Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
175 Cards in this Set
- Front
- Back
How much resistance do up inflated lungs have
|
High
|
|
When does pulmonary resistance drop?
|
Inflation of lungs
|
|
Why does DA contacrt?
|
Po2 and bradykinin from lungs
|
|
What does da convert to
|
Liga,entry, arteriosum
|
|
When breed is it heritable?
|
Poodles
|
|
PDA runs from what to what
|
Between Pulmonary art to aorta
|
|
What direction is shunt in PDA
|
Left to right? Aorta to pul
|
|
What affect does this have on la
|
Volume overload? Compensatory dilation
|
|
What does PDA have on lv
|
Bol overload. Dilation and hypertrophy. Eccentric
|
|
Describe eccentric hypertrophy
|
Thin walls, large chamber
|
|
What happens to right ventricle due to increased Pull pressure
|
Concentric hypertrophy
|
|
When can PDA shunt reverse.
|
If Paul pressure increases
|
|
Signs of shunt reversal in PDA
|
Cyanosis and death. Deoxy to systemic
|
|
What does the turbulent flow at the da predispose to?
|
Thrombosis
|
|
Atrial septal defects are failure to close of what structure
|
Foramen ovale
|
|
Atrial septal defect blood flow is
|
Left to right. High to low pressure
|
|
In asd where do you get vol overload
|
Right a and v
Plus in left atrium due to increase blood coming from pulmonary circuit |
|
Where do you get dilation
|
Ra
|
|
Where do you get eccentric
|
Rv
|
|
Direction of shunt in ventricular defect
|
L to r
|
|
In atrial septal defect where do you get volume overload and compensatory dilation?
|
Both atria
|
|
What is defective in ventricular defects?
|
Interventricular septum defect
|
|
What direction to VSDs normally flow?
|
Left to right
|
|
What chamber do you no get change?
|
Right atria
|
|
As before, how do you get shunt reversal?
|
Pulmonary hypertension
|
|
What else are AVSDs called?
|
endocardial cushion defects
|
|
What do the endocardial cushions help form?
|
Septa and AV valves
|
|
What do AVSDs do?
|
Mixing of blood
High oressure on pulmonary art |
|
What diseases does the failure of valves development include
|
Stenosis
dysplasia |
|
What species is typically affected by Pulmonic stenosis?
|
Dogs
|
|
What are the three forms of pulmonic stenosis?
|
valvular
sub-valvular supra-valvular |
|
What is the most common form of pulmonic stenosis
|
Valvular
|
|
What is the cause of pulmonic valvular stenosis?
|
Disordered fusion and hollowing of valve cushions
|
|
What does this disordered fusion and hollowing lead to?
|
leaflet thickening
fusion hypoplasia excess tissue |
|
What is the cuase of subvalvular stenosis?
|
Ring of connective tissue encircling right outflow tract
|
|
Supravalvular stenosis is
|
narrowing of pulmonic artery
|
|
What happens to pulmonary trunk in valvular stenosis
|
Dilation
|
|
What happens to ventricles
|
Concentric hypertrophy
|
|
What type of dogs ar normally affected by aortic/subaortic stenosis?
|
Large
|
|
Give examples of features of AV valve dysplasias
|
absence of leaflets
Leaflet thickening fusion leaflets short/long tendinae atrophic/hypert papillary muscles |
|
What side is mitral valve?
|
Left
|
|
When does blood flow from atria to ventricles?
|
diastole
|
|
AV valve stenosis will result in
|
Increased atrial pressure
increased atrial blood vol (reduced ventricular filling) |
|
What affect will this have on atria?
|
hypertrophy and dilation
|
|
What can atrial dilation predisposed by?
|
atrial fibrillation
|
|
Blood stasis can predispose to?
|
Thombus
|
|
AV valve insuficiency allows:
|
chronic regurgitation into atria
|
|
When will it regurgitate>
|
systole
|
|
What will happen to atria?
|
Dilation. mild hypertrophy
|
|
What happens to ventricles in insuficiency?
|
eccentric
|
|
Where are valvular hematomas likely to form?
|
AV valves
|
|
What malpositions/anomalies do i need to know?
|
Vascular rings
transpotions common arterial trunks |
|
What structures can vascular rings entrap?
|
oeso and or trachea
|
|
What is most common?
|
PRA
|
|
what is path of common arterial trunk?
|
failure of septum
aorta and pul trunk common |
|
What other conditions affect the cat?
|
endocardial fibroelastosis
|
|
Describe endocardial fibroelastosis
|
Progressive proliferation of fibrous and elastic tissues
|
|
What breeds are predisposed?
|
Burmese and siamese
|
|
What side are moderators bands normally found in in the cat?
|
Right ventricle
|
|
bands in the left will...
|
Impaiur filling and dilation
|
|
PERICARDIAL DISEASE
|
PERICARDIAL DISEASE
|
|
Three types of inflam for percardial disease?
|
Fibrinous
Supporative Constrictive |
|
Usual route for fibrinous?
|
Haematogenous
|
|
What does pneumonia and Pleuritis have to do with it?
|
Possibly an extension of
|
|
If it is grey white what kind of cells are present?
|
Leukocytes
|
|
What type of inflammation is bread and butter pericarditis?
|
Fibrinous
|
|
What is themost common cause of supporative pericarditis?
|
Wire disease! Often fibrinopurulent
|
|
What is constrictive pericarditis?
|
Formation of adhesions and granulation tissue
|
|
What are the main problems with constrictive pericarditis?
|
Impaired expansion
Impaired filling |
|
List the key types of pericardial effusion
|
Hydropericardium
Haemopericardium Heamorraghic |
|
Give 3 causes for Generalised oedema
|
Heart failure
Hypoproteinemia Systemic vascular injury |
|
What type of fluid is found in a hydropericardium
|
Serous transudate
|
|
What is found in a haemopericardium
|
Pure blood
|
|
Give some causes of haemopericardium
|
Aortic, atril rupture
Heamoar from tumour Clotting defects Trauma |
|
In cardiac tamponade how quickly must the fluid fill?
|
Very, heart cannot adapt
|
|
What happens to the heart
|
Restriction and compression
|
|
What does that compression do
|
Inhibitis venous return
|
|
Inhibited veous return means...
|
Reduced cardiac filling therefor reduced output
Cardiogenic shock |
|
What diseas can cause epicardial haemorrage
|
Mulberry
|
|
EndocardIal disease
|
Endocsrdial disease
|
|
Two types of endocarditis
|
Mural and valvular endocarditis
|
|
Which most significant?
|
Valvular
|
|
What side valves are most commonly affected?
|
Left?
Right in cattle |
|
Where do lesions develop?
|
Free margin
|
|
Give some examples of bacteria
|
Staphs
Streps A pyogen |
|
What permits bacterial invasion of valve leaflets?
|
Bacteremia and Endothelial disruption, erosion
|
|
What happens after erosion or ulceration?
|
Inflam and thombus
|
|
What builds up after thobmus
|
Subsequent layers of fibrin deposition. Build up of colonies.
|
|
What happens to thebase layer?
|
Organised with granulation tissue, neutrophils present
|
|
What can predispose to endocarditis?
|
Turbulent blood flow eg subaortic stenosis
|
|
Give 2 pathological conseq of endicarditis
|
Valvular stenosis
Septic emboli can break off |
|
What organ could be associated with endocardiosis?
|
Renal faulure???
|
|
Give 2 examples of degenative disease
|
Endocardiosis
|
|
Another name of endocardiosis
|
Myxomatous valvular degeneration
|
|
What is the most common heart condition of thdog
|
Endocardiosis
|
|
What breed is most predisposed?
|
Cavvies!
|
|
Describe endocardiosis
|
Slowly progressive! Degen.
Unknown aetiology |
|
What valve are normally affected?
|
Av
|
|
Wich valve is normally affected?
|
Left av.(mitral)
One third right trIcuspod |
|
What happens to valve leaflets?
|
Thickened! Irregular smooth nodules
|
|
What are nodules composed of?
|
Fibroblast proliferation deposits poorly staining mucoploysacharide
|
|
What can endocardiosis lead to?
|
Weakening and rupture of tendinae
|
|
Functional consequences
|
Distorted valves lead to regurg or insufiency
Jet lesions |
|
Jet lesions can cause
|
Trauma to endocardium, Leading to foci for Endocardial fibrosis
|
|
Causes of endocardial mineralisation
|
Jet lesions
Vit d tox Healing endocarditis lesions Chronic disease |
|
What disease can cause endocardial mineralisation in cattle?w
|
Asting suchas johnes
Cardiopmyopthy in cats |
|
Myocardial disease
|
Myocardial disease
|
|
When does primary hypertrophy occur?
|
Idiopathic
|
|
When does secondary hypertrophy occur?
|
Adpative response to abnormal increase in Functional demand or trophic stim.
Valvukar defetcs Hyperthyroid |
|
Concentric
|
Small chamber
Tickened walls Response to pressure |
|
Eccentric
|
Large chamber
Tin walls Response to volume |
|
Problems with myocardial hypertrophy
|
Loss compliance
Myocardial blood supply cannot meet demands Interstitial fibrosis Myocardiocyte death |
|
2 issues with feduced compliance
|
Reduced contractiliy? Rduced force
Impaired relaxation. Reduced filling |
|
Outline the process of heart failure
|
Primary or secondary disease
Maladaptive chnages Reduced myocardial function Heartfsilure |
|
When will youseemyocardial atrophy?
|
Wasting diseases, cachexia, starvation
Following injury |
|
List 3 degenerative changes in the myocardium
|
Fatty infiltration
Hydropic change Fatty change |
|
What is lipofuscinosis
|
Old age
Myocard atrophy Dark brown bronzed appearance |
|
What is appearance of myocardial necrosis
|
Pallar at 12-24h
Then mineralised Necrotic replaced by scar |
|
What regions are most prone to ischaemic injury
|
Pappilary muscles
|
|
What is white muscle diseass
|
Selenium vit e defic
|
|
What colour is cytoplasm in necrotic myocardiocytes
|
Pale eosinophillic
|
|
What is basophillic stipling?
|
Minralisation
|
|
How long after injury will you see repair?
|
7-10d
|
|
What will happen first?
|
Proliferation of fibroblasts and new blood vessels
|
|
What type of tissue is deposited?
|
Collagenous
|
|
How can you get supporative myocarditisa.
|
Septicemia
Septic emboli Evalvular endocarditis |
|
When will you see eosinophillic
|
Parasitic. Eg cysticercus ovis
|
|
When might you see lymphocytic inFlammatory response?
|
Viral, eg parvo
|
|
When will ou see a haemorrhagic Inflam
|
Clostridium chauvieii? Blackleg
|
|
What might toxoplasma cause?
|
Myocardial necrosis
|
|
What might cause myocardial necrosis?
|
Huge list
Inflam Nutrional Toxic Ischemia Cns injury Gastric |
|
When might you see pyogranulomatous myocarditis?
|
Fip
|
|
Why does fip cause pyogranulomatous myocarditis?
|
Vasculitis
|
|
Cardiomyopathy
|
Cardiomyopathy
|
|
Primary cardimyopathy is
|
Idiopathic
|
|
What are the 3 main morpholical types of cardiomyopathy?
|
Hypertrophic
Dilated Restricted |
|
What cat breed is predisposed to primary hypertrophic myocardiopathy
|
Maine coon
|
|
What will hcm cause in ventricles
|
Reduced compliance
Inabili to fill in diastole |
|
What is key appearance of hcm histologicslly
|
Haphazard arrangement and hypertrophy
Areas of interstitial fibrosis |
|
What does hcm and dcm predispose to?
|
Thombosis
|
|
Roughtly describe the look of dcm
|
Globular heart
|
|
What side normslly more greatly enlarged?
|
Left
|
|
What might happen to Av valves?
|
Insufiency
|
|
What is the result of dcm
|
Pump failure due to weak contraction.
Arrythmias. Sudden death |
|
Not covering restrictive
|
Not coverting restrictive
|
|
What causes myocardial infarction
|
Throm oembolism in coronary arteries
|
|
What can predispose to heart attack?
|
Diseases of coronary arts such as atherosclerosis and arterisclerosis
|
|
Name common heart tumours
|
Hemangiosarcoma
Lymphoma Chemodectoma Tmour of ectopic thyroid tissue Shwannoma Neurofibroma |
|
Common breed for hemangiosarc
|
Gsd
|
|
Common site for hsa
|
Right atrium
|
|
What shape is hemangiosarc
|
Spindle shaped ! Pleomorphic? Boood filled channels
|
|
Another name for chemodectoma?
|
Aortic body chemo receptor tumour
|
|
Wherer are chemodectomas situated?
|
Base, junction between pul art and aorta
|
|
What are peripheral nerve sheath tumours?
|
Tumours of cardiac nerves.Creamy yellow mass.
Usually incidental Growth alomgside coronary |
|
What is heart failure?
|
Cannot maintain cardiac output to maintain body demands
|
|
Types
|
Acute ir chronic
|
|
Key causes of acute
|
Massive infarction due to thromboembolism
Severe arythmia |
|
Key outcomes of acute
|
Rapid drop in output.
Syncope Compensatory mechanisms |
|
3types of chronic hf
|
Pump failure.
Obstruction to flow Regurg |
|
In pump failure, what type of dysfunction reults in Weak contractions
|
Systolic
|
|
Causes of systolic dysfunction and so weak contractions
|
Infraction
Dcm Conduction dx |
|
Reduced compliance is a ...dysfunction
|
Diastolic dysfunction
|
|
Causes include
|
Hypertrophic or Restrictive Cardiomyopathy
Fribrosis Cardiac tamponade |
|
What can cause obstruction to flow reulting in heart failure?
|
Hypertension, pul or systemic
Stenosis |
|
Regurgitant flow causes
|
Volume overload
|
|
Causes of Regurgitant flow
|
Valvular endocardiosis
Valvular endocarditis Septal defects Pda |
|
What is congestive heart failure?
|
Inability of heart to maintain adequate output and deal with venous return
|
|
What happens to effective circulatory volume in congestive failure?
|
Drops
|
|
Drop in effective volume results in
|
Activation of physiological to increase Vol. despite Total volume being adequate
|
|
Increasing volume will
|
Increase venous return.
Increase co Increase tissue perfusion |
|
Howevere increasing volume will
|
Increase venous pressure, decrease osmotic pressure and cause oedema
|
|
Two ways to characterise conjestive failure
|
Pulmonary and or systemic
|
|
How fast will conjestive heart failure develop?
|
Slow. Common final pathway
|
|
Briefly describe forward failure
|
Reduced Forward cardiac output
|
|
Briefly describe backward failure
|
Damming of blood, causing conjestion and increased pressure
|