Cardiovascular Pathology Flashcards

1
Q

How does systemic disease cause CHF?

A

Whatever the dz, it increases cardiac workload of an otherwise normal heart –> congestion and edema

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2
Q

Describe starling forces and lymphatic system changes relative to edema

A
  • increased capillary hydrostatic pressure
  • increased vascular permability
  • decreased interstitial oncotic pressure
  • decreased lymphatic drainage
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3
Q

Two sequela of left heart failure vs right heart failure

A

LEFT
1. Pumonary congestion
2. Pulmonary edema

RIGHT
1. Hepatic congestion
2. Ascites

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4
Q

Nutmeg Liver

A

chronic, passive congestion of the liver due to RIGHT-sided heart failure

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5
Q

How can you tell which sided heart failure this is?

A

LEFTsided heart failure: diffuse pulmonary edema and congestion:
- The lung is NOT collapsed
- Thickened interlobular septa

pulmonary edema causes thickened interlobular septa b/c of increased pulmonary interstitial edema

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6
Q

What are the 3 most common cardiac anomalies of dogs?

A
  • PDA
  • PS
  • SAS
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7
Q

What are the 2 most common cardiac anomalies of cats?

A
  • VSD
  • Mitral valve dysplasia (malformation)
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8
Q

Congenital Heart Diseases

What are the 5 non-closure anomalies?

A
  1. PDA
  2. ASD
  3. VSD
  4. Patent foramen ovale
  5. Tetralogy of fallot
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9
Q

ID + sequela

A

VSD
- left-sided heart failure (LV to RV/directly into pulmonary trunk –> pulmonary edema)

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10
Q

ID + sequela

A

ASD
- LA -> RA -> vena cava -> right-sided heart failure (ascites)

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11
Q

Tetraology of Fallot: 4 components and the sequela

A

1. VSD
2. Overriding Aorta (blood exits into aorta from both RV and LV due to right displacement)
3. Pulmonic stenosis
4. Right ventricular hypertrophy

Sequela = Cyanosis

overriding aorta
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12
Q

What caused RV hypertrophy

A

Pulmonic stenosis

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13
Q

What 2 species are most likely to get SAS

A

Dogs and swine

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14
Q

Name/cause of this lesion

A

Jet lesions of SAS (caused by turbulent flow hitting the aortic wall)

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15
Q

What species get congenital valvular hematoma/hematocyst?

A

Calves; no functional consequences

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16
Q

ID + pathogenesis

A

NORMAL development of 4th aortic arch: Right branch becomes Rsubclavian a., Left branch becomes aortic arch

Vascular Ring Anomaly: Persistent Right 4th Aortic Arch
- German Shepherds
- Right branch fails to regress into Rsubclav.a.
–> entraps esophagus/trachea –> megaesophagus

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17
Q

What do white lesions in the myocardium indicate?

A

necrosis/mineralization; inflammation, neoplasia

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18
Q

A primary cause of myocardial hypertropy is __?__ cardiomyopathy and is irreversible.

A secondary cause of myocardial hypertrophy is a(n) __?__ response to a(n) __?__ in workload and is reversible.

A

A primary cause of myocardial hypertropy is hypertrophic cardiomyopathy and is irreversible.

A secondary cause of myocardial hypertrophy is a(n) compensatory response to a(n) increase in workload and is reversible.

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19
Q

Concentric hypertrophy: __?__ walls, normal or smaller lumen

Eccentric hypertrophy: __?__ walls, enlarged lumen

A

Concentric hypertrophy: Thick walls, normal or smaller lumen

Eccentric hypertrophy: Normal walls, enlarged lumen

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20
Q

ID + pathogenesis

A

Hypertrophic Cardiomyopathy – cats
- thickened LV walls (fails to relax) –> decr. diastole into LV (less volume capacity) –> incr. backflow into LA –> 2º LA dilation –> left-sided congestion

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21
Q

ID + pathogenesis

A

Restrictive Cardiomyopathy – cats

  • impaired diastole b/c of diffuse myocardial fibrosis or excessive moderator bands –> stiff myocardium but NORMAL ventricular wall thickness –> can lead to 2º, atrial enlargement (bilateral)
22
Q

ID + pathogenesis

A

Dilated Cardiomyopathy – dogs
- 1º systolic dysfunction that leads to 2º dilation

23
Q

Dystrophic myocardial mineralization

A

damage to tissue that causes mineralization, 2º to myocardial necrosis

vs. metastatic which = is multi-focal and 2º to incr. Ca and P levels

24
Q

What species are prone to VitE/selenium deficiency and what is the sequela

A

Herbivores – myocardial mineralization (VitE deficiency = lack of free-radical scavengers –> necrosis)

25
Q

Brain-heart syndrome

A

a type of myocardial necrosis in dogs with brain or SC injury: injury causes catecholamine release increases BP too high, –> overworked heart –> myocardial necrosis

26
Q

What vales are most commonly affect in SA vs LA in vegetative valvular endocarditis?

A

SA: AV valves
LA: semi-lunar valves

hematogenous infection

Blackleg, parvo, etc.

27
Q

Most common neoplasia in dogs vs cattle vs brachycephalic dogs

A

All dogs: hemangiosarcoma (cancer of blood vessels)
Cattle: lymphoma
Brachycephalic dogs: Chemodectoma (aortic body tumor)

28
Q

Common sites of hemangiosarcoma

A

Right auricle, spleen, skin

29
Q

Common sites of lymphoma in cattle (BLV)

A

Heart, LNs, Abomasum Spine, Uterus

30
Q

What virus causes lymphoma in cattle and cats?

A

Leukemia
Cattle: Bovine Leukemia Virus
Cats: Feline Leukemia Virus

31
Q

Where do chemodectomas form?

A

On or around the base of the heart (never in the heart muscle itself) - typicaly near aortic arch or carotid aa.

32
Q

4 types of disease of the pericardium

A
  1. Hydropericardium
  2. Hemopericardium
  3. Fibrinous pericarditis
  4. Suppurative pericarditis (hardware dz)
33
Q

Hydropericardium

A

accumulation of transudate in pericardium by edematous diseases (right-sided HF) –> can lead to cardiac tamponade

34
Q

Cardiac tamponade

A

When fluid in pericardial sac leads to a pressure greater than in the ventricle and therefore compressess the heart –> fatal decr. in CO

35
Q

What causes hemopericadium in dogs vs. horses? Consequence?

A

Dogs: ruptured RA (hemangiosarcoma)
Horses: ruptured aorta

Consequence = cardiac tamponade

36
Q

What causes an increase in epicardial fat?

A

cachexia, anorexia, starvation — chronic negative energy balance

37
Q

3 main causes of fibrinous pericarditis in pigs?

Fibrinous = insoluble mesh network (acute inflammation)

Fibrous = collagenous * sturdy (chronic inflammation

A

hematogenous spread to the heart –> sepsis

  1. Haemophilus parasuis (Glasser’s disease)
  2. Streptococcus suis
  3. Mycoplasma hyorhinus
38
Q

ID

A

Traumatic Reticuloperitonitis // suppurative pericarditis (hardware dz)

SEVERE: thick mat of suppurative exudate
39
Q

Differences in valvular appearance b/w endocardiosis//MMVD and endocarditis

A

Endocardiosis//MMVD = nodular, smooth, glistening

Endocarditis = fibrin! rough, dull granular

Left: Endocardiosis Right: Endocarditis
40
Q

Two factors needed for endocarditis

A
  • bacteremia
  • turbulent blood flow
41
Q

Endocardial fibrosis - type of lesion/name

A

Diffuse lesion of congenital fibroelastosis: fibrin + elaston –> “stretchy”

Recall: fibrosis = collagen / connective tissue

42
Q

Metastatic mineralization

A

multi-focal and is 2º to increased calcium and phosphorus levels

VitD toxicosis, renal failure, Johne’s disease

43
Q

3 factors of thrombosis (Virchow’s Triad)

A

hypercoag: glomerular dz (loss of antithrombin III), cushing’s
abnormal BF: cardiomyopathy
endothelial injury: arteritis/vasculitis

44
Q

How do Dirofilaria immitis cause arteritis and pulmonary hypertension?

A

migration thru pulmonary artery, RA and RV –> endothelial damage to arteries

45
Q

Strongylus vulgaris causes arteritis where in horses? Sequela?

A

cranial mesenteric artery –> leads to ischemic necrosis and colic

46
Q

Arteriosclerosis

often interchanged with Atherosclerosis

A

“hardening of the arteries”

47
Q

What causes atherosclerosis

A

Accumulation of lipid, mø, and fibrous tissue in artery wall

48
Q

ID

A

Aneurysm: local dilaition of a weakened artery caused by copper deficiency or parasites

49
Q

Portosystemic shunt

A

when blood bypasses the liver and goes straight into caudal vena cava (aka does not get detoxified!)

Example of consequence: Due to bypassing the liver, ammonia from GIT does not get transformed into urea (which gets excreted via kidneys) causing–> *hyperammonemia**

50
Q

Lymphangiectasis: definition + causes

A

dilation of lymp vessels
- congenital anomaly
- obstruction of lymph drainage

51
Q

ID + pathogenesis + sequela

A

Chylothorax = accumulation of lymphatic liquid in thorax due to a leakage or rupture of the thoracic duct.

Sequela = pulmonary atelectasis (no more negative pressure in thx –> lungs collapse)