Vascular congestion and edema within the interstitium of tissues and body cavities (chronic)
    • syndrome NOT a dz
  • eventual progression to full failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define acute heart failure

A

Intermittent weakness and syncope caused by substantial change in heart rate or rhythm —> results in drop of precipitous cardiac output —> sudden unexpected death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the causes of left sided heart failure?

A
  • Myocardial loss of contractility (myocarditis, myocardial necrosis, cardiomyopathy)
  • valvular insufficiency (mitral/aortic valve)
  • aortic stenosis
  • systemic hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the sequelae and clinical signs of left sided heart failure?

A

Seq: Pulm congestion/edema/fibrosis and hemosiderosis (heart failure cells)

C/S: cough, dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where does the place of peripheral edema caused by right sided heart failure differ between species?

A
  • Ruminants and horses—> dependent subcutaneous edema
  • Dogs —> peritoneal cavity (ascites)
  • Cats—> thorax (hydrothorax)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

True or False: renal complications occur more frequently with right heart failure than with left heart failure

A

True; leads to incr blood volume, peripheral edema and more marked azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the causes of right sided heart failure?

A
  • Valvular insufficiency (incr preload) - tricuspid, pulmonary
  • pulm hypertension (incr afterload) - obstruction of forward flow
  • pulmonic stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the sequelae of right sided heart failure?

A
  • Hepatic congestion - passive congestion (nutmeg liver)
  • ascites (dogs)/hydrothorax (cats)
  • pleural and pericardial effusion
  • congestion of stomach and intestines—> may impair function —> manifest as diarrhea, splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does the liver look like histologically with right sided heart failure?

A

Sinuosoids are dilated/congested, atrophy of hepatocytes around central veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is cor pulmonale?

A
  • Right heart failure secondary to chronic obstructive pulmonary dz
  • could be d/t dirofilariasis, PTE, neoplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are some congenital heart defects in dogs?

A

PDA, pulmonic stenosis, subaortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some congenital heart defects in cattle?

A

Atrial and ventricular septal defects (VSDs), transpositions of main vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some congenital heart defects in pigs?

A

Subaortic stenosis, endocardium cushion defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are some congenital heart defects in cats?

A

Endocardial cushion defects, mitral valve insufficiency

35
Q

What are the four malformations that can cause left to right shunting?

A

Atrial septal defects, atrioventricular septal defects, ventricular septal defects, PDA

36
Q

Why is a postnatal probe patent foramen ovale not considered an atrial septal defect?

A

Because it is functionally closed during development, even if it’s anatomically patent

37
Q

What are some examples of atrial septal defects?

A

Sinus venous defect, ostium primum defect, and ostium secundum defect (most common)

38
Q

What are the consequences of atrial septal defects?

A

Excessive flow from L to R atrium —> volume overload of RV—>dilation —> elevated CVP —> possible pulm hypertension —> RV hypertrophy —> eventual cyanosis

39
Q

Describe AV septal defects

A

AKA endocardial cushion defects or AV canal defects

  • ostium primum defect (partial AV canal)
  • VSD w/ a cleft in the right AV valve (common)
  • frequent in pigs w/ congenital heart dz and in cats
40
Q

Ventricular septal defects are one of the most common defects in domestic animals.

T or F: most VSD are single and involve the membranous septum

A

True

41
Q

What are the consequences of VSDs?

A

Postnatally - pulm vascular resistance normally drops after birth and leads to left-to-right shunting —> RV and LV pressure equalize —> both ventricles hypertrophy (eccentric) —> eventually pulm hypertension can lead to shunt reversal—> R to L—> cyanosis —> death

42
Q

What is an Eisenmenger complex?

A

VSD cases w/ reversal and R to L shunting

43
Q

At how many days after birth can you officially diagnose a ductus arteriosis as a PDA?

A

After 5 days

44
Q

What are the 3 broad anatomical division of the heart?

A

Mural and valvular endocardium, myocardium and pericardium

45
Q

What are the 3 general rules of mural and valvular endocardial defects?

A
  1. Valvular insufficiency incr the preload to a ventricle
  2. Semilunar valvular stenosis, outflow tract stenosis, and hypertension incr the afterload on the ventricle
  3. AV valvular stenosis and pericardial disorders decr preload on the ventricles
46
Q

When might you see subendocardial hemorrhage?

A
  • Septicemia
  • endotoxemia
  • anoxia
  • electrocution
  • trauma
  • agonal change
47
Q

When might you see subendocardial mineralization?

A
  • Dystrophic (necrotic tissue) or metastatic mineralization (normal tissue w/ hyperCa)
  • vit D toxicity
  • calcinogenic plant toxicosis in cattle
  • Ca/P imbalance
  • Johne’s dz
48
Q

Describe vegetative valvular and mural endocarditis

A
  • Bacteria >>> parasites (Strongylus vulgaris) > fungi
  • Gross: valves have large, adhering, friable yellow-to-gray masses of fibrin ( (= vegetations)
    • can occlude valvular orifice and there is frequently valvular involvement (mitral>aortic>tricuspid>pulm)
49
Q

What is Virchow’s triad of thrombogenesis?

A

Endothelial injury, turbulence, hypercoagulability

50
Q

What is the pathogenesis of vegetative valvular and mural endocarditis?

A
  • Involves Virchow’s triad
  • affected animals often have pre-existing extracardiac infections
  • often septic emboli that lodge in heart,kidneys
51
Q

What are the causes of endocarditis?

A
  • Sepsis (vegetative, valvular, Strep, Staph, Klebsiella, E. Coli)
  • Uremia (ulcerative, LA)
  • can result in embolism of various organs (ie. kidney)
52
Q

Describe uremic endocarditis

A

Occurs in dogs d/t acute or repeated episodes of uremia

  • ulcerative and targets the left atrium
53
Q

What are 4 diseases that distort valves?

A
  1. Endocardiosis
  2. valvular stenosis
  3. valvular dysplasia
  4. hematocysts and lymphocysts
54
Q

What is endocardiosis and what type of animals does it target?

A

Myxomatosis valvular degeneration (mitral > tricuspid)

  • targets small and toy breeds and middle-aged to older dogs
    • Cavies are predisposed
55
Q

What are some possible sequelae of endocardiosis?

A

Valvular incompetency, CHF (R or L), atrial dilation, jet lesions, LA rupture —> hemopericardium, chordae tendinae rupture

56
Q

Describe hematocysts and lymphocysts

A

Occur commonly in ruminants, do not cause problems, and regress within a few months of birth

57
Q

Name 3 common myocardial diseases

A

Myocardial necrosis, myocarditis, and cardiomyopathies

58
Q

What are four potential causes of myocardial necrosis?

A
  • Infectious
  • nutritional myopathies
  • exertional myopathies
  • toxins
59
Q

What are 3 nutritional causes of myocardial necrosis?

A
  1. Vitamin E and Selenium deficiency (lambs, calves, swine - mulberry heart dz, horses)
  2. Thiamine deficiency (carnivores)
  3. Copper deficiency (falling syndrome in AUS/Fl, death)
60
Q

What are some gross and histologically features seen with vitamin E and selenium deficiency-induced myocardial necrosis?

A
  • Pallor = areas of necrosis
  • mineralization of necrotic myofibers
61
Q

What are some toxins that cause myocardial necrosis?

A
  • Monensin (ionophore used as a cocciostat in ruminants)
  • Plants (cardiac glycoside containing plants)
  • Drugs (Doxorubicin)
62
Q

Describe brain-heart syndrome

A

Subendocardial necrosis seen following acute brain/CNS injury

  • caused by coronary artery spasm or excess catecholamine release/functional pheochromocytoma
63
Q

Describe myocarditis

A

Inflammation of the myocardium

  • typically spread hematogenously
  • can result in acute death from focal myocarditis resulting in conduction abnormalities or can lead to CHF
64
Q

What are some causes of myocarditis?

A
  • Viruses (canine herpesvirus, parvo, FMD)
  • bacteria (actinobacillus, bartonella)
  • Protozoa (Neospora, Sarcocystis)
  • helminths (Trichinella spiralis)
65
Q

Describe cardiomyopathies

A

Genetic abnormalities of myocardial contractile, cytoskeleton or mitochrondrial proteins

  • can be responsive to substances such as taurine or carnitine
66
Q

Describe dilated cardiomyopathy

A

Genetic abnormalities in cytoskeletal proteins and mitochondrial genes, characterized by dysfunction of systolic phase of cardiac cycle

  • both atria and ventricles are dilated
67
Q

Describe hypertrophic cardiomyopathy

A
  • Diastolic dysfunction - hypertrophied ventricle is less stiff, resulting in impaired filling
    • commonly inherited as autosomal dominant w/ high prevalence of subclinical dz or sudden death
68
Q

Describe what myocytes look like microscopically with hypertrophic cardiomyopathy

A

Hypertrophied and arranged in a whirled or disorganized pattern

69
Q

Describe restrictive cardiomyopathy

A
  • Impaired filling d/t diastolic dysfunction
  • interstitial or endomyocardial fibrosis
    • occurs most frequently in cats
70
Q

Describe HCM in cats

A

Inherited autosomal dominant trait in Maine Coons and Ragdolls

  • Gross - enlarged heart, massive symmetrical concentric hypertrophy of both ventricles (LV most severe typically)
  • does not = concentric hypertrophy secondary to hyperthyroidism
71
Q

Describe RCM in cats

A
  • Less common than HCM
  • also called LV endocardial fibrosis
  • may be preceded by endomyocarditis
  • seen in older cats with left sided or bilateral heart failure - murmurs and arrhythmias are common
72
Q

Describe the gross and histopathological lesions you see with RCM

A
  • Gross - severe endocardial thickening w/ mural thrombosis
  • Histo - replacement of endocardium and myocardium by granulation tissue and fibrosis +/- macrophages, lymphocytes, plasma cells
  • Bartonella infections and hypereosinophilic syndrome are common causes
73
Q

Describe DCM in cats

A
  • Associated with taurine deficiency, less prevalent
  • Gross lesions: all ventricles are dilated and flabby with thin walls, endocardium may be pale d/t fibrosis
74
Q

Describe the condition of having excessive moderator brands

A

Not technically a cardiomyopathy - likely a congenital defect of older cats

  • excessive moderator bands (false tendons) in LV bridging the ventricular septum to the free wall—> heart failure and death
75
Q

Describe DCM in the dog

A
  • Young to middle aged giant and large breed dogs (ie. Dobies, St. Bernards, Irish wolfhounds, Great Danes)
  • genetic basis - may be X linked
  • heart failure, short onset of C/S, may see unexpected death
76
Q

What are the gross lesions seen in a dog with DCM?

A

L-sided CHF, biventricular failure, all chambers are dilated +/- subendocardial fibrosis, atrial fibrosis

77
Q

What are some common bovine cardiomyopathies?

A
  • DCM in Holsteins, Japanese black calves
  • Cardiomyopathy assoc. w/ tightly curled “wooly” haircoat in polled and horned Hereford calves
  • HCM in Holsteins
78
Q

Describe hydropericardium

A

Excess of clear fluid in pericardial sac - generalized anasarca (edema)

  • causes include - hypoalbuminemia, CHF, neoplasia
  • fluid accumulates slowly allowing stretch of pericardium
79
Q

Describe hemopericardium

A

Accumulation of pure blood in pericardial sac that rapidly results in death

  • if blood is clotted —> true hemopericardium
  • can be due to cardiac rupture or direct trauma
80
Q

Describe the pathogenesis of hemopericardium in horses vs. dogs vs. swine

A
  • Horses: rupture intrapericardial aorta or atria
  • Dogs: atrial rupture d/t endocardiosis, atrial hemangiosarc, ulcerative atrial endocarditis of renal failure
  • Swine: rare, rupture of heart (atrium), coronary artery, aorta
81
Q

What are the microorganisms responsible for fibrinous pericarditis?

A

Usually result of hematogenous microbial infections

  • Cattle - pasteurollosis, blackleg
  • Swine - Glasser’s dz (Haemophilus)
  • Horses: Mycoplasma, mare repro loss syndrome
  • Cats: rare, assoc w/ FIP
82
Q

What causes purulent pericarditis?

A
  • Almost solely occurs in cattle as a result of traumatic perforation from FB originating in the reticulum —> can lead to chronic constrictive pericarditis and severe cardiac dysfunction
  • also seen in cats and horses w/ pyothorax
  • migrating grass awns in western US = another cause
83
Q

What are some neoplasms of the heart?

A

Primary tumors are rare, but mets to the myocardium are common

  • primary tumors of the aortic body (chemodectomas) and ectopic thyroid and parathyroid tumors may arise at heart base in dogs
  • Also rhabdomyomas, metastatic lymphomas
84
Q

What is a rhabdomyoma?

A

Anomalous formations of perinatal cardiac myocytes

  • swine - possible Purkinje cell origi
  • rare but most common in pigs >> cattle, sheep, dogs

Systemic Pathology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions