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22 fall: path > Test 2: lecture 1 heart > Flashcards

Test 2: lecture 1 heart Flashcards

1
Q

3 functions of circulatory system

A

circulation
thermoregulation
fluid homeostasis

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2
Q

what valve in right side of heart

A

tricuspid and pulmonary

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3
Q

what valve in left side of heart

A

mitral and aortic

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4
Q

layers of the heart

A

endocardium
myocardium
pericardium

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5
Q

—- mechanisms operate to help maintain
adequate cardiac output & tissue perfusion

A

Compensatory

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6
Q

dilation of the heart cause

A

increase in chamber volume

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7
Q

hypertrophy of the heart

A

increase in mass of heart, cells get bigger

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8
Q

ischemia

A

decrease in blood flow to tissues

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9
Q

congestion in heart leads to

A

pooling of blood behind the failing chambers, leads to increased hydrostatic pressure and edema

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10
Q

Chronic hepatic
congestion (“nutmeg liver”), Ascites and subcutaneous edema are symptoms of —

A

right sided heart failure

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11
Q

left sided heart failure symptoms

A

pulmonary congestion and edema

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12
Q

right and left sided heart failure symptoms

A

hydrothorax

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13
Q

fluid build up in abdomen

A

ascites

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14
Q

cardiac myocytes look

A

central nuclei
intercalated discs
cross striations

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15
Q

___ hypertrophy due to ↑ workload; REVERSIBLE if underlying cause is removed

A

SECONDARY

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16
Q

— hypertrophy is usually irreversible

A

PRIMARY

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17
Q

concentric cardiac hypertrophy causes

A

increased wall thickness
decreased chamber volume

parallel myocytes are added in response to increased pressure

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18
Q

—- hypertrophy is caused by increased pressure overload

A

concentric

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19
Q

— myocardial hypertrophy is caused by volume overload

A

eccentric

myocytes in series

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20
Q

eccentric myocardial hypertrophy will cause the wall and volume to —

A

increased chamber volume (dilation)

normal or decreased wall thickness

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21
Q

primary vs secondary cardiomyopathy

A

primary- caused by genetics or unknown cause

secondary- caused by something other than genetics

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22
Q

3 types of cardiomyopathy

A

HYPERTROPHIC
DILATED
RESTRICTIVE

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23
Q

HCM is caused by — in maine coons and ragdoll

A

MYBPC3 gene

young male cats

primary cardiomopathy
cause cardiomegaly and concentric hypertrophy

Thick LV wall, ↓ LV volume, LA dilation, thrombosis

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24
Q

HCM cause what gross findings

A

Thick LV wall, ↓ LV volume
LA dilation, thrombosis,
enlarged heart- cardiomegaly

Hypertrophic cardiomyopathy

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25
Q

what has similar gross findings to HCM

A

thyrotoxic cardiomegaly

Thyroid gland hyperplasia → ↑ thyroid hormone production → ↑ production of myocardial contractile proteins → myocardial hypertrophy

can be reversible

Hypertrophic cardiomyopathy

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26
Q

primary dilated cardiomyopathy effects

A

humans, dogs (dobermans, young portuguese water dogs), cattle

caused by genetics

enlarged rounded heart, dilated chambers with thin walls- eccentric hypertrophy

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27
Q

gross findings of dilated cardiomyopathy

A

Enlarged rounded heart

  • Dilated chambers, thin walls (eccentric hypertrophy)
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28
Q

gross findings of thyrotoxic cardiomegaly

A

same of HCM, but reversible if you fix the hyperthyroidism

enlarged heart, thick LV wall, decreased LV volume (concentric hypertrophy), LA dilation and thrombosis

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29
Q

taurine deficiency will cause what heart problem

A

secondary dilated cardiomyopathy

big round heart, dilated chambers, thin walls (eccentric hypertrophy)

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30
Q

boxer dog cardiomyopathy

A

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

variant of DCM

heart cells replaced by fibrous or fat
leads to dilated RV

Predisposed to ventricular arrhythmias, syncope, heart failure, sudden death

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31
Q

symptoms of ARVC

A

Arrhythmogenic right ventricular cardiomyopathy

variant of DCM - boxer dog cardiomyopathy

arrhythmias, syncope, heart failure, sudden death

RV myocytes replaced by adipose tissue (or fibroadipose tissue)
* RV normal or dilated (common)

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32
Q

Restrictive cardiomyopathy will impair —

A

ventricular filling

ventricles not as stretchy- fibrosis, ↑ moderator bands, fibroelastosis

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33
Q

feline LVEF is caused by

A

Sequela of ENDOMYOCARDITIS
(idiopathic inflammation that often follows a stressful event)

Thick opaque endocardium
(usually involving LVOT)

Feline left ventricular endocardial fibrosis

variant of RCM- restrictive

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34
Q

gross findings of Feline left ventricular endocardial fibrosis

A

Thick opaque endocardium
(usually involving LVOT)

variant of RCM- restrictive

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35
Q
A

excessive moderator bands

form of restrictive cardiomyopathy

Endothelial-lined bands of
Purkinje fibers & collagen (“false tendons”) traverse the LV & restrict ventricular filling

  • Congenital defect that
    manifests later in life
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36
Q

excessive moderator bands will cause

A

restricted ventricular filling

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37
Q

hypertrophic vs dilated vs restrictive cardiomyopathy

A
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38
Q

cardiomyopathy can cause

A

arrhythmia
thrombosis
congestive heart failure

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39
Q

what happens when heart muscle injured

A

can’t regenerate
will go through necrosis and form fibrosis

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40
Q
A

Myocardial pallor, dry, gritty texture
(dystrophic mineralization)

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41
Q
A

fibrosis- firm depressed myocardial scar in chronic stage

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42
Q

sheep

A

nutritional myopathy from vitamin E or selenium deficiency

white muscle disease, mulberry heart disease in pigs

leads to decreased antioxidant activity and myocyte necrosis

will cause mineralization

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43
Q

white muscle disease in — and mulberry heart disease in — is caused by —

A

ruminants

pigs

nutritional myopathy from vitamin E or selenium deficiency

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44
Q

inflammation of the myocardium

A

myocarditis

similar in appearance to necrosis

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45
Q
A

Granulomatous myocarditis in a dog Aspergillus terreus fungi infection

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46
Q
A

Suppurative myocarditis in a cow - chronic abcsess

Histophilus somni infection

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47
Q

endocardiosis definition

A

Idiopathic degeneration of valvular collagen

Mitral > tricuspid >aortic & pulmonic

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48
Q

endocardiosis gross findings

A

thickened/nodular valve margins (smooth, glistening, & opaque)

Idiopathic degeneration of valvular collagen

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49
Q

— will commonly get endocardiosis

A

Cavalier King Charles spaniel

old small breed dogs

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50
Q

what valves are normally attacked by endocardiosis

A

Mitral > tricuspid > aortic & pulmonic

Idiopathic degeneration of valvular collagen in old small breed dogs such as Cavalier King Charles spaniel

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51
Q

— valvular degeneration comprised of loose fibroblastic tissue with —

A

Myxomatous valvular degeneration comprised of loose fibroblastic tissue with mucopolysaccharides; non-inflammatory!

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52
Q

Myxomatous valvular degeneration cause

A

loose fibroblastic tissue with mucopolysaccharides; non-inflammatory!

type of endocardiosis on valves of heart

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53
Q

valve insufficiency cause — of blood

A

regurgitation

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54
Q

symptoms of valvular insufficiency

— (turbulent flow)

Atrial volume overload → — and CHF

Atrial subendocardial fibrosis = —

— THROMBOSIS → thromboembolism and infarcts

— RUPTURE

— RUPTURE → hemopericardium

A

HEART MURMUR

ECCENTRIC HYPERTROPHY

“JET LESION”

ATRIAL

corda tendinea

ATRIAL

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55
Q

Atrial subendocardial fibrosis are also called

A

jet lesions

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56
Q
A

Atrial jet lesion (subendocardial fibrosis) where regurgitant jet strikes atrial wall

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57
Q

atrial volume overload will cause — hypertrophy

A

eccentric

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58
Q
A

Atrial thrombosis (top) & chorda tendinea rupture (bottom)

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59
Q

endocardiosis or endocarditis have inflammation

A

endocarditis- inflammation of endocardium

endocardiosis- is degeneration of valves

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60
Q

endocarditis is usually caused by

A

bacterial; rarely fungal or
parasitic

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61
Q

endocarditis effect — valve in cattle and — valve in other species

A

tricuspid

mitral

62
Q
A

endocarditis

Gross findings: thrombi (“vegetations”) on valvular/mural endocardium

63
Q

gross findings of endocarditis

A

thrombi (“vegetations”) on valvular/mural endocardium

64
Q
A

Vegetative endocarditis morphology

Septic thrombi composed of fibrin, bacteria, neutrophils  granulation tissue/fibrosis

65
Q

— composed of fibrin, bacteria, neutrophils and granulation tissue/fibrosis form on valves with endocarditis

A

Septic thrombi

66
Q

how does vegetative endocarditis form

A

bacteria from somewhere in the body will clump onto minor endocardial damage at valves and cause inflammation

can break off and cause thrombosis

67
Q

thrombosis is caused by what three things

A

virchow’s triad

68
Q

vegetative endocarditis will cause —

A

VALVULAR INSUFFICIENCY (leading to CHF) or effects of BACTEREMIA

SEPTIC THROMBOEMBOLI

ISCHEMIA & INFARCTS

INFECTION & INFLAMMATION

69
Q

dystrophic mineralization

A

necrotic tissue that forms mineralization

70
Q

metastatic mineralization is caused by

A

too much calcium in the body

71
Q

endocardial mineralization gross findings

A

gritty white plaques on
endocardium (+/- vascular endothelium)

72
Q

vitamin D toxicosis can be caused by

A

oversupplementation, ingestion of cholecalciferol rodenticides or calcinogenic plants containing vitamin D analogs

will cause endocardial mineralization

73
Q

three causes of endocardial mineralization

A

vitamin D toxicosis
johne’s disease
uremia

74
Q

pericardium is made of the — and —

A

Visceral layer = EPICARDIUM (outermost layer of heart)

Parietal layer associated with outer fibrous portion of
PERICARDIAL SAC

75
Q

serous fluid in pericardial cavity is called

A

HYDROPERICARDIUM

76
Q

blood in pericardial cavity is called

A

HEMOPERICARDIUM

77
Q

inflammatory of the pericardial cavity is called

A

pericarditis

78
Q

rapid fluid accumulation in the pericardial cavity cause

A

CARDIAC TAMPONADE

79
Q

cardiac tamponade is the — of the heart due to —

A

compression

increased pressure in pericardial cavity

80
Q

cardiac tamponade can lead to — and death if not corrected

A

cardiogenic shock

Interferes with cardiac filling, causing venous blood to pool in the splanchnic & systemic vasculature

81
Q

three routes of pathogen entry for pericarditis

A

inflammation of the pericardium

HEMATOGENOUS spread (e.g., septicemia)

DIRECT PENETRATION (e.g., “hardware disease”)

LOCAL EXTENSION from myocardium, pleural cavity, mediastinum

82
Q
A

Acute fibrinous pericarditis (fibrin easily removed from surface)

83
Q
A

Chronic pericarditis (firm fibrous adhesions between pericardial layers)

84
Q
A

Serous atrophy of pericardial fat

Thin translucent gelatinous adipose tissue

85
Q

emaciation

A

the state of being excessively thin and wasted.

86
Q

wasting also called

A

cachexia

87
Q

serous atrophy of pericardial fat gross findings

A

Thin translucent gelatinous adipose tissue

88
Q

Blood is shunted from— (HIGH pressure to LOW pressure)

A

LEFT to RIGHT

89
Q

ductus arteriosus

A

skips fetal lungs

pulmonary artery to aorta

90
Q

foramen ovale

A

hole from left to right side of heart in fetus- skip lungs

91
Q

Reversal of flow (RIGHT to LEFT) may occur later in disease due to —

A

pulmonary hypertension

(normal flow left to right- leads to build up in the lungs)

92
Q
A

patent ductus arteriosus (PDA)

cause lung overload

93
Q
A

ventricular septal defect (VSD)

94
Q

pulmonic stenosis will cause —

A

Pressure overload→ concentric RV hypertrophy

95
Q

aortic stenosis will cause —

A

Pressure overload → concentric LV hypertrophy

96
Q

mitral or tricuspid valve dysplasia will cause

A

regurgitation

atrial volume overload & eccentric hypertrophy

97
Q

left side of heart

A

subaortic stenosis

Raised fibrous ring below aortic valve that narrows the LVOT→ LV pressure overload & concentric hypertrophy

98
Q

subaortic stenosis will cause — hypertrophy

A

concentric

Raised fibrous ring below aortic valve that narrows the LVOT →LV pressure overload & concentric hypertrophy

99
Q

Malformed valve leaflets with short chordae tendineae or direct insertion of valve margin onto papillary muscle → valvular insufficiency → —overload & — hypertrophy

A

atrial volume

eccentric

100
Q
A

persistent right aortic arch (PRAA)

Vascular ring formed around esophagus and trachea → proximal megaesophagus (sequelae: regurgitation, aspiration pneumonia)

101
Q

persistent right aortic arch will lead to

A

Vascular ring formed around esophagus and trachea → proximal megaesophagus (sequelae: regurgitation, aspiration pneumonia)

102
Q

— is anomaly with single blood vessel from RV & LV

A

Persistent truncus arteriosus

103
Q

Ectopia cordis

A

heart outside thoracic cavity)

104
Q

Peritoneal-pericardial diaphragmatic hernia

A

(liver/intestine
translocated into pericardial cavity; may be subclinical

105
Q

4 lesions of Tetralogy of Fallot

A
  1. Pulmonic stenosis
  2. Ventricular septal defect
  3. RV hypertrophy (secondary to PS)
  4. Aortic dextroposition (shifted to right, sit over left and right ventricles)
106
Q

tetralogy of fallot cause

A

Venous blood shunted from R to L through VSD & out aorta into systemic circulation → cyanosis

107
Q

ruminant heart

A

Valvular hemocysts/lymphocysts

incidental finding

Dilated blood- or lymph-filled vascular spaces on AV valves

108
Q

inflammation of blood vessels

A

VASCULITIS

109
Q

inflammation of arteries

A

ARTERITIS

110
Q

inflammation of many arteries

A

POLYARTERITIS

111
Q

inflammation of veins

A

PHLEBITIS

112
Q

inflammation of lymphatic vessels

A

LYMPHANGITIS

113
Q

damage to endothelial & smooth muscle cells will cause

A

edema, hemorrhage, thrombosis

114
Q

vasculitis can be caused by

A

infectious- viral, bacterial, fungal, parasitic

immune-mediated- Polyarteritis nodosa, Idiopathic necrotizing polyarteritis (“beagle pain syndrome”)

115
Q

“hardening of the arteries”

A

ARTERIOSCLEROSIS

116
Q

subset of arteriosclerosis accompanied by plaques of fatty material in the arteries

A

ATHEROSCLEROSIS

uncommon in animals

117
Q

arterial mineralization is caused by

A

vitamin D toxicosis, Johne’s disease, others

118
Q

atherosclerosis in animals is caused by

A

high cholesterol diet

dogs- hypothyroidism and DM

leads to narrowing of the arterial lumen→ ischemia and infarcts

119
Q

gross findings of atherosclerosis

A

fibrofatty + mineralized plaques in vessel walls → thick rigid vessels with narrow lumens

120
Q

Localized vascular dilation due to thinning or weakening of the vessel wall

A

aneurysm

121
Q

what are some causes of aneurysm

A

Copper deficiency

Strongylus vulgaris migration- horse parasite to mesenteric artery

idiopathic

122
Q

tumor of Blood vessel origin that is cancerous vs benign

A

HEMANGIOMA- benign

HEMANGIOSARCOMA

123
Q

Aortic/carotid body tumor are called

A

CHEMODECTOMA

124
Q
A

hemangioma- benign neoplasm of vascular endothelial cells

well differentiated- blood filled spaces

125
Q
A

hemangiosarcoma- malignant neoplasm of vascular endothelial cells

right auricle of dogs- blood filled mass

126
Q

what happens if hemangiosarcoma in dogs burst

A

usually on right auricle of heart

will bleed into pericardial sac- cause cardiac tamponade

127
Q

common primary sites of hemangiosarcoma in dogs

A

Right atrium auricle
* Liver
* Spleen
* Skin/subcutis
* Fat around urinary bladder

128
Q

lymphangisarcoma in cats are usually found —

A

ventral abdomen

oozy- bruisy appearance

Infiltrative endothelial neoplasm affecting ventral abdominal dermis/subcutis in cats

129
Q

dog limb

A

canine perivascular wall tumor

hemangiopericytoma

Infiltrative mesenchymal neoplasm; may recur locally but seldom metastasize

130
Q
A

aortic body tumor (chemodectoma)

Originates from aortic body (chemoreceptor that detects changes in blood O2, CO2, pH, etc.)

131
Q

chemodectoma are found in — type of dogs

A

brachycephalic - boxer

aortic body tumor- found on heart base

may compress great vessels/ atria

132
Q
A

cardiac lymphosarcoma

tan masses- can be seen everywhere

133
Q

common sites of cardiac lymphosarcoma (LSA)

A

right atrium,
abomasum, uterus, spinal
canal, retrobulbar region,
kidney, lymph nodes

134
Q

bovine leukemia virus is associated with what cancer

A

cardiac lymphosarcoma (LSA)

135
Q

Restrictive cardiomyopathy exists is several forms. One common form is left ventricular endocardial fibrosis (LVEF) in cats. The endocardial fibrosis along the outflow tract of the left ventricle makes the ventricle more rigid, “restricting” its ability to dilate and fill with blood.

What is believed to be the preceding lesion of LVEF in cats?

A

endomyocarditis

136
Q

What is the term for enlargement of the heart?

A

cardiomegaly

137
Q

What cell adaptation is usually responsible for increased heart weight?

A

Myocardial hypertrophy

138
Q

what can cause this

A

HCM and thyrotoxic cardiomegaly

139
Q

heart

A

Dilated cardiomyopathy (DCM)

140
Q

What gross abnormalities do you see, and what microscopic changes would you expect to find?

A

The margins of the mitral valve leaflets are thickened, nodular, and opaque with a glistening surface. These features are consistent with endocardiosis, an idiopathic age-related degenerative valvular lesion of dogs characterized by proliferation of loose fibroblastic tissue with a wispy blue-gray mucopolysaccharide matrix.

141
Q

What gross abnormalities do you see, and what microscopic changes would you expect to find?

A

vegetative valvular endocarditis

There are crumbly (friable) red-tan masses attached to the mitral and aortic valve leaflets, consistent with vegetative valvular endocarditis. Microscopically, these masses are septic thrombi consisting of fibrin (F), bacteria (B), and neutrophils (N).

142
Q

Of the two dog hearts, endocarditis or endocardiosis, which would be more likely to have secondary infarcts in other organs and why?

A

endocarditis

The dog in question #2 would be most likely to have infarcts in other organs because the valvular thrombi could fragment, sending thromboemboli into the systemic circulation. These septic thromboemboli can carry bacteria to other organs and potentially block blood flow to those organs, leading to infarcts.

If the lesion were on the right side (tricuspid or pulmonic valve) instead of the left, thromboemboli could enter the pulmonary circulation leading to embolic pneumonia and/or infarcts (though pulmonary infarcts are relatively uncommon).

143
Q

heart

What abnormalities do you see on the atrial endocardium, and what are some possible underlying causes for these findings?

A

endocardial mineralization

There are multifocal raised wrinkled gritty white plaques on the endocardial surface, consistent with endocardial mineralization. A nodular red-tan thrombus adheres to the endocardium next to one of the mineralized plaques (right side of image). Endocardial injury due to necrosis/mineralization or subsequent inflammation likely predisposed to thrombosis at this site.

Endocardial mineralization in dogs can occur due to a variety of causes, including renal failure (uremia) and vitamin D toxicosis (e.g., due to oversupplementation of vitamin D or ingestion of cholecalciferol-based rodenticides). Causes in other species include ingestion of plants containing vitamin D analogs (more common in herbivores) and Johne’s disease in cattle.

144
Q

If the right atrial mass, metastatic hemangiosarcoma, would have ruptured, what clinical impact might it have had on this dog?

A

hemopericardium and cardiac tamponade

145
Q

Inflammation of a vein

A

PHLEBITIS

146
Q

what kind of damage in heart

A

proliferative endarteritis
inflammation of the arterial wall

147
Q

A classic example of PHLEBITIS is —, a mutated form of the feline enteric coronavirus

A

feline infectious peritonitis (FIP)

inflammation of the membrane lining the abdominal wall and covering the abdominal organs.

148
Q

what form of FIP

A

feline infectious peritonitis (FIP)

Effusive (wet) form - characterized by thick stringy yellow cavitary effusions, like this fibrinous effusion in the peritoneal cavity (due to leakage of fluid and protein from injured veins)

149
Q

what form of feline infectious peritonitis (FIP)

A

Non-effusive (dry) form - characterized by perivascular gray-white plaques of pyogranulomatous inflammation (a mixture of neutrophils, epithelioid macrophages, lymphocytes, and plasma cells), like these plaques centered on veins along the surface of a kidney:

150
Q

heart worm will cause what type of right ventricular hypertrophy: concentric or eccentric, and how would this change appear grossly?

A

Pressure overload would lead to concentric hypertrophy of the right ventricle. The ventricular wall would be thickened due to addition of sarcomeres in parallel, and the ventricular chamber would be reduced in size.

151
Q

What is the term for inflammation of the pleural cavity?

A

Pleuritis

22 fall: path (46 decks)

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